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UPON EVISCERATION:
SEGMENT OF ILEUM AND CECUM
o Approx 1.5Liters of clotted blood
The pathologist received a body of a 24- year old male, born in Leyte, whose chief complaint was fever, a non-
specific sign and symptom.
Stomach
Ability to penetrate the epithelial cells
Small Intestine
Thoracic Duct
Carried by macrophages
Bloodstream
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Brain Meningoencephalitis seizure
Typhoid Nodule
Adrenal
1. Less distinct granuloma
2. More Pronounce necrosis
3. Erythrophagocytosis Pancreas
Spleen Splenomegaly
Ileum
Hyperplasia of Peyers
Patches in the Ileum
• Hypotension
• Bradycardia not improved by fluid challenge
Septic Shock
D. REACTIVE SPLENITIS
Ingestion of S. typhi by host Invades through gut Multiplies within mononuclear phagocytic cells
Stool, urine
Colonizes: Inflammation and
• Liver diarrhea
• Spleen
• Lymph nodes
Infect other hosts • Peyer’s Patches
Bile ducts Ulcers,
peritonitis
In receptor- mediated
Gallbladder phagocytosis In gut epithelium:
Submucosa: Macrophage Bacteria- mediated
endocytosis (BME)
• As the illness progresses, fever remains high, and the person may become delirious. Sustained fever is often
accompanied by a slow heartbeat and extreme exhaustion.
• During the second week and last 2 to 5 days: 10% of infected people get clusters of small, pink spots on the
chest and abdomen (Rose spots from typhoid fever)
• At the final stage, a blood infection (bacteremia) occasionally leads to infection of bones (osteomyelitis), heart
valves (endocarditis), kidneys (glomerulitis), the genitourinary tract and tissues covering the brain and spinal
cord (meningitis).
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• Although the history and symptoms of illness may suggest typhoid fever, the diagnosis must be confirmed by
identifying the bacteria in cultures of blood, stool, urine, or other body fluids or tissues.
1. symptoms begin gradually 8 to 14 days after infection. The brassy, nonproductive cough is common.
Nosebleed may occur.
2. This Diarrhea may continue, although some people become constipated. In about 10% of infected people,
clusters of small, pink spots appear on the chest and abdomen during the second week and last 2 to 5
days. After 2 weeks, intestinal bleeding or perforation occurs in 3 to 5% of infected people.
3. Pneumonia usually results from a pneumococcal infection, although typhoid bacteria can also cause
pneumonia.
DISCUSSION
- Causes Self limited food borne and water borne gastroenteritis or typhoid fever
- Vascular congestion
- Mononuclear inflammation
- Peyer patchers inv: swelling, congestion, ulceration with linear ulcers, become sharply
delineated, plateau like elevations upto 8 cm in diameter, enlargement of draining mesenteric
lymph nodes
- Shedding of the mucosa and swollen lymph nodes oval ulcers along the axis of the ileum
Microscopic findings:
- Macrophages containing bacteria
- RBCs
- Nuclear debris
Gross findings:
a. Spleen
- Enlarged, soft and bulging with uniformly pale red pulp, obliterated follicular markings and
prominent sinus histiocytosis and reticuloendothelial proliferation
b. Liver
Typhoid fever
- Marked by fever and systemic symptoms ( S.typhi)
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- Protracted disease that is associated with
- 2nd week: Widespread mononuclear phagocyte involvement with rash, abdominal pain and
prostration
- 3rd week: ulceration of peyer patches with intestinal bleeding and shock
Pathogenesis:
- Salmonella invades intestinal epithelial cells, macrophages
- Invasion is controlled by invasion genes that are induced by low tension found in the gut
- Intramacrophage growth impt. In pathogenecity, mediated by bact. Genes that are induced
by the acid ph within the macrophage pahgolysosome
- Enteric nervous system critical regulator of fluid secretion in the normal gut
- Neural reflex pathways increase epithelial fluid secretion in response to enteric pathogens
Pathophysiology:
• After ingestion by the host, S typhi invades through the gut and multiplies within the
mononuclear phagocytic cells in the liver, spleen, lymph nodes, and Peyer patches
• After successfully passing through the stomach, any Salmonella subspecies may be
phagocytized by the gut's intraluminal dendritic cells, causing inflammation that leads to
diarrhea. Only the subspecies S enterica causes severe disease in the rest of the body. Its
specialized fimbriae adhere to the epithelium that overlies Peyer patches.
• They are the primary mechanism for sampling antigens in the gut and initiating response. S
enterica enters them via 1 of 3 pathways.
• Salmonella insert into eukaryotic cells and intracellular membranes to inject virulence
proteins—to inject proteins SipA and SipC into the epithelial cell. These disrupt the normal
brush border and force the cell to form membrane ruffles. The ruffles engulf the bacilli and
create vesicles that carry them across the epithelial cell cytoplasm and the basolateral
membrane.
• In these havens, it multiplies until some critical density is reached. It causes the apoptosis in
the macrophages and enters the bloodstream to attack the rest of the body. At this stage, the
Vi antigen comes into play. It forms a capsule to protect the bacterium from complement and
from phagocytic immune cells.
• From blood or from the liver via bile ducts, it infects the gallbladder and reenters the
gastrointestinal tract in the bile, spreading to other hosts via stool.
• After primary intestinal infection, further seeding of the Peyer patches occurs through infected
bile. They may become hyperplastic and necrotic with infiltration of mononuclear cells and
neutrophils, forming ulcers that may hemorrhage through eroded blood vessels or perforate
the bowel wall, causing peritonitis.
Chronic Schistosomiasis
Cercarial penetration to maturation of adult worms
Active egg deposition
Immunologic process resulting from cumulative deposition of eggs
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Miracidium hatches out from excreted egg → miracidia infect snails → many cercariae released from
infected snails → people infected by contact with cercariae in water → cercariae enters skin & lose
their tail to become schistosomulae → schistosomulae migrate through tissues, penetrate a blood
vessel → brought to right heart & lungs → they squeeze thru pulmonary capillaries into the systemic
circulation → portal vessels → schistosomule mature in the hepatic portal venules & form pairs →
worms migrate against portal blood flow & deposit eggs into the mesenteric, vesical and pelvic
venules
Pathophysio:
- Granuloma formation and hepatic fibrosis
- Assoc. with dominant Th2 response with persistence of Th1 helper cells
Septic Shock:
Septic shock - due to bacterial toxins thus widespread vasodilation
- no loss of intravascular volume
- high vasodilation
- pooling of venous blood
- low cardiac output