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Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996.

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Medical Microbiology. 4th edition.

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Chapter 100Bone, Joint, and Necrotizing Soft Tissue Infections

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General Concepts

Necrotizing Soft Tissue Infections

Etiology

Anaerobic microorganisms such as Bacteroides species, Peptostreptococcus species, and Clostridium species are largely responsible for these infections. Mixed infections by aerobic and facultative anaerobic organisms are common.

Pathogenesis

Susceptible persons have experienced trauma or surgery and frequently have diabetes and/or vascular insufficiency. Organisms gain entry via direct inoculation. Local hypoxia and decreased oxygen-reduction potentials favor anaerobic growth.

Clinical Manifestations

This signs of disease include production of tissue gas, a putrid discharge, tissue necrosis, fever, (occasionally) systemic toxicity, and absence of classic signs of inflammation.

Microbiologic Diagnosis

These infections are usually diagnosed by clinical presentation. Aerobic and anaerobic wound cultures help identify the major pathogens.

Prevention and Treatment

Immediate surgical debridement of all necrotic tissue is vital. High-dose parenteral antibiotic therapy should be started immediately. Hyperbaric oxygen therapy may be indicated.

Joint Infections

Etiology

Neisseria gonorrhoeae and S taphylococcus aureus are responsible for most cases of bacterial arthritis.

Pathogenesis

Joint infections are usually a result of hematogenous spread, but may also arise from traumatic inoculation or by extension from an adjacent focus of infection. Proteolytic enzymes of polymorphonuclear leukocytes, bacterial toxins, and pressure from joint swelling all contribute to the damage of articular surfaces.

Clinical Manifestations

Joint swelling. pain, warmth (inflammation), decreased range of motion, and fever are the classic symptoms. Disseminated gonococcal infections may also cause migratory polyarthritis, dermatitis, and tenosynovitis.

Microbiologic Diagnosis

Aspiration and culture of synovial fluid usually provides the definite diagnosis.

Prevention and Treatment

Gonococcal arthritis may be prevented by techniques used to decrease the risk for sexually transmitted disease. The treatment for all septic arthritides is administration of parenteral antibiotics. Some cases may require aspiration and/or surgical debridement.

Bone Infections

Etiology

Staphylococcus aureus is the most commonly isolated pathogen. Polymicrobic infections are frequent in contiguous-focus osteomyelitis.

Pathogenesis

Organisms may reach the bones by hematogenous spread, by direct extension from a contiguous focus of infection, or as a result of trauma. A cycle of increased pressure from infection, inflammation, local ischemia, and bone necrosis may establish itself and lead to a chronic infection.

Clinical Manifestations

Hematogenous osteomyelitis classically presents with high fever and pain around the involved bone. Sinus tracts with purulent drainage are evidence of chronic osteomyelitis.

Microbiologic Diagnosis

Bone biopsy and/or debridement cultures are mandatory with rare exceptions. Sinus tract cultures are unreliable.

Prevention and Treatment

Treatment consists of surgical debridement and long-term, culture-directed antimicrobial therapy. Hematogenous osteomyelitis in children may be treated with antibiotics alone.

Introduction

Necrotizing infections of the soft tissues are characterized by extensive tissue necrosis and production of tissue gas. These infections may extend through tissue planes and are not well contained by the usual inflammatory mechanisms. They may develop and progress with dramatic speed, and extensive surgery and systemic antibiotic therapy are required to eradicate them.

Arthritis or inflammation of a joint space may be caused by a wide variety of infectious or noninfectious processes. Non-infectious arthritis is the more common type of arthritis and is usually secondary to degenerative, rheumatoid, or posttraumatic changes within the joint. Infectious arthritis, although less common, is often accompanied by a striking polymorphonuclear inflammatory response and can cause severe destruction of the articular cartilage if not properly diagnosed and treated.

Bone infections are called osteomyelitis (from osteo [bone], plus myelitis [inflammation of the marrow]). Hematogenous osteomyelitis and contiguous-focus osteomyelitis are the two major types of bone infections. Both types can progress to a chronic bone infection characterized by large areas of dead bone.

Bone, joint, and soft tissues, with the exception of the skin, are normally sterile areas. Bacteria may reach these sites by either hematogenous spread or spread from an exogenous or endogenous contiguous focus of infection (Fig. 100-1). Host defenses are important in containing necrotizing soft tissue infections. A systemically or locally compromised host (Table 100-1) is more likely to develop these types of infections and to be unable to contain them.

Figure 100-1. Bacterial spread to bone, joints, and soft tissue.

Figure 100-1

Bacterial spread to bone, joints, and soft tissue.

Table 100-1. Systematic and Local Factors That Adversely Affect the Host Response.

Table 100-1

Systematic and Local Factors That Adversely Affect the Host Response.

Necrotizing Soft Tissue Infections

An exact classification of necrotizing subcutaneous, fascial, and muscle infections is difficult because the distinctions between many of the clinical entities are blurred. Clinical classification is as follows: (1) crepitant anaerobic cellulitis, (2) necrotizing fasciitis, (3) nonclostridial myonecrosis, (4) clostridial myonecrosis, (5) fungal necrotizing cellulitis, and (6) miscellaneous necrotizing infections in the immunocompromised host. These types of infections usually occur in traumatic or surgical wounds or around foreign bodies and in patients who are medically compromised by diabetes mellitus, vascular insufficiency, or both. In the traumatically, surgically, or medically compromised patient, local tissue conditions, hypoxia, and decreased oxidation-reduction potential (Eh) promote the growth of anaerobes. Most necrotizing soft tissue infections have an endogenous anaerobic component. Since anaerobes are the predominant members of the microflora on most mucous membranes, there are many potential pathogens. Hypoxic conditions also allow proliferation of facultative aerobic organisms, since polymorphonuclear leukocytes function poorly under decreased oxygen tensions. The growth of aerobic organisms further lowers the Eh, more fastidious anaerobes become established, and the disease process rapidly accelerates.

Discernible quantities of tissue gas are present in most of these infections. Carbon dioxide and water are the natural end products of aerobic metabolism. Carbon dioxide rapidly dissolves in aqueous media and rarely accumulates in tissues. Incomplete oxidation of energy sources by anaerobic and facultative aerobic bacteria can result in the production of gases that are less water soluble and therefore accumulate in tissues. Hydrogen is presumably the major tissue gas in mixed aerobic-anaerobic soft tissue infections. Its presence indicates rapid bacterial multiplication at a low Eh.

Clinically, the hallmarks of mixed aerobic-anaerobic soft tissue infections are tissue necrosis, a putrid discharge, gas production, the tendency to burrow through soft tissue and fascial planes, and the absence of classic signs of tissue inflammation. Table 100-2 shows the differentiation between the common bacterial necrotizing soft tissue infections.

Table 100-2. Differentiation of the Common Necrotizing Bacterial Soft Tissue Infection.

Table 100-2

Differentiation of the Common Necrotizing Bacterial Soft Tissue Infection.

Crepitant Anaerobic Cellulitis

Nonclostridial and clostridial cellulitides have a similar clinical picture and are discussed together under the term, crepitant anaerobic cellulitis. Crepitant anaerobic cellulitis appears as a necrotic soft tissue infection with abundant connective tissue gas. The condition usually occurs after local trauma in patients with vascular insufficiency of the lower extremities. Multiple aerobic and anaerobic organisms have been isolated, including Bacteroides species, Peptostreptococcus species, Clostridium species, and members of the family Enterobacteriaceae. Crepitant anaerobic cellulitis can be differentiated from more serious soft tissue infections by the abundance of soft tissue gas, lack of marked systemic toxicity, gradual onset, less severe pain, and absence of muscle involvement.

Necrotizing Fasciitis

Necrotizing fasciitis is a relatively rare infection with a high mortality (40 percent). The infection was originally called hemolytic streptococcal gangrene by Meleney in 1924. Although his clinical description was accurate, better culture techniques have demonstrated that organisms other than Streptococcus pyogenes more commonly cause these infections. Clinical manifestations include extensive dissection and necrosis of the superficial and often the deep fascia. The infection undermines adjacent tissue and leads to marked systemic toxicity. Thrombosis of subcutaneous blood vessels leads to necrosis of the overlying skin. Initial local pain is replaced by numbness or analgesia as the infection involves the cutaneous nerves. Most cases of fasciitis follow surgery or minor trauma. The highest incidence is seen in patients with small vessel diseases such as diabetes mellitus. When careful bacteriologic techniques are used, anaerobes, particularly Peptostreptococcus, Bacteroides, and Fusobacterium species, are found in 50 to 60 percent of cases. Aerobic organisms, especially Streptococcus pyogenes, Staphylococcus aureus, and members of the Enterobacteriaceae have also been isolated. Most infections are mixed aerobic-anaerobic infections, but a type of necrotizing fasciitis caused solely by Streptococcus pyogenes has been reported and is referred to by the lay press as “flesh eating bacteria.”

Nonclostridial Myonecrosis

Nonclostridial myonecrosis, called synergistic necrotizing cellulitis by Stone and Martin, is a particularly aggressive soft tissue infection. It is similar to clostridial myonecrosis in that there is widespread involvement of soft tissue with necrosis of muscle tissue and fascia. The prominent involvement of muscle tissue differentiates this infection from necrotizing fasciitis. Subcutaneous tissue and skin are secondarily involved. Clinically, there is exquisite local tenderness, with minimal skin changes, and drainage of foul-smelling “dish-water” pus from small skin surface ulcers. Severe systemic toxicity is found in most patients. Nonclostridial myonecrosis occurs most frequently in the perineal area, as a result of an extension of a perirectal abscess, and in the lower extremities of patients with vascular insufficiency. Multiple organisms have been isolated, including Peptostreptococcus and Bacteroides species and members of the Enterobacteriaceae. Mortality approaches 75 percent.

Clostridial Myonecrosis

Clostridial myonecrosis, or gas gangrene, is a clostridial infection primarily of muscle tissue. Clostridium perfringens is isolated in 90 percent of these infections. Other clostridial species frequently isolated are C novyi (4 percent), C septicum (2 percent), C histolyticum, C fallax, and C bifermentans. Classically, clostridial myonecrosis has an acute presentation and a fulminant clinical course. The infection usually occurs in areas of major trauma or surgery or as a complication of thermal burns. However, it also has been reported following minor trauma, including intravenous administration of drugs, intramuscular injections of epinephrine, insect bites, and nail punctures. Moreover, it may occur in the absence of recent trauma by activation of dormant clostridial spores in old scar tissue. Finally, clostridial myonecrosis may occur in the absence of trauma, by bacteremic spread of the organism from a gastrointestinal or genitourinary site. Clostridium septicum is the major cause of spontaneous, nontraumatic gas gangrene and is often associated with a lesion in the colon such as an adenocarcinoma.

Clostridial myonecrosis is diagnosed mainly on a clinical basis. The infection may be so rapidly progressive that any delay in recognition or treatment may be fatal. The onset is sudden, often within 4 to 6 hours after an injury. Sudden, severe pain in the area of infection is an early clinical finding. Early in the course of infection, the skin overlying the wound appears shiny and tense and then becomes dusky. Within hours, the skin color may progress from dusky to a bronze discoloration, which can advance at a rate of 1 inch per hour. Vesicles or hemorrhagic bullae appear near the wound. A thin, brownish, often copious fluid exudes from the wound. Bubbles occasionally appear in the drainage. This exudate has often been described as having a sweet “mousy” odor. Swelling and edema in the area of infection is pronounced. Within hours the skin overlying the lesion can rupture and the muscle herniate. At surgery, the infected muscle is dark red to black, is noncontractile, and does not bleed when cut. Crepitus, although not prominent, is sometimes detected. Radiographs may show tissue gas outlining fascial planes and muscle bundles.

The rapid tissue necrosis in clostridial myonecrosis is caused by the clostridial toxins. Clostridial species are capable of producing multiple toxins, each with its own mode of action. Clostridium perfringens produces at least 12 different extracellular toxins. The most common of these, a lecithinase called alpha toxin, is hemolytic, histotoxic, and necrotizing. Other toxins act as collagenases, proteinases, deoxyribonucleases (DNases), fibrinolysins, and hyaluronidases. The systemic toxic reaction cannot be fully explained by a single circulating exotoxin. The “toxic factor” may be produced by interaction of the clostridial toxins with infected tissue. The mortality from clostridial myonecrosis ranges from 15 to 30 percent.

Fungal Necrotizing Cellulitis

Phycomyces and Aspergillus species may cause a gangrenous cellulitis in compromised hosts. The hallmark of these infections is the invasion of blood vessels by hyphae, followed by thrombosis and subsequent necrosis extending to all soft tissue compartments. Spores from these fungi are ubiquitous.

The Phycomyces species are characterized by broad-based nonseptate hyphae. Rhizopus, Mucor, and Absidia are the major pathogenic genera within the family Mucoraceae. Serious rhinocerebral, pulmonary, or disseminated infections have been found in patients with diabetes, lymphoma, or leukemia. Phycomycotic gangrenous cellulitis usually occurs in patients with severe burns or diabetes. The characteristic dermal lesion is a black, anesthetic ulcer or an area of necrosis with a purple edematous margin. There is no gas or exudate, and the infection may progress rapidly.

Aspergillus species are characterized histologically by branching septate hyphae. These fungi can cause serious pulmonary or disseminated infections in compromised hosts. Aspergillus gangrenous cellulitis may be primary or from a disseminated infection. The dermal lesion is an indurated plaque that leads to a necrotic ulcer. Gas and exudate are not present.

Joint Infections

Infectious arthritis may arise either from hematogenous spread or by direct extension from an adjacent bone or soft tissue infection. The infection is usually a localized suppurative process. Although any joint can become infected, the knee is most commonly involved (53 percent), followed by the hip (20 percent), shoulder (11 percent), wrist (9 percent), ankle (8 percent), and elbow (7 percent). The infection is monarticular almost 90 percent of the time. However, a bacterial polyarthritis may be seen.

In the normal host, polymorphonuclear leukocytes respond rapidly to the infection and release proteolytic enzymes, which can cause extensive destruction of the articular cartilage within 3 days. The joint may also be damaged directly by the release of bacterial toxins and lysosomal enzymes. Furthermore, an effusion is almost always present and is confined within the joint capsule; this increases intra-articular pressure and interferes with blood supply and nutrition. These complications may occur with almost any type of septic arthritis, but are most common in nongonococcal bacterial infections. Children are especially vulnerable since extension to the epiphyseal growth plate may stunt bone growth.

Several conditions are known to predispose joints to the development of septic arthritis. Corticosteroid therapy, rheumatoid arthritis, and degenerative joint disease are the most common underlying factors. Total joint arthroplasties are susceptible to hematogenous infections. Patients with diabetes mellitus, leukemia, cancer, cirrhosis, chronic granulomatous diseases, or hypogammaglobulinemia or those undergoing cytotoxic chemotherapy or practicing substance abuse also have an increased incidence of infectious arthritis.

Gonococcal Arthritis

The most common cause of bacterial arthritis in healthy young adults in North America is Neisseria gonorrhoeae. Gonococcal arthritis typically follows primary infection of a mucosal site and is thought to spread hematogenously to the joint. Females are affected four times as often as males, and about one-half of all affected females are either pregnant or menstruating. This association supports the theory that endocrine factors play a role in gonococcal arthritis, although the exact mechanism has not been elucidated. Strains of N gonorrhoeae that cause disseminated gonococcal infections differ phenotypically from those that cause simple mucosal infections and are thought to be more virulent.

The disease may manifest itself as part of a disseminated gonococcal infection or as a monarticular joint infection. The presenting symptoms in disseminated gonococcal infections may be mixed, with migratory polyarthralgias, fever, chills, dermatitis, and tenosynovitis. Most of these patients have asymptomatic genital, anal, or pharyngeal gonococcal infections. Skin lesions, when present, begin as small erythematous papules but usually progress to vesicular or pustular stages. Tenosynovitis is characterized by pain, swelling, and periarticular redness. Patients with monarticular disease often have a history of polyarthralgias, and some authorities believe that this represents a continuum from disseminated gonococcal infection.

Nongonococcal Arthritis

Nongonococcal bacterial arthritis is a serious infection with significant sequelae. Mortality as high as 12 percent has been reported, and up to 75 percent of survivors suffer some type of functional loss in the involved joint. Classically, patients present with fever and pain, swelling, warmth, and decreased range of motion in the involved joint. The joint effusion should be aspirated and cultured to determine the exact etiologic agent. There are variations among age groups, but the most common cause of nongonococcal bacterial arthritis is Staphylococcus aureus. In adults, all Gram-negative bacilli together account for about 20 percent of cases. It is generally accepted that Gram-negative infections are the most virulent, with Pseudomonas aeruginosa and Escherichia coli being the most common. Intravenous drug abusers have a significant incidence of infection with Gram-negative organisms. Streptococcal species engender a small but significant proportion of infections (10 to 15 percent). About 10 percent of patients with nongonococcal arthritis have polymicrobial infections. In addition, there are frequent microbiologic associations with concomitant disease states. For example, bacterial arthritis following infectious diarrhea may be caused by Shigella, Salmonella, Campylobacter, or Yersinia species. Streptobacillus moniliformis may cause a migrating polyarthritis; however, this is rare. In children, Haemophilus influenzae is a cause of septic arthritis.

Diagnosis of Bacterial Arthritis

Several laboratory tests are used to diagnose infectious arthritis. The definitive test involves culturing the fluid from the involved joint after aspiration or incision and drainage. Gram stains are often unreliable, although they may provide initial clues. Synovial fluid analysis usually reveals a turbid fluid with leukocyte counts greater than 100,000/mm3 in 30 to 50 percent of cases. In bacterial arthritis, the level of polymorphonuclear leukocytes often approaches 90 percent. Low joint fluid glucose levels and high lactate levels are indicative of septic arthritis, but are nonspecific. Peripheral blood leukocyte counts are usually elevated in children, but are often within normal limits in adults. Finally, radiography may show joint space widening and soft tissue swelling in infections more than 2 weeks old.

Granulomatous Arthritis

Infectious arthritis may be caused by mycobacteria and certain fungi. This disease may be very insidious and may progress for several months before infection is even considered. These organisms usually produce a chronic monarticular arthritis with a granulomatous inflammatory response. Mycobacterium tuberculosis infections of the musculoskeletal system are the most common extrapulmonary manifestation of tuberculosis and result from hematogenous dissemination. Atypical mycobacteria, especially M fortuitum, M chelonae, and M marinum, may cause septic arthritis by inoculation or extension from a contiguous focus of infection. The most common cause of fungal arthritis is Sporothrix schenckii. This infection usually follows traumatic inoculation, but may also result from pulmonary dissemination. Because of its relative rarity and indolent course, the diagnosis is often missed or delayed. Coccidiomycosis, histoplasmosis, and blastomycosis may all affect the joint. In addition, Cryptococcus, Aspergillus, and Candida species may cause infectious arthritis in the immunocompromised host. Diagnosis of all the granulomatous arthritides usually involves a higher index of suspicion and appropriate fungal or mycobacterial cultures.

Bone Infections

On the basis of clinical and pathologic considerations, osteomyelitis may be classified as either hematogenous or secondary to a contiguous focus of infection. Contiguous-focus osteomyelitis can be further subdivided into bone infection with relatively normal vascularity and bone infection with generalized vascular insufficiency. Either major type of osteomyelitis may progress to a chronic bone infection.

Hematogenous Osteomyelitis

Hematogenous osteomyelitis occurs mainly in infants and children but has recently been found with increasing frequency in the adult population. In infants and children the metaphysis of long bones (tibia, femur) is most frequently involved. The anatomy in the metaphyseal region of long bones seems to explain this clinical finding. Nonanastomosing capillary ends of the nutrient artery make sharp loops under the growth plate and enter a system of large venous sinusoids where the blood flow becomes slow and turbulent. Any obstruction of the capillary ends leads to an area of avascular necrosis. Minor trauma probably predisposes the infant or child to infection by producing a small hematoma and subsequent bone necrosis, both of which can be infected by a transient bacteremia. The infection produces a local cellulitis, which results in increased bone pressure, decreased pH, and a breakdown of leukocytes. All of these factors contribute to necrosis of bone. The infection may proceed laterally through the haversian and Volkmann canal system, perforate the cortex, and lift the periosteum. It may also extend into the intramedullary canal. Extension leads to further vascular compromise and bone necrosis. In infants, capillaries penetrate the growth plate. Therefore, the infection may also spread to the epiphysis and into the joint space. In children over 1 year old, the growth plate is no longer penetrated by capillaries, and the epiphysis and joint space are protected from infection. In adults, the growth plate has been resorbed and joint extension of a metaphyseal infection can recur. However, in adults, the diaphysis of the long bones and the lumbar and thoracic vertebral bodies of the axial skeleton are most frequently involved. Adults with axial skeleton osteomyelitis often have a history of preceding urinary tract infection or intravenous drug abuse.

A single pathogenic organism is usually responsible for hematogenous osteomyelitis (Table 100-3). Polymicrobic hematogenous osteomyelitis is rare. Staphylococcus aureus is the most frequent organism isolated, but Streptococcus pyogenes and Streptococcus agalactiae are responsible for a significant number of bone infections, especially in infants. Aerobic Gram-negative organisms are responsible for an increasing number of bone infections. Pseudomonas aeruginosa is often isolated from intravenous drug abusers with vertebral osteomyelitis.

Table 100-3. Commonly Isolated Organisms in Osteomyelitis.

Table 100-3

Commonly Isolated Organisms in Osteomyelitis.

Patients with hematogenous osteomyelitis usually have normal soft tissue around the infected bone. If antimicrobial therapy directed at the pathogen is begun prior to extensive bone necrosis, the patient has an excellent chance of cure.

Contiguous-Focus Osteomyelitis

Osteomyelitis Secondary to a Contiguous Infection with No Generalized Vascular Insufficiency

In contiguous-focus osteomyelitis, the organism either is directly inoculated into the bone by trauma or surgery or reaches the bone from adjacent infected soft tissue. Common predisposing conditions include open fractures, surgical reduction and internal fixation of fractures, and wound infections. In contrast to hematogenous osteomyelitis, multiple bacteria are isolated from the infected bone. The bacteriology is diverse (Table 100-3), but S aureus remains the most commonly isolated pathogen. In addition, aerobic Gram-negative bacilli and anaerobic organisms are frequently isolated. Bone necrosis, soft tissue damage, and loss of bone stability are all common, making this form of osteomyelitis difficult to manage.

Osteomyelitis Secondary to a Contiguous Infection with Generalized Vascular Insufficiency

The small bones of the feet (principally the metatarsal bones and phalanges) are commonly involved in osteomyelitis secondary to a contiguous infection in patients with generalized vascular insufficiency. Most commonly, the infection develops as an extension of a local infection, either cellulitis or a trophic skin ulcer. The inadequate tissue perfusion favors the infection by blunting the local inflammatory response. Multiple aerobic and anaerobic bacteria are usually isolated from the infected bone. Although cure is desirable, a more attainable goal of therapy is to suppress the infection and maintain functional integrity of the involved limb. Recurrent or new bone infections occur in many patients. In time, amputation of the infected area is almost always necessary.

Chronic Osteomyelitis

Both hematogenous osteomyelitis and contiguous-focus osteomyelitis can progress to a chronic bone infection. No exact criteria separate acute from chronic osteomyelitis. Clinically, newly recognized bone infections are considered acute, whereas a relapse of the infection represents chronic disease. However, this simplistic classification is clearly inadequate. The hallmark of chronic osteomyelitis is the presence of large areas of dead bone or sequestra. An involucrum (a reactive bony encasement around the sequestrum) and persistent drainage via one or more sinus tracts are usually present. In chronic osteomyelitis, multiple species of bacteria are usually isolated from the necrotic infected bone (Table 100-3), except in cases of chronic hematogenous osteomyelitis, which usually yield a single organism. Unless the necrotic infected bone can be removed, antibiotic therapy is usually unsuccessful. The prognosis for arresting the infection is worse if there is poor soft tissue integrity surrounding the infection, sclerosis of the involved bone, or bone instability.

Diagnosis of Bacterial Osteomyelitis

The bacteriologic diagnosis of bacterial osteomyelitis rests on isolation of the agent from the bone or the blood. In hematogenous osteomyelitis, positive blood cultures often obviate the need for a bone biopsy when there is associated radiographic or radionuclide scan evidence of osteomyelitis. In chronic osteomyelitis, sinus tract cultures are not reliable for predicting which organism(s) will be isolated from the infected bone. Antibiotic treatment of osteomyelitis should not be based on the results of sinus tract cultures. In most instances, bone biopsy cultures are mandatory to guide specific antimicrobial therapy.

Skeletal Tuberculosis

Skeletal tuberculosis is the result of hematogenous spread of the tuberculosis bacillus early in the course of a primary infection. Rarely, skeletal tuberculosis develops as a contiguous infection from an adjacent caseating lymph node. Either the primary bone infection or a reactivated quiescent primary bone infection elicits an inflammatory reaction, followed by the development of granulation tissue. The granulation tissues erodes and destroys the cartilage and cancellous bone. Eventually the infection causes bone demineralization and necrosis. Proteolytic enzymes that can destroy cartilage are not produced in skeletal tuberculosis. Cartilage is destroyed slowly by granulation tissue, and the joint or disc space is preserved for considerable periods. Healing involves deposition of fibrous tissue. Pain is the most frequent clinical complaint.

Any bone may be involved by skeletal tuberculosis, but the infection usually involves one site. In children and adolescents, the metaphyses of the long bones are most frequently infected. In adults, the axial skeleton, followed by the proximal femur, knee, and small bones of the hands and feet, are most often involved. In the axial skeleton, the thoracic vertebral bodies are most frequently infected, followed by the lumbar and cervical vertebral bodies. Vertebral infection usually begins in the anterior portion of a vertebral body adjacent to an intervertebral disc. Adjacent vertebral bodies may become involved, and a paravertebral abscess may develop. Sixty percent of patients with skeletal tuberculosis have evidence of extraosseous tuberculosis.

Tissue for culture and histology is almost always required for the diagnosis of skeletal tuberculosis. Cultures for Mycobacterium tuberculosis are positive in approximately 60 percent of the cases, but 6 weeks may be required for growth and identification of the organism. Histology showing granulomatous tissue compatible with tuberculosis and a positive tuberculin test are sufficient to begin tuberculosis therapy. However, a negative skin test does not rule out skeletal tuberculosis. Therapy for skeletal tuberculosis involves prolonged chemotherapy and in some cases surgical debridement.

Fungal Osteomyelitis

Bone infections may be caused by a variety of fungal organisms, including Coccidioides, Blastomyces, Cryptococcus, and Sporothrix species. The lesion most often appears as a cold abscess overlying an osteomyelitic lesion. Joint space extension may occur in coccidioidomycosis and blastomycosis. Therapy for fungal osteomyelitis involves surgical debridement and antifungal chemotherapy.

References

  1. Mader, JT, Calhoun, J: Osteomyelitis. p. 1039. In Mandell GL, Bennett JE, Dolin R (eds): Principles and Practice of Infectious Diseases. 4th Ed. Churchill Livingstone, New York, 1995 .
  2. Finegold SM, Bartlett JG, Chow AK. et al. Management of anaerobic infections. Ann Intern Med. 1975;83:375. [PubMed: 1190633]
  3. Mackowiak PA, Jones SR, Smith JW. Diagnostic value of sinus tract cultures in chronic osteomyelitis. J Am Med Assoc. 1978;239:2772. [PubMed: 349185]
  4. Martin DH: Gonococcal arthritis and Reiter's syndrome. p. 233. In D'ambrosia RD, Marier RL (eds): Orthopaedic Infections. Slack, Thorofare, NJ, 1989 .
  5. Meijers KA, Dijkmans BA, Hermans J. et al. Non-gonococcal infectious arthritis: a retrospective study. J Infect Dis. 1987;14:13. [PubMed: 3819454]
  6. Meleney FL. Hemolytic streptococcal gangrene. Arch Surg. 1924;9:317.
  7. Ruthbery AD, Ho G: Nongonococcal bacterial arthritis. p. 213. In D'ambrosia RD, Marier RL (eds): Orthopaedic Infections. Slack, Thorofare, NJ, 1989 .
  8. Smith JW, Piercy EA: Infectious arthritis. p. 1032. In Mandell GL, Bennett JE, Dolin R (eds): Principles and Practice of Infectious Diseases, 4th Ed. Churchill Livingstone, New York, 1995 .
  9. Stone HH, Martin JD Jr. Synergistic necrotizing cellulitis. Ann Surg. 1972;175:702. [PMC free article: PMC1355242] [PubMed: 4555030]
  10. Waldvogel FA, Vasey H. 1980. Osteomyelitis: The past decade. N Engl J Med. 1980;303:360. [PubMed: 6993944]
Copyright © 1996, The University of Texas Medical Branch at Galveston.
Bookshelf ID: NBK8029PMID: 21413289

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