Submitted to: Veterinary Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/18/2017
Publication Date: 3/15/2017
Citation: Jenkins, M.C., Dubey, J.P., Fetterer, R.H., Miska, K.B. 2017. Differences in fecundity of Eimeria maxima strains exhibiting different levels of pathogenicity in its avian host. Veterinary Parasitology. 236:1-6.
Interpretive Summary: Avian coccidiosis is an intestinal disease caused by protozoa in the genus Eimeria. Each year, the disease incurs over $ 350 million loss in the U.S. alone, and over $ 1 billion worldwide due to poor weight gain in infected chickens and the cost of administering anticoccidial drugs and vaccines. The most costly parasite is Eimeria maxima because it not only depresses weight gain and feed utilization, but also predisposes chickens to other diseases such as necrotic enteritis, a bacterial disease causes high mortalities at 2-3 weeks of age. For reasons unknown, different strains of E. maxima have very different pathogenicities. The objective of this study was to determine the underlying cause for these differences. By comparing two strains of E. maxima, namely APU1 and APU2, it was found that weight gain was less and intestinal lesions were greater in the former. Dose response studies showed that infection with E. maxima APU1 produced considerably more parasites than with E. maxima APU2. However, histological examination of intestinal tissue from chickens infected with E. maxima APU1 or APU2 revealed no obvious morphological differences between the strains. This study suggests differences in pathogenicity of E. maxima strains may be due in part to parasite replication, but that other attributes, such as virulence factors may also be involved. This information will be valuable to poultry and pharmaceutical companies that are selecting strains of E. maxima to incorporate into live oocyst vaccines for controlling avian coccidiosis.
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.