The two other filarial causes of lymphatic filariasis are Wuchereria bancrofti and Brugia timori, which both differ from B. malayi morphologically, symptomatically, and in geographical extent.

It is one of the tropical diseases targeted for elimination by the year 2020 by the World Health Organization, which has spurred vaccine and drug development, as well as new methods of vector control.

Abscess formation and ulceration of the affected lymph node occasionally occurs during B. malayi infection, more often than in Bancroftian filariasis.

Blockage of these vessels due to inflammatory induced fibrosis, dead worms, or granulomatous reactions can interfere with normal fluid balance, thus leading to swelling in the extremities.

[2][4] However, clinical manifestations of infection are variable and depend on several factors, including host immune system, infectious dose, and parasite strain differences.

Individuals living in endemic areas with microfilaremia may never present with overt symptoms, whereas in other cases, only a few worms can exacerbate a severe inflammatory response.

[citation needed] 8-1 The infective larvae (L3) migrate to the salivary glands, enter the proboscis and escape onto human skin when the mosquito takes another blood meal.

1-2 The infective larvae (L3) actively penetrate the skin through the bite hole and develop into adults in the lymphatic system over a span of 6 months.

[13] Thus those at greatest risk for infection are individuals living in endemic areas—short term tourists are unlikely to develop lymphatic filariasis.

[14] Tender or enlarged inguinal lymph nodes or swelling in the extremities can alert physicians or public health officials to infection.

[citation needed] PCR based assays are highly sensitive and can be used to monitor infections both in humans and the mosquito vectors.

[18] Successful methods of B. malayi vector control include residual house spraying using DDT and insecticide treated bednets.

While chemical larvicides have only provided partial control, plant removal could prevent vector development, but also potential adverse effects on the aquatic environment.

[19] The Global Alliance to Eliminate Lymphatic Filariasis was launched by the World Health Organization in 2000 with two primary goals: 1) to interrupt transmission and 2) to alleviate the suffering of affected individuals.

Mass drug treatment programs are the main strategy for interrupting parasite transmission, and morbidity management, focusing on hygiene, improves the quality of life of infected individuals.

[2] Microfilariae numbers slowly return many months after treatment, thus requiring multiple drug doses over time in order to achieve long-term control.

[21] Single doses of two drugs (albendazole-diethylcarbamazine and albendazole-ivermectin) have been shown to remove 99% of microfilariae for a year after treatment and help to improve elephantiasis during early stages of the disease.

[2][22] Since the discovery of the importance of Wolbachia bacteria in the life cycle of B. malayi and other nematodes, novel drug efforts have targeted the endobacterium.

Rigorous hygiene practices, including washing with soap and water daily and disinfecting wounds can help heal infected surfaces, and slow and potentially reverse existing tissue damage.

[24] This involves mass drug administration (MDA), where entire at-risk populations are treated annually with safe medicine combinations.

[25] B. malayi infects 13 million people in south and southeast Asia and is responsible for nearly 10% of the world's total cases of lymphatic filariasis.

[2] Regional foci of endemicity are determined in part by the mosquito vectors [citation needed] B. malayi was discovered in 1927 by the Dutch parasitologist Steffen Lambert Brug (1879–1946) (who is commonly known in the scientific literature as S.L.

But the new species of human filaria in North Sumatra was both physiologically and morphologically distinct from the W. bancrofti microfilariae commonly found in Jakarta.

[12] In 1957, two subspecies of human infecting B. malayi were discovered by Turner and Edeson in Malaysia based on the observation of different patterns of microfilaria periodicity.

These two free-living nematodes were incorporated in the study and were important for several reasons:[citation needed] Sequence comparisons between the two genomes allow for mapping of C. elegans orthologs to B. malayi genes.

The drugs often must be taken periodically for years, and the worms can cause a massive immune reaction when they die and releases foreign molecules in the body.

From the genome sequence, several metabolic pathways have been identified, containing dozens of gene products that may be helpful in the discovery of more targeted and effective drug therapies.

It is likely that the mechanism of doxycycline is similar to that in other filarial species, i.e., a predominant blockade of embryogenesis, leading to a decline of microfilariae according to their half-life.

According to Alan L. Scott, Ph.D., a collaborator at Johns Hopkins University, understanding how a particular parasite, such as B. malayi, can adapt to humans, may yield medical benefits far beyond treating elephantiasis.

[citation needed] According to the Filarial Genome Project being done by The Special Programme for Research and Training in Tropical Diseases, the Brugia malayi MIF gene is expressed in all life-cycle stages of the parasite, and results suggest that B. malayi MIF may interact with the human immune system during the course of infection by altering the function of macrophages in the infected individual.