A previously healthy 12-year-old female presented to the emergency department 4 days after completing a 3-day course of trimethoprim/sulfamethoxazole prescribed for a urinary tract infection. She complained of a 9-day history of fever and 3-day history of left hip pain associated with joint movement. The patient denied trauma, erythema, or swelling in the area of pain, but exposure history uncovered prolonged cat contact. Her initial exam revealed full range of motion of all extremities though she exhibited tenderness to palpation of her left hip. The remainder of the exam was unremarkable, including absence of any lymphadenopathy, bruising, erythema, or edema of the affected joint.
The patient's initial workup was significant for normocytic anemia (hemoglobin of 11.9 g/dL and hematocrit of 34.5%) and normal liver function tests. She was noted to have elevated inflammatory markers:an erythrocyte sedimentation rate greater than 120 mm/h and C-reactive protein of 68.6 mg/L. Urinalysis showed small amounts of leukocyte esterase and bacteria but only 0-5 white blood cells (WBCs). Urine and blood cultures were obtained and showed no bacterial growth.
An X-ray of the hip showed no acute abnormalities; however, a subsequent MRI showed a small left sacroiliac joint effusion with mild marrow edema that was concerning for infectious or inflammatory sacroiliitis (Figure 1(a)). Scattered small round lesions replaced bone marrow throughout the iliac architecture.
The patient was admitted with a working diagnosis of septic arthritis and received clindamycin intravenously. Joint fluid obtained via CT-guided aspiration revealed clear fluid with 15 WBCs, 200 red blood cells, and sterile cultures. Antibiotics were discontinued given that these findings were inconsistent with pyogenic arthritis, and she was improving clinically. Concern for possible leukemia based on the abnormal bony lesions led to an oncologic evaluation, including a chest X-ray, peripheral blood smear, and measurement of lactate dehydrogenase and uric acid, all of which were within normal limits.
Due to recrudesce of fever following the discontinuation of antibiotics, Epstein-Barr virus, cytomegalovirus, and B. henselae antibodies were measured. The patient's fever again declined without directed therapy, and she was discharged home with a diagnosis of transient synovitis.
The patient had intermittent low-grade fevers the week following her discharge. Her B. henselae titers were suggestive of recent infection (IgG > 1 : 1024, IgM negative). Due to known hepatic involvement of B. henselae in association with disseminated Bartonella disease, imaging (abdominal ultrasound followed by CT scan; Figure 1(b)) was performed and showed multiple liver lesions thought to be consistent with disseminated B. henselae infection. Cytopathology of the biopsied sample taken from the hepatic lesions revealed scars consistent with resolving Bartonella liver lesions. While we observed inflammation, we did not observe the granulomatous inflammation that is a more classic sign of CSD. PCR of the lesions was negative for B. henselae. Further oncologic evaluations of the hepatic lesions were negative, as was a QuantiFERON-Gold test for tuberculosis.
The patient had clinical resolution after a 6-week azithromycin regimen. An MRI of the patient's pelvis at the end of therapy showed near complete resolution of the abnormalities in the iliac bones, which were fully resolved in an MRI obtained one year later. Furthermore, a CT of the patient's abdomen obtained at the end of therapy revealed that the liver lesions were decreasing in size, consistent with resolving infection. The patient's inflammatory markers also were normal.