[fasteddie]

Gastrointestinal campylobacteriosis, caused by Campylobacter jejuni or C coli , is now recognized as a cause of diarrhea in various animal hosts, including dogs, cats, calves, sheep, ferrets, mink, several species of laboratory animals, and man. In man, it is a leading cause of diarrhea. Campylobacter jejuni and C coli are also recovered from feces of asymptomatic carriers. Animals, including dogs and cats (especially those recently purchased from shelters or pounds) as well as wild animals maintained in captivity, can serve as sources of human infection. The agent(s) also is isolated frequently from the feces of chickens, turkeys, pigs, and other species.

The disease occurs worldwide, and its prevalence appears to be increasing as proper culture techniques for C jejuni and C coli are refined and updated. Clinical manifestations may be more severe in younger animals. In studies using monoclonal and polyclonal antibodies, Campylobacter spp (probably not C jejuni ) have been associated with proliferative ileitis in hamsters, porcine proliferative enteritis, and proliferative colitis in ferrets. However, a cause and effect relationship has not been proved experimentally due to the inability to culture the intracellular Campylobacter sp in vitro.

Etiology: Campylobacter is a gram-negative, microaerophilic, slender, curved, motile bacterium with a polar flagellum. Campylobacter jejuni is routinely associated with diarrheal disease; however, C coli , distinguished from C jejuni on the basis of hippurate hydrolysis, is occasionally isolated from diarrheic animals and is routinely recovered from asymptomatic pigs. More recently, other intestinal, catalase-negative campylobacters, " C upsaliensis " and C helveticus , have been isolated from diarrheic dogs as well as from asymptomatic dogs and cats. Campylobacter (Vibrio) sp was once associated with swine dysentery ( Swine Dysentery), but this is now recognized as being caused by Treponema hyodysenteriae . It is now believed by most that Campylobacter spp do not produce porcine proliferative enteritis ( Porcine Proliferative Enteritis) even though a new organism, Campylobacter hyoilei , has been associated with porcine proliferative enteritis.

Because of the slow growth and microaerophilic requirements of Campylobacter , standard culture methods require selective media that incorporate various antibiotics to suppress competing fecal microflora. Campylobacter jejuni and C coli grow well at 42°C in an atmosphere of 5-10% carbon dioxide and an equal amount of oxygen. Cultures are incubated 48-72 hr; colonies are round, raised, translucent, and sometimes mucoid. The organism can be identified by a series of biochemical tests routinely available in diagnostic laboratories.

Transmission and Epidemiology: As with most intestinal pathogens, fecal-oral spread and food- or water-borne transmission appear to be the principal avenues for infection. One suspected source of infection for pets, as well as mink and ferrets raised for commercial purposes, is ingestion of undercooked poultry and other raw meat products. Asymptomatic carriers can shed the organism in their feces for prolonged periods and contaminate food, water, milk, and fresh processed meats (including pork, beef, and poultry products). The organism can survive in vitro at 41°F (5°C) for 2 mo and can survive in feces, milk, water, and urine. Wild birds also may be important sources of water contamination. Unpasteurized milk has been cited as a principal source of infection in several outbreaks in man.

Clinical Findings: The diarrhea appears to be most severe in young animals. Typical signs in dogs include mucus-laden, watery, and/or bile-streaked diarrhea (with or without blood) that lasts 3-7 days; reduced appetite; and occasional vomiting. Fever and leukocytosis may also be present. In certain cases, intermittent diarrhea may persist >2 wk; in some, it may be present for months. Gnotobiotic puppies inoculated with C jejuni developed malaise, loose feces, and tenesmus within 3 days of inoculation.

In calves, signs vary from mild to moderate. The diarrhea is thick and mucoid with occasionally visible blood flecks; temperature may be normal. Diarrhea with mucus and blood also has been seen in primates, ferrets, mink, and cats. Campylobacter mucosalis and C hyointestinalis have been isolated from pigs with intestinal adenomatosis. Diarrhea and wasting disease are also clinically evident in these animals. Organisms with ultrastructure similar to Campylobacter spp have been seen in hyperplastic ileal epithelial mucosa of hamsters with proliferative ileitis; C jejuni has been isolated from these lesions but has failed to reproduce the syndrome. Organisms with Campylobacter -like morphology also have been associated with proliferative colitis in ferrets and with hyperplastic intestinal lesions in guinea pigs and rats. Campylobacter -like organisms have been described in young rabbits with acute typhlitis; it is now known that these organisms are a Desulfovibrio species.
Lesions: In 3-day-old chickens infected with C jejuni , the organisms were detected within epithelial cells and mononuclear cells of the lamina propria; the jejunum and ileum were the most severely affected. Congested and edematous colons were found in dogs 43 hr after inoculation; microscopically, there was reduction in epithelial height, loss of brush border, and reduced numbers of goblet cells in the colon and cecum. Hyperplastic epithelial glands resulted in a thickened mucosa. Histologic changes in calves primarily involve the jejunum but also can involve the ileum and colon. The lesions can vary from mild changes to severe hemorrhagic enteritis. The mesenteric lymph nodes are edematous. A putative enterotoxin and cytotoxin have been identified in C jejuni infection; however, their role in production of the disease is not known. Experimentally, some strains of C jejuni produce a hepatitis in mice.

Diagnosis: The standard method for diagnosis is microaerophilic culture of feces at 42°C; a special medium is commercially available. Diagnosis is also possible by using darkfield or phase-contrast microscopy, by which fresh fecal samples are examined for the characteristic darting motility of C jejuni . This method is especially useful during the acute stage of diarrhea when large numbers of organisms are more likely to be shed in the feces. Various techniques can detect serum antibodies to different antigens of Campylobacter spp . Heat-stable or heat-labile antigen schemes are used routinely to serotype various strains. Serial serum samples to demonstrate rising antibody titers are helpful in diagnosis. Intestinal viruses as well as other intestinal bacterial pathogens must be ruled out in animals with Campylobacter -associated diarrhea.

Treatment and Control: Isolation of C jejuni or C coli from the diarrheic feces is not, in itself, an indication for antibiotic therapy. Because C jejuni and C coli have only recently been recognized as potential intestinal pathogens in animals, efficacy of antibiotic therapy has been reported infrequently. In certain cases in which animals are severely affected or present a zoonotic threat, antibiotic treatment may be indicated. In general, C jejuni and C coli isolates from animals are similar to those isolates obtained from human populations. Erythromycin, the drug of choice for Campylobacter diarrhea in man, is also effective in other animals. Gentamicin, furazolidone, doxycycline, and chloramphenicol also can be used. Ampicillin is relatively inactive against most strains of Campylobacter . Most strains are also resistant to penicillin. Tetracycline and kanamycin resistance in certain C jejuni strains is reported to be plasmid-mediated and transmissible within C jejuni serotypes. Efficacy of sulfadimethoxine and sulfa combinations is variable. Before therapy is instituted, isolation and sensitivity tests should be done. Some animals continue to shed the organism despite antibiotic therapy. Quinolone antibiotics may be useful in eliminating C jejuni and C coli in asymptomatic carriers, but drug resistance can develop to this class of antibiotics.

NOT A HOAX! HERES PROOF! PLEASE SHARE THIS INFORMATION!!! This is what we suspect is going on.

My Chica. A vaccinated puppy who contracted this illness 3 days after losing BIll. Not knowing about the bacteria present and wasting no time, I treated her with the standard Parvo regiment. She lost half her body weight and nearly died . It took a week, but we saved her. She is completely healthy today.

Amy Arnett's little Nino. Went lethargic and began vomiting later in the day of losing Tobey and Mija. NOW having the information about this bacteria only hours of Mija dying in our arms, he was treated with one cephalexin pill, Nino immediately improved and was normal the following day.

PLEASE, if your animal is exibiting these symptoms, you need to see your vet and have it properly diagnosed to be certain that this is what you are dealing with. We are by no means saying that you should treat without diagnosing, HOWEVER the treatment is simple and if it works, than this is probably the cause.

INTERNET ARTICLES DO NOT REPLACE PROPER VETERNARY CARE!
09-25-04 Update
Oklahoma State University is researching this problem. They are finding these bacterias in animals, and are hearing reports of strange, fast killing parvo-like outbreaks elsewhere. We still do not have a clear picture of what it going on. Phone calls and emails from people losing pets in this manner are still coming in daily. We hope to have answers soon. OSU told us to keep informing the public of the problem and that they are working hard to get us some answers. Until then, PLEASE watch your pets.

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