Abstract Background Sialidase is a well-known virulence factor of other respiratory pathogens, but was only recently documented to occur in some species of <it>Mycoplasma</it>. The sialidase activity expressed can vary quantitatively among strains within a species of mycoplasma, from undetectable to amounts that correlate positively with strain virulence. Very few isolates of <it>Mycoplasma pneumoniae </it>had ever been examined for sialidase activity, so it was unknown whether sialidase may contribute to diseases involving this species. Findings No sialidase activity was detected by spectrofluorometric assay of 15 laboratory strains and 91 clinical isolates of <it>M. pneumoniae </it>banked over many years from patients having radiologically-confirmed, uncomplicated community-acquired pneumonia. Conclusions The annotated genome of strain M129 (GenBank <ext-link ext-link-id="NC_000912" ext-link-type="gen">NC_000912</ext-link>, <ext-link ext-link-id="ATCC29342" ext-link-type="gen">ATCC 29342</ext-link>), also isolated from a patient with pneumonia, accurately represents the absence of sialidase genes from strains of <it>M. pneumoniae </it>typically associated with uncomplicated community-acquired pneumonia. A possible involvement of sialidase in neurologic or other extra-respiratory manifestations of <it>M. pneumoniae </it>mycoplasmosis remains to be investigated.</p

A al-Abassi

B Stamm

Daniel R Brown

DC Krause

DR Brown

F Daxboeck

K Waites

M Del Castillo

M May

M Narita

M Romero-Gómez

Meghan May

ND Walter

P Roggentin

P Vic

R Arav-Boger

R Freeman

S Lee

TP Atkinson

English

PubMed

Abstract Background Sialidase is a well-known virulence factor of other respiratory pathogens, but was only recently documented to occur in some species of Mycoplasma. The sialidase activity expressed can vary quantitatively among strains within a species of mycoplasma, from undetectable to amounts that correlate positively with strain virulence. Very few isolates of Mycoplasma pneumoniae had ever been examined for sialidase activity, so it was unknown whether sialidase may contribute to diseases involving this species. Findings No sialidase activity was detected by spectrofluorometric assay of 15 laboratory strains and 91 clinical isolates of M. pneumoniae banked over many years from patients having radiologically-confirmed, uncomplicated community-acquired pneumonia. Conclusions The annotated genome of strain M129 (GenBank NC_000912, ATCC 29342), also isolated from a patient with pneumonia, accurately represents the absence of sialidase genes from strains of M. pneumoniae typically associated with uncomplicated community-acquired pneumonia. A possible involvement of sialidase in neurologic or other extra-respiratory manifestations of M. pneumoniae mycoplasmosis remains to be investigated.</p

Brown Daniel R

May Meghan

Directory of Open Access Journals

BMC Research Notes

Retrospective survey for sialidase activity in <it>Mycoplasma pneumoniae </it>isolates from cases of community-acquired pneumonia

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SHORT REPORT Open AccessRetrospective survey for sialidase activity inMycoplasma pneumoniae isolates from casesof community-acquired pneumoniaMeghan May1† and Daniel R Brown2*†AbstractBackground: Sialidase is a well-known virulence factor of other respiratory pathogens, but was only recentlydocumented to occur in some species of Mycoplasma. The sialidase activity expressed can vary quantitativelyamong strains within a species of mycoplasma, from undetectable to amounts that correlate positively with strainvirulence. Very few isolates of Mycoplasma pneumoniae had ever been examined for sialidase activity, so it wasunknown whether sialidase may contribute to diseases involving this species.Findings: No sialidase activity was detected by spectrofluorometric assay of 15 laboratory strains and 91 clinicalisolates of M. pneumoniae banked over many years from patients having radiologically-confirmed, uncomplicatedcommunity-acquired pneumonia.Conclusions: The annotated genome of strain M129 (GenBank NC_000912, ATCC 29342), also isolated from apatient with pneumonia, accurately represents the absence of sialidase genes from strains of M. pneumoniaetypically associated with uncomplicated community-acquired pneumonia. A possible involvement of sialidase inneurologic or other extra-respiratory manifestations of M. pneumoniae mycoplasmosis remains to be investigated.FindingsResearch objectiveMycoplasma pneumoniae is primarily associated withinterstitial pneumonitis, tracheobronchitis, desquamativebronchitis and pharyngitis, collectively referred to as pri-mary atypical pneumonia (PAP) [1,2]. Mycoplasmosisaccounts for 20 - 30% of community-acquired pneumo-nia (CAP) cases, constituting significant disease and eco-nomic burdens in North America and Western Europe.Following its initial association with PAP, other diseasesinvolving M. pneumoniae invasion of non-respiratorytissues were reported [Table 1]. Neurologic, dermal,hemotropic, cardiac, arthritic, hepatic, pancreatic,nephritic, and musculoskeletal pathologies have beendescribed[2-12]; many of those diseases occurred secon-darily to PAP, either through dissemination of M. pneu-moniae from the respiratory tract, or followingassociated autoimmune disorders [3]. Primary extra-respiratory M. pneumoniae infections in the absence ofPAP, including meningoencephalitis, hepatitis, andpancreatitis, have also been described [13,14], andM. pneumoniae has been isolated from the urogenitaltract in the absence of clinical signs.The majority of studies on clinical aspects of M. pneu-moniae mycoplasmosis address the diagnosis, treatmentand prevention of CAP, while factors predisposing toextra-respiratory diseases remain virtually unexplored.Extracellular “spreading factors” like sialidase are well-known virulence determinants of other pathogenicmicroorganisms, and are targets for chemotherapy indiseases such as influenza. Sialidase is associated withsystemic dissemination during infection with many bac-terial species, most notably Streptococcus pneumoniaeand Clostridium perfringens, but such glycosidases wereonly recently documented to occur in certain species ofMycoplasma. The sialidase activity expressed by myco-plasmas can vary significantly among strains within aspecies, from undetectable to amounts that correlatepositively with strain virulence. Very few isolates of* Correspondence: drbrown@ufl.edu† Contributed equally2Department of Infectious Diseases and Pathology, College of VeterinaryMedicine, University of Florida, Gainesville FL, USAFull list of author information is available at the end of the articleMay and Brown BMC Research Notes 2011, 4:195http://www.biomedcentral.com/1756-0500/4/195© 2011 Brown et al; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative CommonsAttribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction inany medium, provided the original work is properly cited.M. pneumoniae have been examined for sialidase activ-ity, so it was unknown whether sialidase may contributeeither to PAP or to extra-respiratory diseases involvingthis species. To establish the baseline frequency of itsoccurrance in M. pneumoniae, we conducted a retro-spective survey for sialidase activity in clinical isolatesassociated with respiratory mycoplasmosis.MethodsFifteen laboratory strains of M. pneumoniae, includingthe well-known virulent strain PI1428 (American TypeCulture Collection accession number 29085, from apatient with PAP), SAD03, SAD05, TW11-4, 1RCH,9RCH, 11-61, 104.2, 142-48, 256-8, 541-6, 541-29, 1161,1311 and 15531, plus 91 clinical isolates from cases ofradiologically-confirmed interstitial pneumonia weretested. The de-identified clinical isolates had beenbanked over a period of many years from patients diag-nosed with CAP at various locations in the US. Theywere isolated from four distinct sites in the respiratorytract: 61 were from throat swabs, 4 from nasal swabs, 17from sputum, and 9 from bronchoalveolar lavage fluid.The latter were considered by clinicians to be invasivebecause they were from patients hospitalized with severepneumonia. It was unknown whether any of the patientshad been diagnosed as having pneumonia attributablesolely to M. pneumoniae, or had been treated empiri-cally with viral neuraminidase inhibitors.Frozen stocks of mycoplasma were passaged one timein SP-4 medium supplemented with 10% w/v glucoseand 15% v/v fetal bovine serum at 37°C in ambient air.Sialidase activity of M. pneumoniae cells suspended inconditioned medium was assessed using the fluorogenicsubstrate 2’-(4-methylumbelliferyl)-a-D-N-acetylneura-minic acid (MUAN) as previously described [15]. Briefly,50 μl of stationary phase cultures were added to 50 μlof 0.35% w/v MUAN in 30 mM sodium acetate buffer,pH 4.5. Following 60 min incubation at room tempera-ture, fluorescence at 450 nm was quantitated using aspectrofluorometer (excitation at 350 nm; cutoff filter at420 nm). The positive controls were Mycoplasma alliga-toris strain A21JP2T, which expresses a cell-associatedsialidase [16], and Type VI sialidase purified from Clos-tridium perfringens. The negative controls were Myco-plasma crocodyli strain MP145T, which does not expressany sialidase, and fresh culture medium.ResultsNo sialidase activity was detected in any specimen, thusthere was no evidence that the enzyme contributes toPAP involving M. pneumoniae. However, the undocu-mented clinical significance of M. pneumoniae isolationfrom these patients is a recognized weakness of thisstudy. It seems unlikely that potential empiric treatmentwith viral neuraminidase inhibitors strictly precludedisolation of sialidase-positive strains of M. pneumoniaeTable 1 Diverse outcomes associated with Mycoplasma pneumoniae infectionaAural Dermal Musculoskeletal• otitis externa • bullous exanthema • reactive arthritis• otitis media • cutaneous vasculitis • rhabdomyolysis• myringitis • erythema nodosum • septic arthritisCardiac • Stevens-Johnson syndrome Ocular• arrhythmia • ulcerative stomatitis • conjunctivitis• myocarditis • urticaria • iritis• pericardial effusion • vesicular rash • retinitis• pericarditis Gastrointestinal • uveitisCentral nervous system • hepatitis Renal• ataxia • pancreatitis • glomerulonephritis• Bell’s palsy Hematologic • IgA nephropathy• choreoathetosis • aplastic anemia • interstitial nephritis• encephalitis • hemolytic anemia Respiratory• encephalomyelitis • hemophagocytosis • primary atypical pneumonia• Guillain-Barre- syndrome • intravascular coagulation• meningoencephalitis • lymphadenopathy• meningitis • neutropenia• paralysis • neutrophilia• polyradiculitis • septicemia• psychosis • thrombocytopeniaa The primary disease state generated by M. pneumoniae infection is PAP, although many additional clinical manifestations have been reported [2].Mycoplasmosis due to M. pneumoniae affects numerous organ systems by generating primary lesions in non-respiratory tissues or secondary lesions followingpresumed hematogenous spread from the respiratory tract, or by contributing to autoimmune-related disorders. Differences in bacterial or host phenotypes thatexplain the diverse clinical outcomes remain essentially unknown.May and Brown BMC Research Notes 2011, 4:195http://www.biomedcentral.com/1756-0500/4/195Page 2 of 3from any of these patients, but this remains to be defini-tively established.The ability of certain M. pneumoniae strains to causeextra-respiratory mycoplasmosis may require additionalcellular functions, which can be genetically acquired invivo from the polymicrobial community within thehuman host. The presence of bacterial spreading factorssuch as sialidase might explain the differences in clinicalmanifestations of infection with certain strains of M.pneumoniae. Sialidase is a prominent candidate for thisbecause of its well-documented tendency to be horizon-tally transferred among bacteria [17]. In addition, quan-titative variation of sialidase activity among strains ofother pathogenic mycoplasmas ranges from undetectableto extremely high in significant correlation with straininvasiveness [18]. A possible involvement of sialidase inneurologic or other manifestations of invasive diseaseremains to be investigated, but a bank of those lesscommon specimens will be required to determinewhether PAP-associated strains are less likely to expresssialidase activity than strains associated with other out-comes of M. pneumoniae mycoplasmosis. We concludethat the annotated genome of the well-known virulentstrain M129 (GenBank accession number NC_000912),also isolated from a patient with pneumonia (AmericanType Culture Collection accession number 29342), accu-rately represents the absence of sialidase genes fromstrains of M. pneumoniae typically associated withuncomplicated PAP.AcknowledgementsThe clinical isolates of M. pneumoniae were obtained from Dr. Ken B. Waitesof the University of Alabama at Birmingham, Birmingham AL, USA, andhandled in accordance with a protocol approved by the University ofFlorida’s Institutional Review Board (UF IRB # 89-2009). We thank DinaDemcovitz, Amy Ratliff and Lynn Duffy for technical assistance. This workwas supported by Public Health Service grant 1R01GM076584 from the USNational Institute of General Medical Sciences (DRB). Publication of thisarticle was funded in part by the University of Florida Open-AccessPublishing Fund.Author details1Department of Biological Sciences, Towson University, Towson MD, USA.2Department of Infectious Diseases and Pathology, College of VeterinaryMedicine, University of Florida, Gainesville FL, USA.Authors’ contributionsMM jointly conceived the study and participated in study design; collected,analyzed and interpreted the data; and drafted the manuscript. DRB jointlyconceived the study and participated in study design; reviewed the dataanalysis and interpretation; and revised the manuscript for importantintellectual content. Both authors have read and approved the final versionof the manuscript.Competing interestsThe authors declare that they have no competing interests.Received: 5 January 2011 Accepted: 15 June 2011Published: 15 June 2011References1. Krause DC, Taylor-Robinson D: Mycoplasmas which infect humans. InMycoplasmas: Molecular Biology and Pathogenesis. Edited by: Maniloff J.Washington, DC, American Society for Microbiology Press; 1992:417-444.2. Waites K, Talkington D: New developments in human diseases due tomycoplasmas. In Mycoplasmas: Molecular Biology, Pathogenicity, andStrategies for Control. Edited by: Blanchard A, Browning GF. Norfolk, HorizonBioscience; 2005:289-354.3. Atkinson TP, Balish MF, Waites KB: Epidemiology, clinical manifestations,pathogenesis and laboratory detection of Mycoplasma pneumoniaeinfections. FEMS Microbiol Rev 2008, 32:956-973.4. Freeman R, McMahon M: Acute pancreatitis and serological evidence ofinfection with Mycoplasma pneumoniae. Gut 1978, 19:367-370.5. Arav-Boger R, Assia A, Spirer Z, Bujanover Y, Reif S: Cholestatic hepatitis asa main manifestation of Mycoplasma pneumoniae infection. J PediatrGastroenterol Nutr 1995, 21:459-460.6. Daxboeck F, Blacky A, Seidl R, Krause R, Assadian O: Diagnosis, treatment,and prognosis of Mycoplasma pneumoniae childhood encephalitis:systematic review of 58 cases. J Child Neurol 2004, 19:865-871.7. al-Abassi A: Acute pancreatitis associated with Mycoplasma pneumoniae:a case report of missed diagnosis. Med Princ Pract 2002, 11:112-115.8. Vic P, Blondin G, Blayo M, Finel E, Daaboul M, Queinnec C, Broussine L:Pancréatite aiguë et infection à Mycoplasma pneumoniae [Acutepancreatitis and Mycoplasma pneumoniae infection]. Arch Pediatr 2004,11:154.9. Del Castillo M, D’Giano C, Goicoechea M, Morello F, Salsamendi P, Mora A:Mycoplasma pneumoniae meningoencephalitis in a young adult.Medicina (B Aires) 2005, 65:338-340.10. Stamm B, Moschopulos M, Hungerbuehler H, Guarner J, Genrich G, Zaki S:Neuroinvasion by Mycoplasma pneumoniae in acute disseminatedencephalomyelitis. Emerg Infect Dis 2008, 14:641-643.11. Walter ND, Grant GB, Bandy U, Alexander NE, Winchell JM, Jordan HT,Sejvar JJ, Hicks LA, Gifford DR, Alexander NT, Thurman KA, Schwartz SB,Dennehy PH, Khetsuriani N, Fields BS, Dillon MT, Erdman DD, Whitney CG,Moore MR: Community outbreak of Mycoplasma pneumoniae infection:school-based cluster of neurologic disease associated with householdtransmission of respiratory illness. J Infect Dis 2008, 198:1365-1374.12. Lee S, Yang S, Chang C, Yeh H, Chow W: Mycoplasma pneumoniae-associated acute hepatitis in an adult patient without lung infection. JChin Med Assoc 2009, 72:204-206.13. Narita M, Yamada S, Nakayama T, Sawada H, Nakajima M, Sageshima S: Twocases of lymphadenopathy with liver dysfunction due to Mycoplasmapneumoniae infection with mycoplasmal bacteraemia withoutpneumonia. J Infect 2001, 42:154-156.14. Romero-Gómez M, Otero MA, Sánchez-Muñoz D, Ramírez-Arcos M,Larraona JL, Suárez García E, Vargas-Romero J: Acute hepatitis due toMycoplasma pneumoniae infection without lung involvement in adultpatients. J Hepatol 2006, 44:827-828.15. May M, Brown DR: Secreted sialidase activity of canine mycoplasmas. VetMicrobiol 2009, 137:380-383.16. Brown DR, Zacher LA, Farmerie WG: Spreading factors of Mycoplasmaalligatoris, a flesh-eating mycoplasma. J Bacteriol 2004, 186:3922-3927.17. Roggentin P, Schauer R, Hoyer L, Vimr E: The sialidase superfamily and itsspread by horizontal gene transfer. Mol Microbiol 1993, 9:915-921.18. May M, Kleven SH, Brown DR: Sialidase activity in Mycoplasma synoviae.Avian Dis 2007, 51:829-833.doi:10.1186/1756-0500-4-195Cite this article as: May and Brown: Retrospective survey for sialidaseactivity in Mycoplasma pneumoniae isolates from cases of community-acquired pneumonia. BMC Research Notes 2011 4:195.May and Brown BMC Research Notes 2011, 4:195http://www.biomedcentral.com/1756-0500/4/195Page 3 of 3

Retrospective survey for sialidase activity in Mycoplasma pneumoniae isolates from cases of community-acquired pneumonia

Springer - Publisher Connector

SHORT REPORT Open Access
Retrospective survey for sialidase activity in
Mycoplasma pneumoniae isolates from cases
of community-acquired pneumonia
Meghan May1† and Daniel R Brown2*†
Abstract
Background: Sialidase is a well-known virulence factor of other respiratory pathogens, but was only recently
documented to occur in some species of Mycoplasma. The sialidase activity expressed can vary quantitatively
among strains within a species of mycoplasma, from undetectable to amounts that correlate positively with strain
virulence. Very few isolates of Mycoplasma pneumoniae had ever been examined for sialidase activity, so it was
unknown whether sialidase may contribute to diseases involving this species.
Findings: No sialidase activity was detected by spectrofluorometric assay of 15 laboratory strains and 91 clinical
isolates of M. pneumoniae banked over many years from patients having radiologically-confirmed, uncomplicated
community-acquired pneumonia.
Conclusions: The annotated genome of strain M129 (GenBank NC_000912, ATCC 29342), also isolated from a
patient with pneumonia, accurately represents the absence of sialidase genes from strains of M. pneumoniae
typically associated with uncomplicated community-acquired pneumonia. A possible involvement of sialidase in
neurologic or other extra-respiratory manifestations of M. pneumoniae mycoplasmosis remains to be investigated.
Findings
Research objective
Mycoplasma pneumoniae is primarily associated with
interstitial pneumonitis, tracheobronchitis, desquamative
bronchitis and pharyngitis, collectively referred to as pri-
mary atypical pneumonia (PAP) [1,2]. Mycoplasmosis
accounts for 20 - 30% of community-acquired pneumo-
nia (CAP) cases, constituting significant disease and eco-
nomic burdens in North America and Western Europe.
Following its initial association with PAP, other diseases
involving M. pneumoniae invasion of non-respiratory
tissues were reported [Table 1]. Neurologic, dermal,
hemotropic, cardiac, arthritic, hepatic, pancreatic,
nephritic, and musculoskeletal pathologies have been
described[2-12]; many of those diseases occurred secon-
darily to PAP, either through dissemination of M. pneu-
moniae from the respiratory tract, or following
associated autoimmune disorders [3]. Primary extra-
respiratory M. pneumoniae infections in the absence of
PAP, including meningoencephalitis, hepatitis, and
pancreatitis, have also been described [13,14], and
M. pneumoniae has been isolated from the urogenital
tract in the absence of clinical signs.
The majority of studies on clinical aspects of M. pneu-
moniae mycoplasmosis address the diagnosis, treatment
and prevention of CAP, while factors predisposing to
extra-respiratory diseases remain virtually unexplored.
Extracellular “spreading factors” like sialidase are well-
known virulence determinants of other pathogenic
microorganisms, and are targets for chemotherapy in
diseases such as influenza. Sialidase is associated with
systemic dissemination during infection with many bac-
terial species, most notably Streptococcus pneumoniae
and Clostridium perfringens, but such glycosidases were
only recently documented to occur in certain species of
Mycoplasma. The sialidase activity expressed by myco-
plasmas can vary significantly among strains within a
species, from undetectable to amounts that correlate
positively with strain virulence. Very few isolates of
* Correspondence: drbrown@ufl.edu
† Contributed equally
2Department of Infectious Diseases and Pathology, College of Veterinary
Medicine, University of Florida, Gainesville FL, USA
Full list of author information is available at the end of the article
May and Brown BMC Research Notes 2011, 4:195
http://www.biomedcentral.com/1756-0500/4/195
© 2011 Brown et al; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properly cited.
M. pneumoniae have been examined for sialidase activ-
ity, so it was unknown whether sialidase may contribute
either to PAP or to extra-respiratory diseases involving
this species. To establish the baseline frequency of its
occurrance in M. pneumoniae, we conducted a retro-
spective survey for sialidase activity in clinical isolates
associated with respiratory mycoplasmosis.
Methods
Fifteen laboratory strains of M. pneumoniae, including
the well-known virulent strain PI1428 (American Type
Culture Collection accession number 29085, from a
patient with PAP), SAD03, SAD05, TW11-4, 1RCH,
9RCH, 11-61, 104.2, 142-48, 256-8, 541-6, 541-29, 1161,
1311 and 15531, plus 91 clinical isolates from cases of
radiologically-confirmed interstitial pneumonia were
tested. The de-identified clinical isolates had been
banked over a period of many years from patients diag-
nosed with CAP at various locations in the US. They
were isolated from four distinct sites in the respiratory
tract: 61 were from throat swabs, 4 from nasal swabs, 17
from sputum, and 9 from bronchoalveolar lavage fluid.
The latter were considered by clinicians to be invasive
because they were from patients hospitalized with severe
pneumonia. It was unknown whether any of the patients
had been diagnosed as having pneumonia attributable
solely to M. pneumoniae, or had been treated empiri-
cally with viral neuraminidase inhibitors.
Frozen stocks of mycoplasma were passaged one time
in SP-4 medium supplemented with 10% w/v glucose
and 15% v/v fetal bovine serum at 37°C in ambient air.
Sialidase activity of M. pneumoniae cells suspended in
conditioned medium was assessed using the fluorogenic
substrate 2’-(4-methylumbelliferyl)-a-D-N-acetylneura-
minic acid (MUAN) as previously described [15]. Briefly,
50 μl of stationary phase cultures were added to 50 μl
of 0.35% w/v MUAN in 30 mM sodium acetate buffer,
pH 4.5. Following 60 min incubation at room tempera-
ture, fluorescence at 450 nm was quantitated using a
spectrofluorometer (excitation at 350 nm; cutoff filter at
420 nm). The positive controls were Mycoplasma alliga-
toris strain A21JP2T, which expresses a cell-associated
sialidase [16], and Type VI sialidase purified from Clos-
tridium perfringens. The negative controls were Myco-
plasma crocodyli strain MP145T, which does not express
any sialidase, and fresh culture medium.
Results
No sialidase activity was detected in any specimen, thus
there was no evidence that the enzyme contributes to
PAP involving M. pneumoniae. However, the undocu-
mented clinical significance of M. pneumoniae isolation
from these patients is a recognized weakness of this
study. It seems unlikely that potential empiric treatment
with viral neuraminidase inhibitors strictly precluded
isolation of sialidase-positive strains of M. pneumoniae
Table 1 Diverse outcomes associated with Mycoplasma pneumoniae infectiona
Aural Dermal Musculoskeletal
• otitis externa • bullous exanthema • reactive arthritis
• otitis media • cutaneous vasculitis • rhabdomyolysis
• myringitis • erythema nodosum • septic arthritis
Cardiac • Stevens-Johnson syndrome Ocular
• arrhythmia • ulcerative stomatitis • conjunctivitis
• myocarditis • urticaria • iritis
• pericardial effusion • vesicular rash • retinitis
• pericarditis Gastrointestinal • uveitis
Central nervous system • hepatitis Renal
• ataxia • pancreatitis • glomerulonephritis
• Bell’s palsy Hematologic • IgA nephropathy
• choreoathetosis • aplastic anemia • interstitial nephritis
• encephalitis • hemolytic anemia Respiratory
• encephalomyelitis • hemophagocytosis • primary atypical pneumonia
• Guillain-Barre- syndrome • intravascular coagulation
• meningoencephalitis • lymphadenopathy
• meningitis • neutropenia
• paralysis • neutrophilia
• polyradiculitis • septicemia
• psychosis • thrombocytopenia
a The primary disease state generated by M. pneumoniae infection is PAP, although many additional clinical manifestations have been reported [2].
Mycoplasmosis due to M. pneumoniae affects numerous organ systems by generating primary lesions in non-respiratory tissues or secondary lesions following
presumed hematogenous spread from the respiratory tract, or by contributing to autoimmune-related disorders. Differences in bacterial or host phenotypes that
explain the diverse clinical outcomes remain essentially unknown.
May and Brown BMC Research Notes 2011, 4:195
http://www.biomedcentral.com/1756-0500/4/195
Page 2 of 3
from any of these patients, but this remains to be defini-
tively established.
The ability of certain M. pneumoniae strains to cause
extra-respiratory mycoplasmosis may require additional
cellular functions, which can be genetically acquired in
vivo from the polymicrobial community within the
human host. The presence of bacterial spreading factors
such as sialidase might explain the differences in clinical
manifestations of infection with certain strains of M.
pneumoniae. Sialidase is a prominent candidate for this
because of its well-documented tendency to be horizon-
tally transferred among bacteria [17]. In addition, quan-
titative variation of sialidase activity among strains of
other pathogenic mycoplasmas ranges from undetectable
to extremely high in significant correlation with strain
invasiveness [18]. A possible involvement of sialidase in
neurologic or other manifestations of invasive disease
remains to be investigated, but a bank of those less
common specimens will be required to determine
whether PAP-associated strains are less likely to express
sialidase activity than strains associated with other out-
comes of M. pneumoniae mycoplasmosis. We conclude
that the annotated genome of the well-known virulent
strain M129 (GenBank accession number NC_000912),
also isolated from a patient with pneumonia (American
Type Culture Collection accession number 29342), accu-
rately represents the absence of sialidase genes from
strains of M. pneumoniae typically associated with
uncomplicated PAP.
Acknowledgements
The clinical isolates of M. pneumoniae were obtained from Dr. Ken B. Waites
of the University of Alabama at Birmingham, Birmingham AL, USA, and
handled in accordance with a protocol approved by the University of
Florida’s Institutional Review Board (UF IRB # 89-2009). We thank Dina
Demcovitz, Amy Ratliff and Lynn Duffy for technical assistance. This work
was supported by Public Health Service grant 1R01GM076584 from the US
National Institute of General Medical Sciences (DRB). Publication of this
article was funded in part by the University of Florida Open-Access
Publishing Fund.
Author details
1Department of Biological Sciences, Towson University, Towson MD, USA.
2Department of Infectious Diseases and Pathology, College of Veterinary
Medicine, University of Florida, Gainesville FL, USA.
Authors’ contributions
MM jointly conceived the study and participated in study design; collected,
analyzed and interpreted the data; and drafted the manuscript. DRB jointly
conceived the study and participated in study design; reviewed the data
analysis and interpretation; and revised the manuscript for important
intellectual content. Both authors have read and approved the final version
of the manuscript.
Competing interests
The authors declare that they have no competing interests.
Received: 5 January 2011 Accepted: 15 June 2011
Published: 15 June 2011
References
1. Krause DC, Taylor-Robinson D: Mycoplasmas which infect humans. In
Mycoplasmas: Molecular Biology and Pathogenesis. Edited by: Maniloff J.
Washington, DC, American Society for Microbiology Press; 1992:417-444.
2. Waites K, Talkington D: New developments in human diseases due to
mycoplasmas. In Mycoplasmas: Molecular Biology, Pathogenicity, and
Strategies for Control. Edited by: Blanchard A, Browning GF. Norfolk, Horizon
Bioscience; 2005:289-354.
3. Atkinson TP, Balish MF, Waites KB: Epidemiology, clinical manifestations,
pathogenesis and laboratory detection of Mycoplasma pneumoniae
infections. FEMS Microbiol Rev 2008, 32:956-973.
4. Freeman R, McMahon M: Acute pancreatitis and serological evidence of
infection with Mycoplasma pneumoniae. Gut 1978, 19:367-370.
5. Arav-Boger R, Assia A, Spirer Z, Bujanover Y, Reif S: Cholestatic hepatitis as
a main manifestation of Mycoplasma pneumoniae infection. J Pediatr
Gastroenterol Nutr 1995, 21:459-460.
6. Daxboeck F, Blacky A, Seidl R, Krause R, Assadian O: Diagnosis, treatment,
and prognosis of Mycoplasma pneumoniae childhood encephalitis:
systematic review of 58 cases. J Child Neurol 2004, 19:865-871.
7. al-Abassi A: Acute pancreatitis associated with Mycoplasma pneumoniae:
a case report of missed diagnosis. Med Princ Pract 2002, 11:112-115.
8. Vic P, Blondin G, Blayo M, Finel E, Daaboul M, Queinnec C, Broussine L:
Pancréatite aiguë et infection à Mycoplasma pneumoniae [Acute
pancreatitis and Mycoplasma pneumoniae infection]. Arch Pediatr 2004,
11:154.
9. Del Castillo M, D’Giano C, Goicoechea M, Morello F, Salsamendi P, Mora A:
Mycoplasma pneumoniae meningoencephalitis in a young adult.
Medicina (B Aires) 2005, 65:338-340.
10. Stamm B, Moschopulos M, Hungerbuehler H, Guarner J, Genrich G, Zaki S:
Neuroinvasion by Mycoplasma pneumoniae in acute disseminated
encephalomyelitis. Emerg Infect Dis 2008, 14:641-643.
11. Walter ND, Grant GB, Bandy U, Alexander NE, Winchell JM, Jordan HT,
Sejvar JJ, Hicks LA, Gifford DR, Alexander NT, Thurman KA, Schwartz SB,
Dennehy PH, Khetsuriani N, Fields BS, Dillon MT, Erdman DD, Whitney CG,
Moore MR: Community outbreak of Mycoplasma pneumoniae infection:
school-based cluster of neurologic disease associated with household
transmission of respiratory illness. J Infect Dis 2008, 198:1365-1374.
12. Lee S, Yang S, Chang C, Yeh H, Chow W: Mycoplasma pneumoniae-
associated acute hepatitis in an adult patient without lung infection. J
Chin Med Assoc 2009, 72:204-206.
13. Narita M, Yamada S, Nakayama T, Sawada H, Nakajima M, Sageshima S: Two
cases of lymphadenopathy with liver dysfunction due to Mycoplasma
pneumoniae infection with mycoplasmal bacteraemia without
pneumonia. J Infect 2001, 42:154-156.
14. Romero-Gómez M, Otero MA, Sánchez-Muñoz D, Ramírez-Arcos M,
Larraona JL, Suárez García E, Vargas-Romero J: Acute hepatitis due to
Mycoplasma pneumoniae infection without lung involvement in adult
patients. J Hepatol 2006, 44:827-828.
15. May M, Brown DR: Secreted sialidase activity of canine mycoplasmas. Vet
Microbiol 2009, 137:380-383.
16. Brown DR, Zacher LA, Farmerie WG: Spreading factors of Mycoplasma
alligatoris, a flesh-eating mycoplasma. J Bacteriol 2004, 186:3922-3927.
17. Roggentin P, Schauer R, Hoyer L, Vimr E: The sialidase superfamily and its
spread by horizontal gene transfer. Mol Microbiol 1993, 9:915-921.
18. May M, Kleven SH, Brown DR: Sialidase activity in Mycoplasma synoviae.
Avian Dis 2007, 51:829-833.
doi:10.1186/1756-0500-4-195
Cite this article as: May and Brown: Retrospective survey for sialidase
activity in Mycoplasma pneumoniae isolates from cases of community-
acquired pneumonia. BMC Research Notes 2011 4:195.
May and Brown BMC Research Notes 2011, 4:195
http://www.biomedcentral.com/1756-0500/4/195
Page 3 of 3


A: Mycoplasma pneumoniae meningoencephalitis in a young adult. Medicina (B Aires)

Acute pancreatitis and serological evidence of infection with Mycoplasma pneumoniae. Gut

Acute pancreatitis associated with Mycoplasma pneumoniae: a case report of missed diagnosis. Med Princ Pract

Assadian O: Diagnosis, treatment, and prognosis of Mycoplasma pneumoniae childhood encephalitis: systematic review of 58 cases.

DR: Secreted sialidase activity of canine mycoplasmas. Vet Microbiol

DR: Sialidase activity in Mycoplasma synoviae. Avian Dis

Farmerie WG: Spreading factors of Mycoplasma alligatoris, a flesh-eating mycoplasma.

KB: Epidemiology, clinical manifestations, pathogenesis and laboratory detection of Mycoplasma pneumoniae infections. FEMS Microbiol Rev

MR: Community outbreak of Mycoplasma pneumoniae infection: school-based cluster of neurologic disease associated with household transmission of respiratory illness.

Mycoplasma pneumoniaeassociated acute hepatitis in an adult patient without lung infection. J Chin Med Assoc

Pancréatite aiguë et infection à Mycoplasma pneumoniae [Acute pancreatitis and Mycoplasma pneumoniae infection]. Arch Pediatr

Reif S: Cholestatic hepatitis as a main manifestation of Mycoplasma pneumoniae infection.

S: Neuroinvasion by Mycoplasma pneumoniae in acute disseminated encephalomyelitis. Emerg Infect Dis

Suárez García E, Vargas-Romero J: Acute hepatitis due to Mycoplasma pneumoniae infection without lung involvement in adult patients.

Talkington D: New developments in human diseases due to mycoplasmas. In Mycoplasmas: Molecular Biology, Pathogenicity, and Strategies for Control. Edited by: Blanchard A, Browning GF.

Taylor-Robinson D: Mycoplasmas which infect humans. In Mycoplasmas: Molecular Biology and Pathogenesis. Edited by: Maniloff

Two cases of lymphadenopathy with liver dysfunction due to Mycoplasma pneumoniae infection with mycoplasmal bacteraemia without pneumonia.

Vimr E: The sialidase superfamily and its spread by horizontal gene transfer. Mol Microbiol

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3138463

Retrospective survey for sialidase activity in Mycoplasma pneumoniae isolates from cases of community-acquired pneumonia

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