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Thread: Salmonella[A-Z]Complete Note

  1. #1
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    Lightbulb Salmonella[A-Z]Complete Note


    Over 2000 antigenic types
    Salmonella enterica subspecies enterica serotype Enteritidis = S. Enteritidis.
    They can cause a mild self limiting GI illness ranging to life threatening systemic disease.
    Relative fall in incidence in the UK, although this is still the highest cause of community-associated diahorrea in the developing world.

    Facultatively anaerobic
    Gm(-) bacilli
    Grow on a wide range of simple media
    Highly motile

    ‘O’ antigen: somatic heat stable LPS, anchored on the outer membrane. There is genetic conservation of the lipid A/LPS core region. These are usually just numbers.

    ‘H’ antigen: these are the flagellar protein subunits, and in some microbes two distinct flagellar structures are expressed (Phase I & Phase II genes). These are lower case letters (Phase I) & lower case letters with numbers (Phase II).

    ‘Vi‘ antigen: the virulence factor is expressed in certain serotypes. This protein may encompass the whole bacterium, making detection of ‘O’ antigens difficult.

    Designantion by Kauffmann-White: [’O’ Ag] [Phase I ‘H’] [Phase II ‘H’], e.g. S. Typhi (9, 12, [Vi]: d-). Here only one flagellar phase is expressed.
    Differentiation by phage typing and ABx sensitivity (e.g. S. Typhimurium is very resistant).


    Infects all vertebrates

    Wide range of clinical syndromes

    S. Typhi & S. Paratyphi are essentially human pathogens

    Incubation period = 10-14 days, followed by enteric fever (septicaemic illness).

    Some Salmonellae infect animals
    S. Typhimurium Type 104 = bovine zoonosis

    Infections in the developing world occur from a relatively small number of serotypes.

    Ingested innoculum → colonisation of gut → overgrowth and owerpowering of host defences → infection

    Infective dose: 106 - 109 for S. Typhi (103 suggested for some outbreaks).

    Virulence factors:

    vary amongst strains & serotypes
    depends on the vehicle in ingestion (bacteria can be protected from stomach acid if hiding in food particles)
    Relative increased incidence in <1 yr olds may be due to more aggressive Ix.


    ability to tolerate bile

    S. Typhimurium (ST) expresses Type 1 fimbriae → adhere to α-mannose containing molecules on the surface of ileal microvilli

    S. Enteriditis (SE) express three types of fimbriae (e.g. SEF 14), the expression of which appear to be influenced by environmental conditions

    SE & ST also have non-fimbrial adherence molecules; multiple types expressed in pathogenicity islands (n. DNA sequences that encode several pathogenic mechanisms:-

    Bacterial adhesins
    Adhesin receptors translocated into the host intestine (i.e. they insert their own binding sites into the cells of the gut epithelium)
    Bacterial adhesion leads to degeneration of microvilli and entry into the intestinal epithelia.

    Clinical Syndromes:

    1) Enteric Fever:

    S. Typhi or S. Paratyphi A, B or C
    More severe for S. Typhi
    Penetration of the ileal mucosa allows access to the mesenteric nodes via the lymphatics. After multiplication they drain into the SVC via the thoracic duct.
    1o bacteraemic phase in the first 7-10 days of the incubation period allows infection of the liver, kidneys & bone marrow.
    Multiplication in these organs allows a second phase of heavy bacteraemia leading to fever and clinical illness.
    From the GB, further invasion of the Peyer’s patches leads to gut mucosal infiltration, necrosis and typhoid ulcers.

    Incubation time can vary from 3 - 50 days (usually 14 days)
    Insidious onset: dry cough, dull headache, tender abdomen. Diahorrea uncommon early, and patients mybe constipated.
    Step-wise increase in fever, remains high for 7-10 days.
    Relative bradycardia despite fever, hepato-splenomegaly, rose spots (REM no scar):

    Relapse occurs in 5-10% of untreated cases, with 2o illness being mild.
    Severe intestinal haemorrhage & rupture can occur at any time of the disease.
    Classic typhoid had a mortality of 20%.
    Chronic bacteraemia may occur in endemic areas where schistomiasis co-exsists.
    Some serotypes present as diahorrea.
    2) Gastro-enteritis & Food Poisoning:

    Diahorrea, nausea, headache, malaise. Vomiting is rare.
    8-48 hr incubation.
    Abrupt onset, short course, self-limiting.
    2-3 loose stools → loads of green watery stools, prostration, hypotension, dehydration, ARF.
    Severe infection at the extremes of age and those who are immunocompromised.
    3) Bacteraemia & Metastatic Disease:

    Transient bacteraemia occurs in up to 4% of cases of acute gastroenteritis.
    Localized foci (abscesses)may occur in tissues (salmonellae can survive in macrophages) with pre-exsisting damage:
    Atherosclerotic plaques
    Joint prostheses
    Other implants
    Bony disease (e.g. osteomyelitis & sickle cell disease)
    Suppurative osteomyelitis may occur as part of 2o or 1o infection.
    May cause meningitis in neonates and children.
    Long term survival in the liver, billiary tree, kidneys & bone marrow results in a carrier state.
    4) Prolonged carrier state:

    Organism excreted in the stool for days or weeks after resolution of clinical disease. This ususally leads to complete clearance.
    Chronic carriers excrete salmonella for a year or more - up to 5% of convalscents from typhoid/paratyphoid. GNBs present in the billiary tree and to a lesser extent the urine.
    <1% <20yrs become carriers
    >10% >50yrs.
    Female:male = 2:1.

    Laboratory Diagnosis:

    Desoxycholate-citrate agar or xylose-lysine desoxycholate agar (XLD) can be used to isolate salmonellae from stool.
    Tetrathionate or selenite broth can be used to detect small amounts from environmental samples.

    Suspicious colonies:
    check with O & H antigens, biochemical API testing.
    Negative report after 48 hrs in enrichment cultures.

    Enteric Fever:

    Salmonellae are recovered from the blood in the first 7-10 days and during relapses.
    Can be recovered from clotted blood samples too → digest clot with strep then incubate in broth.

    Stool & urine culture:

    positive results here may mean the patient is a carrier.

    Typhoid fever:

    stool +ve from week 2, urine +ve from week 3.
    Paratyphoid B:
    much shorter clinical course: earlier diarrhoea, stool cultures positive in 1st week.


    IgG difficult to interpret if past infection
    Further confusion with cross reaction of Igs
    Food poisoning:
    Enteriditis/Typhimurium ID’d by: phage typing, ABx resistance, PFGE & plasmid.



    Pharmacotherapy Of Enteric Fever

    Remember Typhoid Mary.

    Chronical asymptomatic carriers:

    If billiary disease: cholecystectomy AND ABx (amoxicillin, ampicillin, septrin, cipro - prolonged courses).
    Adequate sanitation.
    Hand hygiene


    Heat-killed phenol-preserved whole-cell vaccines contain a mixture of cultures of Typhi, Paratyphi A & B (TAB) has been used in endemic countries.
    Now capsular (Vi) polysaccharide or oral live-attenuated vaccines are used.
    Recommended for travellers to Eastern Europe.

    Salmonella Food Poisoning:

    May occur when septicaemic animals are slaughtered.
    Abattoir cross-contamination.
    Poultry - all of our UK eggs are safe (!)
    Cook food well.
    Beware of foods containing raw eggs.
    For prevention all the usual stuff.

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  2. #2
    Join Date
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    Gujarat, India
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    Salmonella Typhi

    Salmonellae are named for the pathologist Salmon, who first isolated S. choleraesuis from porcine intestine.


    More than 2000 serotypes of Salmonella enterica
    Correct name: Salmonella enterica subspecies enterica serotype Typhi
    Shortened to: S. Typhi.


    Gram -ve rod within the family Enterobacteriaceae
    Exposure to food and water (contaminated by faeces) from acutely infected patients or those who are long term carriers
    Significant problems occur in the developing world - most cases affecting children
    No zoonotic reservoirs

    Clinical Features:

    Incubation peroid depends on initial innoculum - can be 1 to 2 weeks
    Minority of patients have diarrhoea during the 1st week of exposure
    First manifestations of the disease may be a fever (40 C)
    Chills, myalgias, headache, sore throat and cough
    Faint rash on the trunk (rose spots)
    Relatively bradycardic despite high fevers
    Abdominal tenderness noted
    Death in the pre-treatment era occured due to multiple perforations in the terminal ileum due to destruction of the Peyer’s patches
    Suppurative complications: pericarditis, meningitis & pneumonitis
    Hepatitis and splenomegaly are noted
    Remember that a state of chronic “carriage” can occur, in contrast to the enteric species where the microbes may be detected in the stool for some time (weeks) after the initial symptoms have settled. This can cause further bacteraemias if neutropenic with mucositis. It is also important in those workers handling unwrapped foods and those with high-risk occupations

    Abnormal LFTs
    Blood culture positive in 50%-70%
    Stool culture in positive in 90%.
    Stool cultures are positive for ~60% of children and ~25% of adults with enteric fever; for the detection of carriers, several samples should be examined because of the irregular nature of shedding .
    Usually positive serology.
    Several serologic tests have been developed to detect S. typhi antibodies. The role of the classic Widal test is controversial, with divergent views on the test’s utility in various areas of endemicity.
    Newer rapid S. typhi antibody tests may be useful in areas where enteric fever is endemic and resources are limited.
    However, no current serologic test is sufficiently sensitive or specific to replace culture-based tests for the diagnosis of enteric fever in developed countries.

    Differentials should include:
    Acute HIV/seroconversion

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