Vibrio cholerae

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Vibrio cholerae
Scientific classification
Domain: Bacteria
Phylum: Proteobacteria
Class: Gammaproteobacteria
Order: Vibrionales
Family: Vibrionaceae
Genus: Vibrio
Species: V. cholerae
Binomial name
Vibrio cholerae
Pacini 1854

Vibrio cholerae is a Gram-negative, comma-shaped bacterium. Some strains of V. cholerae cause the disease cholera. V. cholerae is a facultative anaerobic organism[1] and has a flagellum at one cell pole. V. cholerae was first isolated as the cause of cholera by Italian anatomist Filippo Pacini in 1854,[2] but his discovery was not widely known until Robert Koch, working independently 30 years later, publicized the knowledge and the means of fighting the disease.[3][4]

Pathogenesis[edit]

V. cholerae pathogenicity genes code for proteins directly or indirectly involved in the virulence of the bacteria. During infection, V. cholerae secretes cholera toxin, a protein that causes profuse, watery diarrhea. Colonization of the small intestine also requires the toxin coregulated pilus (TCP), a thin, flexible, filamentous appendage on the surface of bacterial cells. Vibrio cholerae can cause syndromes ranging from asymptomatic to cholera gravis.[4] In endemic areas, 75% of cases are asymptomatic, 20% are mild to moderate, and 2-5% are severe forms like cholera gravis.[4] Symptoms include abrupt onset of watery diarrhea (a grey and cloudy liquid), occasional vomiting and abdominal cramps.[1][4] Dehydration ensues with symptoms and signs such as thirst, dry mucous membranes, decreased skin turgor, sunken eyes, hypotension, weak or absent radial pulse, tachycardia, tachypnea, hoarse voice, oliguria, cramps, renal failure, seizures, somnolence, coma and death.[1] Death due to dehydration can occur in a few hours to days in untreated children and the disease is dangerous for pregnant women and their unborn children during late pregnancy, premature labor and fetal death may occur.[4][5][6] In cases of cholera gravis involving severe dehydration, up to 60% of patients can die; however, less than 1% of cases treated with rehydration therapy are fatal. The disease typically lasts from 4–6 days.[4][7] Worldwide, diarrhoeal disease, caused by cholera and many other pathogens, is the second leading cause of death for children under the age of 5 and at least 120,000 deaths are estimated to be caused by cholera each year.[8][9] In 2002, the WHO deemed that the case fatality ratio for cholera was about 3.95%.[4]

Genome[edit]

V. cholerae has two circular chromosomes, together totalling 4 million base pairs of DNA sequence and 3,885 predicted genes.[10] The genes for cholera toxin are carried by CTXphi (CTXφ), a temperate bacteriophage inserted into the V. cholerae genome. CTXφ can transmit cholera toxin genes from one V. cholerae strain to another, one form of horizontal gene transfer. The genes for toxin coregulated pilus are coded by the VPI pathogenicity island (VPIφ). The entire genome of the virulent strain V. cholerae El Tor N16961 has been sequenced,[1] and contains two circular chromosomes.[4] Chromosome 1 has 2,961,149 base pairs with 2,770 open reading frames (ORF’s) and chromosome 2 has 1,072,315 base pairs, 1,115 ORF’s. It is the larger first chromosome that contains the crucial genes for toxicity, regulation of toxicity and important cellular functions, such as transcription and translation.[1]

The second chromosome is determined to be different from a plasmid or megaplasmid due to the inclusion of housekeeping and other essential genes in the genome, including essential genes for metabolism, heat-shock proteins and 16S rRNA genes, which are ribosomal sub-unit genes used to track evolutionary relationships between bacteria. Also relevant in determining if the replicon is a chromosome is whether it represents a significant percentage of the genome, and chromosome 2 is 40% by size of the entire genome. And, unlike plasmids, chromosomes are not self-transmissible.[4] However it is believed that the second chromosome may have once been a megaplasmid because it contains some genes that are usually found on plasmids.[1]

V. cholerae contains a genomic island of pathogenicity and is lysogenized with phage DNA. That means that the genes of a virus were integrated into the bacterial genome and made the bacteria pathogenic.15 The molecular pathway involved in expression of virulence is discussed in the pathology and current research sections below.

Bacteriophage CTXφ[edit]

CTXφ (also called CTXphi) is a filamentous phage that contains the genes for cholera toxin. Infectious CTXφ particles are produced when V. cholerae infects humans. Phage particles are secreted from bacterial cells without lysis. When CTXφ infects V. cholerae cells, it integrates into specific sites on either chromosome. These sites often contain tandem arrays of integrated CTXφ prophage. In addition to the ctxA and ctxB genes encoding cholera toxin, CTXφ contains eight genes involved in phage reproduction, packaging, secretion, integration, and regulation. The CTXφ genome is 6.9 kb long.[11]

Vibrio pathogenicity island[edit]

The Vibrio pathogenicity island (VPI) contains genes primarily involved in the production of toxin coregulated pilus (TCP). It is a large genetic element (~40 kb) flanked by two repetitive regions (att-like sites), resembling a phage genome in structure. The VPI contains two gene clusters, the TCP cluster and the ACF cluster, along with several other genes. The acf cluster is composed of 4 genes: acfABCD. The tcp cluster is composed of 15 genes: tcpABCDEFHIJPQRST and regulatory gene toxT.

Ecology and epidemiology[edit]

The main reservoirs of V. cholerae are people and aquatic sources such as brackish water and estuaries, often in association with copepods or other zooplankton, shellfish, and aquatic plants.

Cholera infections are most commonly acquired from drinking water in which V. cholerae is found naturally or into which it has been introduced from the feces of an infected person. Other common vehicles include contaminated fish and shellfish, produce, or leftover cooked grains that have not been properly reheated. Transmission from person to person, even to health care workers during epidemics, is rarely documented. V. cholerae thrives in a water ecology, particularly surface water. The primary connection between humans and pathogenic strains is through water, particularly in economically reduced areas that don't have good water purification systems.[9]

Non-pathogenic strains are also present in water ecologies. It is thought that it is the wide variety of strains of pathogenic and non-pathogenic strains that co-exist in aquatic environments that allow for so many genetic varieties. Gene transfer is fairly common amongst bacteria and recombination of different V. cholerae genes can lead to new virulent strains.[12]

Diversity and evolution[edit]

Two serogroups of V. cholerae, O1 and O139, cause outbreaks of cholera. O1 causes the majority of outbreaks, while O139 – first identified in Bangladesh in 1992 – is confined to South-East Asia. Many other serogroups of V. cholerae, with or without the cholera toxin gene (including the nontoxigenic strains of the O1 and O139 serogroups), can cause a cholera-like illness. Only toxigenic strains of serogroups O1 and O139 have caused widespread epidemics.

V. cholerae O1 has 2 biotypes, classical and El Tor, and each biotype has 2 distinct serotypes, Inaba and Ogawa. The symptoms of infection are indistinguishable, although more people infected with the El Tor biotype remain asymptomatic or have only a mild illness. In recent years, infections with the classical biotype of V. cholerae O1 have become rare and are limited to parts of Bangladesh and India.[13] Recently, new variant strains have been detected in several parts of Asia and Africa. Observations suggest that these strains cause more severe cholera with higher case fatality rates. Vibrio cholerae is indigenous to the aquatic environment, and serotype non-O1 strains are readily isolated from coastal waters. However, in comparison with intensive studies of the O1 group, relatively little effort has been made to analyze the population structure and molecular evolution of non-O1 V. cholerae. In this study, high-resolution genomic DNA fingerprinting, amplified fragment length polymorphism (AFLP), was used to characterize the temporal and spatial genetic diversity of 67 V. cholerae strains isolated from Chesapeake Bay during April through July 1998, at four different sampling sites. Isolation of V. cholerae during the winter months (January through March) was unsuccessful, as observed in earlier studies.[14] AFLP fingerprints subjected to similarity analysis yielded a grouping of isolates into three large clusters, reflecting time of the year when the strains were isolated. April and May isolates were closely related, while July isolates were genetically diverse and did not cluster with the isolates obtained earlier in the year. The results suggest that the population structure of V. cholerae undergoes a shift in genotype that is linked to changes in environmental conditions. From January to July, the water temperature increased from 3 °C to 27.5 °C, bacterial direct counts increased nearly an order of magnitude, and the chlorophyll aconcentration tripled (or even quadrupled at some sites). No correlation was observed between genetic similarity among isolates and geographical source of isolation, since isolates found at a single sampling site were genetically diverse and genetically identical isolates were found at several of the sampling sites. Thus, V. cholerae populations may be transported by surface currents throughout the entire Bay, or, more likely, similar environmental conditions may be selected for a specific genotype. The dynamic nature of the population structure of this bacterial species in Chesapeake Bay provides new insight into the ecology and molecular evolution of V. cholerae in the natural environment.

Gallery[edit]

See also[edit]

References[edit]

  1. ^ a b c d e f "Laboratory Methods for the Diagnosis of Vibrio cholerae". Centre for Disease Control. Retrieved 29 October 2013. 
  2. ^ See:
  3. ^ Bentivoglio, M; Pacini, P (1995). "Filippo Pacini: A determined observer". Brain Research Bulletin 38 (2): 161–5. doi:10.1016/0361-9230(95)00083-Q. PMID 7583342. 
  4. ^ a b c d e f g h i Howard-Jones, N (1984). "Robert Koch and the cholera vibrio: a centenary". BMJ 288 (6414): 379–81. doi:10.1136/bmj.288.6414.379. PMC 1444283. PMID 6419937. 
  5. ^ Davis, B (February 2003). "Filamentous phages linked to virulence of Vibrio cholerae". Current Opinion in Microbiology 6 (1): 35–42. doi:10.1016/S1369-5274(02)00005-X. PMID 12615217. 
  6. ^ Boyd, EF; Waldor, MK (Jun 2002). "Evolutionary and functional analyses of variants of the toxin-coregulated pilus protein TcpA from toxigenic Vibrio cholerae non-O1/non-O139 serogroup isolates.". Microbiology (Reading, England) 148 (Pt 6): 1655–66. PMID 12055286. 
  7. ^ Miller, Melissa B.; Skorupski, Karen; Lenz, Derrick H.; Taylor, Ronald K.; Bassler, Bonnie L. (August 2002). "Parallel Quorum Sensing Systems Converge to Regulate Virulence in Vibrio cholerae". Cell 110 (3): 303–314. doi:10.1016/S0092-8674(02)00829-2. 
  8. ^ Nielsen, Alex Toftgaard; Dolganov, Nadia A.; Otto, Glen; Miller, Michael C.; Wu, Cheng Yen; Schoolnik, Gary K. (2006). "RpoS Controls the Vibrio cholerae Mucosal Escape Response". PLoS Pathogens 2 (10): e109. doi:10.1371/journal.ppat.0020109. 
  9. ^ a b Faruque, SM; Albert, MJ; Mekalanos, JJ (Dec 1998). "Epidemiology, genetics, and ecology of toxigenic Vibrio cholerae.". Microbiology and molecular biology reviews : MMBR 62 (4): 1301–14. PMC 98947. PMID 9841673. 
  10. ^ Fraser, Claire M.; Heidelberg, John F.; Eisen, Jonathan A.; Nelson, William C.; Clayton, Rebecca A.; Gwinn, Michelle L.; Dodson, Robert J.; Haft, Daniel H. et al. (2000). "DNA sequence of both chromosomes of the cholera pathogen Vibrio cholerae". Nature 406 (6795): 477–83. doi:10.1038/35020000. PMID 10952301. 
  11. ^ McLeod, S. M.; Kimsey, H. H.; Davis, B. M.; Waldor, M. K. (2005). "CTXφ and Vibrio cholerae: exploring a newly recognized type of phage-host cell relationship". Molecular Microbiology 57: 347–356. doi:10.1111/j.1365-2958.04676.x (inactive 2014-01-31). PMID 15978069. 
  12. ^ Faruque, SM; Nair, GB (2002). "Molecular ecology of toxigenic Vibrio cholerae.". Microbiology and immunology 46 (2): 59–66. doi:10.1111/j.1348-0421.2002.tb02659.x. PMID 11939579. 
  13. ^ Siddique, A.K.; Baqui, A.H.; Eusof, A.; Haider, K.; Hossain, M.A.; Bashir, I.; Zaman, K. (1991). "Survival of classic cholera in Bangladesh". The Lancet 337 (8750): 1125–1127. doi:10.1016/0140-6736(91)92789-5. 
  14. ^ Kaper, J; Lockman, H; Colwell, RR; Joseph, SW (Jan 1979). "Ecology, serology, and enterotoxin production of Vibrio cholerae in Chesapeake Bay.". Applied and environmental microbiology 37 (1): 91–103. PMC 243406. PMID 367273. 

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