 is the characteristic sheath microplarium found in the circulating blood in cases of filiriants. Gravid female worms release these microplaries in the lymphatics. Adult male and female worms causing this disease live in the lymph nodes, lymphatic vessels and their walls. These microplaries, the embryonic stage of the organism, eventually find their way to the circulatory system. When found by blood examination, a diagnosis of filariasis can be made. When a suitable mosquito feeds on a person with circulating microplaries, these embryos are taken up with the blood meal and enter the stomach of the mosquito. The microplary sheds their sheath, penetrates the stomach wall, and migrates to the thoracic muscle of the mosquito, where they develop through three stages to the infected stage. The embryo becomes immoral, shortens, and thickens as the first stage is produced. The internal organs gradually develop, and after a few days the outer cuticle separates. The developing juvenile worm becomes slightly motile as it reaches the second stage. This juvenile continues to grow and molds again to reach the third stage. The third stage then breaks out of the thoracic muscle and begins its migration through the body cavity to the mouth parts of the mosquito. The juvenile in the third stage continues to grow and shortly becomes infective for man. Parasite development in the mosquito takes from eight to 20 days, depending on temperature, humidity, and the species of mosquito. When the mosquito feeds, the infective parasites escape from the labium and enter the new host through the opening made by the mosquito, or through small breaks in the skin. In this more highly magnified view of the labium, infective juveniles can be seen escaping. The course of the disease depends on the number of parasites present and their location within the host. Those that locate in the enginal region may lead to elephantiasis of the scrotum, or of the extremities. In some cases, both. More than 10 percent of those infected will eventually develop the gross abnormalities associated with chronic pyloriases. Two species of pilarioid parasites, wukararia bancrofti, and brugia melei cause pyloriases in man. Pyloriases occurs throughout many of the tropical and sub-tropical parts of the world. Wukararia bancrofti, the most common species causing pyloriases, has two forms. The nocturnal periodic form, in which microphillary are present in the blood in highest concentration at night, and the sub-pyriotic form, in which microphillary are present throughout the day and night, with only a slight rise and fall in numbers in the peripheral blood. The reasons for this variation are not understood. The periodic, or classic form, has the broadest distribution, although endemic localities are often small and separated from each other. In the western hemisphere, pyloriases occurs in the West Indies, El Salvador, Panama, and across the northern coast of South America. In Brazil, the prevalence is high at the mouth of the Amazon. Numerous pockets are found through the Amazon basin. It occurs also in separated foci along the eastern coast, to the southern tip of Brazil. In Europe, it occurs only in southern Spain. In Africa, it is found in Egypt, in several areas across North Africa, and along the West Coast. It extends across tropical Africa to the Republic of Malagasy. In the Middle East, pyloriases has been found in Turkey, Lebanon, Israel, and Saudi Arabia, mostly in immigrants. In Asia, Wukararia-Bancrofty is present in South Korea, Japan, Formosa, Eastern China, Vietnam, Cambodia, the Philippines, Thailand, Malaya, Indonesia, and New Guinea. It occurs also in Burma, Ceylon, and India. The sub-periodic form is limited to an area south of a line between the Gilbert and Ellis Island, and east of the 170-degree line of longitude. Below the 20-degree line of latitude, the line turns westward to include New Caledonia and the Royalty Islands. Rugea-Malayai is limited to Asia. It has been found in the Japanese islands south of Tokyo, in southern Korea, eastern China, Vietnam. The island of the East Coast, Vietnam. The island of Palawan in the Philippines, the Celebes, and adjacent islands west of New Guinea, Indonesia, Malaysia, southern Thailand, and India. Pyloriases in India due to Wukararia-Bancrofty is widely distributed. Pyloriases due to Brugea-Malayai also occurs, and in some localities its occurrence overlaps that of Wukararia-Bancrofty. Calcutta is one focal point for research on Pyloriases in India. Here in the School of Tropical Medicine and in the Hospital for Tropical Diseases, the patients, doctors, and researchers combine to provide a large body of knowledge for the diagnosis, treatment, and prevention of Pyloriases. The raw material for this research can be found throughout the country. Ponds, streams, irrigation ditches, and drainage canals all provide an available source of water where female mosquitoes can lay their eggs. Mosquitoes of the genera-culex and anopheles transmitting the periodic form of the disease live in association with man's habitation. The adult mosquitoes rest during the day in houses, barns, and shelters of various types. Mosquito larvae can be readily collected in the immediate vicinity. The transmission of the periodic form of Pyloriases usually occurs in areas where people are concentrated, such as villages and towns. Infection usually occurs within buildings and at night. Surface water plants such as water hyacinth and pistia offer a source of oxygen for mosquitoes of the genus Mansonia. Adults of this genus act as the intermediate host for the brugia meleae. The Mansonia involved are nocturnal, wild species that will feed during the day in deep shade. Occasionally, mosquitoes enter houses to feed, but seldom rest there during the daylight hours. Infection with brugia meleae is essentially a disease of rural areas, probably because of the habits of the mosquitoes involved in transmission and involvement of animal reservoirs. In order to determine medical problems in India, survey teams are sent into rural areas. There, teams conduct a village census, perform physical examinations, and specific clinical laboratory tests on the villagers. In many areas of India, Pyloriases is one of the major disease problems. Continuous infection leading to chronic Pyloriases and the resulting physical abnormalities interferes with the economic and social life of a community. The clinical manifestations of Pyloriases are not specific, but require differential diagnosis. In the periodic form of Pyloriases, blood samples must be taken at night to detect early cases with circulating micropholaries. Specimens collected in the rural areas are returned to central laboratories. For example, teams from the School of Tropical Medicine in Calcutta return specimens to the laboratory. Here, mosquitoes collected in the field are dissected and infection is often found in female mosquitoes, collected in highly endemic areas, and micropholarie are frequently observed in blood samples from asymptomatic patients. With the bite of the mosquito, the third stage infective parasites escape from the proboscis and enter the tissues of the host. Most of these juveniles die within the first few days after infection. By the end of 72 to 96 hours, only about 20% remain. The worms seek the lymphatics, where they have a better opportunity for survival. Probably another 10% die during the next six to eight weeks. Developing parasites reach maturity in approximately three months. Copulation then occurs between male and female worms, and the female begins extruding micropholarie five months or more after the initial infection. The number of circulating micropholarie rises with their continued extrusion by the female worm. Between five and 10% of the worms invading the host become gravid females, producing micropholarie. Females may continue to produce micropholarie for up to three years. After the death of the adult female parasite, the micropholarie may live as long as six months. Antibodies are continually being produced against the micropholarie that die. Repeated exposure to infective mosquitoes in endemic areas results in superinfection, with the continual repetition of this sequence of events. Clinical symptoms are usually associated with repeated exposure superimposed on an existing infection in a sensitized individual. The serious pathologic effects of human filariasis are associated primarily with the blockage and destruction of the lymphatics. After infection, the worms migrate through the tissues and eventually come to rest in the lymphatics and their walls. During the growth and development of the parasite, histologic changes occurring in the lymph nodes are limited to the formation of a thin fibrous capsule surrounding the worm. The parasite itself is not affected, and few inflammatory cells are present. In cases where parasites live for long periods at a particular site, the fibrotic capsule becomes greatly enlarged, possibly as a result of host reactions to excretions and secretions from the worm, and micropholarie that die in the surrounding tissues. These parasites and their products cause the formation of this small painless nodule associated with the right testis. In cases where worms die soon after reaching maturity, there is a marked inflammatory reaction in the associated tissues, characterized by neutrophils, giant cells, and frequently eosinophils. As the reaction continues, the entire area within the fibrotic capsule becomes involved, including the parasite itself. The lymphangitis becomes chronic, soluble substances seep into the surrounding tissues, and the inflammatory reaction is expanded. The parasite itself is slowly digested by the phagocytic cells. In some lymphatic vessels, parasites become calcified and surrounded by a thick fibrotic capsule. The chronic reaction continues until all of the material originating from the parasite has been removed from the tissue. If the process of inflammation is repeated, the lymphatic vessels become tortuous, fibrotic, and finally fail to function. The chronic signs of filariasis then gradually become evident. During this late chronic stage of the disease, micropholarie are rarely seen in the blood. Gravid female worms produce micropholarie that are released in the tissue and eventually find their way into the blood circulatory system. In many cases of filariasis, micropholarie circulate in the blood without producing any pathologic effect. The earliest symptoms observed are allergic manifestations, probably in response to soluble products of dying and degenerating immature parasites, metabolic products of the growing worm, or dead micropholarie after a prior sensitization of the patient. In Calcutta, at the hospital for tropical diseases, clinics have been set up especially for patients with filariasis. Because of the nature of the disease, clinics for men and women are arranged on separate days. Among these patients are cases varying from the earliest clinical manifestation to the more chronic cases of lymphadenopathy, lymphedema, and elephantiasis. New patients suspected of having filariasis are held at the clinic until late evening when circulating micropholarie are more likely to be found in the blood. The first signs and symptoms are either unilateral or bilateral lymphadenopathy or lymphagitis with tender lumps and red streaks in the lymphatics, usually running from a lesion down the extremities. In this particular case, streaking runs from the thigh to the upper surface of the foot. Recurrent attacks of lymphagitis result in endothelial proliferation and inflammatory thickening of the lymphatic vessels. In rare instances, adult parasites come to rest in the superficial lymphatics. In this case, swelling produced pressure on the ulnar nerve. The resulting pain prevented full extension of the arm. Lymphadenopathy alone may be observed in some cases. This may be accompanied by numbness and weakness in the arms and legs, especially at night after physical exertion. Repeated attacks of transient lymphagitis and lymphadenitis last from three days to two weeks, which relapses every few weeks. Lymphadenopathy is extremely painful and is usually the first symptom to bring patients to the physician. Normal lymph flow takes place through delicate vessels which drain into major lymphatic networks. Finally, to reach thoracic ducts. And then into the blood circulatory system. Lymphedema begins when blockage of the lymphatics is sufficient to cause lymphstasis. This patient has early lymphedema of the right arm and the left leg. Not only is the normal lymph flow prevented, but continual lymphedema causes inflammation and proliferation of fibrotic connected tissues. In some cases, the upper extremities are involved. And lymphedema of the hands and arms appears. Initially, this lymphedema is pitting, but as progressive proliferation of the connected tissues continues, it eventually becomes non-pitting. When the iliac lymph nodes of the enginal region are blocked, as shown in this lymphogram, severe lymphedema of the lower extremities occurs. This may be unilateral or bilateral. Upper extremities as well may be involved in the same patient. Long-standing cases of lymphadenitis, lymphangitis, and lymphedema result in the late grotesque stages of elephantiasis. In patients infected with Brugge MLAI, as in this nine-year-old girl, elephantiasis rarely occurs above the knee. Both legs are involved with the left leg showing typical elephantoid skin. In patients with elephantiasis, even minor injury may result in severe scarring and chiloate formation. This results from poor circulation in the elephantoid limb. The blocking of the superficial iliac lymphatics results in accumulation of the lymph in the scrotal sac or labia and eventually causes elephantiasis. In females, elephantiasis of the labia is frequent, often with the formation of vesicles. In males, lymphedema of the penis and or scrotal sac occurs. In long-standing cases with accumulated lymphedema, elephantiasis of the penis results. The scrotal sac and contents become thickened. Removal of lymph nodes in the inguinal region may result in distortion of the penis and the scrotum and occasionally produces adenol lymphoceles. In this case, they are bilateral. Long-standing lymphedema frequently involves the scrotal sac and the spermatic cord and gradually produces elephantiasis. Secondary infection of the superficial tissues also may accompany this condition. In some cases, lymphangiovarices develop with the formation of vesicles. In older cases, vesicles may be very pronounced. Two types of inguinal involvement may occur, elephantiasis and hydrosil. Thickening of the scrotal sac and its contents has result of long-standing lymph accumulation and low-grade inflammation of the tissues leads to elephantiasis. Elephantiasis may be the end result of scrotal involvement. In this case, the affected part becomes enormously enlarged, representing a solid tumor-like mass. Hydrosil, on the other hand, is a more acute process related to the obstruction of lymphatics as a result of which free fluid and not lymph, per se, collects within the space around the testes. This patient presented with painful bilateral scrotal masses involving each hemiscrotal. In such cases as these, surgical correction is indicated. The procedure is relatively simple and generally leads to permanent relief. Not only does the operation lead to an improvement in physical status, it affects also the patient's psyche since the enlarged scrotum has unfavorable social implications. The fluid usually removed from the hydrosil is clear and straw-colored, although sometimes vessels rupture within the hydrosil and the fluid is bloody. In this case, rupture of the vessels probably occurred during operation. Sometimes removal of hydrosil fluid by syringe is practiced. This procedure should be avoided since it often leads to secondary infection and it may also result in the puncture of a herniated bowel. In any event, it offers only temporary relief. Some cases present with elephantiasis of the limbs and scrotal sac along with hydrosil. As blockage of the lymphatics increases, total obliteration of the lymphatic vessels may occur. In these late stages of filariasis, microfilaree are rarely seen in the blood and diagnosis must be made on a clinical basis. Individuals may become infected when the third stage juveniles migrate from the labium of the mosquito into the tissues of the host at the time the infective mosquito feeds. The surviving parasites eventually reach the lymphatics, generally coming to rest in the capsule of lymph nodes. Here, they grow to maturity and copulate. Shortly after copulation, females become grabbing and begin extruding microfilaree into the lymph spaces. These microfilaree eventually reach the circulatory system. The clinical disease is usually initiated with the death of the immature or adult parasites. Individuals become hypersensitive with continued exposure. Lymphangitis and lymphatiditis are followed by lymphedema. Continuous exposure to the toxic products of dying worms may eventually result in elephantiasis. This is a disease for which there are no satisfactory control measures, no effective prophylactic drugs, and no chemotherapeutic agents to eliminate the parasites and affect the cure. Continued and expanded research is necessary to achieve control of the infection in man. This may be accomplished through specific therapy for individuals having filariasis, effective diagnosis of the disease in the early stages before irreversible changes have occurred, and prevention of the disease through effective control of the vector.