Recurrent hepatitis occurs in the majority of patients undergoing liver transplantation for hepatitis C virus (HCV) cirrhosis, with progression to cirrhosis in up to 30% after 5 years. Based on these data, a decrease in survival can be anticipated with prolonged follow-up. Furthermore, posttransplantation HCV-fibrosis progression has been shown in recent years to increase. Our aims were (1) to describe the natural history of HCV-infected recipients, particularly to determine whether survival has decreased in recent years; (2) to compare this outcome with that observed in non-HCV-infected cirrhosis controls; and (3) to determine the factors associated with disease severity and survival. Among 522 cirrhotic patients undergoing transplantation between 1991 and 2000, 283 (54%) were infected with HCV. Yearly biopsies were performed in these recipients and at 1 and 5 years in the remainder. With similar follow-up, the percentage of deaths in the HCV(؉) group was significantly higher than in the HCV(؊) group (37% vs. 22%, P < .001), and patient survival was lower (77%, 61%, 55% vs. 87%, 76%, 70% at 1, 5, and 7 years, respectively; P ‫؍‬ .0001). Although survival has increased in the HCV(؊) group in recent years, it has significantly decreased in HCV recipients (P < .0001). The main cause of death among the latter was decompensated graft cirrhosis (n ‫؍‬ 23/105, 22%), whereas that of HCV(؊) patients was infections (n ‫؍‬ 10/52, 19%). Reasons for the recent worse outcome in HCV(؉) recipients include the increased donor age and stronger immunosuppression. In conclusion, patient survival is lower among HCV(؉) recipients than among HCV(؊) ones and has been decreasing in recent years. The aging of donors is a major contributor to this worse outcome. (HEPATOLOGY 2002;36:202-210.) H epatitis C virus (HCV)-cirrhosis is the most frequent diagnosis in patients undergoing liver transplantation. 1 Viral recurrence is universal, 2 with development of histologic hepatitis in the majority of patients 3,4 and progression to cirrhosis in up to 30% after 5 years. 5,6 To date, however, most series have revealed no differences in patient or graft survival compared with uninfected controls. [3][4][5]7 Various reasons may explain these supposed discrepancies, one of which is the existence of different end points when assessing the effect of HCV infection on the graft. An indirect way to assess this effect is by calculating the rate of histologic progression posttransplantation, a task easily performed in the posttransplant setting because of the multiple biopsies generally performed and, through assessment of this rate, estimating the median time to development of graft cirrhosis. In one study, this duration was estimated to be 12 years, a duration significantly shorter than that described for the immunocompetent population. 6 From these data, one can anticipate an increase in HCV-related graft loss in the near future as transplant programs reach their second decade of activity. Our center follows a strict policy of performing annual li...

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While hemoplasma infections in domestic cats are well studied, almost no information is available on their occurrence in wild felids. The aims of the present study were to investigate wild felid species as possible reservoirs of feline hemoplasmas and the molecular characterization of the hemoplasma isolates. Blood samples from the following 257 wild felids were analyzed: 35 Iberian lynxes from Spain, 36 Eurasian lynxes from Switzerland, 31 European wildcats from France, 45 lions from Tanzania, and 110 Brazilian wild felids, including 12 wild felid species kept in zoos and one free-ranging ocelot. Using real-time PCR, feline hemoplasmas were detected in samples of the following species: Iberian lynx, Eurasian lynx, European wildcat, lion, puma, oncilla, Geoffroy's cat, margay, and ocelot. "Candidatus Mycoplasma haemominutum" was the most common feline hemoplasma in Iberian lynxes, Eurasian lynxes, Serengeti lions, and Brazilian wild felids, whereas "Candidatus Mycoplasma turicensis" was the most prevalent in European wildcats; hemoplasma coinfections were frequently observed. Hemoplasma infection was associated with species and free-ranging status of the felids in all animals and with feline leukemia virus provirus-positive status in European wildcats. Phylogenetic analyses of the 16S rRNA and the partial RNase P gene revealed that most hemoplasma isolates exhibit high sequence identities to domestic cat-derived isolates, although some isolates form different subclusters within the phylogenetic tree. In conclusion, 9 out of 15 wild felid species from three different continents were found to be infected with feline hemoplasmas. The effect of feline hemoplasma infections on wild felid populations needs to be further investigated.

BackgroundThe Iberian lynx (Lynx pardinus) is considered the most endangered felid species in the world. In order to save this species, the Spanish authorities implemented a captive breeding program recruiting lynxes from the wild. In this context, a retrospective survey on prevalence of selected feline pathogens in free-ranging lynxes was initiated.Methodology/ Principal FindingsWe systematically analyzed the prevalence and importance of seven viral, one protozoan (Cytauxzoon felis), and several bacterial (e.g., hemotropic mycoplasma) infections in 77 of approximately 200 remaining free-ranging Iberian lynxes of the Doñana and Sierra Morena areas, in Southern Spain, between 2003 and 2007. With the exception of feline immunodeficiency virus (FIV), evidence of infection by all tested feline pathogens was found in Iberian lynxes. Fourteen lynxes were feline leukemia virus (FeLV) provirus-positive; eleven of these were antigenemic (FeLV p27 positive). All 14 animals tested negative for other viral infections. During a six-month period in 2007, six of the provirus-positive antigenemic lynxes died. Infection with FeLV but not with other infectious agents was associated with mortality (p<0.001). Sequencing of the FeLV surface glycoprotein gene revealed a common origin for ten of the eleven samples. The ten sequences were closely related to FeLV-A/61E, originally isolated from cats in the USA. Endogenous FeLV sequences were not detected.Conclusions/SignificanceIt was concluded that the FeLV infection most likely originated from domestic cats invading the lynx's habitats. Data available regarding the time frame, co-infections, and outcome of FeLV-infections suggest that, in contrast to the domestic cat, the FeLV strain affecting the lynxes in 2007 is highly virulent to this species. Our data argue strongly for vaccination of lynxes and domestic cats in and around lynx's habitats in order to prevent further spread of the virus as well as reduction the domestic cat population if the lynx population is to be maintained.