Another form of endocarditis is healthcare-associated endocarditis when the infecting organism is believed to be transmitted in a health care setting like hospital, dialysis unit or a residential nursing home. Nosocomial endocarditis is a form of healthcare associated endocarditis in which the infective organism is acquired during stay in a hospital and it is usually secondary to presence of intravenous catheters, total parenteral nutrition lines, pacemakers, etc.

Finally, the distinction between "native-valve endocarditis" and "prosthetic-valve endocarditis" is clinically important. Prosthetic valve endocarditis can be early ( 1 year following valvular surgery).

- Early prosthetic valve endocarditis is usually due to intraoperative contamination or a postoperative bacterial contamination which is usually nosocomial in nature.

- Late prosthetic valve endocarditis is usually due to community acquired microorganisms.

Prosthetic valve endocarditis is commonly caused by "Staphylococcus epidermidis" as it is capable of growing as a biofilm on plastic surfaces.

Pericarditis may be caused by viral, bacterial, or fungal infection.

In the developed world viruses are believed to be the cause of about 85% of cases. In the developing world tuberculosis is a common cause but it is rare in the developed world.

Viral causes include coxsackievirus, herpesvirus, mumps virus, and HIV among others.

Pneumococcus or tuberculous pericarditis are the most common bacterial forms. Anaerobic bacteria can also be a rare cause. Fungal pericarditis is usually due to histoplasmosis, or in immunocompromised hosts Aspergillus, Candida, and Coccidioides. The most common cause of pericarditis worldwide is infectious pericarditis with tuberculosis.

About 30% of people with viral pericarditis or pericarditis of an unknown cause have one or several recurrent episodes.

There are several causes of acute pericarditis. In developed nations, the cause of most (80–90%) cases of acute pericarditis is unknown but a viral cause is suspected in the majority of such cases. The other 10–20% of acute pericarditis cases have various causes including connective tissue diseases (e.g., systemic lupus erythematosus), cancer, or involve an inflammatory reaction of the pericardium following trauma to the heart such as after a heart attack such as Dressler's syndrome. Familial mediterranean fever and TNF receptor associated periodic syndrome are rare inherited autoimmune diseases capable of causing recurring episodes of acute pericarditis.

When properly diagnosed, the mortality of Lemierre's syndrome is about 4.6%. Since this disease is not well known and often remains undiagnosed, mortality might be much higher.

Uremic pericarditis is a form of pericarditis. It causes fibrinous pericarditis. The main cause of the disease is poorly understood.

Uremic pericarditis is correlated to the degree of azotemia in the system. BUN is normally >60 mg/dL (normal is 7–20 mg/dL). The pathogenesis is poorly understood.

The cause of constrictive pericarditis in the developing world are idiopathic in origin, though likely infectious in nature. In regions where tuberculosis is common, it is the cause in a large portion of cases.

Causes of constrictive pericarditis include:

- Tuberculosis

- Incomplete drainage of purulent pericarditis

- Fungal and parasitic infections

- Chronic pericarditis

- Postviral pericarditis

- Postsurgical

- Following MI, post-myocardial infarction

- In association with pulmonary asbestos

Clinical presentation of diseases of pericardium may vary between:

- Acute and recurrent pericarditis

- Pericardial effusion without major hemodynamic compromise

- Cardiac tamponade

- Constrictive pericarditis

- Effusive-constrictive pericarditis

Tuberculous pericarditis is a form of pericarditis.

Pericarditis caused by tuberculosis is difficult to diagnose, because definitive diagnosis requires culturing "Mycobacterium tuberculosis" from aspirated pericardial fluid or pericardial , which requires high technical skill and is often not diagnostic (the yield from culture is low even with optimum specimens). The Tygerberg scoring system helps the clinician to decide whether pericarditis is due to tuberculosis or whether it is due to another cause: night sweats (1 point), weight loss (1 point), fever (2 point), serum globulin > 40g/l (3 points), blood total leucocyte count <10 x 10/l (3 points); a total score of 6 or more is highly suggestive of tuberculous pericarditis. Pericardial fluid with an interferon-γ level greater than 50/ml is highly specific for tuberculous pericarditis.

There are no randomized trials which evaluate the length of anti-tuberculosis treatment required for tuberculous pericarditis. There is a small but not conclusive benefit for treatment with a schedule of steroids with anti-tuberculosis drugs. Open surgical drainage of fluid though effective in preventing cardiac tamponade was associated with more deaths.

Lemierre's syndrome is currently rare, but was more common in the early 20th century before the discovery of penicillin. The reduced use of antibiotics for sore throats may have increased the risk of this disease, with 19 cases in 1997 and 34 cases in 1999 reported in the UK. The incidence rate is currently 0.8 cases per million in the general population, leading it to be termed the "forgotten disease". The disease is known to affect healthy young adults. The disease is becoming less rare with many cases being reported, however it is still known as "the forgotten disease" as many doctors are unaware of its existence, therefore often not even diagnosed which might considerably change the above-mentioned statistics. The mortality rate was 90% prior to antibiotic therapy, but is now generally quoted as 15% once this illness is correctly diagnosed and cured with proper medical treatment, although one series of cases reported mortality as low as 6.4%.

About 33 million people are affected by rheumatic heart disease with an additional 47 million having asymptomatic damage to their heart valves. As of 2010 globally it resulted in 345,000 deaths, down from 463,000 in 1990.

In Western countries, rheumatic fever has become fairly rare since the 1960s, probably due to the widespread use of antibiotics to treat streptococcus infections. While it has been far less common in the United States since the beginning of the 20th century, there have been a few outbreaks since the 1980s. Although the disease seldom occurs, it is serious and has a case-fatality rate of 2–5%.

Rheumatic fever primarily affects children between ages 5 and 17 years and occurs approximately 20 days after strep throat. In up to a third of cases, the underlying strep infection may not have caused any symptoms.

The rate of development of rheumatic fever in individuals with untreated strep infection is estimated to be 3%. The incidence of recurrence with a subsequent untreated infection is substantially greater (about 50%). The rate of development is far lower in individuals who have received antibiotic treatment. Persons who have suffered a case of rheumatic fever have a tendency to develop flare-ups with repeated strep infections.

The recurrence of rheumatic fever is relatively common in the absence of maintenance of low dose antibiotics, especially during the first three to five years after the first episode. Recurrent bouts of rheumatic fever can lead to valvular heart disease. Heart complications may be long-term and severe, particularly if valves are involved. In countries in Southeast-Asia, sub-saharan Africa, and Oceania, the percentage of people with rheumatic heart disease detected by listening to the heart was 2.9 per 1000 children and by echocardiography it was 12.9 per 1000 children.

The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart. This procedure has significant risk involved, with mortality rates of 6% or higher in major referral centers.

A poor outcome is almost always the result after a pericardiectomy is performed for constrictive pericarditis whose origin was radiation-induced, further some patients may develop heart failure post-operatively.

The pleural space can be invaded by fluid, air, and particles from different parts of the body which fairly complicates the diagnosis. Viral infection (coxsackie B virus, HRSV, CMV, adenovirus, EBV, parainfluenza, influenza) is the most common cause of pleurisy. However, many other different conditions can cause pleuritic chest pain:

- Aortic dissections

- Autoimmune disorders such as systemic lupus erythematosus (or drug-induced lupus erythematosus), Autoimmune hepatitis (AIH), rheumatoid arthritis and Behçet's disease.

- Bacterial infections associated with pneumonia and tuberculosis

- Chest injuries (blunt or penetrating)

- Familial Mediterranean fever, an inherited condition that often causes fever and swelling in the abdomen or the lungs

- Fungal or parasitic infections

- Heart surgery, especially coronary-artery bypass grafting

- Cardiac problems (ischemia, pericarditis)

- Inflammatory bowel disease

- Lung cancer and lymphoma

- Other lung diseases like cystic fibrosis, sarcoidosis, asbestosis, lymphangioleiomyomatosis, and mesothelioma

- Pneumothorax

- Pulmonary embolisms, which are blood clots that enter the lungs

When the space between the pleurae starts to fill with fluid, as in pleural effusion, the chest pain can be eased but a shortness of breath can result, since the lungs need room to expand during breathing. Some cases of pleuritic chest pain are idiopathic, which means that the exact cause cannot be determined.

Myopericarditis is a combination of both myocarditis and pericarditis appearing in a single individual, namely inflammation of both the pericardium and the heart muscle. It can involve the presence of fluid in the heart. Myopericarditis refers primarily to a pericarditis with lesser myocarditis, as opposed to a perimyocarditis, though the two terms are often used interchangeably. Both will be reflected on an ECG. Myo-pericarditis usually involves inflammation of the pericardium, or the sac covering the heart.

The ACAM2000 smallpox vaccine has been known to cause myopericarditis in some people.

Libman–Sacks endocarditis (often misspelled Libmann–Sachs) is a form of nonbacterial endocarditis that is seen in association with systemic lupus erythematosus. It is one of the most common heart-related manifestations of lupus (the most common being pericarditis - inflammation of the fibrous sac surrounding the heart).

It was first described by Emanuel Libman and Benjamin Sacks at Mount Sinai Hospital in New York City in 1924. The association between Libman–Sacks endocarditis and antiphospholipid syndrome was first noted in 1985.

A large number of causes of myocarditis have been identified, but often a cause cannot be found. In Europe and North America, viruses are common culprits. Worldwide, however, the most common cause is Chagas' disease, an illness endemic to Central and South America that is due to infection by the protozoan "Trypanosoma cruzi". Many of the causes listed below, particularly those involving protozoa, fungi, parasites, allergy, autoimmune disorders, and drugs are also causes of eosinophilic myocarditis.

It is not practical to test or decontaminate most sites that may be contaminated with "H. capsulatum", but the following sources list environments where histoplasmosis is common, and precautions to reduce a person's risk of exposure, in the three parts of the world where the disease is prevalent. Precautions common to all geographical locations would be to avoid accumulations of bird or bat droppings.

The US National Institute for Occupational Safety and Health (NIOSH) provides information on work practices and personal protective equipment that may reduce the risk of infection. This document is available in English and Spanish.

Authors at the University of Nigeria have published a review which includes information on locations in which histoplasmosis has been found in Africa (in chicken runs, bats and the caves bats infest, and in soil), and a thorough reference list including English, French, and Spanish language references.

The exact incidence of myocarditis is unknown. However, in series of routine autopsies, 1–9% of all patients had evidence of myocardial inflammation. In young adults, up to 20% of all cases of sudden death are due to myocarditis.

Among patients with HIV, myocarditis is the most common cardiac pathological finding at autopsy, with a prevalence of 50% or more.

The pathology is the same as nonbacterial thrombotic endocarditis except focal necrosis with hematoxylin bodies can be found only in Libman–Sacks endocarditis.

Prognosis depends on the pathogen responsible for the infection and risk group. Overall mortality for "Candida" meningitis is 10-20%, 31% for patients with HIV, and 11% in neurosurgical cases (when treated). Prognosis for "Aspergillus" and coccidioidal infections is poor.

These are the typical mechanisms of autoimmunity. Autoantibodies or auto-toxic T-lymphocyte mediated tissue destruction. The process is aided by neutrophils, the complement system, tumor necrosis factor alpha, etc.

Aetiologically, these are most commonly seen in children with a history of sore throat caused by a streptococcal infection. This is similar to the post-streptococcal glomerulonephritis. Here, the anti-bacterial antibodies cross react with the heart antigens causing inflammation.

Inflammatory damage leads to the following:

- Pericarditis: Here the pericardium gets inflamed. Acutely, it can cause pericardial effusion leading to cardiac tamponade and death. After healing, there may be fibrosis and adhesion of the pericardium with the heart leading to constriction of the heart and reduced cardiac function.

- Myocarditis: Here the muscle bulk of the heart gets inflamed. Inflamed muscles have reduced functional capacity. This may be fatal, if left untreated as is in a case of pancarditis. On healing, there will be fibrosis and reduced functional capacity.

- Endocarditis: Here the inner lining of the heart is inflamed, including the heart valves. This may cause a valve prolapse, adhesion of the adjacent cusps of these valves and occlusion of the flow tracts of blood through the heart causing diseases called valve stenosis.

Some strains of group A streptococci (GAS) cause severe infection. Severe infections are usually invasive, meaning that the bacteria has entered parts of the body where bacteria are not usually found, such as the blood, lungs, deep muscle or fat tissue. Those at greatest risk include children with chickenpox; persons with suppressed immune systems; burn victims; elderly persons with cellulitis, diabetes, vascular disease, or cancer; and persons taking steroid treatments or chemotherapy. Intravenous drug users also are at high risk. GAS is an important cause of puerperal fever worldwide, causing serious infection and, if not promptly diagnosed and treated, death in newly delivered mothers. Severe GAS disease may also occur in healthy persons with no known risk factors.

All severe GAS infections may lead to shock, multisystem organ failure, and death. Early recognition and treatment are critical. Diagnostic tests include blood counts and urinalysis as well as cultures of blood or fluid from a wound site.

Severe Group A streptococcal infections often occur sporadically but can be spread by person-to-person contact.

Public Health policies internationally reflect differing views of how the close contacts of people affected by severe Group A streptococcal infections should be treated. Health Canada and the US CDC recommend close contacts see their doctor for full evaluation and may require antibiotics; current UK Health Protection Agency guidance is that, for a number of reasons, close contacts should not receive antibiotics unless they are symptomatic but that they should receive information and advice to seek immediate medical attention if they develop symptoms. However, guidance is clearer in the case of mother-baby pairs: both mother and baby should be treated if either develops an invasive GAS infection within the first 28 days following birth (though some evidence suggests that this guidance is not routinely followed in the UK).

Intensive cardiac care and immunosuppressives including corticosteroids are helpful in the acute stage of the disease. Chronic phase has, mainly debility control and supportive care options.