Clinical Characteristics of the 2019 Eastern Equine Encephalitis Outbreak in Michigan.

Background: Eastern equine encephalitis virus is a mosquito-borne alphavirus responsible for unpredictable outbreaks of severe neurologic disease in animals and humans. While most human infections are asymptomatic or clinically nonspecific, a minority of patients develops encephalitic disease, a devastating illness with a mortality rate of ≥30%. No treatments are known to be effective. Eastern equine encephalitis virus infection is rare in the United States, with an annual average nationwide incidence of 7 cases between 2009 and 2018. However, in 2019, 38 cases were confirmed nationwide, including 10 in Michigan. Methods: Data from 8 cases identified by a regional network of physicians in southwest Michigan were abstracted from clinical records. Clinical imaging and histopathology were aggregated and reviewed. Results: Patients were predominantly older adults (median age, 64 years), and all were male. Results of initial arboviral cerebrospinal fluid serology were frequently negative, and diagnosis was not made until a median of 24.5 days (range, 13-38 days) after presentation, despite prompt lumbar punctures in all patients. Imaging findings were dynamic and heterogeneous, with abnormalities of the thalamus and/or basal ganglia, and prominent pons and midbrain abnormalities were displayed in 1 patient. Six patients died, 1 survived the acute illness with severe neurologic sequelae, and 1 recovered with mild sequelae. A limited postmortem examination revealed diffuse meningoencephalitis, neuronophagia, and focal vascular necrosis. Conclusions: Eastern equine encephalitis is a frequently fatal condition whose diagnosis is often delayed, and for which no effective treatments are known. Improved diagnostics are needed to facilitate patient care and encourage the development of treatments.

Bilateral peripheral facial paralysis during pregnancy: a presentation of acute HIV seroconversion.

A G7P5A1 woman in her 40s presented to the emergency department at 37 weeks 3 days' estimated gestational age (EGA) with headache, lip tingling and several days of difficulty speaking. Physical examination demonstrated bilateral facial weakness in a peripheral distribution, as well as decreased corneal reflexes and cervical lymphadenopathy. Routine fourth generation HIV screening had previously been negative at 14 and 28 weeks' EGA. Brain MRI was unremarkable, and lumbar puncture disclosed a low-grade, mononuclear cerebrospinal fluid pleocytosis; the patient was treated supportively. She returned for induction of labour at 39 weeks, at which time HIV infection was unexpectedly diagnosed. While unilateral idiopathic peripheral facial paralysis is associated with the third trimester of pregnancy and the early postpartum period, bilateral facial paralysis is rare and should prompt work-up for an underlying systemic cause, such as HIV infection.

Diffuse alveolar haemorrhage in the setting of eosinophilic pneumonia.

A 65-year-old woman who presented with a constellation of symptoms, including cough with haemoptysis, fever, chills and hypoxia along with weight loss, was found to have diffuse alveolar haemorrhage. After a myriad of investigations returned normal, an open lung biopsy was performed, which revealed the diagnosis to be subacute eosinophilic pneumonia. This is one of its kind of rare presentations where eosinophilic pneumonia presents as diffuse alveolar haemorrhage and has been reported only five times prior to this.

Dual behavior of N-acetylcysteine during ethanol-induced oxidative stress in embryonic chick brains.

OBJECTIVES: Ethanol (EtOH) causes oxidative stress in embryos. Because N-acetylcysteine (NAC) failures and successes in ameliorating EtOH-induced oxidative stress have been reported, the objective was to determine if exogenous NAC ameliorated EtOH-induced oxidative stress within embryonic chick brains. METHODS: Control eggs were injected with approximately 25 µl of water on day 0, 1, and 2 of development (E0-2). Experimental eggs were injected with dosages of either 3.0 mmol EtOH/kg egg; 747 µmol NAC/kg egg; 3.0 mmol EtOH and 747 µmol NAC/kg egg; 1000 µmol NAC/kg egg; or 3.0 mmol EtOH and 1000 µmol NAC/kg during the first 3 days of development (E0-2). At 11 days of development (E11; late embryogenesis), brains were harvested and subsequently assayed for oxidative stress markers including the loss of long-chain membrane polyunsaturated fatty acids (PUFAs); the accumulation of lipid hydroperoxides (LPO); decreased glutathione (GSH) and glutathione/glutathione disulfide (GSSG) levels; and decreased glutathione peroxidase (GPx) activities. RESULTS: EtOH (3 mmol/kg egg), medium NAC (747 µmol/kg egg), and EtOH and medium NAC promoted oxidative stress. These treatments caused decreased brain membrane long-chain PUFAs; increased LPO levels; decreased GSH levels and GSH/GSSG levels; and decreased Se-dependent GPx activities. High NAC dosages (1000 µmol/kg egg) attenuated EtOH-induced oxidative stress within EtOH and high NAC-treated chick brains. DISCUSSION: Exogenous EtOH and/or medium NAC propagated oxidative stress. Meanwhile, high NAC ameliorated EtOH-induced oxidative stress.