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Chapter: Medical Microbiology: An Introduction to Infectious Diseases: Vibrio, Campylobacter, and Helicobacter

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Campylo Bacter Enteritis

C. jejuni infection typically beginswith lower abdominalpain,which evolvesinto diarrhea over a matter of hours.

CAMPYLO BACTER ENTERITIS

 

C. jejuni infection typically beginswith lower abdominalpain,which evolvesinto diarrhea over a matter of hours. The diarrhea may be watery or dysenteric, with blood and pus in the stool. Most patients are febrile. The illness resolves sponta- neously after a few days to 1 week.

 

EPIDEMIOLOGY

It is humbling to consider how a pathogen as common as C. jejuni could have been missed for decades. Studies from many countries find C. jejuni in 4 to 30% of diarrheal stools, making it the leading cause of gastrointestinal infection in developed countries. Over 2 million cases occur each year in the United States, at a rate roughly double the second most common bacterial enteric pathogen, Salmonella. This high rate of disease is facilitated by the low infecting dose of C. jejuni— only a few hundred cells.

The primary reservoir is in animals and the bacteria are transmitted to humans by in-gestion of contaminated food or by direct contact with pets. Campylobacters are com-monly found in the normal gastrointestinal and genitourinary flora of warm-blooded animals, including sheep, cattle, chickens, wild birds, and many others. Domestic animals such as dogs may also carry the organisms and probably play a significant role in trans-mission to humans. The most common source of human infection is undercooked poultry, but outbreaks have been caused by contaminated rural water supplies and unpasteurized milk often consumed as a “natural” food. Sometimes a direct association can be made as with a sick household pet.

PATHOGENESIS

 

Infection is established by oral ingestion, followed by colonization of the intestinal mu-cosa. The bacteria have been shown to adhere to endothelial cells and then enter cells in endocytotic vacuoles. Once inside, they move in association with the cell’s microtubule structure, rather than the actin microfilaments associated with many other invasive bacte-ria. The search for enterotoxins associated with C. jejuni has thus far been unrewarding. A cytolethal distending toxin arrests cell division while the cytoplasm continues to grow, but how this leads to diarrhea remains to be established. All in all, the virulence determi-nants of this microorganism remain uncertain.

There is an association between C. jejuni infection and the Guillain-Barrésyn-drome, an acute demyelinatingneuropathythatis frequentlypreceded byaninfection.AlthoughC. jejuni is not the only antecedent to this syndrome, it is the most common of identifiable causes. Up to 40% of patients have culture or serologic evidence of Campy-lobacter infection at thetimetheneurologic symptoms occur.Themechanismisbelievedto involve antibody elicited by ganglioside-like structures in the C. jejuni LPS core oligosaccharide that cross-react with similar molecules in the host peripheral nerve myelin. These antiganglioside antibodies are found in the serum of patients with Guillain Barrésyndrome motor neuropathies. This molecular mimicry is similar to the mechanismof rheumatic fever stimulated by the group A streptococcus .

IMMUNITY

Acquired immunity following natural infection with C. jejuni has been demonstrated in volunteer studies, but the mechanisms involved are unknown. Antibodies are formed in the weeks following infection but decline rapidly thereafter. The high rate ofCampy-lobacter infection in patients with acquired immunodeficiency syndrome suggests the im-portance of cellular immune mechanisms.

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