Death From Primary Amebic Meningoencephalitis After Recreational Water Exposure During Recent Travel to India-Santa Clara County, California, 2020.

BACKGROUND: In February 2020, a man returned to the United States after an 11-day trip to India and died of primary amebic meningoencephalitis (PAM), caused by nasal exposure to the free-living ameba Naegleria fowleri found in warm water. We identified potential exposures, confirmed etiology, and described the molecular epidemiology of the infection. METHODS: We reviewed medical records to describe his clinical course and interviewed his family to determine water exposures. Genotyping was performed on the N. fowleri strain and compared with North American strains through repetitive nonpolymorphic nuclear loci analysis to identify differences. We reviewed N. fowleri strains in the National Center for Biotechnology Information database (GenBank) to determine genotypes present in India. RESULTS: The patient became acutely encephalopathic 3 days after returning; the only known nasal water exposure was at an indoor swimming pool in India 5 days earlier. Cerebrospinal fluid (CSF) testing demonstrated neutrophil-predominant pleocytosis and low glucose, but negative gram stain and culture. CSF microscopy revealed trophozoites; N. fowleri was detected by real-time polymerase chain reaction. Classical genotyping confirmed genotype I, common in the United States and among Indian strains in GenBank. The North American N. fowleri strains and the patient's strain varied at 5 nonpolymorphic loci. CONCLUSIONS: A man died from PAM after likely exposure at a vacation rental pool in India. We recommend including PAM in the differential diagnosis when CSF studies suggest bacterial meningitis but gram stain is negative. Genotyping can advance our understanding of N. fowleri molecular epidemiology and support future investigations.

Reintervention After Infant Aortic Arch Repair Using a Tailored Autologous Pericardial Patch.

BACKGROUND: Aortic arch reobstruction is a common complication after aortic repair, with rates of reintervention varying from 0% to 40%, depending on the disease and the institution. This study aimed to determine the reintervention rate in children undergoing aortic arch repair using a tailored autologous pericardial patch at our center (Monroe Carell, Jr Children's Hospital at Vanderbilt, Nashville, TN). METHODS: This retrospective study examined all patients operated on by a single surgeon for aortic arch reconstruction through sternotomy, from 2011 to 2018, with 1 year of follow-up. Our data set was analyzed for normality by using the Shapiro-Wilk test, and nonparametric statistical methods were used. Kaplan-Meier survival analysis was performed, IBM SPSS software version 23 was used to perform all statistical analysis. RESULTS: A total of 171 patients met inclusion criteria. Twenty-three (13.5%) patients underwent aortic arch reinterventions during the study period, 17 (9.9%) catheter based and 3 (1.8%) surgical. Three patients (1.8%) had both. Freedom from reintervention at 1-year follow-up for the univentricular and biventricular patients was 82.1% and 89.4% (P = .174), respectively. To assess the growth of the aortic arch over time, cardiac catheterization measurements were used to index different parts of the aortic arch against the descending aorta. Ascending-to-descending aortic arch measurements revealed that the pre-Glenn median was 2.0 (interquartile range, 1.8 to 2.2), whereas the pre-Fontan median was 2.5 (interquartile range, 2.2 to 2.7) (P < .05). CONCLUSIONS: There was no significant difference in reintervention rates between biventricular and univentricular arches, and catheterization measurements showed significant growth of the arch over time. The use of a tailored autologous pericardial patch for aortic arch repair is comparable to other reported methods of arch repair.

Oculomotor Synkinesis (Aberrant Reinnervation of the Third Cranial Nerve) Associated with Atypical Tolosa-Hunt Syndrome.

A 70-year-old woman with systemic lupus erythematosus developed a painful pupil-involving right third nerve palsy, ipsilateral fourth nerve palsy, and periorbital paraesthesia. Magnetic resonance imaging demonstrated enhancement and thickening of the right third nerve, and she was diagnosed with presumed Tolosa-Hunt syndrome. Repeated imaging seven months later showed resolution of the enhancing thickened oculomotor nerve, but the patient developed signs of oculomotor synkinesis. This presentation demonstrates a rare case of oculomotor synkinesis secondary to inflammation.

Minocycline protects against delayed cerebral ischemia after subarachnoid hemorrhage via matrix metalloproteinase-9 inhibition.

Objective: Delayed cerebral ischemia (DCI) is an independent risk factor for poor outcome after aneurysmal subarachnoid hemorrhage (SAH) and is multifactorial in etiology. While prior studies have suggested a role for matrix metalloproteinase-9 (MMP-9) in early brain injury after SAH, its contribution to the pathophysiology of DCI is unclear. Methods: In the first experiment, wild-type (WT) and MMP-9-/- mice were subjected to sham or endovascular perforation SAH surgery. In separate experiments, WT and MMP-9-/-mice were administered vehicle or minocycline either pre- or post-SAH. All mice underwent assessment of multiple components of DCI including vasospasm, neurobehavioral function, and microvessel thrombosis. In another experiment, rabbits were subjected to sham or cisterna magna injection SAH surgery, and administered vehicle or minocycline followed by vasospasm assessment. Results: MMP-9 expression and activity was increased after SAH. Genetic (MMP-9-/- mice) and pharmacological (pre-SAH minocycline administration) inhibition of MMP-9 resulted in decreased vasospasm and neurobehavioral deficits. A therapeutically feasible strategy of post-SAH administration of minocycline resulted in attenuation of multiple components of DCI. Minocycline administration to MMP-9-/- mice did not yield additional protection. Consistent with experiments in mice, both pre- and post-SAH administration of minocycline attenuated SAH-induced vasospasm in rabbits. Interpretation: MMP-9 is a key player in the pathogenesis of DCI. The consistent attenuation of multiple components of DCI with both pre- and post-SAH administration of minocycline across different species and experimental models of SAH, combined with the excellent safety profile of minocycline in humans suggest that a clinical trial in SAH patients is warranted.