Genetic resistance to experimental Cooperia oncophora infections in calves

The variation in resistance of cattle to gastro-intestinal nematode infection was investigated in three experiments. Bull calves, aged three months and reared under uniform conditions, were artificially infected with infective larvae of Cooperia oncophora, a moderately pathogenic but very abundant parasite of the small intestine. The study aimed to detect a possible genetic effect on resistance and to evaluate the consequences of this resistance for the performance of the animals.Resistance to infection was measured by a number of parasitological and immunological techniques. The course of infection was determined by monitoring faecal egg output and by post mortem examination of the worm burden and characteristics of individual worms. Three immunological tests were used to measure immunological reactions of the calves: an immunofluorescent antibody test (IFAT) on fourth stage larvae and an indirect haemagglutination test (MA) using adult worm extract as the antigen to monitor humoral antibodies in the serum; an intradermal test (IDT) to detect homocytotropic antibodies. Performance of the experimental calves was assessed by recording clinical signs of infection, live weight gain and, for some animals during a limited period, feed intake.In the first experiment 46 calves, comprising 16 half-sib groups (sons of A.I. sires) were infected with a single dose of 100,000 infective larvae. Faecal egg output after this infection, although very variable, showed a basic pattern of logarithmic increase and subsequent logarithmic decrease in most calves. The decrease was due to an initial reduction of individual egg production of female worms and a subsequent expulsion of worms. This expulsion was selective in two ways: female worms were more persistent than males and, among male worms, the polymorph Cooperia surnabada was more persistent than Cooperia oncophora.Resistant calves showed a low faecal egg output that was the result of a small burden of short worms. Egg output and worm length were related significantly to the humoral antibody response of calves as measured by the IFAT technique. There were no relations between the immunological response measured by the IHA test or IDT technique and any of the parasitological parameters. The relation between IFAT antibody level and faecal egg output was curvilinear, suggesting a threshold level of antigenic stimulation which provokes antiparasitic activity of the host.A primary single infection with 100,000 infective larvae caused a mild but significant growth depression which, in the second experiment, appeared to coincide with a notable loss of appetite. However, in experiment I, growth impairment was significantly larger in those calves which showed a higher level of resistance to infection.Analysis of variances between and within sire groups in experiment I showed that the IFAT antibody response was partly genetically determined.From the 16 sires which had provided offspring for expt. I five, which had shown extreme resistance (2) or susceptibility (3) as judged by IFAT antibody titres and faecal egg counts, were chosen for expt. II. Similarly, for expt. III an ultimate selection was made of two extreme sire groups, one being the most resistant and one the most susceptible.Except for a control group, all 93 calves in expts. II and III received a primary dose of either 20,000 or 100,000 infective larvae and, seven weeks later, a secondary infection of either 350,000 larvae as a single dose or multiple doses of 75,000 larvae given at a rate of three doses per week.In expts. II en III the primary infection appeared to have an immunizing effect which was largest for the high primary dose. Thus egg output after secondary infection was severely depressed, mainly due to the low number of gravid female worms present. Generally, adult worms were shorter and were expelled earlier and more rapidly due to this immunizing effect.In contrast to the adult worm burden, the number of fourth stage larvae was greatly enlarged if repeated doses of larvae instead of one single dose were given as secondary infection, irrespective of the primary dose level. The decrease of the number of fourth stage larvae in the course of secondary infection was probably not mainly due to direct expulsion but to a turnover process which consists of development of worms from the early fourth into the adult stage following expulsion of adult worms.As regards the immunological techniques, the IHA and IDT methods proved to be of no value as indicators of resistance of the calves to infection. IFAT antibody titres, on the contrary, were boosted by secondary infection and appeared to be negatively correlated to faecal egg output and worm length.Live weight gains after secondary infection were significantly depressed by about 20 %; feed intake was lower than expected in the absence of infection. Diarrhoea, associated with massive expulsion of worms, occurred simultaneously with a depression of feed intake and live weight gain.In contrast to the findings in a primary infection with 100,000 larvae, resistance to secondary infection (as measured by peak egg output, worm length and IFAT titres) was associated with higher weight gains. As an explanation for this contrast it is suggested that expulsion of adult worms was one of the causes of depressed performance. In primary infection a high level of (acquired) resistance caused a large expulsion, in secondary infection the opposite was true because then a high level of resistance already prevented the establishment of a large worm burden and thereby the necessity to expel it.Thus, in the long run, resistance of calves to Cooperia oncophora infection seems to be a favourable characteristic, whereas in a primary infection it impairs host performance.Genetic differences after secondary infections were found for egg output, worm numbers and worm length, but only if the primary infection had been the small dose of 20,000 larvae rather than the larger dose of 100,000. With regard to IFAT antibody titres a similar difference appeared between the two extreme sire groups ultimately selected. In secondary infections after the small primary dose only the sons of the resistant sire reached a plateau level of maximum antibody titre, whereas after the large primary dose calves of both extreme groups reached this level.Thus, genetic differences in resistance were found only in special cases i.e. for a certain parameter only if a certain level of antigenic stimulation had been present. This result was very similar to the finding that the appearance of differences in resistance due to different levels of infection experience depended on the level of resistance induced and on the sensitivity of the parameter that was used.Nevertheless, this study has clearly shown that genetic differences in resistance of calves to Cooperia oncophora infections do exist. The experimental procedures did not allow an estimation of the heritability, although the results suggest only a minor role of genetic factors. Furthermore, it should be kept in mind, that the expression of genetic differences depends largely on the infection regimen and that resistance to infection is not invariably reflected in a better performance