The signs and symptoms associated with myocarditis are varied, and relate either to the actual inflammation of the myocardium or to the weakness of the heart muscle that is secondary to the inflammation. Signs and symptoms of myocarditis include the following:

- Chest pain (often described as "stabbing" in character)

- Congestive heart failure (leading to swelling, shortness of breath and liver congestion)

- Palpitations (due to abnormal heart rhythms)

- Sudden death (in young adults, myocarditis causes up to 20% of all cases of sudden death)

- Fever (especially when infectious, e.g. in rheumatic fever)

- Symptoms in young children tend to be more nonspecific, with generalized malaise, poor appetite, abdominal pain, and chronic cough. Later stages of the illness will present with respiratory symptoms with increased work of breathing, and is often mistaken for asthma.

Since myocarditis is often due to a viral illness, many patients give a history of symptoms consistent with a recent viral infection, including fever, rash, diarrhea, joint pains, and easily becoming tired.

Myocarditis is often associated with pericarditis, and many people with myocarditis present with signs and symptoms that suggest myocarditis and pericarditis at the same time.

Acute toxoplasmosis is often asymptomatic in healthy adults. However, symptoms may manifest and are often influenza-like: swollen lymph nodes, headaches, fever, and fatigue, or muscle aches and pains that last for a month or more. Rarely will a human with a fully functioning immune system develop severe symptoms following infection. People with weakened immune systems are likely to experience headache, confusion, poor coordination, seizures, lung problems that may resemble tuberculosis or Pneumocystis jiroveci pneumonia (a common opportunistic infection that occurs in people with AIDS), or blurred vision caused by severe inflammation of the retina (ocular toxoplasmosis) Young children and immunocompromised people, such as those with HIV/AIDS, those taking certain types of chemotherapy, or those who have recently received an organ transplant, may develop severe toxoplasmosis. This can cause damage to the brain (encephalitis) or the eyes (necrotizing retinochoroiditis). Infants infected via placental transmission may be born with either of these problems, or with nasal malformations, although these complications are rare in newborns. The toxoplasmic trophozoites causing acute toxoplasmosis are referred to as tachyzoites, and are typically found in bodily fluids.

Swollen lymph nodes are commonly found in the neck or under the chin, followed by the armpits and the groin. Swelling may occur at different times after the initial infection, persist, and recur for various times independently of antiparasitic treatment. It is usually found at single sites in adults, but in children, multiple sites may be more common. Enlarged lymph nodes will resolve within one to two months in 60% of cases. However, a quarter of those affected take two to four months to return to normal, and 8% take four to six months. A substantial number (6%) do not return to normal until much later.

Myocarditis, also known as inflammatory cardiomyopathy, is inflammation of the heart muscle. Symptoms can include shortness of breath, chest pain, decreased ability to exercise, and an irregular heartbeat. The duration of problems can vary from hours to months. Complications may include heart failure due to dilated cardiomyopathy or cardiac arrest.

Myocarditis is most often due to a viral infection. Other causes include bacterial infections, certain medications, toxins, and autoimmune disorders. A diagnosis may be supported by an electrocardiogram (ECG), increased troponin, heart MRI, and occasionally a heart biopsy. An ultrasound of the heart is important to rule out other potential causes such as heart valve problems.

Treatment depends on both the severity and the cause. Medications such as ACE inhibitors, beta blockers, and diuretics are often used. A period of no exercise is typically recommended during recovery. Corticosteroids or intravenous immunoglobulin (IVIG) may be useful in certain cases. In severe cases an implantable cardiac defibrillator or heart transplant may be recommended.

In 2013, about 1.5 million cases of acute myocarditis occurred. While people of all ages are affected, the young are most often affected. It is slightly more common in males than females. Most cases are mild. In 2015 cardiomyopathy, including myocarditis, resulted in 354,000 deaths up from 294,000 in 1990. The initial descriptions of the condition are from the mid-1800s.

Symptoms in eosinophilc myocarditis are highly variable. They tend to reflect the many underlying disorders causing eosinophil dysfunction as well as the widely differing progression rates of cardiac damage. Before cardiac symptoms are detected, some 66% of cases have symptoms of a common cold and 33% have symptoms of asthma, rhinitis, urticarial, or other allergic disorder. Cardiac manifestations of eosinophilic myocarditis range from none to life-threatening conditions such as cardiogenic shock or sudden death due to abnormal heart rhythms. More commonly the presenting cardiac symptoms of the disorder are the same as those seen in other forms of heart disease: chest pain, shortness of breath, fatigue, chest palpitations, light headedness, and syncope. In its most extreme form, however, eosinophilic myocarditis can present as acute necrotizing eosinophilic myocarditis, i.e. with symptoms of chaotic and potentially lethal heart failure and heart arrhythmias. This rarest form of the disorder reflects a rapidly progressive and extensive eosinophilic infiltration of the heart that is accompanied by massive myocardial cell necrosis.

Hypereosinophilia (i.e. blood eosinophil counts at or above 1,500 per microliter) or, less commonly, eosinophilia (counts above 500 but below 1,500 per microliter) are found in the vast majority of cases of eosinophilic myocarditis and are valuable clues that point to this rather than other types of myocarditis or myocardial injuries. However, elevated blood eosinophil counts may not occur during the early phase of the disorder. Other, less specific laboratory findings implicate a cardiac disorder but not necessarily eosinophilic myocarditis. These include elevations in blood markers for systemic inflammation (e.g. C reactive protein, erythrocyte sedimentation rate), elevations in blood markers for cardiac injury (e.g. creatine kinase, troponins); and abnormal electrocardiograms ( mostly ST segment-T wave abnormalities).

Toxoplasmosis is a parasitic disease caused by "Toxoplasma gondii". Infections with toxoplasmosis usually cause no obvious symptoms in adults. Occasionally there may be a few weeks or months of mild flu-like illness such as muscle aches and tender lymph nodes. In a small number of people, eye problems may develop. In those with a weak immune system, severe symptoms such as seizures and poor coordination may occur. If infected during pregnancy, a condition known as congenital toxoplasmosis may affect the child.

Toxoplasmosis is usually spread by eating poorly cooked food that contains cysts, exposure to infected cat feces, and from a mother to a child during pregnancy if the mother becomes infected. Rarely the disease may be spread by blood transfusion. It is not otherwise spread between people. The parasite is only known to reproduce sexually in the cat family. However, it can infect most types of warm-blooded animals, including humans. Diagnosis is typically by testing blood for antibodies or by testing amniotic fluid for the parasite's DNA.

Prevention is by properly preparing and cooking food. It is also recommended that pregnant women do not clean cat litter boxes. Treatment of otherwise healthy people is usually not needed. During pregnancy spiramycin or pyrimethamine/sulfadiazine and folinic acid may be used for treatment.

Up to half of the world's population is infected by toxoplasmosis but have no symptoms. In the United States about 23% are affected and in some areas of the world this is up to 95%. About 200,000 cases of congenital toxoplasmosis occur a year. Charles Nicolle and Louis Manceaux first described the organism in 1908. In 1941 transmission during pregnancy from a mother to a child was confirmed.

Carditis is the inflammation of the heart or its surroundings. The plural of carditis is carditides.

It is usually studied and treated by specifying it as:

- Pericarditis is the inflammation of the pericardium

- Myocarditis is the inflammation of the heart muscle

- Endocarditis is the inflammation of the endocardium

- Pancarditis is the inflammation of the entire heart: the epicardium, the myocardium and the endocardium

- Reflux carditis refers to a possible outcome of esophageal reflux (also known as GERD), and involves inflammation of the esophagus/stomach mucosa

Viral cardiomyopathy occurs when viral infections cause myocarditis with a resulting thickening of the myocardium and dilation of the ventricles. These viruses include Coxsackie B and adenovirus, echoviruses, influenza H1N1, Epstein-Barr virus, rubella (German measles virus), varicella (chickenpox virus), mumps, measles, parvoviruses, yellow fever, dengue fever, polio, rabies and the viruses that cause hepatitis A and C.

Eosinophilic coronary periarteritis is a heart disorder caused by extensive eosinophilic infiltration of the adventitia and periadventitia, i.e. the soft tissues, surrounding the coronary arteries. The intima, tunica media, and tunica intima layers of these arteries remain intact and are generally unaffected. Thus, this disorder is characterized by episodes of angina, particularly Prinzmetal's angina, and sudden death due to heart dysfunction. The disorder is considered distinct from eosinophilic myocarditis.

Dilated cardiomyopathy can be due to pericardial effusion or infective endocarditis, especially in intravenous drug users which are common in the HIV population. However, the most researched cause of cardiomyopathy is myocarditis (myocardial inflammation and infection) caused by HIV-1, which the main subtype of HIV (the other being HIV-2), with greater likelihood of transmission and shorter period between infection and illness. HIV-1 virions infect cardiomyocytes in patches but there is no direct correlation between viral infection and dysfunction of cardiomyocytes.

HIV-related cardiomyopathy is often not associated with any specific opportunistic infection, and approximately 40% of patients have not experienced any opportunistic infection before the onset of cardiac symptoms.

Heart problems are very important in people with Human Immunodeficiency Virus (HIV) as Acquired ImmunoDeficiency Syndrome (AIDS) patients with left ventricular dysfunction have a median survival of 101 days as compared to 472 days in AIDS patients with healthy hearts. HIV is a major cause of cardiomyopathy (problems with the heart muscle that reduce the efficiency with which the heart pumps blood). The most common type of HIV induced cardiomyopathy is dilated cardiomyopathy also known as eccentric ventricular hypertrophy which leads to impaired contraction of the ventricles due to volume overload. The annual incidence of HIV associated dilated cardiomyopathy was 15.9/1000 before the introduction of highly active antiretroviral therapy (HAART). However, in 2014, a study found that 17.6% of HIV patients have dilated cardiomyopathy (176/1000) meaning the incidence has greatly increased.

Before puberty, the disease typically only produces flu-like symptoms, if any at all. When found, symptoms tend to be similar to those of common throat infections (mild pharyngitis, with or without tonsillitis).

Cryptococcosis, also known as cryptococcal disease, is a potentially fatal fungal disease. It is caused by one of two species; "Cryptococcus neoformans" and "Cryptococcus gattii". These were all previously thought to be subspecies of "C. neoformans" but have now been identified as distinct species.

Cryptococcosis is believed to be acquired by inhalation of the infectious propagule from the environment. Although the exact nature of the infectious propagule is unknown, the leading hypothesis is the basidiospore created through sexual or asexual reproduction.

Though caused by different infections, the signs and symptoms of TORCH syndrome are consistent. They include hepatosplenomegaly (enlargement of the liver and spleen), fever, lethargy, difficulty feeding, anemia, petechiae, purpurae, jaundice, and chorioretinitis. The specific infection may cause additional symptoms.

TORCH syndrome may develop before birth, causing stillbirth, in the neonatal period, or later in life.

In adolescence and young adulthood, the disease presents with a characteristic triad:

- Fever – usually lasting 14 days; often mild

- Sore throat – usually severe for 3–5 days, before resolving in the next 7–10 days.

- Swollen glands – mobile; usually located around the back of the neck (posterior cervical lymph nodes) and sometimes throughout the body.

Another major symptom is feeling tired. Headaches are common, and abdominal pains with nausea or vomiting sometimes also occur. Symptoms most often disappear after about 2–4 weeks. However, fatigue and a general feeling of being unwell (malaise) may sometimes last for months. Fatigue lasts more than one month in an estimated 28% of cases. Mild fever, swollen neck glands and body aches may also persist beyond 4 weeks. Most people are able to resume their usual activities within 2–3 months.

The most prominent sign of the disease is often the pharyngitis, which is frequently accompanied by enlarged tonsils with pus—an exudate similar to that seen in cases of strep throat. In about 50% of cases, small reddish-purple spots called petechiae can be seen on the roof of the mouth. Palatal enanthem can also occur, but is relatively uncommon.

Spleen enlargement is common in the second and third weeks, although this may not be apparent on physical examination. Rarely the spleen may rupture. There may also be some enlargement of the liver. Jaundice occurs only occasionally.

A small minority of people spontaneously present a rash, usually on the arms or trunk, which can be macular (morbilliform) or papular. Almost all people given amoxicillin or ampicillin eventually develop a generalized, itchy maculopapular rash, which however does not imply that the person will have adverse reactions to penicillins again in the future. Occasional cases of erythema nodosum and erythema multiforme have been reported.

The heart complications are the most important aspect of Kawasaki disease. It is the main cause of heart disease acquired in childhood in the United States and Japan. In developed nations, it appears to have replaced acute rheumatic fever as the most common cause of acquired heart disease in children. Coronary artery aneurysms occur as a sequela of the vasculitis in 20–25% of untreated children. It is first detected at a mean of 10 days of illness and the peak frequency of coronary artery dilation or aneurysms occurs within four weeks of onset. Aneurysms are classified into small (internal diameter of vessel wall 8 mm). Saccular and fusiform aneurysms usually develop between 18 and 25 days after the onset of illness.

Even when treated with high-dose IVIG regimens within the first 10 days of illness, 5% of children with Kawasaki disease develop at the least transient coronary artery dilation and 1% develop giant aneurysms. Death can occur due either to myocardial infarction secondary to blood clot formation in a coronary artery aneurysm or to of a large coronary artery aneurysm. Death is most common two to 12 weeks after the onset of illness.

Many risk factors predicting coronary artery aneurysms have been identified, including persistent fever after IVIG therapy, low hemoglobin concentrations, low albumin concentrations, high white-blood-cell count, high band count, high CRP concentrations, male sex, and age less than one year.

Coronary artery lesions resulting from Kawasaki disease change dynamically with time. Resolution one to two years after the onset of the disease has been observed in half of vessels with coronary aneurysms. Narrowing of the coronary artery, which occurs as a result of the healing process of the vessel wall, often leads to significant obstruction of the blood vessel and lead to the heart not receiving enough blood and oxygen. This can eventually lead to heart muscle tissue death (myocardial infarction).

MI caused by thrombotic occlusion in an aneurysmal, stenotic, or both aneurysmal and stenotic coronary artery is the main cause of death from Kawasaki disease. The highest risk of MI occurs in the first year after the onset of the disease. MI in children presents with different symptoms from those in adults. The main symptoms were shock, unrest, vomiting, and abdominal pain; chest pain was most common in older children. Most of these children had the attack occurring during sleep or at rest, and around one-third of attacks were asymptomatic.

Valvular insufficiencies, particularly of mitral or tricuspid valves, are often observed in the acute phase of Kawasaki disease due to inflammation of the heart valve or inflammation of the heart muscle-induced myocardial dysfunction, regardless of coronary involvement. These lesions mostly disappear with the resolution of acute illness, but a very small group of the lesions persist and progress. There is also late-onset aortic or mitral insufficiency caused by thickening or deformation of fibrosed valves, with the timing ranging from several months to years after the onset of Kawasaki disease. Some of these lesions require valve replacement.

Idiopathic giant-cell myocarditis (IGCM) is a cardiovascular disease of the muscle of the heart (myocardium).

The condition is rare; however, it is often fatal and there is no proven cure because of the unknown nature of the disorder.

IGCM frequently leads to death with a high rate of about 70% in first year. A patient with IGCM typically presents with symptoms of heart failure, although some may present initially with ventricular arrhythmia or heart block. Median age from the time the disease is diagnosed to the time of death is approximately 6 months. 90% of patients are either deceased by the end of 1 year or have received a heart transplant. Diagnosis is made by endomyocardial biopsy during heart catheterization. Biopsy shows multinucleated giant cells and thus the name. While previously cases universally required heart transplantation, recent studies show that two thirds of patients can survive past one year with high doses of immunosuppressants such as prednisone and cyclosporine. The transplanted heart has a high chance of disease recurrence. Compared to lymphocytic (presumed viral) myocarditis, giant cell myocarditis is much more severe with much more rapid progression.

It is suggested to be caused by T-lymphocytes.

Dependent on the infectious syndrome, symptoms include fever, fatigue, dry cough, headache, blurred vision, and confusion. Symptom onset is often subacute, progressively worsened over several weeks. The two most common presentations are meningitis (an infection in and around the brain) and pulmonary (lung) infection.

Detection of cryptococcal antigen (capsular material) by culture of CSF, sputum and urine provides definitive diagnosis. Blood cultures may be positive in heavy infections. India ink of the CSF is a traditional microscopic method of diagnosis, although the sensitivity is poor in early infection, and may miss 15-20% of patients with culture-positive cryptococcal meningitis. Unusual morphological forms are rarely seen. Cryptococcal antigen from cerebrospinal fluid is the best test for diagnosis of cryptococcal meningitis in terms of sensitivity. Apart from conventional methods of detection like direct microscopy and culture, rapid diagnostic methods to detect cryptococcal antigen by latex agglutination test, lateral flow immunochromatographic assay (LFA), or enzyme immunoassay (EIA). A new cryptococcal antigen LFA was FDA approved in July 2011. Polymerase chain reaction (PCR) has been used on tissue specimens.

Cryptococcosis can rarely occur in the non-immunosuppressed people, particularly with "Cryptococcus gattii".

The initial scratch or wound caused by a bite from a carrier rodent results in mild inflammatory reactions and ulcerations. The wounds may heal initially, but reappear with the onset of symptoms. The symptoms include recurring fever, with body temperature 101–104°F (38–40°C). The fever lasts for 2–4 days, but recurs generally at 4–8 weeks. This cycle may continue for months or years. The other symptoms include regional lymphadenitis, malaise, and headache. The complications include myocarditis, endocarditis, hepatitis, splenomegaly, and meningitis.

Kawasaki disease often begins with a high and persistent fever that is not very responsive to normal treatment with paracetamol (acetaminophen) or ibuprofen. It is the most prominent symptom in Kawasaki disease, is a characteristic sign of the acute phase of the disease, is normally high (above 39–40 °C), is remittent, and is followed by extreme irritability. Recently, it is reported to be present in patients with atypical or incomplete Kawasaki disease; nevertheless, it is not present in 100% of cases. The first day of fever is considered the first day of illness, and the duration of fever is on average one to two weeks; in the absence of treatment, it may extend for three to four weeks. Prolonged fever is associated with higher incidence of cardiac involvement. It responds partially to antipyretic drugs and does not cease with the introduction of antibiotics. However, when appropriate therapy is started – intravenous immunoglobulin and aspirin – the fever is gone after two days.

Bilateral conjunctival inflammation was reported to be the most common symptom after fever. It typically involves the bulbar conjunctivae, is not accompanied by suppuration, and is not painful. It usually begins shortly after the onset of fever during the acute stage of the disease. Anterior uveitis may be present on slit-lamp examination. Iritis can occur, too. Keratic precipitates are another eye manifestation (detectable by a slit lamp but are usually too small to be seen by the unaided eye).

Kawasaki disease presents with set of mouth symptoms, the most characteristic changes are the red tongue, swollen lips with vertical cracking and bleeding. The mucosa of the mouth and throat may be bright red, and the tongue may have a typical "strawberry tongue" appearance (marked redness with prominent gustative papillae). These mouth symptoms are caused by the typical necrotizing microvasculitis with fibrinoid necrosis.

Cervical lymphadenopathy is seen in 50% to 75% of people, whereas the other features are estimated to occur in 90% of patients, but sometimes it can be the dominant presenting symptom. According to the definition of the diagnostic criteria, at least one impaired lymph node ≥ 15 mm in diameter should be involved. Affected lymph nodes are painless or minimally painful, nonfluctuant, and nonsuppurative; erythema of the neighboring skin may occur. Children with fever and neck adenitis who do not respond to antibiotics should have Kawasaki disease considered as part of the differential diagnoses.

In the acute phase of the disease, changes in the peripheral extremities can include erythema of the palms and soles, which is often striking with sharp demarcation and often accompanied by painful, brawny edema of the dorsa of the hands or feet. This is why affected children frequently refuse to hold objects in their hands or to bear weight on their feet. Later, during the convalescent or the subacute phase, desquamation of the fingers and toes usually begins in the periungual region within two to three weeks after the onset of fever and may extend to include the palms and soles. Around 11% of children affected by the disease may continue skin-peeling for many years. One to two months after the onset of fever, deep transverse grooves across the nails may develop (Beau’s lines), and occasionally nails are shed.

The most common skin manifestation is a diffuse macular-papular erythematous rash, which is quite nonspecific. The rash varies over time and is characteristically located on the trunk; it may further spread to involve the face, extremities, and perineum. Many other forms of cutaneous lesions have been reported; they may include scarlatiniform, papular, urticariform, multiform-like erythema, and purpuric lesions; even micropustules were reported. It can be polymorphic, not itchy, and normally observed up to the fifth day of fever. However, it is never bullous or vesicular.

In the acute stage of Kawasaki disease, systemic inflammatory changes are evident in many organs. Joint pain (arthralgia) and swelling, frequently symmetrical, and arthritis can also occur. Myocarditis, diarrhea, pericarditis, valvulitis, aseptic meningitis, pneumonitis, lymphadenitis, and hepatitis may be present and are manifested by the presence of inflammatory cells in the affected tissues. If left untreated, some symptoms will eventually relent, but coronary artery aneurysms will not improve, resulting in a significant risk of death or disability due to myocardial infarction. If treated quickly, this risk can be mostly avoided and the course of illness cut short.

Other reported nonspecific symptoms include cough, rhinorrhea, sputum, vomiting, headache, and seizure.

The course of the disease can be divided into three clinical phases.

- The acute febrile phase, which usually lasts for one to two weeks, is characterized by fever, conjunctival injection, erythema of the oral mucosa, erythema and swelling of the hands and feet, rash, cervical adenopathy, aseptic meningitis, diarrhea, and hepatic dysfunction. Myocarditis is common during this time, and a pericardial effusion may be present. Coronary arteritis may be present, but aneurysms are generally not yet visible by echocardiography.

- The subacute phase begins when fever, rash, and lymphadenopathy resolve at about one to two weeks after the onset of fever, but irritability, anorexia, and conjunctival injection persist. Desquamation of the fingers and toes and thrombocytosis are seen during this stage, which generally lasts until about four weeks after the onset of fever. Coronary artery aneurysms usually develop during this time, and the risk for sudden death is highest.

- The convalescent stage begins when all clinical signs of illness have disappeared, and continues until the sedimentation rate returns to normal, usually at six to eight weeks after the onset of illness.

The presentation between adults and children differs, as adults' neck lymph nodes are more affected (93% of adults versus 15% of children), hepatitis (65% versus 10%), and arthralgia (61% versus 24–38%). Some people have atypical presentations and may not have the classical symptoms. This occurs in particular in young infants; those people are especially at higher risk for cardiac artery aneurysms.

The signs and symptoms of a vertically transmitted infection depend on the individual pathogen. It may cause subtle signs such as a influenza-like illness and may not even be noticed by the mother during the pregnancy. In such cases, the effects may be seen first at birth.

Symptoms of a vertically transmitted infection may include fever and flu like symptoms. The newborn is often small for gestational age. A petechial rash on the skin may be present, with small reddish or purplish spots due to bleeding from capillaries under the skin. An enlarged liver and spleen (hepatosplenomegaly) is common, as is jaundice. However, jaundice is less common in hepatitis B because a newborn's immune system is not developed well enough to mount a response against liver cells, as would normally be the cause of jaundice in an older child or adult. Hearing impairment, eye problems, mental retardation, autism, and death can be caused by vertically transmitted infections. The mother often has a mild infection with few or no symptoms.

The genetic conditions of Aicardi-Goutieres syndrome are possibly present in a similar manner.

Various systems are affected.

- CNS abnormalities – microcephaly, mental retardation, spasticity, epilepsy, periventricular calcification

- Eye – choroidoretinitis and optic atrophy

- Ear – sensorineural deafness

- Liver – hepatosplenomegaly and jaundice due to hepatitis

- Lung – pneumonitis (interstitial pneumonitis)

- Heart – myocarditis

- Thrombocytopenic purpura, haemolytic anaemia

- Late sequelae in individuals asymptomatic at birth – hearing defects and reduced intelligence

Coxsackieviruses-induced cardiomyopathy are positive-stranded RNA viruses in picornavirus family and the genus enterovirus, acute enterovirus infections such as Coxsackievirus B3 have been identified as the cause of virally induced acute myocarditis, resulting in dilated cardiomyopathy. Dilated cardiomyopathy in humans can be caused by multiple factors including hereditary defects in the cytoskeletal protein dystrophin in Duchenne muscular dystrophy (DMD) patients). A heart that undergoes dilated cardiomyopathy shows unique enlargement of ventricles, and thinning of the ventricular wall that may lead to heart failure. In addition to the genetic defects in dystrophin or other cytoskeletal proteins, a subset of dilated cardiomyopathy is linked to enteroviral infection in the heart, especially coxsackievirus B. Enterovirus infections are responsible for about 30% of the cases of acquired dilated cardiomyopathy in humans.

Cytomegalic inclusion body disease (CIBD) is a series of signs and symptoms caused by cytomegalovirus infection, toxoplasmosis or other rare infections such as herpes or rubella viruses. It can produce massive calcification of the central nervous system, and often the kidneys.

Cytomegalic inclusion body disease is the most common cause of congenital abnormalities in the United States. It can also cause pneumonia and other diseases in immunocompromised patients, such as those with HIV/AIDS or recipients of organ transplants.

TORCH syndrome is caused by in utero infection with one of the TORCH agents, disrupting fetal development.

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.