The resistance to re-infection of cats repeatedly inoculated with infective larvae of Brugia pahangi.

Seven microfilaraemic and five amicrofilaraemic cats which had been repeatedly infected with Brugia pahangi were challenged along with normal cats 28, 14 and 1 day before autopsy. The lymphatics of the amicrofilaraemic cats contained no female adult worms originating from the repeat infections and only two adult males (both from the same cat). Only 5.

The ferret (Mustela putorius furo) as an experimental host for Brugia malayi and Brugia pahangi.

Ferrets inoculated subcutaneously with 150--200 infective larvae of Brugia malayi (subperiodic strain) usually developed patent infection during the 3rd month post inoculation. Microfilaremia was transient, and most animals became amicrofilaremic after the 6th month of infection. Ferrets developed a persistent eosinophilia at the time of patency.

The number and distribution of Brugia pahangi in cats at different times after a primary infection.

The number of larvae and adults of Brugia pahangi and their distribution throughout the lymphatics and extra-lymphatic tissue were studied in cats infected by subcutaneous injection of larvae into their hind feet. For the first 20 days approximately 55% of the inoculum is recovered as living worms. After 25 days the recovery falls by a half.

Estimate of the risk of post transfusion hepatitis B in Jakarta, Indonesia.

The prevalences of hepatitis B surface antigen (HBsAg) and antibody to HBsAg (anti-HBs) were determined in blood donors and transfusion recipients in Jakarta, Indonesia. In blood donors the prevalence of HBsAg was 10% while anti-HBs was 43%. In transfusion recipients the prevalence of HBsAg and anti-HBs was 67%.

Effect of treatment with diethylcarbamazine on immune responses to filarial antigens in patients infected with Brugia malayi.

We studied the effect of treatment with diethylcarbamazine (DEC) on immune responses to parasite antigens in humans infected with Brugia malayi. In vitro lymphocyte proliferative responses to microfilarial antigens increased in patients who became amicrofilaremic after treatment with DEC. No changes in reactivity were observed in amicrofilaremic individuals who were given DEC or in a small number of patients who remained microfilaremic after treatment.

Brugia malayi: relationship between anti-sheath antibodies and amicrofilaremia in natives living in an endemic area of South Kalimantan, Borneo.

A seroepidemiological approach was taken to elucidate the relationship between anti-microfilarial antibodies and amicrofilaremia in humans living under natural conditions of exposure to Brugia malayi. Entomological observations indicated that all of the people in the study population in South Kalimantan, Borneo, were exposed repeatedly to filarial infection. A third of the population had antibodies to the sheath of microfilariae.

Immune responses in human infections with Brugia malayi: specific cellular unresponsiveness to filarial antigens.

We evaluated the cellular immune competence of 101 subjects living in an area of South Kalimantan (Borneo) where Malayan filariasis is endemic. All patients with elephantiasis but none with other clinical stages of filariasis reacted with adult worm antigens. The majority of subjects without clinical or parasitological evidence of filariasis and approximately one-half of those with amicrofilaremic filariasis reacted with microfilarial antigens.

Successful vaccination of cats against Brugia pahangi with larvae attenuated by irradiation with 10 krad cobalt 60.

Cats were vaccinated by the inoculation on 10 occasions of approximately 300 larvae of Brugia pahangi which had been irradiated with 10 krad cobalt 60. They were challenged on 3 occasions with normal larvae of either B. pahangior B.

Hybridization between Brugia patei, B. pahangi and sub-periodic B. malayi.

Virgin females of Brugia malayi, B. pahangi and B. patei were mated with males of species other than their own to determine whether they would hybridize.

Studies with Brugia pahangi. 15. Cobalt 60 irradiation of the worm.

Infective larvae of Brugia pahangi were irradiated at 10, 25 or 45 krads by means of a Cobalt 60 source. In cats, 10 krads caused the worms to be stunted and sterile but allowed them to become 5th stage, migrate posteriorly into the afferent lymphatic, and produce pathology. 25 krads prevented the worms from developing beyond the early fourth stage and from migrating away from the popliteal lymph node.

Studies with Brugia pahangi 17. The anthelmintic effects of diethylcarbamazine.

Diethylcarbamazine (DEC) was active in vitro against infective larvae and microfilariae of Brugia pahangi but only at high concentrations. When fed to mosquitoes which were infected with B. pahangi it had little or no activity.

The lethal effects of the cibarial and pharyngeal armatures of mosquitoes on microfilariae.

Microfilariae of Wuchereria bancrofti and Brugia pahangi were killed by the chewing action of the cibarial and pharyngeal armatures and other papillae and spines in the fore-gut of mosquitoes. The proportion of ingested microfilariae that were killed was largely dependent on the presence and shape of the cibarial armature. Anopheles farauti No.

Studies on Brugia pahangi. 13. The anthelmintic effect of compounds F151 (Friedheim), HOE 33258 (Hoechst) and their reaction product.

F151 was a potent filaricide against adult Brugia pahangi in cats and jirds. HOE 33258 did not kill adult worms in cats but had a marginal effect on adult worms in the peritoneal cavity of jirds. It was not immediately microfilaricidal in cats but the microfilarial counts of treated cats fell within a few weeks of treatment.

Studies with Brugia pahangi 10. An attempt to demonstrate the sharing of antigenic determinants between the worm and its hosts.

Infective stage Brugia pahangi that were reared in Aedes aegypti survived equally well in cats that had previously been immunized against mosquito tissue and in a normal cat. The survival of third, fourth, juvenile, adult and microfilarial stages of B. pahangi that were recovered from cats was similar in jirds that had been immunized against cat antigens and in normal jirds.