In July of 2015, a 63-year-old man with 9-month history of nephrotic syndrome was admitted to Shanghai Sixth People's Hospital because of multiple subcutaneous abscesses with intermittent fever for 20 days. Twenty days prior to admission, 2 subcutaneous abscesses presented on his left lower limb.
The subcutaneous abscesses then sequentially spread from the primary infection to the right dorsal hand, the chest wall, the abdominal wall, the left elbow, and the right lower limb. The abscesses appeared as firm and nonfluctuant masses initially, then they gradually grew up and manifested as tender, fluctuant, and erythematous nodules. They were 0.5 to 5 cm in diameter. Some abscesses ruptured and oozed yellow pus. The patient also developed intermittent chills and fever up to 39.7 C. The patient had been admitted to another hospital 15 days before. He was empirically treated with levofloxacin, ceftriaxone, metronidazole, and surgical drainage there. After half a month with no improvement, he was transferred to our hospital.
Medical history: The patient was diagnosed with nephrotic syndrome 9 months ago, and mesangial proliferative glomerulonephritis was confirmed by renal biopsy. He was initially treated with oral methylprednisolone (48 mg/d) and got a remission. Subsequently, his renal disease was stable with a creatinine clearance of 104 mL/min and minimal proteinuria (220 mg/24 h) under low-dose methylprednisolone (8 mg/d). He had developed diabetes after receiving steroids 7 months before this admission. At that time, he also got pneumonia and recovered with empirical antibiotic treatment. He had a history of hypertension and chronic HBV infection. The patient's social and family history were not remarkable.
Physical examination: On admission, T (temperature) 39.5 C, PR (pulse rate) 80/min, RR (respiratory rate) 14/min, BP (blood pressure) 120/81 mm Hg. More than 10 scattered subcutaneous abscesses were found (Figure 1A), and some ruptured or incised abscesses (Figure 1B) with yellowish purulent discharge were observed. The cardiovascular, pulmonary, and neurologic examinations were unremarkable.
Lab test: A complete blood count showed a white blood cell (WBC) of 17.5 x 109/L with 88.4% neutrophils. Erythrocyte sedimentation rate (ESR) 97 mm/h , Procalcitonin 0.340 ng/mL, C-reactive protein (CRP) 130.00 mg/L . 24 h urine protein: 0.22 g. Serum markers of HIV, syphilis, tuberculosis (TB) were all negative. Serum HBsAg, anti-HBc, anti-HBe were positive. Immunology: Antinuclear antigen (ANA), anti-dsDNA, anti-Sm, anti-SSA, anti-SSB and anti-Scl-70: negative. Serum levels of IgG, IgA, IgM, IgE were within normal limits. Serum C3 0.85 g/L , serum C4 0.33 g/L, anti-O: 119.00 IU/ML and serum rheumatoid factor (RF) <9.75 IU/ML. Subset of lymphocytes was almost normal: CD3+ 85.04%, CD4+ 45.01%, CD4+/CD8+ 1.13, CD8+ 39.90%, natural killer (NK) cells 7.97%, CD19+ 5.93%. Immunoelectrophoresis results were normal and M-protein was negative. Liver function tests and the chest radiograph were negative. Ultrasound on sites of abscesses: Subcutaneous anechoic lesions. Blood culture was performed, but it did not yield growth of any bacteria after incubation. In addition, HBsAg and HBeAg staining were both negative on the renal biopsy. There were some infiltrated lymphocytes, but no granulomas were found. Moreover, nocardia was not found on the renal biopsy by wade fite staining
Treatment: The multiple abscesses were incised and drained. Before identification of the pathogen, we used meropenem empirically. Meanwhile, culture of pus was ordered. All of the pus cultures, which were aspirated from 5 different complete abscesses, presented Nocardia consistently, and gene sequencing (Figure 2) confirmed that they were all N. brasiliensis. Further investigations for disseminated disease, including computed tomography of the chest and the brain, were negative. According to drug susceptibility testing, linezolid and TMP-SMX were employed as antibiotic therapy. In addition, the immunosuppression treatment was not halted at the time of nocardia presentation. After 1 week's treatment, his fever resolved. Three weeks later, the abscesses disappeared, and the incisions or wounds had healed (Figure 1C). The WBC and neutrophils count also went down. After 4 weeks of hospitalization, he was sent home on a 6-month course of oral TMP-SMX therapy. He remains well off all treatments, without recurrence. The clinical course is summarized in Figure 3.