to the editor: A 37-year-old black woman with poorly controlled type 1 diabetes and a history of urinary tract infections (UTIs) presented with a three-week history of increasing sharp right flank pain, tactile fever, chills, nausea, anorexia, and a single episode of hematuria. She denied dysuria, frequency, urgency, vomiting, or abdominal pain. Four days earlier, she had been placed on trimethoprim-sulfamethoxazole for a UTI at another hospital. Her past surgeries included tubal ligation, three cesarean sections, and removal of an ectopic pregnancy. Her medical history included hypertension, iron deficiency anemia, depression, and hypercholesterolemia.
Six weeks before admission, she was treated with ciprofloxacin for a UTI by her personal physician; however, urine culture ultimately grew group B streptococcus (GBS) not sensitive to ciprofloxacin. Initial follow-up with her physician indicated she was improving.
Physical examination revealed a slender, uncomfortable woman. Her pulse was 114 and blood pressure was 142/91 mm Hg. She exhibited pale mucosa and a soft cardiac flow murmur, a benign abdominal examination, but significant right flank tenderness. Pelvic examination and wet preparation revealed yeast and trichomonal vaginitis. A bilateral distal peripheral neuropathy was present.
White blood cell count was 10,000 per mm3 (10 × 109 per L), with a differential of 73 percent neutrophils, 10 percent lymphocytes, and 16 percent monocytes; hemoglobin level, 8.6 g per dL (86 g per L); and platelet count, 272 × 103 per mm3 (240 × 109 per L). Urinalysis revealed glucosuria, mild proteinuria, excretion of six to 10 red blood cells and one to five white blood cells per high-powered field, with negative leukocyte esterase and nitrate. Chemistry panel was normal except for a glucose level of 317 mg per dL (17.6 mmol per L). Hemoglobin A1c was 16.3 percent.
A computed tomography scan revealed a 4- to 6-cm right perinephric abscess and non-specific enlargement of both kidneys. This patient recovered with percutaneous drainage of the abscess and intravenous antibiotics directed against GBS, which grew from the abscess drainage.
GBS is a cause of fatal puerperal sepsis. In addition to colonization of the pregnant female genital tract with the risk of early or late onset of neonatal sepsis, GBS causes approximately 2 percent of cystitis, pyelonephritis, and nongonococcal urethritis in adults. Other invasive GBS infections include pneumonia, endocarditis, arthritis, osteomyelitis, skin and soft tissue infections, and, rarely, unusual abscesses and device-related infections.1 These illnesses are more common in blacks and elderly persons.
One report2 describes a 17-year-old black girl with poorly controlled diabetes mellitus and duplication of her upper right ureter–who exhibited signs and symptoms similar to our patient. There also have been case reports of GBS perinephric abscess in a 47-year-old woman,3 a young adult man with diabetes,4 a male newborn,5 and a 61-year-old woman with diabetes who was treated for renal abscess caused by “ß-hemolytic streptococcus.”6
GBS may cause perinephric abscess and other types of invasive infections, particularly in persons with underlying medical problems. It is important that this organism be treated with antibiotics active against GBS when found to be the etiologic agent of UTI.