Tick-induced blood loss leads to regenerative anaemia in the European hedgehog ( Erinaceus europaeus).

Although there is an increasing understanding of the role of parasites in their host dynamics, accurate, quantitative estimates of parasite caused morbidity in wild animals are rare. Here, we examine the possible impact of 2 tick species (Ixodes ricinus, I. hexagonus) on the condition of the European hedgehog (Erinaceus europaeus). For this, we tested for correlations between blood parameters of 36 adult hedgehogs from an experimental population enclosed in a natural habitat and their tick infestation over a period of 8 months (March-October 2007). We found correlations between the tick infestation and the concentration of red blood cells, haemoglobin, haematocrit, MCH, MCHC, thrombocytes, lymphocytes and neutrophils. These results indicate that ticks can induce anaemia in the hedgehog. The peripheral blood characteristics and the erythrocyte indices characterize this anaemia as haemorrhagic and regenerative. During the course of our study the hedgehogs of our population showed below normal mortality but morbidity was found to be high resulting from the blood loss caused by the feeding activity of the ticks.

Synergistic hepatocarcinogenic effect of hepadnaviral infection and dietary aflatoxin B1 in woodchucks.

Interactive hepadnaviral and chemical hepatocarcinogenesis was studied in woodchucks inoculated as newborns with woodchuck hepatitis virus (WHV), which is closely related to the human hepatitis B virus. When the woodchucks reached 12 months of age, aflatoxin B1 (AFB1) was administered in the diet at dose levels of 40 micrograms/kg body weight/day for 4 months and subsequently 20 micrograms/kg body weight/day (5 days/week) for lifetime. WHV DNA was demonstrated by Southern blot hybridization in the serum and by PCR in the serum and/or liver tissue. The histo- and cytomorphology of the liver were investigated by light and electron microscopy. WHV carriers with and without AFB1 treatment developed a high incidence of preneoplastic foci of altered hepatocytes, hepatocellular adenomas, and hepatocellular carcinomas that appeared 6-26 months after the beginning of the combination experiment. Administration of AFB1 to WHV carriers resulted in a significantly earlier appearance of hepatocellular neoplasms and a higher incidence of hepatocellular carcinomas compared to WHV carriers not treated with AFB1. Neither hepatocellular adenomas nor carcinomas (but preneoplastic foci of altered hepatocytes) were detected in woodchucks receiving AFB1 alone, and no preneoplastic or neoplastic lesions were found in untreated controls. These results provide conclusive evidence of a synergistic hepatocarcinogenic effect of hepadnaviral infection and dietary AFB1. Except for the frequent presence of ground glass cells containing surface antigen filaments in the infected woodchucks, the phenotype of preneoplastic foci of altered hepatocytes was similar in WHV carriers with and without exposure to AFB1 and in animals treated with AFB1 alone. Clear cell foci excessively storing glycogen and/or fat, amphophilic cell foci crowded with mitochondria and peroxisomes, and mixed cell foci composed of various cell types including basophilic cells rich in ribosomes predominated. The cellular phenotype in neoplastic lesions varied from clear, amphophilic, and mixed cell populations in highly differentiated adenomas and carcinomas to basophilic cell populations prevailing in poorly differentiated carcinomas. The striking similarities in altered cellular phenotypes of preneoplastic hepatic foci emerging after both hepadnaviral infection and exposure to AFB1 suggest closely related underlying molecular mechanisms that may be mainly responsible for the synergistic hepatocarcinogenic effect of these oncogenic agents.

Monitoring of renal allograft recipients by quantitation of human cytomegalovirus genomes in peripheral blood leukocytes.

The ratio of human cytomegalovirus (HCMV) genomes per cellular genomes in serial peripheral blood leukocyte (PBL) extracts of renal allograft recipients was quantitated by competitive nested polymerase chain reaction (PCR). Patients were also monitored for the development of acute HCMV infection by detection of HCMV pp65 antigenemia, HCMV IgM antibodies, and viruria. Compared to qualitative nested HCMV PCR, the frequency of positive PCR results in renal allograft recipients without further evidence of acute HCMV infection was significantly reduced by quantitative HCMV PCR. HCMV DNA levels > or = 1,000 copies HCMV/10(6) copies beta-globin were found to be highly indicative for the development of a clinically symptomatic HCMV infection following renal allograft transplantation. In patients treated with ganciclovir, quantitation of HCMV target sequences allowed the assessment of the efficacy of antiviral therapy.

The diagnostic significance of the polymerase chain reaction and isoelectric focusing in herpes simplex virus encephalitis.

In this study, serum and CSF samples of 55 neurological patients have been examined to confirm the diagnosis of herpes simplex virus encephalitis (HSVE). Different methods were applied, including serological titer evaluations, determination of intrathecally-produced HSV-specific antibodies by isoelectric focusing with affinity immunoblotting (IEF), as well as HSV-specific ELISA and HSV-specific polymerase chain reaction (PCR). The results of IEF and PCR have been compared and contrasted to develop general directions for virological diagnosis of HSVE. Of 14 patients suffering from clinically diagnosed HSVE, HSVE was confirmed in 12 cases by the demonstration of PCR or IEF positivity. A HSV-specific CNS infection could be excluded in 2 of these 14 patients. In 17 patients suffering from non-HSVE, PCR and IEF results were negative. Twenty-four patients, suffering from other neurological diseases, serving as a control group, were PCR- and HSV-IEF-negative. The study indicated that there are two possibilities for unequivocal demonstration of HSV-specific CNS involvement: first, performance of PCR especially in the acute phase of disease and in suspicious relapses, and second, performance of HSV-specific IEF for determination of intrathecally synthesized HSV-specific antibodies. It is suggested that these two methods should be introduced in routine diagnosis of viral encephalitis.