Inhibition of Nocardia asteroides by neutrophils

Neutrophils are found in lesions of Nocardia asteroides infection, but neutrophils kill few nocardiae in vitro. For determination of neutrophil inhibition of nocardiae, neutrophils and nocardiae were incubated together. Filament formation and amino acid uptake by nocardiae were inhibited for 7.5 hr. Thereafter, nocardiae extended long filaments from within neutrophils to the outside and increased their rate of amino acid uptake. Addition of freshly isolated neutrophils at 7.5 hr of incubation prolonged the inhibition. Electron micrographs revealed that neutrophils phagocytosed nocardiae but that most nocardiae did not appear damaged. Formalin and 2-deoxy-D-glucose abrogated the inhibition by neutrophils. Lysozyme and granule-cationic proteins inhibited amino acid uptake under some conditions. Lactoferrin and lactic acid had no effect, and the oxidative metabolic burst was not required. These findings and clinical observations suggest that inhibition of N. asteroides by neutrophils may be important in vivo.     

Resistance of Nocardia asteroides to oxygen-dependent killing by neutrophils

Nocardia asteroides resists killing by neutrophils despite the occurrence of the oxidative metabolic burst when the organism is phagocytosed. In a study of the apparent resistance of N asteroides to oxygen-dependent killing by neutrophils, this organism and (for comparison) Staphylococcus aureus were exposed to metabolites of the oxidative metabolic burst. N asteroides was more resistant than S aureus to H2O2, hydroxyl radical, and singlet oxygen and to the combination of H2O2, lactoperoxidase, and iodide. The rate of iodination of N asteroides by neutrophils or by the combination of lactoperoxidase and H2O2 was significantly lower than that of S aureus. Lysates of N asteroides had 2.8 times more catalase than lysates of S aureus, but levels of superoxide dismutase were similar in the two lysates. A reduction in the level of catalase activity of N asteroides with aminotriazole or azide resulted in a modest decrease in resistance to oxidative metabolites. Thus, the relative resistance of N asteroides to killing appeared to be due partially but not completely to its relatively high level of catalase activity.     

Acidification of phagosomes in murine macrophages: blockage by Nocardia asteroides

Most strains of Nocardia asteroides are susceptible to the detrimental effects of pH 5 when grown in buffered brain-heart infusion broth. Preventing phagosomal acidification may be a mechanism by which this organism survives the microbicidal activity of macrophages. Fluorescein isothiocyanate was conjugated to the surface of Nocardia and Saccharomyces to form pH-sensitive fluorescent probes. The fluorescent emission, and thus the pH, of this probe was quantitated within individual phagosomes by using a computerized cytospectrophotometer. When either live or dead cells of virulent N. asteroides strain GUH-2 were ingested, the phagosomal pH remained above pH 7 for 2 hr. A nonpathogenic soil isolate, N. asteroides strain 19247, only partially blocked acidification. In contrast, when Saccharomyces was used as a control for normal response, the pH decreased to approximately pH 5. Therefore, virulent N. asteroides blocks phagosomal acidification. Because killed Nocardia act in the same manner, this inhibition of acidification appears to be associated with cellular components. This capacity to prevent phagosomal acidification may be prerequisite to the survival of intracellular pathogens.     

Nocardia asteroides pericarditis in association with HIV

This case report describes Nocardia pericarditis in a newly diagnosed human immunodeficiency virus (HIV) patient as an initial manifestation. Previously, two cases of Nocardia pericarditis were reported in patients with established HIV infection. To our knowledge this is the first case of Nocardia pericarditis as an initial manifestation of HIV infection. This case substantiates and emphasizes the importance of identifying Nocardia as an infectious cause of pericarditis in patients with acquired immunodeficiency. Long-term survival may be achieved with a combined medical and surgical approach.     

First report of submandibular and parotid abscess due to Nocardia asteroides

Herein, we are presenting a first case report where multiple salivary glands abscesses were diagnosed to be due to N.asteroides. Minor trauma of buccal mucosa, due to cleansing of teeth unhygienically, was most probable mode of infection. It was managed successfully by surgical drainage and post surgical co-trimoxazole therapy.     

Bronchiolitis obliterans and Nocardia asteroides infection of the lung

This report describes a patient with right lower lung (RLL) pneumonia of a subacute nature. Sputum and bronchial washings both grew N asteroides. Open lung biopsy showed bronchiolitis obliterans. Both the clinical and radiologic picture dramatically improved during three weeks of treatment with trimethoprim and sulfamethoxazole (TMP - SMX), indicating the possibility that N asteroides infection contributed to bronchiolitis obliterans pneumonia in this patient.     

Lung infection caused by Nocardia asteroides in a renal-transplant patient

A 65-yr-old man developed an acute lung infection while being treated for a rejection episode 2 months after renal transplantation. A chest X-ray revealed a pulmonary infiltrate. Nocardia asteroides was cultured from a percutaneous lung aspirate. The patient was successfully treated with trimethoprim/sulfamethoxazole.     

Failure of trimethoprim/sulfamethoxazole in invasive Nocardia asteroides infection.

A case of pulmonary nocardiosis occurred with progressive involvement of the pleura, pericardium, mediastinum, and sternum. Surgical resection and drainage procedures followed by administration of the drug combination, trimethoprim/sulfamethoxazole, over a six-month period led to clinical recovery. Discontinuation of drug therapy, however, was followed by relapse and further invasion by the same organism. A literature survey of Nocardia asteroides infections treated with trimethoprim/sulfamethoxazole disclosed that posttreatment follow-up is often too brief or unknown, making the ultimate success of therapy uncertain.