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COVID-19 patients are prone to co-infections during their hospitalization. These co-infections are challenging as they involve longer hospital stays, high costs, and higher mortality risk. Here we present a case of a patient with multi-infection by resistant parasites, fungi, and bacteria during his hospitalization in a Peruvian hospital

Lophomonas infection is an emerging parasitic disease causing respiratory infections. After China, Peru is the second country with the highest number of cases. In the bright-field microscopy evaluation of fresh samples, most of them are incorrectly estimated. Therefore, correct identification using cytological stains is to be supplemented. We report a case of a 29-year-old male with typical clinical symptoms of pneumonia, marked eosinophilia, and noninfiltrative pattern in chest X-ray, who had bronchopulmonary lophomoniasis.

Background: Cytological samples are cleared with xylene in two or three baths during a Pap test, however, this solvent has a high degree of toxicity, and being a controlled reagent infers high costs for its purchase and implications for environmental pollution. We estimated the impact of xylene during the Pap test in terms of the number of liters and cost of two baths of xylene, and also estimated the impact with three baths Methods: This cross-sectional study was carried out in four hospitals of EsSalud in Peru in two stages. First, the analysis of the impact due to the use of two baths of xylene was conducted during the period 2015–2019, and second, the estimates were calculated based on the assumption of three baths of xylene for the years 2020–2025. The assumption was based on the recommendations of the 2018 EsSalud cytology guideline. The monthly amount of xylene was ~10 liters per bath/month and the cost per liter was estimated at 8.13 USD (27 soles). Results: For the staining of 594,898 cytology tests, 7,848 liters of xylene were necessary, resulting in a cost of 60,861 USD (202,068 soles) during the period 2015–2019. The estimates showed a maximum assumption of 9,483 liters and 77,110 USD (256,040 soles) for the use of three baths of xylene in the four EsSalud hospitals (p = 0.0025) during the period 2020–2025. Conclusions: We determined that there was a high economic impact of using xylene with two baths from 2015 to 2019 and a dramatic increase in costs with the possible use of three baths of xylene in the Pap test for the following five years.

Introduction Sporadic Creutzfeldt-Jakob disease is a prion disease characterized by rapidly progressive dementia, ataxia and myoclonus. Atypical phenotype masquerading as stroke, movement disorders or autoimmune encephalitis have been described. Here, I report a probable case of sCJD with an atypical presentation associated with anti-Zic4 antibody and review the literature of neuronal antibodies in CJD. Case Report A 70 year-old gentleman is admitted with a 2-month history of recurrent stroke-like symptoms associated with behavioral disturbances, gait ataxia and rapidly progressive dementia. His initial examination demonstrated akinetic mutism, diffuse rigidity, dysautononia, and Cheyne-Stokes respiration. Over the following weeks his condition progressed to profound coma. A comprehensive infectious, metabolic, inflammatory and autoimmune work-up yielded negative results. Empiric immunosuppressive therapy ensued. He expired three months after symptoms onset. Autopsy was not performed. After his demise, prion tests came back abnormal for elevated 14-3-3 protein, total tau and positive RTQuIC. Later on, anti-Zic4 antibodies were found in serum. Conclusion This case underscores the importance of a high index of suspicion for CJD even in case of atypical features or the concurrence of neuronal antibodies. Further larger prospective studies on the prevalence of these neuronal antibodies in CJD and the contribution of these autoantibodies to disease pathophysiology are necessary.

To assess concordance between physician assessment and patient-reported symptoms when screening for depression in Parkinson disease (dPD).Depression in Parkinson disease is highly prevalent (∼40%) and has a significant impact on quality of life and disability, yet physician recognition and treatment remain inadequate.One thousand seventy-six patients with PD completed the Brief Symptom Inventory-18 (BSI-18), a screening questionnaire for psychiatric symptoms, which was compared to item #3 (depression) on the Unified Parkinson's Disease Rating Scale (UPDRS).The mean BSI-18 depression score was 51.4 (9.7). Of the 170 (16%) patients screening positive for dPD on the BSI-18, 104 (61%) were not recognized as depressed by neurologists on the UPDRS. Factors associated with lower neurologist recognition included male gender, better mental health quality of life, and lack of antidepressant use.More than 60% of patients screening positive for depression on self-report were not recognized by neurologists on the UPDRS. A patient-reported screening tool for depression may improve recognition and management of dPD.

To report a case of sporadic Creutzfeldt-Jakob disease (CJD) with bilateral hearing loss at onset and literature review of the scarce cases of CJD with similar audiologic manifestations at presentation.A 67-yr-old man presented to the hospital for evaluation of rapid progression of behavioral decline, unsteady gait, and bilateral hearing loss. Three months before admission, he abruptly developed bilateral hypoacusis without associated tinnitus or vertigo. Shortly after, his family noted an ataxic gait and behavioral changes, for example, paranoid delusions. Initial workup, including a complete autoimmune panel and heavy metals, infectious, toxicology, and paraneoplastic panel (e.g., anti-Hu, anti-VGKC), was conducted. Electroencephalography revealed diffuse generalized slowing without periodic complexes. The presence of distortion product otoacoustic emissions bilaterally was consistent with normal cochlear function, suggesting a retrocochlear origin for symptoms of hearing loss. In the meantime, the patient developed startle myoclonus. The brain magnetic resonance imaging demonstrated asymmetric cortical ribbon along with T2 FLAIR signal hyperintensities of bilateral basal ganglia. Later on, the protein 14-3-3 in the cerebrospinal fluid came back positive, which supported the diagnosis of CJD. Only three cases of CJD with deafness at onset have been published: one sporadic, associated with symptoms suggestive of polyneuropathy; and the other two familial, with the E200K mutation. One presented with symptoms of polyneuropathy and the other with typical features.This case illustrates the phenotypic variability of presentation of CJD in a patient with hearing loss as the initial manifestation. In patients with subacute bilateral hypoacusis and signs of dementia, the differential diagnosis of CJD must be taken into consideration.

A 74-year-old man presented with acute right-sided hemiparesis and epilepsia partialis continua in association with fever and confusion. Initial workup revealed possible cerebritis in the left medial frontal lobe without involvement of the temporal lobes. Cerebrospinal fluid (CSF) analysis revealed minimal lymphocytic pleocytosis but negative real-time herpes simplex virus (HSV) PCR. Acyclovir was discontinued on day 5 due to a negative infectious workup and clinical improvement. On day 9 his condition deteriorated and he was transferred to a higher level of acuity for advanced supportive care. Worsening encephalopathy and refractory status epilepticus ensued despite medical care. Repeat CSF analysis showed mild lymphocytic pleocytosis with negative real-time HSV PCR. Brain MRI revealed progression of cortical enhancement. Immunosuppressive therapy and plasma exchange were attempted without clinical response. On day 24, another lumbar puncture showed only mild lymphocytic pleocytosis. Brain MRI showed involvement of the right medial temporal lobe. Subsequently, acyclovir was resumed. The HSV-1 PCR result was positive on day 30. Unfortunately, the patient expired.

Palatal tremor (PT) is usually considered a movement disorder that presents with recurring rhythmic contractions of the soft palate. The inferior olive shows a characteristic pseudohypertrophy secondary to brainstem lesions in the triangle of Mollaret and Guillain that interrupt dentato-olivary and tegmental pathways. We report a 35-year-old man with a history of uncontrolled hypertension who presented to the emergency department with PT after a left middle cerebral artery ischemic stroke. The diagnostic work-up consisted of brain MRI, which revealed restricted diffusion over the left frontoparietal lobes without involvement of the brainstem. During hospitalization, the patient reported two brief episodes of soft palate and base-of-the-tongue high-frequency, low-amplitude and rhythmic tremor that resolved after intravenous administration of lorazepam. A 2-hour video electroencephalogram showed no abnormalities. After initiation of levetiracetam therapy, no further spells were reported by the patient. At the 2-month follow-up, the patient had had no episodes of stereotypical PT or upper limb tremors since discharge. This report provides further evidence of the central role of the cortex in the generation of PT. The cortical origin of symptomatic palatal tremor (SPT) should be considered in patients presenting after an acute ischemic insult, particularly if there is no evidence of a brainstem lesion. Potential causes of SPT of cortical origin include focal epilepsy and diaschisis.

We describe one patient and review the literature to define delayed posthypoxic leukoencephalopathy, its etiology, pathophysiology and prognosis. We present a 54-year-old man with confusion and diffuse rigidity following a morphine overdose that had required intubation three weeks previously. A brain CT scan showed bilateral globi pallidi hypodensities and diffusion-weighted brain MRI (DWI) was consistent with acute cerebral anoxia. On day 20 after the initial presentation, the patient insidiously progressed to a state of "akinetic mutism". The brain MRI showed diffuse hyperintensity of the white matter on T2-weighted fluid-attenuated inversion recovery sequences. These areas were bright on DWI and were hypointense on the apparent diffusion coefficient map. An extensive autoimmune, metabolic, toxicological, and infectious work-up included arylsulfatase A enzyme levels, which were unremarkable. Therapy with levodopa was initiated with subsequent improvement of the diffuse rigidity. At discharge, the patient continued to be lethargic with moderate rigidity but began to display signs of recovery. He eventually fully recovered with residual mild confusion. Thus, delayed hypoxic leukoencephalopathy is a rare complication of hypoxic-ischemic encephalopathy, occurring in 2.75% of victims of carbon monoxide poisoning. It typically manifests two to 40 days after apparent recovery from an obtunded state. Prognosis is variable, but recovery can be complete. This report brings to light an important syndrome that can easily be misdiagnosed. Patients who present with these clinical and radiographic features should be treated fully and given time to recover without abrupt withdrawal of care.

The authors report a 66 year-old female with past medical history relevant for thoracic abdominal aneurysm who presented with a complaint of chest pain radiating into her neck. The physical examination was significant for the distinctive facial features of wide spaced eyes and V-shaped uvula. Thoracic CT scan revealed a type I aortic dissection which warranted immediate surgical repair. On post-op day one she was noted to be confused and was found to have acute bilateral lower extremity paraparesis with proximal predominance. Furthermore, her left radial artery line had no pulse waves and no brachial, radial, or ulnar pulses could be detected with Doppler ultrasound. Emergent head CT scan revealed bilateral postcentral gyri infarctions and the thoracic CT scan demonstrated extension of the dissection into the aortic branches, including the left brachial and the bilateral carotid arteries. Consequently, surgical brachial artery repair ensued. In the interim, a repeated head CT scan demonstrated new ischemic infarcts involving the bilateral frontal lobes. Anticoagulation was not indicated due to the high risk of bleeding at surgical site. Genetic testing confirmed the presence of a mutation in the TGFBR2 gene at exon 5. Loeys-Dietz syndrome is an autosomal dominant disease caused by heterozygous mutations in the genes encoding type I or II transforming growth factor-β (TGF-β) receptor. Loeys-Dietz syndrome manifests with aggressive vascular pathology. This case underscores the importance of recognition of this spectrum of clinical and pathologic manifestations to identify and manage Loeys-Dietz syndrome.

Neuromyelitis optica (NMO, also eponymously known as Devic's disease) is an immune-mediated demyelinating disease of the central nervous system that can lead to significant disability. Pediatric NMO is a rare disorder often reported after an infection. The authors report a 16 year-old female patient with pemphigus foliaceus who developed subacute optic neuritis followed by cervical transverse myelitis. Restricted distribution of the lesions in the optic nerve and spinal cord was confirmed by ophthalmological evaluation and magnetic resonance imaging of the brain and spinal cord. She was started on intravenous methylprednisolone and then given a maintenance oral prednisone. Subsequently, she was treated with a nonsteroidal immunosuppressant, mycophenolate mofetil, with a target dose of 1000 mg twice a day. Over the course of months, patient noted significant recovery of previous deficits and resolution of the cervical cord enhancement, expansion and cystic dilatation that was previously seen. This case is noteworthy for being the first patient reported with neuromyelitis optica associated with pemphigus foliaceus.

Objective To demonstrate varicella zoster virus (VZV) infection in an asymptomatic extracranial (temporal) artery in a patient with ischemic optic neuropathy produced by VZV vasculopathy in whom the pathological changes were mistakenly identified as giant cell arteritis. Design Case report. Setting Teaching hospital, pathology and virology laboratory. Patient An 80-year-old man with left ophthalmic distribution zoster who developed left ischemic optic neuropathy. Intervention An ipsilateral temporal artery biopsy revealed inflammation that was mistakenly identified as giant cell arteritis. The patient was initially treated with steroids but his condition did not improve. When the diagnosis of VZV vasculopathy was confirmed virologically and the patient was treated with intravenous acyclovir, his vision improved. Results Pathological and virological studies provided proof of VZV vasculopathy in the asymptomatic temporal artery. Varicella zoster virus antigen was abundant in arterial adventitia and scattered throughout the media. With intravenous antiviral therapy, the patient's vision improved. Conclusion Although in previously studied patients who died of chronic VZV vasculopathy after 10 to 12 months, VZV antigen was present exclusively in the intima, collective analyses of chronic cases and the asymptomatic VZV-infected temporal artery suggest that virus enters arteries through the adventitia and spreads transmurally to the intima.

We present a 59-year-old male with early manifestation of opsoclonus associated with gait ataxia as a rare clinical presentation of Hashimoto's encephalopathy. Empiric use of intravenous immunoglobulin followed by intravenous high dose methylprednisolone was initiated with subsequent remittance of opsoclonus, encephalopathy, ataxia, and tremor. Extensive workup for infectious, autoimmune, and paraneoplastic etiologies were undertaken and all studies were negative. Thyroglobulin antibodies (312 U/mL) and thyroid peroxidase antibodies (457 U/mL) were elevated (normal

A 20-year-old man presented to the neurotrauma intensive care unit following blunt head injury. MRI revealed subarachnoid haemorrhage and multiple intraparenchymal haemorrhages suggesting severe brain injury. During recovery, the patient displayed intermittent episodes of alternating hemibody spasms with decerebrate/decorticate dystonic posturing. Episodes presented with autonomic dysregulation including hyperthermia, diaphoresis, tachypnoea, tachycardia and hypertension. Concern for seizure activity prompted simultaneous video monitoring and EEG testing. Results were without epileptiform activity suggesting against seizure as cause for alternating hemibody spasms. Paroxysmal autonomic instability with dystonia (PAID) was considered despite the unusual presentation. Intravenous hydromorphone was used for treatment, which relieved symptoms of autonomic dysregulation and dystonic posturing. PAID syndrome was diagnosed based on presentation with intermittent episodes of dystonia, autonomic dysregulation, absence of epileptiform activity and rapid response to opioid treatment. This case illustrates the clinical variability of this uncommon syndrome because alternating hemidystonia as main manifestation has not been previously described.

Objective: To demonstrate early manifestation of opsoclonus as a rare clinical presentation of Hashimoto9s encephalopathy in a patient with subsequent steroid responsive symptoms and antibody titers. Background Hashimoto9s encephalopathy typically presents in two varieties: relapsing/remitting, which manifests with encephalopathy and stroke-like episodes; and a diffuse progressive type, which has an insidious onset with occasional fluctuations and manifests with psychiatric symptoms and dementia. Either type may also present with tremor, myoclonus, seizures, stupor, or coma. Encephalopathy usually develops over 1 to 7 days. Treatment with corticosteroids is almost always successful, although relapse may occur if this treatment is ceased abruptly. On extensive case review, there has only been one previous case of opsoclonus described as an early manifestation of Hashimoto9s encephalopathy. Design/Methods: Case Report. Results: We present a 59 year old male patient with subacute onset of opsoclonus and gait ataxia. He insidiously developed vertigo associated with gait ataxia and after a few days, vertical diplopia that evolved into involuntary saccadic eye movements. Extensive workup of infectious, autoimmune and paraneoplastic etiologies were undertaken and all studies were negative. Thyroglobulin antibodies and Thyroid peroxidase antibodies were found to be elevated (312 U/ml and 457 U/ml respectively; normal Conclusions: This case underscores the importance of investigating Hashimoto9s encephalopathy as an etiology of opsoclonus in the atypically presenting case. Disclosure: Dr. Salazar has nothing to disclose. Dr. Mehta has nothing to disclose. Dr. Zaher has nothing to disclose. Dr. Miller has nothing to disclose.