INVITED ARTICLE AGING AND INFECTIOUS DISEASES

Thomas T. Yoshikawa, Section Editor

Osteomyelitis in Elderly Patients

Burke A. Cunha
Infectious Disease Division, Winthrop-University Hospital, Mineola, and Department of Medicine, State University of New York School of Medicine, Stony Brook

Downloaded from https://academic.oup.com/cid/article/35/3/287/409096 by guest on 04 March 2022

In elderly persons, osteomyelitis is second only to soft-tissue infection as the most important musculoskeletal infection. Acute
osteomyelitis is usually acquired hematogenously, and the most common pathogen is Staphylococcus aureus. Acute osteomyelitis
can usually be cured with antimicrobial therapy alone. In contrast, chronic osteomyelitis may be caused by S. aureus but is
often due to gram-negative organisms. The causative organism of chronic osteomyelitis is identified by culture of aseptically
obtained bone biopsy specimens. Because of the presence of infected bone fragments without a blood supply (sequestra), cure
of chronic osteomyelitis with antibiotic therapy alone is rarely, if ever, possible. Adequate surgical debridement is the cornerstone
of therapy for chronic osteomyelitis, and cure is not possible without the removal of all infected bone.

Osteomyelitis is a common infectious disease among elderly
patients. Older adults are predisposed to osteomyelitis either
because of an increased incidence of associated disorders that
predispose to osteomyelitis (e.g., peripheral vascular disease,
diabetes mellitus, and poor dentition) or because of surgical
procedures that are frequently performed in the elderly pop-
ulation (e.g., dental extractions, open-heart surgery, and pros-
thetic joint replacement). As with osteomyelitis in other age
groups, osteomyelitis in the elderly population may also be
considered in terms of acuteness of the infectious process (acute
osteomyelitis, subacute osteomyelitis, or chronic osteomyelitis).
Osteomyelitis may be caused by a variety of microorganisms,
but osteomyelitis in the elderly population is most often caused
by pyogenic organisms [1-6] (table 1).
ACUTE OSTEOMYELITIS
General concepts. Acute osteomyelitis is an infection of the
bone that involves the periosteum, cortex, and/or medullary
cavity. Elderly persons frequently fall, which may result in
closed or open bone trauma. Acute osteomyelitis secondary to
closed trauma is usually due to Staphylococcus aureus. Acute
osteomyelitis may be acquired hematogenously after closed
trauma. In acute hematogenous osteomyelitis, the bacteria
Received 9 January 2002; revised 6 March 2002; electronically published 11 July 2002.
Reprints or correspondence: Dr. Burke A. Cunha, Infectious Disease Division, Winthrop-
University Hospital, Mineola, NY 11501.
Clinical Infectious Diseases 2002; 35:287–93
 2002 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2002/3503-0011$15.00
reach the metaphyseal blood vessels of bone to initiate the
infectious process. Pathogenic bacteria in the smaller arterioles
of the metaphyses multiply, which leads to microabscess for-
mation. The abscess formation in acute osteomyelitis within
the medullary cavity of bone, metaphyseal space, or subperi-
osteal space leads to further bone necrosis because of increased
pressure. Eventually, bone fragments are formed (sequestra)
that are, in effect, floating fragments of infected dead bone
without a blood supply. If the process becomes chronic, ex-
tensive bone destruction occurs, which may be accompanied
by fistula formation [1, 6].
Clinical presentation. Patients with acute osteomyelitis
present with pain in the affected bone. There may be point
tenderness over the bone if there is subperiosteal involvement.
In addition to local tenderness, patients may have systemic
symptoms, such as fever or chills. Acute osteomyelitis may be
defined as a first episode of osteomyelitis occurring in a patient
that is cured by medical means in !6 weeks.
The presumptive diagnosis of acute osteomyelitis is clinical
and is confirmed by bone scan. In acute osteomyelitis, soft-
tissue or periosteal elevations are the first changes, followed in
10–12 days by periosteal proliferation and by irregular bone
reabsorption in 3 weeks. Bone sclerosis occurs months later.
The erythrocyte sedimentation rate (ESR) is often elevated
(⭐100 mm/h) in patients with acute osteomyelitis, particularly
in those with vertebral osteomyelitis. If acute osteomyelitis is
hematogenously acquired, blood cultures may yield positive
results early in its course. Plain films are unhelpful diagnosti-
cally in the early phases of acute hematogenous osteomyelitis.
Bone scans yield positive results within the first 2 or 3 days in

AGING AND INFECTIOUS DISEASES • CID 2002:35 (1 August) • 287

Table 1. Clinical types of osteomyelitis among elderly individuals.

Type of osteomyelitis, related disorder Usual pathogen(s) Means of diagnosis

Acute
Open trauma
Closed trauma
Subacute
Vertebral osteomyelitis (excluding spinal tuberculosis)
Infected joint replacement–associated osteomyelitis
Chronic
Sternal osteomyelitis (secondary to open-heart surgery)
Mandibular osteomyelitis (secondary to periapical abscess)
Upper or lower extremity decubitus ulcers (stage 4)
Sacral osteomyelitis
Foot osteomyelitis associated with peripheral vascular disease S. aureus, aerobic or anaerobic gram-negative bacilli
Foot osteomyelitis associated with diabetes mellitus
Staphylococcus aureus, aerobic gram-negative bacilli Clinical finding of exposed infected bone
S. aureus Bone scan, measurement of ESR, blood culture, gallium scan
S. aureus, aerobic gram-negative bacilli Bone or gallium scan, CT, MRI, measurement of ESR, blood
culture
S. aureus, Staphylococcus epidermidis, coagulase-negative Bone scan, CT, measurement of ESR, gallium scan
staphylococci
S. aureus, aerobic gram-negative bacilli Clinical findings of wound dehiscence, unstable sternum,
fistulous drainage
Oral anaerobes Panorex, gallium scan of jaw
S. aureus Clinical finding of exposed bone, plain film, bone scan, CT,
MRI, measurement of ESR
S. aureus, aerobic gram-negative bacilli, Bacteroides fragilis Plain film, measurement of ESR, CT, MRI
Bone scan, CT, MRI, measurement of ESR
S. aureus, group B streptococci, aerobic gram-negative Plain film, CT, MRI, measurement of ESR
bacilli, B. fragilis

NOTE. ESR, erythrocyte sedimentation rate.

Downloaded from https://academic.oup.com/cid/article/35/3/287/409096 by guest on 04 March 2022

acute osteomyelitis and are the preferred diagnostic test. Gal-
lium scans also yield positive results and are useful, but indium
scans often yield false-negative results [2–5].
Therapy. Acute osteomyelitis is usually treated empirically
on the basis of the pathogens most likely to cause osteomyelitis,
or therapy is based on the pathogens identified from culture
material obtained from bone (in open-fracture cases) or blood
(in cases due to closed extremity trauma). The selected anti-
biotic therapy should be active against S. aureus and methicillin-
susceptible S. aureus—for example, antistaphylococcal pen-
icillin, antistaphylococcal cephalosporins, clindamycin, or
vancomycin. If the pathogen is methicillin-resistant S. aureus,
then vancomycin or linezolid may be used. The antibiotic se-
lected should also penetrate the bone in adequate concentration
to eradicate the organism. Most antistaphylococcal antibiotics
given in the usual recommended dose penetrate bone ade-
quately. Oral antibiotics with good bioavailability and the same
or equivalent spectrum of parenteral agents may also be used
to treat acute osteomyelitis or to complete a course initiated
with parenteral antibiotics [1, 6, 7].
SUBACUTE OSTEOMYELITIS
Vertebral Osteomyelitis
General concepts. Subacute osteomyelitis in the elderly pop-
ulation is most commonly due to vertebral osteomyelitis or
osteomyelitis associated with prosthetic joint replacement. Ver-
tebral osteomyelitis may occur through hematogenous dissem-
ination from a distant infected source. Less commonly, in men
with urinary tract infections, aerobic gram-negative bacilli may
ascend via Batson’s plexus and reach the lumbar spine. The
vertebrae are not readily accessible to physical examination,
and the patient’s symptoms or complications (e.g., neurological
or suppurative) may suggest the diagnosis. Rarely, vertebral
osteomyelitis may occur iatrogenically as a complication of
disk-space injections or spinal surgery.
An initial clinical clue to vertebral osteomyelitis may be mus-
cle spasm, which is nonspecific and may occur with a variety
of other disorders. Physical or neurological findings are asso-
ciated with complications, such as perispondylic or epidural
abscess. Pyogenic vertebral osteomyelitis must be differentiated
from tuberculous spinal osteomyelitis, which is also common
among elderly patients. In general, both pyogenic and tuber-
cular vertebral osteomyelitis destroy adjacent vertebral bodies
and involve the disk space. Factors that favor a pyogenic eti-
ology of vertebral osteomyelitis include a rapid rate of disk-
space destruction, a lower incidence of abscess formation, less
osteoporosis or sclerosis, and it is usually limited to a single
disk space or adjoining vertebra. In contrast, tuberculous os-
teomyelitis has a slow and indolent process with a higher in-
cidence of abscess formation. The abscess may extend to the
AGING AND INFECTIOUS DISEASES • CID 2002:35 (1 August) • 289
psoas muscle and dissect to the groin and present as a groin
mass. Typically, but not always, tuberculous osteomyelitis in-
volves 12 contiguous vertebral bodies or disk spaces [8–11].
Clinical presentation. In cases of vertebral osteomyelitis
secondary to hematogenous dissemination, S. aureus is the most
common pathogen. Aerobic gram-negative uropathogens are
associated with vertebral osteomyelitis in elderly men with uri-
nary tract infections that have reached the vertebra via Batson’s
plexus. Spinal tuberculosis is a reactivation of initial hematog-
enous dissemination of Mycobacterium tuberculosis during in-
itial infection. M. tuberculosis localizes in areas of high oxygen
tension, such as the vertebral bodies. Normal host defense
mechanisms contain the organisms until old age, when osteo-
Downloaded from https://academic.oup.com/cid/article/35/3/287/409096 by guest on 04 March 2022
porosis, trauma, or nonmycobacterial infections cause reacti-
vation of latent infection in bone.
The diagnosis of vertebral osteomyelitis is suspected clini-
cally, and the presumptive diagnosis is made on the basis of
radiographic findings. In pyogenic vertebral osteomyelitis, cul-
ture of blood samples frequently yields negative results. Plain
films of the spine usually lack sufficient definition to differ-
entiate tuberculous from pyogenic vertebral osteomyelitis or
from other noninfectious processes involving the spine, such
as sarcoidosis, hemangiomas, or tumors. Bone scans, and, to
a lesser extent, gallium scans, are useful to localize the process,
but they are not always helpful in differentiating tumor from
tuberculosis or from a pyogenic process. The diagnosis of tu-
berculous osteomyelitis is favored by finding evidence of tu-
berculosis elsewhere (e.g., pulmonary tuberculosis). Although
anergy is common with increasing age, 95% of patients with
vertebral osteomyelitis have a positive result of tuberculin pu-
rified protein derivative skin tests. A pulmonary focus of tu-
berculosis is present in ∼90% of patients with tuberculous ver-
tebral osteomyelitis. The ESR is elevated, but this does not help
the examiner differentiate between tumor, tuberculosis, or pyo-
genic osteomyelitis. Although the process in the vertebral bodies
can be localized by noninvasive radiological procedures, a de-
finitive etiologic diagnosis can usually only be made by CT-
guided biopsy or open biopsy of the infected bone or disk space
[12–15].
Therapy. Treatment depends on the causative organism.
Vertebral osteomyelitis due to S. aureus is treated as staphy-
lococcal osteomyelitis in other anatomic locations, and the du-
ration of treatment is 4–6 weeks. Surgical debridement may or
may not be necessary, depending on the degree of bone de-
struction. Antibiotic selection for aerobic gram-negative bacilli
should be based on the susceptibility of the isolate recovered
from a septically collected bone biopsy specimen. The duration
of treatment is ordinarily 4–6 weeks. If the patient is found to
have tuberculous vertebral osteomyelitis, treatment is with dou-
ble-drug antituberculosis therapy (e.g., isoniazid and rifampin),
unless a drug-resistant strain is present. If that is the case, 3
or 4 antituberculous drugs will be necessary and therapy should
be for 6–12 months [7, 16, 17].
Osteomyelitis with Joint Replacement
General concepts. Some elderly persons develop osteomye-
litis following total hip replacement or total knee replacement.
Patients with rheumatoid arthritis are immunocompromised
hosts and are predisposed to a higher incidence of prosthetic
joint–related infections than are patients with osteoarthritis
[18–20].
Clinical presentation. Osteomyelitis associated with in-
fected prostheses in total hip replacement or total knee re-
placement presents with loosening of the prosthesis and with
little or no fever. Prosthetic loosening may be mechanical or
may be a sign of associated osteomyelitis. The patient’s ESR is
not elevated if loosening of the prosthesis is the cause of joint
instability or periprosthetic lucencies are visible on plain film
radiographs, and it is elevated if these findings are because of
prosthetic-associated osteomyelitis. Radiological imaging tech-
niques, such as bone and gallium scans, are useful in differ-
entiating simple mechanical loosening from prosthetic-related
infection [7, 21, 22].
Therapy. If the prosthesis and surrounding bone are in-
fected, then cure necessitates removal of the prosthesis and
debridement of all involved bone, followed by appropriate
antimicrobial therapy. In replacing a prosthetic device, ade-
quate debridement of the surrounding infected bone is es-
sential for cure. There are no good data on the duration of
antimicrobial therapy after reimplantation of the new joint
prosthesis [7, 23, 24].
CHRONIC OSTEOMYELITIS
Chronic osteomyelitis may be defined as osteomyelitis that has
a duration of ⭓6 weeks or as osteomyelitis that recurs or is
not cured after the initial infection. Chronic osteomyelitis is
often accompanied by fistula formation to the skin surface.
Chronic osteomyelitis is, by definition, an indolent, slow pro-
cess with few systemic symptoms. Chronic osteomyelitis has
been associated with performance of certain surgical procedures
(e.g., sternal osteomyelitis after open-heart surgery), has oc-
curred secondary to poor dentition or dental extraction (man-
dibular osteomyelitis), and, more commonly, has been asso-
ciated with systemic disorders (e.g., peripheral vascular disease
and diabetes mellitus). Far and away the most common prob-
lem in the elderly population is chronic osteomyelitis due to
peripheral vascular disease or diabetes mellitus.
Sternal Osteomyelitis
General concepts. Sternal osteomyelitis may complicate any
open-heart surgical procedure that involves dividing the ster-
290 • CID 2002:35 (1 August) • AGING AND INFECTIOUS DISEASES
num. Bone wax and stainless steel sutures are used, which may
become a nidus for bacteria acquired via the wound (e.g., gram-
positive cocci) or from irrigant solutions (e.g., aerobic gram-
negative bacilli) during the thoracic surgical procedure. The
organisms most commonly associated with sternal osteomye-
litis are S. aureus and aerobic gram-negative bacilli. S. aureus
may gain access to the wound via the skin during the surgical
procedure. Aerobic gram-negative bacilli may be the cause of
infection if the irrigation fluids are colonized by these organ-
isms [3, 4, 7].
Clinical presentation. Clinically, sternal osteomyelitis
presents weeks or months after open-heart surgery, as either a
flail sternum or as a draining sinus tract. The draining sinus
Downloaded from https://academic.oup.com/cid/article/35/3/287/409096 by guest on 04 March 2022
tracts in patients with sternal osteomyelitis most commonly
occur at the styloid process or at the top of the incision. Crack-
ing sounds on chest palpation or instability of chest wall seg-
ments suggests sternal osteomyelitis until proven otherwise. In
the diagnosis of sternal osteomyelitis, bone scans and CT or
MRI are usually unhelpful.
Therapy. Sternal osteomyelitis is diagnosed clinically, and
the definitive treatment is surgical with adjunctive antimicrobial
therapy. Because the involved segments are devitalized and have
no blood supply, thorough surgical debridement is necessary
to effect cure in sternal as well as other forms of chronic os-
teomyelitis. If the debridement is inadequate, osteomyelitis will
eventually become clinically manifest again at the sites of in-
adequate surgical debridement. Antimicrobial therapy is ad-
junctive but is directed against S. aureus, coagulase-negative
staphylococci, or aerobic gram-negative bacilli that are asep-
tically cultured from the debrided, surgically removed bone
specimens [7, 25, 26].
Mandibular Osteomyelitis
Mandibular osteomyelitis occurs in elderly patients with poor
dentition or periodontal disease. Periapical abscesses are com-
mon in the elderly population and may present with local symp-
toms or those of intracranial mass lesions. Hematogenous
spread to the brain may be clinically expressed as CNS mass
lesions resembling a neoplasm. It is difficult to differentiate
CNS tumors from abscesses, even with MRI or CT imaging
studies, and often only craniotomy and examination of biopsy
specimens can differentiate these clinical entities. Local exten-
sion of a periapical abscess may result in mandibular osteo-
myelitis. The organisms involved in mandibular osteomyelitis
are those of the oropharyngeal anaerobic flora. Such organisms
as Actinomyces, Eikenella, and Peptostreptococcus species are
commonly isolated from dental abscesses associated with man-
dibular osteomyelitis. Patients present with a swelling or ten-
derness of the jaw, regional adenopathy, and low-grade fever.
Blood culture results are usually negative. Plain film or panorex
radiographs of the jaw are usually diagnostic. Nuclear scanning
or CT imaging is usually unnecessary. Treatment of mandibular
osteomyelitis involves removal of the diseased tooth and root
along with debridement of the involved mandibular bone [3,
4, 27, 28].
Chronic Osteomyelitis Associated with Decubitus Ulcers
Elderly patients who are unable to turn themselves over in bed
frequently develop pressure sores or decubitus ulcers. Pressure
(usually over a bony prominence) may result in a decubitus
ulcer. The severity and depth of a decubitus ulcer depends on
the duration of pressure on the skin over a bony prominence.
Decubitus ulcers are staged by severity and depth. Superficial
decubitus ulcers (i.e., stage 1 or 2) may be treated locally and,
being superficial, are not associated with osteomyelitis. Decu-
bitus ulcers of the deepest variety (i.e., stage 3 or 4) are often
complicated by osteomyelitis. Chronic osteomyelitis is usually
present when bone is visible in a long-standing deep decubitus
ulcer. The organism responsible for osteomyelitis associated
with decubitus ulcers depends on the location of the ulcer.
Decubitus ulcers on the extremities, above and below the waist,
are usually due to S. aureus. Decubitus ulcers involving the
sacrum in the perianal area are usually due to S. aureus or
organisms of the fecal flora, such as Bacteroides fragilis.
Although superficial decubitus ulcers may be managed with
local care and do not require systemic antibiotics, stage-3 de-
cubitus ulcers often require administration of systemic anti-
biotics for control of local extension of infection. However,
stage-4 decubitus ulcers associated with osteomyelitis require
appropriate antimicrobial therapy as well as adequate surgical
debridement for cure. Culture of blood samples usually yields
negative results in cases of sacral osteomyelitis associated with
decubitus ulcers. The patient’s ESR is frequently elevated. The
definitive diagnosis is achieved by means of bone scan or im-
aging studies with CT or MRI. It is often not possible to obtain
an aseptic bone sample for culture during the surgical debride-
ment procedure because of fecal contamination with sacral os-
teomyelitis. For this reason, patients with sacral osteomyelitis
from a decubitus ulcer are treated empirically for S. aureus,
aerobic gram-negative bacilli, and B. fragilis. Debridement is
often superficial or inadequate, resulting in persistence of
chronic osteomyelitis. After bone debridement, plastic surgical
flap procedures are useful in covering large soft-tissue defects
[29–31].
Chronic Osteomyelitis Associated with Peripheral
Vascular Disease
Elderly persons with peripheral vascular disease are at risk for
developing peripheral gangrene as well as osteomyelitis. Os-
teomyelitis due to peripheral vascular disease usually involves
the digits of the foot. The extent and distribution of the os-
teomyelitis is related to the distribution and extent of under-
AGING AND INFECTIOUS DISEASES • CID 2002:35 (1 August) • 291
lying macular vascular compromise. Osteomyelitis due to
peripheral vascular disease is related to an inadequate mac-
rovascular blood supply. These patients clinically present with
cool or cold extremities, often accompanied by gangrenous
changes in 1 or more toes. Diagnosis of osteomyelitis is con-
firmed as it is with other forms of osteomyelitis.
Treatment of peripheral vascular disease associated with os-
teomyelitis depends on adequate debridement of the involved
bone or gangrenous soft tissue, as well as restoration of the
blood supply to the involved extremity. Vascular bypass pro-
cedures are important to prevent extension or recurrence in
the involved extremity and are particularly useful for patients
without diabetes mellitus. Antimicrobial therapy is directed
Downloaded from https://academic.oup.com/cid/article/35/3/287/409096 by guest on 04 March 2022
against skin pathogens is adjunctive and surgical therapy is
primary [32, 33].
Chronic Osteomyelitis Associated with Diabetes Mellitus
General concepts. Elderly patients with osteomyelitis of the
feet present with deep ulcers, usually involving the plantar sur-
face of the foot, or, less commonly, with ulcers between the
toes (table 2). In contrast, other patients present without an
ulcer but with a chronic draining sinus tract. Patients with
diabetes who have chronic, deep-penetrating foot ulcers and/
or a chronic draining sinus tract of the foot should be consid-
ered as having chronic osteomyelitis until proven otherwise.
Studies indicate a high positive correlation between these con-
ditions and chronic osteomyelitis on bone scan [31, 32].
Clinical presentation. Patients with diabetes mellitus and
chronic osteomyelitis of the feet have few systemic symptoms
and slight or no fever. Blood cultures are usually not positive.
Because of diabetic neuropathic changes, pain is usually absent.
Peripheral pulses in the absence of associated peripheral vas-
cular disease are usually normal. Diabetes mellitus is a micro-
vascular disease, and even in the presence of accelerated ath-
erosclerosis, the peripheral pulses, particularly the dorsalis pedis
pulses, are almost always normal. Determination of a highly
elevated ESR (⭓100 mm/h) is an inexpensive but nonspecific
presumptive test for patients who present with a penetrating
foot ulcer or chronic draining sinus tract due to chronic os-
teomyelitis. Definitive diagnosis is achieved by means of plain
film radiography of the foot. Because chronic osteomyelitis is,
by definition, a long-standing process, these patients always
have changes indicative of chronic osteomyelitis on plain films.
Bone scans are not needed unless there are other diagnostic
possibilities in particular cases. The organisms most commonly
associated with chronic foot osteomyelitis in patients with di-
abetes mellitus include S. aureus, group B streptococci, aerobic
gram-negative bacilli, and B. fragilis. Importantly, Pseudomonas
aeruginosa is not associated with chronic foot osteomyelitis in
diabetes mellitus. P. aeruginosa is often cultured from samples
of open ulcers or draining sinus tracts, but this is indicative of
Table 2. Foot infections in patients with diabetes mellitus.

Category of infection

Deep, soft-tissue
Clinical feature Cellulitis infection/fasciitis Chronic osteomyelitis
Usual pathogens Streptococcus (group A, B, C, G), S. aureus, streptococci, coliform bacilli, S. aureus, streptococci, coliform bacilli, B. fragilis
Staphylococcus aureus Bacteroides fragilis
Fever, temperature Variable ⭓38.9C (⭓102F) ⭐38.9C (⭐102F)
Wound appearance Red, tender, warm Extremely tender, warm Erythema, swelling, not warm (fever and other
symptoms may not be apparent except during
flare)
Drainage None Foul Purulent
Crepitance Absent Present Absent
WBC count Elevated or normal Elevated Normal
Findings on plain film No gas Gross gas in the soft tissues Signs of bone destruction

Downloaded from https://academic.oup.com/cid/article/35/3/287/409096 by guest on 04 March 2022

Treatment Antibiotics effective against strepto- Surgical debridement plus appropriate anti- Surgical debridement plus appropriate antibiotics,
cocci and staphylococci, such as biotics, such as meropenem or piperacil- such as meropenem or piperacillin-tazobactam
antistaphylococcal penicillins or lin-tazobactam or a quinolone plus either or a quinolone plus either clindamycin or
cephalosporins clindamycin or metronidazole metronidazole

NOTE. Adapted from [34].

surface colonization, and the organism is not present in bone
biopsy specimens obtained under aseptic surgical conditions.
Clinicians should not base their decisions regarding antimi-
crobial therapy on the results of cultures of samples of foot
ulcers or draining sinus tracts, because such culture information
is not indicative of the infectious process in bone. A bone biopsy
done under aseptic conditions is the preferred way to obtain
culture material on which to base decisions regarding specific
antibiotic therapy [7, 31–33, 35].
Therapy. Empirical treatment with an antibiotic effective
against the usual pathogens in chronic osteomyelitis of the feet
of diabetic patients, in practical terms, is often done pending
the results of or instead of culture of specimens obtained by
bone biopsy. Patients with neuropathic joints (Charcot’s joints)
and chronic osteomyelitis may benefit from orthopedic appli-
ances that shield the foot from further trauma and take the
pressure off the weight-bearing parts of the foot. Chronic os-
teomyelitis in patients with diabetes, in contrast to acute os-
teomyelitis, cannot be cured with antimicrobial therapy alone.
Antimicrobial therapy alone is ineffective, because the infected
bone sequestra have no blood supply, and antibiotics are unable
to penetrate these floating islands of infected bone and eradicate
the infection. The definitive treatment of chronic osteomyelitis
foot infections in persons with diabetes depends on adequate
surgical debridement or amputation of the extremity. In cases
in which adequate surgical debridement is not possible or is
refused, long-term suppressive therapy with orally administered
antimicrobials is an alternative approach. However, chronic
osteomyelitis, over time, may be complicated by systemic non-
infectious disorders, which may threaten the host. Epidermoid
(squamous cell) carcinoma at the site of the ulcer or sinus tract
may occur years later in untreated patients. Similarly, amyloi-
dosis is another late complication of chronic osteomyelitis in
these patients [2, 3, 7, 35].
For patients with diabetes who have foot infections and who
present with deep, persistent ulcers or chronically draining si-
nus tracts, the presumptive diagnosis of chronic osteomyelitis
should be made and tests to confirm the diagnosis should be
ordered. Peripheral vascular bypass procedures are of little use
in treating patients with diabetes and chronic osteomyelitis of
the lower extremities, because diabetes mellitus is a microvas-
cular disease. Patients with chronic osteomyelitis may develop
local suppurative complications, such as surrounding cellulitis,
or systemic complications, such as bacteremia. Long-term com-
plications of chronic osteomyelitis in patients with diabetes
mellitus include squamous cell carcinoma at the ulcer or sinus
site or secondary amyloidosis [6, 7, 27, 36].
Oral versus Intravenous Antimicrobial Therapy for Osteomyelitis
Decisions regarding antimicrobial therapy for osteomyelitis
should be based on the known or presumed pathogens and the
ability of the agents to penetrate bone in sufficient concentra-
tions, whether given intravenously or orally. Because of the
long duration of therapy for treatment of osteomyelitis, treat-
ment is usually begun with intravenously administered agents
and then continued with oral agents. Oral agents selected to
treat osteomyelitis should have a high degree of bioavailability
and the same spectrum and tissue penetration as their par-
enteral counterparts. Chronic osteomyelitis may be treated en-
tirely via the oral route, with clinical outcomes comparable to
those that occur after parenteral therapy. However, the outcome
of chronic osteomyelitis depends primarily on the adequacy of
surgical debridement, and appropriate antimicrobial therapy is
adjunctive [7, 34, 37–40].

292 • CID 2002:35 (1 August) • AGING AND INFECTIOUS DISEASES

References
1. Norman DC, Yoshikawa TT. Infections of the bone, joint, and bursa.
Clin Geriatr Med 1994; 10:703–18.
2. Markus HS. Haematogenous osteomyelitis in the adult: a clinical and
epidemiological study. Q J Med 1989; 71:521–17.
3. Waldvogel FA, Medoff G, Swarz MN. Osteomyelitis: a review of clinical
features, therapeutic considerations, and unusual aspects. N Engl J Med
1970; 282:198–206.
4. Waldvogel FA, Medoff G, Swarz MN. Osteomyelitis: a review of clinical
features, therapeutic considerations and unusual aspects (second of
three parts). N Engl J Med 1970; 282:260–6.
5. Propst-Proctor SL, Dillingham MF, McDougall IR, et al. The white
blood cell scan in orthopedics. Clin Orthop 1982; 168:157–65.
6. Strausbaugh LJ. Vertebral osteomyelitis. In: Jauregui LE, ed. Diagnosis
and management of bone infections. New York: Marcel Dekker, 1995:
174–5.
7. Cunha BA, Dee R, Klein NC, et al. Bone and joint infections. In: Dee
R, Hurst LC, Gruber MA, et al., eds. Principles of orthopaedic practice.
2nd ed. New York: McGraw Hill, 1997:317–42.
8. Sapico FL. Microbiology and antimicrobial therapy of spinal infections.
Orthop Clin North Am 1996; 27:9–13.
9. Torda AJ, Gottlieb T, Bradbury R. Pyogenic vertebral osteomyelitis:
analysis of 20 cases and review. Clin Infect Dis 1995; 20:320–8.
10. Cahill DW, Love LC, Rechtine GR. Pyogenic osteomyelitis of the spine
in the elderly. J Neurosurg 1991; 74:878–86.
11. Thompson D, Bannister P, Murphy P. Vertebral osteomyelitis in the
elderly. Br Med J (Clin Res Ed) 1988; 296:1309–11.
12. Babinchak TJ, Riley DK, Rotheram EB Jr. Pyogenic vertebral osteo-
myelitis of the posterior elements. Clin Infect Dis 1997; 25:221–4.
13. McHenry MC, Easley KA, Locker GA. Vertebral osteomyelitis: long-
term outcome for 253 patients from 7 Cleveland-area hospitals.
2002; 34:1342–50.
14. Chelsom J, Solberg CO. Vertebral osteomyelitis at a Norwegian uni-
versity hospital 1987–97: clinical features, laboratory findings and out-
come. Scand J Infect Dis 1998; 30:147–51.
15. Belzunegui J, Del Val N, Intxausti JJ, et al. Vertebral osteomyelitis in
northern Spain: report of 62 cases. Clin Exp Rheumatol 1999; 17:
447–52.
16. Sapico FL. Microbiology and antimicrobial therapy of spinal infections.
Orthop Clin North Am 1996; 27:9–13.
17. Mader JT, Shirtliff ME, Bergquist S, et al. Bone and joint infections in
the elderly: practical treatment guidelines. Drugs Aging 2000; 16:67–80.
18. Saccente M. Periprosthetic joint infections: a review for clinicians. In-
fect Dis Clin Pract 1998; 7:431–41.
19. Kegel-Szerejko M, Maderazo EB, Cunha BA, Skull E, Gossing HR.
Host factors and prosthetic joint infections. Am J Infect Control
1981; 9:43–39.
20. Cunha BA. Diagnosis of infected joint replacements. Infect Dis Pract
2000; 3:24–65.
AGING AND INFECTIOUS DISEASES • CID 2002:35 (1 August) • 293
21. Cunha BA. Infectious complications in orthopedic surgery: muscu-
loskeletal infections. AIDS Press 1983; 3:1–47.
22. Powers KA, Terpenning MS, Voice RA, et al. Prosthetic joint infections
in the elderly. Am J Med 1990; 88:9N–13N.
23. Tattevin P, Cremieux AC, Pottier JC, et al. Prosthetic joint infection:
when can prosthesis salvage be considered? Clin Infect Dis 1999; 29:
292–5.
24. Bose WJ, Gearen PF, Randall JC, et al. Long-term outcome of 42 knees
with chronic infection after total knee arthroplasty. Clin Orthop
1995; 319:285–96.
25. Shea KW, Cunha BA. Escherichia coli sternal osteomyelitis after open
heart surgery. Heart Lung 1995; 24:177–8.
26. Johnson P, Frederiksen JW, Sanders JH, et al. Management of chronic
sternal osteomyelitis. Ann Thorac Surg 1985; 40:69–72.
27. Bamberger DM. Diagnosis and treatment of osteomyelitis. Compr Ther
2000; 26:89–95.
Downloaded from https://academic.oup.com/cid/article/35/3/287/409096 by guest on 04 March 2022
28. Mader HT, Shirtliff ME, Bergquist S, et al. Bone and joint infections
in the elderly: practical treatment guidelines. Drugs Aging 2000; 16:
67–80.
29. Darouiche RO. Osteomyelitis associated with pressure sores. Arch In-
tern Med 1994; 154:753–8.
30. Kertesz D, Chow AW. Infected pressure and diabetic ulcers. Clin Geriatr
Med 1992; 8:835–52.
31. Braun TI, Lorber B. Chronic osteomyelitis. In: Schlossberg D, ed. Or-
thopedic infection. New York: Springer-Verlag, 1988:9–20.
32. Waldvogel FA, Medoff G, Swarz MN. Osteomyelitis: a review of clinical
features, therapeutic considerations, and unusual aspects. 3. Osteo-
myelitis associated with vascular insufficiency. N Engl J Med 1970; 282:
316–22.
33. Garcia-Lechuz HM, Bachiller P, Vasallo FJ, et al. Group B streptococcal
osteomyelitis in adults. Medicine (Baltimore) 1999; 78:191–9.
34. Cunha BA. Antibiotic selection for diabetic foot infections: a review.
J Foot Ankle Surg 2000; 39:253–7.
35. Harvey J, Cohen MM. Technetium 99–labeled leukocytes in diagnosing
diabetic osteomyelitis in the foot. J Foot Ankle Surg 1997; 36:209–14.
36. Caputo GM, Cavanagh PR, Ulbrecht JS, et al. Assessment and man-
agement of foot disease in patients with diabetes. N Engl J Med
1994; 331:854–60.
37. Bamberger DM, Daus GP, Gerding DN. Osteomyelitis in the feet of
diabetic patients: long-term results, prognostic factors, and the role of
antimicrobial and surgical therapy. Am J Med 1987; 83:653–60.
38. Gentry LO. Antibiotic therapy for osteomyelitis. Infect Dis Clin North
Am 1990; 4:485–99.
39. Cunha BA. Antibiotic tissue penetration. Bull N Y Acad Med 1983;
59:443–9.
40. Black J, Hunt TL, Godley PJ, et al. Oral antimicrobial therapy for
adults with osteomyelitis or septic arthritis. J Infect Dis 1987; 155:
968–72.