Search

Lymphatic filariasis is caused by the nematodes Brugia malayi, Brugia timori, and Wuchereria bancrofti. The disease occurs in developing countries and is more frequent in urban areas. An estimated 4 billion people live in at-risk areas. In Brazil the endemic is caused by W. bancrofti and was first documented in 1878. It was first detected in Recife in 1952. Currently, Recife and Belém are the only cities in Brazil where the endemic is considered a public health problem. The objectives of this study are to discuss the epidemiology and control of lymphatic filariasis and review its control since it was reported by Rachou in 1952. We analyze the "campanhista" or campaign-oriented model employed by the Sucam/FNS institutional program, as well as several proposed innovative methods. We present available strategies for control of filariasis through primary health care services, decentralization to the local level (or "municipalization"), and community-based health programs.

A sensitive and specific polymerase chain reaction (PCR) based on a highly repeated deoxyribonucleic acid (DNA) sequence (188 bp; SspI repeat) was tested for the detection of Wuchereria bancrofti DNA in blood and urine samples collected during the day from individuals in Coque, Recife, Brazil, an endemic area for W. bancrofti. All microfilaraemic individuals were also positive by PCR, irrespective of the samples used. The PCR system was capable of detecting W. bancrofti DNA in amicrofilaraemic individuals: c. 93% were positive by PCR when day blood samples were used and 59.7% when urine samples collected at 07:00 were used. Thus, nocturnally periodic W. bancrofti infection can be detected in blood samples collected during the day, which is convenient for large-scale screening. In addition, non-invasive urine collection provided suitable samples for PCR, which is clearly advantageous for preliminary mass diagnosis.

Bancroftian filariasis is spreading in towns of endemic areas in Recife, northeastern Brazil, where it is a major public health problem. This paper deals with the prevalence of microfilaraemia and filarial disease in two urban areas of Recife, studying their association with individual characteristics and variables related to the exposure to the vectors. The parasitologic survey was performed through a "door-to-door" census and microfilaraemia was examined by the thick-drop technique using 45 microliters of peripheral blood collected between 20:00 and 24:00 o'clock. 2,863 individuals aged between 5 and 65 years were interviewed and submitted to clinical examination. Males aged between 15 and 44 years old presented the greatest risk of being microfilaraemic. Microfilaraemia was also significantly associated with no use of bednet to sleep. The risk of being microfilaraemic was greater among those who had lived in the studied areas for more than 5 years. The overall disease prevalence was 6.3%. Males presented the greatest risk of developing acute disease. The risk of developing chronic manifestations was also greater among males and increased with age. We found no association between time of residence, bednet use, microfilaraemia and acute and chronic disease. We may conclude that in endemic areas there are subgroups of individuals who has a higher risk of being microfilariae carriers due to different behaviours in relation to vector contact.

Despite the common association of filarial infection with elephantiasis, the great majority of those infected are in fact clinically asymptomatic microfilariae carriers. The assumption has been that infection but not disease exists in these presymptomatic persons. In an area Brazil where Wuchereria bancrofti is endemic, flow studies done with dynamic radionuclide lymphoscintigraphy were used to compare 30 limbs from asymptomatic microfilaremic subjects with 16 control limbs. Geometric mean values for T1/2 (19.8 vs. 37.7 min; P < .001), appearance time (7.9 vs. 27.9 min; P < .001), percent uptake at the region of interest (0.67% vs. 0.14%; P < .001), and peak activity (62.6 vs. 2.6 cps; P < .001) each indicated an enhanced pattern of rapid, increased lymph flow in asymptomatic microfilaremic subjects. The abnormal lymphatic function in these subjects indicates that current passive intervention strategies may need to change if the debilitating sequelae of this parasitic infection are to be avoided.

Despite many millions of doses administered over the past 40 years, basic and crucial issues regarding the use, mode of action, and effectiveness of diethylcarbamazine (DEC) in many clinical situations remain unresolved. To directly investigate whether the well-known microfilaricidal and macrofilaricidal actions of DEC actually result in subsequent improvement in existing damage to lymphatic vessels or lymph nodes, 29 study subjects in Recife, Brazil were stratified into three groups according to the severity of clinical manifestations of lymphatic insufficiency. After baseline radionuclide lymphoscintigraphy was performed, subjects were treated with two courses of DEC separated by at least a six-month interval and then rescanned one year after the baseline scan. A side-by-side comparison of images obtained at baseline with those obtained at follow-up in 13 asymptomatic microfilaremic individuals, six individuals with filarial fever, and in 10 individuals with chronic pathology demonstrated essentially unchanged lymphatic morphology in all but one individual whose disease actually progressed in the face of therapy. We conclude that two 12-day treatment courses of DEC did not have a demonstrable direct or indirect effect on existing structural damage to the lymphatic system even in those individuals with preclinical disease.