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Anemia: Introduction
Anemia is a condition characterized by insufficient circulating hemoglobin (Hgb). It results from excessive red blood
cell (RBC) destruction, RBC loss, or decreased RBC production. Anemias can be regenerative or nonregenerative (Table:
Classification of Anemias). Regenerative anemias show evidence of response by the bone marrow to increase the number of
circulating RBC. This response is measured by the quantity of reticulocytes (immature RBC) present in the circulation.
Regenerative anemias have a high reticulocyte count and are due to RBC loss or destruction. In a nonregenerative anemia,
the bone marrow responds poorly and the reticulocyte count is low. Anemias can also be acute or chronic. Most commonly,
acute anemias are due to either RBC loss or destruction. Chronic anemias are usually due to lack of RBC production,
although slow blood loss can also be a cause.
RBC indices are used to further characterize and classify anemias. The mean corpuscular volume (MCV) is an
indication of RBC size. The MCV (femtoliters) = (PCV × 10) ÷ RBC (millions). As RBC precursors mature in the bone
marrow, their volume decreases as the Hgb content increases. Therefore, reticulocytes have a higher MCV, and the MCV is
increased in regenerative anemias. An anemia with a high MCV is classified as a macrocytic anemia. RBC size is
smaller than normal when iron is insufficient, which results in decreased quantities of Hgb and a decreased MCV. An
anemia with a low MCV is classified as a microcytic anemia. A low MCV in an anemic adult animal indicates iron
deficiency from a slow loss of blood (usually GI or renal). A low MCV is seen in the Akita and Shiba Inu, which normally
have small RBC. A low MCV may be seen in some cases of congenital hepatic shunts. The mean corpuscular hemoglobin
concentration (MCHC) indicates the concentration of hemoglobin per unit volume of RBC. The MCHC (g/dL) = (Hgb ×
100) ÷ PCV. It provides similar information as the mean corpuscular hemoglobin (MCH) but is considered to be more
accurate. The MCH (picograms) = (Hgb × 10) ÷ RBC (millions). A low MCHC accompanying macrocytosis is indicative of
a regenerative anemia.
Laboratory diagnosis of anemia is based on the Hgb concentration, the number of RBC, and the hematocrit or packed
cell volume (PCV). The next essential test is the reticulocyte count. Reticulocytes are polychromatic cells when stained with
Wright's stain or a Giemsa-type stain. The vital stain new methylene blue specifically stains reticulocytes. Reticulocytosis is
first seen 72 hr after the onset of significant blood loss or hemolysis. Peak reticulocyte response occurs within 5-7 days.
The reticulocyte index = animal's PCV × % reticulocytes ÷ normal PCV. A value >1 indicates an appropriate response.
Extracorpuscular Abnormalities
Anaplasmosis
Anaplasmosis, formerly known as gall sickness, is a disease of ruminants caused by obligate intraerythrocytic parasites
of the order Rickettsiales, family Anaplasmataceae, genus Anaplasma .
Anaplasmosis occurs in tropical and subtropical regions worldwide
Transmission and Epidemiology:
Anaplasmosis is not contagious. Most transmission occurs via numerous species of tick vectors.
There is a strong correlation between age of cattle and severity of disease. Calves are much more resistant to disease
(though not infection) than older cattle. This resistance is not due to colostral antibody from immune dams. After recovery
from the acute phase of infection, cattle remain chronically infected carriers of the parasite and immune to further clinical
disease. However, these chronically infected cattle may relapse to anaplasmosis when immunosuppressed (eg, by
corticosteroids), when infected with other parasites, or after splenectomy. Carriers serve as a reservoir for further
transmission.
Clinical Findings:
Anaplasmosis is characterized by progressive anemia due to extravascular destruction of infected and uninfected
erythrocytes. Macrocytic anemia with circulating reticulocytes may be present late in the disease. There is moderate
anisocytosis, slight polychromasia, and an increase in unconjugated bilirubin in the serum.
Disseminated intravascular coagulation (DIC) is a syndrome characterized by massive activation and consumption
of coagulation proteins, fibrinolytic proteins, and platelets. It is not a primary disease, but a disorder secondary to
numerous triggering events such as bacterial, viral, rickettsial, protozoal, or parasitic diseases; heat stroke; burns;
neoplasia; or severe trauma. In acute, fulminant DIC, the clinical presentation is uncontrolled hemorrhaging and the
inability to form a normal clot. Classically, all coagulation screening tests (ACT, APTT, PT, thrombin time) are
prolonged, fibrin (or fibrinogen) degradation products are increased, and fibrinogen and platelet concentrations are
decreased. Death is caused by extensive microthrombosis or circulatory failure, leading to single or multiple organ
failure. DIC can usually be identified by the presence of at least three abnormal coagulation test results. Horses, even in
Congenital Thrombocytopenia
Fetal and neonatal alloimmune thrombocytopenia occurs when maternal antibodies are produced against a paternal
antigen on fetal platelets.
1) the end-diastolic volume or preload, which is the volume of blood within the ventricles just before they begin to
contract,
2) myocardial contractility or the inotropic state, which is the rate of cycling of the microscopic contractile units of the
myocardium, and
3) the afterload, which is the interference to ejection of blood from the ventricle into and through the arterial tree. The
afterload is measured as the peak tension the myocardium must generate to eject blood.
The preload is the difference in end-diastolic pressure between the ventricle and the pleural space, divided by the
stiffness of the ventricular myocardium. The preload is regulated predominantly by low-pressure volume receptors in the
heart and large veins. When these receptors are stimulated by an increase in blood volume or by distention of the structures
the receptors occupy, the body responds by making more urine and by dilating the veins—an attempt to decrease blood
volume and lower the pressures in the veins responsible for venous distention.
Myocardial contractility is determined by the rate of liberation of energy from ATP, which is determined, in part, by the
amount of norepinephrine binding to β-1 adrenergic receptors in the myocardium. The afterload is determined by the
relative stiffness of the arteries and by the degree of constriction or dilatation of the arterioles, both of which are determined
by the degree of constriction or relaxation of the arterial and arteriolar vascular smooth muscle. The tone of vascular smooth
muscle depends on many factors, some of which constrict the muscle (eg, α-1, angiotensin II, vasopressin, endothelin) and
some of which relax the muscle (eg, β-2, atriopeptin, bradykinin, adenosine, nitric oxide). Afterload and peak tension are
also determined by the preload and thickness of the ventricular wall just before ejecting. In fact, peak tension is equal to the
preload times the diastolic arterial blood pressure, all divided by the end-diastolic wall thickness of the ventricle.
Oxygen and the Myocardium:
The amount of oxygen delivered to the heart depends on how well the lung functions, how much hemoglobin (Hgb) is
present to carry the oxygen, and how much blood carrying the Hgb flows through the heart muscle via the coronary arteries.
The amount of oxygen consumed by the heart is termed myocardial oxygen consumption. It is determined, principally,
by heart rate, myocardial contractility, and afterload. Myocardial oxygen consumption is higher when each of the
determinants is higher, and lower when each of the determinants is lower. Both heart rate and myocardial contractility are
1) Chronic stretch on myocardial fibers should be minimized because chronic stretch injures and irritates fibers, causes
them to consume excess quantities of oxygen, and leads to their death and replacement by fibrous connective tissue
(remodeling).
2) Edema fluid should be removed because it makes the lung wet, heavy, and stiff, and causes ventilation-perfusion
inequalities and fatigues muscles of ventilation.
3) The circulation should be improved and the amount of regurgitation (most often mitral regurgitation) decreased.
Improved circulation enhances blood flow to important organs, and reducing mitral regurgitation decreases stretch on the
left atrium and pulmonary veins, decreases pulmonary capillary pressure, and decreases edema formation.
4) Heart rate and rhythm should be regulated. A heart beating too slowly fails to eject enough blood. A heart beating
too rapidly does not have time and consumes too much oxygen at a time when there is too little coronary blood flow. A
heart beating too irregularly may deteriorate into ventricular fibrillation and sudden death.
5) Oxygenation of the blood should be improved. Inadequate oxygenation leads to inadequate energy to fuel both
contraction and relaxation of the myocardium. Inadequate oxygenation of the myocardium may also lead to arrhythmia.
6) β1-adrenergic receptors should be “up regulated.” “Down regulation” of β1-adrenergic receptors interferes with the
ability to fight diseases of other organ systems.
7) The likelihood of thromboembolism should be minimized. Cats with hypertrophic cardiomyopathy may shed emboli
from the enlarged left atrium, which may plug up major arterial branches and lead to ischemia and death.
8) Mature heartworms and microfilariae should be killed. Mature heartworms may initiate severe changes in the
pulmonary arteries that ultimately impede blood flow through the lung.
The ultimate goals of therapy for cardiovascular disease are achieved when the animal can be classified as functional
Class I, the respiratory and heart rates are not increased at rest, and there is a respiratory sinus arrhythmia.
Pulmonic Stenosis
Pulmonic stenosis is a common congenital cardiac defect in dogs. It results in obstruction to right ventricular emptying
due, in most cases, to partial fusion and dysplasia of the pulmonic valve cusps.
Pathophysiology:
The right ventricle must generate increased pressure during systole to overcome the stenosis,
which often leads to dramatic right ventricular hypertrophy. As the right ventricle hypertrophies, its compliance
diminishes, which leads to increased right atrial pressures and venous congestion. The jet of blood passing through
the stenosis deforms the wall of the main pulmonary artery and results in a poststenotic dilatation. In severe cases, right-
sided congestive failure is present.
Clinical Findings and Treatment:
Affected animals may have a history of failure to thrive and exercise intolerance. Right-sided congestive heart failure
may be present and is characterized by ascites or peripheral edema. A prominent ejection-type systolic murmur is present
and heard best at the pulmonic valve area. A corresponding precordial thrill is usually present. Jugular distention and
pulsations may also be present. Radiographic abnormalities include right ventricular enlargement, an aneurysmal dilation of
the main pulmonary artery, and diminished pulmonary vasculature. Animals with moderate or severe pulmonic stenosis will
benefit from balloon valvuloplasty or surgical resection. Palliative therapy with diuretics and vasodilators should be
initiated if right-sided congestive heart failure is present.
Tetralogy of Fallot
Tetralogy of Fallot is the most common defect that produces cyanosis. It results from a combination of pulmonic
stenosis, high ventricular septal defect, right ventricular hypertrophy, and varying degrees of dextroposition and overriding
of the aorta. The right ventricular hypertrophy is secondary to the obstruction to right ventricular outflow. The pulmonic
stenosis component may be valvular or infundibular, or both. Canine breeds predisposed to tetralogy of Fallot
include the Keeshond, English Bulldog, miniature Poodle, miniature Schnauzer, and Wirehaired Fox Terrier. A
polygenic trait has been found in the Keeshond. This defect has been recognized in other breeds of dogs and in
cats.
Pathophysiology:
Tricuspid Dysplasia
Congenital malformation of the tricuspid valve complex is seen occasionally in dogs. Breeds predisposed are Labrador
Retrievers and German Shepherd Dogs. Tricuspid dysplasia results in tricuspid insufficiency and systolic regurgitation of
blood into the right atrium .
Pathophysiology:
Malformation of the tricuspid valve results in significant valvular insufficiency. Chronic tricuspid
regurgitation leads to volume overload of the right heart, which results in dilation of the right ventricle and
atrium. Pulmonary blood flow may be decreased and result in fatigue and tachypnea. As the pressure in the right atrium
increases, venous return is impaired, which results in ascites.
Clinical Findings and Treatment:
Clinical signs correlate with the severity of the defect. Affected animals usually display signs of right-sided heart
failure, including jugular distention and pulsation, edema, ascites, tachypnea, and exercise intolerance. Atrial arrhythmias,
especially paroxysmal atrial tachycardia, are common and become serious enough to cause death. Thoracic radiographs
reveal severe right atrial and right ventricular enlargement. The caudal vena cava may be significantly enlarged.
Prognosis for animals with clinical signs is guarded. Periodic abdominocentesis may be needed to control peritoneal
effusions. Diuretics, vasodilators, and digoxin may also be indicated.
The Endocardium
Infective Endocarditis:
Infection of the endocardium typically involves one of the cardiac valves, although mural endocarditis may occur. It is
thought that some sort of endothelial defect must be present for infective endocarditis to develop. When the endothelium is
partially eroded and underlying collagen exposed, platelets adhere and produce a local thrombus. Blood-borne bacteria may
become enmeshed in this thrombic lattice, resulting in a localized infection. This infection, through its own enzymes and
host mediators, causes a progressive destruction of the valve, resulting in valvular insufficiency. In dogs, the aortic valve is
most commonly affected, resulting in aortic insufficiency. The left ventricle cannot tolerate the constant back flow from the
insufficient valve and soon fails. Infective endocarditis of the AV valves (tricuspid and mitral) also occurs but is better
tolerated than aortic endocarditis. In horses, the mitral valve is most commonly affected, while the tricuspid valve is most
frequently involved in cattle. In cats, infective endocarditis is rare, and there are no breed predilections. In dogs, German
Shepherd Dogs and other large-breed dogs are typically affected; there is a significant predilection for males (72%), and the
mean age is 5 yr. Bacteria released from the infected valve enter the circulation and colonize other organs; therefore,
infective endocarditis can produce a wide spectrum of clinical signs that may be neurologic, GI, urologic, orthopedic, or
cardiovascular in nature. A chronic, fluctuating fever is usually present. Shifting leg lameness may occur. Malaise and
weight loss are present in almost all cases. If a right-sided valve is affected (tricuspid, pulmonic), ascites and jugular
pulsations may be present. A murmur is present in most cases, the exact type depending on the valve involved. When there
is aortic endocarditis, a soft diastolic murmur is present, heard best over the left heart base, and arterial pulses are bounding.
Mitral endocarditis results in a murmur similar to that caused by degenerative valve disease, ie, a prominent systolic
murmur heard best over the left cardiac apex.
Bacteria most often isolated from affected small animals include Streptococcus , Staphylococcus , Escherichia coli ,
and Klebsiella . Streptococcus and Actinobacillus equuli are the most common isolates of horses. A complete blood count
often shows a neutrophilic leukocytosis. Radiography demonstrates cardiac chamber enlargement, depending on the
location of the involved valve. If the aortic or mitral valve is affected, there will be left atrial and left ventricular dilatation.
Evidence of left-sided failure may be seen as an increase in the interstitial densities and an alveolar pattern in the lungs. If
the tricuspid or pulmonic valve is affected, right-sided chamber enlargement is expected. Diskospondylitis is a common
sequela of infective endocarditis in dogs and is characterized by irregular, lytic vertebral endplates. Echocardiography is the
ideal test to definitively diagnose infective endocarditis. The affected valve is easily detected. The height of the R waves
may be increased (suggestive of left ventricular enlargement) and the width of the P wave increased (suggestive of left atrial
enlargement).
Therapy must be directed at controlling the CHF, sterilizing the lesion, and stopping spread of infection. The prognosis
is much more favorable when infection is limited to one of the atrioventricular valves. Controlling CHF requires the use of
diuretics (eg, furosemide), vasodilators (eg, enalapril), and digoxin if there is a rapid rate, supraventricular arrhythmias, or
decreased contractility. Initially, parenteral antibiotics are indicated for 1-2 wk, followed by oral antibiotics for 6-8 wk.
Bactericidal antibiotics should be used initially and changed, if needed, based on results of sensitivity studies. The most
common combinations are ampicillin and gentamicin or cephalothin and gentamicin (renal function should be monitored).
Degenerative Valve Disease (Endocardiosis):
This acquired disease is characterized by degeneration and fibrosis of the cardiac valves. As endocardiosis progresses,
the affected valve becomes increasingly insufficient. Insufficiency of the mitral valve allows blood to jet back into the left
atrium during ventricular contraction, which increases the pressure within the left atrium, which decreases venous flow from
the lungs. This results in pulmonary venous congestion and ultimately pulmonary edema. In addition, as the left atrium
dilates, the likelihood that atrial arrhythmias (atrial premature contractions, atrial fibrillation) will occur is high, further
decreasing cardiac output. The constant jetting of blood from the high-pressure left ventricle physically damages the
endocardium of the left atrium and, in chronic cases, may result in left atrial rupture. The decrease in the amount of blood
ejected by the left ventricle (cardiac output) forces several compensatory mechanisms into action. The body responds to
decreases in cardiac output by increasing sympathetic tone and activating angiotensin-converting enzyme (ACE). On a
chronic basis, these compensatory mechanisms become deleterious rather beneficial. Chronic increased sympathetic tone
causes sustained tachycardia, which increases the oxygen demand of the heart and predisposes to arrhythmias. ACE
The Myocardium
The myocardium is affected by a variety of disease processes, including primary muscle disorders (eg, dilated or
hypertrophic cardiomyopathy), degenerative and inflammatory diseases, neoplasia, and infarction. The myocardium is also
sensitive to various toxins, including adriamycin, oleander, and fluoroacetate (1080). Myocarditis occurs in all species and
may be caused by viral, bacterial, parasitic, or protozoal infection. Canine parvovirus, encephalomyocarditis virus, and
equine infectious anemia are viruses with a propensity to cause myocarditis. Myocardial degeneration occurs in lambs,
calves, and foals with white muscle disease and in pigs with mulberry heart disease or hepatosis dietetica. Mineral
deficiencies (eg, iron, selenium, and copper) can also result in myocardial degeneration.
Dilated Cardiomyopathy:
This acquired disease is characterized by the progressive loss of cardiac contractility of unknown cause. Several forms
of secondary dilated cardiomyopathy exist (cause known); for example, it can be due to a taurine deficiency in cats or
induced by adriamycin or parvovirus. As cardiac contractile function is progressively lost, cardiac output decreases.
Increased blood volume and pressure within the chambers causes them to dilate, most dramatically evident in the left atrium
and left ventricle. In response to the decreased contractility and cardiac output, the sympathetic nervous system and the
renin-angiotensin-aldosterone axis are activated. As in degenerative valve disease, these compensatory mechanisms,
although initially beneficial, become deleterious when chronically activated. Constant stimulation of the heart by the
sympathetic nervous system causes ventricular arrhythmias and myocyte death, while constant activation of the renin-
angiotensin-aldosterone axis causes excessive vasoconstriction and retention of sodium and water. In most cases, signs of
left-sided congestive heart failure are seen, although signs of right-sided failure (ascites) can develop.
Dilated cardiomyopathy is common in large-breed dogs and rare in small-breed dogs (English Cocker Spaniel is an
exception). Doberman Pinschers, Great Danes, German Shepherd Dogs, and Labrador Retrievers are particularly at risk.
Pericardial Effusion
When fluid accumulates within the pericardial sac, the pressure within the sac increases and progressively compresses
the chambers of the heart. Because the right-sided chambers have thinner walls than the left-sided chambers, they are
compressed to a greater degree. Compression of the right-sided chambers has two major consequences: venous return is
1) diagnostic evaluations (before therapy) to determine subclinical disease, especially of the liver and kidneys;
2) adulticidal therapy to eliminate mature worms;
3) a rest period of 4-6 wk to allow the dog to recover from the lung injury associated with worm death;
4) microfilaricidal therapy if required;
5) a test for microfilariae to determine success of microfilaricidal therapy;
6) an antigen test to determine success of adulticidal therapy; and
7) preventive medication.
Use of aspirin, aspirin and dipyridamole, serotonin antagonist, short-acting heparin, and high-dose corticosteroids to
decrease the clinical significance of heartworm lesions has been unsuccessful. Because of the pressure overload of
heartworm disease, treatment with digitoxin is usually not recommended. An angiotensin-converting enzyme inhibitor may
be used in severe right ventricle hypertrophy. The interstitial edema associated with acute signs of worm death is not aided
by diuretic therapy.
Adulticidal therapy eliminates the adult heartworms and allows repair of damage where fibrosis has not occurred.
Death of the worms (either spontaneous or induced) in both dogs and cats is associated with severe parenchymal lung
damage, and limitation of exercise is critical after adulticidal therapy. Thiacetarsamide (2.2 mg/kg, four IV doses over 2
days) will kill most male and some female worms but has poor efficacy against immature and young female worms. Dogs
should be rested for 4-6 wk.
Complications of worm death often include impaired pulmonary function and vessel damage, which may initiate
disseminated intravascular coagulation (DIC). Dyspnea after adulticidal therapy is an emergency. Nasal oxygen and an
immediate-acting glucocorticoid at doses used in shock are needed to provide adequate oxygenation and decrease the acute
lung injury. Many dogs will respond within 24 hr. Because of the fragile nature of the capillary beds of the lungs, no
exercise or stress should be allowed during this time.
Ivermectin at 50 µg/kg or milbemycin at the preventive dose is effective within 2-3 wk. Most microfilariae are killed
quickly, and reactions, which usually occur within 1 hr of administration, are associated with high microfilariae counts in
small dogs. Concentration techniques should be used to assess microfilarial status.
Antigen assays 12-16 wk after successful adulticidal therapy should be negative.
Pathophysiology:
The major mechanisms of diarrhea are increased permeability, hypersecretion, and osmosis. Disorders of motility are
often secondary. In healthy animals, water and electrolytes continuously transfer across the intestinal mucosa. Secretions
(from blood to gut) and absorptions (from gut to blood) occur simultaneously. In clinically normal animals, absorption
exceeds secretion, ie, there is net absorption. Inflammation in the intestines can be accompanied by an increase in “pore
size” in the mucosa, permitting increased flow through the membrane (“leak”) down the pressure gradient from blood to the
intestinal lumen. If the amount exuded exceeds the absorptive capacity of the intestines, diarrhea results. The size of the
material that leaks through the mucosa varies, depending on the magnitude of the increase in pore size. Large increases in
pore size permit exudation of plasma protein, resulting in protein-losing enteropathies (eg, lymphangiectasia in dogs,
paratuberculosis in cattle, nematode infections). Greater increases in pore size result in the loss of red blood cells, producing
hemorrhagic diarrhea (eg, hemorrhagic gastroenteritis, parvovirus infection, severe hookworm infection).
Hypersecretion is a net intestinal loss of fluid and electrolytes, which occurs independent of changes in permeability,
absorptive capacity, or exogenously generated osmotic gradients. Enterotoxic colibacillosis is an example of diarrheal
disease due to intestinal hypersecretion; enterotoxigenic Escherichia coli produce enterotoxin that stimulates the crypt
epithelium to secrete fluid beyond the absorptive capacity of the intestines. The villi, along with their digestive and
absorptive capabilities, remain intact. The fluid secreted is isotonic, alkaline, and free of exudates. The intact villi are
beneficial because a fluid (administered PO) that contains glucose, amino acids, and sodium is absorbed, even in the face of
hypersecretion.
Osmotic diarrhea occurs when inadequate absorption results in a collection of solutes in the gut lumen, which cause
water to be retained by their osmotic activity. It occurs in any condition that results in nutrient malabsorption or
maldigestion.
Malabsorption is failure of digestion and absorption due to some defect in the villous digestive and absorptive cells,
which are mature cells that cover the villi. Several epitheliotropic viruses directly infect and destroy the villous absorptive
epithelial cells or their precursors, eg, coronavirus, transmissible gastroenteritis virus of piglets, and rotavirus of calves.
Feline panleukopenia virus and canine parvovirus destroy the crypt epithelium, which results in failure of renewal of villous
absorptive cells and collapse of the villi; regeneration is a longer process after parvoviral infection than after viral infections
of villous tip epithelium (eg, coronavirus, rotavirus). Intestinal malabsorption also may be caused by any defect that impairs
absorptive capacity, such as diffuse inflammatory disorders (eg, lymphocytic-plasmacytic enteritis, eosinophilic enteritis) or
neoplasia (eg, lymphosarcoma).
Other examples of malabsorption include defects of pancreatic secretion that result in maldigestion. Rarely, because of
failure to digest lactose (which, in large amounts, has a hyperosmotic effect), neonatal farm animals or pups may have
diarrhea while they are being fed milk.
Clinical Findings of Gastrointestinal Disease:
Blood and fibrinous casts in the feces indicate a hemorrhagic, fibrinonecrotic enteritis of the small or large intestine, eg,
bovine viral diarrhea, coccidiosis, salmonellosis, or swine dysentery. Black, tarry feces (melena) indicate hemorrhage in the
stomach or upper part of the small intestine. Tenesmus of GI origin usually is associated with inflammatory disease of the
rectum and anus.
Small amounts of soft feces may indicate a partial obstruction of the intestines. Abdominal distention can result from
accumulation of gas, fluid, or ingesta, usually due to hypomotility (functional obstruction, adynamic paralytic ileus) or to a
physical obstruction (eg, foreign body or intussusception). Distention may, of course, result from something as direct as
overeating. A “ping” heard during auscultation and percussion of the abdomen indicates a gas-filled viscus. A sudden onset
of severe abdominal distention in the adult ruminant usually is due to ruminal tympany. Varying degrees of dehydration and
acid-base and electrolyte imbalance, which may lead to shock, occur when large quantities of fluid are lost (eg, in diarrhea
or sequestered in intestinal obstruction) or in gastric or abomasal volvulus.
Abdominal pain is due to stretching or inflammation of the serosal surfaces of abdominal viscera or the peritoneum; it
may be acute or subacute, and its manifestation varies among species. In horses, acute abdominal pain is common (see colic,
Colic In Horses: Introduction). Subacute pain is more common in cattle and is characterized by reluctance to move and by
grunting with each respiration or deep palpation of the abdomen. Abdominal pain in dogs and cats may be acute or subacute
and is characterized by whining, meowing, and abnormal postures (eg, outstretched forelimbs, the sternum on the floor, and
the hindlimbs raised).
Examination of the Gastrointestinal Tract:
Sudan III stain is a sensitive test for steatorrhea in small animals. Cytology of a rectal or colonic mucosal smear stained
with new methylene blue or Wright's stain for fecal leukocytes is useful to detect inflammatory bowel disease.
Principles of Therapy
Campylobacteriosis: Introduction
Campylobacteriosis, caused by Campylobacter jejuni or C coli
Etiology:
Campylobacter is a gram-negative, microaerophilic, slender, curved, motile bacterium with a polar flagellum.
Campylobacter (Vibrio) sp was once associated with swine dysentery, but this is now recognized as being
caused by Treponema hyodysenteriae .
Because of the slow growth and microaerophilic requirements of Campylobacter , standard culture methods
require selective media that incorporate various antibiotics to suppress competing fecal microflora.
Transmission and Epidemiology:
As with most intestinal pathogens, fecal-oral spread and food- or water-borne transmission appear to be the principal
avenues for infection.
Clinical Findings:
The diarrhea appears to be most severe in young animals. Typical signs in dogs include mucus-laden, watery, and/or
bile-streaked diarrhea (with or without blood) that lasts 3-7 days; reduced appetite; and occasional vomiting. Fever and
leukocytosis may also be present. In certain cases, intermittent diarrhea may persist >2 wk; in some, it may be present for
months.
Lesions:
Congested and edematous colons were found in dogs 43 hr after inoculation; microscopically, there was reduction in
epithelial height, loss of brush border, and reduced numbers of goblet cells in the colon and cecum. Hyperplastic epithelial
glands resulted in a thickened mucosa. Histologic changes in calves primarily involve the jejunum but also can involve the
ileum and colon. The lesions can vary from mild changes to severe hemorrhagic enteritis. The mesenteric lymph nodes are
edematous.
Diagnosis:
The standard method for diagnosis is microaerophilic culture of feces at 42°C; a special medium is commercially
available.
Treatment and Control:
Erythromycin, the drug of choice for Campylobacter diarrhea in man, is also effective in other animals. Gentamicin,
furazolidone, doxycycline, and chloramphenicol also can be used. Some animals continue to shed the organism despite
antibiotic therapy.
Salmonellosis: Introduction
Salmonellosis is caused by many species of salmonellae and characterized clinically by one or more of three major
syndromes—septicemia, acute enteritis, and chronic enteritis. Young calves, piglets, lambs, and foals usually develop the
septicemic form (see diarrhea in neonatal ruminants, and diarrheal diseases of foals. Adult cattle, sheep, and horses
commonly develop acute enteritis, and chronic enteritis may develop in growing pigs and occasionally in cattle (see also the
chapters on intestinal diseases in each of the major domestic species, et seq. Pregnant animals may abort. Salmonellosis
occurs infrequently in dogs and cats and is characterized by acute diarrhea with or without septicemia. Transmission to man
occurs via contaminated drinking water, milk, meat, and foods such as cake mixes that use contaminated ingredients;
poultry and eggs are particularly important sources of infection.
Etiology, Epidemiology, and Pathogenesis:
Feces of infected animals can contaminate feed and water, milk, fresh and processed meats from abattoirs, plant and
animal products used as fertilizers or feedstuffs, pasture and rangeland, and many inert materials. The organisms may
survive for months in wet, warm areas such as in feeder pig barns or in water dugouts but survive <1 wk in composted cattle
manure.
The usual route of infection is oral and, after infection, the organism multiplies in the intestine and causes enteritis.
Greater susceptibility of the young may be due to high gastric pH, absence of a stable intestinal flora, and limited immunity.
Penetration of bacteria into the lamina propria and production of cytotoxin and enterotoxin likely contribute to gut damage
and diarrhea. There is a marked inflammatory response, and salmonellae are engulfed by phagocytic cells; however, the
bacteria can survive and multiply in these cells. Septicemia may follow with subsequent localization in brain and meninges,
pregnant uterus, distal aspects of the limbs, and tips of the ears and tails, which can result, respectively, in
meningoencephalitis, abortion, osteitis, and dry gangrene of the feet, tail, or ears.
Infection may persist in lymph nodes or tonsils, with no salmonellae in the feces. Latent carriers may begin shedding
the organism or even develop clinical disease under stress.
Hernias
Hernias involving the abdomen occur when abdominal contents protrude through a natural or abnormal opening in the
body wall. They may be congenital or acquired. In acquired hernias, there is usually a history of trauma. Congenital hernias
may involve the diaphragm or the abdominal wall. Hernias involving the diaphragm are of three main types:
peritoneopericardial, in which abdominal contents are found extending into the pericardial sac; pleuroperitoneal, in which
abdominal contents are found within the pleural cavity; and hiatal, in which the abdominal esophagus, gastroesophageal
junction, and/or portions of the stomach protrude through the esophageal hiatus of the diaphragm into the thoracic cavity.
Clinical signs vary from asymptomatic to severe and depend on the amount of herniated tissue and its effect on the organ it
is displacing. Hiatal hernias may be “sliding” and result in clinical signs of reflux esophagitis (anorexia, salivation, and/or
vomition) that may be intermittent. Diagnosis is through radiology: contrast studies are often needed for confirmation.
Fluoroscopy or endoscopy is useful in the diagnosis of sliding hiatal hernias. Correction of the aforementioned
hernias is best accomplished through surgery. In the case of hiatal hernias, medical therapy, including the use of
systemic antacid preparations and dietary modification, may control signs if mild.
Hernias involving the abdominal wall include umbilical, inguinal, or scrotal. Umbilical hernias are
secondary to failure of the normal closure of the umbilical ring and result in protrusion of abdominal contents into the
overlying subcutis. Size varies depending on the extent of the umbilical defect and the amount of abdominal contents
contained. The etiology in both large and small animals is likely to have a genetic component; however, excess traction on
an oversized fetus or cutting the umbilical cord too close to the abdominal wall are other possible causes. Diagnosis is
usually straightforward, especially if the hernia is manually reducible. If irreducible, it must be differentiated from an
umbilical abscess, which is common in large animals. Umbilical hernia and umbilical abscess often occur together,
especially in cattle and swine. Exploratory puncture may be required for confirmation. Correction is surgical.
Inguinal hernias in the male pig are common and they usually extend into the scrotum. Shaking the suspended piglet
by the forelegs causes even a small hernial bulge to become visible. In female pigs, this defect is invariably accompanied by
arrested genital development; such animals are sterile, and surgery is indicated only when the size of the process is a threat
to the growth of the pig to market weight. Inguinal hernias in male foals often resolve spontaneously during the first year of
life. For this reason, early corrective surgery is not indicated unless the hernia is strangulated or of such a magnitude that it
interferes with gait. Strangulated inguinal hernia in stallions is fairly frequent and is characterized by signs of constant and
severe abdominal pain. It is readily recognized by rectal palpation and may be reduced, under general anesthesia, by rectal
manipulation. If this fails, immediate surgery is necessary. Inguinal hernias in cattle are rare although sometimes seen in
males.
Esophagus
Clinically significant esophageal disorders generally manifest themselves as swallowing dysfunction and regurgitation,
especially evident with the introduction of solid food. These disorders, found predominantly in small animals, can be
classified as congenital megaesophagus, vascular ring entrapment anomalies, and achalasia. Congenital megaesopahagus
is thought to result from developmental anomalies in esophageal neuromuscular innervation. Vascular ring entrapment
anomalies most commonly result from persistence of the right fourth aortic arch during embryonic development, which
results in esophageal entrapment at the heart base by the right fourth aortic arch, left atrium, pulmonic artery, and the
ligamentum arteriosum. This obstructs food passage and results in food retention and subsequent esophageal dilation
anterior to the anomaly. Boston Terriers, German Shepherd Dogs, and Irish Setters have higher breed incidences.
Cricopharyngeal achalasia is a term used to describe a failure, or asynchrony, of the cricopharyngeous muscle to relax
during swallowing, thereby preventing the normal passage of a food bolus from the caudal pharynx to the cranial
esophagus. It has been mainly identified in toy breeds and rarely in cats. Lower esophageal sphincter achalasia is now
considered to be a component of a more generalized esophageal motor disturbance (ie, megaesophagus) and no longer a
distinct entity.
Definitive diagnosis is usually via contrast radiography or fluoroscopy of the swallowing reflex. Treatment is directed
at the primary etiology. Some mildly affected dogs will improve over time; however, those that don't have a poor long-term
prognosis, with aspiration pneumonia being a frequent and often lethal complication.
Esophageal diverticula may involve the cervical esophagus just cranial to the thoracic inlet or be epiphrenic (just
cranial to the diaphragm). Clinical signs depend on severity and are seen in only 10-15% of cases but may include
impaction, esophagitis, and rarely rupture or tracheoesophageal fistula formation. Treatment is via surgical removal.
Irregular Wear
Except for pigs, most large animals have an intermandibular space that is narrower than the intermaxillary space; that
is, they are anisognathic.
Periodontal Disease
In all animals, a degree of inflammatory change occurs during the eruption of both the deciduous and permanent teeth.
However, if malocclusion occurs, severe periodontal disease is inevitable. In horses, this is a common sequela of oral
trauma, dental fractures, impactions, and most importantly irregular wear.
Dental Decay
Infection may be introduced into the pulp chamber of the teeth by various routes, eg, after amputation of teeth (in pigs
or in new world camelids). In horses, hypoplasia of the enamel of the upper cheek teeth may predispose to caries of
cementum and subsequent pulpitis and apical osteitis. Depending on the site of the tooth that is decayed, there
may be accompanying signs of maxillary sinusitis, local cellulitis, periostitis, alveolar periodontitis, and fistula
formation.
When dental decay is advanced, extraction of the affected tooth is recommended.
Periodontal Disease
This bacterial infection of the tissue surrounding the teeth causes inflammation of the gingivae, periodontal ligament,
cementum, and alveolar bone. Ultimately, teeth are lost due to the loss of their supporting tissues. This is the major reason
for tooth loss in dogs.
Etiology and Pathogenesis:
Periodontal disease is caused by gross accumulation of many different bacteria at the gingival margin due in part to a
lack of proper oral hygiene. Over a period of weeks, the flora changes from nonmotile, gram-positive, coccoid, aerobic
bacteria to more motile, gram-negative, rod-shaped, anaerobic bacteria.
As the local bacterial flora increases in mass to 10-20 times normal, gingivitis occurs. The accumulation of bacterial
metabolic products increases epithelial permeability in crevicular epithelial desmosomes and allows antigens to contact
connective tissue. Metabolic products of bacterial metabolism include hydrogen sulfide, ammonia, endotoxin,
hyaluronidase, chondroitin sulfatase, mucopeptides, lipoteichoic acids, acetate, butyrate, isovalerate, and propionate. These
bacterial products and host defense mechanisms cause tissue necrosis. Polymorphonuclear leukocytes (PMN) migrate
through the sulcular epithelium and form a barrier between the subgingival bacteria and the gingiva. With overwhelming
bacterial challenge, PMN die in increasing numbers and release breakdown products. The immune system produces
lymphokines that participate in tissue destruction, which follows the path of the local vascular supply. Accelerated tissue
destruction and inappropriate repair cause loss of periodontal support. Two forms of disease are recognized: gingivitis and
periodontitis.
In gingivitis, the inflammation of the marginal gingival tissues is induced by bacterial plaque and does not affect the
periodontal ligament or alveolar bone. There is a change from coral-pink to red or purple, swelling of the gingival margin,
and a serous or purulent exudate in the sulcus. The gingivae tend to bleed on contact. Fetid breath is common. Gingivitis is
reversible with proper tooth cleaning but, if untreated, may lead to periodontitis.
In periodontitis, the destructive inflammatory process of the periodontium is induced and
driven by bacterial plaque that contains specific bacteria that destroy the gingiva, periodontal
ligament, alveolar bone, and root cementum. It usually occurs after years of plaque, calculus, and gingivitis. It is irreversible
and results in permanent loss of tooth support. There is apical migration of the epithelial attachment and resorption of
supporting alveolar bone. Affected teeth may show increased mobility, concurrent
gingivitis, and subgingival calculus.
Dogs on a hard diet develop fewer problems due to the mechanical cleaning effect
of the food. Caudal teeth have more problems than rostral teeth. The maxilla is affected more severely than the mandible,
and buccal surfaces have more disease than lingual surfaces. Gingivitis often becomes severe at ~2 yr of age but resolves if
treated. Periodontitis usually begins at 4-6 yr of age and, if untreated, progresses to tooth loss.
Treatment:
The basic principle is that active periodontal disease will not develop around a clean tooth.
Gingivitis usually can be treated by thorough cleaning of the teeth, including below the gingival margin.
Gingival Hyperplasia
(Fibromatosis gingivae, Fibromatous epulis, Epulis)
This benign overgrowth of the epithelial and connective tissue of the gums usually originates near the gingival margin.
The tissue is relatively insensitive and tough and has the density of fibrous connective tissue. The growths usually have a
broad base of attachment, are the color of the normal gum or more pale, and may grow large enough to completely cover the
surfaces of several teeth. Predisposition may exist among brachycephalic breeds, in which the condition is termed familial
gingival hypertrophy.
Epulis sometimes refers to giant-cell epulis or tumor of the gum of dogs. This
tumor usually is localized to a single tooth. Biopsy is encouraged to assure proper
diagnosis, treatment, and prognosis.
Gingival hyperplasia is most common in older dogs and is usually asymptomatic. Hair, food, and debris may collect
between the growth and the teeth and cause irritation and halitosis.
Gingivectomy by electrosurgical techniques is the most satisfactory treatment.
Endodontic Disease
Pulpal Hyperemia:
The pulp may become acutely inflamed due to trauma or extension of lesions adjacent to the pulp (eg, caries and
resorption). Because the pulp is totally confined in dentin, inflammatory swelling may result in pressure
necrosis if the insult is prolonged. Severity of the reaction appears to be directly proportional to the extent of
injury. Therefore, small injuries that produce transient hyperemia of the pulp may resolve, and a healthy pulp
may be reestablished. Steroid therapy is indicated immediately after trauma.
Cleaning out carious lesions and placing zinc oxide eugenol into resorptions and former carious areas may allow local
anesthesia and resolution of hyperemia.
Pulpitis:
Inflammation of the pulp with pressure necrosis and abscessation is irreversible. In general, the abscess
cavity is initially sterile unless the tooth has been opened to the oral environment by trauma, resorption, or
caries. Teeth with pulpitis often are acutely painful, and the animal resents manipulation or percussion of the
tooth. As the pulp dies and gas pressure increases in the pulp cavity, blood is forced into the dentinal tubules and the teeth
often change to a reddish brown or dark gray color.
Periapical Lesions:
A periapical abscess is a cavitational lesion at the end of the root due to pulpal disease. These areas generally can be
seen on radiographs as radiolucent circular areas around the end of the root. Such abscesses can sometimes be
palpated over the bony prominence of root ends. Abscesses may extend by pressure drainage into adjacent bone
and soft-tissue areas and exit extraorally into the soft-tissue space between the jaws, beneath the eye, or into the
buccal vestibule. Treatment is endodontic therapy (root canal) on the associated tooth, and the abscess and associated fistula
usually resolve within a few weeks. When endodontic therapy cannot be done, the tooth should be extracted.
Dental Caries
Dental decay is uncommon in dogs and cats, possibly because of differences in oral flora, diets largely free of readily
fermentable carbohydrates, and the slightly alkaline pH of canine saliva. In dogs, decay usually is seen as pits on the flat
surfaces or on the necks of the molar teeth.
Developmental Abnormalities
Malocclusion:
Malposition of the teeth within the jaw can result in a poor bite. Frequently, it occurs when deciduous teeth are retained
and the permanent teeth erupt adjacent to, rather than directly under, them; the roots of the deciduous teeth are not resorbed,
and they tilt the erupting permanent teeth into an abnormal position. Other types of dental malocclusion relate to improper
relationships between the size of the teeth and that of the jaws. For example, a jaw may be too small for the size of the teeth
developing within it, which causes crowding and subsequent malocclusion. Malocclusion may be treated to obtain a
functional bite by early extraction of retained deciduous teeth, selective extraction of permanent teeth, or orthodontics.
Skeletal malocclusions result from an abnormal relationship of the upper and lower jaws to each other, although the teeth
may be properly aligned within the jaw. Treatment is much more difficult and should attempt to achieve a functional bite
rather than perfect occlusion. Selective extractions, orthodontics, and in severe cases, orthognathic surgery may be
necessary.
Enamel Hypoplasia and Dysplasia:
During the development of enamel (both deciduous and permanent teeth), fevers and deposition of chemicals within the
tooth may cause permanent damage. The canine distemper virus is especially damaging in that it attacks the ameleoblasts
(enamel-producing cells) and causes a systemic fever. This results in generalized full-thickness loss of enamel, or enamel
hypoplasia.
Treatment of enamel hypoplasia includes composite bonding and frequent dental prophylaxis. Treatment of enamel
dysplasia includes aggressive polishing of the remaining enamel and possible composite bonding.
Maxillofacial Trauma
Fractured teeth should be inspected for damage to the pulp. If fractures extend into the pulp, endodontic therapy is
required, or extraction must be performed. Lengthwise fractures that extend below the gingival margin can be difficult to
repair; if substantial tooth has been lost, what remains should probably be extracted. Fragmented teeth, especially those with
multiple roots, often are left to “see what happens”; extraction is usually better due to poor general healing.
within a few hours. Thick tissue that has become avascular due to trauma should be removed.
Bone fractures require stabilization. Acrylic splints, arch bars, interdental wiring, and cerclage wires can be used.
Coccidiosis: Introduction
Coccidiosis is a usually acute invasion and destruction of intestinal mucosa by protozoa of the genera Eimeria or
Isospora . Infection is characterized by diarrhea, fever, inappetence, weight loss, emaciation, and sometimes death.
Coccidiosis is a serious disease in cattle, sheep, goats, pigs, poultry, and also rabbits, in which the liver as well as the
Coccidiosis of Goats
The Eimeria spp are host-specific and are not transmitted from sheep to goats.
Eimeria arloingi , E christenseni , and E ninakohlyakimovae are highly pathogenic in kids. Clinical signs include
diarrhea with or without mucus or blood, dehydration, emaciation, weakness, anorexia, and death. Some goats are actually
constipated and die acutely without diarrhea. Usually, stages and lesions are confined to the small intestine, which may
appear congested, hemorrhagic, or ulcerated, and have scattered pale, yellow to white macroscopic plaques in the mucosa.
Histologically, villous epithelium is sloughed, and inflammatory cells are seen in the lamina propria and submucosa. In
addition, there have been several reports of hepatobiliary coccidiosis with liver failure in dairy goats.
Coccidiosis of Pigs
Eight species of Eimeria and one of Isospora infect pigs in the USA.
Isospora suis is prevalent in neonatal pigs. Infection is characterized by a watery or greasy diarrhea, usually yellowish
to white and foul smelling. Piglets may appear weak, dehydrated, and undersized; weight gains are depressed, and
sometimes piglets die. A contributing factor to mortality is that piglets become covered with diarrheic feces and stay damp.
Piglets that recover from infection are highly resistant to reinfection.
Coccidiosis of Sheep
Infections with some species of Eimeria are one of the most economically important diseases of sheep. The parasites
are now considered host-specific.
Cryptosporidiosis
Cryptosporidiosis is an enterocolitis of cosmopolitan distribution caused by the coccidian parasite Cryptosporidium
parvum . It is not host-specific and is common in young ruminants. The disease in calves, characterized by weight loss and
watery diarrhea, is clinically indistinguishable from many other causes of calf diarrhea. Unless the immune system is
compromised, it is self-limiting.
Cryptosporidium parvum infections from animals and other people pose a significant risk to immunocompromised
people, who can develop protracted diarrhea and die.
Etiology and Transmission:
Cryptosporidium parvum is a minute protozoan that is transmitted by the fecal-oral route.
Clinical Findings and Lesions:
Although C parvum can infect virtually the entire intestinal tract, the distal small intestine usually is affected most
severely. Infection in horses is limited to the small intestine. Gross lesions may consist of hyperemic intestinal mucosa and
yellowish intestinal contents. Microscopically, mild to severe villous atrophy with spherical organisms in the brush border is
evident. Unlike Eimeria and Isospora spp , which are intracellular parasites, C parvum is intramembranous and resides
within the brush border of the intestinal epithelial cells.
Treatment and Control:
There is no effective specific treatment; however, because the disease is self-limiting, supportive therapy, such as
rehydration, correction of acidosis, and maintenance of energy requirements, is usually sufficient.
Giardiasis: Introduction
Giardiasis is a chronic, intestinal protozoal infection that occurs worldwide in most domestic and wild mammals, many
birds, and people. There is circumstantial evidence that the Giardia spp that infect domestic animals can infect people.
Perineal Hernia
Perineal hernia is a lateral protrusion of a peritoneally lined hernial sac between the levator ani and either the external
anal sphincter muscle or the coccygeus muscle. Incidence in intact 6- to 8-yr old male dogs.
Etiology and Pathogenesis:
Many factors are involved, including breed predisposition, hormonal imbalance, prostatic disease, chronic constipation,
and weakness of the pelvic diaphragm due to chronic straining. The higher incidence among sexually intact males is
evidence that hormonal influences probably play a primary role. Prostatic hypertrophy attributed to sex-hormone imbalance
has been strongly implicated. Both estrogens and androgens have been cited as causative agents.
Rectal Prolapse
In rectal prolapse, one or more layers of the rectum protrude through the anus due to persistent tenesmus associated
with intestinal, anorectal, or urogenital disease. Prolapse may be classified as incomplete, in which only the rectal mucosa is
everted, or complete, in which all rectal layers are protruded.
Etiology:
Rectal prolapse is common in young animals in association with severe diarrhea and tenesmus. Causal factors include
severe enteritis, disorders of the rectum (eg, foreign bodies, lacerations, diverticula, or sacculation), neoplasia of the rectum
or distal colon, urolithiasis, urethral obstruction, cystitis, dystocia, colitis, and prostatic disease.
Rectal prolapse is probably the most common GI problem in pigs due to diarrhea or weakness of the rectal support
tissue within the pelvis. In cattle, it may be associated with coccidiosis, rabies, or vaginal or uterine prolapse; occasionally,
excessive “riding” and associated traumatic injury may be causative in young bulls. It is common in sheep with short tail
docking or especially in feedlot lambs, in which high-concentrate rations may be causative.
Clinical Findings, Lesions, and Diagnosis:
An elongated, cylindrical mass protruding through the anal orifice is usually diagnostic. However, it must be
differentiated from prolapsed ileocolic intussusception by passing a probe, blunt instrument, or finger between the prolapsed
mass and the inner rectal wall. In rectal prolapse, the instrument cannot be inserted due to the presence of a fornix.
Ulceration, inflammation, and congestion of the rectal mucosa is common. Early, there is a short, nonulcerated,
inflamed segment; later, the mucosal surface darkens and may become congested and necrotic.
Treatment:
In all animals, identifying and eliminating the cause is of primary importance.
In small animals, treatment includes prompt replacement of viable prolapsed tissue to its proper anatomic location, or
amputation if the segment is necrotic. Small or incomplete prolapses can be manually reduced under anesthesia by using a
finger or bougie. Hypertonic sugar solution (50% dextrose or 70% mannitol) applied directly to the mucosa relieves edema
and eases reduction. The placement of a loose, anal purse-string suture for 5-7 days is indicated. Postoperatively, a
moistened diet and a fecal softener (eg, dioctyl sodium sulfosuccinate) are recommended.
In large animals, caudal epidural anesthesia is suggested to reduce straining, facilitate repositioning of the prolapse,
and permit surgical manipulations. Reduction and retention with a purse-string suture is recommended. The suture should
be loose enough to leave a one-finger opening into the rectum in pigs and sheep, and slightly larger in cattle and horses.
Rectal Tears
A separation, rent, or tear in the rectal or anal mucosa occurs as a result of a laceration inflicted within the lumen.
Foreign bodies (eg, sharp bones, needles, and other rough material) have been implicated.
Clinical Findings and Diagnosis:
Constipation and reluctance to defecate are usually attributed to pain. Diagnosis is based on tenesmus and hemorrhage,
perineal discoloration, and inspection of the rectum and anus; fresh blood found on a glove or on feces after rectal
examination is good evidence of a rectal tear.
Treatment:
In all species, treatment should be initiated immediately.
In cattle and horses, accidental perforation during rectal examination necessitates immediate treatment to reduce the
risk of peritonitis and death. Rectal tears in horses have been classified according to the tissue layers penetrated. Grade I
tears involve the mucosa or submucosa. Grade II tears involve rupture of the muscular layers only. Grade III tears involve
mucosa, submucosa, and muscular layers, including tears that extend into the mesorectum. Grade IV tears involve
perforation of all layers of the rectum and extension into the peritoneal cavity.
Grade I tears may be treated conservatively with broad-spectrum antibiotics and IV fluids. Flunixin meglumine may be
given to prevent or treat endotoxic shock. Mineral oil is given via stomach tube to soften feces, and the diet should consist
of pasture grasses or alfalfa. Grade II and III tears require immediate and more extensive surgery. Grade IV tears carry a
Abomasal Ulcers
Abomasal ulcers affect mature cattle and calves and have several different manifestations.
Etiology and Pathogenesis:
Except for lymphosarcoma of the abomasum and the erosions of the abomasal mucosa that occur with viral diseases
such as bovine viral diarrhea, rinderpest, and bovine malignant catarrhal fever, the causes of abomasal ulceration are not
well understood. Many different causes have been suggested. Although abomasal ulcers can occur any time during lactation,
they are common in high-producing, mature dairy cows within the first 6 wk after parturition. This has led to speculation
that the cause is a combination of the stress of parturition, the onset of lactation, and heavy grain feeding.
Abomasal ulcers are common in hand-fed calves after they are weaned from milk or milk replacer and begin to eat
roughage. Most of these are subclinical and nonhemorrhagic. They may be due to consumption of dry food. Occasionally,
milk-fed calves <2 wk old are affected by acute, hemorrhagic abomasal ulcers that may perforate and cause rapid death.
Clinical Findings:
A system of classification is based on the depth of penetration or the degree of hemorrhage or peritonitis caused by the
ulcer: Type I is an erosion or ulcer without hemorrhage, Type II is hemorrhagic, Type III is perforated with acute localized
peritonitis, and Type IV is perforated with acute diffuse peritonitis. There may be only a single ulcer or many acute and
chronic ulcers.
Cattle with bleeding abomasal ulcers may be asymptomatic except for intermittent occult blood in the feces, or they can
die acutely from massive hemorrhage. Common clinical signs include mild abdominal pain, bruxism, sudden onset of
anorexia, tachycardia (90-100 beats/min), and fecal occult blood or melena that may be intermittent. Signs of blood loss
occur with major hemorrhage and may include tachycardia (100-140 beats/min), pale mucous membranes, weak pulse, cool
extremities, shallow breaths, tachypnea, and melena.
Lesions:
Ulceration is most common along the greater curvature of the abomasum. Most of the ulcers occur on the ventral part
of the fundic region, with a few on the border between the fundic and pyloric regions. The single or multiple ulcers measure
from a few millimeters to 5 cm in diameter. Multiple trichobezoars are common in the abomasum of beef calves with
abomasal ulcers.
Diagnosis:
In cases with only slight bleeding and mild clinical signs, diagnosis may require repeated fecal evaluations for occult
blood. Other conditions that can cause partial anorexia and decreased milk production should be ruled out by physical
examination and laboratory tests, including abdominocentesis. In cases with melena, the diagnosis can be based on physical
examination alone. The PCV can help to determine the degree of hemorrhage. Blood from portions of the GI tract distal to
the abomasum reacts on fecal occult blood tests; it is usually bright red if from the large intestine or raspberry-colored if
from the small intestine. Animals with abomasal lymphosarcoma can have a bleeding syndrome similar to that associated
with abomasal ulcers but do not respond to therapy. Occasionally, oral, pharyngeal, and laryngeal lesions bleed, and the
blood is swallowed and appears in the feces.
Diagnosis of perforating abomasal ulcers is based on physical examination and ruling out other causes of peritonitis.
Proximal Enteritis-jejunitis:
The cause is unknown. The affected intestine contains lesions varying from hyperemia to necrosis and infiltration of the
submucosa with inflammatory cells. Often, there is edema and hemorrhage in the various layers of the intestinal wall.
Inguinal Hernia:
Inguinal hernias generally occur in stallions after breeding a mare, trauma, or a hard workout. Hernias appear to be
most common in Tennessee Walking Horses, American Saddlebreds, and Standardbreds. In most cases, the hernia produces
acute colic. The intestine descends through the vaginal ring in most cases and lies next to the testis and epididymis. Rectal
examination will reveal distended loops of small intestine, with one of the loops tracing to the vaginal ring on the affected
side. There will be gastric reflux, and the horse's condition will deteriorate rapidly. Peritoneal fluid generally reflects the
degree of ischemia.
Surgery involves a ventral midline celiotomy and inguinal approach to reduce the hernia. Often, the testicle on the
affected side must be removed, and the affected intestine resected. The prognosis for survival seems to be breed-dependent,
with Standardbred horses having a good prognosis and Tennessee Walking Horses having a fair to poor prognosis.
Presumably, this reflects the fact that many Tennessee Walking Horse stallions with inguinal hernias show little evidence of
pain.
Enterolithiasis:
Enteroliths are concretions composed of magnesium ammonium phosphate crystals around a nidus (eg, wire, stone,
nail). Enteroliths may occur singly or in groups and are commonly found in horses in certain parts of California, the
southwest, Indiana, and Florida. Enterolithiasis commonly affects horses of the Arabian breed, but the fact that these horses
are extremely popular in the aforementioned areas confounds the question regarding breed association.
Many horses with enterolithiasis have a history of recurring colic, presumably indicating that the enterolith(s) had
caused partial or temporary obstruction of the colonic lumen. If the enterolith becomes lodged at the origin of the transverse
colon, the colon proximal to the obstruction distends with gas and the pain is severe. Distention of the abdomen may be
marked. Heart and respiratory rates are increased, and the mucous membranes may be pale or pink. Generally, colonic and
cecal distention is evident on rectal examination, but the mass rarely is palpable because the transverse colon is cranial to
the cranial mesenteric artery. Radiography may be used to identify the enteroliths.
Treatment involves surgery via a ventral midline celiotomy to decompress the colon and cecum and then to remove the
stone(s).
Esophageal Strictures
Idiopathic esophageal strictures occur in foals. Critical cases should be referred to advanced surgical centers, and
esophagomyotomy or esophageal resection and anastomosis may be attempted.
Ascaris sp
Adults of the large roundworm, Ascaris suum , are found principally in the small intestine but may migrate into the
stomach or bile ducts. When the eggs are ingested, the larvae hatch in the intestine, penetrate the intestinal wall, and enter
the portal circulation. After a period in the liver, they are carried by the circulation to the lungs, where they pass through the
capillaries into the alveolar spaces. About 9-10 days after ingestion, the larvae pass up the bronchial tree, return to the GI
tract, and then mature in the small intestine. The first eggs are passed 2-2½ mo after infection.
Clinical Findings:
Adult worms may significantly reduce the growth rate of young pigs; if sufficiently numerous, they may cause
mechanical obstruction of the intestine, or migrate into and occlude the bile ducts, producing icterus.
Migration of larvae through the liver causes hemorrhage and fibrosis that appears as “white
spots” under the capsule. In heavy infections, the larvae can cause pulmonary edema and
consolidation as well as exacerbate swine influenza and endemic pneumonia. Affected pigs show
abdominal breathing, commonly referred to as “thumps.” In addition to the respiratory signs, marked
unthriftiness and weight loss are seen. Permanent stunting may result in pigs up to 4-5 mo old.
Diagnosis:
During the patent period, diagnosis can be made by demonstrating the typical eggs in the feces.
Treatment:
Many drugs have been used to remove adult ascarids. Piperazine preparations have low toxicity and are moderately
priced. The benzimidazoles and probenzimidazoles, dichlorvos, ivermectin, levamisole, and pyrantel are effective and have
a broader spectrum of activity than piperazine.
Tyzzer's Disease
Tyzzer's disease, due to Clostridium piliforme , causes an acute necrotizing hepatitis, myocarditis, and colitis in foals 8-
42 days old.
Etiology:
Cholangiohepatitis is a sporadic cause of hepatic failure in horses and in ruminants. It is occasionally associated with
cholelithiasis in horses. Bacteremia due to an organism (eg, salmonella) eliminated in the bile or an ascending infection of
biliary tract after intestinal disturbance or ileus are thought to be related to the development of cholangiohepatitis. Gram-
negative organisms, including Salmonella sp , Escherichia coli , Pseudomonas , and Actinobacillus equuli are frequently
isolated from the liver.
Clinical Findings:
Depending on the severity of infection and virulence of the organism, clinical signs may be acute with severe toxemia,
or subacute or chronic. Icterus, photosensitivity, and signs of hepatic encephalopathy are variable. SDH, AST, GGT,
bilirubin, and total bile acid concentrations are usually increased. Peripheral WBC counts are variable, depending on the
degree of inflammation and endotoxemia present.
Lesions:
The liver is swollen, soft, and pale. Suppurative foci may be visible beneath the capsule or on cut surface. Lesions in
other systems may reflect septicemia and jaundice. Microscopically in acute cases, neutrophils are present in the portal
triads and degenerate parenchyma. Purulent exudate is evident in the ducts. In subacute or chronic cholangiohepatitis, the
inflammation is more proliferative than exudative. Areas of atrophy, regenerative hyperplasia, and fibrosis may be evident.
Diagnosis:
Liver biopsy should be performed to confirm the diagnosis and to obtain a liver sample for aerobic and anaerobic
culture and sensitivity. Differential diagnoses include other causes of acute to chronic hepatic disease, weight loss, colic, or
sepsis. If neurologic signs are present, cerebral diseases must be considered.
Treatment:
Antimicrobial therapy based on culture and sensitivity results often gives favorable results.
Equine Rhinopneumonitis
Equine rhinopneumonitis due to equine herpesvirus 1 is a sporadic cause of interstitial pneumonia.
Hepatic Abscesses
The primary etiologic agent of liver abscesses in cattle ( Liver Abscesses In Cattle: Introduction) is Fusobacterium
necrophorum . In goats, most abscesses are due to Corynebacterium pseudotuberculosis . Actinomyces pyogenes and
Escherichia coli are also common.
The liver is particularly susceptible to abscess formation because it receives blood from the hepatic artery, the portal
system, and the umbilical vein in the fetus and the neonate.
Hepatic Neoplasia
Primary hepatic tumors are uncommon in horses and ruminants. They include hepatocellular carcinoma,
cholangiocarcinoma, and rarely lymphomas or other neoplasias. Hepatic carcinomas arise from hepatocytes, bile ducts, or
metastasis. Hepatocellular carcinomas generally are found in yearlings to young adult horses and have also been reported in
llamas and goats. Cholangiocarcinoma is primarily found in middle-aged or older horses. Adenomas or adenocarcinomas of
the liver have been reported in cattle.
Lymphosarcoma is the most common neoplasia of the hematopoietic system in horses. As many as 37% of horses with
lymphosarcoma have neoplastic involvement of the spleen, and 41% have neoplastic involvement of the liver.
Clinical Findings:
Liver hepatocellular and biliary enzymes may be increased with hepatic carcinoma or cholangiocarcinoma. Serum GGT
activity in affected horses is usually very high.
Clinical manifestations of lymphosarcoma in horses are variable. Early in the disease, nonspecific signs such as weight
loss, anorexia, and lethargy are seen. Lymphoma occasionally may diffusely infiltrate the liver and produce signs of hepatic
failure, jaundice, and severe depression.
Diagnosis:
The presence and character of the hepatic neoplasia can be confirmed by liver biopsy and microscopical examination of
the tissue. Atypical lymphocytes or lymphoblasts may be seen in peritoneal fluids and peripheral blood of some affected
animals.
Porcine
Edema Disease
(Escherichia coli enterotoxemia)
Edema disease is an acute, highly fatal, neurologic disorder that usually occurs 5 days to 2 wk after weaning and may
be accompanied by diarrhea.
Rotaviral Enteritis
Rotaviral enteritis is a common disease of the small intestine of pigs. All ages are susceptible, but significant diarrheal
disease usually occurs in nursing or postweaning pigs.
Etiology and Pathogenesis:
The causal rotavirus infects and destroys villous enterocytes throughout the small intestine, but lesions are most severe
in the middle third of the intestine. Loss of villous epithelium results in partial villous atropy, malabsorption, and osmotic
diarrhea. Healthy carrier sows may be fecal shedders during the periparturient period, thereby exposing their litters to
infection.
Clinical Findings and Lesions:
If neonatal pigs do not receive protective levels of maternal antibody, they are likely to develop profuse watery diarrhea
in 12-48 hr. More commonly, the infection is endemic in a herd, and sows have varying levels of antibody in the colostrum
and milk, which provide varying degrees of passive protection to nursing pigs. Diarrhea often begins in pigs 5 days to 3 wk
old, or immediately after weaning. The feces of nursing pigs often are yellow or gray and pasty in the early stages and
Swine Dysentery
(Bloody scours)
Swine dysentery is a common, mucohemorrhagic diarrheal disease of pigs that affects the large intestine.
Etiology and Pathogenesis:
The essential causal agent is Serpulina (Treponema) hyodysenteriae , an anaerobic spirochete that produces a
hemolysin, although other organisms may contribute to the severity of lesions. It proliferates in the large intestine and
causes degeneration and inflammation of the superficial mucosa, hypersecretion of mucus by mucosal epithelium, and
multifocal bleeding points on the mucosal surface. The organism does not penetrate beyond the intestinal mucosa.
Decreased ability of the mucosa to reabsorb endogenous secretions from the unaffected small intestine results in diarrhea.
Clinical Findings:
More commonly, a mucoid diarrhea with flecks of blood and mucus develops and progresses to a watery
mucohemorrhagic diarrhea. After several days, the feces are brown and contain flecks of fibrin and debris. Diarrheic pigs
are dehydrated, profoundly weak, gaunt, and emaciated.
Lesions:
The diffuse lesions are confined to the cecum, spiral colon, and rectum. The affected mucosa is covered with a layer of
transparent or gray mucus, often with suspended flecks of blood in early stages; a mixture of blood, fibrin, and necrotic
debris in more advanced cases; and a yellow, necrotic debris late in the course.
Diagnosis:
Clinical signs and necropsy findings are usually sufficient for a presumptive diagnosis. Differential
diagnoses include proliferative enteritis, salmonellosis, and heavy whipworm infections.
Treatment and Control:
Therapeutic use of antibacterials is effective if started early. Bacitracin, carbadox, lincomycin, nitroimidazoles,
tiamulin, and virginiamycin are commonly used.
Transmissible Gastroenteritis
Transmissible gastroenteritis (TGE) is a common viral disease of the small intestine that causes vomiting and profuse
diarrhea in pigs of all ages.
Etiology and Pathogenesis:
The causal coronavirus infects and destroys villous epithelial cells of the jejunum and ileum, which results in severe
villous atrophy, malabsorption, osmotic diarrhea, and dehydration. The incubation period is ~18 hr. Recovered pigs can
carry the virus in their respiratory tract for ≥4 mo. Severe epidemics are more common during winter due to survival of the
virus in colder temperatures.
Clinical Findings:
In nonimmune herds, vomiting often is the initial sign, followed by profuse watery diarrhea, dehydration, and excessive
thirst. Feces of nursing pigs often contain curds of undigested milk. Mortality is nearly 100% in piglets <1 wk old, whereas
pigs >1 mo old seldom die. Gestating sows occasionally abort and lactating sows often exhibit vomiting, diarrhea, and
agalactia.
Immunity from antibody in the sow's milk usually is sufficient to protect pigs until they are 4-5 days old. As the
antibody level in milk decreases, infection and mild disease may occur. If passive protection is sufficient to protect pigs
throughout the nursing period, diarrhea often develops during the first few days after weaning.
Lesions:
Piglets dying of TGE are severely dehydrated, and the skin is soiled with liquid feces. The stomach usually contains
milk curd but may be empty. The small intestine is thin walled, and the entire intestine contains greenish or yellow watery
fluid and clumps of undigested milk. Older pigs have few remarkable lesions except that the colon contains liquid rather
than formed feces. Villous atrophy can be observed by examining the mucosa of the small intestine with a hand lens.
Diagnosis:
In some outbreaks, coronaviral encephalomyelitis may cause similar signs.
Treatment and Control:
Small animal
Mouth Burns
Thermal, chemical, or electrical burns involving the mouth are not uncommon. Chewing on an electrical cord is most
frequently a problem in puppies.
If tissue destruction is marked, ulcerative or gangrenous stomatitis may develop, with secondary bacterial infections. If
contact with a corrosive chemical is seen and the chemical is alkaline, the mouth may be flushed with mild solutions of
vinegar or citrus juice; if the chemical is acidic, a solution of sodium bicarbonate may be used. Copious flushing of the
mouth with water may help remove some of the chemical substances.
Salivary Mucocele:
In a salivary mucocele (or sialocele), mucoid saliva accumulates in the subcutaneous tissue after damage to the salivary
duct or gland. This is the most common salivary gland disorder of dogs. While any of the salivary glands may be affected,
the sublingual and mandibular glands are involved most commonly. Usually the saliva collects at the intermandibular or
cranial cervical area (cervical mucocele).
The cause may be traumatic or inflammatory blockage or rupture of the duct of the sublingual, mandibular, parotid, or
zygomatic salivary gland.
The first noticed sign may be a nonpainful, slowly enlarging, fluctuant mass, frequently in the cervical region. A ranula
may not be seen until it is traumatized and bleeds. A pharyngeal mucocele may obstruct the airways and result in moderate
to severe respiratory distress.
A mucocele is detectable as a soft, fluctuant, painless mass that must be differentiated from abscesses, tumors, and
other retention cysts of the neck. Pain or fever may be present if the mucocele becomes infected. A salivary mucocele
usually can be diagnosed by palpation and aspiration of the characteristic golden or blood-tinged, stringy saliva. Usually,
careful palpation with the animal in dorsal recumbency can determine the affected side; if not, sialography may be helpful.
Surgery is recommended to remove the damaged salivary gland and duct, usually of the mandibular-sublingual gland
complex. Cervical mucoceles can be managed with periodic drainage if surgery is not an option. Drainage,
marsupialization, or gland removal has been recommended for treatment of ranulas. Complete gland and duct removal is
recommended for pharyngeal mucoceles to avoid future life-threatening airway obstruction.
Vomiting: Introduction
Vomiting is the forceful ejection of the contents of the stomach and proximal small intestine. It is a vigorously active
motion signalled by hypersalivation, retching, and forceful contractions of the abdominal muscles and the diaphragm.
Vomiting must be differentiated from regurgitation, which is a passive motion facilitated by gravity and body position of the
animal. In regurgitation, the expelled food and fluid tends to be undigested, has a neutral pH depending on the composition
of the diet, and may have a cylindrical shape reflecting the shape of the esophagus.
Etiology, Pathophysiology, and Clinical Findings:
Vomiting represents a coordinated effort of the GI, musculoskeletal, and nervous systems to expel food, fluid, or debris
from the GI tract. It is initiated by direct stimulation of the vomiting center in the brain stem or indirectly via the
chemoreceptor trigger zone (CTZ) or abdominal afferent nerves. Stimulation of receptors in the semicircular canals of the
vestibular system, or inflammation within the CNS and increases in intracranial pressure, can also promote vomiting. The
CTZ responds to substances in the blood, eg, drugs, ketones, or uremic or bacterial toxins. Most of the receptors involved in
the vomiting reflux are found in the abdominal viscera, especially in the duodenum.
Vomiting can be due to primary GI disease, renal or hepatic failure, electrolyte abnormalities (eg,
hypoadrenocorticism), pancreatitis, or CNS disorders (including toxin ingestion).
Diagnosis:
The diagnostic approach to vomiting varies depending on whether the vomiting is acute or chronic. Chronic vomiting
may be associated with weakness, lethargy, weight loss, dehydration, electrolyte imbalance, and acid-base disorders.
Chronic vomiting, vomiting that occurs more often than once or twice daily, and vomiting accompanied by
hematemesis, abdominal pain, depression, dehydration, weakness, fever, or other adverse clinical signs should be
approached more vigorously. In addition to a detailed history and physical examination, an initial database should include a
complete blood count, biochemical profile (including serum electrolytes), urinalysis, and abdominal radiographs (and
abdominal ultrasound if available).
Treatment and Control:
Symptomatic therapy for acute vomiting includes fasting and withholding water for 24 hr to rest the GI tract. (Water
can be provided in the form of ice.) Animals predisposed to hypovolemia, eg, animals with concurrent renal insufficiency or
cardiac disease, should receive parenteral fluid therapy.
Therapy for chronic vomiting is also directed to elimination of the primary cause and, in addition, to correction of
dehydration, electrolyte imbalances, and acid-base disorders. The vomiting reflex should be suppressed.
Vomiting associated with gastrointestinal obstruction commonly results in hypokalemia, hypochloremia, metabolic
alkalosis, and paradoxical aciduria due to losses of secretions rich in potassium, chloride, and hydrogen. However,
continued vomiting, lack of water intake, insensible water losses, and catabolism of body energy stores contribute to
dehydration, poor tissue perfusion, hypoxia, and lactic acidosis. In the absence of gastric obstruction, the loss of bicarbonate
from duodenal secretions may predispose to metabolic acidosis.
Antiemetic therapy is indicated in animals with intractable vomiting, dehydration, and weakness. Commonly used
antiemetics include antispasmodic medication, agents that depress the CTZ, drugs that suppress the emetic center, drugs that
Hyperadrenocorticism
(Cushing's disease, Cortisol excess)
Hyperadrenocorticism may be the most frequent endocrinopathy in adult to aged dogs but is infrequent in other
domestic animals. The clinical signs and lesions associated with hyperadrenocorticism result primarily from chronic excess
of cortisol. The disease is insidious and slowly progressive. (See also The Pituitary Gland : Introduction .)
Etiology and Pathogenesis:
Increased cortisol levels in dogs may result from one of several pathogenic mechanisms. The most common is an
adenoma or hyperplasia of the adrenocorticotropic hormone (ACTH)-containing cells of the pituitary gland (pars distalis or
pars intermedia), which results in bilateral adrenal cortical hypertrophy and hyperplasia. This form of the disease is referred
to as pituitary-dependent hyperadrenocorticism and occurs in ~90% of cases. Functional adrenal tumors are a far less
frequent cause of hyperadrenocorticism in dogs.
Clinical Findings and Lesions:
Polyuria, polydipsia (PU/PD), and polyphagia are among the most common clinical signs. They occur either as a direct
result of the hypercortisolism or secondary to compression or invasion of the hypothalamus by a pituitary macroadenoma.
The muscles of the extremities and abdomen weaken and atrophy, with gradual abdominal enlargement, lordosis, muscle
trembling, and weakness. Hepatomegaly due to increased fat and glycogen deposition may contribute to the distended, often
pendulous, abdomen. The muscular asthenia and wasting is the result of increased catabolism combined with diminished
protein synthesis.
Alopecia is symmetrical and may involve a significant portion of the body surface. There is atrophy of the epidermis
and pilosebaceous apparatus, combined with loss of collagen and elastin in the dermis and subcutis. Cutaneous
mineralization is a characteristic although infrequent finding in dogs. Although mineral deposition may occur
anywhere in the skin, the dorsal midline, ventral abdomen, and inguinal region are affected most frequently. The
mineral deposits occur despite normal blood calcium and phosphorus levels probably because of the gluconeogenic and
protein catabolic actions of cortisol. Mineralization may also occur in other tissues of the body, most frequently the airways
and blood vessels.
Behavioral problems occur frequently in both dogs and people with hyperadrenocorticism. Signs in dogs include
lethargy, sleep-wake cycle disturbances, panting, and decreased interaction with owners (which may be characterized as
decreased responsiveness to attention or diminished enthusiasm of greeting behavior).
Adenomas of the adrenal cortex are seen most frequently in old dogs and sporadically in horses, cattle, and sheep.
Carcinomas of the adrenal cortex occur less frequently than adenomas and have been reported most often in adult to
older cattle and dogs, with no apparent breed or sex predilection. Adrenal carcinomas are larger then adenomas and more
likely to be bilateral.
Diagnosis:
A complete blood count generally reveals a stress leukogram (mature neutrophilia, lymphopenia, eosinopenia). In dogs,
serum concentrations of sodium, potassium, and chloride are usually normal. Cortisol excess stimulates the synthesis and
release of a steroid-inducible isoenzyme (ciALP) of alkaline phosphatase, and increased levels of alkaline phosphatase are
seen in 80% of dogs. Blood glucose is moderately increased and, occasionally, marked hyperglycemia develops. Diabetes
Hypoadrenocorticism
(Addison's disease)
A deficiency in adrenocortical hormones is seen most commonly in young to middle-aged dogs and occasionally in
horses. The disease may be familial in Standard Poodles. The cause of primary adrenocortical failure usually is not known,
although most cases probably result from an autoimmune process. Other causes can be destruction of the adrenal gland by
granulomatous disease, metastatic tumor, hemorrhage, infarction, or overdose of mitotane.
Clinical Findings:
Although hypoadrenocorticism occurs in dogs of any breed, sex, or age, idiopathic adrenocortical insufficiency is most
common in young female adults. This may be related to its suspected immune-mediated pathogenesis.
A reduction in secretion of aldosterone, the principal mineralocorticoid, results in marked alterations of serum levels of
potassium, sodium, and chloride. Potassium excretion by the kidneys is reduced and results in a progressive rise in serum
potassium levels. Hyponatremia and hypochloremia result from renal tubular loss. Severe hyperkalemia may result in
bradycardia and an irregular heart rate with alterations in the ECG. Some dogs develop a pronounced bradycardia (heart rate
≤50 beats/min) that predisposes to weakness or circulatory collapse after minimal exertion.
Although the development of clinical signs often is not readily apparent, acute circulatory collapse and evidence of
renal failure frequently occur. A progressive decrease in blood volume contributes to hypotension, weakness, and
microcardia. Increased excretion of water by the kidneys, due to decreased reabsorption of sodium and chloride, results in
progressive dehydration and hemoconcentration. Emesis, diarrhea, and anorexia are common and contribute to the animal's
deterioration. Weight loss is frequently severe. Similar clinical signs are seen in cats with hypoadrenocorticism.
Decreased production of glucocorticoids results in several characteristic functional disturbances. Decreased
gluconeogenesis and increased sensitivity to insulin contribute to the development of moderate hypoglycemia. In some
dogs, hyperpigmentation of the skin occurs due to the lack of negative feedback on the pituitary gland and increased release.
The plasma cortisol levels are below the resting reference range, and there is little or no increase in blood cortisol levels
after ACTH administration.
Lesions:
The most common lesion in dogs is bilateral idiopathic adrenocortical atrophy, in which all layers of the cortex are
markedly reduced in thickness.
All three zones of the adrenal cortex are involved, including the zona glomerulosa which is not under ACTH control;
however, no obvious pituitary lesions have been seen in dogs with idiopathic adrenal cortical atrophy.
A destructive pituitary lesion that decreases ACTH secretion is characterized by severe atrophy of the inner two cortical
zones of the adrenal gland; the zona glomerulosa remains intact.
Diagnosis:
A presumptive diagnosis is based on the history and supportive (although not specific) laboratory abnormalities,
including hyponatremia, hyperkalemia, a sodium:potassium ratio of <25:1, azotemia, mild acidosis, and a normocytic
normochromic anemia. Severe GI blood loss has also been reported. Occasionally, mild hypoglycemia is present. The
hyperkalemia results in ECG changes: an elevation (spiking) of the T wave, a flattening or absence of the P wave, a
prolonged PR interval, and a widening of the QRS complex. Ventricular fibrillation or asystole may occur with potassium
levels >11 mEq/L.
Differential diagnoses include primary GI disease (especially whipworm infection), renal failure, acute pancreatitis, and
toxin ingestion. For definitive diagnosis, evaluation of adrenal function is required. After obtaining a baseline blood sample,
ACTH (gel or synthetic) is administered IM and a second blood sample obtained 1-2 hr later. Affected dogs have low
baseline cortisol levels, and there is little response to ACTH administration. This test can be completed in most animals
before replacement hormone therapy is started.
Treatment:
An adrenal crisis is an acute medical emergency. An IV catheter should be inserted and a 0.9% saline infusion begun. If
the dog is hypoglycemic, the saline can include 5% dextrose.
Prednisolone sodium succinate (22-30 mg/kg) or dexamethasone sodium phosphate (2.2-4.4 mg/kg) may be used in the
initial management of shock.
Diabetes Mellitus
Diabetes mellitus is a chronic disorder of carbohydrate metabolism due to relative or absolute insulin deficiency. In
dogs, females are affected twice as often as males.
Etiology and Pathogenesis:
The pathogenic mechanisms responsible for decreased insulin production and secretion are multiple, but usually they
are related to destruction of islet cells, secondary to either severe pancreatitis or selective degeneration. In dogs, chronic
pancreatitis and immune destruction of the pancreatic islets are the most common causes of diabetes mellitus. Chronic
relapsing pancreatitis with progressive loss of both exocrine and endocrine cells and their replacement by fibrous connective
tissue results in diabetes mellitus. Selective infiltration of islets with amyloid, glycogen, and collagen with destruction of
islet cells are less frequent causes of diabetes mellitus in dogs than in cats. In other cases, the numbers of β cells are
decreased, and the cells become vacuolated; in chronic cases, the islets are difficult to find. Insulin resistance and secondary
diabetes mellitus are also seen in many dogs with hyperadrenocorticism, and chronic administration of glucocorticoids or
progestins can predispose to diabetes mellitus. In dogs, but not cats, progesterone leads to release of growth hormone,
resulting in hyperglycemia and insulin resistance. Obesity also predisposes to insulin resistance in both dogs and cats.
Cats with diabetes mellitus usually have specific degenerative lesions localized selectively in the islets of Langerhans,
whereas the remainder of the pancreas appears to be normal. The selective deposition of amyloid in islets, with degenerative
changes in α and β cells, is the most common pancreatic lesion in many cats with diabetes. The amyloid appears to arise
from islet-associated polypeptide (IAPP), which is secreted together with insulin from the β cell. Cats (and 20% of people
with type II diabetes) seem unable to process IAPP normally, which leads to excessive accumulation and conversion into
amyloid. As cats age, a greater percentage of their islets contain amyloid. Cats with diabetes have a greater percentage of
their islets affected with larger amounts of amyloid than age-matched cats without diabetes. The amyloid or IAPP (or both)
lead to both physical disruption of the β cell and insulin resistance, resulting in diabetes.
Infection with certain viruses may cause selective islet damage or pancreatitis and has been suggested to be responsible
for certain cases of rapidly developing diabetes mellitus.
Clinical Findings:
Hypercalcemia of Malignancy
Malignancy is the most common cause of persistent hypercalcemia in dogs and cats. In hypercalcemia of malignancy,
the hypercalcemia primarily results from increased osteoclastic bone resorption, but increased renal tubular resorption and
increased intestinal absorption may also play a role. Factors that may be produced by tumors and result in humoral
hypercalcemia of malignancy include PTH, PTH-related protein, transforming growth factor, 1,25-dihydroxyvitamin D,
prostaglandin E2, osteoclast-activating factor, and other cytokines (interleukin-1, interleukin-2, and gamma interferon).
Although many tumors have been associated with hypercalcemia in man, lymphoma, adenocarcinoma of the apocrine
glands of the anal sac, and multiple myeloma are the most common tumors in animals associated with hypercalcemia of
malignancy.
Lymphoma (Lymphosarcoma):
Lymphoma is the most common tumor associated with hypercalcemia in dogs and cats. The pathogenesis of the
hypercalcemia in lymphoma may involve two general mechanisms: one is local elaboration of an osteolytic factor that
induces resorption of bone and mobilization of calcium when the bone marrow is infiltrated by tumors cells; the other,
probably more important, is humoral hypercalcemia in which neoplastic cells produce a humoral factor that acts at a
distance from the tumor. As evidence for secretion of a humoral substance by tumor cells, increased bone resorption,
phosphaturia, and urinary excretion of cyclic adenosine monophosphate (cAMP) have been documented in dogs with
lymphoma.
Of dogs with lymphoma, 10-40% have been reported to have concurrent hypercalcemia, and a large number of these
cases also have the mediastinal form of lymphoma. Although detectable lymphadenopathy is usually present, hypercalcemia
may be the first abnormality noted. A thorough physical examination, together with thoracic and abdominal radiographs,
abdominal ultrasonography, multiple lymph node aspirates or biopsies, and multiple bone marrow aspirates may be
necessary for diagnosis. Treatment with glucocorticoids (eg, prednisone) will lower the serum calcium concentrations;
however, steroids are lympholytic and will make identification of lymphoma difficult. Although remission rates in dogs
with lymphoma and hypercalcemia are not statistically different from those without hypercalcemia, survival times are
considerably less, indicating that hypercalcemic lymphomas have a poorer prognosis.
Adenocarcinoma of the Apocrine Glands of the Anal Sac:
This tumor usually occurs in older female dogs, with hypercalcemia developing in ~90% of cases. Adenocarcinoma of
the anal sac is usually malignant and has metastasized to regional lymph nodes at the time of diagnosis. Surgical resection is
associated with reduction of serum calcium.
Multiple Myeloma:
Hypercalcemia has been associated with multiple myeloma in dogs and cats in 10-15% of cases. The presence of
extensive bony lysis may also contribute to the increased serum calcium. Although serum protein concentration is usually
increased in multiple myeloma, increased protein binding of calcium rarely accounts for the hypercalcemia.
Primary Hyperparathyroidism
Primary hyperparathyroidism results from excessive secretion of PTH by an abnormal (usually neoplastic) parathyroid
gland(s). Persistent hypercalcemia is characteristic. This disease is relatively rare in dogs and cats.
Etiology:
Solitary adenoma of the parathyroid gland is the most common cause of primary hyperparathyroidism, whereas
parathyroid carcinoma has been infrequently reported.
Clinical Findings:
Polydipsia, polyuria, anorexia, lethargy, and depression are the most common signs, but many animals are
asymptomatic. Constipation, weakness, shivering, twitching, vomiting, stiff gait, and facial swelling are less often reported.
Diagnosis:
Hypercalcemia, normal to low serum phosphorus, and low urine specific gravity are the most consistent findings.
Azotemia commonly develops as a consequence of moderate to severe hypercalcemia. In hypercalcemic animals that still
have relatively normal renal function (normal serum creatinine and BUN concentrations), determination of serum PTH is
helpful in diagnosis.
Hypoparathyroidism
Hypoparathyroidism is a metabolic disorder characterized by hypocalcemia and hyperphosphatemia and either transient
or permanent parathyroid hormone (PTH) insufficiency. The spontaneous disorder is uncommon in dogs and rarely reported
in cats. Iatrogenic injury or removal of the parathyroid glands during thyroidectomy for treatment of hyperthyroidism is the
most common cause of hypoparathyroidism in cats.
Diagnosis:
Diagnosis of hypoparathyroidism is based on history, clinical signs, laboratory evidence of hypocalcemia and
hyperphosphatemia, and exclusion of other causes of hypocalcemia (eg, hypoproteinemia, malabsorption, pancreatitis, renal
failure). Determination of serum PTH concentrations might be helpful in the diagnosis of idiopathic hypoparathyroidism
and may thereby eliminate the need for cervical exploratory surgery and histologic verification.
Treatment:
Treatment of hypoparathyroidism is directed at restoring the serum calcium concentration to the low end of the normal
range. This includes use of calcium supplements and vitamin D for either iatrogenic or idiopathic forms of
hypoparathyroidism. If hypocalcemic tetany or seizures are present, calcium should be administered IV immediately. For
maintenance of normocalcemia, oral calcium should be administered together with a vitamin D preparation.
The major complication associated with treatment of hypoparathyroidism is hypercalcemia, which develops as a
consequence of overtreatment with calcium and vitamin D. If this occurs, calcium and vitamin D therapy should be
temporarily discontinued, and saline and furosemide administered if hypercalcemia is severe (see principles of treatment of
hypercalcemia , above). Principles of Treatment of Hypercalcemia With idiopathic hypoparathyroidism, long-term
management with vitamin D (with or without calcium supplementation) is necessary.
Neurohypophysis:
The neurohypophysis (pars nervosa, posterior lobe) has three anatomic subdivisions. Secretion granules that contain the
neurohypophyseal hormones, ie, antidiuretic hormone (ADH, vasopressin) and oxytocin, are synthesized in the
hypothalamus but are released into the bloodstream in the pars nervosa.
Hyperadrenocorticism
(Cushing's disease)
Clinical Findings:
Miniature Poodles, Dachshunds, Boxers, Boston Terriers, and Beagles are breeds at increased risk of developing
hyperadrenocorticism.
Laboratory Abnormalities:
In dogs, serum chemistry abnormalities associated with hypercortisolemia include increased serum alkaline
phosphatase and ALT, hypercholesterolemia, hyperglycemia, and decreased BUN. The hemogram is often characterized by
evidence of regeneration (erythrocytosis, nucleated red blood cells) and a classic “stress leukogram” (mature neutrophilia,
lymphopenia, and eosinopenia). Basophilia is occasionally seen.
Many dogs have evidence of urinary tract infection without pyuria (positive culture), bacteriuria, and proteinuria
resulting from glomerulosclerosis. Thyroid status is often affected and is evidenced by decreased basal thyroxine (T4) and
triiodothyronine (T3), caused by euthyroid sick syndrome and by an attenuated response to TSH stimulation due to the effect
of cortisol and overcrowding on pituitary thyrotrophs. Overt diabetes mellitus may result from the insulin antagonism
caused by hypercortisolemia in ~25% of dogs with hyperadrenocorticism and in an even higher percentage of cats. In
addition, hyperadrenocorticism can be a cause of insulin resistance and poor glycemic control in diabetic dogs.
Diagnosis:
The low-dose dexamethasone suppression (LDDS) test is the screening test of choice for hyperadrenocorticism in dogs.
As a screening test for the diagnosis of naturally occurring hyperadrenocorticism, the ACTH stimulation test has a
diagnostic sensitivity of ~80-85% and a higher specificity than the LDDS test.
Measurement of endogenous plasma ACTH concentrations is the most reliable method of differentiating between PDH
and adrenal tumors. Dogs with adrenal tumors have low to undetectable ACTH concentrations; in contrast, dogs with PDH
have normal to increased ACTH concentrations. The high-dose dexamethasone suppression (HDDS) test works on the
principle that ACTH secretion has already been suppressed maximally in dogs with functioning adrenal tumors; therefore,
administration of dexamethasone, no matter how high the dose, will not suppress serum cortisol concentrations. In dogs
with PDH, however, high doses of dexamethasone are able to suppress ACTH and hence cortisol secretion. One caveat is
that dogs with pituitary macroadenomas (15-50% of dogs with PDH) fail to suppress on the HDDS test.
Diagnostic imaging of the pituitary or adrenal glands can be accomplished via abdominal radiography, ultrasonography,
computerized tomography, or magnetic resonance imaging. Abdominal radiographs should be performed in all dogs that do
not suppress on an HDDS; in ~30-50% of dogs with adrenal tumors, a mineralized mass in the area of the adrenal glands
can be seen.
Treatment:
Diabetes Insipidus
When target cells in the kidney lack the biochemical machinery necessary to respond to the secretion of normal or
increased circulating levels of ADH, nephrogenic diabetes insipidus results.
Etiology:
The hypophyseal form of central diabetes insipidus develops as a result of compression and destruction of the pars
nervosa, infundibular stalk, or supraoptic nucleus in the hypothalamus. The lesions responsible for the disruption of ADH
synthesis or secretion in hypophyseal diabetes insipidus include large pituitary neoplasms (endocrinologically active or
inactive), a dorsally expanding cyst or inflammatory granuloma, and traumatic injury to the skull with hemorrhage and glial
proliferation in the neurohypophyseal system.
Clinical Findings and Lesions:
Affected animals excrete large volumes of hypotonic urine and drink equally large amounts of water.
Diagnosis:
This is based on chronic polyuria that does not respond to dehydration and is not due to primary renal disease. To
evaluate the ability to concentrate urine, a water deprivation test should be done if the animal is not dehydrated and does not
have renal disease. The bladder is emptied, and water and food are withheld (usually 3-8 hr) to provide a maximum stimulus
for ADH secretion. The animal should be monitored carefully to prevent a loss of >5% body wt and severe dehydration.
Urine and plasma osmolality should be determined; however, because these tests are not readily available to most
practitioners, urine specific gravity is frequently used instead. At the end of the test, urine specific gravity is >1.025 in those
animals with only a partial ADH deficiency or with antagonism to ADH action caused by hypercortisolism. There is little
change in specific gravity in those animals with a complete lack of ADH activity, whether due to a primary loss of ADH or
to unresponsiveness of the kidneys.
If osmolality is measured, the ratio of urine to plasma osmolality after water deprivation is >3 in normal animals, 1.8-3
in those with moderate ADH deficiency, and <1.8 in those with severe deficiency. The ratio of urine osmolality after ADH
administration as compared with water deprivation is >2 in animals with primary ADH deficiency, between 1.1 and 2 in
those with inhibitors to ADH action, and <1.1 in those unresponsive to ADH.
Diabetes insipidus also needs to be distinguished from other diseases with polyuria. The most common are diabetes
mellitus with glycosuria and high urine specific gravity, and chronic nephritis with a urine specific gravity that is usually
low and shows evidence of renal failure (protein, casts, etc).
Treatment:
Polyuria may be controlled using desmopressin acetate, a synthetic analog of ADH.
Feline Acromegaly
Acromegaly, or hypersomatotropism, results from chronic, excessive secretion of growth hormone in the adult animal.
Acromegaly in cats is caused by a growth-hormone-secreting tumor of the anterior pituitary. In cats, these tumors grow
slowly and may be present for a long time before clinical signs appear.
Clinical Findings:
Feline acromegaly occurs in older (8-14 yr) cats, and there appears to be a sex predilection for males. Clinical signs of
uncontrolled diabetes mellitus are often seen as the first sign of acromegaly in cats; therefore, polydipsia, polyuria, and
polyphagia are the most common presenting signs. Net weight gain of lean body mass in cats suffering from uncontrolled
diabetes mellitus is a key sign of acromegaly. Organomegaly including renomegaly, hepatomegaly, and enlargement of
endocrine organs is also seen. Some cats show the classic enlargement of extremities, body size, jaw, tongue, and forehead
that is characteristic of acromegaly in man. Some of the most striking manifestations occur in the musculoskeletal system
Hypothyroidism
In hypothyroidism, impaired production and secretion of the thyroid hormones result in a decreased metabolic rate.
Etiology:
Although dysfunction anywhere in the hypothalamic-pituitary-thyroid axis may result in thyroid hormone deficiency,
>95% of clinical cases of hypothyroidism in dogs appear to result from destruction of the thyroid gland itself (primary
hypothyroidism). The two most common causes of adult-onset primary hypothyroidism in dogs include lymphocytic
thyroiditis and idiopathic atrophy of the thyroid gland. Lymphocytic thyroiditis, probably immune-mediated, is
characterized histologically by a diffuse infiltration of the gland by lymphocytes, plasma cells, and macrophages, and results
in progressive destruction of follicles and secondary fibrosis. Idiopathic atrophy of the thyroid gland is characterized
Hyperthyroidism
Excessive secretion of the thyroid hormones, T4 and T3, results in signs that reflect an increased metabolic rate and
produces clinical hyperthyroidism. It is most common in middle-aged to old cats but also develops rarely in dogs.
Functional thyroid adenoma (adenomatous hyperplasia) is the most common cause of feline hyperthyroidism; in ~70%
of cases, both thyroid lobes are enlarged. Thyroid carcinoma, the primary cause of hyperthyroidism in dogs, is rare in cats
(1-2% of hyperthyroidism cases).
Clinical Findings and Diagnosis:
The most common signs include weight loss, increased appetite, hyperexcitability, polydipsia, polyuria, and palpable
enlargement of the thyroid gland. GI signs are also common and may include vomiting, diarrhea, and increased volume of
feces. Cardiovascular signs include tachycardia, systolic murmurs, dyspnea, cardiomegaly, and congestive heart failure. Of
hyperthyroid cats, 5-10% exhibit apathetic signs (eg, anorexia, lethargy, and depression); weight loss is common.
High serum concentrations of T4 and T3 confirm the diagnosis; however, they are subject to a wide degree of
fluctuation, and more than one basal measurement may be necessary.
Treatment:
Spontaneous hyperthyroidism can be treated by thyroidectomy, radioiodine therapy, or chronic administration of an
antithyroid drug. With unilateral thyroid tumors, hemithyroidectomy corrects the hyperthyroid state, and thyroxine
supplementation usually is not necessary. For bilateral thyroid tumors, complete thyroidectomy is indicated, but
parathyroid function must be preserved to avoid postoperative hypocalcemia. Thyroxine supplementation should be
started 1-2 days after complete thyroidectomy.
Eyelid Disorders
Entropion is an inversion of all or part of the lid margins that may involve one or both eyelids and the canthi. Inversion
of the cilia (or eyelashes) or facial hairs causes further discomfort, conjunctival and corneal irritation, and if protracted,
corneal scarring, pigmentation, and possibly ulceration. Established entropion may require surgical correction with the
Hotz-Celsus procedure or its modifications.
Ectropion is a slack, everted lid margin, usually with a large palpebral fissure. It is a common bilateral conformational
abnormality in a number of dog breeds. Contracting scars in the lid or facial nerve paralysis may produce
unilateral ectropion in any species. Conjunctival exposure to environmental irritants and secondary bacterial
infection can result in chronic or recurrent conjunctivitis. Topical antibiotic-corticosteroid preparations may
temporarily control intermittent infections, but surgical lid-shortening procedures are often indicated. Mild cases
can be controlled by repeated, periodic lavage with mild decongestant solutions.
Lagophthalmos is an inability to fully close the lids and protect the cornea from drying and trauma.
Inflammation
Blepharitis (inflammation of the eyelids) can result from extension of a generalized dermatitis,
conjunctivitis or local infections, or irritants such as plant oils or solar exposure. The mucocutaneous junction of
the skin and conjunctiva can be the site of lesions of immune-mediated diseases such as pemphigus.
In generalized blepharitis, systemic therapy often is indicated in addition to topical treatment. Supportive
therapy of hot packing and frequent cleansing often is indicated in acute cases. Nonophthalmic preparations can be used to
treat the eyelids, but caution in application is indicated to avoid corneal contact and possible irritation.
Keratoconjunctivitis sicca (KCS) is due to an aqueous tear deficiency and usually results in persistent,
mucopurulent conjunctivitis and corneal ulceration and scarring. KCS occurs in dogs, cats, and horses. In
dogs, it is often associated with an autoimmune dacryoadenitis of both the lacrimal and nictitans glands.
Distemper infection, chronic sulfonamide therapy, and trauma are less frequent causes of KCS in dogs. KCS
occurs infrequently in cats and has been associated with chronic feline herpesvirus infections. In horses,
KCS may follow head trauma. Lacrimogenics such as topical cyclosporin A (1-2%, b.i.d.) may increase tear production
in some dogs. Ophthalmic pilocarpine mixed in food may be useful (a 20-30 lb [10-15 kg] dog should be started on 2-4
drops of 2% pilocarpine, b.i.d.). Mucolytic agents (eg, 10% acetylcysteine) lyse excess mucus and restore the spreading
ability of other topical agents.
Conjunctiva
Subconjunctival hemorrhage may arise from trauma or blood dyscrasias and certain infectious diseases.
Chemosis, or conjunctival edema, occurs to some degree with all cases of conjunctivitis, but the most
dramatic examples are seen with trauma, hypoproteinemia, allergic reactions, and insect bites. The
latter are treated with topical corticosteroids and usually resolve rapidly.
Conjunctivitis is common in all domestic species. The etiologic agent(s) may vary
from infectious to environmental irritants. The signs are hyperemia, chemosis, ocular discharge, follicular
hyperplasia, and mild ocular discomfort. In cats, herpesvirus, Mycoplasma , or Chlamydia psittaci
may produce conjunctivitis that begins in one eye and becomes bilateral after ~1 wk. Specific diagnosis is made most
rapidly by demonstrating the inclusions or the agent in conjunctival scrapings. Bilateral conjunctivitis is common in a
variety of viral infections in all species. Herpesviruses produce conjunctivitis in cats, cattle, horses, and pigs. Purulent
discharge indicates a bacterial component, but this may be opportunistic due to debilitation of the mucous membrane.
Environmental irritants and allergens are common causes of conjunctivitis in all species. If a mucopurulent exudate is
present, topical antibiotic therapy is indicated but may not be curative if other predisposing factors are involved. Topical
tetracycline is indicated for chlamydial and mycoplasmal infections; topical antiviral preparations (eg, idoxuridine) are
indicated for herpesvirus infections when both the cornea and conjunctiva are involved.
Ulcerative keratitis may be superficial, deep, deep with descemetocele, or perforating. Pain, corneal
irregularity, edema, and eventually vascularization are signs of ulceration. A dense, white infiltrate at the ulcer
margin indicates strong leukotaxis and bacterial involvement. To detect small ulcers, topical fluorescein may be
required. In dogs and horses, most ulcers are mechanical in origin; in cattle, sheep, and reindeer, infectious agents and
mechanical causes are important; in cats and horses, herpesvirus infection is a frequent cause. All ulcers have the potential
for secondary bacterial contamination or endogenous enzymatic “melting” of the stroma. Therapy for superficial ulcers is
usually medical and consists of topical antibiotic(s), topical atropine for iridocycloplegia, and correction of any mechanical
factors.
Lens
Cataracts are an opacity of the lens or its capsule and should be differentiated from the normal increase in nuclear
density (nuclear sclerosis) that occurs in older animals. Cataracts usually are classified
by their age of onset (congenital, juvenile, senile), anatomical location, cause, degree of
opacification (incipient, immature, mature, hypermature), and shape.
Cataracts (often inherited) occur more commonly in dogs than in other species (Table:
Inherited Cataracts in Domestic Animals ). Other etiologies include diabetes mellitus, malnutrition, radiation,
inflammation, and trauma. In cats and horses, most cataracts are secondary to anterior uveal inflammation. Sight may be
regained in young dogs, cats, and horses when cataracts undergo sufficient spontaneous resorption; congenital nuclear
cataracts in young animals may reduce in size with growth of the lens to permit restoration of vision as the animal matures.
Animals with immature and incomplete cataracts may benefit from topical ophthalmic atropine 2-3 times/wk, which allows
vision around a central cataract. In general, the only definitive therapy for cataracts is surgical removal of the lens.
Lens displacement (subluxation, anterior or posterior luxation) occurs in all species but is common as a primary
inherited defect in several terrier breeds. Lens displacements also can be produced by trauma, enlargement of the globe with
glaucoma, and degenerative zonular changes with chronic cataracts.
Lesions:
Cattle
The most frequent ophthalmic neoplasms in cattle are the squamous cell carcinoma complex and the orbital infiltration
associated with lymphosarcoma ( Bovine Leukosis: Introduction). The latter, with extensive invasion of the orbital
structures, results in progressive exophthalmia, reduced ocular mobility, exposure keratitis, and corneal ulcerations that can
lead to perforation.
It occurs most often in Herefords and rarely in other breeds. The etiology is multifactorial with heritability,
sunlight, nutrition, and perhaps viral involvement. The cancerous or precancerous lesions are bilateral or
multiple in the same eye in ~28% of cases. Ultraviolet radiation and a high plane of nutrition are contributing
influences.
The lesions usually begin as benign, smooth, white plaques on the conjunctival surfaces; they may progress to a
papilloma and then a squamous cell carcinoma, or go directly to the malignant stage. Diagnosis usually is made by the
typical clinical appearance but can be confirmed rapidly by cytologic examination of impression smears. The intraocular
tumor invasion must be differentiated from severely disorganized eyes after trauma or infectious keratoconjunctivitis
( Infectious Keratoconjunctivitis: Introduction).
Surgical excision is indicated for small lesions or for debulking the larger lesions before cryotherapy or hyperthermia.
For advanced lesions confined to the globe, enucleation is recommended.
Owners of problem herds should be advised of the heritability factor, and affected animals and their offspring culled to
decrease the incidence of the tumor.
Actinobacillosis: Introduction
Actinobacillosis is caused by gram-negative coccobacilli that belong to the genus Actinobacillus . It almost always
involves soft tissue, including lymph nodes through which the organisms frequently spread, but also may involve adjacent
bony tissue. Other species of bacteria may be present at the site of infection. In general, therapy should involve surgical
debridement and lavage (when possible), and oral potassium iodide (food safety issues have limited the usefulness of this
product) or an antimicrobial agent to which the pathogen is susceptible and that reaches therapeutic concentrations in active
form at the site of infection.
It has been recommended that this organism be classified as Haemophilus actinomycetemcomitans based on the
similarity of its DNA with other bacteria belonging to the genus Haemophilus .
Actinobacillus lignieresii is the etiologic agent of wooden tongue, primarily seen in cattle but also in sheep, horses,
pigs, and dogs. Wooden tongue is characterized as a hard, tumorous abscess of the tongue.
Pus from the abscesses may contain small colonies of organisms surrounded by club-like processes of calcium
phosphate. The combination of bacteria and club-like processes have the appearance of grayish white “sulfur granules” that
are <1 mm in diameter. The organism is part of the normal flora of the mucous membranes of the animal's upper GI tract. It
causes disease by gaining access to adjacent soft tissue via penetrating wounds and causing localized infections or
spreading, via the lymphatics, to other tissues and organs. Although the disease caused by this organism is distributed
worldwide, it is sporadic in its occurrence and, as such, is difficult to prevent. Treatment involves surgical debridement
(when possible), and potassium iodide administered orally (should not be used in food-producing animals) or systemically
administered antibacterial agents such as the tetracyclines, erythromycin, or tilmicosin.
Actinomycosis: Introduction
Actinomycosis is a disease process caused by gram-positive rods belonging to the genus Actinomyces . Unlike
Mycobacterium or Nocardia spp , Actinomyces are acid-fast negative. These organisms are normal flora of the oral and
nasopharyngeal mucous membranes. As a rule, treatment of actinomycosis should include surgical debridement (when
possible) and antibacterial therapy. Actinomyces spp are susceptible to the β-lactam antimicrobial agents such as penicillins
and cephalosporins but are resistant to sulfas. For animals allergic to penicillin, tetracyclines and erythromycin are
reasonable alternatives.
Actinomyces bovis is the etiologic agent of lumpy jaw in cattle.
Lumpy jaw is characterized as a swelling with draining tracts resulting from a chronic, progressive, indurated,
granulomatous, suppurative abscess that most frequently involves the mandible, the maxillae, or other bony tissues in the
head.
Disease occurs when A bovis is introduced to underlying soft tissue, via penetrating wounds of the oral mucosa from
wire or coarse hay or sticks, and spreads to adjacent bone. Involvement of adjacent bone frequently results in facial
distortion, loose teeth (making chewing difficult), and dyspnea from swelling into the nasal cavity. Culture results and
histopathologic analysis of involved tissue can further confirm the diagnosis. Iodine treatment (tincture of iodine applied
topically) has been used successfully in the past but is no longer recommended due to food safety issues.
Actinomyces (Corynebacterium) pyogenes is the etiologic agent associated with a number of disease entities, primarily
in cattle but also in goats, sheep, and pigs. These include acute and chronic suppurative mastitis, suppurative pneumonia
(usually as a sequelae of acute bovine respiratory disease caused by Pasteurella haemolytica or P multocida ), septicemia,
vegetative endocarditis, endometritis, septic arthritis, wound infections including umbilical infections, seminal vesiculitis
(bulls and boars), and summer mastitis.
Amyloidosis: Introduction
Amyloidosis is a condition characterized by the excessive, extracellular deposition of inert protein fibrils. This material,
called amyloid, may be deposited in a localized fashion or may be widely distributed throughout the body where it can
cause damage by displacement of normal cells. If critical organs such as the kidneys, liver, or heart are involved, the disease
may be fatal. Amyloidosis can affect all domestic mammals, and minor, asymptomatic deposition of amyloid is common in
aged animals.
Anthrax: Introduction
(Splenic fever, Charbon, Milzbrand)
Anthrax is an acute, febrile disease of virtually all warm-blooded animals, including man.
Etiology and Epidemiology:
Bacillus anthracis is a gram-positive, nonmotile, spore-forming bacterium (4-8 × 1-1.5 µm). Strain virulence is
associated with the presence of two plasmids (pX01 and pX02) that carry the genes coding for toxin and capsule production,
respectively.
Bacillus produces an edema toxin (an adenylate cyclase) and a lethal toxin (probably a metalloprotease). Both toxins
gain entry to target cells by competitive binding with a third protein, protective antigen, that has a membrane translocation
function. The toxins and the capsule are the primary virulence factors of the anthrax bacillus.
Outbreaks of anthrax commonly are associated with neutral or alkaline, calcareous soils that serve as “incubator areas”
for the organisms.
Clinical Findings:
Death may occur in cattle, sheep, or goats without any previous evidence of illness.
There may be bloody discharges from the natural body openings.
Lesions:
Rigor mortis is frequently absent or incomplete. Dark blood may ooze from the mouth, nostrils, and anus with marked
bloating and rapid body decomposition. The liver, kidneys, and lymph nodes usually are congested and enlarged.
In pigs with chronic anthrax, the lesions usually are restricted to the tonsils, cervical lymph nodes, and surrounding
tissues. The area around involved lymphatic tissues generally is gelatinous and edematous.
Diagnosis:
Anthrax must be differentiated from other conditions that cause sudden death. In cattle and sheep, clostridial infections,
bloat, and lightning stroke may be confused with anthrax. Also, acute leptospirosis, bacillary hemoglobinuria, anaplasmosis,
and acute poisonings by bracken fern, sweet clover, and lead must be considered in cattle.
Treatment and Control:
When a soil-borne outbreak occurs, it is best to use antibiotics for the sick animals and to immunize all apparently well
animals in the herd and on surrounding premises.
Anthrax in livestock can be controlled largely by annual vaccination of all grazing animals in the endemic area and
implementation of control measures during outbreaks. Animals should not be vaccinated within 2 mo of anticipated
slaughter. Because this is a live vaccine, antibiotics should not be administered within 1 wk of vaccination.
Big Head
infectious disease, caused by Clostridium novyi , C sordellii , or rarely C chauvoei , is characterized by a nongaseous,
nonhemorrhagic, edematous swelling of the head, face, and neck of young rams. Treatment is with broad-spectrum
antibiotics or penicillin.
( Clostridium septicum also causes braxy in sheep, a highly fatal infection characterized by toxemia and inflammation
of the abomasal wall. This disease seems to be confined mostly to European sheep fed on “frosted” pasture.)
Control:
Bacterins are used for immunization. In endemic areas, animals should be vaccinated before they are castrated,
dehorned, or docked. Calves should be vaccinated at ~2 mo of age.
Botulism (Lamziekte)
This rapidly fatal motor paralysis is caused by ingestion of the toxin of Clostridium botulinum .
Etiology:
Botulism is an intoxication, not an infection, and results from ingestion of toxin in food. Like tetanus toxin, botulinum
toxin is a zinc-binding metalloprotease that cleaves specific proteins in synaptic vesicles.
Dogs, cats, and pigs are comparatively resistant to all types of botulinum toxin when administered orally.
Most botulism in cattle occurs in South Africa, where a combination of extensive agriculture, phosphorus deficiency in
soil, and C botulinum type D in animals creates conditions ideal for the disease. Botulism in sheep has been encountered in
Australia, associated not with phosphorus deficiency as in cattle, but with protein and carbohydrate deficiency, which
results in sheep eating carcasses of rabbits and other small animals found on the range.
Toxicoinfectious botulism is the name given the disease in which C botulinum grows in tissues of a living animal and
produces toxins there. The toxins are liberated from the lesions and cause typical botulism. This has been suggested as a
means of producing the shaker foal syndrome.
Clinical Findings and Lesions:
The signs of botulism are caused by muscle paralysis and include progressive motor paralysis, disturbed vision,
difficulty in chewing and swallowing, and generalized progressive weakness. Death is usually due to respiratory or cardiac
paralysis. The toxin prevents release of acetylcholine at motor end-plates. Passage of impulses down the motor nerves and
contractility of muscles are not greatly hindered; only the passage of impulses from nerves to motor end-plates is affected.
No characteristic lesions develop, and pathologic changes may be ascribed to the general paralytic action of toxin,
particularly in the muscles of the respiratory system, rather than to the specific effect of toxin on any particular organ.
Major clinical findings included drooling, inability to urinate, dysphagia, and sternal recumbency that progressed to
lateral recumbency just before death. Skin sensation is usually normal, and withdrawal reflexes of the limbs are weak.
Initially, clinical signs resemble second-stage milk fever ( Parturient Paresis In Cows: Introduction), but the cows do not
respond to calcium therapy.
In the shaker foal syndrome, foals are usually <4 wk old. They may be found dead without premonitory signs; most
often, they exhibit signs of progressive symmetrical motor paralysis. Stilted gait, muscular tremors, and the inability to
stand for >4-5 min are salient features. Other clinical signs include dysphagia, constipation, mydriasis, and frequent
urination. As the disease progresses, dyspnea with extension of the head and neck, tachycardia, and respiratory arrest occur.
Death occurs most often 24-72 hr after the onset of clinical signs. The most consistent necropsy findings are pulmonary
edema and congestion and excessive pericardial fluid, which contains free-floating strands of fibrin.
Diagnosis:
The diagnosis is made by eliminating other causes of motor paralysis. Filtrates of the stomach and intestinal contents
should be tested for toxicity in mice, but a negative answer is unreliable.
Tetanus
Tetanus toxemia is caused by a specific neurotoxin produced by Clostridium tetani in necrotic tissue. Almost all
mammals are susceptible to this disease, although dogs are relatively resistant, and cats seem much more resistant than any
other domestic or laboratory mammal. Birds are quite resistant; the lethal dose for pigeons and chickens is 10,000-300,000
times greater (on a body weight basis) than that for horses. Horses are the most sensitive of all species
Etiology and Pathogenesis:
Clostridium tetani , an anaerobe with terminal, spherical spores, is found in soil and intestinal tracts. In most cases, it is
introduced into the tissues through wounds, particularly deep puncture wounds, that provide a suitable anaerobic
environment. Often in lambs, however, and sometimes in other species, it follows docking or castration.
Suitable conditions for multiplication occur when a small amount of soil or a foreign object causes tissue necrosis. The
bacteria remain localized in the necrotic tissue at the original site of infection and multiply. As bacterial cells undergo
autolysis, the potent neurotoxin is released. The neurotoxin is a zinc-binding protease that cleaves synaptobrevin, a vesicle-
associated membrane protein. Usually, toxin is absorbed by the motor nerves in the area and passes up the nerve tract to the
spinal cord, where it causes ascending tetanus. The toxin causes spasmodic, tonic contractions of the voluntary muscles by
interfering with the release of neurotransmitters from presynaptic nerve endings. If more toxin is released at the site of the
infection than the surrounding nerves can take up, the excess is carried off by the lymph to the bloodstream and thus to the
CNS, where it causes descending tetanus. Even minor stimulation of the affected animal may trigger the characteristic
muscular spasms. The spasms may be so severe as to cause bone fractures. Spasms affecting the larynx, diaphragm, and
intercostal muscles lead to respiratory failure. Involvement of the autonomic nervous system results in cardiac arrhythmias,
tachycardia, and hypertension.
Clinical Findings:
The incubation period varies from one to several weeks but usually averages 10-14 days.
Spasms of head muscles cause difficulty in prehension and mastication of food, hence the common name, lockjaw. In
horses, the ears are erect, the tail stiff and extended, the anterior nares dilated, and the third eyelid prolapsed. Walking,
turning, and backing are difficult. Spasms of the neck and back muscles cause extension of the head and neck, while
stiffness of the leg muscles causes the animal to assume a “sawhorse” stance. Sweating is common. General spasms disturb
circulation and respiration, which results in increased heart rate, rapid breathing, and congestion of mucous membranes.
Sheep, goats, and pigs often fall to the ground and exhibit opisthotonos when startled. Consciousness is not affected.
Usually, the temperature remains slightly above normal, but it may rise to 108-110°F (42-43°C) toward the end of a
fatal attack.
Control:
Active immunization can be accomplished with tetanus toxoid. Mares should be vaccinated during the last 6 wk of
pregnancy and the foals vaccinated at 5-8 wk of age. In high-risk areas, foals may be given tetanus antitoxin immediately
after birth and every 2-3 wk until they are 3 mo old, at which time they can be given toxoid.
When administered in the early stages of the disease, curariform agents, tranquilizers, or barbiturate sedatives, in
conjunction with 300,000 IU of tetanus antitoxin b.i.d., have been effective in the treatment of horses. Good results have
been obtained in horses by injecting 50,000 IU of tetanus antitoxin directly into the subarachnoid space through the cisterna
magna. The horse should be placed in a quiet, darkened box stall with feeding and watering devices high enough to allow
their use without lowering the head. Slings may be useful for horses having difficulty standing or rising. The same approach
as described for horses is used in treatment of dogs and cats, except that caution must be exercised in the IV administration
of antitoxin because the equine antitoxin may induce anaphylaxis. A combination of chlorpromazine and phenobarbital may
be used to reduce hyperesthetic reactions and convulsions.
Erysipelas: Introduction
Erysipelothrix rhusiopathiae (insidiosa) is distributed worldwide and can live in water, soil, decaying organic matter,
slime on the bodies of fish, and in carcasses, even after processing. It causes swine erysipelas in its various forms;
nonsuppurative arthritis in lambs and less frequently in calves and kids; postdipping lameness in sheep; uncommonly, joint-
ill in goats ( Joint-ill); and acute septicemia in turkeys, ducks, and occasionally geese and other birds (see Erysipelas:
It is resistant to certain commonly used antiseptics, such as formaldehyde, phenol, hydrogen peroxide, and alcohol, but
is readily destroyed by caustic soda and hypochlorites. It is very sensitive to penicillin or ceftiofur but less so to the
tetracyclines.
Swine Erysipelas
Clinical Findings:
Acute septicemia, the skin (subacute) form, chronic arthritis, and vegetative endocarditis may occur in sequence, or
separately. Pigs with acute septicemia may die suddenly without previous signs. This occurs most frequently in finishing
pigs (100-200 lb [45-90 kg]). Acutely infected pigs are febrile (104-108°F [40-42°C]), walk stiffly on their toes, and lie on
their sternums separately rather than piling in groups. They squeal plaintively when handled and may shift weight from foot
to foot when standing. Skin discoloration may vary from widespread erythema and purplish discoloration of the ears, snout,
and abdomen, to diamond-shaped skin lesions almost anywhere on the body, but particularly the lateral and dorsal parts.
The lesions may occur as pink or light-purple areas of varying size that become raised and firm to the touch within 2-3 days
of illness.
They may disappear or progress to a more chronic type of lesion such as diamond-skin disease. If untreated, necrosis
and separation of large areas of skin can occur, but more commonly, the tips of the ears and tail may become necrotic and
slough.
Clinical disease is usually sporadic, and affects individuals or small groups, but sometimes larger outbreaks occur.
Mortality is 0-100%, and death may occur up to 6 days after the first signs of illness. Acutely affected pregnant sows may
abort, probably due to the fever, and suckling sows may show agalactia. Untreated pigs may develop chronic arthritis or
vegetative valvular endocarditis; such lesions may also occur in pigs with no previous signs of septicemia. Valvular
endocarditis is most common in mature or young adult pigs and is frequently manifested by death, usually from embolism.
Chronic arthritis, the most common form of chronic infection, produces mild to severe lameness; the affected joints may be
difficult to detect but tend to become visibly enlarged and firm. Mortality in chronic cases is low, but growth rate is
retarded.
Lesions:
In acute infection, in addition to skin lesions, lymph nodes are usually enlarged and congested, the spleen is swollen,
and the lungs are edematous and congested. Petechiae may be found in the kidneys, heart, and occasionally elsewhere.
In chronic cases, there may be erosion of the articular cartilage, and ankylosis may result.
Diagnosis:
Acute erysipelas is difficult to diagnose in pigs showing only fever, poor appetite, and listlessness; however, because
erysipelas responds extremely well to penicillin, a marked improvement within 24 hr supports the diagnosis.
Prevention and Treatment:
Killed bacterins or, in some countries, live-culture immunizing strains of low virulence for pigs are used.
Penicillin is the drug of choice in acutely affected pigs, and it has been used concurrently with antiserum. Treatment of
chronic infection is ineffective, and such pigs should be culled.
All species of deer and antelope, elephant, and giraffe are susceptible to FMD, but camels are resistant to natural
infection, and the smaller camelids such as alpacas and llamas, although susceptible, are probably of no epidemiological
significance.
Etiology:
FMD is caused by an aphthovirus of the family Picornaviridae.
The virus is quickly inactivated outside the pH range of 6.0-9.0 and by desiccation and temperatures > 56°C, although
residual virus may survive a considerable time when associated with animal protein (for instance, a proportion of FMD
virus in infected milk will survive pasteurization at 72°C for 15 sec). The FMD virus is resistant to lipid solvents such as
ether and chloroform. Because of the sensitivity of the virus to acid and alkaline pH, sodium hydroxide, sodium carbonate,
and citric or acetic acid are effective disinfectants.
Transmission, Epidemiology, and Pathogenesis:
Transmission of FMD is generally by contact between susceptible and infected animals. Infected animals have a large
amount of aerosol virus in their exhaled air, which can infect other animals via the respiratory or oral routes. All excretions
and secretions from the infected animal contain virus, and virus may be present in milk and semen for up to 4 days before
clinical signs appear. Aerosol FMD virus can spread a considerable distance as a plume, depending on weather conditions,
particularly when the relative humidity is >60% and when the topography of the surface over which it is dispersing does not
cause turbulence.
Ruminants that have recovered from infection and vaccinated ruminants that have contact with live FMD virus can
remain infected and carry the virus in the pharyngeal region—for up to 2½ years in cattle, 9 mo in sheep, and probably
lifelong in the African buffalo.
Clinical Findings:
The incubation period for FMD is 2-14 days, depending on the infecting dose, susceptibility of the host, and strain of
virus. After the incubation period, a fever of up to 107°F (41.5°C) develops, the animal is anorexic and salivates and stamps
its feet as vesicles develop on the tongue, dental pad, gums, lips, and on the coronary band and interdigital cleft of the feet.
Vesicles may also appear on the teats and udder, particularly of lactating cows and sows, and on areas of skin subject to
pressure and trauma, such as the legs of pigs. Young calves, lambs, kids, and piglets may die before showing any vesicles
because of virus-induced damage to the developing cells of the myocardium. Vesicles in the mouth, even when severe,
usually heal within 7 days, although recovery of the tongue papillae takes longer.
Diagnosis:
In cattle and pigs, the clinical signs of FMD are indistinguishable from those of vesicular stomatitis ( Vesicular
Stomatitis: Introduction), and in pigs from those of swine vesicular disease ( Swine Vesicular Disease: Introduction) and
vesicular exanthema ( Vesicular Exanthema Of Swine: Introduction).
Treatment and Control:
Many countries free of FMD have a policy of slaughter of all affected and in-contact susceptible animals and strict
restrictions on movement of animals and vehicles around infected premises. After slaughter, the carcasses are either burned
or buried on or close to the premises, and the buildings are thoroughly washed and disinfected with mild acid or alkali and
by fumigation. Tracing is carried out to identify the source of the outbreak and premises to which FMD virus could have
already been transmitted by infected animals or animal products, contaminated vehicles or people, or aerosol. In areas or
countries free of FMD in which this is not possible, control is by movement restriction, quarantine of affected premises, and
vaccination around (and possibly within) the affected premises. This has the disadvantage that many carrier animals may
remain after the outbreak, and quarantine may not be sufficiently long to prevent their subsequent movement. FMD in the
Cryptococcosis
This systemic fungal disease may affect the respiratory tract, CNS, eyes, and skin (particularly of the face and neck of
cats). The fungus is found in soil and fowl manure, especially in pigeon droppings. Transmission is by inhalation of spores
or contamination of wounds. Cryptococcosis is most common in dogs and cats but also occurs in cattle, horses, sheep, goats,
birds, and wild animals.
Clinical Findings and Lesions:
Bovine cryptococcosis has been associated only with cases of mastitis, and many cows in a herd may be infected.
Affected cows have anorexia, decreased milk flow, swelling and firmness of affected quarters, and enlarged supramammary
lymph nodes. The milk becomes viscid, mucoid, and gray-white, or it may be watery with flakes.
In cats, upper respiratory signs are most common and include sneezing; mucopurulent, serous, or hemorrhagic
unilateral or bilateral chronic nasal discharge; polyp-like mass(es) in the nostril; and a firm, subcutaneous swelling over the
bridge of the nose. Cutaneous lesions are also common and are characterized by papules and nodules that are fluctuant to
firm. Larger lesions tend to ulcerate, leaving a raw surface with a serous exudate. Neurologic signs associated with
cryptococcosis of the CNS may include depression, changes in temperament, seizures, circling, paresis, and blindness.
Ocular abnormalities may also occur, including dilated unresponsive pupils and blindness due to exudative retinal
detachment, granulomatous chorioretinitis, panophthalmitis, and optic neuritis.
In contrast to cats, dogs tend to have severe disseminated disease, and most have CNS or ocular involvement. Clinical
signs are usually related to meningoencephalitis, optic neuritis, and granulomatous chorioretinitis. Few dogs have been
reported with lesions in the nasal cavity. About 50% of dogs have lesions in the respiratory tract, usually the lungs, and
most have granulomas throughout the body.
The lesion is usually composed of aggregates of encapsulated organisms within a connective tissue reticulum. The
cellular response is primarily macrophages and giant cells with a few plasma cells and lymphocytes. Epithelioid giant cells
and areas of caseation necrosis are less common than with the other systemic mycoses.
Diagnosis:
The most rapid method of diagnosis is cytologic evaluation of nasal exudate, skin exudate, CSF, or samples obtained by
paracentesis of the aqueous or vitreous chambers of the eye or by impression smears of nasal or cutaneous masses. Gram's
stain is most useful; the organism retains the crystal violet while the capsule stains lightly red with safranin.
The capsule does not stain. The best stain for Cryptococcus is Mayer's mucicarmine because of its ability to stain the
capsule. Immunofluorescent staining can also be used. The large capsule and thin cell wall of Cryptococcus differentiate it
from Blastomyces.
Treatment:
Amphotericin has been used to successfully treat dogs and cats. Flucytosine can be used alone or in combination with
amphotericin. However, when flucytosine is used alone, drug resistance may develop, so combination therapy with
amphotericin is recommended. Treatment with orally administered ketoconazole, itraconazole, or fluconazole has become
more popular than amphotericin B and flucytosine. Ketoconazole has been used to successfully treat cats with
cryptococcosis. Ketoconazole has been used less commonly to treat infected dogs, and the response has not been as
consistent as in cats.
Leptospirosis: Introduction
Infections may be asymptomatic or cause various signs, including fever, icterus, hemoglobinuria, renal failure,
infertility, abortion, and death. After acute infection, leptospires frequently localize in the kidneys or reproductive organs
and are shed in the urine, sometimes in large numbers for months or years. Because the organisms survive in surface waters
for extended periods, the disease is often waterborne.
Infection is commonly acquired by contact of skin or mucous membrane with urine and, to a lesser extent, by intake of
urine-contaminated feed or water. If shedder animals are introduced into a herd previously free of the disease, leptospires
are rapidly disseminated. Abortions and stillbirths may occur, most frequently during the middle or last third of gestation.
The microscopic agglutination test (MAT) is the most commonly used serologic test for diagnosis of leptospirosis. It
measures both IgM and IgG antibodies; IgM antibodies usually appear 6-12 days after infection, and IgG after 2-3 wk.
MAT titers rise rapidly, then generally decline over several months to moderate levels that may persist for weeks to years.
Demonstration of leptospires in urine or tissues is helpful in diagnosis.
Leptospirosis in Sheep
Prevalence of leptospirosis in sheep is lower than that in cattle, possibly due to less intensive husbandry methods and
the tendency of sheep to avoid contact with surface water.
Leptospirosis in Pigs
Although pomona was the serovar most commonly found in pigs, recent serologic surveys indicate bratislava is the
most widespread.
Abortions occurring 2-4 wk before term are the most common manifestation of leptospirosis in pigs. Piglets produced
at term may be dead or weak and may die soon after birth. Differential diagnoses include brucellosis, parvovirus, and
SMEDI (stillbirth, mummification, embryonic death, and infertility).
Leptospirosis in Dogs
The most common serovars infecting dogs were reported to be canicola and icterohaemorrhagiae in older studies
Clinical Findings:
The incubation period is 4-12 days. Nonspecific signs such as fever, depression, anorexia, and generalized pain may be
seen during this time. Vasculitis, thrombocytopenia, and a coagulopathy may develop. Within a few days, additional signs
of uremia, such as dehydration, vomiting, and oral ulceration, are seen.
Hematologic abnormalities include leukocytosis, lymphopenia, monocytosis, and thrombocytopenia. Serum chemistry
may reveal azotemia and electrolyte disturbances secondary to the renal failure, including hyponatremia, hypochloremia,
and hyperphosphatemia. Serum levels of hepatic enzymes (AST, ALT, alkaline phosphatase) and serum bilirubin increase if
the liver is affected. Urine sediment usually contains RBC, WBC, and granular casts. Isosthenuria, proteinuria, and
glucosuria reflect tubular damage.
Lesions:
In acute disease, the kidneys or liver, or both, are swollen. Hemorrhages may be present in any organ.
Diagnosis:
In cattle, the course is less acute, and the recovery rate approaches 50%. Lesions are localized in the brain stem, and
the signs indicate dysfunction of the third to seventh cranial nerves.
Initially, affected animals are anorectic, depressed, and disoriented. They may propel themselves into corners, lean
against stationary objects, or circle toward the affected side. Facial paralysis with a drooping ear, deviated muzzle, flaccid
lip, and lowered eyelid often develops on the affected side, as well as lack of a menace response and profuse, almost
continuous, salivation; food material often becomes impacted in the cheek.
Listeriosis is relatively uncommon in pigs.
Neosporosis: Introduction
Neosporosis has been recognized in dogs, cattle, sheep, goats, deer, horses, and experimentally rodents and cats.
Etiology:
Neospora caninum is an obligate intracellular protozoan parasite that has been confused previously with Toxoplasma
gondii . Only asexual stages are known, and they resemble T gondii . The complete life cycle of N caninum is unknown, but
it can be transmitted transplacentally in dogs, cattle, goats, sheep, and cats, and subsequent offspring may be affected.
Tachyzoites are 5-7 × 1-5 µm, depending on the stage of division. They divide by endodyogeny. Tachyzoites are found in
myocytes, neural cells, dermal cells, macrophages, and other cells. Tissue cysts up to 100 µm in diameter are found in
neural cells; the cyst wall is amorphous and up to 4 µm thick. Cysts have no septa and enclose slender 7 × 1.5 µm
bradyzoites.
Clinical Findings and Lesions:
In dogs, both pups and older dogs are affected. Not all littermates are affected. Most severe infections are in young
pups, which typically develop an ascending paralysis of the limbs, particularly the hindlimbs. The paralysis is often
progressive and results in rigid contracture of the muscles of affected limbs. In some dogs, only neural signs are seen. The
syndrome of polyradiculoneuromyositis appears typical of neosporosis. Ulcerative dermatitis, hepatitis, pneumonia, and
encephalitis may also occur.
In dairy cattle, N caninum is a major cause of abortion in many countries, particularly in the USA. Calves may be
aborted, stillborn, born underweight, weak, or paralyzed, or they may become paralyzed within 4 wk of birth.
Nonsuppurative encephalitis is the main lesion in aborted fetal tissues. Abortion can occur throughout gestation, and some
cows may abort again; dams of these calves are clinically normal.
Diagnosis:
An immunoperoxidase test using specific antibodies can identify N caninum in tissue sections or biopsy specimens. An
indirect fluorescent antibody test can be used to detect antibodies.
Treatment and Control:
Drugs used to treat toxoplasmosis (sulfadiazine, daraprim, clindamycin) show some success in treating neosporosis.
Until the definitive host and the sources of infections are identified, control is not possible. There is no vaccine.
Toxoplasmosis: Introduction
Toxoplasma gondii is a protozoan parasite that infects most species of warm-blooded animals, including birds and man,
throughout the world.
Etiology and Pathogenesis:
Members of the cat family are the only known definitive hosts for T gondii and, therefore, serve as the main reservoir.
Three infective stages of T gondii have been identified: tachyzoites (the rapidly multiplying form), bradyzoites (tissue cyst
form), and sporozoites (within oocysts).
In unexposed cats after ingestion of uncooked meat containing tissue cysts, T gondii initiates enteroepithelial
replication. Bradyzoites are released from tissue cysts by digestion in the stomach and small intestine, invade intestinal
epithelium, and undergo sexual replication, culminating in the release of oocysts (10 µm diameter) in the feces. Oocysts are
first seen in the feces at 3 days after infection and may be released for up to 20 days after infection. After exposure to air for
24 hr, oocysts sporulate, become infective, and may persist in the environment for up to 1 yr. Cats generally develop
immunity to T gondii after the initial infection and, therefore, only shed oocysts once in their lifetime.
In all warm-blooded animals, after ingestion of uncooked meat containing tissue cysts (carnivores) or feed
contaminated with cat feces containing oocysts (herbivores), T gondii initiates extraintestinal replication. Bradyzoites and
sporozoites, respectively, are released and infect intestinal epithelium. After several rounds of epithelial replication,
tachyzoites emerge and disseminate via the bloodstream and lymph. Tachyzoites infect tissues throughout the body and
replicate intracellularly until the cells burst, causing tissue necrosis. Tachyzoites measure 4-8 × 2-4 µm in diameter and
stain with Giemsa. Young and immunocompromised animals may succumb to generalized toxoplasmosis at this stage.
Older animals mount a powerful cell-mediated immune response to the tachyzoites (mediated by cytokines) and control the
infection, driving the tachyzoites into the tissue cyst or bradyzoite stage. Tissue cysts are usually seen in neurons and in
cardiac and skeletal muscle. Individual cysts are 50-150 µm in diameter and consist of an argyrophilic wall enclosing
hundreds of sporozoites that stain well with periodic acid-Schiff stain. Tissue cysts remain viable in the host for many years.
Tuberculosis: Introduction
Tuberculosis (TB) is an infectious, granulomatous disease caused by acid-fast bacilli of the genus Mycobacterium .
Etiology:
Three main types of tubercle bacilli are recognized: human, bovine, and avian, respectively, M tuberculosis , M bovis ,
and M avium complex ( M avium-intracellulare-scrofulaceum ). The three types differ in cultural characteristics and
pathogenicity. The two mammalian types are more closely related to each other than to the avian type.
All three types may produce infection in host species other than their own. Mycobacterium tuberculosis is most
specific; it rarely produces progressive disease in the lower animals other than nonhuman primates and occasionally in dogs,
pigs, and birds. Mycobacterium bovis can cause progressive disease in most warm-blooded vertebrates, including man.
Mycobacterium avium complex is the only species of consequence in birds, but it is also pathogenic for pigs, cattle, sheep,
deer, mink, dogs, cats, and some cold-blooded animals.
Pathogenesis:
Inhalation of infected droplets expelled from infected lungs is the usual route of infection, although ingestion,
particularly via contaminated milk, also occurs. Intrauterine and coital methods of infection are recognized less commonly.
Inhaled bacilli are phagocytosed by alveolar macrophages that may either clear the infection or allow the mycobacteria to
proliferate. In the latter instance, a primary focus may form, provoked by cytokines associated with a hypersensitivity
reaction that consists of dead and degenerate macrophages surrounded by epithelioid cells, granulocytes, lymphocytes, and
later, giant cells. The purulent to caseous, necrotic center may calcify, and the lesion may become surrounded by
granulation tissue and a fibrous capsule to form the classic “tubercle.” The primary focus plus similar lesions formed in the
regional lymph node is known as the “primary complex.” In alimentary forms of disease, the primary focus may be found in
the pharynx or mesenteric lymph node or, less commonly, in the tonsil or intestine.
The primary complex seldom heals in animals and may progress slowly or rapidly. Dissemination through vascular and
lymphatic channels may be generalized and rapidly fatal, as in acute miliary TB. Nodular lesions may form in many organs,
The delayed-type hypersensitivity response of the host, responsible for much of the pathology of TB, is fundamental to
the tuberculin skin test that is widely used for diagnosis in large animals. The single intradermal (SID) test involves
inoculation of mycobacterial antigen prepared from a filtrate of cultures of either M bovis or M tuberculosis . Purified
protein derivative (PPD) preparations of the mycobacteria improve specificity.
In a reactor, the antigen stimulates a local infiltrate of inflammatory cells and causes skin swelling that can be detected
by palpation and measured by calipers. The reaction is read between 48 and 72 hr for maximum sensitivity and at 96 hr for
maximum specificity. Test sites used vary in sensitivity and between countries and include the neck region, anal or caudal
fold at the tail base, and vulval lip.
Control:
The main reservoirs of infection are man and cattle;
The three principal approaches to the control of TB are test and slaughter, test and segregation, and chemotherapy. The
test and slaughter policy is the only one assured of eradicating TB and relies on the slaughter of reactors to the tuberculin
test. In an affected herd, testing every 3 mo is recommended to rid the herd of individuals that can disseminate infection.
Test and slaughter used only in the final stages of eradication.
Treatment of cases of TB has been attempted using drugs that have had some success in man, eg, isoniazid,
streptomycin, and para-aminosalicylic acid. Efficacy is limited, and there are overriding arguments against therapy, based
on the removal of infected animals, zoonotic risks, and the danger of encouraging drug resistance. Treatment is therefore not
advisable and is illegal in some countries. The BCG (bacille Calmette-Guérin) vaccine, sometimes used to control TB in
man, has proved to be poor at protecting most animal species, and inoculation often provokes a severe local granulomatous
reaction.
it tends to become an inapparent infection but occasionally results in death. In horses with active disease, the PCV and
platelet count are decreased and monocytes are increased. In chronic infections, blood may contain WBC with stainable iron
and have increased gamma globulin.
Lesions:
In acute cases, the spleen and splenic lymph nodes are enlarged.
Microscopically, there is proliferation of reticuloendothelial cells in many organs, and periportal and perisinusoidal
collections of round cells in the liver with accumulations of hemosiderin in Kupffer's cells.
Diagnosis:
Clinical diagnosis should be confirmed by the immunodiffusion or Coggins test, a simple and highly accurate serologic
test to detect infection. EIA should be suspected if a horse has a history of weight loss accompanied by periodic fever, or if
several horses in a group develop similar signs after introduction of new animals into a herd or death of a horse on pasture.
Treatment and Control:
No specific treatment or vaccine is available. General supportive therapy may help in an individual case, but an infected
horse, especially one exhibiting clinical signs, should be considered a likely source of infection for other horses. Whenever
a diagnosis is established, the infected horse should be promptly isolated from other horses and maintained in isolation if it
is not to be euthanized. Because the horse fly is an important vector, stabling during the fly season helps to prevent spread
of infection.
Bluetongue: Introduction
Etiology and Transmission:
Bluetongue virus is the prototype virus of the genus Orbivirus , family Reoviridae. The distribution of the disease is
limited by the culicoid insect vector that serves as the principal means of transmission between ruminant species. The
viruses are biologically transmitted between ruminants by the biting midge Culicoides variipennis sonorensis , in the USA.
Cattle develop prolonged viremias lasting for as long as 70-90 days. The viruses have an affinity for RBC and survive in the
infected cattle until the cells are catabolized. Thus, cattle serve as reservoirs for the virus. Semen that contains RBC or
WBC infected with bluetongue virus may infect susceptible cattle.
Clinical Findings:
The usual incubation period in sheep is 5-10 days. In chronological sequence of appearance, clinical signs include
dyspnea with panting; hyperemia of the lips, muzzle, and ears; pyrexia (reaching 107.5°F [42°C]); depression; and
inflammation, erosions, and ulceration of the oral mucous membranes, particularly the dental pad. Other signs include
swollen cyanotic tongue, lameness due to coronitis and widespread muscle necrosis, torticollis, vomiting, pneumonia,
conjunctivitis, and alopecia. Cattle more commonly have inapparent infections. The rare clinical case in cattle is
characterized by vesicular and ulcerative lesions in the oral cavity, hyperesthesia, and a vesicular and ulcerative dermatitis.
These lesions are mediated by an IgE hypersensitivity reaction. The malformations include hydranencephaly or
porencephaly, which results in ataxia and blindness at birth.
Diagnosis:
Clinical signs are presumptive, and confirmation is based on identification of virus by isolation in embryonated chicken
eggs, susceptible sheep, or cell cultures, or by polymerase chain reaction (PCR) technology.
Bluetongue viremia is associated with RBC, and the virus can coexist with high neutralizing antibody titers.
Affected sheep have increased CK levels, which often appear before signs of stiffness and are associated with muscle
necrosis. On necropsy, lesions include mucosal erosions and ulceration, coronitis, hemorrhage in the pulmonary aorta, and
necrosis of the striated muscles.
Prevention and Control:
Vaccines are widely used only in southern Africa. The modified live virus vaccines should not be used during the
vector seasons because the culicoid vectors may pick up the vaccine virus and transmit it to other animals. There is
mounting evidence that vaccine viruses may reassort with field strains, giving rise to new virus strains. Pregnant ewes
should not be vaccinated during the first 100 days of gestation; otherwise, fetal malformations may occur. Passive immunity
in lambs may last 4-6 mo. Control of vectors by using ear tags with insecticides, controlling water levels by raising or
lowering the levels in lagoons every week, or moving animals into barns during the evening hours tends to lower the risk of
culicoid exposure and subsequent bluetongue infection.
Enzootic leukosis is a disease of mature cattle, and most cases occur in animals that are 4-8 yr old. The tissues most
commonly affected include lymph nodes, abomasum, heart, spleen, kidneys, uterus, spinal meninges, and retrobulbar
lymphatic tissue.
Diagnosis:
A presumptive diagnosis of leukosis can be made if there is clinical evidence of lymphadenopathy or tumor in a
commonly affected tissue. Sometimes, leukemia can be demonstrated in the calf form, but thymic and skin cases are usually
aleukemic. The serological test is not appropriate for calf, thymic, and skin leukosis, because the sporadic forms are not
caused by BLV.
Control:
There is no treatment for leukosis or for BLV infection in individual animals. Virus can be eliminated from a herd if all
cattle are tested serologically at 2- to 3-mo intervals, and positive animals removed immediately.
Hypertonia and hyperreflexia are also common. Over time, signs progress to paraparesis or tetraparesis and paralysis.
Depression, head tilt, circling, opisthotonos, torticollis, and paddling have also been seen in affected goats. The “hard
udder” syndrome attributed to CAE virus infection is characterized by a firm, swollen mammary gland and agalactia at the
time of parturition. Milk quality is usually unaffected.
Lesions:
Pathologic lesions of CAE virus infection are generally described as lymhoproliferative with degenerative mononuclear
cell infiltration. Lesions in joints are characterized by thickening of the joint capsule and marked proliferation of synovial
Systemic Pasteurellosis
The systemic form of pasteurellosis is caused by P haemolytica biotype T. Systemic pasteurellosis results when the
organism moves from the tonsils to the lungs and passes into the blood. This results in septicemia or localization of the
infection in one or more tissue such as the joints, udder, meninges, or lungs. Systemic pasteurellosis is most common in
young, weaned sheep (~6 mo old) during the late fall and winter after transport or a sudden feed change, but it can occur in
sheep of any age throughout the year. Sheep with septicemia often die quickly without premonitory signs. In some animals,
The oculonasal discharge becomes mucopurulent, and the muzzle becomes dry and cracked. Diarrhea, the final clinical
sign, may be watery and contain blood, mucus, and mucous membrane. Animals show severe abdominal pain, thirst, and
dyspnea and may die from dehydration. Convalescence is prolonged and may be complicated by concurrent infections due
to immunosuppression.
Lesions:
Gross pathological changes are evident throughout the GI and upper respiratory tracts, either as areas of necrosis and
erosion, or congestion and hemorrhage, the latter causing classical “zebra-striping” in the rectum. Lymph nodes may be
enlarged and edematous, with white necrotic foci in the Peyer's patches. Histological examination reveals lymphoid and
epithelial necrosis with viral syncytia and intracytoplasmic inclusions.
Diagnosis:
In areas where the disease is uncommon or absent, laboratory tests must be used to differentiate rinderpest from bovine
viral diarrhea in particular, as well as East Coast fever, foot-and-mouth disease, infectious bovine rhinotracheitis, and
malignant catarrhal fever. ELISA, for detecting viral antigens or serum antibodies, is also a valuable diagnostic test.
Control:
Treatment usually is not attempted, but supportive nursing care with fluid and antibiotics may aid recovery of valuable
animals. Active immunity is usually lifelong; maternal immunity lasts 6-11 mo. Control in endemic areas is by
immunization of all cattle and domestic buffalo >1 yr old with attenuated cell culture vaccine.
Feline Leukemia Virus And Related Diseases: Introduction (Feline lymphoma and leukemia, Lymphosarcoma)
Canine Ehrlichiosis
The classical disease is an acute to chronic disease that is caused by infection of mononuclear cells by Ehrlichia canis
and is transmitted by the brown dog tick, Rhipicephalus sanguineus . Ehrlichia platys is the cause of infectious cyclic
thrombocytopenia and infects only platelets; it results in minimal if any hemorrhagic tendencies in dogs. The discussion
below primarily describes infection in dogs caused by E canis .
Etiology:
The causative agent is seen rarely, appearing as colonies of coccoid bodies in the cytoplasm of usually monocytes. The
brown dog tick ( Rhipicephalus sanguineus ) is the primary vector and reservoir and may transmit the disease for up to 5 mo
after engorgement. Blood transfusions, or other means by which infected WBC are transferred, also transmit the disease.
Clinical Findings:
Signs arise from the involvement of the hemic and lymphoreticular systems and commonly progress from acute to
chronic, depending on the strain of organism and immune status of the host. In acute cases, there is reticuloendothelial
hyperplasia, fever, generalized lymphadenopathy, splenomegaly, and thrombocytopenia. Variable signs of anorexia,
depression, loss of stamina, stiffness and reluctance to walk, edema of the limbs or scrotum, and coughing or dyspnea may
occur. Most acute cases occur in the warmer months, coincident with the greatest activity of the tick vector.
In the acute phases, the hemogram is usually normal but may reflect a mild normocytic, normochromic anemia;
leukopenia; or mild leukocytosis. Thrombocytopenia is common, but petechiae may not be evident, and platelets may not be
obviously decreased on a blood smear. Vasculitis and immune-mediated mechanisms induce a thrombocytopenia and
hemorrhagic tendencies. Lymph node aspiration reveals hyperplasia.
Allergic asthma is less common in other animals than in man. Among animals, it is most frequent in cats, in which
the signs are similar to those in man. It occurs more frequently in summer and after going outdoors; individual attacks can
be transient and mild, or protracted and severe (status asthmaticus). Mild attacks may manifest as wheezing and coughing;
in severe attacks, there may be expiratory dyspnea, hyperinflation of the lungs, aerophagia, cyanosis, and frantic attempts to
obtain air.
Intestinal allergies (food allergies) are principally seen in dogs and cats, particularly kittens. Allergic gastritis is
manifest by vomiting, which occurs 1 to >12 times weekly, within 1-2 hr of eating. The vomitus may be tinged with bile. In
cats, vomiting may be the sole sign; dogs may also have loose feces intermittently. Skin lesions and poor coat are
commonly associated with food allergies in cats but less commonly in dogs. Food allergy may be a cause of diarrhea in
newly weaned piglets, although the supporting evidence is not clear; the diarrhea is usually treated as an infection rather
Because the epidermis of animals is relatively thin (compared with human skin), the bullae rupture rapidly and form
erosions; consequently, characteristic bullae are seldom seen. The bullae occur as a result of suprabasilar acantholysis.
Secondary bacterial infection often complicates the lesions, and if untreated, the disorder is often fatal. It is treated with
high doses of glucocorticoids alone or in combination with other drugs such as cyclophosphamide, azathioprine, or gold
salts. The disease is difficult to maintain in remission, and the long-term prognosis is fair to poor.
Pemphigus foliaceus is more common in dogs than in cats and horses but is still an uncommon disease. It is
characterized clinically by erosions, ulcerations, and thick encrustations of the skin and mucocutaneous junctions.
The absence of lesions in the mouth, and the widespread thick, crusty nature of the skin lesions, tend to differentiate
pemphigus foliaceus from pemphigus vulgaris. As in pemphigus vulgaris, autoantibodies are present in the skin and react
with intracellular cement substance. These autoantibodies cause a separation of the cornified from uncornified cell layers.
High doses of glucocorticoids are used initially, but low-dose, alternate-day therapy is used once the disease is under
control. More potent immunosuppressive drugs such as cyclophosphamide or azathioprine are used with glucocorticoids in
cases unresponsive to steroids. Gold salts, in conjunction with low doses of glucocorticoids, are sometimes helpful in
maintaining remission in animals in which steroids alone are ineffective. Animals that respond poorly to initial therapy, or
require high dosages of drugs to control lesions, have a poor long-term prognosis.
Bullous pemphigoid has been recognized in dogs, most often in Collies and Doberman Pinschers. Lesions are often
widespread but tend to be concentrated in the groin. The involved skin resembles a severe scald. Bullae also may be seen;
they are subepidermal and may be full of eosinophils.
Anterior uveitis ( Anterior Uvea) often involves immune-complex-mediated reactions; it frequently occurs in the
recovery stage of infectious canine hepatitis ( Infectious Canine Hepatitis: Introduction) due to the reaction of serum
antibodies with uveal endothelial cells that contain canine adenovirus 1. Similarly, equine uveitis ( Equine Uveitis:
Introduction) or anterior uveitis of horses may be associated with immunologic reactions to Leptospira or Onchocerca spp .
Uveitis caused by Toxoplasma and feline infectious peritonitis virus infections of cats also has an immunologic basis.
Deficiencies in phagocytosis often manifest as an increased susceptibility to bacterial infections of the skin,
respiratory system, and GI tract. These infections respond poorly to antibiotics.
Selective Immunodeficiencies
Rottweiler puppies have a breed predilection for severe and often fatal canine parvovirus infections.
Persian cats have a predilection toward severe, and sometimes protracted, dermatophyte infections. In some Persian
cats, the fungal infections invade the dermis and cause granulomatous disease (mycetomas).
Mink with the Aleutian coat color mutation are susceptible to chronic parvovirus infection and develop a disorder
called Aleutian mink disease. Other strains of mink are susceptible to infection with this virus but do not develop clinical
disease.
Long-nosed breeds, in particular German Shepherd Dogs and shepherd-crosses, are prone to develop focal
aspergillosis in the nasal passages. Systemic aspergillosis is seen almost exclusively in German Shepherd Dogs, and more
commonly in Western Australia than elsewhere. It is characterized by fungal pyelonephritis, osteomyelitis, and
diskospondylitis.
Viral-induced Immunodeficiencies
Canine distemper virus causes a profound combined immunodeficiency in affected puppies. The infection is
associated with a progressive decline in levels of antibody globulin and increased susceptibility to agents normally
contained by cellular immunity, eg, Toxoplasma , Nocardia .
Parvoviral infection in both dogs and cats causes a profound and transient depression in the number of neutrophils and
in lymphocyte responsiveness.
Feline leukemia virus (FeLV) infection is associated with acquired immunodeficiency and increased incidence of
secondary and opportunistic infections. Acquired immunodeficiency in FeLV infection is multifactorial and broad in nature.
Infected cats can have deficiencies of neutrophils, decreased synthesis of antibodies (especially to bacterial antigens),
decreased cellular immunity, and variable levels of complement. Immune responses to FeLV infection also appear to inhibit
ongoing feline infectious peritonitis (FIP) virus immunity specifically, which leads to reactivation of quiescent FIP.
Simian immunodeficiency virus (SIV) is a lentivirus with considerable genetic homology to human
immunodeficiency virus (HIV), the cause of AIDS in man.
Transmission between infected and noninfected monkeys is probably by bites and in utero exposure. SIV is not
present in native populations of Asian primates. The immunosuppression associated with SIV can last for weeks or years.
Encephalitis (usually asymptomatic except for wasting) and lymphomas are frequent sequelae of SIV infection in macaques.
Infected animals, whether healthy or diseased, carry the infection for life. Because the infection is lifelong, the presence of
serum antibodies to SIV indicates the presence of virus in the body.
Feline immunodeficiency virus (FIV, originally feline T-lymphotropic lentivirus) is a related lentivirus that has been
identified in domestic cats and cheetahs. The virus is shed mainly in the saliva, and the principal mode of transmission is
through bites. Free-roaming (feral and pet), male, and aged cats are at the greatest risk of infection. After infection, there is
a transient period of fever, lymphadenopathy, and neutropenia. Cats with acquired immunodeficiency induced by FIV suffer
from chronic secondary and opportunistic infections of the respiratory, GI (including mouth), and urinary tracts, as well as
the skin. FIV-infected cats have a higher than expected incidence of FeLV-negative lymphomas, usually of the B-cell type,
and myeloproliferative disorders (neoplasias and dysplasias). Cats remain infected for life; the presence of serum antibodies
is directly correlated with the ability to isolate virus from blood cells and saliva.
Dermis:
Except in horses, apocrine glands do not appear to be innervated.
Appendageal System:
The hair follicles of dogs, cats, sheep, and goats are compound, ie, the follicles have a central hair surrounded by 3-15
smaller hairs all existing from a common pore. The hair follicles of horses and cattle are simple, ie, the follicles have one
hair emerging from each pore. Animals with compound hair follicles are born with simple hair follicles that develop into
compound hair follicles.
The growing stage of the hair is referred to as anagen and the resting stage (mature hair) is referred to as telogen. The
transitional stage between anagen and telogen is catagen. Animals normally shed their hair coat in response to changes in
temperature and photoperiod; most animals undergo a shed in the early spring and early fall. Hormones have a significant
effect on hair growth. Thyroxine initiates hair growth, and glucocorticoids inhibit hair growth. The effect of sex hormones
on hair growth is not well understood; the primary function of sex hormones is not to produce hair.
Sebum is a complex lipid material containing cholesterol, cholesterol esters, triglycerides, diester waxes, and fatty
acids. Sebum is important for keeping the skin soft and pliable and for maintaining proper hydration. Sebum gives the hair
coat a sheen and has antimicrobial properties.
There is some clinical evidence to suggest that limited sweating occurs in dogs and cats, and that it may have a minor
role in cooling of the body. Dogs and cats thermoregulate primarily via panting, drooling, and spreading saliva on their
coats (cats).
Alopecia
(Hair loss)
Alopecia is the partial or complete lack of hairs in areas where they are normally present.
Etiology:
There are many causes of alopecia; any disease that can affect hair follicles can cause hair loss. There are two broad
etiologic categories of alopecia—congenital or hereditary and acquired.
Congenital or hereditary alopecia has been described in cows, horses, dogs, cats, and pigs. Hairless breeds of mice,
rats, cats, and dogs have been bred and developed for personal and research interests. Congenital alopecia may or may not
be hereditary; it is caused by a lack of development of hair follicles and is apparent at or shortly after birth.
Acquired alopecia encompasses all of the other causes of hair loss. In this type of alopecia, the animal is born with a
normal hair coat, has or had normal hair follicles at one time, and is/was capable of producing structurally normal hairs.
Acquired alopecia can develop because the disease destroys the hair follicle or hair shaft, interferes with the growth of hair
or wool, or causes the animal discomfort (eg, pain, pruritus) leading to self-trauma and loss of hair.
Diseases that can directly cause destruction or damage to the hair shaft or follicle include bacterial skin diseases,
dermatophytosis, demodicosis, severe inflammatory diseases of the dermis (eg, juvenile cellulitis, deep pyoderma),
traumatic episodes (eg, burns, radiation), and (rarely) poisonings caused by mercury, thallium, and iodine.
Diseases that can directly inhibit or slow hair follicle growth include nutritional deficiencies (particularly protein
deficiencies), hypothyroidism, hyperadrenocorticism, and excessive estrogen production or administration
(hyperestrogenism, Sertoli cell tumors, estrogen injections for mismating). Temporary alopecia in horses, sheep, and dogs
can occur during pregnancy, lactation, or several weeks after a severe illness or fever.
Pruritus or pain is a common cause of acquired alopecia in animals. Diseases that commonly cause pruritus or pain
include infectious skin diseases (eg, bacterial pyoderma and dermatophytosis), ectoparasites, allergic skin diseases (eg,
atopy, food allergy, contact, insect hypersensitivity), and less commonly neoplastic skin diseases.
Clinical Findings and Lesions:
Congenital or hereditary hair loss is commonly symmetrical and not accompanied by many inflammatory changes; in
some cases, the areas of hair loss are localized to one region (eg, ear flaps) or to well-demarcated areas.
The clinical signs of acquired hair loss are varied and often influenced by the underlying cause(s); the pattern of hair
loss may be focal, multifocal, symmetrical, generalized, depending on the underlying cause(s). Inflammatory changes such
as hyperpigmentation, lichenification, erythema, and pruritus are common. In endocrine alopecias, the hair loss usually
develops in a symmetrical pattern, often in wear areas first; pruritus is uncommon unless there is a secondary infection. Hair
loss is not generally an early clinical sign of an endocrine alopecia.
Many owners seek veterinary assistance because of perceived excessive shedding. Shedding may be abnormal
(excessive) if it results in obvious loss of the hair coat and areas of alopecia. A common cause of abnormal shedding is
Dermatitis
The most common sign is scratching, followed by skin lesions that progress from edema and erythema to papules,
vesicles, oozing, and crusting or scaling. Secondary infection may occur. As dermatitis becomes chronic, the erythema
decreases and there are fewer papules, but the lesions are drier and the skin may develop fissures.
Chronic dry dermatitis is usually helped by application of a corticosteroid ointment. To remove scales or crusts, a
sulfur and salicylic acid or tar and sulfur shampoo may be used. Tar products are contraindicated in cats.
Unfortunately, topical medications often are licked or rubbed off; systemic therapy with anti-inflammatory doses of
corticosteroids is usually the best alternative.
Restraining devices, such as hobbles or Elizabethan collars, and sedatives should be used only as last resorts in the
therapy of pruritus.
Pruritus
(Itching)
The nature of the mediators of pruritus is controversial but is believed to include both histamines (released from mast
cell degranulation) and proteolytic enzymes (proteases). Proteases are released by fungi, bacteria, and mast cell
degranulation, and during antigen-antibody reactions. Leukotrienes, prostaglandins, and thromboxane A2, which are broken
down from arachidonic acid, are pro-inflammatory. Essential fatty acids, particularly γ-linolenic acid, have been used to
counter the inflammation mediated by leukotrienes and thromboxane A2.
Feline Atopy
Feline atopy is similar to canine atopy, with several important distinctions. Feline atopy is a pruritic disease in which
affected cats have a hypersensitivity reaction to inhaled environmental allergens and positive reactions to intradermal
allergy testing. No studies have compared serologic testing with intradermal allergy testing for feline atopy. Clinical
presentations include miliary dermatitis, feline symmetrical alopecia, eosinophilic granuloma complex (primarily the
eosinophilic plaque), and severe head and neck pruritus. The pruritus and dermatologic lesions may be seasonal or year
round. Response to steroids is excellent in most cases initially; however, efficacy decreases over time in most cases.
Intradermal allergy testing and hyposensitization procedures are similar to those used in dogs, but the testing is more
difficult to read because the reactions to intradermal injections of allergens are less dramatic in cats than in dogs. The
hyposensitization response is similar to that seen in dogs.
Dermatophilosis: Introduction
( Dermatophilus infection, Cutaneous streptothrichosis, Lumpy wool, Strawberry footrot)
The lesions are characterized by exudative dermatitis with scab formation. Dermatophilus congolensis has a wide host
range. Among domestic animals, cattle, sheep, and goats are affected most frequently;
horses occasionally; and pigs, dogs, and cats rarely.
Etiology, Transmission, and Epidemiology:
Dermatophilus congolensis is a gram-positive, non-acid-fast, facultative anaerobic
actinomycete. It is the only species in the genus, but a variety of strains can be present within a group of animals during an
outbreak. It has two characteristic morphologic forms—filamentous hyphae and motile zoospores. The hyphae are
characterized by branching filaments (1-5 µm in diameter) that ultimately fragment by both transverse and longitudinal
septation into packets of coccoid cells. The coccoid cells mature into flagellated ovoid zoospores (0.6-1 µm in diameter).
The natural habitat of D congolensis is unknown. Attempts to isolate it from soil have been unsuccessful, although it
is probably a saprophyte in the soil. It has been isolated only from the integument of various animals and is restricted to the
living layers of the epidermis. Asymptomatic chronically infected animals are considered the primary reservoir.
Epidemics usually occur during the rainy season. Moisture facilitates release of zoospores from preexisting lesions
and their subsequent penetration of the epidermis and establishment of new foci of infection. High humidity also contributes
indirectly to the spread of lesions by allowing increases in the number of biting insects, particularly flies and ticks, that act
as mechanical vectors. Infection can be spread by shearing, dipping, or introducing an infected animal into a herd or flock.
Dermatophilosis is contagious only in that any reduction in systemic or local skin resistance favors establishment of
infection and subsequent disease.
Pathogenesis:
To establish infection, the infective zoospores must reach a skin site where the normal protective barriers are reduced
or deficient. The respiratory efflux of low concentrations of carbon dioxide from the skin attracts the motile zoospores to
susceptible areas on the skin surface. Zoospores germinate to produce hyphae, which penetrate into the living epidermis and
subsequently spread in all directions from the initial focus. Hyphal penetration causes an acute inflammatory reaction.
Natural resistance to the acute infection is due to phagocytosis of the infective zoospores, but once infection is established,
there is little or no immunity. In most acute infections, the filamentous invasion of the epidermis ceases in 2-3 wk, and the
lesions heal spontaneously. In chronic infections, the affected hair follicles and scabs are sites from which intermittent
invasions of noninfected hair follicles and epidermis occur. The invaded epithelium cornifies and separates in the form of a
scab. In wet scabs, moisture enhances the proliferation and release of zoospores from hyphae. The high carbon dioxide
concentration produced by the dense population of zoospores accelerates their escape to the skin surface, thus completing
the unique life cycle.
Clinical Findings:
Dermatophilosis occurs in animals at all ages but is most prevalent in the young. Lesions are not at the same stage of
progression and, in an individual animal, can vary from acute to chronic. Variation also occurs because of age, sex, and
breed. Few animals exhibit pruritus, and most recover spontaneously within 3 wk of the initial infection or during dry
weather. Uncomplicated skin lesions heal without scar formation. These infections usually have little effect on general
health. Animals with severe generalized infections often lose condition, and movement and prehension are difficult if the
feet, lips, and muzzle are severely affected; these animals are often sent to slaughter as incurable. Deaths occasionally
occur, particularly in calves and lambs, because of generalized disease with or without secondary bacterial infection and
secondary fly or screwworm infestation. The primary economic consequences are damaged hides in cattle, wool loss in
sheep, and lameness and loss of performance in horses when severely affected around the pastern area.
Lesions:
Distribution of the gross lesions on cattle, sheep, and horses usually correlates with the predisposing factors that
reduce or permeate the natural barriers of the integument. In cattle, the lesions can be observed in three stages: 1) hairs
matted together as “paintbrush” lesions, 2) crust or scab formation as the initial lesions coalesce, and 3) accumulations of
cutaneous keratinized material forming “wart-like” lesions that are 0.5-2 cm in diameter. Typical lesions consist of circular,
dome-shaped scabs 2-8 mm in diameter. Most lesions associated with prolonged wetting of the skin are distributed over the
head, dorsal surfaces of the neck and body, and upper lateral surfaces of the neck and chest. Cattle that stand for long
Pyoderma: Introduction
Pyoderma is a pyogenic infection of the skin. Pyodermas are common in dogs but uncommon in cats. They are
classified as primary or secondary, superficial or deep. Most skin infections are superficial and secondary to any of a variety
of other conditions, most notably allergies (flea allergy, atopy, food allergy), internal diseases (particularly endocrinopathies
Dermatophytosis: Introduction
(Ringworm)
Dermatophytosis is an infection of keratinized tissue (skin, hair, and claws) by one of the three genera of fungi
collectively called dermatophytes— Epidermophyton , Microsporum , and Trichophyton . (See also fungal infections ,
Fungal Infections: Introduction). In developed countries, the greatest economic and human health
consequences come from dermatophytosis of domestic cats and cattle. The most important animal
pathogens worldwide are M canis , M gypseum , T mentagrophytes , T equinum , T verrucosum , and M
nanum . These species can be spread to and cause ringworm in people, especially M canis infections of domestic
cats and T verrucosum of cattle and lambs.
Under most circumstances, dermatophytes grow only in keratinized tissue, and advancing infection stops on reaching
living cells or inflamed tissue. Infection begins in a growing hair or in the stratum corneum, where threadlike hyphae
develop from the infective arthrospores or fungal hyphal elements. Hyphae can penetrate the hair shaft and weaken it, which
together with follicular inflammation, leads to patchy hair loss. As the infection matures, clusters of arthrospores develop on
the outer surface of infected hair shafts. Broken hairs with associated spores are important sources for spread of the disease.
In young or debilitated animals and, to some extent, in longhaired breeds of domestic cats, infection may be persistent and
widespread.
Dermatophytosis is diagnosed by fungal culture, examination with a Wood's lamp, and direct microscopical
examination of hair or skin scale. Fungal culture is the most accurate means of diagnosis. Dermatophyte test medium
(DTM) may be used in a clinical setting.
The Wood's lamp is useful in screening examinations for M canis infections in cats and dogs. Infected hairs fluoresce
yellow-green; however, only 80% of M canis infections fluoresce, and other fungal species in animals do not. Therefore,
negative Wood's lamp examinations are not meaningful. False-positive examinations may occur and are especially likely in
oily, seborrheic skin conditions. Fluorescing hairs should always be cultured to confirm the diagnosis.
Cutaneous Habronemiasis
(Summer sores, Jack sores, Bursatti)
Cutaneous habronemiasis is a skin disease of Equidae caused in part by the larvae of the spirurid stomach worms
( Habronema spp). When the larvae emerge from flies feeding on preexisting wounds or on moisture of the genitalia or eye,
they migrate into and irritate the tissue, which causes a granulomatous reaction. The lesion becomes chronic, and healing is
protracted. Diagnosis is based on finding nonhealing, reddish brown, greasy skin granulomas that
contain, yellow, calcified material the size of rice grains. Larvae, recognized by spiny knobs on their
tails, can sometimes be demonstrated in scrapings of the lesions. Many different treatments have
been used, most with poor results. Symptomatic treatment, including use of insect repellents, may be of benefit,
and organophosphates applied topically to the abraded surface may kill the larvae. Surgical removal or cauterization of the
excessive granulation tissue may be necessary. Treatment with ivermectin (200 µg/kg) has been effective, and although
Lice: Introduction
(Pediculosis)
Various species of biting or chewing lice (order Mallophaga) and sucking lice (order Anoplura) infest domestic
animals. Sucking lice infest mammals only, but biting lice infest both mammals and birds (see also ectoparasites of poultry,
Bedbugs , Examination for Ectoparasites , Ectoparasites ).
Etiology:
Lice are wingless, flattened insects, usually 2-4 mm long. The claws of the legs are adapted for clinging to hairs and
feathers. Anoplura are blood feeders. The three mouthpart stylets are retracted within the head when not in use. Mallophaga
have ventral chewing mandibles and live on epidermal products; some species feed on blood and exudates when available.
Louse eggs or "nits" are glued to hairs and are pale, translucent, and suboval. Nymphal lice (three stages) are smaller
than adults but otherwise resemble them in habits and appearance. About 3-4 wk are required to complete one generation,
but this varies with species.
Clinical Findings and Diagnosis:
Extreme infestation with sucking lice can cause anemia. Sucking lice cause small wounds that may become infected.
The constant crawling and piercing or biting of the skin causes nervousness in hosts.
Diagnosis should be based on the presence of lice. The hair should be parted, and the skin and proximal portion of the
coat examined with the aid of light if indoors. On small animals, the ova are readily seen. Occasionally, when the coat is
matted, the lice can be seen when the mass is broken apart. Biting lice are active and can be seen moving through the hair.
Sucking lice usually move more slowly and are often found with mouthparts embedded in the skin.
Pediculosis of livestock is most prevalent during the winter; severity is greatly reduced with the approach of summer.
Infestations, particularly of sucking lice, may become severe.
Transmission usually occurs by host contact.
Treatment:
Louse control usually requires treatment with an effective insecticide or drug.
Both dipping and thorough spraying with an insecticide provide excellent coverage of animals, and usually two
treatments 2 wk apart effectively control lice. Dipping consistently provides the most thorough coverage, but the number of
formulations that can be applied by this method is limited. Examples of formulations that may be applied via dipping
include phosmet, which is approved for beef cattle, and coumaphos, which may be applied as a dip to beef cattle,
nonlactating dairy cattle, sheep, and goats.
Many compounds are effective when applied as a whole body spray for lice control. A light, mist application of some
formulations may be effective, while others may require soaking the hair to the skin. As much as 12 L may be required on
large, long-haired cattle.
Zero to very low residue tolerances for pesticides in milk limit the insecticides that may be applied to dairy cattle and
dairy goats. Permethrin spray may be applied to these animals for control of lice. Additionally, dairy cattle may be sprayed
with permethrin synergized with piperonyl butoxide, coumaphos, tetrachlorvinphos plus dichlorvos, and amitraz.
In lactating dairy cattle, the appropriate milk withdrawal time must be observed.
Because of ease of application and reduced stress to the treated animal, the pour-on method has become a popular
means of applying a variety of products. Beef cattle, lactating dairy cattle, sheep, and nonlactating goats may be treated with
pour-on formulations of permethrin for louse control.
The paste formulation of famphur is approved for control of both biting and sucking lice. Ivermectin, injectable and
premix, is effective against the sucking louse of swine.
Dogs can be treated with dips, washes, sprays, or dusts. Effective compounds include permethrin, pyrethrins,
rotenone, methoxychlor, lindane, diazinon, malathion, or coumaphos. Doses of ivermectin high enough to be effective for
lice are not recommended in dogs. On cats, only carbaryl, rotenone, or pyrethrins should be used.
Soft-tissue Sarcomas
This group of malignancies includes equine sarcoids, fibromatoses, fibrosarcomas, malignant fibrous histiocytomas,
neurofibrosarcomas, leiomyosarcomas, rhabdomyosarcomas, and variants of liposarcomas, angiosarcomas, synovial cell
sarcomas, mesotheliomas, and meningiomas. As a group, sarcomas are widely recognized, yet poorly characterized
neoplasms. Consequently, it is widely accepted that the cell of origin of all soft-tissue sarcomas is a primitive mesenchymal
cell that can differentiate in many different directions. This makes it difficult to define histopathologic criteria necessary for
making an unequivocal diagnosis of specific spindle-cell sarcomas. Most spindle-cell sarcomas of domestic animals are
locally infiltrative, difficult to excise, and yet seldom metastasize. Because, by definition, only malignant tumors have
metastatic potential, these tumors should be considered benign; however, again by definition, benign neoplasms are not
infiltrative, and those tumors should be considered malignant. In human pathology, infiltrative but nonmetastasizing
mesenchymal spindle-cell tumors have been defined as “sarcomas of intermediate malignancy,” a concept used below.
Clinically, four general principles relate to spindle-cell sarcomas and soft-tissue sarcomas:
• The more superficial the location, the more likely the tumor is to be benign (deep tumors tend to be malignant).
• The larger the tumor, the more likely it is to be malignant.
• A rapidly growing tumor is more likely to be malignant than one that develops slowly.
• Benign tumors are relatively avascular, whereas most malignancies are hypervascular.
Excision is the treatment of choice; wide excision or amputation should be performed when anatomically feasible
because spindle-cell sarcomas often infiltrate along fascial planes, making it difficult to determine from gross examination
the peripheral margins of the tumor. The best, if not only, opportunity to completely remove a spindle-cell sarcoma is
during the first surgical attempt; those that recur have a greater potential for metastasis, and the time between recurrence
often shortens with each subsequent attempt at excision. In addition, many soft-tissue tumors have a “pseudocapsule,”
which on gross examination gives the impression of complete encapsulation; these tumors should not be “shelled out”
because neoplastic cells are usually present in the pericapsular connective tissues. Except for equine sarcoids, cryosurgery is
usually not used for these tumors because some types, most notably fibrosarcomas, are resistant to freezing. Spindle-cell
sarcomas generally do not respond well to conventional doses of radiation; however, higher doses have been reported to
control ~50% of them for 1 yr. Surgical debulking followed by radiation is also an option for local control. Recently,
Vascular Tumors
Hemangiomas of the skin and soft tissues are benign proliferations that closely resemble blood vessels. Whether
these are neoplasms, hamartomas, or vascular malformations remains undefined, and no clear criteria exist that allow for
their separation. They are most commonly identified in dogs, occasionally in cats and horses, and rarely in cattle and pigs;
they are an exceptional finding in other domestic animals. In dogs, they are tumors of adult dogs and most commonly
develop on the trunk and extremities. Cats most frequently develop hemangiomas when they are adults. Lesions are most
common on the head, extremities, and abdomen. In horses, they are most common on the distal extremities of young (<1 yr
old) animals. In cattle, they may be seen as congenital lesions or in older animals. Hemangiomas are single to multiple,
circumscribed, often compressible, red to black nodules. The lining epidermis may be unaffected or ulcerated or papillated.
Small, superficial hemangiomas that often appear as a “blood blister” are known as angiokeratomas. When erythrocytes are
sparse or absent within vascular lumens, the term lymphangioma is applied. Hemangiomas are benign, but their tendency to
Seborrhea: Introduction
Seborrhea is usually a chronic disease of dogs that is characterized by a defect in keratinization. Clinically, it results in
increased scale formation, occasionally excessive greasiness of the skin and hair coat, and sometimes by secondary
inflammation.
Etiology, Clinical Findings, and Diagnosis:
Primary seborrhea is an inherited skin disorder characterized by faulty keratinization of the epidermis, hair follicle
epithelium, hair follicle cuticle, or the claw. The disease begins at a young age (usually <18-24 mo) and progresses
Metabolic diseases are either inherited or acquired and acquired ones are more important. These diseases are of
clinical significance because they affect energy production or damage tissues important for survival of the animal.
Prevention of Fatigue
Training:
Physical training is the most effective way of reducing fatigue and increasing the ability to exercise. There are many
physiological responses to training, including increases in the maximal rate of oxygen transport, stroke volume, capillary
density in muscle, blood volume, and total Hgb content of blood. Hypertrophy of muscle cells occurs, along with increases
in concentrations of mitochondria, glycogen, and enzymes concerned with energy production. Sprint training can result in
decreased proportions of slow-twitch fibers, and endurance training can result in increased oxidative capacity of fast-twitch
fibers. Training also increases the strength of supportive tissues (such as ligaments, tendons, and bones) and decreases the
likelihood of muscle soreness in response to exercise. Training therefore results in functional and structural adaptations that
enable an animal to run faster or longer.
Nutrition:
Energy supply and hydration are frequently manipulated in human athletes to limit fatigue during endurance exercise.
Dehydration before exercise results in higher core temperatures during exercise in horses. It would be inappropriate for an
animal to begin endurance exercise with suboptimal hydration or glycogen concentrations in liver and muscle. Whether or
not hyperhydration before exercise or carbohydrate “loading” has a role in endurance exercise in animals is unknown.
Horses are more susceptible to hyperthermia during prolonged exercise because of their high body mass to surface area
ratio.
Glucose supplementation may be important in limiting fatigue in endurance exercise in horses. This may be due to
increased glucose availability, reduced reliance on anaerobic energy production, lower core temperature, and better
maintenance of plasma volume.
Horses should not be given large meals 1-2 hr before competition because plasma volume is decreased for at least 1 hr
after a large meal. Feeding small portions every 4 hr does not affect plasma volume.
The use of fat as a dietary supplement in horses has been suggested to increase performance.
Carnitine supplements have been used in the expectation of faster rates of fat metabolism in muscle.
Buffering agents, such as sodium bicarbonate, have been popular as ergogenic aids, especially in horse racing.
Exhaustion
Horses that have competed in 3-day events or endurance rides may present with life-threatening exhaustion. Horses
may lose sweat at 10-15 L/hr during prolonged exercise, and urgent treatment of fluid and electrolyte deficits and
hyperthermia (rectal temperatures >40.5° C) may be required.
Isotonic balanced electrolyte solutions can be administered PO and IV for dehydration. Initially, 8 L can be given PO,
followed by subsequent administration of 4-8 L every 1-2 hr. Hypertonic, hypotonic, or alkaline solutions should not be
used. About 30 L of Ringer's solution is required to replace a sodium deficit of 4000 mmol.
The transmission of a nerve impulse at the neuromuscular junction involves massive release of acetylcholine from
small synaptic vessels, where it is stored. The acetylcholine fills the synaptic cleft between the nerve terminal and the
muscle fiber membrane, where most of it is destroyed by cholinesterase within a fraction of a second. This short period of
activity is sufficient to excite the muscle fiber membrane, which results in a significant increase in membrane permeability
to sodium ions and allows rapid influx of sodium into the muscle fiber. The sodium ion increases the endplate potential,
which elicits electrical currents that spread to the interior of the fibers where they cause a release of calcium ions from the
sarcoplasmic reticulum. The calcium ions initiate, in turn, the chemical events of the contractile process. When this occurs
in all the muscle fibers innervated by each motor neuron (possibly thousands), muscle contraction results.
Disorders that affect the neuromuscular junction (eg, myasthenia gravis, hypocalcemia, hypermagnesemia) can
result in muscle fatigue, weakness, and paralysis. The neuromuscular junction can also be affected by muscle-relaxing drugs
(eg, curare, succinylcholine, M99), certain antibiotics, and toxins (eg, botulism, tetanus, venoms).
Disorders primarily of the muscle membrane and, to some extent, of the actual muscle fibers are called myopathies.
Muscle membrane disorders may be hereditary (eg, myotonia congenita in goats) or acquired (eg, vitamin E and selenium
deficiencies, hypothyroidism, and hypokalemia).
Bone diseases are generally congenital or hereditary, nutritional, or traumatic.
Articulations are divided into synarthroses, in which the osseous components are united by fibrous tissue or
cartilage, and diarthroses, in which the opposing bone ends are covered with hyaline cartilage and are separated by a joint
cavity filled with synovial fluid. Synarthoses are practically immovable and are rarely associated with joint disease other
than fractures. In most cases, diarthroses are movable joints, with a variable degree of mobility depending on the anatomic
location of the joint.
Chronic inflammation of joints and surrounding structures is most common in articulations associated with
locomotion, although other joints, such as the temporomandibular, may occasionally be affected as well. Normal synovial
fluid lubricates the synovial tissues in a joint through boundary lubrication, whereas articular cartilage lubrication is
provided by weeping lubrication, through a glycoprotein expressed from the cartilage during weight bearing.
Arthritis: Overview
Arthritis is a nonspecific term denoting inflammation of a joint. All joint diseases of large animals have an
inflammatory component to varying degrees. Arthritic entities of importance in horses include traumatic arthritis,
osteochondritis dissecans, subchondral cystic lesions, septic (or infective) arthritis, and osteoarthritis (also called
degenerative joint disease).
Traumatic Arthritis
Traumatic arthritis includes traumatic synovitis and capsulitis, intra-articular chip fractures, ligamentous tears
(sprains) involving periarticular and intra-articular ligaments, meniscal tears, and osteoarthritis.
Clinical Findings and Diagnosis:
Traumatic synovitis and capsulitis is inflammation of the synovial membrane and fibrous joint capsule associated
with trauma. Typically, the horse is an athlete and presents with synovial effusion in the acute stage, along with general
thickening and fibrosis in the more chronic stage. Clinical signs of osteochondral fractures are similar to those of synovitis
and capsulitis, as well as those of osteoarthritis; differential diagnosis of these entities is based on radiographs and, in some
cases, arthroscopy.
As a generalization, arthritis results in pain and altered function of the joint. If the process is active or acute, there is
usually synovial effusion, and the surrounding tissues are swollen and warm. In more severe cases, manipulation of the joint
causes pain.
Treatment:
Treatment of acute traumatic synovitis and capsulitis includes rest and physical therapy regimens such as cold water
treatment, ice, passive flexion, and swimming. Nonsteroidal anti-inflammatory drugs (usually phenylbutazone) are used
routinely. In more severe cases, lavage of the joint is done to remove inflammatory products produced by the synovial
membrane, as well as articular cartilage debris that exacerbates the synovitis. Joint drainage alone, without lavage or
injection of medication, provides only short-term relief. Various intra-articular medications have been used. Corticosteroids
are the most potent anti-inflammatory agents and are effective in acute traumatic arthritis. However, there are differences in
the side effects between various corticosteroids and various dosages. Betamethasone products and triamcinolone acetonide
are effective with no deleterious side effects. Methylprednisolone acetate is more potent and longer acting than the other
two drugs but excessive use could lead to degenerative changes in the articular cartilage. Intra-articular sodium hyaluronate
has been used effectively for mild to moderate synovitis but has minimal effect on articular cartilage damage or when intra-
articular fractures are present. Polysulfated glycosaminoglycans (PSGAG) are also used frequently for traumatic arthritis
entities.
Osteochondritis Dissecans
Etiology and Epidemiology:
The most common sites of osteochondritis dissecans (OCD), which usually occurs in young animals, are the
femoropatellar joint, tibiotarsal (tarsocrural) joint, fetlock (metacarpophalangeal and metatarsophalangeal) joints, and the
shoulder. See also Osteochondrosis: Introduction , Osteochondrosis , Osteochondrosis .
Clinical Findings and Diagnosis:
Animals with OCD of the shoulder usually present when <1 yr old with severe forelimb lameness and possibly some
muscular atrophy. Animals with OCD in the other joints usually present with synovial effusion and varying degrees of
lameness. Diagnosis is confirmed with radiographs.
Treatment:
The treatment of OCD depends on the location and degree of involvement.
Septic Arthritis
(Infective arthritis)
Etiology and Epidemiology:
Septic or infective arthritis results from sequestration of bacterial infection in a joint. An infected joint develops in
three main ways: 1) hematogenous infection, which is common in foals, calves, and lambs (commonly referred to as navel
ill); 2) traumatic injury with local introduction of infection; 3) iatrogenic infection associated with joint injection or surgery
(usually in horses). Navel ill is only one example of a hematogenous route of infection, which can also be gained from GI or
pulmonary sources.
Clinical Findings and Diagnosis:
Septic arthritis is usually characterized by severe lameness and distention of the joint with cloudy, turbid synovial
fluid that contains >30,000 WBC/mm3 and a total protein level of >4 g/dL. In foals, hematogenous osteomyelitis often
accompanies septic arthritis. Septic arthritis in foals has been classified into type S (septic joint only), type P
(involving osteomyelitis of the adjacent growth plate as well), or type E (involving osteomyelitis of the epiphyseal
and subchondral bone). Control is best directed toward reducing the possibility of infection from the environment.
Treatment:
Septic arthritis requires prompt treatment to avoid irreparable damage.
Osteoarthritis
(Degenerative joint disease)
Etiology and Epidemiology:
Osteoarthritis represents the end stage of most of the other diseases discussed above if treatment is ineffective or the
initial problem is too severe. The sine qua non of osteoarthritis is progressive degradation of articular cartilage—a
permanent condition.
Clinical Findings and Diagnosis:
Lameness occurs and can be localized with analgesia to the affected joint. There will be varying degrees of synovial
effusion, joint capsule fibrosis, and restricted motion (decreased flexion).
Treatment:
Treatment of osteoarthritis is most commonly palliative and includes the use of nonsteroidal anti-inflammatory
drugs, polysulfated glycosaminoglycans, intra-articular corticosteroids, and IV hyaluronic acid. Physical therapy regimens
are also gaining popularity. In advanced cases, surgical fusion (arthrodesis) may be performed on selected joints.
Chlamydial Polyarthritis-serositis
(Transmissible serositis)
This infectious disease affects sheep, calves, goats, and pigs.
Etiology and Epidemiology:
Tendinitis
(Bowed tendon)
Inflammation of a tendon can be acute or chronic, with varying degrees of tendon fibril disruption. Tendinitis is
most common in horses used at fast work, particularly racehorses. The problem occurs in the flexor tendons and is more
common in the forelimb than in the hindlimb.
Etiology:
Tendinitis usually appears after fast exercise and is associated with overextension and poor conditioning, fatigue,
poor racetrack conditions, and persistent training when inflammatory problems in the tendon already exist. Improper
shoeing may also predispose to tendonitis. Poor conformation and poor training also have been implicated.
Clinical Findings and Diagnosis:
During the acute stage, the horse is severely lame and the involved structures are hot, painful, and swollen. In
chronic cases, there is fibrosis with thickening and adhesions in the peritendinous area. The horse with chronic tendinitis
may go sound while walking or trotting, but lameness may recur under hard work.
Treatment:
Tendinitis is best treated in the early, acute stage. The horse should be stall-rested, and the swelling and
inflammation treated aggressively with cold packs and systemic anti-inflammatory agents. The horse should be brought
back slowly into an exercise regimen to try to minimize the formation of adhesions. Superior check ligament desmotomy
has been used more recently as an adjunctive treatment to minimize recurrence of the problem when the horse is returned to
training.
Splints
(Interosseous desmitis)
Splints primarily involve the interosseous ligament between the large (third) and small (second) metacarpal (less
frequently the metatarsal) bones. The reaction is a periostitis with production of new bone (exostoses) along the involved
splint bone. Trauma from concussion or injury, strain from excess training (especially in the immature horse), faulty
conformation, or improper shoeing may be contributory factors.
Splints most commonly involve the medial rudimentary metacarpal bones. Lameness is seen only when splints are
forming and is seen most frequently in young horses. Lameness is more pronounced after the horse has been worked. In the
Dyschondroplasia
Dyschondroplasia of genetic origin occurs in most breeds of cattle. The forms range from the so-called Dexter
“bulldog” lethal, in which the calf is invariably stillborn, to those animals that are mildly affected.
Dyschondroplasia of the appendicular and axial skeletons also occurs in dogs. The former is reported in Poodles, and
Scottish Terriers, the latter in Alaskan Malamutes, Basset Hounds, Dachshunds, Poodles and Scottish Terriers. In some
breeds (Bassets, Dachshunds, Pekingese), the appendicular dyschondroplastic characters are an important feature of breed
type. In Malamutes, the condition is accompanied by anemia.
Interdigital Dermatitis
(Stable footrot, Slurry heel, Scald)
Interdigital dermatitis is a low-grade infection of the interdigital epidermis that causes a slow erosion of the skin
with discomfort but no lameness unless the lesion becomes complicated. It is seen worldwide but
is most prevalent under poor hygienic conditions in intensive dairy production.
In tied systems, the hindlegs are more often affected than the forelegs. In loose housing
systems, the distribution between fore and hindlegs is about equal. Animals on slatted floors are
affected less often than animals on solid floors.
Etiology and Pathogenesis:
Interdigital dermatitis is caused by a mixed bacterial infection, but Dichelobacter nodosus has been considered to be
the most active component. The disease is most commonly seen when the humidity is high, in temperate climates, and under
poor hygienic conditions, especially in housed dairy cattle. The source of the infection is the cow itself, and the infection
spreads from affected to nonaffected animals through the environment. Dichelobacter nodosus cannot survive >4 days on
the ground but will persist in filth that is caked onto the claws. The bacteria invade the epidermis, but the organisms do not
penetrate to the dermal layers. As the condition progresses, the border between the skin and soft heel horn disintegrates,
producing lesions similar to ulcers or erosions. At this stage, the lesions causes discomfort.
Clinical Findings:
Digital Dermatitis
Digital dermatitis is a highly contagious, erosive and proliferative infection of the epidermis proximal to the
skin/horn junction in the flexor region of the interdigital space.
The condition was first seen in European countries but, in recent years, it has spread across the dairy-
producing areas of the USA. The incidence in beef cattle appears to be minimal. The incidence is highest in loose-
housed herds that are not kept clean. The prevalence is highest in the fall and winter and is lowest if the animals
are pastured.
Etiology and Pathogenesis:
Two main types of lesions occur, one is erosive/reactive, the other is proliferative or wart-like. Both forms cause
varying degrees of discomfort and may give rise to severe lameness. The two forms likely represent different stages of the
disease process. Some of the variation may be due to concurrent interdigital dermatitis (see Interdigital Dermatitis , Ovine
Interdigital Dermatitis).
Deep in the epidermis of erosive/reactive lesions, two types of spirochetes can be demonstrated using Warthin-
Starry stain. It is thought that there is a multifactorial etiology with multiple organisms being involved. Dichelobacter
nodosus is likely to be implicated. Strong circumstantial evidence suggests that a virus plays a part in the pathogenesis of
the disease, but to date, none has been isolated.
Clinical Findings:
Lesions are most common in the region of the flexor commissure of the interdigital space. Less typically, lesions
have been seen on the dorsal surface of the foot as well as around the dewclaws. One or both hindfeet are most commonly
involved, although both hind and forefeet can be affected.
Small, early lesions are clearly separated from surrounding healthy skin by a white line of raised tissue. Typically,
they are round or oval and ~0.5-2.0 cm in diameter. The surface of the lesion may be flat or concave, raw, moist, and red,
yellow, or gray with a finely tufted or granular surface. The lesion is often referred to as being “strawberry-like.” Mature
lesions are usually raised by as much as 2-4 cm, with the surface covered by gray, brown, or black hair-like papillary
growths.
The lesions are usually extremely tender to the touch. An affected animal may hold its foot off the ground or walk
on its toes.
Digital dermatitis is distinctly different in appearance from footrot because swelling and fever are normally absent.
Treatment:
In advanced cases, individual treatment may be necessary. The foot, especially the interdigital area, should be
thoroughly cleansed to remove the prolific population of spirochetes. Some caustic preparations have been effective, eg, a
single topical paint of 36% muriatic acid or formaldehyde. The dressing must be applied carefully to the infected tissue and
protected by a waterproof bandage. A one-time treatment is likely to be effective, and repeated dressing with the caustic
preparation is not advisable.
Topical dressing of the lesion and surrounding surfaces with soluble oxytetracycline produces good results.
Lincomycin-spectinomycin (66 g and 132 g/L of water, respectively) can be highly effective.
Herd outbreaks are best treated with a footbath containing oxytetracycline or lincomycin-spectinomycin.
Control:
Digital dermatitis is exacerbated by filthy, wet conditions. Slurry removal and improved standards of hygiene are
essential for control. In herds in which this condition is not yet a problem, animals should be isolated for 1 mo before being
introduced into a herd. Vaccines are not available.
Enzootic Calcinosis
This disease complex of ruminants and horses is caused by plant poisoning or mineral imbalances and characterized
by extensive calcification of soft tissues.
Etiology and Pathogenesis:
Known causes fall into two categories: plant poisonings and mineral imbalances in the soil, the first probably being
the more important. Cestrum diurnum (wild jasmine, day-blooming jessamine, king-of-the-day), Trisetum flavescens
(golden oats or yellow oat grass), Nierembergia veitehii , Solanum esuriale , S torvum , and S malacoxylon (glaucophyllum)
contain 1,25-dihydroxycholecalciferol (calcitriol) glycoside or a substance that mimics its calcinogenic action. Studies
indicate that S malacoxylon has the required enzyme systems for the synthesis of calcitriol from vitamin D3. No concrete
evidence incriminating other plants is available.
The imbalance of minerals in certain soils in Hawaii, India, Austria, and possibly elsewhere has been thought to be
the main etiologic factor; dietary mineral imbalance may contribute to the calcification chiefly associated with plant
poisoning. Excessive phosphate or calcium, absolute or conditioned magnesium deficiency, and deficiency of potassium and
nitrogen have all been incriminated or suspected.
Osteodystrophy of bulls after prolonged intake of excessive calcium is a similar condition; calcification of the
cardiovascular system associated with aging and such cachectic diseases as tuberculosis is not identical. Excessive vitamin
D3 and normal or excessive calcium intake induces aortic calcification and atherosclerosis in ruminants.
Normally, the conversion of 25-hydroxycholecalciferol (calcifediol) to calcitriol in the kidney is controlled by a
feedback mechanism. The calcitriol-like factor in the leaves of plants bypasses this mechanism, and more calcium is
absorbed than can be accommodated physiologically. Hypercalcemia promotes calcitonin production, calcinosis, and
osteoporosis.
Clinical Findings:
The disease is progressive and chronic, extending over weeks or months. The earliest signs are stiffened and painful
gait, which is most pronounced when the animal rises after prolonged rest. Forelimbs are particularly affected, and some
animals even walk or graze on their knees. When standing, the forelimbs bow forward because the joints cannot be extended
completely. The animal shifts weight to the forepart of the hooves or, alternatively, to each forelimb to ease stress on the
carpus, which is thickened and painful. The distal joints become abnormally straight. When affected animals are forced to
walk, their gait is awkward, stiff, and slow, and their steps are short. After walking only short distances, breathing becomes
shallow and diaphragmatic, the nostrils are flared, and the head and neck are extended. Varying degrees of heart murmur are
detectable, usually as a double or blurred second sound; these are exaggerated after exercise. Pulse rate is increased after
slight exercise. Jugular pulse is prominent in some cases.
Calcification of vessels is palpable on rectal examination.
Lesions:
Degeneration and calcification of soft tissues occur, with emaciation and varying amounts of excess fluid in the
thoracic and abdominal cavities and pericardial sac. The cardiovascular system is the first to be involved, followed by lung,
kidney, and tendons. The heart and aorta show the most marked effects. The left side of the heart is more affected than the
right.
Control:
Removal of the causal factor(s) is essential, but when the disease is associated with the mineral content of the soil,
control may be difficult. Change of pasture, forage, and environment may effect clinical improvement and even diminish
the soft-tissue mineral deposits. Experimentally, daily administration of 15 g of aluminum hydroxide, PO, prevented the
development of calcinosis in sheep fed Trisetum flavescens .
Primary Hyperparathyroidism
Hypoparathyroidism
In hypoparathyroidism ( Hypoparathyroidism), either subnormal amounts of parathyroid hormone (PTH) are
secreted, or the hormone secreted is unable to interact normally with target cells. It has been recognized primarily in dogs,
particularly in smaller breeds such as Miniature Schnauzers, but other breeds may be affected.
Etiology and Pathogenesis:
Various pathogenic mechanisms can result in inadequate secretion of PTH. Parathyroid glands may be damaged or
inadvertently removed during thyroid surgery.
Idiopathic hypoparathyroidism in adult dogs usually is the result of diffuse lymphocytic parathyroiditis that
causes extensive degeneration of chief cells and replacement by fibrous connective tissue. Other possible causes of
hypoparathyroidism include destruction of parathyroids by primary or metastatic neoplasms in the anterior cervical area,
and atrophy of parathyroids associated with chronic hypercalcemia. The presence of numerous distemper virus particles in
chief cells of the parathyroid gland may contribute to the low blood calcium in certain dogs with this disease. An immune-
mediated mechanism may be involved, because a similar destruction of secretory parenchyma and lymphocytic infiltration
has been produced experimentally in dogs by repeated injections of parathyroid tissue emulsions.
Clinical Findings and Lesions:
The functional disturbances and clinical manifestations of hypoparathyroidism primarily are the result of increased
neuromuscular excitability and tetany. Bone resorption is decreased because of the lack of PTH, and blood calcium levels
diminish progressively (4-6 mg/dL). Affected dogs are restless, nervous, and ataxic, with weakness and intermittent tremors
of individual muscle groups that progress to generalized tetany and convulsions. Blood phosphorus levels are increased
substantially, owing to increased renal tubular reabsorption. Calcification of microvasculature, intracerebral calcification,
decreased mental function, cataracts, osteopenia, and ligamentous ossification have been associated with chronic
hypoparathyroidism.
Regional Analgesia
Intravenous regional analgesia is the method of choice of analgesia for most digital surgical procedures.
Footbaths
Routine use of a footbath can reduce the incidence of lameness by up to 10%. If footrot (interdigital phlegmon) is a
major herd problem, there has been some success with using footbaths on a regular basis. For digital dermatitis, an
antibiotic footbath is often used for treatment.
Many types of footbaths are used, including those containing formalin, copper and zinc sulfate (which are more
expensive and slightly less effective than formalin), and antibiotics.
Formalin (3-5%) is the least expensive footbath solution; it lasts longer in the bath than other products and has good
bacteriostatic activity as well as having some potential for hardening the epidermis. However, the fumes from formalin are
an irritant and, under certain conditions, milk can be tainted. In many areas, local laws prohibit the use of formalin.
Formalin is also ineffective at temperatures <13°C.
The stronger the formalin solution used, the more effective it will be, but the danger of a chemical burn on the cow's
skin will also be greater. Therefore, the status of the hair around the claw should be carefully monitored. If the hair appears
to be standing on end or the skin is pink, treatment should be suspended.
Pododermatitis Circumscripta
(Sole Ulcer)
A sole ulcer is a lesion located in the region of the sole/bulb junction, usually nearer the axial than abaxial
margin. Damage to the dermis is associated with a circumscribed zone of localized
hemorrhage and necrosis.
Sole ulcers are common in dairy herds in which animals are managed in loose-
housing systems, particularly if conditions are unhygienic as is often the case during winter
months. The incidence is variable, but in some herds, >50% of the mature cows can be affected.
Etiology and Pathogenesis:
It is widely thought that subclinical laminitis is a major predisposing factor. Laminitis damages horn-producing
tissues, resulting in softer than normal sole horn. The horn is further softened if it is exposed to moisture, while the chemical
agents in slurry are thought to disrupt the integrity of the horn. Excess wear of the softened sole horn flattens and thins the
sole. Weight bearing beneath the flexor process of the distal phalanx causes the sole to squeeze the corium in the region and
leads to an ischemic necrosis occurring over a small area. Horn production ceases in this specific area, and as the
surrounding horn continues to grow, the damaged area continues to persist as a perforation. The damaged corium undergoes
repair until the granulation tissues erupts through the sole.
Clinical Findings:
Because the lateral digit is usually involved, the limb is often held slightly abducted with weight bearing on the
unaffected medial digit.
Toe Ulcer
Double Sole
In a double sole, a superficial sole is separated by a space from a second sole that is attached directly to
the dermis.
Etiology and Pathogenesis:
A double sole may result from a short-term nutritional insult. A sudden disturbance in the microcirculation of the
dermis probably results in an effusion of serum that separates the dermis from the epidermis. The condition has been seen in
animals suddenly changed from a mainly forage diet to one rich in concentrates and in beef cattle turned out in the spring on
lush grass after a winter ration of forage. The etiology is similar to that causing toe ulcer or digit rotation.
Treatment and Control:
The sole beneath is extremely soft and vulnerable to damage; therefore, the animal should be confined to a well-
strawed loose stall until the new horn has hardened, after which more of the sole may be removed.
For control, sudden changes from forage to concentrate or lush grass should be avoided.
Vertical Fissures
(Sandcrack)
A vertical fissure is a crack in the wall of the claw that has been classified into four types: Type I is confined to the
coronary band, Type II is from the coronary band to the middle of the claw, Type III is from the coronary band to the
bearing surface of the wall, and Type IV is from the middle of the wall to the bearing surface.
Etiology:
The etiology remains uncertain. Most fissures occur in the front outside claw. Heavy
cows and animals with overgrown claws are more likely to be affected.
Traumatic injury of the coronary band is likely to be the main cause of type I fissures.
Many type II and III fissures are associated with horizontal fissures. The horizontal fissure is a point of structural weakness
at which the claw will bend once the fissure has grown out to a point halfway between the coronary band and the apex of
the toe. The stability of the wall is compromised, and vertical fissures apparently result from mechanical stress. Type IV
fissures are quite rare and probably represent the resolving stages of type II and III fissures.
Treatment:
Most sandcracks are not painful and require no treatment.
Type I fissures are only dangerous if they are located in the region where dorsal and abaxial surfaces meet. At this
location, the dorsal pouch of the distal interphalangeal joint lies immediately beneath the coronary band. If such a fissure is
infected, the risk of a septic joint is considerable. In these cases, a small segment of horn should be dissected from either
side of the fissure, and the cavity dressed with antibiotic powder.
Type II and III fissures often have ragged edges that may be twisted and gape open.
Horizontal Fissures
Horizontal fissures result from disruption of horn production at the dermis beneath the coronary band, which results
in a defect in the integrity of the wall running parallel to the coronary band. The defect varies in severity from a shallow
groove (hardship groove) to a complete fracture (fissure) of the wall. The fissure moves distally as
the claw grows, and the distal portion becomes progressively more mobile (thimble)
until it fractures, leaving a “broken toe.” A series of grooves can destabilize the vertical
strength of the dorsal wall causing it to bend (buckled toe).
Etiology:
Heel Erosion
Heel erosion is an aberration in the appearance of the surface of the bulb of the heel.
The incidence of heel horn erosion (“slurry heel”) is most common during the winter,
particularly when the claws are exposed to an unhygienic, moist environment (such as exists in
intensively managed dairy units). Because heel erosion does not cause lameness per se, the true
incidence is unknown.
Etiology and Pathogenesis:
During the destructive phase, heel erosion occurs most frequently when interdigital dermatitis is present, and
Dichelobacter nodosus is likely involved.
Claws exposed to slurry appear to have a higher incidence of erosions than those that are kept clean and dry.
Moisture undoubtedly softens horn, and slurry contains a huge bacterial burden as well as an undetermined number of
irritants.
In the secondary phase, it is thought that changes in the distribution of weight bearing occur as the result of heel
horn loss. This in turn causes an increase in the rate of horn produced beneath the heel. The excessive horn growth is often
more pronounced in the lateral claw and causes the hock to turn in (cow-hocked stance).
Interdigital Phlegmon
(Footrot, Foul in the foot)
Footrot is a subacute or acute necrotic infection originating from a lesion in the interdigital skin that leads to a
cellulitis in the digital region. Pain, severe lameness, fever, anorexia, loss of condition, and reduced milk
production are major signs of the disease.
Etiology and Pathogenesis:
Injury to the interdigital skin provides a portal of entry for infection. Maceration of the skin by
water, feces, and urine may predispose to injuries. Fusobacterium necrophorum is considered to be the
major cause of interdigital phlegmon. It can be isolated from feces, which may explain why control is difficult. Other
organisms, such as Staphylococcus aureus , Escherichia coli , Actinomyces pyogenes , and possibly Bacteroides
melaninogenicus , can also be involved.
Clinical Findings:
Both the fore or, more commonly, the hind digits can be affected, but it is rare that more than one foot is affected at
the same time in dairy cows. However, the disease can occasionally occur in several feet in calves. The first sign is swelling
and erythema of the soft tissues of the interdigital space and the adjacent coronary band. The inflammation may extend to
the pastern and fetlock. Typically the claws are markedly separated, and the inflammatory edema is uniformly distributed
between the two digits. The onset of the disease is rapid, and the extreme pain leads to increasing lameness. In severe cases,
the animal is reluctant to bear weight on the affected foot. The body temperature is increased and appetite is reduced. The
skin of the interdigital space first appears discolored; later, it fragments with exudate production. As necrosis of the skin
progresses, sloughing of tissue is likely to follow. A characteristic foul odor is produced.
If the disease proceeds unchecked, there will be severe weight loss and a significant reduction in milk yield. Milk
production may not recover during the current lactation. Open lesions can be infected with secondary invaders. If the
necrotic lesion is located in the anterior region of the interdigital space, the distal interphalangeal joint can become infected
because of its proximity.
Hematogenous infection of the tissues of the interdigital space may account for peracute cases of interdigital
phlegmon, which are referred to as either “blind” or “super foul.” This form of the disease is characterized by the initial
absence of a skin lesion, extreme pain, and the tendency to progress despite aggressive therapy.
Diagnosis:
Laminitis: Overview
Laminitis is a pathophysiologic disturbance of the microvasculature of the corium that compromises the function of
the tissues, particularly those of the horn-producing cells. Laminitis can be subclinical, acute, or chronic, depending on the
severity of the several causative variables.
Subclinical Laminitis
This form of laminitis has the greatest economic importance; it produces no immediately obvious clinical signs but
is suspected to be present in a herd if there is a high incidence of diseases such as sole ulcer. Subclinical laminitis has been
reported mostly in mature dairy cows.
Etiology:
The classic hypothesis for the etiology of laminitis in cattle is similar to that of laminitis in horses ( Laminitis:
Overview , Laminitis , Laminitis , Septic Laminitis). High levels of carbohydrate in the rumen invoke an increase of
Streptococcus bovis and Lactobacillus spp , which in turn lead to a state of acidosis in the rumen. It is further hypothesized
that this environment is hostile to gram-negative organisms and, as they die, vasoactive endotoxins are released. Rumenitis
is frequently associated with ruminal acidosis. High levels of histamine in the blood have been found in the early stages of
the disease. Fiber and the frequency of feeding are extremely important factors.
A second hypothesis involves the receptors for epidermal growth factor (EGF) that are present in the corium of the
claw. Because EGF is liberated in large quantities from the GI tract that has been insulted, it could be involved in the
pathogenesis of laminitis. In addition to its mitogenic effect, EGF can inhibit the differentiation of keratinocytes in vitro.
Inhibited differentiation of keratinocytes of the hoof matrix is a dominant morphologic feature in the early stages of
laminitis. This hypothesis might account for the irregularities in horn production that are seen in some cases of laminitis.
Pathogenesis:
The pathophysiologic process causing laminitis may be summarized as a toxic influence on capillary walls that
results in insufficient nutrient supply to the keratin-producing cells and synthesis of structurally incompetent keratin. It is
believed that when vasoactive toxins reach the corium, the arteriovenous shunts are paralyzed. Pressure inside the claw
rises, and the vessels are damaged, which allows blood or blood fluids to escape and soak into the horn claw staining it
either pink or yellow. Hemorrhagic staining of the horn tubules of the sole give a “brush mark” appearance. Increased blood
pressure inside the claw (intraungular pressure) and the associated reduced blood flow, is usually followed by thrombus
formation. This is a characteristic feature of laminitis. Thrombi form as fine layers inside the walls (mural thrombi) of the
vessels. Because of reduced blood flow, fewer nutrients reach horn-producing tissues, and horn quality deteriorates. The
blood vessels can eventually become completely blocked, causing ischemic changes followed by scar tissue formation.
Frequently, young animals appear to recover from a laminitic incident. This may be because new blood vessels
develop to form collateral circulation and take over the function of those that have been damaged. Nevertheless, each time
an animal has a bout of laminitis, more scar tissue is formed and the animal will be less able to recover from the next insult.
Clinical Findings:
Some animals appear to walk in a deliberate, careful manner, with a delayed appearance of hemorrhages in the sole.
Erythema and edema of the coronary band above the heel and around the dewclaws in freshly calved cows may be an
Chronic Laminitis
Chronic laminitis is assumed to be caused by a series of laminitic insults. It is seen most commonly in dairy cows >5
yr old.
Foot Abscess
(Infective bulbar necrosis, Heel abscess, Bumblefoot)
A foot abscess is a necrotizing or purulent infection involving the distal interphalangeal joint. The incidence is
usually sporadic, but up to 15% of rams or ewes in late pregnancy may be affected.
The two organisms most consistently recovered from foot abscess are Fusobacterium necrophorum and
Actinomyces pyogenes . Most commonly, foot abscess develops as a complication of ovine interdigital dermatitis (see Ovine
Interdigital Dermatitis) by extension of the necrotic process into the subcutis and then into the distal interphalangeal joint.
This joint is vulnerable to infection on the interdigital aspect where the joint capsule protrudes above the coronary border as
the dorsal and volar pouches. At these two sites, the joint capsule is protected only by the interdigital skin and a minimal
amount of subcutaneous tissue. Sporadic cases may also develop after penetration by sharp objects or careless paring of the
hoof.
Foot abscess develops most often when the soil and pastures are wet. Rams, particularly in their first winter, and
ewes during late pregnancy are affected most commonly. The disease causes an acute lameness that is usually restricted to
one foot. In the early stages, it may be possible to express necrotic material through an opening in the interdigital skin via
the channel caused by the bacterial invasion. In ~50% of the cases, movement of the affected digit is exaggerated, which
indicates that the ligaments about the distal interphalangeal joint have ruptured; it is likely that there will be displacement of
the digit during locomotion, and permanent deformity.
Acute lameness, swelling of one digit, and discharging sinuses distinguish foot abscess from footrot.
The clinical appearance is characteristic, but similar conditions such as benign or virulent footrot must be excluded.
Dermatophilosis (strawberry footrot, Dermatophilosis: Introduction) affects the hairy skin of the coronet and pastern. Viral
diseases such as ulcerative dermatitis, contagious ecthyma, and foot-and-mouth disease may be excluded by flock history,
clinical signs, and serology. Fusobacterium necrophorum may also infect the lesions caused by these diseases.
Treatment and Control:
Most lesions heal rapidly with the advent of dry conditions or removal to drier pastures.
Interdigital Fibroma
An interdigital fibroma is a mass of fibrous tissue between the toes that may resemble a papilloma. If not removed, it
grows upward between the first phalanges and may cause severe lameness. If it is detected early, surgical removal
(cryosurgery and electrocautery) is successful.
Lameness in Horses:
Navicular Disease
(Podotrochlosis, Podotrochlitis)
Navicular disease is essentially a chronic degenerative condition of the navicular bursa and navicular bone that
involves damage to the flexor surface of the bone and the overlying deep digital flexor tendon with osteophyte formation on
the lateral and proximal borders of the bone. Thus, it is a syndrome with a complex pathogenesis rather than a specific
disease entity. It is one of the most common causes of chronic forelimb lameness in horses but is essentially unknown in
ponies and donkeys.
Etiology:
The exact cause is unknown, but it is likely to be multifactorial involving the navicular bone and its blood supply,
the suspensory ligament, the coffin joint, the navicular bursa, and the deep digital flexor tendon. It is considered to be a
disease of the more mature riding horse, but radiographic signs have been seen in 3-yr-olds. It may be partially hereditary; it
is certainly associated with upright conformation of the forefoot. The conformation of the foot in chronic cases becomes
abnormal; it is upright and narrow and has a small frog. Defective shoeing that inhibits the action of the frog and the
quarters may be contributory. Concussion between the flexor tendon and the navicular bone can cause a local bursitis that
leads to hyperemia and rarefaction of the bone with resultant alteration of the flexor surface of the bone.
Clinical Findings and Diagnosis:
Usually, the disease is insidious in onset. Attention is first directed to the affected foot or feet by the attitude of the
horse when at rest. The horse relieves the pressure of the deep digital flexor tendon on the painful area by pointing or
advancing the affected foot with the heel off the ground. If both forefeet are affected, they are pointed alternately. An
intermittent lameness is manifest early in the course of the disease. The stride is shortened, and the horse may tend to
stumble. A flexion test involving the distal forelimb usually produces a transient exacerbation of lameness. There may be
soreness in the brachiocephalic muscles secondary to the changes in posture and gait, thus the frequent complaint of
“shoulder lameness.”
Clinical diagnosis is reasonably straightforward and is based on a complete history and careful physical
examination. The lameness can be eliminated by palmar digital nerve block. Radiographic changes include a range of
degenerative changes involving the navicular bone.
Treatment:
Because the condition is both chronic and degenerative, it can be managed in some horses but not cured.
Nonsteroidal anti-inflammatory drugs such as phenylbutazone, along with proper foot management, extend
serviceable soundness in some horses. Another therapy is isoxsuprine hydrochloride (0.27 mg/lb [0.6 mg/kg], PO, b.i.d. for
6-14 wk) in a paste form, which acts as a peripheral vasodilator, but recurrences follow cessation of therapy.
Palmar digital neurectomy may render relief from pain and prolong the usefulness of the horse, but no neurectomy
should be considered curative. Digital neurectomy can be accompanied by severe complications such as painful neuroma
formation. Volar and higher neurectomy should never be done.
A technique of desmotomy of the collateral sesamoidean ligament has also been described. By cutting this ligament,
the concussive forces between the navicular bone and the deep digital flexor tendon are thought to be reduced. The results
are preliminary and unsubstantiated.
Laminitis
(Founder, Fever in the feet)
Traditionally defined as inflammation or edema of the sensitive laminae of the hoof, laminitis is now thought to be a
transient ischemia associated with coagulopathy that leads to breakdown and degeneration of the union between the horny
and sensitive laminae. In refractory cases, rotation of the pedal bone is a common sequela that may progress to perforation
of the sole. The disease is a local manifestation of a more generalized metabolic disturbance, and the hoof problems are
classified as acute, subacute, or chronic. It can occur in the forefeet, all four
feet, or occasionally only in the hindfeet.
Etiology:
The most common causes of laminitis are ingestion of excess
carbohydrate (grain overload), grazing of lush pastures (especially in ponies), and excess
exercise and concussion in an unfit horse. It also may occur secondary to postparturient metritis, endotoxemia, colic and
enteritis, or administration of an excess of corticosteroid or some other medicament. The risk is higher in ponies and in
horses that are overweight and unfit. There is a higher incidence of the acute and subacute forms whenever there is a flush
of new grass.
The initial change in acute laminitis is ischemia of the lamellar arterioles and venules. The arterial blood is then
shunted to the venous return via the many anastomotic blood vessels in the foot (especially at the coronary band) and
bypasses the corium; the result is stagnation of blood and functional congestion and thromboembolism of the capillary beds.
Laminar necrosis contributes to rotation.
These disturbances in the circulation to the foot, which initially are reversible, probably cause the exhibited pain.
However, if the condition becomes protracted and there is chronic hypoxia and a lack of essential sulfur-containing amino
acids for the corium, then slowing or cessation of keratinization occurs between the stratum germinativum and keratogenous
zone. The end result, in mild cases, is production of “laminitic rings”; in severe cases, pedal rotation or complete separation
of the hoof from the underlying tissues occurs. The separation of the horny and sensitive laminae is due to ischemia, faulty
keratinization, and the constant pull of the deep flexor tendon on the pedal bone, along with the upward push of the toe as
the horse stands. There is some support at the back of the pedal bone from the deep digital flexor tendon and the digital
cushion; however, these supportive structures may serve as a fulcrum, resulting in pedal bone rotation. If the separation
occurs rapidly, the pedal bone may “sink” within the hoof. In chronic cases, the corona of the pedal bone may penetrate the
sole just in front of the frog. The prognosis in severe cases is poor because the changes become irreversible and secondary
infection is common. In subacute and chronic cases, the rotation of the pedal bone occurs relatively slowly. The sole tends
to become convex and thicken, and the hoof alters shape to accommodate the new position.
Clinical Findings:
In acute laminitis, the horse is depressed and anorectic and stands reluctantly. Resistance to any exercise is marked,
and the normal stance is altered in attempts to relieve the weight borne by the affected feet. If forced to walk,
the horse shows a slow, crouching, short-striding gait. Each foot, once lifted, is set down as quickly as possible.
Usually, heat is apparent in the whole hoof, especially near the coronary band. An exaggerated and
bounding pulse can be palpated and may be visible in the digital arteries. Pain can cause muscular trembling, and a fairly
uniform tenderness can be detected when pressure is applied to the feet. The pedal bone may rotate during or after the acute
stage if efficacious treatment is not given rapidly. Radiographic evidence of rotation can be present as early as the third day.
The subacute case may exhibit any or all of the above clinical signs but to a lesser degree. The acute and subacute
forms of laminitis tend to recur at varying intervals and may develop into the chronic form.
Chronic laminitis is characterized by changes in the shape of the hoof and usually follows one or more attacks of the
acute form. Bands of irregular horn growth (laminitic rings) may be seen in the hoof, close at the toe and
diverging at the heel. The hoof itself becomes narrow and elongated, with the wall almost vertical at the heel
and horizontal at the toe.
Diagnosis:
In acute and severe laminitis, diagnosis is based on the history (eg, grain overload) and posture of the horse,
increased temperature of the hooves, a hard pulse in the digital arteries, and reluctance to move. Divergence of ≥11°
indicates a guarded to unfavorable prognosis for return to performance.
Treatment:
Acute laminitis constitutes a medical emergency because pedal rotation can occur rapidly. In acute laminitis,
especially in cases of grain overload, mineral oil is indicated; 1 gal. (4 L) PO acts as a laxative and tends to prevent
absorption of toxic material from the GI tract.
Traditionally, cold packs or ice packs applied to the affected feet have been advocated, but recent evidence suggests
that hot packs used early in the course of the disease may be more beneficial. Antihistamines are of doubtful value during
Thrush
Thrush is a degeneration of the frog with secondary bacterial infection that begins in the central and collateral sulci.
It results from poor management and hygiene that permit horses to stand in wet conditions for prolonged periods and from
failure to clean the hooves regularly. It is more common in the hindfeet.
Treatment should begin by providing dry, clean standings and cleaning out the hoof with removal of all macerated
horn.
Bucked Shins
(Sore shins, Saucer fractures)
Bucked shins is a painful, acute periostitis on the cranial surface of the large metacarpal or metatarsal bone. It is seen
most often in the forelimbs of young Thoroughbreds (2-yr-olds) in training and racing and is much less common in
Standardbreds.
This injury is generally brought about by concussion in young horses in which the bones are not fully conditioned.
Microfractures (ie, stress fractures) are believed to be involved. There is a warm, painful swelling on the cranial surface
of the affected bone. The horse is usually lame initially, the stride is short, and the severity of the lameness increases
with exercise.
Suspensory Desmitis
Injuries of the suspensory ligament (superior sesamoidean ligament or interosseous muscle) are common injuries in
both forelimbs and hindlimbs of horses. Lesions are frequently restricted to the proximal one-third of the ligament, to the
body or middle one-third, or to one or both branches.
Proximal Suspensory Desmitis:
The term proximal suspensory desmitis is restricted to lesions confined to the proximal one-third of the
metacarpus (or metatarsus). It is relatively common and affects both forelimbs and hindlimbs of horses of all
ages. In contrast to lesions involving the body or branches (or both) of the suspensory ligament, there is usually associated
lameness or poor performance or poor action. The condition may occur unilaterally or, less commonly, bilaterally. It
sometimes occurs in association with more distal limb pain (eg, navicular disease) and is frequently seen in horses with poor
Gonitis
Gonitis is an inflammation of the stifle leading to degenerative joint disease. The joint is complex, and gonitis may
be precipitated by multiple causes, including osteochondrosis, persistent upward fixation of the patella, injuries to the
medial or lateral collateral ligaments, injuries to the cruciate ligaments or the menisci, erosions of the articular cartilage, or
bacterial infection of the joint from puncture wounds or of hematogenous origin (eg, pyosepticemia).
Signs vary with the cause and extent of the pathologic changes.
Patellar Luxation
True dislocation of the patella is uncommon in horses. When it does occur, it is usually a serious injury and the
lateral luxation is readily apparent. In some breeds, a congenital form of lateral luxation occurs similar to that seen in small
dogs ( Patellar Luxation). The most frequent problem involving the patella is upward fixation or locking of the medial
patellar ligament over the proximal part of the medial femoral trochlear ridge. Some pony breeds may have a hereditary
predisposition, but patellar luxation is also seen in immature animals with poorly developed thigh muscles. It may be uni- or
bilateral.
In many cases, a general improvement in fitness and muscle tone of the hindquarters effects a cure. In the more
severe and persistent cases, desmotomy of the medial patellar ligament is indicated. However, desmotomy, which has been
commonly used in the past, is currently in disfavor. A fragmentation of the distal extremity of the patella is believed to
follow the surgery, particularly if postoperative exercise is initiated early. When surgery is done, rest should be sufficient
(eg, 4-6 wk) to permit complete healing before training is resumed.
Osteochondrosis
(Osteochondritis dissecans, Dyschondroplasia)
Osteochondrosis (see also Osteochondrosis: Introduction , Osteochondrosis) is one of the most important and
prevalent developmental orthopedic diseases of horses. Although its specific etiology is not known, it is considered to arise
from a focal disturbance in endochondral ossification. The term osteochondrosis is currently used to describe the clinical
manifestation of the disorder; however, the term dyschondroplasia is preferred when referring to early lesions because
primary lesions occur in cartilage.
Osteochondrosis has a multifactorial etiology that includes rapid growth, overnutrition, mineral imbalance, and
biomechanics (ie, trauma to cartilage). Genetics has been implicated in some breeds (eg, Standardbred and Swedish
Warmblood). The condition mainly affects articular growth cartilage, but the metaphysis may also be involved. If the
physeal metaphyseal cartilage is affected, bone contours and longitudinal growth are disturbed (see physitis , Physitis).
Involvement of articular cartilage at the periphery of joint surfaces leads to regressive changes at the joint margins,
dissecting lesions, and the formation of flaps (osteochondritis dissecans). Central articular lesions, because of weight-
bearing effects, involve focal retention of cartilage within the subchondral bone (see subchondral cysts, Subchondral Cystic
Lesions). Axial skeletal involvement includes vertebral articular facets, and this may lead to stenosis of the vertebral canal
and, ultimately, ataxia and proprioceptive deficits (ie, wobbler syndrome).
Clinical Findings:
The clinical signs of equine osteochondrosis are difficult to characterize specifically because of the wide range of
lesions and sites involved. In severe cases, other signs of developmental orthopedic disease also may be apparent.
Furthermore, lesions of dyschondroplasia do not always progress to osteochondrosis and produce clinical signs. These signs
may begin with mild stiffness or lameness, but if there is superimposed biomechanical trauma, the joint damage progresses
to pain and lameness or loss of performance.
The most common sign of osteochondrosis is a nonpainful distention of an affected joint (eg, gonitis, bog spavin).
Clinical signs may be divided broadly into two categories; those occurring in foals <6 mo old and those occurring in older
animals. Often the first sign noted in foals is a tendency to spend more time lying down. This is accompanied frequently by
joint swelling, stiffness, and difficulty keeping up with other animals in the paddock. An accompanying sign may be the
development of upright conformation of the limbs, presumably as a result of rapid growth. Fetlock osteochondrosis is
particularly seen in younger foals (<6 mo old).
Marked lameness is not usually a feature of equine osteochondrosis, although it does occur with damage in some
sites. For example, lesions in the shoulder frequently produce moderate to severe lameness, muscle atrophy, and pain on
joint flexion. The true origin of pain in osteochondrosis is unknown. Horses often exhibit severe pathologic changes without
showing much pain or distress in contrast to some situations seen in some other species and sites (eg, canine elbow).
The main signs in yearlings or older horses are stiffness of joints, flexion responses, and varying degrees of
lameness. These signs are usually associated with the onset of training and, therefore, suggest a biomechanical influence
and an activation of subclinical or “silent” lesions.
Diagnosis:
Clinical diagnosis can often be made on the basis of signalment and signs. More definitive diagnosis requires the use
of some specific clinical aids. Radiographic examination has been the traditional method of confirming diagnosis;
however, early lesions involving cartilage without significant subchondral bone damage will not be visualized. In
the distal limb, oblique views may be helpful; in the hock, because the most common site of a lesion is the distal
Erysipelas:
Although acute erysipelas can occur in nursery pigs, it may be more typical of the growing/finishing pigs .
Vertebral Deformities:
Kyphosis or lordosis and cuneiform deformities of vertebrae have been seen in weaned pigs, but a cause has not
been identified. “Humpy back” pigs are seen sporadically in some herds; the spine is curved in the vertical plane such that
the lumbar vertebrae are higher than the thoracic vertebrae, and there is a “kink” between the two segments. The condition
may have a genetic predisposition.
Hip Dysplasia
Hip dysplasia is a multifactorial abnormal development of the coxofemoral joint in large dogs that is characterized
by joint laxity and subsequent degenerative joint disease. Excessive growth, exercise, nutrition, and hereditary factors affect
the occurrence of hip dysplasia. The pathophysiologic basis for hip dysplasia is a disparity between hip joint muscle mass
and rapid bone development. As a result, coxofemoral joint laxity or instability develops and subsequently leads to
degenerative joint changes, eg, acetabular bone sclerosis, osteophytosis, thickened femoral neck, joint capsule fibrosis, and
subluxation or luxation of the femoral head.
Clinical signs are variable and do not always correlate to the radiographic abnormalities. Lameness may be mild,
moderate, or severe, and is pronounced after exercise. A “bunny-hopping” gait is sometimes evident. Joint laxity (Ortolani's
Degenerative Arthritis
(Degenerative joint disease)
Progressive deterioration of articular cartilage in diarthrodial joints is characterized by hyaline cartilage thinning,
joint effusion, and periarticular osteophyte formation. Joint degeneration can be caused by trauma, infection, immune-
mediated diseases, or developmental malformations. The inciting cause initiates chondrocyte necrosis, release of
degradative enzymes, synovitis, and continued cartilage destruction and inflammation. Abnormal cartilage congruency and
joint capsule anatomy can further lead to alteration in normal joint biomechanical function. Pain and lameness develop
secondary to joint dysfunction or muscle atrophy and to limb disuse.
Clinical signs of degenerative joint disease include lameness, joint swelling, muscle atrophy, pericapsular fibrosis,
and crepitation. Radiographic changes in the joint include joint effusion, periarticular soft-tissue swelling, osteophytosis,
subchondral bone sclerosis, and possibly narrowed joint space. Arthrocentesis may be unremarkable or yield
minor changes in color, turbidity, or cell counts of synovial fluid.
Treatments can be medical or surgical. Nonsurgical therapies include weight reduction, controlled
exercise on soft surfaces, and therapeutic application of warm compresses to affected joints. Nonsteroidal
anti-inflammatory drugs (eg, aspirin, phenylbutazone, or carprofen) will reduce pain and inflammation.
Corticosteroids will also suppress prostaglandin synthesis and subsequent inflammation, but short-term use is advised to
prevent iatrogenic Cushing's syndrome, cartilage degeneration, and intestinal perforation. Joint fluid modifiers such as
glycosaminoglycans or sodium hyaluronate prevent cartilage degradation, although results of objective clinical trials are not
available. Surgical options include joint fusion (arthrodesis), most frequently performed on the carpus and tarsus; joint
replacement, such as total hip replacement; joint excision, such as femoral head and neck osteotomy; and amputation.
Prognosis is variable and depends on the location and severity of the arthropathy.
Septic Arthritis
Infectious arthritis is most frequently associated with bacterial agents such as staphylococci, streptococci, and
coliforms. Causes include hematogenous spread or penetrating trauma, including surgery. Other agents producing a septic
arthritis include rickettsia (Rocky Mountain spotted fever, ehrlichiosis) and spirochetes (borreliosis).
Clinical signs of septic arthritis include lameness, swelling, pain of affected joint(s), and systemic signs of fever,
malaise, anorexia, and stiffness. Radiography may reveal joint effusion in early cases and degenerative joint disease in
chronic conditions. Arthrocentesis will reveal increased WBC, especially neutrophils. The synovial fluid may be grossly
purulent. Bacterial culture and antimicrobial sensitivity testing may confirm the diagnosis. Serologic testing is used for
nonbacterial agents. Treatment is with appropriate IV and oral antibiotics, joint lavage, and surgical debridement in severe
cases.
Immune-mediated Arthritis
Inflammatory polyarthritis secondary to deposition of immune complexes can produce erosive (destruction of
articular cartilage and subchondral bone) or nonerosive (periarticular inflammation) forms of joint diseases. Rheumatoid
arthritis, Greyhound polyarthritis, and feline progressive polyarthritis are examples of erosive arthritides. Systemic lupus
erythematosus (SLE) is the most common form of nonerosive arthritis.
Clinical signs are lameness, multiple joint pain, joint swelling, fever, malaise, and anorexia. Clinical signs
commonly wax and wane.
Diagnosis is aided by radiography, biopsy, arthrocentesis, and serologic testing. Radiography reveals periarticular
swelling, effusion, and joint collapse plus subchondral bone destruction in erosive conditions. Arthrocentesis reveals
Neoplastic Arthritis
Synovial cell sarcoma is the most common malignant tumor involving joints. The tumor arises from primitive
mesenchymal cells outside of the synovial membrane. Clinical signs include lameness and joint swelling. Radiography
reveals soft-tissue swelling and a periosteal reaction. Pulmonary metastasis is detected in ~25% of animals at initial
examination. Biopsy reveals evidence of a soft-tissue tumor. Limb amputation is the treatment of choice.
Hypertrophic Osteodystrophy
Hypertrophic osteodystrophy is a developmental disorder of the metaphyses in long bones of young, large, and giant
breeds of dogs. The exact etiology is unknown, but vitamin C deficiency, excessive dietary supplementation, and infection
have been suspected. The pathophysiology is based on metaphyseal vascular impairment leading to a failure in ossification
and trabecular necrosis and inflammation.
Clinical signs include bilateral metaphyseal pain and swelling in the distal radius and ulna, fever, anorexia, and
depression. Clinical signs may be periodic. Angular limb deformities may develop in severely affected dogs. Radiography
reveals metaphyseal bone lucencies and circumferential periosteal bone formation.
Therapy is symptomatic and aimed at relieving pain (eg, aspirin), reducing dietary supplementation, and providing
supportive fluid care.
Panosteitis
Panosteitis is a spontaneous, self-limiting disease of young, rapidly growing, large and giant dogs that primarily
affects the diaphyses and metaphyses of long bone. The exact etiology is unknown, although genetics (in German Shepherd
Dogs), stress, infection, and metabolic or autoimmune causes have been suspected. The pathophysiology of the disease is
characterized by intramedullary fat necrosis, excessive osteoid production, and vascular congestion. Endosteal and
periosteal bone reactions occur.
Clinical signs are acute, cyclical, and involve single or multiple bone(s) in dogs 6-16 mo old. Animals are lame,
febrile, inappetent, and have palpable long bone pain.
Ionophore Toxicity
Monensin, lasalocid, salinomycin, maduramicin, and narasin may cause myopathy. Horses are highly susceptible,
and reports of toxicity also exist for cattle, sheep, pigs, dogs, chickens, turkeys, and guinea fowl. Toxicity has generally
resulted from exposure to undiluted premixes or from mixing errors. Toxicosis may be potentiated by various antibiotics
and sulfonamides incorporated into feeds in combination with ionophores. Affected horses and cattle may develop anorexia,
cardiac failure with tachycardia, dyspnea, diarrhea, stiffness, muscular weakness, and myoglobinuria. At necropsy, pale
areas of myocardial necrosis and pulmonary congestion are usually prominent in horses and cattle. Pigs and sheep tend to
have mainly skeletal muscle lesions that appear quite similar grossly and histologically to those of nutritional myopathy.
Diagnosis requires history of exposure with development of characteristic clinical and pathologic alterations.
Plant Intoxication
Degeneration of skeletal and cardiac muscles results when cattle and some other animals, notably goats, consume
the fruit or beans of certain plants. Karwinskia humboldtiana (coyotillo) and Cassia spp (sennas) have been incriminated.
Osteochondrosis: Introduction
Osteochondrosis is a disturbance in endochondral ossification that is sometimes classified as dyschondroplasia. It
may involve the separation of the immature articular cartilage from the underlying epiphyseal bone, which sometimes
Osteochondritis Dissecans
In osteochondritis dissecans, a focal area of the immature articular cartilage is retained, and the matrix in the basal
area of this region becomes chondromalacic and acellular. The immature articular cartilage separates from the underlying
trabecular bone. The chondral fracture extends horizontally and vertically until a flap is formed. Synovial fluid gains
entrance to the underlying medullary space and subchondral cysts may form (usually only in larger animals). The flap of
immature articular cartilage may break away completely (joint mice), or may reattach by endochondral ossification to the
underlying bone, especially in pigs, and result in a wrinkled articular surface. The latter occurs only if the joint is rested or
protected, which permits reestablishment of the circulation necessary for endochondral ossification. If the flap is torn free
by joint motion, it may be ground into smaller pieces during locomotion and disappear, while the larger plaques may
become attached to the synovial membrane, become vascularized, and ossify. The resultant articular defect, in time, fills
with fibrocartilage.
Etiology:
The exact cause is unknown, but it is assumed to be multifactorial. Trauma due to excessive biomechanic stresses in
focal areas has been implicated. In pigs, complementary lesions in the immature articular cartilage and the adjacent physeal
cartilage are not uncommon. The inheritance of predisposing characteristics (rate of growth, excitability, size of skeleton,
muscle mass, etc) is not known. The joint most commonly affected varies among species (eg, shoulder in dogs, elbow in
pigs). The stifle (medial or lateral condyle) and hock (caudal aspect of medial trochlea of the talus) also may be involved.
Clinical Findings:
Osteochondrosis causes an insidious and usually persistent lameness beginning, in dogs, at 4-8 mo of age. Lameness
is often unilateral, even though the lesions can be bilateral. Occasionally, several joints are affected. The animal may be stiff
after resting, and lameness is aggravated by exercise. Depending on which joint is affected, pain can be elicited by
hyperextension or hyperflexion (eg, shoulder joints are most painful on hyperextension). Untreated, the lameness persists
and becomes permanent due to secondary osteoarthritis. The joint is crepitant, and muscular atrophy develops in the chronic
condition. When the articular cartilage does not fracture, the condition may go undetected; however, the silent lesions may
be demonstrated radiographically.
Diagnosis:
The history, age, breed, sex, and clinical signs provide useful information; however, radiographs are required to
substantiate the diagnosis. The shoulder lesion is observed on a lateral radiograph as a flattened irregularity of the central
caudal half of the humeral articular surface. Osteochondrosis of the femoral condyles in the dog is observed best from a
lateral radiograph in which the condyles are not superimposed. Craniocaudal radiographs of the hock in full extension
reveal the characteristic depression of the affected surface. The specific lesions in the elbow and hock are not visible on
radiographs until after proliferative osteoarthrosis develops.
Treatment:
A few animals recover spontaneously with 4-6 wk of rest and restricted exercise. Anti-inflammatory
drugs are not indicated because they promote physical activity, and thus aggravate the condition. If surgery of affected
shoulder joints is performed soon after diagnosis, the prognosis is good. Joint bodies should be removed and the lesion in
the subchondral bone curetted. Lesions involving the stifle, elbow, and hock also should be treated surgically; however, the
prognosis for these joints is guarded.
Sarcocystosis: Introduction
(Sarcosporidiosis)
In sarcocystosis, the endothelium and muscles and other soft tissues are invaded by protozoans of the genus
Sarcocystis . As the name implies, Sarcocystis spp form cysts in various intermediate hosts—man, horses, cattle, sheep,
goats, pigs, birds, rodents, and reptiles. The cysts vary in size from a few micrometers to several centimeters, depending on
the host and species.
Etiology, Transmission, and Pathogenesis:
Sarcocystis spp normally develop in two-host cycles consisting of an intermediate host (prey) and the final host
(predator).
About 1 wk after ingesting muscle tissue that contains Sarcocystis cysts (sarcocysts), the final host begins to shed
infective sporocysts in the feces; shedding continues for several months. After ingestion of sporocysts by a suitable
intermediate host, sporozoites are liberated and initiate development of schizonts in vascular endothelia. Merozoites are
liberated from the mature schizonts and produce a second generation of endothelial schizonts. Merozoites from this second
generation subsequently invade the muscle fibers and develop into the typical sarcocysts. Initially, sarcocysts contain only a
few metrocytes—round, noninfective parasites that give rise to the banana-shaped infective zoites found in mature cysts
beginning 2-3 mo after infection. Sarcocysts of some species grow so large that they are easily visible with the unaided eye.
The presence of such sarcocysts can cause condemnation of the carcass during meat inspection. Sarcocystis cruzi is
probably most important in condemnation of beef cattle for human consumption. However, S hirsuta was primarily
responsible for dairy cattle condemnation for visible sarcocysts. Sarcocystis meischeriana is usually the species responsible
for sarcocyst condemnation of pork and may affect meat quality. Sarcocysts are easily recovered from esophagus,
diaphragm, and heart muscle. Sarcocysts of some species remain microscopic even though tremendous numbers of cysts
may be present in the muscles.
“Immunization” using small doses of sporocysts appears to prevent development or reduce severity of clinical
disease in sheep when challenged with large doses later (premunitive immunity).
History
The primary complaints for neurologic problems often include behavioral changes, seizures, tremors, cranial nerve
deficits, ataxia, and paresis or paralysis of one or more limbs. Congenital and familial disorders are most common in
purebred animals at birth or within the first few years of life. Inflammatory, metabolic, toxic, and nutritional disorders can
occur in any species, breed, or age; tend to have an acute or subacute onset; and are usually progressive. Vascular and
traumatic disorders have an acute onset and rarely progress after 24 hr. Most degenerative and neoplastic disorders tend to
occur in older animals (except for familial neuronal degeneration) and have a chronic onset and progressive course. Many
idiopathic disorders begin acutely and improve over a short time.
Physical And Neurologic Examinations: Overview
If abnormalities are found on evaluation of the head, then an initial attempt should be made to explain all limb
abnormalities by a lesion above the foramen magnum (C1). If no abnormalities are found on evaluation of the head, but
thoracic limb abnormalities are present, then an attempt should be made to explain the abnormalities by a cervical lesion
(C1-T2 ). Paralysis or paresis of all four limbs with loss of all spinal reflexes (with or without cranial nerve deficits) is often
associated with diffuse peripheral nerve or neuromuscular junction disease
Principles of Therapy
Seizure Control:
Status epilepticus (continuous or cluster seizures) in dogs and cats may be interrupted by diazepam. Sodium
pentobarbital to effect, not to exceed 3-15 mg/kg, IV, may also be used, followed by phenobarbital at 2-4 mg/kg, IM, every
6 hr.
Recommended maintenance anticonvulsant therapy in dogs is phenobarbital at 2-4 mg/kg, PO, every 8-12 hr as needed
to control seizures or to maintain serum levels at 25-30 µg/mL, 2-4 hr after medication. In addition, potassium bromide
(KBr), 22 mg/kg, s.i.d. with food, may be given to dogs if seizures continue or occur in clusters. Because KBr is toxic to
people, owners are advised to wear gloves while medicating the dog. KBr has proved more efficacious in seizures in dogs
than any other anticonvulsant except phenobarbital.
Acute Spinal Cord Injury:
Hyperkalemic periodic paralysis occurs in Quarter horses 2-3 yr old and is due to an inherited mutation of the
sodium channel. It causes episodes of muscle tremor and sometimes recumbency, both of which may be precipitated by
exercise. Hyperkalemia is usually present during an attack, and electromyography can also be helpful for diagnosis.
Acetazolamide (0.5-2.2 mg/kg, PO, b.i.d.) and hydrochlorthiazide (0.5 mg/kg, PO, b.i.d.) may lessen the frequency and
severity of attacks.
Degenerative Diseases
Dancing Doberman disease is a neuromuscular disease that occurs in Doberman Pinschers of either sex, 6 mo to 7 yr
old. Initially, affected dogs intermittently flex the hip and stifle of one pelvic limb while standing. Within several months,
most dogs alternately flex and extend both pelvic limbs in a dance-like fashion. They often prefer to sit rather than stand.
The etiology is unknown. Pathologic changes have been reported in pelvic limb muscles as well as peripheral nerves, and
whether this is a primary muscle or nerve disease remains to be clarified. There is no treatment.
Distal denervating disease is a common polyneuropathy of dogs in the UK but has not been reported elsewhere.
Distal polyneuropathy of Rottweiler dogs is characterized by paraparesis that slowly progresses to tetraparesis,
hyporeflexia, and muscle atrophy. Male and female Rottweilers 1-4 yr old have been affected. The cause is unknown.
Prognosis is poor.
Metabolic Disorders
Diabetic neuropathy is an uncommon complication of diabetes mellitus ( Diabetes Mellitus) in cats and rarely dogs.
Hyperchylomicronemia in cats is a suspected autosomal recessive disorder characterized by fasting hyperlipemia,
lipemia retinalis, and peripheral neuropathy. There is a deficiency of lipoprotein lipase, resulting in increased serum
triglycerides, cholesterol, and very low-density lipoproteins.
Idiopathic facial paralysis is a common disorder resulting in unilateral or bilateral paresis or paralysis of the facial
muscles in dogs and cats.
Neoplasia
Nerve sheath tumors include those tumors referred to as schwannomas, neurilemmomas, and neurofibromas. They
occur in most domestic animals but are most common in dogs and cattle. In dogs, tumors often arise in the nerves of the
brachial plexus, initially causing unilateral thoracic limb lameness and pain that may be confused with musculoskeletal
disease. The trigeminal nerve is the most frequently affected cranial nerve. This results in unilateral atrophy of the
temporalis and masseter muscles and facial dysesthesia or anesthesia. Eventually, brain-stem compression can occur.
Nutritional Disorders
Pantothenic acid deficiency may occur in pigs on rations of corn. Clinical signs include pelvic limb ataxia and a
“goose-stepping” gait in which the stifles remain extended and the hips flex to lift the limbs off the ground.
Riboflavin deficiency in chickens (curled toe paralysis) can occur if feed is not formulated properly.
Brain Tumors:
Primary tumors of the nervous system in dogs and cats occur more often in the brain than in the spinal cord or
peripheral nerves. Commonly reported primary brain tumors in dogs are meningiomas, gliomas (astrocytomas,
oligodendrogliomas), undifferentiated sarcomas, pituitary tumors, and ventricular tumors (choroid plexus papillomas and
ependymomas).
Secondary tumors extending into the brain from the nasal sinuses are relatively common in dogs, as are metastatic
brain tumors. Hematogenous metastases in dogs frequently originate from carcinomas of the mammary glands, thyroid,
bronchopulmonary epithelium, kidneys, chemoreceptor cells, nasal mucosa, squamous epithelium of the skin, prostate,
pancreas, adrenal cortex, and salivary glands. In dogs, common metastases include hemangiosarcomas, lymphosarcomas,
fibrosarcomas, and melanoblastomas. In cats, metastases most frequently originate from mammary carcinomas and
lymphosarcomas.
Meningiomas are one of the most common intracranial tumors in dogs and are the most commonly reported brain
tumor in cats.
Meningiomas in dogs and cats usually are benign tumors that tend to grow slowly under the dura mater. They may be
irregular, nodular, globular, ovoid, lobulated, or plaque-like masses ranging in size from a few millimeters to several
centimeters in diameter. Meningiomas often are firm, rubbery, encapsulated, and discrete. They can contain granular
calcifications known as psammoma bodies. Independently of these bodies, there can be focal or massive calcification of the
tumor. Most meningiomas are usually of the endotheliomatous type, fibromatous type, or mixed endotheliomatous
fibromatous type.
Meningiomas also occur commonly over the convexities of the cerebral hemispheres and over the cerebellum. In cats,
common locations include the tela choroidea of the third ventricle and the supratentorial meninges. Thickening of bone
adjacent to meningiomas, termed hyperostosis, may occur in dogs and cats. Meningiomas may extend into paranasal
regions, rarely metastasize outside the brain, and may occur as primary extracranial masses as a result of embryonic
displacement of arachnoid cells or meningocytes
Astrocytomas are probably the most common neuroectodermal brain tumor in dogs. They are common in
brachycephalic breeds and are usually found in middle-aged or older dogs but have been reported in dogs <6 mo old.
Astrocytomas were not distinguished easily from oligodendrogliomas because of their similar features and poorly defined
tumor margins.
Oligodendrogliomas are also common tumors in dogs, especially brachycephalic breeds. These tumors consist of
densely packed, chromatin-rich, round cells with perinuclear halos. Most oligodendrogliomas grow by infiltration and
destroy invaded tissue. Capillaries tend to proliferate within these tumors, producing glomerular-like structures. Regressive
changes are similar to those in astrocytomas.
Glioblastoma multiforme is a relatively common tumor in dogs and occurs most commonly in brachycephalic breeds.
Most are of considerable size and are most commonly located in the cerebrum.
Ependymomas are rare neuroglial tumors that occur more frequently in brachycephalic breeds. They are soft, gray to
reddish, lobular masses that tend to invade the ventricular system and the meninges.
Choroid plexus papillomas are common tumors in dogs with a reported frequency similar to that of glioblastomas
(~12% of neuroglial tumors). There is no apparent predilection for brachycephalic breeds. These tumors are reddish,
papillary growths that tend to bleed.
Pituitary tumors may be nonfunctional or functional. Tumors of either type can cause hypopituitarism by mechanical
or functional impairment of remaining pituitary tissue (although uncommon). Nonfunctional pituitary tumors are common
in dogs (perhaps less common in cats) and are usually chromophobe adenomas, although pituitary adenocarcinomas have
been reported. Functional pituitary tumors associated with the adenohypophysis are typically characterized by pituitary
dependent hyperadrenocorticism (PDH). The tumors are usually chromophobic microadenomas (<1 cm in diameter) that do
not produce neurologic signs. Up to 30% of dogs with PDH have large, chromophobic macroadenomas (>1 cm in diameter)
that may become invasive.
Because most pituitary tumors in dogs tend to grow dorsocaudally, consequent compression of the hypothalamus and
median eminence may result in central diabetes insipidus. Disturbance of water balance is the result of interference with the
synthesis of antidiuretic hormone in the supraoptic nucleus or release of the hormone into capillaries of the pars nervosa.
Polioencephalomalacia: Introduction
(Cerebrocortical necrosis)
Pseudorabies: Introduction
(Aujeszky's disease, Mad itch)
Rabies: Introduction
Rabies is an acute viral encephalomyelitis that principally affects carnivores and insectivorous bats, although it can
affect any mammal. It is almost invariably fatal once clinical signs appear.
Etiology and Epidemiology:
Rabies is a rhabdovirus that characteristically is confined to one species in a given geographic area, although extension
to other species is common.
No cat-to-cat transmission of rabies has been recorded, and no feline ecotype is known. However, cats are very
susceptible to all ecotypes, and extension is common.
Transmission and Pathogenesis:
Transmission is almost always by introduction of virus-laden saliva into the tissues, usually by the bite of a rabid
animal. However, virus from saliva or tissue fluids may be introduced into fresh wounds or through intact mucous
membrane (eg, ingestion). Virus may be present in the saliva and transmitted by an infected animal several days before
onset of clinical signs (usually 3-5 days in domestic dogs and cats and up to 8 days in striped skunks). Rabies virus has not
been isolated from skunk musk (spray).
The incubation period is both prolonged and variable; typically, the virus remains at the inoculation site for a
considerable time. The unusual length of the incubation period is why postexposure treatment, including in man the practice
Scrapie: Introduction
(Tremblante du mouton, Rida)
Scrapie is a fatal neurologic disease that produces subacute spongiform encephalopathy in adult sheep.
Etiology, Transmission, and Pathogenesis:
Two possible structures for the causal neuropathogen have been proposed: 1) the prion—a small exogenous particle
consisting of proteinase-resistant protein (PrP), which is an abnormal form of a host cellular protein and that can act as a
catalyst to convert more of the host's protein to the abnormal form, and 2) the virino—a hybrid particle consisting of a small
agent-specific core of nontranslated nucleic acid (which exists only to replicate itself) associated with host cellular proteins
(which may include PrP). Whatever the nature of the infectious agent, one of its most striking features is its resistance to
conventional physical and chemical treatments that destroy bacteria, spores, fungi, and viruses.
In the course of the disease, the cellular form of PrP undergoes a conformational change, resulting in increased β-sheet
folding and subsequent appearance of scrapie-associated fibrils (SAF). Amino acid substitutions in three regions of the host
PrP influence how rapidly the disease progresses.
Scrapie is frequently transmitted in family lines in flocks, which indicates that some form of maternal transmission may
occur at a pre- or postnatal stage. The infected placenta may also be eaten by other sheep or contaminate pastures, which
may account for horizontal transmission.
Clinical Findings:
The onset is insidious. Behavioral changes may include increased excitability, nervousness, or aggressiveness,
particularly elicited by sudden noise or movement. Fine tremors of the head and neck (tremblante du mouton) and
occasional convulsions may be seen. Lack of coordination of the limbs with a tendency to move at the trot or to hop like a
rabbit are characteristic.
Water metabolism is altered; sheep drink small quantities frequently, and urination may be abnormal with voiding of
small quantities of urine. n some cases, the pruritus makes it difficult for the animal to feed and rest normally, which is a
major factor in emaciation and weakness. Different breeds of sheep may not show the full range of clinical signs.
Lesions:
Pathologic lesions are restricted to microscopic changes in the CNS.
Diagnosis:
This is based on clinical signs and microscopical examination of the CNS. Further confirmation is provided by
immunoblotting to detect proteinase K-resistant PrP or by electron microscopy to detect protease-resistant SAF. No test is
available for detecting infection of carrier animals or those incubating disease.
Epidemiology and Control:
There is no treatment, and currently there are no practical methods of controlling the spread of scrapie in flocks in
which it is endemic.
Goats can be infected by contact with scrapie-infected sheep, either directly or by exposure to contaminated pastures.
The Testes:
Spermatogenesis is stimulated by FSH and augmented by androgens, primarily testosterone. Leydig cells, under the
influence of LH, produce testosterone and, in some species (eg, equine), also estrogens.
Nonantibiotic Alternatives:
Drugs of primary interest for evacuation of the uterus are oxytocin, ergonovine, estrogens, and in some species (eg,
dogs), PGF2α. Of these drugs, estrogens and PGF2α may have a dual beneficial effect, stimulating both the contractions of the
uterus (eg, in cases of retained lochia or placenta, or postpartum metritis) and the local cellular defense. In addition to its
contractile effect on the myometrium, PGF2α causes regression of the CL in several species. This allows estrus to occur,
which reinforces the effect on the myometrium and produces endogenous estrogen.
Cryptorchidism
is a failure of one or both testicles to descend into the scrotum. Testes retained within the abdomen suffer thermal
suppression of spermatogenesisBilateral cryptorchidism results in sterility; unilateral cryptorchidism is more common,
and fertility is usually near normal because of normal sperm production from the testicle located in the scrotum.
Cryptorchidism is seen in all domestic animals but is most common in stallions and boars. It is reported that
cryptorchidism in the horse is inherited as a dominant trait, while in other species it is a recessive trait.
Because of the inherited nature of the condition, unilateral cryptorchids should not be used for breeding. Because
cryptorchid testicles may become neoplastic, affected animals should be castrated.
Infectious Causes
Neospora Infection:
Leptospirosis:
Leptospira interrogans , serovars grippotyphosa , pomona, hardjo, canicola , and icterohaemorrhagiae usually cause
abortions in the last trimester, 2-6 wk after maternal infection. Although the dam may show clinical signs of leptospirosis,
most abortions are in otherwise healthy cows. The leptospires cause a diffuse placentitis with avascular, light tan cotyledons
and edematous, yellowish intercotyledonary areas.
Brucellosis:
Brucellosis (Bang's disease) is a threat in all countries where cattle are raised. Brucellosis causes abortions in the
second half of gestation (usually ~7 mo), and ~80% of unvaccinated cows in later gestation will abort if exposed to
Brucella abortus . The organisms enter via mucous membranes and invade the udder, lymph nodes, and uterus, causing a
placentitis. The placentitis may be acute or chronic, with abortion or stillbirth occurring 2 wk to 5 mo after initial infection.
Affected cotyledons may be normal to necrotic, and red or yellow. The intercotyledonary area is focally thickened with a
wet, leathery appearance. The fetus may be normal or autolytic with bronchopneumonia.
Brucellosis is a serious zoonosis and a reportable disease.
Mycotic Abortion:
Fungal abortion due to Aspergillus sp (septic fungi, 60-80% of cases), or to Mucor sp , Absidia , or Rhizopus sp
(nonseptate fungi) is an important cause of bovine sporadic abortion. Abortions occur from 4 mo to term. Mycotic abortions
occur more often in winter. Placentitis is severe and necrotizing. Cotyledons are enlarged and necrotic with turned-in
margins. The intercotyledonary area is thickened and leathery. The fetus seldom is autolyzed, although it may be
dehydrated; ~30% have gray ringworm-like skin lesions principally involving the head and shoulders. The diagnosis is
based on the skin lesions, hyphae associated with fetal dermatitis (especially eyelids), bronchopneumonia, abomasal
contents, and placental lesions.
Actinomyces pyogenes:
Actinomyces (Corynebacterium) pyogenes causes sporadic abortion in the last trimester. The fetus is usually autolyzed,
with fibrinous pericarditis, pleuritis, or peritonitis possible.
Trichomoniasis:
Trichomonas (Tritrichomonas) foetus infection causes a venereal disease that usually results in infertility but
occasionally causes abortion in the first half of gestation. Placentitis is relatively mild with hemorrhagic cotyledons and a
thickened intercotyledonary area covered with flocculent exudate.
Campylobacteriosis:
Campylobacter fetus venerealis infection causes a venereal disease that usually results in infertility
Listeriosis:
Listeria monocytogenes can cause placentitis and fetal septicemia. Abortion is at any stage of gestation, and the dam
may have fever and anorexia before the abortion. The fetus is retained for 2-3 days after death, so autolysis may be
extensive. The fetal liver is shrunken and gray and contains pinpoint microabscesses. There is necrosis of the cotyledons
Abortion in Sheep
The major infectious agents causing abortions in sheep are Campylobacter , Chlamydia , Toxoplasma , Listeria ,
Brucella , and Salmonella .
Toxoplasmosis:
Toxoplasmal placentitis causes cotyledonary lesions consisting of gray-white foci, 1-3 mm in diameter. The
intercotyledonary area is normal or slightly edematous.
Abortion in Goats
Major infectious causes of abortion in goats are toxoplasmosis, chlamydiosis, leptospirosis, brucellosis, and listeriosis.
Abortion in Horses
The most common noninfectious cause of abortion in horses is twinning.
Bacterial Abortion:
Potomac horse fever ( Potomac Horse Fever) caused by Ehrlichia risticii may be followed by abortion in mid to late
gestation.
Salmonella spp and Leptospira sp have been implicated in equine abortions.
Brucellosis in Cattle
(Contagious abortion, Bang's disease)
Etiology and Epidemiology:
The disease in cattle, water buffalo, and bison is caused almost exclusively by Brucella abortus ; however, B suis or B
melitensis is occasionally implicated in some cattle herds. Brucella suis does not appear to be contagious from cow to cow.
Infection spreads rapidly and causes many abortions in unvaccinated herds. Typically, in a herd in which disease is
endemic, an infected cow aborts only once after exposure; subsequent gestations and lactations appear normal. After
exposure, many cattle become bacteremic for a short period and develop agglutinins and other antibodies; others resist
infection, and a small percentage of infected cows recover.
Clinical Findings:
Abortion is the most obvious manifestation.
Seminal vesicles, ampullae, testicles, and epididymides may be infected in bulls; therefore, organisms are in the semen.
Diagnosis:
Diagnosis is based on bacteriology or serology. Most cows cease shedding organisms from the genital tract when
uterine involution is complete. Foci of infection remain in some parts of the reticuloendothelial system, especially
supramammary lymph nodes, and in the udder.
Serum agglutination tests have been the standard diagnostic method. Agglutination tests may also detect antibodies in
milk, whey, semen, and plasma.
Screening Tests:
1) Brucella milk ring test (BRT): Cows in herds with a positive BRT are individually blood tested, and reactors are
slaughtered.
2) Market cattle testing: Nondairy and dairy herds in an area may also be screened for brucellosis by testing serum
samples collected from cattle destined for slaughter or replacements through intermediate and terminal markets, or at
abattoirs. Reactors are traced to the herd of origin, and that entire herd is tested.
Control:
Efforts are directed at detection and prevention because no practical treatment is available. Eventual eradication
depends on testing and eliminating reactors.
Noninfected herds must be protected.
Brucellosis in Sheep
Brucella melitensis infection in certain breeds of sheep causes clinical disease similar to that in goats (see Brucellosis
in Goats). However, B ovis produces a disease unique to sheep, in which epididymitis and orchitis impair fertility—the
principal economic effect.
Primary manifestations are lesions of the epididymis, tunica, and testis in rams; placentitis and abortion in ewes; and
occasionally perinatal death in lambs. After regression of the acute phase—which may be so mild as to go unobserved—
lesions may be palpated in the epididymis and scrotal tunics. Epididymal enlargement may be unilateral or bilateral. The tail
of the epididymis is involved more frequently than the head or body, and the most prominent lesion is spermatoceles of
variable size containing partially inspissated spermatic fluid. The tunics frequently become thickened and fibrous, and
extensive adhesions develop between them.
Serologic tests used for eradication of disease and certification of animals have included ELISA, complement fixation,
hemagglutination inhibition, indirect agglutination, and gel diffusion.
Because infection in ewes apparently originates almost exclusively from service by infected rams, lamb losses through
infection of ewes may be controlled economically by restricting vaccination to rams. There is no recommended vaccination
in the USA.
Chlortetracycline and streptomycin used concurrently have effected bacteriologic cures. However, treatment is not
economical except in especially valuable rams, and even if infection is eliminated, fertility may remain impaired.
Brucellosis in Goats
Staphylococcal Mastitis:
Staphylococcus aureus causes both acute and chronic mastitis that responds poorly to treatment. It is easily transmitted
at milking time and colonizes the teat canal but, contrary to prior opinion, does not colonize the skin.
In herds in which staphylococcal mastitis is a problem, >50% of the cows may have chronic, subclinical infections.
Staphylococcus aureus may cause peracute mastitis; peracute gangrenous mastitis (in which the skin of the quarter and teat
becomes cold and bluish and eventually sloughs); as well as acute, subacute, and chronic subclinical mastitis. Infections
lasting more than a few months often are refractory to treatment because of the development of a tissue barrier between the
antibiotic and the organism.
Treatment of cows with subclinical infections during lactation is not as successful as dry-cow treatment; hence, these
cows should be treated at drying off with an approved dry-cow infusion product (eg, penicillin-streptomycin preparations,
cephalosporin, novobiocin, or benzathine cloxacillin).
Peracute and acute staphylococcal mastitis may be treated systemically with an appropriate antibiotic (eg,
erythromycin, oxytetracycline). For intramammary therapy, cloxacillin is recommended, but sensitivity tests may reveal that
other infusions, such as erythromycin or penicillin, may be effective.
Coagulase-negative staphylococci cause subclinical and clinical mastitis.
Streptococcal Mastitis:
The mammary gland is required for perpetuation of Streptococcus agalactiae in nature. All other streptococci, whether
saprophytes or potential pathogens, enter the mammary gland by chance and do not depend on it for survival. Therefore, S
agalactiae mastitis is a specific infectious disease that can be eradicated from dairy herds. The organism enters the gland
through the teat opening and resides in the milk and on the surface of the milk channels. It does not penetrate the tissue.
Initially, it multiplies rapidly, causes an outpouring of neutrophils into the ducts, and damages the ductal and acinar
epithelium, which leads to ductal obstruction with cells and cellular debris. Fibrosis of interalveolar tissue and involution of
acini in affected lobules quickly follow and lead to a loss of secretory function.
Because S agalactiae spreads from cow to cow during milking, shedder cows should be milked last. Some believe that
calves fed on milk containing S agalactiae may transmit it to the immature glands of penmates if they are permitted to
suckle each other. For this reason, milk-fed calves are housed separately. Streptococcus agalactiae is most likely to
contribute substantially to unacceptable bacterial counts in milk.
Mastitis caused by S agalactiae responds well to penicillin, but some of the other streptococci appear to be more
resistant. The antibiotic is infused into the infected gland through the teat canal after thorough disinfection of the teat
orifice. Cephalosporin or sodium cloxacillin also may be used. Benzathine cloxacillin, penicillin-novobiocin, cephalosporin,
or long-acting penicillin preparations may be used in dry-cow treatment. Postmilking teat dipping will reduce new
infections by 50%, and total dry-cow therapy will cure >90% of S agalactiae infections.
Streptococcus uberis , S dysgalactiae , and other environmental streptococci pose threats of mastitis infections on most
farms. These infections arise from environmental exposure of the teat after milking and from contamination of teat skin
between milkings. Most environmental streptococcal infections last 14-30 days. Subclinical mastitis caused by
environmental streptococci may result in high somatic cell counts on individual cows for short periods (≤30 days).
Coliform Mastitis:
The most common coliforms are Escherichia coli , Enterobacter aerogenes , and Klebsiella spp . In quarters with low
cell counts, coliforms multiply rapidly. The inflammatory reaction that follows destroys the coliform population, thereby
releasing endotoxin. The resulting toxemia produces the local and systemic signs of acute or peracute mastitis (including
gangrene in occasional cases), and death may occur. Rectal temperature in acute or peracute mastitis is 103-108°F (39-
42°C). Milk secretion ceases (even though usually only one gland is infected), and anorexia, depression, dehydration, and
Treatment:
Treatment is almost always recommended when clinical mastitis occurs. Penicillin is the drug of choice for
streptococcal mastitis and nonresistant staphylococci. However, in some herds, most staphylococcal isolates are resistant, so
that semisynthetic penicillins (such as cloxacillin, which is not affected by staphylococcal penicillinase) are more effective.
Although treatment usually hastens return of production, a high percentage of staphylococcal infections may not be
eliminated during lactation. A somewhat better cure rate results from dry-cow therapy. Coliforms vary widely in their
antibiotic sensitivity and may respond best to supportive therapy without antibiotics. Mastitis caused by Mycoplasma does
not respond to therapy.
Certain antibiotics, such as erythromycin, reach much higher levels in the milk than in plasma after systemic
administration and may be useful in acute and peracute cases due to susceptible organisms. Clinical infections should be
treated as they occur, and subclinical infections at drying off (especially Staph aureus and streptococcal infections). Use of
parenteral antibiotics and nonsteroidal anti-inflammatory drugs is recommended in toxic cases.
Mastitis in Sows
Mastitis can be important in swine-raising units. Peracute mastitis can affect sows and gilts and is most commonly
associated with coliform ( Escherichia coli , Enterobacter aerogenes , and Klebsiella ) infections. It is most common at or
just after parturition, and affected sows have a moderate to severe toxemia. The sow's temperature may be increased to
107°F (42°C) or may be subnormal. The affected glands are swollen, purple, and have a watery secretion. Sow mortality is
high, and the piglets will die unless fostered or fed artificially. Milk production of recovered sows may be impaired in the
next lactation. The treatment of peracute coliform mastitis in sows is similar to that in cows. Ampicillin,
dihydrostreptomycin, or oxytetracycline administered systemically has been used.
Subacute mastitis may occur in older sows and lead to induration of one or more glands and impair the sow's ability to
nurse a large litter. This form of mastitis is more likely to be associated with infection by streptococci or staphylococci.
Granulomatous lesions in the mammae of sows have been associated with Actinobacillus lignieresii , Actinomyces bovis ,
and Staph aureus infections.
The control of mastitis in sows has not been extensively investigated, but isolating sows in adequately disinfected pens
before, during, and for an adequate period after farrowing should help prevent the severe losses associated with coliform
mastitis.
Mares:
Although profound endometritis accompanies contagious equine metritis ( Contagious Equine Metritis) in mares, most
breeding problems are related to endometritis caused by nonspecific infections. In mares, the most common etiologic agent
of endometritis is Streptococcus zooepidemicus , but several other organisms may be involved, including Escherichia coli ,
Pseudomonas aeruginosa , and Klebsiella pneumoniae . Yeasts and fungi are incriminated in some cases, particularly in
mares with reduced resistance, or as a sequela of exuberant antimicrobial therapy. Visible exudate is rarely a feature of
endometritis in mares.
Intrauterine therapy is still commonly used in mares.
Sows:
A form of endometritis characterized by profuse vaginal discharge at the onset of estrus has been described in Europe
and other countries. The causative agent is usually Staphylococcus hyicus or Escherichia coli , and the disease seems to be
transmitted at mating or artificial insemination; signs are seen 15-25 days later during the subsequent proestrus or estrus.
Other Species:
Endometritis has been seen in sheep, goats, and camelids. In commercial sheep and goat flocks, diagnosis is seldom
made antemortem, and treatment is generally impractical. In animals with a persistent uterine discharge, remnants of a
macerated fetus should be considered as a nidus of chronic infection. Endometritis in camelids is usually treated empirically
based on treatments for cattle and horses.
Pyometra
Pyometra is characterized by the accumulation of purulent or mucopurulent exudate in the uterus. In cows, it is
invariably accompanied by the persistence of an active corpus luteum and interruption of the estrous cycle. In
affected mares, the cervix is often found to be fibrotic, inelastic, affected with transluminal adhesions, or in
some other way impaired. Mares may continue to cycle normally, or the cycle may be interrupted. Discharge
from the genital tract may be absent or intermittent and corresponding to periods of estrus. As a rule, affected
animals do not exhibit any systemic signs of illness, but affected mares may be in poor condition. In both cows and
mares, pyometra must be distinguished carefully from pregnancy before treatment is undertaken.
The treatment of choice in cows is administration of PGF2α or its analogs at normal luteolytic doses. No
intrauterine treatment is recommended in conjunction with the prostaglandin.
Lavage of the uterus using large volumes of fluid is recommended, but the condition frequently recurs, and permanent
cure in these cases requires hysterectomy.
Cows:
Normal expulsion of fetal membranes occurs within 3-8 hr after delivery of the calf. Retention of fetal membranes
usually is defined as failure to expel fetal membranes within 24 hr after parturition. The incidence is 5-15% in healthy dairy
cows and lower in beef cows. The incidence is increased by abortion, dystocia, hypocalcemia, twin birth, high
environmental temperature, advancing age of the cow, premature birth or induction of parturition, placentitis, and nutritional
disturbances.
The precise pathogenesis of retained fetal membranes is poorly understood, but normal maturation and loosening of the
placenta begin during late pregnancy and are marked by alterations in the collagen of the placentome. During parturition,
changes in uterine pressure, diminution of blood flow, and physical flattening of the placentome during uterine contractions
contribute to final loosening and expulsion of the fetal membranes.
Diagnosis is usually straightforward—degenerating, discolored, ultimately fetid membranes are seen hanging from the
vulva >24 hr after parturition. Occasionally, the membranes may be within the uterus and not readily apparent, in which
case their presence may be detected by a foul-smelling discharge. In most cases, there are no signs of systemic illness.
When systemic signs are seen, they are related to toxemia. However, such cows are at increased risk of developing metritis,
ketosis, mastitis, and even abortion in a subsequent pregnancy. Cows that have once had retained fetal membranes are at
increased risk of developing the condition at a subsequent parturition.
Manual removal of the retained membranes is no longer recommended and is potentially harmful. Trimming of excess
tissue that is objectionable to animal handlers and contributes to gross contamination of the genital tract is permissible.
Untreated cows expel the membranes in 2-11 days. Routine use of intrauterine antimicrobials has not been found to be
beneficial and may be detrimental. Although oxytocin, estradiol, and prostaglandin F2α have all been advocated at various
Mares:
The equine fetal membranes are normally expelled within 3 hr after parturition, but expulsion may be delayed for 8-12
hr or even longer without signs of illness.
Retention of fetal membranes may mediate development of metritis or even peritonitis. Laminitis is a potential sequela.
In cases of prolonged retention of fetal membranes, antimicrobials should be administered prophylactically along with
nonsteroidal anti-inflammatory drugs and other therapeutic strategies to prevent laminitis.
Trichomoniasis: Introduction
Trichomoniasis is a venereal protozoal disease of cattle characterized primarily by early fetal death and infertility,
resulting in extended calving intervals. Distribution is probably worldwide.
Etiology and Epidemiology:
The causative protozoan, Trichomonas (Tritrichomonas) foetus , is pyriform and ordinarily 10-15 × 5-10 µm, but there
is considerable pleomorphism. Although T foetus can survive the process used for freezing semen, it is killed by drying or
high temperatures.
Trichomonas foetus is found in the genital tracts of cattle. When cows are bred naturally by an infected bull, 30-90%
become infected. By contrast, most cows are free of infection within 3 mo after breeding. However, immunity is not long-
lasting and reinfection does occur. Transmission can also occur when the semen from infected bulls is used for artificial
insemination.
Clinical Findings:
Trichomonas foetus has been found in vaginal cultures taken as late as 8 mo of gestation and, apparently, live calves
can be born to infected dams. Pyometra occasionally develops after breeding.
Diagnosis:
History and clinical signs are useful but are essentially the same as those of campylobacteriosis. Douching with saline
or lactated Ringer's solution (without preservatives) can be used. Studies suggest that 90-95% of infected bulls will be
positive on culture, and that three successive cultures at weekly intervals will detect ~99.5% of infected bulls. Vaginal pus
(after treatment of pyometra) or vaginal mucus (obtained toward the end of a luteal phase) may also be of diagnostic value.
Treatment and Control:
Various imidazoles have been used to treat bulls, but none is both safe and effective. Ipronidazole is probably most
effective but, due to its low pH, frequently causes sterile abscesses at injection sites. Trichomonas foetus can be safely
eliminated from semen with dimetridazole. Vaccines have been developed for use in cows but none is highly effective.
Dystocia
Difficult birth may result from myometrial defects, metabolic abnormalities such as hypocalcemia, inadequate pelvic
diameter, insufficient dilation of the birth canal, fetal hormone (corticosteroid) deficiency, fetal oversize, fetal death, or
abnormal fetal presentation and posture.
Dystocia should be considered in any of the following situations: 1) an animal has a history of previous dystocia or
reproductive tract obstruction; 2) parturition does not occur within 24 hr after the drop in rectal temperature (to <100°F
[37.7°C]); 3) strong abdominal contractions for 1-2 hr without passage of a puppy or kitten; 4) active labor for 1-2 hr
without delivery of subsequent puppies or kittens; 5) the resting period during active labor exceeds 4-6 hr; 6) the bitch or
queen is in obvious pain (crying, licking, or biting the vulva); 7) there is a black, purulent, or hemorrhagic vaginal
discharge; 8) there are signs of systemic illness; or 9) gestation is prolonged.
To determine the appropriate therapy, the cause of the dystocia (obstructive versus nonobstructive) must be determined
and the condition of the animal assessed. The animal should be examined for signs of systemic illness which, if present,
may necessitate immediate cesarean section. The normal vaginal discharge at parturition is a dark green color; abnormal
color or character indicates immediate attention is needed.
Oxytocin (3-20 u in bitches, 2-5 u in queens) given IM up to three times at 30-min intervals, with or without 10%
calcium gluconate (3-5 mL, IV slowly, once) may be given in an attempt to promote uterine contractions. If no response
follows, a cesarean section should be performed.
Forceps may be used (carefully) to remove dead fetuses or to facilitate delivery of malpresented or partially delivered
fetuses. Gentle manipulation and adequate lubrication must be used to prevent injury or death to living fetuses. Episiotomy
may be helpful.
Surgery is indicated for obstructive dystocia, if dystocia is accompanied by shock or systemic illness, for primary
uterine inertia, when active labor is prolonged, and/or if medical management has failed.
False Pregnancy
(Pseudopregnancy, Pseudocyesis)
False pregnancy is common in bitches and uncommon in queens. It occurs at the end of diestrus and is characterized by
hyperplasia of the mammary glands, lactation, and behavioral changes. Some bitches behave as if parturition has occurred,
“mothering” by nesting inanimate objects and refusing to eat. The possibility of true pregnancy should be eliminated by the
history, abdominal palpation, and abdominal radiographs and ultrasonography.
If owners are distressed by repeated bouts of pseudopregnancy, the bitch should either be bred or undergo
ovariohysterectomy. Ovariohysterectomy prevents recurrence.
Pyometra
Pyometra is a hormonally mediated diestrual disorder characterized by an abnormal uterine endometrium with
secondary bacterial infection. In the normal bitch, the corpora lutea produce progesterone for 9-12 wk after ovulation in
each estrous cycle. If pregnancy does not occur after a cat is induced to ovulate, the life span of the corpora lutea is ~45
days.
Etiology:
Factors associated with occurrence of pyometra include administration of long-lasting progestational compounds to
delay or suppress estrus, administration of estrogens to mismated bitches, and postinsemination or postcopulation infections.
Progesterone promotes endometrial growth and glandular secretion while decreasing myometrial activity. Cystic
endometrial hyperplasia and accumulation of uterine secretions ultimately develop and provide an excellent environment for
bacterial growth. Progesterone may also inhibit the WBC response to bacterial infection. Bacteria from the normal vaginal
flora or subclinical urinary tract infections are the most likely source of uterine contamination. Escherichia coli is the most
common bacterium isolated in cases of pyometra, although Staphylococcus , Streptococcus , Pseudomonas , Proteus spp ,
and other bacteria also have been recovered. Because queens require copulatory stimulation to ovulate, form corpora lutea,
and produce progesterone, pyometra is less common in queens than in bitches.
Estrogen, by itself, does not contribute to the development of cystic endometrial hyperplasia or pyometra. However, it
does increase the stimulatory effects of progesterone on the uterus. Administration of exogenous estrogens to prevent
pregnancy (ie, “mismate shots”) during diestrus greatly increases the risk of developing pyometra and should be
discouraged.
Clinical and Laboratory Findings:
Clinical signs are seen during diestrus, usually 4-8 wk after estrus, or after administration of exogenous progestins. The
signs are variable and include lethargy, anorexia, polyuria, polydipsia, and vomiting. When the cervix is closed, there is no
discharge and the large uterus may cause abdominal distention. Signs can progress rapidly to shock and death.
Physical examination reveals lethargy, dehydration, uterine enlargement, and if the cervix is patent, a sanguineous to
mucopurulent vaginal discharge. Only 20% of affected animals have a fever. Shock may be present.
The leukogram of animals with pyometra is variable and may be normal; however, leukocytosis characterized by a
neutrophilia with a left shift is usual. Leukopenia may be found in animals with sepsis. A mild, normocytic, normochromic,
nonregenerative anemia (PCV of 28-35%) may also develop. Hyperproteinemia due to hyperglobulinemia may be found.
Results of urinalysis are variable. With E coli uterine infection, isosthenuria due to endotoxin-induced impairment of renal
tubular function or to insensitivity to antidiuretic hormone (or both) may develop. A glomerulonephropathy caused by
immune-complex deposition may result in proteinuria. These renal lesions are potentially reversible once the pyometra is
resolved.
Diagnosis:
Pyometra should be suspected in any ill, diestrual bitch or queen, especially if polydipsia, polyuria, or vomiting is
present. The diagnosis can be established from the history, physical examination, and abdominal radiography and
ultrasonography. Vaginal cytology is often helpful in determining the nature of the vulvar discharge. The
complete blood count, biochemical profile, and urinalysis help exclude other causes of polydipsia and polyuria
and vomiting; they also evaluate renal function, acid-base status, and septicemia.
Treatment and Prognosis:
Vaginal Hyperplasia
In vaginal hyperplasia, a proliferation of the vaginal mucosa, usually originating from the floor of the vagina anterior to
the urethral orifice, occurs during proestrus and estrus, as a result of estrogenic stimulation. The most common sign is a
mass protruding from the vulva. Initially, the mass is smooth and glistening, but with prolonged exposure, the surface
becomes dry and fissures develop, so it has a tongue-like appearance. A slight vaginal discharge may be present. Although
the hyperplastic tissue originates near the urethral orifice, dysuria is uncommon. Vaginal hyperplasia interferes with
copulation. Reluctance to breed or failure of intromission may be the only clinical sign if the hyperplastic tissue is contained
within the vaginal vault. Vaginal hyperplasia resolves spontaneously as soon as estrogen declines. The diagnosis is made by
the history (stage of the estrous cycle) and examination of the vagina. Estrogenic stimulation could be confirmed by vaginal
cytology if the history is questionable. The two differential diagnoses are vaginal prolapse (excluded by the history and
physical findings) and neoplasia (excluded by biopsy).
If the hyperplastic tissue is not causing problems, therapy is not indicated. However, if it protrudes from the vulva,
it should be kept clean and moist and an antibiotic ointment applied. An Elizabethan collar may be necessary to
prevent self-trauma. These animals may be bred by artificial insemination. The hyperplasia regresses as soon as the
follicular phase of the estrous cycle has passed. Rarely, the hyperplasia recurs at parturition, presumably associated
with a burst of estrogen.
Vaginitis
Inflammation of the vagina may occur in prepubertal or mature (intact or spayed) bitches. It is rare in queens. Vaginitis
usually is due to bacterial infection, which may be secondary to conformational abnormalities such as vestibulovaginal
strictures. Viral infection (eg, herpes), vaginal foreign bodies, neoplasia, hyperplasia of the vagina, androgenic steroids (eg,
mibolerone), or intersex conditions also may cause vaginitis.
The most common clinical sign is a vulvar discharge. Licking of the vulva, attraction of males, and frequent micturition
also may be seen. Signs of systemic illness are not present, and the hemogram and biochemical profile are normal. The
absence of these abnormalities helps differentiate vaginitis from open-cervix pyometra, the most important differential
diagnosis. Prepubertal animals often do not require treatment because the vaginitis nearly always resolves with the first
estrus. Therefore, it may be wise to delay elective ovariohysterectomy in affected animals until after their first estrous cycle.
Prostatitis
Inflammation of the prostate gland usually is suppurative and may result in abscesses. It may be associated with
prostatic hyperplasia (see Benign Prostatic Hyperplasia). Various organisms, including Escherichia coli , Staphylococcus ,
Streptococcus , and Mycoplasma spp , have been incriminated. Infection may be hematogenous or ascending from the
urethra. Because prostatic fluid normally refluxes into the bladder, urinary tract infection often accompanies prostatic
infection.
The signs resemble those of prostatic hyperplasia. In addition, malaise, pain, and fever are common. Dehydration,
septicemia, and shock may occur in severe cases of acute bacterial prostatitis or prostatic abscess.
The historical, physical, and radiographic findings are suggestive of acute bacterial prostatitis and abscesses.
Neutrophilia with a left shift, monocytosis, and/or toxic WBC may be seen. Ultrasonography shows hypoechoic areas
consistent with pockets of fluid. Ideally, prostatic material is obtained by prostatic massage, ejaculation, or fine-needle
Neoplasms
Adenocarcinoma is the most common neoplasm of the prostate. Transitional cell carcinoma arising from the bladder
occasionally invades the prostate.
The clinical signs of prostatic neoplasia are similar to those of other prostatic diseases. Pain and fever may be present.
If the neoplasm infiltrates the urethra, dysuria or urethral obstruction is likely. Prostatic adenocarcinoma metastasizes to the
regional lymph nodes, lumbar vertebrae, and bony pelvis.
Diagnosis is made by biopsy.
There is no effective curative treatment. Consultation with a veterinary oncologist is recommended.
The three main groups of species that have anatomically similar respiratory tracts are 1) cattle, sheep, and pig; 2) dog,
cat, monkey, rat, rabbit, and guinea pig; and 3) horse and man.
Marked physiologic variations also exist between different species. For example, cattle are prone to retrograde drainage
from the pharynx, are predisposed to pulmonary hypertension and reduced ventilation in a cold environment, have relatively
small lungs with low tidal volume and functional residual capacity, and are more sensitive to changes in environmental
temperatures than are most other species. These anatomic and physiologic differences largely determine why some
pathogens affect only some species (eg, Pasteurella haemolytica affects cattle but not pigs) and why pneumonia is very
important in some species (cattle, pigs) but less so in others (dogs, cats).
Clinical Signs of Respiratory Malfunction:
Nasal discharge may be serous, catarrhal, purulent, or hemorrhagic, depending on the degree of mucosal damage. It
indicates increased production of normal secretions, sometimes supplemented by neutrophils (purulent) or blood
(hemorrhage). It probably also indicates decreased “grooming” of the nostrils with the tongue when animals are ill.
Epistaxis (hemorrhage from the nose) is often caused by vascular rupture, such as in mycotic infection of the guttural pouch
or exercise-induced pulmonary hemorrhage in horses, or by intranasal fungal infection or neoplasia, systemic coagulopathy,
vasculitis, thrombocytopenia (immune-mediated or result of rickettsial infection), hyperviscosity syndrome, or nasal trauma.
Hemoptysis (the coughing up of blood) occurs after rupture of pulmonary aneurysms in the lungs of cattle with chronic
lung abscesses. Bleeding may also result from polyps, neoplasms, granulomas, trauma, thrombocytopenia, and bracken fern
or sweet clover toxicity.
Hyperpnea (an increase in rate and depth of pulmonary ventilation) becomes dyspnea when the breathing appears
labored and to be causing distress. Labored inhalation seen with obstructive diseases above the thoracic inlet (eg, tumors or
exudates) or with pleural effusions is termed inspiratory dyspnea; labored expiration seen with obstructive diseases below
the thoracic inlet (eg, diffuse bronchitis or emphysema) is termed expiratory dyspnea. Other responses include coughing,
clear exudates, and shallow breathing with grunting, often associated with the pain of pleuritis. Fixed airway obstructions
(eg, tracheal neoplasia or stenosis) or a combination of upper and lower obstructive airway diseases will result in both
inspiratory and expiratory dyspnea.
Principles of Therapy
Respiratory disease is often characterized by abnormal production of secretions and exudates and by a reduced ability
to remove them. The primary goal is to reduce the volume and viscosity of the secretions and to facilitate their removal.
This can be accomplished by controlling infection, modifying the secretions, and when possible, improving postural
drainage and mechanically removing the material. Therapeutic methods include altering the inspired air and administering
expectorants, antitussives, bronchodilators, antimicrobials, diuretics, and other drugs.
Hydration should be maintained. Inhalation of humidified air may facilitate removal of airway secretions. Expectorants
are sometimes used with the intention of liquefying these secretions. However, they should be used in conjunction with
ancillary respiratory therapy such as improved postural drainage, mild exercise, and thoracic percussion, which (in addition
to coughing) encourages expectoration and removal of secretions. The value of expectorants at traditional dosages is
questioned. Mechanical removal of tenacious and viscid secretions by aspiration may be necessary in severe airway
obstruction.
Antitussive agents are indicated to relieve the discomfort associated with unproductive coughing but are
contraindicated when secretion of airway mucus is excessive. Products that contain atropine also are contraindicated, at
least in theory, because atropine increases the viscosity of airway secretions.
Increased airway resistance caused by bronchial smooth muscle contraction can be alleviated with bronchodilators,
which may be indicated in animals with asthma-like conditions and chronic respiratory disease. Methylxanthines, such as
theophylline and aminophylline, are effective bronchodilators in species other than cattle. Isoproterenol, clenbuterol, and
epinephrine are also generally effective, and sodium cromoglycate is used in horses for treating small airway disease (eg,
heaves). The use of corticosteroids is justified in allergic conditions. Antihistamines can be used to alleviate the
bronchoconstriction caused by histamine release. Bronchospasm also can be reduced significantly by removing irritating
factors, using mild sedatives, or reducing periods of excitement.
Laryngeal Paralysis
This disease of the upper airway is common in dogs and rare in cats. Signs include a dry cough, voice changes, noisy
breathing that progresses to marked difficulty in breathing with stress and exertion, stridor, and collapse. Regurgitation and
vomiting may occur. Progression of clinical signs is slow, usually taking months to years before respiratory distress is
evident. It is a common acquired problem in middle-aged to older, large and giant breeds of dogs, eg, Labrador Retrievers,
Irish Setters, and Great Danes.
Diagnosis is based on clinical signs; laryngoscopy under light anesthesia is needed for confirmation. Laryngeal
movements are absent or paradoxical with respiration. Electromyography shows positive sharp waves, denervation
potentials, and sometimes myotonia. Radiographs are not diagnostic. Denervation atrophy is seen on histologic sections of
laryngeal muscles.
Differential diagnoses include myositis, recurrent laryngeal or vagal nerve tumor, inflammation, myasthenia gravis,
severe hypothyroidism, trauma, and more widespread generalized neurologic degeneration. Therapy is directed at relieving
signs of airway obstruction. Severe obstruction may require tracheotomy. Definitive therapy is surgical and is directed at
enlarging the glottic opening.
Necrobacillosis: Introduction
The term necrobacillosis is used to describe any disease or lesion with which Fusobacterium necrophorum (
Sphaerophorus necrophorus ) is associated. It includes calf diphtheria, necrotic rhinitis of pigs, footrot of cattle, foot
abscess of sheep, postparturient necrosis of the vagina and uterus, focal necrosis of the liver of cattle and sheep, quittor of
horses, and numerous other necrotic lesions in ruminants and (less commonly) pigs, horses, fowl, and rabbits. The organism
is probably a secondary invader rather than a primary cause and is usually part of a mixed infection. However, its
necrotizing exotoxin undoubtedly plays a role in the production of characteristic lesions. It is part of the normal flora of the
mouth, intestine, and genital tract of many herbivores and omnivores and is widespread in the environment. It is thought to
gain entry to the body through wounds in the skin or mucous membranes.
Calf Diphtheria
(Necrotic laryngitis, Laryngeal necrobacillosis)
Calf diphtheria is a disease of young cattle characterized by fever, inspiratory dyspnea, and stertorous breathing.
Inflammation of the laryngeal mucosa and cartilage, caused by invasion of F necrophorum into laryngeal contact ulcers, is
responsible for the clinical signs. Calf diphtheria primarily affects feedlot cattle between 3 and 18 mo of age; however,
cases in calves as young as 5 wk and in cattle as old as 24 mo have been documented. Necrotic laryngitis has a worldwide
distribution.
Etiology:
The primary etiologic agent is uncertain because F necrophorum , which is commonly isolated from lesions of affected
cattle, is unable to penetrate intact mucous membranes.
Transmission, Epidemiology, and Pathogenesis:
Necrotic laryngitis is most common where cattle are housed in dirty environments or in feedlots.
Clinical Findings:
Initially, a moist, painful cough is noticed. Severe inspiratory dyspnea, characterized by open-mouth breathing with the
head and neck extended and loud inspiratory stridor are common findings. Ptyalism; frequent, painful swallowing motions;
bilateral, purulent nasal discharge; and a fetid odor to the breath may also be present. Systemic signs may include pyrexia
(106°F [41.1°C]), anorexia, depression, and hyperemia of the mucous membranes. Untreated calves die in 2-7 days from
toxemia and upper airway obstruction. Long-term sequelae include aspiration pneumonia and permanent distortion of the
larynx.
Lesions:
Lesions are typically located over the vocal processes and medial angles of arytenoid cartilages. Acute lesions are
characterized by edema and hyperemia surrounding a necrotic ulcer in the laryngeal mucosa; lesions may spread along the
vocal folds and processes to involve the cricoarytenoideus dorsalis muscle. In chronic cases, lesions consist of necrotic
cartilage associated with a draining tract surrounded by granulation tissue.
Diagnosis:
Clinical signs are usually sufficient to establish a diagnosis. However, because numerous other conditions can cause
signs of upper airway obstruction, the larynx should be visually inspected to confirm a diagnosis. Differential diagnoses
include pharyngeal trauma; severe viral laryngitis (eg, infectious bovine rhinotracheitis); actinobacillosis; and laryngeal
edema, abscesses, trauma, paralysis, or tumors.
Treatment and Control:
Pneumonic Pasteurellosis
Etiology:
Pasteurella haemolytica biotype A, serotype 1 is the bacterium most frequently isolated from the lungs of cattle with
BRD. Although less frequently cultured than P haemolytica , P multocida is also an important cause of bacterial pneumonia.
Haemophilus somnus is being increasingly recognized as an important pathogen in BRD; these bacteria are normal
inhabitants of the nasopharynx of cattle (see also Haemophilus Somnus Disease complex: Introduction ). When pulmonary
abscessation occurs, generally in association with chronic pneumonia, Actinomyces pyogenes is frequently isolated.
The increased bacterial growth rate and colonization of the lungs may be due to suppression of the host's defense
mechanism related to environmental stressors or viral infections. It is during this log phase of growth that virulence factors
are elaborated by P haemolytica , such as an exotoxin that has been referred to as leukotoxin. The interaction between the
virulence factors of the bacteria and host defenses results in tissue damage and development of pneumonia.
Clinical Findings:
Clinical signs of bacterial pneumonia are often preceded by signs of viral infection of the respiratory tract. With the
onset of bacterial pneumonia, the severity of clinical signs increases and are characterized by depression and toxemia. There
will be pyrexia (104-106°F [40-41°C]); serous to mucopurulent nasal discharge; moist cough; and a rapid, shallow
respiratory rate. Auscultation of the cranioventral lung field reveals increased bronchial sounds, crackles, and wheezes. In
severe cases, pleurisy may develop, which is characterized by an irregular breathing pattern and grunting on expiration. The
animal will become unthrifty in appearance if the pneumonia becomes chronic, which is usually associated with the
formation of pulmonary abscesses.
Lesions:
Pasteurella haemolytica causes a severe, acute fibrinous pneumonia or fibrinonecrotic pneumonia. The pneumonia has
a bronchopneumonic pattern. Grossly, there is extensive reddish black to grayish brown cranioventral regions of
consolidation with gelatinous thickening of interlobular septa and fibrinous pleuritis. There are extensive thromboses, foci
of lung necrosis, and limited evidence of bronchitis and bronchiolitis.
Pasteurella multocida is associated with a less fulminating fibrinous to fibrinopurulent bronchopneumonia. In contrast
to P haemolytica , P multocida is associated with only small amounts of fibrin exudation, some thromboses, limited lung
necrosis, and suppurative bronchitis and bronchiolitis.
Haemophilus somnus infection of the lungs results in purulent bronchopneumonia that may be followed by septicemia
and infection of multiple organs. Occasionally, H somnus is associated with extensive pleuritis.
Pulmonary abscessation can occur as the pneumonia becomes chronic. Abscesses develop in ~3 wk but do not become
encapsulated until 4 wk. Actinomyces pyogenes is frequently cultured from these abscesses.
Diagnosis:
Generally, neither serologic testing nor direct means of detection of bacteria are performed, and diagnosis relies on
bacterial culture.
Treatment:
Early recognition and treatment with antibiotics is essential for successful therapy. It is important that antibiotic therapy
extend beyond apparent recovery to avoid relapses. Mass medication in feed or water generally is of limited value because
sick animals do not eat or drink enough to achieve inhibitory blood levels of the antibiotic. If pulmonary abscessation has
occurred, it is difficult to achieve resolution with antimicrobials, and culling of the animal should be considered.
Mycoplasmal Pneumonia
Mycoplasmas are sensitive to several antibiotics, including the tetracyclines and macrolides.
Equine Influenza
Etiology and Epidemiology:
Equine influenza causes an acute, highly contagious, febrile respiratory disease. Two immunologically distinct
influenza viruses have been found in horse populations worldwide except in Australia and New Zealand. The clinical
outcome after viral exposure largely depends on immune status; in susceptible animals, this may vary from a mild,
inapparent infection to severe disease that is rarely fatal except in young, old, or otherwise debilitated horses and in
donkeys. Transmission occurs by the respiratory route through contact with infective respiratory secretions.
Clinical Findings and Lesions:
The incubation period is usually 1-3 days but ranges from 18 hr to 5 or, rarely, 7 days. Onset is abrupt, with fever up to
107.5°F (42°C) that usually lasts <3 days in uncomplicated infections. Coughing, usually dry, harsh, and nonproductive, is a
significant feature; it develops early in the course of the disease and may persist for several weeks, especially if bacterial
infection supervenes. Nasal discharge, although scant and serous initially, usually becomes profuse and mucopurulent later
in the presence of a superimposed streptococcal infection. Depression, anorexia, and weakness are frequent. Lacrimal
discharge, enlargement of the lymph nodes in the head, limb edema, stiffness, laminitis, expiratory dyspnea, and pneumonia
are sometimes present. Mildly affected horses recover uneventfully in 2-3 wk; severely affected horses may convalesce for
up to 6 mo. Recovery from the cough and incapacitating sequelae of the disease are hastened by complete restriction of
strenuous physical activity. Respiratory tract epithelium takes much longer to heal than clinical signs take to abate. During
this time, horses may be susceptible to the development of complicating secondary problems. The risk of complications or
serious sequelae such as pneumonia, pleuropneumonia, chronic bronchitis, and chronic obstructive pulmonary disease, are
minimized by restricting exercise, controlling dust, providing superior ventilation, and practicing good stable hygiene.
Diagnosis:
Laboratory assistance is often required to differentiate influenza from equine viral rhinopneumonitis, equine viral
arteritis, and other respiratory infections. However, occurrence of a rapidly spreading respiratory infection in a group of
horses characterized by rapid onset, high fever, depression, weakness, and widespread coughing is usually sufficient to
make a presumptive diagnosis of equine influenza. Confirmation is based on virus isolation or serology of acute and
convalescent sera. Nasopharyngeal swabs are the clinical specimens of choice for attempted virus isolation; they should be
taken as soon as possible after the onset of illness.
Treatment and Control:
Pleuropneumonia
(Pleuritis, Pleurisy)
Pleuropneumonia is an acute or chronic inflammation of the pleural membranes, presumably originating in the lung(s),
and characterized by signs related to pleural pain and pleural effusion.
Etiology and Pathogenesis:
Pleural effusion can be idiopathic but usually is associated with pneumonia, lung abscessation, penetrating thoracic
wounds, esophageal rupture, neoplasia, or peritonitis. In North America, pleuropneumonia is the most common cause of
pleural effusion, with horses involved in regular competition or long distance travel being most susceptible. A recent viral
respiratory infection, plus stress associated with transportation, exercise, or surgery and anesthesia, are important
predisposing factors.
Microbes can be isolated in about two-thirds of horses with parapneumonic pleural effusion. Typical organisms include
Streptococcus equi zooepidemicus , Escherichia coli , Pasteurella spp , Klebsiella spp , and anaerobes such as Bacteroides
and Clostridium spp . Mycoplasma felis and other Mycoplasma spp also have been isolated. In certain dry dusty regions,
lung infections with Coccidioides immitis and Nocardia spp have been associated with pleural effusion.
Clinical Findings and Diagnosis:
Early signs include fever, inappetence, depression, dyspnea, standing with abducted elbows and reluctance to move,
and subcutaneous edema of the ventral thorax and limbs. A flinching response to thoracic percussion indicates pleural pain.
Often, horses with pleuropneumonia appear to have colic or myositis. In chronic cases, there is often anorexia, weight loss,
intermittent fever and cough, abnormal respiratory effort, and in horses with sterile or neoplastic effusion, reduced exercise
tolerance.
Definitive diagnosis usually requires detection of pleural effusion and collection of samples for gross and cytologic
evaluation, Gram's stain, and culture. Cytologic examination allows differentiation of infectious from neoplastic and other
noninfectious causes of pleural effusion. A foul odor to the breath or pleural fluid is strongly suggestive of anaerobic
infection. Occasionally, horses manifest pleural pain in the absence of effusion. This is usually very early in the
development of the disease and precedes the development of the effusion. This form of the disease is sometimes referred to
as subacute pleuropneumonia.
Ultrasonography is useful to estimate the quantity of pleural fluid, to monitor the response to treatment, and to ascertain
the degree of loculation within the effusion by fibrinous adhesions. Gas bubbles within the fluid are indicative of anaerobic
infection. Radiography is of limited value until the pleural cavity is drained. Radiographs often confirm coexisting
pulmonary pathology and are useful for monitoring the resolution of pneumonic lesions after the effusion has resolved.
Hematologic findings are relatively nonspecific and usually indicate inflammation or infection. Hyperfibrinogenemia,
mild anemia, neutrophilic leukocytosis, hyperproteinemia, hypoalbuminemia, and hyperglobulinemia are usually seen.
Abnormal lung sounds include complete absence of air movement, inspiratory wheezes and crackles, friction rubs, and
musical sounds. Careful auscultation with and without the aid of a rebreathing bag, combined with outlining regions of
abnormal sound and fluid levels on the chest wall, are important for monitoring progression of the disease.
Treatment:
Drainage of the pleural cavities combined with antibiotics, anti-inflammatory agents, analgesics, and supportive nursing
care are important. Broad-spectrum antimicrobial therapy (penicillin and gentamicin) should be used initially and changed if
culture results indicate more appropriate antibiotics. Tetracycline is indicated for Mycoplasma spp infection, and
metronidazole may be required for some anaerobic infections. In many cases, the latter is used empirically until an
anaerobic infection has been ruled out. The pleural space can be drained by intermittent thoracentesis as fluid reaccumulates
or by continuous drainage with tube thoracostomy and a one-way Heimlich chest drain valve or an underwater seal. Open
chest drainage is indicated when the fluid is too viscous to drain through a tube or if it is contained within a well-
demarcated abscess cavity.
Pleural effusion secondary to peritonitis requires identification and appropriate treatment of the cause of the peritonitis.
Malignant pleural effusions are often refractory to treatment because the neoplastic process is usually advanced by the time
signs become evident. Effusion secondary to esophageal perforation and rupture requires recognition and repair of the site
of the esophageal defect. Extensive contamination of the mediastinal space with feed material often precludes successful
repair. Penetrating thoracic wounds should be debrided vigorously and repaired. Lavage of the affected hemithorax,
aspiration of the pneumothorax, and broad-spectrum antimicrobial therapy are important to minimize empyema. Prognosis
in these cases is guarded to poor.
Strangles
(Distemper)
Strangles is an infectious, transmissible, worldwide disease of Equidae characterized by inflammation of the upper
respiratory tract and most often by abscessation of the adjacent lymph nodes.
Etiology and Pathogenesis:
The causal agent, Streptococcus equi equi , is a gram-positive, capsulated, β-hemolytic Lancefield group C coccus that
forms chains. Affected animals are infectious for≥4 wk after onset. While primarily a disease of the young, animals of any
age without previous infection or immunization may be affected.
Infection is by inhalation or ingestion, followed by invasion of upper respiratory and pharyngeal mucosa in which
enzymes and toxins released by the organism induce inflammation. The organism then spreads to local lymph nodes, where
it causes lymphadenitis and abscessation. Bacteremia may occur, which disseminates the organism to lymphoid tissues
throughout the body. Local spread may cause guttural pouch inflammation and sinusitis. Production of specific antibodies
(secretory IgA and IgG) by the nasopharyngeal mucosa and maturation and drainage of the abscesses effect recovery.
Immunity after recovery is not long-lasting, usually persisting for no more than 2 yr.
Clinical Findings:
The incubation period is 3-6 days. Inappetence and fever up to 106°F (41°C) are the first signs. Inflammation of the
upper respiratory mucosa and lymphoid tissue of the pharynx occurs within 1-2 days, which makes swallowing painful. A
serous or mucopurulent bilateral nasal discharge and, sometimes, ocular discharge follow. Lymphadenopathy is the major
clinical finding. The infection spreads to the intermandibular and parapharyngeal lymph nodes and often to the
anterior cervical and parotid nodes. Abscessation of the nodes then occurs. The hemogram of infected horses is
nonspecific and shows neutrophilia with or without a left shift and hyperfibrinogenemia. The normal course of
the disease is 10-14 days when the abscesses mature and drain.
Morbidity may approach 100% in a previously unexposed population, although mortality is <2%. Death may result
from a CNS infection, pneumonia, abscessation of viscera, or asphyxiation due to compression of the pharynx or larynx.
Myocarditis and pericarditis may occur. Equine purpura may accompany or follow the disease. Empyema of the guttural
pouch ( Empyema) occurs in a few animals either through primary diverticulitis or drainage of local lymph node abscesses
into the pouch.
“Bastard strangles” is characterized by abscessation in other areas of the body, particularly of the lymph nodes in the
abdomen and less frequently the thorax. However, any lymph node can be affected. Rupture of mesenteric or mediastinal
Laryngeal Hemiplegia
(Roaring, Recurrent laryngeal neuropathy)
Permanent paresis or paralysis of the left arytenoid cartilage and vocal fold manifests clinically by exercise intolerance
and abnormal respiratory noise—primarily inspiratory stridor (whistling or roaring)—during exercise. Right-sided and
bilateral involvement (laryngeal paraplegia) are uncommon.
Etiology and Pathogenesis:
This is a distal axonopathy, usually congenital (and likely heritable), that affects the recurrent laryngeal nerves and
possibly the peroneal nerves and long fibers of the CNS. The cause of the axonal degeneration is unknown. Progressive loss
of the large myelinated fibers in the distal portion of the recurrent laryngeal nerves results in neurogenic atrophy of the
intrinsic laryngeal muscles, except for the cricothyroid muscle, which is innervated by the cranial laryngeal nerve. Initially,
the adductor muscles, notably the lateral cricoarytenoid muscle, are affected, and clinical signs become evident with
involvement of the principal abductor, the dorsal cricoarytenoid muscle. The left recurrent nerve is thought to be involved
more commonly because of its longer length, and the initial involvement of the lateral cricoarytenoid muscle because of the
larger fibers distributed to this muscle. Less common causes include direct trauma to the vagus or recurrent laryngeal nerve,
accidental perivascular injection of irritating substances, and plant ( Cicer arietinum [chick peas] and Lathyrus spp ) and
chemical (lead, organophosphate) intoxications.
Although all breeds can be affected, there appears to be a higher prevalence in long-necked and larger breeds and in
males and larger horses within a breed. Estimates of the prevalence in Thoroughbreds are 2-95% depending on the
diagnostic criteria.
Loss of neuromuscular control of the abductor muscle results in collapse of the associated arytenoid cartilage and vocal
fold, which reduces the glottal cross-sectional area. The increased impedance to flow necessitates greater effort by the
accessory muscles of respiration to maintain the airflow necessary for gas exchange. Because of the pliable nature of the
glottis, the exaggerated collapsing forces result in further collapse of the arytenoid cartilage and exacerbation of the
impedance to airflow. During strenuous exercise the affected side collapses completely so that the left arytenoid cartilage is
drawn across the midline until it abuts the abducted normal arytenoid, effectively occluding the airway (dynamic collapse).
The characteristic inspiratory whistle results from resonance within the open ventricle on the affected side. The
harsher stridor, or roar, is produced by vortex shedding from the edges of the arytenoid cartilage and vocal fold.
Clinical Findings and Diagnosis:
Affected horses are usually asymptomatic at rest. Abnormal respiratory noise during exercise and exercise intolerance
are the principal clinical signs. Diagnosis is confirmed by endoscopic observation of abnormal motion of the arytenoid
cartilage and vocal fold. With laryngeal hemiplegia, the arytenoid cartilage and vocal fold are located in a median position
within the laryngeal lumen and are immobile. Incomplete abduction, or early adduction after complete abduction, is
Nasal Polyps
Nasal polyps are pedunculated growths that arise from the mucosa of the nasal cavity and also from the nasal septum or
tooth alveolus. Polyps are usually unilateral and single but can be bilateral and multiple.
Clinical signs are dyspnea, unilateral mucopurulent nasal discharge with a foul odor, occasionally epistaxis, and a mass
that extends rostrally until it protrudes beyond the nostrils. Polyps can be seen on both endoscopic and radiographic
examinations.
Choanal Atresia
Choanal atresia is caused by persistence of the bucconasal membrane that separates the primitive buccal or oral cavity
from the nasal pits during embryonic development. Bilateral and unilateral cases have been described in horses.
Sinusitis
Primary sinusitis is caused by an upper respiratory tract infection that has involved the paranasal sinuses; it usually
involves all sinus cavities but can be confined to the ventral conchal sinus where it forms an abscess that is difficult to
detect on radiographs and is not readily accessible at surgery. Secondary sinusitis is caused by a tooth infection; in some
horses, more than one tooth may be involved. The teeth involved in decreasing order of frequency are the first molar, fourth
premolar, and third premolar. The nasal discharge may be fetid, and sinus tracts can extend from the cheek teeth to the skin.
Treatment of secondary sinusitis involves removal of affected cheek teeth.
Ethmoid Hematoma
Ethmoid hematoma is a progressive and locally destructive mass of unknown cause in the paranasal sinuses that
resembles a tumor in appearance and development but is not neoplastic. Large hematomas usually arise from the ethmoid
labyrinth, but smaller ones can arise from the floor of the sinuses. The hematoma usually extends into the nasal passage.
Sinus Cysts
Sinus cysts are single or loculated fluid-filled cavities with an epithelial lining. They develop in the maxillary sinuses
and ventral concha and can extend into the frontal sinus. Radiographs are more helpful than endoscopic examination for
diagnosis, and they can demonstrate multiloculated densities and fluid lines in the sinuses, occasionally with dental
distortion and displacement.
Empyema
In empyema of the guttural pouch, pus may accumulate secondary to upper respiratory tract infections in horses,
especially those caused by streptococci, or as a complication of other guttural pouch diseases. Bacterial infection in one or
both pouches produces an intermittent nasal discharge, painful swelling in the parotid area, and in severe cases, stiff head
carriage and stertorous breathing. Body temperature is increased, and depression and anorexia occur often. Diagnosis can be
made by endoscopy of the pharynx and affected guttural pouch, and radiographs can demonstrate partial obliteration of the
normal guttural pouch contour by accumulated fluid.
Treatment with antibiotics alone is frequently unsuccessful, although a course of penicillin therapy
combined with daily lavage of the guttural pouches with a nonirritating solution usually is effective.
Atrophic Rhinitis
Atrophic rhinitis is characterized by sneezing, followed by atrophy of the turbinate bones, which may be accompanied
by distortion of the nasal septum, and shortening or twisting of the upper jaw.
Etiology:
The etiology is complex and involves at least two organisms. Various infections (eg, inclusion body rhinitis and
pseudorabies) and noninfectious agents (eg, dust or high ammonia levels) may cause sneezing and tear-staining,
usually without leading to atrophic rhinitis. Bordetella bronchiseptica has long been implicated as a major cause.
This bacterium is not host-specific, although strains that cause atrophic rhinitis are generally isolated only from pigs. Dogs,
cats, rodents, and other species may harbor B bronchiseptica for long periods, but their role in the spread of atrophic rhinitis
in pigs is uncertain. Certain toxigenic strains of Pasteurella multocida (types A and D), often acting with B bronchiseptica ,
cause permanent turbinate atrophy and nasal distortion. Both organisms can cause clinical atrophic rhinitis. The disease has
been divided into two forms: regressive atrophic rhinitis, due to B bronchiseptica , is mild and transient and probably does
not greatly affect the animal's growth and performance; progressive atrophic rhinitis, caused by toxigenic P multocida , is
severe, permanent, and usually accompanied by poor growth.
Outbreaks of disease usually follow either the introduction of infected pigs or mixing of pigs from different sources.
Piglets may become affected at any age, especially with P multocida , which also may infect mature animals. Crowding,
Mycoplasmal Pneumonia
(Enzootic pneumonia, EP)
Mycoplasmal pneumonia is a chronic, clinically mild, infectious pneumonia of pigs, characterized by its ability to
become endemic in a herd and to produce a persistent dry cough, retarded growth rate, sporadic “flare-ups” of overt
respiratory distress, and a high incidence of lung lesions in slaughter pigs. It occurs worldwide.
Clinical outbreaks of mycoplasmal pneumonia may impair growth rate and feed conversion. This effect is enhanced
when large numbers of pigs are closely confined in poorly ventilated buildings under poor husbandry conditions.
Etiology and Epidemiology:
The terms “virus pneumonia” and “enzootic pneumonia” are frequently used to describe a characteristic disease
syndrome now known to be caused primarily by Mycoplasma hyopneumoniae .
Clinical Findings and Lesions:
In herds in which the disease is endemic, morbidity is high, but clinical signs may be minimal and mortality is low.
Coughing is the most common sign and is most obvious when pigs are roused. Sporadically, individual pigs or groups
develop severe pneumonia. A common predisposing factor is a change of weather, but other stresses (eg, transient viral
infections, parasitic migration, and mixing pigs) may also cause outbreaks.
Affected lungs are gray or purple, most commonly in the apical and cardiac lobes.
Diagnosis:
Clinical, pathologic, and epidemiologic findings are usually adequate for diagnosis. Mycoplasma hyopneumoniae can
be demonstrated in impression smears of the cut surface of the affected lung, identified by fluorescent antibody technique,
and sometimes isolated and identified in culture. Serologic tests, principally the complement fixation test, and ELISA are
occasionally used on a herd basis, but results may be difficult to interpret.
Swine Influenza
(Hog flu, Pig flu)
Swine influenza is an acute, highly contagious, respiratory disease that results from infection with type A influenza
virus. Field isolates of variable virulence exist, and clinical manifestation may be determined by secondary organisms.
Etiology:
Swine influenza virus is an orthomyxovirus of the influenza A group with hemagglutinating antigen H1 and
neuraminidase antigen N1 (ie, H1N1) and also H3N2 and their recombinants. Influenza B and C viruses have been isolated
from pigs but have not caused the classic disease. The classic type A infection with isolates of mild virulence may favor
replication of pseudorabies virus, Haemophilus parasuis, Actinobacillus pleuropneumoniae, and Mycoplasma
hyopneumoniae, any of which may complicate outbreaks. The mixing of carrier and nonimmune pigs is an important
predisposing factor. The virus is unlikely to survive outside living cells for >2 wk except in cold conditions. It is readily
inactivated by disinfectants.
Transmission and Epidemiology:
In North America, outbreaks are most common in fall or winter, often at the onset of particularly cold weather. In
warmer areas of the world, infection may occur at any time. Usually, an outbreak is preceded by one or two individual cases
and then spreads rapidly within a herd, mainly by aerosolization and pig-to-pig contact. The virus survives in carrier pigs for
up to 3 mo and can be recovered from clinically normal animals between outbreaks. In antibody-positive herds, outbreaks of
infection recur as immunity wanes.
Pathogenesis:
The spectrum of infection ranges from subclinical to acute. In the classic acute form, the virus multiplies in bronchial
epithelium within 16 hr of infection and causes focal necrosis of the bronchial epithelium, focal atelectasis, and gross
hyperemia of the lungs. Bronchial exudates and widespread atelectasis, seen grossly as plum-colored lesions affecting
individual lobules of apical and intermediate lobes occur after 24 hr. The lesions continue to develop until 72 hr after
infection, after which the virus becomes more difficult to demonstrate. Losses in reproduction associated with primary
outbreaks appear to be secondary as virus has been recovered only rarely from the fetus.
Clinical Findings:
A classic acute outbreak is characterized by sudden onset and rapid spread through the entire herd, often within 1-3
days. The main signs are depression, fever (to 108°F [42°C]), anorexia, coughing, dyspnea, weakness, prostration, and a
mucous discharge from the eyes and nose. Mortality is generally 1-4%. Some pigs may become chronically affected. In
herds that are in good condition, the principal economic loss is from stunting and delay in reaching market weight. Some
increase in piglet mortality has been reported, and effects on herd fertility, including abortions in late pregnancy, may
follow outbreaks in nonimmune herds.
Lesions:
In uncomplicated infections, the lesions usually are confined to the chest cavity. The pneumonic areas are clearly
demarcated, collapsed, and purplish red. They may be distributed throughout the lungs but tend to be more extensive and
confluent ventrally. Nonpneumonic areas are pale and emphysematous. The airways contain a copious mucopurulent
exudate, and the bronchial and mediastinal lymph nodes are edematous but rarely congested.
Diagnosis:
In typical outbreaks, a presumptive diagnosis can be made on clinical and pathologic findings, but confirmation
depends on isolation of the virus or demonstration of virus-specific antibody. Virus can be isolated from nasal secretions in
the febrile phase or from affected lung tissue in the early acute stage. A retrospective diagnosis can be made by
demonstrating a rise in virus-specific antibodies in acute and convalescent serum samples, using the hemagglutination
inhibition test. Both H3 and H1 subtype antigens should be included. This test is also used for herd surveys. To diagnose
uncomplicated influenza infection, conditions such as pasteurellosis; pseudorabies; porcine reproductive and respiratory
syndrome; and chlamydial and Haemophilus infections must be eliminated.
Treatment and Control:
Progressive Pneumonia
(Maedi, Zwoegersiekte, La bouhite, Graaff-Reinet disease, Marsh's progressive pneumonia)
This chronic, progressive, viral disease of sheep and goats is caused by a lentivirus. In sheep, the virus affects
principally the lungs and udder, but the CNS and joints also may be affected. A similar disease in goats caused by a closely
related lentivirus usually involves the nervous system and joints and less commonly the lungs.
Etiology:
The causal lentivirus (family Retroviridae), which persists in lymphocytes, monocytes, and macrophages of infected
sheep in the presence of a humoral and cell-mediated immune response, can be detected by several serological tests.
Seropositive sheep and goats must be considered infected and capable of transmitting the virus. Transmission is considered
to occur either orally, usually by ingestion of colostrum or milk that contains virus, or by inhalation of infected aerosol
droplets. Intrauterine infection is thought to occur infrequently.
Clinical Findings:
Signs rarely occur in sheep <2 yr old and are most common in sheep >4 yr old. The disease progresses slowly, with
wasting and increasing respiratory distress as the main signs. Coughing, bronchial exudate, depression, and fever are seldom
evident unless secondary bacterial infection occurs. Affected sheep may die from secondary Pasteurella pneumonia. Other,
but rarer, forms of disease produced by this virus are encephalitis and arthritis. All are low-grade, progressive infections. In
the encephalitic form (visna), ataxia, muscle tremors, or circling progresses to paresis and eventually to complete paralysis.
Acute neurologic disease is a frequent occurrence in 1- to 6-mo old kids on farms where there is a high incidence of
arthritis in lactating does. Unlike the slowly progressive arthritic disease in adults, infected kids show signs of ataxia within
1 mo of birth, which may progress to paralysis within the following 2 mo.
Lesions:
Macroscopic lesions of progressive pneumonia are confined to the lungs and associated lymph nodes. The lungs do not
collapse when the thorax is opened and are abnormally firm and heavy (2-4 times normal weight). Early lung changes may
be difficult to detect, but later in the disease, lungs are mottled by gray and brown areas of consolidation. The mediastinal
and tracheobronchial lymph nodes are enlarged and edematous. Interstitial pneumonia, perivascular and peribronchial
lymphoid hyperplasia, and hypertrophy of smooth muscle are seen throughout the entire lung. CNS lesions, when they
occur, are those of meningoleukoencephalitis with secondary demyelination. All lesions are progressive and result from the
cellular immune response of the host, and not directly from viral damage.
Diagnosis:
Clinical diagnosis of progressive pneumonia cannot be made with certainty. Pulmonary adenomatosis, verminous
pneumonia, and pulmonary caseous lymphadenitis are differential diagnoses. Necropsy can rule out both of the latter and, in
most cases, pulmonary adenomatosis also. Listeriosis, scrapie, louping ill, rabies, and space-occupying lesions should be
considered when neurologic signs are seen. In flocks experiencing progressive pneumonia for the first time, the diagnosis
should be confirmed by histopathology, serology, or isolation of the virus.
Control:
There is no effective treatment.
Pneumonia
Pneumonia is an acute or chronic inflammation of the lungs and bronchi characterized by disturbance in respiration and
hypoxemia and complicated by the systemic effects of associated toxins. The usual cause is primary viral infection of the
lower respiratory tract.
Canine distemper virus, adenovirus types 1 and 2, parainfluenza virus, and feline calicivirus cause lesions in the distal
airways and predispose to secondary bacterial invasion of the lungs. Parasitic invasion of the bronchi, as by Filaroides ,
Aelurostrongylus , or Paragonimus spp may result in pneumonia. Tuberculous pneumonia, although uncommon, is seen
more often in dogs than cats. The incidence of mycotic granulomatous pneumonias is also higher in dogs than in cats.
Cryptococcal pneumonia has been described in cats. Injury to the bronchial mucosa and inhalation or aspiration of irritants
may cause pneumonia directly and predispose to secondary bacterial invasion. Aspiration pneumonia may result from
persistent vomiting, abnormal esophageal motility, or improperly administered medications (eg, oil or barium) or food
(forced feeding); it may also follow suckling in a neonate with a cleft palate.
Clinical Findings:
The initial signs are usually those of the primary disease. Body temperature is increased moderately, and there may be
leukocytosis.
Diagnosis:
Analysis of bronchoalveolar lavage fluid is valuable for the diagnosis of bacterial infections. Leukopenia, often
expected, may not be seen in many viral respiratory infections (eg, canine infectious tracheobronchitis, feline calicivirus
pneumonia, feline infectious peritonitis pneumonia). A history of recent anesthesia or severe vomiting indicates the
possibility of aspiration pneumonia. Acutely affected animals may die within 24-48 hr of onset. Mycotic pneumonias are
usually chronic in nature. Miliary nodules seen at necropsy may suggest protozoal pneumonia.
Tracheobronchitis: Overview
Tracheobronchitis is an acute or chronic inflammation of the trachea and bronchial airways; it may be primary or
secondary depending on the etiologic agent. Bronchitis may extend from the bronchioles to the lung parenchyma.
Etiology:
Canine infectious tracheobronchitis is often secondary to viral infection of the respiratory system. Other causes of
tracheobronchitis include parasites, eg, Aelurostrongylus abstrusus (cats and dogs), Capillaria aerophila (dogs),
Crenosoma vulpis (dogs), and Oslerus osleri (dogs).
Tracheitis may be secondary either to diseases of the oropharynx or to chronic coughing related to heart disease or
noncardiac pulmonary disease. Other causes include smoke aspiration and exposure to noxious chemical fumes.
Exacerbation of a chronic bronchitis affecting middle-aged and older dogs may follow sudden changes in the weather or
other environmental stresses. Bronchial asthma (allergic bronchitis) is a syndrome in cats with similarities to asthma in man.
Young cats and Siamese and Himalayan breeds are most affected. Foreign bodies in the airway and developmental
abnormalities such as laryngeal deformities may predispose to bronchitis. Chronic bronchitis most often affects small breeds
of dogs and is characterized by persistent cough for at least two consecutive months in absence of specific pulmonary
disease.
Clinical Findings:
Spasms of coughing are the outstanding sign. These are most severe after rest or a change of environment or at the
beginning of exercise. On auscultation, the respiratory sounds may be essentially normal. In advanced cases, sonorous rales
are heard. Severe bronchitis and pneumonia are difficult to differentiate; the former often extends into the lung parenchyma
and results in pneumonia. Feline bronchial asthma may result in cyanosis and dyspnea and is accompanied by eosinophilia.
Lesions:
During the acute and subacute inflammatory stages, the air passages are filled with frothy, serous, or mucopurulent
exudate. In chronic bronchitis, they contain excessive viscid mucus. The epithelial linings are roughened and opaque, a
result of diffuse fibrosis, edema, and mononuclear cell infiltration. There also is hypertrophy and hyperplasia of the
tracheobronchial mucous glands and goblet cells.
Diagnosis:
The diagnosis is made from the history and clinical signs and by elimination of other causes of coughing. In chronic
bronchitis, chest radiographs may show an increase in linear and peribronchial markings. Bronchoscopy reveals inflamed
epithelium and tacky, often mucopurulent mucus in the bronchi. Bronchial washing is an additional diagnostic aid that may
demonstrate causative agents or significant cellular responses, eg, eosinophils.
Treatment:
Broad-spectrum antimicrobial chemotherapy is indicated for treatment of cough. Persistent, productive coughing is best
controlled by expectorants or similar antitussives that contain codeine. Transtracheal wash for cytology and culture
sensitivity may be indicated to identify an etiologic agent and to determine appropriate antimicrobial chemotherapy. A
bathroom environment with steam from a hot shower may be substituted for nebulization.
Pollakiuria must be differentiated from polyuria; polydipsia suggests polyuria. A full neurologic examination should be
performed on all animals with micturition disorders.
Urinalysis:
This is the most important diagnostic test in evaluation of urinary tract disease. (See also Urinalysis: Overview.)
Cystocentesis is the preferred method of obtaining a urine sample because it precludes contamination of the sample from the
urethra or genital tract.
A urinalysis should include evaluation of color, turbidity, specific gravity, and pH. The presence of protein, occult
blood, glucose, ketones, bilirubin, and urobilinogen may be assessed using a dipstick. A dipstick cannot differentiate
between hemoglobinuria, myoglobinuria, or hematuria; however, examination of the urine sediment can confirm hematuria.
Proteinuria should be evaluated in light of the urine specific gravity; very concentrated urine may have an increased protein
concentration without pathologic significance.
Urine sediment should be examined for RBC, WBC, epithelial cells, renal casts, crystals, parasitic ova, and bacteria.
Exfoliated neoplastic cells may be seen in the urine sediment of animals with a renal or lower urinary tract neoplasm. A
quantitative culture yielding >100 colony-forming units (CFU)/mL is considered evidence of infection. If a catheterized
sample must be used, a quantitative culture of >100,000 CFU/mL is the best indication of infection; cultures of 10,000-
100,000 CFU/mL may be seen with contamination.
Complete collection of urine for a specific period provides information on fractional excretion of electrolytes,
glomerular filtration rate (GFR), and protein excretion. The urine protein to creatinine ratio is normally <0.4 in dogs and
cats. A ratio >0.4 indicates a protein-losing nephropathy. Although animals with amyloidosis ( Amyloidosis: Introduction ,
Feline Hepatic Amyloidosis) tend to have higher ratios than those with glomerulonephritis, the ratio cannot be relied on as
an accurate differentiating test due to the large degree of overlap.
Other Diagnostics:
Evaluation of serum chemistries, including BUN, creatinine, calcium, phosphorus, and serum electrolytes, is required to
confirm renal dysfunction.
Principles of Therapy
Diseases of the urinary system can result from a variety of pathologic processes, and appropriate therapy depends on
the location, severity, and etiology of the problem. Therapy should be instituted only after an accurate history, a complete
physical examination, and a minimal laboratory data base (complete blood count, serum chemistry analysis, urinalysis, and
urine culture) are assessed. The best therapy is to remove the specific cause; however, often this is not possible, and
nonspecific or supportive therapy must be instituted.
Acute urinary obstruction is commonly an emergency. Relief of mechanical obstruction is usually accomplished by
manipulation or surgical removal of the cause. Medical therapy to replace fluid deficits and to correct acidosis and
hyperkalemia is commonly required to alleviate azotemia. Clinical improvement is usually seen in 24-48 hr because urinary
obstruction does not result in permanent parenchymal injury to the kidneys. Treatment of chronic obstruction is more
complicated because it requires a thorough search for the site and cause of obstruction; surgery may be required to eliminate
the cause.
Treatment commonly includes administration of parenteral fluids to control fluid balance and correction of acidosis,
hyperkalemia, hyperphosphatemia, and possibly hypertension. In anuria, osmotic diuretics or the use of vasodilators such as
dopamine may be helpful. If these conservative measures are inadequate, peritoneal dialysis or hemodialysis may be
instituted to maintain homeostasis while the kidneys are undergoing repair.
Therapy for chronic renal failure is complex and may require continual changes as the disease progresses. Special long-
term nutritional support may be necessary to control hyperphosphatemia, restrict protein, maintain calcium balance and
vitamin intake, and supply adequate calories in an animal with anorexia and intermittent vomiting. Other considerations
may include controlling hypertension, treating acidosis, and promoting hematopoiesis by using anabolic steroids or
recombinant erythropoietin.
Glomerular diseases in animals are difficult to treat, particularly if the animal is also in renal failure; if the animal is not
in renal failure, removing the cause of chronic antigenic stimulation of inflammation can be considered. Effective treatment
has been rare in animals with either glomerulonephritis or amyloidosis. Dietary protein restriction may reduce proteinuria
and, paradoxically, improve protein balance. Plasma transfusions have only transient effects and are rarely indicated.
Chronic, recurring infections are usually associated with pyelonephritis, prostatitis, urolithiasis, or bladder atony.
Medical therapy for urolithiasis is a matter of dissolving calculi and preventing their recurrence. A mineral-deficient
diet has been effective in control of struvite calculi. Other types of uroliths, such as cystine and urate, require specific
medical treatment.
Renal tubular acidosis may require bicarbonate therapy, depending on the form of acidosis.
Cystitis
Signs are pollakiuria, hematuria, and dysuria; some animals may break housetraining. Hematuria may be most
prominent in the last part of the voided urine. The bladder wall may be palpably thickened or tender.
Cystocentesis is preferred to catheterization. The urinalysis in a typical urinary tract infection reveals increased Hgb
and protein and increased numbers of RBC, WBC, and bacteria; the pH may be alkaline, especially if the infection is caused
by urease-positive bacteria such as Staphylococcus or Proteus spp . Fungal infections are usually diagnosed by observation
of fungal elements in the urine sediment; confirmation is by fungal culture.
Predisposing causes must be considered in chronic or recurrent bacterial cystitis. Persistence of clinical signs despite
appropriate antimicrobial therapy suggests additional disease in the lower urinary tract, eg, urolithiasis or neoplasia. Double
contrast cystourethrography or ultrasonography is used to diagnose calculi, neoplasia, and anatomic defects. Pyelonephritis
(see Pyelonephritis , Bovine Cystitis and Pyelonephritis) should be ruled out. Chronic prostatitis ( Prostatitis ) in dogs can
be diagnosed by cytology and culture of prostatic fluid (obtained by ejaculation or prostatic massage) or by prostatic biopsy
for histopathology and culture. A complete blood count and serum chemistry profile should be done to rule out predisposing
systemic diseases, eg, diabetes mellitus or hyperadrenocorticism.
First episodes of cystitis should be treated for 2-3 wk with an antibiotic, preferably based on culture and sensitivity;
without a culture, broad-spectrum antibiotics that achieve high concentration in the urine should be used. Ampicillin or a
trimethoprim-sulfonamide combination may be administered because most urinary pathogens are sensitive to these agents.
A urine culture should be performed 3-5 days after therapy ends. If the culture is negative, no further treatment is indicated;
if the culture is positive, a second course of antibiotics is given for a minimum of 3 wk.
Pyelonephritis
Acute pyelonephritis can cause systemic signs such as fever, anorexia, depression, vomiting, and pain during palpation
of the kidneys. Chronic pyelonephritis may be subclinical; cause intermittent fever, anorexia, and depression; or result in
uremia if sufficient renal tissue is destroyed. Decreased ability to concentrate the urine may result in polydipsia and
polyuria. Concurrent cystitis may cause signs of lower urinary tract disease.
The history and physical findings may be suggestive of acute pyelonephritis but usually are not helpful in chronic
infections. Increased serum urea nitrogen and creatinine concentrations, as well as other laboratory abnormalities associated
with renal failure, may be present. The urinalysis in most animals is consistent with bacterial infection (see cystitis, Bovine
Cystitis and Pyelonephritis , Cystitis ) and yields a positive bacterial culture. Bacterial or WBC casts in the urine are
strongly suggestive of pyelonephritis. In those few animals in which the infection is localized to the renal parenchyma, the
urinalysis is normal and urine cultures are negative.
Confirming pyelonephritis can be difficult. Radiographs and ultrasonography may demonstrate enlarged kidneys in
acute pyelonephritis, small and irregular ones in chronic pyelonephritis.
Antibiotic therapy, based on results of urine or renal biopsy culture and sensitivity, for a minimum of 4-6 wk is
necessary. Chronic infections can sometimes be controlled with antibiotic suppression therapy (see cystitis, Bovine Cystitis
and Pyelonephritis , Cystitis ).
Animals with renal failure secondary to pyelonephritis should be given appropriate fluid and medical therapy (see renal
failure , Renal Failure: Overview , Renal Failure).
Interstitial Nephritis
Acute interstitial nephritis in dogs may be due to leptospiral infections.
Obstructive Uropathy
Even though the kidneys would otherwise be able to function normally, obstruction to urine flow at any point below the
level of the kidneys leads to accumulation of metabolic wastes and acute renal failure. Obstruction of the urethra by uroliths
in dogs and by crystalline and mucoprotein plugs in cats is the most common cause, although tumors or blood clots in the
urethra or ureters also may be responsible.
Hydronephrosis is characterized by dilatation of the renal pelvis as the result of partial or complete obstruction to
outflow of urine from one or both kidneys. When the obstruction is acute, complete, and bilateral,
changes in the kidneys are less extensive because the period of survival is short. In unilateral or partial
obstruction, the animal survives long enough for severe pressure atrophy of the renal parenchyma and
cystic enlargement of the affected kidney to develop. Hydroureter is a common accompaniment seen when the
obstruction occurs lower in the tract. Increased hydrostatic pressure results in atrophy of functional renal
parenchyma. The papillae of the medulla disappear first; later, even the cortex may atrophy. The affected kidneys eventually
become grossly enlarged, functionless sacs, filled with urine or serous fluid.
Clinical Findings:
Animals with urethral obstruction have stranguria and frequently hematuria; abdominal pain may be marked, especially
if the obstruction is bilateral. Signs of renal failure develop rapidly and include vomiting, dehydration, hypothermia, and
severe depression. The bladder is distended and painful on palpation, and a catheter cannot be passed into it. Bradycardia or
cardiac arrhythmias due to acidosis and hyperkalemia may be present.
Diagnosis:
The history, clinical signs, and physical examination usually provide a straightforward diagnosis of urethral
obstruction. An IV pyelogram or abdominal ultrasonography is necessary in ureteral obstruction. Serum potassium levels
should be determined immediately in animals with cardiac arrhythmias. An ECG can provide presumptive evidence of
hyperkalemia (bradycardia; tall, peaked T waves; increased P-R interval; widened QRS complex; atrial standstill) if
laboratory results are delayed.
Treatment:
Normal saline is the fluid of choice; sodium bicarbonate is added to correct acidosis and hyperkalemia. In animals with
severe hyperkalemia and cardiac arrhythmias, dextrose or regular insulin and dextrose infusions can be given to drive
potassium intracellularly.
Glomerular Disease
Damage to the glomerular basement membrane results in albuminuria, which may lead to hypoalbuminemia. Animals
may exhibit signs related to hypoalbuminemia rather than uremia. Glomerulopathies are uncommon in dogs and even less
common in cats.
Glomerulonephritis is an immune-mediated disease characterized by deposition or in situ formation of immune
complexes in the glomerular capillary wall, which then incite inflammatory changes (see also Diseases Involving Immune
Complexes). In cats, the mean age at presentation is 4 yr, 75% are males, and there is no breed predisposition. It is
frequently associated with infection by feline leukemia virus (FeLV) or feline infectious peritonitis (FIP) virus. In dogs, the
mean age at presentation is 7 yr, with no breed or sex predilection. It has been associated with adenovirus, pyometra,
neoplasia, systemic lupus erythematosus (SLE), and heartworm disease.
Amyloid is the name given to any of several chemically inert fibrillar protein subunits that can be deposited in tissue
and interfere with normal organ function. (See also amyloidosis , Amyloidosis: Introduction , Feline Hepatic Amyloidosis.)
All of these proteins are deposited in a β-pleated sheet conformation, which results in the unique appearance and chemical
properties of amyloid. Most cases of amyloidosis in dogs and cats, including familial amyloidosis in Shar Pei dogs and
Abyssinian cats, are reactive, or secondary, amyloidosis. In this form of the disease, amyloid A protein is deposited in
various tissues after serum levels are increased as the result of inflammation. When the kidneys are affected, amyloid
deposition usually occurs in the glomerulus. However, in Shar Pei dogs, at least 25% of Abyssinian cats, and in a number of
domestic cats, amyloid is found primarily in the medullary interstitium. Amyloidosis usually affects middle-aged to older
dogs and cats. Beagles, Collies, and Walker Hounds are reported to be at increased risk. Animals with the familial form of
the disease are usually diagnosed at a younger age.
Clinical Findings:
Disorders of Micturition
Disorders of micturition can result from any dysfunction in urine storage or voiding, which may be neurologic or non-
neurologic in origin.
The most common non-neurologic incontinence is attributed to deficiency of sex hormones in neutered animals,
particularly females. Idiopathic urethral sphincter incompetence also occurs. Urge incontinence is seen with detrusor
irritability, usually associated with cystitis. Destruction of urethral smooth muscle by infection or neoplasia can cause
incontinence. Animals with unilateral congenital ectopic ureters may void normally and “dribble” urine intermittently, while
animals with bilateral ectopic ureters are less likely to void normally. Paradoxical urinary incontinence may occur when
there is a partial obstruction of the urethra.
Inability to urinate is characterized by frequent attempts to urinate, stranguria, and passage of only small amounts of
urine. Animals with complete obstruction rapidly become uremic. Inability to urinate can be due to mechanical obstruction
of the urethra by calculi, tumors, or strictures; to detrusor atony from overdistention of the bladder; or to neurologic disease.
Neurologic causes of micturition disorders can be categorized as upper (UMN) or lower motor neuron (LMN) lesions
to the bladder. Lesions in the sacral spinal cord, trauma to the pelvic nerve, and detrusor atony lead to LMN signs, which
are characterized by a distended, easily expressed bladder. Damage to the thoracolumbar spinal cord or disease of the
cerebrum, cerebellum, or brain stem can lead to UMN signs, which are characterized by a distended bladder that is difficult
to express. Another neurologic cause of inability to urinate is functional obstruction (reflex dyssynergia), which occurs
when there is incoordination of the normal micturition reflex; this is believed to result from overdischarge of sympathetic
nerve impulses to the urethral sphincter.
Diagnosis:
Clinical signs are usually suggestive of a micturition disorder. A catheter can easily be passed into the bladder in
animals with functional obstruction but will not pass in animals with mechanical obstruction. Plain and contrast radiography
are necessary to determine the type and location of mechanical obstruction.
Treatment:
Animals with hormonal incontinence are treated with the appropriate sex hormone—diethylstilbestrol in females and
testosterone in males. The dose should be adjusted to the minimum required to maintain continence. Alternatively, an α-
adrenergic agonist drug (eg, phenylpropanolamine, 2-4 mg/kg/day in divided doses) can be given. This also may be
beneficial in animals with urethral sphincter incompetence. Urge incontinence is treated with anticholinergic drugs such as
propantheline (dogs <20 kg, 7.5 mg daily; dogs >20 kg, 15 mg daily; cats, 7.5 mg every 72 hr). Cholinergic drugs such as
bethanechol are used in animals with detrusor atony. Functional obstruction is treated with sympatholytic drugs (eg,
phenoxybenzamine, 2.5-10 mg, 1-3 times daily); cholinergic drugs may also be necessary.
Urolithiasis: Overview
One function of the urinary system is the removal of body wastes in liquid form. However, some mineral wastes are
only slightly soluble and may precipitate to form crystals. If the transit time of crystal movement through the urinary system
is prolonged, crystals may interact and grow to macroscopic size, at which time they are known as uroliths. Urolithiasis is a
general term referring to stones located anywhere within the urinary tract. Uroliths can occur in the kidney, ureter, bladder,
or urethra and are referred to as nephroliths, ureteroliths, urocystoliths, and urethroliths, respectively. Stones generally
contain an organic matrix, which is believed to vary minimally among stones and which constitutes ~2-10% of the stone's
chemical composition. The remaining 90-98% of a stone's chemical structure comprises crystalline mineral that varies
depending on the type of stone.
Mechanisms involved in stone formation are not well understood.
Canine Urolithiasis
Struvite Stones:
The most common urinary stones in dogs are composed of struvite. The mineral composition is
mostly struvite (MgNH4PO4·6H2 O), but frequently, small amounts of hydroxyapatite crystals
(Ca10[PO4]6 [OH]2) are included. In most cases, struvite uroliths form in association with urinary
tract infections with urease-producing Staphylococcus intermedius or Proteus sp ; dogs that form struvite stones in the
absence of infection may do so because of a renal acidification defect, or because they tend to pass very concentrated urine.
Extreme supersaturation occurs in urine when urease produced by bacteria hydrolyzes urea. The action of urease on urea
increases urinary ammonium ion concentration and urine pH. Increased urine alkalinity increases trivalent phosphate ion
availability and, as a result, urine becomes supersaturated with respect to struvite. Diets rich in protein contribute to struvite
urolithiasis by undergoing digestion, catabolism, and eventual urea formation. The increased blood urea concentrations lead
to increased urea excretion and increased renal medullary tonicity.
Medical management involves dissolution and prevention of stone formation. In both instances, the aim of treatment is
to reduce the concentrations of NH4 +, Mg+ 2, and PO4 -3 in urine. For dissolution, urine should be extremely undersaturated
for struvite; for prevention, the degree of struvite saturation should be sufficiently low to make crystallization unlikely. The
choice between surgical and medical treatment may not be easy.
Dissolution Protocol:
A commercially available prescription diet for stone dissolution (eg, Canine s/d® [Hill's]) should be fed. When fed to
provide the daily energy requirements (45-75 calories/kg/day), dogs have reduced intake of protein, phosphate, and
magnesium and a high intake of sodium. The diet causes the production of acidic urine, which reduces the proportion of
urinary phosphate in the trivalent form. The low urinary urea concentration may also reduce ammonia production by the
action of urease-producing bacteria.
The urease-producing urinary tract infection should be treated. Most Staphylococcus and Proteus infections are
sensitive to amoxicillin or ampicillin.
A urease inhibitor can be given but is not usually necessary. Concurrent treatment with a urease inhibitor such as
acetohydroxamic acid enhances the rate of struvite stone dissolution, particularly when antibiotic resistance precludes
effective antibacterial sterilization of the urine.
Stones that fail to reduce in size after 8 wk of treatment should be treated another way because they are probably not
composed of struvite. Renal stones tend to dissolve more slowly than do bladder stones.
Once the urinary tract is free of stones, prevention strategies are much more likely to be successful.
Prevention Protocol:
The concentration of major struvite solutes in urine should be reduced.
An acidic urine should be maintained. Dogs are at risk for struvite stone formation only when the urine is alkaline.
Urease-producing infections should be eliminated, after which owners should regularly check the pH of the first voided
urine in the morning after an overnight fast; in most dogs on a normal diet, the urine will be acidic. Provided the urine
remains acidic, struvite stone formation is very unlikely.
Urate Stones:
Silicate Stones:
Early reports indicated a predominance of silicate stones in German Shepherd Dogs, but many breeds have now been
implicated. Urethral obstruction in males is the most common presenting problem. The mean age of occurrence is ~6 yr.
The stones are usually multiple and in the bladder and urethra. Silicate uroliths are radiopaque. The calculi frequently, but
not always, have a very characteristic “jack-stone” appearance.
Only general management principles can be suggested for silicate urolithiasis. Additional salt should be administered in
the diet to induce diuresis and to lower the urine solute concentration. When present, urinary tract infection should be
eliminated. The effects of urine pH on silicate solubility are not established; therefore, no recommendation can be made
concerning therapeutic alteration of urine pH.