Fatal outcomes in family transmission of Mycoplasma pneumoniae

Abstract

Background: Mycoplasma pneumoniae continues to be a significant cause of community-acquired pneumonia and, on rare occasions, manifests as fulminant disease that leads to mortality, even in healthy individuals.

Methods: We conducted a retrospective study on members of a family who were quarantined by the Centers for Disease Control and Prevention in 2002 for respiratory failure and death of a 15-year-old brother (sibling 1) and a 13-year-old sister (sibling 2). Collected airway, cerebrospinal fluid (CSF), and serum samples from both deceased siblings and serum samples from both parents and the remaining 3 ill siblings (sibling 3-5) were tested using a range of diagnostic assays. Autopsy lung tissue samples from sibling 2 were also assessed using immunohistochemical and immunoelectron microscopic methods.

Results: Autopsy evaluation of sibling 1 revealed cerebral edema consistent with hypoxic ischemic encepatholopathy and pulmonary findings of bronchiolitis obliterans with organizing pneumonia (BOOP). Postmortem lung examination of sibling 2 revealed lymphoplasmacytic bronchiolitis with intraluminal purulent exudate, BOOP, and pulmonary edema. Results of diagnostic assays implicated the household transmission of M. pneumoniae among all 5 siblings and both parents. Further analysis of lung tissue from sibling 2 demonstrated the presence of M. pneumoniae organisms and community-acquired respiratory distress syndrome toxin. M. pneumoniae was cultured directly from sibling 2 autopsy lung tissue.

Conclusion: Evidence is provided that M. pneumoniae was readily transmitted to all members of the household and that the resulting infections led to a spectrum of individual responses with variation in disease progression, including lymphoplasmacytic bronchiolitis, BOOP, and death.

Figure 1.

Timeline graph showing the onset of symptoms and time of diagnosis of the siblings. Further details of the siblings are included in Table 1.

Figure 2.

Immunolocalization of Mycoplasma pneumoniae and community-acquired respiratory distress syndrome (CARDS) toxin in lung specimen of sibling 2. In focal peribronchiolar sites, intra-alveolar collections of alveolar macrophages and monocytes were present, some of which showed positively-immunostained intracytoplasmic mycoplasma aggregates and CARDS toxin. Bold arrows indicate immunostained aggregates of mycoplasma organisms (Mp panel) and CARDS toxin (CARDS panel) that are similar in size and distribution (original magnification ×40). Insets indicate the higher magnification of same (original magnification ×60).

Figure 3.

Immunogold electron microscopic detection of Mycoplasma pneumoniae in lung tissue of sibling 2. M. pneumoniae cells were gold-particle-labeled with anti–M. pneumoniae antibodies (arrows) as described in the Materials and Methods. Mycoplasma cells were visualized with a JEOL 1230 transmission electron microscope. Gold labeling (arrows) reveals M. pneumoniae with its characteristic tip organelle (scale bar, 0.1 μm).