Vibrio parahaemolyticus Food Poisoning

Vibrio parahaemolyticus food poisoning is an acute or subacute illness caused by eating food contaminated with or containing this bacterium. V. parahaemolyticus is a common food poisoning pathogen accounting for a substantial proportion of bacterial food poisoning, with gastrointestinal symptoms such as nausea, vomiting, abdominal pain, diarrhea, and watery stool as the main manifestations. This food poisoning has the common features of bacterial food poisoning: fulminant onset (same time, same area, same or similar symptoms, same contaminated food), short incubation period (hours to days), and seasonality (mostly summer and autumn).

Common Symptoms

Toxic manifestations; abdominal discomfort; ...; diarrhea; mucoid stool; abdominal pain; nausea

Causes and Pathogenesis

(1) Etiology: V. parahaemolyticus is a Gram-negative encapsulated bacillus of the genus Vibrio, family Vibrionaceae, a pleomorphic coccobacillus and slightly curved vibrio, 0.7 to 1.0 μm long, with a single polar flagellum and active motility. It is halophilic, growing best in media containing 2% to 4% salt at 37°C, pH 7.4 to 8.5. It dies within 1 to 3 minutes in vinegar, is inactivated in 5 to 10 minutes at 56°C, and dies in 5 minutes in 1% hydrochloric acid. Colony morphology varies with culture conditions, mostly oval on SS agar or blood agar, and coccobacillary on salt peptone agar. Its pathogenic factors are thermostable direct hemolysin (TDH) and thermostable-related hemolysin (TRH). TDH has a molecular weight of 42×10^3 and is not inactivated by 10 min at 100°C; human, monkey, dog, and rat erythrocytes are sensitive to TDH. V. parahaemolyticus isolated from diarrheal patients shows positive Kanagawa phenomenon on Wagatsuma agar, suggesting the disease may relate to thermostable hemolysin; it also has cardiac toxicity in experimental mice, killing them within seconds after small intravenous doses. TRH has a molecular weight of 48×10^3, composed of two 24×10^3 subunits; TRH shares 68.6% gene homology with TDH but is heat-labile, inactivated in 10 min at 60°C. Both hemolysins cause intestinal mucosal congestion, edema, and mild erosion, and can cause secretory intestinal fluid retention and diarrhea via cAMP and cGMP pathways. V. parahaemolyticus is acid-sensitive, not growing below pH 6 and dying within 1 to 3 min in vinegar; it multiplies rapidly in 3% to 6% NaCl with a generation time of 8 to 9 min. Its halophilic mechanism relates to the K-H antiport system. It has little heat resistance, dying in 5 to 10 min at 65°C, within 1 day in room-temperature tap water, within 2 days in river, pond, or well water, but surviving 47 days in seawater and continuing to survive for 11 weeks in peptone water at -20°C. It has weak resistance to common disinfectants, killed by low-concentration phenol and cresol soap solution. V. parahaemolyticus has flagellar (H), capsular polysaccharide (K), and somatic (O) antigens; H antigen is common to all strains and not useful for typing, so O and K antigens form the basis of serotyping. There are 12 known O antigens and at least 59 K antigens; 25 serotypes based on O and H antigens, with B, E, and H being the main food poisoning serotypes; at least 9 phage types have been identified in China. (2) Pathogenesis: The pathogenicity for humans is established but the mechanism is not fully clear. Ingestion of 10^5 to 10^7 viable organisms can cause disease; bacteria can invade intestinal epithelial cells, and pathological damage found at autopsy confirms direct invasion. TDH and TRH both have hemolytic activity and enterotoxic effects, causing intestinal loop swelling, congestion, and fluid retention leading to diarrhea. The diarrhea mechanism is thought closely related to the vibrio lipopolysaccharide enterotoxin component, similar to V. cholerae heat-labile toxin (CT), causing secretory diarrhea via cAMP and cGMP mediation. Thermostable hemolysin also has specific cardiac toxicity, causing myocardial lesions in rats and guinea pigs, and human atrial fibrillation and premature beats. Pathological changes are acute enteritis, most prominent in the duodenum, jejunum, and upper ileum, with diffuse mucosal congestion and edema extending to the muscularis and serosa, mild erosion but no ulcers, and neutrophil infiltration histologically; internal organs (stomach, liver, spleen, lung) are congested. Urease has recently been linked to the diarrhea. Clinical manifestations vary in severity depending on patient constitution and immunity; infection in mountainous or inland residents traveling to coastal areas tends to be more severe and typical, while coastal cases are generally milder.

Treatment

Drug therapy, supportive therapy

Preventive Measures

Professional guidance: Prevention is similar to other bacterial causes; the key is strengthening health education and improving hygiene awareness. (1) Strengthen hygienic handling of seafood; washing, salting, cold storage, and transport should strictly follow hygiene regulations. (2) Prevent cross-contamination between raw and cooked foods; do not eat raw seafood. Keep raw and cooked foods separate to prevent cross-infection. Cook seafood thoroughly. Re-cook stored food thoroughly before eating. Do not eat raw crabs, raw swimming crabs, or salted roasted shrimp; if eaten raw, soak in vinegar for 5 min to kill pathogens.

Department to Visit

It is recommended to visit the Emergency department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.