The pneumococcus is a human pathogen that produces pneumonia, sepsis, and meningitis.1 Less frequently, pneumococci may cause other manifestations such as cellulitis, cutaneous abscesses, or intra-abdominal abscesses.2,3 We recently cared for a patient who presented with an intra-abdominal abscess and cutaneous abscesses with cellulitis. We describe the clinical course of our patient and discuss diagnosis and management of this condition.
A 55-year-old woman with rheumatoid arthritis, type I neurofibromatosis, and a penicillin allergy presented to the emergency department with a 3-day history of abdominal pain and decreased urinary output. She also related a 4-month history of weight loss (an estimated 15 kg) and multiple cutaneous abscesses. The cutaneous abscesses usually occurred on the extremities and resolved spontaneously, but she had recently developed a similar lesion on a buttock. On 3 occasions, incision and drainage of the lesions was required. She received several 1- to 2-week courses of clindamycin (300 mg by mouth 4 times daily). She stated that the skin lesions began shortly after she received a 2-week course of clindamycin for otitis media. She denied fever or chills. Her home medications included prednisone 2 mg by mouth daily and leflunomide 20 mg by mouth daily. She had not previously received polyvalent pneumococcal immunization.
On examination, her temperature was 38.4°C, blood pressure was 97/40 mm Hg, pulse was 114 beats per minute, and respiratory rate was 20/min. She appeared chronically ill and had numerous scattered neurofibromas. No evidence of otitis media was noted on examination. The chest was clear, and there was no cardiac murmur noted. Abdominal examination was normal. A fluctuant right gluteal abscess with perirectal extension was noted. A 1 × 2 × 1-cm abscess on the right knee was noted. Erythema surrounded both cutaneous abscesses. Examination of the extremities revealed extensive rheumatoid changes including ulnar drift, swan neck deformity, and synovial thickening.
A contrasted abdominal computed tomogram (CT) revealed a 6 × 4 × 5-cm abscess involving the right psoas muscle and a 3 × 1.25 × 3-cm abscess extending from the level of the hip to the left renal pole (Fig. 1). A 6 × 4 × 5-cm right perirectal abscess and multiple small pelvic abscesses adjacent to the bladder were also noted. The intra-abdominal abscesses were drained via CT-guided catheter placement. The cutaneous abscesses and perirectal abscess were incised, drained, and cultured. All cultures grew pneumococci, which were resistant to clindamycin and erythromycin, but susceptible to ceftriaxone, levofloxacin, penicillin, trimethoprim/sulfamethoxazole, and vancomycin. The bacteria from all cultures were very slow growing, and 5 to 6 days of incubation were required for identification. The bacterial colonies were very mucoid in appearance. Efforts to maintain the strain in culture for additional testing were unsuccessful.
Antibody testing for infection with human immunodeficiency virus was negative. Screening tests for deficiencies in complement and immunoglobulins (with subclasses) were normal. Serum protein electrophoresis was normal. Absolute CD4− lymphocyte count was 0.33 × 109/L. The absolute CD4− lymphocyte count was found to be 0.54 × 109/L on a repeat assessment obtained 5 days after the initial value.
The patient was begun on cefazolin 1 g intravenously every 8 hours and drainage of the abscesses via catheter continued. Additional CT-guided drainage procedures were intermittently required during the next 12 days until adequate drainage of the fluid collections was accomplished. The patient was discharged to home to complete an 8-week course of intravenous cefazolin and also received pneumococcal immunization. One year after completion of treatment, she has experienced no further infections.
Pneumococci commonly are implicated as the cause of pneumonia, sepsis, and meningitis.1 Less commonly, skin or intra-abdominal infections result from this organism.2,3 Mechanisms for extrapulmonary manifestations of pneumococcal disease include direct inoculation or spread either hematogenously or from contiguous structures.
Although rare, soft-tissue infections due to pneumococci are usually associated with predisposing factors.2,4 Parada and Maslow described 2 distinct clinical syndromes of pneumococcal cellulitis in adults.5 Patients with a history of active substance abuse (ethanol or intravenous drugs) and diabetes mellitus more commonly presented with pneumococcal cellulitis of the limbs, whereas patients who presented with pneumococcal cellulitis of the face and neck were more likely to have connective tissue disease, nephrotic syndrome, or a hematologic disorder.
We speculate that our patient's initial disease was otitis media caused by S. pneumoniae with subsequent hematologic spread to the other sites. Regrettably, we were unable to sustain growth of the isolate for additional testing, but the slow rate of growth and gross morphological appearance of the colonies suggest that the bacterial strain may have had unusual properties that contributed to the chronic course. The role of the patient's rheumatologic disease and immunosuppressive therapy in the pathological process is also speculative. Leflunomide is reported to be an "immunomodulatory" agent6; however, there are only rare reports of serious infections occurring in patients taking leflunomide.7,8 These reports are not overly suggestive of leflunomide imparting a major risk of subsequent serious infection. Likewise, the significance and origin of the transient decrease in absolute CD4 count is unknown.
This case illustrates that pneumococci can cause unusual clinical manifestations. Isolation of pneumococci from an extrapulmonary source should prompt consideration for an evaluation for an underlying comorbid condition or additional foci of pneumococcal infection.
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