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Title: Invasion of host tissue by infective larvae of Ascaris suum (Goeze, 1782)
Author: Arene, Felix Ofodile Ifeanyichukwu
ISNI:       0000 0004 2698 8643
Awarding Body: University of Wales, Bangor
Current Institution: Bangor University
Date of Award: 1980
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The strategy by which infective A. suum larvae gain entry into their hosts' intestinal tissue has been investigated. The infective larvae develop in the egg between the temperatures 16 °+ 1°C and 34° + 1°C. Within this temperature range, increase in temperature increased the rate of development. The maximum rate of development of the eggs was attained at 31° + 1°C. Eggs embryonated at 280 + 1°C and above gave rise to infective larvae which had a lesser ability to hatch in vitro, shorter longevity when aged in phosphate buffered saline (pH 7.2) at 37°C, and a limited ability to penetrate tissue membranes in vitro, compared with those embryonated at lower temperatures. Maximum larval viability was achieved when eggs were embryonated at 220 +1 °C. These results suggest that the optional temperature for rate of development and larval viability or survivability are not the same. In mice, given large oral infections, eggs hatched mainly in the small intestine. In vitro studies showed that the infective larvae (13 /um in diameter) actively emerged through a hole in the egg shell wall 9.7/um in diameter. This hatching mechanism is considered to contract with the situation in some hookworm eggs where the infective larva is liberated from the egg following splitting of the egg shell under high internal pressure. The egg shell retained its shape during and after hatching. There was no major configurational change in the structure of the egg shell. The inner lipid layer of the shell was broken down during hatching. The location of the hole on the egg shell through which the infective larva emerged varied and was not restricated to any one position. How the hole is made was not obvious. The presence of an opercular structure in the egg shell has been suggested but clear evidence for this was not found. Ultrastructural study indicated that the infective larva possessed no specialised cuticular structures that might either assist its emergence from the egg shell or entry into the host tissue. Soon after hatching, the infective larvae invaded the host intestinal tissue mainly in the regions of the posterior third of the small intestine, the caecum and the colon. Penetration of the larvae into the host tissue was principally via the crypts of liberakun. Direct penetration via the villi appeared to be non-existent. Entry into and subsequent passage of the infective larvae through the tissues was related to the production of larval secretions which caused changes in the acellular materials of the host tissue. These made it easier for the larvae to separate the cells and fibres as they migrated. Passage of the infective larvae did not involve any extensive digestion of the host tissue. Enzymatic studies of the larvae revealed a correlation between the larval secretions and the ability to cause these changes. Incubation with azocoll revealed that the larvae produced secretions which are capable of releasing dye from azocoll. These secretions were neither gelatinolytic nor histolytic. The time course of penetration and subsequent migration to the liver and lungs of mice was followed and a possible mechanism for migration postulated. The results are discussed in relation to the epidermiology of ascariasis and the known biology of the parasite.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available