New measles exposures in Palisades mall, Spring Valley as outbreak spreads

Two places in Spring Valley and a store at the Palisades Center are the latest locations health officials said may have been exposed to measles over Thanksgiving weekend.

With 83 measles cases in Rockland and eight more under investigation, health officials are cautioning that anyone in the county could be affected and everybody should check their immunization status.

Officials said the latest exposures happened at Compare Supermarket in Spring Valley between 7 and 9:30 p.m. on Nov. 22, Jalapa Express in Spring Valley between 5:30 and 7:45 p.m. on Nov. 24 and Best Buy at the Palisades Center between 7 and 9:30 p.m. on Nov. 24.

These times reflect when the infected person was in these locations and the two-hour period after they left, officials said. The Palisades Center exposure was only in Best Buy and not the rest of the mall.

https://www.lohud.com/story/news/local/rockland/2018/11/29/measles-spring-valley-palisades-mall-outbreak/2147114002/

Best Buy, Supermarket Shoppers May Have Been Exposed to Measles, NY Health Officials Say

Officials say there have been 83 confirmed measles cases in Rockland County and nearly a dozen other cases are being investigated

https://www.nbcnewyork.com/news/local/Measles-Outbreak-New-York-Rockland-County-501556391.html

Measles diagnosis closes Passaic yeshiva for girls; 3 cases confirmed in one household

The state Department of Health is working with local officials as it investigates an ongoing outbreak of measles that totals 18 cases, three confirmed in one household in the city of Passaic.

The household in Passaic County has a direct epidemiological link to the outbreak in Ocean County, where 15 cases have been confirmed.

Individuals infected with the virus range in age from 6 months to 59 years, according to the state Department of Health.

On Wednesday, the girls division of the Yeshiva Ktana of Passaic was closed after a "member" of the school's community was diagnosed with the measles, said state health officials. The "member" is one of the three confirmed cases in the city, said officials.

The decision to shut down Bais Yaakov for the day was made by the school, state health officials said. The Pennington Avenue school was re-opened Thursday, according to an employee who answered the phone but would not give her name.

https://www.dailyrecord.com/story/news/health/2018/11/29/measles-diagnosis-closes-yeshiva-ktana-passaic-school-girls-bais-yaakov/2147440002/

Where is the measles coming from?

AFM info

This review highlights clinical features of the increasing cases of acute flaccid paralysis associated with anterior myelitis noted in the United States from 2012 to 2015. Acute flaccid myelitis refers to acute flaccid limb weakness with spinal cord gray matter lesions on imaging or evidence of spinal cord motor neuron injury on electrodiagnostic testing. Although some individuals demonstrated improvement in motor weakness and functional deficits, most have residual weakness a year or more after onset. Epidemiological evidence and biological plausibility support an association between enterovirus D68 and the recent increase in acute flaccid myelitis cases in the United States.

From 2012 to 2015, increasing reports of a distinct syndrome of acute flaccid paralysis with anterior myelitis were noted in the United States, prompting increased surveillance.1,2 Previously, the terms “poliomyelitis” or ‘polio-like syndrome” were used to refer to this clinical presentation. In order to avoid confusion with disease caused by poliovirus, the terms “acute flaccid paralysis with anterior myelitis” and eventually “acute flaccid myelitis” (AFM) were coined to refer to cases of acute flaccid weakness with spinal cord gray matter lesions on imaging or evidence of spinal cord motor neuron injury on electrodiagnostic testing.1,3 The term AFM will be used throughout this review for consistency.

This review focuses on clinical features of the recent increase in AFM cases in the United States from 2012 to 2015. In this review, we provide a detailed description of published AFM cohorts in the United States from California, Colorado, and Utah, as well as epidemiological data from the Centers for Disease Control and Prevention (CDC) nation-wide surveillance and international case reports. We review the epidemiology, clinical characteristics, diagnostic testing, and therapeutic recommendations for AFM. We highlight distinguishing features that can be used to differentiate AFM from other known neurological causes of paralysis and compare the recently reported AFM cases to other infectious acute flaccid paralysis syndromes. Last, we weigh the evidence for and against the association of the recent increase in cases of AFM with enterovirus D68 and suggest areas for future research.

In the fall of 2012, the California Department of Public Health (CDPH) received three reports of cases of unexplained sudden paralysis; in 2 cases, poliovirus testing was requested. In response, the CDPH initiated enhanced state-wide surveillance in California for cases meeting a definition of acute-onset flaccid limb weakness with spinal gray matter lesion on magnetic resonance imaging (MRI) or electrodiagnostic studies consistent with anterior horn cell damage. From June 1, 2012 to July 31, 2015, 59 reported cases met the CDPH case definition.6

In August 2014, a cluster of children with a similar neurological syndrome presented to Children’s Hospital Colorado (CHCO) in Aurora, Colorado, in the midst of an outbreak of enterovirus D68 respiratory disease.2 A case definition of any patient presenting to CHCO with acute-onset focal limb weakness and/or cranial nerve dysfunction associated with MRI findings of predominantly gray matter lesions in the spinal cord and/or brainstem was used to identify children with this syndrome. From August to October of 2014, 12 children met the case definition.7

In response to the CDPH and CHCO reports, the CDC established a case definition for enhanced nationwide surveillance of AFM, which included individuals less than 21 years of age with acute flaccid limb weakness and MRI involvement of predominantly the gray matter of the spinal cord without identified etiology presenting after August 1, 2014. Between August and December of 2014, 120 children from 34 US states met the criteria.8 Ten children meeting the CDC AFM case definition and 1 additional child with cranial nerve dysfunction presenting to Primary Children’s Hospital (PCH) in Utah during the 2014 enterovirus D68 outbreak were subsequently reported.10 Tables 1 and ​and22 summarize clinical characteristics of the CDPH, CHCO, and PCH cohorts of AFM described above, as well as nation-wide CDC epidemiological data. Of note, CDC nation-wide epidemiological data include 24 CDPH, 9 CHCO, and 10 PCH cases. Following reports of the public health investigation of AFM cases associated with enterovirus D68 in the United States, cases of acute flaccid paralysis associated with enterovirus D68 have been reported from Canada,11,12 France,13 Norway,14 and Great Britain15,16 (Supplementary Table).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5098271/

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Management

Immunomodulatory and/or antiviral agents were administered to most AFM cases in the United States, though the retrospective nature of data from these cohorts does not allow systematic assessment of response to treatment. The majority of AFM patients received intravenous immune globulin (IVIG), many received high-dose intravenous steroids, several underwent plasmapheresis, and some received antiviral therapy (Table 3).6–8,10 No significant clinical improvement or deterioration was noted with any of these therapies.

In November 2014, the CDC drafted interim suggestions for management of children with AFM, based primarily on expert opinion.5 Because of the possibility of an active neuroinvasive infectious process without effective antiviral therapy, the CDC recommended reducing immunosuppression medications, when possible, and discouraged the use of steroids and plasmapheresis. However, there is incomplete understanding of the pathophysiology of AFM and no clinical trial data available to guide therapeutic recommendations. It remains uncertain whether AFM is an active infectious process or a postinfectious inflammatory process; therefore, the use of immunomodulatory therapies remains controversial. In cases of severe cord edema, judicious use of steroids may be necessary to limit additional cord injury.

Given the lack of a clear indication for efficacy in treatment of AFM, use of IVIG was not endorsed in the CDC interim recommendations. IVIG has been shown to help prevent poliovirus poliomyelitis when administered before exposure, but fails to prevent or impact severity of paralysis when administered after poliovirus infection in cases of preparalytic poliomyelitis.21–23 In agammaglobulinemic children, IVIG has efficacy in treatment of chronic enteroviral central nervous system (CNS) infections, suggesting a role for antibody-mediated immunity.24 IVIG has also been shown to modulate systemic and CNS cytokine production in enterovirus A71 encephalitis, though effect on clinical outcomes has not been systematically evaluated.25 In 2014, all commercially available preparations of IVIG tested contained high levels of neutralizing antibody against the circulating strains of enterovirus D68 in the United States.26 It is the opinion of these authors that in the absence of alternative effective therapies, IVIG may be the safest available therapy with the potential for efficacy if given very early in the course of disease or in immunocompromised patients with enterovirus-associated AFM.

In the absence of a confirmed viral etiology and in vitro susceptibility of available antivirals at the time of publication of the CDC interim recommendations, there were insufficient data to recommend antiviral treatment.5 However, fluoxetine has since been confirmed to have in vitro antiviral activity against enterovirus D68 (including the 2014 outbreak strain) and other enteroviruses.27–29 A recent case report describes favorable response to fluoxetine in a patient with X-linked agammaglobulinemia and chronic enterovirus (coxsackie B virus) encephalitis.30 Fluoxetine has been proposed as a potential therapeutic agent to be investigated in enterovirus-associated cases of AFM.31

Vigilant supportive care was identified by the CDC recommendations as the mainstay of AFM management. This includes mechanical ventilation in cases of impaired airway protection attributed to bulbar weakness or respiratory failure resulting from diaphragmatic paralysis, as well as feeding support in cases of loss of bulbar function. Physical and occupational rehabilitation therapies are recommended as soon as the patient is clinically stable in order to prevent atrophy and contractures and maximize functional outcomes. Rehabilitation needs of AFM patients can be extensive and may require inpatient and outpatient therapies at a dedicated center with multidisciplinary experience. Nerve or muscle transfers have been used for brachial plexus polio-like paralysis cases.32 These transfer procedures have been proposed as a possible therapeutic option in patients with no innervation of functional muscle groups, though no reports exist on the use of this procedure for AFM. Furthermore, the timing of when the procedure may be of highest yield and minimal risk is not known. Support for the psychological as well as physical effects of disability should be provided for those afflicted.

>>4078894

Course

Nearly all patients diagnosed during the acute phase of their illness were hospitalized. A significant proportion required invasive or noninvasive ventilatory support because of bulbar weakness and inability to protect the airway, or for respiratory failure attributed to paralysis of the respiratory musculature.6–8,10 Ventilated patients required prolonged intensive care unit stays, and some continued to be ventilator dependent at the time of hospital discharge.6,7,10 The CDPH reported two deaths among their cohort, both in immunocompromised adults.6

Most patients developed significant muscle atrophy in the affected limbs in the weeks to months following onset of weakness.33 Some patients experienced persistent pain for weeks to months after onset. Extent of recovery has varied greatly.6 Of 45 patients in the CDPH cohort with follow-up data available at a median of 9 months, complete recovery was noted in 7 (16%). All children in the PCH cohort showed improvement in neurological abnormalities, though 9 of 10 (90%) had residual motor deficits at last follow-up (median, 6 months).10 At 1-year follow-up in the CHCO cohort, minimal to no improvement in strength was observed in the most profoundly affected proximal muscle groups, whereas less-affected distal muscle groups and cranial nerve impairments were noted to improve or resolve.34 Functional gains were noted with rehabilitation therapies involving recruitment of surrounding muscle groups, even in cases with no objective improvement in strength of affected muscles. Nationwide, only 3 (5%) of 56 AFM patients reported complete recovery of strength and 10 (18%) reported being fully functional at a median of 4.2 months after onset.8

Comparison With Known Neurological Entities

The combination of hypotonic weakness and radiographical or electrophysiological evidence of anterior horn cell disease are the most specific findings in AFM. Factors that help to clinically differentiate AFM from other neurological causes of limb paralysis, such as idiopathic transverse myelitis, acute inflammatory demyelinating polyneuropathy (Guillain Barré Syndrome), and acute disseminated encephalomyelitis, are presented in Tables 3 and ​and4.4. The pattern of tropism for spinal cord motor neurons in recent AFM cases in the United States is clinically, radiographically, and electrophysiologically similar to other infectious acute flaccid paralysis syndromes (such as poliovirus, enterovirus A71, enterovirus D70, West Nile virus, and Japanese encephalitis virus), suggesting a common pathophysiology.35–41 Indeed, these other infectious acute flaccid paralysis syndromes would all meet the current AFM case criteria. Hopkins’ syndrome may be a historical clinical description of AFM. First described in 1972, Hopkins’ syndrome is a rare disorder of children presenting with asymmetric flaccid limb weakness following an asthma-like acute respiratory illness with clinical features and imaging similar to recent AFM cases in the United States.42–44

Etiological Investigations

Given that the vast majority of AFM cases had received the recommended schedule of vaccines and that wild-type or vaccine strain poliovirus was not identified in any AFM case in the United States, poliovirus is unlikely to have contributed to the increase in AFM cases in the United States. No infectious agents of clinical significance have been identified in the CSF of any of the 2012–2015 AFM cases in the United States, despite extensive microbiological investigations, including next-generation sequencing for novel pathogens, with the exception of enterovirus D68 identified in the CSF of 1 patient with a bloody lumbar puncture.8,9,45 A variety of nonenteroviral respiratory viruses was identified in respiratory specimens from individual cases, including a variety of rhinoviruses, respiratory syncytial virus, influenza virus, parainfluenza virus, and adenovirus.6–8,10 Several nonpolio enteroviruses were identified in respiratory or stool specimens from AFM cases.3,6,7,46 Of these, enterovirus D68 was the most commonly identified infectious agent and the only virus identified in ≥2 cases.8 Five of 11 (45%) AFM cases at CHCO and 9 of 41 (22%) AFM cases from the CDPH with respiratory specimens tested were positive for enterovirus D68, whereas none of the PCH cases had enterovirus D68 identified.6,7,10 Of 17 nation-wide AFM cases reported to CDC with respiratory specimens collected within 7 days, 8 (47%) were positive for enterovirus D68.3