Micdadei Pneumonia Research Articles

An outbreak of Legionella micdadei pneumonia in transplant patients: evaluation, molecular epidemiology, and control

purpose: To describe a nosocomial outbreak of Legionella micdadei pneumonia in transplant patients and to characterize the source of the outbreak and the control measures utilized. subjects and methods: We performed retrospective Legionella micdadei serologic testing to enhance case finding in transplant patients with pneumonia that lacked a documented microbial etiology, as well as prospective environmental surveillance of water sites and testing for Legionella in clinical specimens. results: During a 3-month period, 12 cases of Legionella micdadei pneumonia were identified either by culture or serologic testing among 38 renal and cardiac transplant patients. Legionella micdadei isolates from hot water sources were found by pulsed-field gel electrophoresis to have a DNA banding pattern that was identical to the isolates from the first 3 culture-positive cases and from 2 cases that occurred 16 months later. conclusions: Hospitals caring for organ transplant recipients and other immunosuppressed patients must be aware of the possibility of environmental sources of outbreaks of Legionella infection. A first-line screen with the Legionella urine antigen test will identify Legionella pneumophila serogroup 1. However, specific cultures in outbreak situations should be considered to identify other Legionella pneumophila serotypes and the nonpneumophila Legionella species.

Community-acquired Legionella micdadei pneumonia presenting as acid fast bacilli in sputum

Community-acquired Legionella micdadei pneumonia presenting as acid fast bacilli in sputum

Pneumonia Due to Legionella micdadei in Bone marrow Transplant Recipients

Legionella micdadei has previously been described as a cause of nosocomial pneumonia, particularly in kidney transplant recipients. Cell-mediated immunity is the principal host defense against this pathogen. A common clinical scenario in the immunocompromised host is that of septic pulmonary embolus, but asymptomatic infections have also been reported. The organism is weakly acid-fast in clinical specimens but loses this property when grown on solid media. We report two cases of L. micdadei pneumonia, differing markedly in clinical severity and outcome, in bone marrow transplant recipients. Additionally, we note the growth of the organism in liquid culture media with preservation of its acid-fast property.

EVALUATION OF ULTRAVIOLET LIGHT FOR DISINFECTION OF HOSPITAL WATER CONTAMINATED WITH LEGIONELLA

An epidemic of nosocomial Legionella micdadei pneumonia occurred among renal transplant patients in the University of Virginia hospital between 1978 and 1982. Although no further cases were diagnosed after 1982, filters and ultraviolet light (UVL) fittings were installed in 1985 as an attempt to disinfect water piped to rooms of transplant patients, because of concern about persistence of L micdadei in hospital water. Water samples were obtained from eight UVL-treated rooms and eight control rooms. 26 of 95 control samples were culture positive for L micdadei compared with 0 of 71 samples of filtered, UVL-treated water (p <0·0001, Fisher's exact test). After the UVL fitting and filter had been bypassed because of a leak, 9 of 33 samples from the UVL rooms were positive (p<0·0001). These data suggest that UVL treatment may be useful in continuous disinfection of water in the hospital rooms of high-risk patients.

Legionella micdadei and Legionella dumoffii monoclonal antibodies for laboratory diagnosis of Legionella infections.

Two different monoclonal antibodies directed against Legionella micdadei and L. dumoffii (Genetic Systems Corp., Seattle, Wash.) were evaluated for their specificity and ability to detect L. micdadei and L. dumoffii in human and animal clinical samples and bacterial isolates in an indirect immunofluorescence assay. All three frozen sputum samples and all three Formalin-fixed sputum and liver samples from patients with culture-documented L. micdadei pneumonia were positive when tested with the L. micdadei monoclonal antibody. A Formalin-preserved lung sample from a patient with culture-documented L. dumoffii pneumonia was positive with its homologous monoclonal antibody. No cross-staining reactions were found with either monoclonal antibody on any of 25 human sputum samples tested from patients without Legionella infections. A total of 66 Legionella strains and 56 non-Legionella strains including 22 Pseudomonas strains and 34 other bacterial strains were studied. No cross-staining reactions were found except in Staphylococcus aureus Cowan 1 ATCC 12598. The lower limit of detection in seeded sputum samples was about 7 X 10(4) cells per ml for both monoclonal antibodies. Lung and tracheal lavage specimens from L. micdadei- or L. dumoffii-infected guinea pigs showed specific staining only with their respective monoclonal antibodies. The monoclonal antibodies stained homologous bacteria slightly less intensely than did the polyclonal antisera, but the signal-to-noise ratio was considerably higher for the monoclonal antibodies. No differences in sensitivity of staining of clinical specimens or bacterial isolates were noted between the monoclonal antibodies and the polyclonal reagents for L. micdadei and L. dumoffii (Centers for Disease Control, Atlanta, Ga., and BioDx, Denville, N.J. These monoclonal antibodies ae sensitive and specific, making them good candidates for laboratory diagnostic purposes.

Role of the alveolar macrophage in host defense and immunity to Legionella micdadei pneumonia in the guinea pig

Guinea pigs develop a lethal pneumonia after intratracheal infection with Legionella micdadei, and the lung displays pathological changes similar to those observed in humans. To investigate the role of the resident alveolar macrophage in the pathogenesis of L. micdadei pneumonia, guinea pig alveolar macrophages obtained by bronchoalveolar lavage were cultured in vitro and infected with L. micdadei. In the absence of opsonins L. micdadei was phagocytized by, and multiplied within, alveolar macrophages with greater than a 100-fold increase in cell-associated colony forming units over 20 h. L. micdadei opsonized with complement or antibody multiplied within alveolar macrophages at the same rate as unopsonized bacteria. Guinea pigs which were treated with antimicrobials after infection with L. micdadei and recovered from the pneumonia were immune to challenge with an otherwise lethal inoculum of L. micdadei. However, the growth curve of both unopsonized and opsonized L. micdadei in the alveolar macrophages from immune animals was essentially identical to that in macrophages from susceptible animals. Thus, the resident alveolar macrophage is not capable of limiting the growth of Legionella. Rather, the alveolar macrophages appear to be the primary site of Legionella multiplication within the lung. Although alveolar macrophages may participate in other aspects of pulmonary immunity to the legionellae, these data indicate that the alveolar macrophage alone does not act as an effector cell in cell-mediated immunity to Legionella.

Acid-fast bacilli in sputum: a case of Legionella micdadei pneumonia

Legionella micdadei has been implicated as a cause of nosocomial pneumonia. There are no reports of L. micdadei pneumonia diagnosed by acid-fast stain of expectorated sputum. We report a case of L. micdadei pneumonia in which expectorated sputum harbored acid-fast bacteria that reacted specifically with fluorescent antiserum to L. micdadei, confirmed by culture. In a patient at risk for nosocomial infection, the differential diagnosis of a positive sputum stain for acid-fast bacilli should include L. micdadei in addition to mycobacteria. Therapy for L. micdadei infection should be considered pending confirmation of the diagnosis.

Antimicrobial therapy of experimental Legionella micdadei pneumonia in guinea pigs.

Several antimicrobial agents were evaluated for activity against experimental Legionella micdadei pneumonia in guinea pigs. Erythromycin, rifampin, doxycycline, and sulfamethoxazole-trimethoprim produced significant reductions in mortality. Penicillin, cefazolin, cefoxitin, chloramphenicol, and gentamicin were not efficacious even though, at the doses administered, the peak concentrations of these agents in serum substantially exceeded their MICs for the test strain. It is suggested that the poor performance of the latter group of agents resulted from poor penetration into cells in which L. micdadei was multiplying.

Infections caused by Legionella micdadei and Legionella pneumophila among renal transplant recipients.

In an analysis of legionellosis at Presbyterian-University Hospital in Pittsburgh during the 28 months after the original outbreak of pneumonia caused by Legionella micdadei , 101 consecutive renal-allograft recipients were studied. The prevalence of elevated titers of antibody to Legionella pneumophila or L. micdadei among the patients at the time of transplantation (21.6%) was not significantly different from that among kidney donors (13.4%; P greater than .25). Seroconversion occurred in 21 (23.6%) of 89 recipients during the six months after transplantation. Seven recipients who seroconverted were diagnosed as having legionella pneumonia, eight had fever and pneumonitis attributed to other causes but compatible (on clinical grounds) with legionella infection, and six had no clinical evidence of infectious pneumonia. The interval from transplantation to onset of pneumonia was shorter for recipients with evidence of L. micdadei pneumonia than for patients with L. pneumophila pneumonia (P = .006); this finding suggested that the former disease occurred when the recipients were most immunocompromised. The original outbreak of L. micdadei pneumonia was found to have subsided nine months after the last formally recognized case, but infections with L. pneumophila continued to occur thereafter.

The use of Tracheal and Pulmonary Aspiration to Diagnose Legionella Micdadei Pneumonia

Legionella micdadei (Pittsburgh pneumonia agent) pneumonia was diagnosed in three patients by transtracheal aspiration and in a fourth patient by percutaneous lung aspiration on two occasions. The organism was identified by direct fluorescent antibody staining and by culture in each case. Diagnosis by aspiration of the respiratory tract was rapid, specific, and safe. This allowed early institution of specific antimicrobial therapy in a group of severely ill, immunocompromised patients. These techniques should be considered whenever the diagnosis of L micdadei pneumonia is likely.

Successful treatment of Legionella micdadei (Pittsburgh pneumonia agent) pneumonia with erythromycin

Optimal treatment of Legionella micdadei pneumonia has not been established, although in vitro studies have shown the pathogen to be sensitive to erythromycin. At our institution, L. micdadei pneumonia was diagnosed in six patients over a one and one-half year period. All patients were immunocompromised and had a typical clinical syndrome; in four of six, diagnosis was made by isolation of the pathogen. All patients received erythromycin (2 to 4 g daily) for 12 to 27 days, and five of six recovered completely. One patient improved initially but died four weeks later from Serratia marcescens pneumonia and septicemia. Although L. micdadei may cause life-threatening pneumonia in immunocompromised hosts, prompt diagnosis and institution of erythromycin therapy can result in a favorable outcome.

Legionella micdadei (Pittsburgh pneumonia agent): direct fluoresent-antibody examination of infected human lung tissue and characterization of clinical isolates.

Legionella micdadei (Pittsburgh pneumonia agent) was identified by direct fluorescent-antibody (DFA) examination of lung tissue in six of seven persons diagnosed previously as having L. micdadei pneumonia only by histopathology and in four persons who also had positive cultures of the organism. No cross-reactions occurred with monospecific DFA conjugates prepared against Legionella pneumophila serogroups 1 to 6, Legionella bozemanii, Legionella dumoffii, and Legionella gormanii. One person had L. pneumophila serogroup 6 identified by DFA examination of lung tissue and subsequent culture of stored pulmonary secretions. Characterization of the four strains of L. micdadei revealed specific DFA reactions, bacteriological behavior, and cellular fatty acid composition that allow identification of the organism. DFA testing appears to be a sensitive method for identifying L. micdadei prescent in human lung tissue or cultured on artificial media.