Anaerobes have traditionally been viewed as uncommon causes of osteomyelitis because they are difficult to isolate from infectious sites due to their fastidious nature. However, due to the development of methods for detecting anaerobes, reports of anaerobic osteomyelitis have been increasing; up to 39% of cases of osteomyelitis were associated with anaerobic infections in a previous study [
9]. Anaerobic osteomyelitis has typically been reported in patients with complicated bone fractures or underlying chronic disease, usually as a result of non-hematogenous spread. The predominant anaerobes causing osteomyelitis are
Bacteroides spp
., Peptostreptococcus spp
., Fusobacterium spp
., Clostridium spp
. and
Propionibacterium acnes[
9,
10].
Fusobacterium spp
., which are members of the normal oral flora, are most frequently isolated from cranial or facial infections [
10]. The species most commonly isolated is
F. necrophorum[
6,
7,
11]. Cases of
F. nucleatum are relatively rare [
1,
9]. Table
1 shows cases of
Fusobacterium osteomyelitis at sites other than the head and neck that have been reported in the medical literature. As indicated, most of the cases are children or patients with predisposing factors for anaerobic hematogenous osteomyelitis. To our knowledge, our patient is the first case of long bone osteomyelitis caused by
F. nucleatum in an immunocompetent adult. Many patients with anaerobic osteomyelitis have an anaerobic infection elsewhere in the body that is the source of the organisms involved in osteomyelitis. Osteomyelitis of long bones is generally due to hematogenous spread, trauma, or the presence of a prosthetic device [
10]. Our patient had no specific infection source except a history of recurrent periodontitis. Patients with periodontal disease are predisposed to systemic infections with anaerobic bacteria such as
Fusobacterium spp. There are a few case reports of long bone osteomyelitis following oral infection [
12]. In our patient, his poor dentition may have caused
F. nucleatum bacteremia, leading to hematogenous osteomyelitis of the lower leg with an abscess of the adjacent muscle.
Table 1
Cases of osteomyelitis caused by Fusobacterium spp. reported in the medical literature
| M/7 | Sickle cell disease | Tibia |
F.nucleatum
| Tissue | Nafcillin + Ceftriaxone → Clindamycin 6w (IV) | Cured |
| M/6 | None | Pelvis |
F.nucleatum
| Tissue | Clindamycin 10 w (IV 4w, PO 6w) | Cured |
| F/78 | Recent dental work | Vertebra, L5-S1 |
F.necrophorum
| Blood and tissue | Clindamycin 12 w (IV 4w, PO 8w) | Cured |
| M/62 | Arterial hypertension | Vertebra, L4-L5 |
F.necrophorum
| Blood | Amoxicillin-clavulanic acid → Clindamycin 8w (IV 4w, PO 4w) | Cured |
| M/61 | Diabetes mellitus, Arterial hypertension | Vertebra, T6-T8 |
F.nucleatum
| Blood and tissue | Penicilin G 4w (IV) → Clindamycin 8w (PO) | Cured |
| M/16 | None | Pubic symphysis |
F.necrophorum
| Blood | Imipenem → Amoxicillin-clavulanic acid 6w | Cured |
| M/13 | None | Fibula |
F.necrophorum
| Tissue | Penicilin G 6w (IV) | Cured |
Management of osteomyelitis includes symptomatic therapy, immobilization for some patients, adequate drainage of purulent material, and antibiotic therapy consisting of parenteral administration of antibiotics for at least four to eight weeks. In some cases, even longer antibiotic treatment is necessary [
13].
Fusobacterium spp
. are commonly sensitive to the usual anti-anaerobic antibacterial agents including penicillin G, clindamycin, metronidazole, chloramphenicol, imipenem, and cefoxitin [
7]. However, there is evidence of emerging resistance of some
Fusobacterium spp
. isolates to penicillins, carbapenems, and clindamycin [
13,
15]. The first description of a β-lactamase in
Fusobacterium spp
. was reported in 1985, and this was shown to primarily be a penicillinase with little activity against cephalosporins [
15]. Since then, several studies have reported β-lactamase production by
Fusobacterium spp
. Fatal sepsis due to a β-lactamase-producing strain occurred in an immunocompromised patient [
16]. In studies done from 1999 to 2008, 0–14.6% of
Fusobacterium spp
. isolates were found to be nonsusceptible to penicillin [
17‐
24]. The nonsusceptibility to β-lactam-β-lactamase inhibitors was found to be much lower (0-3.3%) [
18‐
22]. There were regional differences between species in terms of penicillin resistance, but resistance to β-lactam-β-lactamase inhibitors was similarly low in different regions [
24]. Recently, as
Bacteroides spp
. have become more resistant to carbapenem, carbapenem resistance in
Fusobacterium spp. has also been reported. In a study from Taiwan, 4% of
Fusobacteria isolates were “nonsusceptible” to imipenem and 8% were “nonsusceptible” to meropenem [
17]. Our patient was successfully treated with β-lactam-β-lactamase inhibitors. The duration of antibiotic therapy is debated, but prolonged duration of high-dose β-lactam therapy is recommended because of the endovascular nature of the infection. Surgical debridement is crucial given the tendency toward abscess formation [
7].