<i>Mycoplasma felis</i>-associated meningoencephalomyelitis in a cat

Beauchamp, Dustin J.; Costa, Ronaldo C. da; Premanandan, Christopher; Burns, Colby G.; Cui, Jing; Daniels, Joshua B.

doi:10.1016/j.jfms.2010.10.004

Cited by 12 publications

(10 citation statements)

References 24 publications

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“…Similar pathologies have been attributed to other species of mycoplasmas that gained entry into the brain (62)(63)(64). The profile of cytokine secretion by DH82 cells following exposure to M. canis isolates UF31 and UF33, characterized by high TNF-␣/IL-10 ratios, clearly contrasted with the responses to strains PG14 T , LV, and UFG1, characterized by high IL-10/IFN-␥ ratios (Fig.…”

Section: Discussionsupporting

confidence: 63%

Cellular Microbiology of Mycoplasma canis

et al. 2016

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M ycoplasma canis infects many mammalian hosts but is usually thought of as a commensal or opportunistic cofactor in respiratory or urogenital tract diseases of dogs (1). We found unexpectedly that M. canis was also detectable by culture or PCR in a majority of brain tissue specimens in a retrospective case-control study of canine granulomatous meningoencephalitis (ME) (GME) and necrotizing ME (NME) (2). The presence of M. canis in brain tissue was associated with both GME and NME (both P Ͻ 0.05, as determined by a 2 test). The clinical signs of this common idiopathic neurological disease of dogs include seizures, proprioceptive deficits, circling, and blindness. Immunosuppressive therapy may be palliative, but the syndrome is progressive and uniformly fatal (3). The extensive search for a presumed viral cause of canine GME and NME has been fruitless (4).In humans, bacterial meningitis and encephalitis are multifactorial lethal infections with often severe sequelae for survivors. New detection methods have shown that the variety of bacteria associated with human ME is much more extensive than usually appreciated (5-9). Additional animal models of bacterial ME are necessary to study this broader spectrum of pathogens (10). Since a possible association between M. canis and canine ME was discovered, our objective has been to help fill the void of basic knowledge about the organism's virulence factors, the host responses that it elicits, and its potential roles in pathogenesis. Our working hypotheses were that M. canis is capable of evoking host cell responses that favor dissemination from mucosal surfaces to secondary sites of infection, possibly in a strain-dependent fashion, and also that, regardless of how it might reach those sites, the presence of M. canis there modulates inflammation and direct injury to host cells. Understanding this potential can be expected to help evaluate the cause of canine ME and other diseases.(Portions of these data were presented in abstract form at Congresses of the International Organization for Mycoplasmology [90,91].) MATERIALS AND METHODSMycoplasma strains and cultivation. Strain PG14 T of M. canis (ATCC 19525) was first isolated from the throat of a normal dog (11). Strains UF31, UF33, LV, 5, 26, Cal, and Mara were first isolated from vaginal swabs of dogs without ME (12). Strains UFG1, UFG2, UFG3, and UFG4 were isolated from frozen brain tissues from cases of canine NME (2). Mycoplasma cynos strain H-831 T (ATCC 27544) was first isolated from the lung of a dog with pneumonia (13). Mycoplasma arginini strain G230 T , Mycoplasma bovigenitalium strain PG11 T , Mycoplasma edwardii strain PG24 T , Mycoplasma maculosum strain Skotti B, Mycoplasma molare strain H542 T , Mycoplasma opalescens strain MH5408 T , and Mycoplasma spumans strain PG13T , representing other species that have been isolated from dogs (1), were obtained from The Mollicutes Collection. All strains were propagated under standard conditions (14) in ATCC 988 medium supplemented with fetal bovine serum (FBS) and glu...

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Section: Discussionsupporting

confidence: 63%

Cellular Microbiology of Mycoplasma canis

et al. 2016

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“…Mycoplasmas have been infrequently associated with CNS disease and the virulence factors that would allow M . canis to invade and colonize the CNS are unknown.…”

Section: Discussionmentioning

confidence: 99%

Broadly Reactive Polymerase Chain Reaction for Pathogen Detection in Canine Granulomatous Meningoencephalomyelitis and Necrotizing Meningoencephalitis

Barber¹,

Porter

Li³

et al. 2012

Veterinary Internal Medicne

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Background: Granulomatous meningoencephalomyelitis (GME) and necrotizing meningoencephalitis (NME) are common inflammatory conditions of the central nervous system of dogs. Infectious pathogens, particularly viruses, are suspected to contribute to the etiopathogenesis of GME and NME.Hypothesis: Broadly reactive PCR might aid in the identification of infectious agents in GME and NME. Animals: Sixty-eight client-owned dogs evaluated by necropsy at 1 university referral hospital. Methods: A mixed prospective/retrospective case-control study was performed. Brain tissue prospectively collected at necropsy from GME, NME, and control cases was evaluated by broadly reactive polymerase chain reaction (PCR) for adenoviruses, bunyaviruses, coronaviruses, enteroviruses, flaviviruses, herpesviruses, paramyxoviruses, and parechoviruses. In addition, these tissues were retrospectively evaluated for the presence of mycoplasmas by PCR, culture, and immunohistochemistry (IHC).Results: Brain tissue was collected from 11 GME and 27 NME cases and 30 controls. Viral nucleic acids were not identified in the 6 GME cases, 25 NME cases, and 2 controls evaluated by viral PCR. Mycoplasma canis was identified by Mycoplasma genus PCR in 1/5 GME and 4/25 NME cases and subsequently was cultured from 4/5 GME and 4/8 NME cases as well as 2/9 controls. The IHC did not detect M. canis in any of the 11 GME and 27 NME cases or 14 controls evaluated with strain PG14 polyclonal antiserum.Conclusions and Clinical Importance: The negative results suggest that viral pathogens are not common in the brain tissue of dogs with GME and NME. Further investigation is warranted to determine the importance of M. canis in cases of GME and NME.

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“…Other naturally occurring and clinically significant CNS infections A variety of organisms have been seen very occasionally as a cause of CNS disease in cats, including Bartonella henselae, which typically causes cat scratch disease in humans, but can also cause CNS disease in cats, 63 Mycoplasma felis, 64 feline herpesvirus (FHV-1), feline calicivirus (FCV), Aujeszky's disease virus, Aspergillus species and dematiaceous fungi (Cladophialophora bantiana), and nemotodes (eg, cuterebral larval migration, Sarcocystis neurona). A number of different arboviruses (the arthropod-borne encephalomyelitis group) have also been shown to infect cats (eg, BDV -see above), St Louis encephalitis virus, Japanese encephalitis virus, Yellow fever virus and Rift Valley fever virus, to name just a few.…”

Section: Highly Pathogenic Avian Influenzamentioning

confidence: 99%