Two Cases of Fulminant Mycoplasma pneumoniae Pneumonia within 4 Months

Baum, Heike von; Strubel, Andreas; Nollert, J.; Layh‐Schmitt, Gerlinde

doi:10.1007/s150100050077

Cited by 9 publications

(7 citation statements)

References 8 publications

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“…There are several descriptions of severe cases of My coplasma pneumoniae pneumonia with and without associated multi-organ failure [15][16][17][18][19]. Clinically severe cases of M. pneumoniae pneumonia published before 1995 have been reviewed by Chan and Welsh [13].…”

Section: Discussionmentioning

confidence: 99%

Fatal Mycoplasma pneumoniae pneumonia in a previously healthy 18-year-old girl

Daxboeck

Eisl

Burghuber

et al. 2007

Wien Klin Wochenschr

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A case of fatal Mycoplasma pneumoniae pneumonia in a previously healthy 18-year-old girl is reported. On hospital day 9, the antibody titer to M. pneumoniae was 1:512 in the complement fixation test and 1:5120 in the microparticle agglutination assay. After five weeks in the intensive care unit, the patient died from necrotizing hemorrhagic pneumonia with multi-organ failure. No significant superinfections occurred during ICU treatment. Corticosteroids (hospital day 8 onward) did not influence the course of the disease. It is noteworthy that, as in some previously reported cases, the clinical state deteriorated during presumably adequate antibiotic treatment (2 days before admission onward), and despite documented eradication of the pathogen from the respiratory tract (PCR from bronchoalveolar fluid on hospital day 22 was negative). However, the illness had lasted for several days before admission to the hospital, therefore the potentially beneficial effect of antibiotic treatment at an early stage of the disease cannot be assessed. Clearly, in default of other treatment options, correct diagnosis and early treatment of mycoplasma community-acquired pneumonia seems mandatory. This is the third case of fatal mycoplasma pneumonia reported from Austria in recent years, making this topic worthy of further scientific attention.

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Section: Discussionmentioning

confidence: 99%

Fatal Mycoplasma pneumoniae pneumonia in a previously healthy 18-year-old girl

Daxboeck

Eisl

Burghuber

et al. 2007

Wien Klin Wochenschr

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“…Layh-Schmitt et al (6,(39)(40)(41)(42)(43)(44)(45)66) showed that MGPC gene products (accessory proteins B and C) are essential for M. pneumoniae cytadherence. MGPC gene products are found in close proximity to ADP1 as well as to other cytadherencerelated molecules, such as HMW1, HMW3, p65, and p30 in M. pneumoniae (42,45,66).…”

Section: Discussionmentioning

confidence: 99%

GapA and CrmA Coexpression Is Essential for Mycoplasma gallisepticum Cytadherence and Virulence

et al. 2002

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It was previously demonstrated that avirulent Mycoplasma gallisepticum strain R high (passage 164) is lacking three proteins that are expressed in its virulent progenitor, strain R low (passage 15). These proteins were identified as the cytadhesin molecule GapA, the putative cytadhesin-related molecule CrmA, and a component of a high-affinity transporter system, HatA. Complementation of R high with wild-type gapA restored expression in the transformant (GT5) but did not restore the cytadherence phenotype and maintained avirulence in chickens. These results suggested that CrmA might play an essential role in the M. gallisepticum cytadherence process. CrmA is encoded by the second gene in the gapA operon and shares significant sequence homology to the ORF6 gene of Mycoplasma pneumoniae, which has been shown to play an accessory role in the cytadherence process. Complementation of R high with wild-type crmA resulted in the transformant (SDCA) that lacked the cytadherence and virulence phenotype comparable to that found in R high and GT5. In contrast, complementation of R high with the entire wild-type gapA operon resulted in the transformant (GCA1) that restored cytadherence to the level found in wild-type R low . In vivo pathogenesis trials revealed that GCA1 had regained virulence, causing airsacculitis in chickens. These results demonstrate that both GapA and CrmA are required for M. gallisepticum cytadherence and pathogenesis.Mycoplasma gallisepticum is one infectious agent initiating the chronic respiratory disease complex in chickens and is the primary agent of infectious sinusitis in turkeys (74). This bacterium has developed a wide array of surface molecules that are involved in cytadherence to host cells (9,17,22,51). GapA is considered the primary cytadhesin. Goh et al. (21) identified its gene in M. gallisepticum based on its nucleotide sequence homology to the Mycoplasma pneumoniae cytadhesin ADP1 gene. Subsequent studies showed that anti-GapA Fab fragments were able to significantly inhibit M. gallisepticum cytadherence (22). Troy (69) reported that GapA was absent in avirulent M. gallisepticum. These data led us to hypothesize that complementation of GapA expression in strain R high via Tn4001 might restore cytadherence and perhaps virulence. Neither cytadherence nor virulence was restored upon the gapA-complemented strain R high , transformant GT5 (56, 57). This indicated that other factors might play an important role in M. gallisepticum cytadherence. Protein profile comparison between virulent and avirulent strains showed that, in addition to GapA, two other proteins are absent in R high (69). One of these proteins was found to be encoded by the second gene of the gapA operon. Its gene product shows significant sequence homology with the precursor of M. pneumoniae ORF6 gene products, which are known to play accessory roles in P1 (ADP1)-mediated cytadherence (35,36,40,66 The aim of this study was to evaluate the role of CrmA in M. gallisepticum cytadherence and virulence. We demonstrate that coexpr...

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“…Fewer than 10% of cases are clinically apparent and fewer than 5% of those cases requiring hospitalization. [3][4][5] Of those requiring hospitalization, 10% will require admission to an intensive care unit (ICU) with mechanical ventilation as a result of Acute Respiratory Distress Syndrome (ARDS).…”

Section: Introductionmentioning

confidence: 99%

“…The literature presents cases where a previously healthy subject, between the ages of 18 and 37, progressed to ARDS and the associated severe complications. [4][5][6][7][8] Many of these cases presented for medical treatment after up to 10 days of non-specific symptoms such as fatigue, myalgia, and low-to high-grade fever. The majority of these cases received appropriate medical care, including antibiotic therapy, at time of presentation.…”

Section: Introductionmentioning

confidence: 99%