 |
Campylobacter spp are spiral, microaerobic gram-negative bacteria that cause gastroenteritis in people and animals. Several Campylobacter spp are zoonotic. Many domestic animals develop acute gastroenteritis after ingestion of C jejuni, including dogs, cats, calves, sheep, pigs, ferrets, mink, monkeys, several species of laboratory animals, and people. (see also Bovine Genital Campylobacteriosis.) Infection with C jejuni is one of the most common causes of gastroenteritis in people worldwide.
Etiology
Campylobacter spp are spiral or curved rods that exhibit a characteristic corkscrew darting motility, mediated by a single polar flagellum. These are slow growing, with a generation time of ~90 min, fastidious, and require enriched medium and microaerobic conditions with increased CO2 (3–15% O2, 3–10% CO2, 85% N2) for growth.
The family Campylobacteraceae contains two genera: Campylobacter and Arco-bacter. The genus Campylobacter currently includes 14 species. The thermophilic Campylobacter spp, C jejuni or C coli, have the highest prevalence and disease impact. However, another 12 species of Campylobacter can also be pathogenic for people and animals: C fetus fetus, C fetus venerealis, C hyointestinalis, C lari, C upsaliensis, C helveticus, C concisus, C curvus, C showae, C gracilis, C sputorum, C rectus, and C mucosalis. At least 2 of these species, including C fetus fetus and C upsaliensis, are acquired through the GI tract but are most often associated with extra-intestinal infections. Also, several species, including C concisus, C curvus, C showae, C gracilis, and C rectus can cause periodontal disease. Some closely related species have been removed from the genus, including Campylobacter-like organisms (CLO) (Helicobacter cinaedi [CLOIA] and H fennelliae [CLO2]) and H pylori. Ileal symbiont Heliobacter intracellularis, originally called Campylobacter-like, was reclassified as an Arcobacter, C nitrofragilis as A nitrofragilis, and C cryaerophilus as A cryaerophilus. Finally, subspecies of C jejuni exist, including C jejuni jejuni and C jejuni doylei.
Transmission and Epidemiology
Transmission is food- or waterborne or via fecal-oral spread. Animals serve as reservoir hosts for Campylobacter spp infections in both animals and people throughout the world. The predominant ecologic niche for Campylobacter spp is the GI tract of a wide variety of domesticated and wild vertebrates, and zoonotic transmission from animals to people in meat of animal origin, especially chicken, is a food safety issue. Campylobacter spp are also commonly isolated from free-living birds, including migratory birds and waterfowl, crows, gulls, and domestic pigeons, which can contaminate environments of grazing animals. Wild rodents and insects such as flies have also been reported to harbor and transmit C jejuni. Fecal contamination of the environment provides a ubiquitous source of these organisms under appropriate conditions for their survival. Campylobacter spp can persist for long periods in feces, milk, water, and urine, especially at temperatures close to 4ºC. In adverse conditions, C jejuni converts to a viable nonculturable form that can be reactivated when ingested.
Human foods documented as contaminated with Campylobacter include chicken, turkey, beef, pork, fish, and milk. Domesticated poultry are the most significant reservoir of C jejuni for people, causing 50–70% of cases; chicken meat is the number one source. Dogs and cats are commonly infected similar to their owners when they ingest undercooked poultry.
Pathogenesis
Bacterial motility, mucus colonization, toxin production, attachment, internalization, and translocation are among the processes associated with C jejuni virulence. Infection begins with ingestion of the C jejuni in contaminated foods or water. Gastric acid provides a barrier, and the bacteria must reach the small and large intestines to multiply; C jejuni invades both epithelial cells and cells within the lamina propria.
Clinical Findings
Abdominal pain, fever, diarrhea, frank blood in feces, and inflammatory cells in feces demonstrate the inflammatory nature of the infection. Natural infections with C jejuni resulting in enteritis have been reported in juvenile macaques, weaning-age ferrets, dogs, cats, and swine. Chickens, rodents, ferrets, dogs, primates, rabbits, and pigs have been inoculated experimentally by various routes with C jejuni and subsequently developed enteritis. Clinical reports describe primary infections with systemic spread, infection with mucosal disease, infection without disease but with short-term bacterial persistence, and infection with resistance and no bacterial persistence. These reports support the idea that C jejuni produces a spectrum of disease scenarios, depending on the immune status of the host, bacterial virulence, gene expression, and other factors.
C jejuni, C coli, C jejuni, C upsaliensis, and C helveticus are the Campylobacter spp that have been associated with intestinal disease in companion animals. C jejuni causes diarrhea in dogs and cats, which are considered a significant source of the bacterium for the human population. Diarrhea is usually acute but can be recurrent. Exposure of dogs to C jejuni causes mild diarrhea followed by bacteremia. 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%). C jejuni was cultured from feces of 3 of 206 (1.5%) cats in a western USA study designed to identify enteric zoonotic organisms. The bacterium was detected in samples from cats with and without diarrhea. Additionally, C jejuni has been isolated in pure culture from the vaginal discharge from 3 German Shepherd bitches after late-pregnancy abortion; the main clinical sign was a profuse and odorless hemorrhagic vaginal discharge.
Dogs and cats commonly have clinical signs after C jejuni infection. Diarrhea lasting 5–15 days is the most common clinical sign in dogs <6 mo old. It may be watery to bloody with mucus and is sometimes bile-stained. Occasionally, the diarrhea becomes chronic and may be accompanied by fever and an increased WBC count. Cats <6 mo old commonly have diarrhea, which may be bloody. Most cats have other infectious agents present, eg, Toxoplasma or Giardia. Some infected cats show no signs.
In cattle and sheep, C jejuni can cause enteritis and abortion. However, in studies that compared C jejuni prevalence in healthy cattle and cattle considered “sick” because of diarrhea, the frequency of Campylobacter spp was not significantly different. However, in studies of abortion rates, 3.2% of cattle and 21.7% of sheep had Campylobacter spp abortions attributed to C jejuni. Beef and dairy cattle can have significant levels of Campylobacter, with prevalences of 2.5–60%. In a number of studies, cattle checked at slaughter harbored Campylobacter in gallbladders, large and small intestines, and liver. Fecal shed in cattle leads to contamination of milk and beef.
C jejuni has been associated with abortion in sheep. Campylobacter spp isolated from cases of sheep abortion and typed for biochemical, antigenic, and genetic differences demonstrated 15 isolates of Campylobacter spp (14 C jejuni and 1 C fetus fetus) present during a single lambing season.
Campylobacters can contribute to colitis in weaning aged pigs. Swine commonly carry C coli and C jejuni as intestinal commensals, and studies in the USA, Netherlands, Great Britain, and Germany show that more than half of commercially raised pigs excrete the organisms. C coli strains comprise most isolates from pigs. Gnotobiotic or colostrum-deprived piglets inoculated orally with pathogenic strains of C jejuni develop acute enteritis. Pigs have anorexia, fever, and diarrhea for 1–5 days followed by remission of clinical signs but continue to shed C jejuni in the feces. However, immunocompetent pigs with a full complement of enteric bacteria exposed early in life are resistant to reinfection with C jejuni. Concurrent infections with viruses, bacteria, and parasites increase the disease and pathology caused by C jejuni in swine.
Birds appear to have a higher infection rate and carriage of Campylobacter spp especially C jejuni, than other animals. In broilers, the organism may colonize the palatine lymphoid tissues and the crop, leading to extremely rapid transmission through communal water troughs and standard fecal-oral spread. However, the organism has been isolated from the small intestines of clinically ill birds, especially psittacines (parrots) and passeriforms (finches and canaries), with hepatitis, lethargy, loss of appetite, weight loss, and yellow diarrhea. Mortality may be high. Campylobacter spp have also been isolated from free-living birds, including migratory birds and waterfowl, crows, gulls, and domestic pigeons. Despite the high rate of bacterial colonization, disease due to C jejuni in naturally infected birds is rare.
Campylobacter GI disease has been reported in exotic pets (eg, ferrets, mink, primates, hamsters, guinea pigs, mice, and rats). Although clinical signs vary in these species, they generally include mucoid, watery, bile-streaked diarrhea (sometimes with blood), anorexia, vomiting, and fever. Prolonged infections are possible but uncommon; most infections are self-limiting with mild signs. Ferrets develop Campylobacter induced diarrheal disease similar to that seen in people. Various strains of mice also develop disease after oral ingestion of C jejuni, with specific defects in immune system components leading to watery or bloody diarrhea and typhlocolitis.
Lesions
C jejuni can stably colonize the small and large intestines, although most animals show cecal and colonic lesions with typhlocolitis. In swine and mice, gross lesions observed in C jejuni enteritis include enlarged and fluid-filled ceca and proximal colons with thickened walls. Lymph nodes (ileocecocolic and mesenteric) draining infected sites become significantly enlarged. Infection with particular strains of C jejuni produces bloody exudates with mucus. Histopathologic features include a marked inflammation of the lamina propria, dominated by neutrophilic polymorphonuclear cells and mononuclear cells that sometimes extend into submucosa. Immune cells such as plasma cells, macrophages, and mononuclear cells have been found in smaller numbers in the lamina propria. Damage to, sloughing of, and ulceration of the epithelial surface and edema have also been observed in most infected species. In pigs and mice, damage to the epithelial surface is associated with the presence of C jejuni at the basolateral surface of the epithelium, in paracellular junctions of the epithelium, and in erosive and ulcerative lesions of the epithelium; there is often a mucopurulent neutrophilic exudate with sloughed and lysed epithelial cells and erosive or ulcerative lesions where C jejuni is associated with the basolateral aspect of sloughing villous tip cells in the colon. Crypt abscesses and damage to the crypt epithelium are also common findings.
Diagnosis
Diagnosis of C jejuni is based on isolation of the organism on selective media under microaerophilic conditions. Fresh fecal samples should be collected; if transport to the laboratory is delayed, transport media and storage at 4ºC produce the best results. Campylobacter spp are sensitive to low pH (<5), drying except under refrigeration, NaCl concentrations >2%, and long periods at temperatures of 10–30ºC. In unfavorable growth conditions, spiral rods undergo a degenerate conversion to coccoid forms. Thermophilic Campylobacter spp, C jejuni, C coli, and C lari grow best at 42ºC, although they are capable of growth at 37ºC. Enrichment is required for most clinical sampling unless material can be transported to the laboratory immediately.
PCR-based methods are effective in identifying infection especially if cultivation is difficult or if the sample has been somewhat mishandled. However, a positive test is not sufficient evidence to determine causation and must be considered in conjunction with clinical signs.
Treatment and Control
Clindamycin, gentamicin, tetracyclines, erythromycin, and fluoroquinolones are effective against Campylobacter spp. Penicillins, cephalosporins, and trimethoprim are generally ineffective. Resistance to the fluoroquinolones, tetracycline, kanamycin, and some other antibiotics has been documented among the Campylobacter spp, mediated by both chromosomal and plasmid mechanisms. Culture-dependent diagnosis can provide isolates for antibiotic sensitivity testing. However, some animals remain colonized and become persistent shedders despite antibiotic therapy. If the goal of treatment is to decrease the risk of zoonotic transmission to a susceptible household member, antibiotic treatment alone may be inadequate. Control involves treatment, removal to a clean environment, and prospective fecal testing to ascertain shedding status; even so, low infective doses and the ubiquitous distribution of the organism pose significant challenges.
Last full review/revision March 2012 by Linda S. Mansfield, MS, VMD, PhD
| |
|
