Shigella, salmonella & yersinia

Non-Lactose Fermenters

Prof. Alaa Al-Charrakh

Babylon University, Iraq

Enterobacteriaceae\ Non-lactose fermenters

Pale-colour colonies on MacConkey agar

ProteusShigellaSalmonella Yersinia

Shigella:

Gram-negative, non-motile rodsNon lactose fermentersNot a member of normal colonic flora

Classification of Shigella 4 groups on the basis of :• Different somatic (O) antigens &• Fermentation of glucose & mannitol

1. Group A – S. dysenteriae – 10 serotypes °(Type I – Shiga bacillus) – causes severe dysentery

2. Group B – S. flexneri 3. Group C – S. boydii 4. Group D – S. sonei

Pathogenesis• Very low Infective Dose (ID50)°Ingestion of as few as 100 bacilli can cause disease as bacteria are not easily killed by stomach acid°Vibrio cholerae and Salmonella typhi – 105 bacilli.

• Transmission from person to person by “Four Fs” fingers, flies, food, faeces• Causes Shigellosis (dysentery) • Only a human disease• Disease of GIT – invasion of mucosa of distal ileum

and colon.

Shigella are taken up by M cells in the large intestine by endocytosis.

Bacteria are quickly released from endosomes and leaving shigella free in the cytoplasm. The bacteria multiply & enter the inferior and lateral aspects of the epithelial cells

Actin filaments quickly form a tail and push the bacteria into next cell where they multiply. Macrophages that take up Shigella are killed and release organism.

Infected cells die and slough off. Acute inflammatory response occurs with bleeding and abscess formation.

Pathogenesis of ShigellaEpithelial cellM cell Shigella

Endosome

Macrophages

Pathogenesis• Some strains of S. dysenteriae produce “Shiga toxin” like

EHEC- contributes to severity of disease. • The toxin has a strong association with hemolytic uremic

syndrome (HUS). In this, RBCs break up in tiny blood vessels resulting in anemia and kidney failure.

Clinical features of shigellosisCommonly called bacillary dysenteryIncubation period : 3-4 daysInitially abdominal cramps followed by diarrhoea

(watery at first) and later on dysentery (contains blood, pus and mucous) – small volume of bloody mucoid stools.

S. dysenteriae – most severe, S. sonei – mildFeverDisease is self-limiting within few days.

Lab identificationSpecimen : stoolMicroscopy• Methylene blue staining to see PMNLs : if present

(Invasive organisms like Shigella, Salmonella, Camphylobacter rather than: toxin producing organisms like V. cholerae, E. coli, C. perfringens).

Culture on:• MacConkey or Salmonella – Shigella agar (SS Agar) Non-lactose fermenting colonies identified by:° Motility (non-motile)° TSI – Butt – acidic, Slant – alkaline; no H2S Serological Grouping : A-D subtypes

TreatmentRehydrationAntibiotics - Ciprofloxacin is drug of choice

- AmpicillinAntispasmodics are contraindicatedImmunity: Short lived; Preparation of oral live attenuated vaccine is on the

way to stimulate mucosal IgA.

PreventionSanitary precautions Good personal hygiene (hand-washing)

SalmonellaComprises of about2,500 serotypes Parasite of intestine of poultry and animals (cattles)S. typhi and paratyphi – human are the only hosts

Antigenic structure• Somatic (O) antigen• Flagellar (H) antigen• Virulence (Vi) antigen – by S. typhi &

S. paratyphi C

ClassificationA. Ewing’s classificationThree species:

1) S. typhi (one serotype)

2) S. choleraesuis (one serotype)

3) S. enteritidis (> 2,400 serotypes)

Kaufman-White classificationEach serotype given a species name

(>2,400 species e.g. S.dublin, S.tamale etc)

SalmonellaImportant members are:• S.typhi• S. parathyphi A,B,C• S. typhimurium• S. choleraesuis

Diseases caused by salmonella1. Gastroenteritis - S. typhimurium

2. Enteric fever - S. typhi (typhoid fever)

- S. paratyphi A,B,C (paratyphoid fevers)

3. Bacteremia -mostly S. choleraesuis, S. typhi

Transmission

• Animal food stuffs • Poultry – (eggs infected trans-ovarially)• Contaminated water and vegetables• Ingestion of raw milk has been associated with outbreak• Seasonal variation – peak in summer – fall

Diseases caused by Salmonella

Gastroenteritis (Enterocolitis)• Most common cause is S. typhimurium• Infective dose : 10,000 bacilli or more.

Patients on antacid drugs – a smaller dose.• Incubation period : 24-48 hours.

PATHOGENESIS• After ingestion → bacilli are internalized by induced

endocytosis in the epithelial cells of ileum & colon → penetrate to lamina propria → inflammation and poor absorption.• PMNL response limits infection to gut • Bacteremia is infrequent.

CLINICAL FEATURES:Nausea & vomiting Abdominal cramps & diarrhea

Salmonella are taken up by M cells in the small intestine by endocytosis.

Bacteria multiply within endosomes and kill M cells. Bacteria are discharged from base of cell and are taken up by macrophages inPeyer’s patches.

The bacteria multiply inside cells leading to death of macrophages. Are carried via lymphatics to macrophages in mesenteric LN, liver, spleen, bone marrow where they multiply and cause bacteremia.

Symptoms of the disease probably due to Endotoxins.

Pathogenesis of Typhoid FeverEpithelial cellM cell Salmonella

Endosome

Macrophages

Enter RES Cause bacteremia Infection of Gall Bladder

Infection of intestinal lymph follicles

Clinical features of enteric feverFirst WeekGradual increase in fever-step-ladder pattern Generalized aches & pains Anorexia & constipation Relative bradycardiaSecond Week High-grade feverAbdominal pain & diarrhea, weaknessEnlarged spleen, rose spots on abdomenThird Week: If no complications – recovery starts.

Lab identification

Specimen : stool or bloodMicroscopy• Methylene blue staining to see PMNLs : if present

Culture on:• MacConkey or Salmonella – Shigella agar (SS Agar) Non-lactose fermenting colonies identified by:° Motility (motile)° TSI – Butt – acidic, Slant – alkaline; with H2S

Complications of enteric fever

• Intestinal perforation in terminal ileum• Abscess formation• Pneumonia• Myocarditis, damaged heart valves• Thrombophlebitis, IVC• Carrier state (3%)

Yersinia pestis: The agent of Plague

Plague – infection of wild rodents, transmitted interspecies occasionally from rodents to humans, by bites of fleas.

Outbreak: seen in India, Africa, North/South of America

and S.E. Asia.

Black death – pandemic that killed 2/3 of Europeans (~75 millions people) in late 1340s.

Plague is caused byYersinia pestis G-ve rod; exhibits striking bipolar staining with Wright-Giemsa stain; non-motile.

Pathogenesis

By coagulase

1

Polymorphs→ killed

Monocytes→ survive

Clinical findings

After 2-7 days of incubation, patients presented with high fever, painful lymphadenopathy, enlarged, tender nodes (buboes) in groin and axillae. Sometimes with vomiting and diarrhoea.

Later disseminated intravascular coagulation (DIC) leads to hypotension, altered mental status, renal & cardiac failures.

As a result, the patient develops a severe

bacterial pneumonia, exhaling large numbers of

viable organisms into the air during coughing

fits. Up to 90 percent of untreated patients will

die representing a highly contagious health

hazard to nursing staff.

Diagnostic: important to recognize early, confirms with lab.Specimens: taken from blood, aspirates of enlarged lymph nodes and sputum.

Control:

(1) streptomycin, alternatively tetracycline; (2) destruction of plague-infected rodents, (3) vaccine (formalin-killed) for travelers.

Thank you