TYPHOID FEVER AND

AMOEBIASIS

DR A.O. OLUWASOLA
 Epidemiology
• Typhoid is a pyrexial systemic disease
caused by intestinal infection with certain
Salmonella species viz.
• S. typhi, S. paratyphi A, B and C.
• Humans are the only host of S typhi, which is
shed in the feaces, urine, vomitus and oral
secretions of acutely ill persons and feaces
of chronic carriers.
• S.typhi is transmitted through food, water,
diary products and flies,
• While others species are via commercial
meats.
 Epidemiology ctd.
• Typhoid has a worldwide distribution
• Endemic only in communities (Developing
countries) where the standards of sanitations
and personal hygiene are low.
• All ages and both sexes are susceptible.
• About 2-4% of typhoid patients become
chronic carriers of the infection-
• Mostly feacal carriers while some are urinary
carriers.
 PATHOGENESIS

• Following ingestion;
• The bacilli multiply in the second part of the
duodenum;
• Salmonellae invade non-phagocytic intestinal
epithelial cells & tissue macrophages;
• Invasion of intestinal epithelial cells is
controlled by different invasion genes:
-ity genes
• It occurs via adhesion and internalisation
processes.
 Phases of infection
• I. Incubation period (10-14 days):
• Transcytosis in peyer’s patches;
• Then lymphatic dissemination via thoracic
duct and transient bactaraemia;
• Clearance and multiplication in MPS;
• II. Septicemia – Ist week of clinical disease:
• Parasitized MPS cells undergo necrosis;
• Blood is flooded with bacilli;
• Diagnosis depends on obtaining positive
blood culture.
• III. 2nd week of clinical dx:-
• Via the liver they pass into bile,
• Multiply rapidly,
• Enter intestinal tract for the second time.
• Heavy reinfection of the lymphoid tissue
occurs;
• Local Ab production occurs.
• Stages involve Hyperemia, Necrosis,
Ulceration, Haemorrhage and perforation or
healing of Peyer’s patches.
• 2nd and 3rd weeks- Diagnosis depends on
culture of feaces.
• 3rd –4th wks- Diagnosis is by urine culture.
• After about the tenth day the widal test.
• (O & H agglutinin) becomes positive and
rises progressively.
• Vi reaction is of no value either in the
diagnosis of acute attack or forecasting
clinical relapse but of help in detection of
carrier state.
 Clinical course
• Onset may be insidious
• Wk1. Malaise, headache, fever, stepladder
temperature pattern, chills.
• Wk 2. Abdominal Symptoms esp. cramps
constipation and then diarrhea, prostration,
• Rose red spots (hyperemic macules in lower
chest and upper abdomen).
• Disappears after 2nd wk.
• Hyperplasia of MPS.-
• Hepatosplenomegally (mild to moderate).
 The typical ‘Face of Typhoid’
•
• Wk 3: Ulcer, Bleeding – shock; & perforation
• Other signs include- Bradycardia &
Leucopenia, relative lymphocytosis.
• As toxaemia increases delirium, Coma &
death.
• In those who recover, temperature falls by
lysis, and appetite returns etc.
• Diagnosis:–
• As above i.e. B. F.U. culture and widal test.
 Complications:
• Haemorrhages and perforation at end
of 2nd wk or during third wk.
• Pneumonia,
• Thrombophlebitis,
• Myocarditis, myositis, arthritis,
osteomyelitis, meningitis, and
cholecystitis.
 Morphology
• I GIT:- Macro:
• Shows hyperplasia of lymphoid tissue in the
small and large intestine.
• Especially terminal ileum + jejunum or
ascending colon.
• Paratyphoid B infection may cause ulcers in
stomach & rectum.
• Longitudinal as in yersinia enterocolitica.
• Four stages occur – hyperaemia, necrosis,
ulceration and healing
LONGITUDINAL ULCERS
 Microscopically:
• There is infiltration of large monocytes with
pale eosinophilic cytoplasm,
• Eccentric nucleus with erythrophagocytosis
+ bacilli, lymphocytes and cellular debris in
cytoplasm called mallory cells or typhoid
cells;
• Monocytes; lymphocytes; plasma cells and
rarely neutrophils.
• Mesenteric lymphadentis occurs,
• Healing is without fibrosis + fibrinous
exudates; haemorrhage; perforation;
ileus; intussusception.
TYPHOID CELLS
 II.LIVER & GALLBLADDER
• Hepatomegally:
• Striking feature is the presence of typhoid
nodules in the liver-
• Consists of collection of macrophages,
lymphocytes + central necrosis + bacilli,
• Also seen in Bone marrow and lymph nodes.
• + Typhoid abscesses,
• Cholangitis is rarer;
• Gall bladder is the usual seat of carrier +
chronic cholecystitis + Gall stone.
TYPHOID NODULES IN ILEUM
• III. SPLEEN –
• Enlarged, Soft, pale red pulp,
• Sinus histiocytosis; reticulo-endothelial
proliferation (prominent malpighian corpuscles) +
typhoid nodules.
• IV. GENITOURINARY SYSTEM.
• Toxic nephrosis + typhoid nodules;
• Orchitis –typhoid nodules.
• V. RESPIRATORY SYSTEM –
• Ulceration and oedema of the larynx, Pneumonitis +
lung abscesses, & mild bronchitis,
• VI. CVS-
• Pericarditis, Fatty degeneration of myofibrils
due to toxaemia.
• VII. CNS
• Meningism, (N) CSF due to toxaemia
• VIII. SKIN:
• Rose Spots- hyperaemia of dermis with an
associated monocytic infiltration + bacilli.
• 8. MUSCULOSKELETAL SYSTEM
• Osteomyelitis of long bones in SCD- SS &SC.
• Typhoid osteitis – typhoid nodules in
marrow.
• Zenkers degeneration in Skeletal muscle e.g.
• Rectus abdominis,
• -A focal hyaline degeneration with
fragmentation of the muscle fibres caused by
the toxaemia.
 AMOEBIASIS
• Agent:- Protozoan Entamoeba histolytica.
• It has a world wide distribution but clinical
disease occurs most frequently in tropical
and sub-tropical regions.
• E. histolytica cyst is the infectious form of
the parasite because they are resistant to
gastric acid.
• In the colonic lumen, cysts release
trophozoites,
• When there is no diarhoea the amoebae
cease feeding and encyst.
 PATHOGENIC MECHANISM
• Amoebae cause dysentery – bloody diarrhoea,
intestinal pain, fever –
• When they attach to the colonic epithelium, they lyse
colonic epithelial cells and invade the bowel wall.
• Amoebae proteins involved in tissue invasion
include:-
• Lectins on parasite bind carbohydrate on colonic
epithelium and RBC
• Channel forming proteins (amoebopore) form holes
on colonic epithelial cells- plasma membrane and
lyse them.
• Cysteine proteinases, -break down proteins of
extracellular matrix.
AMOEBIC TROPHOZOITES

Figure 17-35 Entamoeba histolytica in colon. High-power view of the organisms. Note some of the organisms ingesting red blood cells.

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© 2005 Elsevier
 EPIDEMIOLOGY

• Only 10% of persons infected develop diarrhea,

possibly non virulent strains exist (e.g. E. dispar is
avirulent).
• Trophozoites containing ingested red cells- a
virulent strain.
• Diseases spread by cyst passers, either in the
convalescent period or much later after attacks.
-directly through contaminated hands or indirectly
through foods or flies or water large outbreaks.
• The disease appears in fulminating forms in
pregnant and peuperal women and may be severe in
mal-nourished children.
Life Cycle of Entamoeba histolytica:
 Clinical Features
• Depends on site; intensity of lesion produced; host
immune competence and protozoal virulence.
• a. Intestinal -fever, malaise, nausea, vomiting,
diarrhea, cramps, abdominal tenderness,
dehydration and incapacitation & weight loss.
• OR asymptomatic until immunity falls or
malnutrition ensues.
• b. Extra intestinal –Liver: tender hepatomegally;
more than half give no hx of intestinal infection.
Others - abscesses in brain, lung, & spleen.
+Discharging sinus- draining through body wall.
DISCHARGING SINUS FROM
AMOEBIC LIVER ABSCESS
 DIAGNOSIS
• Fresh and warm fluid feaces can be taken
for immediate examn. for motile
trophozoites- staining with iodine reveals 1-
4 nuclei and glycogen mass, & cysts.
• Scrapings and biopsies obtained by
sigmoidoscopy
• Liver abscess aspirate for trophozoites
• Blood for serologic tests- complement
fixation & indirect haemaglutination tests,
indirect fluorescent antibody test (IFAT),
counter immunoelectrophoresis (CIEP) and
(ELISA)
 MORPHOLOGY
• Amoebiasis most frequently involves the
ceacum and ascending colon.
• In severe cases the entire colon is affected
and rarely ileum.
– Trophozoites resemble macrophages; contain
vacuoles, have smaller nucleus and stain +ve with
PAS stain.
– Amoebae invade through the crypts of lieberkuhn;
burrow through the lamina propia and are halted
by the muscularis mucosa.
 Morphology ctd.
– Fan out laterally to create small pin point flask shaped
ulcers with a narrow neck, and broad base and over
hanging edges.
– Overlying mucosa sloughs off.
– Usually a low-grade inflammatory reaction initially
neutrophilic then with lymphocytes and macrophages
predominating.
– + Amoebae in submucosa and muscularis propia.
Neutrophils are rare.
– Trophozoites may penetrate muscle coat and cause
perforation(rarely) with:
– Haemorrhage , amoebic & bacterial peritonitis and paralytic
ileus & abscesses.
– Rectal and anal fistulae may follow penetrating deeper
lesions + stricture.
FLASK SHAPED ULCERS
PAS+VE TROPHOZOITES
 Amoeboma
• An uncommon lesion seen in areas of
stasis in the large bowel viz – ceacum,
rectum, sigmoid & trans colon –
• A napkin-like constrictive lesion which
consists of a core of necrosis with
acute and chronic inflammatory cells
surrounded by granulation tissue.
• It can be mistaken for a colonic
tumour.
 Amoebic Liver Abscess
– In about 40% of cases amoebae embolize through
portal circulation to liver.
– To produce usually solitary or less often multiple,
discrete abscesses, usually in the right lobe,
– Liver abscess is the most common extra-
intestinal complication of intestinal amoebiasis.
– It has scant inflammatory reaction and shaggy
fibrinous linning. –contains a chocolate
colour/anchovy sauce material.
– usually sterile, but 20 infection purulent material.
Amoebae may be present in the periphery.
AMOEBIC LIVER ABSCESS
• Rare complications include:
• empyema thoracis, broncho-pleural fistulas,
pericardial abscesses, and perianal skin
infection (amoebiasis cutis)
• Metastatic abscesses in kidney and brain.
• There is risk of systemic spread and
widespread dissemination when patients
with underlying amoebiasis or carriers
undergo surgical procedures e.g.
appendisectomy.