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The International Agency for Research on Cancer (IARC) identifies ten infectious agents (viruses, bacteria, parasites) able to induce cancer disease in humans. Among parasites, a carcinogenic role is currently recognized to the digenetic trematodes Schistosoma haematobium, leading to bladder cancer, and to Clonorchis sinensis or Opisthorchis viverrini, which cause cholangiocarcinoma. Furthermore, several reports suspected the potential association of other parasitic infections (due to Protozoan or Metazoan parasites) with the development of neoplastic changes in the host tissues. The present work shortly reviewed available data on the involvement of parasites in neoplastic processes in humans or animals, and especially focused on the carcinogenic power of Cryptosporidium parvum infection. On the whole, infection seems to play a crucial role in the etiology of cancer.

Parasitic diseases constitute the most common infections among the poorest billion people, entailing high mortality rates and leading to long-term infirmities and poverty. Although the setting-up of public health programs implies many ethical consequences, the range of specific questions in parasitology that can be attributed to bioethics remains, to a large extent, unexplored. From the present analysis, it emerged three main issues which characterize ethical stakes in parasitology: accounting the complexity of the field of intervention, putting the principle of justice into practice and managing the changing context of research. From the research angle, medical parasitology-mycology, as other biological disciplines, is undergoing tensions derived from biological reductionism. Thanks to its links with the history and philosophy of the sciences, bioethics can help to clarify them and to explain the growing hold that technologies have over scientific thinking. On the whole, researchers as well as clinicians are called on to assume a specific responsibility, proportional to their competence and their place in the making of scientific, health, economic and social decisions.

Airborne transmission of Pneumocystis sp. from host to host has been demonstrated in rodent models and several observations suggest that interindividual transmission occurs in humans. Moreover, it is accepted that the Pneumocystis organisms infecting each mammalian species are host specific and that the hypothesis of an animal reservoir for Pneumocystis jirovecii (P. jirovecii), the human-specific Pneumocystis species, can be excluded. An exosaprophytic form of the fungus cannot be strictly ruled out. However, these data point toward the potential for the specific host to serve as its own reservoir and for Pneumocystis infection in humans as an anthroponosis with humans as a reservoir for P. jirovecii. This review highlights the main data on host-to-host transmission of Pneumocystis in rodent models and in humans by the airborne route and provides a rationale for considering the occurrence of nosocomial infections and measures for their prevention

It has been suggested that patients with pulmonary surfactant impairment are more susceptible to Pneumocystis infection than healthy controls. Owing the fact that most patients with pulmonary surfactant impairment also suffer from hypoxia, we explored the effect of intermittent hypobaric hypoxia conditions on the ability of non-immunocompromised rats infected by endotracheal route with P. carinii to clear the infection from their lungs. Control rats, inoculated or not with P. carinii, were maintained in normobaric normoxic conditions, and were submitted or not to dexamethasone administration. It was found that even if hypobaric hypoxia weakened host immune mechanisms and impaired significantly the surfactant composition, mainly of surfactant proteins A and D, these changes were not enough to favour the Pneumocystis growth or to inhibit the clearing of Pneumocystis organisms from the lungs of non-immunocompromised rats. The potential influence of surfactant protein changes on Pneumocystis infection is discussed.

A longitudinal study was undertaken to determine the prevalence of Cryptosporidium in a dairy farm in Sfax, Tunisia. 480 faecal samples were obtained from 30 calves under one month of age. All faecal samples were analysed for Cryptosporidium oocysts by microscopic examination of smears stained by modified Ziehl Neelsen technique. The parasite was detected in 26 calves (86.7 %). Infection was significantly associated with diarrhoea. A molecular characterization, performed in seven calves, confirmed that isolates were C. parvum. This work is the first report on Cryptosporidium in calves in Tunisia.

1,001 faecal samples were obtained from 89 sheep (lambs and adult), 184 goats, 190 horses, 178 rabbits, 110 camels, 200 broiler chicken and 50 turkeys housed in farms from different localities in Tunisia. All samples were analysed for Cryptosporidium oocysts by microscopic examination of smears stained by modified Ziehl Neelsen technique. The parasite was detected in ten lambs and adult sheep (11.2 %) and nine broiler chicken (4.5 %). Molecular characterization, performed in four animals, identified C. bovis in three lambs and C. meleagridis in one broiler chicken. This work is the first report on Cryptosporidium in farm animals in Tunisia.

Cette revue rappelle les connaissances actuelles relatives à la biologie de Cryptosporidium, notamment sa biodiversité et son mode de transmission. Elle fait état de la présence du parasite chez les différentes espèces d'hôtes mammifères qui l'hébergent et analyse les risques réels et potentiels de la transmission à l'homme. Le rôle probable d'une transmission mécanique par les insectes est évoqué sur la base d'expérimentations originales. Enfin, les coûts sanitaires et économiques de la cryptosporidiose, tant chez l'espèce humaine que chez le bétail, sont rappelés, ce qui souligne à nouveau l'importance de la détection du parasite dans l'environnement et la faune sauvage, son identification à l'aide d'outils moléculaires spécifiques et les moyens à mettre en oeuvre pour lutter efficacement contre la parasitose.

Previous studies have provided histological evidence of an association between primary Pneumocystis infection and sudden infant death syndrome (SIDS). The aim of this work was to determine the species of clustered Pneumocystis organisms found in formalin-fixed paraffin-embedded (FFPE) lung tissue sections from Chilean sudden infant death (SID) victims. This approach needed first to optimize a DNA extraction method from such histological sections. For that purpose, the QIAamp DNA Isolation from Paraffin-Embedded Tissue method (Qiagen) was first tested on FFPE lung tissue sections of immunosuppressed Wistar rats inoculated with rat-derived Pneumocystis. Successful DNA extraction was assessed by the amplification of a 346 bp fragment of the mitochondrial large subunit rRNA gene of the Pneumocystis species using a previously described PCR assay. PCR products were analysed by direct sequencing and sequences corresponding to Pneumocystis carinii were found in all the samples. This method was then applied to FFPE lung tissue sections from Chilean SID victims. Pneumocystis jirovecii was successfully identified in the three tested samples. In conclusion, an efficient protocol for isolating PCR-ready DNA from FFPE lung tissue sections was developed. It established that the Pneumocystis species found in the lungs of Chilean SID victims was P. jirovecii.

Pneumocystis carinii has a multigene family, PRT1, that encodes proteins with homology to KEX2-like proteases. PRT1 genes cluster with MSG genes near the telomeres and, like MSG, PRT1 proteins seem to be surface-expressed. The clustering of PRT1 and MSG genes suggested that expression of the two multigene families might be coordinated. Studying gene expression in P. carinii has been hampered by the lack of a culture system, and by lack of clonality in P. carinii populations in naturally infected rats, the host of this fungus. Heterogeneity can be reduced, however, by low-dose intratracheal inoculation, which can produce P. carinii populations dominated by organisms derived from a single progenitor. To study PRT1 expression, nude rats were inoculated with approximately 10 P. carinii each. The clonality of the P. carinii populations from inoculated rats was assessed by analysis of the UCS locus, a site in the genome that is known to be very heterogeneous in naturally infected rats, but nearly homogeneous in rats infected by low-dose intratracheal inoculation. Each of the populations had the same MSG gene at the UCS locus in at least 80 % of the organisms. To investigate PRT1 gene expression, RNA was amplified using primers that amplify numerous PRT1 genes. Seventy-four cloned cDNAs were sequenced, including at least 12 clones from each population of P. carinii. Many differently expressed PRT1 sequences were identified in each population, and a total of 45 different sequences were detected. However, the same PRT1 sequence was present in 15 of 74 plasmids and was found in 3 of the 5 P. carinii populations, suggesting that some PRT1 genes may be either more commonly expressed or expressed at a higher level. These data show that many members of the PRT1 gene family can be expressed in populations of P. carinii derived from few progenitors and suggest that the regulation of this family is different from that governing expression of the MSG gene family.

Research has been conducted on Cryptosporidium spp. The primers for detection Cryptosporidium known to amplify the diagnostic DNA fragment and the extent of sequence heterogeneity of this fragment among Cryptosporidium human isolates have been investigated and the results are presented.