Shigellae DNA analysis has determined that 4 species of shigella are biogroups within E.coli Pathogenic species of shigella S.dysenteriae S.Flexneri S.Boydii S.Sonnei type A type B type C type D
shigellae lactose (-) non- motile Glucose fermentation without Gas production H 2 S production (-) Many share common antigens with species or with other enteric bacteria (Hafnia alvei, P.shigelloides) Cause of bacterial dysentery Shiga toxin acts like enterotoxin and neurotoxin (meningismus and coma)
Shigella Virulence : Endotoxin, genes for adherence, invasion and intracellular replication Permeability barrier of outer membrane Exotoxin (shiga toxin) disrupt protein synthesis and produces endothelial damage (S.dysenteriae) Hemolytic colitis and hemolytic- uremic syndrome associated with shigella
Pathogenesis of shigella Shigella appear unable to attach to differentiated mucosal cells. They first attach and invade the M cells located in peyer patches. Type III secretion system mediates secretion of 4 proteins (IpaA, IpaB, IpaC, IpaD) into epithelial cells and macrophages. These proteins induce membrane ruffling on the target cell, leading to engulfment of the bacteria. Shigellae lyse the phagocytic vacuole and replicate in the cell cytoplasm
Pathogenesis of shigella With the rearrangement of actin filaments in the host cell, the bacteria are propelled through the cytoplasm to immunemediated adjacent cells, where cell-to-cell passage occurs. Organism are protected from clearance.
Pathogenesis of shigella Shigellae survive phagositosis by inducing apoptosis, leads to the release of IL-1β, resulting in the attraction of PMN into the infected tissues. This in turn destabilizes the integrity of the intestinal wall and allows the bacteria to reach the deeper epithelial cells
Pathogenesis of shigella S.dysenteriae produce shiga toxin that have one A subunit and 5 B subunit. B subunits bind to host cell glycolipid (GB3), facilitate transfer of the A subunit into the cell. A subunit cleaves the 28S rrna in the 60S ribosomal subunit, Preventing the binding of aminoacyltransfer RNA and disrupting protein synthesis. Toxin activity damage the intestinal epithelium, mediate damage to the glomerular endothelial cells, resulting in renal failure (HUS)
Epidemiology of shigellosis human are only reservoir for shigella S.flexneri is predominant in developing countries S.dyesnteriae is the most virulent species (mortality 5%-15% in Africa) Shigellosis is a pediatric disease %60 of all infections in children <10 years Out breaks occur in daycare centers, nurseries, Spread from person to person by fecal-oral route (Transmitted by food, finger, feces and fly) The infective dose is 10 2 organism Highest risk for children
Diseases of Shigella Gastroenteritis (shigellosis) (bacterial dysentery) Incubation period: 1-3 days initial watery diarrhea( by enterotoxin) progressing bloody diarrhea ( by invasion), abdominal cramp, tenesmus) Abundant neutrophils, erythrocytes and mucus are found in the stool. Asymptomatic carriage,reservoir for future infections ( rare ) Diagnosis: Culture (SS,SF,XLD, ), latex agglutination
Klebsiella Have a capsule that is responsible for the mucoid appearance of colonies and enhanced virulence factor Non-motile Lactose+ LIA+ Urease + Virulence factors: Capsule (K antigen): persistent to immune response, 80 type of k.pneumoniae
Klebsiella K.pneumoniae: cause community-or hospital acquired lobar pneumonia (40-60% mortality), production of blood-tinged sputum. wound,soft tissue and UTI( in immune suppressive or catheterized patients) K.oxytoca: cause community-or hospital acquired lobar pneumoniae, production of blood-tinged sputum. wound,soft tissue and UTI( in immune suppressive or catheterized patients) K.granulomatis (Donovania granulomatis, Calymatobacterium granulomatis): cause granuloma inguinale (donovanosis) transmitted by trauma or STD K.ozaenae: cause chronic atrophic rhinitis K.rhinoscleromatis: cause rhinoscleroma (granulomatous disease of nose)
Diagnosis and Treatment of Klebsiella UTI: K.pneumoniae causes pyelonephritis and cystitis in catheterized patients.specimen collection and culture like E.coli Pneumoniae : caused by K.pneumonia in immune suppressive patients. bloody sputum, apses, necrosis and septicemia. Specimens: sputum, blood and tracheal aspirate Rhinitis: culture of secretions Rhinoscleroma: microscopy: Gram staining Treatment : Antibiotic susceptibility testing must be done before treatment. Klebsiella is resistant to many antibacterial agents
Enterobacter A part of intestinal normal flora Thin capsule and less mucoid than klebsiella Motile Ornithin decarboxylase + 11 species E.aerugenes E.cloacae Serotyping by O,H,K antigens
Enterobacter Diseases: Primary infections are rare in immunocompetent patients, are more common in neonates and immunocompromised patients. UTI: in catheterized patients. Pneumonia, Wound, sepsis in hospitalized patients Treatment: Resistance is a particularly serious problem with Enterobacter species. Betalactamase class 1 producing E.cloacae
Proteus Lactose(-) Urease(+) Phenylalanine deaminase(+) Motility(+), Growing on KCN medium(+) Xylose(-) Swarming movment on solid media unless CLED agar (cystine-lactoseelectrolyte-deficient) (best medium for urine culture), phenylethyl alcohol agar and sometimes EMB. P.mirabilis P.vulgaris
P.mirabilis : UTI is most common disease Produce six different types of fimbriae Proteus Produce large quantities of urease Urea urease ammonia + CO2 PH Ca + Mn struvite (calsium magnasium hydroxide) +apatite crystals renal (kidney) stones Alkalinity of urine is toxic for uroepithelium Bacteremia, pneumonia, focal lesions in patients receiving intravenous infusions
P.vulgaris nosocomial infections Infection occur in immunocompromised patients. Proteus Bacteremia, pneumonia, focal lesions in patients receiving intravenous infusions O antigens of P.vulgaris cross react with Rickettsial antigens (weil-felix test)