Mass Gatherings and Diarrheal Disease Transmission Among Rural Communities in Coastal Ecuador.

Mass gatherings exacerbate infectious disease risks by creating crowded, high-contact conditions and straining the capacity of local infrastructure. While mass gatherings have been extensively studied in the context of epidemic disease transmission, the role of gatherings in incidence of high-burden, endemic infections has not been previously studied. Here, we examine diarrheal incidence among 17 communities in Esmeraldas, Ecuador, in relation to recurrent gatherings characterized using ethnographic data collected during and after the epidemiologic surveillance period (2004-2007). Using distributed-lag generalized estimating equations, adjusted for seasonality, trend, and heavy rainfall events, we found significant increases in diarrhea risk in host villages, peaking 2 weeks after an event's conclusion (incidence rate ratio, 1.21; confidence interval, adjusted for false coverage rate of ≤0.05: 1.02, 1.43). Stratified analysis revealed heightened risks associated with events where crowding and travel were most likely (2-week-lag incidence rate ratio, 1.51; confidence interval, adjusted for false coverage rate of ≤0.05: 1.09, 2.10). Our findings suggest that community-scale mass gatherings might play an important role in endemic diarrheal disease transmission and could be an important focus for interventions to improve community health in low-resource settings.

Acute Flaccid Myelitis of Unknown Etiology in California, 2012-2015.

IMPORTANCE: There has been limited surveillance for acute flaccid paralysis in North America since the regional eradication of poliovirus. In 2012, the California Department of Public Health received several reports of acute flaccid paralysis cases of unknown etiology. OBJECTIVE: To quantify disease incidence and identify potential etiologies of acute flaccid paralysis cases with evidence of spinal motor neuron injury. DESIGN, SETTING, AND PARTICIPANTS: Case series of acute flaccid paralysis in patients with radiological or neurophysiological findings suggestive of spinal motor neuron involvement reported to the California Department of Public Health with symptom onset between June 2012 and July 2015. Patients meeting diagnostic criteria for other acute flaccid paralysis etiologies were excluded. Cerebrospinal fluid, serum samples, nasopharyngeal swab specimens, and stool specimens were submitted to the state laboratory for infectious agent testing. MAIN OUTCOMES AND MEASURES: Case incidence and infectious agent association. RESULTS: Fifty-nine cases were identified. Median age was 9 years (interquartile range [IQR], 4-14 years; 50 of the cases were younger than 21 years). Symptoms that preceded or were concurrent included respiratory or gastrointestinal illness (n = 54), fever (n = 47), and limb myalgia (n = 41). Fifty-six patients had T2 hyperintensity of spinal gray matter on magnetic resonance imaging and 43 patients had cerebrospinal fluid pleocytosis. During the course of the initial hospitalization, 42 patients received intravenous steroids; 43, intravenous immunoglobulin; and 13, plasma exchange; or a combination of these treatments. Among 45 patients with follow-up data, 38 had persistent weakness at a median follow-up of 9 months (IQR, 3-12 months). Two patients, both immunocompromised adults, died within 60 days of symptom onset. Enteroviruses were the most frequently detected pathogen in either nasopharynx swab specimens, stool specimens, serum samples (15 of 45 patients tested). No pathogens were isolated from the cerebrospinal fluid. The incidence of reported cases was significantly higher during a national enterovirus D68 outbreak occurring from August 2014 through January 2015 (0.16 cases per 100,000 person-years) compared with other monitoring periods (0.028 cases per 100,000 person-years; P <.001). CONCLUSIONS AND RELEVANCE: In this series of patients identified in California from June 2012 through July 2015, clinical manifestations indicated a rare but distinct syndrome of acute flaccid paralysis with evidence of spinal motor neuron involvement. The etiology remains undetermined, most patients were children and young adults, and motor weakness was prolonged.

Influenza-associated intensive-care unit admissions and deaths - California, September 29, 2013-January 18, 2014.

The California Department of Public Health (CDPH) conducts surveillance on severe influenza illness among California residents aged <65 years. Severe cases are defined as those resulting in admission to an intensive care unit (ICU) or death; reporting of ICU cases is voluntary, and reporting of fatal cases is mandatory. This report describes the epidemiologic, laboratory, and clinical characteristics of ICU and fatal influenza cases with symptom onset on or after September 29, 2013, and reported by January 18, 2014 of the 2013-14 influenza season. At the time of this report, local health jurisdictions (LHJs) in California had reported 94 deaths and 311 ICU admissions of patients with a positive influenza test result. The 405 reports of severe cases (i.e., fatal and ICU cases combined) were more than in any season since the 2009 pandemic caused by the influenza A (H1N1)pdm09 (pH1N1) virus. The pH1N1 virus is the predominant circulating influenza virus this season. Of 405 ICU and fatal influenza cases, 266 (66%) occurred among patients aged 41-64 years; 39 (10%) severe influenza illnesses occurred among children aged <18 years. Only six (21%) of 28 patients with fatal illness whose vaccination status was known had received 2013-14 seasonal influenza vaccine ≥2 weeks before symptom onset. Of 80 patients who died for whom sufficient information was available, 74 (93%) had underlying medical conditions known to increase the risk for severe influenza, as defined by the Advisory Committee on Immunization Practices (ACIP). Of 47 hospitalized patients with fatal illness and known symptom onset and antiviral therapy dates, only eight (17%) received neuraminidase inhibitors within 48 hours of symptom onset. This report supports previous recommendations that vaccination is important to prevent influenza virus infections that can result in ICU admission or death, particularly in high-risk populations, and that empiric antiviral treatment should be promptly initiated when influenza virus infection is suspected in hospitalized patients, despite negative results from rapid diagnostic tests.

Pregnancy and severe influenza infection in the 2013-2014 influenza season.

OBJECTIVE: To describe the epidemiologic and clinical characteristics of critically ill pregnant and postpartum women with influenza infection reported in the 2013-2014 season. METHODS: The California Department of Public Health conducts surveillance for patients with laboratory-confirmed influenza who die or require hospitalization in intensive care units. For this case series, we reviewed data on pregnant and postpartum (6 weeks or less from delivery) women reported in the 2013-2014 influenza season. RESULTS: From September 29, 2013, through May 17, 2014, 17 pregnant women with severe influenza were reported. The median age was 29 years (range 17-44 years). Sixteen (94%) were in the second or third trimester. Fifteen (88%) patients were hospitalized, nine (53%) required mechanical ventilation, five (29%) required emergent cesarean delivery, and four (24%) died. Of 14 patients with available information, only two (14%) received influenza vaccination during pregnancy. Seven patients who tested positive by polymerase chain reaction also had rapid influenza diagnostic testing performed; only one (14%) had a positive rapid influenza diagnostic test results. Fifteen patients received antiviral treatment; four (27%) began treatment within 48 hours of symptom onset. One additional patient was 36 days postpartum and required intensive care unit admission and mechanical ventilation for influenza-associated acute respiratory distress syndrome. CONCLUSION: Influenza remains a significant cause of morbidity and mortality in pregnant and postpartum women; in our series, a majority were not vaccinated. During the influenza season, pregnant women with suspected influenza should receive prompt empiric antiviral therapy, regardless of rapid influenza diagnostic test results or vaccination status. LEVEL OF EVIDENCE: III.

Contact hypersensitivity to oxazolone provokes vulvar mechanical hyperalgesia in mice.

The interplay among pain, allergy and dysregulated inflammation promises to yield significant conceptual advances in immunology and chronic pain. Hapten-mediated contact hypersensitivity reactions are used to model skin allergies in rodents but have not been utilized to study associated changes in pain perception in the affected skin. Here we characterized changes in mechanical hyperalgesia in oxazolone-sensitized female mice challenged with single and repeated labiar skin exposure to oxazolone. Female mice were sensitized with topical oxazolone on their flanks and challenged 1-3 times on the labia. We then measured mechanical sensitivity of the vulvar region with an electronic pressure meter and evaluated expression of inflammatory genes, leukocyte influx and levels of innervation in the labiar tissue. Oxazolone-sensitized mice developed vulvar mechanical hyperalgesia after a single labiar oxazolone challenge. Hyperalgesia lasted up to 24 hours along with local influx of neutrophils, upregulation of inflammatory cytokine gene expression, and increased density of cutaneous labiar nerve fibers. Three daily oxazolone challenges produced vulvar mechanical hyperalgesic responses and increases in nerve density that were detectable up to 5 days post-challenge even after overt inflammation resolved. This persistent vulvar hyperalgesia is resonant with vulvodynia, an understudied chronic pain condition that is remarkably prevalent in 18-60 year-old women. An elevated risk for vulvodynia has been associated with a history of environmental allergies. Our pre-clinical model can be readily adapted to regimens of chronic exposures and long-term assessment of vulvar pain with and without concurrent inflammation to improve our understanding of mechanisms underlying subsets of vulvodynia and to develop new therapeutics for this condition.