Transverse Myelitis Associated With Cat-Scratch Disease in an Adult

Transverse myelitis (TM) includes a pathobiologically heterogeneous syndrome characterized by acute or subacute spinal cord dysfunction resulting in paresis, a sensory level, and autonomic (bladder, bowel, and sexual) impairment below the level of the lesion. Etiologies for TM can be broadly classified as parainfectious, paraneoplastic, drug/toxin-induced, systemic autoimmune disorders, and acquired demyelinating diseases. We discuss the clinical evaluation, workup, and acute and long-term management of patients with TM. Additionally, we briefly discuss various disease entities that may cause TM and their salient distinguishing features, as well as disorders that may mimic TM.

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“…Bacteria reported to cause PITM 155,195,[201][202][203][204][205][206][207][208][209][210][211][212][213][214] are listed in Box 5.…”

Section: Vogt-koyanagi-harada Syndromementioning

confidence: 99%

Transverse Myelitis

et al. 2013

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“…However, a human study that sought to identify the cause and characterize signs of encephalitis in California over a 2 year period found Bartonella species to be the most common bacterial agent associated with encephalitis (Glaser et al 2003). Signs of neurological dysfunction include encephalopathy (Carithers 1985, Carithers and Margileth 1991, Margileth 1993, Noah et al 1995, transverse myelopathy (Pickerill and Milder 1981), demyelinating polyneuropathy (McNeill et al 2000), facial nerve paralysis (Walter and Eppes 1998), aseptic meningitis (Wong et al 1995), cerebral arteritis (Selby and Walker 1979), neuroretinitis (Ormerod and Dailey 1999) and radiculopathy (Marra 1995). Encephalopathy is considered one of the most serious complications of CSD (Noah et al 1995, Chomel et al 2003 and can manifest with fever, headaches, mentation changes (aggression, confusion and excitability), combative behavior, tonic-clonic seizures, status epilepticus and occasionally, coma that develops 1e8 weeks after the onset of lymphadenopathy (Carithers 1985, Carithers and Margileth 1991, Weston et al 2001.…”

mentioning

confidence: 99%

Prevalence of Bartonella henselae antibodies in serum of cats with and without clinical signs of central nervous system disease

Pearce

Radecki

Brewer

et al. 2006

Journal of Feline Medicine and Surgery

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Bartonella henselae is occasionally associated with neurological dysfunction in people and some experimentally infected cats. The purpose of this study was to determine whether B henselae seroprevalence or titer magnitude varies among cats with neurological disease, cats with non-neurological diseases, and healthy cats while controlling for age and flea exposure. There was no difference in B henselae seroprevalence rates between cats with seizures and cats with other neurological diseases. Cats with non-neurological disease and healthy cats were more likely than cats with neurological disease to be seropositive. While the median B henselae antibody titer was greater in cats with seizures than in cats with other neurological disease, the median B henselae antibody titer was also greater in healthy cats than cats with seizures. The results suggest that titer magnitude cannot be used alone to document clinical disease associated with B henselae infection and that presence of B henselae antibodies in serum of cats with neurological disease does not prove the clinical signs are related to B henselae.

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Granulomatous Hepatitis in Three Children due to Cat-scratch Disease Without Peripheral Adenopathy

Malatack¹

1993

Am J Dis Child

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Transverse Myelitis Associated With Cat-Scratch Disease in an Adult

Cited by 21 publications

References 6 publications

Transverse Myelitis

Transverse Myelitis

Prevalence of Bartonella henselae antibodies in serum of cats with and without clinical signs of central nervous system disease

Granulomatous Hepatitis in Three Children due to Cat-scratch Disease Without Peripheral Adenopathy

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