Lecture 13-Entero-Shigella-Yersinia

Lecture 13-Entero-Shigella-Yersinia - gram negative rods...

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Unformatted text preview: gram negative rods General Characteristics CORRECTION!!! motile, peritrichous flagella produce abundant hydrogen sulfide (opposed to Shigella\E.coli)­ ­ S. paratyphi , cholerasusis are exceptions and produce low amount of H2S Resistant to bile Non­lactose fermenter (MacConkey agar/colorless colony) several surface antigens: O, Vi (subunit vaccine), H Enterobacteriaceae Part III Shigella and Yersinia Lecture 13 Classification Classification Family Genus Species Enterobacteriaceae Shigella S. dysenteriae most severe disease S. flexneri most common in underdev. countries S. boydii rare S. sonnei most common in dev. countries New DNA analysis found the shigella species to be serogroups of E.coli!!! General Characteristics General Characteristics gram negative rods usually non­motile lactose fermentation negative ­McConkey Agar non­H2S producers (contrast to Salmonella) have capsule K antigen grouped according to O antigen Epidemiology World ~ 165 million cases 99% in underdeveloped countries Of those ~70% in children under 5 ~ 1 million deaths (60% in children<5) S. flexneri most common in underdeveloped countries Epidemiology /Shigellosis Epidemiology USA > 12,000 reported cases in US in 2006­2007/ estimated 450,000 S. sonnei most common infection in developed nations Epidemiology Epidemiology USA MMWR October 2010 Epidemiology /Shigellosis Epidemiology /Shigellosis USA In 2005, Kansas, Kentucky, and Missouri reported increases in shigellosis cases associated with day care centers caused predominantly by multidrugresistant (MDR) (i.e., resistant to ampicillin and trimethoprim/sulfamethoxazole [TMP/SMX]) strains of S. sonnei. general: day care center are important settings for shigellosis outbreaks! Epidemiology Transmission 4 Fs (Fingers, food , flies and feces) Fecal­oral route consumption of contaminated food or water no seasonal variance mostly pediatric cases (>70%) low doses required (1­100 CFUs) May be asymptomatic to severe bacillary dysentery Clinical Manifestation Clinical Manifestation Early onset (after 1­3 days) watery diarrhea Abdominal cramps Fever Bloody stools (frequently with mucus, leukocytes, pus) Usually self limiting Systemic infections very rare Hemolytic Uremic Symptom is possible complication (Renal Failure; EHEC) Laboratory diagnosis Laboratory diagnosis Shigella are very fragile ex vivo culture rectal swab or stool immediately use selective media (HE, XLD) both inhibit gram­pos. biochemical tests serology Overview: Bacteria induced host cell Overview: Bacteria induced host cell actin rearrangement Shigella and Listeria : general mechanisms of infection, replication and spreading are similar Shigella Actin tails of Shigella Actin tails of Actin tails induced by different Actin tails induced by different pathogens Actin Tail Formation Actin Tail Formation Listeria: direct activation of Arp2/3 via bacterial protein (ActA) Shigella: indirect activation of Arp2/3 via cellular protein N­WASP Shiga Toxin Shiga Toxin Stx­1 & ­2 (present also in STEC) The A subunit cleaves 28S rRNA in 60S ribosomal subunit Disrupts protein synthesis Leads to cell death Shiga Toxin Shiga Toxin S. dysenteriae and certain EHEC (Stx­1 and Stx­2→HUS) Binds glycosphingolipid Inactivates 28S ribosomal RNA AB Structure: catalytic A subunit, noncovalent bond to B­subunit pentamer 5 Cholera toxin /LT­1 in ETEC Cholera toxin /LT­1 in ETEC Pathogenicity Pathogenicity Endotoxin/LPS TTSS Invasion (“trigger mechanism” phagocytosis) Enterotoxins ­Induces cell death of macrophages ­cell to cell spread (IcsA) ­escape from phagosome Exotoxin (Shiga toxin) in S. dysenteriae only; most serious forms of shigellosis ­mediates endothelial damage and hemolytic colitis ­in some cases Hemolytic Uremic Syndrome (Stx­2 expression) Ipa A, B, C, D Treatment/Prevention Treatment/Prevention Rehydration Antibiotic treatment in sever cases In vitro susceptibility testing required Start Trimethoprim/sulfamethoxazole (TMS) or Ciprofloxacin Proper sewage disposal Proper hygiene of child care workers (and everyone else!)­Frequent hand washing Water chlorination No vaccine available Salmonella vs. Shigella Salmonella vs. Shigella Yersinia Yersinia Classification Classification Family Genus Species Enterobacteriaceae Yersinia Y. pestis Y. enterocolitica Y. pseudotuberculosis General Characteristics General Characteristics Wayson staining General Characteristics General Characteristics gram negative, short, plump rods usually non­motile lactose negative grouped according to O antigen have capsular K antigen Yersinia Pestis Yersinia Pestis Bubonic Plague “The Dance of Death” From Toggenburg bible 1411 541­542 first pandemic (~100 million death) 1346 to 1350, the second pandemic started in China and moved along the trade routes South to Europe. This pandemic killed more than one third of the population of Europe (~35million) and a total of ~ 200million 1629­1631 Italian plague (Venice “Quaranta” orig. Quarantine) 1855 third pandemic started in China killing 15million China+India alone Bubonic Plague Bubonic Plague (Black Death) Plague: “Prevention” Plague: “Prevention” " Der Doctor Schnabel von Rom " (English: "The Doctor Beak of Rome") engraving by Paul Fürst (after J Columbina). The beak is a primitive gas mask, stuffed with substances (such as spices and herbs) thought to ward off the plague Epidemiology Epidemiology Epidemiology/World Epidemiology/World 1,000­3,000 cases per year About 10 countries affected ~100­200 death per year Local epidemic possible (India 1994) Plague outbreak in India; Newsweek 1994 Epidemiology/USA Epidemiology/USA •~13 cases per year • mostly in NM, AZ, CO and CA •Last epidemic in 1924­25 in Los Angeles Reservoir/Transmission Reservoir/Transmission Natural host for all Yersinia spp. is animal (zoonotic infections!) Y. pestis primarily in wild rodents (rats) Y.pestis is mostly vector­borne disease (transmitted by bite of intermediate host; flea) Pulmonary Plague: highly infectious, transmitted person­to­person via aerosol Rodent flea Rodent flea Disease Manifestation Disease Manifestation Swollen lymph glands termed "buboes" caused by plague bacteria (bubonic plague). Bubonic plague (primary infection in lymphe) ­onset after 2­6days ­enlarged, tender lymph nodes (buboes), fever chills ­can become septicemic Septicemic plague (blood): fever, chills, abdominal pain, bleeding into skin (black) and other organs Both above can lead to Pneumonic Plague: fever, chills, cough, difficulty breathing, rapid death (highly contagious) Disease Manifestation Treatment Bubonic/Septicemic plague: 50% mortality rate if untreated (5% if treated) Pneumonic plague: 90% mortality if untreated, survival rate depends on start of treatment (within 24h!) Recommended chemotherapy: streptomycin, chloramphenicol (good tissue penetration) Treatment/Prevention Plague Scientists wear protective suits when examining a mouse with fleas that can harbor plague bacteria. Avoid wild rodents Pest control programs in urban areas Monitor plague in rodent populations Use of insecticides to kill fleas Preventive drug treatment for person at risk Vaccine no longer commercially available Many antibiotics work for treatment (streptomycin, ciprofloxacin) Treatment/Prevention Plague Yersinia: Dissemination Yersinia Overview: Bacteria induced host cell Overview: Bacteria induced host cell actin rearrangement “Zipper” mechanism for induced phagocytosis into endothelial cells Invasin Yersinia: YOPs help to avoid host cell Yersinia macrophages YopH, inhibition of phagocytosis YopJ/P, induction of apoptosis Pathogenicity determinants Pathogenicity determinants Endotoxin/ LPS Invasin (Adhesion) TTSS Multitude of specific virulence factors Yersinia Outermembrane Proteins (YOPs) Enteric Yersinia infections Enteric Yersinia infections Gastroenteritis Quite rare 1 in 100,000 Mostly Y. enterocolitica Associated with consumption of contaminated food (meat, milk, water) Infection more common during winter months! Zoonotic infections (pigs) Enteric Yersinia infections Most often in young children Onset 4­7 days after exposure May last 1­3 weeks Fever, abdominal pain (right sided, Appendicitis!), bloody diarrhea Bacteremia rare Usually self limiting If not use TMS or aminoglycosides Bacteremia/Septic shock Bacteremia/Septic shock Y. enterocolitis can grow at 40C Can grow to large numbers in contaminated blood samples Cause septic shock and/or bacteremia after blood­transfusion No rapid diagnostic test available to screen for contamination ...
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This note was uploaded on 01/24/2011 for the course BSCI 424 taught by Professor Staff during the Fall '08 term at Maryland.

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