Cat scratch disease (CSD), caused by Bartonella henselae, is a common cause of self-limited lymphadenopathy in children and young adults. About 10% of patients with CSD develop systemic complications such as hepatic granuloma, splenic abscess, or encephalitis. Severe systemic diseases occur in 2% of all cases with prolonged or recurrent symptoms that persist for weeks or months.1
In recent years the number of published reports of patients presenting with atypical manifestations of CSD has increased and among them glomerulonephritis has been reported albeit rarely.2–4
We report a child who developed bilateral renal microabscesses caused by B. henselae.
A previously healthy 9-year-old female presented with a 12-day history of fever as high as 104°F. Associated symptoms were lethargy, fatigue, and headaches. The patient had had a tooth extraction 1 month earlier and had a recent history of travel to Colorado. There was a history of exposure to older cats but no history of animal scratches. The patient also had a history of contact with dogs and horses during a trip to Colorado. On physical examination, the patient was well nourished, active, alert, and oriented. She was febrile but otherwise had an unremarkable physical examination. There was no lymphadenopathy, hepatosplenomegaly, costovertebral tenderness, or skin rash.
Initial laboratory evaluation revealed a white blood cell count of 14,200/mm3 with 68% segmented neutrophils, 9% lymphocytes, 11% bands, 10% monocytes, and 2% eosinophils. The hemoglobin was 13.1 mg/dL and the platelet count was 303,000/mm3. Her erythrocyte sedimentation rate (ESR) and serum C-reactive protein (CRP) were both elevated at 36 mm/h and 9.6 mg/dL, respectively. Heterophile antibody test, rapid influenza test, and throat culture for group A β-hemolytic streptococcus were negative. An initial blood culture remained sterile. Urine culture was sterile as well and urinalysis done twice was normal. The blood urea nitrogen remained between 5 to 14 mg/dL and creatinine between 0.4 to 0.6 mg/dL during hospitalization. B. henselae serology was ordered.
An ultrasound examination of the abdomen and pelvis, chest radiograph, and echocardiogram done on day 2 of hospitalization were reported as normal. Her fever persisted with daily spikes as high as 103°F and ESR and CRP increased to 135 mm/h and 23 mg/dL, respectively. Four days after hospitalization she developed shaking chills and a fever spike of 104°F. Three sets of blood cultures were obtained and therapy was empirically started with intravenous vancomycin and meropenem, but she remained febrile. A computerized tomograph (CT) with contrast enhancement of the abdomen done on day 5 of hospitalization revealed multiple hypodense lesions scattered within the cortical portion of both kidneys consistent with microabscesses (Fig. 1). No abnormalities of the liver, spleen, adrenal glands and intra-abdominal or pelvic lymph nodes were seen. Her antibiotic regimen was changed to intravenous gentamicin and oral rifampin on day 5 of hospitalization because of suspicion of cat scratch disease. Bartonella serology done as part of her initial evaluation for prolonged fever was reported as IgG 1:640 (negative <1:320) and IgM 1:100 (negative <1:40). One week later, the IgG was >1:2560 and IgM was >1:800. She remained febrile during her 7 days of hospital stay although both the frequency and height of the fever spikes were lower. Her fatigue improved and she looked much better overall. ESR and CRP decreased to 95 mm/h and 9.1 mg/dL, respectively. The patient was discharged home on intravenous gentamicin and oral rifampin, to complete a total antibiotic course of 3 weeks. She was seen in the office 9 days after discharge from the hospital and was afebrile, active, without fatigue or headache, and back to her baseline status. Her ESR and CRP 2 weeks after discharge were 16 mm/h and <0.5 mg/dL, respectively. Her convalescent Bartonella serology 1 month after the last serology showed an IgG of 1:1024 and IgM of 1:40. A repeat abdominal CT scan with contrast enhancement showed the microabscesses had resolved without calcification and the liver, spleen, pancreas, and kidneys were normal.
To our knowledge this is the first reported case of isolated renal abscesses associated with Bartonella infection. Renal abscesses have been previously reported in a child with systemic CSD and abscesses in liver, spleen, and both kidneys.5 Typically CSD follows a scratch usually by cats, however, in many cases, including our patient, a history of a scratch cannot be elicited. Lymphohematogenous dissemination of Bartonella may occur in some cases, leading to a variety of complications, including osteomyelitis, encephalitis, and hepatosplenic lesions. Sometimes Bartonella infection may present as a fever of unknown origin.6
Renal involvement with CSD has previously been reported as postinfectious glomerulonephritis with complete resolution within 3 weeks to 8 months.2–4 Our patient's history and physical examination did not suggest renal disease and laboratory evaluation showed normal urinalysis, urine culture, blood urea nitrogen, and serum creatinine. The renal lesions were not visualized on ultrasound examination but were present on a contrast enhanced CT scan.
Intra-abdominal lesions with CSD can often be seen on ultrasound, however, as this case illustrates a CT scan may sometimes be necessary. Reports of hepatic CSD usually have normal liver enzymes and no hepatomegaly.7 This form of CSD does resolve spontaneously in 6 months and may leave residual calcifications.
Conservative management of uncomplicated CSD is recommended since mild CSD resolves spontaneously within approximately 6 weeks. When hepatosplenic CSD is treated with antibiotics it is often with intravenous gentamicin until fever resolves followed by oral trimethoprim-sulfamethoxazole and rifampin for 2 to 4 weeks.8–10
The authors thank the Radiology Department for their assistance in providing the images and Andrew Margileth, MD for critical review.
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