Clostridium ramosum is one of the anaerobes commonly implicated in soft tissue and intra-abdominal infections. Invasive systemic infections and bacteremias are rare, however, because C. ramosum is less virulent compared with C. perfringens and other clostridia . We report a case of osteomyelitis and bacteremia caused by C. ramosum in a patient with multiple pressure sores.
A 91-year-old nursing home resident, with hypertension and diabetes, was referred for evaluation of fever. Initial assessment revealed a demented, bedridden patient who appeared toxic, with a temperature of 102°F. She had multiple pressure sores, including stage IV ulcers over the left hip (9 × 7 cm) and sacrum (9.5 × 8 cm) and a stage III ulcer over the right hip (4 × 3.5 cm). The ulcer over the hip extended to the bone and had a foul-smelling purulent discharge and necrotic debris at the base. Further examination was unremarkable except for scattered rales and a short aortic ejection systolic murmur.
Laboratory results showed leukocytosis (18.9) with a left shift and anemia (hematocrit 22.7). Urinalysis was normal, and a chest roentgenogram did not reveal any infiltrates. Blood cultures were drawn, and the patient began receiving ampicillin-sulbactam and gentamicin.
The two sets of blood cultures performed at different time intervals, from different sites, both yielded C. ramosum. Blood cultures were incubated in the BACTEC 9240 system (Becton Dickinson, Sparks, MD) and subcultured on a blood agar plate and CDC’s blood agar plate media with a gas pack pouch anaerobic system (BBL Becton Dickinson Microbiology systems, Cockeysville, MD). The identity of the organism was established with the API 20 A anaerobic strip (bioMerieux, Hazelwood, MO).
A computed tomographic scan of the abdomen and pelvis, although negative for abdominal pathology, revealed a large ulcer over the left hip, intramedullary gas in the femoral head, and a small pocket of fluid anterior to the hip consistent with osteomyelitis. Gas was also seen in the soft tissue surrounding the ulcer.
Antibiotics were continued and surgical debridement was done. The patient received a packed red blood cell transfusion for anemia, and blood sugars were controlled with multiple daily doses of regular insulin. A transthoracic echocardiogram showed mild aortic stenosis but did not reveal any evidence of vegetations. The patient responded well to treatment and was afebrile by the third day. Subsequent blood cultures were negative for C. ramosum. Two weeks later, the patient remained afebrile, the pressure sores appeared to be healing, and she was discharged to the nursing home on antibiotics.
C. ramosum is an anaerobic, spore-forming, non-motile, thin, gram-positive rod, which occurs singly, in pairs, or in short chains. It was first isolated by Veillon and Zuber in 1898 . Holdeman et al.  found that it was a spore-forming anaerobe and placed it in the genus Clostridia. It is indigenous to the human intestinal tract and has been isolated from human feces . C. ramosum has frequently been implicated in wound infections after intraabdominal trauma, acute bowel perforation, and colorectal abscesses [4,5]. However, it has seldom been isolated from pressure sores . Infected pressure sores can cause metastatic or contiguous osteomyelitis. Anaerobic osteomyelitis is increasingly recognized in this setting, but clostridia have not often been implicated . In our patient, bacteremia probably resulted from the severely infected pressure sores. Evidence of infection with a gas-forming organism in soft tissues around the hip and isolation of C. ramosum from two separate sets of blood cultures lend credence to our assumption. The incidence of clinically significant clostridial bacteremias has been increasing, and isolated cases of unusual clostridial bacteremias have been reported in patients with pressure sores . C. ramosum bacteremia has been reported in a patient with acute bowel perforation and in a renal allograft recipient with mural endocarditis [5,9]. Our report demonstrates C. ramosum as a pathogen causing soft tissue infection, osteomyelitis, and bacteremia in the setting of pressure sores. C. ramosum is often resistant to penicillin and shows varying susceptibility to clindamycin and cephalosporins. This can potentially result in therapeutic failure . Infected pressure sores should be recognized as a source of deep-seated clostridial infections, including bacteremia and osteomyelitis. We also emphasize the importance of species identification, if not antibiotic susceptibility testing, in clostridial infections.
1. Gorbach SL. Clostridium perfringens
and other clostridia. In: Gorbach SL, Bartlett JG, Blacklow NR, editors. Infectious diseases. 2nd ed. Philadelphia: W.B. Saunders; 1998. p. 1925–30.
2. Veillon A, Zuber A. Recherches sur quelques microbes strictement anaerobies et leur role en pathologic. Arch Med Exp Anat Pathol 1898; 10:517–45.
3. Holdeman LV, Kato EP, Moore WEC, editors. Anaerobe laboratory manual. 4th ed. Blacksburg, VA: VPI Anaerobe Laboratory, Virginia Polytechnic Institute and State University; 1977.
4. Gorbach SL, Thadepalli H. Isolation of clostridium in human infections: evaluation of 114 cases. J Infect Dis 1975; 131:S81–5.
5. Peranio VA, Cross SA, Goldstein EJC. Incidence and clinical significance of anaerobic bacteremia in a community hospital. CID 1993; 16:S288–91.
6. Gaplin JE, Chow AW, Bayer AS, Guze LB. Sepsis associated with decubitus ulcers. Am J Med 1976; 61:346–50.
7. Brook I, Frazier EH. Anaerobic osteomyelitis and arthritis in a military hospital: a 10-year experience. Am J Med 1993; 94:21–8.
8. Poduval RD, Mohandas R, Unnikrishnan D, Corpuz M. Clostridium cadaveris
bacteremia in an immunocompetent host. Clin Infect Dis 1999; 29:1354–5.
9. Muakkassa WF, Mohanty PK, Kipreous B, Lee HM, Goldman MH. Left ventricular mass with septic (Clostridium ramosum
) arterial emboli in a renal allograft patient: report of a case and review of the literature. Transplant Proc 1983; 15:1715–9.
10. Citron DM, Appelbaum PC. How far should a clinical laboratory go in identifying anaerobic isolates, and who should pay? Clin Infect Dis 1993; 16(Suppl 4):S435–8.