Chyluria: Another of the chronic filarial syndromes, Chyluria, is caused by the intermittent discharge of intestinal lymph (chyle) into the renal pelvis and subsequently into the urine. The mechanisms underlying this discharge have not been well defined, though the clinical course is known to be intermittent, sometimes remitting after treatment with DEC, sometimes after lymphangiography (owing to the scelerosing effects of the injected contrast material) or sometimes spontaneously. Nutritional compromise can, however, be severe in patients with chronic chyluria; special low-fat, high-protein diets supplemented with fluids that minimize the intake and subsequent loss of medium-chain triglycerides when possible can be helpful.

Non-invasive management of chyluria relies on nutritional support, especially substitution of foods fat-rich by high protein, high fluid diets supplemented where possible with medium- chain triglycerides. 'Correction' of the lymphatic defect can be effected through surgery, but even the sclerosing effects of lymphangiography or, often, time alone can lead to the cessation 

Tropical pulmonary eosinophilia: An acute filarial syndrome is tropical pulmonary eosinophilia, caused by an immunologic hyper-responsiveness to filarial infection. It is characterized by extremely high levels of peripheral blood eosinophilia, asthma-like symptoms, restrictive (and often obstructive) lung disease, very high levels of specific anti-filarial antibodies and an excellent therapeutic response to appropriate anti-filarial treatment (DEC). It occurs with a frequency of less than 1% of all filariasis cases, but it is a severe condition that can lead to chronic interstitial fibrosis and pulmonary failure.

Patients have extraordinarily high levels of total serum IgE (almost always in excess of 10,000ng/ml), and their levels of specific anti-filarial antibodies (both IgG and IgE) are extremely high, the absolute levels depending on the specific tests used. For other amicrofilaraemic syndromes serologic findings based on detecting IgG4 antibodies have proven helpful, since this subclass has greater diagnostic specificity and is stimulated by the presence of active infection. Such antibody analyses are also especially helpful in diagnosing the expatriate syndrome' where 'background (i.e., pre-exposure) levels' of IgG and especially IgG4 antibodies to filarial antigens will be very low, so that elevated levels have significant diagnostic implications in association with the clinical presentations.

Acute inflammatory reaction: The least commonly recognized form of acute inflammatory reaction is caused by filarial infection that is seen early after infection particularly in expatriates exposed to, and acquiring, the infection for the first time, as when military missions have been sent to filariasis-endemic areas. Lymphangitis occurs around developing larval and early adult stages in these individuals, and an extensive set of biopsies of such lesions has indicated clearly their acute, eosinophilic inflammatory nature and their association with the presence of immature filarial worms.

Expatriate Syndrome: Recently, a 'new' filarial syndrome has been described as one of clinical and immunologic hyper-responsiveness found in expatriate visitors to regions endemic for loiasis. This clinical syndrome is, of course, not new, nor is it limited to loiasis (tropical eye worm), as similar clinical descriptions of patients with onchocerciasis, lymphatic filariasis, and other filarial infections also have been recorded previously. Instead of developing the commonly described chronic clinical manifestations of their filarial infections, individuals who have grown up outside endemic regions and then moved to these regions and acquired a filarial infection manifest prominent signs and symptoms of inflammatory (including allergic) reactions to the mature or maturing parasites. In loiasis, these manifestations have included primarily Calabar swellings, hives, rashes and occasionally asthma; and in bancroftian filariasis (when military personnel or other migrants to endemic areas have acquired these infections), symptoms have usually been lymphangitis, lymphadenitis, genital pain (from inflammation of the associated lymphatics), along with hives, rashes and other 'allergic-like' manifestations, including blood eosinophilia. The reason for these different clinical presentations lies almost certainly in the different immunoregulatory responses to filarial antigens between those with long (including prenatal) exposure to these antigens and those meeting them for the first time.