Submitted to: Veterinary Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/12/2017
Publication Date: 1/20/2017
Citation: Jenkins, M.C., Dubey, J.P., Miska, K.B., Fetterer, R.H. 2017. Differences in fecundity of Eimeria maxima strains exhibiting different levels of pathogenicity in its avian host. Veterinary Parasitology. 236:1-6.
Interpretive Summary: Major losses to the poultry industry are caused by Eimeria parasites that induce a disease known as coccdiosis, and which predispose chickens to damaging bacterial infections as well. The purpose of this study was to determine the underlying cause of differences in pathogenicity between two strains of Eimeria maxima, which vary in the severity of resulting lesions and reduced weight gain. To do so, ARS researchers in Beltsville, Maryland conducted dose response studies of each parasite strain. Peak oocyst production was nearly identical for both strains; however, total oocyst production was 1-2.6 fold higher for the more virulent strain. No obvious differences were noted in the histological sections recovered from the two strains. Therefore, variation in fecundity explains, in part, the observed differences in pathogenicity. Other factors may also contribute to differences in observed clinical effects. Efforts to manage fecundity, for example through improved vaccination, may offer effective means to manage the deleterious outcomes of disease. These data will be of interest to veterinarians, poultry producers, and epidemiologists interested in animal welfare and sustainable food production.
Technical Abstract: The purpose of this study was to determine the underlying cause of differences in pathogenicity of two Eimeria maxima strains (APU1 and APU2) observed during coccidiosis infection. At identical challenge doses, E. maxima APU1 always produces greater intestinal lesions and lower weight gain compared to E. maxima APU2. A dose response study of E. maxima APU1 and APU2 was conducted in the present study. It was found that median and mean intestinal lesion scores in E. maxima APU1-infected chickens were greater by a score of 1 – 1.5 compared to chickens infected with E. maxima APU2. Likewise, weight gain depression in E. maxima APU1-infected chickens was 20-25% greater (equivalent to 110 – 130 g body weight) than in E. maxima APU2-infected chickens. In order to understand the underlying cause of these observed clinical effects, 120 broiler chicks (5 oocyst levels, 6 replicates/level) were inoculated with various doses of E. maxima APU1 or APU2 oocysts. In order to examine the dynamics of oocyst shedding, fecal material was collected every 12 h from 114 – 210 h post-inoculation and every 24 thereafter from 210 – 306 h post-inoculation, and then processed for measuring E. maxima oocyst output. Oocysts were first observed at 138 h post-inoculation, and time of peak oocyst production was nearly identical for both E. maxima APU1 and APU2 at about 150-162. However, total oocyst production was measurably higher (1.1 – 2.6 fold) at all dose levels for E. maxima APU1 compared to E. maxima APU2, being significantly higher (P < 0.05) at the log 1.5 dose level. Other groups of chickens were infected with high doses of E. maxima APU1 or APU2 oocysts, and intestinal tissue was recovered at 72, 96, 120, and 144 h for histological examination. Although schizonts, gametes, and oocysts were observed at expected time-points, no obvious differences were noted between histological sections recovered from the two E. maxima strains. This study showed that the greater fecundity of E. maxima APU1 compared to E. maxima APU2 explains in part the observed differences in pathogenicity of the two E. maxima strains, but that other factors may contribute to differences in observed clinical effects.