Biomedical subjects

B H Kwa

Publications and source records attributed to B H Kwa.

At least 19 recordsLinked to original sources

PubMed2003

Observations of Breinlia booliati in a new host, Rattus rattus jalorensis, from Kuantan, state of Pahang, Malaysia.

Breinlia booliati Singh and Ho, 1973 is described from the Malaysian wood rat, Rattus rattus jalorensis Bonhote. The parasites presented here were originally discovered in 1955 in Kuantan, Malaysia, but were not classified until now. On the basis of morphological observations of anatomical structures and comparisons with other species of Breinlia, it was determined that the parasites were B. booliati. The parasites discussed here show slight deviation from B. booliati, but they do not warrant a new species classification. There is some variation in anatomical measurements, the number of male caudal papillae, and the morphology of the microfilariae. Breinlia booliati from a new host is described in this article, with a brief discussion on Rattus species that are hosts of B. booliati and vectors that transmit the parasite. The occurrence of B. booliati in R. r. jalorensis represents the first report of the parasite in this host.

Animals↗

PubMed1996

Regulatory cytokines in the lymphatic pathology of athymic mice infected with Brugia malayi.

To investigate whether Brugia malayi-induced lymphatic inflammation is due to production of pro-inflammatory cytokines, we determined the lymph and serum levels of interleukin (IL)-1, IL-6, tumor necrosis factor (TNF)-alpha and granulocyte-macrophage colony stimulating factor (GM-CSF) using enzyme immunoassays. Serum from normal and infected mice did not show elevated cytokine concentrations. Samples of lymph from parasitized lymphatics had significantly increased levels of IL-1 (range = 6-1620 pg/ml), IL-6 (19-17,800 pg/ml), TNF-alpha (19-2000 pg/ml) and GM-CSF (4-275 pg/ml). The anti-inflammatory cytokine IL-4 (7-12 pg/ml) was in the normal range and no increase in interferon (INF)-gamma was detected in lymph samples. The data suggest that increased levels of mediators or cytokines localized in the lymphatics may be important contributors to massive lymphatic dilation and inflammation.

Animals↗

PubMed1996

Effect of Brugia malayi on the growth and proliferation of endothelial cells in vitro.

Athymic mice (C3H/HeN) parasitized by Brugia malayi develop massively dilated lymphatics. The lymphatic endothelial lining is perturbed, and numerous mononuclear and giant cells are closely apposed to the endothelium. The hyperplastic endothelial cells and low opening pressure of the lymphatics suggest abnormal multiplication of these cells may be important in the dilation. We studied the in vitro growth rate of human umbilical vein endothelial cells cultured with adult worms and microfilariae of B. malayi. The tetrazolium salt reduction assays were used to quantify possible direct mitogenic or inhibitory effects. The growth factor-induced proliferation of endothelial cells was significantly suppressed by 44-51% on day 1, 46-81% on day 3, and 45-79% on day 5 in cultures containing adult female worms, which had greater suppressor activity on endothelial cell proliferation than male worms, microfilariae, or soluble adult worm extract. Culture supernatant containing female worm excretory-secretory products significantly inhibited the growth and multiplication of cells, suggesting that adult female worms release antigens or proteins that have inhibitory activity on growth factors necessary for endothelial cell proliferation in vitro. Excess human recombinant epidermal growth factor and bovine brain extract partly reversed the inhibitory activity of worms in culture and restored the endothelial cell proliferation when incubated with worm culture supernatant. Indomethacin and BW 775Hcl failed to restore normal endothelial proliferation in the presence of female worms, suggesting that parasite-derived prostanoids and cyclooxygenase products did not cause the inhibition. Lymph from dilated lymphatics, but not serum from infected mice, increased the proliferation of cells in vitro. Together, these data demonstrate that excretory-secretory products of B. malayi parasites suppress vascular endothelial proliferation in vitro. Furthermore, increases in the number of these cells in vitro in the presence of lymph suggest that parasite-induced host factors may be important in modulating the degree of proliferation.

Animals↗

PubMed1994

Evaluation of different medium supplements for in vitro cultivation of Brugia malayi third-stage larvae.

Growth and development of Brugia malayi (Nematoda: Filarioidea) third-stage larvae (L3) were compared in 5 medium supplements. The basic culture medium (NI) consisted of a 1:1 (v/v) mixture of NCTC-135 and Iscove's modified Dulbecco's medium, an antibiotic/antimycotic mixture, and 1 of the following 5 supplements: 25 mg/ml bovine albumin fraction-V (BAF), 10% fetal bovine serum (FBS), 10% commercially obtained human serum (CHS), 10-15% pooled human serum from hospital patients (PHS), and 10-15% human serum from a single individual (SHS). Cultures were maintained at 37 C in an atmosphere of 5% CO2 in air. NI-BAF and NI-CHS did not support molting of L3 to fourth-stage larvae (L4), whereas NI-FBS, NI-PHS, and NI-SHS did support molting of L3 to L4 but only the larvae in NI-SHS attempted the fourth molt. Growth and development of in vitro larvae in NI-PHS and NI-SHS were comparable to that observed in jirds for the first 28 days, after which the in vitro larvae lagged behind in vivo larvae. Optimal growth and development may be dependent on certain as yet unidentified components of specific human serum.

Animals↗

PubMed1992

Effect of carrageenan on the resistance of congenitally athymic nude and normal BALB/c mice to infective larvae of Brugia malayi.

Resistance of BALB/c mice to infective third-stage larvae (L3) of the human filarial parasite Brugia malayi is thymus-dependent, although the actual effector mechanisms that mediate larval killing are unknown. The present study examined the effect of carrageenan (CGN) on the mechanisms of resistance to B. malayi infection in heterozygous (nu/+) and nude (nu/nu) mice. Mice were treated with CGN at a single dose of 20 or 200 mg/kg and were inoculated intraperitoneally 1 day later with 100 L3. The results showed a dose-dependent increase in the numbers of L4 and L5 that were recovered from nu/+ and nu/nu mice. CGN treatment also enhanced the recovery of mature adult worms from nu/nu mice and appeared to abolish partially the dichotomy of resistance between the usually more susceptible male and the more resistant female nu/nu mouse. Microfilariae were found in the peripheral blood and the peritoneal cavity of CGN-treated male and female nu/nu mice and in the peritoneal cavity of male but not female nu/+ mice. Fewer larval granulomas were recovered from the peritoneal cavity of treated mice. CGN-treated, parasitized nu/+ and nu/nu mice showed high titers of IgM and IgG antibodies. An experimental compound, CGP 20376, showed 100% larvicidal activity following the administration of a single dose of 20 mg/kg to CGN-treated mice. From this study, we conclude that macrophages alone or in conjunction with other cells are actively involved in the resistance of mice to B. malayi L3.

Animals↗

PubMed1992

Brugia malayi: ivermectin inhibits the exsheathment of microfilariae.

Brugia malayi-infected microfilaremic jirds (Meriones unguiculatus) were treated with ivermectin at a single dose of 200 micrograms/kg of body weight injected subcutaneously. Susceptible Aedes aegypti mosquitoes were fed on treated jirds 24 hours later. Mosquitoes fed on untreated jirds served as controls. Infected mosquitoes were dissected at 1, 3, 24, 48, 72, and 96 hr after the blood meal, and differential counts of sheathed microfilariae, exsheathed microfilariae, and cast sheaths were performed using fluoresceinated wheat germ agglutinin. Microfilariae failed to exsheath in mosquitoes fed on ivermectin-treated jirds. Microfilariae from ivermectin-treated jirds also did not exsheath in vitro in the presence of 10 mM CaCl2, whereas 85-90% of sheathed microfilariae from untreated jirds exsheathed in vitro. In addition, sheathed microfilariae from untreated jirds, when pretreated in vitro with ivermectin at 0.25, 0.5, or 1 microgram/ml, lost their ability to exsheath in vitro in the presence of 10 mM CaCl2. However, ivermectin treatment had no effect on exsheathing of microfilariae when incubated with papaya protease. Thus, ivermectin appears to inhibit the intrinsic exsheathing process of microfilariae in the mosquito host, thereby blocking their development and further transmission of infection.

Aedes↗

PubMed1991

Histopathology of Brugia malayi-infected nude mice after immune-reconstitution.

Long term (greater than 200 day) Brugia malayi-infected nude mice with grossly dilated lymphatics were reconstituted with 10(8) primed spleen cells from heterozygous donors. Histological and ultrastructural examination at 7, 14, 21 and 28 days post-reconstitution revealed progressive fibrosis, obliterative lymph thrombus formation, interstitial infiltrates and extensive perilymphangitis. Formation of lymph thrombi/granulomas was associated with killing of adult worms and microfilariae, and the predominant cell types involved were large granular macrophages. Langhan's giant cells and eosinophils. Thus, the ability to initiate the formation of obstructive lesions in the dilated lymphatics of chronically parasitized nude mice by immunological reconstitution, suggests that several complex mechanisms might operate in stages to cause filarial elephantiasis.

Animals↗

PubMed1991

Variations in complement activation of Brugia patei, B. malayi and B. pahangi microfilariae.

The complement of fresh normal heterozygotic BALB/C (nu/+) and nude (nu/nu) mice was activated by sheathed microfilariae (Mf) of Brugia malayi and B. pahangi but not by B. patei. Mouse C3 was detected by immunofluorescence on the sheathed surface of B. malayi and B. pahangi Mf but not on B. patei Mf. The bound complement promoted macrophage and neutrophil mediated adherence and cytotoxicity to these Mf. However, BALB/C nu/+ or nu/nu mouse macrophages and neutrophils adhered to exsheathed Mf of B. patei and killed them in the presence of fresh normal mouse serum (NMS). C3 molecules were detected on the cuticle of exsheathed Mf of B. patei and B. malayi. Fresh NMS (nu/+ or nu/nu) depleted of complement factors by heating or by zymosan or anti-mouse C3, failed to promote cell adherence to these parasites. EDTA but not EGTA abolished the adherence activity to sheathed and exsheathed Mf of B. malayi, whereas both EGTA and EDTA abolished the adherence activity to exsheathed Mf of B. patei and sheathed Mf of B. pahangi suggesting the different pathways of complement activation by these closely related species. Macrophages and neutrophils from peritoneal exudate cells of nu/+ or nu/nu were equally potent in adherence and killing of Mf. Transfused B. patei but not B. malayi or B. pahangi Mf were recovered from the peritoneal cavity of BALB/C mice with no cell adherence and cytotoxicity.

Animals↗

PubMed1991

Cultured endothelial cells from lymphatics of nude mice parasitized by Brugia malayi.

Endothelial cells from dilated inguinal lymphatics of congenitally athymic nude mice, parasitized by adult Brugia malayi, were placed in culture. Cells formed a loose monolayer and exhibited a typical cobblestone appearance. When microfilariae were present in cultures, they frequently appeared to be attached to the monolayer by one end. Approximately 75% of the primary explant cells were positive for Factor VIII-associated antigen, comparable to bovine artery endothelial cells used as a control. With few exceptions, cultures were uncontaminated with fibroblasts or other non-endothelial cell types. Large granular cells with characteristics of mononuclear/macrophage cells appeared in long term and unpassaged cultures. Cells remained viable in culture for an average of 60 days, 5 to 6 passages, before becoming highly vacuolated and assuming a rounded configuration. Viability of the cells was dependent upon heparin, serum and endothelial cell growth factor. The propensity of the lymphatics of nude mice to become greatly dilated in the presence of viable adult worms of B. malayi will prove to be important not only for the study of the effects of the parasite and its products upon endothelial cells, but also because a source of murine lymphatic endothelial cells can be readily available for functional studies.

Animals↗

PubMed1990

Brugia malayi and Brugia pahangi: transmission blocking activity of ivermectin and brugian filarial infections in Aedes aegypti.

Brugia malayi- or Brugia pahangi-infected, microfilaremic jirds (Meriones unguiculatus) were treated with ivermectin at a single dose of 200 micrograms/kg body weight, administered subcutaneously. After different time intervals, Aedes aegypti mosquitoes were fed on treated or untreated jirds. Sausage stage, L2, and L3 larvae failed to develop in mosquitoes that fed on jirds from 15 to 30 days post-treatment. After 1 month, the numbers of L3 larvae recovered from mosquitoes fed on treated B. pahangi jirds were comparable to controls. However, the number of L3's recovered from mosquitoes fed on B. malayi jirds remained significantly lower than controls, 2 and 3 months after treatment. This reduction suggests that ivermectin may be more effective in blocking transmission of B. malayi than B. pahangi. Ivermectin treatment had no effect on the mean number of circulating microfilariae in treated jirds. Therefore, mosquitoes ingested comparable numbers of microfilariae when compared to those mosquitoes fed on untreated controls. Only in the case of jirds infected with B. malayi did the circulating microfilarial counts fall 30 days after treatment. The failure of microfilariae to develop to the L3 stage in mosquitoes fed on jirds within 30 days of treatment was not due to failure of mosquitoes to ingest microfilariae. Brugia malayi microfilariae also failed to develop to L3 in mosquitoes that were allowed to feed on microfilaremic jird blood treated with ivermectin (50 ng/ml) in vitro, indicating its efficacy at low concentrations. In addition to N-acetyl glucosamine, microfilariae obtained for a period of 15 days from ivermectin-treated but not control jirds showed D-mannose, N-acetyl galactosamine, and L-fucose moieties on the surface of the sheath.(ABSTRACT TRUNCATED AT 250 WORDS)

Aedes↗

PubMed1990

A direct fluorescence technique for the rapid detection of sheathed microfilariae in blood smears.

Thick and thin blood smears containing microfilariae of Wuchereria bancrofti, Loa loa, Brugia malayi, Brugia pahangi, Brugia patei or Acanthocheilonema viteae were prepared from either cryopreserved blood samples or from freshly collected blood, fixed in methanol and treated with a fluoresceinated lectin wheat germ agglutinin. Sheathed microfilariae of W. bancrofti, L. loa, B. malayi, B. pahangi and B. patei in the blood smears could be easily detected and counted using a fluorescence assay. The unsheathed microfilaria of Acanthocheilonema viteae did not fluoresce. The possibility of adapting this technique, which does not require the use of parasite specific antibody for the sensitive, parasitological detection of filarial infections, is discussed.

Animals↗

PubMed1990

Ophthalmic dirofilariasis.

Dirofilaria tenuis infection involving the eye and ocular adnexae is rare. We report a patient from Florida with a subconjunctival worm which was surgically removed and identified as immature D. tenuis. Ophthalmic involvement of this organism is found most commonly in Florida and the southeastern United States. Raccoons are a natural host and mosquitoes a natural vector for D. tenuis.

Aged↗

PubMed1989

Lectin binding to larval stages of Brugia patei.

Surface properties of microfilariae (mf) and infective larvae of Brugia patei were investigated to compare them to previous studies with the other brugian species. Of all the lectins tested, only wheat germ agglutinin (WGA) binds to the sheath surface of mf indicating the presence of N-acetyl-D-glucosamine as a major surface carbohydrate. However, cuticle of infective larvae failed to show binding of these lectins. Enzyme treatment of mf with N-acetyl-D-glucosaminidase and L-fucosidase has exposed D-mannose, N-acetyl-D-galactosamine and L-fucose on the sheath surface. The binding of lectins to intact mf and to enzyme-treated mf appeared to be specific as pretreatment with specific inhibitory sugars completely abolished the binding activity. This is the first study conducted with this filarial parasite and it established that B. patei is similar to other species of Brugia but differs from Wuchereria in its surface-lectin binding properties.

Animals↗

PubMed1987

Human in vitro immune reactions to animal filariids.

Infective third stage larvae of animal filariids Brugia pahangi and Breinlia booliati incubated in vitro in the presence of normal human peripheral leucocytes and sera from human filariasis subjects resulted in decrease in motility, cell adherence, and formation of precipitates around the larvae. Strongest immune reactions were seen with sera from amicrofilaraemic symptomatic subjects, normal exposed individuals, and patients with tropical pulmonary eosinophilia syndrome (TPE). Weaker reactions were observed with sera from patients with elephantiasis. In all cases, reactivity to B. pahangi larvae was considerably higher than against B. booliati. Sera from microfilaraemic patients and unexposed control subjects were nonreactive. The implication of these human in vitro immune reactions against filarial parasites of animal origin is discussed in the context of the hypothesis of "zooprophylaxis" previously suggested by other workers.

Animals↗

PubMed1984

The presence of blocking factors in Brugia malayi microfilaraemic patients.

Serum from microfilaraemic patients have been shown to be unable to promote the antibody-dependent, cell-mediated adherence reaction to infective larvae of Brugia malayi in vitro. In this study, it was found that peripheral leucocytes from microfilaraemic patients were also incapable of promoting the adherence reaction even when incubated with serum of tropical pulmonary eosinophilia (TPE) patients. The TPE sera would normally promote the most intense adherence reaction. It was further shown that preincubation of normal human peripheral leucocytes with sera of microfilaraemic patients would similarly render them incapable of adherence. Such preliminary studies suggest that blocking factors may be present in microfilaraemic patients.

Antibody-Dependent Cell Cytotoxicity↗

PubMed1983

Immunoglobulin levels in various clinical groups of human Brugian filariasis in Malaysia.

Quantitation of serum immunoglobulin M, G, A, D and E levels was carried out in Malaysians with Brugia malayi infections. Results showed highly elevated levels of IgM and IgE as well as moderately elevated levels of IgG. These were most significant in patients with tropical pulmonary eosinophilia or elephantiasis. Serum IgE levels were extremely high in microfilaraemic patients (6,060 +/- 3,958 IU ml) probably due to a constant antigenic stimulation by dead and dying microfilariae.

Adolescent↗

PubMed1983

Effects of serum from treated patients on antibody-dependent cell adherence to the infective larvae of Brugia malayi.

Adherence assays were used to demonstrate the in vitro effect of serum-dependent cellular adherence of human buffy coat cells to infective larvae of Brugia malayi in filariasis patients treated with antifilarial drugs. In this study, microfilaraemic patients were treated with either diethylcarbamazine citrate (DEC), mebendazole or levamisole hydrochloride. It was found that DEC and mebendazole decreased the motility of infective larvae due to a direct action of the drugs. Sera of levamisole-treated patients caused increased adherence of human buffy coat cells to infective larvae, leading to a decrease in motility and cuticular damage as confirmed by scanning electron microscopic studies. However, serum of levamisole-treated patients alone could cause a similar lethal effect on infective larvae. Studies with the indirect fluorescent antibody test suggested that IgM was involved in this phenomenon. Complement did not appear to be important.

Anthelmintics↗

PubMed1983

Experiences in the management of chest injuries and a review of current management.

Eleven cases of chest trauma managed in the Intensive Care Unit (ICU), Alexandra Hospital were reviewed. Common manifestations were: rib fractures, haemothorax, pneumothorax, pulmonary contusion and flail chest. Nine patients had fractures on other sites of the body and three patients had associated abdominal injuries requiring laparotomy. Patients were referred to the ICU only when they were in respiratory distress. Transfer to the ICU occurred one to three days after admission to the hospital. Eight patients subsequently had to be ventilated. Two patients died. Respiratory failure in chest trauma is often the result of damage to the parenchyma, atelectasis and infection. Whilst the extent of parenchyma lung damage is dependent upon the severity of the injury and therefore not medically preventable, atelectasis and infection can be avoided. Patients with significant chest trauma should therefore be admitted directly to the Intensive Care Unit and the 'Expectant Therapy' instituted.

Critical Care↗