Nocardial Cerebral Abscess Associated with Mycetoma, Pneumonia, and Membranoproliferative Glomerulonephritis

Abstract

Nocardial brain abscesses remain a clinical challenge. We successfully treated a patient with nocardial brain abscess, mycetoma, pneumonia, and glomerulonephritis. Nocardial soft tissue involvement, mycetoma, is well known. However, the fact that actinomycetoma can metastasize may not be as well appreciated. The association between nocardiosis and glomerulonephritis should be better clarified. CASE REPORTA 49-year-old male, a businessman, was admitted to our hospital with complaints of severe edema of the lower extremities. Clinically, the diagnosis was nephrotic syndrome. Light microscopy of a renal biopsy showed fibrosis with mesangial hypercellularity and tubular atrophy. Immunofluorescence staining revealed deposition of immunoglobulin G and C 3 at the glomeruli, basal membranes, and mesangia. The diagnosis of a membranoproliferative glomerulonephritis was established, and the patient received oral treatment with prednisolone at 60 mg/kg per day. Because of persistent proteinuria, he underwent monthly intravenous pulse cyclophosphamide therapy. When the patient was hospitalized for his third course of cyclophosphamide therapy 9 months later, he was febrile, and physical examination revealed a tender mass in the anterolateral region of the left thigh. Laboratory findings revealed the following: white blood cell count, 13,360/mm 3 (normal range, 4 ϫ 10 9 to 10 ϫ 10 9 /liter); hemoglobin, 10.4 g/dl (normal range, 11 to 16 g/dl); hematocrit, 32.1% (normal range, 37 to 50%); erythrocyte sedimentation rate, 63 mm/h (normal range, Ͻ25 mm/h); cyclic AMP receptor protein, 16.2 mg/dl (normal range, Ͻ0.8 mg/dl); urea, 35 mg/dl (normal range, 10 to 50 mg/dl); creatinine, 0.8 mg/dl (normal range, 0.7 to 1.2 mg/dl); aspartate aminotransferase, 68 U/liter (normal range, 14 to 36 U/liter); and alanine aminotransferase, 116/liter (normal range, 9 to 52 U/liter). There was 5 g/day of proteinuria. Magnetic resonance imaging of the left lower extremity showed a mass lesion within the vastus lateralis muscle (Fig. 1). The mass had cystic characteristics and was multiloculated. The microbiological diagnosis was made from the aspirated pus of the mass lesion in the left lower extremity. The specimens, cultured on sheep blood agar, brain-heart infusion agar, and Sabouraud dextrose agar plates, were incubated at 37°C in the presence of 10% CO 2 plus air. Direct microscopic examination of aspirated Gram-stained pus showed gram-positive cocci, gram-positive filamentous branching bacilli, and polymorphonuclear neutrophils. The smear was stained with modified acid fast. After a 24-h incubation, typical smooth, yellow-pigmented, hemolyzed colonies were tested with the catalase, oxidase, coagulase, and ID 32 Staph tests (bioMérieux, Nutingen, Germany) and oxacillin on Mueller-Hinton agar. Methicillin-sensitive Staphylococcus aureus was identified. After 3 days of incubation, typical dry, chalky, dull, tough colonies appeared on the media. All species were gram-positive branching bacilli. These bacilli were identified as Nocardia species. ...

Membranoproliferative Glomerulonephritis — A New Look at an Old Entity

“…[14][15][16][17][18] Bacteria associated with MPGN include staphylococcus, Mycobacterium tuberculosis, streptococci, Pro-pionibacterium acnes, Mycoplasma pneumoniae, brucella, Coxiella burnetii, nocardia, and meningococcus. [19][20][21][22][23][24][25][26][27][28][29][30]…”

Soil-acquired cutaneous nocardiosis on the forearm of a healthy male contracted in a swamp in rural eastern Virginia

“…The drained pus contains white or yellowish granules which are actually microcolonies of the infecting organism surrounded by masses of inflammatory cells. Mycetomas are almost always painless and there are few or no constitutional symptoms 35,36. Most cases of mycetoma are found in tropical and subtropical regions.…”

Membranoproliferative glomerulonephritis complicatingPropionibacterium acnesinfection

“…There is paucity of data, but some cases of suspected primary MPGN may later prove to be secondary to low-grade infections. However, it is often difficult to know whether subclinical low-grade infections lead to the subsequent glomerulonephritis or whether infection is secondary to prolonged immunosuppressive medication due to glomerulonephritis [16]. …”