A genetic defect of granulocyte oxidative metabolism in a man with disseminated aspergillosis. J Lab Clin Med 1981 May;97(5):730-8
Date
05/01/1981Pubmed ID
6783713Scopus ID
2-s2.0-0019510817 (requires institutional sign-in at Scopus site) 13 CitationsAbstract
A 26-year-old man presented with progressive pneumonia, and Aspergillus was grown from cultures of lung, cutaneous nodules, and urine. His PMNs had a poor CL response after exposure to phagocytic stimuli (S. aureus, latex, aggregated IgG and IgG-coated latex) (p less than 0.01 vs. controls) and soluble stimuli (PMA, sodium fluoride, and Con A) (p less than 0.05). His PMNs failed to reduce NBT, oxidize 14C-1 glucose (p less than 0.001), or iodinate proteins (p less than 0.001), normally, compared with controls, and his PMNs killed Candida albicans and Staphylococcus aureus abnormally (p less than 0.05). The patient was anergic; his plasma inhibited responsiveness of his lymphocytes to stimulation with Aspergillus and Candida antigens. His lymphocytes failed to produce the lymphokine LMIF normally. The patient's 10-month-old daughter was demonstrated to have the same defects of PMN metabolism and function. The findings in this patient were similar to those in CGd, but transmission of the defect from father to daughter and the presence of lymphocyte abnormalities make this diagnosis unlikely. Inhalation of Aspergillus by patients with defective PMN oxidative metabolism may be associated with development of significant infection.
Author List
Chusid MJ, Sohnle PG, Fink JN, Shea MLAuthor
Peter G. Sohnle MS, MD Emeritus Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AdultAspergillosis, Allergic Bronchopulmonary
Aspergillus
Blood Bactericidal Activity
Candida albicans
Enterococcus faecalis
Granulocytes
Humans
Leukocyte Migration-Inhibitory Factors
Luminescent Measurements
Lymphocyte Activation
Male
Neutrophils
Nitroblue Tetrazolium
Phagocytosis
Staphylococcus aureus
