{'fraction_non_alphanumeric': 0.013040901007705987, 'fraction_numerical': 0.007113218731475993, 'mean_word_length': 5.59375, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Genetic resistance to helminths. The influence of breed and haemoglobin type on the response of sheep to primary infections with Haemonchus contortus

Summary The possible existence of strain and breed differences in the response of sheep to primary infections with Haemonchus contortus was examined by comparing the establishment and pathogenic effects of the parasite in Scottish Blackface and Finn Dorset sheep grouped according to haemoglobin type and infected with 7–10000 3rd-stage larvae. Homozygous haemoglobin A-type sheep of both breeds had lower worm burdens and faecal egg outputs, and suffered less severe clinical and pathophysiological disturbances than animals homozygous for haemoglobin B. In addition, Scottish Blackface sheep displayed similar advantages over Finn Dorsets with the same haemoglobin type and variations in the severity of the disease as judged by a variety of pathophysiological indices correlated closely with parasite numbers. It was therefore concluded that genetic resistance operated primarily against worm establishment and that, barring the unlikely involvement of non-specific physiological factors, this was controlled by the immune response elicited. The nature of this response is unknown, but appeared to operate only against the larval stages, since the size and metabolic activities of the surviving worms were similar in all animals. In a subsequent experiment, designed to examine the response of Scottish Blackface sheep to heavy infection (45000 larvae), there was no correlation between worm establishment and haemoglobin type. This was possibly due to a delayed immune response arising from exposure to excessive amounts of antigen.