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MYCOPLASMA PNEUMONIAE AND HEMORRHAGIC PERICARDIAL EFFUSION

St. Joseph’s Regional Medical Center, Paterson, NJ

INTRODUCTION: Mycoplasma pneumoniae is one of the most common respiratory pathogens. The most common presentation is community acquired pneumonia in which it accounts for more than 20% of cases, but is responsible for upper respiratory illness as well. It is usually considered a noninvasive organism. Extrapulmonary disease especially in terms of cardiac involvement is unusual. Mycoplasma pneumoniae-associated pericarditis is one such manifestation that can lead to life threatening pericardial effusion and tamponade. Pericarditis as a complication has been reported in 4.5 % of all serologically diagnosed cases of acute mycoplasmal infection. The lack of feasible culture methods and under appreciation of the pathogen’s ability to cause invasive disease is responsible for reduced number of diagnosed Mycoplasma pneumoniae related complications.

CASE PRESENTATION: A previously healthy 53 year old Hispanic male presented with 3 days duration sharp epigastric pain associated with nausea and vomiting. Physical examination was found to be significant for tachycardia, jugular venous distension, muffled heart sounds, pulsus paradoxus, diminished breath sounds at lung bases and ascitis. Chest x-ray demonstrated enlarged cardiac silhouette with bilateral pleural effusions. EKG showed sinus tachycardia and electrical alternans. Bedside Echocardiogram revealed large pericardial effusion with evidence of tamponade. Subsequently, patient was taken to operating room for pericardial window but the patient went into cardiopulmonary arrest requiring cardiopulmonary resuscitation, following which open sternotomy was performed. Twenty five hundred cc of bloody fluid was drained which was sent for analysis. Analysis showed mostly blood with white blood cells and rare atypical cells, possibly reactive mesothelial origin. Pericardial biopsy showed dense fibrocollagenous tissue and adipose tissue with inflammatory cell infiltration. No neoplastic or granulomatous process was noted. Work up for autoimmune etiology was negative. Serology demonstrated significantly elevated mycoplasma pneumoniae IgG titers > 600. There was no evidence of any other causative agents in repeated stains, cultures or pathological examination. Hospital stay was further complicated with upper gastrointestinal bleed which was managed conservatively, seizures and deep vein thrombosis with pulmonary embolism requiring Greenfield filter insertion. Patient was discharged home in stable condition on azithromycin and antiseizure medication. On subsequent outpatient follow-ups patient remains asymptomatic and has been doing well.

DISCUSSIONS: Mycoplasma pneumoniae in the repiratory tract has been suggested to reach the pericardium through the bloodstream, the bronchiolar lymphatics or by direct seeding, when the pleural-pericardial barrier is breached by a tumor or surgery. Mycoplasma pericarditis may result in pronounced morbidity unless appropriate antibiotic therapy is administered. Some cases diagnosed as idiopathic pericarditis could have a mycoplasmal etiology. Large pericardial effusions, especially in immunocompromised patients or those with previous cardiac surgery are more likely to be suspicious of mycoplasma associated pericarditis. Serology is the mainstay of laboratory diagnosis. IgM is a reliable indicator of recent Mycoplasma pneumoniae infection, but since this antibody is produced less frequently during reinfection, a negative result could be expected in patients over the age of 45 years, as in our case. The culture of mycoplasma species usually requires 1–2 weeks, thus limiting the role of this modality in guiding diagnostic and therapeutic decisions. When available, PCR, which can be done rapidly and has a high specificity, may be helpful, especially when combined with serology.

CONCLUSION: As appropriate treatment is significant for the outcome of mycoplasma associated pericarditis, serologic testing for the mycoplasma species should be part of the routine workup for pericarditis of unknown cause.

DISCLOSURE: Sharad Bajaj, No Financial Disclosure Information; No Product/Research Disclosure Information

REFERENCES

1. Waites KB, Talkington DF: Mycoplasma pneumoniae and its role as a human pathogen. Clin Microbiol Rev2004; 17 (4):697 –697[Abstract/Free Full Text]
2. Kenney RT, Li JS, Clyde WA Jr, Wall TC, O’Connor CM, Campbell PT, et al. Mycoplasma pericarditis: Evidence of invasive disease. Clin Infect Dis1993; 17 (Suppl 1)):S58 –S62[Medline]