1 Typhoid fever You Chengcheng Dept. of pathology China Three Gorges University.

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Transcript of 1 Typhoid fever You Chengcheng Dept. of pathology China Three Gorges University.

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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