The mainstay of treatment for tenosynovitis includes symptom alleviation, antibiotic therapy, and surgery. Mild tenosynovitis causing small scale swelling can be treated with non-steroidal anti-inflammatory drugs (NSAIDs) to reduce inflammation and as an analgesic. Resting the affected tendons is essential for recovery; a brace is often recommended. Physical or occupational therapy may also be beneficial in reducing symptoms.

Most infectious tenosynovitis cases should be managed with tendon sheath irrigation and drainage, with or without debridement of surrounding necrotic tissue, along with treatment with broad-spectrum antibiotics. In severe cases, amputation may even be necessary to prevent the further spread of infection. Following surgical intervention, antibiotic therapy is continued and adjusted based on the results of the fluid culture.

No specific cure is known. Treatment is largely supportive. Nonsteroidal anti-inflammatory drugs (NSAIDs) are indicated for tender lymph nodes and fever, and corticosteroids are useful in severe extranodal or generalized disease.

Symptomatic measures aimed at relieving the distressing local and systemic complaints have been described as the main line of management of KFD. Analgesics, antipyretics, NSAIDs, and corticosteroids have been used. If the clinical course is more severe, with multiple flares of bulky enlarged cervical lymph nodes and fever, then a low-dose corticosteroid treatment has been suggested.

Bisphosphonate therapy has been suggested as a first-line therapeutic option in many case reports and series.

Treatment with tumor necrosis factor alpha antagonists (TNF inhibitors) have been tried in few patients with limited success. Other drugs that are used in psoriatic arthritis, to which SAPHO syndrome is closely related, have also been used in this condition. They include NSAIDs, corticosteroids, sulfasalazine, methotrexate, ciclosporin and leflunomide.

Some patients have responded to antibiotics. The rationale for their use is that Propionibacterium acnes, a bacterium known for its role in acne, has been isolated from bone biopsies of SAPHO patients.

Treatment for infectious tenosynovitis is more effective the earlier the condition is identified and treated. Factors that worsen patient outcomes include being older than 43, having diabetes mellitus, and a polymicrobial infection.

Treatment consists of rest, non-weightbearing and painkillers when needed. A small study showed that the nonsteroidal anti-inflammatory drug ibuprofen could shorten the disease course (from 4.5 to 2 days) and provide pain control with minimal side effects (mainly gastrointestinal disturbances). If fever occurs or the symptoms persist, other diagnoses need to be considered.

Paracetamol (acetaminophen) and NSAIDs, such as ibuprofen, may be used to reduce fever and pain. Prednisone, a corticosteroid, while used to try to reduce throat pain or enlarged tonsils, remains controversial due to the lack of evidence that it is effective and the potential for side effects. Intravenous corticosteroids, usually hydrocortisone or dexamethasone, are not recommended for routine use but may be useful if there is a risk of airway obstruction, a very low platelet count, or hemolytic anemia.

There is little evidence to support the use of antivirals such as aciclovir and valacyclovir although they may reduce initial viral shedding. Although antivirals are not recommended for people with simple infectious mononucleosis, they may be useful (in conjunction with steroids) in the management of severe EBV manifestations, such as EBV meningitis, peripheral neuritis, hepatitis, or hematologic complications.

Although antibiotics exert no antiviral action they may be indicated to treat bacterial secondary infections of the throat, such as with streptococcus (strep throat). However, ampicillin and amoxicillin are not recommended during acute Epstein–Barr virus infection as a diffuse rash may develop.

Infectious mononucleosis is generally self-limiting, so only symptomatic or supportive treatments are used. The need for rest and return to usual activities after the acute phase of the infection may reasonably be based on the person's general energy levels. Nevertheless, in an effort to decrease the risk of splenic rupture experts advise avoidance of contact sports and other heavy physical activity, especially when involving increased abdominal pressure or the Valsalva maneuver (as in rowing or weight training), for at least the first 3–4 weeks of illness or until enlargement of the spleen has resolved, as determined by a treating physician.

Synovitis symptoms can be treated with anti-inflammatory drugs such as NSAIDs. An injection of steroids may be done, directly into the affected joint. Specific treatment depends on the underlying cause of the synovitis.

No treatment has been found to be routinely effective. NSAIDs and COX-2 inhibitors are not generally helpful other than for general pain relief. They do not seem to help reduce effusions or prevent their occurrence. Low-dose colchicine (and some other ‘anti-rheumatic’ therapies e.g. hydroxychloroquine) have been used with some success. (Use of methotrexate and intramuscular gold have not been reported in the literature). More aggressive treatments such as synovectomy, achieved using intra-articular agents (chemical or radioactive) can provide good results, with efficacy reported for at least 1 year.

Reducing acute joint swelling:

Arthrocentesis (or drainage of joint) may be useful to relieve joint swelling and improve range of motion. Local steroid injections can also reduce fluid accumulation short-term, but do not prevent onset of episodes. These treatments provide temporary relief only. Bed rest, ice packs splints and exercise are ineffective.

A single case report of a patient with treatment-refractory IH describes the use of anakinra, an interleukin 1 receptor antagonist. At the first sign of any attack, a single 100 mg dose was given. With this dosing at onset of attacks, each episode of effusion was successfully terminated.

Reducing frequency and severity of IH episodes:

Case reports indicate some success using long-term, low-dose colchicine (e.g. 0.5 mg to 1 mg daily). A recent single case report has shown hydroxychloroquine (300 mg daily) to be effective too.

Small-sized clinical trials have shown positive results with (1) chemical and (2) radioactive synovectomy. (1) Setti et al. treated 53 patients with rifampicin RV (600 mg intra-articular injections weekly for approximately 6 weeks) with good results at 1 year follow-up. (2) Top and Cross used single doses of intra-articular radioactive gold in 18 patients with persistent effusions of mixed causes including 3 with IH. All 3 patients with IH responded well to treatment at one-year follow-up.

Once PVNS is confirmed by biopsy of the synovium of an affected joint, a synovectomy of the affected area is the most common treatment. Bone lesions caused by the disorder are removed and bone grafting is performed as needed. Because diffuse PVNS has a relatively high rate of recurrence, radiation therapy may be considered as a treatment option. In some cases, a total joint replacement is needed to relieve symptoms when PVNS causes significant joint destruction.

Because any medication that could reduce the inflammation of CPPD bears a risk of causing organ damage, treatment is not advised if the condition is not causing pain.

For acute pseudogout, treatments include intra-articular corticosteroid injection, systemic corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), or, on occasion, high-dose colchicine. In general, NSAIDs are administered in low doses to help prevent CPPD. However, if an acute attack is already occurring, higher doses are administered. If nothing else works, hydroxychloroquine or methotrexate may provide relief.

Research into surgical removal of calcifications is underway, however this still remains an experimental procedure.

Disease-modifying antirheumatic drugs (DMARDs) are the primary treatment for RA. They are a diverse collection of drugs, grouped by use and convention. They have been found to improve symptoms, decrease joint damage, and improve overall functional abilities. DMARDs should be started early in the disease as they result in disease remission in approximately half of people and improved outcomes overall.

The following drugs are considered as DMARDs: methotrexate, hydroxychloroquine, sulfasalazine, leflunomide, TNF-alpha inhibitors (certolizumab, infliximab and etanercept), abatacept, and anakinra. Rituximab and tocilizumab are monoclonal antibodies and are also DMARDs.

The most commonly used agent is methotrexate with other frequently used agents including sulfasalazine and leflunomide. Sodium aurothiomalate (gold) and cyclosporin are less commonly used due to more common adverse effects. Agents may be used in combinations. Methotrexate is the most important and useful DMARD and is usually the first treatment. Adverse effects should be monitored regularly with toxicity including gastrointestinal, hematologic, pulmonary, and hepatic. Side effects such as nausea, vomiting or abdominal pain can be reduced by taking folic acid.

A 2015 Cochrane review found rituximab with methotrexate to be effective in improving symptoms compared to methotrexate alone. Rituximab works by depicting levels of B-cells (immune cell that is involved in inflammation). People taking rituximab had improved pain, function, reduced disease activity and reduced joint damage based on x-ray images. After 6 months, 21% more people had improvement in their symptoms using rituximab and methotrexate.

Biological agents should generally only be used if methotrexate and other conventional agents are not effective after a trial of three months. They are associated with a higher rate of serious infections as compared to other DMARDs. Biological DMARD agents used to treat rheumatoid arthritis include: tumor necrosis factor alpha (TNFα) blockers such as infliximab; interleukin 1 blockers such as anakinra, monoclonal antibodies against B cells such as rituximab, and tocilizumab T cell co-stimulation blocker such as abatacept. They are often used in combination with either methotrexate or leflunomide. Abatacept should not be used at the same time as other biologics. In those who are well controlled on TNF blockers decreasing the dose does not appear to affect overall function. Persons should be screened for latent tuberculosis before starting any TNF blockers therapy to avoid reactivation.

TNF blockers and methotrexate appear to have similar effectiveness when used alone and better results are obtained when used together. TNF blockers appear to have equivalent effectiveness with etanercept appearing to be the safest. Abatacept appears effective for RA with 20% more people improving with treatment than without but long term safety studies are yet unavailable. However, there is a lack of evidence to distinguish between the biologics available for RA. Issues with the biologics include their high cost and association with infections including tuberculosis.

Glucocorticoids can be used in the short term and at the lowest dose possible for flare-ups and while waiting for slow-onset drugs to take effect.

Non-NSAID drugs to relieve pain, like paracetamol may be used to help relieve the pain symptoms; they do not change the underlying disease.

NSAIDs reduce both pain and stiffness in those with RA but do not affect the underlying disease and appear to have no effect on people's long term disease course and thus are no longer first line agents. NSAIDs should be used with caution in those with gastrointestinal, cardiovascular, or kidney problems. Use of methotrexate together with NSAIDS is safe, if adequate monitoring is done. COX-2 inhibitors, such as celecoxib, and NSAIDs are equally effective.

RS3PE responds excellently to low dose corticosteroids, with sustained and often complete remission. Non-steroidal anti-inflammatory drugs (NSAIDs) have also been used. Hydroxychloroquine has proven effective in some cases.

When infection attacks the body, "anti-infective" drugs can suppress the infection. Several broad types of anti-infective drugs exist, depending on the type of organism targeted; they include antibacterial (antibiotic; including antitubercular), antiviral, antifungal and antiparasitic (including antiprotozoal and antihelminthic) agents. Depending on the severity and the type of infection, the antibiotic may be given by mouth or by injection, or may be applied topically. Severe infections of the brain are usually treated with intravenous antibiotics. Sometimes, multiple antibiotics are used in case there is resistance to one antibiotic. Antibiotics only work for bacteria and do not affect viruses. Antibiotics work by slowing down the multiplication of bacteria or killing the bacteria. The most common classes of antibiotics used in medicine include penicillin, cephalosporins, aminoglycosides, macrolides, quinolones and tetracyclines.

Not all infections require treatment, and for many self-limiting infections the treatment may cause more side-effects than benefits. Antimicrobial stewardship is the concept that healthcare providers should treat an infection with an antimicrobial that specifically works well for the target pathogen for the shortest amount of time and to only treat when there is a known or highly suspected pathogen that will respond to the medication.

Peri-ocular injection of corticosteroids (injection of corticosteroids very close but not into the eye). In resistant cases oral administration of corticosteroids, immunosuppressive drugs, and laser or cryotherapy of the involved area may be indicated.

Steroid implants have been explored as a treatment option for individuals with non-infectious uveitis. Research comparing fluocinolone acetonide intravitreal implants to standard-of-care treatments (prednisolone with immunosuppressive agents) found that while the steroid implant treatment possibly prevents the recurrence of uveitis, there may be adverse safety outcomes, such as the increased risk for needing cataract surgery and surgery to lower intraocular pressure.

Antibiotic ointment is typically applied to the newborn's eyes within 1 hour of birth as prevention against gonococcal ophthalmia. This maybe erythromycin, tetracycline, or silver nitrate.

Prophylaxis needs antenatal, natal, and post-natal care.

- Antenatal measures include thorough care of mother and treatment of genital infections when suspected.

- Natal measures are of utmost importance as mostly infection occurs during childbirth. Deliveries should be conducted under hygienic conditions taking all aseptic measures. The newborn baby's closed lids should be thoroughly cleansed and dried.

- If it is determined that the cause is due to a blocked tear duct, a gentle palpation between the eye and the nasal cavity may be used to clear the tear duct. If the tear duct is not cleared by the time the newborn is one year old, surgery may be required.

- Postnatal measures include:

- Chemical ophthalmia neonatorum is a self-limiting condition and does not require any treatment.

- Gonococcal ophthalmia neonatorum needs prompt treatment to prevent complications. Topical therapy should include

Systemic therapy: Newborns with gonococcal ophthalmia neonatorum should be treated for seven days with one of the following regimens ceftriaxone, cefotaxime, ciprofloxacin, crystalline benzyl penicillin

- Other bacterial ophthalmia neonatorum should be treated by broad spectrum antibiotics drops and ointment for two weeks.

- Neonatal inclusion conjunctivitis caused by Chlamydia trachomatis responds well to topical tetracycline 1% or erythromycin 0.5% eye ointment QID for three weeks. However systemic erythromycin should also be given since the presence of chlamydia agents in conjunctiva implies colonization of upper respiratory tract as well. Both parents should also be treated with systemic erythromycin.

- Herpes simplex conjunctivitis should be treated with intravenous acyclovir for a minimum of 14 days to prevent systemic infection.

Treatment can include topical steroids to diminish the inflammation. Antibiotics to diminish the proportion of aerobic bacteria is still a matter of debate. The use of local antibiotics, preferably local non-absorbed and broad spectrum, covering enteric gram-positive and gram-negative aerobes, can be an option. In some cases, systemic antibiotics can be helpful, such as amoxicillin/clavulanate or moxifloxacin. Vaginal rinsing with povidone iodine can provide relief of symptoms but does not provide long-term reduction of bacterial loads. Dequalinium chloride can also be an option for treatment.

Treatment of rheumatoid nodules is rarely a priority for people with rheumatoid arthritis. However, surgical removal is often successful, even if there is a tendency for nodules to regrow. Of the drug therapies commonly used in rheumatoid arthritis, methotrexate has the disadvantage of tending to make nodules worse. TNF inhibitors do not have a very reliable effect on nodules. B cell depletion with rituximab often leads to disappearance of nodules but this is not guaranteed.

People affected by the severest, often life-threatening, complications of cryoglobulinemic disease require urgent plasmapharesis and/or plasma exchange in order to rapidly reduce the circulating levels of their cryoglobulins. Complications commonly requiring this intervention include: hyperviscosity disease with severe symptoms of neurological (e.g. stroke, mental impairment, and myelitis) and/or cardiovascular (e.g., congestive heart failure, myocardial infarction) disturbances; vasculitis-driven intestinal ischemia, intestinal perforation, cholecystitis, or pancreatitis, causing acute abdominal pain, general malaise, fever, and/or bloody bowel movements; vasculitis-driven pulmonary disturbances (e.g. coughing up blood, acute respiratory failure, X-ray evidence of diffuse pulmonary infiltrates caused by diffuse alveolar hemorrhage); and severe kidney dysfunction due to intravascular deposition of immunoglobulins or vasculitis. Along with this urgent treatment, severely symptomatic patients are commonly started on therapy to treat any underlying disease; this treatment is often supplemented with anti-inflammatory drugs such as corticosteroids (e.g., dexamethasone) and/or immunosuppressive drugs. Cases where no underlying disease is known are also often treated with the latter corticosteroid and immunosuppressive medications.

Treatment of mixed cryoglobulinemic disease is, similar to type I disease, directed toward treating any underlying disorder. This includes malignant (particularly Waldenström's macroglobulinemia in type II disease), infectious, or autoimmune diseases in type II and III disease. Recently, evidence of hepatitis C infection has been reported in the majority of mixed disease cases with rates being 70-90% in areas with high incidences of hepatitis C. The most effective therapy for hepatitis C-associated cryoglobulinemic disease consists of a combination of anti-viral drugs, pegylated INFα and ribavirin; depletion of B cells using rituximab in combination with antiviral therapy or used alone in patients refractory to antiviral therapy has also proven successful in treating the hepatitis C-associated disease. Data on the treatment of infectious causes other than hepatitis C for the mixed disease are limited. A current recommendation treats the underlying disease with appropriate antiviral, anti-bacterial, or anti-fungal agents, if available; in cases refractory to an appropriate drug, the addition of immunosuppressive drugs to the therapeutic regimen may improve results. Mixed cryoglobulinemic disease associated with autoimmune disorders is treated with immunosuppressive drugs: combination of a corticosteroid with either cyclophosphamide, azathioprine, or mycophenolate or combination of a corticosteroid with rituximab have been used successfully to treated mixed disease associated with autoimmune disorders.

The cause of the infection determines the appropriate treatment. It may include oral or topical antibiotics and/or antifungal creams, antibacterial creams, or similar medications. A cream containing cortisone may also be used to relieve some of the irritation. If an allergic reaction is involved, an antihistamine may also be prescribed. For women who have irritation and inflammation caused by low levels of estrogen (postmenopausal), a topical estrogen cream might be prescribed.

The following are typical treatments for trichomoniasis, bacterial vaginosis, and yeast infections:

- Trichomoniasis: Single oral doses of either metronidazole, or tinidazole. "Sexual partner(s) should be treated simultaneously. Patients should be advised to avoid sexual intercourse for at least 1 week and until they and their partner(s) have completed treatment and follow-up."

- Bacterial vaginosis: The most commonly used antibiotics are metronidazole, available in both pill and gel form, and clindamycin available in both pill and cream form.

- Yeast infections: Local azole, in the form of ovula and cream. All agents appear to be equally effective. These anti-fungal medications, which are available in over the counter form, are generally used to treat yeast infections. Treatment may last anywhere between one, three, or seven days.

There is no standard treatment for PLC. Treatments may include ultraviolet phototherapy, topical steroids, sun exposure, oral antibiotics, corticosteroid creams and ointments to treat rash and itching.

One study identified the enzyme bromelain as an effective therapeutic option for PLC.

There is usually an indication for a specific identification of an infectious agent only when such identification can aid in the treatment or prevention of the disease, or to advance knowledge of the course of an illness prior to the development of effective therapeutic or preventative measures. For example, in the early 1980s, prior to the appearance of AZT for the treatment of AIDS, the course of the disease was closely followed by monitoring the composition of patient blood samples, even though the outcome would not offer the patient any further treatment options. In part, these studies on the appearance of HIV in specific communities permitted the advancement of hypotheses as to the route of transmission of the virus. By understanding how the disease was transmitted, resources could be targeted to the communities at greatest risk in campaigns aimed at reducing the number of new infections. The specific serological diagnostic identification, and later genotypic or molecular identification, of HIV also enabled the development of hypotheses as to the temporal and geographical origins of the virus, as well as a myriad of other hypothesis. The development of molecular diagnostic tools have enabled physicians and researchers to monitor the efficacy of treatment with anti-retroviral drugs. Molecular diagnostics are now commonly used to identify HIV in healthy people long before the onset of illness and have been used to demonstrate the existence of people who are genetically resistant to HIV infection. Thus, while there still is no cure for AIDS, there is great therapeutic and predictive benefit to identifying the virus and monitoring the virus levels within the blood of infected individuals, both for the patient and for the community at large.