Pathophysiology of infections by the gastric trichostrongylid Obeliscoides in a rabbit model system

Abstract

The gastric trichostrongylid parasite Obeliscoides sp. was isolated from Alaskan snowshoe hares (Lepus americanus) and passaged 3 times in laboratory rabbits (Oryctolagus cuniculus). Despite its low fertility, the isolate persisted, often as occult infections, for up to 45 weeks and produced physiologic effects in clinically normal rabbits. Prominent eosinophilic and hyperplastic lesions of the gastric mucosa occurred during post-inoculation weeks (PIW) 2-15, while mononuclear aggregations were seen in older infections. Gastric lesion severity was directly related to size of the Obeliscoides population, which declined over time and was smaller in secondary infections. Anorexia occurred within 3 weeks of infective larval inoculation in 12 (of 21) primary and 2 (of 10) secondary infections. Serum total protein, albumin, and the A/G ratio were significantly reduced in anorectic infected rabbits compared to fasted uninfected rabbits. Fecal N excretion was significantly increased between PIW 1 and 5 in rabbits with primary infections, and during PIW 1 and 2 for those with secondary infections. Nitrogen absorption was enhanced during PIW 5-15 of primary infection. Serum gastrin concentrations, determined for the first time in Obeliscoides-infected rabbits by radioimmunoassay, were significantly elevated in primary infections during PIW 6 and 7, while hypokalemia was apparent during PIW 5. Hypermagnesemia occurred in both primary and secondary infections between PIW 8 and 15. Other serum constituents and concentrations of N, Ca and P in the gastrointestinal tract and feces remained largely unchanged. Total mean retention time (TMRT), 31.8 h, and GI turnover time (GITT), 26.3 h, of the fiber component (determined with Ce-141-marked fiber $>$355 microns) were significantly prolonged in secondary infections during PIW 16 to 26. TMRT (53.0 h) and GITT (57.0 h) of the liquid component (using Cr-51 EDTA), were determined for the first time in rabbits, and were not significantly changed by Obeliscoides infection. Persisting populations of this Obeliscoides isolate caused physiologic and pathologic alterations in clinically healthy rabbits. Because these effects were similar to those seen in ruminant Ostertagia spp. infections, this laboratory model could be useful in understanding the pathophysiology of costly production losses that occur in parasitized commercial livestock.