The genus Vibrio comprises Gram-negative, oxidase-positive, facultatively anaerobic rods. Differentiation from Aeromonas may be made on the basis of the sensitivity of most vibrios to the vibriostat O/129. Cells are often curved, or comma-shaped, and motile by a characteristic sheathed, polar flagellum. With the exception of V. costicola, the genus is of estuarine, or marine origin, many species having an obligate requirement for the Na+ ion. Some species, including V cholerae, may be more prevalent in fresh water than has previously been thought. Enteropathogenic Vibrio spp. are generally found in greater numbers in warm waters and may show a marked seasonal variation in occurrence, which correlates with temperature (Varnam and Evans, 2000). The genus is among those able to enter the putative viable non-recoverable (VNR) state (Oliver et al., 1995), which can complicate the epidemiology of infections.
The genus Vibrio contains a number of species, of which 11 have a proven association with intestinal or extraintestinal disease. The main species of importance with respect to foods are V. cholerae, V. parahaemolyticus and V. vulnificus. Seafood is the most common vehicle of foodborne infection, although water is historically associated with V. cholerae infection. Vibrio vulnificus is also an important cause of wound infections.
Foodborne infections with Vibrio spp. are most common in Asia. Infections are rare in Europe and usually associated with imported foods, or travellers returning from affected areas. Not all US states report Vibrio infections, but 30 to 40 cases of V. parahaemolyticus infection occur each year in Gulf Coast states, such as Texas and Alabama. Vibrio vulnificus infection is less common, ca 300 cases being reported between 1988 and 1995.
14.14.2 Enteropathogenic species (V cholerae, V. parahaemolyticus, V. vulnificus): infection and epidemiology
The three main enteropathogenic species are distinguishable on the basis of phenotypic properties, have a distinct ecology within the aquatic environment and cause illness of different types and severity.
The cause of serious human disease since antiquity, V. cholera is the causative agent of Asiatic cholera. The current cholera pandemic is the eighth and the disease is present in many parts of the world. Cholera is classically a waterborne disease, but food is also an important vehicle, especially in countries with a sea-coast. Classic Asiatic cholera is caused only by strains of V. cholerae serogroup O1 and O139, which also produce cholera toxin. Serogroup O1 has two biotypes, classic and El Tor, and three serotypes, Inaba, Ogawa and Hikojima. The incubation period of cholera varies from 6 hours to as long as 3 days. Although initial symptoms may be mild, the infection rapidly progresses to copious diarrhoea ('rice water stools'), with rapid loss of body fluids and mineral salts, especially potassium. Fluid loss is up to 1 litre/hour, resulting in dehydration, hypertension and salt imbalance. Where treatment is unavailable, death may be rapid, but recovery in 1 to 6 days is normal where rehydration and salt replacement are possible.
Other illness is caused by V. cholerae other than O1 and O139, or by strains of these serotypes which lack the ability to produce cholera toxin. Symptoms are usually milder, but severity varies and can approach that of cholera. Gastroenteritis produced by V. cholerae other than O1 and O139 is characterised by diarrhoea, which is bloody in ca 25% of cases, abdominal cramps and fever (ca 70%). Nausea and vomiting accompany diarrhoea in ca 20% of cases. Illness caused by non-toxigenic strains of O1 and O139 usually involves diarrhoea only. Mild diarrhoea is also caused by a separate species within the V. cholerae group; V. mimicus.
V. cholerae adheres to the surface of the small intestine, little being known of the mechanism of adhesion, although there is an important role for cell-associated haemagglutinins. Cells grow, producing cholera toxin, a true enterotoxin, which is an oligomeric protein (MW 84000), composed of two subunits, A1 (MW 21 000) and A2 (MW 7000), which is linked by covalent bonds to five B subunits (MW 10 000). The B subunits bind to a receptor ganglioside in mucosal cell membrane, while the A1 subunit enters the cells, irreversibly activating adenylate cyclase, leading to increased intracellular levels of cyclic AMP, and a biochemical reaction cascade, resulting in hypersecretion of water and salts. The role of the A2 subunit is probably in mediating entry into the cell.
Other toxins are produced by V. cholerae, although their significance is uncertain. These include heat-stable (ST) and heat-labile (LT) enterotoxins, a Shiga-like cytotoxin, a haemolysin similar to that of V. parahaemolyticus and an endotoxin. This is produced in significantly greater quantities by non-toxigenic strains. At least some of the pathogenic mechanisms of V. cholerae are shared by V. mimicus.
V. parahaemolyticus causes a predominantly diarrhoeal syndrome. Typical symptoms are diarrhoea, abdominal cramps and nausea. Vomiting occurs in ca 50% of cases and there may be a headache. Mild fever and chills occur in ca 25% of cases. Onset is usually after 4-24 hours, although longer and shorter periods have been reported. Symptoms usually abate within 2-3 days and death is very rare. A second, more severe, dysenteric form has been described (Twedt, 1989), which is characterised by bloody, or mucoid, stools. Human pathogenicity of V. para-haemolyticus usually correlates with presence of direct, thermostable haemolysin activity (Kanagawa reaction). Kanagawa-negative strains can be a cause of diarrhoea, however, and are important outside tropical countries.
Vibrio parahaemolyticus differs from V. cholerae in being invasive and in not producing a classic enterotoxin. Much attention has been paid to the role of the direct, thermostable haemolysin (Vp-TDH), but relatively little is known of other aspects of pathogenicity. Both flagella and cell-associated haemagglutinins are involved in adhesion to the epithelial cells before entry and penetration to the lamina propria. The direct, thermostable haemolysin promotes in vitro vascular permeability and has enterotoxin properties, but its precise role in induction of diarrhoea is unknown. Other toxins may be produced, including a Shiga-like cyto-toxin, which may be involved in the less common dysenteric form of infection. Pathogenicity in these strains is associated with production of a second haemolysin, Vp-TDH related haemolysin.
Foodborne V. vulnificus infections are almost invariably associated with underlying medical conditions (see below). Although similar to V. parahaemolyticus, V. vulnificus differs from this, and other enteropathogenic vibrios, in having a sep-ticaemic rather than an enteric human pathology. In healthy persons, infection may involve no more than mild and self-limiting diarrhoea, but most cases involve primary septicaemia with fever, chills and, in many cases, nausea. Hypotension occurs in ca 33% of cases and ca 66% of patients develop skin lesions on extremities and trunk. The normal incubation period of V. vulnificus infection is 16-48 hours, septicaemia progressing rapidly and being difficult to treat. Mortality is 40-60%.
Invasion occurs rapidly after adhesion and is accompanied by extensive tissue damage. The organism has a number of virulence factors which protect against host defences. These include cell-associated factors protective against normal serum and complement-induced lysis and a surface component (capsule) which is antiphagocytic and anticomplementary. Vibrio vulnificus also produces active siderophores, which facilitate iron acquisition and which are associated with enhanced virulence when blood iron levels are high.
A number of products may be responsible for tissue damage. At least two haemolysins, which possess cytotoxic activity, are produced but, while contributing to virulence, these are not essential determinants. Specific proteinases, collagenase and phospholipases are also produced, which affect vascular permeability and cause tissue destruction.
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