Do Wolbachia infections play a role in unidirectional incompatibilities in a field cricket hybrid zone?

Two closely related field crickets, Gryllus firmus and G. pennsylvanicus, hybridize along an extensive north-south zone in the eastern United States. Crosses between G. firmus males and G. pennsylvanicus females produce viable and fertile F1, but the reciprocal cross consistently fails to produce offspring. Wolbachia, a bacterial parasite of arthropods that causes unidirectional incompatibilities in a variety of insect species, has been suggested as the cause of the observed incompatibility between G. pennsylvanicus and G. firmus. We examine the presence/absence of Wolbachia strains, defined by sequencing the ftsZ gene, in four cricket populations from the north-eastern United States. Most G. firmus individuals are infected (100% in Guilford, Connecticut; 65% in Seaside Park, New Jersey) and > 95% of those infected harbour a single strain of Wolbachia. All individuals in G. pennsylvanicus populations (Ithaca, New York; Sharon, Connecticut) are infected; the majority of individuals carry a second strain of Wolbachia, but a significant fraction carry the same strain found commonly in G. firmus. The presence of an apparently identical Wolbachia strain in crickets of both species means that some crosses between G. pennsylvanicus males and G. firmus females should be compatible. We have no evidence of such compatibility. Furthermore, if Wolbachia infections are responsible for the observed incompatibility between species, then incompatibilities must also exist within G. pennsylvanicus, because this species harbours both Wolbachia strains. Although some single pair crosses within G. pennsylvanicus do fail to produce offspring, the proportion is lower than expected if Wolbachia were responsible. Therefore, Wolbachia is unlikely to be involved in reproductive isolation between the two cricket species.

Detection of herpes simplex and varicella-zoster infection from cutaneous lesions in different clinical stages with the polymerase chain reaction.

BACKGROUND: The polymerase chain reaction (PCR) can be used to diagnose a variety of infectious processes. OBJECTIVE: We sought to determine whether Tzanck smear debris, vesicle fluid swabs, crusts, or fixed tissue specimens are the best source for template herpes simplex virus (HSV) or varicella-zoster virus (VZV) DNA for the PCR. METHODS: Patients with both clinical and histologic evidence of HSV (n = 6) or VZV (n = 16) infection were examined. Stained Tzanck smears, vesicle fluid swabs, dried crusts, and skin biopsy specimens were obtained at the same time from each patient. DNA was extracted from the different clinical specimens and then examined for HSV or VZV DNA with PCR. Fifteen control subjects did not have clinical or histologic evidence of herpesvirus infection. RESULTS: In cases of suspected VZV infection, PCR detected VZV DNA sequences from all 15 Tzanck smears, all 15 vesicle swabs, one of one crust, and 14 of 16 fixed tissue specimens. HSV DNA sequences were detected from all six Tzanck smears, all four vesicle fluid swabs, two of two crusts, and five of six fixed tissue specimens. CONCLUSION: PCR can detect VZV and HSV DNA sequences from a variety of sources including formalin-fixed tissue specimens. Although viral DNA was detected slightly more frequently from Tzanck smear debris, crusts, and vesicle fluid swabs compared with fixed tissue specimens, each was an excellent source of target DNA for the PCR to confirm the diagnosis of herpesvirus infection.

Effect of ultraviolet radiation and PUVA on mediator release from purified mast cells.

Exposure of highly purified rat serosal mast cells to UVA (34-340 kJ/m2), in the presence or absence of 8-methoxypsoralen (100 ng/ml), or to UVB (160-640 J/m2), resulted in dose-dependent releases of mast cell preformed mediators, as measured by the release of radioactivity from 3H-serotonin-labeled cells. The net release ranged from 2.3% to 14.2%. The above treatments had no effect on mediator release induced by subsequent incubation with calcium ionophore A23187 (0.4 and 4.0 mumol/l) or with compound 48/80 (1.0 microgram/ml), with the exception that exposure to UVB did suppress the release induced by the latter. These results indicate that under clinically relevant conditions, the direct effect of in vitro ultraviolet radiation on mast cells did not alter the ability of these cells to respond to subsequent stimulation with secretagogues.