Very few clinical reports have been published about C. pneumoniae as a cause of myocarditis/perimyocarditis since C. pneumoniae was established as a distinct Chlamydial species(3) (see Table I). Most publications are case studies, where patients often have concomitant pneumonia or other complicating factors. The diagnosis has been made by serology in most cases; cultures for C. pneumoniae have been uniformly negative in all cases where culture was attempted. C. pneumoniae has been diagnosed by PCR in four individual cases, of which three had fatal outcomes. In two of these cases,(19,20) and in the fourth case,(21) the results of serology were suggestive of C. pneumoniae infection.

Reports of C. pneumoniae in Cases With Myocarditis, Perimyocarditis,

Diagnosis made by

Year of Number Concomitant _

Author (s) publication of cases Disease^ disease (s) Serology PCR IHC

Gran et al. 1993 1 M Pneumonia, arthritis +

Gnarpe et at. 1998 I Mh PM Earlier pneumonia +

Etienoe et aL 1992 10 E +

Norton et al. 1995 1 E Pneumonia +

Song et aL 2001 26 DCM +

"M = myocarditis, PM = perimyocarditis, E = endocarditis, DCM = dilated cardiomyopathy.

Wesslen et al.(19) reported a series of six cases of myocarditis with fatal outcome among Swedish elite orienteers aged 17-29 between 1989 and 1992. All cases had degenerative changes in the myocardium in addition to lymphocytic infiltrates and patchy fibrosis but no obvious other pathological changes at autopsy. The last of the six cases, a 26-year-old man, was described in more detail. He had pneumonia a couple of months earlier with a cough that lasted almost 2 months, and did not train during this period. He died suddenly after a skiing tour with teammates a few months later.

The heart showed small foci of lymphocyte infiltration, degenerative changes within myocytes, and some focal fibrosis in the left ventricle and in the septum at autopsy. He had both specific C. pneumoniae IgM (1:64) and IgG (1:512) antibodies demonstrated by MIF and a low titer of IgM antibodies (1:16) to C. psittaci, which wasjudged as cross-reactive. PCR was positive for C.pneumo-niae in specimens obtained from the septum and lung. Analyses of antibodies to a number of other possible viral and bacterial agents were negative.

Gran et al.(22) reported a case of pneumonia, myocarditis, and reactive arthritis in a 37-year-old male patient in 1993. The patient's illness started with a sore throat, malaise, and fever followed by erythema nodosum in the lower extremities and reactive arthritis of both ankles and the right wrist. He was admitted to a hospital and diagnosed with pneumonia and myocarditis in addition to arthritis. Echocardiography showed a dilated heart with decreased contractility. He had an increased ESR (78 mm/h) and his CRP was >200. Serology for Yersinia enterocolitica, Widal's test, and AST were negative, as was a test for HLA B27. Routine bacteriological cultures were negative for pathogenic bacteria. A complement fixation test showed a titer of 1:256 to Chlamydia and a MIF test for C. pneumoniae showed a specific IgG titer of 1:2048 and IgM of <1:8. Specific IgA antibodies were not investigated. He was given treatment with high dosages of i.v. penicillin and netilmicin. His clinical condition improved, and no clinical signs remained after 1 month, but he complained of fatigue when exposed to physical activity. The authors conclude that his condition was caused by C. pneumoniae. Although not mentioned, it is plausible that his myocarditis was secondary to reactive arthritis and pneumonia.

Tong and coworkers(23) reported a case of C. pneumoniae myocarditis, possibly in combination with influenza. The patient was an 18-year-old male who was admitted with vomiting, myalgia, and fever after participating in a 400-m race. His condition worsened with generalized convulsions; chest X-rays showed widespread unilateral shadowing, indicating consolidation or alveolar hemorrhage, but bronchoscopy did not reveal any hemorrhage. He required mechanical ventilation for several days and treatment for renal failure with hemofil-tration. The management of the patient was complicated by repeated episodes of pulmonary edema. ECGs were abnormal. A wide variety of serological tests for viral and bacterial agents were negative, except a rising CFT titer to influenza A and to Chlamydia spp. Specific Chlamydia serology (MIF) showed a rising titer of specific IgG and positive IgM antibodies to C. pneumoniae.

The patient improved after being treated with i.v. erythromycin and ce-fotaxime. He was given a course of doxycycline to prevent relapse. Cardiac and renal functions were normalized at follow-up. The authors conclude that

C. pneumoniae was the likely cause of his myocarditis. They speculate that intense physical exercise may have been a triggering factor.

We have investigated a material of 20 male patients, 13-43 years of age (median 28, mean 27.5) with a clinical diagnosis of myocarditis (n = 7), perimy-ocarditis (n = 9), and pericarditis (n = 4) .(24) All patients had ECGs suggestive of myocarditis. Sera from these patients were compared to sera from new, healthy male blood donors aged 18-43 (median 30, mean 31) (n = 111). All sera were analyzed using MIF for specific antibodies to C. trachomatis D-K, C. psittaci, and C. pneumoniae. All sera initially positive for IgM or IgA antibodies were absorbed with protein A-Sepharose CL-4B to remove possible interference from IgG and retested.(25) Thirty percent of the patients (6/20) had specific C. pneumoniae IgG antibodies in titers of 1:512 or more compared with 4.5% of blood donors (5/111). Sixty percent of the patients (13/20) had increased specific C. pneumoniae IgA antibodies compared with 8.1% (9/111) of the blood donors. The patients with myocarditis, perimyocarditis, or pericarditis had also much higher geometric mean titers (GMT) of specific antibodies to C. pneumoniae than the age- and sex-matched blood donors (363 vs. 107 for IgG; 65 vs. 13 for IgA). We concluded that C. pneumoniae was the likely cause for some of the cases.

We have also reported a case of perimyocarditis with multiorgan failure and a fatal outcome in a 51-year-old male teacher with a presumed year-long C. pneumoniae infection.(26) He was admitted to the hospital suffering from pronounced fatigue, hypotension, and a CRP value of >200 mg/l. He had bilateral pneumonia on admittance and an enlarged heart compared with chest X-ray 1 month earlier. He was given i.v. penicillin and fluid substitution because of low diuresis. He suddenly collapsed the next morning. During attempts at resuscitation, 500 ml of pericardial fluid was removed. Serum electrophoresis showed low C3 and C4, suggesting complement activation. Chlamydia serology (MIF) showed a specific C. pneumoniae IgG titer of 1:256 and IgA of 1:64 but no IgM; no specific antibodies to C. trachomatis or C. psittaci were seen. Serology for Legionella spp., Mycoplasma, CMV, EBV, and enteroviruses were all negative. Antinuclear factors, Goodpasture's antigen, c-ANCA, and p-ANCA were negative. Rheumatoid factor was not found.

The autopsy revealed a fibropurulent pericarditis with mild myocardial hypertrophy and mild to moderate coronary atherosclerosis. There was mild chronic portal inflammation ofthe liver. Immunohistochemical staining ofspec-imens taken from the heart and lung revealed the presence of C. pneumoniae and a massive inflammatory infiltrate both in the heart and in the lung.

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