Mycoplasmas in the etiology of multifactorial respiratory disease

Kleven, S. H.

doi:10.1093/ps/77.8.1146

Cited by 146 publications

(97 citation statements)

References 41 publications

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“…Infection can produce disease that ranges from subclinical to severe, and clinical outcome can be influenced by co-infection with other agents [4,5,6,7,8]. The majority of prior studies have focused on cytadherence and/or hemadsorption as pathogenic mechanisms of M. synoviae, with particular attention to antigenically-variable hemagglutinins, although the molecular basis of M. synoviae pathogenicity is still not well-understood [9,10].…”

Section: Introductionmentioning

confidence: 99%

Genetic variation in sialidase and linkage to N-acetylneuraminate catabolism in Mycoplasma synoviae

May

Brown

2008

Microbial Pathogenesis

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We explored the genetic basis for intraspecific variation in mycoplasmal sialidase activity that correlates with virulence, and its potentially advantageous linkage to nutrient catabolism. Polymorphism in N-acetylneuraminate scavenging and degradation genes (sialidase, Nacetylneuraminate lyase, N-acetylmannosamine kinase, N-acetylmannosamine-6-phosphate epimerase, N-acetylglucosamine-6-phosphate deacetylase, and glucosamine-6-phosphate deaminase) was evident among eight strains of the avian pathogen Mycoplasma synoviae. Most differences were single nucleotide polymorphisms, ranging from 0.34 ± 0.04 substitutions per 100 bp for N-acetylmannosamine kinase to 0.65 ± 0.03 for the single-copy sialidase gene nanI. Missense mutations were twice as common as silent mutations in nanI; 26% resulted in amino acids dissimilar to consensus; and there was a 12-base deletion near the nanI promoter in strain WVU1853 T , supporting a complex genetic basis for differences in sialidase activity. Two strains had identical frameshifts in the N-acetylneuraminate lyase gene nanA, resulting in nonsense mutations, and both had downstream deletions in nanA. Such genetic lesions uncouple extracellular liberation of sialic acid from generation of fructose-6-phosphate and pyruvate via intracellular N-acetylneuraminate degradation. Retention of nanI by such strains, but not others in the M. synoviae phylogenetic cluster, is evidence that sialidase has an important non-nutritional role in the ecology of M. synoviae and certain other mycoplasmas.

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Section: Introductionmentioning

confidence: 99%

Genetic variation in sialidase and linkage to N-acetylneuraminate catabolism in Mycoplasma synoviae

May

Brown

2008

Microbial Pathogenesis

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“…Clinical manifestations vary by strain, and some appear to have a greater tropism for synovial membanes or the respiratory tract than others (21). Disease is often complicated by co-infection with other pathogens, most notably Newcastle disease virus, infectious bronchitis virus, infectious bursal disease virus, Escherichia coli, Mycoplasma gallisepticum and Mycoplasma meleagridis (11,20,32,37,38). The molecular basis of M. synoviae virulence is not well-understood.…”

Section: Introductionmentioning

confidence: 99%

Sialidase Activity in Mycoplasma Synoviae

May¹,

Kleven

Brown³

2007

Avian Diseases

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SUMMARYEleven strains of the avian pathogen Mycoplasma synoviae were evaluated for the presence of sialidase activity by using the fluorogenic substrate 2′-(4-methylumbelliferyl)-α-D-Nacetylneuraminic acid and the sialidase inhibitor 2-deoxy-2,3-didehydro-N-acetylneuraminic acid. The kinetics of in vitro growth in modified Frey's medium were also assessed for each strain. Five strains had been isolated from clinically symptomatic chickens, and strains WVU1853 T and K3344 have been demonstrated to be capable of reproducing disease in specific pathogen-free chickens. All strains exhibited sialidase activity, although the amount varied 65 fold (P < 0.0001) from 1.3 x 10 −7 to 2.0 x 10 −9 activity units/colony-forming unit among strains. Strains originally isolated from clinically symptomatic birds had more (P < 0.05) sialidase activity than strains from asymptomatic birds. Strain WVU1853 T exhibited the most sialidase activity (P < 0.0001) and grew to the highest culture density (P < 0.0001) among strains, but across strains the rank correlation of growth rate with sialidase activity was not significant. Negligible activity was detected in conditioned culture supernatant fluid. This is the first report of sialidase activity in pathogenic strains of M. synoviae, which suggests a potential enzymatic basis for virulence of the organism.

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“…Notably, penicillin G-exposed Chlamydiae can reenter the normal developmental cycle upon drug removal ( There might be a pathogenic interaction between C. psittaci and other viral and/or bacterial respiratory pathogens. Interactions between respiratory pathogens have already been demonstrated for M. gallisepticum and NDV in experimentally infected chickens (reviewed by Kleven, 1998) The presence of C. psittaci in empty barns and in 1-day-old broilers remains intriguing. Vertical transmission occurs in chickens (Wittenbrink et al, 1993) and bio-aerosol monitoring during hatching revealed increasing numbers of C. psittaci (Dickx & Vanrompay, 2011).…”

Section: Discussionmentioning

confidence: 99%

Longitudinal monitoring for respiratory pathogens in broiler chickens reveals co-infection of Chlamydia psittaci and Ornithobacterium rhinotracheale

Boeck

Kalmar

Dumont

et al. 2015

Journal of Medical Microbiology

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Chlamydia psittaci is prevalent in broiler chicken production. However, the role of C. psittaci in the respiratory disease complex needs to be clarified. Our aim was to identify the time point when a C. psittaci infection appeared on a broiler farm and to examine the presence of other respiratory pathogens at that time. We focused on the 'major' respiratory pathogens occurring in Belgian broilers, namely infectious bronchitis virus (IBV), avian metapneumovirus (aMPV), Ornithobacterium rhinotracheale, Mycoplasma gallisepticum and Mycoplasma synoviae, and examined their co-occurrence with C. psittaci on three commercial broiler farms. For all farms, 1-day-old broilers showed high maternal antibody titres against C. psittaci in the presence of viable C. psittaci. Maternal antibodies seemed to protect against respiratory signs. Maternal antibodies declined and clinical outbreaks could be identified serologically even before maternal antibodies completely disappeared. Mixed infections with genotypes B/C and B/C/D were observed. Broilers with C. psittaci antibody increases showed conjunctivitis, signs of upper respiratory disease and dyspnoea. C. psittaci always preceded an O. rhinotracheale infection. Infections with aMPV, IBV or Mycoplasma spp. were not observed. Evidence was provided that C. psittaci could occur at an early age in broilers without a predisposing respiratory infection. Both C. psittaci and O. rhinotracheale should be considered when developing prevention strategies for respiratory disease in broilers

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Mycoplasmas in the etiology of multifactorial respiratory disease

Cited by 146 publications

References 41 publications

Genetic variation in sialidase and linkage to N-acetylneuraminate catabolism in Mycoplasma synoviae

Genetic variation in sialidase and linkage to N-acetylneuraminate catabolism in Mycoplasma synoviae

Sialidase Activity in Mycoplasma Synoviae

Longitudinal monitoring for respiratory pathogens in broiler chickens reveals co-infection of Chlamydia psittaci and Ornithobacterium rhinotracheale

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