Case Report: Late Reactivation of Herpes B Virus After a Monkey Bite: A Case of Severe Meningoencephalitis.

Macacine alphaherpesvirus 1, also known as herpes B virus (BV), is an alphaherpesvirus endemic to several macaque species, capable of causing zoonotic infections in humans, with high mortality rates. Evidence of reactivation in humans has rarely been reported. Here we depict a case of BV reactivation after 54 years, leading to severe meningoencephalitis. This case supports the use of antiviral prophylaxis in patients surviving a confirmed BV central nervous system infection. We sequenced DNA from BV obtained from the patient's cerebrospinal fluid. Phylogenetic analysis showed significant divergence in the clustering of this particular BV strain compared with other known BVs. Therefore, additional efforts are needed to obtain a broader sequence landscape from BVs circulating in monkeys.

Impact of a restrictive antibiotic policy on the acquisition of extended-spectrum beta-lactamase-producing Enterobacteriaceae in an endemic region: a before-and-after, propensity-matched cohort study in a Caribbean intensive care unit.

BACKGROUND: High-level antibiotic consumption plays a critical role in the selection and spread of extended-spectrum beta-lactamase-producing Enterobacteriaceae (ESBL-E) in the ICU. Implementation of a stewardship program including a restrictive antibiotic policy was evaluated with respect to ESBL-E acquisition (carriage and infection). METHODS: We implemented a 2-year, before-and-after intervention study including all consecutive adult patients admitted for > 48 h in the medical-surgical 26-bed ICU of Guadeloupe University Hospital (French West Indies). A conventional strategy period (CSP) including a broad-spectrum antibiotic as initial empirical treatment, followed by de-escalation (period before), was compared to a restrictive strategy period (RSP) limiting broad-spectrum antibiotics and shortening their duration. Antibiotic therapy was delayed and initiated only after microbiological identification, except for septic shock, severe acute respiratory distress syndrome and meningitis (period after). A multivariate Cox proportional hazard regression model adjusted on propensity score values was performed. The main outcome was the median time of being ESBL-E-free in the ICU. Secondary outcome included all-cause ICU mortality. RESULTS: The study included 1541 patients: 738 in the CSP and 803 in the RSP. During the RSP, less patients were treated with antibiotics (46.8% vs. 57.9%; p < 0.01), treatment duration was shorter (5 vs. 6 days; p < 0.01), and administration of antibiotics targeting anaerobic pathogens significantly decreased (65.3% vs. 33.5%; p < 0.01) compared to the CSP. The incidence of ICU-acquired ESBL-E was lower (12.1% vs. 19%; p < 0.01) during the RSP. The median time of being ESBL-E-free was 22 days (95% CI 16-NA) in the RSP and 18 days (95% CI 16-21) in the CSP. After propensity score weighting and adjusted analysis, the median time of being ESBL-E-free was independently associated with the RSP (hazard ratio, 0.746 [95% CI 0.575-0.968]; p = 0.02, and hazard ratio 0.751 [95% CI 0.578-0.977]; p = 0.03, respectively). All-cause ICU mortality was lower in the RSP than in the CSP (22.5% vs. 28.6%; p < 0.01). CONCLUSIONS: Implementation of a program including a restrictive antibiotic strategy is feasible and is associated with less ESBL-E acquisition in the ICU without any worsening of patient outcome.

Neurally adjusted ventilatory assist during weaning from respiratory support in a case of guillain-barré syndrome.

We report a case of Guillain-Barré syndrome complicated by respiratory failure requiring mechanical ventilation. Neurally adjusted ventilatory assist (NAVA) allowed proper patient-ventilator synchronization by pressure support proportional to the electrical activity of the diaphragm (Edi). Prolonged ventilation with NAVA seems feasible in patients with neuromuscular impairment, but the weaning process conducted by a continuous monitoring of Edi for pressure support titration needed to be assessed in a Guillain-Barré syndrome patient. Beginning on day 12 after hospital admission, the patient was ventilated with NAVA for 8 d. The NAVA level (pressure support per unit of Edi) was decreased from 1.2 cm H2O/µV to zero over the 8-d period. A simultaneous decrease in the tidal volume/Edi ratio was interpreted as a sign of recovery. A spontaneous breathing trial was successfully performed on day 20, followed by decannulation 4 d later. In conclusion, NAVA should be further investigated in patients with Guillain-Barré syndrome, particularly during the weaning period.

Inverted (Reverse) Takotsubo Cardiomyopathy following Cerebellar Hemorrhage.

Background. First described in 2005, inverted takotsubo is one of the four stress-induced cardiomyopathy patterns. It is rarely associated with subarachnoid hemorrhage but was not previously reported after intraparenchymal bleeding. Purpose. We reported a symptomatic case of inverted takotsubo pattern following a cerebellar hemorrhage. Case Report. A 26-year-old woman presented to the emergency department with sudden headache and hemorrhage of the posterior fossa was diagnosed, probably caused by a vascular malformation. Several hours later, she developed acute pulmonary edema due to acute heart failure. Echocardiography showed left ventricular dysfunction with hypokinetic basal segments and hyperkinetic apex corresponding to inverted takotsubo. Outcome was spontaneously favorable within a few days. Conclusion. Inverted takotsubo pattern is a stress-induced cardiomyopathy that could be encountered in patients with subarachnoid hemorrhage and is generally of good prognosis. We described the first case following a cerebellar hematoma.

Partly reversible central auditory dysfunction induced by cerebral vasospasm after subarachnoid hemorrhage.

The authors describe a rare case of central auditory dysfunction induced by cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). A 55-year-old woman who was admitted after aneurysmal SAH developed cerebral vasospasm on Day 3 affecting mainly the right middle cerebral artery (MCA) and partly the left MCA. The vasospasm became refractory to conventional therapy and was ultimately improved by intraarterial infusion of nimodipine in the right MCA and angioplasty. Severe auditory dysfunction was apparent from Day 10 as the patient was not reactive to speech or environmental sounds. Brain MRI on Day 17 demonstrated infarcted areas mainly in the right hippocampus, medial occipital lobe, and thalamus. The patient underwent further examination using audiometry, speech testing, auditory evoked potentials, functional MRI, and cerebral PET. The initial diagnosis was extended nonverbal agnosia and total pure word deafness. The central auditory dysfunction improved over 6 months, with persisting hyperacusis, tinnitus, and amusia. Central auditory dysfunction is a rare complication after SAH. While cortical deafness may be associated with bilateral lesions of the temporal cortex, partly reversible central auditory dysfunction was observed in this patient after prominently unilateral right temporal lesions. The role of the interthalamic connections can be discussed, as well as the possibility that a less severe vasospasm on the left MCA could have transiently impaired the left thalamocortical auditory pathways.

Severe acute cardiomyopathy associated with venlafaxine overdose and possible role of CYP2D6 and CYP2C19 polymorphisms.

INTRODUCTION: Venlafaxine (VEN) is a serotonin-norepinephrine-dopamine reuptake inhibitor that causes usually a mild cardiotoxicity when ingested in overdose. We report a patient who developed acute heart failure following overdose. As the toxicokinetic data suggested a prolonged metabolism, genetic polymorphisms for cytochrome P450 isoenzymes CYP2D6 and CYP2C19 were also investigated. CASE REPORT: A 34-year-old woman was admitted to the hospital 10 hours after the ingestion of an 11.25 g overdose of VEN. She was comatose and suffered two self-limited seizures. The electrocardiogram showed diffuse ST segment depression, but normal QRS and QTc duration. The plasma levels on admission were 18,015 and 3,846 ng/ml for VEN and the metabolite O-desmethylvenlafaxine (ODV), respectively. The patient developed severe cardiodepression. The left ventricular shortening fraction was only 9% on echocardiography. The patient was oliguric and required continuous venovenous hemofiltration. The administration of milrinone was required for 12 days, and norepinephrine for 10 days. Left ventricular function recovered. The calculated elimination half-life was 30.8 and 72.2 hours for VEN and ODV, respectively. The patient genotype was CYP2D6*1/*5, the *5 allele corresponding to a complete deletion of CYP2D6 gene. CONCLUSIONS: Severe and sustained cardiotoxicity following VEN overdose may be related to the amount ingested, as well as to the genetic polymorphism for CYP2D6 leading to a delayed elimination of active metabolite.