Male reproductive success of Schistosoma mansoni-infected Biomphalaria glabrata snails.

Infection of Biomphalaria glabrata by Schistosoma mansoni results in a dramatic reduction in the snail's ability to produce eggs. We studied the ability of such parasitically castrated snails to fertilize the eggs of uninfected snails. Pigmented B. glabrata snails (13141 stock) were infected with S. mansoni miracidia and reared individually until they ceased laying eggs. These infected snails were then given the opportunity to mate with uninfected albino (NMRI) snails. Each of the infected snails was paired with a different albino partner each subsequent week. Sperm transfer by the infected snails was evident from the production of pigmented progeny by the uninfected albino snails. Infected snails successfully acted as males for up to 6 wk after parasitic castration had occurred. The duration of allosperm use by uninfected recipients was lengthy, regardless of the infection status of the pigmented sperm donor.

Use of RAPD-PCR to differentiate genetically defined lines of an intermediate host of Schistosoma mansoni, Biomphalaria glabrata.

The genetic differentiation among several laboratory-maintained pedigree snail lines of Biomphalaria glabrata (with different susceptibility phenotypes to Schistosoma mansoni infection) was assessed with the random amplified polymorphic DNA method. Out of the 20 primers tested, 2 (OPA-01 and OPA-06) gave reproducible markers with either individual or bulked DNA samples from resistant (BS-90, 10-R2, LAC-line) and susceptible (M-line) snails. Arbitrary primer, OPA-01, amplification of BS-90 DNA identified a 180-bp strain-specific fragment and a 400-bp marker in the susceptible M-line stock. In the 10-R2 and LAC snail lines, OPA-01 specific markers of 200 bp and 550 bp were identified. Amplification with primer OPA-06 identified several major strain-specific markers in the BS-90 (150 bp, 400 bp, 800 bp) and M-line (1,100 bp) snails. The heritability of the RAPD markers was evaluated in progeny snails derived from a cross between the BS-90 and M-line stocks. Results showed that markers were inherited in a dominant or codominant fashion. The 1,100-bp M-line marker was inherited in all susceptible progeny snails analyzed.

Direct stimulation of lymphokine production by cephalothin.

Cephalothin significantly suppressed in vitro DNA and total protein synthesis in human peripheral blood lymphocytes stimulated by antigens or mitogens. However, similar concentrations of this antibiotic enhanced streptokinase-streptodornase-stimulated production of the lymphokine leukocyte-migration-inhibition factor (LMIF) and directly stimulated production of this lymphokine by otherwise unstimulated lymphocytes from 10 of 12 normal human subjects. Penicillin did not appear to produce these effects. Cephalothin did not interfere directly with neutrophil migration or the interaction of preformed LMIF with neutrophils. Stimulation of LMIF production by cephalothin required viable lymphocytes and was inhibited by puromycin. These results suggest that cephalothin is capable of inducing lymphokine production by human lymphocytes in a manner that appears to be nonspecific in nature. This type of effect could be the basis of some apparently immunologic reactions to this antibiotic.

Failure of lymphokine-producing lymphocytes from aged humans to undergo activation by recall antigens.

In order to understand better the causes of diminished delayed hypersensitivity in the elderly, we studied lymphocyte function in 10 healthy subjects over 80 years of age. Markedly decreased antigen-stimulated lymphokine production (3 of 30 assays positive versus 24 of 31 in young control subjects) was the most significant finding in the elderly subjects and appeared to be the best explanation for their reduced cutaneous responses to recall antigens. Although mitogen-stimulated lymphocyte transformation in the elderly group was more sensitive to suppression by prostaglandin E2 than that of the young group, direct prostaglandin action did not appear to explain the diminished antigen-stimulated lymphokine responses. The nonspecific mitogen concanavalin A elicited normal lymphokine responses in 9 of 10 elderly subjects, indicating that lymphocytes from the elderly have a normal capacity for lymphokine production when activated by a sufficient stimulus. Therefore, diminished delayed hypersensitivity in aged humans may be related to deficient lymphokine production, which in turn appears to involve a decreased capacity of the lymphocytes producing these mediators to undergo activation by recall antigens.