The three basic types of skeletal infections are:
Osteomyelitis - infection
of the bone
Septic arthritis - infection of the joint
Mycetoma - a local, chronic and progressive infectious disease of the skin, subcutaneous
tissues and bone
Osteomyelitis is a purulent inflammation of bone caused most often by bacteria and only occasionally by other microorganisms. In order of frequency of infection the bacterial species are:
Streptococcus spp. ) Long bone and spine infections
Members of the Enterobacteriaceae )
Bacteroides spp. - mandibular infections
Most osteomyelitis is of hematogenous origin. The clinical picture varies with age. In children through the age of puberty the long bones of the extremities are most often involved with the metaphysis as the initial infected site. In adults hematogenous osteomyelitis most often affects the spine. This age-dependent preference for bone relates to the vasculature and blood flow to the site. In children, the metaphysis is very active metabolic tissue with a large blood flow and with vasculature predisposed to infection. Phagocytes lining the capillaries in this region are deficient in number and function. The nutrient arteries near the epiphyseal cartilage are nonanastomosing, thereby allowing any blockage to produce tissue necrosis and the sinusoids (venous side of capillary) have slow, turbulent flow predisposing to thrombosis. As aging occurs metaphysis metabolism slows down, blood flow decreases and phagocytic activity increases. Concomitant with these changes the vertebrae become more vascular with maturation (senile hyperemia) and bacteremias seed vertebral bodies preferentially at the more vascular anterior vertebral end plates. In addition, lumbar paracentral veins communicate freely with pelvic veins by valveless anastomoses. Theoretically, retrograde flow from pelvic tissues (urethra, prostate, bladder) to lumbar vertebrae explains the spread of pelvic infections preferentially to lumbar vertebrae.
In about 25% of patients with osteomyelitis, the
predisposing factor is trauma to the bone at or near the site of infection.
Infections of the mandible are often due to traumatic dental procedures
while the installation of prosthetic devices, such as artificial joints,
predisposes to long bone infection.
The host responds to the presence of bacteria in the metaphysis with a local increase in vascular permeability, resulting in edema, increased vascularity and the influx of polymorphonuclear leukocytes. Pressure increases as pus collects and is confined within rigid bone. Exudation through Volkmann's canals and the haversian canal affords little relief, although the relatively inelastic periosteum may become elevated. The blood supply to the area of involvement is decreased secondary to the pressure; necrosis of the infected bone may result in the formation of a sequestrum. A protein-rich liquid containing inflammatory cells may collect in an adjacent joint but such effusions are sterile.
After the vascular supply to the involved area has been interrupted and necrosis has occurred, the chronic phase of osteomyelitis is established. The residual dead bone acts as a foreign body, making the eradication of bacteria impossible until the sequestrum is removed.
If the infected area becomes well demarcated and the infection is contained, the acute inflammatory process may subside, leaving a subperiosteal accumulation of pus which may be discovered by tenderness on palpation. This relatively quiescent form of subperiosteal infection is termed a Brodie's abscess. After some time, there is deposition of new bone, the involucrum, under the elevated periosteum.
In osteomyelitis of the spine, infection most often
involves the vertebral body. It spreads readily through the anastomotic
venous system to adjacent ligaments and vertebral bodies. It is common
for more than one vertebral body to be involved. Pus may accumulate between
the vertebral periosteum and dura mater, forming an extradural abscess.
Compression of the spinal cord may result, yielding a paraplegia. If a
subdural abscess ruptures into the subarachnoid space, meningitis results.
Hematogenous osteomyelitis is often preceded by the signs and symptoms of bacteremia:
This phase of the illness may last for several days.
The second phase of the disease is the clinical onset of involvement of bone. This gives rise to:
Soft tissue around the inflamed bone which is
Diagnosis is based upon:
Clinical symptoms of an infection
Laboratory evidence of an infection:
of an organism
Increase in antibody titer
Presence of bone pain
Soft tissue swelling
Limited motion of extremity
Roentgenographic changes occur late in disease and should not be waited for to make the diagnosis; this would allow the development of chronic osteomyelitis. A differential diagnosis should include:
Rheumatic fever - there is severe pain and limitation
of joint motion in this disease but there is no
Monoarthritic rheumatoid arthritis - the major swelling
and tenderness is limited to the joint,
without local tenderness on palpation over the adjacent metaphysis.
Poliomyelitis - tenderness of the bone in an apparently
paralyzed extremity indicates
osteomyelitis. There is no bone tenderness in polio.
Septic arthritis - joints are exquisitely tender
and painful, whereas the swollen joint associated
with osteomyelitis may be gently manipulated through a limited range of motion.
Bacterial cellulitis - there is warmth, erythema,
pain and edema of the soft tissue but it is clearly
demarcated whereas in osteomyelitis it is not clearly demarcated.
Acute osteomyelitis should be treated with a parenterallyadministered antibiotic based on the infecting organism:
Staphylococcus aureus - nafcillin
Streptococcus pyogenes - penicillin G
Gram-negative rods - ampicillin, gentamicin or chloramphenicol
Bacteroides spp. - clindamycin
Chronic osteomyelitis requires surgical procedures
as well as antibiotic therapy. This includes full debridement and excision
of all dead bone and necrotic tissue (sequestrectomy).
Septic arthritis, the invasion of the synovial membrane
by microorganisms, usually with extension into the joint space, is generally
secondary to infection elsewhere in the body. In young adults, the primary
infection is generally a genital lesion caused by Neisseria gonorrhoeae.
In all other age groups the most common agent is Staphylococcus aureus,
which spreads from a cutaneous lesion. Several other agents may cause septic
arthritis but their frequency of infection is low.
There is no microorganism that shows a tropism for
synovial membrane and/or joints. During a septicemia, caused by an infection
at a site outside of the joint, organisms are deposited in or on the synovial
membrane and only rarely proliferate to cause a septic arthritis. When
they do grow, the infection may spread to the joint space and then spread
to bone and cartilage.
When joint infection occurs as a result of bacteremia, the initial growth of microorganisms is either in the synovial membrane or in the adjacent bone. In either case, an inflammation of the synovial membrane is quickly established and results in a marked increase in leukocytes in the synovial fluid, even though the fluid itself is sterile. When the microorganisms have spread into the joint fluid, culture of the fluid reveals the etiology of the infection. The pathologic findings are varied and depend on the duration of the infection, the organism and the resistance of the host. Early in the infection, only inflammatory changes in the synovium are seen. Late in the course of untreated septic arthritis, destruction of joint structures is marked. Articular cartilage is particularly vulnerable because it is an avascular tissue.
In acute, pyogenic arthritis, the cartilage characteristically dissolves first at points of articular contact to expose the underlying bone. As destructive changes occur several abnormalities appear in the synovial fluid:
Low concentration of glucose
Activation of proteolytic enzymes
Presence of mucin precipitate
The clinical manifestations of septic arthritis are variable and related to many factors: the etiologic agent, the joint involved and the age of the patient. In gonococcal arthritis one sees:
A prominent prodrome consisting of fever, chills,
headache, anorexia and malaise
Migratory polyarthralgia or polyarthritis prior to localization in one or more joints
Skin lesions of gonococcemia
Small joint effusions
Tenosynovitis in about 1/3 of patients
Large joints are most involved
In nongonococcal septic arthritis the clinical picture
is variable. At one extreme, the patient may complain of an acutely painful,
swollen joint that is exquisitely tender and rigidly limited in range of
motion but no manifestations of infection elsewhere. At the other extreme
there may be little or no signs of inflammation.
The definitive diagnosis of septic arthritis requires examination of the synovial fluid. This fluid will show:
Presence of microorganisms
Presence of antibody directed against the microorganisms
More than 10,000 pmns/mm3
Decreased glucose concentration (< 0.6% of blood glucose)
Increased lactic acid concentration (> 65 mg/dl)
Treatment consists of both drainage of the synovial
fluid and administration of an antibiotic systemically.
Mycetoma is caused by at least 20 species of actinomycetes
and fungi. The most common infecting agents are Nocardia spp and
Mycetoma is a local chronic and progressive infection
of the skin, subcutaneous tissues and bone. It is characterized by swelling
that is often grotesque and disfiguring and by multiple sinus tracts that
drain granule-containing pus.
PATHOLOGY AND CLINICAL SYMPTOMS:
The disease is acquired by traumatic implantation in the skin. The microorganisms grow through the subcutaneous tissue into the bone. As this occurs, there is hyperplasia of the tissues, formation of pus containing granules (which are actually colonies of microorganisms), expression of pus to the surface of the skin and granuloma formation at the periphery of the infected area. The classical triad of symptoms is:
Gross deformity of the infected
Granules in the pus
DIAGNOSIS AND TREATMENT:
Diagnosis is made by the presence of the classical
triad of symptoms and by culture of the pus draining from the wound. Treatment
is initially with sulfonamides for Nocardia or Amphotericin B for
fungi. If the fungal infection does not respond to amphotericin B then
amputation is required.