1 typhoid fever you chengcheng dept. of pathology china three gorges university
TRANSCRIPT
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Typhoid feverTyphoid fever
You ChengchengDept. of pathology
China Three Gorges University
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Contents
Introduction Pathogenesis Pathological changes Symptoms Complication
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First, let me tell a story of typhoid Mary……
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Prevalent in the third world countryOutbreaks are rare,but in some areas such as in
Indonesia and New Guinea,it ranks among the 5
most common causes of death Bacterial infection of the intestinal tract and
occasionally the bloodstreamThe ileum is most affected
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Mononuclear Phagocytic System(MPS):
Monocytes and its derivationsmononuclear cells (blood) macrophages (connective tissue) kupffer cells (liver) ………..
Typhoid fever is characterized by macrophages
Proliferation of MPS, which are particularly
predominant in ileum.
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The germ that causes typhoid is a unique
human strain of salmonella called Salmonella
typhi
Gram negative bacillus.
O-Ag, H-Ag, vi-Ag
(Widal reaction)
Pathogenesis
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Infection source : typhoid fever patient and carrier
route of transmission : fecal-oral route
susceptible population:children and young people
Food, fly, finger, water
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Salmonella typhi
Contaminanted food
Proliferate in ileum tissue bacteremia
First contact Whole body
Gall bladder
second contact
Lymph tissue in ileum
Septicaemia
Hyperplasia stage (1w)
Toxemia
Excretion
Necrosis and ulceration (2w)
Healing (1w)
Incubation period(10 d)
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Pathological changesHallmark histologic finding:the infiltration of tissue by typhoid cells
typhoid cells:large macrophages contain Phagocytized erythrocytes, lymphocytes,bacteria and necrotic cellular debris
Typhoid nodule (typhoid granuloma) :the aggregates of typhoid cells
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Typhoid nodule can present in the lymph tissue
of small intestine, mesenteric lymph node, the
liver, spleen and marrow,
its typical changes often occur in the lower
part of ileum , especially in the Peyer‘s
patches and Isolated lymphonodulus.
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typhoid cell
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typhoid cell
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typhoid cell
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Typhoid granulomaTyphoid granuloma
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Intestinal pathological changes
The principal lesions are those of lymphoid tissue of terminal small intestine.
(1) Hyperplasia Stage ( Peyer’s patches)
(2) Necrosis Stage;
(3) Ulceration Stage;
(4) Healing Stage.
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Hyperplasia stage : the 1st w after onset the 1st w after onset
lymphoid tissue swelling protrude out the mucosa , lymphoid tissue swelling protrude out the mucosa ,
looks like looks like cerebral convolution
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Showing the hyperplasia of Peyer’s patches of ileum, which is button-like elevation
Hyperplasia stage
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Hyperplasia stage
looks like looks like cerebral convolution
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Hyperplasia stage
looks like looks like cerebral convolution
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Hyperplasia stage
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Microscopy:
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•Necrosis stage : the 2nd w after onset the 2nd w after onset multi-focal necrosis in lymphoid tissuemulti-focal necrosis in lymphoid tissue
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Ulceration stage :the 3rd w after onsetthe 3rd w after onset ,,
necrosis tissue fall off and ulcer formation, necrosis tissue fall off and ulcer formation,
longitudinal ulcerlongitudinal ulcer is parallel with the axis ofis parallel with the axis of
intestinal canal ,intestinal canal , deep to the muscularis layer deep to the muscularis layer
and involve the artery ,which will result in and involve the artery ,which will result in bleedingbleeding
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Key features :• Round or oval
•Elevated margins
•Uneven bottom
•Parallel to the axis of intestine
ulceration stage
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ulceration stage
Key features :• Round or oval
•Elevated margins
•Uneven bottom
•Parallel to the
axis of intestine
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ulceration stage
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DifferenceDifferenceTyphoid feverTyphoid fever TuberculosisTuberculosis
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Healing stage : the 4th w after onset the 4th w after onset
Granulation tissue proliferation ,Granulation tissue proliferation ,
scar formationscar formation
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Changes in other MPS
Typhoid nodule formation and ulceration in
mesenteric lymph node, the liver, spleen
and marrow.
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Lesions in other organ
Gall bladder: carrier
Heart: slower pulse
Kidney: Albuminuria
Skin: rose rashes
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SYMPTOMS Fever (some as high as 40 Degrees)
Weakness
Headache
Loss of Appetite
Stomach pains
Rose Rashes
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Complications:
intestinal bleeding
intestinal perforation
lobular pneumonia
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Bacillary DysenteryBacillary Dysentery
Chengcheng You Dept. of pathology
China Three Gorges University
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Bacillary dysentery is an acute bacterial infection caused by the genus Shigella resulting in colitisaffecting predominantly the rectosigmoid colon.
The disease is characterized by diarrhea, dysentery, fever, abdominal pain, and tenesmus.
It is usually limited to a few days.
Mainly occur in infants and young childrenMainly occur in infants and young children
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•Pathogen
Shigellae are nonmotile
gram-negative bacilli belonging
to the family Enterobacteriaceae
•Four species:
S. dysenteriae (group A),
S. flexneri (group B),
S. boydii (group C),
S. sonnei (group D).
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Incidence
•most cases of shigellosis occur in children ofdeveloping countries
•S. flexneri is the predominant species
•Children between 1 and 4 years old
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• Infection source : patient and carrier
• route of transmission : fecal-oral route
• Susceptible population:children and young people
• seasonal patterns: autumn and summer
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PATHOGENESISPATHOGENESIS
•organisms traverse the small bowel, penetrate colonic epithelial cells and multiply intracellularly
•acute inflammatory response•pseudomembranous type of colitis
•Epithelial cells containing bacteria are lysed, resulting in superficial ulcerations and sheddingof shigella organisms into stools
•Diarrhea results because of impaired absorption ofwater and electrolytes by the inflamed colon
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Feature Location: predominantly the rectosigmoid colon
Clinical type :
Acute bacillary dysenteryAcute bacillary dysentery
Chronic bacillary dysenteryChronic bacillary dysentery
Toxic bacillary dysenteryToxic bacillary dysentery
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Acute bacillary dysenteryAcute bacillary dysentery
Fibrinous inflammation
Serous inflammationMucus secretion increasediffuse hyperemiaerosion
Map-like ulcer
healingbloody mucoid diarrhea
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•Gross: Affect the colon, producing an acuteinflammation with diffuse hyperemia 、edema and multiple superficial ulcers.
•Pseudomembrane formation: exudate fibrin,neutrophils, necrotic debris, bacteria
•MI: epithelial cell necrosis, fibrin exudationmonocytes and neutrophils infiltration
abscess formation
•The lesions are often self-limited and can recover completely
Acute bacillary dysenteryAcute bacillary dysentery
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Pseudomembrane
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pseudomembranous inflammation
Gross: showing the pseudomembrane and irregular ulcers
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bacillary dysenterybacillary dysentery
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Microscopy:
Bacillary dysentery
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Complications
•Intestinal Bleeding
•Intestinal Perforation(seldom)
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Clinic Feature Symptoms begin with sudden onset of high grade fever,
abdominal cramps and watery diarrhoea.
Subsequently diarrhea become mucoid, of small volume and
mixed with blood. This is accompanied
by abdominal pain and tenesmus.
Physical signs are those of dehydration beside fever, lower
abdominal tenderness and normal or increased bowel sounds.
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Chronic bacillary dysenteryChronic bacillary dysentery•lasting more than 2 months ,
infected by S.flexneri(福氏菌 ).
•Clinical features: Mild symptom of abdominal pain ,diarrhea
Infectious source
•pathological changes: ① chronic ulcers;
② forming polypi ;
③ intestinal wall are fibrosis.
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Toxic bacillary dysenteryToxic bacillary dysentery
Children at the age of 2-7 years old are sensible
most are result from S.sonnei and S.flexneri.
clinical features:
① toxic symptom all over the body:
Toxic shock 、 respiratory or circulation failure.
② intestinal symptom: mild
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Questions for the class
1.What kind of inflammation is involved in
bacillary dysenterybacillary dysentery?
2.The definition of typhoid granulomatyphoid granuloma