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At least 19 recordsLinked to original sources
PubMed1977

The microfilaria of Brugia timori (Partono et al. 1977 = Timor microfilaria, David and Edeson, 1964): morphologic description with comparison to Brugia malayi of Indonesia.

The microfilaria of Brugia timori was compared with microfilariae of Indonesian strains of periodic and subperiodic Brugia malayi using alcohol-fixed (stained) and formalin-fixed (unstained) preparations. As noted by other observers of the Timor microfilaria, the absence of a stained sheath in Giemsa preparations, a long cephalic space with a length-to-width ratio of about 3:1, and a great overall body length are features which most readily distinguish this parasite. Additionally, B. timori has greater numbers of single row nuclei in the terminal column of body cells and a lesser bulge of the cuticle surrounding nuclei in the distal portion of the tail than does B. malayi. About 60% of B. timori microfilariae were exsheathed in haemalum-stained thick blood films. Brugia timori microfilariae were found to be distinct from microfilariae of B. malayi by comparing percentages of total body length included between the cephalic tip and major internal anatomic markers.

Animals↗
PubMed1976

Infective larvae of Brugia: escape from mosquitoes into water and subsequent oral infectivity in jirds.

Published work showed that third-stage larvae (L-3s) escape into water from dead or dying, Brugia pahangi-infected, Aedes aegypti. The present study revealed the same escape phenomenon among B. pahangi-infected Armigeres subalbatus, Anopheles quadrimaculatus, and Aedes togoi, and among Brugia malayi-infected Ae. aegypti and Ae. togoi. L-3s maintained in water or in Lum's solution for 3 hours retained infectivity when tested in orally or subcutaneously exposed jirds; furthermore, L-3s recovered from mosquitoes dead for 24 to 48 hours were also infective by either portal of entry in jirds. Since L-3s may escape and remain infective in the field, it is conceivable that natural filarial infections might thus be acquired orally by definitive hosts.

Aedes↗
PubMed1977

Distribution of acid phosphatase activity in the larval stages of Wuchereria bancrofti, Brugia malayi, B. pahangi and Dirofilaria immitis in the mosquito.

The histochemical distribution of acid phosphatase in microfilariae and in the larval stages of four mosquito-borne filariae: Wuchereria bancrofti, Brugia malayi, B. pahangi and Dirofilaria immitis was studied using naphthol AS-TR-hexazonium technique and light microscopy. Accurate differentiation between microfilariae of the four species could be made on the basis of their patterns of acid phosphatase activity. In contrast to microfilariae in the blood, the larval stages in the mosquito exhibited different patterns of acid phosphatase activity which were characteristic for each developmental stage. In the first-stage larva, maximum acid phosphatase activity was found in the anal vesicle, the growing anal membrane (anal plug), buccal cavity, forming intestine and rectum. In the second-stage larva, acid phosphatase activity was present throughout the alimentary canal, particularly in the section of the intestine and rectum. In the infective third-stage larva, the whole body stained densely red. The reaction for acid phosphatase in the excretory cell complex of W. bancrofti and of both species of Brugia gradually decreased in intensity and disappeared completely towards the end of the first-larval stage, whereas in D. immitis a strong reaction in this area persisted throughout the larval life in the mosquito. The presence or absence of enzymic activity in the excretory cell complex and in the Mundgebilde (amphids) of the developing larvae can be used as an adjunctive diagnostic method.

Acid Phosphatase↗
PubMed1978

Studies with Brugia pahangi. 18. Anthelmintic effects of stibocaptate.

Stibocaptate (Asiban, Hoffman--La Roche) killed third stage larvae of Brugia pahangi in vitro at 50 p.p.m. but had no effect on microfilariae at 1 X 10(4) p.p.m No larvae developed in infected mosquitoes fed 1% stibocaptate in 10% sucrose. It was neither micro-nor macrofilaricidal in either jirds or cats but did affect embryogenesis.

Animals↗
PubMed1975

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. Host antigenic determinants were not detected on the surface of larvae in substantial amounts using fluorescent antibody techniques. It is unlikely that B. pahangi evades the immune response of its vertebrate hosts by masquerading as "self" behind host antigens.

Aedes↗
PubMed1976

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. The reaction product, or mixture, of these two compounds (V5851 = E) was strongly macrofilaricidal in cats and jirds.

Animals↗
PubMed1977

Flight muscle ultrastructure of susceptible and refractory mosquitoes parasitized by larval Brugia pahangi.

On parasitization with larval Brugia pahangi the infected flight muscle fibres of "resistant" Anopheles labranchiae atroparvus undergo the following ultrastructural changes. The fibres become almost totally devoid of glycogen, their sarcoplasmic reticulum becomes elongate and closely associated with muscle fibrils. These fibrils degenerate and vesicles appear both within the degenerate fibril and within elements of the sarcoplasmic reticulum. Vesicles accumulate around the worm and degenerate to a uniform mass which eventually becomes melanized from its inner edge (next to the parasite) outwards. The infected flight muscle fibres of both "resistant" Aedes aegypti and "susceptible" Aedes togoi are almost totally devoid of glycogen granules, but show no other ultrastructural change from the uninfected state.

Aedes↗
PubMed1977

Sensitivity and specificity of skin reactivity to Brugia malayi and Dirofilaria immitis antigens in Bancroftian and Malayan filariasis in the Philippines.

Saline antigen extracts of microfilariae, adult worms and third-stage larvae of subperiodic Brugia malayi maintained in gerbils were prepared for use as skin test reagents. Patients were studied on three different islands in the Philippines, one endemic for Bancroftian filariasis (Sorsogon, Luzon), another endemic for Malayan filariasis (Palawan) and the third without endemic filariasis (Cebu). A dose-response curve was established initially in patients with Bancroftian filariasis: thereafter 1.0 microng of the B. malayi antigens and 0.05 microng of Dirofilaria immitis FST antigen (obtained from Dr. T. Sawada) were used. Sizes of reactions were measured by recording the diameters of wheals at 20 minutes, 24 and 48 hours. There was a very high correlation in immediate hypersensitivity reactions among the three B. malayi antigens. Reaction sizes followed a normal distribution. When an area of an antigen-induced wheal 3 X that of the saline control was considered a positive reaction, 99% of 150 patients with Bancroftian filariasis and 96% of 45 subjects with Malayan filariasis reacted to B. malayi larval antigen. Only 68% of patients with Bancroftian filariasis but 90% of those with Malayan filariasis reacted to D. immitis FST antigen. There was no relationship between skin reactivity and age, sex, microfilaremia or severity of clinical disease. Approximately half of 50 patients who lived in an endemic area for W. bancrofti but had neither patent infection nor clinical disease reacted to B. malayi antigens. A maximum of 7% of 120 age- and sex-matched controls from Cebu gave false positive reactions with any of the antigens. Only a small proportion of patients gave 24- and 48-hour reactions. It is concluded that the use of antigens prepared from a human parasite, subperiodic B. malayi, which is easily maintained in a laboratory animal host, improves the ability to diagnose filarial infections by immunological means.

Adult↗
PubMed1977

The carbohydrate metabolism of Brugia pahangi microfilariae.

Evidence is presented that the microfilariae of Litomosoides carinii, Dipetalonema viteae and Brugia pahangi have an aerobic requirement for motility, but possibly not for survival. In addition, the data suggest that in an in vitro anaerobic environment, B. pahangi microfilariae ferment glucose only as far as lactate. In an aerobic environment, however, the data are consistent with a portion of glucose being dissimilated via a one step oxidative decarboxylation of pyruvate formed from glycolysis to acetate and CO2. In addition, a low level of complete oxidation, possibly via a tricarboxylic acid cycle pathway, may be occurring. Finally, if B. pahangi microfilariae are immobilized with levamisole in an aerobic atmosphere, the drug appears to alter the aerobic glucose metabolism of the parasite both qualitatively and quantitatively. A decreased glucose utilization occurs, together with a shift to a more nearly homolactate fermentation. It is suggested that the effects of levamisole on the metabolism of the microfilariid are secondary to the observed paralysis.

Aerobiosis↗
PubMed1977

Experimental Brugia timori and Wuchereria bancrofti infections in certain species of mosquitoes.

Laboratory reared Aedes aegypti (black eye and Jakarta strains), Aedes togoi, (Taiwan), Aedes albopictus, (Jakarta), wild caught Anopheles barbirostris, (Java) and Mansonia uniformis, (Jakarta) were fed on a carrier with mixed infection of Brugia timori and Wuchereria bancrofti. B. timori and W. bancrofti were able to develop in A. aegypti (black eye) and A. togoi, with development proceeding more rapidly for of B. timori than W. bancrofti. Both species of parasites were readily distinguishable in each of their developmental stages. A. barbirostris from Java was able to support development of B. timori as well as A. barbirostris from Flores. B. timori and W. bancrofti did not develop in M. uniformis, A. aegypti (Jakarta strain) and A. albopictus.

Aedes↗
PubMed1978

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. In jirds it was inactive against B. pahangi microfilariae and adults when administered at 300 mg/kg for 5 days either by the intraperitoneal or oral route. In cats given 25 or 50 mg DEC/kg intraperitoneally on 3 or 5 occasions it was not microfilaricidal, but most of the adult worms died within 30 days of the end of treatment. Although most microfilariae disappeared from the blood of cats immediately (i.e., within an hour) after treatment, they reappeared within a few hours in the same numbers. Microfilarial levels were reduced after treatment but there was no precipitate decline as occurs in human B. malayi patients.

Animals↗
PubMed1978

The vectors of Brugia malayi in Southern Thailand.

Mansonia uniformis, with an infective rate of 0.02, was incriminated as the vector of periodic Brugia malayi in Pattani province. Mansonia bonneae and Ma. dives, with infective rates of 0.18 and 0.20 respectively, were the vectors of B. malayi in Narathiwat, where the microfilarial periodicity was the subperiodic form.

Aedes↗
PubMed1979

Incorporation of radioactive precursors into filarial larvae of Brugia developing in susceptible and refractory mosquitoes.

The incorporation of tritiated precursors injected into mosquito hosts parasitized by developing filarial larvae of Brugia patei has been studied by autoradiography in 2 species of mosquito, Aedes togoi in which filarial development was normal and Anopheles labranchiae atroparvus in which filarial development was abnormal. In both mosquito hosts there was significant incorporation into 4--5-day-old developing larvae of uridine and amino acids (isoleucine, leucine, valine, arginine, lysine, cystine, methionine, phenylalanine, tyrosine, tryptophan, histidine, and proline), although lower incorporation of methionine, tyrosine, and tryptophan was found during abnormal development. No incorporation of thymidine, hydroxytryptophan, dopa, or carbohydrate was found at this stage of larval development. Some incorporation of glucose and dopa was found in or around earlier stages of development in An. l. atroparvus. Mosquito flight muscle showed lower incorporation of glucose, but not of amino acids, around the site of filarial parasite development. The flight muscle of An. l. atroparvus showed a higher level of incorporation of lysine compared to that in A. togoi and higher levels of lysine and valine were found in the abnormally developing filarial larvae in the refractory mosquito.

Aedes↗
PubMed1979

The effect of diethylcarbamazine in a murine model of Brugia malayi microfilaraemia.

The effect of diethylcarbamazine was tested in a murine model of Brugia malayi microfilaraemia. A course of therapy similar to that used to treat human infection led to more than a 90% decrease in circulating parasites. Experiments in which different amounts of diethylcarbamazine were given as a single dose indicated that its microfilaricidal activity is dose-dependent. The animal model of B. malayi microfilaraemia may be useful for studies of the mechanism of action and pharmacology of diethylcarbamazine and may be applied to the screening of new microfilaricidal drugs.

Administration, Oral↗
PubMed1979

Studies on human filariasis in Malaysia: immunoglobulin and complement levels in persons infected with Brugia malayi and Wuchereria bancrofti.

Levels of immunoglobulins G, A, M and E as well as complement components C3c and C4 have been determined in populations in various endemic areas in Peninsular Malaysia and also in filariasis patients. High immunoglobulin levels were seen. In the microfilarial-negative group IgG was 2009 mg% while IgE was 3967 I.U./ml. In the filariasis group, Wuchereria bancrofti patients had significantly higher levels of IgG, IgM and IgE, namely, 3314 mg%, 804 mg% and 18400 I.U./ml respectively. The significance of these levels is discussed.

Adolescent↗