Legionella-Like and Other Amoebal Pathogens as Agents of Community-Acquired Pneumonia

Thomas J. Marrie, Department of Medicine University of Alberta, Edmonton, Alberta, Canada; Didier Raoult, Bernard La Scola, Richard J. Birtles, Faculté de Médecine de Marseille, Marseille, France; Emidio de Carolis, Pfizer Canada Inc., Montreal, Quebec, Canada; the Canadian Community-Acquired Pneumonia Study Group(1)

Disclosures

Emerging Infectious Diseases. 2001;7(6) 

In This Article

Conclusions

In August 1986, Rowbotham[19] isolated LLAP 1 from the sputum of an 82-year-old woman with persistent pneumonia, by cocultivation with A. polyphaga. Seroconversion was demonstrated to LLAP 3. He screened >5,000 serum specimens submitted for Legionella antibody testing and found that 10 patients met the criteria for infection with LLAP 3[19].

The only other study similar to ours is a study by Benson et al.[20], who examined 500 patients with community-acquired pneumonia and determined antibody titers to LLAP 1,2,3,4,6,7,9, and Hall's coccus; 94 (18.9%) had a fourfold rise in antibody titer of 128 to any LLAP; 36 (7.2%) had a titer rise to ≥1,024. In contrast, 1.4% of our 255 hospitalized patients with community-acquired pneumonia had evidence of recent infection with a LLAP or Hall's coccus. As in our series, LLAP 4 was the most common cause of infection in the Benson study, which also found that in 10 (10.6%) of 94 patients with LLAP or Hall's coccus infection a copathogen had been implicated as cause of the pneumonia. Likewise, almost all our patients with LLAP infection were infected with another pathogen.

One of the most interesting findings in our study was a fourfold rise in antibody titer to BN 19 in a patient with presumed adult-onset Kawasaki syndrome, an acute vasculitis of unknown cause found predominantly in infants and young children. The diagnostic criteria include fever of >5 days plus four of the following five features: bilateral conjunctivitis without exudate; polymorphous eruption; cervical lymph node >1.5 cm in diameter; changes in the extremities, including edema of the hands or feet, palm or sole erythema, and periungual desquamation during convalescence; and changes in the oropharynx, including fissured red lips, strawberry tongue, and diffuse erythema of the oropharyngeal mucosa[21]. Our patient met this definition. An association between an antecedent respiratory infection and Kawasaki syndrome has been described[21,22], as has exposure to freshly cleaned carpets[23,24]. It is possible that the gamma globulin administered to our patient contained antibody to BN 19. However, there was no seroconversion or high titer of antibody to any of the other antigens included in our test panel. A possible association between infection with BN 19 and Kawasaki syndrome is easily tested.

Strengths of this study are its size and the comprehensiveness of the diagnostic work-up. Its limitations include the following: the three populations were enrolled in different periods; we tested only a subset of the patients hospitalized with community-acquired pneumonia and these patients were from multiple centers across Canada; our comparison groups (healthy persons and patients with ambulatory pneumonia) were Nova Scotians. However, the inferences that we are making are limited to the rate of infection in these three separate groups and are not intended to indicate differences temporally or geographically.

Our data suggest that LLAPs play a role, albeit an infrequent one, in community-acquired pneumonia. Usually they are a copathogen, but in some cases they are the sole pathogen. The possible association between BN 9 and Kawasaki disease requires further study.

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