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Shigella, Salmonellaand Yersinia
Anne Rompalo, M.D., Sc.M.
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February 10, 2012 2
Med J Malaysia. 2002 Mar;57(1):24-30.
Bacterial enteropathogens isolated in childhood diarrhoea in Kuala Lumpur--the changing trend.
Lee WS, Puthucheary SD.
Department of Paediatrics, University of Malaya Medical Centre, 50603, Kuala Lumpur.
Abstract
A retrospective review of all stool samples obtained from children aged < 16 years with diarrhoea
from University of Malaya Medical Centre (UMMC), Kuala Lumpur, from 1978 to 1997 wasundertaken to ascertain the pattern of bacterial pathogens causing diarrhoea in children in an urban
area in Malaysia. Of 26444 stool samples processed, 2989 (11%) were positive. The five most
common bacterial pathogens isolated were non-typhoidal Salmonella (57%), enteropathogenic E.
coli (EPEC) (14%), Shigella spp. (11%), Campylobacter spp. (5%) and Aeromonas spp. (4%). There
was a significant reduction in the average percentage of positive isolation during the last 5 years of
the study period as compared to the first 5 years (15.0% vs. 7.2%; r = -0.92, p = 0.0001). EPEC and
Shigella spp. were less commonly isolated in the last five years compared with the first five years ofthe study (6% vs 21% p < 0.001 for E. coli; 7% vs 22%, p < 0.001 for Shigella spp.). This information
is important for public health education in reducing the incidence of childhood diarrhoea further, and
in the selection of appropriate antimicrobials in the management of extra-intestinal complications of
childhood diarrhoea.
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Lecture Objectives
This presentation is a continuation of the discussion on
the Enterobacteriaceaethat cause gastrointestinalinfections. At the conclusion of this lecture the
student will know:1) how Shigella, Salmonellaand Yersiniacause gastrointestinal
infections.
2) the major clinical manifestations of these GI infections.
3) the optimum methods for specimen collection and diagnosis4) the essentials of patient treatment and management for each
infection.
3
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Shigella
Closely related to E. colibiochemically andantigenically
Non-lactose fermenter
Nonmotile
Does not produce gas when fermenting glucose
Shigella are divided into 4 species based ondifferences in O antigens and some biochemical
reactions Shigella dysenteriae(A)
Shigella flexneri(B)
Shigella boydii(C)
Shigella sonnei(D)
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ShigellosisEpidemiology
Never a commensal in the human GI tract
Highly adapted to humans
Important factors in transmission
Feces FoodFingers Flies
High infectivity rate: < 200 organisms cause disease
Secondary attack rates are high: 20-60%
Shigellosis in the US Largely a pediatric disease
Associated with day care centers
Typically caused by S. sonnei
Worldwide epidemics ofS. dysenteriaetype I (Shigabacillus) have high mortality
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ShigellaPathogenesis
Fundamental event in disease: invasion ofcolonic mucosa, a multistep process
Entryorganism directed endocytosis
Escape from phagocytic vacuole Actin polymerization
Propulsion through cytoplasm by actin tails
Passage into adjacent cells
Shiga toxin
Not essential for invasion
Contributes to severity of disease: cytotoxin
Can lead to hemolytic uremic syndrome
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ShigellaClinical Features
Classic bacillary dysentery Fever
Abdominal cramps
Tenesmus
Bloody, mucoid, small volumestools
S. sonneidiarrhea in theU.S. Fever
Systemic symptoms
Watery diarrhea
With both entities stoolmicroscopy shows largenumbers of fecal leukocytes
Appearance of rectosigmoid colon by
sigmoidoscopy showing loss of lumen due to
bowel wall edema, mucous, areas of
hemorrhage and yellow exudates (leukocytes)
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ShigellaDiagnosis
Stool culture on non-selective and selectivemedia
XLD (xylose-lysine-deoxycholate agar) OR
Hektoen enteric agar(HE)
AND Broth enrichment (GN or
selenite)
Shigella on XLD agar
E coli on
XLD agar
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Shigella Treatment
Disease is usually self limited
Antibiotics are indicated to prevent
disease transmission
Ampicillin resistance is common
Alternative agents: TMP/SXT, quinolones,
third generation cephalosporins,azithromycin
Avoid antispasmodic agents
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Salmonella sp. Bacteriology
Non-lactose fermenters
Produce hydrogen sulfides from sulfur-
containing amino acids
Selective media is used to recover
organisms from stool
Panels of biochemicals are used to
confirm identification
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Salmonella Classification
More than 2500 distinct serotypes existbased upon antigenic analysis of O/K/Hantigens
CDC 2000 classification Two species
Salmonella enterica: includes subspecies I(contains most of the human pathogens), II, IIIa,IIIb, IV, VI
Salmonella bongori(formerly subspecies V)
Subspecies/serotypes if named before 1966 retainthat name e.g. Salmonellaserotype Typhi
(Previously Salmonella typhi)
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Salmonella GastroenteritisEpidemiology Ubiquitous pathogens found in humans,
livestock, mammals, reptiles, birds andinsects
Gastroenteritis (non-typhoidal) Related to improper food handling Poultry products, including eggs, are the most
common vehicles of infection
1.4 million cases occur annually in the U.S.
Peak incidencesummer/fall Highest attack rates are in children < 5 yrs. and
adults > 70 yrs.
S. serotypeTyphimurium and S. enteriditisserotypes are the major causes of disease
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Salmonella GastroenteritisPathogenesis
Major pathogenic mechanism: invasion
Sequence of events
Bacteria adhere to brush border of
intestinal cells and cause membrane
ruffles
Bacteria are internalized by pinocytosis Bacteria enter lamina propriaendure
inflammatory response
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Salmonella GastroenteritisClinical Manifestations
Symptoms begin 6-48h following
ingestion of contaminated food or water
Nausea, vomiting, cramping diarrhea:food poisoning
Diarrhea persists 3-7 days, resolves
spontaneously Fever is present in 50% of patients
Infecting dose is > 105 bacilli
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Salmonella Diagnosis
Salmonella on HEK agar
note H2S (black colonies)
Salmonella species TSI
reaction
Confirm with serotype
agglutination
Send to State Lab
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Salmonella GastroenteritisTreatment
Fluid and electrolyte balance
Control of nausea and vomiting
Antibiotics are recommended for certain groups at riskof invasive disease:
Neonates up to 3 months
Patients > 50 yrs. of age
Patients with lymphoproliferative disorders
Patients with bone or joint disease
Patients with sickle cell disease
Patients post transplantation
Symptomatic patients with HIV
Ampicillin, trimethoprim sulfamethoxazole, quinolones
third generation cephalosporins are potentially usefula ents
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Typhoid Fever
Worldwide cause of morbidity and mortality
Contaminated water is the vehicle of
transmission in endemic areas
Food contaminated by a carrier is the most
frequent source of infection in non-endemic
areas
In U.S. disease is seen primarily in travelers toMexico, Asia, Latin America, India
S. typhiand S. paratyphiinfect only humans
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Typhoid FeverPathogenesis
S. typhienter and kill M cells
Organisms invade macrophages,
multiply
Spread to reticuloendothelial system
and reach the blood stream
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Typhoid Fever
Multi-organ system infection
Incubation period 14 days
Symptoms
Fever Relative bradycardia
Headache
Rash (Rose spots)
Constipation
Bacteremia may lead to infection at othersites
Intestinal perforation may occur
Infection in biliary tree may lead to carrierstate
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Typhoid Fever
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Typhoid FeverDiagnosis
High index of clinical suspicion
Early: positive blood cultures
Late: positive stool, urine cultures
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Typhoid FeverTreatment
Antimicrobials are effective and required: Ampicillin
Ceftriaxone
Quinolones
Trimethoprim/sulfamethoxazole Azithromycin
Chloramphenicol
Vaccines Live attenuated vaccine
Parenteral Vi capsular polysaccharide vaccine Efficacy ranges from: 50-80%
Preventive measures Treatment of carriers
Provision of safe water
Travelers beware
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Yersinia
Coccobacilli that demonstrate bipolar staining
Some strains grow
best at temperatures < 37C--Survive at refrigerator temps
Species of major clinical
significance Yersinia pestis
Y enterocolitica
Y pseudotuberculosisY enterocolitica in blood
showing bipolar staining
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Yersinia
PathogenesisEnteropathogenic Y. enterocolitica
and Y. pseudotuberculosis
Ingestion
Invasion of M Cells ofPeyers Patches
Proliferation in Lymph nodes
Small intestinal inflammation
and ulceration
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YersiniaClinical Manifestations
Enterocolitis
Fever
Abdominal pain
Diarrhea
Acute mesenteric lymphadenitis
Terminal ileitis
Septicemia
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YersiniaDiagnosis
Use selective differentialmedia for recovery CIN (cefsulodin-irgasan-
novobiocin agar)
Incubate at 32 C or lowerfor 24-48 h
Colonies appeartranslucent with dark redcenters
TSI reactions:alkaline/acid without H2S
Urea positive
NLF on MacConkey agar
Yersinia enterocolitica on CIN agar
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Treatment and Prevention ofYersinia Infections
Prevention
Avoid eating
undercooked pork orother meats
Appropriate food safety
Screening blood donors
for recent fever or GI
illness
Treatment
Enteric disease is
usually self-limited Treat sepsis with
parenteral antibiotics: Aminoglycosides
TMP-SXT
Ciprofloxacin
Doxycycline