Curs Engleza Partea 2 Corectat - Lari

SPECIAL VETERINARY
PATHOLOGICAL ANATOMYCOURS
FOR FOREIGN STUDENTS
EDITURA AGROPRINT
TIMISOARA 2014
1
Scientific referens:
-
Professor Romeo Cristina DvD, PhD

Professor Valeria Grieco DvD, PhD
Associated professor Marius Pentea DvD,
PhD
Contents
2
1.
CARDIOVASCULAR MORPHOPATHOLOGY.....................11
1.1. Heart morphopathology.....................................................................11

1.1.1. Congenital anomalies of the heart and vessels 11
1.1.2. Pericardium injuries
11
1.1.3. Myocardial injury
20
1.1.4. Endocardial lesions
26
1.2. Pathology of the arteries, veins and lymphatic vessels.....................29
1.2.1. Artery lesions 29
1.2.2. Veins injuries 33
2.1. Bone marrow morphopathology........................................................37
2.1.1. Developmental disorders
37
2.1.2. Bone marrow atrophies and dystrophies 37
2.1.3. Circulatory changes
38
2.1.4. Inflammation of bone marrow 38
2.1.5. Hyperplastic noninflammatory changes 38
2.1.6. Tumors of bone marrow
39
2.2. Thymic pathology................................................................................39
39
2.2.2. Thymic involution and atrophy 39
2.2.3. Thymus dystrophies
40
40
2.2.5. Inflammations of the thymus 40
2.2.6. Thymic tumors 41
2.3. Morphopathology of the Fabricius bursa.........................................41
2.3.1. Changes congenital
41
2.3.2. Involutions and bursal atrophy 41
2.3.3. Dystrophies of Fabricius bursa 42
2.3.4. Inflammation of Fabricius bursa42
2.3.5. Tumors of Fabricius bursa
43
2.4. Pathology of the spleen.......................................................................43

2.4.1. Spleen abnormalities 43
2.4.2. Atrophies and dystrophies of the spleen 44
45
2.4.4. Spleen inflammations 46
2.4.5. Hyperplastic changes of the spleen
48
2.4.6. Spleen tumors 48
2.5. Lymph nodes Pathology......................................................................48
48
2.5.2. Atrophies and dystrophies
49
50
2.5.4. Lymph nodes inflammations 50
2.5.5. Tumors of lymph nodes 52
2.6. The morphoathology of mucosa associated lymphoid tissue...........52
3. THE MORPHOPATHOLOGY OF THE RESPIRATORY SYSTEM54
3.1. Pathology of the respiratory tract in mammals................................54
3.1.1. Airway abnormalities 54
3.1.2. Nasal cavity lesions
54
3.1.3. Paranasal sinus lesions 57
3.1.4. Injuries of the auditory tubes diverticulum
58
3.1.5. Lesions of the larynx and trachea
58
3.1.6. Bronchial lesions
60
3.2. Lung pathology in mammals..............................................................61
3.2.1. Volumetric changes
61
3.2.2. Dystrophies of the lungs
63
64
3.2.4. Lung inflammation
65
.2.5. Lung tumors.......................................................................................70
3.3. Morphopathology of thoracic cavity in mammals............................70
3.3.1. Content changes
70
71
3.3.3. Inflammation of the pleura
71
3.3.4. Mediastinal lesions
72
3.3.5. Injuries of diphragm
72
3.4. Respiratory pathology in birds..........................................................72

3.4.1. Airway lesions 72
3.4.2. Lung lesions 73
3.4.3. Air sac lesions 74
4. THE MORPHOPATHOLOGY OF DIGESTIVE TRACT................76
4.1. Oral cavity morphopathology...........................................................76
4.1.1. Malformations of the mouth
76
4.1.2. Dystrophies of the mouth
77
4.1.3 Necrosis of the mouth 77
77
4.1.5. Inflammations of the mouth cavity
78
4.1.6. Tumors of the oral cavity
81
4.1.7. Changes in dental aparatus
81
4.2. Pharynx morphopathology.................................................................83
4.2.1. Inflammation of the pharynx 83
4.2.2. Pharyngeal tumors
84
4.3. Esophagus morphopathology.............................................................84
4.3.1. Changes in lumen
84
4.3.2. Esophagus dystrophies 85
4.3.3. Inflammation of the esophagus 85
4.3.4. Esophagus tumors
86
4.4. Goiter morphopathology....................................................................86
4.4.1. Topographic changes 86
4.4.2. Goiter inflammation
87
4.4.3. Goiter tumors 87
4.5. Pre-stomach morphopathology..........................................................87
4.5.1. Changes in prestomachs content87
4.5.2. Volumetric changes..........................................................................87
4.5.3. Prestomach dystrophies 88
4.5.4. Prestomach inflammations
89
4.5.5. Prestomach tumors
90
4.6. Morphopathology of mammalian stomach.......................................90

90
91
4.6.4. Gastric ulcers 91
4.6.5. Stomach inflammation 93
4.6.6. Stomach tumors
95
4.7. Morphopathology of the stomach in birds........................................95
4.7.1. Injuries of the proventriculus 95
4.7.2. Ventricle lesions
97
4.8. Bowel pathology..................................................................................98
4.8.1. Bowel abnormalities 98
4.8.3. Bowels dystrophies
100
4.8.4. Changes in blood flow 101
4.8.5. Inflammation of the intestines 101
4.8.6. Bowel tumors 104
4.9. Salivary gland pathology..................................................................105
4.9.1. Dystrophies of the salivary gland
105
4.9.2. Cystic changes 105
4.9.3. Inflammation of the salivary glands
106
4.9.4. Salivary gland tumors 106
4.10. Pancreas morphopathology............................................................106
4.10.1. Anomalies of pancreas106
4.10.2. Dystrophies of the pancreas 107
4.10.3. Pancreatic necrosis 107
4.10.4. Circulatory changes 108
4.10.5. Inflammation of the pancreas 108
4.10.6. Tumors of the pancreas
109
4.11. Liver Pathology...............................................................................109
4.11.1. Liver abnormalities 109
109
4.11.3. Hepatic necrosis
113
4.11.4. Changes in the liver circulation
113
4.11.5. Inflammation of the liver
114
4.11.6. Liver Tumors 119

4.12. Pathology of the gallbladder (gallbladder)....................................120
4.12.2. Dystrophies of the gallbladder120
4.12.3. Gallbladder inflammation
121
4.12.4. Gallbladder Tumors 121
4.13. Abdominal pathology......................................................................122
4.13.1. Content changes of the abdominal cavity
122
4.13.2. Dystrophies of the peritoneum 122
4.13.4. Inflammation of the peritoneum
123
4.13.5. Peritoneal tumors
125
5. MORPHOPATHOLOGY OF THE EXCRETION SYSTEM........126
5.1. Kidney lesions....................................................................................126
5.1.1. Congenital anomalies 126
126
129
5.1.4. Kidney Inflammation 130
5.1.5. Renal Tumors 135
5.2. Urinary lesions..................................................................................135
5.2.1. Common urinary injuries
135
5.2.2. Ureteral injuries
136
5.2.3. Urinary bladder lesions 136
5.2.4. Urethra injuries 138
6.1. Congenital abnormalities common to both sexes............................140
6.2. The morphopathology of the male reproductive system................140
6.2.1. Testicular lesions
140
6.2.2. Lesions of the epididymis and deferens channel 143
6.2.3. Injuries of tunica vaginalis
144
6.2.4. Spermatic cord lesions 145
6.2.5. The injuries of genital glands 146
6.2.6. Injuries of penis and prepuce 146
6.3. The morphopathology of mammalian female genital system........148
6.3.1. Ovarian lesions 148

6.3.2. Salpinx lesions (fallopian tube) 150
6.3.3. Uterine lesions 151
6.3.4. Lesions of the vulva and vagina 154
6.3.5. Mammary gland morphopathology
156
6.4. Morphopathology of birds female genital system..........................160

6.4.2. Ovarian dystrophies
160
6.4.3.
Topographic changes
161
6.4.4.
Female genital inflammation in birds
161
6.4.5. Female genital tumors in birds 162
7. THE MORPHOPATHOLOGY OF NERVOUS SYSTEM.............163
7.1. Nervous system abnormalities..........................................................163
7.2. Injuries of meninges.........................................................................164
7.2.1. Meningeal dystrophies 164
164
7.2.3. Meninges inflammations
164
7.2.4. Meningeal tumors
165
7.3. Brain and spinal cord injuries..........................................................165
165
7.3.2. Nervous system necrosis
166
7.3.3. Changes in blood flow 166
7.3.4. Changes in cerebrospinal fluid circulation
167
7.3.5. Encephalon and bone marrow inflammation
167
7.3.6. Nervous system tumors
169
7.4. Nerve damage....................................................................................170
170
7.4.2. Nerve inflammation
170
7.4.3. Nerve Tumors 171
8. PATHOLOGICALLY SKIN AND SENSE ORGANS....................172
8.1. Skin lesions........................................................................................172
8.1.1. Congenital anomalies of the skin and appendages

8.1.2. Skin dystrophies
172
8.1.3. Gangrene and skin necrosis
174
8.1.4. Changes in skin circulation
174
8.1.5. Skin Inflammation
175
8.1.6. Skin Tumors 179
172
8.2. Visual organ lesions...........................................................................179

8.2.1. Injuries eyeballs
179
8.2.2. Accessory eye organs injuries 181
8.2.3. Tumors of the visual organ
181
8.3. Auditory organ lesions......................................................................182
8.3.1. Ear necrosis
182
8.3.2. Ear Inflammation
182
8.3.3. Ear tumors
182
9. THE MORPHOPATHOLOGY OF THE ENDOCRINE SYSTEM. 183
9.1. The morphopathology of the endocrine glandular system............183
9.1.1. Pituitary lesions
183
9.1.2. Epiphyseal lesions
184
9.1.3. Thyroid lesions 185
9.1.4. Parathyroid lesions
188
9.1.5. Adrenal lesions 189
9.2. The morphopathology of the diffuse endocrine system..................191
9.2.1. Diffuse endocrine system
191
9.2.2. Diffuse endocrine tumors
191
10. THE MORPHOPATHOLOGIY OF THE LOCOMOTOR
APPARATUS..................................................................................191
10.1. Muscle injuries................................................................................192
10.1.2. Muscular dystrophies 192
10.1.4. Muscle inflammation 193
10.1.5. Somatic muscle tumors
194
10.2. Injuries of tendons, synovial sheaths and synovial bursas...........195

10.2.1. Inflammation of the tendons 195
10.3. Joint lesions.....................................................................................196
10.3.1. Dystrophies of the joints
196
10.3.3. Inflammation of joints 197
10.4. Bone lesions.....................................................................................199
199
10.4.2. Bone dystrophies
199
10.4.4. Bone inflammation 201
10.4.5. Bone Tumors 202
'
202
BIBLIOGRAPHY............................................................................203
1. CARDIOVASCULAR MORPHOPATOLOGY
1.1. Heart morphopathology
1.1.1. Congenital anomalies of the heart and vessels
10
Heart malformations are determined by various factors, some with

severe movement disorders and oxygen that are incompatible with life, other
compatible although initially not generally allow a long-term survival. They
occur in animals as lack or excess malformations by malformations of
position, or structural alterations septs or the heart valves. Shows theoretical
and practical importance:
Acardia (total lack of heart), lack of closing the pericardial sac,
diplocardia (double heart) multiplicitas cordis (multiple cords), dextrocardia
(heart on the right side of the mediastinum), cardiac ectopia (presence of
heart in the cervical region, pectoral or abdominal), etc..
Septs structural defects are common to all species. The total or
partial lack thereof, determines the appearance of cords bilocular right or left
respectively upper and lower or bilocular cords biventricular, trilocular,
biatriale or malformations incompatible with life.
Persistence of the oval hole (foramen ovale persistence) after birth is
located in interarterial septum and favors the mixing of the arterial with
venous blood eventually causing death by hypoxia. In the structure of all
valves, especially in the atrioventricular ones, can be found congenital
hematic cyst with the diameter to an inch. (5, 11, 16, 19)
1.1.2. Pericardium injuries
1.1.2.1. Pericardium dystrophies
Dystrophic lesions of the pericardium is of less importance in
mammals, while in birds they produce irreversible changes sometimes
incompatible with life.
Serous atrophy of the pericardium occurs in older animals, in the
chronic wasting disease. Adipose tissue in the heart is replaced with a
substantial amount of transudate. The lesion is also known as gelatinous
edema or "ex edema vacuo".
Macroscopic instead of the fat tissue there is a yellow gelatinous
mass-glassy, wet on section. Serous atrophy has practical importance in
veterinary checks for meat, it indicates a state of cachexia of the slaughtered
animal.
11
Fat infiltration of epicardium is the opposite of serous atrophy. It is

characterized by excessive storage of fat in this stage, and sometimes fat
necrosis. It is found mainly in animals subjected to the process of fattening
(cattle, pigs, poultry).
Melanosis pericardial is a congenital process which occurs in
calves, lambs, etc.. macroscopically characterized by the presence of brownblackish outbreaks of varying sizes (melanosis stained). Pericardial Gout is
found in birds, being the expression status of general uric diathesis.
Macroscopic, first,by the transparency of the pericardium is noticed
in the pericardial cavity the presence of a white deposit like chalk more or
less adherent to pericardium. Epicardium appears sprinkled with white
paint.
Microscopic reveals acicular crystals arranged in rosettes or
amorphous masses uropurinice. In longest developments on the outskirts of
uric deposits a lymphohystocytar mesenchymal reaction is observed with the
appearance of giant cells, ultimately resulting in foreign body granulomas
(granulomatous pericarditis). Installing the inflammatory process is possible
only in cases where the bird holding a long "uric poisoning", facilitating the
emergence and development of granulomatous inflammation.
1.1.2.2. Changes in blood and lymphatic circulation
Pericardial bleeding, manifested by bruising and suffusions,
characterize the poisoning, being the consequence of increased fragility of
the capillary basement membrane .
Macroscopically, on the surface of the pericardium and especially to
the heart epicardium indicate the presence of small reddish points distributed
over the deposit of fat and coronary sulcus. Such lesions are found in
diseases like:
- bacterial septic emice: anthrax, pasteurellosis, streptococci;
- virotic: classical and African swine fever, Newcastle disease;
- toxic: warfarin poisoning or with derivatives.
12
Haemopericardium occurs as a result of breaking the great vessels

of the heart with blood accumulation in the pericardial cavity, followed by
clotting and blocking movements of the heart. It is found in all species, but
especially horses, pigs and dogs.
Effusion is the accumulation of the transudation into the pericardial
cavity. Pericardium and epicardium is shiny and smooth. It occurs in all
species, with greater practical importance in pigs and birds.
Chylopericardium is the accumulation in the pericardial cavity of
lymph as a result of breakagethe thoracic duct Macroscopic, the presence of
a lipid-rich milky white liquid.
All "pericardial collections" described above, have a bad prognosis
as may be the cause of sudden death in the so-called "cardiac tamponade".
(5, 11, 16, 19)
1.1.2.3. Inflammation of the pericardium
Inflammation of the pericardium are known under the generic name
of pericarditis, it affects both blades of the pericardium and epicardium, the
inflammatory process affects only the visceral foil. Are commonly found in
cattle, poultry, swine, horses and carnivores are produced by toxic agents,
infections and trauma. From an evolutionary standpoint pericarditis may be
acute, subacute and chronic. Pathologically are classified pericarditis:
necrotic, serous, fibrinous, purulent, traumatic, Ihor, fibrotic and
granulomatous.
Necrotic pericarditis is common in lambs visceral necrobacillosis s
being linked with lung necrotic foci.
Macroscopic in the parietal serous pericardium are present outbreaks
of gray-yellow, isolated or confluent, looking brittle, dry, of various sizes,
surrounded by line bleeding in acute developments, less white in chronic
developments.
Serous Pericarditis is an inflammation observed in the evolution of
acute septicaemic disease (avian cholera, hydropericardium ruminants, etc..).
13
Macroscopic the pericardial cavity indicate the presence of increased

amounts of liquid citrine, which immediately coagulates in contact with air.
Parietal and visceral pericardial blades are congested, shiny and wet.
Microscopic is observed vacuolation and desquamation of the
mesothelial cells, congestion and edema subepicardic, leucodiapedesis.
Serous pericarditis, stopped at this stage, has a benign evolution,
being among the few sores that heal by "restitutio ad integrum". In general, it
evolves into a serofibrinous inflammation and fibrinous (eg avian cholera),
or the serohemorhagic inflammation (eg coal emphysematous).
Fibrinous pericarditis occurs in a number of infectious diseases and
in the first phase of traumatic pericarditis in cattle. It is characterized by the
appearance and accumulation of fibrinous exudate in the pericardial cavity.
Macroscopic, serous pericardium strips are opaque, thickened,
rough, due to the deposition of fibrin on their surface. Pericardial cavity is
enlarged and contains appreciable quantities of yellowish fibrin. Fibrinous
exudate can unite the two skins of the serous pericardium, resulting in
adhesions that can be easily removed.
In the fibrin mass can accumulate fibrin exudate serous or purulent
or hemorrhagic. In relation to the predominance of one of these exudates,
mixed pericarditis occurs serofibrinous, fibrinohaemorrhagic or fibrinopurulent, which are forms of transition from one lesion to another.
These specific pathological aspects are specific of acute (2-4 days)
pericarditis. In developments longer resorption occurs partially liquid,
organizing fibrinous exudate on account of conjunctive tissue subepicardic,
ending with the appearance on the epicardial surface of some gray-white
filaments, or villi-like hairs, printing the heart a matter of "villous heart" or
"hairy heart." Gradually connective scar tissue welding will produce two
blades pericardial, if at this stage is a forced separation of the two serous
same appearance is found like "villous heart."
14
Microscopic in the acute forms are found degeneration and peeling

of the mesothelium, bare land cover with fibrinous exudate rich in micro-and
macrophages, edema and swelling of capillary subepicardic. In longer
developments (5-10 days), when there is organization, there is connective
tissue proliferation and capillary forming the junction between the parietal
and visceral tabs of the serous pericardium. Appearing tissue is scar tissue
that creates synechiae epicardo-pericardial ,pathologic characteristic aspect
of the fibrous pericarditis.
Purulent or suppurative pericarditis occurs most often as a further
unfavorable fibrinous pericarditis, or occurs as a metastatic purulent
pericarditis (in Gurm and piosepticemia foals, piglets piobacillosis).
Macroscopic the pericardial sac is increased in volume to the
palpation ,can be feel sometimes a liquid consistency, fluctuating,
sometimes more viscous. On section, the pericardiumblades are much
thickened and in the pericardial cavity is found varying amounts of purulent
exudate.
Microscopic pericardial blades are covered with purulent exudate,
mesothelium is flaky or turned in piophage, subserous connective tissue is
heavily infiltrated with granulocytes, capillaries are ectasies and with an
intense leucodiapedesis process.
Purulent pericarditis is a very serious, often being lethal. It is known
as the piopericard or pericardial empyema.
Traumatic pericarditis commonly found in cattle, is determined by
the penetration of sharp metal body of the network through the diaphragm
into the heart. Foreign bodies carry with them a wide range of germs
including pyogenic and anaerobic. Following the initial pericardial traum
first occure a serofibrinous inflammation then purulent, the last form being
able to turn into gangrenous pericarditis. These forms are dependent by the
circulated microbial flora .
Macroscopic appearance is dependent on the morphological form in
which is surprised the evolution of the traumatic pericarditis. In general,
evolution is chronic, proliferation processes dominated conjunctiva, with the
advent of synechiae between the two pericardium skins(fibroadhesive
pericarditis).
15
Pericarditis gangrenous or Ihor is, in most cases, the consequence of

traumatic pericarditis, or occurs as a complication of purulent pericarditis.
Macroscopic volume of the pericardial sac is increased occurs by
gas (pneumopericard) and by ihor exudate. When the he pericardial cavity is
opened a distinct odor of gangrene is smelled. Ihor effusion is greenishbrown fluid, heterogeneous, and sometimes being able to detect foreign
bodies or fragments thereof. Pericarditis is gangrenous and sapremia death
by heart failure that it determines.
Pericarditis fibrous hyperplastic or fibroblast is an evolving chronic
productive inflammation, the result, in general, of the exudative pericarditis:
serous, fibrinous or purulent.
Fibrous pericarditis occurs in all species pasteurellosis,
salmonellosis in pigs and poultry in the hemofilosis of swine mycoplasmosis
in colibacillosis and avian mycoplasmosis etc.
Macroscopic, it appears pericardial thickening due to a proliferative
process with the starting base in the the subseries pericardial connective
tissue (fibrous pericarditis simple). Thickened pericardium sometimes has
some hairs on the surface (pericarditis viloasa). The two blades of the
pericardium will stick together by clamps and synechiae, taking the
appearance of "fibro-adhesive pericarditis" common in pigs. Other times, the
process is limited to small outbreaks gray-whitish appearance called
"maculae albidae".
Granulomatous pericarditis occurs in tuberculosis in cattle and
carnivores in aspergillosis and gout in birds, have different morphological
aspects in relation to aetiology.
In tuberculosis, it may be predominantly effusive (caseous
tuberculosis) characterized by large caseum in the serous pericardium, or
may develop in the form of lumps of various shapes and sizes, caseous and
calcified (pearl tuberculosis or fungal serous), expression of productive
tuberculosis. In carnivores can be foun epicardial nodules associated with
serous exudation .
Granulomatous Aspergillus pericarditis in birds is rare and is
manifested by gray-white nodules with yellowish center.
16
Uric granulomatous pericarditis is observed in birds chronic gout

developments
Macroscopic nodular foci are found to grainy, chalky and dry.
1.1.2.4. Pericardium Tumors
Pericardial tumors have a low incidence. Primary tumors can result
in serous cells (mesothelioma) and connective tissue (fibroids, lipomas).
Secondary tumors occur in avian and bovine enzootic leucosis manifested by
hyperplasia of the pericardium (limfosarcoma), being a continuation of
neoplastic processes in cardiac structure. Tumors can cause compression of
great vessels and heart in general.
1.1.3. Myocardial injury
1 .1.3.1. Myocardial dystrophies
Myocardial atrophy occurs in animals undergoing chronic diseases
exhausting (infectious, parasitic or neoplastic) in states of malnutrition in
older animals, the lesion is observed in all species, but especially in cattle.
Macroscopic, the heart is reduced in volume, consistency is
maintained or slightly increased, fat tissues from the coronary groove and
interventricular septum is gone and the coloring is darker, brownish closed.
Microscopic there is narrowing (atrophy) of myocardial fibers with
lipofuscin deposits at the two poles of the nucleus, where it is more abundant
sarcoplasm, lesion known as "brown atrophy of the heart." Dystrophies of
the myocardium are known as generic myocardosis.Fat myocardosis or
myocardum steatosis occurs in animals for fattening and in phosphorus
poisoning, copper, arsenic, lupine poisoning etc.
Macroscopic the myocardum is yellowish, diffuse or circumscribed
and brittle.
Microscopic on the sections on ice and stained with Sudan are seen
in sarcoplasm lipid droplets. Myocardial steatosis is considered basic lesion
in round heart disease in chickens.
17
Granular myocardosis is common during infectious diseases, toxic

and deficiency.
Macroscopic infarction of gray, lacking luster, brittle, can affect the
body in its entirety, or only area.
Hyaline myocardosis occurs in young animals, calves, lambs,
piglets, foals. is generated by deficiencies (vitamin E and / or selenium)
poisoning, transport etc .
Macroscopic infarction with areas or striped gray-yellow with
increased friability. The diagnosis is established by histological examination.
Microscopic myocardial fibers are swollen, homogenized,
fragmented and vacuolated in imminent state of necrobiosis (hyalinosis
intracellular). This lesion is found in youth nutrition myodystrophy , also
known as white muscle disease. Also, myocardial intracellular hyalinosis is
the base lesion from Herztod, or heart death of swine . Sometimes,
especially affecting the medium-caliber vessels, hyaline depositing the initial
subendothelial and then, invading the whole vascular wall (interstitial
hyalinosis) lesional aspect found in " mulberrylike heart disease." The walls
are fragile and myocardial bleeding occurs. Fibrinoid myocardosis structure
is observed in small caliber vessels evolved in parallel with hyaline
degeneration. The main reason seems to be the hypovitaminosis E.
Pigmentation myocardosis are found either as brown atrophy of the
myocardium in all animals cachectic and tracked, whether congenital
melanosis stained, seen in lambs and calves as dark brown spots well
defined. Microscopic stands melanofore accumulation in myocardial
interstitium .
Limestone myocardosis is rare. Occurs in cattle in hypovitaminosis
D derivatives mercury poisoning, hypomagnesemia, etc.. Diagnosis is
established based microscopic aspect,of calcareous incrustations in
myocardial fibers and fibers and Purkinje cells.
18
All degenerative processes (myocardosis) in all species can evolve

to myocardial necrosis generally small. Causes of necrosis may be vascular
obstructions, poisoning and infections, self and exogenous intoxications,
hypovitaminosis and endocrine disorders (catecholamines), initially
producing ischemia and ultimately myocardial necrosis of various sizes. (5,
11, 16, 19, 31, 33, 35, 41, 43)
1.1.3.2. Circulatory changes
Circulatory changes are of great importance in veterinary medicine
are represented by hyperemia, hemorrhage and stroke.
Myocardial hyperemia is observed in poisoning and the
development of infarction. Especially the superficial myocardial vessels are
swollen and obvious form of "red ropes".
Parenchymal hemorrhages of the myocardium are seen as bruising,
or petechiae, located in the heart subepicardic in avian pasteurellosis, in
describe mulberrylike heart disease heart as in most septicemic diseases .
Bleedings through a ruptured myocardial wall can be produced
either by sharp foreign bodies or serious developments of the myocardosis
resulting ultimately necrosis processes. Rupture can span several inches,
causing rapid death through internal bleeding (haemopericardium).
Myocardial infarction appear after coronary artery thrombosis,
injury found in horse in 24.4% of cases of infectious anemia. The incidence
of infarcts is related to the duration of febrile accesses.
Macroscopic foci are found on the surface of the myocardium,
yellow elongated in the direction of the myocardial fibers, loose, with
irregular edges, defined in acute forms of hemorrhagic congestivo reaction
(reddish), and n isubacute and chronic developments of a fibrous reaction
(off-white) . On he section is shaped with large base on the outskirts of
targeted organ.
Microscopic, central is seen an area of coagulation necrosis
surrounded by a leukocyte reaction. Gradually, there is granulation tissue by
fibrosis and scar repair occurs (for small infarcts).
19
Evolution and severity of myocardial infarction is given by the

location and its extension. Large infarcts,
produce multiple
myocardiocytolysis ,local expansion and sometimes even perforation of the
myocard wall , followed by haemopericardium acute and sudden death
by"cardiac tamponade".
1.1.3.3. Volumetric changes of the myocardium
Volumetric changes of the myocardium are represented by dilation
and cardiac hypertrophy.
Dilated heart is characterized by increasing the volume of the heart
as a result of the increase ventricle space.
Macroscopic, the heart is increased in volume, consistency is loose
(to flatten when you put it on the table), the color gray. On section, the
myocardium is thin, lacking tone, while the cardiac cavities are widen very
much. in hens are found relatively frequently, and especially dilated right
heart atrium. Sometimes, the lower limit of the right ventricle reaches the tip
of the heart, resulting in heart with "double apex". Cardiac dilatation can be
observed in animals depleted ,cachectic, in cardiac deficiencies, iron
deficiency anemia in piglets etc. Must be differentiated the compensatory
dilatetions by the ones non compensatory or myogenic. The first is an
adjustment to an amount of blood and therefore can develop rapidly. The
second form is determined mainly by myocardial atrophy and degenerative
changes. Cardiac dilation lasting entails chronic congestive lesions in
various organs (liver, lung) and peripheral edema often emphasized.
Cardiac hypertrophy is characterized by the size increasing of the
volume of the heart by increasing myocardial mass, due to thickening of
muscle fibers. Stenosis of the atrioventricular orifices produce the
hypertrophy of the atrial wall, while the aortic and pulmonary hole stenosis
causes hypertrophy of ventricular myocardium.
Macroscopic, the heart is increased in size, and the consistency is
increased. The cross sections are found thickening of the walls while
decreasing cardiac chambers.
1.1.3.4. Myocardial inflammation
20
Myocardial inflammation are called myocarditis. They may be

secondary to the expression of general disease of the body or may have a
primary location (if traumatic myocarditis).
Among domestic animals, in cattle are the most myocardial
inflammation. Pathologically, there are the following forms of myocarditis:
parenchyma, necrotic, hemorrhagic, necrotic, purulent,lymphohistocytic ,
eosinophilic, fibrous and granulomatous.
Myocarditis parenchymal arises from the toxic action of bacteria . It
is difficult to distinguish macroscopically from pelleting myocardosis.
Macroscopic in the forms supraacute, it is possible that the
myocardium does not show changes. In longest developments, on the
myocardium is seen of outbreaks or striped gray-white, alternating with
areas of normal appearance. This image of the myocardium is also known as
"tiger heart".
Microscopic is observed hyaline a granulocyte-degeneration of
-myofibrils, edema and infiltration between. This morphological form is seen
in phosphorus , copper and arsenic poisoning. Necrotizing myocarditis is
found in ruminants following podal necrobacillosis metastasis and birds in
some forms of avian cholera.
Macroscopic stands yellowish gray areas, of varying sizes, dry bulk
and delineated.
Microscopic is highlighted elements necrosis , accompanied by
vascular and leukocyte reaction .
Myocarditis hemorrhagic-necrotic or emphysematous, found in
emphysematous coal of the cattle.
Macroscopic foci stands brownish-red, alternating with yellowish
gray areas, loose and crackles.
Microscopic, there is a rich infiltrate serohemoragic that will
produce dilacerations and necrosis of myocardial fibers.
21
Purulent or suppurative myocarditis in most cases, is a secondary

localization processes, evolving primary
elsewhere in the body:
omfaloflebite in calves, purulent nephritis and metritis in cattle.
Macroscopic on the surface and the depth of the myocardium is
found gray-yellow foci (abscesses) of various sizes. On section, there is the
presence of pus, bounded on the periphery by a capsule.
Microscopic it shows all the elements that enter into the structure of
the "pyogenic membrane."
Myocarditis lymphohitocitaris presents two aspects lesions: diffuse
and nodular. Meets most frequently in birds pulorosis, and listeriosis.
Macroscopically, the surface of the myocardium is observed or graywhite nodule ("nodule pulorici '), of various sizes, sometimes prominent or
diffuse infiltration. Surface section bacon lesions character.
Microscopic nodules and diffuse infiltrations correspond to
lymphohistocytic interstitial hyperplasia, producing atrophy and necrosis of
myocardial fibers.
Eosinophilic myocarditis is reported in cattle, as an expression of
disseminated eosinophilic myositis with obscure etiology.
Microscopic
myocardial fibers.
there is a rich
fibrous tissue, which reduces the
Fibrous myocarditis is a continuation and completion of other forms

of myocarditis , heart attacks, etc..
Macroscopic
it highlights the gray-white areas of sclerosis
(scarring) of different sizes, compared with myocardial brown background.
Outbreaks are difficult on sectioning, making a sound like "creak
Microscopic fibro-connective hyperplasia more or less extensive.
22
Granulomatous myocarditis is relatively rare. It can be observed in

tuberculosis in pigs and cattle, in the form of lumps or caseous foci, and in
fungi (aspergillosis, mucormycosis), aspects of which are dependent on the
morphology of the causative agent.
In echinococcosis and cysticercosis, are seen macroscopically cystic
parasitic granulomas, the diagnosis is easily established (cystic
granulomatous myocarditis). In sarcosporidiosis, more common in sheep,
cattle and pigs, are seen microscopic lesions, the diagnosis is established by
histological examination. (5, 6, 11, 16, 19, 33)
1.1.3.5. Myocardium tumors
Fibroid tumors are the primary tumors,having as departure point the
epicardium or neurofibroma frequently diagnosed in cattle. Secondary
tumors are observed in all species, but especially in cattle and poultry.
Are common the myocariac sites of avian leukosis and Marek's
disease, sometimes more than 50% of myocardial mass being replaced by
tumor tissue (limfosarcoame). In cattle leucosis, in the myocardial mass,
especially in the structure of the atria, it appears striped or gray-white foci
(sarcomas) with greasy look. (7, 11, 16)
1.1.4. Endocardial lesions
1.1.4.1. Dystrophies endocardial
Endocardial dystrophies are known as generic endocardosis. The
best known are: fibroelastosis, uric dystrophy of birds and endocardial
calcification.
Fibroelastosis is characterized by diffuse or circumscribed
thickening of the endocardium, which is whitish, opaque.
Microscopic there is hyperplasia of elastic fibers. It meets relatively
infrequently in calves, dogs and cats.
Uric dystrophy /endocardic gout , can be seen in birds, locating on
the atrioventricular valves in the form of dots or striped white, causing
endothelial necrosis.
23
Endocardial calcification was observed in all species, both in the

structure of valves (mitral) and the parietal endocardium, atrial or
ventricular.
Macroscopic, on the endocardium surface is seen whitish streaks or
plates, gently raised, the rough part due to the precipitation of calcium ions.
Microscopic limestone deposits produce atrophy and necrosis of
connective fibers, elastic fibers and Purkinje cells even. Endocardial
calcification occurs in phosphocalcic imbalances, hypervitaminosis D,
hyperparathyroidism, and in some poisoning hypermagnesaemia. In South
America there has been a syndrome in cattle, characterized by fibroelastic
tissue calcification of the heart and lungs.
1.1.4.2. Endocardial circulatory changes
Circulatory changes a most common of endocardium are
hemorrhages. They are represented by suffusions orsubendocardial sugilaii (
romanian)development of toxic conditions, sepsis or hypoxic injury.
Macroscopic appear as reddish spots, relatively large, irregular
stretched both on surface and deep.
1.1.4.3. Endocardial inflammation
Endocardial, parietal and valvular inflammations are known as
endocarditis. They are found in all animal species,having in general
poisoning etiology. Classification endocarditis can be done according to
several criteria:
-
Pathogenetic: primary and secondary endocarditis;

Evolution: acute and chronic endocarditis;
Topographical: valvular endocarditis, parietal, trabecular, papillary;
Etiology: rujetic endocarditis, streptococcal, fungal etc.;
Pathology: simple endocarditis, warty, ulcerovegetant .
Simple endocarditis is characterized by endocardial thickening

associated with the loss of its transparency, especially on the free edge of
valves.
24
Microscopic there is serous infiltration, endothelial desquamation,

fibrinocellular network. It develops acutely and can be observed in horses,
dogs, chickens in poisoning and allergic conditions.
Verrucous endocarditis is the following of the simple endocarditis and
consists in the appearance on the parietal or valvular endocardium, of
deposits (Blood clots) with irregular surface, isolated of various sizes.
Microscopic, there is peeling endothelial, platelets adhesion and fibrin
deposit in the form of warts. It is found more frequently in carnivores.
Ulcerovegetant endocarditis is the most important in veterinary
pathology, as seen in many infectious diseases. Is produced by :
- rujet bacillus, swine and horses;
- of pyogenic bacillus in cattle and swine;
- streptococci, in equine, swine and poultry,by leptospire in carnivores
etc. Evolving usually as valve endocarditis and affect particularly the
bicuspid valve.
Macroscopic there is voluminous vegetation, irregular surface,
alternating with extremely varied locales ulcerations. Ulcers can perforate
the valves.
Microscopic the process begins with an ulcer on its the surface
accumulates
abundant fibrinocellular deposits (mixed thrombus) and
colonies of germs. Ulcerovegetant Endocarditis is the most serious, since it
is followed by embolism and white infarcts , both with fatal outcome.
Fibrous endocarditis endocarditis is usually the result of simple and warty
endocarditis.
Macroscopic there is initially excessive endocardial thickening,
which becomes white and opaque, and ultimately thins and retract valve.
Microscopically, there is connective hyperplasia, cellular initially
and then fibrillation.
25
Clinic is signaled the existence of recurrent endocarditis, which is

manifested by periodic rebound effect.
Endocarditis consequences are severe in most cases for the body, by
producing emboli and infarcts, or by the occurrence of stenosis and heart
failure, which will cause changes in the volume of the heart.
Stenosis of the atrioventricular orifices entail hepatopulmonary
stasis and the hypertrophy of atrial walls, while holes aortic or pulmonary
stenosis results in ventricular myocardial hypertrophy and pulmonary stasis.
Valvular insufficiencies (incomplete closure of openings) arising
from the shortening of tendon strings and valves, causing blood stasis by
blood dischargin inside cavities. Myocardium will shrink ,the cavities will
expand progressively the consequence being cardiac dilatation. (5, 11, 16,
19, 31, 33, 35, 41, 43)
1.2. Pathology of the arteries, veins and lymphatic vessels
1.2.1. Artery lesions
Assessment of arterial lesions must always be interpreted according
to age of the animals.
Ageing of the arteries is characterized microscopic by intima
thickening, progressive disorganization of the average elastic fibers, muscle
hyperplasia and mean fibrosis ultimately . The process is affectin the entire
arterial system and have a diffuse character. These changes have adverse
repression for the metabolic changes manifested morphologically by
generalized atrophy specific to older animals.
1.2.1.1. Arteries dystrophies
Of the dystrophic processes, the most important are: fatty
dystrophy, mucoid, fibrinoid, hyaline, amyloid ,elastosis and elastolysis,
calcification etc. Except steatosis and mean arterial calcification, all
dystrophies are only visible microscopically putting on specific aspects of
these processes.
26
Fatty arteries in animals is less important compared to human

medicine. Lipid deposition in cattle are befrore arterial wall calcifications.
Macroscopic especially in large arteries at the origin of branches is
observed spots or striped yellow slightly raised marginal.
Microscopic lipids are seen in intimate, with or without a peri-focal
reaction.
Mean aortic calcification is common in cattle and horses, aged 10
years. Meets the conditions of hypervitaminosis D, hyperparathyroidism,
hypermagnesemia, chronic illness, etc..
Macroscopic, plates or granules are found, whitish, hard to
palpation, protruding to intimate that endothelial prints look rough.
Microscopic, the deposit of calcium salts are noted in the
fundamental substance and elastic fibers, which arise dissect, fragmented
and non-specific corrugations.
Arteriosclerosis and atheromatosis, frequently found in humans, is a
dystrophic process, which apparently has no counterpart in animals.
Atherosclerosis is the deposit of substances in the intima and media of the
large and medium arteries with aterom plaque formation.
Macroscopic there is circumscribed thickening of the intima,
yellowish-white. On section, there is a yellowish mass, composed of
cholesterol crystals that produce muscle-elastic fibers necrosis frommedia
artery.
Microscopic in the development process are described four stages:
edema intima lipid streak, fibrous plaque and aterom plaque, the last stage is
irreversible and is predominant fatty softening.
27
The ethiopathogenesis is not understood even today, but it is

believed that the disease could be the consequence of hypercholesterolemia,
with lipids deposit in vascular walls. Currently, the disease is considered
plurifactorial. Location of atherosclerosis is increased in aortic arch and
abdominal aorta. Evolution is progressive and irreversible ,the complications
varied depending on the location and size of the affected artery. Was
diagnosed in poultry, rabbit, dog, pig, etc..
Differential diagnosis must
arteriosclerosis and atherosclerosis.
be
made
between
the
terms
Atherosclerosis is an arterial non-ateromatose , diffuse structures

characterized by atrophy of the myoelastic fibers and substitution fibrosis
with an increase in arterial wall structure and rigidity. It affects arterioles,
small arteries and arteries medium rare. The etiology of hypertension is
assigned a role. Arteriosclerosis can evolve associated with atherosclerosis.
(5, 11, 16, 19, 31, 33)
Circulatory changes of the arteries is represented by localized and
generalized thrombosis.
Arterial localized thrombosis is the result of the intimal endothelial
damage caused by trauma (digital arteries horse) parasites endovascular
action, (eg vermin endarteritis horse) different maneuvers iatrogenic etc.
Macroscopic deformation of the artery is found and the presence on
the section of the wall of adherent thrombus, parietal or obliterated.
In cattle, and especially in horses, thrombosis occurs relatively
frequently on the descending aorta, morphoclinical manifested by lameness,
which suddenly set. Thrombus may calcify, in which is called arteriolit .
Total obstruction of the arteries can cause intestinal colic which in
horses are deadly and necrosis of the intestinal wall.
28
Generalized arterial thrombosis are affecting the microcirculation

and is known as disseminated vascular coagulation (DIC). It is found in
various diseases as:viral, bacterial, parasitic, cancer etc. (5, 11, 16, 19, 41,
43)
1.2.1.3. Volumetric changes
Volumetric changes are represented artery aneurysms and
dilatations. Aneurysms are permanent dilations circumscribed or segmentar,
produced by structural changes of the arterial wall. They are more common
in horses strongyles larvae parasitism, is the most common etiologic factor.
Macroscopic are found arterial deformations sometimes gigantic,
with fibrotic or calcified walls. In the "vasa vasorum" and around can be
found larvae of parasites. Headquarters of parasitic aneurysms ,most
commonly in horses is a cranial mesenteric arteryetc.
According with their shape , aneurysms can be sacciforme when
forming an outer bag, fusiform, when dilatation is limited without outer bag
and dissect when the intimate break and blood infiltrates diffuse in the wall
forming false cavities.
The first two aneurysms (sacciforme and fusiform) are considered
true aneurysms, produced by structural changes in the walls, while dissecting
aneurysms are considered false, because they are the result of infiltration of
blood into arterial walls.
Microscopic there is myolysis and elastolysis a substitute fibrosis
and even calcification. In birds, known dissecting aneurysm of the
abdominal aorta caused by latirism (pea poisoning) and copper deficiency.
Artery dilation is widening the lumen without structural wall
changes. To capillary dilation is use the name ectasia (gr. extasis =
expansion). These changes are observed in active hyperemia, the result of
vasomotor disturbances.
1.2.1.4. Inflammation of the arteries
29
Inflammation of the arteries are generically called arteries. After the

caliber of vessels, variable nomenclature: arteries, and capillaries ,arteriolite,
as the inflammatory process affects large arteries, medium and small, or
capillaries. After the inflammations locations may be endoarterite,
mezoarterite and priarterite, when the process is localized predominantly in
intimate, medium or advent. When inflammation is affecting the entire
arterial wall panarteritis term is used. In general, for small vessel vasculitis
nomenclature is used, namely, endo-or perivasculittis.
Etiology, including causative agents of arteritis are listed bacteria
suppurative ,necrosis bacillus, viruses, parasites, etc.. In the pathogenesis of
arteritis, the endothelial dystrophy, thrombosis and reactive processes are
steps preceding the inflammatory process. From the point of view:
- view of morphopathology, arthritis can be necrosant, serous,
fibrinous, purulent and granulomatous.
- view
of etiology can be viral arteritis, parasitic, bacterial and
fungal. For medical and veterinary practice are important viral and
parasitic arteries.
Viral arteritis is characterized by fibrinoid degeneration and / or hyaline
of intima and media associated with lymphoid infiltration resulting in
obliteration of the lumen.
Parasitic arteritis, or vermin, are seen more often in mesenteric trunks in
horse and thoracic aorta in dogs. They are caused by Strongylus vulgaris in
horses, wolves Spirocerca respectively in carnivores.
Macroscopic there is thickening of the arterial wall, necrosis and
fibrosis in the form of lumps of various sizes. In these areas, under the action
of blood pressure may occur aneurysms.
Microscopic stands arterial wall necrosis and thrombotic masses,
which can identify the parasite. In more advanced forms, there is
replacement fibrosis.
In horses from the blood clots can break off fragments (embolusuri)
which circulated into the bloodstream, giving rise to thromboembolic colic.
30
In dogs, the lesions consist of thickening and deformation of the

aorta, without producing thrombosis and without parasites as larvae migrate
to the digestive tract.
In the literature are cited and immune vasculitis manifested by
fibrinoid necrosis and nonspecific inflammatory reactions caused by immune
complexes, their etiology and morphopathogenesis is the least studied in
animals. (16, 19)
1.2.2. Veins injuries

Phlebosclerosis senile or aging of the veins is diagnosed in older
animals, but its importance is much lower compared to aging arteries.
Localized vein thrombosis is more common than arterial thrombosis.
Morphological aspects are generally similar to those outlined in the arteries,
affecting the propensity v. cava caudal v. harbor and vv. limbs. It can be
associated with phlebitis, evolving as thrombophlebitis. Formed thrombus
may calcify, in which case it is called flebol.
Macroscopic venous thrombi are similar to reddish coagulant, are
hard to the touch, with rough surface and adhesion to the vascular wall.
1.2.2.2. Changes in volume
Changes in the size of the veins have a small importance in animals
then in humans.
Phlebectaisaa is dilated lumen of a vein without altering the
structure of the vein wall, a process often met in passive hyperemia (stasis).
Varicose veins is correspondent of aneurysm characterized by
dilation of veins,consecutive alteration of vascular walls.
Macroscopic the affected veins are greatly increased in volume,
deformed, fluctuating, sometimes with a tortuous course.
31
Microscopicare observed myoelastic fiber necrosis and substitution

fibrosis.
As examples may be mentioned environmental varicose of the
saphenous vein in horse and cow mammary veins , the scrotum in dogs.
Testicular varicose veins on the horses and rams, especially in the
pampiniform plexus is called varicocele. Locating the varices
in
hemorrhoidal veins, called piles, lesion observed in dogs. It is accompanied
by intense perianal itching, forcing the animal to rub the ground. The causes
of varicose are varied: shortness return venous blood, venous wall
dystrophies, damage venous valves, cardiac disorders etc. (5, 11, 16, 19, 49,
50)
1.2.2.3. Inflammation of the veins
Inflammation of the veins is called phlebitis. The etiology of
phlebitis is, in most cases, poisoning and may develop acute or chronic.
Topographically can be endo-and periphlebitis and pathologically
phlebitis are: fibrinous, hemorrhagic, purulent, Ihor, fibrotic and
granulomatous. In most cases, it is accompanied by secondary thrombosis,
process known as thrombophlebitis. Their relationship with the organs in
which arose make the diagnosis easier.
In veterinary pathology are reported two important phlebitis : new born umbilical-phlebitis, suppurative phlebitis .
Umbilical-phlebitis is inflammation of the umbilical cord, although
its anatomical structures (veins, arteries, connective tissue). It occurs as a
consequence of failure of the rules of hygiene at birth and the cutting of the
umbilical cord. Common pathological form of development is purulent.
Macroscopic, the cord is thick and hard to palpation, and on the
section, there is a magma-purulent necrotic, which is found in veins and
adjacent structures. In developments longer the inflamed vein is converted
into a fibrous cord. It is commonly seen in calves.
32
Suppurative drug phlebitis drug is found on the external jugular

vein in horses and cattle or lateral saphenous vein in carnivores, due to
intravenous drug solutions with irritation character (eg formalin,
sulfathiazole, calcium chloride, calcium gluconate) , wrongly executed
(perivenously). Drugs will cause a suppurative inflammation of connective
tissue perivenously, which will include the venous wall, manifested by
swelling the jugular vein into the groove.
Initially, suppurative phlebitis is an inflammation aseptic , but if not
treated in time can turn into septic phlebitis with bad prognosis. (5, 11, 16,
19, 41, 51)
1.2.3. Lesions of the lymphatic vessels

Thrombosis lymphatic is the result of coagulation of lymph in the
lymphatic vessels or hyaline appearance of fibrin clots. From their structure
can detach fragments that can achieve lymphatic metastasis.
Lymphatic-ctasies are dilatations of the lymphatic vessels to to
regional stasis . It is found most frequently in rear interlobular lung in the
first phase of croupal bronchopneumonia.
1.2.3.3. Inflammation of the lymphatic vessels
The most common injuries are inflammation of the lymphatic
vessels, known as lymphangitis.
Etiology is almost exclusively poisoning. Evolution, can be acute
and chronic, depending on location, there are endo-and perilymphagitis, and
after the morphological characters are lymphangitis: serofibrinous,purulent
ulcerous, thrombosis and granulomatous.
33
Most important for the practice of veterinary medicine are

granulomatous lymphagitis seen in glanders, tuberculosis, ulcerative
lymphangitis, epizootic and sporotrichosis .
Macroscopic lymph vessels are dilated, protruding from the skin, on
their path seen in the presence of nodules, ulcers or diffuse thickening
(appearance of "lymphocytic chord").
Microscopic stands aspects specific to each etiologic agent, which
allows a diagnosis of certainty.
Their importance in the diagnosis of disease is reduced. Mentioned
that regional lymphagitis can be the starting point for metastasis of the
infectious processes.
1.2.3.4. Tumors of blood and lymphatic vessels

Vascular tumors are found in various organs, especially in cattle,
being identified as surprises for slaughter or necropsy. The most common are
hemangiomas.
Hemangiomas are especially common in dogs after the age of 8-9
years, but has been diagnosed in young dogs and breed Boxer, Airedale,
Scottisch.
In dogs, the location of the scrotum skin is more common in
pigmented races. (5, 11, 16, 19, 41, 43)
34
2. THE MORPHOLOGY OF THE HEMATOPOETIC AND

LYMPHORETICULAR ORGANS
2.1. Bone marrow morphopathology
Bone marrow hyperplasia, is found frequently in young hipotrepsic.
It is characterized by scarcity of islands erythroblasts, anisocytosis,
anizocromie, RBCs with high volume and hemoglobin less (especially the
lamb
Senile involution. Senile involution of the bone marrow are found in
old animals ,and is characterized macroscopically by yellowish-gray,
generalized color.
2.1.2. Bone marrow atrophies and dystrophies
Serous atrophy or "ex edema. Vacuo" occurs in cachectic animals, a
change that prints a gelatinous appearance, gray-yellow to the bone marrow.
Atrophy of the bone marrow may be due to prolonged irradiation, as well as
poisoning with bezon followed by decreasing of the leukocytar
myelinogenesis.
Bone marrow dystrophies are called osteomyelosis. More important
are lipid dystrophies, porphyrinic and marrow fibrosis.
35
Fatty osteomyelosis is found in chickens fed with feed

contaminated with citrinin, a toxic metabolite of Penicillium and
Aspergillus species.
Porphyrin ostepmyelosis can occur in pigs and cattle, by storing
porphyrin pigments in reticular cells and macrophages free of marrow, its
printing yellowish coloring with reddish reflexes. The process differs from
hemosiderosis by the negative reaction of iron.
Osteomyelosclerosis is a degenerative process in piglets of
primarily iron deficiency (iron deficiency anemia). It is characterized by a
gradual reduction of medullary parenchyma and replacement by fibrous
connective tissue. Osteomieloscleroza and subsequent precipitation of
calcium salts (calcification of the bone marrow) causes a microcytic
hypochromic anemia, which produces losses through mortality, or failure to
gain weight. The lesion was diagnosed also in birds.
Bone marrow can be the headquarter for congestion, ischemia and
even bleeding (fractures, hypovitaminosis K, septicaemic disease, poisoning
coumarin derivatives).
Marrow hyperemia has a red or red-vine blackish-gray or whitish
coloration in ischemic states.
Medullary hemorrhages are observed mainly in the marrow of the
loneg bone (femur, tibia). They are characterized by uniform fillingof the
spaces with erythrocytes and disappearance of the fatty elements from the
hemorrhagic outbrreak.
2.1.4. Inflammation of bone marrow
Inflammation of the bone marrow are called osteomyelitis.
Pathology of the osteomyelitis include: haemorrhagic, purulent, hyperplasia
and granulomatous. Bleeding and purulent forms are rare.
Hyperplasticor hyperplastic osteomyelitis seen in salmonellosis of
calves, in the long bones in the form of small gray-white foci of
reticuloendothelial proliferation with fibrosis trend.
Granulomatous osteomyelitis is found in over 90% of cases of
generalized avian tuberculosis.
Macroscopic especially in the bone marrow of the femur and tibia
ash stands nodules up to the size of a pea, easily enucleated, caseous on
section, occupying large areas of bone.
36
Microscopic granulomas are observed with central caseous

reaction and an epithelio-giant reaction at the periphery.
Granulomatous osteomyelitis can be seen in the spongy bone
tuberculosis in cattle and in cattle actinomycosis.
2.1.5. Hyperplastic noninflammatory changes
Regenerative hyperplasia are hyperplasic noninflammatory
conditions of the bone marrow, which is found in equine infectious anemia
and in some hemosporidiosis (babesiosis, theilerioze) and are intended to
supplement the loss of hematic cells, a phenomenon that occurs consistently
in these diseases (compensatory hyperplasia).
These regenerative hyperplasia consist of yellow marrow return to
the phase of red bone marrow . It is not done entirely ,only in some areas,
so that the lesion is called "islands of fetalisation" or " marrow fetalisation ".
Macroscopic is seen the presence of foci or areas of red bone
marrow on the general yellow background.
2.1.6. Tumors of bone marrow
Bone marrow tumors are common and visible in all species,
especially birds. They are represented by leukemias, lymphomas, myelomas.
In birds, lymphoid leucosis and myeloid appear as gray or reddish-gray
outbreaks of varying sizes. Bone marrow is light, and the aqueous was often
replaced with fat. (5, 8, 11, 16, 19, 53)
2.2. Thymic pathology
Thymic hypoplasia is the result of poor nutrition in pregnant
females that give birth to immature morphophysiological producs.
In piglets, the thymus is reduced to small yellowish gelatinous
mass on the base of the neck and cranial mediastinum.
Microscopic the, lobules are small, dissociated by edema and
represented only by the bone marrow.
Microscopic lobules surface is 2.5 times smaller, the number of
corpuscles Hass is three times higher, and their volume is almost double.
There is a clear trend towards fibrosis (Coman, M. 1989). (15) Cases of
thymic hypoplasia were observed in calves, chickens, kids, dogs. Congenital
37
thymic hyperplasia is characterized by the multiplication of cells in bone

marrow lesion may be due to dystocic parturition. Occurs in calves, and
other species.
2.2.2. Thymic involution and atrophy
Irreversible or physiological involution occurs with age, in 4-6
years in cattle, horses 2-2.5 years, 1-2 years for sheep, goats, swine, dogs
(90), 3-10 months hen, duck. Morphologically, there is gradual regression of
the thymus, evidenced by the reduction in size, lipid deposition in the gaps,
fibrosis.
Thymic atrophy, stress thymus or reversible involution occurs in
young animals at different ages and in all species. It is the destruction of the
cell. It installs relatively quickly in power imbalances, infectious diseases,
chronic poisoning, radiation, nonspecific stress (physical and mental).
Regeneration is possible (reversible).
Macroscopically, hardly can identify small pockets of thymic
parenchyma, sometimes it can be diagnosed only microscopically. Both
congenital hypoplasia and thymic atrophy, contributes to the depression of
the cellular immune response of the body. The practical importance of the
diagnosis of these thymic changes is special and should be taken into
account when interpreting the morbid states that occur in livestock units. (5,
11, 15, 16, 19, 41, 43)
2.2.3. Thymus dystrophies
Thymic dystrophies are little known. It states:
reticular dystrophy of the fat cells and corpuscles Hass;
medulla amyloidosis in cattle;
hyalinosis intracellular thymic cortex in foxes;
melanosis of the corpuscles hassle from pig and cattle etc.
calcification of vascular walls and Hass corpuscles in calves and
goats.
-

Circulatory changes, manifested by congestion, hemorrhage and
edema are found in infectious diseases and intoxications.
38
Thymic bleeding point, are of great practical value in poisoning

with strychnine and cyanuric acid in dogs.
In young dogs, especially under 2 years ,are evolving deadly with
bleeding in the thymic parenchyma and mediastinal cavity. It is assumed that
vessels with thin walls can break (bleeding per rhexis) to the tension for
various reasons (nervousness, physically onerous, strychnine poisoning,
etc..) and lead to fatal bleeding. After the second year of life the lesion is
very rare, because the vessels are sclerosed by gradual involution of the
thymus.
2.2.5. Inflammations of the thymus
Thymus inflammations are called thymitis. In animals are not
observed frequently. Pathologic it can be :
- hemorrhagic, in infectious pleuropneumonia in swine;
- fibrinous in pasteurellosis of calves;
- purulent metastatic strangles in foals and calves;
- granulomatous, the generalized avian tuberculosis.
2.2.6. Thymic tumors
Primary tumors of the thymus are known as generic timoame. They
are: epithelial, lymphoid, and mixed , the latter being the most common.
They are relatively rare in veterinary pathology, except avian leucosis and
and juvenile of the cattle.
Macroscopic in the both morbid conditions are produced nodular
or diffuse tumor proliferation looking greasy, externalized by oversizing the
thymus.
Microscopic they are made up of epithelial and lymphoid cells
wich are much hyperplasiated.
Thymic tumors cause serious circulatory disorders, atrophy by
compression of adjacent organs and major imbalances of immune status.
2.3. Morphopathology of the Fabricius bursa
At hatching the bursa has the size of a cherry pit and achieve
maximum development in 2-3 months, with the size of a cherry. With the
installation of sexual maturity it gradually regresses and disappears entirely.
39
The bursa's function is to develop immune competence of

synthesis of humoral antibodies (B lymphocytes).
cells for
2.3.1. Changes congenital

Hypoplasia of fabricius bursa is described in hypotrepsic chickens.
The organ is less developed and microscopically are observed cystic
formations. Chicken presents a development of the areas dependent on the
bursa,in secondary lymphoid organs and severe defects of the humoral
immune response wich lead to infections resulting in death.
2.3.2. Involutions and bursal atrophy
Involution irreversible, or physiological of FB occurs after 4.5-6
months to hen, ducks 9-10 months, 2 years in geese. It is the almost
complete disappearance of the organ, except the ostrich and raptors in which
the bursa is persists throughout life.
A trophic exchange, or accidental regression is the result of a
number of factors: food (hypovitaminosis A), infections (infectious bursal
virus, Marek's disease virus, E. coli) and numerous stress factors. The birds
are susceptible during maturation of the bursa (weeks 3-12 of life) while
animals with already devolved bursa are no longer making the disease
Macroscopically, bursa is reduced to a mere membranous
formation, predominantly fibrous, without the specific folds. Atrophy is done
either by bursa'l cells migration or by their cytoclasia. Termination of the
aggresion is followed by repopulation with bursal cells (reversible).
Microscopic in the bursa are observed circumscribed necrosis,
particularly lymphoid cells and macrophages.
Frequent diagnosis in young avian bursal atrophy is particularly
important because it may explain some failures of specific prevention
activity (low immunization after vaccination).
2.3.3. Dystrophies of Fabricius bursa
Bursal corneus epithelium metaplasia is seen in hypovitaminosis A
that is multi-layered and cornified epithelium.
Macroscopic, the scholarship is dilated 2-3 times than normal and
contains a mucinous mass in lumen. Bursal folds are flattened, have
brownish-yellow color, representing the cornified epithelium.
40
Epithelium cystisation is found in hypotrepsic chickens, in relation

to pathogens insufficiently known. Their incidence increases in experimental
infection with infectious bursal virus and possibly other immunosuppressive
effect. It highlights only histologically.
2.3.4. Inflammation of Fabricius bursa
Inflammation of Fabricius bursa are called lymphobursitisp.
Pathologically, they are: catarrh, edematous, fibrinous, hemorrhagic and
granulomatous. Presents practical importance only the ones serous,
fibrinous and hemorrhagic.
Serous lymphobursitis, edematous form is characteristic of
infectious bursal disease or Gumboro.
Macroscopic, there bursa is enlarged 2-3 times, edematous
infiltration and small hemorrhages. Color can be whitish to yellowish or red
(bleeding). On section the bursal folds are swollen and dotted sometimes
with small hemorrhages. Exchange content can be liquid, with striated
mucosal blood be consistent with fibrin deposits.
Microscopic there is redness, swelling and even necrosis (wet) of
follicles,serhohemorhagic infiltration and reticulohystocytaris proliferation.
Fibrinous lymphobursitis is found in colibacillosis and is
characterized by fibrinous exudate in the lumen of the organ.
Hemorrhagic lymphobursitis occurs in parasitic diseases such as
coccidiosis and prostogonimosis, morphologically manifested by the
presence of hemorrhagic exudate in the wall and in the lumen of the organ.
Parasites Eimeria tenella and Prostogoninus sp. in private households do not
produce outstanding clinical manifestations. (5, 11, 16, 19, 41, 43)
2.3.5. Tumors of Fabricius bursa
Tumors of Fabricius bursa are found frequently in lymphoid
leukosis, bursal localisation is a criterion for differential diagnosis between
avian leucosis and Marek's disease.
In leucosis the Fabricius bursa is hypertrophied while in
Marek's disease is atrophied and chystic. In leucosis, the bursa is increased
in volume and weight, is gray-white and have a greasy look at inspection
and section.
41
2.4. Pathology of the spleen

Spleen of young animals is relatively rich in lymphoid tissue. With
age this tissue regresses spleen shrinks capsule becomes wrinkled.
2.4.1. Spleen abnormalities
Congenital anomalies of the spleen are common and can be in
shape, position, number and volume.
Flexion and torsion of the spleen, also the double spleen and are
considered trivial anomalies especially for pigs species. in horses are
reported spline accessories and cows, horses and pigs, cases of splenic
aplasia.
In lambs hypotrepsia are found constantly, cases of splenic
hypoplasia, the organis lower than normal, low lymph nodes and lymphatic
sheaths, while conjunctive stroma is hyperplasiated (Coman, M.1989). The
same lesion was observed in piglets and rabbits. (15)
2.4.2. Atrophies and dystrophies of the spleen
Spleen atrophy occurs in animals cachectic, as a result of eating
disorders, in the tracks, from the compressions, etc.. Occurs in old dogs.
Macroscopic spleen is small and soft as a result of lymphoid tissue
involution. Capsule and trabeculae are thickened.
Spleen dystrophies are called lienosis. The practical importance is
own by protides lienosis such as: fibrinoidosis, hyalinosis, amyloidosis,
hemosiderosis.
Fibrinoid lienosis (fibrinoidoza spleen) occurs more frequently in
birds and mink, with predominant lymph nodes location . Initially, the
fibrinoid appears as a highly branched network among spleen cells. By
accumulating successive the lymphnodes elements disappear, resulting in
areas of fibrinoid necrosis.
Macroscopic there was a slight enlargement of the spleen,
associated with a dry, granular appearance on the surface of section. Correct
diagnosis is established by microscopic examination.
Hyaline lienosis (Splenic hyalinosis) is found frequently in
swine,in which is produced hyalinisation of artery of the lymph nodes,
weakening and breaking them, appearing as red infarcts marginal.
Macroscopic aspects of hyaline lienosis are uncharacteristic.
42
Amyloid lienosis (Splenic amyloidosis) is predominantly

lymphonodular, amyloid deposits start from the periphery to the center of
their lymph nodes. It is frequently found in birds, carnivores and horses.
Macroscopic, in advanced cases, are particularly remarkable on the
surface of the section, the presence of small lumps translucent ,size of a
grain of rice, as a result of precipitation of amyloid in the spleen lymph
nodes (lienoza amyloid in focus, "spleen ago").
Hemosiderin lienosis (Splenic hemosiderosis) occurs in poisoning
diseases, parasitic (hemosporidioze) and in states of chronic anemia as a
result of destruction of red blood cells. Hemosiderin is deposited in red pulp
in siderocite. The infectious anemia in horses, there was a decrease in splenic
hemosiderin, instead increasing hepatic hemosiderosis. At the very young
animals up to six months as well as in fetal spleen is usually free of
hemosiderin, while the contents of the adult animals, the increase
hemosiderin.
Macroscopic the spleen is a dark brown and a relatively high
consistency.
Uric lienosis commonly occurs in birds visceral gout and gout
generalized.
Macroscopic the spleen is mottled characterized by the presence of
foci pearly white, barely visible amid the congestion of the organ. In long
evolution may arise inert foreign body granulomas.
Minerals lienosis (calcification of the spleen). The lesion may
develop as dystrophic calcification as tuberculosis and parasitic nodules or
as metastatic calcification (eg canine leptospirosis).
Spleen necrosis form of yellowish-gray miliary foci, is one of the
characteristic lesions of the Aujeszki's disease in piglets. Necrosis is a
terminatio way of the majority of dystrophic processes.
Circulatory changes are represented by congestion, ischemia,
hemorrhage, myocardial infarction red and white.
Congestion , stasis hyperemia passive or spleen stasis occurs in
chronic cardiac insufficiencies ,in stasis after abdominal venous system, the
torsion of the spleen etc.
Macroscopic in the acute form, the spleen is enlarged in volume,
turgid, red-violet, with a fload tending to sectioning. On section, drain a
large amount of dark venous blood, white pulp is no longer observed, the
43
consistency is low. Chronic form is characterized by hypertrophy and

increased splenic pulp consistency. On section, the color is reddish-brown,
sometimes with white lines, fibrosis.
Spleen ischemia is common in birds and piglets (iron deficiency
anemia). It is caused by cold by contraction of the leiocitelor trabecular .
Spleen hemorhagies apear in swine fever as subcapsular
ecchymoses and petechiae, or bruising..
Red or hemorrhagic infarcts of the spleen appear in swine, but also
in the case of live virus vaccination.
Macroscopic red infarcts are multiple located more marginal in the
ventral third of the spleen. They are triangular, with the tip pointing toward
the hilum of the spleen and the base to periphery, blackish-red color and are
slightly protruding from the surface of the organ. The section is dry and
rough.
Microscopic necrotic areas observed and a strong hemorrhagic
infiltration,. In he developments subacute and chronic hemorrhagic necrosis
is accomplished through proliferation of the conjunctiva. Splenic infarction
can occur from other causes arterial spasm, thrombosis, compression etc..
Are pestous infarction over only those that show on microscopic
examination hyaline vascular endothelium. Red marginal infarcts are lesions
characteristic for swine fever, as infarctions of other origin than the pest are
very rare.
White infarcts are ischemic , may be observed in all species. They
follow endocarditis ulcerovegetant, and warty.. The embolic particles
detached from rujet endocarditis in pigs can cause obstructions in the
terminal arterioles of the spleen, with the occurence of white infarcts.
Macroscopic their imageis similar with the one in the red infarcts
except the gray-yellow color. Also, they are well separated from the
periphery by a leukocyte barrier and by a congestive zone. (5, 11, 13, 16,
19, 41, 43)
2.4.4. Spleen inflammations
Spleen inflammations are called lienitis or plenitis and the ones of
the capsule ore perisplenitis, Evolutionarily speaking, the spleen
inflammations may be: acute, subacute and chronic, and by their pathology
can be necrotic,hemorrhagic , purulent, gangrenous, hyperplasia and
granulomatous.
Necrotic spleen is frequently found in birds in pasteurellosis,
Listeriosis, Spirochaetosis, histomoniasis and in ruminants necrobacillosis .
44
Macroscopic, the spleen, of the bird is much larger in volume, and

is found in the parenchyma of small foci of necrosis, ash-colored. Around
them, in acute form are observed a reddish ring, and in chronic forms, one
white representing perifocal fibrosis.
In ruminants, necrotic spleen is of metastatic origin,and points 10
to 15 mm diameter, gray-yellow, brittle, dry and surrounded by a white ring.
Microscopic, in all species, there is central coagulation necrosis,
bounded by a mesenchymal reaction.
Splenic bleeding is one of the most frequent forms but also the
most controversial. Some researchers consider it as being more an acute or
chronic congestion, while others define it as acute infectious of the spleen.
Macroscopic splenic bleeding can evolve through three presentations: diffuse
and hemorrhagic-necrotic, and in outbreaks.
Diffuse hemorrhagic spleen, the spleen is enlarged in volume, the
color is uniform dark red-brown and the lymphnodular drawing is deleted or
absent. Consistency is increased ,elastic in diplococci of calves, pigs and
acute in babesiosis and low muddy in anthrax.
Microscopic, there is a sharp expansion of the venous sinuses and
splenic lymph nodes disappearance through dispersion, due to infiltration of
hemorrhagic exudate. Splenic reticulum is preserved in rujet and diplococci
and destroyed in anthrax.
Splenic bleeding in outbreaks is seen in some forms of anthrax in
horses, by the appearance of macroscopic outward gray-blackish bumps
called carbuncles.
Hemorrhagic-necrotic spleen occurs in acute forms of
salmonellosis of piglets and calves, as in some cases of streptococci in
piglets.
Macroscopic stands coagulation necrosis foci of varying sizes,
diffuse bleeding due to inflammation of the spleen.
Purulent spleen is generally of metastatic nature, characterized by
the presence of multiple abscesses. Sometimes evolving with diffuse
character, phlegmon (eg piobaciloza pig metastases from other purulent foci
uterus, mammary gland or navel).
Splenic gangrenous (Ihor) is a particular form specifies cattle,
which occurs as a result of migration or foreign bodies in the spleen
network, either from empirical practices.
Macroscopic is observed in hypertrophied spleen abscesses, or
phlegmons with gray-purple walls that deforming the organ surface. On
section, exudate has low consistency and a bad smell.
45
Granulomatous spleen is particularly common in tuberculosis,

brucellosis, glanders, pseudotuberculosis, coligranulomatosis or parasitic
infestations, etc..
In infections arenobserved miliary or nodular granulomas with
central caseum area. Splenic tuberculosis in birds, has an incidence of over
90% of cases of disease, and chronic forms of tuberculosis in cattle and
horses, it is noted tuberculous nodules in the spleen.
Granulomatous spleen in pigs is similar macroscopic with
brucellosis and tuberculosis. Brucella spleen is relatively more common than
tuberculosis. Lesion requires careful differential diagnosis (histological
structure of granuloma and etiologic agents).
2.4.5. Hyperplastic changes of the spleen
A special place must be given in veterinary to the pathology of
splenic lesion called splenomegaly. Splenomegaly is a hypertrophy of the
spleen can lead to double size, sometimes even more. It must be
distinguished from inflammation of the spleen. The morphologic base for
splenomegaly is:
proliferation of lymphoid elements (follicular hyperplasia);
- elements reticulo-histiocytic proliferation (hyperplasia pulp).
Pulp hyperplasia occurs in acute and subacute forms, the follicle in more
chronic infectious processes. Are included in this changes category the
splenomegaly from infectious anemia of horse,from babesiosis etc..
Perisplenitis are inflammation of the splenic capsule. In clinical practice
perisplenita most important are:
- fibrinous encountered
in colisepticemie, mycoplasmosis and
Glasser's disease in pigs;
- fibrous, form viloasa representing the end of all perisplenitis
- granulomatous , fungal, or pearly observed in tuberculosis.
2.4.6. Spleen tumors
Primary splenic tumors are:

lymphomas are relatively common in older dogs and seem to be free
of malignancy.
leiomioame of cows and dogs;
fibromas in cows.
46
Secondary spleen tumors are frequent in Marek's disease, avian leukosis

and taurine, sarcomas, etc.., Characterized by diffuse or circumscribed tumor
hyperplasia.
2.5. Lymph nodes Pathology
Hypoplasia of lymph nodes is almost constant lesion in hypotrepsic
lambs (also in other species), which affects both the muscle lymph nodes and
the visceral ones (Coman, M. 1989). (15)
Atrophy of lymph nodes are found in undernourished animals in
various stress nonspecific chronic inflammation in older animals etc..
Cortical atrophy particular substance.
Dystrophies lymph nodes are represented mostly by hoarding
processes (deposition of substances) and less by dystrophic changes
themselves. Of particular importance are the pigment dystrophy, among
which anthracosis hemosiderosis and lymph nodes.
Hemosiderosis of the lymph nodes is a pigmentation that prints
reddish or greenish coloration to all lymphoid nodules in hemolytic diseases
(infectious anemia of horses, leptospirosis, babesiosis, etc..) Or can be
observed only in certain lymph nodes (lymph port ruminants acute
fasciolosis in various bleeding tissue, etc.).
Microscopic, there is phagocytosed hemosiderin granules in the
cells and reticular endothelial sinus, to be drawn into the lumen of the
sinuses thus giving.
Remember that administration of preparations antianemic in piglets
(Ferdextran, Ferrovie, Myofer)prints to the lymph nodes a rusty tint
(exogenous siderosis). Overdose of these preparations will induces siderin
intoxication, affecting all lymph nodes or lymph nodes only close to the
ingvinale inoculation site.
Anthracosis of lymph nodes is an exogenous pigmentation,
frequent bronchial and mediastinal lymph nodes in cattle and carnivores, or
in mesenteric lymph nodes in pigs following administration of antidiarrheal
coal in the treatment of enteritis.
47
Macroscopic, the lymph nodes are increased in volume, especially

in the cortical area, many fine points blackish as a result of the antocitosis of
the coal dust particles by the reticuloendothelial cells.
Emphysema of the lymph nodes is a particular lesion that occurs
most often from in pig mesenteric lymph nodes, intestinal and mesenteric
often accompany the emphysema. The lesion is attributed to bacillus coli
fermentation products, or the anaerobic (intestinal pneumatosis). The lesion
is encountered in cattle in tracheobronchial and mediastinal lymph nodes by
air absorption in case of pulmonary emphysema.
Macroscopic, the hypertrophied lymph nodes, crackles on
palpation, seen gas bubbles of various sizes, and observed microscopically
sharp sinus dilatation with atrophy of lymphatic parenchyma.
Emphysema of the lymph nodes cause the occurence of
inflammatory processes as gas gas bubbles act as foreign bodies.
Lymph circulatory changes are common but, their are lacking the
diagnostic specificity. Swelling of lymph nodes are found in processes of
stasis, caecsie and direct destruction due to toxins action on the capillary
walls. Lymphnodes hemorhages as petechiae and ecchymoses are found in
many infectious diseases with fatal sepsis in many poisoning and for
vascular bleeding diatheses.
Accurate diagnosis between lymph congestion and hemorrhage is
determined only by microscopic examination:
congestion: vascular dilation and hematic mass excess;
- haemorrhage: massive erythrocyte extravasation in extravascular
spaces. (5, 11, 16, 19, 41, 43)
2.5.4. Lymph nodes inflammations
Inflamed lymph nodes are called limforeticulitis since lymph
nodes are not glands, but lymphoreticular organs. Term lymphadenitis,
although quite widespread, we consider outdated inappropriate. Instead the
term of lmphonodulitis
could be discussed, being more scientific
correspondant. Lymphoreticulitis are the result of the inflammatory process
diffusion, in the region or lymph organs that they serve. Morphopathologic
can be described the following forms: necrotic, serous, hemorrhagic,
purulent, hyperplasic, granulomatous.
48
Necrotic lymphoreticulitis occurs more frequently in piglets

salmonellosis, toxoplasmosis, necrobacillosis.
Macroscopic lymph nodes are hypertrophied, and the section of
coagulation necrosis foci gray-yellow, of various sizes, separated by
mesenchymal reaction.
Simple lymphoreticulitis
is the most common form of
lymphnodes inflammation
Macroscopic lymph nodes are enlarged in volume and succulents
reddish-in section.
Microscopic there is redness, peeling endothelium,dilated sinuses
Serous lymphoreticulitis is found in retrofagiene and mandibular
lymph nodes in acute pasteurellosis of pigs and cattle, and in the mesenteric
lymph nodes in pigs in edema disease.
Macroscopic lymph nodes are enlarged in volume and embedded
in a yellow gelatinous mass. On section, are wet and drain an appreciable
amount of serous exudate.
Microscopic sinus dilation is observed, peeling sinus endothelium,
infiltrating lymph nodes with serous exudate rich in fibrin and granulocytes.
Haemorrhagic lymphoreticulitic may develop as a circumscribed
inflammation "in outbreaks" in swine often called "ganglion mottled or
mosaic", or diffuse, observed in the majority of septicaemic disease and not
so often as haemorrhagico-necrotic, found in anthrax in pigs in the lymph
nodes retropharyngeal and mesenteric.
Macroscopic aspects were presented in exudative inflammation
chapter.
Microscopic there is inflammation and bleeding of the perinodular
subcapsular sinuses (as circumscribed), extending and enhancing
hemorrhagic inflammation respectively necrosis in the other two forms.
Purulent lymphoreticulitis strangles occurs more frequently in
foals, affecting mandibular lymph nodes, retropharyngeal, and so on, can
develop diffuse or circumscribed.
Macroscopic lymphnodes are enlarged in volume (eg child's head)
on the outside and on section are seen abscesses or collections diffuse,with
low consistency (fluid) containing purulent. Sometimes the entire lymph
node is transformed into a large collection purulent inflammatory process
affecting lymphoid node capsule and even skin. In the case of superficial
limphnodes it comes to fistulization .
Microscopic in the lymphnodes abcesses case are found all the
characteristics elements,and in , and diffuse inflammation, advanced stands
purulent exudate masses and lymphnodes structure destruction (necrosis).
49
Hyperplasic lymphoreticulitis is characterized by enlarged lymph

nodes, following intense lymphnodes hyperplasia .On section, there is
increased emphasis on thwe lymphnodes design that prints the section a
mulberrylike look whitish. In chronic forms, is found missing the
lymphnodes drawing as hyperplasia of the reticuloendothelial lymphoblastic
joins. In other cases, hyperplasic cells are differentiated in fibroblasts and
fibrocitar direction, moving toward sclerosis. It is found in some viruses,
vaccinations or substances revealing (tuberculin malein etc.).
In pigs, in chronic rujet was observed a particular form of
hyperplastic lymphoreticulitis Macrophagic lymphoreticulitis -characterized by the emergence in
the sinuses of numerous cells with macrophagic character, derived by
multiplying and swelling of endothelial cells.
Granulomatous lymphoreticulitis with giant cells found in
tuberculosis, paratuberculosis, actinobacilosis, glanders, brucellosis, etc..
Tuberculosis lymphoreticulitis occurs more frequently in the bronchial and
mediastinal lymph nodes and can take three forms of presentation: caseous,
nodular and diffuse.
Caseous form is an exudative lesion type is characterized by the
radial provision of the caseous masses.
Nodular form shows gray-white miliary foci points, or nodules of
various sizes with caseum central aspect cheesy, yellowish. Nodules may
coalesce, taking the form of tubers, which subsequently can calcify. This
form is found more frequently in cattle.
Diffuse form, is the most benign, the surface of section is glossy
without looking fat. It is the result of hyperplasia epiteioido- giant diffuse
type, called "large cell proliferation." This form is found in avian bacilli
infections, especially in horses, dogs, cats, and other species. Also in
ruminant paratuberculosis, mesenteric lymph dress this lesion (diffuse
granulomatous mesenteric lymphoreticulitis).
Actinobacillar lymphoreticulitis is found in mandibular and
retropharyngeal lymph nodes in cattle and recognized semifluid character,
yellowish necrosis of the area delimited by a connective capsule hard on
palpation. (14, 19, 22)
2.5.5. Tumors of lymph nodes
Lymph node tumors can be primary specific to the lymphoid tissue
and secondary , which develop after localized tumor metastasis in various
tissues and organs (especially carcinomas).
50
The category of primary tumors, lymphosarcoma and

reticulosarcomul mention, while secondary tumors may be sites of
mammalian lymphoid leucosis.
Whatever the form, the affected lymph nodes are greatly increased
in volume (5-10 times), the section looking greasy and sometimes with
intratumoral hemorrhage and necrosis (malignant forms).
Microscopic, there is a strong lymphoblastic and reticular
hyperplasia, which causes loss of the lymhoreticular design. In the center
are frequent outbreaks haemorrhagic or necrotic.
2.6. The morphoathology of mucosa associated lymphoid tissue
MALT is represent the whole lymphoid clusters nodular or
diffuse scattered in various locations organics. Thus associated lymphoid
tissue:
bronchus (BALT - Associated bronchial lymphoid Tissue);
- gut (GALT - Gut Associated lymphoid Tissue);
- conjunctival mucosa (tow - Conjunctivitis Associated lymphoid
Tissue);
nasal mucosa (high - Nassau Associated lymphoid Tissue);
- Harder gland (HALT - Harderian Associated lymphoid Tissue) in
birds.
MALT provides a very effective local immune response to
infectious mucosal defense. Reduction or absence of mucosal lymphoid
elements populating be construed as processes immunosuppressive or
immune deficiencies. MALT morphopathology is closely linked to the
organs they serve. (5, 11, 16, 19, 41, 43)
51
3. THE MORPHOPATHOLOGY OF THE RESPIRATORY SYSTEM

Morphological features of the respiratory system in mammals and
birds, forces us to present separately the structural changes of this device, on
the two categories of creatures.
3.1. Pathology of the respiratory tract in mammals
The airways include: nasal cavity, paranasal sinuses, larynx,
tracheea, bronchi and fallopian aids (guttural pouches) in horses.
From the pathologic point of view of the respiratory tract disease
is one of the main portal of entry into the body of various pathogens. Airway
structure is perfectly suited to serving local defense. The mucosa is made of
pseudostratified epithelium lining, ciliated and at the same time being
mucus manufacturer. Film of mucus on the surface of the respiratory
epithelium ,fixes the inhaled pathogens , incorporates local aged cell and
physiological scaling undulating movements of cilia, aiming to continue
treatment through the act airway sputum. Cilia movement is under dineinei
action, a protein with similar properties to myosin existing inside cilia
structure.
52
Several relatively recent studies noted that populating the chorion

or lamina with immunocompetent elements. Their number increases in
direct relation to environmental pollution, ie the age of the animal.
3.1.1. Airway abnormalities
Higher brahignatism is relatively frequently observed in some
breeds of dogs and pigs wherein the muzzle or snout is shorter than normal.
Overshot mouth in which the muzzle or snout is longer than normal. Other
developmental disorders of the respiratory tract are rare and can be
represented by nostril atresia, cleft palate, stenosis of the larynx, trachea and
bronchi, tracheo-oesophageal fistula, etc..
3.1.2. Nasal cavity lesions
3.1.2.1. Atrophies and dystrophies
Nasal concha atrophy occurs in atrophic rhinitis of pigs, and may
be the result off compressions exerted by tumors, abscesses, cysts, etc.. The
lesion may be unilateral or bilateral. Macroscopic areas appear brown
atrophied.
Amyloidosis of nasal cavities are found very rarely in horses and
dogs, externalized through gray-white nodules, often ulcerated, confluent or
solitary , located in the cranial cavity of the nose, septs or cornet.
Microscopic deposits identifying with Congo red .
Mucinous dystrophy is relatively common, either as a result of
goblet cells hyperproduction or enhanced their multiplication. It is found in
flu states.
Circulatory changes of nasal mucosa lesions are commonly seen in
various forms.
Active congestion accompanies inflammatory processes, whem the
lining is red-lit living or passive congestion characteristic of cardiac
insufficiencies, the lining is cyanotic and thickened.
Epistaxis is nasal bleeding nasal in drops, occurs from trauma,
poisoning or in case of pronounced vascular fragility (hypovitaminosis C
and K in swine infectious diseases, parasitic infestations or Oestrus ovis).
It is observed in piglets in infectious atrophic rhinitis and horses
due to rupture of pulmonary vessels (bilateral epistaxis) or nasal cavities of
53
capillary (unilateral epistaxis). In cattle epistaxis may result of the imperial

fern poisoning. Rinorrhagia is the nasal bleeding following in continuous jet
after efforts ,cough or consequence of trauma. The horses are cited cases of
deadly rinoragie during competitions. ( 11, 16, 17, 18, 19, 41)
3.1.2.3. Inflammation of the nasal mucosa
Nasal inflammation is called rhinitis. They can be acute or chronic
and infectious etiology, infectious and parasitic. Are known the following
forms of rhinitis:catarrhal, pseudomembranous bleeding, purulent and
granulomatous.
Catarrhal rhinitis is the most common form, the nasal mucosa is
swollen, red-purple and covered with an exudate, whose character varies
from lesion development (serous, mucous, mucopurulent). It notes estrosis in
mild forms of infectious rhinotracheitis of cattle etc. Although it is very
common diagnosis is meaningless.
Serous rhinitis occurs in cattle with FMD usually vesicular form
(rhinitis disease).
Macroscopic, the nasal mucosa is moist and red diffused amid
thrush is observed that burst taking birth pale reddish erosions.
Microscopically, the epithelial cells show vacuolar dystrophy,
goblet cells are hyperactivity, and lamina propria vessels are congested and
infiltrated with inflammatory cells serous.
Pseudomembranous rhinitis evolves either superficial as rhinitis or
as croupal rhinitis, or as profound rhinitis, rhinitis diphtheroids.
Croupla rhinitis is seen in horse, ruminants and pigs,lesion in
which the nasal mucosa is swollen and covered with gray-yellow fibrinous
membrane, slightly loose.
Diphtheroids rhinitis may be following of the croupal one, the
deposits of fibrin are more circumscribed and highly adherent to the
submucosa. It is found in cattle in MCF, in the worst forms of infectious
rhinotracheitis of cattle. In diphtheria of calves and piglets, necrotic foci may
occur, or ulcers.
Haemorrhagic rhinitis, respectively haemorrhagico-necrotic found
in MCF, or may be likely traumatic. It is characterized by the appearance on
the surface of the nasal mucosa of outbreaks of intense red. Purulent rhinitis
is usually caused by streptococci, being constantly observed strangles foals.
Evolves as abscesses or phlegmons that may ulcerate. Granulomatous
rhinitis occurs in glanders in horses in tuberculosis in cattle and fungi of all
species.
54
Glanders rhinitis is the most common, representing one of the main

locations of this disease.
Macroscopic, on the nasal mucosa is observed granulomas of
different sizes that openness will lead to the primary ulcer. Ulcers resulting
from their confluence wider (secondary), which scars, giving the mucosa a
stellate appearance, called "stellate scars." All these aspects (nodules, ulcers,
scars) can be seen on the nasal mucosa, giving it an appearance similar to the
relief map (cartographic aspect).
We complete the inflammations list with some aspects not found
in the classic patterns such as atrophic rhinitis of pigs, parasitic or allergic
inflammation.
Pigs atrophic Rhinitis is an inflammation with chronic evolution,
called "crooked nose ringing disease" in which the nasal mucosa is
atrophied, the headquarters of either leukocyte inflammation or hyperplasia.
Chronic transform of the disease causes atrophy of the cornet osteofibrosis
and diversion nose ringing in different directions. Is a polyfactorial a
syndrome in which Bordetella bronchiseptica and / or Pasteurella strains,
phosphocalcic imbalances, environmental factors, etc. breed predisposition.,
can cause chronic nasal mucosa inflammation.
Allergic rhinitis is characterized histologically by hyperplasia of
the epithelium with its erosion and infiltration with eosinophils chorion.
Sometimes in severe cases there is fibrinoid necrosis and local vessels. It
occurs more frequently in cattle, sheep and hunting dogs.
Parasitic inflammations of previous airway are relatively common
in sheep and goats caused by Oestrus ovis in April-August period known as
the "north nasal and sinus". Debuts as a catarrhal inflammation rich in mucin
due to irritation produced by larval cuticle thorns for then to turn into
purulent joint inflammation, often with blood strii. (5, 11, 16, 19, 20, 21)
3.1.2.4. Tumors of the nasal cavity
Nasal cavity tumors have an incidence generally low, often being
reported in dogs. They are caused by chronic irritation caused by the
polluted environment and the onset of lesions occurring nasal mucosal
epithelial metaplasia.
In dogs, the incidence of benign tumors (adenomas and
papillomas) is much lower compared with malignant neoplasms. Malignant
forms, carcinomas, are more numerous than sarcomas. The average age of
dogs with nasal neoplasms is around 9 years with a very wide variation.
55
In cats, nasal tumor incidence is much lower than that of the dog.
The most common carcinomas were diagnosed scvamous ones,most having
location on the outside of the nostrils. In horse nasal tumor incidence
increases with age. Most commonly diagnosed tumors were squamous and
glandular epithelium coverage.
Benign tumors, nasal polyps have a high incidence.
In bovine nasal tumor incidence is low reaching only 0.1% of all
respiratory neoplasms. Adenocarcinomas and squamous cell carcinomas are
cited. In sheep and goats were reported sporadic neoplasms like those from
cattle. Mention the existence of a oncogen virosis, adenopapillomatosis of
the respiratory mucosa of sheep, morphoclinical externalized through
mucous gland adenomas of the nasal cavity. (5, 11, 16, 19, 24, 41, 43)
3.1.3. Paranasal sinus lesions
Practical importance are shown by sinus inflammatory lesions
called sinusitis. They are the result of the release of inflammation of the
nasal cavities and in sheep by the action of the circulation of injury and
microbial by the parasite Oestrus ovis.
Sinusitis develops usually chronic because by closing holes, or
purulent exudate seromucos not eliminated. Chronicity result is sinus
mucosal atrophy and dissemination of the inflammatory process to the wall
and even bone to the meninges. The most important and most commonly is
the frontal sinusitis of sheep.
3.1.4. Injuries of the auditory tubes diverticulum
Auditory tubes diverticulum or guttural pouches are usually referred
as aerocistite and are the site of inflammation.
Bluetongue aerocystitis is characterized by serous-mucous
hypersecretion and its accumulation in the guttural pouches where
fermentation gives rise to large quantities of gas. It follows timpanism or
pneumatosis of the guttural pouches.
Purulent aerocystisis or guttural pouches empyema is the most
important lesion and occurs almost always as a complication of acute
pharyngitis. It is found as a complication in, glanders or mycosis trivial.
Purulent collection deformed region, causing compression and necrosis of
adjacent organs.
56
In chronic developments, purulent contents dehydration occurs,

sometimes precipitating salts limestone, forming calcified concremente
called guturolite.
3.1.5. Lesions of the larynx and trachea
3.1.5.1. Laryngeal atrophy
Ciliary immobility syndrome has been reported more common in
veterinary medicine due to congenital lack of dineinei the substrate of cell
mobility (ciliary). Consequently purifying respiratory tract by respiration is
reduced or absent.
Laryngeal muscle atrophy, especially cricoaritenoidian dorsal
muscle occurs after recurrent laryngeal nerve degeneration is the basis for
morphological laryngeal hemiplegia. The lesion is observed more frequently
in horses, usually unilateral, on the left side. It seems that regional irritant
injections lead to nerve degeneration that causes paralysis of laryngeal
muscles.
Macroscopic, there is discoloration of the laryngeal muscles and
reducing their size, even up to very thin foil. Entry is asymmetric larynx and
vocal chords are very close of air passing favor of horn noise (lat. Cornus =
trumpet, horn).
Laryngotracheitis circulatory changes represented by congestion
and haemorrhage, occur during septicaemic infectious diseases, such as:
swine, pasteurellosis, anthrax, etc.
Bleeding laryngotracheitis in some cases (eg avian infectious
laryngotracheitis, singamoza birds) are very severe, occurring not only
intramural lumen but also where some clots can form cylindrical especially
in the trachea. Bleeding occurs in the trachea (free) when after severe
inflammation and blistered epithelium covering such capillaries get "free" in
the trachea.
Laringoglotic edema is another important circulatory change
caused by irritants (gases, fumes, foreign bodies, caustic), allergic factors
(serum sickness, urticaria) and infectious factors (pasteurele, B. anthracis).
57
Macroscopic laryngeal mucosa appears thickened by a bright

yellow gelatinous mass, reducing the laryngeal cavity. Edema of this region
produce death by asphyxia by reducing bronchial lumen lines. (5, 11, 16, 19,
23, 41, 43)
3.1.5.3. Inflammation of the larynx and trachea
Inflammation of the larynx is called laryngitis, and those of trachea
tracheitis. They often evolve with rhinitis and bronchitis. Its athology are:
catarrh, bleeding, pseudomembranous purulent and granulomatous. Presents
practical importance pseudomembranous inflammation, purulent,
granulomatous.
Pseudomembranous laryngotracheitis is found in calves diphtheria s
and piglets, externalized by the presence of yellow-gray pseudomembrane
on the mucosal dark red background.
Laryngotracheitis purulent evolving as phlegmon and found
predominantly in strangles in horses after trauma caused by sampling.
Laryngotracheitis granulomatous is found in tuberculosis in cattle
and glanders in horses.
Laryngotracheitis tuberculosis in cattle usually progress through
fungible form, the outward appearance of nodules protruding into the lumen
of the trachea, greasy on sectors, either as colitis, characterized by the
appearance of ulcers, with raised edges and base covered with caseous
masses.
Laryngotracheitis glanders shows a similar pattern with glanders
rhinitis, which can evolve togheter(nodules, ulcers primary and secondary
stellate scars).
3.1.5.4. Laryngeal tumors
Tumors of the larynx have been reported in cats aged 6 months and
14 years were diagnosed squamous cell carcinomas. In cattle the most
common are laryngeal polyps. Tracheal mucosal tumors are carcinomas
mentioned as in horse, or adenocarcinoma in the lower trachea in dogs.
3.1.6. Bronchial lesions
3.1.6.1. Changes in lumen
58
Bronhostenosis (gr. bronchus + Stenos = contraction) or bronchial

lumen narrowing occurs after external compressions exerted by
inflammatory processes or tumors located adjacent bronchus (bronhostenoza
compression) or located in the bronchial wall (bronhostenoza obstruction).
Large bronchial obstruction can be caused by foreign bodies and small
bronchi (partial or total) of fribrino-muco-purulent exudates. When the
bronchial lumen is completely obliterated, atelectasis occurs.
Bronchiectasis (specific gravity = ektasis bronchus and expansion) is
an increase in the bronchial lumen, due to the expansion of the total and a
higher tensile walls (bronchiectasis cilindroid), and only limited portions
(bronchiectasis saciform).
In bronchiectasis pathogenesis of degenerative or inflammatory
changes occur that cause destruction of muscle and elastic fibers and their
replacement by connective tissue. Bronchiectasis meet in tuberculosis in
cattle, being called "caverns bronchiectasis" or chronic parasitic
bronchopneumonia in sheep and cattle (strongilosis).
3.1.6.2. Bronchial inflammation

Inflammation of the bronchi is called bronchitis. They usually
progress with previous tract and lung inflammation. In animals, unlike the
human, there is no pure bronchial inflammation, bronchial narrowed down at
the walls, but they evolve in most cases of pulmonary alveolar inflammation,
referred to as bronchopneumonia. Initially, for a short period of time can be
observed and pure bronchitis but spreading rapidly in alveolar tree.
Bronchitis morphological characters fall in the general table of
bronchopneumonia and can be: catarrhal, pseudomembranous purulent and
granulomatous and lymphohystocytaris. (5, 11, 16, 19, 41, 43)
3.2. Lung pathology in mammals
Changes in lung volume are represented by atelectasis and
emphysema.
59
3.2.1.1. Atelectasis
Atelectasis (gr. Ateles = incomplete and extazis = Large) is
characterized by reduced alveolar space without breathing air and
transforming into a parenchymal tissue unbreathable. After the installation
atelectasis may be: congenital or gained.
Congenital atelectasis is found in death fetuses and is widespread
throughout the organ. Occurs in calves, piglets and foals, because of the lack
of secretion of pulmonary surfactant during intrauterine development, or as a
result of inhalation by the fetus, fetal quantities of fluids (amniotic fluid),
when the births dystocic that can neutralize the action of the surfactant.
Bilateral atelectasis, is found in the dead babies.
Macroscopic the lungs are small, dark blue, compact and free of
crepitation. Docimasia is positive. The newborn who lived a few hours, on
the lung surface areas are observed red-blue clogged body mass (density),
non-aerated, with no crepitation.
Atelectasis earned or acquired during life,is produced
by
obliterating the bronchus
(atelectasis by obstruction) or external
compression exerted on the lung (atelectasis compression).
Atelectasis by obstruction occurs after acute and complete
obliteration of the large bronchi by mucopurulent discharge,
pseudomembrane, parasites, endobronchial tumors, foreign bodies, etc.. The
remaining air is absorbed slowly (2-3 hours) while progressively collapses
alveoli.
Macroscopic it is found smaller depressed areas of red-violet color,
lack of elasticity and without crepitation. On section, the lesion is shaped
like a cone, with the base toward the pleura and docimasia is positive.
Microscopic, the alveoli are collapsed with close walls close, the
lumen was absent, or barely noticeable. Alveolar walls are thickened,
congested histostructural aspect that confers territories macroscopic
atelectasis purplish-red coloration.
Compression atelectasis is a result of external compression,
externalized the lung parenchyma by pleural effusion and gas, and
inflammation of the pleural tumors, mediastinal, aortic aneurysms, etc..
Macroscopic, the color is lighter and microscopic alveolar walls
are very thin. The other aspects are similar to the obstruction atelectasis.
60
Whatever t heir form, surface hematosis reduces, followed by

respiratory failure and dyspnea appearance. Winning atelectasis may be
complicated by pulmonary edema and pneumonia. (11, 16, 19, 26, 27, 43)
3.2.1.2. Emphysema
Emphysema (gr. emphysao = to blow into something) is the opposite
of atelectasis and is characterized by increased above the normal of the
volume of breathing spaces of the distal terminal bronchioles. It arises from
the accumulation of excessive amounts of air (forced inspiration and
expiration deficiency).
Classification of emphysema is done after following criteria:
- after anatomical microstructures : alveolar and interstitial;
- etiopathogenesis: essential and clearing or vicars;
- evolution: acute and chronic.
Alveolar emphysema is characterized by excessive dilation of
pulmonary alveoli, with or without breaking the alveolar walls.
Macroscopic in the essential emphysema the lungs are affected
entirely, they are much increase in volume, white and crackles on palpation.
Alveolar vicar emphysema are evolving acute and on areas shown
in the structure intact when lungs develops various pneumopathies
(congestion, inflammation, tumors, and so on).
Macroscopic, there is a overdistention of the normal lung alveoli,
in the form of outbreaks around the compaction zones (pulmonary
atelectasis, bronchial pneumonia, cancer, lung fibrosis and so on).
Microscopic, alveolar spaces are dilated, septa interalveolare
thinned, but without breaking them, as observed in chronic emphysema,
respiratory large areas of alveolar walls due to breakage.
Bullous emphysema is a chronic form of emphysema, in which the
respiratory spaces newly formed in the lung parenchyma, in particular
subpleural, reach an unusual size and protrudes from the surface of lungs. At
this horse is due to the lower elasticity of the tissues in these areas.
Interstitial emphysema is air into thick interlobular septs and
spaces by alveolar walls rupture and terminal bronchioles.
Macroscopic, there are vesicles with air unde pleura, in the form of
small beads or, along interlobular space of blood vessels. This form of
emphysema can be found in cattle in the parainfluenza, interstitial
pneumonia atypical around hydatid cysts as a result of respiratory effort of
the animals (attacks of coughing, shortness of breath with the forced
inspiration).
61
Lower emphysematous drop the lung surface oxygenation and

hypoxia in the body is installed installation.
In corpses the volume changes can not always be highlighted
because after postmortem hypostasis, lesion picture changes a lot.
3.2.2. Dystrophies of the lungs
Dystrophies of the lungs are represented by endo-and exogenous
pigmentation (jaundice, melanosis, anthracosis) and calcification.
Anthracosis pulmonary is frequent in animals and working dogs
living in heavily polluted atmosphere of the great industrial centers. Particles
less than 5 mm diameter airways pass the barrier and reach the pulmonary
alveoli, where they are phagocytosed by macrophages.
Macroscopically, the lungs of small foci isolated or confluent, the
blackish color, and histologically observed islands of macrophages loaded
with dust particles of coal. Anthracosis lung is followed by limfonodular
anthracosis.
Other dystrophies of lung are caused by inhalation of dust
exogenous called pneumoconiosis (gr. air and konis = dust) have less
importance in veterinary pathology. Silicosis of sheep in very sandy areas
(Dobrogea, Arab countries) by inhaling silica dust. Siderosis is representing
the inhalation of iron oxide, iron fine particles.
Pulmonary melanosis is found as a surprise in necropsy or
slaughter examination of small ruminants. Lung with melanosis, on surface
and depth, appears with black or brown-green well defined.
Dystrophies limestone more common in ruminants and carnivores
can perform either as:
- dystrophic calcification in the case of infectious or parasitic
granuloma;
- metastatic calcification, manifested by the presence of alveolar walls
inlaid limestone of easily discernible to the touch (pneumocalcinosis).
Dystrophic calcification of the lungs is usually the result of chronic
circulatory disorders and primary biting preceded by elastic fibers.
Circulatory changes in the lungs are found in all species manifested
by congestion, hemorrhage, embolism and thrombosis, hemorrhagic
infarction and pulmonary edema.
Pulmonary congestion, is characterised by excess of blood in the
pulmonary capillaries, or together with the increased speed of movement in
62
the case of increased muscle (active congestion) or to slow the stagnation of

blood in the vessels (passive congestion). Appears under the influence of
numerous and varied biological, chemical, physical, factors
Macroscopic the lungs are increased in volume and weight, vivid
red-black-red active congestion in passive congestion and elasticity is
reduced. On section, drain a large amount of blood, sparkling, red or
blackish vines. Docimasia is negative in active congestion and "between two
waters" in passive congestion.
Microscopic, in the active form alveolar capillaries are dilated and
filled with red blood cells in the lumen well individualized and there is a
liquid seroproteic, while in passive congestion is noted in addition diffuse
septal fibrosis, interstitial, perivascular and peribronhic.
Complications of the pulmonary congestion is pulmonary edema,
acute or chronic, and bronchopneumonia.
Pulmonary hemorrhage are common in pigs and have traumatic or
toxic nature. They are located mainly under pleura, interlobular, or lungs in
the form of bruises thickness of various sizes.
Hemoptysis is a pulmonary haemorrhage caused by the rupture of a
large vessel caliber, or result in the formation of pulmonary tuberculosis
caverns. Blood, in hemoptysis, is mixed with numerous bubbles of gas, as it
comes from the pulmonary alveoli.
Thrombosis and pulmonary embolism are seen in horses after
mobilization of fragments of clots from jugular vein, the posterior vena cava
and uterine veins. Thrombi inside the lungs of the large veins of the systemic
circulation in pulmonary arteries stop. In view of the fact that the lungs have
a double movement and the anastomosis between blood vessels,
thromboembolism consequences are minimal. The most common
consequence of pulmonary embolism and thrombosis is the formation of
hemorrhagic infarcts.
Pulmonary infarction occurs more frequently in horses, cattle and
pigs, especially in diaphragm lobes as red infarcts (hemorrhagic)
Macroscopic are observed compact areas, blackish-red, dense
comprising several lobules, and the cone-shaped section, based on the
pleura. In acute developments, protrudes from the surface, and on section
has the appearance of coagulated blood. In chronic form appear in thr lung
parenchyma clogged, dry and sometimes pleuropleurale fibrosis with
adhesions in the right infarcted area.
Pulmonary edema occurs either due to slower blood flow in small or
large circulation (stasis edema, inflammatory) or following alteration of
vascular permeability in poisoning disease (inflammatory edema).
63
Macroscopic, there are no large differences between the

inflammatory edema and stasis except the color. Lungs are increased in
volume and weight, lobular design is very obvious, pasty consistency and the
color is gray in stasis edema and red in the inflammatory one. On section
and pressure, there is a whitish or reddish liquid aerated, which occupies the
entire respiratory tree is sometimes observed in animal nose, or where the
animal stayed.
Microscopic indicate the presence of edema fluid in the pulmonary
alveoli, bronchi, interlobular space that appears larger in size. The
inflammatory edema observed in addition, capillary congestion, leukocytes
and endothelial cells exfoliate and blended into a homogeneous liquid. The
evolution is rapid in pulmonary edema, death can be installed in minutes,
through suffocation or heart isufficiency.
3.2.4. Lung inflammation
Inflammation of the lungs is called pneumonia (gr. pneumonia =
lung) and bronchopneumonia by locating process only in alveolar tissue, or
both microlayers of the lung (bronchi and alveoli).
In view of the fact that in animals, in most cases, the inflammatory
process develops in the bronchi and alveoli at the same time, the logic
requires more accurate name for this process is the bronchopneumonia.
We note that lately they were diagnosed and pure pneumonia in
animals (eg giant cell pneumonia, pneumonia macrophages).
The etiology of bronchopneumonia is polymorphic (bacteria,
viruses, fungi, parasites, foreign bodies, etc..), And the starting point is the
device bronchial or lobar bronchi. Locating inflammatory lung disease is
prevalent in the cranial lobes in viral infections, chlamydiene, mycoplasmal
and bacterial predominant diaphragm lobes (caudal) in parasitic infestations.
Over time, there have been several classifications of lung
inflammation following:
- etiology : bronchopneumonia bacterial, viral, parasitic, foreign body
aspiration and so on;
- extent and topography of lesions: lobular (bronchopneumonia), lobar
(pneumonia) and interstitial (pneumonia);
- morphological criteria, it may find the following forms of
bronchopneumonia: necrotic, tongue, bleeding, cereal, festering, gangrenous,
lymphohystocytic fibrotic and granulomatous.
Necrotizing bronchopneumonia is characterized by the appearance
on the surface and thickness of the lungs, of some necrotic foci, grayyellow, dry, of different sizes (5 mm - 10 cm), separated by a reddish ring in
64
acute developments respectively whitish in forms chronic. Occurs in cattle,

sheep and horses, usually as a secondary lesion (metastatic) in
necrobacillosis.
Microscopic there is the coagulation necrosis zone surrounded by a
leukocyte reaction. In chronic forms, there is a fibro connective reaction with
a encapsulation trend.
Macroscopic, the affected lung lobes or territories are slightly
increased in volume, have purplish-red uniform color, obvious lobular
drawing and increased consistency. The section has a wet pressure of
exudate in bronchi appearing gray or grayish-yellow.
Microscopic, there is desquamation of alveolar cells, exudate with
a high content of inflammatory cells simultaneously with serous effusion, or
serofibrinous.. Descuamation processes occur in the structure of the bronchi.
In longer developments, the color of inflamed territories becomes
lighter, the volume decreases, increases consistency, lobular design becomes
more apparent. Originally inflamed areas have a color reddish-mottled (
splenization phase), and subsequently that of the pancreas, gray-whitish
(phase pancreatization), typical forms of chronic bronchopneumonia. On a
microscopic peribronchial mesenchymal tissue, interlobular septal and the
spaces, thus reducing the volume territories proliferating inflamed, increased
consistency, while reducing alveolar lumens. These issues are commonly
seen in pigs.
Hemorrhagic bronchopneumonia may protrude through outbreaks
of hemorrhagic infiltration, predominantly interlobular in swine, respectively
intralobular in some forms of anthrax. Form of joint inflammation,
hemorrhagic-necrotic meets supraacute developments and acute infectious
swine pleuropneumonia.
Microscopic, heamorrhage infiltration is observed with the loss of
cellular design, whether or not accompanied by other types of exudate, or to
areas of necrosis.
Fibrinous bronchopneumonia or groats, also called lobular
pneumonia occurs in all ages and species, is produced by bacteria or viruses
pathogenic saprophytic condition, in which an important role is played by
pasteurella infection. Fibrinous inflammation is characterized by a large
parts of the lungs, with a cyclical trend, with relatively fixed duration, 9-13
days to horse. In other species, this development stage is not respected.
In the evolution of croupal bronchopneumonia, by analogy with
human pathology, differ four successive phases: acute congestion, red and
gray hepatisation and resolution.
65
Congestion phase , filling or prehepatisation stage is the initial phase

and lasts 1-2 days.
Macroscopic thr affected lobules are reddish, have increased the
volume and consistency, and on section wet dripping reddish liquid foam.
Docimasia is "between two waters."
Microscopic, there is septal capillary congestion and intraalveolar
serous exudate.
In the red hepatisation phase (2-4 days), lung territories resembles
inflamed liver tissue, the red-brown, firm consistency, without crepitation.
The surface of the section is dry, dull and particulate, due to fibrin deposition
in the alveoli. Granular aspect is the fact that the elastic bucking of lung
parenchyma shrinks and printing this macroscopic fibrin sectioned.
Docimasia is positive.
Microscopic, it is noted capillary congestion and intraalveolar
fibrinous exudate, bronchial, as in interlobular spaces with many rare red
blood cells and leukocytes and desquamated alveolar cells. Congestion and
the large amount of red blood cells in the alveoli in this stage.
The gray hepatisation phase (3 days), lung areas affected have the
same physical characteristics as the macroscopic and the previous phase,
except the color, which gradually becomes gray-reddish or yellowish due to
the disappearance of congestion and intraalveolar erythrocytes. Surface
section initially granular gradually becomes glossy and smooth, docimasia is
positive.
Microscopic, it is found primarily in the exudate, neutrophil
granulocytes that will produce enzymatic lysis of fibrin, there is no
congestion and alveolar epithelium.
In general, the phase of "block lung", red and gray hepatisation takes
5-6 days.
In the phase of resolution the lung parenchyma returns to its
original shape by "restutio ad integrum". Alveolar fibrin exudation was
broken completely and absorbed by macrophage activity, or eliminated
through the bronchial alveolar epithelium is restored and air flows back into
the alveolar lumen.
Lungs regain normal color, consistency decreases and docimasia
becomes negative. This feature of croupal bronchopneumonia outwardly,
macroscopic, with a mottled appearance (full color), both on the surface and
the organ section.
In animal the healing is quite rare because the processes of
resorption due to blood circulation disorders, thrombosis of lymphatic
66
vessels, occurs more slowly triggering a process of proliferating connective

organization .
Pulmonary complications of croupal bronchopneumonia are
suppuration and carnificarea (the conjunctiva organizing fibrinous exudate)
and the neighborhood are pleural.
Suppurative bronchopneumonia can occur as a complication of
catarrhal bronchopneumonia and croupal, the metastasis of purulent
infection of any outbreak festering in the body, or may be caused by
pyogenic germs through the Air-borne route.
Macroscopic on the surface and in the mass of the lung ,abscesses
are seen in either multiple sizes, depending on the etiology and length of the
process, either a single bulky abscess. Recent content is purulent abscesses,
yellow-green, while that old and young can be caseous and calcified. It
occurs more frequently in ruminants and swine, especially in youth and in
infectious bronchopneumonia foals.
Gangrenous bronchopneumonia may be due to ingress of foreign
matter into the lungs through ingestion or administration forced (hence the
name of bronchopneumonia "ab ingestis" or suction), or may be the result of
unfavorable evolution of fibrinous bronchopneumonia, or the purulent.
Macroscopic, it appears foci containing gray-green fluid, dirty,
Ihor, or caverns
Microscopic, there is an ihor exudate that obliterates bronchi and
alveoli. It differs from the amount of purulent bronchopneumonia the
exudate leukocyte is reduced or absent.
Lymphohistocytaric
bronchopneumonia is an interstitial
inflammation, predominantly productive occurring after viral infections
chlamydiene and mycoplasmal, or immune sensitization processes.
Macroscopic the lesion is located in the cranial lobes and is difficult
to diagnose resembling catarrhal bronchopneumonia.
Microscopic, there is hyperplasias peribronchial, perivascular,
interlobular septal, viral inclusions, sparkling pneumocytes (in
chlamydioz). This form is found in adeno- and respiratory reovirosia in
chlamydian bronchopneumonia in piglets etc enzotic pneumonia. It is also
called interstitial pneumonia .
Recently,in mink youth was identified a particular form of interstitial
pneumonia, characterized by hyperplasia and macrophage metaplasia of
advential cells of the artery called also
macrophage pneumonia.
macrophages can reach 200-300 m size.
67
In parainfluenza virus infections (cattle, pigs), alveolar macrophages

and bronchial epithelial hyperplasia is fragmented and give rise to
multinucleated giant cells, characteristic to pneumococcal giant cell.
Bronchopneumonia fibrous or sclerosing pneumonia occurs as a
result of the chronicity of acute, catarrhal,or fibrinous bronchopneumonia,.
Parasites of the lung (strongyles and metastrongili) may be another
important cause of the bronchopneumonia.
Macroscopic there is a gray-whitish foci endured and microscopic,
thickening of the alveolar septs ,hyperplasia generally poor in cells. alveolar
lumens reduces to extinction. Granulomatous bronchopneumonia occurs in
all species:
- either as compact granulomas in bacteriosis (tuberculosis, glanders)
in mycosis (aspergillosis) in parasites (in mlerioza sheep);
- or in the form of granuloma parasitic cysts in echinococcosis.
Among such granulomatous bronchopneumonia infectious and
parasitic in nature macroscopic differences. In the first, granulomas formed
is adhered to the lung tissue, with a necrotic center and a perifocal side ,
while in the case of parasitic bronchopneumonia, well defined granulomas
formed, which can be easily enucleated surrounding lung tissue, leaving a
disposal site smooth membrane. Removal workmanship is called parasitic
granuloma .
Characteristic aspects of granulomatous bronchopneumonia are
dependent on the etiologic agent and will be exhibited in the
etyomorphopathology.
A common characteristic for all pathological forms of
bronchopneumonia, regardless of etiology, is positive docimasia except
rump state of congestion, from croupal bronchopneumonia, which is
"between two waters." (5, 11, 16, 19, 41, 43)
.2.5. Lung tumors
In animals of rent, the frequency of lung tumors is significantly
lower, which is explained by the much shorter life.
In the dog lung carcinomas occur almost constantly around the age
of 10 years, very rarely under 6. The average age in cats with lung
carcinoma, is about 12.
Incidence of neoplasms in dogs appears to be influenced by race or
gender, although greater sensitivity is own by Boxer and German Shepherd
breed.
68
In cattle, the incidence was 2.8% of all neoplasms, mostly

adenocarcinomas. It signaled EBL pulmonary location. (19)
Particular importance should be given to pulmonary adenomatosis of
sheep and goats, viral oncogene characterized by alveolar epithelial
hyperplasia and bronchial tumor.
3.3. Morphopathology of thoracic cavity in mammals
3.3.1. Content changes
Internal and external injuries of thoracic cavity, can lead to
excessive amounts of liquid, solid foreign bodies, gas in the pleural cavity..
Foreign bodies commonly found in cattle, from network by perforating the
diaphragm. Air or gas from digestion, accumulated in the pleural cavity,
producing spontaneous or traumatic pneumothorax and compression
atelectasis occurs.

Circulatory changes are represented by congestion and
haemorrhage,in sepsis and in poisoning, but also as hollow collections
(Hydrothorax, hemothorax, chylothorax), all processes can cause atelectasis.
3.3.3. Inflammation of the pleura
Pleural inflammation bearing different names, depending on the
presence or absence of exudate. Inflammation in the pleural cavity in which
large amounts of exudate is found, is call pleurisy, while the dry
inflammation or with small amounts of exudate are called pleuritis.
Pleurisy are generally acute inflammation predominantly exudative.
Pathologically, they are:
- serous effusion in ruminants, swine pleuropneumonia infectious
acute form;
- fibrinous in pasteurellosis in calves and piglets;
- purulent in pasteurellosis in rabbits.
69
Pleuritis are inflammations with subacute or chronic evolutions,

morphological externalized by pleuritis necrotic (in necrobacillosis lambs),
fibrotic and granulomatous.
Fibrous pleuritis are polymorphic and can take the following
forms:
- fibrous pleuritis simple - when the pleura is thickened, and the
surface is smooth;
- pleuritis viloasa - the pleura is thickened with many "hairs"
connective tissue printing surface looks rough serous;
- adhesive pleuritis or fibroadhesive - When pleural adhesions
between the two skins.
- maculae albidae focused as thickening whitish.
They appear as a way to end the pleurisy. Occur more frequently
in chronic evolution of infectious pleuropneumonia and swine pasteurellosis.
Granulomatous pleuritis is found in cattle tuberculosis and glanders in
horses, nodular form, fungal, pearl or as largecaseum area. Particular
mention pearls and fungal tuberculosis pleuritis of cattle. (5, 11, 16, 19, 41,
43)
3.3.4. Mediastinal lesions

Mediastinal emphysema occurs in case of breakage departure hatred.
Mediastinitis is inflammation caused by foreign bodies in the esophagus or
proventriculus, or by spontaneous opening of mediastinal lymphoreticulitis.
3.3.5. Injuries of diphragm
Diaphragm congenital non-stiching favors herniation of abdominal
organs (liver, stomach, etc..) In the chest cavity or, more rarely, of the chest
(heart, lung) in the abdominal cavity. Unraveling and diaphragm rupture
occurs after trauma, the macroscopic lesions are found on the edges of the
tear hemorrhagic infiltration.
Pleural mesothelioma is pleural primary tumor diagnosed in cattle,
dogs, horses, cats and goats. The tumor is rare and affects both skins
(visceral and parietal) of the thoracic cavity. The main cause of these tumors
is exposure to asbestos, but there is evidence that can be offending
ferruginous particles.
70
3.4. Respiratory pathology in birds

3.4.1. Airway lesions
3.4.1.1. Respiratory dystrophies
Corneus etaplasia dystrophy is the most important dystrophy of the
air found in hypovitaminosis A, which is exhibited by whitish miliary
nodules, especially in the trachea.
Of lesser importance are cited dystrophy uric gout if generalized, ie
mucinous dystrophy as a result of inadequate microclimate (increased
amount of ammonia). The latter is manifested morphologically by an excess
of mucus as a result of airways irritation .
3.4.1.2. Airway inflammation
Inflammation of airways: rhinitis, sinusitis and laringotraheits are
common in birds, being of viral, bacterial, mycoplasma, etc. . For
concomitant inflammation of the nasal passages and sinuses can use the term
coryza. Catarrhal rhinitis and sinusitis are found in the early stages of
infectious coryza and mycoplasmosis. Rhinitis and sinusitis
pseudomembranous meet in infectious coryza, mycoplasmosis, etc..
Serocatarhal laryngotracheitis can be seen in avian infectious
bronchitis. Heamorrhagic laringotracheitis is observed in the acute form of
infectious laryngotracheitis in chickens singamoza the last two being
diagnosed only in the private sector.
Pseudomembranous larynotracheotos meet in difterovariola,
infectious laryngotracheitis, mycoplasmosis and hypovitaminosis A.
Granulomatous laryngotracheitis are found in subacute and chronic
developments of singamosis, especially in turkeys, pheasants, peacocks and
more rarely in chickens.
Macroscopic, it is noted in the trachea military granulomas, which
are formed at the mucosa of the male fastening.
Microscopic differential diagnosis of laryndotrachotos is
determined by the following criteria:
- in difterovariola, intracytoplasmic inclusions observed acanthosis
and Bollinger;
- in infectious laryngotracheitis, there is exudation, proliferation and
syncytial gigantocelulare with intranuclear inclusions Seifried;
71
- in mycoplasmosis, mucous gland hyperplasia is highlighted as an

amphora or Tubes;
- in hypovitaminosis A, we notice the horny epithelium metaplasia. (5,
11, 16, 19, 41, 43)
3.4.2. Lung lesions
Congestion of the lungs in chickens may be due to cold and heat,
sudden temperature variations, inhalation of irritant substances in poisoning,
infections, etc.. Evolution of pulmonary congestion is rapid (minutes, hours),
being seconded by pulmonary edema, which produce death by asphyxia.
3.4.2.2. Lung inflammation
Morphological lung inflammation outwardly through the following
forms: catarrhal, fibrinous, lymphohisocytic, granulomatous.
Catarrhal bronchopneumonia is the result of deficiencies in nutrition
and hygiene, physiological states of debilitation (moulting), infections,
infestations (singamoza in chickens and pheasants, trichomoniasis in pigeons
etc.).
Macroscopic the lungs are enlarged, reddish, wet look on section.
Fibrinous bronchopneumonia is seen in subacute and chronic
pasteurellosis.
Macroscopic the lungs are increased in volume, red-purple, had
increased consistency and on section is observed dry matter, highlighting the
parabronchia design due to fibrinous exudate, yellow, dry filling the lumens.
Lymphohistocytic
ronchopneumonia
are
diagnosed
only
microscopically (in mycoplasmosis, salmonellosis, viral) and are confused
with pulmonary localizations of Marek's disease. It is considered as
pathological and lymphoid hyperplasia of parabronhia walls.
Granulomatous bronchopneumonia meet in aspergillosis,
coligranulomatosos rarely in tuberculosis. in adult birds have nodular
character, while in chikens they affect large areas with predominantly
caseous aspect.
3.4.2.3. Lung tumors
72
Lung tumors, diffuse or nodular-looking bacon, meet in Marek's

disease in avian leucozele etc.
3.4.3. Air sac lesions
The most important lesions of the air sacs are inflammation called
airsaculitis. In their etiology, have a special role bacterial and fungal
infections, and causes irritation: gases, particularly ammonia, carbon
dioxide, or particulate (dust) and pathology are described airsaculitis serous,
fibrinous and granulomatous.
Airsaculitis serous, meets in early forms of colibacillosis.
Macroscopic air sacs walls are congested and within them there is a
serous exudate, which sometimes fibrin.
Airsaculitis fibrinous is a common lesion in mycoplasmosis, but
also in colibacillosis. In micoplasmosis the initial exudat has a sero fibrinous
aspect, but by later dehydration takes ayellowish look , consistent, like
'greaves'. Walls of the air sacs are thickened, cloudy, with rough surface due
to massive infiltration of serofibrinos exudate. In colibacillosis, exudate is
serofibrinos, or fibrinopurulent, which identifies concremente brittle
yellowish, smelly.
Granulomatous airsaculitis the most frequent and characteristic
found in aspergillosis.
Macroscopically, the surface of the air bag is observed military
nodes, yellow, well defined, protruding into the lumen thereof, and the inner
surface of the bag is covered with a layer of mold in the form of a yellowgreen fine spray.
Microscopic, the presence of hyphae mycelium in an necrotic foci
surrounded by epithelioid cells and giant cells in PAS staining is
pathognomonic lesion for the diagnosis of aspergillosis.
Of the granulomatous aerosaculitele with parasitic origin ,we
mention
mite infestation Cytodites nudus in chickens, manifested
macroscopically by small dots, gray resembling sand surface on air bags,
representing colonies of mites ("lungs sprinkled with sand"). (5, 11, 16, 19,
29, 41, 43)
73
4. THE MORPHOPATHOLOGY OF DIGESTIVE TRACT

4.1. Oral cavity morphopathology
4.1.1. Malformations of the mouth
Macrocheilia (Gr. macros = big cheilo = lip) is malformation in
which lips are unusually high.
Microcheilia (Gr. micros = small) is the anomaly in which the lips
are too small or hypoplastic.
Macrostomia (gr. macro and stoma = mouth) is when mouth opening
is unusually high. It is very rare and is due to incomplete fusion of the
mandibular jaw bud, either unilaterally or bilaterally.
Microstomia is damage the mouth hole is too small. It is
exceptionally rare.
Cleft (Gr. cheilo and schist = crack) or cleft lip can be simple when
only interested cleft upper lip or be full when there is lack of unity and
alveolar ledge. Occurs in calves, lambs and puppies.
Gnathoschizis (gr. gnathos = jaw and schist) lack of welding jaws.
Cheilognatoschizis - lack of union co lips and jaws.
74
Cleft palate is cleft palate can be localized only to the soft palate,
Staff iloschizis, or may involve the soft palate and hard palate
simultaneously, uranoschizis, in which case the oral cavity communicates
with the nasal cavity.
Cheilognatopalatoschizis or mouth of the wolf is the absence of a
union bud lips, jaw and palate you.
Agnathia (gr. a = lacking and gnathos), lack jaws.
Brahignatia (gr. brachys = short) or the presence of maxillary
micrognathia shorter compared to normal peers. In dogs bulldogs there is
often a high brahignatie.
Prognation (gr. pro = before and Gnat) - jaws longer than normal.
On the pathological brahignatia or prognatia not ensure normal incidence of
the dental arches. Kampilognatia (gr. kampylos = bending and Gnat) is cross
beak abnormality incompatible with prehension feed. It is only found in
birds, especially chickens turkeys. (5, 11, 16, 19, 25, 41, 43)
4.1.2. Dystrophies of the mouth

Oral cavity dystrophies have little practical importance in animals.
Hyperkeratosis mouth, reported in hypovitaminosis A in poultry, pigs and
calves. They appear as Cretaceous plate the size of a grain of wheat or
higher. By removing the epithelium, lamina propria remains uncovered. In
these areas the existing bacterial flora in the mouth can easily penetrate and
cause necrosis and inflammation. Balloning vacuolar dystrophy and
epithelial cells contribute to blistering mouth and canker sores (aphthous
fever).
In all species are found dystrophies pygmies entation, jaundice, and /
or melanin pigment accumulation.
4.1.3 Necrosis of the mouth
Necrosis lingual fossa occurs in taurine through the accumulation of
feed. In some diseases such as foot and mouth disease, mucosal disease,
rinderpest, etc.. extensive necrosis occurs in the mouth and tongue. At
carnivores necrosis is found in uremic poisoning complicated with oral
ulcerative inflammation.
75
Macroscopic necrosis appear as areas more or less extensive, the

gray-yellowish mucosa can be outlined as flaps leaving denuded chorion
(ulcers).
Circulatory disorders that appear in this section are determined by
the direct action of foreign bodies, improper food, parasites or indirect action
that hypovitaminosis C, K, general stasis disease, septicemia, etc..
Anemia of the mouth mucosa accompanying general it may be less
the result of localized circulatory disorders. Mucosa appears pale, whitishlooking.
Cyanosis tongue as a practical matter lesions characteristic of sheep
bluetongue, called "blue tongue" and in pellagra in dogs (tongue black, blue
tongue) caused by lack of nicotinic acid or avitaminei PP.
Sublingual bleeding related to increased vascular fragility is found in
equine infectious anemia.
Bleeding in the mouth appear in septicaemic diseases, poisoning,
vitamin C deficiency (scurvy dogs, guinea pigs and monkeys, located mainly
on the gums).
4.1.5. Inflammations of the mouth cavity
Inflammation of the mouth are known by the generic name of the
Stomatitis (gr. stoma = mouth). Most times they evolve located on certain
structures, or parts of the cavity, bearing their names corresponding to the
inflamed area.
The lips inflammation are called cheilitis , gingivitis is inflammation
of the gums, palatinitis is palate inflammation, Gnat is inflammation
buccelor, glossitis is inflammation of the tongue, tonsils or tonsillitis is
inflammation of the tonsils, angina is inflammation of the entire pharyngeal
lymphoid ring.
Stomatitis etiology is diverse and confused with the inflammation
in general. Stomatitis can be classified in terms of:
Et. iopatogenetic: primary or secondary;
Evolution: acute, subacute or chronic;
Pathology: catarrhal, papular, serous, ulcerative,
pseudomembranous, festering, gangrenous and granulomatous.
Catarrhal stomatitis is characterized by the accumulation of graywhite deposits, Filante, the internal faces of the oral vestibule wall or on the
tongue forming the so-called aloin layer showing a characteristic
76
morphoclinical aspect language called Sabur (lat. saburra=ballast, ballast).

Under these confounding mucus hyperproductio with desquamated epithelial
cells lining is red-hot, swollen and edematous. Chronic catarrhal stomatitis
lead to proliferation of submucosal tissue.
Papular stomatitis, is found mainly in cattle in disease of the same
name, papular stomatitis in cattle, but also sheep ectima contagious.
Macroscopic the surface of the mucosa is found nodular formations
of different dimensions (about 1-3 cm in diameter) yellow-red. The papules
are often bounded by a circle reddish brown.
Microscopic balloning degeneration observed in the upper layers of
the epithelium, papillary edema and intracytoplasmic viral inclusions glued
nuclear membrane.
Serous stomatitis develops in most cases,in outbreaks of vesicular
stomatitis form and more rarely, diffuse edematous form of stomatitis (eg
glossitis edematous of pasteurellosis).
Vesicular stomatitis is a result of either the action of heat or
chemical factors, or more often the result of viruses epiteliotrope as the
FMD, vesicular stomatitis, swine vesicular disease, vesicular exanthema,
ectima contagious disease of sheep and goats etc.
Vesicles appear as bumps containing clear fluid and in older
formations, called thrush, is slightly opalescent liquid. Further, they are
white, opaque, turning into pustules. Thereafter, they are broken, resulting in
erosion more or less flat. Both blisters, canker sores and erosions,
surrounded by a reddish ring.
Ulcerative stomatitis is characterized by the appearance of
excavations (ulcers) superficial or deep, round, oval, or irregular edges
highlighted located on the gums, the sides of the tongue, or the inside of the
cheek. Center ulcer is covered by a yellow-brown deposit, reddish color.
It found as the primary lesion in leptospirosis stahiobotriotoxicosis
in lead poisoning, mercury or phosphorus, or may occur as a complication of
stomatitis, which evolved earlier (vesicular disease). The fund hemorrhagic
uremia occurs in dogs and hypovitaminosis C. The intensity of damage
depends on the concentration of chemical substances as well as their
duration of action, or necrotic complications caused by such infectious
pathogens.
Microscopic, there is a central area withdeposits of fibrin an
leukocytes.
Pseudomembranous stomatitis (fibrinous) is characterized by the
formation of yellowish-white membrane on the surface of the mucosa. can
evolve as stomatitis or diphtheroids. It occurs more frequently in birds
77
difterovariola, Newcastle, trichomoniasis, candidiasis, or swine in

salmonellosis and necrobacillosis.
In birds, pseudomembrans are more apparent as compared to
mammals which prevails necrotic nature of the lesions. Please note that
pseudomembrans are relatively shallow (stomatitis croup) in Newcastle,
difterovariol and candidiasis, respectively deep (stomatitis diphtheroids) in
trichomoniasis in pigeons and mammals youth diphtheria. By removing
pseudomembrans, denuded mucosa and bleeding occurs.
Microscopic, epithelial necrosis is observed in the presence of a
surface deposit fibrin oxifil.
Purulent stomatitis can be found in all species, as abscesses,
phlegmons or chronic suppurative catarrh. Most often evolves as tonsillar
abscess in foals strangles.
Gangrenous stomatitis (noma), in most cases, occurs as a
complication of suppurative stomatitis with anaerobes, leptospire, canine
distemper virus, etc.. It occurs more frequently in dogs and more rarely in
piglets and calves.
Macroscopic is observed a process of deep necrosis, accompanied
by edema and characteristic odor.
Granulomatous stomatitis is more common in cattle and pigs, as in
most cases actinobacilar and parasitic nature. Actinobacilosis, in cattle,
evolving form of nodules, ulcers, or more frequently as mesenchymal
proliferation, diffuse macroscopic consistency throughout the printing tough
body, hence the name "wooden language".
Parasitic granulomatous stomatitis canbe diagnosed, macroscopic, in
cattle and pigs, in the masseter muscles, as in the tongue muscles in
cysticercosis.
Macroscopic, the muscles appear to be sprinkled with grains of rice,
representing granulomas parasitic cyst. Sometimes cysts can be diagnosed
and in the lingual and masseter muscles in cattle and sheep, as trichinelice
granulomas in pigs.
Glositis. Usually inflammation of oral mucosa and tongue include
being able to speak in such cases of glossitis. A special form of glossitis is
deep parenchymal infection in the etiology of which some may be favored
by a bee or wasp stings, trauma or burns. It's also good to know the
particular aspects that we the thongue takes in various diseases.
Sabur language, loaded ,found in gastric dyspepsia;
- tongue dry roasted in febrile diseases, diabetes, liver cirrhosis;
- tongue brown, blackish are found in pneumonia;
- yellow in jaundice;
78
- tongue pale in anemia, equine infectious anemia;

- language purplish-blue states asphyxia.
Tonsillitis may develop simultaneously, or as a consequence of
stomatitis, but can also occur as a symptom of viral diseases (eg swine).
The gloss-anthrax in pigs in nature hemorrhagic-necrotic tonsillitis,
the tonsils were infiltrated with exudate serohemoragic which includes
submaxillary region.
In swine fiber the lesion is necrotic or fibrous (diphtheroids) and, in
most cases, lesions precede the digestive tract. Tonsils are cyanotic and the
outbreaks round, oval or scalloped white-gray areas bounded failure. In
calves and dogs there is a purulent tonsillitis. (5, 11, 16, 19,30, 41, 43)
4.1.6. Tumors of the oral cavity
Mouth tumors are represented by lingual and gingival papillomas in
dogs, rabbits and horses, and fibroids, carcinomas and sarcomas. A particular
form of sarcoma is the so called "epulis" observed in dogs boxers and
bulldogs, externalized through cauliflower growths, greasy located along the
gums, sometimes presenting with papillary extension into the oral cavity.
Melanoma is the most common oral tumor localization in the dog. The
average survival time is 3 months.
4.1.7. Changes in dental aparatus
4.1.7.1. Abnormalities of teeth
Disorders of tooth development in animals can be represented by:
numerical abnormalities (oligo-and poliodontia);
abnormal size (micro-and macroodontia);
abnormal position (torsional rotations, deployments in horses and
dogs);
- abnormally shaped (coronary dysmorphia, root);
abnormal structure (enamel, dentin) etc..
4.1.7.2. Wear hanges
Abrasion is the loss of tooth substance in contact tooth- tooth during

mastication. It may be physiological or pathological.
Macroscopic it externalizes by the molars worn in scale, teething
wavy blunt teeth on the lingual or the labial edge, corner of molars etc.
79
This abrasion pathological produced on the one hand, trauma of

oral mucosa, followed by inflammation (stomatitis different), and, on the
other hand, makes it difficult to mastication and facilitate the emergence of
gastropathy (ulcers).
Etiology, in taurine pathological process due to excessive abrasion
silage, insufficient intake of digestible protein, macro-and microelements,
etc.. (5, 11, 16, 19, 41, 43)
4.1.7.3. Dystrophies of the teeth
Dystrophies of the teeth are known as odontodystrophies (gr. odontis
= tooth). They appear as disturbances of enamel and dentin in
hypovitaminosis A and D or chronic fluoride poisoning.Fluoride
odontodystrophie (dental fluorosis) occurs fluoride poisoning.
Macroscopic the teeth appear brown-blackish looking porous
occlusal surface is irregular and sometimes peeling enamel notes ..
Odontolitiasis or dental calculus is a process characterized by the
formation of dystrophic mineral concretions (in particular calcium
carbonates and phosphates) and deposited in the form of black-brown
deposit on the lingual tooth, particularly in older animals (dogs, cats, horses,
and so on). It is considered an important factor in the etiology of
periodontitis (inflammation and ulceration of the gums).
Dental caries (caries lat. = rot) is a destructive-necrotic lesion
evolving from the surface into the depth of cavities of the permanent tooth.
Ethiomorphopathogenesis of dental caries is not fully elucidated,
although several theories have been formulated (acidogenic, proteolytic
proteolysis-chelation). Neither is entirely satisfactory. The decisive role they
have acidifying bacteria and putrefaction processes of food debris and causes
favoring ,interdental spaces are represented by enlarged so occlusal
irregularities faces.
Caria can locate on the occlusal faces ,the contact one ,or on the
cervix or teeth and are more commonly seen in horses, and sheep.
After the intensity decay can be:
- Grade I, they are only interested in enamel;
- Grade II, affecting enamel and dentin;
- Grade III, characterized by opening the pulp cavity and pulp
infection (caries penetrating);
Grade IV, with the opening range of dental cavity associated with
pulp necrosis and gangrene.
80
Macroscopic on the occlusal tooth face are found foci or cavities

of various sizes, a gray-brown or blackish, brittle and obnoxious odor.
Odontodystrophies , dental caries as strong trauma exerted by
mastication of hard bodies sometimes meet with dental fractures.
4.1.7.4. Inflammation of dental aparatus
Inflammation of the dental aparatus, in animals, are periodontitis and
pulpitis. Periodontitis is calld improperly inflammation of the gums and
dental alveoli. The inflammatory process starts in the gums and then include
alveolodentar ligament.In chronic developments are found gum retraction
and discovery tooth root, thus facilitating their fall.
In cattle the chronic pulp and paradental inflammation are of
actinomicotic or tuberculosis origines.
In horse and the dog in the lower jaw especially youth dental plaque
notes storage. Periodontal disease is more frequent in sheep and dogs and
other small species.
Pulpitis is pulp inflammation, as in most cases a continuation and a
complication of tooth decay or tooth fracture. Pulpitis may be serous,
purulent or gangrenous.
4.1.7.5. Tumors of the teeth
Tumors of animal teeth are rare and can be represented by
ameloblastoame and odontoame.
Ameloblastomul or adamantinoma, ameloblastelor tumor, which are
producing enamel, is non invasive character by infiltration of the
odontogenic epithelium through stromal connective tissue fibers. Occur at
any age and is most commonly located on the lower jaw in horses, dogs and
cattle. Odontomul is composed of a disordered association of enamel, dentin,
cement, with a low degree of mineralization. (5, 11, 16, 19, 41, 43)
4.2. Pharynx morphopathology
4.2.1. Inflammation of the pharynx
The most important lesions are inflammatory processes called
pharyngitis . They evolve simultaneously with stomatitis. in acute
pharyngitis,hypermia is accompanied by edematous infiltration of the
81
pharynx and epiglottis covering. Pathology differ pharyngitis: serous,

seroheamorrhagic , pseudomembranous purulent and granulomatous
hyperplasia.
Serous pharyngitis is characterized by swelling of the pharynx and
regional lymph nodes. It is found in pasteurellosis in cattle and pigs.
Seroheamorrhagic pharyngitis is accompanied by necrotic foci with
gelatinous aspect extension to adjacent tissues. Occurs in localized form of
anthrax, called glosantrax.
Pseudomembranous pharyngitis ,found in diphtheria youth in
mammals, in Newcastle in chickens, pigeons trichimonosis respectively.
Purulent pharyngitis, diffuse or circumscribed, may occur in
pyogenic infections. In strangles, horse, frequently evolve phlegmonous
form.
Hyperplastic pharyngitis or lymphohistocytaric is exhibited by the
appearance of miliary nodules, gray-yellow, representing lymphoid
hyperplasia formations at this level, following the "conflict" with various
pathogens.
Pharyngitis granulomatous found in tuberculosis in cattle and in
youth and mycoses glanders in horses. Evolves as nodular or ulcerative.
In chronic pharyngitis is seen the gland atrophy.
4.2.2. Pharyngeal tumors
Are cited melanomas and epidermoid carcinomas (squamous cell)
located in the tonsils, especially those in dogs.
4.3. Esophagus morphopathology
4.3.1. Changes in lumen
Esophageal lumen changes are observed in all species represented
by esophageal stenosis and dilatation.
Esophageal stenosis caused by inflammation or tumors are located
either in the wall of the esophagus, or in the periesophageal area, where the
development exert a compressive, resulting in reduced lumen ( stenosis
compression ). Other injuries due to foreign bodies (food, etc..) That can
obliterate the lumen of the esophagus ( stenosis the obstruction ) are
sequelae of esophagitis.
Esophageal dilation can be generalized for the entire length of the
organ damage observed in pigs and dogs, called megaesophagus
82
segmentation can be in the form of a diverticulum, more common in cattle (

ruffles esophagus ).
Megaesophagus apears after a motor dysfunction (absence of
primary peristalsis) of the esophagus especially in dogs that has no real
sfinter between the esophagus and stomach.
Jabo esophagus is the result dilacerrii musculoasei esophageal
mucosa in space followed by herniation periesofagian form of diverticular
pouches that communicates with the body lumen. It is also found in horses
and dogs, consecutive esophageal muscle damage. It occurs more frequently
in cervical and thoracic region of the cattle and the size range of a few
centimeters, to that of an orange. Evolution esophageal diverticulelor is
always accompanied by atrophy of the esophageal wall, which may end up
with esophageal necrosis and perforation.
4.3.2. Esophagus dystrophies
Corn gland metaplasia of esophageal submucosa glands in bird is
most characteristic lesion in hypovitaminosis A and at the same time, the
most important oesophageal dystrophy.
Macroscopic , the upper segment of the esophagus are found graywhite nodules, the size of the needle , well defined and slightly protruding
from the mucosal surface. Microscopic these nodules are represented by
submucosal glands metaplasia corneum.
Parakeratosis of the esophageal mucosa is found in pigs in the
terminal portion and evolve simultaneously with gastroesophageal ulcers.
Occur with hypovitaminosis A.
4.3.3. Inflammation of the esophagus
Inflammation of the esophagus are called esophagitis and install
again with sore mouth. They can be: tongue, papular, vesicular,
pseudomembranous festering, gangrenous, ulcerative and granulomatous.
Presents practical importance forms purulent gangrenous and parasitic.
Purulent esophagitis can be a complication of catarrhal esophagitis
or esophageal wall is the result of trauma by foreign body retention
(potatoes, beets), and by brutal poll conducted for esophageal obstruction. in
esophageal wall is formed abscess or phlegmons (most commonly), which
cause erosion, ulcers or fistulas.
Gangrenous esophagitis is likely (iatrogenic) traumatic, in most
cases, suppurative complications of esophagitis.
83
Macroscopic , it appears gray-green foci on the surface of the lining,

or it is detached flaps as large, smelly, leaving bleeding submucosa. The
danger of these two forms is the possibility of extending purulent or
gangrenous inflammation in other organs of the mediastinum.
Parasitic esophagitis is found in ruminants and pigs
sarcosporidiosis,in spirocercosis in dogs in locating larvae (L 1 ) of
Hypoderma lineatum in ruminants.
Macroscopic in evolved sarcosporidiosis \ in cattle and sheep stands
fusiform nodules, whitish, of 8-10 mm long and 3-4 mm thick in all
esophageal muscles (myositis oesophageal granulomatous cystic).
Microscopic identifying characteristic cystic granulomas in the
muscle fibers.
In canine spirocercosis in the thoracic portion of the esophagus is
observed nodules of varying size, sometimes reaching the size of a pigeon
egg, a firm consistence, and on section identifies parasites floating in
purulent substance.
Fungal esophagus (esophageal candidiasis) reported in young
animals in the form of pseudomembrans (pseudomembranous esophagitis).
4.3.4. Esophagus tumors

Esophageal tumors are rarely cited in animals, except papilloma.
Benign tumors are represented by multiple papillomas,(papilloma ) in cattle
in certain geographical areas.
Macroscopic the papillifer vegetation spread over the lining of the
esophagus. It is the result of infection with bovine papillomavirus type.
Reported tumors in dogs are malignant fibrosarcoma and osteosarcoma.
4.4. Goiter morphopathology
4.4.1. Topographic changes
Goiter ptosis or swinging goiter is observed more frequently in
turkeys being driven by a genetic predisposition for ptosis ingluvial.
Etiologic, occure repeated overloading of the goiter fermentation yeasts of
the genus Sacharomyces products for rations rich in carbohydrates, etc.
vagus nerve degeneration.
84
Macroscopic the crop is much larger in volume fallen below normal

and hanging like a diverticulum prepectoral, something that justifies the
name " chaps swinging . " the goiter consistency is increased.
4.4.2. Goiter inflammation
Goiter inflammations are called ingluvitis and have generally
polymorphic etiology (infectious, parasitic, nutritional). Pathologically there
is ingluvite climbing pseudomembranous and very rarely granulomatous.
Presents practical importance the pseudomembranous ingluvitis.They are
found in: candidiasis, capilariosis, hypovitaminosis A, etc..
4.4.3. Goiter tumors
Goiter tumors are very rare (papillomas, sarcomas).
4.5. Pre-stomach morphopathology
4.5.1. Changes in prestomachs content
Foreign bodies, Ruminants are characterized by a chewing
superficial, which facilitates ingestion of foreign bodies existing in feed or
pasture. Sometimes they can stop into the esophagus causing esophageal
obstruction, but most notably prestomachs reach the network. Have been
identified mostly metal body (nails, wire, pins, etc..), Pieces of wood, stones,
bricks, broken glass, rubber balls, rags and even clumps of string, etc..
Gradually they are impregnated with phosphates
forming large
conglomerates approx. 5-10 kg (bezoar) that can cause obstruction of the
orifice and cause timpanism secondary ruminal atony. Prestomachs sharp
corpus, especially from the network can perforate the wall with the intention
of making cranial way to heart. Throughout the route cause localized
inflammation (reticulopericarditis traumatic). Necropsy identifies only
"channel migration" like a cord that goes from the wall to the pericardial sac
network. (5, 11, 16, 19, 28, 41, 43)
Prestomachs volumetric changes are represented by timpanism and
overloading the rumen and omasum.
85
Timpanism or acute ruminal bloating is the consequence of

increased amounts of gas, either by their inability to eliminate, whether they
are formed in excessive amounts. Etiopathogenetic, obstruction of the cardia
and esophagus, proventriculus torque, reduced motility, inflammation and
chronic poisoning, as consumers summer crops (alfalfa, clover), fresh,
polluted or dewy, and so on, can be causes of timpanism
Macroscopic, there is excessive distension of the rumen, consistency
fluctuating, and on section there is a heavy fine foam. Venous stasis occurs
in the thorax and cardiac dilatation. Evolution is usually fatal acute .
Overloading (pulping) rumen and omasum , is characterized by the
accumulation of coarse fodder, stationed more than their digestion time.
Etiopathogenetic is determined by atonia of proventriculus, poisoning, or
due to fault the food.
Macroscopic, the observed increase in volume associated with an
increase of substances (almost hard). On section, impressive aspect of the
content of dry food, sticking blades omasum, lining may be hemorrhagic,
necrotic or ulcerated.
Both prestomachs changes have resulted atrophy ruminal walls, or
the omasum. Morphologically, the mucosa is congested decreases rumen
papillae, omasum blades are thinner, and the section, greatly reduce their
profile prestomacelor wall thickness.
4.5.3. Prestomach dystrophies
Ruminal parakeratosis in young ruminants occurs in fattening, feed
only, chopped or pelleted feed with low abrasive power, is considered a
"disease focused." The etiology of the lesion is complex and associated with
hypovitaminosis A, changes in local pH, meals etc finely ground.
Macroscopic, rumen papillae are enlarged, increased consistency,
brown-blackish and often stuck together.
Microscopic , there is parakeratosis, incomplete cornification with
retention of nuclei in the superficial layers, hyperkeratosis, interstitial
edema, cellular infiltration or hyperplasia fibroconjunctive, especially in the
submucosa. These changes explain the increased permeability of the ruminal
wall, which favors the development of local suppurative infection and the
metastasis may cause liver abscesses particular.
Ruminal globiform dystrophy, gastrointestinal malignancy is found
in the form of FMD in cattle.
Macroscopic, it is noted erosions or ulcers of different sizes,
especially in the ruminal pillars.
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Prestomachs mineral dystrophies, externalized by Tricho-, phyto-and

lanobezoare as mineralizable core may be composed of hair, vegetable fiber
or wool yarn. They are mainly observed in calves and lambs, causing
obstruction to the passage openings from one compartment to another. Are
determined mainly by deficient rations (quantity, quality) and overcrowding.
(5, 11, 16, 19, 32, 41, 43)
4.5.4. Prestomach inflammations
Prestomachs inflammation, depending on the affected compartment
is called rumen , reticulum and omasitis (the omasum).
The main causes are caustic substances, adulterated or frozen foods,
or they appear as secondary events in the development of general diseases
like foot-and necrobacillosis etc. In terms of pathology, differ necrotic
inflammation,
blistering,
bleeding,
purulent
limfohistiocitare,
pseudopapilomatoase and granulomatous.
Ruminal necrotic, meets necrobacillosis cattle and locate the passage
of rumen pillars or to network and deciduous.
Macroscopically , the foci gray or yellowish brown, brittle, slightly
raised and surrounded by a reddish ring of various sizes (2 mm-2 cm
diameter). The lining of necrosis, ulcers arise that can scar gradually.
Ruminal vesicular (disease) foot is characteristic malignant lesion,
but it may be the result of the action of irritating chemicals. It evolves into a
ruminal erosive and / or ulcerative.
Heamorrhage uminal and omasitis , characterized by reddish
outbreaks in the ruminal pillars and areas with small papillae, and the
deciduous blade faces. Can evolve and hemoragiconecrotic character.
Sometimes, it can diagnose the transparency serous. It is caused by trauma,
intoxication and especially for fungicides.
Traumatic purulent reticulitis is the most common, more serious
and complex prestomach inflammation in cattle. It phlegmon or gangrenous
evolving nature, depending on the microbial flora that is carried by the
foreighn body perforating the network wall.
Initially, local occure a heamorrhagic inflammation then a fibrous
exudate appears that later become purulent exudate and form abscesses in
the wall or phlegmons network. They produce wall thickening and even the
appearance of peritoneal adhesions.
If the foreign body pitched forward into the chest cavity, the
infection may spread by continuity, producing reticuloperitonitis or traumatic
reticulopericarditis. As chronic suppurative reticle turns proliferative
87
inflammation, resulting in the final fiber paths with hard edges which often
hosts foreign body
Pseudopapillomatoas ruminitis is a productive inflammation
characterized by the appearance on the surface lining of the rumen, of
whitish nodules,
increased consistency, following annexation by
neighboring papillae fibrosis peaks with demarcation of territory corneum. It
will gradually increase in size by scaling unable to format horn.
Granulomatous inflammation is relatively rare . (5, 11, 16, 19, 41, 43)
4.5.5. Prestomach tumors
Prestomach tumors are represented by papillomas, fibromas,
leiomioame as benign forms, namely carcinomas and sarcomas, as
malignancies. Latest usually occur in enzootic leucosis of
cattle.
Prestomachs tumors are rare except papillomas and fibropapiloamelor. They
are associated with oral papillomatosis and / or esophagus.
4.6. Morphopathology of mammalian stomach
Topographic changes of the stomach, are found in ruminants, horses
and carnivores and are represented by moving, twisting or
transdiaphragmatic hernias.
Moving ruminant stomach, abomasul or clot can migrate into left
paralombar sep sometimes with torsion and in small animals are found quite
frequently stomach twisting .
Stomach torsion is followed by exaggerated timpanism, thereof from
the fermentation of food. Stomach walls are thickened, red-purple, as a
result of congestion stasis.
Transdiaphragmatic hernia occurs due to the diaphragm rupture,
followed by entry of a part of the stomach in the thoracic cavity.
Dilated stomach, or gastrectasia, is characterized by excessive
accumulation of food in the stomach. It has particular importance in horses
and cattle, but can be found in the other species.
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Macroscopic the stomach is much increased in volume, increased

consistency, and on section, there is undigested food and gas conglomerate
smelly. Stomach wall is much thinned and gastric folds are missing. In more
severe cases, it can be seen even rupture of the stomach, especially the
greater curvature in all monocavity stomachsand especially in horses.
Ruptured stomach is found most commonly in horses or following
an acute gastric dilatation (aerophagia, overload) or after a colic slams the
animal. It easily recognize by plaguq lip infiltration with blood, gastric wall
layers are dissect. The peritoneal cavity is a reddish liquid with repulsive
odor. Perforation of the monogastric stomach is the result of sharp foreign
bodies ingested with food or other consequences of gastric ulcers
(perforated). Foreign bodies can cross the gastric wall to the abdominal
cavity causing a localized gastroperitonitis
Changes in blood flow of stomach bleeding are represented by
congestion, edema and infarction (the topographic changes).
Flushing is often associated with inflammatory processes. May be
such traumatic, toxic or infectious nature. Bleeding suffusions as bruising or
accompanying diseases septicemia. Presents practical importance linear
serous bleeding of stomach in dogs canine infectious hepatitis and swine
gastrorrhagias following gastroesophageal ulcers.
Stomach bleeding or gastrorrhagia can be produced by the ingestion
of sharp foreign bodies, parasites, toxic substances, infectious agents, etc..
gastrorrhagias occur most frequently as a complication of gastric ulcers and
are externalized by haematemesis or melaena.
Inflammatory edema of the gastric wall is caused by portal
hypertension or other common causes edema and edema inflammatory
edema disease in pigs is specific. (5, 11, 16, 19, 41, 43)
4.6.4. Gastric ulcers
Stomach wall can be established both the processes of actual
necrosis with diffuse aspect, that of circumscribed necrosis with no
superficial or deep tissues of the stomach wall, called ulcers.
Necrosis itself, arising from the action of caustic substances. Thus,
arsenic and corrosive sublimate produce coagulative necrosis of the lining,
while the ammonia and sodium hydrate, causes liquefaction necrosis.
89
Macroscopic, the gastric mucosa is a gray-yellow, the dry matter, if

sublimate, that is swollen, wet, red-brown, in sodium hydroxide.
Microscopic observed color tissue loss and persists only in the
stomach lining glandular tubule basement membranes and some of chorion
connective fibers.
Gastric ulcers are characterized by circumscribed necrosis, followed
by removing the lining, submucosa, musculoas, or sometimes even
perforation serous. Last, called perforated gastric ulcer. In comparative
pathology, peptic ulcers are encountered more frequently in calves and pigs.
In the occurrence of ulcers, an important role is given to the states
of hyperchlorhydria, quantitative and qualitative changes of protective
mucus, masticatory deficiencies due to a defective dentition, traumatic
factors, stress, etc..
In terms of the intensity of the necrotic process and the degree of
removal of necrotic layers, ulcers can be shallow and deep.
Ulcers, superficial with epithelium removal and chorion are also
known as erosion, while the deep ulcers, requires the removal of mucosa,
submucosa, and / or the musculoas.
In animals, ulcers may be:
- primary or idiopathic peptic ulcers (ulcers of hunger, peptic ulcer
and gastroesophageal ulcers);
- secondary ulcers, following the action of mechanical factors,
physical, chemical or circulatory lesions, inflammatory or neoplastic etc.
Hunger ulcer is characterized by the initial appearance of small outbreaks
heamorrhagico-necrotic, which turns into ulcers. It is found in calves in the
first 24-40 hours after birth, if the calf colostrum was not breastfed as exam
slaughterhouse because animals before slaughter are subjected to diet at least
24 hours. Peptic ulcers themselves, meet in descending order in calves, pigs
and dogs. They are located in the fundus of the stomach and pyloric portion,
shaped like a funnel with large circumference to mucous and serous pointing
to are well circumscribed, and margins are usually smooth. Base ulcer is redbrown initially and then becomes gray-whitish scar tissue from developing.
Ulcer size ranging from the size of a pepper up to the approximately 2-3 cm
in diameter
Microscopic, there is necrosis of the mucosa and submucosa,
reduced cellular infiltration in the absence of ulcers and inflammatory
reaction.
Gastroesophageal ulcer is specifically to pigs reared intensively.
Etiology is unclear. Hypovitaminosis A, stress factors, and even biotic agents
90
(Candida albicans) are only some of the causes incriminated in the

occurrence of these ulcers.
Macroscopic in , the stomach is a large blood volume and in the
area on the portion nonglandular , mucosal ulcers are observed single or
multiple, always profound, sometimes affecting the entire esophageal
mucosa. It seems that the first ulcers appear borderline glandular portion of
the stomach lining.
Microscopic there is parakeratosis association with esophageal
mucosal ulcers and loss of epithelium at the boundary between the two
portions. Blood vessels of the corium are affected by ulcers can become fatal
massive outpouring of blood in the stomach cavity.
Traumatic ulcer is an ulcer secondary type, which can be found in
all species due to trauma to the gastric mucosa roughage (4-14 weeks calves,
lambs), or various foreign bodies challenge. In calves is serious and rapid
development since abomasale ulcers can become perforant, death occurring
within 2-3 days due to acute peritonitis.
In pigs and dogs some parasites in massive infestations in horses,
causes gastric mucosal injury resulting ultimately superficial ulcers or deep,
more or less flat.
Ulcers can develop differently. The acute or chronic infection can be
cured. In cases of chronic can cause stenosis of the gastric segment
affected.
4.6.5. Stomach inflammation
Inflammation in animals with monocavity stomach is called gastritis
and for the ones with more stomach cavities is called, abomasitis.
Etiologic gastritis are caused by mechanical, physical, chemical and
infectious agents. Morphopathologic there are catarrhal gastritis, serous,
hemorrhagic, ulcer,, pseudomembranous emphysematous, purulent,
hyperplasia and granulomatous.
Evolution, manifested by acute gastritis catarrhal inflammation,
serous, hemorrhagic colitis, pseudomembranous, purulent and
emphysematous, while chronic gastritis may be atrophic hyperplasia,
granulomatous.
Catarrhal gastritis is nonspecific in the lining appears thickened, red
and covered with a whitish coating, sticky mucus.
Desquamated cells are observed microscopically trapped in a mass of
mucus with rare leukocytes and obvious hyperemia and submucosal
interglandular chorion.
91
Serous Gastritis occurs in pigs in edema disease (hemolytic E. coli)

and malignant edema (Cl. septicum), externalized through edematous form.
thickened gastric wall (3-4 cm thick), especially on the greater curvature due
to infiltration and accumulation of serous exudate in all layers. The gastric
mucosa is swollen, congested and infiltrated. Hemorrhagic gastritis can
evolve in two forms: diffuse and in outbreaks.
Macroscopic diffuse hemorrhagic gastritis, gastric mucosa has
swollen, edematous, red to dark purplish-uniform over large areas that are
not washed in water stream. The process is very evident in the gastric
mucosal folds. Hemorrhagic exudates may be present at the mucosal surface
and, in some cases impregnated in food content.
Occurs in acute forms of salmonellosis and swine fever in
leptospirosis, uremia and chemotherapy treatments to dogs at various
poisoning in all species.
Hemorrhagic gastritis in outbreaks, characterized by the appearance
of the gastric mucosal surface areas generally small, red-purple-black.
Ulcerative gastritis may be in pigs the consequence of
heamorrhagic-necroticgastritis, but can be found in young cattle as a result
of septic complications of peptic ulcers. It can be caused by caustic
substances, mycotoxins, parasites (Gasterophilus sp.).
Macroscopic, it appears circular ulcers of various sizes, with raised
edges and in the middle-fibrinous catarrhal secretion.
Microscopic there is necrosis of the mucosa and submucosa and
around the lesion is noted leukocyte infiltration, acute poorly expressed due
to rapid evolution.
Pseudomembranous gastritis evolves in pest croupal form,
salmonellosis and swine candidiasis, the emergence of the fibrinous
membrane ulcerated gastric mucosa. Membranes peel easily and affects only
a small part of the mucosa. Deep form of gastritis pseudomembranous is
found in necrobacillosis and after the action of toxic necrosis.
Gastritis (abomazita) emphysematous, found in the lambs in
bradsot by Cl. septicum. Injuries occur in the early stages of infection with
anaerobic germs entering the submucosa, where they multiply and produce a
pronounced emphysema of the stomach wall, manifested by thickening the
mucous folds. Subsequently, there is exudation, necrosis and ulceration of
the mucosa.
Purulent gastritis, is rare. Mucosal trauma caused by parasites may
be the site of penetration of pyogenic bacteria. It can also be observed in
foals strangles the form of abscesses or phlegmons.
92
Hyperplastic gastritis is an inflammation productive with chronic

evolution.
Macroscopic characterized by diffuse or nodular thickening of the
gastric wall. Fundic mucosa has numerous irregularities grainy, papillary or
cerebriform.
Granulomatous gastritis is generally rare. It can be found in
paratuberculosis in cattle in, habronemoza of the horses (H. megastoma) in
spirocercosis in dogs. (5, 11, 16, 19, 36, 37, 38)
4.6.6. Stomach tumors
Stomach tumors are rare in animals. benign forms are adenomas
and papillomas mention and among the malignant carcinomas and sarcomas.
Scvamoas carcinomas were diagnosed in horses, which produce gastric wall
thickening and ulceration of the mucosa in their own right.
Among the domestic species the most affected is the dog being
diagnosed with benign and malignant neoplasms.
4.7. Morphopathology of the stomach in birds
4.7.1. Injuries of the proventriculus
Proventriculus dilation is found in birds reared in intensive system
of feeding due to errors associated with atonia of the proventriculus. In
broilers is observed malabsorption.
Macroscopic proventriculus is much dilated, and on section, there is
an abundant food conglomerate, almost dry, while thin wall.
4.7.1.2. Dystrophies proventriculus wedge
Mucinous dystrophy is relatively common and usually develops in
catarrhal inflammation. It is the result of irritation of the most diverse nature.
It is recognized by excessive production of mucus at the mucosal surface.
93
Heamorrhagias are the most important circulatory changes of

proventriculus.seen in Newcastle, but also poisoning hypovitaminosis K,
uricemia etc.
Proventricular edema is found in salt poisoning. Proventriculus is
slightly thickened wall and looks wet and glossy section.
4.7.1.4. Inflammations of the proventriculus
Inflammations of the proventriculus are called proventriculitis and
are the most important lesions of this organ.
Pathologically, they are similar to those in mammals. Of greater
practical importance is etiology. Distinguish so proventriculitis: traumatic,
nutritional, viral, bacterial, fungal and parasitic.
Traumatic proventriculitis is an accidental injury ,observed only in
the individual sector, especially in ducks, caused by ingestion of sharp
foreign bodies.
Macroscopic, it appears haemorrhagic infiltration, erosion, ulcers, or
even perforation of the wall.
Proventriculitis of nutrition is determined by roughage or,
conversely, too finely ground, as well as altered feed.
Macroscopic proventriculus wall is much thickened, whether as a
result of cystic transformation of the secretion channels of the deep glands.
Lining the seepage erosion and even seroheamorrhagic.
Viral proventriculitis haemorrhagic outwardly through or
pseudomembranous inflammation encountered in Newcastle, according to
evolution.
Proventriculus hemorrhagic lesions is one of the most important for
the diagnosis of Newcastle.
Macroscopic, the lining of the proventriculus is observed bleeding
point located to the tip of papillae, interpapilar, but often occur in clusters in
the form of a belt or ring at the entrance and at the exit of the proventriculus.
The longest developments amid bleeding necrosis.
Bacterial proventriculitis found in tuberculosis either as primary
effect, either due to its generalization.
Macroscopic, it develops nodular, or in the form of ulcers.
In pseudomonosis, is thickening of the proventriculus, and the
section, there is an appreciable quantity of liquid, highly colored in green,
which prints the same color to the lining.
Fungal proventriculitis
candidiasis can meet, manifested
macroscopically by pseudomembranous inflammation.
94
Parasitic proventiculitis outwardly or by heamorrhagic inflammation

in fissispina Tetrameres infestations ,in grouse and palmipeds or by cystic
swelling in the palmipeds, tricolor Histrichis infestations, particularly in
ducks. Those parasites identification facilitate diagnosis. (5, 11, 16, 19, 41,
43)
4.7.1.5. Proventriculus tumors
Tumors of the pr oventriculus are represented by malignant forms,
carcinomas and sarcomas, .
4.7.2. Ventricle lesions
Inactivity atrophy of the stomach muscle is produced by feeding the
feed too finely grinded without sand, in chronic poisoning (Pb, caustic, etc..),
Undernourishment, etc.. It is known that the stomach muscle of poultry
observed pebbles or sand, which contributes to the smooth muscle and the
development of gastric motility. Their absence causes the so-called "disease
of lack of stones" with implications of the ventricle muscle . In
ethiopathogenetic terms the lack of stone disease is a inactivity atrophy by
decreasing the characteristic tonus. The cuticle is thin, loses its consistency .
4.7.2.2. Dystrophies ventricle
Hyaline ventricular muscle dystrophy is evident in the muscles,
especially to young turkeys.
Macroscopic discoloration uneven of the muscle (white muscle
disease) and hyalinosis observed microscopically in smooth muscle fibers. It
is the most obvious lesion in hypovitaminosis E in this species.
Heamorrhagies are the main blood circulation disorders. They
may have three locations:
- cuticular: hypovitaminosis K, coccidiostats;
subcuticulare in Newcastle disease;
peristomacale in septicemic cholera.
95
4.7.2.3. Ventricular necrosis

Necrosis and erosions cuticle, are common in chickens in
hypovitaminosis K and in lead poisoning.
Macroscopic cuticle magma turns into a blackish brown and
microscopic necrosis observed .
4.7.2.4. Ventricle inflammations
Ventricles inflammations are called ventriculitis and the ones of the
cuticle, cuticle.
Etiology, ventriculitis may be of traumatic or infectious, parasitic
pathologically speaking describing ventricular necrotic, cathhar, , ulcerative
and granulomatous.
Necrotic ventriculitis
occurs in chickens salmonellosis and
exhibited by the appearance of the thick muscles of outbreaks yellowish
gray, isolated ,small (2-4 mm) called puloric nodules.
In avian pseudomonosis the cuticle is frequently colored green or
green-blue associated with the presence of a fluid into the lumen of the same
color.
Ventricular tumors are generally rare, benign leiomioame being
represented and by malignant undifferentiated sarcomas.
4.8. Bowel pathology
4.8.1. Bowel abnormalities
Congenital anomalies of the bowel, in mammals, are more common in
their caudal segment, externalized by:
dolichocolon, colon too long;
- megacolon, colon too widely described in pigs, dogs and cats;
- atresia ani, most common in piglets and calves;
- bowel stenosis (narrowing of the lumen).
In birds is found agenesis and unilateral or bilateral hypoplasia of
the checks, or rather the appearance of three or more bags cecal.
96
Topographic changes of the intestines are diverse, represented by:

torsion, volvulus, bending, intussusception, hernias, incisional hernias and
rectal prolapse.
Intestinal pathogenesis is complex dystopia in which: disorders of
intestinal tone and motility (peristalsis), pre-existing or created openings
accidental mechanical compression exerted on the bowel (sudden changes in
body position in case of colic, uneven load of chances, tumors, etc.).
Torsion is twisting a part of the bowel around the longitudinal axis.
It is found most commonly in horses, in the ascending colon.
Volvulus is a segment of bowel knotting around the mesentery or
pedunculated tumors. It has an incidence of between 7-9% in the horse and
is found more often in the jejunum. Volvulus may be ligament (jejunum
knotting around mesenteric ligament) or nodosum (by bending the jejunal
loops and knotting them).
Flexion, bending occurs dorsal or ventral side of the great colon
normal to the longitudinal axis. Following the ileocecal ligament rupture, tip
check can bend it backwards (retroflex). These lesions are found all the
horses.
Intussusception, consists of on intestinal loops entering the next
loop . The most common intussusception in horses are the jejunal and
ileocecal.
Hernias are traveling under the protection of some intestinal loops
parietal peritoneum through natural orifices or incidental abdominal cavity.
Topographic include: abdominal hernia, umbilical, inguinal, inghinoscrotale,
transdiaphragmatic. Umbilical hernias are most commonly found in cattle,
horses and carnivores, while inguinal hernias and inghinoscrotale have
higher incidence in pigs.
Eventration represents penetration and displacement of abdominal
viscera through a crack in the peritoneum and muscle fibers in the
subcutaneous connective tissue.
Rectal prolapse, rectal output is the outside through the anus. It can
be total or partial (only interesting the mucosa).
Macroscopic Prolab territories are congested, edematous, ulcerated
or gangrenous.
In birds, cloacal prolapse is a risk factor of cannibalism.
Some enteropathies topographical evolving acute (volvulus,
torsion) in horses and can cause death in less than 1-2 days, the image is
relevant or occlusive shock.
Other dystopian enteropathies have a chronic course (hernia) and
have a poor prognosis.
97
Regardless of topographic changes, in terms of local circulatory

disorders occur pathologically manifested by venous stasis, resulting finally
with infarction of the injured segments.
4.8.3. Bowels dystrophies
Bowels dystrophies are weak outward macroscopic, although they
quite common. Their importance is low.
Steatorrhea is an intestinal lipodystrophy observed in piglets of 2-3
weeks as a result of malabsorption of lipids and thus increase the content of
intestinal fat (fatty stools).
Bowels lipofuscinosis is characterized by brownish pigmentation of
the intestinal muscles due to aging pigment accumulation (lipofuscin).
Dystrophies limestones are represented either by intestinal wall
calcification of the older rabbits in hypervitaminosis D, either by apearence
in the intestinal lumen, of the stones (enterolite) and pseudocalculi (Bezoar),
most common in horses and ruminants.
The enterolitis and pseudocalculus influence by their sizes the
bowel transit, causing local necrosis, or perforation of the intestinal wall,
which outward clinical by syndromes colic.
In colon of horse can form so-called fecaloame or conglobata,
pulping of fibrous feed which can produce bowel blockage morphoclinical
manifested by violent colic.
Sablosis, is characterized by the accumulation and storage of sand in
the enteric mucosa. It meets most commonly in pigs, in the ascending colon
and sometimes in horses produce local compression, resulting finally with
mucosal atrophy.
Anthracosis is frequently, in birds, the duodenum and young porcine
receiving antidiarrheal charcoal or coal, combating enteritis.
Macroscopically, the duodenal mucosa is observed blackish color
with fine dots.
Intestinal emphysema or intestinal cystic pneumatotosis, is a
particular state, characterized by the presence in the subseries of the
jejunum and ileum of small vesicles transparent gas filled mainly to limit
insertion of the mesentery. Is encountered quite frequently in pigs in
anaerobic dysentery of piglets, jejunal accompanying necrotic, probably due
to anaerobic germs entering the lymphatic circulation.
Microscopic ectasia is found in the submucosal lymphatic capillaries
that produce dilacerations of all intestinal wall layers.
98
4.8.4. Changes in blood flow

Bowel circulatory changes are diverse, externalized by congestion,
hemorrhage, stroke, thrombosis and embolism.
Active Congestion typically occurs in digestion and passive
congestion is the result of topographic changes, toxicosis, intestinal
parasitism. In passive hyperemia , the intestine is red-violet highlighting fine
venous vasculature, the mucosa is infiltrated with blood and edema fluid.
Bleeding usually occurs in hemorrhagic diatheses. Enterorrhagias
may be traumatic or ulcerative . Macroscopically, they are recognized by the
dark red color (melena) printed to the lining and intestinal contents.
Venous infarcts intestinal obstruction involving total intestinal
vessels are rare in animals, except for changes due to topographical or
mesenteric venous circulation blocking other processes (thrombus,
inflammation, tumors). Numerous anastomoses blood that exists in
mesenteric area allow deviations of the blood flow , preventing the
stagnation total circulation. Therefore bowel infarctions are rare.
Usually in these cases are involved several intestinal loops, the
process being called infarction. The lesion is a local circulatory disorder
characterised first by venous stasis and arterial then, exudation HIV-bleeding
and in that the end portion necrosis.
Macroscopic the affected anse are thikenned , red-violet, consistency
of rotten cloth containing dark red and Ihor smell. The wall is crisp and
blistered mucosa. Thrombosis and embolism parasite is found in horse in
mesenteric arteries in strongilosis. Originally formed trombarterite obliterans
and thereafter aneurysms of various sizes starting at mesenteric arteries.
These changes are morphological substrate of thromboembolic colic in
horses. (5, 11, 16, 19, 41, 43)
4.8.5. Inflammation of the intestines
Inflammation of the intestines are generically called enteritis. On segment
bears their names: the duodenum, jejunum, ileitis, snook (a check), colitis,
rectal proctor (anus) and cloaca. The etiology is diverse: toxic, infectious,
parasitic, nutrition.
Classification of the enteritis after the following criteria:
Etiopathogenetic: primary and secondary;
Evolution: acute, subacute and chronic
Pathology: catarrhal, edematous, hemorrhagic, pseudomembranous
pus, eosinophilic, lymphohistiocytic, hyperplasic and granulomatous.
99
Catarrhal enteritis is caused by the superficial irritation caused by

improper diet , which facilitates intestinal flora exacerbation by virulence of
viruses /coli, parasites (ascarids), particular in the youth.
Macroscopic there is a viscous deposit abundant, gray-whitish, in
which the mucosa is swollen and congested.
Microscopic there is no large territories epithelium cells and necrosis
exfoliate the surface villi and in chorion and submucosa congestion and
leukocyte infiltration.
Enteritis serous, edematous form, occurs in the cecum and colon in
edema disease in pigs.
Macro scopic is , observed swelling of the intestinal walls and
mesenteries, gelatinous looking, yellowish due to serous exudate that
accumulates in the submucosa, muscular and serosa.
Haemorrhagic enteritis may develop diffuse or circumscribed.
Diffuse hemorrhagic enteritis affect large areas, especially in the
colon.
Macroscopic the mucosa is red-purple, edematous . It is found in
anaerobic enterotoxiemia, leptospirosis, canine parvovirus, anthrax
poisoning, coccidiosis (diffuse hemorrhagic typhoid in chickens).
Observed microscopically hemorrhagic exudate, blood clots,
vascular leukocyte infiltration in the submucosa and chorion. Coverage and
glandular epithelium is removed and necrotic and hemorrhagic exudate
intricate with.
Haemorrhagic enteritis in outbreaks is characteristic of anthrax and
is exhibited by the appearance of red-blackish patches, edematous, necrotic
central images called "intestinal carbuncles".
Pseudomembranous enteritis, is found in all species evolved either
as croup (surface) or as diphtheroids (deep).
Croup enteritis is found in salmonellosis in cattle and cats infectious
leucopenia. Is localized, in particular, in the small intestine, the mucosa is
swollen and flushed, and the surface has a thin coating of fibrin, which is
located superficial and has a yellowish surface.
Microscopic stands capillary moderate swelling, fibrin clot, fibrin
thrombi, leukocyte infiltration and exudate serofibrinos dilacerations the
structures.
Enteritis diphtheroids, begins as a fibrinous inflammation that
affects the entire mucosa, producing its coagulation necrosis (fibrinous
exudate with lining forms a joint). The process is usually located in the large
intestine and may be limited (in plates or foci) and diffuse.
100
Enteritis diphtheroids in outbreaks is found in fish and swine

balantidiosis , respectively Newcastle in birds.
Macroscopic
are observed in swine "buttons" with concentric
layered look on the submucosal lymphoid hyperplasia, fibrinous exsudation
and necrosis of Peyer plaques. They bulge in the intestinal lumen and are
located mostly around the ileocecal valve and helicoidal colon. If
complications arise easily excavated areas of necrosis in the center of the
button.
In birds, the location of the feature button to diagnose Newcastle is
the duodenojejunal.
Enteritis diphtheroids diffuse is found in subacute and chronic
forms of salmonellosis and treponemosis of piglets.
Macroscopic intestinal walls (check and colon) are thickened,
longitudinal section and the lining is covered with fibrin finely shredded
(necrosis), printing an issue of "gut sprinkled with bran". In treponemoz is
affected check, colon and ileum end, hemoragiconecrotic inflammation in
character.
Purulent enteritis. It can evolve reduced incidence and diffuse
(phlegmons), or as abscesses.
In piglets we mention nodular colitis due to infection of the
submucosal glands. The lesion is attributed to Treponema hyodisenteriae,
Balantidium coli, Campylobacter sputorum.
Nodules observed macroscopically are cyellowish-gray, translucent
subseries (2-3 mm) protruding from its surface.
Hyperplastic enteritis, is a consequence of the chronicity of acute
enteritis, can develop diffuse or circumscribed.
Macroscopic there is either a thickening of the bowel wall in the
form of gray-white foci in proliferative enteritis.
Granulomatous enteritis, is found in the evolution of several
infectious diseases or parasitic. May develop diffuse in paratuberculosis
(diffuse granulomatous enteritis), the mucosa is thickened and stressed "look
cerebriform" or it may manifest character circumscribed in tuberculosis and
coligranulomatosis of the birds.
In paratuberculosis microscopically are observed epithelial cell
proliferation and the formation of syncytial giant with chorion and
submucosal thickening. The Ziehl-Nielsen stain will highlight many acidresistant bacilli phagocyted.
The parasites usually nodular form is found. As follows:
- in strongilosis of the horse stands nodules the size of a peanut in
colonic submucosa;
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- in esofagostomosis in cattle, nodules can be the size of millet grain,

or as a cherry;
- in teniasis of the chickens have needle size, located in submucosa
jejunum. Parasites facilitate etiologic diagnosis. Reveal microscopic
parasite debris, rich leukocyte influx and presence of erythrocytes. In the
literature are described in dogs immune substrate enteritis, and eosinophilic
and lymphohistiocytic characterized by cell hyperplasia characteristic of
this inflammation, especially in chorion and externalized intestine,
especially by ulcerative forms. Inflammatory enteropathy involving great
losses both mortality and decreased weight gain and productions.
Diarrhea in infants processes are located in the small intestine while
the young adult animals weaned at the starting point of diarrhea in most
cases in the colon. Youth is more severely affected, survivors remain
weakness, prone to various diseases intercurrent so worthless. (5, 11, 16, 19,
41, 43)
4.8.6. Bowel tumors
Intestinal tumors are rare, mostly epithelial malignancies. Exception
rectal polyps in dogs that can be adenomas or carcinomas.
Lymphomas are found in all species, but with a higher frequency in
cat.
The old dogs are diagnosed more frequently with perianal gland
tumors (hepatoide).
4.9. Salivary gland pathology
4.9.1. Dystrophies of the salivary gland
Horny metaplasia of the epithelium of excretory ducts parotid
gland in cattle, is found in hypovitaminosis A, or some toxic states (chloronaphthalene, tar), establishing the diagnosis by microscopic examination.
Mucosal epithelia are replaced with horny epithelium.
Salivary stones is found in horses and usually occurs in the parotid
channel, following participation desquamated epithelium calcium salts
mixed with mucus.
Etiology, animal feed barley occurs. Salivary calculi can be single
or multiple, isolated or prepared in the form of strings of beads in the
channel lumen (canalicular stones). Secondary containment is found salivary
102
calculi formation with the appearance of glandular atrophy and local

inflammatory processes.
Sialolite or salivary stones consist of 80% calcium carbonate,
calcium phosphate, 6% sodium carbonate and 1% magnesium, organic
matter 12%. Have an average weight of 25-50 g and can reach up to 800 g or
even more. (19)
4.9.2. Cystic changes
Peasant (sialocel) frequently occurs in carnivores, and in horses and
cattle, and represent cystic dilatation of the excretory channels maxillary and
sublingual glands.
Etiology are caused by blockage of a segment of glandular excretory
system (foreign bodies, calculi obliterans, inflammatory processes and so
on).
Macroscopic, the peasant or frog sublingual tongue is displaced by
one or more cystic formations, fluctuating, reddish, smooth surface or
multilobs developed between the tip of the tongue and dental arch. It is
called sialocel and have serous content. The size of cystic formations can
reach the size of a chicken egg.
4.9.3. Inflammation of the salivary glands
Inflammation of the salivary glands are called Sialoadenitis and
salivary gland channel, sialodochite. Are more common in horses, cattle and
carnivores, mostly located in the parotid glands (parotid), sublingual and
submaxillary gland (maxilla).
Sialoadenitis sublingual and submaxillary evolves toghether with
stomatitis. Pathology may be: Sialoadenitis catarrhal ,,purulent, hyperplasic.
with morphological aspects of these types of inflammation.
Sialoadenitele especially maxillitis is more common in dogs and
cats. Can evolve into complicating acute suppurative processes. In
sialoadenitele chronic hyperplastic gland fibrosis are the predominant
process. Acute parotitis are founf in horse streptococci infections and in
cattle is found actino=micotic parotiditis.
4.9.4. Salivary gland tumors
103
Salivary gland tumors are rare in all animal species. Have been
reported in cattle, sheep, goats, horses, dogs and cats, but not in pigs.
The location of the tumor may be in the parotid salivary glands and.
It was found that these tumors occur in animals that are mostly older and are
malignant in most of the cases.
Malignant tumors are fast growing, fastened to the skin, are very
painful and cause metastases in regional lymph nodes.
4.10. Pancreas morphopathology
4.10.1. Anomalies of pancreas
Congenital aplasia and hypoplasia of the islands Langherhans,
causes of diabetes in dogs 2-3 months.
Ectopic pancreas in dogs can be found in the form of small nodules
in submucosa or muscular stomach, intestine, liver parenchyma in the
mesentery, etc..
Dilatation of the pancreatic ducts causes a blister-like pancreatic
gallbladder. This anomaly is cited in cats (often die by uremic poisoning).
Pancreatic hypoplasia is diagnosed more frequently in dogs and
calves. In calves, the pancreas is underrepresented small, imprecisely
defined and pale. (5, 11, 16, 19, 41, 43)
4.10.2. Dystrophies of the pancreas
Dystrophies of the pancreas are predominantly histological order
and found in many febrile diseases, toxic and wasting.
Steatosis, granular dystrophy, vacuolar and hyaline, are seen in
some poisoning of birds in aflatoxicosis hypovitaminosis E and
hiposelenosis.
Their importance is relatively low, the diagnosis being established
by microscopic examination.
Pancreatic atrophy occurs quite frequently and has two
morphological forms: primary and secondary.
Primary diffuse atrophy progresses without obvious changes of the
pancreas.
Secondary pancreatic atrophy is manifested by chronic interstitial
fibrosis associated with pancreatic degenerative changes.
104
Macroscopic, the pancreas has an irregular shape, it is hard and

fell, sometimes nodular structure.
Pancreatic stones appears as a surprise for slaughter or necropsy,
being diagnosed mainly in cattle aged 7-10 years, although it can be
diagnosed in young animals.
Macroscopic main channel is thickened on palpation feels hard
formations. Gallstones are white ,round, oval or angular, small (up to pea),
their number is very large and sometimes looking gritty.
Microscopic there is catarrh, pericanalicular fibrosis, atrophy of the
glandular acini.
Microlithiasis of the pancreatic ducts is cited in selenium poisoning
in chickens.
4.10.3. Pancreatic necrosis

Pancreatic necrosis, or citosteatonecrosis is due to a process of
intra vitam autolysis by digestion, of the pancreatic tissue caused by
pancreatic enzymes (lipase, trypsin, amylase), issued its parenchyma.
Etiologic factors incriminated are autoimmune, toxic, infectious,
obesity etc.
Macroscopic, it appears yellowish-white foci, miliary or larger, dry
and brittle on the section. Frequent location is the tail of the pancreas which
is hypertrophy through an interstitial exudative serous.
Microscopic, there is necrosis of glandular acini, of interstitial
tissue surrounded by leukocyte reaction.
Lesion of importance in dogs is rarely reported in pigs.
In dogs were found also the necrosis of Langherhans islands,
which causes hyperglycemia or diabetes.
The current state of knowledge there is no precise morphological
boundary between pancreatic necrosis, pancreatitis and pancreatic atrophy.
Punctate hemorrhages, pancreatic great diagnostic value in oral
strychnine poisoning in dogs (in 80% of cases of poisoning). Please note that
105
such bleeding can occur in poisoning with hydrocyanic acid in uremia, in

rabies.
4.10.5. Inflammation of the pancreas
Pancreatitis, pancreatic inflammation are produced in most cases by
extending the inflammatory process in the intestine, through the pancreatic
duct. Pathology may be necrotic pancreatitis, bleeding, pus and proliferative,
diffuse or nodular.
Presents an importantance the purulent hemorrhagic pancreatitis
caused by penetration of parasites, ascarids (Ascaris suum) or strongyles
(Strongyllus ecvinus) in the pancreatic duct and circulate with them a rich
pyogenic flora. These forms are found in swine and horses.
In chronic forms, there is induration or sclerosing pancreatitis cases
that changes with cirrhosis characterized by a granular aspect of pancreas
lesion allowed to call "pancreatic cirrhosis." It is commonly reported in cats
and occasionally in horses.
In birds, pancreatitis dress morphological aspects that does not
overlap with the classification of lesions in mammals.
Necrotizing pancreatitis, miliary in outbreaks is associated with
some viral infections :pancreatitis reoviral of chickens, broiler etc.
adenoviral necrotizing pancreatitis.
Lymphohistocytar nodular or diffuse pancreatitis is found in avian
infectious bursitis, pancreatitis with inclusions of chickens and guinea fowl
salmonellosis.
Granulomatous pancreatitis occurs in avian tuberculosis and in some
visceral mycosis (aspergillosis).
4.10.6. Tumors of the pancreas
Exocrine pancreas tumors occurring in Marek's disease in lucosis of
birds and the mammals. As their benign tumors can occur in dogs and cows
adenomas or adenocarcinomas as malignancies, most common in the dog,
cat, cow and horse. Pancreatic endocrine tumors are represented by
adenomas (insuloame) or adenocarcinoma common in older dogs (5-12
years). Both sexes are affected equally. (5, 11, 16, 19, 41, 43)
106
4.11. Liver Pathology

4.11.1. Liver abnormalities
Congenital anomalies of the liver in animals are very rare and can be
represented by: Liver hypoplasia, which can affect one lobe or more liver
lobes; Congenital hepatic cysts occur in all species are described several
morphological types. Biliary atresia is the absence of the gallbladder and / or
extrahepatic bile ducts. in dog is manifested by jaundice and vitamin D
deficiency.
Atrophy of the liver, are secondary lesions of other processes or
pathological conditions. They may be generalized or localized.
Generalized liver atrophy, occurs in cachectic animals due to chronic
diseases in the state of starvation or old animals. In animals tracked atrophy
and pigment accumulation is accompanied by wear brown coloration
printing liver, lesion called "brown atrophy of the liver."
Macroscopic the organ is reduced in volume, thickened capsule
color is gray and the interstitial connective tissue is increased and visible
macroscopically.
Microscopic liver histoarhitectonic is maintained, but there is a
decrease in all lobules, including cell components. Liver cells are loaded
with pigment wear lipofuscin.
Localized liver atrophy is the result of lobes compressions exerted
by various pathological processes that develop in the liver parenchyma:
hydatid cysts, tumors, etc. granulomas. Sometimes it arises from
compression of adjacent organs. in horse lobe atrophy can occur due to
compression exerted by the colon, and the left lobe of the cattle.
Macroscopic affected lobe is reduced in volume, flattened, dark
gray and sharp edges. The compensatory hypertrophy of the remaining liver
is found.
Liver dystrophies are called hepatosis and have a higher incidence
in veterinary pathology. They may include all or lobule are seen
predominantly in the centrilobular or exolobular area.
Lipid dystrophies, also called hepatic steatosis are observed in all
species in various pathological conditions.
We mention the presence of liver dystrophy in the following
pathologies:
107
- hepatic steatosis in neonates as a result of parsimony nutrition of

mothers during pregnancy (maternal-fetal toxicosis);
- fat cow syndrome, caused mainly by excessive feeding silage of
poor quality;
- toxiemia (ketosis) pregnancy, sheep, rabbits and mink produced
mainly by carbohydrate deficiency;
- fatty liver and kidney syndrome in chickens 1-10 days favored by
excess fat and protein deficiency;
- laying hens steatosis or fatty liver hemorrhagic syndrome due to
hormonal dysfunction induced by food , stuffed birds (geese), etc..
For all species, we point toxic hepatosis produced by, carbon
tetrachloride, phosphorus, arsenic and the Micotox caused by aflatoxins,
ochratoxin etc.
From pathological presentation, it is found hepatic steatosis,
resulting all cases this process may induce dystrophic ie overeating,
unbalanced diets, starvation, exo-and endointoxications, ketosis,
hypovitaminosis E, circulatory disorders (hipoxiemii) etc.. The process can
be hastened or worsened by the absence or inadequacy of lipotropic factors,
defense of hepatocytes: methionine, choline, biotin.
Herbivores containing the lowest amount of fat compared to
omnivores and carnivores. Also, in newborn animals to weaning, and is
found in pregnant females increase the amount of fat in the liver.
Macroscopic, the liver is increased in size, brittle, yellowish on the
whole surface or only in certain areas of the organ. Because of brittleness,
especially in birds can be observed rupture of the liver with the production of
internal bleeding (per rhexis), sometimes lethal.
In pigs, where limited storage with lipid lobular design is very
obvious, being able to distinguish a centrilobular hepatic steatosis, or
exolobular, depending on the lipid deposition.
The centrilobular form is observed in the center lobe, a yellowish
color that contrasts with its periphery, the red-brown.
By contrast, in hepatic steatosis exolobular the center lobe is dark
red-brown due to stasis in the centrilobular vein and periphery is yellowish.
Microscopic in the cytoplasm of hepatocytes by ice tehnique the
lipids appear as small droplets (reversible stage), sometimes as large drops,
occupying the entire cell (irreversible stage), or cysts as fat of stuffed birds.
The technique to color ice deposits (drops) is different depending on the dye
used.
108
In paraffin technique is found in the cytoplasm of hepatocytes a

variable number of small vacuoles or vacuole can occupy one entire
cytoplasm.
Fatty liver is extremely sensitive to the action of toxic factors and
nutritional disorders, situations in which foci of necrosis are installed much
faster.
Protides dystrophies are commonly found in liver structure
represented by hepatosis granular, hyaline, fibrinoid, amyloid, pigmentation
and nucleoprotidic.
Hepatosis granular prints the organ a gray coloration with the
appearance of "organ boiled" (without gloss). It is found in toxiemie,
septicemia disease in poisoning, etc. hipoxiemice states.
Microscopic hepatocytes are increased in volume with numerous
fine granules in the cytoplasm (mitochondrial swelling) and nuclei are intact
or in various stages of necrobiosis.
Hepatosis amyloid can be found in animals with chronic
suppurative inflammation, malignant tumors, in horses producing
hyperimmune serum, in chronic poisoning, hiperprotidic ratios, especially in
chickens.
Macroscopic, the liver is increased in volume, gray-white, low
consistency in mammals and higher in birds, and the appearance of the
section is smooth and translucent.
Microscopic amyloid deposits stands Disse spaces gradually
causing capillary obliteration and compression atrophy coordoanelor
Remack.
Hepatosis hyaline and fibrinoid are detectable only
microscopically, the first frequent in hepatocytes (carbon tetrachloride
poisoning, etc..) And intralobular biliary epithelium in Dicroceliosis in sheep
and second in poultry has increased incidence in chronic diseases
(tuberculosis, coligranulomatosis).
Pigmentation hepatosis may protrude through jaundice,
hemosiderosis, melanosis and lipofuscinosis.
Jaundice prints, macroscopic liver characteristic yellowish
coloration. The most common is mechanical jaundice, determined after bile
duct obstruction (computer, ascarids, bile thrombi, etc..), Found in pigs. Can
occur after massive hemolysis.
Hemosiderosis gives the liver a rust stain. Found in infectious
anemia in horses in ruminant fasciolosis in babesiosis in Siderin intoxication
of piglets.
109
Microscopic identification of isolated siderocitelor in sinusoidal

capillary lumen, is an important criterion for the diagnosis of infectious
anemia in horses. In other diseases, siderocite are grouped around bleeding,
or connective bays. Liver cells and Kupffer cells are loaded with
hemosiderin. Highlighting iron deposition is by Perls staining.
Melanosis of the liver, brown-blackish coloration print, distribute or
stained, observed more frequently in young ruminant and sometimes in
horses. Melanin pigment deposition occurs in the connective cromatoforelor
in Kupffer cells and liver cells .
Liver lipofuscinosis is specific to the old animals, gives a brownishblackish color and evolves frequently, with reducing the volume of the organ
(brown atrophy of the liver). Pigment lipofuscin or wear occurs abundantly
in liver cells around the nucleus. The melamine can be distinguished by the
fact that do not change under the action of silver nitrate.
Nucleoprotidic dystrophy manifested by Gouty hepatosis has
increased incidence in birds, manifested macroscopically by dots, striped or
white-Cretaceous deposits of urate fibrous on the capsule surface and deep
organ parenchyma.
Mineral dystrophies are exhibited by:
- dystrophic calcification of tuberculous granulomas or parasitic;
- biliary stones in fasciolosis in cattle;
- biliary calculus, observed more frequently in pigs and carnivores.
4.11.3. Hepatic necrosis
Hepatic necrosis are common to all species. They succeed usually
dystrophic processes and evolve before or concurrently with inflammation .
Etiologic necrosis produced by toxic bacteria, viruses, parasites,
etc..
Macroscopic necrosis outwardly by yellowish-gray discoloration
of shapes and sizes, in the surface and the depth of the organ.On section, are
generally dry or brittle, some area bounded by a failure.
Microscopic, are coagulation necrosis manifested by lysis of liver
cells associated with dystrophic images, pronounced swelling of the Disse
space, granulocyte at periphery outbreaks.
4.11.4. Changes in the liver circulation
110
Liver circulatory changes are represented by acute and chronic

congestion, hemorrhage and angioma macula.
Acute hepatic congestion, minor in terms of pathologic liver gives a
blackish-red color, and passive hyperemia or stasis, where the lobular
design becomes very obvious, because centrilobular vein dilatation, in
contrast to the periphery of a yellowish tint due to fatty dystrophy ( muscad
liver and heart). In both forms the section running a substantial amount of
blood different colors.
Microscopic centrilobular veins and capillaries in the center of the
lobe are dilated and filled with blood.
Hemorrhages are the result of toxic states, infectious, dystrophic
(steatosis) and visible throughout the liver mass in the form of dots or spots,
uneven red.
Microscopic spaces occur full high blood bordered by liver cells.
In birds, in the case of liver rupture, occur in the fibrous capsule
hematoma of various sizes, and if the cap is cut, blood will invade
thoracoabdominal cavity causing death (haemoperitoneum).
Macular angioma or stained teleangiectasia occurs in cattle and red
foci exhibited by black-sponge, easy cord, spread over the surface and in
depth. The section has red open and look cavernous.
Microscopic there is hyperplasia of sinusoidal capillaries their
expansion (teleangiectazie) they continue with the portal vein. Lesion was
observed in cows with multiple gestation with twin gestation,being the
result of circulatory disorders during pregnancy.
4.11.5. Inflammation of the liver
Inflammation of the liver is called hepatitis, the ones of the fibrous
capsule glisonite or perihepatitis, and the bile ducts, angiocolitis or
cholangitis.
Etiopathogenetic, hepatitis are likely the result of infective agents,
parasitic or toxic liver that can address about hematogenous (via the hepatic
artery, umbilical vein and veins goal) by biliary through contiguity and
trauma caused by the larvae, or foreign bodies penetrating the fibrous
capsule.
Hepatitis can systematize the following criteria:
- evolution: Hepatitis can be acute, subacute and chronic
- etiologic, there are toxic hepatitis, infectious and parasitic diseases;
pathology differ parenchymal hepatitis, necrotic, serous,
hemorrhagic, purulent lymphohistocytic, fibrous and granulomatous.
111
Hepatitis parenchymal, also called acute toxic hepatitis, is the result

of exogenous poisoning,minerals (arsenic, phosphorus, mercury, chloroform,
carbon tetrachloride), plant toxic plants, lupine, or other inappropriate fodder
poisoning (fermented corn), but may appear that image is relevant (the toxic
products resulting from gastrointestinal disorders).
Macroscopically, the liver is increased in volume, rusty yellow,
brittle, sometimes can notice a perilobular edematous connective tissue.
Microscopic there is serious granulo-fat dystrophy, necrosis,
congestion and reduced mesenchymal reactions.
Necrotic hepatitis have an increased incidence in comparative
pathology, as in most cases such infectious or parasitic.
Macroscopic foci of necrosis of various sizes, gray-yellow. They
may be small, miliary, barely visible in Aujeszki's disease in cholera,
streptococcus, Vibrio listeriosis and hepatitis, birds, and this was known as
"miliary necrotizing hepatitis". Sometimes it may evolve in the form of well
defined large outbreaks in sheep necrobacillosis, campylobacteriosis in
mammals, respectively Spirochaetosis and histomoniasis in birds.
Microscopic as acute coagulation necrosis stands of hepatic cords
including Kupffer cells, and chronic developments, establish a peripheral
mesenchymal reaction. In the center of the necrosis can be distinguished by
appropriate etiologic agents.
Serous hepatitis has acute development is common in birds and
diagnosis may be made only microscopic. May develop diffuse swelling it
appears Disse spaces, separation of Kupffer cells, hepatic subcapsular
dissociation insulation seams and clear delimitation of hepatocytes, and can
evolve as circumscribed in the initial stages of colibacillosis and avian
mycoplasmosis. Indication, the plan macroscopic liver is enlarged and
congested wet.
Hepatitis bleeding may develop circumscribed (the foci) in the
form of punctate hemorrhages in canine infectious hepatitis and viral
hepatitis freshmen to duck, or as hemoragiconecrotic in subacute avian
colibacillosis. In acute fasciolosis by young fasciols migration through the
capsule and liver parenchyma is found Strii sinuous red-purple of 3-4 mm
(hemoragiconecrotical hepatitis).
Microscopic liver cords are missing, appear erythrocytes, necrotic
cell migration along the whole length of the parasite. In subacute and chronic
developments show numerous eosinophils.
Hepatitis purulent outwardly as abscesses, single or multiple,
roughly equal (hepatitis aposteomatoas).
112
Macroscopic, the shape, size and number of abscesses may vary

from case to case. The appearance of pus is dependent by the bug that
caused the injury. It is generally held metastatic from other primary foci
(omphaloflebitis, metritis, pyelonephritis) or can be caused by foreign bodies
coming from the digestive tract. The fattening of calves, is the result of
complex paracheratosis-rumen, which favors disseminating germs to the
liver.
Microscopic stands central areas of necrosis and pus and abscess
wall known structure.
Liver abscesses should be distinguished from purulent collections,
resulting in overgrowth and softening necrotic foci of tuberculosis,
necrobacillosis, or hydatid cysts. Differentiation is made only by
microscopic examination.
Hepatitis aposteomatoas has increased incidence in calves and
foals following umbilical infection. Abscesses are located mainly on the left
whereas umbilical vein opens into the left branch of the portal vein.
Gangrenosum and necrotizing hepatitis may occur as a primary
process after direct trauma by foreign bodies or secondary in some
anaerobic processes(coal emphysematous, malignant edema).
Macroscopic, the liver has gray-green with dirty appearance,
consistency becomes extremely brittle and make a stange noise on palpation
due to gas bubbles.
Microscopic, there is complete lysis of liver, bile capillaries and
the channels while maintaining broadly perilobular structure.
Necrotizing hepatitis outbreaks are characterized by round, varying
in size (about 5-8 cm in diameter), yellowish surrounded by a reddish area. It
swells the surface of the body, are for homogeneous and dry the surface of
the section. Some outbreaks confluence, invading new territories. The
process ends with acute toxic-septic peritonitis and death of the animal.
Microscopic, in the center identifies the cellular total lysis during
which only the outline thereof is observed (shaded cells). At the periphery,
accuses various degrees of hepatic cords necrobiosis, among them numerous
bacilli are observed. Bacilli can be highlighted using basic common stains.
The toxins produced in the whole liver will suffer degeneration necrosis
granulocyte-acids.
Lymphohistocytic hepatitis is considered to be produced,
especiallyby Salmonella, but it can also be found in other bacteriosis
(pasteurellosis, colibacillosis), as well as various viral infections.
Morphological basis of this inflammation is the intralobular mesenchymal
113
hyperplasia or portobiliare the premises under the influence of Salmonella

endotoxin.
Macroscopic, the surface of the liver, is congested or dystrophic
indicate the presence of miliary foci, gray-white, slightly protruding and
greasy on the section.
In birds due to toxins in the intestinal origin differs liver lymphoid
nodules mass a large number of eosinophils defining eosinophilic interstitial
hepatitis.
The mink proliferation and differentiation of mesenchymal
substrate is suggesting predominantly plasma cell immune inflammation plasma cell hepatitis in mink plasmocitosis.
Fibrotic liver or liver cirrhosis is a chronic inflammation, diffuse,
characterized by proliferation of connective tissue in the liver parenchyma
damage, loss of micro-and macroscopic characteristic architecture.
Is has varied etiology: infectious (viral, microbial), toxic, parasitic
power failures, circulatory disorders etc. hypoxia phenomena. May be
secondary to various liver cirrhosis, the degenerative, circulatory and
inflammatory or inflammation occur as primary factors when infectious and
parasitic toxic, acting moderate but long.
Etiopathogenetic, hepatitis fibrous produced by toxic and
infectious factors are called cirrhosis itself, or poisoning, while inflammation
caused by parasites are called interstitial hepatitis.
Cirrhosis itself is the result of active proliferation of connective
tissue, predominantly intralobular from the premises pericapilare, resulting
finally with pronounced fibrosis liver parenchyma. Under the action of
pathogens occur necrobiosis, hepatic necrosis followed them.
Inability regenerative of hepatocytes destroyed ,leads gradually to
neogenesis conjunctiva. It is a degree of fibrosis, regeneration Islands
(neoformation hepatocytes) can not compensate the parenchymal shortfall by
printing cirrhosis general character of the disease. The presence of
lymphocytes in the outbreak, is suggesting stationary or progressive
development of cirrhosis, (prognosis) as the aggressiveness of the process is
directly related to the number of lymphocytes.
In terms of pathology, cirrhosis itself may be atrophic and
hypertrophic.
Atrophic cirrhosis stage begins with hypertrophic ephemeral
precirotic, followed by atrophic. Etiology, chronic toxicity and acute
infectious hepatitis and mycotoxins, are the main causes that produce these
liver.
114
In the atrophic stage, the liver reaches a third of its normal size,
hence the name of atrophic cirrhosis. The color is yellow-brown, depending
on the conjunctiva hyperplasia accompanying degenerative changes.
Consistency is greatly increased, even harsh, cutting making it difficult.
Liver surface is uneven because of yellow nodules, which range in
size from a grain of hemp (cirrhosis granular) to that of a nut (nodular
cirrhosis). Sometimes the body surface is crossed by numerous grooves with
a depth of 5-10 mm, lobes subdivided pseudolobi of the liver (lobar
cirrhosis).
Microscopic stands marked intralobular fibrosis with lobe split into
two or more pseudolobuli (coordoane centrilobular hepatic vein free),
hepatocellular dystrophy and necrobiosis.
Atrophic necrosis is more common in carnivores and swine, but
can be found in other species. In cattle is more common in the left hepatic
lobe, which reaches a degree of atrophy exaggerated, leaving the fibrous
band whitish-reddish, hard, sharp edges against right hepatic lobe that
hypertrophy.
Cirrhosis hypertrophic occurs in calves with Salmonella etiology,
in swine feeding due to industrial waste or waste from the cafeteria, the
rabbits in some viruses, in aflatoxicoz.
Macroscopic, the liver is increased in volume, smooth surface, high
consistency and color variable, gray, yellow, or green.
Microscopic proliferation in the conjunctiva of Disse space is
particularly intense and diffuse, isolating groups of hepatocytes, or liver
almost every cell that will undergo necrobiosis by anoxia and compression.
This type of cirrhosis in cattle can be installed even during
intrauterine development due to moldy feed containing aflatoxin and other
mycotoxins, namely feeding cows with feed acid (borhoturi storage).
In light of current knowledge it seems there is a connection between
liver cirrhosis and hepatocellular carcinoma.
Interstitial hepatitis is characterized by theconnective proliferation
starts initially at portobiliare spaces, hence the name of this liver. They are
found in all species and are parasitic in nature.
Macroscopic evolve in two anatomoclinical ways:
- interstitial hepatitis multiple or outbreaks;
- diffuse interstitial hepatitis. Whatever form of presentation, their
morphogenesis is similar.
Initially, there is a traumatic phase, manifested macroscopically by
tracks or foci hemoragiconecrotic ,produced by parasite migration of
nehapatofili /hepatofili parasites through the liver parenchyma. Then follows
115
a phase of leukocyte exudation, predominantly eosinophilic, with antitoxin

and resorptive role, printing trajectory outbreaks and a greenish tint. Finally,
fibrous phase through connective organizing trajectory.
Intestial
multiple hepatitis, or "hepatitis eosinophilic" is
characterized by healing phase (fiber) by outbreaks white pearl, the surface
having a diameter of 1-3 cm, irregular, often focusing a reddish point located
on the surface of the body .found more frequently in piglets, the result of
migration of ascaris larvae of cysticerci, and even metastrongili
esophagostomy.
In rabbits and lambs, and tracks can be observed thin, whitish,
reddish-centered line.
Diffuse interstitial hepatitis occurs in ruminants fasciolosis and
Dicroceliosis exhibited by the appearance on the surface of liver of white
tracks representing either much thickened bile ducts by fibrisation or trauma
scarring produced by parasites.
Granulomatous hepatitis is found in all species, with infectious
etiology: tuberculosis in all species actinobacilosis in cattle, glanders in
horses, birds coligranulomatosis and fungi, or parasitic in nature, in
echinococcosis and cysticercosis.
Macroscopic , in all cases, the size and the weight of the liver, cystic
compacted granuloma is observed (the parasitic), of various sizes, separate
or enclosed by a capsule, the more or less pronounced.
Of cystic echinococcosis granulomatous hepatitis occurs more
frequently in ruminants and swine. Cysts may be unilocular or multilocular,
and the numbers can reach several tens, twisting and greatly increasing liver
weight. Depending on developments of the cysts, cystic granulomatous
hepatitis may be evolving when vesicle cyst fluid contains large quantities of
membrane is good compliance (larvae are alive). Sometimes the vesicle or
cyst lose the fluidthe proliger membrane it collapses, the larvae die.
Regressed cyst may calcify or cazeifiction.
Microscopic around cyst liver atrophy associated with
mesenchymal reaction consists in:
- interior of giant cells and epithelioid in contact with the parasite;
- intermediate zone rich in histiocytes, lymphocytes, plasma cells;
- periphery area rich fibrous connective fibers that are seen among
many mast cells and eozinocite.
Perihepatitis evolve, with hepatic parenchymal inflammation.
Mention two pathological forms of diagnostic importance, namely:
perihepatitis fibrinous in avian colisepticemia respectively perihepatitis fiber
, called viloasa observed in older horses, as a result of parasitic irritation
116
(Settaria equine), or compression of the liver processes . in perihepatitis

viloasa Glisson capsule surface highlights the presence of gray-white
filaments, like hairs, formed of the fibrous connective tissue.
Colangitis or angiocolitis have parasitic etiology, being produced by
coccidia (Eimeria stiedae) in rabbits and trematodes (Fasciola hepatica,
Dicrocelium lanceolatum) in ruminants, pigs ascaridiosis. Chronic catarrhal
cholangitis presents practical importance of fasciolosis most apparent on the
visceral liver.
Macroscopic , the bile ducts are much thickened, whitish and
increased consistency. On section, the wall is thickened and narrowed lumen
of flowing viscous content consists of bile, desquamated epithelium, bile
salts precipitated and parasites.
Microscopic, the walls much thickened bile duct lymphocytic
reaction is observed, and mast cells. Epithelium is necrotic and partially
peeling, can see rush of bile salts. (1, 5, 9, 11, 16, 19)
4.11.6. Liver Tumors

From the tumors of the liver we, mention adenomas,
adenocarcinomas, and all forms of tumor metastases.
Hepatoamele affects several species: old dogs, cows, sheep, pig and
poultry.
Macroscopic nodules are found slightly protruding .
Microscopic observed hepatocyte hyperplasia-adenoma compact
solid.
Biliary adenomas have a higher incidence in ducks and chickens
being produced by aflatoxins. We may encounter in other species (calves).
Macroscopic initially cysts appear green, and then gray-white
nodules can reach the size of a walnut.
Microscopic, initially, there is a tubular adenoma, then, is papilifer
and sometimes cystic dilation of these cavities. Finally, changes in
fibroadenoma emphasized developing stroma.
Adenocarcinoma of the liver epithelial tumor is malignant, it is
more common to carnivored and cattle. Appears as multiple tumors
contoured, yellow or gray-brown, which protrudes from the surface of the
organ. The section distinguishes stroma separating the tumor cell masses,
taking an acinous look .
117
Microscopic tumor cell multiplication shows that acinar or

trabecular ordering.
Liver tumors are common in birds and mammals leucosis.
4.12. Pathology of the gallbladder (gallbladder)
4 .12.1. Atrophy of the gallbladder wall
Gallbladder wall atrophy arises from the excessive accumulation of
bile ectasies (colecistomegalie). It is triggered by biliary stasis obstruction
caused by calculi, tumors, parasites (fascial sheep).
4.12.2. Dystrophies of the gallbladder
Calculus bile (gr. chole = bile + kystis = bladder) or cholelithiasis, is
characterized by the formation of calculi, usually in the gallbladder and bile
ducts rarely. Occurs in cattle, swine and dogs in the form of multiple calculi.
Gallstones are composed of cholesterol, bilirubin and calcium
carbonate. Composition of gallstones can be:
- cholesterol, white and crumbly;
- bilirubin, dark and crumbly;
- limestone, chalky and high consistency (hard);
- mixed, the most frequent.
An important role in the occurrence of cholestasis seems to have
some infectious factors (Pseudomonas aeruginoasa).
4.12.3. Gallbladder inflammation
Inflammation of the gallbladder is called cholecystitis. They have
etiology parasitic and microbial in cattle, swine. By pathology we have
cholecystitis:
- catarrhal (in fasciolosis, Dicroceliosis);
- serous bleeding (sometimes in Newcastle disease);
pseudomembranous (especially pigs);
lymphohystocytic(in salmonellosis);
granulomatous (in tuberculosis).
Serous cholecystitis, edematous form is a characteristic lesion in
canine infectious hepatitis, in African swine fever and Superphosphate
poisoning in cattle.
118
Macroscopic gallbladder walls are edematous and perivesical

connective tissue has a gelatinous, shiny look.
Pseudo cholecystitis is the most common inflammatory form of
swine.
Macroscopic fibrin deposits occur on mucous hyperemia which
reveals marginal form of studs and plates yellow-green areas bounded
cyanotic.
Microscopic mucosal necrosis is found associated with moderate
fibrinous exudation.
4.12.4. Gallbladder Tumors
Adenoma occurs in older dogs, cats and mink, tumor incidence is
average, and the other species occurs sporadically. Appear as nodules (0.5 to
1 cm diameter) bright, brittle rough surface. Adenocarcinoma is a malignant
epithelial tumor of the gallbladder with papilifer character. The tumor is soft
with cauliflower appearance and tends to expand. Occurs in cows older than
10 years with the location in the gallbladder neck. (5, 11, 16, 19, 38, 43, 52)
4.13. Abdominal pathology
Lesions in the abdominal cavity organs directly affect serous
peritoneal visceral and parietal processes remarking be located next to the
affected visceral or generalized over the whole cavity surface.
4.13.1. Content changes of the abdominal cavity
Into the abdominal cavity, in certain pathological conditions, one can
find:
floaters tough, coming from a ruptured abdominal wall, or from the
digestive tract;
home fluids urinary, digestive, blood, lymphatic;
female genital products (calves in poultry and eggs, mammalian
fetuses and fetal fluids);
transudate and exudates.
In birds we mention an abnormality of the abdomen characterized
by the presence of "pedicle cyst" on the right side of the cloaca and whose
size can reach up to 15 cm in diameter. They can compress the digestive
organs and cause cachexia syndrome.
119
4.13.2. Dystrophies of the peritoneum

Uric dystrophies birds is the most important process dystrophic off
the peritoneal serous macroscopic externalized through points, striated or
uric deposits white-cretaceous.
Steatonecrosis of abdominal fat appears by expanding pancreatic
steatonecrosis. It is frequently found in sheep and sometimes in pignlooking gray-white isolated outbreaks of 2-3 mm in diameter.
Peritoneal melanosis in pigs and ruminants appears as blackishbrown spots scattered especially on the parietal serous.
Circulatory changes of peritoneum is found in most infectious
diseases or toxic nature, manifested by congestion and hemorrhages located
in the abdominal wall (subperitoneal). Hemoperitoneum occur after trauma
or spontaneous rupture of organs, especially the liver steatosis common in
birds, but also for warfarin poisoning in other species.
Macroscopic non-coagulated blood or blood clot formed around the
organ like a capsule and continue between intestines.
Hydroperitoneum or ascitid e is the accumulation of transudate in
the peritoneal cavity. It occurs as a complication of stasis, whether due to
central causes (valvular insufficiency, myocardial) or related causes portal
circulation (liver cirrhosis, liver tumors, spleen, liver tuberculosis, etc..). It
occurs more frequently in dogs, pigs and ruminants.
Macroscopic in, the abdominal cavity accumulates significant
amounts of fluid (transudate) clear or yellowish, which relaxes the walls of
the abdominal cavity. The amount of fluid collected varies with the size of
the animal.
Chiloperitoneul, or ascites, is the accumulation of lymph in the
abdominal cavity due to rupture of the regional lymphatic vessels. In chilous
ascites fluid has a milky appearance.
Other collections peritoneal rarer uroperitoneul can be observed in
newborn foals and lambs in fattening due to bladder wall rupture (in
urolithiasis lamb) and characterized by infiltration of urine and hence the
visceral peritoneum.
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4.13.4. Inflammation of the peritoneum

Inflammation of the peritoneum is called peritonitis, the omentum,
epiploic, and when are affected more organs the polyserositis term is used.
Peritonitis classification is according to several criteria:
Etiology: infectious, parasitic, traumatic, chemical;
morphogenetic: are primary and secondary;
after stretching: localized and generalized;
Evolution: acute and chronic
following address: visceral and parietal;
pathology: serous, serofibrinoas, fibrinous, purulent, gangrenous,
Issues, macro-and microscopic, of peritonitis set, correspond to all
forms of classical inflammatory.
Serous peritonitis is specific in goslings parvovirosis (Derszy's
disease) in which all the organs seem to be coated with a substance similar to
egg white.
Sero-fibrinous peritonitis if commonly found in piglets in Glasser's
disease in some cases of mycoplasmosis and colibacillosis. Abdominal
organs, especially the liver and intestines are covered by yellowish exudate
serofibrinos. .
Fibrinous peritonitis presents practical importance in piglets as a
result of mycoplasma infection respectively fibrinopurulent in avian
colisepticemia .
Macroscopic in both cases there is moderate fibrinous deposits on
Glisson capsule and mesentery (in colisepticemie ooze fermentative odor).
Purulent peritonitis occurs more frequently in cattle after
transabdominal trauma or digestive tract, either in the form of abscesses, or
in the fistula. It is found in piglets in Corinebacterium pyogenes infections,
and the horses strangles.
Macroscopic intestines, internal organs are coated with
fibrinopurulent diffuse deposits. Sometimes changing the form of abscesses
varying in size.
Gangrenous peritonitis is rare and is found in the intestines
localized topographic changes more common in horses.
Macroscopic is recognized by the amount of exudate large orange,
with flakes of fibrin and intensely putrid smell.
Stercorale and biliary peritonitis found in the mammalian due to
gastrointestinal walls breakage, respectively gall bladder with overflow
121
specific content into the peritoneal cavity. It is recognized by a large amount

of exudate and putrid smell /
Fibrous peritonitis is a subacute-chronic inflammation which ends
with the appearance of synechiae parieto-visceral and viscero-visceral,
making so-called "organic blocks" (adhesive peritonitis). Sometimes, in the
form of peritonitis viloasa, externalized by the presence of whitish hairs on
the surface of serous, common lesion in horses and attributed migration of
parasites (Settaria equine) through the abdominal cavity.
Granulomatous peritonitis occurs more frequently in tuberculosis in
cattle, are productive aspect, tuberculosis or fungal pearl or as exudative
inflammation, caseous tuberculosis of the serous membranes.
The chickens have a high peritonitis incidence, an important cause
of losses in industrial growth (15-60% of mortality cases in this species).
Substrate morphology is the outpouring of calves in the peritoneal cavity by
breaking the membrane of the ovisacs after some degenerative and
inflammatory processes of the ovary, called yolk peritonitis.
Macroscopic, are found on the surface of intestinal loops, some
deposits yellowish oily consistent in pure form or in complicated forms,
accompanied by a repulsive odor.
Microscopic there is a foreign body granulomatous reaction
consists of a crown around the calves in giant cells containing numerous
colonies of germs. At the periphery of granulomas is highlighted
serofibrinoase exudates, fibrin and fibrinopurulent.
Macroscopic there is congestion in the yolk sac, softening and
non-resorbsion of the vitelus. Sometimes stands wall lysis bag with overflow
vitelus in the peritoneal cavity of the yolk peritonitis resulting chicks.
4.13.5. Peritoneal tumors
Peritoneal cavity may be the seat of numerous tumor processes:
Benign tumors are the lipomas, fibromas, myxomas and malignant
mesothelioma manifests as, liposarcoame, fibrosarcoma, mixosarcoame.
Both forms have their origin in the structural elements of the composition of
peritoneal serous.
Mesothelioma is the most common primary peritoneal tumors.
Affects mainly cattle and dogs. The incidence is relatively low. Lipomas are
located mainly in the mesentery and omentum, most frequently cited in the
horse and dog. (5, 10, 11, 16, 19, 43)
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5. Morphopathology of the excretion system

5.1. Kidney lesions
5.1.1. Congenital anomalies
Congenital anomalies are developmental disorders of the kidney in
all species, the most common affected being birds and pigs. They are:
numerical renal agenesis and aplasia, unilateral or bilateral,
especially in birds;
volumetric bilateral renal hypoplasia, unilateral renal
hypertrophy;
the position, outward through Ectopies renal unilateral or
bilateral (location-outside the lodge renal kidney);
form, or ring horseshoe kidneys, by joining one or both
extremities, fetal kidney, preserving traces of intrauterine lobules, frequently
observed in piglets and foals;
structure, manifested either by solitary congenital cysts,
polycystic kidney either, the last having hereditary aspect in Landrace pigs.
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Atrophied kidneys have an increased incidence in veterinary

pathology may be unilateral or bilateral, partial or total, and in terms
etiopathogenetic are:
- compression (hydronephrosis, stones, cysts, inflammation, tumors,
parasites).
- inactivity, in case of circulatory disorders (amyloidosis and
glomerular sclerosis).
Macroscopic, the kidney, or the affected areas are reduced in size,
sometimes to a low parenchymal strip.
Microscopic atrophic area to reduce their number and volumetric
uriniferi tubules and renal corpuscles.
Dystrophies of the kidney are called nephrosis. After locating the
predominant lesions (glomeruli, tubules, gaps) nephrosis are:
- glomerular or glomerulonephrosis (lipids, amyloid);
- tubular or tubulonephrosis (carbohydrates, granular, hyaline,
vacuolated, pigmentation, uric Melanie).
Presents practical importance the following nephrosis: fat, granular,
hyaline, amyloid, pigmentation, uric limestone.
Nephrosis fatty, nephrosteatosis or renal steatosis, is found in all
species, is the result of toxic agents, such as endo-and exogenous. It is found
in ketosis and pregnancy toxiemia of ruminants, liver and kidney syndrome
in chickens, enterotoxiemia etc.
Macroscopic the kidneys are slightly enlarged, yellow (partially or
totally) on section presents lipid gloss.
Microscopic fat affects all kidney structures (tubules, glomeruli,
gaps) and can be identified by staining elective, and by breaking the apical
pole of the cells is formed in the tubule lumen the so-called "adipose
cylinder."
Nephrosis granular is the consequence of the toxic and infectious
factors,brief and low intensity and the starting point or the other protides
nephrosis or of nephritis.
Macroscopical the kidneys are enlarged, gray (area or in full) and
lack of gloss-look "body oils" like parenchymatous nephritis.
Hyaline nephrosis or renal hyalinosis is a
tubulonephrosis
diagnosticable only microscopic. Found in piglets in colisepticemie in
ocratoxicosis, or if fetal kidney.
Microscopic is observed hyaline under the form oof small balls in
the cytoplasm of renal cells (hyalinosis intracellular), or as "hyaline
cylinders" in the lumen of the tubules (interstitial hyalinosis). In chronic
124
swine rujet is observed hyaline glomerular capillary, and hypovitaminosis E

and hiposelenosis,the hyaline stands in the artery and interstitial capillaries.
Amyloid nephrosis or renal amyloidosis, occurs mainly in cattle and
poultry in chronic inflammation (suppurative tuberculosis) in malignant
tumors (enzootic) in horses producing serums and vaccines etc.
Macroscopic, the kidneys are enlarged, yellowish and sometimes
with outbreaks glassy, translucent needle size evident in the cortical area. In
birds, the consistency of the kidneys is similar to a block of wax.
Microscopic is observed amyloid deposition in glomerular
capillaries in related and efferent arterioles and sometimes the basal
membrane of urinary tubules .
Pigmentation nephrosis are, in most cases tubulonephrosis that
occur when massive renal elimination of hemoglobin, myoglobin,
hemosiderin, porphyrins, bile pigments.
Tubulonephrosis hemoglobinuric ormyoglobinuric is found , after
the red blood cells massive distruction or muscle tissue observed in
infectious diseases and acute supraacute, in piroplasmosis and babesiosis,
poisoning, in myopathy paralytic myoglobinuria horse etc. Hemoglobin or
myoglobin, the excess is eliminated by the kidneys, with the formation of
cylinders hemoglobin or myoglobin in the tubule lumen.
Macroscopic, the kidneys are red to dark metallic luster and the
color uniformity on section.
Microscopic crystalline or granular cylinders are observed mainly
in the lumen l of Henle loop.
Tubulonephrosis hemosiderin, or hemosiderosis, is the result of
chronic hemolysis. as in the horse infectious anemia if bleeding resulting in
great damage to red blood cells and the release of hemosiderin, which is
excreted through the kidneys.
Macroscopic, the kidneys have a rusty color and microscopic
hemosiderin is found in the form of:
- granules in the cytoplasm of renoepithelium (hemosiderosis
intracellular);
- "cylinders hemosiderin" in the tubule lumen (extracellular
hemosiderosis);
- in renal interstitial macrophages - siderocite - (hemosiderosis
interstitial). Hemosiderin gives positive Perls reaction due to iron that turns
bluish-green.
Porphyrin tubulonephrosis occurs in cattle and swine kidney with a
brown or brownish-green. Microscopic porphyrinic granules are brown or
125
yellow-green, the same locations as hemosiderin, which are distinguished by

Perls reaction negative (not containing porphyrins iron).
Nucleoproteids tubulonephrosis are represented by gout, tubular
dystrophic process, frequently encountered in birds and rarer in piglets and
calves.
Nephrosis uric of the bird is the starting point of visceral gout.
Macroscopic the kidneys are enlarged, the surface and observing
mass points and ribbed white-Cretaceous fine.
Microscopic there is the presence of uric acid and urate crystals in
the tubule lumen, along with necrosis and desquamation of the
renoepitheliums, in developments chronic uric nephrosis by mesenchymal
hyperplasia will arise, it will turn into inert foreign body granulomatous
nephritis.
Gouty nephrosis in piglets (guaninoza) has as biochemical substrate
of guanine nucleotides and special.
Macroscopic the kidneys are pale and on section are found in the
basin deposits whitish yellowish-white and ridged, radial, the renal papilla
tip. Renal guaninosis impairment occurs in viral gastroenteritis of pigs, in
pig ocratoxicosis and morphofunctional immaturity syndrome of the kidney
(fetal kidney).
Gouty nephrosis in cattle, (xantinoza) is the consequence of
excessive feeding or exclusive with bird droppings. Biochemical substrate is
represented by uric acid, xanthine, and tyrosine.
Macroscopic there is white dots and ribbed Cretaceous in cortical.
Calcar nephrosis are found in all species, either as pathological
calcifications or as urolithiasis.
Pathological dystrophic calcification can be observed in areas of
necrosis of tuberculosis, parasites, fungus, or it may be metastatic, as in the
case of vitamin D deficiency, hyperparathyroidism and characterized by the
deposition of calcium in the renal parenchyma.
Nephrocalcinosis and metastatic calcification appears as dots or
stripes, white, in the cortical area, especially in the medulla. Sometimes the
cattle can be distinguished white calcium deposits, surrounded by a
congestivo hemorrhagic areas, lesions called infarcts limestone.
Nephrolithiasis are found most frequently in the pelvis, outgoing,
or in the form of small granules (sand urine) and / or in the form of stones
(calculus).
Uric stones, or urolithiasis, is found in ruminants, carnivores and
birds. Urinary stones can form in the kidneys, pelvis and along the whole
length excretourinare ways, by precipitating urinary constituents around
126
small nuclei organic (microbial colonies, necrotic material, fibrin, foreign

bodies etc). In ruminants, as well as in other species, the stones are formed
of calcium phosphate or carbonate, ammonium and magnesium.
Macroscopic on section can be seen in the medulla ,strii bright
white and the pelvis identify precipitates (crystals) yellowish-white.
Microscopic is a tubulonephrosis is most apparent in the distal and
collecting tubules with degeneration and necrosis of the renoepithelium.
Epithelial cells are affected on the one hand due to the toxic effects of drugs,
on the other hand due to the crystals. These crystals were dissolved in water,
so that in the histological sections often can not be distinguished.
Nephropathies circular nature are represented by congestion,
hemorrhage and renal infarcts.
Active renal congestion, found in septicaemic disease in all
species, and the pig is a constant lesion rujet. It can affect kidney entirely or
only prevail in one of two areas: cortical or medullary. Intense color is red,
both on the outside and on the section.
The venous congestion (passive), kidney color is red-brown,
gradually evolving toward stasis sclerosis (nephrosclerosis). In both forms,
the section there is a considerable amount of blood to different shades
depending on the type of congestion.
Renal haemorrhage are common injuries in septic or toxic
disease.They can be located subcapsular, parenchymal mass in the lumen of
the renal pelvis.
Subcapsular hemorrhages are usually traumatic in nature, or toxic
(warfarin).
Bleeding cortical (cortex corticis) meet in Swine salmonellosis.
Corticomedullar hemorrhages are found in swine, leptospirosis,
equine infectious anemia.
In the renal parenchyma, the heamorrhages are of ecchymotic
type, are localized either in gaps or glomerulus.
Microscopic, the kidneys appear sprinkled with fine reddish dots
scattered throughout the parenchyma thickness, or only in the cortical area.
Intrabasinetal hemorrhages are characteristic of swine, although they
can also have a toxic etiology (warfarin). In the form of bloody collection, or
as intrabasinetal hematoma.
Renal infarction is typically white or anemic, are generally the
consequence of croup endocarditis.
127
Macroscopic on inspection are found gray-yellow areas , surrounded

by a small reddish ring. On section, triangular in shape, with the base facing
the periphery and separated by a reddish lizereu. Multiple infarcts, scarred,
deformed body surface due to numerous retractile scars that arise from
connective organizational phenomena.
5.1.4. Kidney Inflammation
Inflammation of the kidney is called nephritis, of capsule are called
perinephritis,,of the connective tissue from renal box is called paranephritis,
of the pelvis and renal tissue is called pyelonephritis. By way of
introduction of pathogens, nephritis can be:
- downward when the subjects are circulated through blood;
- upward when pathogens come in the urinary ways (urethra, bladder,
ureters).
A. Descending nephritis
Nephritis down (marrow), is characterized by quartering the
glomerular inflammatory process or tubules, interstitial connective tissue, or
all of the structural components. After locating predominant inflammatory
process, descending nephritis may be:
- predominantly glomerular or glomerulonephritis;
predominantly tubular or tubulonefrite;
- predominantly interstitial or interstitial nephritis;
- mixed nephritis.
Glomerulonephritis
Glomerulonephritis are inflammatory processes in which the
primary lesion is in the renal glomerulus, (Bowman capsule, capillary
endothelium, basement membrane, mesangial) other changes being
secondary to glomerular injury.
In veterinary pathology, macroscopic aspects are quite removed,
which makes it appear that they have a low incidence in animals.
Microscopic examination disproves this claim, showing
glomerulonephritis: serous cyst, hemorrhagic, purulent, hyperplastic,
membranous.
Serous glomerulonephritis is characterized by glomerular
dilatation, after accumulation in glomerular area of appreciable amounts of
128
serous exudate. Area glomerulus appears increased and decreased vascular

glomeruli. in longer developments due to the compressive effect exercised
by serous exudate, vascular glomeruli atrophy and concomitant serous
glomerulonephritis turns into a cystis glomerulonephritis.
Macroscopic in the serous glomerulonephritis, the kidneys are
normal or slightly increased in volume, and on section is cortical graywhitish liquid .Acute developments are more common in equine and chronic
ones in cattle and pigs.
Cystic glomerulonephritis is the result of evolution of subacute and
chronic glomerulonephritis serous. In the cortical cystic formations are
found 4-5 small (2-3 mm) printing a spongy appearance of the area.
Microscopic vascular glomeruli atrophy, sometimes to extinction.
Hemorrhagic glomerulonephritis occurs in rujet,septicemia, acute
salmonellosis and in poisoning.
Macroscopic, the kidneys due to congestion in cortical are
observed small red spots the size of pin needle (dilated glomeruli).
Microscopic it shows a glomerulitis::
- intracapilar observed in pigs rujet, characterized by vascular
congestion of the glomerulus with glomerular space reduction, respectively;
- extracapilar, seen more frequently in cattle as hemorrhagic exudate
accumulates in the glomerular space in the form of a crescent, and vascular
glomeruli is reduced.
Purulent glomerulonephritis is the result of bacterial emboli and
metastases from other primary pyogenic foci (omfaloflebite, endometritis,
mastitis, etc..). Subsequently, purulent inflammation of glomerular by
continuity affects renal tubules and interstitium. Occurs in cattle, in C.
pyogenes infections in foals strangles etc.
Macroscopic on, the kidney area and the section in the cortical are
found foci yellowish needle size , surrounded in acute forms, of a reddish
ring (microabscesses).
Microscopic, there is accumulation of purulent exudate in
glomerular space, compressing vascular glomeruli. The pole of glomerular
urine, pus dripping tubules, forming so-called "leukocyte cylinders" or
purulent.
Glomerulonephritis or mesangial hyperplasia is characterized by
endothelial and mesangial cell proliferation of vascular ball, leading to
enlargement of the glomerulus, while the glomerular space is reduced or
absent.
Macroscopic , on the red-brown babground due to renal cortex, we
observe the presence of whitish foci, greasy, needle size.
129
Microscopic , it shows a glomerular hypercellularity. It is observed

more frequently in cattle and horses, but have obscure etiology.
Membranoproliferative glomerulonephritis, have immune substrate
and is characterized by capillary basement membrane damage predominant
compared with cell proliferation, which is reduced.
Capillary basement membranes on the outside become irregular
and thickened with deposition of immunoglobulins (IgG, IgM), losing
selective filtration function. Glomeruli is relatively poor in cells.
It is often found in dogs due to pyometra, infectious viral hepatitis,
lupus erythematosus.
Tubulonephritis
Tubulonephritis are inflammation of the kidney, primary lesions
occur predominantly in the tubular system. Pathology may be epithelial or
cystic. Epithelium tubulonephritis , also called nephritis, toxic or
parenchymal is characterized by severe degeneration, cytolytic or epithelial
peeling, the formation of "epithelial cylinder" in the lumen of the tubules.
Macroscopic, there is discoloration in the form of grooves,
indistinguishable from those of nephrosis. It occurs in all species with toxic
etiology (copper, phosphorus, lead, ochratoxin etc.) Or in some
toxisepticemice disease (kidney disease soft lambs).
Cystic tubulonephritis is found only in cattle.
Macroscopic, the surface and the kidney mass is observed
numerous cysts, set a spongy appearance to the organ. Microscopic, urinary
tubules are dilated, filled with fluid and desquamated cells. It has been
described by Paul I, 1990. (45)
Interstitial nephritis
Interstitial nephritis is inflammation of kidney, the initial lesion and
dominant conjunctive-vascular interstitial tissue. Some acute evolving only
other acute and subacute and chronic others . Can be exudative and
productive .
Nephritis interstitial bleeding occurs, as lesion feature, classical
swine fever, and in some cases of salmonellosis and leptospirosis in pigs and
dogs.
Macroscopic on a light background of the kidney, there is reddish
points of unequal size, particularly in cortical of the body printing fowl egg
appearance.
130
Microscopic, there is interstitial hemorrhagic exudate, and

intertubular integlomerular, hyalinosis vessel wall and thrombosis (the main
type of bleeding infarctiform).
Suppurative interstitial nephritis is characterized by the appearance
of yellowish-white foci of various sizes, sometimes prominent, with purulent
content per section. Is likely metastatic.
Microscopi, it is notes granulocytic hyperplasia accompanied by
lytic areas, the more or less flat. It is found more frequently in infections
with C. pyogenes.
Lymphohistocytic interstitial nephritis is one of the most common
nephropathies seen in animals with toxic etiology, infection (leptospirosis,
salmonellosis), running etc.. Occurs due interleukins, biologically active
substances released in the early stages of the inflammatory process. Can
evolve circumscribed (in focus), or diffuse. Interstitial nephritis
lymphohistiocytic in foci, is characterized by the appearance on the surface
of the kidneys, whitish-gray outbreaks of up to 5 mm in diameter, in the
acute form , slightly protruding. On section, outbreaks appear as parallel
bands, white and greasy, mainly in cortical area.
In the subacute form, outbreaks are larger, appearing in the form of
spots (macules) gray-white, hence the name of nephritis macula (the
macula).
Fibrous interstitial nephritis , has chronic evolution and can be
further of the lymphohistocytic nephritis, or other acute nephropathy. It is
known as " little kidneys rippled ".
Macroscopic, the kidney is reduced in volume, or cerebriform
irregular surface due to numerous deep scar retraction. Color is gray uniform
and greatly increased consistency. On section, it is noted ribbed or white
islands of connective tissue.
Microscopic, there is marked hyperplasia of fibrous connective
tissue that causes atrophy by nephron compression (tubules and corpuscles).
Mixed nephritis, granulomatous
Mixed or granulomatous nephritis is exhibited differently depending
on the etiologic agent. May be of infections, tuberculosis, parasitic renal
coccidiosis in geese and inert foreign body in gout disease.
Microscopic , lesions observed in glomeruli, tubules and in renal
interstitium. Morphological aspects specific to each etiologic agent will be
presented at the disease.
B. Ascending nephritis
131
Ascending nephritis (urinogene) are the result of infections, about

canalicular progressing from distal urinary tract (urethra, bladder, ureters).
Meet less frequently than descending nephritis, starts the skin and
later by impaired renal parenchyma arise pyelonephritis.
Purulent pyelonephritis occurs more commonly in cows after
calving, abortion, or endometritis secondary. Etiopathogenetic,
Corynobacterium of the kidney has an important role, but it can be produced
by a polymicrobial flora (Streptococcus, Staphylococcus, Arcanobacter,
Proteus).
Macroscopic , the kidneys are increased in volume, yellowish,
purulent foci through and consistency is fluctuating. On section, pelvis and
affected lobes are turned into real purulent collections. In severe cases, the
entire kidney may be a bag of pus. (5, 11, 16, 19, 34, 41, 43)
5.1.5. Renal Tumors

Renal tumors are more common in swine, poultry and carnivores
as either primary process or as metastatic.
Primary tumors are represented by adenomas and malignancies of
the carcinomas and nephroblastoama seen in carnivores. Adenoma is rare in
cattle and horses. Renal carcinomas are more common in dogs and cattle
while nephroblastoma have a higher incidence in pigs, dogs and calves.
Mammalian and avian leukosis and Marek's disease may produce
nodular or diffuse tumor proliferation. They are the most common renal
secondary tumors in animals.
5.2. Urinary lesions
5.2.1. Common urinary injuries
Hydronephrosis (Gr. hydor = water = nephric kidney oz =
noninflammatory disease) is retention of urine in the pelvis and renal pelvis
caused by an obstruction or decrease in tonicity pelvis followed by its
expansion. The lesion may be unilateral or bilateral and is most commonly
found in cattle, sheep, swine and carnivores.
Causes of hydronephrosis are ureters obliterations by calculi, scar
stenosis, tumors, etc. . When the obstacle is located in the caudal portion,
132
and dilated ureter occurs upstream, resulting uretero-hydronephrosis.

Urinary stasis in the ureter causes atrophy and even rupturing wall with
overflow urine into the peritoneal cavity (uroperitoneu).
Macroscopic p pelvis are dilated ,variable ,after the degree and
duration of obstruction. Dilation may be minimal or can reach impressive
sizes, sometimes entire kidney can be converted into a bag filled with urine.
Mucoureter in birds are found relatively frequently the existence
of excessive mucinous secretions at this level. This injury occurs due to lack
pelvis, collecting tubules opening into a dilatation of the ureter. Mucoureter
is the starting point of ureteral stones in birds.
Urinary stones or urolithiasis is commonly observed in ruminants,
carnivores and birds and more rarely in other species.
Contributing factors are represented by anatomical conformation of
the urethra, sigmoid flexure in cattle or narrowing of the urethra and
vermicular appendix to ram lumen reduction in bone penile urethra in dogs
etc.
In ruminants phosphate granulation process begins by Amoni
acomagnezieni and especially struvite (NH 3 MgPO 4 6 H 2 O) which
usually obliterates induce urethra and urinary retention with bladder
distention and death in uremia. It is more common in males than in females,
affecting calves, lambs.
In carnivores the damage occurs more frequently in dogs, both
sexes are affected in equal proportions. Urolithiasis in dogs is a predisposing
factor for urinary tract infection. The first are the type phosphate calculi, and
the type urate and cystine than those pests.
Is a proven breed predisposition, respectively basets and young Irish
consisting of cystine calculi, Dalmatians for those of ammonium urate;
German Shepherd calculi based on silicon, etc.
5.2.2. Ureteral injuries
Dystrophies of ureters are represented by urolithiasis (sand and / s
are calculated).
In chickens and in adults is found in the lumen ureteral calculi
uric obliterans (gout impairment).
Macroscopic , ureters are increased in volume, white-like cords
with a diameter of about 5 mm with high consistency. The lumen is found
cilindroide whitish deposits (uric calculi obliterans).
Inflammation of ureters are called ureteritis. They can be
downward or upward, and in terms of pathology, the most common are
forms serous, hemorrhagic and purulent.
133
5.2.3. Urinary bladder lesions

Bladder dilation is a consequence of excessive accumulation of urine
in the bladder because of inability to escape it. It can be caused by ureteral
obstruction, represented by calculi, processes tumor ,stenotic scars, parasites,
or may be due to external compressions etc.
5.2.3.2. Dystrophies of the urinay bladder
Bladder epithelium dystrophies can be granular, vacuolar,
cornous(hypovitaminosis A). Bladder stones, it is most important dystrophic
process manifested either by sand either by bladder calculi, single or
multiple.
The presence of gallstones, causes irritation of the mucous
membrane, initially manifested by bleeding, and then, through inflammatory
process.
Circulatory changes of the bladder can be represented by
hemorrhage bladder (poisoning, infections, gallstones, PPA) and infarction,
compared with the intensity of blood stasis.
5.2.3.4. Bladder Inflammation
Urinary tract infection or cystitis is called urocistite. Their etiology
is varied: mechanical, toxic, infectious and parasitic. Pathology may be
urocystitis, bleeding, pseudomembranous purulent
(diffuse polyps),
granulomatous.
Catarrhal urocystitis manifested by epithelial desquamation and
leukocyte exudation processes that will give a yellowish-gray color. Occurs
in all species.
Heamorrhagic urocystitis is characterized by thickening of the walls
of the bladder as a result of accumulation of blood exudate. Found in
poisoning, trauma (rough stones) etc..
In this form morphological score and the first phase of hemorrhagic
cystitis cattle known as "chronic bladder hematuria."
134
Haemorrhagic cystitis of the cattles is a disease of the cattle in

northwestern foothill regions of our country (Maramures). The disease is
probably caused by the consumption of imperial fern (Pteridium spp) and
other factors indicate incomplete. The main symptom is hematuria in this
disease, where it gets its name.
Histological investigations have shown that hemorrhagic
inflammation is present only in the early stages of the disease and later
becomes chronic inflammatory process and turns into a process of malignant
or sarcomatous tumor type.
Pseudomembranous urocystitis (fibrinous) is common in
carnivores and cattle either fibrinous deposits on mucosal surface or by
necrosis deep into the lining.
Purulent urocystitis is characterized by massive leucodiapedesis
determining the cloudiness of urine (flakes of pus). It may be superficial in
lamina propria and subepithelial microabscesses and diffuse as it affects the
entire mucosa (phlegmonous form).
Urocystitis hyperplastic (follicular) are observed more frequently
in dogs and cattle by lymphoid hyperplasia outbreaks as a result of
prolonged irritation of the bladder mucosa.
Sometimes inflammatory hyperplasia may progress through the
formation of polyps (urocistit polyps) that the peak union may give rise to
cystic formations (urocistita cystic).
Granulomatous urocystitis is rare. It has been described in
tuberculosis in cattle and carnivores.
5.2.3.5. Urinary bladder Tumors
Bladder tumors are rare. Have greater importance in cattle,
whereas more advanced stages of the cattle hemorrhagic cystitis,
inflammatory process turns into one tumor (malignant epithelial and / or
neepiteliale). Were diagnosed papillomas, carcinomas, aden ocarcinoame,
fibroids, leiomioame.
5.2.4. Urethra injuries
5.2.4.1. Congenital anomalies
Hypospadias is the urethra opening on the underside of the penis
and epispadias urethra opening is on the dorsal side of the penis.
135
5.2.4.2. Dystrophies of the urethra

Dystrophies urethra can be represented by kidney stones or bladder
stones, which can stop the penis from bulls S's, penile bone in dogs or
vermicular appendix to ram them causing obliteration.
These anatomical segments may be often the points formation of
urolithiasis.
5.2.4.3. Inflammation of the urethra

Inflammation of the urethra is called urethritis, being in relation to
inflammation of the penis and prepuce. Pathology differ catarrhal urethritis,
purulent, hemorrhagic and ulcerated, with their own issues these types of
inflammation. (5, 11, 16, 19, 39, 41, 43)
136
6. The morphopathology of the genital system

6.1. Congenital abnormalities common to both sexes
Hermaphrodism or intersexuality is characterized by the presence of
organs of both sexes, fully represented in the same individual. It may be:
- true (H versus) both sexes are represented;
- alse when the gonads belong to one sex and the secondary gonads
belongs to the other sex.
True hermaphroditism is generally rare and may be:
- biglandular bilateral represented by both testes and ovaries,
separated or joined (ovotestis or ovariotestis);
biglandular unilaterally when on one side there are both
gonads
(ovary and testis) united or separated, and on the other, only the ovary or
testicle only and will be called testicular or ovarian after gonadal
predominant;
- biglandular alternating on one side of the animal has ovary and testis
another.
Pseudohermaphroditism is characterized by the fact that gonads
belongs to one sex and external genitalia of another sex. These are:
- masculine when the animal shows testes and further, clitoris and
vagina was observed in pigs 0.2%, to 0.1% goat less than that in other
species;
- female, characterized by the ovaries, a rudimentary uterine tube and
the outside, penis and foreskin.
Fremartinismul is a state of a particular intersexuality of females
from opposite-sex twin gestation, characterized by the presence of female
137
and male sexual organs fully developed. It is found most commonly in

ruminants.
6.2. The morphopathology of the male reproductive system
6.2.1. Testicular lesions
6.2.1.1. De development disorders
Congenital anomalies can occur through:
- anorhie (anorhidie), lack of testes observed in horses and dogs;
monorhie the presence of one testicle;
triorhie, the presence of three balls.
Cryptorchidism is the most important abnormality of testis
development, characterized by the absence of migration, migration
incomplete or erratic migration of the testis seen in stallions, boars, dogs and
tomcats. It can be abdominal, groin and extragenital.
Macroscopic there is no uni-or bilateral scrotal testes of bags.
Cryptorchid testis is reduced in volume, increased consistency and
microscopic interstitial Leydig cells are developed at the expense of the
seminiferous tubules.
Testicular hypoplasia occurs more frequently in bulls and rams and
defines lack of development of testes to sexual maturity.
Macroscopic
the testes were smaller and microscopic
differentiation highlights the lack of differentiation or incomplete sperm
cells.
Etiology, testicular hypoplasia is the result of impaired youth
nutrition for maintenance and reproduction, but may be caused by some
genetic factors.
6.2.1.2. Testicular atrophy and dystrophy
Testicular atrophy is characterized by a decrease in testicular
volume after installing sexual maturity. It can be caused by disruption
(castration) by compression malnutrition in pituitary senility. Testicular
atrophy is the most common dystrophy of the testicular parenchyma.
Vacuolar degeneration of the seminiferous epithelium, ends with
necrobiosis and necrosis more or less stretched and impregnation with
calcium salts (calcification).
138
Fatty degeneration of germinal epithelial cells is reported in

zearalenone intoxication in male guinea fowl with total cessation of
spermiogenesis. (Vanya and Szki, 1980 quoted by Paul). (45)
Calcareous degeneration or calcification testicular found in bull,
ram and being secondary to necrosis, hemorrhage or chronic inflammation.
Macroscopic, it appears whitish points, hard to the touch, and
microscopic observed calcified seminiferous tubules.
Interstitial melanosis occurs in fowls, turkeys and canaries.
Testicular circulatory changes are relatively common, manifested
by congestion, hemorrhage, hematoma or infarction, first observed in the
evolution of infectious diseases, and seconds are usually the result of
spermatic cord torsion, or after inguinal hernia.
6.2.1.4. Testicle inflammations
Inflammation of the testicles is called orchitis, and ones of the
coverings are called periorchitis. In their etiology is determined mainly
include trauma to the testicles swinging ruminant position, plus various
infectious agents: brucella, salmonella, coli, mycobacteria, etc..
Morphopathologic orchitis may be necrotic (in salmonellosis
duck), serous, fibrinous, hemorrhagic, purulent,lymphohistocytic, fibrotic
and granulomatous.
Orchitis serous and heamorrhagic are generally traumatic nature,
and is characterized by infiltration serous, fibrinous or / and of testicular
interstitial bleeding.
It presents diagnostic importance in mammals,the purulent and
granulomatous orchitis.
Purulent orchitis may protrude, in "outbreaks" (abscesses) or
diffuse, with the latter being the result of purulent orchitis . It can be caused
by corynebacteria, actinobacili, brucella, salmonella, pseudomonas, etc.. It
was described in rams, bulls, stallions and dogs.
Fibrous orchitis is a consequence of acute inflammation is
associated with adhesive periorchitis .
Granulomatous orchitis is seen in brucellosis, glanders,
tuberculosis, actinobacilosis, externalized through nodular foci of different
sizes.
139
6.2.1.4. Testicular Tumors

Primary testicular tumors are very common in older dogs, to a lesser
extent the old bulls and exceptionally in other species.
Males develop criptorhizi 10 times more testicular tumors compared
with normal dogs. Canine testicular tumors are commonly located in the
right testicle, which is valid for cryptorchidism. Sertolinomul is the tumor of
the sertolu cells.
Macroscopic, it is limited by the large capsule. The section is
whitish, hard consistency, sometimes with cystic appearance.
Microscopic there is a relatively abundant stroma, Sertoli cells in
early forms are similar to normal cells, and in more advanced forms, the
cells are less differentiated.
Seminoma is the tumor of the germinal cells (spermatogenic series).
Macroscopic appears as nodules, sometimes with a diameter of 6
cm distorting albugineea. The color and structure closely resembles that of
the lymphoid tissue.
Microscopic differ in two forms: intratubular seminoma and
seminoma diffuse type.
Leydigomul is the interstitial Leydig cell tumor . It is presented as a
multiple tumor, and solitary. It has small, well-encapsulated, yellowish, and
are frequently hemorrhagic necrosis.
Microscopic differ a leydigom: compact diffuse type, a vascular-type
cystic pseudoadenomatos. (5, 11, 12, 16, 19, 40)
6.2.2. Lesions of the epididymis and deferens channel
Congenital anomalies of the epididymis can be represented by
aplasia, hypoplasia, or congenital obstruction of the channel epididimar,
especially in rams.
Spermatocele are dilated epididymis, following the accumulation of
increased amounts of sperm. This injury occurs as a result of congenital or
acquired obstruction, of epididimar channel. Over time, this can cause
rupture of the walls, resulting in discharge sperm into the interstitial spaces
140
where the mycolic acid it contains, triggers an inflammatory process (sperm

granuloma).
6.2.2.3. Dystrophies of the epididymis
Cornous metaplasia of the epithelium epididimar and of the
deferens vessel is the only dystrophy, which can be observed in these
segments. Occurs in rams and bulls in hypo-and avitaminosis A. is diagnosed
only microscopically.
6.2.2.4. Inflammation of the epididymis

Inflammation of the epididymis is called epididymitis. They
precede or co-evolve with testicular inflammation (orhiepididimite). Presents
practical significance rams infectious epididymitis caused by Brucella ovis,
manifested as acute testicular tunics by swelling and accumulation of
exudate serofibrinos in the vaginal cavity and in the chronic form, the
appearance of epithelioid and giant cell granulomas. The process is
localized, usually in epididymal tail. (5, 11, 12, 16, 19, 41)
6.2.3. Injuries of tunica vaginalis
Circulatory changes accompanying the tunica vaginalis are usually
those of the parietal peritoneum.
Hydrocele is the accumulation of a transudate into the vaginal cavity
or due to ascites or as a result of local compression caused by tumors or
inflammation.
Chilocelul, is the accumulation of lymph in the sheath of the vagina
as a result of trauma.
Hematocelul is the accumulation of blood in the sleeve vaginal
trauma due to circulatory changes found in all of the tunica vaginalis.
Macroscopic there is an increase in vaginal cavity volume and
consistency is low or fluctuating.
6.2.3.2. Inflammations of the tunica vaginalis
141
Inflammations are called vaginalite. They follows orchitis

epididimitis and peritoneitis. Morphopathologic differ serous, fibrinous,
hemorrhagic, in acute forms respectively vaginalite fibrous adhesive in
chronic developments.
6.2.4. Spermatic cord lesions
Sperm cord (Funiculi) consists of spermatic arteries, veins, nerves
and cremaster m.
Congenital anomalies can be identified sometimes with segmental
aplasia of the vas deferens, encountered in bulls.
Spermatic circulatory changes are represented by varicocele,
testicular veins characterized in rams and stallions, especially in the
pampiniform plexus.
6.2.4.3. Topographic changes
Spermatic cord torsion is a change in terrain, found mainly in dogs
manifested by congestion, edema and hemorrhage in mild forms respectively
by infarction and necrosis in severe forms.
6.2.4.4. Inflammation of the spermatic cord
Inflammation of the sperm cord (Funiculi)
is a septic complication following castration of boars
other species. Mofopatologic, funiculitis may be
suppurative and granulomatous. After locating
inflammation, funiculitis can be:
intrascrotal (in stock scrotal bag);
inguinal (in the groin);
abdomen (the abdominal cavity).
is called funiculitis. It
and stallions, rarely in
serous, hemorrhagic,
the spermatic cord
142
In boars, they have evolved and acute purulent necrotic nature,

propagating rapidly to the abdominal cavity, producing acute suppurative
peritonitis, which can lead to death of the animal.
In stallions, funiculitis have a chronic course, manifested by
marked proliferation of connective tissue, and subsequently abscesses, ulcers
and fistulas effusion.
Macroscopic spermatic cord occurs much increased in volume,
hard to palpation, sometimes reaching a diameter of 10-15 cm. Castrating
wounds and scars do not have a fistula, which is running a purulent exudate.
This proliferative funiculitis is known as the botriomicosis or
"castrating fungus." A leading role in its occurrence rests of Staphylococcus
aureus.
6.2.5. The injuries of genital glands
Accessory genital glands of male genitalia are represented by the
seminal glands, prostate and bulbouretral glands (Cowper).
They have been little studied in veterinary medicine, the existing
data originated, mostly, from the investigations carried out on bulls.
Changes in volume can protrude through atrophy or hypotrophy of
the prostate gland and seminal due to hormonal disorders.
Dystrophies glands genital are represented by seminal gland
metaplasia of the epithelium in hypovitaminosis A diagnosed only
microscopically.
Inflammation ofseminal glands are called spermoadenitis or
spermatocystitis and prostate, prostatitis. Etiology, are produced by a
polymicrobial flora and evolving, they may be acute, subacute and chronic.
Spermoadenitis most common are type catarrhal and prostatitis, in
most cases, are of aposteomatos (old dogs). Genital gland tumors are rare in
animal pathology. Prostate tumors are found especially in dogs with a higher
incidence in age from 6 to 15 years with an average of 10 years. They are
represented by adenomas, adenocarcinomas, respectively mesenchymal
tumors: leiomyoma, fibroma, fibrosarcoma and leiomyosarcoma. (5, 11, 16,
19, 41, 43)
6.2.6. Injuries of penis and prepuce
143
Congenital anomalies can be represented by micropenis, poor

orientation of the penis by phimosis and paraphimosis.
Phimosis is strait preputial orifice, preventing protrusion of the
penis.
Paraphimosis Strait and constricting preputial orifice is behind the
glans, making it impossible to enter the sheath preputial gland. The last two
abnormalities are more common in dogs.
Circulatory changes may be manifested by hemorrhage on the dorsal
side of the corpora cavernosa of the penis, due to the breaking of the vessels.
I found in bull and sometimes can take aspect of hematoma.
6.2.6.3. Inflammations of the penis
Inflammation of the glans is called Balan and mucosal preputial
post. They usually evolve together, as the balanopostitis.. Pathologic the
balanopostitis may be catarrhal, vesicular, pustular, purulent ulcers, follicular
and granulomatous.
Balanopostitis catarrhal manifested by congestion and catarrh
infiltration.
Balanopostitis purulent characterized by congestion and swelling
of the preputial mucosa, accompanied with purulent exudate which by
dehydration, is transformed into a pseudo. It is more common in bulls, being
found in trichomoniasis, the infection with C. pyogenes, staphylococci,
streptococci, etc..
Ulcerous balanpostitis is characterized by the emergence of ulcers,
preputial first round hole, and thereafter the preputial cavity, with or without
closing the orifice.
It occurs more frequently in rams and goats, being favored by high
protein diet that provides optimal living conditions of Corynebacterium . It
hydrolyzes urea to ammonia, which is proscribed metabolite production
ulcers .
Follicular balanpostitis (limfohistiocitar) is exhibited by the
appearance of gray-whitish nodules, barely visible, as a result of the
proliferation of lymphoid in penile mucous membrane structure. It is a nonspecific inflammation caused by viruses, as well as polymicrobial flora.
144
Granulomatous balanpostitis it manifests itself macroscopically by

the appearance of nodules, often ulcerated. It occurs more frequently in
summer stallions in habronemoza skin caused by the larval form of parasites.
Morphoclinical, balanopostititis can be complicated by phimosis
and paraphimosis gained when inflammation is accompanied by preputial
orifice .
6.2.6.4. Penis and preputial tumors

Penis and preputial tumors are represented by Sticker's sarcoma in
dogs by fibropapiloama of the bulls or the squamous papilloma and
squamous cell carcinoma in stallions.
6.3. The morphopathology of mammalian female genital system
6.3.1. Ovarian lesions
Are rare and often related to intersexuality. We may encounter:
unilateral or bilateral ovarian agenesis;
supernumerary ovaries;
Aryan paraov cysts (cystic dilatation of some scrap channel Wolf);
- ovarian hypoplasia, solitary or associated with the entire female
genital apparatus (genital infantilism).
Ovarian hypoplasia is one of the most common abnormalities seen
in females of all species and particularly those maintained in poor
zoohygiene conditions and poor diet.
. Etiologic criminalizing fetal vasculature disorders, endocrine
disorders, genetic defects and multiple failures.
Macroscopic the , ovaries were smaller than normal, and in serious
cases, are represented only by a conjunctive-vascular tissue, devoid of
germinal epithelium. Ovarian hypoplasia is common in heifers.
All these abnormalities are pathological elements of sterility in
females.
145

Ovarian atrophy following the onset of sexual maturity (adult
females), being an important lesion as it determines estrous disorders and
sterility.
Etiopathogenetic, ovary atrophies are: compression (cysts, tumors),
hormonal and senility.
Macroscopic, the ovaries are much reduced in size, the surface
appears wrinkled longitudinally, and the consistency is increased.
Dystrophies ovaries are represented by cystic degeneration and
persistent corpus luteum.
Cystic degeneration or ovarian cysts are the most common
ovariopaties in all species. Ovarian cysts may be unilateral or bilateral,
solitary or multiple, very small or very large (orange). Once the starting
point is different follicular cysts, corpus luteum and luteal.
Follicular cysts are formed in the complete absence of LH
producing cystic degeneration of de Graaf follicle.
Macroscopic, there is thin-wall and translucent vesicles of different
sizes containing serous fluid, yellow, which maintains the capsule under
pressure.
Microscopic, the walls are constituted either internal sheath cells
(they have small, secret estrogen) or in granulosa cells (have large).
Luteum cyst or luteinizing, the birth of a Graafian follicle in the
presence of sufficient amounts of LH, which produces partial luteinization
granulosa. Cyst walls are uneven in thickness, and the content is slightly
reddish, rich in progesterone. It is more common in sows.
Corpus luteum cyst is formed from a Graafian follicle in which
ovulation occurred but was incomplete luteal transformation. Thus remain in
the center of the yellow body cavity filled with liquid citrine surrounded by a
thick wall and evenly. These cysts contain large amounts of estrogen and
progesterone.
A particular case of cysts are found in mares, if it does not form the
corpus luteum, although the ovulation has occurred. They are called
"hematocysts" their causes are multiple.
Persistent corpus luteum is the result of a hormonal imbalance,
characterized by the absence of degeneration and involution of the corpus
luteum of heat and especially the gestation. Is encountered relatively
frequently in cows and appears as a yellowish nodule, prominent about 2-4
cm in diameter.
146
Corpus luteum persistent corpus luteum differs from physiological

(heat or pregnancy), only by microscopic examination, we observed an
enhanced vacuolar degeneration, necrobiosis and fibroblast hyperplasia.
Circulatory changes are represented by bleeding that may be of
infectious, toxic (mycotoxins, warfarin) and traumatic (for manual
enucleation of the persistent corpus luteum).
6.3.1.4. Inflammations of the ovary
Ovarian inflammation are called ovaritis, and of serous ovarian
periovaritis. They are relatively rare, and may take forms pathological:
serous, hemorrhagic, purulent, fibrotic and granulomatous.
Serous and hemorrhagic ovaritisare generally traumatic or
hormonal nature, the purulent are the result of infection with C. pyogenes;
fibrinous ovaritis evolves as periovaritis adhesive , and granulomatous, are
found in tuberculosis, brucellosis in cows and sows.
6.3.1.5. Tumors of the Ovary
Ovarian tumors have higher incidence in the bitch, and the cow,
horse and sheep. The tumors are bilateral bitch while in cow, sheep and
horse are one-sided. Ovarian tumors in cats are few.
Can also be observed teratomas, ovaries being the election
headquarters of embryonic tumors. In mammalian leucosis the ovarian
localizations can be observed more frequently in cattle, making a meal ovary
greasy, whitish gray. (4, 5, 11, 16, 19, 41, 43)
6.3.2. Salpinx lesions (fallopian tube)
Are mentioned in the literature unilateral or bilateral agenesis,
stenosis, and even supernumerary fallopian tubes.
147
6.3. 2.2. Dystrophies of salpinx

Salpinx dystrophies are little known in animals and their diagnosis
is made only microscopic.
Vacuolated epithelial cylinder distrophy is characterized by loss of
cilia and flaking cells on sterile cows and old.
Cystic dystrophy of the epithelium, can be seen in sterility mare,
bitch and sow after castration.

Salpinx circulatory changes can be represented by hydro-and
hematosalpinx.
Hydrosalpinx is accumulating in the lumen of the salpinx of
transudation.
Macroscopic, there is a sharp expansion salpinx, pending issues
pseudocyst. Content is serous cyst, citrine and oviduct wall is thinned.
Hydrosalpinx is likely the result of dystrophic or inflammatory stenosis,
followed by dilatation, segmental or total upstream of the oviduct.
Hematosalpinxul is the accumulation of blood in the lumen salpinx
by mucosal vessels rupture in case of torsion, but can be inflammatory in
nature.
6.3.2.4. Inflammations of the salpinx
Salpinx inflammations are called salpingitis, and ones of the
serous perisalpingite. Salpingitis may be upward or downward, uni-or
bilateral. Pathologically, there is special salpingitis:
catarrhal (nonspecific);
- purulent form of piosalpinx in C. pyogenes infections, staphylococci
(especially cows);
- fibrous (hypertrophic, atrophic or as salpingoovarite adhesive);
- granulomatous (in tuberculosis, miliary or nodular form). (5, 11, 16,
19, 41, 43)
148
6.3.3. Uterine lesions

Congenital anomalies of the uterus is externalized in particular by
infantilism cervical or uterine hypoplasia, solitary or associated with female
genital hypoplasia at all appear, making genital infantilism syndrome.
Are also mentioned uterine agenesis (absence of uterus), uterus
unico rnual, double uterus, which are found mainly in pigs, changes easily
diagnosed with adverse implications for animal breeding.
6.3.3.2. Dystrophies of the uterus
Dystrophies of the uterus are almost unknown in veterinary
medicine. Are mentioned:
- melanosis ligaments and uterine serous;
- hemosiderosis chorionic villi, both sheep;
- elastosis uterine artery observed in older cows, still known as
"sclerosis of gestation."
Uterine torsion may protrude by turning the uterus along its
longitudinal axis.
Uterine prolapse uterus is manifested externally output as a result
of laborious parturition, placental retention, hypocalcemia, etc.. Both injuries
result in serious circulatory disorders.
Circulatory changes are represented by uterine hemorrhage and
infarction. Uterine haemorrhages can develop, either in the form of
metrorrhagia, with elimination of blood through the vagina on the outside,
or in the form of hematometru, the accumulation of blood in the uterine
cavity through the cervical canal obstruction. Cervical canal obstruction may
be congenital or acquired (postinflammatory adhesions, tumors, etc..). The
uterus is enlarged in volume, but the uterine cavity is filled with blood.
149
Infarction uterus is found in its topographic changes (torsion,

prolapse), macroscopic manifested by thickening the walls, red-purple or
blackish and putrid odor. Content is fluid, dark red and the same smell
repulsive. (5, 11, 16, 19, 41, 43)
6.3.3.5. Inflammations of the uterus
Inflammation of the uterus are called metritis, it affects all layers of
the lining,;; the endometrium, the musculoasei, myometrium, the serous, the
perimetritis. the tissues around the uterus including ligaments broad is called
parametritis..
Metritis are found in all species, resulting in single or combined
action, mechanical factors, physico-chemical, infectious and parasitic. They
may be ascending or descending, and after development, can be acute,
subacute and chronic.
After morphological appearance, differ inflammation: catarrhal,
hemorrhagic, purulent, gangrenous necrosis, hyperplasia and granulomatous.
Endometritis catarrhal is the surface inflammation of the uterine
lining, characterized by the presence of mucous or mucocelular deposit
(whitish) under the mucosa is congested and edematous. It is difficult to
diagnose because its aspects are similar morphological changes in estrous.
Haemorrhagic endometritis occurs only in gog females being the
result of an excess follicular.
Purulent endometritis in acute form is evolving diffuse and in
subacute and chronic forms is manifested by the formation of the chorion
microabcesses or by the accumulation of pus in the lumen of the uterus
(pyometra or uterine empyema). Uterine cervix is more wide open than
normal.
Pyometra occurs more frequently in cows and one being the
consequence of post-partum infections with staphylococci, C. pyogenes,
colibacili (every) etc..
Macroscopic, there is an enlarged uterine horns affected, and the
section is observed the presence of excessive amounts of pus, its color and
composition, is dependent upon the etiologic agent. Mucosa is edematous,
infiltrated purulent, with areas of necrosis and fragmentation.
Damage capillary tubes, favor the passage of germs and even pus
in the great movement, causing metastatic processes (embolism is Ptiie,
piemie).
Gangrenous metritis is the most serious disease of puerperium, the
result of two factors, tissue trauma and anaerobic flora (Cl. perfringes etc.).
150
The uterus is enlarged in volume, edematous, crackles on palpation

and very brittle. Uterine contents is liquid, red-brown, pungent and putrid
odor with small fragments of necrotic tissue. It meets frequently in
ruminants following dystocic births.
Necrotizing metritis is caused by staphylococci or C. pyogenes
bacillus in association with necrosis and can be localized to the wattles in
ruminants ( necrotizing metritis) or extended over the entire endometrial
mare, sow and bitch ( necrotizing endometritis).
Hyperplasic metritis is characterized by enhanced proliferation and
mesenchymal They are exhibited either by diffuse thickening or outbreaks
(meters polyps) or by closing glands with epithelial atrophy and retention
forming microcysts (meters cystic). In chronic developments glands
disappear lining thins and hyperplastic process differentiates in a fibrocitic
direction (meters atrophic).
Granulomatous metritis is found brucellosis in pigs, externalized
through miliary granulomas scattered throughout the mucosal surface.
6.3.3.6. Uterine tumors
Uterine tumors in domestic animals are common, often described
leiomyoma of the cows and cow uterine adenocarcinoma.
Leiomionul is diagnosed in about 85-90% of uterine malignancies
in dogs and cats.
Macroscopic, it can reach 10-12 cm in diameter. Initially, when the
tumor is small fleshy consistency then becomes firm or hard. Sectioning
surface is wet, glossy pink or white .
Microscopic, the tumor is composed of smooth muscle, anarchic
arranged in a mass of tissue.
Uterine adenocarcinoma is found in older cows after age 7 is
difficult to diagnose.
Macroscopic, in the form of multiple small nodules of firm, was
uniformly disseminated uterine horns compared with cervical uterine body.
It can reach up to 10 cm with a concentric arrangement, which causes more
narrowing of the lumen.
Microscopic, the cow's uterus c arcinomul schiros character,
infiltrative growth in the myometrium, being heavily vascularized. It grows
in deep uterine glands and contrast with normal structures.
151
6.3.4. Lesions of the vulva and vagina

Hypoplasia of the vagina, cervix agenesis as persistent hymen are
developmental disorders that are found in "white heifers disease."
6.3.4.2. Dystrophies of vagina
Dystrophies of the vulva and vagina have little significance,
represented by mucosal dystrophy and cystic (the cervix and Bartholin
Grtner channels) sometimes observed in cows.
Vestibulovaginale cervix and cysts represent cystic degeneration or
Bartholin's glands or glands channel chistizri Grtner (cysts are multiple
and symmetrically arranged on two parallel strings of one side of the center
line of the vagina).
Vaginal and cervical prolapse is characterized by the exit to the
outside of the vaginal and cervical sometimes including vulvar labia. It is the
consequence of increased intra-abdominal pressure by fetal volume.
increased timpanism etc.Is frequently found ante-or post-partum in gilts
before puberty, and the cows.
Macroscopic , the mucosa is swollen congested, edematous,
sometimes with necrosis more or less flat.
Vaginal bleeding and perivaginal are consequences of trauma
(vaginal fissures) caused by calving dystocic.
Vulvar edema is a common medical condition where consumption
of feed contaminated with Fusarium graminearum (fusariotoxicoz).
Macroscopic there is swelling and redness of the vulva sharp,
something only seen before puberty gilts.
6.3.4.5. Inflammation of the vagina and vulva
152
Inflammation of the cervix are called cervicitis, , vaginitis -ones of

the vagina ;;vestibule -, vestibulitis, of the vulva-, vulvitis, Bartholin's
glands-bartholinitis; Grtner's glands-, grtmetritis. Often they evolve
together, especially as vulvovaginitis.
Cattarhal vulvovaginitis is similar macroscopic, with inflammation
of other mucous membranes (catarrh, congestion, swelling).
Vesiculo-purulent vulvovaginitis , evolve macroscopic through the
mucosal surface appearance of red-yellow pustules, slightly protruding, that
the break or rise to erosions and ulcers. It meets in the equine coital
exanthema, and in
cattle in the complex infectious rhinotracheitis
-vulvovaginitis.
Purulent vulvovaginitis is characterized by the appearance of
purulent exudate in the ventral vaginal fornix. Occurs in cows, in
trichomoniasis and genital campylobacteriosis, and the sheep in vulvar north
side.
Necrotizing vulvovaginitis is a consequence of trauma and infection
with bacillus crushed tissue necrosis (Fusobacterium necrophorum), which is
normally found in the digestive tract through defecation pollutes the vulvar
labia.
Macroscopic necrotizing territories covered by yellowish-gray
pseudomembrane.
Vulvovaginal gangrenous, is more common in ruminants, as a
consequence of anaerobic flora (Cl. septicum, Cl. Perfringes), which thrives
in injured tissues (dystocia).
Macroscopically, there is a swelling of the vulva crackles that
rapidly invades neighboring regions. Mucosal surface is covered initially by
a seriousness yellow, and bloody, emitting an odor Ihor.
Follicular or granular vulvovaginitis is characterized by hyperplasia
of lymph nodes vaginal vestibular mucosa. It is caused by Mycoplasma sp.
Vulvovaginal granulomatous is seen in tuberculosis in cattle, but its
incidence is low. It usually occurs in the form of lumps and vulvar ulcers.
6.3.4.6. Tumors of the vagina and vulva
Vulvovaginitis tumors have a higher incidence in bitches. Are
venereal tumors of viral origin, known as Kaposi's Stickers. Tumors of the
vulva and vagina are similar in morphology to those of the penis and uterus.
6.3.4.7. Uterine tumors
153
6.3.5. Mammary gland morphopathology

6.3.5.1. Mammary gland abnormalities
Congenital anomalies of the mammary gland are observed more
frequently in cattle, represented by:
polimastie = nipels supernumerary;
- politelie and oligotelie = mameloame over or infranumerare;
hypotelie and hypertelie = mameloame shorter or longer;
- aplasia and hypoplasia of the lack of development mamma = total,
partial breast;
papillary duct aplasia or atresia = no, narrowing, or papillary
imperforarea channel.
Gynecomastia (gr. gynaikos = female; mastos = mamma) is
characterized by excessive growth of the mammary gland in the male.
6.3.5.2. Mammary gland dystrophies
Dystrophies of the mammary gland are called mastosis and
generally are likely protides (horny and colloids).
Mamelar epithelial hyperkeratosis is seen in cows and sheep, as a
consequence of mechanical milking, of hypovitaminosis A, a permanent
stress etc.
Colloid mastosis is manifested by arenacei corpus formation,
formations, concentric layers fully or partially impregnated with calcium
salts, as evidenced in the lumen acini or sometimes in ways galactofere
(aged).
Udder necrosis can be caused by physical factors (excessive cold),
infectious and toxic. Are observed in ruminants (cows and sheep especially)
and the other species (pigs).
Gangrene nipples of newborn piglets is determined by mycotoxic
estrogenism of sows (zearalenone), which favors the development of Cl.
perfrigens. The pigs died in the early days by enterotoxemia secondary to
anaerobic gangrene nipples.
Macroscopically, pigs survive, there is total or partial shortening of
the nipples, female in question is unsuitable for breeding.
154
Circulatory changes are represented by congestion, hemorrhage,

edema, thrombosis of mammary veins . They are dependent on the estrous
cycle and the act of parturition, and on the other hand, various diseases of
the female genital tract.
Mammary edema of special importance in dairy cows. He appears
physiological ante-and postpartum and can turn pathological edema. In
practice farming is considered a sign of good lactation period ahead.
Macroscopic the udder is enlarged in volume, paste, and the
thickened section shown connective stroma, gelatin, swelling due to fluid
citrine yellow color which is in excess.
Microscopic , there is transudation the presence of both the gaps
and the lumen of the mammary acid.
Breast edema is produced by neuroendocrine disorders. If you do
not withdraw udder edema after calving, it can turn into a pathological
edema, which is compounded with mastitis.
Breast edema following installs pathological disorders stasis,
arising from the growth in volume and weight of the udder that cause
compression of vessels departing from mamma.
6.3.5.4. Udder inflammation
Are called mastitis or mastitis, the nipples, telitis, and the milk
ducts, lactiferous. Mastitis etiology is varied, traumatic, toxic, hereditary,
mostly starring role of infectious factors. In terms of pathology, may be
catarrhal mastitis, serous, hemorrhagic, fibrinous, gangrenous, fibroblasts
and granulomatous.
Catarrhal mastitis
is the result of ascending infection,
inflammatory process affecting the epithelium lining of the milk ducts and
acini.
Macroscopic, the gland is enlarged in volume, turgid, and at the
nipples are found nodules of various sizes, representing sinuses lactifere
much dilated due to a serous exudate, fibrinous or purulent.
Microscopic epithelial desquamation observed in the lumen of the
milk ducts and acini, hyperemia and interstitial edema. This morphological
form can be found in the early stages of streptococcal mastitis of cows.
Mastitis serous or inflammatory edema is characterized by
infiltration of the subcutaneous tissue and breast gap with a serous exudate.
Macroscopic gland is enlarged in volume, asymmetric, and
consistency is increased. The section is wet, glossy due serous exudate.
155
Microscopic, there is the presence of serous exudate in the gaps

and secretory channels.
hemorrhagic mastitis is characterized by the appearance of
hemorrhagic exudate in the interstitial tissue, alveolar and milk ducts.
Macroscopic volume of the udder is enlarged, and on section has a
reddish dry. Both haemorrhagic mastitis and the serous, acute inflammation
are nonspecific nature.
Mastitis fibrin exhibited by mammary hypertrophy, and the section
is found predominantly fibrinous exudate, most abundant in the lumen of the
mammary cistern.
Microscopic is observed fibrinocelular exudate in the lumen of
acini ,in connective interstices, but especially in the milk ducts. Meets in
colibacillosis in cattle.
Purulent mastitis is caused by staphylococci and especially C.
pyogenes. In the acute form, evolve as catarrhal purulent mastitis, and
chronic form, forming abscesses or phlegmons. On section, the chronic
forms, it highlights a gray-whitish or greenish pus. Purulent mastitis caused
by C. pyogenes is known as mastitis or mastitis piobacilar or summer
mamitis.
Microscopic is observed initially in the presence of purulent
exudate in the lumen of the milk ducts and acini, and subsequently specific
mesenchymal reaction abscesses.
Gangrenous mastitis incidence has increased in sheep is caused by
Staphylococcus aureus and sometimes cows in infection with Cl. perfringes,
C. pyogenes etc.
Macroscopic udder is hypertrophied, red-violet, and the notes
section serohemoragic rich edema, which affects the connective tissue under
the skin and breast parenchyma.
Gangrenous mastitis of sheep and goats is deadly trend. The sheep
that resist infection, gangrene area is deleted (amputation or mutilation of
spontaneous mammary gland).
Microscopic mammary acini are necrosis, lysed and the gaps are
noted congestion, edema, hemorrhage and thrombosis.
Fibroblasts Mastitis is usually the result of chronicity of acute
mastitis, exudative. It is found in the second phase of streptococcal mastitis
in brucellosis, and other chronic infections. Initially, there is hyperplasia in
milk ducts lumen and subsequently progresses to fibrosis process. The newly
formed tissue mass is noted rare islands of glandular acini.
Macroscopic udder is reduced in volume, consistency is greatly
increased, and cutting is difficult.
156
Frequent use of antibiotics to treat mastitis mastitis occurrence

favored allergic conjunctiva manifested by a proliferation predominantly
eosinophilic, something for which they are also called "eosinophilic
mastitis."
Granulomatous mastitis can be found in tuberculosis, the fungus,
or staph infections. Granulomatous mastitis progresses, microscopic,
predominantly nodular.
All morphological forms of mastitis is accompanied by
inflammation of the mammary lymph nodes.
6.3.5.5. Mammary gland tumors
Mammary gland tumors are common in dogs and cats appear
sporadically in other species.
Clinical breast tumors appear as single or multiple nodules in the
parenchyma, with or without nipple involvement. Give rise to metastases in
mammary lymph nodes, liver and lungs. (3, 5, 11, 16, 19, 42, 44)
6.4. Morphopathology of birds female genital system
Congenital anomalies can be represented by hypoplasia congenital
cysts or genital infantilism.
Congenital cysts are located on the right side of the cloaca are
pedunculated and various sizes. They are reminiscent of the right channel of
Mller. Large cysts may cause compression atrophy of the digestive organs,
resulting in cachexia syndrome.
Genital tract hypoplasia that it remains in a state of "infantilism" is the
result of poor nutrition in chickens.
6.4.2. Ovarian dystrophies
Ovarian dystrophies are represented by the cystic degeneration and
yolk and the oviduct lumen is observed pseudoconcremente eggs, soft eggs
and training without lime peel.
Yolk dystrophies is found in vitaminoza A, E in Salmonella
infections in prolonged use of coccidiostats, etc.. Whatever the causes, there
is hyperpermeabilisation of the membrane of sacs ovarian .
157
Macroscopic the yolk sacs are reduced in volume, lack of tone,

sometimes pedicle containing semifluid, brownish-green color. Most times,
softening leads to membrane rupture of vitelul in ovarian sacs, followed by
pouring into the peritoneal cavity.
Follicular cystic dystrophy is characterized by vitelus resorption
and its replacement with a transparent albuminous fluid.
Macroscopic ovarian sacs are 2-3 times increase in volume, usually
pedicles (ovarian pedicles elongate ovisacilor underweight).
Egg pseudoconcrements are the result of the oviduct segmentation
dyskinesias caused by power failures or induced by various infectious agents
(coli, salmonella, etc..). Dyskinesias oviduct, followed by inability to
eliminate eggs and their accumulation in the lumen. After the portion of the
oviduct at which the atonia, pseudoconcrements may be predominant
- vitelogene consisting only of vitelus, the color yellow;
- albuminogene formed only in albumen, whitish;
mixed set of calves in, albumen and limestone.
Macrososcopic, they are impressive sizes (10-20 cm diameter)
with different structure, depending on the portion in which the atony.
Oviduct mucosa atrophy, and in more serious cases, the wall is the only who
can break resulting in serous yolk peritonitis.
6.4.3.
Topographic changes
Oviduct prolapse is a topographic change observed in female

genital laying hens. Oviduct mucosa, externalized, is congested and
hemorrhagic necrosis more or less flat.
Prolapse oviduct ends mortality (20%) or favor the emergence of
cannibalism, behavioral syndrome manifested by pinching the sick birds by
healthy birds . A special role in the development of prolapse oviduct estrogen
plays syndrome, especially in turkeys caused by rich feed zearalenone
(fusariotoxicosis).
6.4.4.
Female genital inflammation in birds
Female genital inflammation are particularly common in birds, both

the ovaries or oophoritis externalized and by salpingitis.
Ovaritis are the result of food deficiencies, or can be caused by
various infectious agents: Salmonella, colibacili, pasteurele, mycoplasma,
staphylococci, streptococci, etc. infectious bronchitis virus.
158
Macroscopic ovaritis are difficult to diagnose because the issues

are very similar to the morphology of ovarian dystrophies. Red-brown or
greenish appearance of bags and ovarian pedicle of variables lenghs are
indicative elements for inflammatory processes.
In acute developments fibrinous exudate is noted, hemorrhagic or
purulent, covering and infiltrating ovarian bags and occupies the space
between them.
Correct diagnosis is established by microscopic examination. The
developments longer (salmonellosis) and ovaries are found chronic atrophic
type (atrophic ovaries).
In most cases, the ovarian sac membrane rupture content flows into
the peritoneal cavity giving birth to yolk peritonitis.
Salpingitis have similar etiology to the ovaritis and pathology may
be catarrhal, hemorrhagic, pseudomembranous, hyperplastic and
granulomatous.
Catarrhal salpingitis is the most frequent diagnosis but its
importance is very low.
Hemorrhagic salpingitis is characterized by outbreaks of
hemorrhagic infiltration in the caudal segment of the oviduct. It meets in the
summer months, only individual sector, led by infestations with
prostogonimus sp.
Pseudomembranous salpingitis
evolves superficial with the
emergence of yellow casts in the lumen of oviduct, being observed
micoplasmosis youth and adult colibacillosis in chickens.
Hyperplastic salpingitis externalizes the outbreak of mucosal
hyperplasia in thickness and sometimes even muscular, resulting in motility
disorders of the oviduct, which facilitates formation in the lumen of the
oviduct eggs pseudoconcrements. Hyperplastic salpingitis is responsible for
the appearance of a high proportion of eggs with rough bark, strangled, or
fissure (avian infectious bronchitis feature). It is also found in salmonellosis,
mycoplasmosis, viruses etc.
Granulomatous salpingitis occurs more frequently as inert foreign
body inflammation, caused by the remnants of shells stored in thick mucous
membranes and less frequently, such as infections, and tuberculosis seen
only in the individual. In both cases, the correct diagnosis is established by
microscopic examination.
6.4.5. Female genital tumors in birds
159
At the ovary level is found frequent location Marek's disease in

young (4-6 months) and at adult sites of avian leucosis (sarcomas and
adenocarcinomas).
Rarely, can be identified and ovarian cystic adenomas. In the
oviduct, in adults can be seen fibromas of the oviduct ligaments. (5, 11, 16,
19, 41, 43, 46)
7. The morphopathology of nervous system

7.1. Nervous system abnormalities
Malformations of central nervous system are the result of primary
disorders regarding the nervous tissue development and "closing defects"
(disrafiile) of the skull or spinal canal.
Anencephaly is the complete absence of encephalitis, associated or
not with acrania, lack of development of the skull.
Microcephaly characterized by very low volume of encephalitis. It
may relate to all or only body segments (cerebellum).
Cerebellar hypoplasia is one of the most common malformations of
the nervous system as a result of viral infections, or copper deficiency in
sheep and goats.
Amelia is the absence of the spinal cord that is associated with
anencephaly.
Agir, microgiria, macrogiria are changes in brain circumvolutions
(absent, low, or higher than normal).
Porencephaly is the lack of a circumscribed portion of the cerebral
hemispheres, which is replaced with a clear liquid, resulting in a cavity
pseudocyst. It is most frequent in calves and lambs.
Cranioschizisul or ne-closure of the skull favors herniation of a
portion of the meninges - meningocele (gr. meninx = membrane + kele =
hernia) or the meninges and part of the forebrain, called anomaly
meningoencefalocel.
160
Rahischisisor Spina bifida is the lack of closure of the spinal canal

with or without a skin crack.
Congenital Hydrocephalus is an excessive accumulation of fluid in
the brain ventricles c (internal hydrocephalus) or subarachnoid cavity
(external hydrocephalus), both resulting in atrophy of the cerebral
hemispheres. Does hereditary in calves and some breeds of dogs.
7.2. Injuries of meninges
7.2.1. Meningeal dystrophies
Meningeal dystrophies are defined anatomically and histologically
in all species.
Calcar dystrophies or meningeal calcification is observed in the
structure of the dura-mater especially in dogs, cats, chickens.
Macroscopic we find large areas, or hardboard, pearly-white.
Microscopic it is noted mainly calcareous impregnation connective
fibers which will cause spleen and cranial nerve compression in places
where crosses meninges.
Cholesterinc dystrophy or colesteatosis, apears in the choroid
plexus structure in the form of granules or of larger formations, pearly-white
color.
Occurs in older horses as a result of deposition of cholesterol esters.
Melanic dystrophy or meningeal melanosis is seen in lambs and
calves for slaughter comes as a surprise. externalized by blackish-brown
spots (melanosis stained).
Microscopically, we can identify hyaline and amyloid dystrophy, but
their practical significance is reduced.
Meninges circulatory changes manifested by hyperemia and
hemorrhage with generally traumatic etiology or poisoning.
Bleeding after issue, are: bruising, or hematoma suffusions and by
location: epidural, subdural, subarachnoid and subpiale.
7.2.3. Meninges inflammations
Inflammation of the meninges are known as meningococcal
meningitis. After un meningitis, they can be pahimeningitis, duramater
161
predominantly affects the inflammation process, and the inflammation is

located at the arachnoid and the skins m ater.
After location, meningitis include: brain, spinal cord and
cerebrospinal and morphological point of view, they are:
exudative, fibrinous, hemorrhagic, purulent;
productive (fibrous and granulomatous ).
Because of the close link with the nervous tissue of the meninges,
meningitis inflammation changes with this form of meningoencephalitis,
meningomielitis or meningoencefalomielitis.
7.2.4. Meningeal tumors
Are called meningiomas and meningeal tumors are relatively rare
in veterinary medicine.
Meningiomas were diagnosed in cats and dogs in the previous dorsal
forebrain.
Macroscopic the tumor can be round, oval, flat or lobular, firm
consistency and white-gray.
Microscopic has less uniform structure with complex layout and
fibroid endoteliomatoase areas that may prevail in each case. The average
age of occurrence in cats and dogs was 10 years. (5, 11, 16, 19, 41, 43)
7.3. Brain and spinal cord injuries
Forebrain atrophy occurs as secondary lesions, mainly due to
compression (inflammation, tumors, hydrocephalus, parasitic cysts,
meningeal fibrosis and calcification, etc..
Macroscopic, the brain is reduced in volume, yellowish-white color
and design circumvoluiilor brain is altered.
Dystrophies of the nervous system can affect all three structural
elements of nervous tissue: neurons and nerve fibers nevroglias. They are
called encefalosis for encephalitis, neuromielosis on the spinal cord, axonal
dystrophy or if nerve branches. All dystrophies of nervous system are
particularly important, their diagnosis being established only by microscopic
examination.
The nerve cells can be observed cytoplasmic damage manifested
by:
- tigrolysis depolymerization tigroizi corpus RNA (Nissl);
162
- fibrilolysis, melting neurofibrils;

- vacuolar dystrophy observed in most poisonings and infections
(scrapie sheep, subacute spongiform encephalopathy in cattle - esste).
Axonal dystrophy is particularly remarkable in the structure of
peripheral nerves, manifested by the gradual disappearance of axonal
structure , from nerve cell to the periphery, called Wallerian degeneration.
Hyaline dystrophy. In the structure of blood vessels, particularly in
forebrain in pigs, there is the hyaline vascular walls dystrophies caused by
hypovitaminosis E (microangiopathy diet).
In old animals can be identified vascular amyloidosis.
7.3.2. Nervous system necrosis

Central nervous system necrosis occurring as a result of poisoning,
after stopping by thrombosis or embolism the arterial blood pressure. They
defined by the term macroscopic softening.
Macroscopic cerebral senility, based on the etiology and the
mechanism may be red or yellow. Both forms are characterized by
pathological decrease consistency.
Red softening occurs after trauma caused by parasitic larval
migration (acute form). In necrotic areas exhibited by impregnation with
blood and its degradation products.
Yellowish softening it is found in subacute and chronic
developments in which the nervous tissue liquefaction is associated with a
slight vascular response .
Occurs in enzootic ataxia of lambs, calves corticocerebral necrosis
in lead poisoning in cattle.
To define necrosis of nervous system with microscopic substrate,
on the topographic name of the affected tissue is added the suffix malacia
(eg, brain or spinal malacia).
Encephalomalacia of the animals are found in primary or secondary
copper deficiency (enzootic ataxia of lambs) in hypovitaminosis B 1
(necrosis polioencephalomalacia corticocerebral of
calves) in
hypovitaminosis E (encephalomalacia of chickens).
7.3.3. Changes in blood flow
163
Changes in blood flow of the nervous system are represented by

congestion, edema and hemorrhage.
Stroke outwardly by dilating meningoencephalitis nerve giving a
reddish substance.
Cerebral edema is the accumulation of transudate in the
subarachnoid spaces, perivascular brain ventricles and the cerebral
substance.
Macroscopic , the brain appears wet, shiny, glassy reflections due
to a liquid is present in the trenches gray hemispheres (the appearance is
significant swelling only six hours after death).
Microscopic the cerebral edema is observed broadening VirchowRobin spaces, vacuolation and sponginess nerve substance spongy
appearance.
Cerebral hemorrhages are the result of vascular rupture . They have
traumatic etiology, toxic or infectious, and after locations include:
intracerebral, intraventricular and intraspinal intraependimare.
Macroscopic, there is petechiae, in particular in the small
hemorrhages in the white matter, or blood clots in the major bleeding.
7.3.4. Changes in cerebrospinal fluid circulation
Circulation changes of cerebrospinal fluid is manifested by the
accumulation of excessive amounts of CSF in the brain ventricles or
subarachnoid space, causing internal hydrocephalus respectively external.
Macroscopic the encephals shows an image of enlarged brain. The
section is observed widening and thinning of the cerebral hemispheres
ventricles from white matter.
7.3.5. Encephalon and bone marrow inflammation
Inflammations of the encephalon are called encephalitis the ones of
the marrow are called myelitis and the ones of the entire nervous sitem are
called encephalomyelitis. Predominant localization of inflammation in white
matter is defined by the terms of leucoencephalitis, respectively
leucomyelitis and for gray matter inflammation, use words polioencephalitis
respectively poliomyelitis.
If they are contained in both the gray and white matter, the
inflammation is defined panencephalitis. Inflammations of forebrain may be
extended to the meninges and vice versa, reasons for them will be described
164
separately, because in practice they play together as a meningoencephalitis,

or even meningoencephalomyelitis..
Etiology, such as encephalomyelitis can be toxic, infectious,
parasitic, traumatic, etc..
Pathology
can
distinguish
the
following
types
of
meningoencephalitis: bleeding serofibrinoas, purulent thromboembolic ,
Haemorrhagic meningoencephalitis are exhibited by outbreaks of
hemorrhagic infiltration associated with softening of nerve substance. It is
found in anthrax in sheep in viral arteritis horse and especially infectious
meningoencephalitis of horse. In sheep, the parasitic larval migration (eg
Coenurus cerebralis) shows a bleeding or hemorrhagic, necrotizing
encephalitis.
Serofibrinous meningoencephalitis
is characterized by
accumulation of fibrinous exudate especially in meningeal spaces. Found in
Glasser's disease in piglets, caused by Haemophilus parasuis (alone or in
combination).
Purulent meningoencephalitis develops usually in the form of
single or multiple abscess, phlegmon.
Macroscopic foci stands yellowish or gray, reddish ring bounded
by a generally small. Found in listeriosis, streptococci, staphylococci, etc.
corynebacteriosis.
Microscopic in listeriosis in acutely monocytes predominate, while
in listeriosis subacute and pyogenic infections predominate flora neutrophil
granulocytes.
Thromboembolic meningoencephalitis
outwardly through
necroticohaemorrhagic outbreaks on the surface and in depth. Microscopic
necrotizing meningoencephalitis is highlighted, and exudate perivenously
vein thrombosis. It is found in thromboembolic meningoencephalitis in
cattle, caused by Haemophilus somnus.
Lymphohistocytic meningoencephalitis, are the most important
inflammation of the nervous system. They are found in all neurotropic and
pantrope virosis as well as is toxoplasmosis, clamydiosis, etc..
Macroscopic lesions are uncharacteristic, manifested by
meningoencephalitis vascular congestion, edema and increased CSF etc.
Microscopic, under the influence of agents, it is found
characteristic changes evident in the structure of nerve cells and the blood
vessels.
Neurons suffer irreversible degenerative processes and become a
non-self to the body. They are surrounded by gliocite, called satelitosis stage.
165
Then gradually degenerating neurons by phagocytosis is achieved with the

neuronophagia appearance.
At the capillary level is found swelling of the endothelium and /
or congestion in Virchow-Robin space of local cells migrated from the
bloodstream, making the appearance of perivascularitis or perivascular
sleeves that will cause narrowing or obliteration of the lumen and
compression atrophy of adjacent nervous tissue.
In neurotrope virosis, along with neuronal degeneration in the
cytoplasm and / or nucleus are shown corpuscles viral various shapes and
sizes generally oxifili, pathognomonic for certain diseases (rabies, terminal
disease, Aujeszky's disease, etc..).
In subacute and chronic forms, if the animal survives, the
lymphohitocytic inflammation progresses to fibrosis.
Eosinophilic meningoencephalitis shown diagnostic importance in
NaCl poisoning in swine, and where parasitic larval migration. It is
characterized by the appearance of leukocyte infiltration, predominantly
eosinophilic perivascular nervous tissue and meninges structure.
Fibrous meningoencephalitis are the result,of chronicity other
forms of meningoencephalitis. It is characterized by hyperplasia congestivoglial outbreaks of softening of the brain, associated with thickening by
fibrosis of the meninges. Found in the hens passed through Newcastle.
Granulomatous meningoencephalitis may be of infectious parasitic,
or fungal. In tuberculosis in cattle (calves) have compact structure
granulomas (nodular), while in the parasitic infections of cystic granulomas
are found (eg cenuroza sheep, swine cysticercosis and echinococcosis in
cattle).
The literature mentioned demyelinating and allergic encephalitis.
Allergic encephalitis is found in dogs after rabies vaccination, due to the
formation of an excess of antibodies .
Microscopic plasma cells in the presence of glial nodules and
perivascular sleeves are key elements suggestive of this lesion.
Demyelinating encephalitis is characterized by large areas of
demyelination (see dystrophies lipid complex) seen in some forms of
distemper in sheep Visna in infectious meningoencephalitis in old dog. In
these diseases antimyelin antibodies were detected. (5, 11, 16, 19, 41, 43,
47, 48)
7.3.6. Nervous system tumors
166
Nervous system tumors in animals were considered, until recently,

as low-incidence. Comparative Oncology mention a higher incidence of
nervous system tumors in dogs.
The dog breed Boxer, English Bulldog have a higher incidence of
gliomas, which are twice more to meningeal or peripheral nerve tumors,
especially at the age of 10-14 years.
The most common neuroglial tumor of the nervous system is
astrocytoma was localized mainly in the cerebral hemispheres, and the
thalamus, hypothalamus, cerebellum, etc..
Macroscopic astrocytoma has variable dimensions and consistency
can be from soft to firm. The rapidly growing section are edematous, with
hemorrhage and necrosis.
Microscopic
differ
differentiated
and
undifferentiated
astrocytomas.
We mentioned tumor diseases system very often enzootic bovine
located around lumbosacral spinal cord. (5, 11, 16, 19, 41, 43)
7.4. Nerve damage
Nerve atrophy may be due to compression effects or the result of
toxicities, poisonings, deficiency (Hypovitaminosis A, B 1, B 2), etc.. The
most notable is the nerve myelin, which is found low levels of myelin sheath
of Schwann cells and multiplying.
Fucosidosis nerve dystrophies are represented by Walerian and
Gudden degenerations.
Fucosidosis dystrophy is a hereditary carbohydrate, found in dogs.
Macroscopically manifested by thickening the vagus nerve, as well as other
cranial and spinal nerves.
Walerian and Gudden dystrophies recognize same causes and
evolve under the same conditions as in the central nervous system.
Necrosis of peripheral nerves can be caused by trauma (bruising,
lacerations, accidental nevrotomii), the physical, chemical or infectious. The
process starts with the disappearance of the myelin sheath, the sheath of
Schwann, the nerve being gradually replaced by fibrous connective tissue.
Microscopically it is found damaged nerve related muscle necrosis.
7.4.2. Nerve inflammation
167
Nerve inflammations are called neuritis, nerve root, radiculitis, and

the lymph, lymph or ganglionevritis. Neuritis may have unique locations
(mononeuritis) or multiple (polyneuritis), and from an evolutionary
standpoint may be: acute, subacute and chronic.
More often meet radiculoganglionitis. They accompany central
nervous system inflammation.
Pathologically, are different forms of neuritis following: serous,
hemorrhagic, purulent .
Mention the so-called "neuritis of the cauda equina" which is a
pathological progressive radiculoganglionevritis characterized by
inflammation and demyelination of the cauda equina nerve (fillum
terminals), caudal spinal cord.
7.4.3. Nerve Tumors
Nerve Tumors of proliferation concern or amielinice myelinated
nerve fibers, the sheath of Schwann and connective tissue of nerve structure.
Schwannoama or neuroma is the sheath of Schwann cell tumors.
Macroscopic stands whitish nodular or fusiform thickening of the
nerve, and microscopic sheath of Schwann cells are arranged in palisade.
They are more common in cattle, dog brachial plexus in thoracic
nerves and acoustic nerve. Sometimes its malignancy and invasiveness and
metastasis in the lungs.
In birds, note the presence of tumors in Marek's disease (as nervous)
in the line of nerves: sciatic and brachial etc. Macroscopically, there is
cilindroide thickening or nodular, whitish, with greasy on character section.
Microscopically, the lesion is predominantly initial inflammatory
that ultimately turn into a lawsuit tumor (schwannoma).
Neurofibromas are tumors of connective tissue in the nerve
structure. They can be single or multiple peripheral nerve damage,
(neurofibromatosis). Most affected are the nerves of the brachial plexus,
intercostal nerves, cardiac nerves, spleen, etc..
Macroscopically, the brachial plexus can achieve size tails like a
hatchet, and nerves on the bodies of a finger, both locations have numerous
nodular proliferation on their path.
Microscopically observed fascicular connective tissue hyperplasia,
nerves are reduced or absent. In neurofibromatosis cattle in tumor structure
appears gelatinous material, bounded by fibrous tissue with persistent nerve
fibers. (5, 11, 16, 19, 41, 43)
168
8. Pathologically skin and sense organs

8.1. Skin lesions
8.1.1. Congenital anomalies of the skin and appendages
Congenital anomalies of the skin is manifested at birth by
incomplete form of the skin, absence of hair or skin pigmentation disorders.
Mentioned as important following developmental disorders:
Skin aplasia (gr. a = without, plaissein = to form) (epiteliogeneza
imperfect) is a hereditary anomaly resulting from an autosomal recessive
gene, frequently observed in calves and piglets.
It is exhibited by the appearance of areas where skin is missing,
located in calves more frequently in distal limb in piglets may be more
affected body regions (head, back, thighs, etc..). Territories in which the
epidermis is absent causing death quickly becomes infected animals.
Congenital ichtiosis (gr. ichtys = oz = fish and noninflammatory
disease) more common in calves and dogs, is a generalized or localized
hyperkeratosis.
Macroscopic outward by thickening the form of plates horny
hairless, including deep cracks, imitating the appearance of fish scales.
Alopecia (Gr. Alopex, alopecis = fox atrich oz or atrichia defines the
absence of hair or wool on areas of varying sizes (eg lines of mice, rats and
nude rats used as experimental animals).
Domestic animals, alopecia is found in piglets, foals, calves,
puppies. May be localized or diffuse.
169
Albinism (Gr. melas = black) is a form of congenital achromat

skin, hair and iris due to lack of melanin pigment. It can be localized or
generalized. It is an inherited disease.
Melanosis is a hyperpigmentation of the skin, most commonly seen
in dogs, particularly in the form of circumscribed (melanosis stained).
8.1.2. Skin dystrophies
Dystrophies are called dermatitis skin. They can be predominantly
epidermal and predominantly dermohipodermice.
8.1.2.1. Dermatoses pre dominant epidermal

Predominantly epidermal dermatosis are represented by
discheratosis and discoloration.
Discheratosis are disorders of cornification process and is
manifested by hyperkeratosis and paracheratosis.
Hyperkeratosis (gr. hyper = more; Kerasia = horn + oz) can develop
diffuse or circumscribed, with the latter may take the form of callousness,
plates, or cutaneous horns, seen especially in ruminants and horses.
Macroscopic, the skin is dry and thickened (leather).
In dogs, state workers digital hyperkeratosis (bearings planting) to
"strong heel disease" and muzzle skin observed after distemper virus
association with staphylococci and streptococci.
Parakeratosis (gr. para = beyond + Kerasia = horn + oz) is
characterized by thickening of the horny layer of the epidermis, but cell
cornification is incomplete, resulting in a soft corn. The disease occurs most
commonly in piglets with deficiency etiology, no zinc, hypovitaminosis A,
etc..
Macroscopically observed initially reddish areas, then brown and
finally, crusting, located at the distal limbs, head, tail, ventral side of the
abdomen, etc..
The skin parasites and dermatomycosis preserved are secondary
hyper-and parakeratosis.
Discoloration (Gr. dys = unpleasant, chroma = color) or acquired
pathological pigmentation are: leucoderma, vitiligo and mugs.
Leucoderma (gr. leukos = white, derma = skin) occurs as a result of
wounds, radiation, infectious or parasitic diseases, while vitiligo is a
170
discoloration of neuroendocrine nature. Both processes are a zonal

depigmentation of the skin, called "white skin".
Noggin (Latin canus = gray) depigmentation or whitening hair is
more or less obvious. This occurs skin diseases, generally, or as a
consequence of aging. (5, 11, 16, 19, 41, 43)
8.1.2.2. Dermatoses mostly dermohypodermic
Dystrophies predominantly dermohypodermic are represented by
pachyderm and cutaneous calcinosis.
Pachyderm (gr. pahy = thick dermis) is characterized by a marked
thickening of the skin due to dermal connective tissue hyperplasia.
Injuries occur after lacunar circulation stasis, which facilitates
precipitation fundamental substance .
Dermal calcinosis is calcification circumscribedof the connective
tissue under the skin, in the form of hard nodules, single or multiple,
frequently located in the extremities (limbs).
Sometimes, the lesion may evolve as generalized calcinosis. It has
been described in dogs.
8.1.3. Gangrene and skin necrosis
May consider use of the term corresponding to skin gangrene,
tissue necrosis as defined in direct contact with the external environment,
and the necrosis may be used only for subcutaneous fat mortification.
Skin gangrene stands in all species in
fusariotoxicosis,
leptospirosis and swine in chronic rujet and necrobacillosis.
Weakened animals with chronic diseases, sores prolonged dry
gangrene will appear in the right areas of bony prominences (eg coxal tuber,
art. Temporomandibular art. Coxofemoral) due to compression of the skin
between the bone and the supporting surface.
In longest developments, the gangrene is off and remove, leaving
uncovered the deeper layers (muscles, joints, bones), inflammatory processes
occur.
8.1.4. Changes in skin circulation
Circulatory changes of the skin may occur as a result of local
circulation disorders, or be externalization of general diseases. They are
represented by hyperemia, hemorrhage and edema.
171
Skin redness or erythema (Gr. erythema = redness) occurs

frequently in pigs in different toxic or infectious disease known as the "red
disease" (fever, rujet, acute salmonellosis). In active hyperemia, skin color is
bright red, while passive hyperemia, skin color is red-purple (cyanotic
aspect) and include large areas or entire organ surface.
Skin hemorrhages occur in various animals for poisoning,
infectious diseases, some allergic conditions, from insect bites, etc..
Hypopigmented animals, conspicuous hemorrhages are as bruising,
petechiae, vibices (when the linear form) and hematoma when forming
deeper (dermis or hypodermis).
The presence of bruising or petechiae all over the body in pigs,
called purpura and thrombocytopenic purpura observed izoimune of piglets
(see general part).
In warfarin poisoning in dogs and cats are found extensive
hemorrhage subcutaneous connective tissue, especially periarticular.
Skin Edema is the expression of tissue fluid movement disorders,
which occurs in toxic states, allergic, infectious, in dysproteinaemias in
endocrine disorders, etc..
Skin edema may be limited to certain physical areas, such as:
eyelid edema, the edema disease in pigs.
- chin edema in chronic pasteurellosis in poultry.
- abdominal edema, scrotal edema, or the localized limb when called
elephantiasis.
Sometimes edema is invading nature, encompassing multiple
regions or even the entire body surface, a process called anasarca (gr. ana =
through, over + Sark = meat).
Microscopic skin edema may be localized to the dermal papilla and
corresponding epithelium or connective tissue under the skin. (5, 11, 16, 19,
41, 43)
8.1.5. Skin Inflammation
Dermatitis is the primary inflammation of the skin and exanthema
is a secondary dermatitis characteristic to an infectious disease and appears
as macules or papules.
From the evolutionary point of view, they may be acute or chronic
and as interesting layers can be superficial and deep dermatitis. After
predominance of structural changes, dermatitis dermatitis can be classified
into: epidemic, allergic, exudative, productive, parasitic and photosensitivity.
172
8.1.5.1. Dermatitis epidemic

Dermatitis or e xantemele are secondary inflammation of the skin
that occur in diseases of the body that: foot-Vario, eczema contagious,
piglets salmonellosis. Exanthema evolving stage in the form of: macula,
papule, vesicle, pustule and crust.
The macula is a red spot, due to congestion in the dermal papilla.
Papule appears as a projection of the skin, due to the serous
exudate which penetrates through the stratum spinosum cells producing at
the same time and their balloning degeneration.
Microcavity intraepidermal vesicle is formed by the confluence
rupture cell membranes and liquid contents of several cells degenerate.
When vesicles are small, like the bubbles, called pemphigus (gr. pemphix =
bubbles, blisters).
Pimple occurs due to leukocyte diapedesis of dermal vessels in
vesicle content, the liquid became white and cloudy.
Scale is a yellow or brown film, which is formed by breaking the
extravasated pustules and coagulation liquid along with dirt and grease
particles existing on the surface of the skin.
Compared to classical dynamics exanthema in some diseases found
some evolutionary features.
Thus, veterinary pathology is identified:
- vesicular exanthema - prevails in foot;
- papular exanthema - pustular - is found in sheep pox;
- exanthema varioloid - as blackish bumps due to the penetration of
erythrocytes in epidermal blistering (eg swine subacute, chronic
salmonellosis);
- exanthema acanthosis - manifested by marked hyperplasia of
epidermal cells (eg myxomatosis rabbit pox in birds).
8.1.5.2. Allergic Dermatitis
Allergic dermatitis, atopic eczema, skin inflammation substrate are
immune, recurrent reactions characterized by eruptive dermoepidermice
accompanied by accumulation of varying amounts of IgE in circulation and
skin structure.
In terms of topography, eczema can be interdigital, scrotal, the
eyelids, corners etc. beak birds.
Morphoclinical, eczema can evolve in different ways:
173
erythematous;
papular;
vesicular
pustular or impetiginoase (they participate and pyogenic flora);
crusted;
scvamoas e (pronounced desquamation evolving);
warty, externalized by the appearance of skin growths;
lichenoid characterized by cracking cornified epidermis.
Hives (Latin urtica = stinging nettle) is an immediate-type allergic
dermatitis, caused by some toxic, insect bites (hives exogenous) or may be
due to ingested or inhaled produced by animals (hives endogenous).
Macroscopically observed itchy patches and blisters at the contact of
the agent sensitized and affected skin area.
8.1.5.3. Exudative dermatitis
Exudative dermatitis are represented by purulent and gangrenous
inflammation.
Or purulent dermatitis pyoderma by location can be superficial and
deep.
Superficial suppurative dermatitis.
This category is part intertrigo and impetigo.
Intertrigo (Latin inter = between and Terere = a fruit) is purulent
inflammation of the skin of the folds or pleats. Macroscopically observed
with depilation and reddish areas covered by an exudate seropurulent,
smelly.
Pyodermatitis in this category is noted in the folds of obese animals,
the dogs of the labial folds Cocker, the Pekingese and Bulldog facial folds.
They are of infectious origin (bacteria, fungi, yeasts) are favored skin
moisture (sweating).
Impetigo (lat. = ringworm ringworm) is characterized by the
appearance of blisters on the skin surface (microabscesses) in the stratum
corneum of the epidermis, that burst and form crusts content clots.
It is observed in distemper in puppies and adult dogs is likely to
traumatic plus pyogenic germs (staphylococcus, streptococcus).
Deep purulent dermnatitis are is characterized by purulent exudate
in all layers of the skin (epidermis, dermis, hypodermis). From this category
includes: folliculitis, furuncle and phlegmon.
Folliculitis (lat. folliculus = bag) is a purulent inflammation of the
hair follicle root.
174
Observed macroscopically small pustules, centered by a hair and

surrounded by a ring failure. It is produced by pyogenic microbes (eg,
staphylococcus) or fungi.
Boil (lat. furunculus = Carbuncle) is a purulent inflammation of
hair follicles and perifollicular structures (follicle pilosebaceu) produced by
staphylococci. It is found most commonly in pigs, dogs and horses.
The boil should never be handled, pressed to remove pus may
cause (risk of dissemination of microbes).
Phlegmon (gr. phlegmon = phlegmon) or phlegmonous dermatitis
is diffuse purulent inflammation of the skin and subcutaneous tissue that
may extend to skin necrosis. and sometimes has a tendency to invade large
areas as phlegmon not as abscess. Worst danger is septicopiemia.
In a few cases, purulent dermatitis can evolve and form deep
abscess subcutaneous tissue disorders more common in piglets.
8.1.5.4. Gangrenous dermatitis
Gangrenous dermatitis is the consequence of the anaerobic germs
of the genus Clostridium.
Javartul skin of horses and cattle belong to this category.
Macroscopically, after removing necrotic areas remains the ulcer,
covered with a purulent exudate Ihor odor. The process is localized mainly in
the limbs (pastern, coronet, and interdigital space).
8.1.5.5. Dermatitis productive
Productive dermatitis are represented mainly by granulomatous
inflammation encountered in various diseases such as tuberculosis,
actinobaciloza, glanders, fungi etc. Their pathological aspects we present in
the above mentioned diseases.
8.1.5.5. Parasitic Dermatitis
Parasitic dermatitis exhibited pathological picture very different as
they are determined by a large number of ectoparasites.
Psoriasis (psoriasis Gr = itch) is an erythematous, scaly dermatitis
with chronic evolution, manifested by pronounced stratum corneum
exfoliation, redness and scaling. The etiology is unknown, seems to have the
issue one way to skin a particular reaction.
175
The disease is rebellious to treatment, recurrent, is exacerbated by

infections or strong emotions.
Other parasites may produce dermatitis:
- free products, mosquito bites, flies, fleas;
- mitching caused by different types of Heaven (scabies);
- granulomatoase seen in habrenomosis of horses and cattle
hyperdermosis.
Macro-and microscopic aspects will be presented in the section on
parasites.
8.1.5.6. Photosensitivity dermatitis
Photosensitivity dermatitis (photodynamic or solar) is inflammation
of the skin caused by the action of sunlight (UV) by photodynamic
substances stored in the skin. It is found mainly in cattle, pigs and cats
depigmented skin.
Macroscopically, depigmented areas, depending on the duration of
exposure to the sun is observed following lesions: erythema, papules,
vesicles, crusting, scaling epidermal flaps and ulcers. (2, 5, 11, 16, 19, 41,
43)
8.1.6. Skin Tumors
There are many skin tumors, both benign and malignant tumors
observed in all species, in particular in dogs, horses, cattle, and cats.
Among benign tumors, we mention:
papillomatosis in cattle;
- fibroidsin horse (grows in areas that come in contact with
harnesses);
- adenoma is much rarer and found the dog in the perianal region.
Among malignant tumors mention:
- epidermioid carcinoma (squamous cell) observed in horse, dog and
cattle, especially around the natural orifices;
- melanomas encountered, especially in horses, in the form of
subcutaneous nodules.
8.2. Visual organ lesions
176
To understand more easily the visual apparatus morphopathology

,we present separately eyeballs llesions and then the ones of eye accessories
organ
8.2.1. Injuries eyeballs
Development of congenital anomalies are:
anophthalmia (total absence of the eyeball);
microphthalmia (small eye socket);
- cyclopia (presence of only one eye sitting on the median plane of the
head).
They are more commonly observed in piglets originating from
sows deficient in vitamin A.
An congenital omaliile position eyeballs are:
protruding eyeballs are out beyond the orbit;
enophthalmos is moving eyeballs in deep orbit.
Strabismus defining the visual axis of the eye deviation, or both, to
normal the axis of the species.
These are:
convergent when the focus is shifted towards the midline;
- divergent when the optical axis is tipped out.
8.2.1.2. Dystrophies of eyeballs
Dystrophies of eyeballs are represented by cataracts, jaundice and
uric dystrophy in birds (in serious cases of gout).
Cataract remains the most important of eyeballs dystrophic process
characterized by opacificarea lens. It is frequently found in horses, cattle and
carnivores. It can be partial or total.
8.2.1.3. Inflammations of eyeballs
Inflammation eyeballs of names, depending on the affected
structures of the eyeball. The cornea is called keratitis inflammation, iris,
iritis, ciliary, retina, retinitis , optic nerve, optic neuritis.
Inflammation entire eyeball is called ophthalmia and inflammation
eyeballs and their additions are known as panophtalmia . In their etiology are
177
criminalized traumatic factors, physical, chemical, toxic, food, biological

(viruses, bacteria, parasites), etc..
Keratitis may develop acute or chronic, superficial or deep.
Acute keratitis, pathologically speaking, may be catarrhal and
suppurative.
Macroscopically, the cornea and / or conjunctival sacs, are found
climbing, and purulent exudate.
Purulent exudate present in corneal thickness destructive acts
(ulcers), favoring herniation outside the bar limiting posterior (Descemet's
membrane) a Microvesicles, lesion called cheratocel.
nefeli on (gr. nephele = cloud) or nubecul the bleaching occurs
circumscribed the cornea (corneal macula);
- albugo (Latin albus = white), the specification is larger and more
intense;
- leucoma, the cornea is completely opacified (keratoleucom).
Relapsing iridocyclitis is found in chronic equine leptospirosis
reason for this form is known as the periodic ophthalmia horse.
Accumulation of purulent exudate in the anterior chamber of the eye latch as
crescent is called hipop ion and a hemorrhagic exudate, hipohema,
pathological aspects that produce deformation of the iris.
8.2.2. Accessory eye organs injuries
All accessory organs of the eye lesions are inflammatory in nature.
Blepharitis is inflammation of the eyelids, externalized through
thickening and deformation especially their free edges. Changes with
inflammation of the conjunctiva (blefaroconjunctivitis).
In chronic forms thereof, there is free beading eyelid or out
(ectropion) or turning them inwards (entropion).
Conjunctivitis is inflammation often associated with conjunctivitis
and keratitis evolving form of keratoconjunctivitis. Pathologically, it can be
catarrhal, purulent, pseudomembranous follicular and granulomatous.
Their etiology is varied. It is more common in ruminants:
keratoconjunctivitis chlamydian of ruminants, telsiosis of
bovine
,contagious agalactia of sheep and goats etc.
Dacrioadenitis lacrimal gland inflammation is observed more
frequently in periodic ophthalmia horse. Macroscopically, there is a swelling
in the orbit superexternal.
Dacryocystitis is inflammation of the lacrimal sac, externalized
through a subconjunctival swelling medial angle of the eye.
178
Encantis is hypertrophy wattles tear. It may be inflammatory or

neoplastic.
8.2.3. Tumors of the visual organ
Visual organ primary tumors are found as often in cattle aged 6-10
represented by carcinoma epidermoid (squamous cell) with eyelid location,
the tumor cells of the epidermis layer Malpighi. Metastasis of squamous cell
carcinoma occurs in parotid lymph nodes.
The horse mentioned melanomas, located in the eyelids.
Of metastatic tumors, the most common are sarcomas. In
generalized leucosis in cattle, dogs and cats can occur intraocular
limfosarcoma. (5, 11, 16, 19, 41, 43)
8.3. Auditory organ lesions
8.3.1. Ear necrosis
Gangrene of the auricle (Pinna) are found most commonly in
piglets and finished, to the animals several times mutilation. It can be caused
by traumatic agents, physical (frostbite) and infection (bacillus necrosis,
leptospire, mycotoxins, etc..).
8.3.2. Ear Inflammation
Ear perichondritis is inflammation of the auricle. In terms of
pathology, may be serous, purulent and myxomatoas. The first two forms,
one can see on one or both sides of the roof, as seen in rabbits myxomatous
perichondritis is located in particular on the edges of the flag, in the form of
swelling of different sizes linked in the form of "bead".
Otitis media is inflammation of the external ear canal and is
common in dogs and cats. From the morphological point of view, it can be
suppurative, the bacterial etiology is, as otitis fungal and parasitic diseases
are characterized by epidermal exfoliation. The parasitic external otitis, there
is a dark brown earwax hyper rich in parasites (genus Otodectes, Psoroptes).
8.3.3. Ear tumors
Tumors of the auricle are rare, and their location in the auricle are
common to those described in the skin (epidermoid carcinoma).
Ceruminous gland neoplasms in dogs and cats meet old are the
adenomas and carcinomas them with a structure similar to that of sweat
179
glands. Auditory canal polyps appear amid chronic inflammation, most

commonly in older cats.
9. The morphopathology of the endocrine system

9.1. The morphopathology of the endocrine glandular system
Endocrine glandular system is a highly specialized complex
represented by the pituitary gland, epiphysis, thyroid, parathyroid, adrenal
and endocrine pancreas (islets Langherhans).
9.1.1. Pituitary lesions
It is known that the pituitary gland is great variability in the species,
breed and physiological status of the animal, that fact must be taken into
account in interpreting the morphology of the pituitary.
Thus, youth anterior dominant chromophores acidophilic cells from
old animals while they are replaced by the atrophy is gradually basophilic
cells, is similar to cell.
9.1.1.2. Pituitary abnormalities
Abnormalities most common are cystic formations derived from
duct craniofaringeal or representing remnants of Rathke's pouch.
They have varying sizes and a high content of mucin. Were
diagnosed in some dog breeds.
9.1.1.3. Pituitary dystrophies
Pituitary atrophy is caused by compression performed by
cerebrospinal fluid (CSF) in high quantity in case of internal or external
hydrocephalus. It can be caused by tumors or cysts of parasitic nature
(Coenurus cerebralis).
180
Pituitary atrophy, partial or total, causes dwarfism in youth and

adult animals.
Pituitary dystrophies are found in the anterior lobe. They are
caused by infection, poisoning or compression. They are hyaline
degeneration, lipid vacuolar, hipofuscin limestone deposit.
9.1.1.4. Inflammations of pituitary

Pituitary gland inflammations are called pituitaritis. They are more
frequently reported in halves (posterior lobe), while adenohipofiza is more
resistant to infection.
Inflammations of pituitary are rare and are associated with
inflammation of the meninges or central nervous system.
Purulent pituitaritis are found under the form of microabscesses
in cattle, caused by Listeria or C. pyogenes, etc..
Granulomatous pituitaritis were observed in actinobacilosis,
tuberculosis in cattle and pigs, putting on morphological aspects pathogen
determinants.
9.1.1.5. Pituitary tumors
Primary pituitary tumors are rare in animals. Are reported mainly
in dogs and horses. Pituitary tumors can be divided into two groups:
- representing functional pituitary tumors secreting ACTH and MSH
cells;
- is inactive pituitary tumors are non-secretory and exerts its more
compression. May have as a starting point any cell type. (5, 11, 16, 19, 41,
43)
9.1.2. Epiphyseal lesions
Epiphysis or pineal gland has been less studied so that data gland
morphology and pathophysiology are relatively few.
The structure of the epiphysis is found structural changes in the
species and age. In old animals fibrosis occurs more or less extended.
181
9.1.2.1. Dystrophies of epiphysis

Epiphyseal dystrophies are represented by concrete and melanosis.
Concretions are characterized by the appearance of the poles in the central
gland of homogeneous or slightly stratified formations initially focus
basophils, and oxifile, PAS-positive.
Sometimes round or oval located near blood vessels and cells calcify
and components are called calcosferitis,
Sometimes very irregularly shaped concretions. The process of
calcification begins in blood vessels. Vascular wall thickening, lumen and
vessel it obliterates turns into a arteriolit calcosferit or better.
Finally in terms of pathogenetic epiphyseal concretions can be
calcosferite and arteriolite.
Melanosis is characterized by accumulation of melanin pigment in
the structure of epiphyseal capsule, connective cells immediately
surrounding the capsule and less frequently throughout the gland
parenchyma. Melanocytes have shapes and sizes, the pigment is present as
granular.
9.1.2.3. Inflammation epiphysis
Epiphysis inflammations are called pinealitis. They were found in
slaughtered animals: cattle, sheep and pigs. In most cases pinealitis are a
continuation of meningeal inflammatory processes.
Lymphohistocytic pinealitis evolve in the form of endo-vessels and
perivascular varying intensities in neurotrope virosis.
Granulomatous pinealitis were reported in cattle in tuberculosis.
9.1.2.4. Tumors of the epiphysis
Epiphyses gland tumors are rarely reported. They are the epiphyseal
adenomas or pinealomul , rarely other tumors.
9.1.3. Thyroid lesions
And in the tyroid case must take into account the morphological
variations depending on the species, breed, physiological status, etc..
Hyperfunction of thyroid or hyperthyroidism is characterized by
small follicles, high epithelium and basophilic colloid with numerous
resorptive vacuole near the epithelium.
182
Hypofunction thyroid or hypothyroidism is manifested by large

follicles, flattened epithelium, intense colid Acidophilic and lack resorptive
vacuole.
9.1.3.1. Thyroid abnormalities

Thyroid abnormalities are:
- hyroid aplasia and hypoplasia , is rare in all species especially as
hypoplasia;
- Accessory thyroid in the structure of the lungs, mediastinum,
periaortic adipose tissue and peritraheal;
- Congenital thyroid cysts, reminiscent of tiroglos channel. Were
diagnosed in pigs and dogs.
9.1.3.2. Dystrophies of the thyroid
Thyroid atrophy occurs if the gland compression exerted by
inflammation and / or tumor laryngotracheitis region, the accumulation of
which gives rise to thyroid colloid cyst formation (cyst).
Microscopic thyroid follicles become asymmetric follicular
epithelium is uneven and flat, meaning gland inactivity. The walls of
follicles can break releasing colloidal infiltrates in interfoliculare spaces.
Thyroid atrophy has been described in all species, particularly in
carnivores . In older dogs or obese is observed related thyroid hypofunction
of pituitary atrophy.
Dystrophies thyroid meet in infectious diseases in pigs , dog,
chicken.
Amyloid dystrophy interstitial location is exerting compressive
effect on hair follicles. It was reported in cattle, dogs and cats.
Cornea epithelial metaplasia is observed in follicular and
hypovitaminosis A in poisoning with naphthenic products.
In all species, particularly the dog, there is accumulation of colloid
impregnated with mineral salts called " corpus arenacei "(improperly
amilacei corpus) without functional significance.
9.1.3.3. Hyperplasia of the thyroid or goiter
183
Goiter or struma (Latin struma = goiter) is a process thyroid

hyperplasia in all species. In other words goiter is a thyroid hypertrophy due
to noninflammatory hyperplasia. It can be congenital or acquired. The cause
is lack of iodine in drinking water or the presence of antithyroid principles in
some feed.
Congenital goiter affects both thyroid lobes are symmetrical
increase in volume, small-cell follicles were high, without colloid. The
process occurs in Corriedale breed lambs, Merino, Romney , Sanen breed.
Lambs with congenital hypothyroidism have low stamina, slow growth,
reduced pilose coverage often presents myxedema.
Winning goiter occurs in all species are implicated in the
emergence of iodine deficiency and compounds that interfere with goiter
production of thyroid hormones (thiocyanates, nitrates, fluorides, etc..)
Pathologically, is systematized into two groups: parenchymal and
colloid goiter.
In parenchymal goiter (hyperplasia) is increased total thyroid
volume (diffuse goiter) or its mass nodules of various sizes (nodular goiter).
Both forms are the result of thyroid follicular epithelial hyperplasia. Gland
color is brownish-gray or whitish.
Microscopic in this form is observed follicles of different sizes, with
cubic or cylinder hyperplastic epithelium in several layers. Colloid is very
little or absent.
The colloid goiter thyroid is enlarged in volume, discolored and
shiny on the back of massive accumulations of colloid. The section appears
cavities filled with gelatinous fluid.
Microscopic, there is large follicles with abundant colloid flattened
follicular epithelium and smooth, even appearance of cysts in the basal
membrane rupture.
Nodular goiter occurs in older animals (horse, dog). Nodules of
various sizes are bounded by connective tissue and are the expression of type
cystic follicular hyperplasia (with or without colloid).
9.1.3.4. Inflammations of the thyroid
Thyroid inflammations are called thyroiditis or struma . Thyroiditis
arising from the direct action of external trauma, the position of this gland
favors action traumatic factors. Other causes include bacterial metastasis and
spread of the inflammatory process in regions vaccine. They are generally
rare in animals, the thyroid gland is resistant to infection.
In birds have been reported:
184
- lymphohistocytar thyroiditis were found in colibacillosis and

mycoplasmosis;
- granulomatous thyroiditis seen in tuberculosis, thyroid location is
relatively common.
In mammals were diagnosed following forms:
purulent
thyroiditis under the form of microabscesses, are
generally metastatic;
- immune thyroiditis substrate diagnosed in dogs and in certain breeds
of poultry, particularly in the obese.
9.1.3.5. Thiroid tumors
Most thyroid tumors have folicullar origine . The incidence is
higher in dogs and cats, and the lowest for the horses, cattle, sheep.
Thyroid tumors are represented mostly by adenomas and
adenocarcinomas.
Adenomas were found in dog an average frequency between 10
and 12 years and horses for over 10 years. Adenocarcinomas are rare,
occurring at a later age (dog 9-15 years) and can be compact follicular
papilifere or undifferentiated.
In birds leucosis we mention thyroid locations. It requires a
careful differential diagnosis to lymphohistocytic thyroiditis.
9.1.4. Parathyroid lesions
Parathyroid atrophy evolves concomitantly generally similar to
those found in the thyroid gland.
Morphologically manifested by the reduction in size of the
parathyroid predominance of atrophic cells and stroma rich. The presence of
atrophic cells (dark cells atrophied) denotes the excess of calcium and
vitamin D.
Hypercalcemia occurs in diseases in hypervitaminosis D, as well
as diets rich in calcium from the secretion of parathyroid hormone is not
necessary.
Also is observed in dogs, cats and horses with tumors (gastric
carcinoma, anal) that produce parathyroid hormone-like peptide with
persistent hypercalcemia.
Parathyroid hyperplasia is characterized by enlarged glands and is
the most important pathological process.
185
Microscopic indicate the presence of hyperactive cells (clear cell

hypertrophic) acinar or follicular arranged around a lumen containing an
amorphous or granular substance. The presence of these cells indicates
chronic stimulation of the gland by renal and nutritional disorders.
The reflecting secondary hyperparathyroidism in dogs, cats, horses,
birds following diets deficient in calcium or phosphorus excess.
Parathyroid cysts have been identified in cattle and dogs have
different sizes and containing clear or slightly opalescent liquid (colloidal
cysts).
Interstitial edema of the parathyroid gland in dogs with experimental
administration of large amounts of vitamin D 2 .The lesion is associated with
calcium deposition in renal medulla.
Paratiroiditis are the inflammation of the parathyroid glands. They
were raised in chickens. It was described parathyroid granulomatous ,
tuberculous nature.
In mammals paratiroiditis are rare, even when in the vicinity of
large territories there gland inflammation.
Parathyroid tumors are rare in animals. However were diagnosed
adenomas and carcinomas .
9.1.5. Adrenal lesions
For microscopic study of these glands, examination and sampling
should be no more than 30 minutes after the slaughter or death of the animal,
as postmortem changes (cell lysis) occur very early, especially in the
medulla structure.
9.1.5.1. Adrenal abnormalities
-
Disorders of adrenal development are:

unilateral agenesis indicated in dogs;
bilateral agenesis is fatal but is rare;
adrenals accessories seen in cattle.

Adrenal atrophy occurs secondary pituitary lesions and manifested
by reducing the volume of the gland, especially due to the beam area.
186
In horses there is a bluish secondary adrenal atrophy due to

degenerative processes pituitary and in dogs was reported bilateral atrophy
in all cortical areas are reduced in volume.
Dystrophies of the adrenal glands are observed in all species are
represented by the following dystrophies:
- lipid dystrophies are difficult to interpret, fat is a normal constituent
of the adrenal cortex. It is observed more frequently in cattle fattening made
in horse, cat and pig;
- hyalinosis intracellular found in medulla of the pigs with classical
swine fever (European);
- amyloidosis is observed in all species with initial deposits sinusoidal
capillaries of the beam and then the rest of the gland. Development amyloid
compression leads to atrophy of the cells in the area;
- pigmentation are the hemosiderosis, melanosis and lipofuscinosis.
These injuries fall within the types of lesions described in the general;
- calcification of the adrenal occurs in older animals (cattle,
carnivores, primates, etc..). They are the result of dystrophic calcification
in these species are commonly observed cortical necrosis.
9.1.5.3. Circulatory disorders of the adrenal
Haemorrhagias of the adrenalis found in infectious diseases,
poisoning microbleeds in the form of the beam.
9.1.5.4. Inflammations of the adrenal
We believe that the term adrenal correct, which is why we will
continue to use. The main pathological forms are:
Suprarenalitis necrotic found in Aujeszky's disease in pigs, in
some viruses in cattle (infectious rhinotracheitis).
Suprarenalitis purulent occur most often in the form of cattle
products microabcess C. pyogenes.
Suprarenalitis lymphohistocytaris
is observed in
poultry
colibacillosis and mycoplasmosis.
Suprarenalitis granulomatous tuberculosis in cattle are present as
in some fungi of carnivores (histoplasmosis).
9.1.5.5. Adrenal tumors
187
Tumors of the adrenal adenomas and adenocarcinomas are

represented by cortical and medullary phaeochromocytomas.
Cortical adenoma may be unilateral or bilateral, are rich in fat and
yellowish or yellowish-red. It has been described in dogs over 8 years of age
as well as horses, cattle and sheep.
Cortical carcinoma is more common in cattle, horses older and rarer
in other species. In cattle the notes section of calcification or ossification foci
metaplasia.
Medullary pheochromocytoma is the most common tumor of adrenal
medulla in domestic animals. It was reported in cattle and dogs, rarely in
other species. Cell morphology consists of a more or less similar to those of
the adrenal medulla, hence very different functional influences. (5, 11, 16,
19, 41, 43)
9.2. The morphopathology of the diffuse endocrine system
9.2.1. Diffuse endocrine system
Diffuse endocrine system was identified in 1966 by Pearle and
system called APUD (Amine Precursor Uptake and Decarboxylation).
Whatever the name, this system cells have the ability to capture biogenic
amines precursors precursors generating stimulatory or inhibitory peptide
surrounding cells. (11, 16)
9.2.2. Diffuse endocrine tumors
These groups endocrine cell tumors, disseminated structures of
organs or tissues were diagnosed long before their functions are well
defined.
Explanation on endocrine cell tumors may be driven by two main
issues:
- inappropriate secretion of hormones seen in some tumors that do
not secrete specific hormones that formed neoplasm cells (eg pancreatic
tumors may produce calcitonin etc.).
- ectopic hormone secretion occurs in tumors which arise from
endocrine cells but acquire property to secrete hormones (eg lung
adenocarcinomas and squamous carcinomas may secrete ACTH and ADH).
188
Tumors of the diffuse endocrine system are named after hormonal

secretion products (eg insulinomas, which secrete insulin gastrinoame which
secrete gastrin, etc..).
10. The morphopathologiy of the locomotor apparatus

Musculoskeletal organ meets very different structures, such as bones
with joints, muscles and tendons, which in normal and pathologic plan
provides a close interdependence.
10.1. Muscle injuries
Congenital anomalies of the muscles were better studied in swine
species .
Miofibrilar hypoplasia of piglets is characterized by reduction of
myofibrils of adductors muscles of limbs, removal of lesion externalized
through exaggerated hind legs ( feet distant disease ).
Etiologic factors involved are hereditary, toxic (mycotoxins) and
deficiency.
10.1.2. Muscular dystrophies
Atrophy of the skeletal muscle are injuries of varied etiology,
atrophy of inactivity, cachexia, neurotic, compression, etc. o. Macroscopic
muscle mass decreases its volume, thus highlighting the contours of different
muscle groups and muscle becomes darker color (brownish ).
Muscular dystrophies called myodystrophies
or dystrophic
myopathies. they are the consequence of metabolic disorders through food
rations unbalanced and deficient in vitamins and trace elements.
Youth myodystrophy nutrition called " white muscle disease "is
caused by hypovitaminosis E and hiposelenosis.
189
Macroscopic , it appears gray-white or striped areas, dry, brittle, and

in various muscle groups, alternating with normal areas. At other times, the
process can be generalized.
Microscopic , it shows a marked hyaline affected muscle fibers.
Occurs in all species.
Myopathy of equine paralytic myoglobinuria is characterized by
necrobiosis and fragmentation of muscle fibers, followed by the release of
myoglobin and its elimination by the kidney. Etiology, involving several
factors: diet rich in carbohydrates, rest, effort, cold etc..
Macroscopic , the affected muscle mass is increased in volume, bulk
and yellow color, due to the high content of lactic acid. On section, it is
noted bleeding or rupture of muscle fibers and run a pink liquid. The lesions
are located mainly in the muscles: psoas, thigh adductors, sural triceps,
buttocks, chest, etc..
Swine exudative myopathy and pigmentation is s visible
myodystrophie,at 12-24 hours after slaughter decline in the ability of muscle
fibers to retain water of constitution. In terms of etiology, stress plays an
important role.
Macroscopic , the muscles appear discolored, soft and moist.
Longissimus dorsal muscle first and most affected are the muscles of the
pelvic limbs.
Fatty muscle or lipomatous pseudohypertraphy occurs more
frequently in fattening of cattle, swine and sheep. Macroscopic , there is
enlargement of the muscle territories following the replacement of muscle
with fat bundles. Etiology process is not yet specified.
Pigmentation myodystrophies are represented by melanosis,
jaundice and lipofuscinosis whose macro-and microscopic characteristics do
not differ from those described in the general section.
Limestone myodystrophy or muscle calcification occurs in muscle
fibers undergoing various degenerative or necrotic processes. In
sarcosporidiosis and trichinosis, calcification is very common.
Muscle necrosis is found after intramuscular vaccination of
animals, externalized by area yellowish-gray, dry and brittle. Sometimes it
can be observed and necrotic processes more serious (wet gangrene, gas),
but only in the initial stages, as they are usually of gangrenous inflammation.
They can be ischemic or toxi-infectious.
190
Muscle circulatory changes are represented by active and passive

congestion , ie the muscle bleeding . The last category is found in
intoxication with warfarin ,urea in hypovitaminosis K, in case of injuries and
poisonings in various disease (Gumboro disease, and so on).
Macroscopic, bleeding can be in the form of petechiae, or bruising
suffusions.
10.1.4. Muscle inflammation
Inflammation of muscles called myositis . Etiologic factors are
determined traumatic myositis, toxic, infectious and parasitic. In terms of
pathology, differ myositis: serous, serofibrinoase, fibrinohemoragice,
festering, gangrenous, eosinophilic, fibrous and granulomatous.
Myositis serous , serofibrinos and fibrinohaemorrhagic evolves as
localized swelling from trauma or generalized form for poisoning, parasitic
larval migration etc.
Macroscopica , the territories affected are enlarged congested and
the skirt section is infiltrated with serous effusion, or fibrinohemoragic
serofibrinos.
Purulent myositis occurs in all the species or by phlegmonous
form (eg, phlegmon withers the horse), whether in the form of abscess (eg
piobaciloza pigs).
Myositis gangrenous or emphysematous, meets the coal produced
by Clostridium emphysematous .
Macroscopic , hind limb muscles (thighs, buttocks etc..) is much
swollen, and the section is observed serohemoragic and gas formation that
dilacerate the muscles, printing a spongy appearance and crackles on
palpation. The color is purplish-blackish, low consistency and smell Ihor.
Eosinophilic myositis occurs in cattle, swine and carnivores.
Macroscopic , there is yellow with greenish outbreaks, pearly white
areas bounded by increased consistency.
Microscopic denotes a fibrous connective tissue rich in eosinophils,
while muscle fibers are atrophied or necrotic. The lesion appears to be
allergic in nature.
Myositis fiber is the way to end all forms of myositis. Macro-and
microscopic diffuse conjunctival hyperplasia is found in muscle tissue
damage. Areas is pearly white color, consistency greatly increased, and the
bucking is subject to a "creak".
Granulomatous myositis can be infectious in nature (eg in
brucellosis, glanders), or parasitic in nature (eg sarcosporidiozsis,
191
cisticerosis, trichinosis). Parasitic granulomas are important in veterinary

medicine because they have implications for expertise meat.
A particular form of granulomatous myositis is the so-called "
Roeckl's granuloma . " It was described in cattle in cervical muscles,
especially the shoulders and tail region.
Macroscopic , multiple muscle granulomas stands, off-white, of
various sizes, hard to palpation.
Microscopic , there is a necrotic center leukocyte surrounded by a
granulomatous reaction. Its etiology is not understood: some say that is
produced by Hypodermis bovis larvae (parasitic etiology), while others
argue for infectious etiology - C. pyogenes.
10.1.5. Somatic muscle tumors
Skeletal muscle tumors in mammals, are represented by:
- benign : rabdomyoama, fibroids, lipomas;
malignancies:
rabdomyosarcoama,
liposarcoame
and
fibrosarcomas in different body regions. Tumor proliferation striated muscles
have a low incidence in animals. Forms benign retains features throughout
evolution without malignant transformation trend. Forms malignancies are
strongly aggressive and destructive, the virtues of metastasis and lymphatic
or venous generalizations.
In birds, note the location of muscle, relatively frequent in the acute
form of Marek's disease. (5, 11, 16, 19, 41, 43)
10.2. Injuries of tendons, synovial sheaths and synovial bursas
The main fundamental pathological processes affecting the tendons,
synovial sheaths and bursas are serous inflammation.
10.2.1. Inflammation of the tendons
Inflammation of the tendons are called tendonitis , sinvoiale sheath,
tenosynovitis or tendovaginite and bursa inflammations are called bursitis .
Tendonitis are determined by mechanical, traumatic, infectious and
parasitic. It is more common in horses and racehorses particularly affecting
flexor muscle tendons metacarpus.
Pathology differ tendinitis exudative ( serous, serofibrinoase,
purulent ) and productive ( fibroblasts ).
192
Macroscopicy, the exudative tendinitis, the tendon is increased in

volume, tone is low (soft), and the space peritendinous, and tendon structure,
it is noted that exudate. In fibroblasts tendonitis, tendon region is slightly
enlarged, and on section the tendon is "caught" in a mass of connective
tissue peritendinous space due to chronicity of exudative forms.
In horses, there is parasitic tendinitis caused by Onchocerca
crosslinked.
Macroscopically , the tendon path is found nodules composed of
clumps of parasites. The most frequent location is the tendons of the flexor
muscles of the limbs.
Tenosinovitis were predominantly exudative: serous and purulent
serofibrinoase.
Macroscopic , there is accumulation of exudate in sacs along with
thickening of the synovial layer. In chronic developments can be observed
tenosynovitis fibroblasts. Their incidence is increased in cattle and pigs,
because stabulaiei.
Bursitis is also known as the higroame (eg elbow hygroma). Meet
the horses, pigs and carnivores. The main morphological types: serous,
serofibrinoase, bleeding, pus, and developments chronic bursitis fibroblasts.
In birds, we mention sternal bursitis observed in complex avian
great technological factors over (grates various batteries to increase).
10.3. Joint lesions
10.3.1. Dystrophies of the joints
Dystrophies of the joints are called osteoarthritis or degenerative
arthropathy. etiology is not fully elucidated. Some consider an infection
outbreak, others blame the chronic rheumatism, vascular factors, endocrine
and metabolic diseases.
Osteochondrosis arthropathy is a chronic, progressive,
characterized by articular cartilage depolymerization.
Macroscopically , it appears erosions and ulcers of various shapes
and extensive articular cartilage, bone is discovered, hemorrhagic or necrotic
process. The etiology of osteochondrosis is still discussed (excess synovitis,
biochimism changed traumatic factors etc..).
Slipped epiphyses (epiphyseal separation) is a degenerative process
followed by necrosis of articular cartilage detachment. It occurs more
frequently in pigs, the proximal end of the femur. Sometimes there is
193
separation of the femoral head remains attached articular acetabular cavity

round ligament. There are cases when metaphysics remains in contact with
the epiphysis, maintaining it is provided by the periosteum.
Spondylosis (lat. spondillus = vertebra, osis = disease) is a
degenerative arthropathy of vertebrae and intervertebral discs observed in all
species, especially in the lumbar region.
Initially, it causes thinning of the intervertebral disc with its ventral
herniation, and in later stages of the edges of two neighboring vertebrae bone
proliferation begins, the union achieved by joint stiffness.
Microscopic, there is intervertebral disc degeneration, followed by
progressive fibrosis of the nucleus pulposus mucilaginous.
Osteoarthritis of the knee is the knee joint osteoarthritis, chronic
process complicated by profound alterations followed by limiting joint
mobility.
Osteoarthritis is characterized by degenerative processes and
proliferative both cotiloid cavity and the femoral head and neck. The disease
occurs mostly in adults and older pigs and is usually the result of joint wear.
Hock arthritis is the most common clinical form in industrial
complexes growing and fattening pigs. May result rujetului chronic
periarticular chronic infections, improper climate, with negative
repercussions on the movement of intra-articular and periarticular.
Macroscopic , there is cartilage thinning, loss of elasticity and
normal color. Articular surface wear occurs on the other hand by erosion,
cracks and separation of articular cartilage, on the one hand, productive
processes (osteophytes) that lead to hypertrophy expifizelor joints.
Uric arthritis or gout joint is found in poultry, as a result of the
precipitation mass uropurinice in the joint cavity.
Macroscopic , joints legs appear slightly thickened, and on section
is observed crystals or small deposits pearly white, pasty, which is easily
separated from the synovial membrane.
Circulatory changes in the joints are represented by hidrartrosis
and haemarthrosis.
Hidrartrosis or circulatory arthropathy is characterized by the
accumulation transudation into the joint cavity.
Haemarthrosis or intraarticular bleeding occurs as a result of
trauma to warfarin poisoning in some states septicaemic etc.
194
The evolution of these two chronic arthropathy occurs dystrophic

process of cartilage covering called velvet degeneration , resulting in the
final joint appearance of ulcers.
10.3.3. Inflammation of joints
Inflammation of joints is called arthritis or osteoarthritis , the
inflammatory process extends to bone rays. Location inflammation
predominantly in synovial layer is called synovitis at articular tissue,
periarthritis , and damage several joints, polyarthritis.
Spondylitis is inflammation of the vertebrae, and spondilartrita is
arthritis of the spine.
Arthritis etiology is varied. Two categories of factors seem to have
a leading role, infection and trauma. Arthritis can develop acute (serous and
purulent serofibrinoase) or chronic (deforming, and granulomatous
spondylitis).
Serous arthritis manifested by the appearance of serous exudate in
the joint cavity.
Macroscopic, the joint is increased in volume and on opening
stands a yellowish liquid, or slightly reddish. Synovial layer is thickened and
congested. It appears frequently in chlamydiene and mycoplasmal infections
(contagious agalactia of sheep and goats).
Serofibrinoas arthritis involves the presence of a joint effusion in
the joint cavity.
Macroscopic, the joint is much thicker, and the section is observed
cloudy synovial fluid, the floating flocs of fibrin. Synovial layer is swollen
and covered with fibrin. In chronic developments fibrin organization
undergoes found in Glasser's disease, colibacillosis, etc. rujet.
Purulent arthritis occurs as a result of direct infection,
intraarticular, if trauma or blood may be due to metastases.
Macroscopic , the joint is increased in volume due to swelling
periarticular, and the section is observed purulent collection in the joint
cavity. Synovial layer is swollen and may show erosions or ulcers.
Periarticular inflammation can extend the form of abscesses or phlegmons. It
is found in streptococci, the lambs and piglets, pigs etc Deforming arthritis is
characterized by the appearance of hyperplastic reaction of the synovial
layer (proliferation polyps) and cartilage neoformations (chondral) and bone
osteophytes).
195
Macroscopically , these issues proliferative outwardly through

hypertrophy and deformation usually asymmetric joint.
Spondylitis Arthritis is the result of deforming arthritis.
Granulomatous arthritis is predominantly infectious nature, but may
evolve as arthritis uric birds. The first category, mention of tuberculosis and
arthritis in cattle and swine brucellosis, miliary granulomas externalized
through the synovial layer.
In birds, inert foreign body granulomatous arthritis results from
deposits chronicity uropurinice mass in the joint cavity, which causes
mesenchymal reactions resulting in the formation of deposits and
encapsulation of the so-called tophi , or uric granulomas .
Macroscopic, joints, limbs are increased in volume, and the large
warehouses n (tophi). Articular gout in birds, begins as dystrophic process,
which gradually turns into an inflammatory process, thereby establishing the
unity and interdependence of the various fundamental pathological
processes.
10.4. Bone lesions
Bone development disorders have genetic etiology, deficiency or
unknown. They can be generalized and localized.
Chondrodystrophy fetal or micromelia is a generalized abnormality
characterized by abnormal enchondral ossification of the limb bones,
externalized through thick and short limbs (dwarfism).
It has been described in calves, dogs and chickens.
Of localized anomalies we mention:
- amelia - lack of development of one or more limbs;
abrahia - lack of development of thoracic limbs;
apodia - lack of development of limbs;
adactilia - no fingers;
syndactyly - Union fingers;
polydactyly - is the existence of several fingers.
10.4.2. Bone dystrophies
Bone dystrophies are called osteodystrophy or dystrophic
Osteopaths. they can be grouped in two categories:
196
- protein-mineral osteodystrophy (rickets, osteomalacia,

osteoporosis, osteofibroza);
- osteodystrophy pigmentation .
Rickets is a disease characterized by the inability of young bone
and cartilage to fix calcium.
Etiologic factors involved more vitamin D deficiency, imbalances
P/Ca, deficiency of calcium, phosphorus, etc.. Morphological spans the areas
of bone ossification not calcify and remain osteoid character.
Macroscopically, the young of all species are observed:
- bowing of long bones, with thickening of the epiphyseal ends;
- lateral deflection mammalian spine ( scoliosis ) and sternal keel
birds;
- joint hypertrophy chondrocostal-looking "bead" called "rachitic
rosary";
- welding lack of skull bones or delay it.
All the bones are devoid of rigidity, easy to break and cut, which is
called the " soft bone disease ".
Microscopic there is an excess of osteoid tissue, "erosion line"
(between bone and cartilage) is irregular, broad and vague area.
Osteomalacia (Gr. osteon = bone and Malak = softening) is a
process specific dystrophic adulthood, characterized by progressive
decalcification. Rahistism is considered equivalent to adult animals. The
etiology of the disease, failure occurs calcium, phosphorus, vitamin D, as
well as the excessive food for cattle feed acid (silos). It occurs more often in
cows, sheep and chickens.
Macroscopic , there is bowing of long bones (especially the femur)
in weight, multiple fractures can occur spontaneously. Consistency bone is
much lower.
The bird stands sternal deflection hull ( osteodystrophy deformans
) and produce eggs with thin skin and fragile.
Microscopic observed increasing number of osteoclasts, which
cause increased resorption of bone minerals and an excess of osteoid tissue.
Osteoporosis is a generalized or localized osteopathy characterized
by insufficient bone matrix (ossein). It is more common in young people and
carnivores, but occurs in all species and all ages. It is found more frequently
in the ribs, vertebrae and pelvic bones.
Etiology, low intake of protein is the main cause of low
oseinogenesis. Osteoporosis does not involve a primary disorder of
metabolism phosphocalcic.
197
Macroscopic , the bones are light, without stiffness, and often

deformed fractures. On section, the cortical bone is thinned (sometimes up to
a simple leaf), medullary canals are much enlarged, and the periosteum is
thickened.
Microscopic , there is reduction of osteoid tissue and osteoblasts.
There is increasing transparency radiological bone.
Osteofibrosis or fibrous osteodystrophy, and in all animals of all
ages, are characterized by the replacement of bone with fibrous connective
tissue.
The etiology is polifactorial, the nutritional secondary
hyperparathyroidism, caused by excess phosphorus in the ration (imbalance
P / Ca) plays the main role.
Macroscopic , the most characteristic changes are found in the
bones of the face. Deformation jaw in horses, goats and dogs sometimes
gives the impression of large head, hence the name " big head disease ".
Move teeth dental alveoli. Lightweight bones, and their consistency is
rubbery.
Microscopic , there is abundant resorptive role of osteoblasts in the
fiber hyperplasia in the form of foci of various sizes.
Osteodystrophy pigmentation are the melanosis and bone
porphyria.
Melanie osteodystrophy , or bone melanosis is recognized
macroscopically bluish-blackish staining of the periosteum.
Osteodystrophy porphyrins is a bone pigmentation more common
in cattle and pigs. It is also known as " green bone disease . "
Macroscopic, it appears reddish-brown coloration of the bones. In
cross section, there is a mosaic-rings given by the alternation of red-brown
and crisp.
Osteopaths dystrophic rare, may occur in fluorosis, dental injuries
and externalized through bone.
Circulatory changes in the bones are less known and studied in
animals.
Active hyperemia bone occurs as a consequence of trauma, and the
passive restraint too tight for dressings or bandages plaster.
Bone hemorrhages are usually traumatic in nature (bleeding
postfracturale). They may be surface (subperiosteal) and deep localized in
endosteal.
198
The bone fractures open, bleeding is external, as in the unopened

blood fractures with bone fragments, contribute to the formation of callus
possible transient and the occurrence of pulmonary embolism.
10.4.4. Bone inflammation

Bone inflammation are known under the generic name of osteitis.
Inflammation of the periosteum is called periostitis and bone marrow
osteomyelitis. Concomitant damage of the three components (periosteum,
bone, bone marrow) defines the term panosteitis . Frequently there is
inflammation of bone and periosteum called osteoperiostitis .
Etiologic , osteitis are produced, in most cases,by traumatic and
infectious factors.
Osteoperiostis serous, fibrinohaemorrhagic,e sero-fibrinosr arise as a
result of strong trauma.
Macroscopic, affected bone region is red-purple, low consistency
and, observed better in spongy bones.
Osteoperiostis purulent exudative can result from other forms, or
may be due to the intervention of pyogenic germs. It is most commonly
observed in limb bones, jaws, etc. interscapular region.
Macroscopic, there is festering subperiosteal collections, or the
epiphyseal plates. Pyobacilosis is found in streptococcus swine and foals.
Osteitis thin or corrosive, is characterized by a pronounced bone
resorption, which leads to abnormal fragility of the bones.
Microscopic, there is increasing number of osteoclasts a. The
affected regions are congested. Differential diagnosis should be made to
osteoporosis.
Osteitis ossificans or condensed, phenomena manifested by bone
hyperplasia, externalized by the appearance of circumscribed horns of
various sizes located on the surface of bone (exostosis), medullary canal
(enostoze), or near a joint (osteophytes). These forms are more common in
horse limb bones. If bone proliferation is diffuse bone thickens greatly
partially or totally, the lesion being called hyperostosis .
Granulomatous osteitis is characterized by pronounced destruction
of bone and filling the space with granulomatous foci. It is found in
actinomycosis, tuberculosis and brucellosis.
199
10.4.5. Bone Tumors

Primary bone tumors are common in dogs, and cats and more rarely
in other species.
In birds, mention osteoporosis, bone lymphomatosis, viral
oncogene characterized by thickening and deformation of long bones. (5, 11,
16, 19, 41, 43)
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SPECIAL VETERINARY

Professor Romeo Cristina DvD, PhD

1.1. Heart morphopathology.....................................................................11

2.3.5. Tumors of Fabricius bursa

2.4. Pathology of the spleen.......................................................................43

3.3.5. Injuries of diphragm

3.4. Respiratory pathology in birds..........................................................72

4.6. Morphopathology of mammalian stomach.......................................90

4.11.6. Liver Tumors 119

6.3.1. Ovarian lesions 148

6.4. Morphopathology of birds female genital system..........................160

8.1.1. Congenital anomalies of the skin and appendages

8.2. Visual organ lesions...........................................................................179

10.2. Injuries of tendons, synovial sheaths and synovial bursas...........195

Heart malformations are determined by various factors, some with

Fat infiltration of epicardium is the opposite of serous atrophy. It is

Haemopericardium occurs as a result of breaking the great vessels

Macroscopic the pericardial cavity indicate the presence of increased

Microscopic in the acute forms are found degeneration and peeling

Pericarditis gangrenous or Ihor is, in most cases, the consequence of

Uric granulomatous pericarditis is observed in birds chronic gout

Granular myocardosis is common during infectious diseases, toxic

All degenerative processes (myocardosis) in all species can evolve

Evolution and severity of myocardial infarction is given by the

Myocardial inflammation are called myocarditis. They may be

Purulent or suppurative myocarditis in most cases, is a secondary

fibrous tissue, which reduces the

Fibrous myocarditis is a continuation and completion of other forms

Granulomatous myocarditis is relatively rare. It can be observed in

Endocardial calcification was observed in all species, both in the

Pathogenetic: primary and secondary endocarditis;

Simple endocarditis is characterized by endocardial thickening

Microscopic there is serous infiltration, endothelial desquamation,

Clinic is signaled the existence of recurrent endocarditis, which is

Fatty arteries in animals is less important compared to human

The ethiopathogenesis is not understood even today, but it is

Atherosclerosis is an arterial non-ateromatose , diffuse structures

Generalized arterial thrombosis are affecting the microcirculation

Inflammation of the arteries are generically called arteries. After the

In dogs, the lesions consist of thickening and deformation of the

1.2.2. Veins injuries

Microscopicare observed myoelastic fiber necrosis and substitution

Suppurative drug phlebitis drug is found on the external jugular

1.2.3. Lesions of the lymphatic vessels

Most important for the practice of veterinary medicine are

1.2.3.4. Tumors of blood and lymphatic vessels

2. THE MORPHOLOGY OF THE HEMATOPOETIC AND

Fatty osteomyelosis is found in chickens fed with feed

Microscopic granulomas are observed with central caseous

thymic hyperplasia is characterized by the multiplication of cells in bone

2.2.4. Circulatory changes

Thymic bleeding point, are of great practical value in poisoning

The bursa's function is to develop immune competence of

2.3.1. Changes congenital

Epithelium cystisation is found in hypotrepsic chickens, in relation

2.4. Pathology of the spleen

Amyloid lienosis (Splenic amyloidosis) is predominantly

consistency is low. Chronic form is characterized by hypertrophy and

Macroscopic, the spleen, of the bird is much larger in volume, and

Granulomatous spleen is particularly common in tuberculosis,

Primary splenic tumors are:

Secondary spleen tumors are frequent in Marek's disease, avian leukosis

Macroscopic, the lymph nodes are increased in volume, especially