We report on the first case of documented Helicobacter cinaedi septic arthritis in an immunocompetent heterosexual young man. The patient presented no identified risk factor except for contact with animals that have been incriminated as a possible source of infection, particularly for these patients. Despite prolonged bacteremia, the response to long-term therapy with ciprofloxacin and rifampin was excellent.
Helicobacter cinaedi (previously called Campylobacter-like organism) was first isolated from rectal swabs of homosexual men with proctocolitis [1]. H. cinaedi is also responsible for bacteremia complicated with cellulitis or monoarticular arthritis. Forty-seven cases of H. cinaedi bacteremia have been reported, most of which occurred in HIV-infected homosexual men or in patients with underlying immunosuppressive factors (e.g., alcoholism, cancer, immunosuppressive therapy, pregnancy, or neonate) [2–5]. Only 3 cases of H. cinaedi infection have been observed in heterosexual immunocompetent men [3]. We report a case of H. cinaedi bacteremia and septic arthritis in an otherwise healthy immunocompetent man and discuss the clinical and laboratory features pertinent to its recognition.
A 20-year-old man was hospitalized in August 1998 with a 24-h history of fever (temperature, 38.1°C) and an acute inflammation of the right knee with synovial effusion. The remainder of the physical examination was normal except for a scab on the anterior surface of the opposite knee. Radiography of the right knee was normal. Laboratory findings showed a WBC count of 13,600 cells/μL (77% neutrophils) and a high level of C-reactive protein (98 mg/L). There was no humoral immunity defect, and HIV serology was negative. The microscopic examination of the right knee joint fluid showed 25,000 nucleated cells/μL (85% neutrophils), but no bacteria were seen. Bacterial culture was performed on the joint liquid and blood samples on solid media and by inoculation in Bact-Alert bottles (Organon Teknika, Durham, the Netherlands). After 36–72 h of incubation, aerobic bottles with blood and joint fluid flagged positive, whereas cultures on solid media remained negative, even after a 5-day incubation. The microscope examination revealed a motile, 10 μ-spiraled, faintly gram-negative bacterium. It mimicked a spirochete, but Lyme serology and Borrelia burgdorferi PCR were negative.
Subcultures from Bact-Alert bottles yielded growth on Campylobacter selective media after a 4-day incubation under microaerobic conditions. However, further subcultures showed no growth. Biochemical test results revealed the organism to be oxidase-positive, catalase-positive, and nitrate reductase-positive, but urease and hippurate hydrolysis were negative; this suggested that the bacterium was H. cinaedi. Complete identification and susceptibility testing using a disk diffusion technique was performed by the French National Reference Center of Campylobacter and Helicobacter. The isolate was susceptible to nalidixic acid, rifampin, and tetracycline but resistant to erythromycin and cephalotin. The 16S rRNA gene nucleotide sequence, determined as described elsewhere [6], confirmed the identification.
Antimicrobial therapy against spirochete (iv penicillin G, 12 million U/d) was first initiated in combination with analgesics, joint immobilization, and drainage. When an H. cinaedi infection was suspected, ciprofloxacin (1g/d) and rifampin (1.2 g/d) were given for 12 weeks (because of the severity of infection and the delay in making the diagnosis). After 2 weeks of treatment, the joint fluid became sterile and the synovitis of the knee disappeared without any joint sequelae.
The clinical spectrum of H. cinaedi bacteremia is broad: patients usually present with a mild fever associated with dermatological and/or rheumatologic manifestations. Four cases of large-joint involvement have been reported: 2 cases of reactive arthritis [2] and 2 cases of septic arthritis (although no information concerning the joint fluid culture was provided) [7]. Concerning our case, the septic arthritis was proven by the laboratory findings and by the clinical improvement after appropriate therapy. The patient presented none of the identified risk factors associated with H. cinaedi bacteremia. The mode of acquisition has not been fully elucidated. However, the patient reported that he worked occasionally as a shepherd and had contact with cows and farm animals. These contacts have been incriminated as possible sources of infection by Kiehlbauch et al. [3]; indeed, all 3 of the immunocompetent patients with H. cinaedi bacteremia that they described had been in contact with animals or had eaten raw eggs [3]. Orlicek et al. [4] reported that H. cinaedi was responsible for bacteremia and meningitis in a newborn whose mother cared for pet hamsters (which is the normal host of this bacterium [8]) during her pregnancy.
Several previous reports have related that the laboratory diagnosis of H. cinaedi is critical [2, 9, 10]. Our experience is identical. We were unable to sustain culture growth of the organism and consequently were unable to perform characterization and antimicrobial-susceptibility tests. However, the diagnosis of bacteremia was not hampered by the slow growth of the organism: indeed, we used a Bact-Alert blood culture system, and our bottles flagged positive in 36–72 h. (vs. >7 days for Burman et al. [2]), which confirms its superiority over the Bactec system, as reported elsewhere [2, 4].
Our experience confirms that the Bact-Alert system allows a more rapid growth of H. cinaedi than the Bactec system. Clinically, H. cinaedi bacteremia should also be considered in immunocompetent patients. In these patients, the clinical presentation is frequently subtle and may cause the diagnosis to be missed or delayed. Investigation of contact with animals may be useful for patients with no identified risk factor to detect this infection.
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