An enzyme-linked immunosorbent assay was adapted to measure immunoglobulin A (IgA), IgG, and IgM classes of human serum antibody to Campylobacterjejuni. Sera were tested from healthy controls, from ill persons at various intervals after exposure to an epidemiologically implicated vehicle for Campylobacter sp. enteritis, from persons exposed to these same vehicles who remained well, and from persons who chronically drank raw milk. The major antigens in the C. jejuni acid-washed antigen preparations from three different strains all migrated at about 30,000 and 63,000. Persons with Campylobacter enteritis developed rising serum IgA, IgG, and IgM antibodies during the second week after infection; IgG and IgM elevations persisted longer than did IgA. Exposed persons who remained well showed similar, but lower, antibody rises. Chronic raw milk drinkers had elevated IgG levels, but not IgM or IgA levels, whether or not they were acutely exposed to an implicated vehicle.
In Bangladesh and other developing countries, isolation of Campylobacter jejuni is common in healthy children, and the illness/infection ratio falls with age. To determine whether specific serum antibodies correlate with this phenomenon, using an enzyme-linked immunosorbent assay, we studied sera from 93 healthy Bangladeshi children and 121 healthy U.S. children under 15 years of age. For each age group (<1, 2 to 4, and 5 to 14 years) studied, specific serum antibody levels were significantly higher in the Bangladeshi children. Among Bangladeshi children, for each of the three immunoglobulin subclasses, the change in antibody levels with age was different. Specific immunoglobulin A antibody levels rose linearly with age, immunoglobulin G levels peaked in the 2to 4-year age group and then fell, and immunoglobulin M levels peaked in the 2to 4-year age group and then plateaued. Elevated serum antibody levels to C. jejuni in Bangladeshi children may be protective in themselves or may reflect other protective phenomena.
The serologic responses to Campylobacter jejuni in persons involved in two clusters of infection and in control subjects were studied. In the first cluster, in which previously unexposed persons drank raw milk, the attack rate was high and elevated complement-fixing (CF) and specific IgG and IgM antibodies were demonstrated. In the second cluster, involving farmers who chronically drank raw milk, the attack rate was low, but titers of CF and IgG antibodies were high in both affected and unaffected persons. At a control dairy farm, where raw milk was drunk regularly, asymptomatic infection and high CF titers were demonstrated. In contrast to the findings in the first cluster, the titers of IgM antibody among the dairy farmers were low. These studies suggest that chronic exposure to C. jejuni may lead to immunity that may possibly be mediated by IgG.
HA-ICR adult mice were studied to develop an animal model for Campylobacter jejuni enteritis in humans. Fecal and ileal cultures made by selective and nonselective methods showed that C. jejuni and related organisms are not bowel commensals. Intragastric feeding of 108 CFU of three different strains of C. jejuni produced infection in 100% of the animals, and infection rates were dose dependent. Pretreatment with antibiotics or opiates was not necessary to induce infection. Fresh isolates and strains passed on artificial media yielded similar infection rates. Infected mice did not show signs of illness, but transient bacteremia within 10 min of oral infection was observed in nearly 100%. The small intestine was the principal target organ, with epithelial inflammation seen 48 h after infection. Control mice offour species had undetectable serum immunoglobulin G antibody specific for the infecting strain, but infected mice showed peak titers at 1 week with rapid decline. Immunoglobulin M titers rose minimally, and immunoglobulin A titers did not rise. Infected mice uniformly became chronic asymptomatic excretors, shedding 104 to 106 CFU/g of feces; a minority were biliary carriers. Intestine carriage was most pronounced in the stomach and proximal small intestine. Because this experimental infection led to bacteremia, transient pathological changes, and immunoglobulin G titer rises, this model may be useful for evaluating the effects of prophylactic and therapeutic interventions.
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