Cat-scratch encephalopathy

Wheeler, Steven W.; Wolf, Sheldon M.; Steinberg, Evan A.

doi:10.1212/wnl.49.3.876

Cited by 38 publications

(26 citation statements)

References 5 publications

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“…CIDP is an autoimmune process in which both humoral and cellular factors are thought to participate in the pathogenesis. Wheeler et al also suggested an immune response as a pathophysiological mechanism responsible for CSD encephalopathy 1. In our patient a delayed myelin destruction is induced by sensitised macrophages, originally activated by the Bartonella infection.…”

supporting

confidence: 59%

“…However, neurological complications associated with CSD are rare, with encephalopathy being by far the most common form (90%) of nervous system involvement. Encephalopathy occurs in 2%–3% of patients and is more common in adults than in children with the onset varying from a few days to months after diagnosis of CSD 1. Other known neurological manifestations, often in combination with encephalopathy, are neuroretinitis, oculoglandular disease of Parinaud, myelopathy, radiculopathy or abducens nerve, and facial nerve paresis.…”

mentioning

confidence: 99%

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Chronic inflammatory demyelinating polyneuropathy as a complication of cat scratch disease

Mcneill¹,

Verrips²,

Mullaart³

et al. 2000

Journal of Neurology, Neurosurgery &Amp; Psychiatry

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to run) and manifested as spasm of the left side of the face and flexor spasm of the left arm and left leg. There were no premonitory symptoms and consciousness was normal during the attack. Attacks lasted for a few seconds only and he felt perfectly well afterwards. Neurological examination was normal. Brain MRI was normal and three EEGs performed over the course of the next year were all normal. There were no biochemical or haematological abnormalities; copper studies were normal. A diagnosis of paroxysmal kinesigenic choreoathetosis was made. He was allergic to carbamazepine and did not respond to sodium valproate.Lamotrigine(3,5-diamino-6-[2,3-dichlorophenyl]-1,2,4-triazine) is a use dependent blocker of voltage gated sodium channels and has a similar anticonvulsant profile to phenytoin and carbamazepine in animal models. 5Lamotrigine at a dose of 50 mg twice daily, completely abolished the involuntary movements. On two occasions, these returned on stopping lamotrigine and were abolished by reinstituting treatment. Our patient has taken this for over 2 years without ill eVect. He now only experiences symptoms of paroxysmal kinesigenic choreoathetosis if he omits his medication. The response to lamotrigine may provide insight into the pathogenesis of the disease, suggesting that it may be caused by an ion channel defect; these are known to be responsible for some paroxysmal neurological conditions.6 As far as we are aware, this is the first report of the successful use of lamotrigine to treat paroxysmal kinesigenic choreoathetosis.

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supporting

confidence: 59%

mentioning

confidence: 99%

Chronic inflammatory demyelinating polyneuropathy as a complication of cat scratch disease

Mcneill¹,

Verrips²,

Mullaart³

et al. 2000

Journal of Neurology, Neurosurgery &Amp; Psychiatry

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“…5 Infection of the central nervous system (CNS) with B. henselae is uncommon and typically presents with an encephalopathy and seizures. [6][7][8][9] In a study of 1200 cases of CSD there was neurological involvement in only 2% of cases, with encephalopathy being the most common complication. 3 In a series of 76 patients with CSD and neurological complications, 80% had an encephalopathy.…”

Section: Discussionmentioning

confidence: 99%

Encephalopathy with retinitis due to cat‐scratch disease

Smith

Scott

Beverley

et al. 2007

Develop Med Child Neuro

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Cat‐scratch disease is one of several diseases known to be caused by Bartonella species. Some infections due to Bartonella resolve spontaneously without treatment with antibiotics, but in other cases the disease can be fatal without treatment. This case study reports a 7‐year‐old male who presented with an unexplained encephalopathy and unusual retinal findings associated with evidence supporting infection by B. henselae. The 7‐year‐old male presented with a 2‐week history of general malaise and cervical lymphadenopathy progressing onto fever, headache, vomiting, and confusion associated with meningism. Lumbar puncture revealed a raised cerebrospinal fluid protein, low glucose, and raised white cell count. Abnormal retinal findings and raised antibodies titres to B. quintana indicated a diagnosis of cat‐scratch disease. He was treated with azithromycin orally for 3 weeks and made a complete recovery.

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“…II νόσος των αμυχών της γάτας αποτελεί το συχνότερο αίτιο μονήρους λεμφαδενοπάΟειας σε νεαρά άτομα με εξαίρεση επιχώριες λεμφαδενίτιδες λόγω εμφανών τοπικών φλεγμονών. Σε ασθενείς με ανοσοκαταστολή έχει αναφερθεί εξάπλωση του βακτηρίου και εντόπιση του στο ήπαρ και το σπλήνα (Slater et al 1990, Noah et al 1995, Wheeler et al 1997, Spach et al 1998, Margileth 2000, Roux et al 2000, Fournieretal. 2001, Koehler et al 2003, Eremeeva et al 2007, Florin et al 2008, Chomel et al 2009, Dietrich et al 2010.…”

Section: θεραπευτικη αντιμετωπισηunclassified

Feline bartonellosis· A review

Athanasiou¹,

Chatzis²,

Κοντου)

et al. 2017

J Hellenic Vet Med Soc

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ABSTRACT, Bartonella infection is caused by Gram negative bacteria commonly isolated from domestic cats. Cats are the major reservoir of Bartonella henselae, B> clarridgeiae and B. koehlerae which are transmitted to humans, while they are accidental host of B, quintana. Β, bovis και Β, vìmonìi subsp. berkhoffìi. The pathogen is transmitted among cats mainly by fleas while other vectors are also suspicious for transmission since the bacteria have been isolated from ticks and flies. The bacterial pathogenicity may be emphasized by the strain of the bacterium and the immune status of the infected host Most of the infected eats remain asymptomatic. In the natural occurring cases of feline bartonellosis uveitis, chronic gingivostomatitis and endocarditis have been reported. Mild anemia and leucocitosi s in the early phase of the infection has been also reported. Diagnosis is based on the detection of the specific anti-bartoneila antibodies by the inderict immunofluorescent test, ELISA and Western blot assays. Molecular biology techniques mainly PCR, cytology, histopathology and blood culture have also been employed for the direct detection of the pathogen. Prolonged antimicrobial therapy results to the reduction of bacterial burden without total elimination of the pathogen.Bartonella henselae is the causative agent of cat scratch disease, a human infection usually characterized by persistent regional lymphadenopathy and less frequently fever while angiomatosis or hepatic peliosis have been reported mainly in immunocompromised patients. It is transmitted to humans by cat scratches or bites. The most effective means of protection is regular flea control Additionally, commonsense precautions and hygiene such as washing hands after handling pets and clean any cats and bites or scratches promptly are recommended especially in population at great risk.

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Cat-scratch encephalopathy

Cited by 38 publications

References 5 publications

Chronic inflammatory demyelinating polyneuropathy as a complication of cat scratch disease

Chronic inflammatory demyelinating polyneuropathy as a complication of cat scratch disease

Encephalopathy with retinitis due to cat‐scratch disease

Feline bartonellosis· A review

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