A DNA sequence specific for forest form Onchocerca volvulus.

Onchocerciasis, or river blindness, is caused by infection with Onchocerca volvulus, a filarial parasite which infects about 40 million people in Africa and Latin America. Epidemiological, clinical, entomological and serological studies of African onchocerciasis led to the hypothesis that Onchocerca volvulus exists in different forms in the forest and savannah. It is uncertain if these differences are due to genetic differences within O. volvulus itself, or to epigenetic factors, such as differences in the host populations. To date no basic biochemical differences between the forest and savannah populations of O. volvulus has been found, although isoenzyme studies have shown that differences in allele frequency between forest and savannah populations exist. Here we describe the isolation of a DNA sequence that seems to be specific for the forest form of O. volvulus, the first indication of a basic genetic difference between the savannah and forest forms.

Malaria falciparum resistente a cloroquina e ao fansidar tratada com minociclina. / Chloroquine and fansidar resistant falciparum malaria treated with minocycline

Em abril de 1978 uma infeccao malarica causada por Plasmodium falciparum foi diagnosticada em um paciente adulto do sexo masculino, nativo da Amazonia brasileira. O parasito foi resistente in vitro a cloroquina e in vivo a associacao pirimetamina + sulfadoxina (Fansidar R). O paciente foi tratado com minociclina (Minomax R); contudo, sua resposta imune ao parasito pode ter tido um importante papel na eficacia do tratamento com a minociclina

Fansidar prophylaxis, therapy, and immune responses in rodent malaria (Plasmodium berghei).

In order to determine the effect of Fansidar on plasmodial infection in mice, outbred, adult, Swiss-Webster mice were treated with Fansidar (20 mg sulfadoxine and 1 mg pyrimethamine/kg body weight) at various intervals before and/or after inoculation with blood stages of Plasmodium berghei. Drug therapy resulted in cure if it was given before the parasitemia rose to 53%. Oral administration of Fansidar was more effective in reducing or preventing parasitemia than intramuscular injection. Fatal infections were prevented if mice were treated orally with one dose of Fansidar 2 days before inoculation with P. berghei, whereas only partial protection occurred in animals treated 4 or more days before inoculation. Fansidar administered on two consecutive days provided protection if the drug was given at 3 and 2 days before inoculation. Administration of Fansidar for three consecutive days protected all animals if given on days 8 to 6 before inoculation. After oral administration of Fansidar, the parasitemia dropped dramatically and was undetectable at 60 hr. At 12 hr after oral treatment, schizonts and trophozoites were numerous, but there were few merozoites. Schizonts were the predominant stage at 24 hr, whereas merozoites predominated at 36 hr. Swiss-Webster and C57BL/6 mice became immune to a lethal dose of P. berghei after 4 cycles of inoculation and drug cure. Protective immunity was still present at 472 days after the fifth parasite inoculation.

Adoptive transfer of resistance to Plasmodium berghei with spleen cells and serum from Fansidar-cured mice.

The ability of splenic leukocytes or serum to transfer immunity to Plasmodium berghei was studied in C57BL/6 mice. Splenic leukocytes or serum was removed from mice which had been inoculated previously 1 to 4 or 5 times with P. berghei and cured 1 to 4 or 5 times with Fansidar (pyrimethamine plus sulfadoxine) and transferred to syngeneic recipients 1 or 2 days before parasite challenge. Partial protection was observed in recipients of immune serum or unfractionated splenic leukocytes. Significantly more protection was observed in recipients of preparations from immune mice enriched for immunoglobulin-positive (B-lymphocyte) cells or B-lymphocyte plus immunoglobulin-negative (T-lymphocyte) cells than in recipients of preparations enriched for T-lymphocytes. Recipients of B- or B+T-lymphocyte-enriched spleen cells from immune mice had significantly longer survival times than did recipients of T-lymphocyte-enriched spleen cells and recipients of spleen cells from normal mice. Transferred immunity lasted less than 2 months and did not protect recipients against death induced by the malarial parasite. The ability of splenic leukocytes to transfer resistance to recipients was independent of the number of times donors were inoculated with P. berghei and cured with Fansidar.

Resistencia do Plasmodium falciparum ao fansidar, quinina e tetraciclina. / Resistance of Plasmodium falciparum to fansidar, quinine and tetracycline

Descreve-se pela primeira vez uma cepa amazonica de Plasmodium falciparum resistente ao Fansidar (pirimetamina mais sulfadoxina) e quinino mais tetraciclina simultaneamente. O paciente, com 13 anos de idade, residia ha cinco anos em Ariquemes, Estado de Rondonia, na Amazonia brasileira. A infeccao foi curada com dose elevada de cloroquina administrada em dose unica intravenosa (IV). E evidenciado o alto valor da cloroquina na cura da malaria falciparum resistente, quando administrada em doses maiores que as usadas nos esquemas convencionais de tratamento

Prevalencia de anticorpos contra os agentes causadores da hepatite, malaria, sifilis e toxoplamose em cinco populacoes humanas distintas da Amazonia Brasileira. / Prevalence of antibodies against agents causing hepatitis,malaria syphilis and toxoplasmosis in 5 different human populations of the Brazilian Amazonia

Um total de 866 amostras de soros de cinco populacoes humanas distintas da Amazonica brasileira foram examinadas para a deteccao de anticorpos contra o virus da hepatite B, Plasmodium falciparum, Toxoplasma gondii e Treponema pallidum pelas tecnicas de hemaglutinacao passiva, imunofluorescencia indireta, hemaglutinacao indireta e floculacao (VDRL) respectivamente. Cada populacao foi classificada de acordo com o padrao socio-economico e grau de contacto com outras civilizacoes. Hepatite, malaria falciparum, sifilis e toxoplasmose apresentaram prevalencias de 38,1 - 27,3 - 21,9 e 73,9%, respectivamente, na populacao de Manaus. A populacao de Barcelos apresentou valores correspondentes a 40,7 - 33,8 - 22,1 e 63,8%; A tribo Mayongong 1,3 - 80,1 - 4,5 e 66%; A tribo Mundurucu 20,2 - 17,3 - 15,4 e 70,8%. A tribo Sanoma 0,9 - 77,7 - 1,8 e 56,2%. Malaria e toxoplasmose foram as infeccoes mais prevalentes entre as cinco populacoes de pouco contacto com a civilizacao, especialmente nas tribos indigenas mais isoladas. Baixa prevalencia de positividade para as quatro infeccoes foi observada nos individuos idosos de todas as cinco localidades

Prevalence of chloroquine-resistant falciparum malaria in the Brazilian Amazon.

The prevalence of chloroquine-resistant falciparum malaria was determined for humans living at 28 different sites in the Brazilian Amazon. Blood samples obtained from each patient were defibrinated, placed in vials containing 0.5% glucose and or chloroquine and incubated for 24 hours at 39-40 degrees C without agitation. In vitro sensitivity of the parasite to four different concentrations of chloroquine was determined for each sample. After 24 hours of incubation, trophozoites of Plasmodium falciparum developed to schizonts in all control cultures (no chloroquine) as well as in 80.6, 48.4, 11.8 and 7.5% of the cultures containing 0.5, 1.0, 2.0, and 3.0 nmol chloroquine/ml blood, respectively. Chloroquine-resistant P. falciparum was found in blood samples from all 28 locations, indicating that such resistance is widely spread in the Brazilian Amazon.