SHIGELLA

SHIGELLA
• Most important agent of bacillary dysentery.
• 1896 - Japanese microbiologist Kiyoshi Shiga isolated the first
member, S.dysenteriae serotype-1 from epidemic dysentery.
• Differ from E. coli being nonmotile & not fermenting most sugars
except mannitol.
 CLASSIFICATION

• Based on a combination of biochemical and serological characteristics

- four species;
- S. dysenteriae, S. flexneri, S. boydii and S. sonnei.
• Serotypes are distinguished within the species.
 MORPHOLOGY
• Shigellae are short, gram negative rods.
• Measures 0.5 x 1-3 μm in size.
• Non motile, non-sporing and non capsulated.
• Fimbrae may be present.
 ANTIGENS AND SEROTYPING OF
SHIGELLA
• S. dysenteriae (group A):
- Has 15 serotypes.
- Does not ferment mannitol.
Serotype 1 (S. shigae): only Shigella to produce Shiga toxin. Only
member of family Enterobacteriaceae to be catalase negative, Indole
negative.
Serotype 2 (S. schmitzi) forms indole and ferments sorbitol and
rhamnose.
ANTIGENS AND SEROTYPING OF
SHIGELLA
• S.flexneri (group B): has 6 serotypes.
- Most complex antigenically.

• S.boydii (group C): has 19 serotypes.

- First described by Boyd.
- Isolated least frequently from cases of bacillary dysentery.

• S.sonnei (group D): antigenically homogeneous and has only one

serotype.
 ANTIGENS AND SEROTYPING OF
SHIGELLA
• K antigen - present in some serotypes, covers O antigen and makes it
inagglutinable by homologous O antisera.

• Fimbrial antigens found in some strains.

• Flagellar H antigen is absent.

Cross reactivity:
- Shigella (other than S.sonnei) cross-react with E. Coli.
- S. sonnei cross react with Plesiomonas shigelloides.
 PATHOGENESIS
• One of the important causes of bacillary dysentery

Mode of transmission:
- Ingestion - contaminated fingers (most common), food, and water or
rarely flies.
• Minimum infective dose: 10–100 bacilli are enough.
 PATHOGENESIS
• Entry via M cell: mucosa via M cells engulfed by macrophages 
macrophages release bacilli  recruitment of inflammatory cells to
infected site  acute colitis

• Invasion: Once inside the submucosa, shigellae induce their own

uptake into the adjacent epithelial cells virulence plasmid codes for ipa
proteins and type III secretion system

• Direct cell-to-cell spread: by inducing actin polymerization of host cells

- IcsA proteins.
 EXOTOXINS:
• Shigella enterotoxin (ShET1 and 2)
- ShET1 - structurally similar to cholera toxin and found in S.flexneri 2a
- ShET2 - present in all S.flexneri isolates, helps in iron uptake
• Shiga toxin: cytotoxin produced by S.dysenteriae type 1
- Similar to verocytotoxin of EHEC
- Inhibits protein synthesis by inhibiting 60S ribosome
- Enhances local vascular damage – intestine, kidney and brain
• Endotoxin: induces intestinal inflammation and ulcerations.
 CLINICAL MANIFESTATIONS
1. Incubation period: 1–4 days
2. Initial phase - watery diarrhea with fever, malaise, anorexia and
vomiting
3. Phase of dysentery:
- Frequent passage of bloody mucopurulent stools with increased
tenesmus and abdominal cramps.
- Endoscopy - edematous and hemorrhagic mucosa, with ulcerations
and overlying exudates.
- Mostly self-limiting.
 CLINICAL MANIFESTATIONS
4. Phase of complication: children < 5 years
- Intestinal complications - toxic megacolon, perforations and rectal
prolapse.
- Metabolic complications - hypoglycemia, hyponatremia, and
dehydration.
- Ekiri syndrome or toxic encephalopathy: altered consciousness,
seizures, delirium, abnormal posturing and cerebral edema.
- Bacteremia - rare and can lead to meningitis and pneumonia.
 CLINICAL MANIFESTATIONS
5. Postinfectious phase:
- HLA-B27  autoimmune reaction months after shigellosis
- Reactive arthritis, ocular inflammation and urethritis
- Seen only after S.flexneri infection (3% of cases)

HUS (Haemolytic Uremic Syndrome): may occur as a complication in

severe cases due to microangiopathic haemolytic anaemia,
thrombocytopenia & renal failure.
 EPIDEMIOLOGY
• Risk factors - overcrowding, poor hygiene & children <5yr
• Epidemics in developing countries

• S.flexneri – MC (60%) in the developing areas.

• S.sonnei – MC (77%) in developed and industrialized world.
• S.dysenteriae type-1 : high mortality, epidemics of dysentery,
particularly in refugee camps.
 EPIDEMIOLOGY
• No animal reservoirs & cases are the only source of infection
• Chronic carriage - rare except in malnourished children or AIDS
patients
• World: most communicable among bacterial diarrheas
• 80 million cases of bacillary dysentery with 7 lakh deaths annually
• Children (<5 years) accounts for nearly 60% of the cases
• Development of drug resistance among Shigella strains
 LABORATORY DIAGNOSIS
• Specimen collection: Fresh stool (Rectal swabs are not satisfactory)
• Transport media: Sach’s buffered glycerol saline
• Wet mount : large number of pus cells, erythrocytes & macrophages
• Culture:
• Enrichment broth:Selenite F broth, tetrathionate broth and gram-
negative broth  Uniform turbidity appears in 24 hours 
subcultures onto selective media
 LABORATORY DIAGNOSIS
Selective media:
• Mildly selective media:
- MacConkey agar - Non-lactose fermenting colonies
• Highly selective medium
• DCA (Deoxycholate citrate agar): translucent colonies
• XLD agar (Xylose lysine Deoxycholate): red without black center
• SS agar (Salmonella Shigella agar)
• Hektoen enteric agar
 LABORATORY DIAGNOSIS
• Culture smear & motility testing: short, gram-negative bacilli
nonmotile, noncapsulated and non-sporing
• Biochemical reactions:
• Catalase: catalase positive except S. dysenteriae serotype-1 and S.
flexneri serotype- 4a
• Oxidase test - negative
• Mannitol fermentation: All species ferment mannitol except S.
dysenteriae, Newcastle biotype of S. flexneri serotype-6 and
rabaulensis biotype of S. flexneri serotype-4a
 BIOCHEMICAL REACTIONS
• Do not Lactose and sucrose fermentation: except S.sonnei which is a
late fermenter of both
- Gas production: All are anaerogenic except—Manchester and
Newcastle biotypes of S. flexneri type 6
• Indole production: Most shigellae do not produce indole.
• Urease and citrate negative
• TSI - alkaline/acid, no gas and no H2S
 LABORATORY DIAGNOSIS
• Decarboxylase test: Lysine, arginine and ornithine Negative (except S.
sonnei which decarboxylates ornithine)
• ONPG test - negative (except S. Sonnei)
• Slide agglutination test: Confirmation using group specific & species
specific antisera
• Bacteriocin or colicin typing - done for S. sonnei
• Antimicrobial susceptibility testing
 TREATMENT SHIGELLA
• Every case of shigellosis should be treated with antibiotics
• Ciprofloxacin - drug of choice.
• Alternative drugs - ceftriaxone, azithromycin, pivmecillinam and some
fifth-generation quinolones
• Duration - 3 days except for:
- S. dysenteriae type 1 infection—5 days
- Infections in immunocompromised patients—7–10 days
• Oral rehydration solution (ORS)
 PREVENTION
• Strict infection control measures of contact precaution
• Handwashing - single most important measure, must after handling
of children’s feces and before handling food
• Stool decontamination (e.g. with sodium hypochlorite)
• No vaccine available against shigellosis
 EDWARDSIELLEAE
• Commensal in the gut of reptiles and fishes
• Human infection - rare, ingestion of inadequately cooked aquatic
animals
• E. tarda - most frequently isolated species
• Gastroenteritis (most common presentation)
• Others - septic shock, liver abscess and infections related to trauma
and aquatic environment
 EDWARDSIELLEAE
• E. tarda - biochemically slow
• Motile and biochemical properties similar to E. Coli with some
exceptions:
- Ferments fewer sugars (only glucose and maltose)
- Non-lactose fermenter
- Produces H2S
E. tarda has been isolated from wounds, urine, blood & from CSF in cases of fatal
meningitis.
- Treatment: susceptible to most antimicrobials used for gram-negative
bacilli
 CITROBACTEREAE
• Mostly environmental contaminants isolated from water, soil, food
and feces of man and animals
• Urinary tract, gallbladder and middle ear infections and neonatal
meningitis (C.koseri)

Identification:
- Motile, ferment lactose
- Citrate positive
- Lysine decarboxylase negative
 CITROBACTEREAE
• C. freundii—indole negative and H2S positive
• C. koseri (previously, C. diversus)—indole positive and H2S negative
• C. amalonaticus—indole positive, H2S negative and grows in KCN
medium
• Ballerup-Bethesda group - possess Vi antigen, antigenically similar to
that of salmonellae
• Treatment: Most are MDR