enteric fever
TRANSCRIPT
ENTERIC FEVER
Prabin ShahBScMLT, MSc(Biochemistry)
Enteric fever 2
Typhoid fever, commonly just typhoid, is a
common worldwide illness, transmitted by the ingestion of food or water contaminated with the feces of an infected person.
This fever received various names, such as gastric fever, the bends, abdominal typhus, infantile remittent fever, slow fever, nervous fever, pathogenic fever, etc.
INTRODUCTION
The salmonella bacilli was first described by Salmon and Smithin the year 1885.
In 1906, Irish immigrant Mary Mallon worked as a cook and was a carrier. Thus earned the nickname "Typhoid Mary. She died of a stroke after 23 years.
History
The term enteric fever or typhoid fever refers to a communicable disease, found only in man and includes both typhoid fever caused by S.Typhi and paratyphoid fever caused by S.Paratyphi A, B and C .
It is an acute generalized infection of the reticulo-endothelial system, intestinal lymphoid tissue, and the gall bladder.
DEFINITION
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GNB Motile Non sporing Non capsulated
MORPHOLOGY
6
Killed at 60°C in 15 mins
Boiling, chlorination of water and pasteurisation of milk also destroys the bacilli.
Survive in water and ice for weeks
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RESISTANCE
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3 types of antigens;1. Flagellar antigen ‘H’2. Somatic antigen ‘O’3. Surface antigen ‘Vi’
ANTIGENIC STRUCTURE
"O"-group
Sero type "O" antigensPhase 1 (motile)
"H" antigens
Phase 2 (non-motile) "H"
antigensOld New
A 2 S.Paratyphi A 1,2,12 a no phase 2 antigen
B 4 S. Paratyphi B 1,4,5,12 b 1,2
S. Typhimurium 1,4,5,12 i 1,2
C1 7 S. Paratyphi C 6,7 c 1,5
S. Colerae-suis 6,7 c 1,5
C2 8 S.muenchen 6,8 d 1,2
S.newport 6,8,20 e, h 1,2
D 9 S. Typhi 9,12,Vi d no phase 2 antigen
S. Enteritidis 1,9,12 g,m no phase 2 antigen
S. Gallinarum 1,9,12 no phase 1 antigen no phase 2 antigen
S. Pullorum (1),9,12 no phase 1 antigen no phase 2 antigen
E1 3,10 S. Anatum 3,10 e,h 1,6
H antigen( flagellar antigen)Ag is present in the flagellaHeat labile proteinStrongly immunogenicProduces large, loose, fluffy clumps.
O antigenLipo polysaccharideIdentical to endotoxinHeat stableProduces compact, chalky, granular clumps.Less immunogenic
Vi antigen
Surface antigen enveloping the O Ag is
referred to as Vi Ag.
Heat labile
Acts as virulence factor by inhibiting
phagocytosis, resisting complement activation
and bacterial lysis.
Poorly immunogenic.
Not helpful in the diagnosis of enteric fever.
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1. ENTERIC FEVER
i. TYPHOID FEVER
ii. PARATYPHOID FEVER
2. SEPTICAEMIA
3. GASTROENTERITIS
PATHOGENESIS
1. TYPHOID FEVER
The name typhoid was coined by Louis in 1829.
Caused by S.typhi
Acquired by the ingestion of contaminated food and
water
IP: 7-14 days
ENTERIC FEVER
Enteric fever is endemic in all parts of india.
Typhoid fever occurs in 2 epidemiological types;
1. endemic( occurs through out the year)
2. epidemic( occur in endemic or non-endemic areas)
Epidemiology
1. Convalescent carriers shed the bacilli in feces for 3 weeks to 3 months.
2. Temporary carriers Shed the bacilli for more than 3 months but less than a year.
3. Chronic carriers Shed the bacilli over an year
4. Fecal carrier the bacilli that persist in kidney or gall bladder are eliminated through feces
5. Urinary carrier bacilli eliminated through urine, associated with urinary lesion such as calculi.
Types of carriers
Bacilli attaches to the epithelial cells of the
intestinal villi in the small intestine.
Penetrates to the lamina propria and sub mucosa
Phagocytosed by the neutrophils and macrophages
Bacteria resists and it enters into the mesenteric lymph nodes and multiply there via the thoracic
duct and enters into the blood stream.
A transient bacteremia follows and the internal organs like liver, gall bladder, spleen, bone marrow,
lungs and kidney get infected.
Sequence of infection
Clinical features include; Mild pyrexia Headache Malaise Anorexia Coated tongue Abdominal discomfort with
constipation/diarrhea Congestion of mucous membranes Hepatosplenomegaly with soft and palpable
spleen. Step ladder pyrexia with relative bradycardia
and leucopenia. Skin rashes known as rose spots may appear
on the 2nd and 3rd week.
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Rose spots
2. PARATYPHOID FEVER
Milder form than typhoid fever. Caused by S.paratyphi A,B and C
Other salmonella causing enteric fever are;
S.dublinS.bariellyS.sendaiS.enteritidisS.typhimuriumS.eastbourneS.saintpaulS.panama
I. Specimen collection
BloodFaecesUrineAspirated duodenal fluidBileBone marrowRose spotsPus from suppurative lesionsCSFSputumAt autopsy cultures may be obtained from the gall bladder, liver, spleen, and mesenteric lymph nodes.
LAB DIAGNOSIS
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Duration of disease Specimen examination
% positivity
1st week Blood culture 90
2nd week Blood cultureFaeces cultureWidal test
7550Low titre
3rd week Widal testBlood cultureFaeces culture
80-1006080
Specimens collection based on different phases of enteric fever
Gram stain is done
GNBNon capsulatedMotile with peritricous flagella except gallinarum and pullorum.
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II. Microscopy
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Grows on ordinary media Opt temp: 37°C pH: 6-8 Aerobic and facultative anaerobic.
On nutrient agarColonies are 2-3mm in diameter, circular, translucent, grey white in color, low convex and smooth.
III. Culture
On MacConkey’s agar and DCAColorless colonies due to NLF colonies.
Selective mediaWilson and Blair bismuth sulphite medium
Jet black colonies with metallic sheen are formed due to formation of hydrogen sulphide.
Xylose lysine deoxycholate (XLD)Red colonies with black centres are seen
Enrichment mediaSelenite F brothTetrathionate broth (TTB)
Ferments glucose and mannitol forming acid and
gas except S.typhi produces only acid but no gas. Catalase positive Oxidase negative Indole is not produced
Produces H2S in TSI agar except S. paratyphi A
and S. cholerae-suis. Utilise citrate (except S.typhi & S.paratyphi A) MR positive VP negative Urea not hydrolysed Nitrate reduction test is positive
IV. BIOCHEMICAL REACTIONS
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S.typhi
S.Paratyphi A
S.Paratyphi B
S.Paratyphi C
Glucose A AG AG AG
Mannitol A AG AG AG
Lactose - - - -
Sucrose - - - -
Indole - - - -
Citrate - - + +
MR + + + +
VP - - - -
H2S + - ++ +
Biochemical rxns to differentiate btw salmonella species
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Positive in 90% of the cases in the first week of fever. 75% in second week 60% in third week
Procedure
10ml of blood collected under aseptic conditions and transferred into blood culture bottles.
Blood culture
Blood has to be diluted with the culture media in
the ratio of 1:10.
Then incubated at 37°C overnight.
Subculture done on BA and MCA
More preferred method is the Castaneda’s method of blood culture.
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Salmonella are shed in faeces during the infection and
convalescence phase too.
Generally faeces culture turn positive in the second
week of infection.
Sample is inoculated into one tube each of selenite
and tetrathionate broth(enrichment media)
Plated onto MCA, DCA, XLD, and Wilson-Blair medium.
Faeces culture
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Frequency of getting a positive result is less
when compared to that of blood and faeces.
Generally seen as positive in the 2nd and 3rd
weeks.
Urine samples are centrifuged and deposit is
inoculated into both enrichment and selective
medium.
Urine Culture
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5ml of blood is withdrawn aseptically into
sterile container and allowed to clot.
Clot is broken up with a sterile glass rod and added to bile broth containing streptokinase(100units/ml) which digests the clot causing its lysis and thereby the bacteria are released from the clot.
Clot culture
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It is an agglutination test for the detection of
agglutinins (H and O) in patients with enteric fever.
The antibodies begin to appear in serum at the end of 1st week and rise during the 3rd week of enteric fever.
2 specimens of sera are collected at an interval of 7 to 10 days to demonstrate the rising Ab titre.
WIDAL TEST
2 types of tubes; Dreyer’s tube Felix tube
Equal vol of 0.4ml of serial dilution of the serum(1:10 to 1:640) and the H and O antigens are mixed and incubated at 37°C for 4 hrs and read after overnight incubation in room temp.
Control tubes with antigen and normal saline are included to check for auto agglutination.
Procedure
H agglutination - formation of loose, cotton wool clumps
O agglutination – granular deposit at the bottom of the tube
High dilution with carpet formation indicates the antibody titre against that particular Ag.
Control tubes will show a compact deposit (button formation).
A loopful of the growth from nutrient agar slope is emulsified in 2 drops of saline on a slide.
One emulsion acts as a control and other as a test.
Agglutination is first carried out with the polyvalent O and the polyvalent H antisera.
Positive agglutination indicates that the isolate belong to genus salmonella.
Then if S.typhi is suspected, agglutination with O anti serum is done.
Prompt agglutination indicates that the isolate belong to group D salmonella.
S.typhi is confirmed by the agglutination with O anti serum.
SLIDE AGGLUTINATION TEST
Vaccinations
i. TAB vaccine heat killed Polyvalent vaccine Dose schedule: 2 doses of 0.5ml at an interval of
4-6 weeks S/C followed by booster every 3 years.
ii. Purified Vi polysaccharide vaccine(typhim-Vi) Dose schedule: single dose of 25µg injected I/M or
S/C Causes minimal reaction.
PROPHYLAXIS
iii. Live Oral typhoid vaccine
Stable mutant of S.typhi
Dose schedule: 3 doses on days 1,3,5 should be taken an hour before food, with a glass of water or milk.
Oral (typhoral) vaccine is available as capsule.
On ingestion, it initiates infection but self destructs after 4-5 cell divisions and thus cannot induce any illness.
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Antibiotics such as;
Chloramphenicol Streptomycin Tetracycline Ampicillin Amoxycillin Cotrimoxazole
Are found effective in the treatment of typhoid fever.
Treatment
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Showed resistance to chloramphenicol.
Chloramphenicol resistant typhoid fever
appeared in kerala in 1972.
Multi drug resistant S.typhi is also becoming a
major problem in india.
These may cause nosocomial salmonellosis as
septicaemia, meningitis, and suppurative lesions.
Drug resistance
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A zoonotic disease
Caused by S.typhi, S.typhimurium,
S.enteritidis, S.indiana, S.newport, S.agona.
Sources: poultry, meat, milk, eggs.
Clinical features: diarrhea, vomiting, fever,
abdominal pain.
Gastroenteritis
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Certain salmonella may cause septicaemia with
suppurative lesions such as deep abscess,
osteomyelitis , pneumonia, endocarditis and
meningitis.
S.cholerae suis is the most important causative agent
of salmonella septicaemia.
Fulminating blood infection.
Treatment with chloramphenicol.
Septicaemia
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1. Text book of microbiology
Ananthnarayan and Paniker’s
2. Text book of microbiologyC.P. Baveja
3. Mackie and McCartney4. google
REFERENCE
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