Vibrio parahaemolyticus

Vibrio parahaemolyticus
SEM image of V. parahaemolyticus
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gamma Proteobacteria
Order: Vibrionales
Family: Vibrionaceae
Genus: Vibrio
Species: V. parahaemolyticus
Binomial name
Vibrio parahaemolyticus
(Fujino et al. 1951)
Sakazaki et al. 1963

Vibrio parahaemolyticus is a curved, rod-shaped, Gram-negative bacterium found in brackish[1] saltwater, which, when ingested, causes gastrointestinal illness in humans.[1] V. parahaemolyticus is oxidase positive, facultatively aerobic, and does not form spores. Like other members of the genus Vibrio, this species is motile, with a single, polar flagellum.[2]

Contents

Pathogenesis

While infection can occur via the fecal-oral route, ingestion of bacteria in raw or undercooked seafood, usually oysters, is the predominant cause the acute gastroenteritis caused by V. parahaemolyticus.[3] Wound infections also occur, but are less common than seafood-borne disease. The disease mechanism of V. parahaemolyticus infections has not been fully elucidated.[4]

Clincal isolates usually possess a pathogenicity island (PAI) on the second chromosome. The PAI can be acquired via horizontal gene transfer and contains genes for several virulence factors. There are two fully sequenced variants of the Vibrio parahaemolyticus PAI with distinctly different lineages[5][6]. Each pathogenicity island variant contains a genetically-distinct Type III Secretion System (T3SS), which is capable of injecting virulence proteins into host cells to disrupt host cell functions or cause cell death via apoptosis. There are two known T3SS variants on Vibrio parahaemolyticus chromosome 2, known as T3SS2α and T3SS2β. These variants correspond to the two known PAI variants. Aside from the T3SS, two genes encoding well-characterized virulence proteins are typically found on the PAI, the thermostable direct hemolysin gene (tdh) and/or the tdh-related hemolysin gene (trh). Strains possessing one or both of these hemolysins exhibit beta-hemolysis on blood agar plates. There seems to be a distinct correlation between presence of tdh, trh, and the two known T3SS variants: observations have shown T3SS2α correlating with tdh+/trh- strains, while T3SS2β correlates with tdh-/trh+ strains [7] .

Epidemiology

Outbreaks tend to be concentrated along coastal regions during the summer and early fall when higher water temperatures favor higher levels of bacteria. Seafood most often implicated includes squid, mackerel, tuna, sardines, crab, shrimp, and bivalves like oysters and clams. The incubation period of ~24 hours is followed by explosive, watery diarrhea accompanied by nausea, vomiting, abdominal cramps, and sometimes fever. Vibrio parahaemolyticus symptoms typically resolve with-in 72 hours, but can persist for up to 10 days in immunocompromised individuals. As the vast majority of cases of V. parahaemolyticus food infection are self-limiting, treatment is not typically necessary. In severe cases, fluid and electrolyte replacement is indicated.[2]

Additionally, swimming or working in affected areas can lead to infections of the eyes or ears[8] and open cuts and wounds. Following Hurricane Katrina, there were 22 vibrio wound infections 3 of which were caused by V. parahaemolyticus and 2 of these led to death.

Hosts

Hosts of Vibrio parahaemolyticus include:

References

  1. ^ a b CDC Disease Info vibriop
  2. ^ a b Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 0-8385-8529-9. 
  3. ^ Finkelstein RA (1996). Cholera, Vibrio cholerae O1 and O139, and Other Pathogenic Vibrios. In: Barron's Medical Microbiology (Barron S et al., eds.) (4th ed.). Univ of Texas Medical Branch. (via NCBI Bookshelf) ISBN 0-9631172-1-1. 
  4. ^ Baffone W, Casaroli A, Campana R, Citterio B, Vittoria E, Pierfelici L, Donelli G (2005). "'In vivo' studies on the pathophysiological mechanism of Vibrio parahaemolyticus TDH(+)-induced secretion". Microb Pathog 38 (2-3): 133–7. doi:10.1016/j.micpath.2004.11.001. PMID 15748815. 
  5. ^ Makino, Kozo; Kenshiro, Oshima, Ken Kurokawa, Katsushi Yokoyama, Takayuki Uda, Kenichi Tagomori, Yoshio Iijima, Masamoto Najima, Masayuki Nakano, Atsushi Yamashita, Yoshino Kubota, Shigenobu Kimura, Teruo Yasanaga, Takeshi Honda, Hideo Shinigawa, Masahira Hattori, Tetsuya Iida (March 1, 2003). "Genome sequence of Vibrio parahaemolyticus: a pathogenic mechanism distinct from that of V. cholerae". The Lancet 361: 743-479. PMID 19543642. 
  6. ^ Okada, Natsumi; Tetsuya Iida, Kwon-Sam Park, Naohisa Goto, Teruo Yasunaga, Hirotaka Hiyoshi, Shigeaki Matsuda, Toshio Kodama, Takeshi Honda (Feb 2009). "Identification and Characterization of a Novel Type III Secretion System in trh-positive Vibrio parahaemolyticus Strain TH3997 Reveal Genetic Lineage and Diversityt of Pathogenic Machinery beyond the Species Level". Infection and Immunity 77 (2): 904–913. PMID 19075025. 
  7. ^ Noriea, Nicholas; CN Johnson, KJ Griffitt, DJ Grimes (September 2010). "Distribution of type III secretion systems in 'Vibrio parahaemolyticus from the northern Gulf of Mexico". Journal of Applied Microbiology 109 (3): 953–962. PMID 20408916. 
  8. ^ Penland RL, Boniuk M, Wilhelmus KR (2000). "Vibrio ocular infections on the U.S. Gulf Coast". Cornea 19 (1): 26–9. doi:10.1097/00003226-200001000-00006. PMID 10632004. 
  9. ^ a b Kumazawa NH, Kato E, Takaba T, Yokota T. (August) 1988. Survival of Vibrio parahaemolyticus in two gastropod molluscs, Clithon retropictus and Nerita albicilla. Nippon Juigaku Zasshi. 50(4): 918-24.

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