A 44-year-old Indian housewife presented with prolonged cough, intermittent fever, loss of weight and shortness of breath on exertion. Physical examination revealed a thin lady with fine crackles on both lungs. Marked eosinophilia and elevated erythrocyte sedimentation rate were noted on peripheral blood. Chest radiograph showed characteristic bilateral infiltrates affecting the periphery of both lungs. Treatment with corticosteroid resulted in dramatic improvement in symptoms, signs and radiographic changes within a few days.
Tropical pulmonary eosinophilia (TPE) is considered to be a variant of human filarial infection. The pulmonary manifestations of TPE have been well described. Extra-pulmonary features of the disease, although not commonly seen, have been reported previously. A 9-year-old Malay girl with a history of recurrent cough and wheezing was admitted because of cardiac failure. Physical examination revealed a very sick girl with tachypnoea, central cyanosis, finger clubbing, elevated jugular venous pulse, generalized crackles and rhonchi in the chest, a loud second heart sound and hepatosplenomegaly. A chest radiograph showed cardiomegaly and right pleural effusion. Laboratory investigations revealed hypochromic, microcytic anaemia with persistent blood eosinophilia (absolute eosinophil counts varied from 1.9 to 5.5 x 10(9)/1). The ELISA test for antifilarial IgG antibodies was strongly positive. She responded promptly to treatment with diethylcarbamazine. In summary, this is a patient with TPE who presented with cor pulmonale, probably due to late-stage interstitial pulmonary fibrosis. In order to prevent the long term morbidity of cardiorespiratory disability, the early signs of TPE should be recognized and the infection treated.
Quantitation of serum immunoglobulin M, G, A, D and E levels was carried out in Malaysians with Brugia malayi infections. Results showed highly elevated levels of IgM and IgE as well as moderately elevated levels of IgG. These were most significant in patients with tropical pulmonary eosinophilia or elephantiasis. Serum IgE levels were extremely high in microfilaraemic patients (6,060 +/- 3,958 IU ml) probably due to a constant antigenic stimulation by dead and dying microfilariae.
Brugia malayi and Wuchereria bancrofti infections cause lymphatic filariasis in Malaysia. About 2.5 million people live in endemic areas of filariasis, of whom 5% have microfilaraemia and probably twice as many are infected. There is a wide clinical spectrum of response to the infection. While some have asymptomatic microfilaraemia, others have episodic attacks of fever, lymphadenitis, retrograde lymphangitis and lymphoedema. Elephantiasis is a late complication. Tropical pulmonary eosinophilia and other forms of occult filariasis are due to hyper allergic reactions to microfilarial antigens. Parasitological and serological tests aid in confirming the clinical diagnosis. The drug of choice is diethylcarbamazine citrate.
Developing and adult worms of the human lymphatic filarial parasites (Wuchereria bancrofti,
Brugia malayi, and Brugia timori) are located mainly in the lymphatic system and occasionally in aberrant sites like subcutaneous and conjunctival cysts. Lymphatic
pathology ranging from dilatation of lymphatic channels and lymphangiectasia are detected on ultrasonography in apparently healthy, amicrofilaraemic, but filarial antigen positive individuals in endemic areas. Microfilariae are distributed in various organs and may be associated with immune mediated pathology at these sites; tropical pulmonary eosinophilia is characterized by intense immune mediated destruction of microfilariae in the lung parenchyma. In the spleen and other sites, nodular granulomatous lesions can occur where microfilariae are trapped and destroyed. The finding of Wolbachia endosymbionts in all stages of lymphatic filarial parasites has provided new insight on the adverse reactions
associated with anti-filarial chemotherapy. Inflammatory molecules mainly lipopolysaccharide (LPS)-like molecules released from endosymbionts on death of the
parasites are largely responsible for the adverse reactions encountered during anti-filarial chemotherapy. Prenatal tolerance or sensitization to parasite derived molecules can immune-modulate and contribute to both pathology and susceptibility/resistance to infection. Pathological responses thus depend not only on exposure to filarial antigens/infection, but also on host-parasiteendosymbiont factors and to intervention with antifilarial treatment. Treatment induced or host mediated death of parasites are associated with various grades of inflammatory response, in which eosinophils and LPS from endosymbionts play prominent roles, leading to death of the parasite, granulomatous formation, organization and fibrosis. The non-human primate (Presbytis spp.) model of
Brugia malayi developed for the tertiary screening of anti-filarial compounds has provided unique opportunities for the longitudinal study of the pathology associated with lymphatic filariasis. The pathology in this non-human primate model closely follows that seen in
human lymphatic filarial infections and correlates with clinical evidence of lymphatic pathology as detected with ultrasonography. These studies also show that successful treatment as detected by loss of motility and calcification of worms on ultrasonography is associated with reversal of early dilatations of lymphatic channels.