Hodgkin's disease causing a reversible nephrotic syndrome by compression of the inferior vena cava.
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Biomedical subjects
Publications and source records attributed to W F Piessens.
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To determine the extent of lymphatic disease in persons infected with Wuchereria bancrofti who were microfilaraemic, we examined the superficial lymphatics of the legs by scintigraphy. In 4 endemic control subjects and in 10 of 14 clinically asymptomatic microfilaraemic individuals, lymphoscintigraphy revealed one major channel of lymphatic drainage in each leg. However, while trunk lymphatics were bilaterally symmetrical in the control, marked differences in the calibre of lymphatic vessels were observed in the microfilaraemic persons. Non-discrete lymphatics and a diffuse symmetrical distribution of collateral vessels in both legs were observed in all of 5 amicrofilaraemic patients with grade 2 lymphoedema. A similar diffuse drainage pattern was also seen in 3 previously microfilaraemic persons who had remained amicrofilaraemic and asymptomatic following treatment with diethylcarbamazine citrate (DEC). Thus, clearance of microfilaraemia by DEC therapy did not appear to reverse the type of lymphatic pathology observed in microfilaraemic subjects. The lymphoscintigraphy patterns did not correlate with serum levels of antibodies to 3 recombinant filarial antigens. Virtually all the asymptomatic microfilaraemic individuals infected with W. bancrofti examined had subclinical lymphatic disease detected by the non-invasive imaging technique of lymphoscintigraphy.
The value of the polymerase chain reaction (PCR) in the diagnosis of Wuchereria bancrofti infection was evaluated in comparison to microscopical examination of night blood smears, Nuclepore filtration, serology and ultrasonography. No correlation was found between PCR-based deoxyribonucleic acid (DNA) probing and serology. We did not find any evidence of free filarial DNA in either blood plasma or chylocoele fluid. We conclude that the 2 PCR-based techniques evaluated are not more sensitive than Nuclepore filtration for detection of W. bancrofti microfilaraemia, need at least 1 intact microfilaria in the volume of blood used for DNA extraction, and were much inferior to ultrasonography for detection of amicrofilaraemic adult worm carriers.
The ability of diethylcarbamazine (DEC) to kill adult Wuchereria bancrofti worms was evaluated by examining lymphatic nodules formed after treatment with 4 different treatment schedules of 193 males living in the endemic area of Greater Recife, Brazil. Lymphatic nodules appeared in the spermatic cord or upper extremities in 43 of 138 microfilaraemic individuals, in 3 of 30 amicrofilaraemic patients with filarial disease manifestations, and in 1 of 25 asymptomatic amicrofilaraemic residents of the endemic area treated with DEC. Fourteen of these nodules were surgically removed 10-150 d after the start of treatment. Regardless of the DEC dosage and schedule used, all nodules contained damaged and degenerating adult worms. An exuberant granulomatous process with large numbers of eosinophils and progressive fibrosis gradually developed around the dead parasites. The mechanism(s) by which DEC killed adult W. bancrofti could not be determined.
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Studies using conventional angiography or non-invasive scintigraphy have revealed widespread abnormalities in the lymphatics of the legs of patients with bancroftian filariasis, regardless of whether clinical lymphoedema is present. To determine if the observed changes were specific for filarial infections, we imaged the lymphatics of both legs in native residents of an area in Brazil where filariasis is not endemic. Study participants were matched by age, socioeconomic status and physical activities to patients with filariasis in Recife, evaluated in parallel. Based on textbook criteria, only one of 15 study participants had a completely normal lymphoscintigram. Modest to severe pathology of the leg lymphatics was observed in the remaining 14 residents of the non-endemic area and in 49 of 50 patients with bancroftian filariasis. These results indicated that factors other than filarial worms are a common cause of subclinical pathology of the leg lymphatics in north-eastern Brazil, and that the latter is not specific for bancroftian filariasis.
The natural history of lymphatic disease in human filariasis remains unclear, but recurrent episodes of acute lymphangitis are believed to constitute a major risk factor for the development of chronic lymphoedema and elephantiasis. Prospective analysis of 600 patients referred to the filariasis clinic of the Centro de Pesquisas Aggeu Magalhães/FIOCRUZ in Recife, Brazil, indicated that 2 distinct acute syndromes accompanied by lymphangitis occur in residents of this filariasis-endemic area. One syndrome, which we call acute filarial lymphangitis (AFL), is caused by the death of adult worms. It is relatively uncommon in untreated persons, usually is asymptomatic or has a mild clinical course, and rarely causes residual lymphoedema. The second syndrome, of acute dermatolymphangioadenitis (ADLA), is not caused by filarial worms per se, but probably results from secondary bacterial infections. ADLA is a common cause of chronic lymphoedema and elephantiasis in Recife as well as in other areas of Brazil where lymphatic filariasis is not present. The syndromes of AFL and ADLA can be readily distinguished from each other by simple clinical criteria.
Treatment with the antifilarial drug diethylcarbamazine (DEC) results in a rapid decline in the number of microfilariae circulating in the blood of infected hosts. DEC induces morphological changes in the surface layers of microfilariae, but these alterations alone are probably insufficient to cause the death of the parasite, because the drug fails to reduce microfilaraemia in animals lacking filarial antibodies, and also does not shorten the survival of microfilariae in vitro. The effect of DEC in vivo is thought to result from the trapping of microfilariae in the liver, where they undergo lysis.
The identification of Mycobacterium tuberculosis is a lengthy process. Attempts were made to develop a more rapid, specific, and sensitive assay for identifying tubercle bacilli in biologic specimens by differentially screening plasmid libraries of Sau3AI-digested M. tuberculosis H37Rv (ATCC 25618) DNA with homologous and heterologous DNA for clones that hybridized strongly with M. tuberculosis DNA alone. Three clones, pMTB1, pMTb2, and pMTb3, were selected for further study. Southern analysis indicated that these clones reacted strongly with DNA from strains of M. tuberculosis isolated in different parts of the world, weakly with DNA from other mycobacterial species, and not at all with Escherichia coli or human DNA. Smaller fragments of mycobacterial DNA contained in plasmid pMTb3 were subcloned into pBR322 (pMTb4) or pUC12 (pMTb5). These recombinant plasmids hybridized with DNA from M. tuberculosis, Mycobacterium bovis, and Mycobacterium bovis BCG (bacille Calmette-Guérin) Montreal and may provide the reagents needed for the development of new methods for rapid diagnosis of M. tuberculosis infections.
This paper serves to introduce some concepts of modern immunobiology that are relevant to the understanding of the complex interactions between mycobacteria and the infected host. Six topics are discussed: (1) the phenotypic markers and functions of human T lymphocyte subsets; (2) the nature of antigen receptors on T cells; (3) antigen processing and presentation; (4) adhesion molecules that facilitate cellular interactions; (5) surface molecules on phagocytes that promote the entry of pathogens into cells; and (6) compartmentalization of the immune system in vivo.