Viral Arthritis

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Practice Essentials

Viral arthritis is inflammation of the joints from a viral infection. Approximately 1% of all cases of acute arthritis are thought to have a viral etiology. Infection from a broad range of viruses can result in arthralgias and arthritis. In some cases the specific virus involved can be identified on the basis of the clinical features of systemic infection, but in many cases serologic testing is necessary for diagnosis, guided by clinical and epidemiologic data.[1] See Etiology, Presentation, and Workup.

In general, viral arthritis is mild and requires only symptomatic treatment with analgesics or nonsteroidal anti-inflammatory drugs (or, occasionally, low-dose prednisone). In some cases, antiviral treatment is available for the underlying systemic disease. See Treatment.

For patient education resources, see the Arthritis Health Center.

Pathophysiology

Viruses can cause infection or act as cofactors in the development of rheumatic diseases. Viral infection depends on both host and viral factors. Key host factors include age, sex, genetic background, infection history, and immune response. Key viral factors include mode of host entry, tissue tropism, replication, effects of cytokines, 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, human T-lymphotropic virus [HTLV]-1, or hepatitis C virus [HCV]). Molecular mimicry may cause abnormal self-reactivity by altering immune tolerance.[2]

Etiology

Viruses that can give rise to viral arthritis include the following[3] :

Parvovirus B19

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 about 12% of cases of sudden-onset polyarticular arthritis, especially in adults frequently exposed to children (eg, schoolteachers and pediatric nurses, who have a 50% risk of 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.

Respiratory secretions are a vector for transmission. The use of blood products, especially clotting factor concentrates, is another mode of transmission.[4] Vertical transmission may occur from mother to fetus. The highest morbidity to the fetus is during the first or second trimester.

Hepatitis viruses

HAV 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.

HBV is an enveloped, double-stranded DNA virus. HBV infection causes 20-25% of cases of viral arthritis. Transmission can be parenteral or sexual.

HCV is an enveloped, single-stranded RNA virus. HCV infection occurs worldwide. Transmission can be parenteral or, uncommonly, sexual.

Rubella virus

Rubella 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 is transmitted via nasopharyngeal secretions, with a peak incidence in late winter and spring. Approximately 50-75% of rubella virus infections are symptomatic; the rest are subclinical.

Alphaviruses

Alphaviruses constitute a genus of the Togaviridae family. Approximately five to six types of alphavirus infection cause rheumatic symptoms and fever as major features; all are mosquito-borne. Geographic distributions are as follows:

Chen and colleagues found that alphavirus infection results in bone loss in a mouse model of Ross River virus, and that bone loss was prevented by inhibition of interleukin-6 (IL-6). Alphaviruses may disrupt bone homeostasis, and osteoblasts may contribute to alphavirus-induced arthritis by regulating IL-6 and contribute to bone loss by disrupting the receptor activator of nuclear factor-kappaB ligand/osteoprotegerin balance.[7]

Retroviruses

HIV infection is associated with several rheumatic manifestations, of which arthralgia is the most common (25-40% of cases).[8] Other manifestations include the following:

Arthritis (ie, arthralgia and arthritic syndromes) in association with HIV infection has been reported in the United States, Europe, and Africa. It can occur at any stage of HIV infection. The pattern of HIV-associated arthritis is similar to that of arthritis associated with other viral disorders: acute onset, short duration, recurrences, and no erosive changes. Patients infected with HIV are not at increased risk for the development of septic arthritis but they do have an increased frequency of pyomyositis.

Diffuse infiltrative lymphocytosis syndrome (DILS) resembles Sjögren syndrome, with sicca symptoms, salivary gland enlargement, and lymphocytic infiltration involving the lungs, gastrointestinal (GI) tract, and kidneys. To make the diagnosis, there needs to be histological confirmation of salivary or lacrimal lymphocytic infiltration, with granulomatous or neoplastic etiologies excluded. In contrast to Sjögren syndrome, the lymphocytes infiltrating these sites in diffuse infiltrative lymphocytosis syndrome are predominantly CD8+ (rather than CD4+) T cells and the presence of elevated titers of circulating and infiltrating CD8+ lymphocytes is a key feature of the pathophysiology.[9]

Reactive arthritis 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.  Human leukocyte antigen (HLA)–B27 is found in 80–90 % of Caucasians with HIV-associated reactive arthritis, while studies of Africans with HIV-associated reactive arthritis have found nearly all to be HLA-B27-negative. As in HIV-uninfected patients, antecedent history of genitourinary and gastrointestinal infection is common. This point could hold the key to explaining the geographical differences observed in the prevalence of reactive arthritis – countries with higher rates of HIV contracted through intravenous drug use for example, rather than sexual contact, have observed lower rates of reactive arthritis.[10]

Psoriasis and psoriatic arthritis tend to occur late in the course of HIV infection. They are often severe.

Human T-cell lymphotropic virus – 1 (HTLV-1) is a type C retrovirus (an RNA virus in the Oncovirinae subfamily) that infects millions of people worldwide, particularly in the Caribbean, southern Japan, South Africa, and South America. It is transmitted through ingestion of breast milk, sexual intercourse, and use of blood products. HTLV-1 infection is associated with Sjögren syndrome, as well as with the following diseases:

Other viruses

A number of other viruses have also been found to be capable of causing arthritis, including the following:

Epidemiology

United States and international statistics

Although viral arthritis clearly is not uncommon in the United States, its exact incidence and prevalence are unknown and vary with the type of virus and the age range of specific population groups. It is estimated that approximately 2.7 million people are infected with HCV in the United States, and perhaps 0.01% of the population is infected with HBV.

Viral arthritis is known to occur worldwide, though its exact international incidence and prevalence are unknown,. The rate of HBV infection is higher in Asia (especially China [10% of the population]), the Mideast, and sub-Saharan Africa. HCV infection rates are higher in Africa and Asia.

Age-, sex-, and race-related demographics

Viral infection rates may be higher in adults than in children or the reverse, depending on the virus under consideration. HBV infection rates in childhood may be as high as 5% annually in some parts of the world. In adulthood, HBV is transmitted through sexual activity or needle exposures. Children are more susceptible to infection with parvovirus B19 than adults are, although they rarely experience arthritis. As many as 60% of adults have serologic evidence of past parvovirus B19 infection.

Parvovirus B19 infection is more common in women than in men. Whether HAV or HCV has a predilection for either sex is unknown. Viral arthritis has no recognized racial or ethnic predilection.

Prognosis

Viral arthritis is generally mild and self-limited, typically lasting no longer than a few weeks. There is no specific treatment for the arthritis; simple symptomatic measures (eg, analgesics, nonsteroidal anti-inflammatory drugs [NSAIDs], or, occasionally, low-dose prednisone) are sufficient.[12]

The major morbidity of viral arthritis is joint dysfunction. Mortality depends on the type of virus causing the arthritis and on the duration of infection.

History

Viral arthritis occurs during the viral prodrome, when the characteristic rash develops. In the United States, patients with the most common viral arthritides generally present with symmetrical small-joint involvement, though different patterns of joint and soft-tissue involvement occur with different viral infections. Many of the viruses that can cause arthritis have specific geographic niches (eg, HTLV-1 in Japan and the Caribbean), so a travel history will be important in some cases.

 

Physical Examination

Physical findings in patients with viral arthritis vary substantially, depending on the type of virus causing the arthritis.

Parvovirus B19

Clinical features of arthritis associated with parvovirus B19 infection in children include the following:

Clinical features in adults include the following:

Rare clinical features include the following:

Hepatitis viruses

Clinical features of arthritis related to hepatitis B virus (HBV) infection include the following:

Clinical features of arthritis related to hepatitis C virus [HCV] infection include the following:

Rubella virus

Clinical features of arthritis associated with rubella virus infection (in both children and adults) include the following:

In children, the following 2 syndromes may occur with either natural infection or vaccination:

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.

Alphaviruses

Clinical features of arthritis associated with alphavirus infection include the following:

Laboratory Studies

Parvovirus B19

The incubation period for parvovirus B19 is 7-18 days, and the state of viremia lasts 5-6 days. The following studies are indicated:

The immunoglobulin G (IgG) antibody titer is of little diagnostic significance. Low-to-moderate titers for rheumatoid factor (RF), anti-DNA, antinuclear antibodies (ANAs), and anticardiolipin antibodies are possible in some patients.

Hepatitis viruses

The following tests may be ordered for hepatitis A virus (HAV):

The following tests may be ordered for hepatitis B virus (HBV):

The following tests may be ordered for hepatitis C virus (HCV):

Rubella virus

The following tests may be ordered for rubella virus:

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 of alphavirus infection is confirmed by specific serology results.

Retroviruses

In persons with HIV infection, laboratory abnormalities generally are common but nonspecific, including the following:

Human T-lymphotropic virus (HTLV-1) infection is diagnosed on the basis of detection of antibodies by means of enzyme-linked immunosorbent assay (ELISA), with confirmation by Western blot and the observation of “flower cells” on the peripheral smear.

Other Tests

Radiologic findings in patients with viral arthritis depend on the specific condition. Most of the virus-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.

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

Approach Considerations

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

Surgical drainage is not indicated unless septic arthritis is considered likely. Most septic joints are managed effectively with a single surgical debridement. However, Hunter and colleagues reported that the risk factors for failure of a single surgical debridement included the following[14] :

No dietary restrictions are necessary. Gentle mobilization may be initiated after a few days of rest.

In patients with rheumatoid arthritis (RA), the elevated risk of infection due to relative immunosuppression must be carefully assessed.[15] A better understanding of the cause of flareups would help predict patient responses to various therapies.[16]

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

Preventive measures include the following:

Pharmacologic Therapy

Parvovirus B19

Treatment of arthritis associated with parvovirus B19 infection is symptomatic, consisting primarily of administration of analgesics and NSAIDs. In severe cases, aspiration of fluid from the affected joint may relieve pain.

Hepatitis viruses

Treatment of arthritis associated with hepatitis A virus (HAV) is symptomatic, consisting primarily of administration of analgesics and NSAIDs. Prophylaxis for contacts is an important element of management.

No evidence indicates that early treatment of acute hepatitis B virus [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. Management of acute HBV infection should be focused on avoidance of further hepatic injury and prophylaxis of contacts.

For hepatitis C virus (HCV) infection, treatment continues  to evolve rapidly. HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C contains the most recent recommendations of the American Association for the Study of Liver Diseases (AASLD) and Infectious Diseases Society of America (ISDA).

Rubella virus

Treatment of arthritis associated with rubella virus infection is symptomatic, consisting primarily of administration of analgesics and NSAIDs. Some investigators have recommended giving corticosteroids at low to moderate doses to control symptoms and viremia.

Alphaviruses

Treatment of arthritis associated with alphavirus infection is symptomatic, involving the use of analgesics and NSAIDs, but aspirin should be avoided so as to prevent the development of a hemorrhagic component with alphavirus rashes. When NSAIDs are not effective, chloroquine phosphate 250 mg/day may be considered.

Chronic chikungunya arthritis shares several characteristics with rheumatoid arthritis such as persistent debilitating arthralgia and exacerbated inflammatory response. Because of these parallels, hydroxychloroquine (HCQ) and disease‐modifying antirheumatic drugs (DMARDs) such as methotrexate (MTX) and sulfasalazine have been evaluated in some peri‐epidemic clinical trials of treatments. However, these studies have produced conflicting outcomes and it remains unclear whether specific DMARDs are effective in treating chronic chikungunya arthritis.[17]

Retroviruses

For cases involving HIV infection, use currently recommended antiretroviral regimens, and treat symptoms with analgesics and NSAIDs. Administer sulfasalazine and methotrexate to patients who have conditions refractory to NSAID therapy. Prednisone, antimalarials, and other agents have been used successfully in patients with polymyositis, reactive arthritis, Sjögrenlike syndrome, psoriatic arthritis, and vasculitis.

Antiretroviral and prophylactic therapy, trimethoprim-sulfamethoxazole, and pentamidine help improve associated rheumatic symptoms. Intravenous immune globulin (IVIg), interleukin (IL)–12, IL-2, interferon gamma, or sargramostim may be effective in some HIV-infected patients with arthritis.

For human T-lymphotropic virus–1 (HTLV-1) infection, current treatment options are poor.

Consultations

In general, patients can initially be seen by their family doctors. In patients who do not improve or in whom the treatment response is poor, the following practitioners may be consulted:

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Agents used to treat patients with viral arthritis include the following:

Naproxen (Anaprox, Naprelan, Aleve, Naprosyn)

Clinical Context:  Naproxen is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which is responsible for prostaglandin synthesis.

Ibuprofen (Motrin, Advil, Adapin, Caldolor)

Clinical Context:  Ibuprofen is the drug of choice for mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. Many doses are available, either with or without a prescription.

Ketoprofen

Clinical Context:  Ketoprofen is used for the relief of mild to moderate pain and inflammation. Small doses are indicated initially in patients with small body size, elderly patients, and persons with renal or liver disease. Doses of over 75 mg do not increase therapeutic effects. Administer high doses with caution, and closely observe the patient for response.

Flurbiprofen

Clinical Context:  Flurbiprofen may inhibit cyclooxygenase, thereby inhibiting prostaglandin biosynthesis. These effects may result in analgesic, antipyretic, and anti-inflammatory activities.

Diclofenac (Voltaren XR, Cataflam, Cambia)

Clinical Context:  This is one of a series of phenylacetic acids that has demonstrated anti-inflammatory and analgesic properties in pharmacological studies. It is believed to inhibit the enzyme cyclooxygenase, which is essential in the biosynthesis of prostaglandins. Diclofenac can cause hepatotoxicity; hence, liver enzymes should be monitored in the first 8 weeks of treatment. It is absorbed rapidly; metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation. The delayed-release, enteric-coated form is diclofenac sodium, and the immediate-release form is diclofenac potassium.

Tolmetin

Clinical Context:  Tolmetin inhibits prostaglandin synthesis by decreasing the activity of the enzyme cyclooxygenase, which, in turn, decreases the formation of prostaglandin precursors. The pediatric dosage is 20 mg/kg/d PO divided tid/qid initially, then 15-30 mg/kg/d, not to exceed 30 mg/kg/d.

Celecoxib (Celebrex)

Clinical Context:  Celecoxib inhibits primarily COX-2. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, the incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions may be decreased when compared with nonselective NSAIDs.

Seek the lowest dose for each patient. The adult dosage is 100-200 mg PO bid; the pediatric dosage has not been established for patients younger than 2 years, is 50 mg PO bid for patients 2 years or older whose weight ranges from 10 kg to no heavier than 25 kg, and is 100 mg PO bid for patients 2 years or older who weigh more than 25 kg.

Indomethacin (Indocin)

Clinical Context:  Indomethacin is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.

Class Summary

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanisms of action are unknown, 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.

Hydroxychloroquine (Plaquenil)

Clinical Context:  Hydroxychloroquine inhibits chemotaxis of eosinophils and locomotion of neutrophils and impairs complement-dependent antigen-antibody reactions. Hydroxychloroquine sulfate 200 mg is equivalent to 155 mg hydroxychloroquine base and 250 mg chloroquine phosphate.

Class Summary

Antimalarial agents are derivatives of 4-aminoquinoline and are active against various autoimmune disorders.

Immune globulin, intravenous (Carimune NF, Gammaplex, Octagam, Gammagard)

Clinical Context:  Neutralizes circulating myelin antibodies through antiidiotypic antibodies; down-regulates proinflammatory cytokines, including INF-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; promotes remyelination; may increase CSF IgG (10%).Immune globulin, intravenous (Carimune NF, Gammaplex, Octagam, Gammagard)

Intravenous immune globulin (IVIg) neutralizes circulating myelin antibodies through anti-idiotypic antibodies; down-regulates proinflammatory cytokines, including interferon gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells while augmenting suppressor T cells; blocks the complement cascade; promotes remyelination; and may increase immunoglobulin G (IgG) in cerebrospinal fluid (CSF) (10%).

Class Summary

Immunoglobulins are used to improve clinical and immunologic aspects of the disease. They may decrease autoantibody production and increase solubilization and removal of immune complexes.

Interferon alfa-2b (Intron A)

Clinical Context:  Interferon alfa-2b is a protein product manufactured by means of recombinant DNA technology. The mechanism of its antitumor activity is not clearly understood; however, direct antiproliferative effects against malignant cells and modulation of host immune response may play important roles.

Class Summary

Interferons are naturally produced proteins with antiviral, antitumoral, and immunomodulatory actions. Interferons alfa, beta, and gamma may be given topically, systemically, and intralesionally.

Prednisone

Clinical Context:  Prednisone is an immunosuppressant used for treatment of autoimmune disorders; it may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte (PMN) activity. Prednisone stabilizes lysosomal membranes and suppresses lymphocyte and antibody production.

Prednisolone (Millipred, Orapred, Orapred ODT, Prelone)

Clinical Context:  Corticosteroids act as potent inhibitors of inflammation. They may cause profound and varied metabolic effects, particularly in relation to salt, water, and glucose tolerance, in addition to their modification of the immune response of the body. Alternative corticosteroids may be used in equivalent dosage.

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body’s immune response to diverse stimuli.

Cyclophosphamide

Clinical Context:  Cyclophosphamide is an alkylating agent that depresses T- and B-cell function.

Methotrexate (Folex PFS, Rheumatrex)

Clinical Context:  Unknown mechanism of action in treatment of inflammatory reactions; may affect immune function. Ameliorates symptoms of inflammation (eg, pain, swelling, stiffness). Adjust dose gradually to attain satisfactory response.

Class Summary

These agents inhibit key factors responsible for deregulated cell proliferation.

Sulfasalazine (Azulfidine, EN-tabs)

Clinical Context:  Sulfasalazine is useful in the management of ulcerative colitis and acts locally in the colon to decrease the inflammatory response. It systemically inhibits prostaglandin synthesis.

Class Summary

Anti-inflammatory agents inhibit key factors responsible for inflammation.

Acetaminophen (Aspirin-Free Anacin, FeverAll, Rapimed Junior, Tylenol)

Clinical Context:  Acetaminophen is the drug of choice for managing pain in patients who have documented hypersensitivity to aspirin or NSAIDs, who have upper gastrointestinal (GI) disease, or who are taking oral anticoagulants.

Class Summary

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.

Ribavirin (Rebetol, Virazole, Copegus)

Clinical Context:  Ribavirin is indicated for chronic hepatitis C virus (HCV) infection. It inhibits replication of RNA and DNA viruses; in addition, it inhibits initiation and elongation of RNA fragments, resulting in inhibition of viral protein synthesis.

Class Summary

Nucleoside analogues are initially phosphorylated by viral thymidine kinase (TK) and eventually form a nucleoside triphosphate. These molecules inhibit herpes simplex virus (HSV) polymerase with 30-50 times the potency with which they inhibit human alpha-DNA polymerase.

Pentamidine (Pentam-300, NebuPent)

Clinical Context:  Pentamidine inhibits the growth of protozoa by blocking oxidative phosphorylation and inhibiting incorporation of nucleic acids into RNA and DNA, causing inhibition of protein and phospholipid synthesis.

Trimethoprim-sulfamethoxazole (Septra DS, Bactrim, Bactrim DS)

Clinical Context:  Trimethoprim-sulfamethoxazole (TMP-SMZ) inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. The antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except for Pseudomonas aeruginosa.

Class Summary

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

What is viral arthritis?What is the pathophysiology of viral arthritis?What are the most common causes of viral arthritis?How does parvovirus B19 cause viral arthritis?How do hepatitis viruses cause viral arthritis?How does rubella virus cause viral arthritis?Which alphaviruses cause viral arthritis?Which retroviruses cause viral arthritis?Which viruses are less common causes of viral arthritis?What is the US prevalence of viral arthritis?What is the global prevalence of viral arthritis?Which patient groups have the highest prevalence of viral arthritis?What is the prognosis of viral arthritis?Which clinical history findings are characteristic of viral arthritis?Which physical findings are characteristic of viral arthritis?Which physical findings are characteristic of parvovirus B19-caused viral arthritis?Which physical findings are characteristic of HBV-caused viral arthritis?Which physical findings are characteristic of HCV-caused viral arthritis?Which physical findings are characteristic of rubella-caused viral arthritis?Which physical findings are characteristic of alphavirus-caused viral arthritis?What are the differential diagnoses for Viral Arthritis?What is the role of lab tests in the workup of parvovirus B19-caused viral arthritis?What is the role of lab tests in the workup of HAV-caused viral arthritis?What is the role of lab tests in the workup of HBV-caused viral arthritis?What is the role of lab tests in the workup of HCV-caused viral arthritis?What is the role of lab tests in the workup of rubella-caused viral arthritis?What is the role of lab tests in the workup of alphavirus-caused viral arthritis?What is the role of lab tests in the workup of HIV-caused viral arthritis?What is the role of imaging studies in the workup of viral arthritis?What is the role of aspiration in the workup of viral arthritis?How is viral arthritis treated?What is the role of surgery in the treatment of viral arthritis?Which dietary and activity modifications are used in the treatment of viral arthritis?What are considerations in the treatment of viral arthritis in patient with RA?When should specialists be consulted in the treatment of viral arthritis?How is viral arthritis prevented?How is parvovirus B19-caused viral arthritis treated?How is HAV-caused viral arthritis treated?How is HBV-caused viral arthritis treated?How is HCV-caused viral arthritis treated?How is rubella-caused viral arthritis treated?How is alphavirus-caused viral arthritis treated?How is HIV-caused viral arthritis treated?Which specialist consultations are beneficial to patients with viral arthritis?What is the role of medications in the treatment of viral arthritis?Which medications in the drug class Antibiotics are used in the treatment of Viral Arthritis?Which medications in the drug class Antiviral agents are used in the treatment of Viral Arthritis?Which medications in the drug class Analgesics are used in the treatment of Viral Arthritis?Which medications in the drug class 5-Aminosalicylic Acid Derivatives are used in the treatment of Viral Arthritis?Which medications in the drug class Antineoplastic Agents are used in the treatment of Viral Arthritis?Which medications in the drug class Corticosteroids are used in the treatment of Viral Arthritis?Which medications in the drug class Immunomodulators are used in the treatment of Viral Arthritis?Which medications in the drug class Immunoglobulin agents are used in the treatment of Viral Arthritis?Which medications in the drug class Antimalarial agents are used in the treatment of Viral Arthritis?Which medications in the drug class Nonsteroidal Anti-inflammatory Drugs are used in the treatment of Viral Arthritis?

Author

Rabea Ahmed Khouqeer, MD, FRCPC, FAAAAI, Consultant, Department of Medicine, Division of Allergy and Clinical Immunology/Rheumatology, Saad Specialist Hospital, Saudi Arabia

Disclosure: Nothing to disclose.

Coauthor(s)

Martin Cohen, MD, FRCPC, Adjunct Professor, Department of Medicine, McGill University Health Center

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD, Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate Medical Center; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Disclosure: Nothing to disclose.

Acknowledgements

Elliot Goldberg, MD Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine

Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology

Disclosure: Nothing to disclose.

Kristine M Lohr, MD, MS Professor, Department of Internal Medicine, Center for the Advancement of Women's Health and Division of Rheumatology, Director, Rheumatology Training Program, University of Kentucky College of Medicine

Kristine M Lohr, MD, MS is a member of the following medical societies: American College of Physicians and American College of Rheumatology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Viral arthritis. Typical "slapped cheek" appearance. Courtesy of Brenda Moroz, MD, Montreal Children's Hospital.

Viral arthritis. "Slapped cheeks" with typical reticulated erythema of arms. Courtesy of Brenda Moroz, MD, Montreal Children's Hospital.

Viral arthritis. Typical "slapped cheek" appearance. Courtesy of Brenda Moroz, MD, Montreal Children's Hospital.

Viral arthritis. "Slapped cheeks" with typical reticulated erythema of arms. Courtesy of Brenda Moroz, MD, Montreal Children's Hospital.