Pericarditis and myocarditis are increasingly diagnosed by the consequences of campylobacter infection. Despite the rarity, these manifestations are of great importance, since misdiagnosis threatens the inappropriate appointment of thrombolytics or angioplasty with all the potential complications.

Enteritis caused by Campylobacter jejuni is the most common infection in developed countries, with an annual incidence exceeding 1 case per 1000 people. Campylobacter fetus has been identified as the causative agent of pericarditis in at least 10 documented cases. In all of these cases, patients generally had a history of nonspecific symptoms for several weeks, including fever, weight loss, cough, and chest pain. A key fact was the lack of data on the association with gastrointestinal symptoms in these cases. C.jejuni -pericarditis is also an extremely rare manifestation, which is reported in only one case, in a patient with congenital immunodeficiency, X-linked agammaglobulinemia. Pericarditis was one component of the picture of systemic campylobacteriosis, in which the lungs and pericardium were significantly affected. C.jejuni has been isolated from blood, pleural aspirate and pericardial effusion.

There are also reports of six cases of myocarditis associated with C.jejuni and six cases of myopericarditis associated with C.jejuni in the literature. All have developed in patients without immunodeficiency. Typical clinical manifestations included transient acute chest pain with concomitant ECG changes and increased enzyme levels, in combination with anterior or concomitant enteritis. Patients showed short-term signs of acute left ventricular failure and, in one case, persisted for several months after infection.

The mechanism of development of campylobacterial myopericarditis remains unknown. It is believed that there is a direct effect on the pericardium and myocardium of bacteria or their toxin due to an episode of bacteremia. Although C. fetus is almost always released from the blood when a pathogen is associated with myopericarditis, this cannot be said for C.jejuni. There has not been one case of myocarditis and myopericarditis associated with C.jejuni out of 12 documented in which the microorganism would be isolated from the blood (only positive fecal culture and / or serological analysis).

Differences in the manifestations of the infectious process can be associated with the peculiarities of the pathogenicity of these pathogens. There are many extraintestinal manifestations of C. fetus infection, usually caused by a direct invasion of the pathogen: septic abortion, meningoencephalitis, brain abscess, subdural empyema, septic arthritis, arthritis vertebral, osteomyelitis and pulmonary abscess. The ability to "escape" from the action of the host's immune system is associated with the presence of a surface protein which prevents the binding of complement C3b to the surface of the microbial cell and gives the pathogen resistance to antibodies. and the attack of phagocytes. This, apparently, allows C. fetus to use the blood freely as a transport route from the intestine to secondary foci, especially if the immune system is partially weakened by chronic diseases (rheumatism, lymphoma, hypothyroidism, polycystic kidney disease, beta thalassemia and diabetes with hypertension in half of the documented cases). C. fetus -pericarditis appears following colonization of the pericardium due to bacteremia and septicemia (confirmed by the appearance of fever, malaise and weight loss). C.jejuni has no surface protein and can only cause malignant bacteremia in people with severe immunodeficiency. However, such a mechanism does not explain the pathogenesis of C.jejuni -myopericarditis.

Another hypothesis is linked to the role of type II hypersensitivity reactions, when the antigens of campylobacter and / or its toxin cross-react with or are similar to pericardial antigens. Thus, the antibodies produced against the pathogen also damage the pericardium. In this case, a typical period of several weeks is typical between the primary infection and the development of hypersensitivity reactions. It should be noted that C.jejuni has been shown to be associated with certain pathologies, involving immunological mechanisms of pathogenesis. Reactive arthritis is a complication detected in 1% of the manifest forms of C.jejuni enteritis. Enteriitis C.jejuni is a previous pathology in 26 to 41% of patients suffering from Guillain-Barré syndrome, while a period of several weeks between the symptoms of enteritis and development syndrome is also typical.

Thus, extraintestinal campylobacter infection and the pathogenicity of pathogens remain a problem in the 21st century, particularly in connection with the general increase in the number of immunocompromised patients.