Lawsonia intracellularis proliferative enteropathy in a foal
D. J. Feary1, C. J. Gebhart2, N. Pusterla3
Medical Teaching Hospital and 3Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA, 2Department of Veterinary Biosciences, University of Minnesota, College of Veterinary Medicine, St.Paul, MN, USA
Equine proliferative Enteropathie durch Lawsonia intracellularis
A weanling foal was diagnosed with proliferative enteropathy caused by Lawsonia intracellularis based on history, clinical findings of depression, anorexia, weight loss, colic, diarrhea, and ventral edema, and a combination of serology and fecal PCR. An epidemiological investigation on the premisesrevealed that many of the other foals and adult horses were seropositive for L. intracellularis, despite being clinically normal, and identified a dog as a potential carrier and source of infection for the foal.The foal was successfully treated with a combination of azithromycin and rifampin.
In einem Fohlen wurde aufgrund der Vorgeschichte, der klinischen Befunde (Apathie, Anorexie, Abmagerung,Kolik, Diarrhoe und Unterbauchödem) und der diagnostischen Ergebnissen (Serologie und PCR) eine proliferative Enteropathie durch Lawsonia intracellularis diagnostiziert. Um den möglichen Erregerkontakt zu identifizieren, wurden Kot- und Blutproben von gesunden Tieren (Pferde, Hunde) aus der Umgebung mittels Serologie und PCR untersucht. Die Ergebnisse zeigen, dass zahlreiche Fohlen, adulte Pferde undein Hund seropositiv für L. intracellularis waren. Die Bedeutung des Hundes als Übertraeger wird diskutiert. Das erkrankte Fohlen wurde mit einer Kombination von Azithromycin und Rifampin erfolgreich behandelt.
Schlüsselwörter: Equine proliferative Enteropathie, Lawsonia intracellularis, Fohlen, Epidemiologie
Keywords: equine proliferative enteropathy, Lawsonia intracellularis, foal,epidemiology
A 6-month-old Quarter Horse filly was admitted to the Veterinary Medical Teaching Hospital, School of Veterinary Medicine, University of California in Davis with a 7 day history of lethargy, anorexia, mild weight loss, fever, ventral edema, mild colic, weakness, and intermittent diarrhea. The foal was observed to drink and urinate excessively during this time. Prior treatmentwith trimethoprim-sulfamethoxazole and long-acting ampicillin by the referring veterinarian did not result in clinical improvement. The foal had been growing well and was active, bright, and vigorous until recent illness. The foal had been administered ivermectin at 4-weeks interval since birth and had not been vaccinated.The foal was in contact with 3 other foals between 6 and 10 months old, and13 adult horses between 3 and 26 years old. There had been no recent history of movement of horses on or off the premises and no other foals or adult horses had shown any signs of illness in the past 6 months. There were 2 pigs between 4 and 12 months of age on the premises for 10 months prior to illness in the foal. All four foals were housed together in a foaling stall with a run for 4 weeksprior to development of clinically apparent disease in the aforementioned foal. Both pigs had been previously housed in this stall for an 8 day period just 7 days prior to introduction of the foals into the stall. There were 3 cows, 2 dogs, 3 zebra and various wildlife (rabbit, deer, raccoon, skunk) on the premises.
Clinical and laboratory findings
At the time of admission the foal waslethargic, depressed, and reluctant to move. The foal was well grown with a moderate body condition score of 5/9, and weighed 203 kg. Mild pectoral, ventral abdominal, and distal limb edema was present. Physical examination revealed mild tachycardia (60 beats/min), normal rectal temperature (37.9ºC) and respiratory rate (18 breaths/min). Jugular refill was normal and peripheral pulses were strong. Oral...
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