Viral and bacterial pathogens | Myocarditis

Viral and bacterial pathogens

In the case of infectious myocarditis, viruses are most likely to be involved in developed countries. Mainly enteroviruses, especially Coxackie viruses and ECHO viruses, are found in microbiological detection. Other pathogens such as parvovirus B19 are also important as pathogens of rubella, adenoviruses and herpes viruses, especially human herpes virus six.

More rarely, the HI virus and cytomegalovirus (CMV) come into question. Usually following infections localized elsewhere, such as in the upper respiratory tract or gastrointestinal tract, there is a low risk of spreading in the heart muscle. Possible sources of infection are, through contact with faeces, contaminated hands, toys, drinking water and many more.

Bacterial causes of myocarditis include the pathogens causing diphtheria, tuberculosis, Lyme borreliosis or pneumococcus. However, persons with a weakened immune system are more likely to be affected by bacterial myocarditis. Single-celled organisms (protozoa) such as the pathogen of Chagas’ disease are found as the main cause in South America, and that is why they hardly play a role in Europe. Parasites and moulds or yeast fungi are also able to cause such a disease, but in terms of numbers they only make up a small proportion.

Chronic Myocarditis

Decisive for the course and healing of myocardial inflammation is the persistence or survival of the pathogen in the tissue. If viral genetic information (RNA) or virus components remain, the immune response and thus the inflammation is maintained. A chronic course is more likely to develop, which is associated with the conversion of muscle tissue into connective tissue (fibrosis) and can lead to an enlargement of the heart chambers within a few years.

This would manifest itself as typical symptoms of heart failure. As a rule, the immune system eliminates the pathogen without any problems and spontaneous, effective healing occurs – the infection remains without consequences. It is assumed that a genetically determined susceptibility or receptivity of the affected person clearly favors the transition to a chronic course.