Heart & Lung: The Journal of Acute and Critical Care
Volume 38, Issue 5 , Pages 444-449, September 2009

Mycoplasma pneumoniae community-acquired pneumonia (CAP) in the elderly: Diagnostic significance of acute thrombocytosis

  • Burke A. Cunha, MD

      Affiliations

    • Corresponding Author InformationReprint requests: Burke A. Cunha, MD, Chief, Infectious Disease Division, Winthrop-University Hospital, Mineola, NY 11501
  • ,
  • Francisco M. Pherez, MD

Infectious Disease Division, Winthrop-University Hospital, Mineola, New York; and State University of New York School of Medicine, Stony Brook, New York

published online 22 January 2009.

The most common cause of nonzoonotic atypical community-acquired pneumonia (CAP) is Mycoplasma pneumoniae. M. pneumoniae CAP is most common in young adults but may occur at any age. Like other atypical CAPs, M. pneumoniae is associated with a characteristic pattern of extrapulmonary organ involvement and nonspecific laboratory tests. M. pneumoniae CAP is frequently accompanied by gastrointestinal manifestations (eg, loose stools/diarrhea), nonexudative pharyngitis, or skin involvement (ie, erythema multiforme). Central nervous system involvement with M. pneumoniae is rare and accompanied by highly elevated cold agglutinin titers. Cardiac, hepatic, and renal involvement are not features of M. pneumoniae CAP. Because M. pneumoniae CAP is most frequent in ambulatory young adults, it is an easily overlooked diagnosis in elderly patients hospitalized with CAP. The hallmark clinical finding of M. pneumoniae CAP is protracted nonproductive cough. The characteristic nonspecific laboratory test finding uniquely associated with M. pneumoniae CAP is elevated cold agglutinin titers. Seventy-five percent of patients with M. pneumoniae infection have elevated cold agglutinin titers. However, the absence of elevated cold agglutinin titers does not argue against the diagnosis of M. pneumoniae. If cold agglutinins are present in a patient with CAP, the higher the cold agglutinin titer is (>1:64), the more likely the cold agglutinins are due to M. pneumoniae. Q fever is the only other atypical CAP that is rarely associated with cold agglutinins. We present a hospitalized patient with CAP in whom all microbiologic and serologic diagnostic test results were negative during the first week of her hospitalization. M. pneumoniae CAP was not suspected because of her age. Her initial M. pneumoniae immunoglobulin-M and cold agglutinin titers were negative. During the second week of hospitalization, an increased platelet count was noted. It is a common misconception that acute thrombocytosis is an acute phase reactant. Her acute thrombocytosis increased and persisted. The diagnostic clue to the cause of this hospitalized patient with CAP was acute thrombocytosis. In a patient with CAP, acute thrombocytosis is usually associated with Q fever pneumonia and less commonly with M. pneumoniae. If Q fever can be excluded on the basis of a recent/proximate zoonotic vector contact history, then acute thrombocytosis is an important clue to M. pneumoniae CAP. Acute thrombocytosis due to M. pneumoniae and Q fever occurs during weeks 1 and 2 of the infection. In patients with CAP, acute thrombocytosis that occurs during weeks 1 and 2 of the illness should suggest M. pneumoniae in patients without recent zoonotic vector contact history.

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PII: S0147-9563(08)00195-7

doi:10.1016/j.hrtlng.2008.10.005

Heart & Lung: The Journal of Acute and Critical Care
Volume 38, Issue 5 , Pages 444-449, September 2009