Impact and management of Campylobacter in human medicine: European perspective. Discussion

Viruses, enteric bacteria and parasites can all produce similar syndromes of acute enteritis, although the pathophysiology and molecular pathogenesis may vary widely. The severity of acute enteritis varies greatly, and only a small fraction of cases undergo medical evaluation. There are over 200 000 000 episodes of acute enteritis annually in the USA, of which approximately 75 000 000 are foodborne. Fewer than 20% of estimated cases have a known etiology. Nearly half of the more than 4 000 000 cases of known foodborne bacterial enteritis are attributed to Campylobacter infections. The FoodNet active population-based surveillance system has demonstrated geographic variation in the incidence of Campylobacter infection, and generally declining incidence since 1996. Campylobacter jejuni infections vary in severity and duration. Antimicrobial therapy, especially if administered early, may hasten clinical resolution by 2-3 days. Therapy is generally restricted to individuals with moderate-to-severe disease and high-risk individuals (underlying immunodeficiency, chronic illness, extremes of age, etc.). Approximately 10-15% of C. jejuni isolates are fluoroquinolone resistant, although most strains are macrolide susceptible. Several acute intra-abdominal as well as extraintestinal complications can occur following C. jejuni enteritis, although bacteremia and metastatic infection are rare, except in high-risk patients. Post-infectious syndromes include post-dysenteric bowel dysfunction, the less frequent but more severe reactive arthritis (1%), and Guillain-Barre syndrome (0.1%). The recent demonstration that antibiotic administration for Escherichia coli O157:H7 hemorrhagic enteritis increases the risk of hemolytic-uremic syndrome 5-10-fold forces reconsideration of empirical broad-spectrum antibiotic therapy for acute hemorrhagic enteritis, and supports narrow-spectrum erythromycin therapy for acute enteritis.