An epidemiological survey of filariasis and malaria in Banggi Island and Upper Kinabatangan, Sabah, revealed microfilarial rates of 7.2% and 8.6% respectively and malaria prevalence of 9.7% and 16.9% respectively. Wuchereria bancrofti was a rural nocturnally periodic type with a periodicity index of 137.2 and average peak hour at 01.32 hrs; 9.2% of microfilaremic carriers as compared to 2.4% amicrofilaremic subjects had clinical filariasis. The Plasmodium falciparum: P. vivax: P. malariae ratios were 1:1:0.17 and 1.4:1:0.12 for Banggi and Upper Kinabatangan respectively. Anopheles flavirostris was incriminated as a new malaria vector in Banggi where the well-known primary malaria vector is An. balabacensis. The latter was also found for the first time to be a vector of rural W. bancrofti in Upper Kinabatangan. Experimental feeding also showed that L3 larvae of W. bancrofti were recovered at low rates from An. balabacensis. Aedes togoi appeared to be a suitable laboratory vector for W. 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.
Developing and adult worms of the human lymphatic filarial parasites (Wuchereria bancrofti,
Brugia malayi, and Brugia timori) are located mainly in the lymphatic system and occasionally in aberrant sites like subcutaneous and conjunctival cysts. Lymphatic
pathology ranging from dilatation of lymphatic channels and lymphangiectasia are detected on ultrasonography in apparently healthy, amicrofilaraemic, but filarial antigen positive individuals in endemic areas. Microfilariae are distributed in various organs and may be associated with immune mediated pathology at these sites; tropical pulmonary eosinophilia is characterized by intense immune mediated destruction of microfilariae in the lung parenchyma. In the spleen and other sites, nodular granulomatous lesions can occur where microfilariae are trapped and destroyed. The finding of Wolbachia endosymbionts in all stages of lymphatic filarial parasites has provided new insight on the adverse reactions
associated with anti-filarial chemotherapy. Inflammatory molecules mainly lipopolysaccharide (LPS)-like molecules released from endosymbionts on death of the
parasites are largely responsible for the adverse reactions encountered during anti-filarial chemotherapy. Prenatal tolerance or sensitization to parasite derived molecules can immune-modulate and contribute to both pathology and susceptibility/resistance to infection. Pathological responses thus depend not only on exposure to filarial antigens/infection, but also on host-parasiteendosymbiont factors and to intervention with antifilarial treatment. Treatment induced or host mediated death of parasites are associated with various grades of inflammatory response, in which eosinophils and LPS from endosymbionts play prominent roles, leading to death of the parasite, granulomatous formation, organization and fibrosis. The non-human primate (Presbytis spp.) model of
Brugia malayi developed for the tertiary screening of anti-filarial compounds has provided unique opportunities for the longitudinal study of the pathology associated with lymphatic filariasis. The pathology in this non-human primate model closely follows that seen in
human lymphatic filarial infections and correlates with clinical evidence of lymphatic pathology as detected with ultrasonography. These studies also show that successful treatment as detected by loss of motility and calcification of worms on ultrasonography is associated with reversal of early dilatations of lymphatic channels.