CAMPYLOBACTER

Members of the genus Campylobacter are gram-negative, slender, spiral to curved rods (Figures 28-1 and 28-2). Many were formerly in the genus Vibrio, leading to continuing references to the diseases they cause as vibriosis. Campylobacter spp. are motile, with a characteristic darting or corkscrew motion, best seen by darkfield or phase contrast microscopy. They are microaerophilic and require 3% to 5% CO₂ and 3% to 15% O₂ for growth. They are distinguished from true Vibrio species by their lack of oxidation and fermentation of carbohydrates. All are oxidase positive, some produce catalase, and most reduce nitrate. Urease negativity is common, and this trait is useful in distinguishing them from many members of the genus Helicobacter.

FIGURE 28-1 Gram-stained cells of Campylobacter fetus ssp. fetus.

(Courtesy J. Glenn Songer.)

FIGURE 28-2 Campylobacter sp. viewed by darkfield microscopy. Note the chaining of individual organisms, which are often mistaken for spirochetes.

(Courtesy J. Glenn Songer.)

Campylobacter spp. frequently live as commensals in the intestinal tracts of mammals and birds. Campylobacter jejuni, the leading cause of bacterial food-borne illness, and Campylobacter coli, which contributes a minor share of cases, colonize food animals without producing illness. Non-jejuni and non-coli species have a role in animal disease. Animal-derived foods, especially those from poultry, are the major source of Campylobacter spp. for infection of humans. Species encountered in veterinary medicine are presented in Table 28-1.

TABLE 28-1 Campylobacter Species Encountered in Veterinary Medicine

* Zoonotic agent.

Diseases, Epidemiology, And Pathogenesis

Campylobacter fetus.

Subspecies of C. fetus have been recognized causes of ovine and bovine abortion for decades and, before the mid-1970s, were the major organisms of interest in the genus. Sheep infected with Campylobacter fetus ssp. fetus, by ingestion of the organism in contaminated food or water, develop bacteremia. Infection is sporadic, but in at least some cases, deposition of C. fetus ssp. fetus in placenta initiates an inflammatory process that is followed by abortion, usually in the third trimester (Figure 28-3). Infection by Campylobacter fetus ssp. venerealis, known as bovine venereal campylobacteriosis, is transmitted from bulls to cows in the normal process of breeding or by way of artificial insemination. The organism can typically be recovered from the glans penis and distal urethra of infected bulls, and deposition in the female reproductive tract results in ascend ing colonization that extends to the fallopian tubes. The syndrome usually manifests as infertility, and abortion occurs in less than 10% of infected cows.

FIGURE 28-3 Ovine abortion resulting from Campylobacter fetus ssp. fetus.

(Courtesy J. Glenn Songer.)

Serum resistance probably plays a major role in virulence of C. fetus, and high-molecular-weight proteins composing the S (surface)-layer are the key components in this resistance. The S-layer is not effectively opsonized by complement component C3b, so neutrophil phagocytosis is limited. A 135-kD protein mediates resistance to phagocytosis by preventing binding of O-specific antibody. Mutants lacking the S-layer are serum sensitive and have reduced virulence in mice, suggesting that the S-layer masks Campylobacter lipopolysaccharide (LPS), perhaps in a bacterial strategy to decrease immunogenicity. S-layer proteins of C. fetus ssp. venerealis may be subject to antigenic shifts over time in experimentally infected heifers, and genetic analysis suggests that the basis for this phenomenon is in genomic rearrangements. The sapA promoter is on an invertible DNA fragment, which allows expression of two oppositely oriented S-layer gene cassettes, and recombination of 5′ conserved regions of multiple sapA homologs also contributes to antigenic variation. The S-layer is not required for adherence to epithelial cells in vitro.

Campylobacter jejuni and Campylobacter coli.

Campylobacter jejuni and C. coli occur in large numbers (as many as 10⁷ colony-forming units [CFUs] per g) as commensals in the intestinal tract of companion and food animals. Humans are infected by consumption of undercooked meats, especially poultry, contaminated by either C. jejuni (95%) or C. coli(5%); an incubation period of 24 to 72 hours is followed by severe diarrhea, with blood and leukocytes in feces, fever, vomiting, and abdominal pain. Illness is usually self-limiting.

Prevalence of campylobacters in companion animals varies inversely with age. Nonetheless, dogs and cats may be involved in transmission of campylobacteriosis to humans. Healthy dogs harbor C. jejuni, but there is a strong correlation between the occurrence of diarrhea and recovery of C. jejuni from these animals. The organism is found in clinically normal cats. Symptoms of campylobacteriosis are mild in food animals, consisting of soft to watery feces with mucus and flecks of blood.

Extraintestinal infections with C. jejuni have been reported in sheep, goats, cattle, and pigs. The organism can cause abortion in sheep and goats, with symptoms similar to those of C. fetus abortions, and mastitis in cattle. Campylobacter jejuni is frequently isolated from milk contaminated by feces or via mastitic infections, and is a major source of infection in countries where raw milk is consumed. Campylobacter jejuni and C. coli infections have been associated with abortion in sheep and pigs, but infections in these species are usually more benign.

Pathogenesis of C. jejuni infections is initiated when the organism penetrates the intestinal mucus layer and invades enterocytes. This adherence facilitates resistance to elimination by peristalsis, and is mediated by constitutively expressed proteins. Attachment factors include a fibronectin binding protein (CadF), a lipoprotein (JlpA), and possibly flagellin, pilus proteins, and LPS. Binding is followed by invasion, the extent of which is highly strain dependent; environmental isolates are much less invasive than clinical isolates, and isolates from noninflammatory diarrheal disease are less invasive than those from colitis patients. Internalization of C. jejuni is by directed endocytosis, and requires fully functional bacterial metabolism. Cia proteins play an important but undefined role in pathogenesis. They are synthesized on bacterium-cell contact, and reach the cytoplasm via a type III secretion system. Intracellular membrane-bound C. jejuni initially decreases in numbers, but then undergoes exponential growth over a 72-hour period. It gains access to deeper tissues by transcytosis, and can be found in granulocytes, parenchymal cells, and mononuclear cells in the lamina propria and submucosa. Experimental disease in newborn piglets mimics human campylobacteriosis. Macrophages and neutrophils appear in the lamina propria and submucosa within three days of infection, and many contain internalized C. jejuni. In vitro, uptake is strain and host dependent, and is facilitated by antibodies.

Survival of C. jejuni in macrophages may contribute to disease severity, duration of symptoms, and rate of relapse. Campylobacter superoxide dismutase (from sod B) might be expected to facilitate intracellular survival of C. jejuni, but survival of a sod B mutant was no different than that of the parent strain. In contrast, a catalase (kat A) mutant was susceptible to intracellular killing, whereas the parent strain remained viable through 72 hours of intracellular residence.

< div class='tao-gold-member'>

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Join