Lecture 20 Vibrio and Aeromonas

Lecture 20 Vibrio and Aeromonas - Vibrio and Aeromonas...

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Unformatted text preview: Vibrio and Aeromonas Lecture 20 Classification Classification Family Genus Species Aeromonodaceae Aeromonas A. hydrophila A. caviae A. veronii biovar sobria Aeromonas Aeromonas Gram­neg., rod shaped Facultative anaerob Resembles members of Enterobacteriaceae Motile with monotrichious flagellum Can grow in temp as low as 4C Aeromonas: Epidemiology Aeromonas: Epidemiology Bacteria are ubiquitous in fresh and brackish (intermediate salt concentration) water Aeromonas are mainly a serious pathogen for fish and amphibians In Humans: (mostly affects immunocompromised ) Food borne infections (water/food) cause of gastroenteritis Contact with contaminated water (swimming) cause of wound infections Epidemiology Epidemiology Bacteria are common in environment and cause serious disease but no outbreaks recorded Frequency of Aeromonas infections in US unknown Aeromonas: Pathology Gastroenteritis Wound infections Systemic disease Aeromonas: Pathology/treatment Gastroenteritis Acute Gastroenteritis in children Is self­limiting; only supportive treatment Aeromonas: Pathology/treatment Chronic Gastroenteritis mostly in adults (lasts for weeks ) Systemic Infections and/or wound infections Both require antimicrobial treatment with Fluoroquinole (Ciprofloxacin) Resistance to penicillins , cephalosporins and erythromycin Classification Classification Family Genus Species Vibrionaceae Vibrio >60 species V. cholerae V. parahaemolyticus V. Vulnificus V. alginolyticus General Characteristics General Characteristics Broad temp. range (140­400C) Gram­negative, curved rods Tolerate high pH (basic) but susceptible to acid environment (stomach!) Single, polar flagellum (monotrichous) LPS (O­antigen) for serum ID (serogroups) V. parahaemolyticus,V. vulnificus Food­borne disease (Raw fish); Gastroenteritis Wound infections; Tissue necrosis, Septicemia infections rare in US but most common form of bacterial gastroenteritis in Japan/Southeast Asia (V. parahaemolyticus) Gastroenteritis: self­limited disease Wound infections/Septicemia: potentially fatal­ prompt antibiotic treatment (V. vulnificus) V. vulnificus can lead to septicemia following gastroenteritis!! Vibrio infections (non tox Cholera) Vibrio infections (non tox Cholera) in USA Foodborne Vibrio infections in the Foodborne Vibrio infections in the US (2004) hy seasonal variance (mostly during summer) of vibrio infections: ) Higher risk of contamination in seafood (more bacteria in ocean) ) Bathing season; higher risk of infection during recreational water usage V. cholerae V. cholerae Morphology V. cholerae important human pathogen, discovered in 1884 by R. Koch First correlation between water quality and cholera outbreaks observed by J. Snow in England in 1854 Serotypes O1 and O139 (first described in 1992) are associated with epidemics, both produce cholera toxin V. cholerae O1 does not produce capsule (no disseminating disease) uring the second Cholera pandemic in Paris 20,000 people die (650,000 total population) Epidemiology/History V. cholerae 7 major pandemics since 1816 Last one started 1961 in Asia, spread to Europe/Africa during 70s and 80s and reached South America in the 90s, caused by serotype O1 (El Tor strain) August 2007, outbreak reported in Iraq (~2,000 cases) Cholera Epidemic in the Americas Initial epidemic: January 1991 August 1991 February 1992 March 1993 Reported Cases of Cholera Reported Cases of Cholera (Region of the Americas, 1991­2002) 400,000.00 350,000.00 300,000.00 250,000.00 200,000.00 150,000.00 100,000.00 50,000.00 0.00 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 Cases 57,312 534 24 2008–2009 Zimbabwean cholera 2008–2009 Zimbabwean cholera outbreak Spread of 2008–2009 Zimbabwean Spread of 2008–2009 Zimbabwean cholera outbreak RED= Deaths recorded Orange= Infections recorded 2008–2009 Zimbabwean cholera 2008–2009 Zimbabwean cholera outbreak By 23 July 2009 there had been 98,592 reported cases and 4,288 deaths making it the deadliest African cholera outbreak in the last 15 years Haiti: Cholera confirmed in Haiti: Cholera confirmed in Port­au­Prince Comparing the population figures of Peru and Haiti and factoring in the number of cholera cases in Peru during the outbreak in the 1990s, the organization thinks that 270,000 people in Haiti could fall ill. 1990 outbreak in Peru spread to 16 countries Cholera bacteria established in Haiti’s river system Outbreak caused by V.cholera O1 Nov. 9 2011 Nov. 9 th Epidemiology : World Epidemiology : World 3­5 million cases 100,000 to 120,000 deaths Cholera in the US Cholera in the US Bacteria multiply in water (salt and fresh water) Bacteria shed in high amounts in feces of patients and asymptomatic infected (75%) or recovering patients for 7­14days! Spread most often via consumption of contaminated water (leaky sewage system) In USA rare cases of cholera are due to returning travelers or consumption of contaminated seafood (shell fish) No person­to­person infections Requires high infectious does (106­108 bacteria) Sporadic outbreaks mostly in underdeveloped countries (disaster areas, refugee camps) Epidemiology/Transmission V. cholerae Incidence of Cholera by Incidence of Cholera by Gross National Product (per capita GNP) 500 450 400 350 300 250 200 150 100 50 0 Incidence Rate per 100,000 inhabitants Ecuador Bolivia Guatemala Nicaragu Hondura s Guyana El Salvador Panamá Colombi M éxico Brasil Chile 0 1000 2000 3000 Per capita GNP 4000 5000 6000 GENERAL: The principal cause of the outbreak is lack of access to safe water. This is often due to the collapse of the urban water supply, sanitation and garbage collection systems, along with the onset of the rainy season leading to faeces with cholera bacteria being washed into water sources, in particular public drains, as well as providing readily available but contaminated water. Zimbabwe: Due to a shortage of purification chemicals, such as chlorine, the capital city of Harare stopped receiving piped water on 1 December 2008.[17] By that date, many suburbs had not had any water supply for much longer.[18] Many households cannot even afford sufficient fuel to boil all of their water.[23] According to Medecins Sans Frontieres, the spread of cholera from urban to rural areas from December 2008 onwards was due to infected city­dwellers visiting their families' rural homes for Christmas and the burial of infected city­dwellers in rural areas.[24] 2008–2009 Zimbabwean cholera 2008–2009 Zimbabwean cholera outbreak http://en.wikipedia.org/wiki/2008–2009_Zimbabwean_cholera_outbreak Background: Background: Seasonal occurrence of cholera epidemics in Ganges delta region of Bangladesh/India Twice during year Highest incidences just after monsoon (Sept­ Dec) Second peak during spring (March­May) Faruque et al. PNAS 2005 vol 102/ no. 5 and no.17 Conclusion: Conclusion: Seasonal occurrence of cholera epidemics correlates with prevalence of cholera phages (Title) Reservoirof Vibrio species in water is important Impact of global/local aquatic condition (global warming?!) Outbreaks when new V.cholera is introduced in environment without phages (Flooding) Cholera phages could be used as biological control agents in water Cholera: (only serotypes O1 and O139) Abrupt onset (2­3days after ingestion) of watery diarrhea and vomiting (only in 20% of patients) “rice­water” stools: colorless/odorless, speckled with mucus (contains large amounts of bacteria!) Up to 1 liter (1/4 gallon) of fluid loss per HOUR is possible (ADHERENCE is key for virulence) Sever dehydration, cardiac and renal failure possible 60% mortality in untreated; 1% in treated Gastroenteritis: Caused by serotypes which do not express cholera toxin Milder diarrhea, self­limited infection Clinical Manifestation Clinical Manifestation V. cholerae Pathogenesis Pathogenesis Cholera toxin (severe loss of electrolytes, water) Toxin co­regulated pilus (Adherence) Colonization Factor (Adhesin) Other toxins that increase intestinal fluid secretion (diarrhea by non­toxigenic V. cholera) Toxins are grouped in pathogenic island on chromosome and co­regulated (ToxR regulator)­common feature of virulence factors ETEC/V.cholerae ETEC/ LT­I, Cholera toxin Laboratory diagnosis Laboratory diagnosis Organisms survive poorly in dry or acidic environments! Inoculate promptly into culture media McConkey agar; non­lactose fermenter Specific enrichment medium (Thiosulfate Citrate Bile Salts Sucrose) TBCS Isolates identified with special biochemical tests PCR based detection of toxin gene presence Serology (O­antigen) Cholera: Rehydration Treatment Cholera: Rehydration Treatment Rule of thumb: drink as much as you loose; can be up to 1l/hour (=1/4 gallon) Treatment Treatment Replacement of fluids and salts!! ­Prepackaged mixtures of salt/sugar, mixed with water and drunk in large amounts (results in <1% mortality) Sometimes IV (intravenous) fluid replacement Antibiotics shorten course and reduce severity of disease (Doxycycline) for adults and TMS for children (cases of drug resistance have been reported), e.g. current strain in Haiti is resistant to TMS Prevention and Control Strategies Prevention and Control Strategies Epidemiological surveillance Environmental sanitation (sewage system) Food safety 1) (“cook it, boil it, peel it”) 2) in US; FDA testing of imported shell fish Social communication and health/sanitary education 1) importance of clean drinking water and proper sewage disposal 2) in US check out http://www.cdc.gov/travel Oral Vaccine available but not recommended by CDC Factors Favoring Eradication Factors Favoring Eradication Fragility of the organism. Large dose required for infection (106) lack of person­to­person transmission. Short incubation period. Factors Impeding Eradication Factors Impeding Eradication Persistence of V. cholerae in the aquatic environment!! Increase in population density. Non­existence of an adequate vaccine, limited protection from natural immune system. (chemoprophylaxis, quarantine, trade embargos). Failure of other traditional public­health measures Development of an effective treatment. Flexibility and variety of V. cholerae toxigenic strains. ...
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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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