shigella, salmonella and yersinia 2012

7/29/2019 Shigella, Salmonella and Yersinia 2012

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1

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.

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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

shigella, salmonella and yersinia 2012

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