Effects on inhibition of development of the transfer of Ostertagia ostertagi between geographical regions of Australia

Abstract

SUMMARYPasture plots in a warm coastal region were separately contaminated in the autumn, winter and spring with eggs of a coastal strain of Ostertagia ostertagi derived from dairy calves. At the same times, a parallel set of plots was contaminated by a strain transferred from within a beef cattle management system in a cooler tablelands region. A reciprocal transfer of the coastal strain was also made to the tablelands, where pasture plots were contaminated with eggs of both strains of O. ostertagi in winter. Successive groups of parasite-free calves were grazed on the plots for 10–14 days at 4-week intervals and then killed for worm counts 14 days after their removal from pasture. In both environments, irrespective of the season of pasture contamination, inhibition of development reached a maximum in spring and the two strains differed only in the proportion of the population inhibited, which was significantly greater for the table- lands strain. There was no strain difference for either numbers of infective larvae on pasture or total O. ostertagi numbers. This suggested that the difference between coastal and tablelands populations in the extent of inhibition is genetically determined. If an environmental stimulus was implicated in the spring occurrence of inhibition, the stimulus was provided equally in coastal and tablelands environments and it cannot be exposure to low temperatures.

Strains of cattle parasites in the netherlands with different propensities for inhibited development

“…Recent studies by Smeal and Donald (1981) in Australia showed results which were sometimes at variance with earlier observations in Great Britain. They showed that after reciprocal transfer of parasite populations in calves from different geographical regions, no strain differences could be found with the exception of a significantly greater proportion of inhibited larvae in one of the populations of O. ostertagi.…”

The epidemiology of Ostertagia ostertagi and other gastrointestinal nematodes of cattle in Louisiana

“…Michel, Lancaster & Hong (1976a) reported that just as inhibited development may be induced by more than one cause, resumption of development might be induced in at least 3 circumstances: (a) a small, constant number resumes its development every day, (b) the rate is very greatly increased during March (northern temperate conditions) and (c) the increase may also occur earlier, apparently through a breakdown of host resistance. Other investigators (Bowen, 1979;Smeal, Hotson, Mylrea, Jackson, Campbell & Kirton, 1977;Smeal & Donald, 1981) have indicated the occurrence of variations of the 0. ostertagi population structure during the time of larval inhibition (mid-summer onward in Australia), but their conclusions were primarily concerned with adult worm burdens being supplied by summer transmission of new infection as well as by maturation of inhibited larvae. The present data indicate an early triggering of maturation of large numbers of spring-acquired EL 4 during May, followed by persistence of smaller numbers of EL 4 during summer, and lastly, a concommitant final decrease in numbers of EL 4 and substantial rise in numbers of adult worms during August-October 1981.…”

“…If cessation of weather conditions inimical to development and survival of free-living stages marks the period when inhibited larvae resume development (Armour & Ogbourne, 1983;Smeal & Donald, 1981), then the late spring deviation in temperature and rainfall pattern could have triggered the magnitude of maturation observed in May 1981. The residual of reduced numbers of EL 4 and large numbers of IXL 4 observed each month of summer may have been maintained by the extension of new infection through June and subsequent continuation of usual weather conditions.…”

Hypobiosis induction alters the protein profile of Ostertagia ostertagi (Nematoda: Trichostrongylidae)

“…There are two theories explaining the causes of hypobiosis: the first one proposes that the effect is produced by the host on the L 4 via the immune response; the second one suggests that the seasonal effect acts directly upon the free-living stages, resulting in the arrested development as early L 4 in the host (Armour 1978, 1980, Smeal and Donald 1981, Anderson 1986). …”