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Report on a boy, now 3 years old, who presented the typical clinical picture of a BCG generalization during infancy. The BCG agents were verified in the lymph node. Intensive tuberculostatic therapy in combination with the transfer factor failed. The negative NBT test revealed a progressive septic granulomatosis.
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Chronic granulomatous disease, in which abnormal susceptibility to infection is caused by an inherited defect in phagocytic cells, has been diagnosed in three brothers. Two brothers had repeated bacterial infections of the skin, superficial lymph nodes and lungs from infancy and died aged 27 months and 13 months. Characteristic suppurating granulomata were found in many organs. The diagnosis was established in both during life, and in the third asymptomatic brother shortly after birth, by studies of phagocytic function which included tests for nitroblue-tetrazolium reduction, hexose monophosphate shunt activity and bactericidal capacity. Their mother and a maternal aunt, both Maoris with no known Caucasian ancestry, were identified as carriers of the presumed sex-linked recessive gene. The clinical features of the disease and the laboratory methods for diagnosis are described.
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The present investigation has compared the influences of phorbol myristate acetate (PMA) and heat-killed bacteria (HKB) on oxygen consumption and glucose oxidation by polymorphonuclear leukocytes (PMN) from carriers of sex-linked chronic granulomatous disease (CGD). PMA or HKB caused neutrophils from CGD carriers, considered as a group, to consume oxygen and oxidize glucose-1-14C at rates that were statistically distinguishable from rates of normal controls and affected CGD hemizygotes. PMA at a final concentration of 1.0 micrograms per milliliter wass more effective and reproducible than a ratio of 50 HKB: 1 PMN in discriminating the partial abnormality of carrier PMN from normal PMN. Moreover, a deficiency in glucose oxidation by the PMN of one individual carrier was detectable using PMA stimulation when no defect was apparent with HKB. Results of the present investigation confirm and extend previous observations which have demonstrated the similarity in responses of PMA-treated normal and CGD PMN to the reactions produced by particulates under similar conditions.
Several little-emphasized manifestations of familial chronic granulomatous disease are considered: destructive chorioretinal lesions may be as constant as the pigmented histiocytosis seen in reticuloendothelial organs and could be related to a defect in the phagocytic activity of the retinal pigment epithelium; pigmented histiocytes with the staining characteristics of sea-blue histiocytes may be present in the bone marrow; patients may present with lesions resembling eosinophilic granuloma. Also discussed are some observations related to the sequestration of bacteria within phagocytic cells and the use of continuous antimicrobial therapy.
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A brief clinical and a rather detailed histological decription is given of three male siblings suffering from chronic granulomatosis. Two types of granulomas were indentified. One of them occurring extrapulmonally resembled the specific tuberculous granuloma with caseation, but tuberculous bacilli not demonstrated. The other type of granuloma was found in the lungs and was composed of a leucocytic core surrounded by an epithelioid cellular rim containing giant cells. In all the three cases such granulomas were shown to contain mould filaments of the aspergillus type.
Stress substantially modulates the mononuclear phagocytic system (its center and periphery), the time of changes in granuloma formation in animals infected with BCG vaccine. This determines the specific features of development of vaccine-induced granulomatous inflammation as a reflection of changes in the host's resistance system and possibly mycobacteria. An additional influence (to Mycobacteria tuberculosis) of stresses during 30 days enhances destructive processes in the hepatic parenchyma.
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