Causes of Infectious arthritis
List of causes of Infectious arthritis
Following is a list of causes or underlying conditions
(see also Misdiagnosis of underlying causes of Infectious arthritis)
that could possibly cause Infectious arthritis includes:
Infectious arthritis Causes: Book Excerpts
Infectious arthritis as a complication of other conditions:
Other conditions that might have
Infectious arthritis as a complication may,
potentially, be an underlying cause of Infectious arthritis.
Our database lists the following as having
Infectious arthritis as a complication of that condition:
Related information on causes of Infectious arthritis:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Infectious arthritis may be found in:
Causes of Infectious arthritis: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the causes of Infectious arthritis.
Arthritis – Multiple Joints:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
- Infectious
–Reactive arthritis (postenteric or genital including Reiter syndrome, postviral, poststreptococcal)
–Acute rheumatic fever (ARF): Migratory, painful; usually affects large joints; diagnosis is based on Jones criteria, which includes five major (arthritis, carditis, Sydenham chorea, erythema marginatum, subcutaneous nodules) and several minor (fever, arthralgia, elevated ESR or CRP, prolonged P-R interval) manifestations
–Lyme disease: Arthritis is monoarticular or oligoarticular, is rarely symmetric, and is the second most common manifestation of Lyme disease after erythema migrans
–SBE-related arthritis
–Septic polyarthritis (unusual)
- Rheumatic
–Polyarticular JRA: Arthritis in five or more joints in first 6 months of disease, insidious onset, symmetric involvement, may be RF+ (erosive, similar to adult RA) or RF-
–Systemic-onset JRA: Presents with severe systemic involvement (fever, rash, serositis), which may precede the arthritis, usually oligoarticular
–Juvenile ankylosing spondylitis (JAS): Initially affects lower extremity joints; later affects axial skeleton, also affects tendons
–Psoriatic arthritis
–Arthritis of IBD: Usually more transient than JRA
–SLE: May present only with arthritis, may be misdiagnosed as JRA
–Other connective tissue diseases (scleroderma)
–Vasculitis (HSP, Kawasaki disease)
-
Malignancy such as leukemia
-
Other systemic disorders: Serum sickness, sarcoidosis, Behçet disease, Ehler-Danlos syndrome, mucopolysaccharidoses, Noonan syndrome, Turner syndrome
-
Medications (minocyline, carbamazapine)
-
Sickle cell disease
» READ BOOK EXCERPT ONLINE »
Source: In A Page: Pediatric Signs and Symptoms, 2007
Arthritis – Single Joint:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
- Septic arthritis
–Rapid diagnosis critical: Untreated septic arthritis causes irreversible joint and bone destruction
–Usually presents hyperacutely with very tender, swollen, warm, red joint with severely restricted range of motion
–Usual pathogens: Haemophilus influenzae type b, Staphylococcus aureus, group B strep in neonates, and Neisseria gonorrhoeae in adolescents; fungal and mycobacterial arthritis are seen rarely, may have chronic course
-
Lyme arthritis
–Second most common manifestation of Lyme disease (after erythema migrans)
–Monoarthritis of a knee occurs in about two-thirds of children with Lyme disease
-
Reactive arthritis
–Probably the most common etiology of childhood rheumatic diseases
–Transient sterile arthritis following a bacterial GI infection
–Usually full resolution, but a few children have a chronic course
-
Trauma, overuse, fracture
–Often acute onset with significant pain
-
Malignancy such as leukemia, neuroblastoma and osteogenic sarcoma
-
Pauciarticular juvenile rheumatoid arthritis (JRA)
-
Spondyloarthropathies (SpA)
-
Congenital hip dysplasia
-
Slipped capital femoral epiphysis (SCFE)
–Most common adolescent hip disorder
–Separation of the femoral growth plate
–More common in obese males
-
Spontaneous osteonecrosis of the joint
–Mostly in hip (Legg-Calvé-Perthes disease), shoulder, and knee
–More common in males
-
Internal structural abnormality
–Discoid meniscus, osteochondritis dissecans, synovial chondromatosis
-
Hemarthrosis due to trauma, bleeding disorder such as hemophilia, or benign tumors such as hemangiomas and pigmented villonodular synovitis
-
Periodic fever syndromes such as familial Mediterranean fever
» READ BOOK EXCERPT ONLINE »
Source: In A Page: Pediatric Signs and Symptoms, 2007
Psoriatic arthritis:
Causes
(Professional Guide to Diseases (Eighth Edition))
Evidence suggests that predisposition to psoriatic arthritis is hereditary; 20% to 50% of patients are human leukocyte antigen-B27 positive. However, onset is usually precipitated by streptococcal infection or trauma.
About 5% to 7% of patients with psoriasis develop psoriatic arthritis. It occurs in up to 1% of the general population.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Septic arthritis:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
In most cases of septic arthritis, bacteria spread from a primary site of infection — usually in adjacent bone or soft tissue — through the bloodstream to the joint. Common infecting organisms in children are group B Streptococcus and Haemophilus influenzae. Adults are usually infected by Staphylococcus, Streptococcus (pneumonia), and group B Streptococcus, whereas chronic septic arthritis is caused by Mycobacterium tuberculosis and Candida albicans.
Various factors can predispose a person to septic arthritis. Any concurrent bacterial infection (of the genitourinary or the upper respiratory tract, for example) or serious chronic illness (such as malignancy, renal failure, rheumatoid arthritis, systemic lupus erythematosus, diabetes, or cirrhosis) heightens susceptibility. Consequently, elderly people and those who abuse I.V. drugs run a higher risk of developing septic arthritis. Of course, diseases that depress the immune system and immunosuppressive therapy increase susceptibility. Other predisposing factors include recent articular trauma, joint arthroscopy or other surgery, intra-articular injections, and local joint abnormalities.
Septic arthritis may be seen at any age in children, but it occurs most often in children younger than age 3. It’s uncommon from age 3 until adolescence, at which time the incidence increases again.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Juvenile rheumatoid arthritis:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
The cause of JRA remains puzzling. Research continues to test several theories, such as those linking the disease to genetic factors or to an abnormal immune response. Viral or bacterial (particularly streptococcal) infection, trauma, and emotional stress may be precipitating factors, but their relationship to JRA remains unclear.
Considered the major chronic rheumatic disorder of childhood, JRA affects an estimated 150,000 to 250,000 children in the United States; overall incidence is twice as high in females, with variation among the types of JRA.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Rheumatoid arthritis:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
RA occurs worldwide, striking three times more females than males. Although it can occur at any age, it begins most often between ages 25 and 55. This disease affects more than 7 million people in the United States alone.
What causes the chronic inflammation characteristic of RA isn’t known, but various theories point to infectious, genetic, and endocrine factors. Currently, it’s believed that a genetically susceptible individual develops abnormal or altered immunoglobulin (Ig) G antibodies when exposed to an antigen. This altered IgG antibody isn’t recognized as “self,” and the individual forms an antibody against it — an antibody known as RF. By aggregating into complexes, RF generates inflammation. Eventually, cartilage damage by inflammation triggers additional immune responses, including activation of complement. This in turn attracts polymorphonuclear leukocytes and stimulates release of inflammatory mediators, which enhance joint destruction.
Much more is known about the pathogenesis of RA than about its causes. If unarrested, the inflammatory process within the joints occurs in four stages. First, synovitis develops from congestion and edema of the synovial membrane and joint capsule. Formation of pannus — thickened layers of granulation tissue — marks the second stage’s onset. Pannus covers and invades cartilage and eventually destroys the joint capsule and bone. Progression to the third stage is characterized by fibrous ankylosis — fibrous invasion of the pannus and scar formation that occludes the joint space. Bone atrophy and malalignment cause visible deformities and disrupt the articulation of opposing bones, causing muscle atrophy and imbalance and, possibly, partial dislocations or subluxations. In the fourth stage, fibrous tissue calcifies, resulting in bony ankylosis and total immobility.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Acute Monoarticular Arthritis:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Injury
❑ Gout
❑ Osteoarthritis
❑ Lyme disease
❑ Gonococcal arthritis
❑ Seronegative spondyloarthropathy
❑ Septic arthritis
❑ Pseudogout
❑ Septic bursitis
❑ Avascular necrosis
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Arthritis/Dermatitis:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑Lyme disease
❑Erythema nodosum
❑Rheumatoid arthritis
❑Systemic lupus erythematosus
❑Psoriatic arthritis
❑Disseminated gonococcemia
❑Sarcoidosis
❑Scleroderma
❑Dermatomyositis
❑Reiter syndrome
❑Rheumatic fever
❑Behçet syndrome
❑Still disease
❑Hypersensitivity vasculitis
Clinical Findings
Lyme disease Erythema migrans, a rapidly expanding annular rash with a clearing center, is the key early finding. The site of the ixodid tick bite at the center of the lesion is usually intensely indurated, vesicular, or necrotic. The arthritis is an asymmetric oligoarthritis that usually occurs after the rash has resolved.
Erythema nodosum A prodromal syndrome of fever, chills, malaise, and polyarthralgia is followed by the development of lesions that are discrete, tender, slightly raised subcutaneous nodules on the shins or ankles. They represent a hypersensitivity reaction to group A streptococcal infection, tuberculosis, sarcoidosis, inflammatory bowel disease, or drugs such as oral contraceptives and sulfonamides.
Rheumatoid arthritis Symmetric polyarticular arthritis with synovial proliferation, especially of the wrist, and morning stiffness lasting more than 1 hour characterize the early joint involvement. Rheumatoid nodules appear over extensor surfaces. Vasculitic lesions are frequently found on the digits, appearing as small red or purpuric macules that progress to painful nodules or ulcers.
Systemic lupus erythematosus A classic butterfly rash occurs in 40% and is exacerbated by sun exposure. A diffuse maculopapular rash in areas exposed to the sun heralds disease flares. Discoid lesions and scaling plaques that range in color from red to violaceous, with central atrophy and telangiectasias, occur in 20%. Vasculitis, in the form of painful ulcers on the extremities, palpable purpura, or lupus profundus (firm nodules in the subcutaneous fat on the forehead, cheeks, buttocks, and upper arms) are found. The arthritis is typically one of symmetric fusiform swelling of the proximal interphalangeal and metacarpophalangeal joints, diffuse puffiness of the hands, and tenosynovitis.
Psoriatic arthritis Psoriatic plaques, erythematous with a silvery scale, are critical to diagnosis, but may be hidden in the scalp, umbilicus, or gluteal folds. Nail changes such as pitting or yellow discoloration of the nail plate are other clues. The arthritis typically involves the proximal interphalangeal and distal interphalangeal joints, creating sausage digits. The arthritis may become erosive, leading to telescoping of the hands. One-fourth of patients have axial skeletal arthritis.
Disseminated gonococcemia Acral lesions are typically hemorrhagic pustules, but petechiae, hemorrhagic papules, or hemorrhagic bullae can occur. Fever, rigor, tenosynovitis, and polyarthritis are other findings.
Sarcoidosis Transient maculopapular eruptions of the trunk, face, and extremities are often accompanied by uveitis, adenopathy, and parotid enlargement. Translucent reddish-brown to purple indolent plaques may develop on the face (lupus pernio), buttocks, or extremities. Joint symptoms consist of migratory transient arthralgias.
Scleroderma Early findings are primarily Raynaud phenomenon and puffy fingers. Later findings include sclerodactyly (smooth, shiny, tapered fingers with taut, bound-down skin); contractures with “claw hand” deformity; expressionless face (with thin lips, a beak-like nose, and sunken cheeks); microstomia; mat telangiectasias on the nail folds, face, lips, oral mucosa, or trunk; and calcinosis with leathery crepitation over the joints.
Dermatomyositis The classic skin manifestation is a lilac-colored heliotrope rash on the eyelids and in a butterfly distribution. Gottron papules are violaceous, scaly, flat lesions on the extensor aspect of the interphalangeal joints, elbows, knees, and medial malleoli; these occur as a late manifestation. Proximal muscle aching/weakness, not arthritis, is prominent. The patient is unable to reach overhead or arise from a chair. Neck flexors are more involved than extensors.
Reiter syndrome Arthritis, urethritis, conjunctivitis, and mucocutaneous ulcers are found. The arthritis is asymmetric, usually involving the lower extremity joints. Solitary sausage digits may be seen. Tendinitis and fasciitis are common. The mucocutaneous lesions are eroded red vesicles or papules of the corona and glans, which when confluent are called circinate balanitis. Pustules may change into thick hyperkeratotic plaques on the palms and soles, keratoderma blennorrhagicum.
Rheumatic fever There is an acute migratory polyarthritis with fever. Subcutaneous nodules appear over the bony prominences of the elbows, knuckles, ankles, scapulae, and occiput. They are associated with carditis. Erythema marginatum, appearing as evanescent pink lesions with serpiginous borders, is also associated with carditis.
Behçet syndrome The classic triad is arthritis, iritis, and oral and genital ulcerations. Recurrent aphthous ulcers are a sine qua non. They begin as macular erythema that develops into superficial gray ulcers. Scrotal or labial ulcerations are also found. Hypopyon uveitis, a hallmark, is a rare finding. The arthritis is primarily of the knees and ankles.
Still disease Skin lesions are red, flat, and less than 1 cm in diameter. Lesions are evanescent, occurring with fever spikes. A migratory polyarthralgia occurs.
Hypersensitivity vasculitis After an upper respiratory infection, young adults may develop palpable purpura over the extensor surfaces and buttocks. Arthritis, edema, and colicky abdominal pain, followed by bloody stools, suggests the diagnosis.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Polyarticular Arthritis:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Osteoarthritis
❑ Rheumatoid arthritis
❑ Lyme arthritis
❑ Systemic lupus erythematosus
❑ Psoriatic arthritis
❑ Polyarticular gout
❑ Viral arthritis
❑ Scleroderma
❑ Reiter syndrome
❑ Inflammatory bowel disease
❑ Gonococcal arthritis
❑ Ankylosing spondylitis
❑ Systemic vasculitis
❑ Sarcoidosis
❑ Pseudogout (CPPD)
❑ Acute rheumatic fever
❑ Still disease
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Psoriatic arthritis:
Causes
(Handbook of Diseases)
Evidence suggests that predisposition to psoriatic arthritis is hereditary; 20% to 50% of patients are human leukocyte antigen-B27-positive. However, its onset may be precipitated by streptococcal infection or trauma.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Septic arthritis:
Causes
(Handbook of Diseases)
In most cases of septic arthritis, bacteria spread from a primary site of infection, usually in adjacent bone or soft tissue, through the bloodstream to the joint.
Common infecting organisms include four strains of gram-positive cocci — Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, and Streptococcus viridans — and two strains of gram-negative cocci — Neisseria gonorrhoeae and Haemophilus influenzae. Various gram-negative bacilli — Escherichia coli, Salmonella, and Pseudomonas, for example — also cause infection.
Anaerobic organisms such as gram-positive cocci usually infect adults and children older than age 2. H. influenzae most often infects children younger than age 2.
Risk factors
Various factors can predispose a person to septic arthritis. Any concurrent bacterial infection (of the genitourinary or the upper respiratory tract, for example) or serious chronic illness (such as cancer, renal failure, rheumatoid arthritis, systemic lupus erythematosus, diabetes, or cirrhosis) heightens susceptibility. Consequently, alcoholics and elderly people run a higher risk of developing septic arthritis.
Of course, susceptibility increases with diseases that depress the autoimmune system or with prior immunosuppressant therapy. I.V. drug abuse (by heroin addicts, for example) can also cause septic arthritis.
Other predisposing factors include recent articular trauma, joint surgery, intra-articular injections, and local joint abnormalities.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Juvenile rheumatoid arthritis:
Causes
(Handbook of Diseases)
JRA is thought to be an autoimmune disorder. Research has linked causation to genetic and immune factors. Viral or bacterial (particularly streptococcal) infection, trauma, and emotional stress have been identified as precipitating factors.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Rheumatoid arthritis:
Causes
(Handbook of Diseases)
What causes the chronic inflammation characteristic of RA isn’t known. One theory states that abnormal immune activation (occurring in a genetically susceptible individual) leads to inflammation, complement activation, and cell proliferation within joints and tendon sheaths. Although no single environmental factor has been found to be a consistent and reproducible cause of this response, infection (viral or bacterial), hormonal factors, and lifestyle factors may all influence disease onset.
Some RA patients develop an immunoglobulin (Ig) M antibody against their body’s own IgG, which is called RF. Increased production of this antibody may also play a role in genetic inflammation.
Pathogenesis
Much more is known about the pathogenesis of RA than about its causes. If unarrested, the inflammatory process within the joints occurs in four stages.
In the first stage, synovitis develops from congestion and edema of the synovial membrane and joint capsule. Infiltration by lymphocytes, macro-phages, and neutrophils perpetuates the local inflammatory response. These cells, as well as fibroblast-like synovial cells, produce enzymes that help to degrade bone and cartilage.
Formation of pannus — thickened layers of granulation tissue — marks the onset of the second stage. Pannus covers and invades cartilage and eventually destroys the joint capsule and bone.
Progression to the third stage is characterized by fibrous ankylosis — fibrous invasion of the pannus and scar formation that occludes the joint space. Bone atrophy and malalignment cause visible deformities and disrupt the articulation of opposing bones, causing muscle atrophy and imbalance and, possibly, partial dislocations or subluxations.
In the fourth stage, fibrous tissue calcifies, resulting in bony ankylosis and total immobility.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
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