
%0 Journal Article
%A Roberts, FHS 
%A Elek, P 
%A Keith, RK 
%T Studies on resistance in calves to experimental infections with the nodular worm, <I>Oesophagostomum radiatum</I> (Rudolphi, 1803) Railliet, 1898
%J Australian Journal of Agricultural Research
%D 1962/06/01
%V 13
%N 3
%P 551-573
%K 
%R https://doi.org/10.1071/AR9620551
%U https://www.publish.csiro.au/paper/AR9620551 
%X In calves reared free of Oesophagostomum radiatum and given a single infection of this helminth, the third ecdysis in the life cycle was completed in the gut wall in 5-7 days. The fourth stage larva moved into the gut lumen between the seventh md 14th days, where the fourth ecdysis occurred between 17 and 22 days. The prepatent period was 32-42 days. Egg production reached its peak usually during the sixth to 10th weeks, and in most calves this rate of production persisted for only 1-4 weeks. The subsequent decline in the egg count to low levels was very rapid, and was accompanied by the elimination of most of the adult worms. Reinfection with large doses of larvae, either during the period of peak egg production or some weeks later when the egg count was at low levels, did not produce any increase in the egg count, except on rare occasions. In these instances only a small increase was detected. Egg counts of calves given daily doses of larvae showed a trend similar to that resulting from a single dose, and attempts at reinfection with massive doses when the egg count had declined to low levels were also unsuccessful in producing any appreciable rise in the egg count. The failure of the egg count to respond to a challenge dose of larvae is regarded as evidence that a resistance to reinfection had been acquired. Resistance was apparent following a single dose as low as 1000 larvae and a daiIy dose as low as 50 larvae. Necropsies confirmed this conclusion and indicated that, whereas the host resistance mechanism could be responsible for the encapsulation of some reinfecting larvae in the gut tissues and their subsequent death, such mechanism was directed mainly against fourth stage larvae shortly after they had moved back to the gut lumen. The reaction here resulted in the elimination of all or most of the larvae and was accompanied by diarrhoea. While some reinfecting larvae survived in nodules for many weeks in the third or fourth stage, it would seem that the majority of those successfully penetrating the tissues completed the histotrophic phase within the normal period. The few reinfecting larvae which survived to maturity in the gut lumen completed their development also within the normal period. Infection was followed by the production of circulating antibodies detectable by both the haemagglutination and complement fixation tests. With calves infected with a single dose of larvae, all developed haemagglutinins, but complement-fixing (C. F.) antibodies were detected only in some, and these had become infected with Cooperia spp. prior to the experiment. Levels of both types of antibody were low, only exceeding in a few calves a titre of 1/80 for haemagglutinins and of 1/20 for C. F. antibodies. Following reinfection, C. F. antibodies were detected in all animals. They appeared simultaneously with haemagglutinins and there was little evidence that reinfection had stimulated any significant secondary rise in either type of antibody. The available data gave no definite indication of any effect of these antibodies in host-parasite reactions. They suggest, however, that haemagglutinins may be indicative merely of a state of infection, and that C.F. antibodies are stimulated more readily after reinfection. 
