Other Pathogenic Vibrios

Vibrio species are ubiquitous in estuarine waters in the temperate zones. Plankton blooms and temperature upshifting in the spring are followed by rapid outgrowth of most vibrios. Molluscan shellfish, which are filter feeders, acquire vibrios as part of their normal microbiota during the warmer months. Shellfish contamination by these vibrios thus occurs as a consequence of the normal climate-associated changes in Vibrio prevalence in coastal waters. In addition to this mechanism, sewage contamination of shellfish beds in epidemic cholera can contribute significantly to disease burden.

In the United States, illnesses caused by the commonly isolated pathogenic vibrios have a marked seasonal peak, with more than 90% of cases occurring between April and October. This presumably reflects seasonal changes in shellfish consumption, recreational water exposure, and the increase in densities of vibrios in marine waters during the warmer months. The incidence of vibriosis in the United States has been increasing despite prevention efforts. This may be reflective of both host and exposure factors, such as increases in water-related outdoor activities (swimming, boating), natural disasters (hurricanes, flooding), increased consumption of seafood, and more persons living with chronic liver disease and immunocompromising conditions. Recently, more widespread use of DNA amplification panels for detection of diarrheal pathogens has led to a 54% increase in the number of Vibrio infections reported in 2017 compared with the prior 2 years.

In addition to Vibrio cholerae serotype O1 and Campylobacter fetus (formerly known as Vibrio fetus ), other vibrios have been clearly associated with human disease. The best known among the halophilic (salt-requiring) vibrios are V. parahaemolyticus and V. vulnificus, both of which can cause serious illness and death. Three other halophilic vibrios, V. alginolyticus, V. fluvialis, and V. furnissii, cause infections of appreciable frequency but lesser clinical severity. The former V. hollisae and V. damselae have been reclassified and are now Grimontia hollisae and Photobacterium damselae, respectively. V. metschnikovii, V. cincinnatiensis, and V. harveyi ( V. carchariae ) rarely cause human illness. The nonhalophilic vibrios include non-O1/O139 V. cholerae and V. mimicus; like V. cholerae, they cannot grow at higher salt concentrations. They are worldwide in distribution and have frequently been incriminated in human illness.

Vibrio parahaemolyticus

V. parahaemolyticus, a halophilic vibrio, is a major cause of acute diarrheal disease in Japan. In the United States, V. parahaemolyticus was the most commonly isolated Vibrio species and the most common of the speciated vibrios reported. This pathogen was the most common bacterial cause of foodborne disease in Taiwan, accounting for 35% of all outbreaks ; in less-developed countries, it has been incriminated in up to 20% of acute diarrheal illnesses. A specific serotype, V. parahaemolyticus O3:K6, emerged as an important cause of human illness in Southeast Asia and, since 1996, became established globally by a pandemic clone. In 1998, this serotype first appeared in the United States, causing a large multistate outbreak that prompted regulatory changes in programs for bacteriologic monitoring of shellfish. In 2004, an outbreak of gastroenteritis caused by serotype O6:K18 was traced to raw oysters from the Gulf of Alaska, harvested when the water temperature was higher than 15°C. Whether global warming trends portend locally acquired V. parahaemolyticus infection even at high northern latitudes is a concern and emphasizes the need for surveillance and appropriate diagnostics, a recurring theme in emerging infectious diseases.

The genome of V. parahaemolyticus has been sequenced. Like V. cholerae, V. parahaemolyticus has two circular chromosomes, but unlike V. cholerae, a type III secretion system has been found on both of the two chromosomes of V. parahaemolyticus. This finding likely underlies the inflammatory diarrhea seen in V. parahaemolyticus, but not V. cholerae, infection, and suggests distinctly different mechanisms for diarrhea from these two pathogenic vibrios.

As suggested both by clinical manifestations and by animal studies, V. parahaemolyticus has the genetic endowment to produce an enterotoxin and to cause an inflammatory reaction in the small bowel mucosa. Major degrees of intestinal fluid loss are seldom seen, and the tissue damage that this vibrio causes is generally less extensive than that observed in shigellosis. Two hemolysins, thermostable direct hemolysin (TDH) and TDH-related hemolysin, have enterotoxin activity; strains negative for TDH and TDH-related hemolysin are usually avirulent.

Epidemiology

Because of lack of specificity of the clinical features of the illness, the epidemiologic history usually provides the most important clue to diagnosis. V. parahaemolyticus is ubiquitous in coastal waters, although it typically is not recovered from estuarine waters during winter months in temperate zones. During periods of low temperature or nutrient deprivation, it enters a viable but nonculturable state.

Consumption of raw or undercooked shellfish is the most common means of acquiring V. parahaemolyticus infection. In the United States, raw oysters are the most common vehicle. In a microbiologic survey of oysters harvested from US waters, the frequency of V. parahaemolyticus contamination was consistently greater than that for V. vulnificus. Inadequately cooked seafood can harbor small numbers of surviving vibrios, as can food contaminated by seawater on ships. V. parahaemolyticus can proliferate rapidly to reach high colony counts in contaminated foods held at ambient temperature for a few hours. This presumably contributes to the high attack rates seen in common source outbreaks.

Person-to-person transmission has not been documented, suggesting that the infective dose for normal persons is relatively high. V. parahaemolyticus has rarely been cultured from asymptomatic people, and no carrier state has been identified.

Clinical Manifestations

Gastroenteritis is the most common clinical illness associated with V. parahaemolyticus infection; wound infections and septicemia may be seen, but much less frequently. Enteric illness ranges from mild watery diarrhea to a frank dysentery-like syndrome. Illness commonly begins with the acute onset of explosive watery diarrhea, generally within 24 to 72 hours of ingestion of the contaminated seafood. Often, the diarrhea is accompanied by mild to moderately severe cramping and abdominal pain; low-grade fever, mild chills, and headache occur in fewer than half of infected people. The fluid loss is rarely severe, and death caused by V. parahaemolyticus is rare, usually occurring in very young children, older adults, or people with underlying disease.

Laboratory Findings

The diarrheal fluid is characteristically watery, sometimes mucoid, and occasionally bloody (<15% of cases). Fecal leukocytes are often present. V. parahaemolyticus is a pleomorphic gram-negative rod that is a facultative anaerobe. It is readily identified on the selective thiosulfate citrate–bile salts–sucrose (TCBS) agar, on which it appears as distinct opaque green colonies. While culture-independent diagnostic testing has greater sensitivity (lower limit of detection) compared with stool cultures, it does not provide antibiotic susceptibility or molecular subtyping results to compare isolates. Reflex cultures from fecal specimens positive for Vibrio species by DNA amplification panels were only positive in 38% of cultures.

Nearly all clinical isolates of V. parahaemolyticus cause β-hemolysis of human erythrocytes (the Kanagawa reaction), which is caused by the production of TDH. Interestingly, growth in bile salt–containing environments enhances the expression of several virulence traits in V. parahaemolyticus.

In patients with V. parahaemolyticus enteric infection, both serum and coproantibody responses to lipopolysaccharide and to TDH were detected. Mucosal biopsies from the duodenum and rectum showed inflammatory changes, suggesting that the small and large intestines are affected. Tumor necrosis factor-α (TNF-α) levels were noted to be elevated acutely in V. parahaemolyticus infection, similar to observations in shigellosis but in contrast to cholera infections, in which TNF-α levels are not elevated.

Differential Diagnosis

Because V. parahaemolyticus is ubiquitous in coastal waters throughout the temperate and tropical zones of the world, this pathogen must be considered in the differential diagnosis of all acute diarrheal illnesses that follow the ingestion of seafood. There are no clinical features that, in the individual case, reliably distinguish diarrhea caused by V. parahaemolyticus from that caused by enterotoxigenic Escherichia coli or from milder cases of shigellosis or salmonellosis. Vomiting is characteristically less prominent than in disease caused by staphylococcal enterotoxin, and the cramping abdominal pain is generally less severe than that typical of food poisoning caused by Clostridium perfringens.

Therapy

No treatment is required by most patients because the gastroenteritis is usually self-limited. However, antimicrobial therapy could be considered for those patients with diarrhea lasting longer than 5 days. Therapy with doxycycline or a quinolone would be expected to shorten the clinical course and duration of pathogen excretion. In the United States, 16% to 20% of patients with V. parahemolyticus infection were hospitalized; the overall case fatality rate was <1%. Occasionally patients, usually at the extremes of age, may become sufficiently dehydrated that oral or intravenous rehydration is needed. Wound infections due to V. parahaemolyticus are managed similarly among all the vibrios causing soft tissue infection, including antibiotic treatment and débridement as needed.

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