Campylobacter Enteritis

Campylobacter enteritis is an acute intestinal infectious disease caused by Campylobacter. It is clinically characterized by fever, abdominal pain, and bloody stool with numerous neutrophils and red blood cells. Campylobacter was first isolated in 1909 from aborted cattle and sheep as Vibrio fetus, and first isolated from humans in 1947.

Common Symptoms

Dysentery; muscle aches; diarrhea; delirium; tenesmus; sepsis; abdominal pain; fatigue; nausea; dizziness

Causes and Pathogenesis

(1) Etiology: Campylobacter species causing human disease include C. jejuni, C. coli, C. lari, C. fetus subspecies fetus, and C. sputorum subspecies mucosalis. These are Gram-negative, spiral or S-shaped, non-spore-forming bacteria with a single polar flagellum at one or both ends, actively motile, microaerophilic, invasive, containing endotoxin and secreting exotoxins such as enterotoxin. C. jejuni is hardy in vitro, surviving 160 days in milk at 4°C and over 2 months at room temperature, but is sensitive to common disinfectants and killed within 5 min at 58°C. (2) Pathogenesis: After oral infection, Campylobacter multiplies in the bile and microaerophilic environment of the upper small intestine. The pathogenesis is not fully understood; current evidence suggests intestinal disease depends mainly on direct invasiveness. Chicken embryo cell invasion tests and chick inoculation tests demonstrate invasiveness; bloody diarrhea, intestinal mucosal pathology, and bacteremia in patients also suggest mucosal epithelial invasion. The bacterial flagellum was once considered the key virulence factor, but opinions differ. It is now established that the soluble protein PEB1 and chemotactic proteins play a role in adhesion and colonization. PEB1 directly participates in bacterial adhesion to and invasion of HeLa cells; it is on the bacterial surface, encoded by the peb1A gene. In animal models, the A site of peb1 enhances adhesion and invasion of intestinal epithelial cells, while inactivation of peb1A significantly reduces adhesion. CheY-mediated chemotaxis is also critical for intestinal colonization. Some strains also produce enterotoxin similar to cholera enterotoxin causing watery diarrhea; bacterial lysis releases large amounts of endotoxin causing fever and systemic symptoms. Pathological changes are mainly in the jejunum, ileum, and colon, with diffuse hemorrhagic, edematous, and exudative lesions of the mucosa; microscopically, small intestinal villi show degeneration and atrophy, with abundant neutrophil and mononuclear infiltration in the lamina propria, sometimes ulcers and crypt abscesses, and enlarged mesenteric lymph nodes with inflammation.

Treatment

Drug therapy, supportive therapy

Preventive Measures

Prevention is similar to other intestinal infections. The most important source of C. jejuni infection is animals; controlling animal infection and preventing contamination of water and food by animal excreta is critical. Pay attention to food and personal hygiene to cut transmission. Isolate patients enterically. Strengthen management and treatment of infected poultry and livestock. Food and drinking water should be boiled. Attenuated live and heat-killed vaccines are under research, expected to play an important role in eliminating sources of infection and preventing disease.

Department to Visit

It is recommended to visit the Infectious Diseases 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.