AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Identifying and understanding the pathophysiologic mechanisms by which viral arthritis causes acute and chronic arthropathies is crucial to understanding its immunopathogenesis. Alterations of the immune system can lead to acute forms of arthritis, which can be followed by chronic arthralgia or arthritis (ie, overrepresentation of CD8⁺ T lymphocytes in the synovial fluid of individuals with rheumatoid arthritis or Epstein-Barr virus infection). The number of patients diagnosed with acute viral arthritis is relatively low because of its late presentation. New technologies now provide simpler, faster, more reliable, and more sensitive tests for viral diagnosis; additionally, antiviral treatment is now available.

Pathophysiology

Viruses are agents that cause infection or are cofactors in the development of rheumatic diseases. Viral infection depends on host and viral factors. Host factors are very important and include age, sex, genetic background, infection history, and immune response. Viral factors include the mode of host entry, tissue tropism, replication, the effects of cytokines, the ability to establish persistent or latent viral infections, and alterations of host antigens. Infected cells can undergo apoptosis (programmed cell death). The immune complexes from an antibody response can be deposited at sites of viral infection or in the synovium. Virus-induced autoimmunity, polyclonal B-cell activation, and immunodeficiency may result in opportunistic infection, largely because of an inability of the immune system to eliminate the virus (eg, HIV-1, human T-lymphotropic virus 1 [HTLV-I], hepatitis C virus [HCV]). Molecular mimicry may cause abnormal self-reactivity by altering immune tolerance.

Frequency

United States

Although not uncommon, exact incidence and prevalence rates of viral arthritis are unknown and vary with the type of virus and the age range of specific population groups. However, approximately 2.7 million people are infected with HCV in the United States, and perhaps 0.01% of the population is infected with hepatitis B virus (HBV).

International

Although precise international incidence and prevalence rates are unknown, viral arthritis occurs worldwide. The rate of HBV infection is higher in Asia (China, 10% of the population), the Mideast, and sub-Saharan Africa. HCV infection rates are higher in Africa and Asia.

Mortality/Morbidity

The major morbidity of viral arthritis is dysfunctional joints. The mortality rate depends on the type of virus and duration of infection.

Race

No racial or ethnic predilection is recognized.

Sex

Parvovirus B19 infection is more common in women than in men. Whether hepatitis A virus or HCV has a predilection for either sex is unknown.

Age

Adulthood infection rates may be higher than in childhood or vice versa, depending on the virus. HBV infection rates in childhood may be as high as 5% annually. In adulthood, HBV infection occurs through sexual activity or needle exposures. Children are more susceptible to infection with parvovirus B19 than adults, although arthritis rarely occurs in children. Up to 60% of adults have serologic evidence of past parvovirus B19 infection.

CLINICAL

Section 3 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

Viral arthritis occurs during the viral prodrome, when the characteristic rash arises. In the United States, patients with the most common viral arthritides generally present with symmetrical small joint involvement, although different patterns of joint and soft tissue involvement occur with different viral infections. In all instances, the arthritis associated with viral infections is nondestructive and does not lead to any currently recognized form of chronic disease.

• Parvovirus B19: Discovered in 1975, parvovirus B19 is a small, single-stranded DNA virus that replicates in dividing cells and thus has a remarkable tropism for human erythroid progenitor cells. It may be responsible for causing approximately 12% of the cases of sudden-onset polyarticular arthritis, especially in adults with frequent exposures to children, such as schoolteachers and pediatric nurses, who have a 50% risk of acquiring infection. Outbreaks of erythema infectiosum commonly occur in late winter and spring, but the condition can be observed during summer and fall, with sporadic cases occurring throughout the year.
• • Clinical features in children
  • • Up to 70% may be asymptomatic.
    • A few may have flulike symptoms (eg, fever, headache, sore throat, cough, anorexia, vomiting, diarrhea, arthralgia).
    • A bright red rash is typically noted, often characterized as "slapped cheeks" (see Images 1-2).
    • Joint symptoms are rare (5-10%).
  • Clinical features in adults
  • • Rash is rare.
    • Joint symptoms occur in up to 60%. Arthralgia is more common than frank arthritis. Arthralgia is usually self-limited; symmetrical; and in peripheral small joints, hands (ie, proximal interphalangeal and metacarpophalangeal), wrists, knees, and ankle joints, with prominent morning stiffness and swelling.
    • Parvovirus B19 is emerging as a pathogen responsible for several diseases, including erythema infectiosum (fifth disease), transient aplastic crisis (especially in patients with sickle cell disease, thalassemia, or HIV-induced anemia), and fetal hydrops in infected mothers.
  • Rare clinical features
  • • Henoch-Schönlein purpura is rare but possible.
    • Thrombotic thrombocytopenic purpura is unlikely but may be present.
    • Polyarteritis nodosa is rare.
    • Wegener granulomatosis is possible but rare.
  • Transmission
  • • Respiratory secretions are a vector for transmission.
    • Blood products, especially clotting factor precipitants, are modes of transmission.
    • Vertical transmission may occur from mother to fetus. The highest morbidity to the fetus is during the first or second trimester.
• Hepatitis A virus: This infection accounts for 10-14% of cases of viral arthritis. Arthralgia and skin rash occur during the acute phase. Transmission is via the fecal-oral route.
• Hepatitis B virus: HBV is an enveloped, double-stranded DNA virus. HBV infection causes 20-25% of cases of viral arthritis.
• • Clinical features
  • • Symmetric arthritis may be migratory or additive; the hand and knee joints are most commonly affected. Significant morning stiffness and fusiform swelling are associated with HBV-induced arthritis.
    • Arthritis and urticaria may precede jaundice by days to weeks and may persist several weeks after jaundice resolves.
    • Recurrent polyarthralgia or polyarthritis can occur in patients with chronic active hepatitis or chronic HBV viremia.
    • Polyarteritis nodosa may be associated with chronic HBV viremia.
    • Patients may have arthritis-dermatitis syndrome.
    • Nephropathy is described.
    • Systemic necrotizing vasculitis is also a clinical feature.
  • Transmission: This can be parenteral or sexual.
• Hepatitis C virus: HCV is an enveloped, single-stranded RNA virus. HCV infection occurs worldwide.
• • Clinical features
  • • It is a rapidly progressive acute arthralgia (but rarely arthritis) in a rheumatoid distribution affecting the hands, wrists, shoulders, knees, and hips.
    • Myalgia is common.
    • Essential mixed cryoglobulinemia, a triad of arthritis, palpable purpura, and cryoglobulinemia, is associated with HCV in most cases.
    • Necrotizing vasculitis with cryoglobulinemia is a clinical feature.
    • Essential mixed cryoglobulinemia type II or III is associated with more severe skin disease, such as Raynaud phenomenon, purpura, livedo-reticularis, distal ulcers, gangrene, and peripheral neuropathy.
    • Sjögren syndrome has been described in a number of HCV patients.
    • Several recent reports describe a possible association between fibromyalgia and HCV infection.
  • Transmission: This can be parenteral or, uncommonly, sexual.
• Rubella virus: This virus is the sole member of the Rubivirus genus (Togaviridae family) and is a single-stranded RNA virus. Rubella virus naturally infects humans, primarily women, and transmission is by nasopharyngeal secretions, with peak incidence in late winter and spring. Approximately 50-75% of rubella virus infections are symptomatic; the rest are subclinical.
• • Clinical features (in both children and adults)
  • • Patients have a low-grade fever, malaise, and coryza.
    • Rash (acute mild-to-severe viral exanthema [maculopapular rash]) appears first on the face, then the trunk and upper extremities, and then lower extremities, sparing the palms and soles.
    • Significant lymphadenopathy (posterior cervical, postauricular, and occipital) may be noted.
    • Arthritis is usually sudden in onset 1 week before or after the rash. Morning stiffness is symmetric and polyarticular in distribution (eg, fingers, knees, wrists), brief in duration (a few days to weeks), and without residua.
    • Arthritis may also occur within a few weeks of vaccination by attenuated rubella virus, which is similar to that of natural infection. The HPV77/DK12 strain is the most arthrogenic of the vaccine strains available in the United States. The RA27/3 strain is used currently and causes postvaccination joint symptoms in approximately 15% of recipients.
    • In children, 2 syndromes, with either natural infection or vaccination, may occur. In "arm syndrome," a brachial radiculoneuritis causes arm and hand pain and dysesthesias that worsen at night. In "catcher's crouch" syndrome, a lumbar radiculoneuropathy causes popliteal fossa pain upon arising in the morning. Both syndromes occur 1-2 months after vaccination. The first episode may last up to 2 months, but recurrence is usually shorter in duration. Catcher's crouch syndrome may recur for up to a year but causes no permanent damage.
  • Transmission: It is transmitted via nasopharyngeal secretions, with a peak incidence in late winter and spring.
• Alphaviruses: These viruses are a genus of the Togaviridae family. Approximately 5-6 types of alphavirus infection have rheumatic symptoms and fever as major features. All are mosquito borne. Although alphaviruses are not endemic in the United States, an outbreak of West Nile virus has recently spread across the country. Arthralgia is common with West Nile virus infection (76%), but arthritis has not been described.
• • Geographic distribution: The distribution includes Chikungunya (East Africa, India, Southeast Asia, Philippines), O'nyong-nyong (East Africa), the Ross River (Australia, New Zealand, South Pacific islands), Mayaro (South America), Sindbis (Europe, Asia, Africa, Australia, Philippines), and the Barmah Forest (Australia).
  • Clinical features
  • • Fever is reported, with temperatures from 102.2-104°F (39-40°C)
    • Arthritis or a migratory polyarthralgia of the small joints of the hands, wrists, elbows, knees, feet, and ankles occurs, along with stiffness and swelling. The arthritis is generally symmetric and polyarticular. In most alphavirus infections, joint symptoms resolve over 3-7 days, but they can persist for more than a year, albeit with no evidence of permanent joint damage.
    • Maculopapular rash may be itchy to some patients.
• Retroviruses
• • Human immunodeficiency virus
  • • HIV infection is associated with several rheumatic manifestations. The most common (25-40%) is arthralgias.
    • Others include psoriatic arthritis, painful articular syndrome (10%), undifferentiated spondyloarthropathy, inflammatory myopathy, systemic vasculitis, diffuse infiltrative lymphocytosis syndrome (5%), fibromyalgia (30%), avascular necrosis, and gout.
    • Infections may include septic arthritis, osteomyelitis, or pyomyositis or other conditions may be related to soft tissue rheumatism (eg, tendinitis, bursitis).
    • Arthritis (ie, arthralgia, arthritic syndromes) in association with HIV infection has been reported in the United States, Europe, and Africa. Arthritis can occur at any stage of HIV infection. The pattern of HIV-associated arthritis is similar to that of other viral disorders, with an acute onset, short duration, recurrences, and no erosive changes. Interestingly, patients infected with HIV are not at an increased risk for the development of septic arthritis, but they do have an increased frequency of pyomyositis.
    • Diffuse infiltrative lymphocytosis syndrome resembles Sjögren syndrome with sicca symptoms, salivary gland enlargement, and lymphocytic infiltration involving the lungs, gastrointestinal tract, and kidneys. In contrast to Sjögren syndrome, the lymphocytes infiltrating these sites are predominantly CD8⁺ (rather than CD4⁺) T cells.
    • Reiter syndrome in association with HIV infection occurs in 0.5-3% of cases. Oligoarthritis of the lower extremities and urethritis is common, but conjunctivitis is rare. Severe erosive arthritis is possible and can be very debilitating. The frequency of HLA-B27 in HIV-infected Reiter syndrome patients is the same as that found in Reiter syndrome patients of the same race without HIV infection.
    • Psoriasis and psoriatic arthritis tend to occur late in the course of HIV infection. This is often severe.
  • Human T-lymphotropic virus 1: HTLV-1 is a type C retrovirus (an RNA virus in the Oncovirinae subfamily). It infects millions of people worldwide, particularly in the Caribbean, southern Japan, South Africa, and South America. HTLV-1 is transmitted by breast milk, sexual intercourse, and blood products. HTLV-1 infection is associated with Sjögren syndrome and the following diseases:
  • • Adult T-cell leukemia/non-Hodgkin lymphoma may develop, with a 5% lifetime risk, and is commonly associated with hypercalcemia and skin involvement.
    • Chronic inflammatory syndromes develop at a lifetime risk of 2%. These include a seronegative oligoarthritis or polyarthritis with tenosynovitis and nodules with fibrinoid necrosis. Other syndromes include polymyositislike disease, dermatitis, uveitis, or transverse myelitis (known as tropical spastic paraparesis).
• Other viruses: Several patients have been discovered to have infections with other viruses that can cause arthritis, as follows:
• • Epstein-Barr virus: This infection is usually associated with polyarthralgia, but monoarthritis of the knee and ruptured Baker cysts may occur.
  • Varicella-zoster virus: This infection in children rarely develops into pauciarticular arthritis.
  • Mumps virus: In infected adults, it is associated with small or large joint synovitis that lasts for several weeks. Arthritis may precede or follow parotitis by up to 4 weeks.
  • Adenovirus or coxsackieviruses A9, B2, B3, B4, and B6: These infections have been associated with recurrent episodes of polyarthritis, pleuritis, myalgia, rash, pharyngitis, myocarditis, and leukocytosis.
  • Echovirus: This infection can be associated with polyarthritis, fever, and myalgias.
  • Herpes simplex virus or cytomegalovirus: These infections are also rare. Cytomegalovirus arthritis has been reported in patients after bone marrow transplantation. Vaccinia virus has been associated with postvaccination knee arthritis in only 2 reported cases.

DIFFERENTIALS

Section 4 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

WORKUP

Section 5 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
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Lab Studies

• Parvovirus B19: The incubation period is 7-18 days, and the state of viremia lasts 5-6 days.
• • CBC count (to assess hemoglobin, neutrophils, lymphocytes)
  • High immunoglobulin M antibody levels 4-6 days after the initial viremia
  • Viral B19 DNA by polymerase chain reaction
  • Immunoglobulin G antibody titer (of little diagnostic significance)
  • Low-to-moderate titer values for rheumatoid factor, anti-DNA, antinuclear, and anticardiolipin antibodies possible in some patients
• Hepatitis A virus
• • Elevated bilirubin and transaminases values
  • Immunoglobulin M–specific anti–hepatitis A virus
• Hepatitis B virus
• • Elevated bilirubin and transaminases values (may be normal in early stage of disease when arthritis is present)
  • Serum hepatitis B surface antigen, hepatitis B early antigen, anti–hepatitis B surface antigen immunoglobulin M (indicates acute infection), viral DNA, polymerase
• Hepatitis C virus
• • Elevated bilirubin and transaminase values (Normal transaminase levels do not exclude HCV infection.)
  • Anti-HCV
  • HCV-RNA by polymerase chain reaction methods
  • Cryoglobulins, rheumatoid factor
• Rubella virus
• • Anti–rubella virus immunoglobulin M (peaks 8-21 d after symptoms, then wanes by 5 wk)
  • Anti–rubella virus immunoglobulin G (rises rapidly over a period of 1-3 wk and is of long duration)
  • More recently, rubella virus has been isolated from lymphocytes and synovial fluid of patients who had vaccine-induced disease or who experienced rubella virus–associated arthritis years earlier.
• Alphaviruses: Diagnosis is confirmed by specific serology results.
• Human immunodeficiency virus: Generally, laboratory abnormalities are common but nonspecific in persons with HIV infection.
• • Elevated levels of serum immunoglobulins, moderate elevation of erythrocyte sedimentation rate, circulating immune complexes, low-grade complement activation, low-titer antinuclear antibody, rheumatoid factor, false-positive test result for syphilis and anticardiolipin antibodies, and lupus anticoagulants
  • CD8⁺ T cell and P-24 antigen possibly detected in synovial fluid.
• Human T-lymphotropic virus: Diagnosis of HTLV-1 is achieved by the detection of antibodies with enzyme-linked immunosorbent assays, with confirmation by Western blot and the observation of "flower cells" on the peripheral smear.

Imaging Studies

• Radiologic findings depend on the condition. Most of the virally associated arthropathies are nonerosive and show only soft tissue swelling. However, with HIV-related seronegative or psoriatic-type arthropathy, erosions, ankylosis, narrowing of joint spaces, whittling, osteolytic lesions, periostitis, sacroiliac joint-space widening, and syndesmophyte formation can be seen.

Procedures

• Aspiration of the joint is useful to help rule out other conditions such as crystal arthropathy or bacterial infection.

TREATMENT

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Medical Care

In general, viral arthritis is mild and patients require only symptomatic treatment with analgesics or nonsteroidal anti-inflammatory drugs (NSAIDs). Occasionally, a brief course of low-dose prednisone may be used.

• Parvovirus B19: Treatment is symptomatic with analgesics and NSAIDs. In severe cases, aspiration of fluid from the affected joint may relieve pain.
• Hepatitis A virus: Treatment is symptomatic with analgesics and NSAIDs. Prophylaxis for contacts is an important element of management.
• Hepatitis B virus: No evidence indicates that early therapy for acute HBV infection with interferon alfa or antiviral agents decreases the rate of chronicity or speeds recovery. Most patients with acute icteric HBV infection recover without residual injury or chronic hepatitis. Focus management of acute HBV infection on avoidance of further hepatic injury and prophylaxis of contacts.
• Hepatitis C virus: Administer interferon alfa-2b (3-5 million U 2-3 times/wk for 6 mo). Combination therapy with ribavirin (1000-1200 mg/d) is recommended and has been shown to yield better response rates. Patients with complications of cryoglobulinemia are best treated with antiviral therapy. However, corticosteroids and cyclophosphamide may be required initially for patients with more active, severe vasculitic complications.
• Rubella virus: Treatment is symptomatic with analgesics and NSAIDs. Steroids at low-to-moderate doses to control symptoms and viremia are suggested by some investigators.
• Alphaviruses: Treatment is symptomatic with analgesics and NSAIDs, but avoid aspirin in order to prevent a hemorrhagic component with alphavirus rashes. Chloroquine phosphate (250 mg/d) has been used when NSAIDs are not effective.
• Human immunodeficiency virus
• • Use a combination of newer antiretroviral therapy.
  • Treatment is symptomatic with analgesics and NSAIDs.
  • Administer sulfasalazine and methotrexate for patients with conditions refractory to NSAID therapy.
  • Prednisone, antimalarials, and other agents have been successfully used in patients with polymyositis, Reiter syndrome, Sjögrenlike syndrome, psoriatic arthritis, and vasculitis.
  • Antiretroviral and prophylactic therapy, sulfamethoxazole-trimethoprim, and pentamidine help improve associated rheumatic symptoms.
  • Intravenous immune globulin, interleukin-12, interleukin-2, interferon gamma, and/or sargramostim may be effective for some HIV-infected patients with arthritis.
• Human T-lymphotropic virus 1: Treatment options are poor.

Surgical Care

Surgical drainage is not indicated unless septic arthritis is considered likely.

Consultations

In general, patients can initially be seen by their family doctors. If no improvement or poor response ensues, the following practitioners may be consulted:

• Rheumatologists
• Hepatologists (if HBV or HCV infection is considered)
• Infectious disease specialists
• Immunologists

Diet

No restrictions are necessary.

Activity

Recommend gentle mobilization after a few days of rest.

MEDICATION

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The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Nonsteroidal anti-inflammatory drugs

Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanisms of action are not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may be present, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Drug Category: Antimalarial agents

Derivatives of 4-aminoquinoline are active against various autoimmune disorders.

Drug Category: Immunoglobulin agents

Used to improve clinical and immunologic aspects of the disease. May decrease autoantibody production and increase solubilization and removal of immune complexes.

Drug Category: Interferons

Naturally produced proteins with antiviral, antitumoral, and immunomodulatory actions. Alfa-, beta-, and gamma-interferons may be given topically, systemically, and intralesionally.

Drug Category: Corticosteroid agents

Have anti-inflammatory properties and cause profound and varied metabolic effects. Modify body's immune response to diverse stimuli.

Drug Category: Antineoplastic agents

Inhibit key factors responsible for deregulated cell proliferation.

Drug Category: Anti-inflammatory agents

Inhibit key factors responsible for inflammation.

Drug Category: Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience pain.

Drug Category: Antiviral agents

Nucleoside analogs are initially phosphorylated by viral thymidine kinase to eventually form a nucleoside triphosphate. These molecules inhibit HSV polymerase with 30-50 times the potency of human alpha-DNA polymerase.

Drug Category: Antibiotics

Therapy must cover all likely pathogens in the context of this clinical setting. Indications include Pneumocystis carinii pneumonia and HCV infection.

FOLLOW-UP

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Further Inpatient Care

• Individuals with viral arthritis are usually treated in an outpatient setting. Order physical therapy as indicated. Follow-up care may be conducted by family practitioners and rheumatologists. If the patient's condition proves refractory, appropriate specialists can be consulted.

Further Outpatient Care

• Patients can be seen by their family practitioners.

In/Out Patient Meds

• Nonsteroidal anti-inflammatory drugs
• Acetaminophen

Deterrence/Prevention

• Vaccination
• Safe sex
• Clean food and drinking water
• Education

Complications

• Rarely, viral infections cause damage to the joints.

Patient Education

• For excellent patient education resources, visit eMedicine's Arthritis Center and Bacterial and Viral Infections Center.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Failure to diagnose septic arthritis: This can lead to permanent damage to the joint and medicolegal liability. If septic arthritis is considered in the differential diagnosis, obtaining a sample of joint fluid for culture is essential.
• Failure to diagnose and appropriately treat cryoglobulinemic syndromes secondary to HCV infection (ie, with antiviral therapy)

MULTIMEDIA

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Media file 1:  Viral arthritis. Typical "slapped cheek" appearance. Courtesy of Brenda Moroz, MD, Montreal Children's Hospital.
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Media type:  Photo

Media file 2:  Viral arthritis. "Slapped cheeks" with typical reticulated erythema of arms. Courtesy of Brenda Moroz, MD, Montreal Children's Hospital.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
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• Follow-up
• Miscellaneous
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• References

• Albert LJ, Inman RD. Molecular mimicry and autoimmunity. N Engl J Med. Dec 30 1999;341(27):2068-74. [Medline].
• Gutierrez K. Bone and joint infections in children. Pediatr Clin North Am. Jun 2005;52(3):779-94, vi.
• Heegaard ED, Taaning EB. Parvovirus B19 and parvovirus V9 are not associated with Henoch-Schonlein purpura in children. Pediatr Infect Dis J. Jan 2002;21(1):31-4. [Medline].
• Koturoglu G, Kurugol Z, Cetin N, et al. Complications of varicella in healthy children in Izmir, Turkey. Pediatr Int. Jun 2005;47(3):296-9. [Medline].
• McCarthy JJ, Dormans JP, Kozin SH, Pizzutillo PD. Musculoskeletal infections in children: basic treatment principles and recent advancements. Instr Course Lect. 2005;54:515-28. [Medline].
• Medina Rodriguez F. Rheumatic manifestations of human immunodeficiency virus infection. Rheum Dis Clin North Am. Feb 2003;29(1):145-61, viii. [Medline].
• Moylett EH, Shearer WT. HIV: clinical manifestations. J Allergy Clin Immunol. Jul 2002;110(1):3-16. [Medline].
• Murphy FA, Fauquet CM, Bishop DHL, et al, eds. Virus Taxonomy. The Sixth Report of the International Committee on Taxonomy of Viruses. New York, NY: Springer-Verlag; 1995.
• Naides SJ. Viral Arthritis. In: Ruddy S, Sledge CB, Harris ED, eds. Kelley's Textbook of Rheumatology. Vol 2. New York, NY: Elsevier Science; 2000:. 1519-27.
• Naides SJ. Viral Arthritis. In: Klippel JH, Crofford L, eds. Primer on the Rheumatic Diseases. 12th ed. Atlanta, Ga: Arthritis Foundation; 2001:. 265-8.
• Naides SJ. Viral Arthritis. In: Koopman WJ, ed. Arthritis and Allied Conditions: A Textbook of Rheumatology. Philadelphia, Pa: Lippincott Williams & Wilkins; 2001:. 2649-68.
• Pinals RS. Polyarthritis and fever. N Engl J Med. Mar 17 1994;330(11):769-74. [Medline].
• Scott M. Viral causes of arthritis. Family Practice Notebook.com [online]. Available at: http://www.fpnotebook.com/ID192.htm. 2002. [Full Text].
• Siegel LB, Gall EP. Viral infection as a cause of arthritis. Am Fam Physician. Nov 1 1996;54(6):2009-15. [Medline].
• Tan LC, Mowat AG, Fazou C, et al. Specificity of T cells in synovial fluid: high frequencies of CD8(+) T cells that are specific for certain viral epitopes. Arthritis Res. 2000;2(2):154-64. [Medline].
• Ytterberg SR. Viral arthritis. Curr Opin Rheumatol. Jul 1999;11(4):275-80. [Medline].

Article Last Updated: Dec 4, 2006