Publications by authors named "Jeffrey Ratto"

7 Publications

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The Effects of an Integrated Community Case Management Strategy on the Appropriate Treatment of Children and Child Mortality in Kono District, Sierra Leone: A Program Evaluation.

Am J Trop Med Hyg 2017 Sep 19;97(3):964-973. Epub 2017 Jul 19.

Health Unit, International Rescue Committee, New York, New York.

Integrated community case management (iCCM) aims to reduce child mortality in areas with poor access to health care. iCCM was implemented in 2009 in Kono district, Sierra Leone, a postconflict area with high under-five mortality rates (U5MRs). We evaluated iCCM's impact and effects on child health using cluster surveys in 2010 (midterm) and 2013 (endline) to compare indicators on child mortality, coverage of appropriate treatment, timely access to care, quality of care, and recognition of community health workers (CHWs). The sample size was powered to detect a 28% decline in U5MR. Clusters were selected proportional to population size. All households were sampled to measure mortality and systematic random sampling was used to measure coverage in a subset of households. We used program data to evaluate utilization and access; 5,257 (2010) and 3,649 (2013) households were surveyed. U5MR did not change significantly (4.54 [95% confidence interval [CI]: 3.47-5.60] to 3.95 [95% CI: 3.06-4.83] deaths per 1,000 per month ( = 0.4)) though a relative change smaller than 28% could not be detected. CHWs were the first source of care for 52% (2010) and 50.9% (2013) of children. Coverage of appropriate treatment of fever by CHWs or peripheral health units increased from 45.5% [95% CI: 39.2-52.0] to 58.2% [95% CI: 50.5-65.5] ( = 0.01); changes for diarrhea and pneumonia were not significant. The continued reliance on the CHW as the first source of care and improved coverage for the appropriate treatment of fever support iCCM's role in Kono district.
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http://dx.doi.org/10.4269/ajtmh.17-0040DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5590598PMC
September 2017

Nodding syndrome may be an autoimmune reaction to the parasitic worm .

Sci Transl Med 2017 02;9(377)

Section of Infections of the Nervous System, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.

Nodding syndrome is an epileptic disorder of unknown etiology that occurs in children in East Africa. There is an epidemiological association with , the parasitic worm that causes onchocerciasis (river blindness), but there is limited evidence that the parasite itself is neuroinvasive. We hypothesized that nodding syndrome may be an autoimmune-mediated disease. Using protein chip methodology, we detected autoantibodies to leiomodin-1 more abundantly in patients with nodding syndrome compared to unaffected controls from the same village. Leiomodin-1 autoantibodies were found in both the sera and cerebrospinal fluid of patients with nodding syndrome. Leiomodin-1 was found to be expressed in mature and developing human neurons in vitro and was localized in mouse brain to the CA3 region of the hippocampus, Purkinje cells in the cerebellum, and cortical neurons, structures that also appear to be affected in patients with nodding syndrome. Antibodies targeting leiomodin-1 were neurotoxic in vitro, and leiomodin-1 antibodies purified from patients with nodding syndrome were cross-reactive with antigens. This study provides initial evidence supporting the hypothesis that nodding syndrome is an autoimmune epileptic disorder caused by molecular mimicry with antigens and suggests that patients may benefit from immunomodulatory therapies.
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http://dx.doi.org/10.1126/scitranslmed.aaf6953DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5434766PMC
February 2017

Notes from the Field: Ebola Virus Disease Response Activities During a Mass Displacement Event After Flooding--Freetown, Sierra Leone, September-November, 2015.

MMWR Morb Mortal Wkly Rep 2016 Feb 26;65(7):188-9. Epub 2016 Feb 26.

Since the start of the Ebola virus disease (Ebola) outbreak in West Africa, Sierra Leone has reported 8,706 confirmed Ebola cases and 3,956 deaths. During September 15-16, 2015, heavy rains flooded the capital, Freetown, resulting in eight deaths, home and property destruction, and thousands of persons in need of assistance. By September 27, approximately 13,000 flood-affected persons registered for flood relief services from the government. On September 17, two stadiums in Freetown were opened to provide shelter and assistance to flood-affected residents; a total of approximately 3,000 persons stayed overnight in both stadiums (Sierra Leone Ministry of Health and Sanitation, personal communication, September 2015). On the same day the stadiums were opened to flood-affected persons, the Ministry of Health and Sanitation (MoHS) and Western Area Ebola Response Center (WAERC) staff members from CDC, the World Health Organization (WHO), and the African Union evaluated the layout, logistics, and services at both stadiums and identified an immediate need to establish Ebola response activities. The patient in the last Ebola case in the Western Area, which includes Freetown, had died 37 days earlier, on August 11; however, transmission elsewhere in Sierra Leone was ongoing, and movement of persons throughout the country was common.
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http://dx.doi.org/10.15585/mmwr.mm6507a4DOI Listing
February 2016

Ebola Virus Disease--Sierra Leone and Guinea, August 2015.

MMWR Morb Mortal Wkly Rep 2015 Sep 11;64(35):981-4. Epub 2015 Sep 11.

The Ebola virus disease (Ebola) outbreak in West Africa began in late 2013 in Guinea (1) and spread unchecked during early 2014. By mid-2014, it had become the first Ebola epidemic ever documented. Transmission was occurring in multiple districts of Guinea, Liberia, and Sierra Leone, and for the first time, in capital cities (2). On August 8, 2014, the World Health Organization (WHO) declared the outbreak to be a Public Health Emergency of International Concern (3). Ministries of Health, with assistance from multinational collaborators, have reduced Ebola transmission, and the number of cases is now declining. While Liberia has not reported a case since July 12, 2015, transmission has continued in Guinea and Sierra Leone, although the numbers of cases reported are at the lowest point in a year. In August 2015, Guinea and Sierra Leone reported 10 and four confirmed cases, respectively, compared with a peak of 526 (Guinea) and 1,997 (Sierra Leone) in November 2014. This report details the current situation in Guinea and Sierra Leone, outlines strategies to interrupt transmission, and highlights the need to maintain public health response capacity and vigilance for new cases at this critical time to end the outbreak.
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http://dx.doi.org/10.15585/mmwr.mm6435a6DOI Listing
September 2015

Prevalence of nodding syndrome--Uganda, 2012-2013.

MMWR Morb Mortal Wkly Rep 2014 Jul;63(28):603-6

Nodding syndrome (NS) is a seizure disorder of unknown etiology, predominately affecting children aged 3-18 years in three sub-Saharan countries (Uganda, South Sudan, and Tanzania), with the primary feature of episodic head nodding. These episodes are thought to be one manifestation of a syndrome that includes neurologic deterioration, cognitive impairment, and additional seizure types. NS investigations have focused on clinical features, progression, and etiology; however, none have provided a population-based prevalence assessment using a standardized case definition. In March 2013, CDC and the Ugandan Ministry of Health (MOH) conducted a single-stage cluster survey to perform the first systematic assessment of prevalence of NS in Uganda using a new consensus case definition, which was modified during the course of the investigation. Based on the modified definition, the estimated number of probable NS cases in children aged 5-18 years in three northern Uganda districts was 1,687 (95% confidence interval [CI] = 1,463-1,912), for a prevalence of 6.8 (CI = 5.9-7.7) probable NS cases per 1,000 children aged 5-18 years in the three districts. These findings can guide the MOH to understand and provide the health-care resources necessary to address NS in northern Uganda, and provide a basis for future studies of NS in Uganda and in other areas affected by NS.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5779414PMC
July 2014

Clinical, neurological, and electrophysiological features of nodding syndrome in Kitgum, Uganda: an observational case series.

Lancet Neurol 2013 Feb 8;12(2):166-74. Epub 2013 Jan 8.

Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA, USA.

Background: Nodding syndrome is an unexplained illness characterised by head-bobbing spells. The clinical and epidemiological features are incompletely described, and the explanation for the nodding and the underlying cause of nodding syndrome are unknown. We aimed to describe the clinical and neurological diagnostic features of this illness.

Methods: In December, 2009, we did a multifaceted investigation to assess epidemiological and clinical illness features in 13 parishes in Kitgum District, Uganda. We defined a case as a previously healthy child aged 5-15 years with reported nodding and at least one other neurological deficit. Children from a systematic sample of a case-control investigation were enrolled in a clinical case series which included history, physical assessment, and neurological examinations; a subset had electroencephalography (EEG), electromyography, brain MRI, CSF analysis, or a combination of these analyses. We reassessed the available children 8 months later.

Findings: We enrolled 23 children (median age 12 years, range 7-15 years) in the case-series investigation, all of whom reported at least daily head nodding. 14 children had reported seizures. Seven (30%) children had gross cognitive impairment, and children with nodding did worse on cognitive tasks than did age-matched controls, with significantly lower scores on tests of short-term recall and attention, semantic fluency and fund of knowledge, and motor praxis. We obtained CSF samples from 16 children, all of which had normal glucose and protein concentrations. EEG of 12 children with nodding syndrome showed disorganised, slow background (n=10), and interictal generalised 2·5-3·0 Hz spike and slow waves (n=10). Two children had nodding episodes during EEG, which showed generalised electrodecrement and paraspinal electromyography dropout consistent with atonic seizures. MRI in four of five children showed generalised cerebral and cerebellar atrophy. Reassessment of 12 children found that six worsened in their clinical condition between the first evaluation and the follow-up evaluation interval, as indicated by more frequent head nodding or seizure episodes, and none had cessation or decrease in frequency of these episodes.

Interpretation: Nodding syndrome is an epidemic epilepsy associated with encephalopathy, with head nodding caused by atonic seizures. The natural history, cause, and management of the disorder remain to be determined.

Funding: Division of Global Disease Detection and Emergency Response, US Centers for Disease Control and Prevention.
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http://dx.doi.org/10.1016/S1474-4422(12)70321-6DOI Listing
February 2013

Effects of multiday exposure to ozone on airway inflammation as determined using sputum induction.

Environ Health Perspect 2006 Feb;114(2):209-12

Lung Biology Center, University of California San Francisco, San Francisco, California 94143-0843, USA.

Single short-term exposures to ozone are known to cause acute changes in pulmonary function and neutrophilic airway inflammation. The respiratory health effects of repeated exposures are not as well studied. Pulmonary function decrements are known to attenuate, but it is less clear how injury and inflammation are affected. Using sputum induction (SI) to sample respiratory tract lining fluid after single- and multiday exposures, we designed a study to test the hypothesis that neutrophils would increase after multiday exposure compared with single-day exposure. In a randomized, crossover design, 15 normal healthy subjects were exposed to O3 (0.2 ppm) under two conditions: for 4 hr for 1 day (1D) and for 4 hr for 4 consecutive days (4D). Pulmonary function testing was performed immediately before and after each 4-hr exposure. The SI was performed 18 hr after the end of the 1D and 4D conditions. The symptom and pulmonary function data followed a pattern seen in other multiday O3 exposure studies, with the greatest changes occurring on the second day. In contrast to previous studies using bronchoalveolar lavage, however, there was a significant increase in the percentage of neutrophils and a significant decrease in the percentage of macrophages after the 4D condition compared with the 1D condition. Given that SI likely samples proximal airways better than distal lung, these results add to the body of evidence that differential airway compartmental responses to O3 occur in humans and other species.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1367833PMC
http://dx.doi.org/10.1289/ehp.8341DOI Listing
February 2006
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