[Bacterial and viral epidemics of zoonotic origin; the role of hunting and cutting up wild animals]. / Epidémies bactériennes et virales d'origine zoonotique. Rôle de la chasse et du dépeçage d'animaux sauvages.

Since the Prehistoric times hunting has been a vital activity for man. However, this may account for the contamination of the hunter, his family and relatives. Infections may occur by direct contact with blood or tissues of infected animal during handling and cutting up preys and when preparing or eating meat, or also when bitten by injured animal. Apes and antelopes hunting in sub-Saharan Africa proves to be particularly important since it has been well established that the recent or previous emergence of some viral zoonosis (Ebola, Aids, T lymphotropic viruses and Monkeypox) resulted from hunting and poaching. Moreover predation among different species of non human primates such as that practised by chimpanzees against monkeys, has led to the construction of recombinant simian Lentiviruses, such as SIV cpz able to infect man and then spread over the entire mankind as it was the case with HIV-1. SARS is another possible example of the zoonotic risks represented by the sale, handling and cutting up Chinese wild animals such as Himalayan civets for culinary purposes.

[Human transmission and plasmodium resistance]. / Transmission humaine et résistance des plasmodies.

There is no longer malaria transmission in Europe and North America, while the transmission decreases in sub-tropical areas and increases in tropical countries. Most of malarias are now due to Plasmodium falciparum and happen in Africa. In the regions where the transmission is high, malaria is stable, baby mortality is high, and protective immunity is achieved in early childhood. Falciparum resistant malaria originates from mutations on drug target decreasing affinity to antifols, or mutations preventing accumulation of chloroquine in parasitized red blood cells. Resistance is a rapid event following large use of antifols, even associated, while falciparum chloroquine resistance is now widespread. Resistance to quinine, mefloquine and halofantrine is still at low levels out of Thailand, as their use remains through medical hands. Non resistance was observed yet with artemisinin derivatives.

[Reserve treatment for malaria: pros and cons]. / Le traitement de réserve du paludisme: le pour et le contre.

Any discussion of stand-by treatment will raise several questions: to whom should it be prescribed? which drugs are advised for stand-by treatment, according to the expected sensitivity of the parasites, the chemoprophylaxis and the possible side effects of the drugs chosen? what information should be given to a potential user? under what circumstances should stand-by treatment be used? how can the use of stand-by treatment and its efficacy be evaluated? are there any data for the stand-by treatment in literature? what are the pros and cons for the use of stand-by treatment? what is the place for stand-by treatment in today's array of antimalarial treatment? All of these questions were discussed at a round table stating that while stand-by treatment is an important element in malarial prevention for travellers, it must not become synonymous with self-treatment. An initial prescription of stand-by treatment is essential with the physician informing the user of the conditions for its use and its risks. The use of stand-by treatment does not exempt the traveller from rigourously carrying out the extensive recommended preventive measures. If, in spite of these precautions, a traveller does come down with a presumed malarial fever, the use of stand-by treatment should not prevent him from consulting a physician. A physician is in the best position to indicate an available stand-by treatment which should be considered as a back-up treatment. Self-treatment should only be considered as a last resort given its limitations. In all cases, it is indispensable to consult a physician.

Possible prognostic significance of a brief rise in parasitaemia following quinine treatment of severe Plasmodium falciparum malaria.

An increase in parasitaemia is not uncommon after initiation of treatment for Plasmodium falciparum malaria, but its exact significance is unknown. The time-course of parasitaemia was assessed retrospectively in 33 patients with severe imported malaria. In 19 patients (group 1) mean parasitaemia (+/- SEM) fell promptly after starting quinine treatment, from 24.9 +/- 4.1% on day 0 to 9.7 +/- 2.3% on day 1 and 1.8 +/- 0.7% on day 2. In 14 other patients (group 2), parasitaemia did not change significantly or increased, with mean parasitaemia (+/- SEM) of 9.5 +/- 2.1% on day 0, 17.2 +/- 2.6% on day 1, and 3.7 +/- 1.8% on day 2. Simplified acute physiology scores on admission (mean +/- SEM) were 17.4 +/- 1.4 in group 1 and 11.7 +/- 1.0 in group 2 (P = 0.006). The mean number of complications of malaria per patient (+/- SEM) was 2.9 +/- 0.5 in group 1 and 1.6 +/- 0.3 in group 2 (P = 0.046). Two group 1 patients died. Initially, more than 95% of peripheral blood parasites were tiny and small rings in both groups, and this distribution was unchanged on day 1, suggesting that the parasitaemia increase in group 2 was not due to release of sequestered mature parasites. In severe falciparum malaria, a rise in parasitaemia after treatment initiation may be of favourable prognostic significance and should not lead to aggressive therapeutic approaches such as exchange transfusion.

[Effects of chloroquine on the replication of a murine retrovirus]. / Effets de la chloroquine sur la réplication d'un rétrovirus murin.

The wide use of chloroquine (Cq) for prophylaxis and chemotherapy of malaria in Africa, and the increased spread of AIDS in areas of this continent where malaria is endemic, raised the question of a possible interaction between chloroquine intake and HIV infection. Indeed, hydroxychloroquine and chloroquine itself have been shown to inhibit HIV-1 replication in vitro, hydroxychloroquine being proposed as a potential useful adjunctive therapy in the treatment of HIV-1 infection. On the other hand, chloroquine has been reported to enhance the replication of Semliki forest and encephalomyocarditis viruses in a mouse model. In an attempt to elucidate Cq effect on retroviral replication, we have studied the effect of various concentrations of chloroquine in vitro (0.1 nmol/l to 25 mumol/l) on Friend retrovirus (FV)-infected fibroblasts of mice and in vivo (2 to 30 mg/kg) on FV-infected mice. No reduction in the number of virus foci was found in chloroquine-treated fibroblasts cultures. In chloroquine treated-infected mice, no differences were observed in the spleen weights, except an increase at 10 mg/kg. A decrease in splenocyte virus titer was only observed at 10 and 30 mg/kg. No differences in the median survival time was observed up to 30 mg/kg. The authors concluded that chloroquine seemed to have variable effects on viral replication in vivo depending on the dosage, but has no influence on the course of FV-induced disease.

[Treatment of bilharziasis]. / Le traitement des bilharzioses.

Specific treatment of bilharziosis is obviously simplified by praziquantel which, unfortunately, is not easily available in endemic areas. Nevertheless, the major problem is an early treatment before the occurrence of severe sequellae. Mass chemoprophylaxis remains needed and, if possible, with praziquantel. For economic purposes, we have often to use either oxamniquine or niridazole-metrifonate combination.

[Contribution of molecular genetics to the understanding of chemoresistance of Plasmodium falciparum]. / Apport de la génétique moléculaire à la compréhension des chimio-résistances de Plasmodium falciparum.

Resistance to pyrimethamine and proguanil is due to a single point mutation in the gene that codes for dihydrofolate reductase. A single mutation gives rise to resistance to only one of the drugs. Resistance to both drugs results from several mutations. Chloroquine resistance phenotype is due to a rapid efflux of the drug from the parasite's digestive vacuole. This efflux is associated with a transmembrane permeability glycoprotein, or P-gp, which is similar to the protein implicated in the multidrug resistant phenotype of some cancer cells. However, one or several other poorly understood major gene(s) may be involved. Drugs which can inhibit the supposed affinity of P-gp for chloroquine are under study.

[Geographic approach to the epidemiology of chloroquine-resistance of Plasmodium falciparum in tropical Africa]. / Abord géographique de l'épidémiologie de la chloroquino-résistance de Plasmodium falciparum en Afrique tropicale.

Plasmodium falciparum chloroquine-resistance occurred initially in 1978 in East Africa. Its step by step propagation towards West Africa is due to several factors which coincide with a high increase of population migration and urbanization since the seventies. Several maps show the dynamics of chloroquine-resistance in Africa during that era.

[Hemolytic anemia associated with minor salmonellosis in an HIV positive, G6PD deficient Congolese woman]. / Anémie hémolytique associée a une salmonellose mineure chez une congolaise VIH positive déficitaire en G6PD.

Haemolytic anaemia in G6PD-deficient patients with thyphoid fever is well known, but there is only one case-report associated with non-typhic salmonella fever. We report here a case observed in a black african young woman whose HIV infection has been discovered on this occasion. Because of the high prevalence of HIV infection, salmonellosis and G6PD deficiency in sub-saharian Africa, an increasing number of such haemolytic anaemias should be expected in this geographic area.