Which individual is most at risk to develop osteomyelitis caused by Staphylococcus aureus?

Osteomyelitis can be defined as an inflammation of the bone marrow with a tendency to progress, often involving periosteal tissues and adjacent cortical plates.

From: Facial Trauma Surgery, 2020

Osteomyelitis

John E. Bennett MD, in Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 2020

Summary

Despite important medical and surgical advances in management of patients, osteomyelitis remains extremely difficult to treat. The relapse rate can be as high as 20%. The optimal management of osteomyelitis requires a multidisciplinary team of physicians, including an orthopedic surgeon, neurosurgeon, oral surgeon, plastic surgeon, vascular surgeon, invasive radiologist, and infectious disease specialist. The usual goal of therapy is the eradication of the infection and restoration of function. Treatment of chronic osteomyelitis usually requires aggressive surgical débridement and prolonged antimicrobial therapy.

Osteomyelitis

Fred F. Ferri MD, FACP, in Ferri's Clinical Advisor 2022, 2022

Treatment

Surgical debridement in biopsy-positive cases will guide direction for antibiotic therapy. This will vary with type of osteomyelitis. Duration of therapy is usually 4 to 6 wk for acute osteomyelitis; chronic osteomyelitis may need a longer course of medication

Orthopedic hardware should be removed if possible

S. aureus (MSSA): Cefazolin IV, nafcillin IV, vancomycin IV (in patient allergic to penicillin)

S. aureus (MRSA): Vancomycin IV, linezolid IV or PO, daptomycin IV

Streptococcus spp: Ceftriaxone, IV penicillin G in sensitive species

P. aeruginosa: Cefepime, imipenem/cilastatin, or meropenem

Enterobacteriaceae: Ceftriaxone or ertapenem

Anaerobes: Clindamycin, piperacillin-tazobactam, cefotetan, or metronidazole

Table 2 summarizes antimicrobial therapy for selected microorganisms in osteomyelitis. A retrospective analysis1 revealed that in diabetic foot osteomyelitis adjunctive rifampin is associated with improved amputation-free survival

Hyperbaric oxygen therapy: May be useful in chronic osteomyelitis

Wound-assisted vacuum device may help closure of wound

Surgical debridement of all devitalized bone and tissue

Immobilization of affected bone (plaster, traction) if bone is unstable

Disposition

Acute hematogenous osteomyelitis usually resolves without recurrence or long-term complications, but contiguous focus osteomyelitis, bone infections from open fractures, or osteomyelitis frequently recurs.

Referral

To an orthopedic surgeon if chronic osteomyelitis with need for bone debridement, bone grafting, or stabilization of infected tissue adjacent to a bone fracture

To an infectious disease specialist for appropriate treatment for difficult-to-treat or recalcitrant infections

To a hyperbaric oxygen chamber service for nonhealing, chronic osteomyelitis

INFECTION OF SPECIFIC ORGAN SYSTEMS

Paul Krogstad, in Feigin and Cherry's Textbook of Pediatric Infectious Diseases (Sixth Edition), 2009

FUNGI

Osteomyelitis may be caused by numerous endemic and opportunistic fungal agents, including C. immitis, cryptococci, Candida spp., Blastomyces spp., and Aspergillus spp. Coccidioidomycosis may be characterized by cough, chest pain, night sweats, and anorexia, and it often is associated with erythema nodosum or erythema multiforme. This disease commonly is found in the southwestern United States. Extrapulmonary involvement is suggested by persistent high temperature and toxicity. C. immitis occurs primarily in cancellous bone (e.g., vertebral bodies, distal tubular bones, and the skull).167 These lesions are not radiographically distinct from the lesions seen in osteomyelitis from other causes.183 Débridement of bone lesions often is needed initially, and years of therapy are required. Oral triazole agents generally are recommended.74

Blastomycosis may mimic coccidioidomycosis, but the pulmonary involvement is much more varied, and fusion of the vertebral bodies rarely occurs. A propensity for the development of verrucous, reddened, weeping skin lesions has been noted, and prostate involvement may be seen. Bone involvement occurs frequently, with the skull and vertebral bodies being infected most often. Distinguishing it from other forms of osteomyelitis is impossible by radiographic examination.

Aspergillus osteomyelitis is being recognized with increasing frequency.35 Most commonly, it is a disease of immunosuppressed patients, with Aspergillus pneumonia seen initially followed by disseminated disease. Bone disease occurring by hematogenous spread has developed, however, in normal individuals and after injectable drug use.43,172 Aspergillus osteomyelitis developing after trauma also has been reported.

Other fungi are causes of osteomyelitis. The medical literature contains dozens of reports of osteomyelitis caused by C. neoformans, generally in immunocompromised patients and in the setting of disseminated or pulmonary infection. The few reports in pediatric patients generally have involved immunocompromised adolescents. In adolescents and adults, usually only one bone is involved. The lesions generally are slowly destructive, very discrete lesions occurring primarily in the long tubular bones without marginal sclerosis. This radiologic reaction is confused most commonly with tumor and, occasionally, with tuberculosis. Infection of the ribs and skull also has been reported. Although experience with this disease is limited, débridement of the lesions and medical therapy seem to be highly effective.14,30,37,84,131,132 Cases of Rhizopus osteomyelitis have been reported intermittently and apparently are hematogenous in origin.57

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Osteomyelitis

Robert M. Kliegman MD, in Nelson Textbook of Pediatrics, 2020

Differential Diagnosis

Distinguishing osteomyelitis from cellulitis or trauma (accidental or abuse) is the most common clinical circumstance. Myositis or pyomyositis can also appear similar to osteomyelitis with fever, warm and swollen extremities, and limping; tenderness to palpation of the affected soft tissue area is generally more diffuse than noted in acute osteomyelitis. Nevertheless, distinguishing myositis and pyomyositis from osteomyelitis clinically may be difficult. Myositis and pyomyositis may be isolated but are often found adjacent to an osteomyelitis on MRI. Pyomyositis is most often caused byS. aureus, followed by group A streptococcus. The pelvic muscles are a common site of pyomyositis and can mimic a pelvic osteomyelitis. MRI is the definitive study to identify and localize pelvic pyomyositis (Fig. 704.5). An iliopsoas abscess can manifest with thigh pain, limp, and fever and must be considered in the differential diagnosis of osteomyelitis. The iliopsoas abscess may be primary (hematogenous:S. aureus) or secondary to infection in adjacent bone(S. aureus), kidney(E. coli) or intestine (E. coli,Bacteroides spp.).Mycobacterium tuberculosis has been reported in patients with HIV infection. Any child with negative x-ray imaging and a negative hip aspiration, who presents with fever, limp, and elevated inflammatory marks should be evaluated for pyomyositis.

Appendicitis, urinary tract infection, and gynecologic disease are among the conditions in the differential diagnosis of pelvic osteomyelitis. Children with leukemia commonly have bone pain or joint pain as an early symptom. Neuroblastoma with bone involvement may be mistaken for osteomyelitis. Primary bone tumors need to be considered, but fever and other signs of illness are generally absent except in Ewing sarcoma. In patients with sickle cell disease, distinguishing bone infection from infarction may be challenging.

Chronic recurrent multifocal osteomyelitis (CRMO) is a nonpyrogenic, sterile inflammatory bone disease that is considered an autoinflammatory disorder (seeChapter 188). It is also associated with a family history of autoimmune disease; the affected patient may also have other inflammatory diseases such as Crohn disease, Sweet syndrome, psoriasis, and palmar plantar pustulosis. CRMO in children has many similarities with synovitis, acne, pustulosis, hyperostosis, and osteitis syndrome (SAPHO), seen in adults. In addition, CRMO has similarities to Majeed syndrome, an autosomal recessive disorder with a microcytic dyserythropoietic anemia and with a deficiency of interleukin-1 receptor antagonist, an autosomal recessive autoinflammatory disease.

In contrast to infectious osteomyelitis, CRMO is multifocal and recurrent and may involve bones not typical of osteomyelitis (spine, pelvis, clavicle, mandible, calcaneus). Plain radiographs reveal osteolytic lesions or sclerosis; whole body short tau inversion recovery MRI imaging is the diagnostic study of choice (Fig. 704.6).

Oral and Maxillofacial Infections

Shahrokh C. Bagheri DMD, MD, ... Chris Jo DMD, in Clinical Review of Oral and Maxillofacial Surgery, 2008

DISCUSSION

Osteomyelitis is an inflammatory condition involving the medullary cavity of bone that begins as a bacterial infection and can cause significant bony destruction. The microorganisms cause host tissue injury from direct cellular attack and through enzymatic degradation. The host responds by recruiting neutrophils to the area to digest the pathogens via release of enzymes and phagocytosis. When purulence (composed of necrotic tissue, dead bacteria, and WBCs) accumulates, it causes an increase in the intramedullary pressure, causing collapse of the vessels, venous stasis, and congestion. Vessels within the haversian system and Volkmann's canals of the cortical bone may undergo thrombosis or experience stasis and congestion, resulting in the surrounding bone becoming ischemic and thereby permitting the extension of osteomyelitis. If purulence continues to accumulate, the periosteum is penetrated and mucosal or cutaneous fistulas develop.

The establishment of an infection within bone is related to the compromise in the bone's vascular supply, but other factors, such as the virulence of the organism and the integrity of the host defenses, are also important. Host factors include systemic diseases with a microvascular component (e.g., diabetes), blood dyscrasias (e.g., sickle cell disease), immunosuppression (e.g., HIV infection), and collagen vascular disorders or bone dysplasias (e.g., osteopetrosis).

Initially, Staphylococcus aureus and Staphylococcus epidermidis accounted for 80% to 90% of osteomyelitis of the jaws. However, the frequency of S. aureus involvement in osteomyelitis has decreased due to the improved culture methods used to identify organisms, especially anaerobes. Anaerobes are frequently associated with aerobic organisms in osteomyelitis. Currently, osteomyelitis is recognized as a disease commonly caused by streptococci (α-hemolytic) and oral anaerobes such as Peptostreptococcus, Fusobacterium, and Prevotella.

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Clinical Syndromes and Cardinal Features of Infectious Diseases: Approach to Diagnosis and Initial Management

Kathleen M. Gutierrez, in Principles and Practice of Pediatric Infectious Disease (Third Edition), 2008

SPECIAL CLINICAL SITUATIONS

Neonatal Osteomyelitis

Osteomyelitis is uncommon in the neonatal period. The incidence is unknown but is estimated to be approximately 1 to 3 cases for every 1000 intensive-care nursery admissions.83

Associated risk factors include prematurity, low birthweight, preceding infection, bacteremia, exchange transfusion, and the presence of an intravenous or umbilical catheter.84–87 Osteomyelitis of the skull secondary to contiguous spread of infection has occurred as a complication of fetal scalp electrode monitoring88–90 and in association with infected cephalohematoma.91,92 Osteomyelitis of the calcaneus has complicated heel lancet puncture.85,93

The diagnosis of osteomyelitis in neonates is often delayed because of nonspecific symptoms.94 Signs and symptoms include fever, irritability, swelling or decreased movement of a limb (pseudoparalysis), erythema, and tenderness over the affected bone.83–85,95 Preterm infants are more likely than term infants to manifest symptoms of septicemia.96

Approximately 20% to 50% of neonates with osteomyelitis have infection of multiple bones,83,84,97 and about 75% have suppurative arthritis of contiguous joints84 (Figure 80-5).

Staphylococcus aureus (including CA-MRSA98), GBS, and enteric gram-negative bacilli are the most common causes (Table 80-4); fungi,99 Ureaplasma urealyticum,100 S. epidermidis,101 Neisseria gonorrhoeae,95 and anaerobic88 bacteria are unusual causes.

Infants with GBS bone infection have usually had an uncomplicated neonatal course and have infection of a single bone. There is as a predilection for involvement of long bones on the right, particularly the right proximal humerus.101,102 This predilection may be secondary to trauma to the upper arm as it passes below the symphysis pubis during vaginal delivery.101 Misdiagnosis of bone infection as trauma in these mildly ill infants is common. Since the release of the 1996 consensus guidelines for prevention of GBS disease, the incidence of early-onset perinatal GBS disease has declined in the United States.103

The white blood cell count is commonly normal; ESR and CRP are often elevated.104 In most infants, an osteolytic lesion is visible on plain radiograph 10 to 12 days after onset of symptoms (frequently at the time of diagnosis).76,84,85,95,105,106 Radionuclide bone scans may be positive44,83,94 but sometimes are less sensitive than plain radiographs.85

Neonatal osteomyelitis can lead to permanent joint abnormalities or disturbance in skeletal growth secondary to damage to the cartilaginous growth plate, including arthritis, decreased range of motion, limb length discrepancy, and gait abnormalities.107 The reported incidence of permanent sequelae varies from 6% to 50%.84,85,96,101

Vertebral Osteomyelitis

Vertebral osteomyelitis accounts for approximately 1% to 3% of cases of osteomyelitis in children.12,17,108,109 Boys are affected twice as frequently as girls.110 Infection usually occurs as a result of bacterial seeding of the vertebral bodies by hematogenous arterial or venous spread. It can also result from extension of soft-tissue infection or complication of a surgical procedure.15,111

Clinical manifestations can be indolent and nonspecific, leading to delayed diagnosis. Young infants can have nonspecific signs of septicemia.112 Symptoms in older children include back, chest, abdominal, or leg pain as well as loss of normal curvatures.108,113 Rarely, children manifest dysphagia secondary to a paravertebral or retropharyngeal abscess or acute spinal cord paralysis due to paraspinal compression.108,114 Fever is common, and tenderness over the involved vertebrae is expected. Neurologic deficits are found in 15% to 20% of cases.108,110

S. aureus is isolated in most cases.15,108,110,115 In one review, Salmonella spp. caused 12% of cases of childhood vertebral osteomyelitis.108 Gram-negative bacilli such as Escherichia coli cause vertebral osteomyelitis in adults, particularly those with a history of recent urinary tract infection or instrumentation. Vertebral osteomyelitis in intravenous drug users is commonly caused by Pseudomonas aeruginosa and less commonly by Staphylococcus aureus, Serratia spp., Klebsiella spp., Enterobacter spp., or Candida spp.116,117 Tuberculosis and brucellosis should be considered if symptoms and radiographs suggest chronic infection.118,118a

Characteristic findings on plain radiograph consist of narrowing of the involved disk space, lucency of the adjacent vertebral bodies, and, eventually, reactive sclerosis of the bone with fusion of vertebral bodies.15,108,115 Vertebral osteomyelitis is differentiated from diskitis radiographically by the minimal vertebral endplate involvement associated with diskitis (see Chapter 82, Diskitis). MRI is reported to be highly sensitive (96%) and specific (92%) for diagnosis of vertebral osteomyelitis.119,120

Blood culture results are positive in only about 30% of acute cases. When blood culture results are negative, strong consideration should be given to obtaining a biopsy specimen from the vertebral body for culture and histologic examination.120

Children with uncomplicated vertebral osteomyelitis and no evidence of abscess formation should be treated with at least 4 weeks of parenterally administered antibiotics.108 Treatment of shorter duration is associated with therapeutic failure.110 Surgical decompression or debridement or both are indicated in the presence of spinal epidural abscess, signs of spinal cord compression, or extensive bony destruction.

Complications of vertebral osteomyelitis include neurologic deficits secondary to epidural abscess,121 paravertebral abscess,122 and infected aneurysms of the aorta.123

Pelvic Osteomyelitis

Approximately 6% to 9% of all cases of hematogenous osteomyelitis involve the bones of the pelvis.34,124,124a The ilium and ischium are most commonly involved124; infection of the sacrum, acetabulum, or pubic symphysis is rare.124–126 Pathogenesis is not clearly defined, but risk factors include a history of pelvic trauma, intravenous drug use, and genitourinary procedures.124,126

Most patients with pelvic osteomyelitis have fever, gait abnormalities, and pain that is often localized to the hip, groin, or buttock.124,126–129 Pain with hip movement and point tenderness over the affected bone is often observed. Clinical features can mimic those of pyogenic arthritis of the hip124; however, pelvic osteomyelitis is more likely to be associated with near-normal range of motion of the hip, absence of referred pain to the knee, specific point tenderness over the affected bone (or pain on rocking of the pelvic girdle), and abnormal rectal findings.129 Responsible pathogens are similar to those that cause osteomyelitis of long bone.

Plain radiographs of the pelvis are often normal. Technetium scanning,124,124a,127–129 MRI, or CT can suggest the correct diagnosis and may be useful for differentiating osteomyelitis from bacterial infection of the muscles of the pelvic girdle.

Patients should be treated for at least 4 weeks with antibiotics.124–126,129 Surgical drainage or debridement should be considered in cases of extraosseous abscess formation or in patients whose symptoms do not respond rapidly to intravenous antibiotic therapy.

Children with Sickle Hemoglobinopathies

Children with sickle-cell disease have increased susceptibility to bacterial infections, including osteomyelitis.130 Although the pathogenesis of osteomyelitis is poorly understood, microscopic areas of infarction in the intestinal mucosa and bone probably develop during sickling, resulting in bacteremia and focal bone infection. Splenic hypofunction, impaired opsonization, impaired macrophage function, and microembolism as well as tissue infarction are likely contributing factors in osteomyelitis.131,132

Salmonella spp. plus other gram-negative enteric bacilli cause > 70% of cases of osteomyelitis in children with hemoglobinopathies.133–136 Staphylococcus aureus is also an important cause of osteomyelitis in this population. Other organisms causing osteomyelitis in children with sickle hemoglobinopathies are listed in Box 80-1.

Manifestations of osteomyelitis in children with sickle-cell disease are difficult to differentiate from those of acute vaso-occlusive crisis. Fever, bone pain, and leukocytosis are common to both conditions. Temperature >39°C, toxic appearance, and an absolute band count > 500 cells/mm3 are more consistent with infection; however, there is considerable clinical and laboratory overlap.133

Distinctive features of osteomyelitis in children with sickle-cell disease are frequent involvement of the diaphyses of long bones, flat bones, and small bones of the hands and feet as well as multifocal, symmetrical bone involvement.131,137

Plain radiograph, technetium scanning, and MRI cannot differentiate infarction from infection.137,138 Therefore, if fever and bone pain have not improved after supportive care has been given for vaso-occlusive crisis, needle aspiration of the affected area of bone for Gram stain and culture should be performed.

Prolonged courses of parenteral antibiotic therapy (6 to 8 weeks) may be necessary for treatment of osteomyelitis in patients with sickle hemoglobinopathy; oral therapy can be substituted for parenteral treatment once a pathogen has been confirmed and there is clinical improvement.131,133

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Osteomyelitis

DOYLE J. LIM MD, STEPHEN C. EPPES MD, in Pediatric Infectious Diseases, 2008

Chronic Recurrent Multifocal Osteomyelitis

Chronic recurrent multifocal osteomyelitis (CRMO) is generally considered to be noninfectious, occurs more commonly in girls younger than 10 years old, and is associated with palmoplantar pustulosis, psoriasis vulgaris, and Sweet's syndrome (acute febrile neutrophilic dermatosis). CRMO is characterized by recurrent episodes of fever, swelling, and pain, usually at more than one site. Plain radiographs often demonstrate multiple areas of osteolysis and sclerosis, especially in the long bones and clavicles. Diagnosis may be difficult, but long-term prognosis is generally good. Treatment includes nonsteroidal anti-inflammatory agents and possibly steroids; in most cases antibiotics are not helpful.

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Osteomyelitis

In Diagnostic Imaging: Pediatrics (Third Edition), 2017

DIAGNOSTIC CHECKLIST

Consider

Imaging after treatment: Uncomplicated osteomyelitis may require 6 months for MR normalization

Nonspecific for ongoing bone infection vs. resolving inflammation/healing

Drainable collections can be sampled to guide therapy

Image Interpretation Pearls

For aggressive bone masses, generally consider

Infection: Nonenhancing fluid > solid enhancing tissue; moderate to marked surrounding soft tissue edema

Tumor: Solid enhancing tissue > nonenhancing fluid; surrounding soft tissue edema typically mild

Coronal ultrasound of the proximal right humerus in a 5-month-old boy shows a subperiosteal fluid collection

with disruption of the metaphyseal cortex & disturbed underlying medullary echotexture . Compare the normal left humeral sonographic architecture .

Coronal STIR MR of the same patient with osteomyelitis shows abnormal fluid signal throughout the right humerus

plus a nondisplaced pathologic metaphyseal fracture . A subperiosteal fluid collection is noted .

Coronal T1 (top) & T1 C+ FS (bottom) MR images in a 1 year old with a fever & a limp show abnormal poorly defined marrow heterogeneity of the proximal right femur

with surrounding soft tissue edema , typical of osteomyelitis.

Coronal T1 (left), STIR (middle), & DWIBS (right) MR images in a 9 year old with MRSA bacteremia & septic emboli show right distal tibial osteomyelitis

, pulmonary nodules, & numerous foci of myositis & fasciitis with muscular abscesses.

Lateral radiograph (left) & sagittal STIR MR (right) in an infant with ulnar osteomyelitis show soft tissue edema

, a large subperiosteal abscess , & marrow heterogeneity . A small subperiosteal globule followed fat signal on all sequences, consistent with marrow lipocyte necrosis.

Coronal PD FS (left) & T1 C+ FS (right) MR images in a neonate with femoral osteomyelitis show focal loss of normal low signal ZPC

with poor enhancement of unossified epiphyseal cartilage & overlying soft tissue edema .

Coronal T2 FS MR of the ankle in a 7-year-old boy with osteomyelitis shows abnormal heterogeneous marrow signal intensity of the distal tibial metaphysis & diaphysis

with mild overlying periosteal & soft tissue edema .

Sagittal T2 FS MR in a 2-year-old boy shows abnormal marrow signal of the distal femoral metaphysis

& epiphyseal ossification center . A fluid collection within the epiphyseal ossification center extends into the overlying unossified epiphyseal cartilage .

Lateral radiograph of the knee in a teenager shows a focus of proximal tibial cortical destruction anteriorly

with overlying soft tissue edema & a subjacent lucent, permeative lesion .

Sagittal T1 C+ FS MR of the same patient shows a Brodie abscess with a target-like appearance of central nonenhancing pus

surrounded by hyperenhancing granulation tissue & a faint outer low signal intensity rim of sclerotic bone . An internal rim of precontrast T1 hyperintensity (not shown) is often seen in patients with a Brodie abscess (the penumbra sign).

Lateral radiographs in a 5-year-old boy obtained after 1 day (left) & 8 days (right) of knee pain initially show edema of the prefemoral fat

without any bony abnormality. Subsequently, a lytic femoral metaphyseal lesion developed with increased soft tissue edema & a joint effusion .

Sagittal T1 C+ FS MR shows an abscess at the site of the lytic lesion

with surrounding marrow & soft tissue edema . A suprapatellar joint effusion is noted, which could be reactive or due to septic arthritis.

AP radiograph shows lucent foci of osteomyelitis

in the great toe distal phalanx 12 days after a Salter-Harris II fracture , an injury that must be treated as an open fracture (with antibiotics) when there is an accompanying nail bed injury.

Sunrise radiograph shows lucent, poorly defined foci of patellar osteomyelitis

due to Staphylococcus aureus.

AP (left) & lateral (right) radiographs of the distal femur in a teenager with months of thigh pain show numerous central, elongated lucent lesions

of the distal femur, some of which have narrow zones of transition & some of which do not. There is mild expansile remodeling of the distal femur with foci of endosteal scalloping intermixed with generalized cortical thickening.

Coronal T1 MR in the same patient shows a high signal intensity rim

surrounding a central medullary lesion, the typical penumbra sign of granulation tissue in a Brodie abscess in subacute to chronic osteomyelitis. An outer rim of poorly defined low signal intensity corresponds to fibrosis & sclerosis.

Coronal STIR MR in the same patient shows that the high signal intensity intramedullary collection is surrounded by a hypointense outer rim of fibrosis &/or sclerosis

, a feature not seen with acute infections. There is surrounding poorly defined marrow edema .

Coronal T1 C+ FS MR in the same patient shows intense rim enhancement

of the medullary abscess of the distal femur with surrounding poorly defined marrow edema. The periosteal & soft tissue edema in this case of subacute to chronic osteomyelitis is less pronounced than is typically seen with acute cases of infection that have such extensive bony abnormalities.

Lateral radiograph shows an area of osteomyelitis

in the dorsal cortex of the index finger proximal phalanx 32 days after an accidental laceration by an opponent's teeth during a basketball game.

AP radiograph shows a lucent lesion

of the distal humeral metaphysis in a 3 year old with Streptococcal osteomyelitis. The margins of the lesion are somewhat poorly defined.

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INFECTIOUS ARTHRITIS AND OSTEOMYELITIS

Ross E. Petty, Ronald M. Laxer, in Textbook of Pediatric Rheumatology (Fifth Edition), 2005

Definition and Classification

Osteomyelitis is an intraosseous infection with bacteria or, rarely, fungi. It is classified as acute, subacute, or chronic. Acute osteomyelitis is of recent onset and short duration. It is most often hematogenous in origin but may result from trauma such as a compound fracture or puncture wound. It can be metaphyseal, epiphyseal, or diaphyseal in location. Subacute osteomyelitis is of longer duration and is usually caused by less virulent organisms. Chronic osteomyelitis results from ineffective treatment of acute osteomyelitis and is characterized by necrosis and sequestration of bone.

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How does Staphylococcus aureus cause osteomyelitis?

Osteomyelitis occurs when bacteria from nearby infected tissue or an open wound circulate in your blood and settle in bone, where they multiply. Staphylococcus aureus bacteria (staph infection) typically cause osteomyelitis. Sometimes, a fungus or other germ causes a bone infection.

Why is osteomyelitis common in elderly?

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 population (e.g., ...

Which is the most common organism's causing osteomyelitis in all age groups?

Staphylococcus aureus is the most common cause of acute and chronic hematogenous osteomyelitis in adults and children.

Why is osteomyelitis common in children?

In children, an infection in the blood is a common cause of osteomyelitis. This is because a child's growing bones have an increased blood supply. That makes it easier for the bacteria to get into the bone. An infection from nearby soft tissue or from a wound may also lead to osteomyelitis.

What is the most common route of disease causation of chronic osteomyelitis?

Most commonly, chronic osteomyelitis is secondary to direct inoculation of pathogens into the bone at the time of trauma, as a result of surgical trauma (i.e. following open reduction and internal fixation of fractures), from chronic overlying open wounds or contiguous soft tissue infections.