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PEDIATRICS Vol. 112 No. 1 July 2003, pp. 87-95

Mycoplasma Disease and Acute Chest Syndrome in Sickle Cell Disease

Lynne Neumayr, MD^*, Evelyne Lennette, PhD, Dana Kelly, MPH^*, Ann Earles, RN/PNP^*, Stephen Embury, MD, Paula Groncy, MD^¶, Mauro Grossi, MD^||, Ranjeet Grover, MD^#, Lillian McMahon, MD, Paul Swerdlow, MD^**, Peter Waldron, MD and Elliott Vichinsky, MD^*

^* Hematology/Oncology Department, Children’s Hospital Oakland, Oakland, California
Virolab, Inc, Berkeley, California
Department of Medicine, San Francisco General Hospital, San Francisco, California
^¶ Hematology Department, Long Beach Memorial Hospital, Long Beach, California
^|| Pediatric Hematology Department, Children’s Hospital of Buffalo, Buffalo, New York
^# Comprehensive Sickle Cell Center, St Luke’s/Roosevelt Hospital, New York, New York
^** Division of Hematology, Wayne State University, Detroit, Michigan
Health Sciences Center, Department of Pediatrics, University of Virginia, Charlottesville, Virginia
Boston Medical Center, Boston, Massachusetts

Background. Acute chest syndrome (ACS) is the leading cause of hospitalization, morbidity, and mortality in patients with sickle cell disease. Radiographic and clinical findings in ACS resemble pneumonia; however, etiologies other than infectious pathogens have been implicated, including pulmonary fat embolism (PFE) and infarction of segments of the pulmonary vasculature. The National Acute Chest Syndrome Study Group was designed to identify the etiologic agents and clinical outcomes associated with this syndrome.

Methods. Data were analyzed from the prospective study of 671 episodes of ACS in 538 patients with sickle cell anemia. ACS was defined as a new pulmonary infiltrate involving at least 1 complete segment of the lung, excluding atelectasis. In addition, the patients had to have chest pain, fever >38.5C, tachypnea, wheezing, or cough. Samples of blood and deep sputum were analyzed for evidence of bacteria, viruses, and PFE. Mycoplasma pneumoniae infection was determined by analysis of paired serologies. Detailed information on patient characteristics, presenting signs and symptoms, treatment, and clinical outcome were collected.

Results. Fifty-one (9%) of 598 episodes of ACS had serologic evidence of M pneumoniae infection. Twelve percent of the 112 episodes of ACS occurring in patients younger than 5 years were associated with M pneumoniae infection. At the time of diagnosis, 98% of all patients with M pneumoniae infection had fever, 78% had a cough, and 51% were tachypneic. More than 50% developed multilobar infiltrates and effusions, 82% were transfused, and 6% required assisted ventilation. The average hospital stay was 10 days. Evidence of PFE with M pneumoniae infection was seen in 5 (20%) of 25 patients with adequate deep respiratory samples for the PFE assay. M pneumoniae and Chlamydia pneumoniae was found in 16% of patients with diagnostic studies for C pneumoniae. Mycoplasma hominis was cultured in 10 (2%) of 555 episodes of ACS and occurred more frequently in older patients, but the presenting symptoms and clinical course was similar to those with M pneumoniae.

Conclusions. M pneumoniae is commonly associated with the ACS in patients with sickle cell anemia and occurs in very young children. M hominis should be considered in the differential diagnosis of ACS. Aggressive treatment with broad-spectrum antibiotics, including 1 from the macrolide class, is recommended for all patients as well as bronchodilator therapy, early transfusion, and respiratory support when clinically indicated.

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Key Words: sickle cell • acute chest syndrome • Mycoplasma pneumoniae • Mycoplasma hominis • pulmonary fat embolism • pneumonia

Abbreviations: ACS, acute chest syndrome • PCR, polymerase chain reaction • PFE, pulmonary fat embolism • SCD, sickle cell disease • VOC, vaso-occlusive crisis • Ig, immunoglobulin • IL, interleukin

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Received for publication Jul 2, 2002; Accepted Nov 22, 2002.

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