The elicci of mouse strain, age, sex, and the size of infective dose on the susceptibility to infection with the coccidium Cryptosporidium, parvum Tyzzer, 1912 was determined using several murine models. Mice were infected with C. parvum oocysts originally of cervine origin, maintained by repeat passage in calves. All mice in the experimental groups proved susceptible to infection, though this resulted asymptomatic in all cases. C. parvum infection in BALB/c and Porton mice exhibited some variation. BALB/c mice demonstrated a longer prepatent period than Porton mice. They also produced a greater oocyst output over the patent period, though the differences were not statistically significant. Differences were observed between mice infected at either 3 or 4 weeks of age. Prepatent period was shorter in those mice infected at 3 weeks of age, reaching 100% infection rate by day 7 post-inoculation. The patent period was longer in younger mice showing that age at time of infection can modify the oocyst shedding profile. However, no sex related differences in the course of infection were observed. The effect of different infective doses of oocysts was analysed. The three doses used (l-O4, IO5, 106) proved infective for all mice, there were no statistical differences in either prépaient or patent periods, or in the oocyst shedding profiles. Experimental cryptosporidiosis was also induced in cyclophosphamide-immunosuppressed mice. Cyclophosphamide was orally administered by stomach lube at a dose of 50 mg/kg/day starting 10 days before the intragastric inoculation of 10fi oocysts of C. parvum per mouse and continuing until the end of the experiment, Immunosupprcsscd mice had a shorter prepatent period, remained infected longer and shed more oocysts than immunocompetent mice. Immunosuppression produced high mortality rates; during the course of the experiment 44% of immunosuppressed-infcctcd and 30% of immunosuppressed-uninfccted mice died. There were no deaths in the untreated groups. Differences in the clinical course of the infection were also observed between immunosuppressed and immunocompetent mice; however, some mice recovered without immunosuppression withdrawal.
The effect of repeated infestations of BALB/c mice with Ixodes ricinus (L.) nymphs on tick borne encephalitis (TBE) virus infection was studied. Enhancement of nymphal feeding, occurring in noninfected mice during the quaternary infestations, was less apparent or absent in female nymphs engorged on TBE virus infected mice. The mice infected with TBE virus during quaternary tick infestation survived significantly longer (P < 0.01) than mice infected with TBE virus during the primary tick infestation. The mean titre of virus in murine blood (determined by plaque assay) was significantly lower (P < 0.01) and the number of nymphs acquiring virus was reduced (P < 0.05) when feeding on hosts infected during the quaternary infestation. The results indicate that repeated infestations of I. ricinus nymphs on BALB/c mice, although enhancing tick feeding, reduced infection with TBE virus when inoculated intraperitoneally.
Solid organ transplantation is an established treatment modality in patients with end-stage organ damage in cases where other therapeutic options fail. The long-term outcomes of solid organ transplant recipients have improved considerably since the introduction of the first calcineurin inhibitor (CNI) - cyclosporine. In 1984, the potent immunosuppressive properties of another CNI, tacrolimus, were discovered. The immunosuppressive effects of CNIs result from the inhibition of interleukin-2 synthesis and reduced proliferation of T cells due to calcineurin blockade. The considerable side effects that are associated with CNIs therapy include arterial hypertension and nephrotoxicity. The focus of this article was to review the available literature on the pathophysiological mechanisms of CNIs that induce chronic nephrotoxicity and arterial hypertension. CNIs lead to activation of the major vasoconstriction systems, such as the reninangiotensin and endothelin systems, and increase sympathetic nerve activity. On the other hand, CNIs are known to inhibit NO synthesis and NO-mediated vasodilation and to increase free radical formation. Altogether, these processes cause endothelial dysfunction and contribute to the impairment of organ function. A better insight into the mechanisms underlying CNI nephrotoxicity could assist in developing more targeted therapies of arterial hypertension or preventing CNI nephrotoxicity in organ transplant recipients, including heart transplantation., L. Hošková, I. Málek, L. Kopkan, J. Kautzner., and Obsahuje bibliografii