Campylobacter

Etiologic agent = Campylobacter spp.

There are a variety of zoonotic Campylobacter species (see below), but C. jejuni is clearly the most important in terms of its impact on human health.

The Campylobacters are gram (-), uniquely curved ("gull wing") rods.

Sources of Campylobacter:

* Dogs and cats:
o Infection is most common in puppies and kittens, but Campylobacter spp. can also be isolated from clinically normal adult dogs and cats (up to 30%), as well.
o Epidemiologically, living with dogs and cats has been documented to be a specific risk factor for Campylobacter infection.
* Poultry, ruminants and swine:
o This organism is part of the GI tract normal flora of these animals. Infection of humans can occur via direct contact with animal feces or, much more commonly, via ingestion of contaminated, undercooked meat or raw milk.
+ A recent study found C. jejuni in the intestinal contents of up to 76% (mean 31%) of market swine in Texas. However, poultry represent the most significant public health concern.
# From 22-100% of commercial poultry products are contaminated, and this source accounts for 50-70% of all human cases. If the meat is thoroughly cooked, it poses no risk.
# A recent study in the U.K. found that 100% of chickens raised organically outdoors carried Campylobacter, versus 58% of indoor conventionally raised birds.
# A concern above and beyond the frequency of contamination is the occurrence of antibiotic-resistance among Campylobacter isolates from poultry. Studies have documented 14-84% resistance to antibiotics, including fluoroquinolones, and it appears that resistance to fluoroquinolones develops rapidly in antibiotic-treated chickens. In addition, there is concern for macrolide resistance among human isolates and a suggestion that this may be related to macrolide use in animals.

Campylobacteriosis in humans:

Campylobacter jejuni is the most common agent of bacterial diarrheal disease among humans in the U.S., with an estimated 2 million cases each year in this country. It produces an enteritis lasting 1-7+ days, characterized by a prodrome of fever and malaise that progresses to varying degrees of diarrhea and abdominal pain (even pseudo-appendicitis).

* The incubation time is inversely related to the inoculum dose.
* Anti-motility drugs for diarrhea increase the severity of symptoms and prolong the course of disease.
* Campylobacteriosis is generally self-limiting, except in immunocompromised patients.

Campylobacter infection and Guillain-Barre syndrome:

In addition to gastrointestinal disease, C. jejuni is considered one of the most common triggering factors for Guillain-Barre syndrome (GBS), an immune-mediated myelitis/neuropathy in human beings. Recent work by Prendergast et al. (1998) specifically indicates that lipopolysaccharides from C. jejuni contain antigens that mimic GM1 or GQ1b gangliosides in human CNS tissue. However, other host factors may also be important in development of GBS (e.g., certain HLA genotypes).

* Approximately 1/1000 Campylobacter infections result in GBS.
* ~40- 66% of GBS cases have premonitory C. jejuni infections.
* GBS that follows Campylobacter infection is more severe and more likely to be irreversible.
* GBS may be associated with infection with certain serotypes of C. jejuni and strains with unique sequences in their fla A flagellar genes.

Campylobacter infection is also associated with another immune-mediated disease called "Reiter's syndrome" (tenosynovitis with accompanying skin lesions, uveitis and urethritis). This is estimated to occur in ~7% of patients with campylobacteriosis.

Campylobacter infection has also been associated with development of myocarditis as a post-gastroenteritis sequelae, and fatal septic shock in a splenectomized patient, reflecting the potential severity of infection in immunocompromised individuals.

Campylobacteriosis in dogs and cats:

* Clinical signs of ileocolitis are most common in puppies and kittens <6 months of age.
* The chief presenting sign is diarrhea.
o The diarrhea is thought to be due to the action of a cholera-like enterotoxin and a cytotoxin.
o Other signs such as vomiting, anorexia and fever are uncommon.
* The clinical course of disease is 1-3 weeks (generally closer to 1 week).
o Severity varies from case to case and clinical signs are exacerbated by stress.

Diagnosis:

* fecal culture (requires specific media and reduced oxygen culture conditions at 42C)

Treatment:

* erythromycin (chloramphenicol is less efficacious) for 7 (to 28) days
o Renewed shedding after completion of the course of antibiotics is possible, hence the importance of follow-up fecal cultures.