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Title: Studies on the host-parasite relationship of Strongyloides ratti in rats
Author: Moqbel, R.
ISNI:       0000 0001 3418 8943
Awarding Body: London School of Hygiene & Tropical Medicine
Current Institution: London School of Hygiene and Tropical Medicine (University of London)
Date of Award: 1976
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Studies were conducted on the host-parasite relationship in Strongyloides ratti infections in rats. During initial infection, rats acquired a strong immunity against this parasite and 1. production and the expulsion of adult Infected rats were strongly resistant to reinfection and this immune response lasted for a period of three months, independent of the residual worm population. The immune response during initial infection caused a reduction in the size of adult worms after day 18 PI. Adult worms, which occupied the anterior half of the small intestine in the first 18 days, shifted to the posterior half before they were expelled. The Immune response affected the adult worm in the intestine during a primary infection, the migratory larvae in the lung during a secondary infection and the skin stage following multiple infections. In heavily infected rats, larvae disseminated and were detected in the brain tissue. A full infection with S. ratti induced complete resistance to reinfection, but adult worms were a major souroe of protective antigens, while migratory larvae did not stimulate an immune response against reinfection. "Normal" worms obtained on days 8-16 PI were able to continue their larval production when transferred to new, clean, rats; "damaged" worms obtained on days 18-25 PI were unable to do so. Worm damage during initial infection was irreversible. Short non-fertile worms found in rats early after challenge were able to resume their egg production and survive in new hosts. The possibility of adaptation was discussed. 22 day-old worms were examined under the electron microscope and were compared with 10 day-old worms. Damaged worms were smaller in size and showed vacuolation and tissue disorganisation, particularly the gut cells. Peculiar whorls were observed inside the gut lumen of damaged worms, and were suggested to be immune complexes. Precipitates were persistently observed surrounding the mouths of damaged worms. It was proposed that worm damage is instigated by immune complexes plugging the mouth and causing a state of starvation through inhibition of food intake. Worm expulsion was demonstrated to be an imrtunological event. Antibody mediated worm damaqe, in S. ratti, as an essential step in worm expulsion, was argued immume MINC alone, given on days 6 or 12 PI, were capable of inducing worm expulsion. Serum alone repeatedly induced auto-infection. A variety of factors were suggested to explain the action o f transferred antibodies. Co-operation between immune MLNC and serum in inducing worm expulsion was only evident when MLNC were given on day 12 PI. The tissue eosinophils Increased in the mucosa of Infected intestines immediately before worm expulsion, during initial and challenge infections. The percentage of degranulating mesenteric mast cells increased during the period of expulsion, and the introduction of histamine into the gut of infected rats caused a significant acceleration of worm damage and expulsion. Aspirin, a potent inhibitor of prostaglandins, delayed the action of expulsion for 5 days suggesting a possible role of prostaglandins in this process. Corticosteroid treatment caused the long persistanoe of S. ratti worms in the rats and indicated that worm damage was due to an immune response, and not to the worm's senescence. Levels of tissue eosinophils and degranulated mesenteric mast cells were also suppressed. No auto-infection was demonstrable when cortico steroid treatment commenced with the infection , but it was evident when the treatment started immediately prior to worm expulsion. Corticosteroids suppressed all manifestations of acquired immunity to reinfection. An attempt was made to render rats unresponsive to S. ratti infection by treating with corticosteroids at strategic periods during an initial infection.
Supervisor: Nelson, G. S. Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral