Acute ischemic strokes from small vessel vasculitis due to disseminated histoplasmosis infection

Bolen, Robert D.; Bushnell, Cheryl; Reynolds, Patrick

doi:10.1016/j.jns.2015.03.037

Cited by 4 publications

(4 citation statements)

References 7 publications

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“…Emerging evidence suggests that stroke-induced peripheral immune suppression is a major factor that predisposes the host to infections. Immune suppression can be characterized by loss of lymphocytes through apoptosis, shift of T-helper cell 1-type to T-helper cell 2-type cytokine production, decreased monocyte count and function, and IFN-g deficiency, which begins a few hours after ischemia and lasts for several weeks (7,(16)(17)(18). Several studies have reported on the potential roles of lymphocytes in host susceptibility during poststroke infection (7,19,20).…”

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confidence: 99%

Activation of JAK/STAT3 restores NK‐cell function and improves immune defense after brain ischemia

et al. 2018

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Stroke-induced immune suppression predisposes the host to infections and can contribute to high morbidity and mortality in stroke patients. Because ischemic stroke has a profound effect on the systemic immune response, which may explain the increased susceptibility of stroke patients to infection, an urgent need persists for a better understanding of mechanisms associated with immune suppression; new and effective treatments for stroke can then be identified. NK cells play a key role in early host defense against pathogens by killing infected cells and/or producing cytokines such as IFN-γ. Because the phenotype and function of peripheral NK cells have been widely investigated in ischemic stroke, nCounter Inflammation Gene Array Analysis was used to build immune-related gene profiles of NK cells to comprehensively analyze the molecular signature of NK cells after ischemic brain injury. We observed distinct gene expression profiles reflecting different splenic NK-cell phenotypes and functional properties across the time course of transient middle cerebral artery occlusion (MCAO). Based on gene expression and pathway-network analysis, lower expression levels of signal transducer and activator of transcription-3 (STAT3) were observed in animals with MCAO compared with sham control animals. Genetic activation of STAT3 through the introduction of STAT3 clustered regularly interspaced short palindromic repeats (CRISPR) plasmid prevented the loss of NK-cell-derived IFN-γ production after MCAO, together with reduced bacterial burden and mortality. Our data suggest that brain ischemia impairs NK-cell-mediated immune defense in the periphery, at least in part through the JAK-STAT3 pathway, which can be readdressed by modulating STAT3 activation status.-Jin, W.-N., Ducruet, A. F., Liu, Q., Shi, S. X.-Y., Waters, M., Zou, M., Sheth, K. N., Gonzales, R., Shi, F.-D. Activation of JAK/STAT3 restores NK-cell function and improves immune defense after brain ischemia.

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confidence: 99%

Activation of JAK/STAT3 restores NK‐cell function and improves immune defense after brain ischemia

et al. 2018

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“…A complex presentation of histoplasmosis is the involvement of the central nervous system (CNS), most commonly seen in disseminated histoplasmosis infection with an incidence rate of 5%-10% [ 7 ]. CNS manifestations can include meningitis involving the basilar meninges, acute meningitis, encephalitis, small ring-enhancing lesions, abscess, and stroke due to infected emboli [ 8 ]. Brain imaging is abnormal in most cases, with MRI being more sensitive than CT scan, although, in one study, greater than 20% of patients had no significant findings on head imaging [ 7 ].…”

Section: Discussionmentioning

confidence: 99%

Miliary Histoplasmosis in a Renal Transplant Patient

Verdecia¹,

Coyne²,

Patel³

et al. 2021

Cureus

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Solid organ transplant (SOT) recipients are at increased risk of opportunistic infections due to significant T-cell immune dysfunction. The incidence of clinical disseminated histoplasmosis is rare, and its variable clinical presentation and response to therapy make it challenging to treat with resultant high mortality. A high index of clinical suspicion is necessary, especially in non-endemic areas. We report our clinical experience treating a 63-year-old renal transplant patient on immunosuppressive therapy with late-onset acute miliary histoplasmosis initiated on liposomal amphotericin B (L-AmB).

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“…The clinical presentation of CNS histoplasmosis encompasses multiple neurological syndromes that tend to overlap. Those include: chronic meningitis with or without hydrocephalus, cerebritis, cerebral or spinal cord histoplasmoma, CNS vasculitis with ischemic infarcts of small caliber arteries, and rarely, cardioembolic stroke syndromes secondary to Histoplasma endocarditis [6] , [15] , [16] , [17] . According to early studies, the rates of CNS involvement among subjects with disseminated histoplasmosis approach 10% [6] , [15] , however, the diagnosis is often obscured when neurological manifestations are the only presenting signs/symptoms and there are no specific epidemiological risk factors.…”

Section: Discussionmentioning

confidence: 99%

“…The pathophysiology of cerebrovascular disease in CNS histoplasmosis is not fully understood. Evidence to date suggests that brain infarctions can occur in two different settings: [1] granulomatous small vessel vasculitis with lacunar infarcts predominantly in the brainstem and deep white matter [15] , [16] and [2] mycotic emboli and microemboli to arteries of various calibers secondary to Histoplasma endocarditis [19] , [20] . These syndromes may coexist in severe disseminated disease [20] .…”

Section: Discussionmentioning

confidence: 99%

Ischemic brain infarcts and vasculitis in histoplasmosis of the central nervous system: A case report and review of the literature

Pineda-Reyes

Guiance

Landman

et al. 2021

IDCases

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Histoplasmosis is one of the most common endemic mycoses affecting immunocompromised individuals in the United States and Latin America. Involvement of the central nervous system carries higher mortality rates and worse prognosis, given its resemblance to stroke, vasculitis, and meningitis of other etiologies. The diagnosis is challenging, due to its subtle clinical presentation and the poor sensitivity of the cerebrospinal fluid culture. Herein the authors present a case of a middle-aged man with HIV, who presented with intermittent headaches exacerbated by an oculomotor nerve palsy, concerning for acute stroke. A diagnosis of central nervous system histoplasmosis was made, and his neurological deficits subsided after initiation of treatment. The stroke-like syndrome in this scenario may be secondary to granulomatous vasculitis of small caliber cerebral blood vessels. Histoplasmosis of the central nervous system remains a challenging diagnosis, which requires a high index of suspicion by the clinician for an early institution of therapy in order to improve outcomes.

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Acute ischemic strokes from small vessel vasculitis due to disseminated histoplasmosis infection

Cited by 4 publications

References 7 publications

Activation of JAK/STAT3 restores NK‐cell function and improves immune defense after brain ischemia

Activation of JAK/STAT3 restores NK‐cell function and improves immune defense after brain ischemia

Miliary Histoplasmosis in a Renal Transplant Patient

Ischemic brain infarcts and vasculitis in histoplasmosis of the central nervous system: A case report and review of the literature

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