Experimental animal models in vaccination against schistosomiasis.

Contrary to previous expectations, innate resistance to a primary schistosome infection is mediated predominantly in the lungs of many laboratory rodents. In addition, the phenomenon of non-permissiveness seen in a sub population of 129 strain mice, is associated with worm relocation from the liver to the lungs and is facilitated by dramatic alteration to the lung and liver vasculature; lung located adult worms exhibit gut damage and are ultimately destroyed within eosinophil-rich inflammatory focal reactions. It is now clear that the immunity induced by exposure to radiation-attenuated cercariae can be affected in the skin (mice), the lungs (mice and rats) or the liver (guinea pigs) of laboratory rodents. Moreover, the fact that skin phase resistances involves radio-sensitive cells, while lung and liver phase immunity centres on radio-resistant leucocytes, resolves current discord in the literature. Immobilisation and trapping of challenge larvae within focal inflammatory infiltrates is nevertheless common to both skin and lung phase attrition. Hyperimmunisation of rodents with irradiated cercariae is associated with a switch in immunoglobulin isotype and serum harvested from such donors is able to protect naive recipients passively; transferred serum recruits effector cells. Challenge parasites exhibit a broader window of sensitivity to vaccine immunity than was originally envisaged; stages ranging from the 3 to 4 day old skin/lung stage larva to the 3 week old juvenile liver worm constitute targets of protective resistance in vivo. This is at variance with the fact that newly transformed schistosomula constituting the primary targets of in vitro effector mechanisms, a feature perhaps related to our inability to mimic the process of intravascular parasite immobilisation and trapping in the test tube. Finally, schistosomicidal drugs such as Praziquantel can, by re-exposing disguised parasite antigens, facilitate the expression of vaccine immunity in sites additional to those at which resistance is normally mediated.

Comparative surface ultrastructure of adult Onchocerca volvulus recovered from human nodules by dissection or collagenase digestion.

The surface ultrastructure of male and female adult worms of Onchocerca volvulus obtained from human nodules by the technique of collagenase digestion has been compared with that of worms excised manually without the aid of enzyme treatment. No topographical differences have been identified.

Ultrastructural observations on the in vitro interaction between rat eosinophils and some parasitic helminths (Schistosoma mansoni, Trichinella spiralis and Nippostrongylus brasiliensis).

Rat eosinophils form an intimate association with the surfaces of parasitic helminths, in vitro, in the presence of immune serum. The parasite presents a non-phagocytosable surface to the cell. The initial response of the eosinophil is degranulation which leads to the formation of large cytoplasmic vacuoles. Peroxidase, an enzyme localized in the matrix of the crystalloid secretion granules, is discharged into these vacuoles as a consequence of degranulation. The vacuoles eventually become connected to the adherent basal plasma membrane of the eosinophil, and peroxidase is secreted directly onto the surface of the parasite. There is no morphological evidence to suggest that this particular secretion affects the integrity of the parasite surface.

Nippostrongylus brasiliensis: further properties of antibody-damaged worms and induction of comparable damage by maintaining worms in vitro.

When adult Nippostrongylus brasiliensis were maintained in vitro they became damaged. Using the criteria of ultrastructural morphology, acetylcholinesterase isoenzyme pattern and the behaviour of the worms after transfer to a normal rat, this damage appeared to be similar to that produced by the in vivo action of antibodies. Antibodies were shown to be responsible for the anterior migration of adult worms which occurs during primary infections in mature rats and in the prolonged infections seen in lactating and immature rats. Antibody damaged worms and worms unaffected by antibodies were equally able to stimulate the immune response required for worm expulsion. Apparently antibody damage is not required for the initiation of the second immune component necessary for expulsion of this parasite.