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Fig. 26.3. Lymphatic filariasis. The distribution of W. bancrofti (A) and B. malayi (B). B. timori is confined to parts of Indonesia

Bancroftian filariasis (Fig. 26.3) has no known reservoir, whereas B. malayi, which occurs in South and Southeast Asia, has a large animal reservoir. Lymphatic filariasis affects people living in both rural and urban environments. It is generally acquired as a teenager or young adult, and more often affects men than women. Other Brugia spp. are principally animal parasites, and only occasionally infect humans (e.g., B. pahangi). The B. malayi zoonotic infection is difficult to control because both domestic and wild animals act as a source for human infection. Hence, the mass chemotherapy programs which are used in peoples infected with W. bancrofti may not be as effective in B. malayi. The mosquito Culex quinquefasciatus is a significant vector of bancroftian filariasis: Anopheles spp. and Aedes spp. are also important vectors with different biting habits. Culex quinquefasciatus breeds in tropical urban areas and in polluted water and, like Anopheles spp., feeds largely at night and is endophilic. Urban malaria spray control programs are therefore also effective for some filariasis. Aedes spp., transmitting lymphatic filariasis in Southeast Asia and the South Pacific, are more difficult to control because they are diurnal, exophilic, and breed in tiny deposits of water in man-made objects in cities as well as tree holes or crab holes in rural environments. Mansonia spp. are important vectors of B. malayi in the Orient. The larvae of these mosquitoes puncture the submerged portions of certain species of water plants to obtain oxygen. This, together with the adults' variable feeding and resting behavior, makes Mansonia spp. a particularly difficult vector to control. Chemical larviciding spray programs have met with success in some regions along with the use of chemical impregnated clothing and anti-mosquito bed nets. Biological control continues to be investigated.

Most of our understanding of the pathogenesis of lymphatic filariasis comes from patients with W. bancrofti infection. Prior to World War II, little was known about this disease. During and following the South Pacific campaign, numerous U. S. soldiers infected with W. bancrofti were treated and studied. Histological studies from biopsies of these servicemen, together with experimental studies of animals, suggest that the host inflammatory response to the worms in the lymphatics is important in pathogenesis and is both humoral and cell-mediated. Animal studies with brugian parasites have shown that, in addition to the tissue reaction caused by the host immune response to infection, lymphatic damage is also the result of the direct mechanical or toxic effects of the nematode within the lymphatic vessels or lymph nodes.

The degree of immunity or immunological responsiveness to filarial parasites is different between people native to an endemic region and those people arriving from nonendemic areas. The endemic individual, who is hyporesponsive, will have a relatively mild lymph node response and may therefore not develop the same lymphatic pathology as the nonendemic person, or it may progress at a slower rate. Human and animal studies both suggest that secondary bacterial infections aggravate preexisting lymphatic pathology in filariasis and cause exacerbation of lymphedema.

The dead worms are of more significance than the living, although neither are desirable guests. Adult male and female filarial worms reside in different sites of the body (Fig. 26.4), usually in afferent channels or cortical sinuses of lymph nodes. Abdominal, pelvic, femoral, inguinal, supraclavicular, and epitrochlear lymph nodes can all be involved. The larval or adult worms first cause dilatation of the lymphatics, an effect which is likely in part mechanical as these lymphatic channels are tiny and intraluminal valves are easily damaged (Fig. 26.5). Hypertrophy of the vessel wall occurs next, followed by endothelial and connective tissue proliferation which ultimately protrudes into the lumen. The lymph vessels tend to remain patent as long as the nematodes are alive, but tortuosity and development of early collateral vessels also occur even at this stage.

It is the dead or dying worms which elicit the most severe inflammation, and it is during these episodes that lymphatics become completely obstructed. Lymphatic endophlebitis may ensue and, although there is some collateralization and recanalization, obstruction persists and increases in severity. The common end result is an inguinal or femoral lymphadenovarix.

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Fig. 26.4. A Microfilariae in the cutaneous tissues with an adult nematode in subcutaneous tissue. B Adult nematodes in antecubital fossa in a Puerto Rican patient. C An adult W. bancrofti in an inflamed and dilated distal lymphatic.

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Fig. 26.5 A,B. Surgical specimens from patients with W. bancrofti infections. A An abscess within the breast slowing gravid female worms. Note thin cuticle, paired uteri containing microfilariae, and single intestine. x75. B Chronic orchitis with gravid female worm in dilated testicular lymphatic. x55. (From Marty and Anderson 1995).

The histopathological changes in lymph nodes include:

- Dilatation of lymphatic channels and subcapsular sinusoids
- Capsular fibrosis
- Infiltration with histiocytes and eosinophils
- Fibrosis of trabeculae

In early infection, lymph node follicles are hyperplastic, while later, in chronic disease, the follicles are atrophic. These lymph node changes are so characteristic that the diagnosis of filariasis may be suggested confidently even though adult or larval worms are not identified. The most common site to find larval or adult nematodes is in prenodal afferent channels, in capsular lymphatics, or in subcapsular sinusoids. Necrotizing granulomas may be found around dead or dying nematodes and are composed of eosinophils and giant cells. Healing may occur with calcification and scarring around degenerating worm fragments.

Although the lymphatic pattern is well described, the pathogenesis of renal disease is only partially understood. Microfilariae have been seen in glomerular capillaries and when alive do not cause renal lesions. Chronic antigenemia or circulating immune complexes result in a membranoproliferative glomerulonephritis which can cause the acute nephrotic syndrome.

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