The standard treatment is with a minimum of four weeks of high-dose intravenous penicillin with an aminoglycoside such as gentamicin.

The use of high-dose antibiotics is largely based upon animal models.

Leo Loewe of Brooklyn Jewish Hospital was the first to successfully treat subacute bacterial endocarditis with penicillin. Loewe reported at the time seven cases of subacute bacterial endocarditis in 1944.

Prophylaxis and treatment with an anti-inflammatory agent may stop progression of the reaction. Oral aspirin or ibuprofen every four hours for a day or 60 mg of prednisone orally or intravenously has been used as an adjunctive treatment . However, steroids are generally of no benefit. Patients must be closely monitored for the potential complications (collapse and shock) and may require IV fluids to maintain adequate blood pressure. If available, meptazinol, an opioid analgesic of the mixed agonist/antagonist type, should be administered to reduce the severity of the reaction. Anti TNF-a may also be effective.

The first line treatment for polymyositis is corticosteroids. Specialized exercise therapy may supplement treatment to enhance quality of life.

Treatment usually involves high doses of steroids such as dexamethasone. While high doses of steroids may risk laminitis, low doses are associated with refractory cases. Antibiotics are used to treat any residual nidus of "S. equi". Non-steroidal anti-inflammatory drugs (NSAIDs), such as phenylbutazone or flunixin, may be useful to reduce fever and relieve pain. Intravenous DMSO is sometimes used as a free-radical scavenger and anti-inflammatory. Additionally, wrapping the legs may reduce edema and skin sloughing. Supportive care with oral or IV fluids may also be required.

Recovery from an anaerobic infection depends on adequate and rapid management. The main principles of managing anaerobic infections are neutralizing the toxins produced by anaerobic bacteria, preventing the local proliferation of these organisms by altering the environment and preventing their dissemination and spread to healthy tissues.

Toxin can be neutralized by specific antitoxins, mainly in infections caused by Clostridia (tetanus and botulism). Controlling the environment can be attained by draining the pus, surgical debriding of necrotic tissue, improving blood circulation, alleviating any obstruction and by improving tissue oxygenation. Therapy with hyperbaric oxygen (HBO) may also be useful. The main goal of antimicrobials is in restricting the local and systemic spread of the microorganisms.

The available parenteral antimicrobials for most infections are metronidazole, clindamycin, chloramphenicol, cefoxitin, a penicillin (i.e. ticarcillin, ampicillin, piperacillin) and a beta-lactamase inhibitor (i.e. clavulanic acid, sulbactam, tazobactam), and a carbapenem (imipenem, meropenem, doripenem, ertapenem). An antimicrobial effective against Gram-negative enteric bacilli (i.e. aminoglycoside) or an anti-pseudomonal cephalosporin (i.e. cefepime ) are generally added to metronidazole, and occasionally cefoxitin when treating intra-abdominal infections to provide coverage for these organisms. Clindamycin should not be used as a single agent as empiric therapy for abdominal infections. Penicillin can be added to metronidazole in treating of intracranial, pulmonary and dental infections to provide coverage against microaerophilic streptococci, and Actinomyces.

Oral agents adequate for polymicrobial oral infections include the combinations of amoxicillin plus clavulanate, clindamycin and metronidazole plus a macrolide. Penicillin can be added to metronidazole in the treating dental and intracranial infections to cover "Actinomyces" spp., microaerophilic streptococci, and "Arachnia" spp. A macrolide can be added to metronidazole in treating upper respiratory infections to cover "S. aureus" and aerobic streptococci. Penicillin can be added to clindamycin to supplement its coverage against "Peptostreptococcus" spp. and other Gram-positive anaerobic organisms.

Doxycycline is added to most regimens in the treatment of pelvic infections to cover chlamydia and mycoplasma. Penicillin is effective for bacteremia caused by non-beta lactamase producing bacteria. However, other agents should be used for the therapy of bacteremia caused by beta-lactamase producing bacteria.

Because the length of therapy for anaerobic infections is generally longer than for infections due to aerobic and facultative anaerobic bacteria, oral therapy is often substituted for parenteral treatment. The agents available for oral therapy are limited and include amoxacillin plus clavulanate, clindamycin, chloramphenicol and metronidazole.

In 2010 the American Surgical Society and American Society of Infectious Diseases have updated their guidelines for the treatment of abdominal infections.

The recommendations suggest the following:

For mild-to-moderate community-acquired infections in adults, the agents recommended for empiric regimens are: ticarcillin- clavulanate, cefoxitin, ertapenem, moxifloxacin, or tigecycline as single-agent therapy or combinations of metronidazole with cefazolin, cefuroxime, ceftriaxone, cefotaxime, levofloxacin, or ciprofloxacin. Agents no longer recommended are: cefotetan and clindamycin ( Bacteroides fragilis group resistance) and ampicillin-sulbactam (E. coli resistance) and ainoglycosides (toxicity).

For high risk community-acquired infections in adults, the agents recommended for empiric regimens are: meropenem, imipenem-cilastatin, doripenem, piperacillin-tazobactam, ciprofloxacin or levofloxacin in combination with metronidazole, or ceftazidime or cefepime in combination with metronidazole. Quinolones should not be used unless hospital surveys indicate >90% susceptibility of "E. coli" to quinolones.

Aztreonam plus metronidazole is an alternative, but addition of an agent effective against gram-positive cocci is recommended. The routine use of an aminoglycoside or another second agent effective against gram-negative facultative and aerobic bacilli is not recommended in the absence of evidence that the infection is caused by resistant organisms that require such therapy.

Empiric use of agents effective against enterococci is recommended and agents effective against methicillin-resistant "S. aureus" (MRSA) or yeast is not recommended in the absence of evidence of infection due to such organisms.

Empiric antibiotic therapy for health care-associated intra-abdominal should be driven by local microbiologic results. Empiric coverage of likely pathogens may require multidrug regimens that include agents with expanded spectra of activity against gram-negative aerobic and facultative bacilli. These include meropenem, imipenem-cilastatin, doripenem, piperacillin-tazobactam, or ceftazidime or cefepime in combination with metronidazole. Aminoglycosides or colistin may be required.

Antimicrobial regimens for children include an aminoglycoside-based regimen, a carbapenem (imipenem, meropenem, or ertapenem), a beta-lactam/beta-lactamase-inhibitor combination (piperacillin-tazobactam or ticarcillin-clavulanate), or an advanced-generation cephalosporin (cefotaxime, ceftriaxone, ceftazidime, or cefepime) with metronidazole.

Clinical judgment, personal experience, safety and patient compliance should direct the physician in the choice of the appropriate antimicrobial agents. The length of therapy generally ranges between 2 and 4 weeks, but should be individualized depending on the response. In some instances treatment may be required for as long as 6–8 weeks, but can often be shortened with proper surgical drainage.

Once a diagnosis of JDMS is made, the treatment is often a 3-day course of Intravenous ("pulse") steroids (methylprednisolone, Solu-Medrol), followed by a high dose of oral prednisone (usually 1–2 mg/kg of body weight) for several weeks. This action usually brings the disease under control, lowering most lab tests to or near normal values. Some minor improvement in muscle symptoms may also be seen in this time, but normally it takes a long time for full muscle strength to be regained.

Once the disease process is under control, oral steroids are tapered gradually to minimize their side effects. Often, steroid-sparing drugs, such as methotrexate (a chemotherapy drug) or other DMARDs, are given to compensate for the reduction in oral steroids. Once the oral steroids are reduced to a less toxic level, the sparing agents can also be gradually withdrawn. Lab results are closely monitored during the tapering process to ensure that the disease does not recur.

In the cases where steroids or second-line drugs are not tolerated or are ineffective, there are other treatments that can be tried. These include other chemotherapy drugs, such as ciclosporin, infliximab, or other DMARDs. Another is intravenous immunoglobulin (IVIg), a blood product that has been shown to be very effective against JDMS.

To treat the skin rash, anti-malarial drugs, such as hydroxychloroquine (Plaquenil) are usually given. Topical steroid creams (hydrocortisone) may help some patients, and anti-inflammatory creams (such as tacrolimus) are proving to be very effective. Dry skin caused by the rash can be combated by regular application of sunscreen or any moisturizing cream. Most JDM patients are very sensitive to sun exposure, and sunburn may be a disease activity trigger in some, so daily application of high-SPF sunscreen is often recommended.

Polymyositis and dermatomyositis are first treated with high doses of a corticosteroids

Prognosis is good with early, aggressive treatment (92% survival in one study).

There is no cure for dermatomyositis, but the symptoms can be treated. Options include medication, physical therapy, exercise, heat therapy (including microwave and ultrasound), orthotics and assistive devices, and rest. The standard treatment for dermatomyositis is a corticosteroid drug, given either in pill form or intravenously. Immunosuppressant drugs, such as azathioprine and methotrexate, may reduce inflammation in people who do not respond well to prednisone. Periodic treatment using intravenous immunoglobulin can also improve recovery. Other immunosuppressive agents used to treat the inflammation associated with dermatomyositis include cyclosporine A, cyclophosphamide, and tacrolimus. Physical therapy is usually recommended to prevent muscle atrophy and to regain muscle strength and range of motion. Many individuals with dermatomyositis may need a topical ointment, such as topical corticosteroids, for their skin disorder. They should wear a high-protection sunscreen and protective clothing. Surgery may be required to remove calcium deposits that cause nerve pain and recurrent infections.

Antimalarial medications, especially hydroxychloroquine and chloroquine, are used to treat the rashes, as they are in similar conditions.

Rituximab is used when people don't respond to other treatments.

As of 2016, treatments for amyopathic dermatomyositis in adults did not have a strong evidence base; published treatments included antimalarial medications, steroids, taken or orally or applied to the skin, calcineurin inhibitors applied to the skin, dapsone, Intravenous immunoglobulin (IVIG), methotrexate, azathioprine, and mycophenolate mofetil. None appear to be very effective but among them, IVIG has had the best outcomes.

Treatment is directed toward the underlying cause. However, in primary eosinophilia, or if the eosinophil count must be lowered, corticosteroids such as prednisone may be used. However, immune suppression, the mechanism of action of corticosteroids, can be fatal in patients with parasitosis.

In severe cases of PM and DM with systemic signs, an initial three to five days on intravenous corticosteroid (methylprednisolone) may be used; but normally treatment begins with a single daily (after breakfast) high dose of oral corticosteroid (prednisone). After a month or so the strength of every second day's dose is very gradually reduced over three to four months, to minimize the negative effects of the prednisone. When a high dose of prednisone cannot be reduced without losing muscle strength, or when prednisone is effective but it is producing significant complications, "steroid sparing" oral immunosuppressants such as azathioprine, mycophenolate mofetil, methotrexate and cyclosporine, may be used in combination with reduced prednisone. Some of these steroid sparing drugs can take several months to demonstrate an effect.

To minimize side effects, patients on corticosteroids should follow a strict high-protein, low-carbohydrate, low-salt diet; and with long-term corticosteroid use a daily calcium supplement and weekly vitamin D supplement (and a weekly dose of Fosamax for postmenopausal women) should be considered.

For patients not responding to this approach there is weak evidence supporting the use of intravenous immunoglobulin, ciclosporin, tacrolimus, mycophenolate mofetil and other agents; and trials of rituximab have indicated a potential therapeutic effect.

Fulminant infection from meningococci bacteria in the bloodstream is a medical emergency and requires emergent treatment with adequate antibiotics. Benzylpenicillin was once the drug of choice with chloramphenicol as a good alternative in allergic patients. Ceftriaxone is an antibiotic commonly employed today. Hydrocortisone can sometimes reverse the adrenal insufficiency. Plastic surgery and tissue grafting are sometimes needed to treat tissue necrosis resulting from the infection.

Antibiotics are the treatment of choice for bacterial pneumonia, with ventilation (oxygen supplement) as supportive therapy. The antibiotic choice depends on the nature of the pneumonia, the microorganisms most commonly causing pneumonia in the geographical region, and the immune status and underlying health of the individual. In the United Kingdom, amoxicillin is used as first-line therapy in the vast majority of patients acquiring pneumonia in the community, sometimes with added clarithromycin. In North America, where the "atypical" forms of community-acquired pneumonia are becoming more common, clarithromycin, azithromycin, or fluoroquinolones as single therapy have displaced the amoxicillin as first-line therapy.

Local patterns of antibiotic-resistance always need to be considered when initiating pharmacotherapy. In hospitalized individuals or those with immune deficiencies, local guidelines determine the selection of antibiotics.

In cases of viral adenoiditis, treatment with analgesics or antipyretics is often sufficient. Bacterial adenoiditis may be treated with antibiotics, such as amoxicillin - clavulanic acid or a cephalosporin. In case of adenoid hypertrophy, adenoidectomy may be performed to remove the adenoid.

"Streptococcus pneumoniae" — amoxicillin (or erythromycin in patients allergic to penicillin); cefuroxime and erythromycin in severe cases.

"Staphylococcus aureus" — flucloxacillin (to counteract the organism's β-lactamase).

Despite its very similar clinical presentation to PM, IBM does not respond to the drugs that effectively treat PM, and there is no proven effective therapy for IBM. Alemtuzumab is being studied but as of May 2013 it had not demonstrated clinical effectiveness in IBM. Dysphagia (difficulty swallowing) may be improved by intravenous immunoglobulin, though more trials are needed. Non-fatiguing, systematic strength-building exercise has demonstrated benefit. Occupational and rehabilitation therapists can offer good advice on walking without falling and performing fine motor tasks, and can provide appropriate canes, braces and wheelchairs. Speech pathologists can provide advice on preventing choking episodes and reducing the anxiety of an immanent aspiration for both patients and carers.

Antibiotic therapy has to overcome the blood/prostate barrier that prevents many antibiotics from reaching levels that are higher than minimum inhibitory concentration. A blood-prostate barrier restricts cell and molecular movement across the rat ventral prostate epithelium. Treatment requires prolonged courses (4–8 weeks) of antibiotics that penetrate the prostate well. The fluoroquinolones, tetracyclines and macrolides have the best penetration. There have been contradictory findings regarding the penetrability of nitrofurantoin , quinolones (ciprofloxacin, levofloxacin), sulfas (Bactrim, Septra), doxycycline and macrolides (erythromycin, clarithromycin). This is particularly true for gram-positive infections.

In a review of multiple studies, Levofloxacin (Levaquin) was found to reach prostatic fluid concentrations 5.5 times higher than Ciprofloxacin, indicating a greater ability to penetrate the prostate.

Persistent infections may be helped in 80% of patients by the use of alpha blockers (tamsulosin (Flomax), alfuzosin), or long term low dose antibiotic therapy. Recurrent infections may be caused by inefficient urination (benign prostatic hypertrophy, neurogenic bladder), prostatic stones or a structural abnormality that acts as a reservoir for infection.

In theory, the ability of some strains of bacteria to form biofilms might be one factor amongst others to facilitate development of chronic bacterial prostatitis.

Escherichia coli extract and cranberry have a potentially preventive effect on the development of chronic bacterial prostatitis, while combining antibiotics with saw palmetto, lactobacillus sporogens and arbutin may lead to better treatment outcomes.

Bacteriophages hold promise as another potential treatment for chronic bacterial prostatatis.

The addition of prostate massage to courses of antibiotics was previously proposed as being beneficial and prostate massage may mechanically break up the biofilm and enhance the drainage of the prostate gland. However, in more recent trials, this was not shown to improve outcome compared to antibiotics alone.

The addition of a prokinetic drug to an antibiotic regime reduces the incidence of spontaneous bacterial peritonitis possibly via decreasing small intestinal bacterial overgrowth.

For the allergic type, cool water poured over the face with the head inclined downward constricts capillaries, and artificial tears sometimes relieve discomfort in mild cases. In more severe cases, nonsteroidal anti-inflammatory medications and antihistamines may be prescribed. Persistent allergic conjunctivitis may also require topical steroid drops.

Viral conjunctivitis usually resolves on its own and does not require any specific treatment. Antihistamines (e.g., diphenhydramine) or mast cell stabilizers (e.g., cromolyn) may be used to help with the symptoms. Povidone iodine has been suggested as a treatment, but as of 2008 evidence to support it was poor.

Cefotaxim s DOC. After confirmation of SBP, patients need hospital admission for intravenous antibiotics. They will often also receive intravenous albumin. A repeat paracentesis in 48 hours is sometimes performed to ensure control of infection. Once patients have recovered from SBP, they require regular prophylactic antibiotics as long as they still have ascites.

Corticosteroids remain the main treatment modality for IOI. There is usually a dramatic response to this treatment and is often viewed as pathognomonic for this disease. Although response is usually quick, many agree that corticosteroids should be continued on a tapering basis to avoid breakthrough inflammation.

Although many respond to corticosteroid treatment alone, there are several cases in which adjuvant therapy is needed. While many alternatives are available, there is no particular well-established protocol to guide adjuvant therapy. Among the available options there is: surgery, alternative corticosteroid delivery, radiation therapy, non-steroidal anti-inflammatory drugs, cytotoxic agents (chlorambucil, cyclophosphamide), corticosteroid sparing immunosuppressants (methotrexate, cyclosporine, azathioprine), IV immune-globin, plasmapheresis, and biologic treatments (such as TNF-α inhibitors).

Over time, the relapse rate is high, exceeding 50%. However, recent research indicates that combination therapies offer a better prognosis than antibiotics alone.

A 2007 study showed that repeated combination pharmacological therapy with antibacterial agents (ciprofloxacin/azithromycin), alpha-blockers (alfuzosin) and Serenoa repens extracts may eradicate infection in 83.9% of patients with clinical remission extending throughout a follow-up period of 30 months for 94% of these patients.

A 2014 study of 210 patients randomized into two treatment groups found that recurrence occurred within 2 months in 27.6% of the group using antibiotics alone (prulifloxacin 600 mg), but in only 7.8% of the group taking prulifloxacin in combination with Serenoa repens extract, Lactobacillus Sporogens and Arbutin.

Of the children diagnosed with and treated for JDM, about half will recover completely. Close to 30 percent will have weakness after the disease resolves. Most children will go into remission and have their medications eliminated within two years, while others may take longer to respond or have more severe symptoms that take longer to clear up.

A common lasting effect of JDM is childhood arthritis.

It is usually caused by a form of streptococci viridans bacteria that normally live in the mouth ("Streptococcus mutans, mitis, sanguis "or "milleri").

Other strains of streptococci can also cause subacute endocarditis, streptococcus intermedius:

acute and subacute infection ( can causes about 15% of cases pertaining to infective endocarditis). Additional enterococci (urinary tract infections) and coagulase negative staphylococci can also be causative agents.