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Horner Syndrome induced by toxoplasmosis infection in a patient with AIDS and disseminated herpes simplex virus.

ABSTRACT: Purpose:This case report describes a case of Horner syndrome resulting from central nervous system (CNS) toxoplasmosis in an immunocompromised patient. Horner Syndrome is a neurological condition characterized by unilateral miosis, ptosis with apparent enophthalmos, and anhidrosis due to inhibition of the sympathetic pathway. The ocular sympathetic pathway runs from the posterolateral hypothalamus to the ophthalmic branch of the trigeminal nerve (cranial nerve V1). Central nervous system (CNS) toxoplasmosis infection is typically only seen in immunocompromised patients. To our knowledge, toxoplasmosis has never been reported as a cause of Horner syndrome. Observations:A forty-four-year-old Caucasian male was admitted to the hospital for left upper extremity paresthesias, gait instability, and painful vesicular skin lesions, and Horner syndrome. Upon review, he had an 18-year history of HIV initially controlled on anti-retrovirals but had been lost to follow-up for several years until he developed severe headaches determined to be caused by Toxoplasmosis lesions in his brain. Over several months he was treated for the Toxoplasmosis but had poor adherence to medications. After subsequent admission and workup, we found multi-focal ring enhancing lesions on MRI in the basal ganglia, hypothalamus, thalamus, and internal capsule. We postulated that the hypothalamic lesion was the cause of his Horner syndrome. After treatment for both toxoplasmosis and HSV his Horner syndrome and other neurologic symptoms resolved. Conclusions and Importance:This is the first reported case of Horner syndrome resulting from CNS toxoplasmosis. This case report and the accompanying questions provide an opportunity to review and explore the neuroanatomy and subtle symptomatic differences between various etiologies of Horner syndrome (primary, secondary, tertiary) in the context of a novel presentation. In conclusion, toxoplasmosis should be considered when investigating Horner syndrome in immunocompromised patients.

SUBMITTER: Straehley I

PROVIDER: S-EPMC7183101 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

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Horner Syndrome induced by toxoplasmosis infection in a patient with AIDS and disseminated herpes simplex virus.

Straehley Ian I Varada Neilmegh N Prokop Ingmar I Muxen Cassandra C

American journal of ophthalmology case reports 20200408

<h4>Purpose</h4>This case report describes a case of Horner syndrome resulting from central nervous system (CNS) toxoplasmosis in an immunocompromised patient. Horner Syndrome is a neurological condition characterized by unilateral miosis, ptosis with apparent enophthalmos, and anhidrosis due to inhibition of the sympathetic pathway. The ocular sympathetic pathway runs from the posterolateral hypothalamus to the ophthalmic branch of the trigeminal nerve (cranial nerve V1). Central nervous system ...[more]

PMID: 32346650

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Project description:Herpes simplex virus 1 (HSV-1) infects eye corneal tissues leading to herpetic stromal keratitis (HSK), which is one of the leading causes of blindness. Here in our study, we found that 6-thioguanine (6-TG), a once clinically approved medication for child acute myelogenous leukemia, inhibited multiple strains of HSV-1 infection in vitro and in vivo. 6-TG is more potent than acyclovir (ACV) and ganciclovir (GCV), with the 50% inhibitory concentration (IC50) of 6-TG at 0.104 μM with high stimulation index (SI) (SI = 6,475.48) compared to the IC50 of ACV at 1.253 μM and the IC50 of GCV at 1.257 μM. In addition, 6-TG at 500 μM topically applied to the eyes with HSV-1 infection significantly inhibits HSV-1 replication, alleviates virus-induced HSK pathogenesis, and improves eye conditions. More importantly, 6-TG is effective against ACV-resistant HSV-1 strains, including HSV-1/153 and HSV-1/blue. Knockdown of Rac1 with small interfering RNA (siRNA) negatively affected HSV-1 replication, suggesting that Rac1 facilitated HSV-1 replication. Following HSV-1 infection of human corneal epithelial cells (HCECs), endogenous Rac1 activity was upregulated by glutathione S-transferase (GST) pulldown assay. We further found that Rac1 was highly expressed in the corneal tissue of HSK patients compared to normal individuals. Mechanistic study showed that 6-TG inhibited HSV-1 replication by targeting Rac1 activity in HSV-1 infected cells, and the Rac1 is critical in the pathogenesis of HSK. Our results indicated that 6-TG is a promising therapeutic molecule for the treatment of HSK. IMPORTANCE We reported the discovery of 6-TG inhibition of HSV-1 infection and its inhibitory roles in HSK both in vitro and in vivo. 6-TG was shown to possess at least 10× more potent inhibitory activity against HSV-1 than ACV and GCV and, more importantly, inhibit ACV/GCV-resistant mutant viruses. Animal model studies showed that gel-formulated 6-TG topically applied to eyes locally infected with HSV-1 could significantly inhibit HSV-1 replication, alleviate virus-induced HSK pathogenesis, and improve eye conditions. Further study showed that HSV-1 infection upregulated Rac1 expression, and knockdown of Rac1 using siRNA markedly restricted HSV-1 replication, suggesting that Rac1 is required for HSV-1 replication. In addition, we also documented that Rac1 is highly expressed in corneal tissues from HSK patients, indicating that Rac1 is associated with HSK pathogenesis. In view of the high potency of 6-TG, low cytotoxicity, targeting a distinct therapeutic target, we suggest that 6-TG is a potential candidate for development as a therapeutic agent for HSK therapy.

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Horner Syndrome induced by toxoplasmosis infection in a patient with AIDS and disseminated herpes simplex virus.

Publications

Horner Syndrome induced by toxoplasmosis infection in a patient with AIDS and disseminated herpes simplex virus.

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