Polio Outbreak Investigation and Response in The Horn of Africa: 2013-2016.

BACKGROUND: There has been civil strife, spanning more than two decades in some countries and recurrent natural disasters in the Horn of Africa (HoA). This has consistently maintained these countries in chronic humanitarian conditions. More important however is the fact that these crises have also denied populations of these countries access to access to lifesaving health services. Children in the difficult terrains and security compromised areas are not given the required immunization services to build their immunity against infectious diseases like the poliovirus. This was the situation in 2013 when the large outbreaks of poliovirus occurred in the HoA. This article reviews the epidemiology, risk, and programme response to what is now famed as the 2013-204 poliovirus outbreaks in the HoA and highlights the challenges that the programme faced in interrupting poliovirus transmission here. METHODS: A case of acute flaccid paralysis (AFP) was defined as a child <15 years of age with sudden onset of fever and paralysis. Polio cases were defined as AFP cases with stool specimens positive for WPV. RESULTS: Between 2013 and 2016, when transmission was interrupted 20,266 polio viruses were in the Horn of Africa region. In response to the outbreak, several supplementary immunization activities were conducted with oral polio vaccine (OPV) The trivalent OPV was used initially, followed subsequently by bivalent OPV, and targeting various age groups, including children aged <5 years, children aged <10 years, and individuals of any age. Other response activities were undertaken to supplement the immunization in controlling the outbreak. Some of these activities included the use of various communication strategies to create awareness, sensitize and mobilize the populations against poliovirus transmission. CONCLUSIONS: The outbreaks were attributed to the existence of clusters of unvaccinated children due to inaccessibility to them by the health system, caused by poor geographical terrain and conflicts. The key lesson therefore is that the existence of populations with low immunity to infections will necessary constitutes breeding grounds for disease outbreak and of course reservoirs to the vectors. Though brought under reasonable control, the outbreaks indicate that the threat of large polio outbreaks resulting from poliovirus importation will remain constant unless polio transmission is interrupted in the remaining polio-endemic countries of the world.

Lessons Learnt from Interregional and Interagency Collaboration in Polio Outbreak Response in the Horn of Africa.

Following the outbreak of poliovirus in the countries in the Horn of Africa, Somalia, Kenya and Ethiopia, in two WHO regions, an outbreak response involving the WHO Africa and WHO East and Mediterranean Regions and partner agencies like the UNICEF in East and Southern African was developed. This paper documents response to polio virus outbreak in the Horn of Africa and the lessons learnt for the interregional and inter-agency collaboration on the response. This collaboration led to speedy interruption of the outbreak and within a period of one year the total virus load of 217 in 2013 was brought down to mere six. This resulted from collaborative planning and implementation of activities to boost the hitherto low immunity in the countries andimprove surveillance among others. A number of lesson were generated from the process. Some of the lessons is critical role such collaboration plays in ensuring simultaneous immunity boosting, information and resources sharing, among other. Some challenges were equally encountered, chiefly in the appropriation of authorities. In conclusion, however, one is safe to note that the collaboration was very fruitful given the timely interruption of transmission.

Effectiveness of the Horn of Africa Polio Outbreak Coordination Office in Nairobi, Kenya.

Background: The WPV1, first detected in Somalia in April 2013, quickly spread to Kenya and Ethiopia and triggered a multi-country coordinated effort. In February 2014, a formal HoA Polio Outbreak Coordination Office was established by WHO AFRO and WHO EMRO in Nairobi to provide technical and managerial leadership. An independent assessment was conducted to ascertain the usefulness of the HoA Coordination in response to the outbreaks. Methods: The independent assessment team conducted desk review of the rules and guidelines forming the HoA Coordination office and committee. It also reviewed minutes of meetings and interviewed various stakeholders at the Regional levels. Results: This independent review of the work of the office, in September 2016, showed that the office was fully functional and had benefited from financial and technical support from regional and global GPEI partners. The office is based in the WHO Kenya Country Office which also provides administrative, logistics and until August 2016, data management support. The close working relationship with technical partners ensured alignment and close coordination of outbreak response activities. The mechanism also allowed partners to identify areas of work based on their expertise and avoided duplication of efforts at the local level. Overall, the office was effective in close monitoring of implementation of the outbreak response, strengthening of cross-border activities, monitoring implementation of the TAG recommendations, improving SIA planning and quality, and expanding independent monitoring in Somalia and South Sudan. Key constraints included limited office space for day-to-day operations, and disruption of some activities due to interruption of contracts of technical staff. However, the closure of the HoA outbreak in August 2015 led to some complacency, resulting in a lost sense of urgency, negatively impacting the coordination. Conclusions: The HoA Coordination Office should continue to function into the foreseeable future. To ensure sustainability of activities, the technical staff should be given contracts for a minimum of 12 months. The Office should reintroduce and schedule the Joint Polio Outbreak Response team meetings at least once every three months.

The effectiveness of N-acetyl-L-cysteine (L-NAC) in the prevention of severe noise-induced hearing loss.

Three groups of chinchillas were exposed to a nonGaussian continuous broadband noise at an Leq=10 5dB SPL, 8h/d for 5d. One group (N=6) received only the noise. A second group (N=6) received the noise and was additionally treated with L-NAC (325 mg/kg, i.p.). Treatment was administered twice daily for 2d prior to exposure and for 2d following the exposure. During exposure the animals received the L-NAC just prior to and immediately after each daily exposure. The third group (N=4) was exposed to the noise and received saline injections on the same schedule as the L-NAC treated animals. Auditory evoked potential recordings from the inferior colliculus were used to estimate pure tone thresholds and surface preparations of the organ of Corti quantified the sensory cell population. In all three groups PTS exceeded 50 dB at 2.0k Hz and above with severe sensory cell loss in the basal half of the cochlea. There was no statistically significant difference among the three groups in all measures of noise-induced trauma. Treatment with L-NAC did not reduce the trauma produced by a high-level, long duration, broadband noise exposure.

Hearing loss from interrupted, intermittent, and time varying non-Gaussian noise exposure: The applicability of the equal energy hypothesis.

Sixteen groups of chinchillas (N=140) were exposed to various equivalent energy noise paradigms at 100 dB(A) or 103 dB(A) SPL. Eleven groups received an interrupted, intermittent, and time varying (IITV) non-Gaussian exposure quantified by the kurtosis statistic. The IITV exposures, which lasted for 8 hday, 5 daysweek for 3 weeks, were designed to model some of the essential features of an industrial workweek. Five equivalent energy reference groups were exposed to either a Gaussian or non-Gaussian 5 days, 24 hday continuous noise. Evoked potentials were used to estimate hearing thresholds and surface preparations of the organ of Corti quantified the sensory cell population. For IITV exposures at an equivalent energy and kurtosis, the temporal variations in level did not alter trauma and in some cases the IITV exposures produced results similar to those found for the 5 day continuous exposures. Any increase in kurtosis at a fixed energy was accompanied by an increase in noise-induced trauma. These results suggest that the equal energy hypothesis is an acceptable approach to evaluating noise exposures for hearing conservation purposes provided that the kurtosis of the amplitude distribution is taken into consideration. Temporal variations in noise levels seem to have little effect on trauma.

Hearing loss from interrupted, intermittent, and time varying Gaussian noise exposures: the applicability of the equal energy hypothesis.

Eight groups of chinchillas (N=74) were exposed to various equivalent energy [100 or 106 dB(A) sound pressure level (SPL)] noise exposure paradigms. Six groups received an interrupted, intermittent, time varying (IITV) Gaussian noise exposure that lasted 8 h/d, 5 d/week for 3 weeks. The exposures modeled an idealized workweek. At each level, three different temporal patterns of Gaussian IITV noise were used. The 100 dB(A) IITV exposure had a dB range of 90-108 dB SPL while the range of the 106 dB(A) IITV exposure was 80-115 dB SPL. Two reference groups were exposed to a uniform 100 or 106 dB(A) SPL noise, 24 h/d for 5 days. Each reference group and the three corresponding IITV groups comprised a set of equivalent energy exposures. Evoked potentials were used to estimate hearing thresholds and surface preparation histology quantified sensory cell populations. All six groups exposed to the IITV noise showed threshold toughening effects of up to 40 dB. All IITV exposures produced hearing and sensory cell loss that was similar to their respective equivalent energy reference group. These results indicate that for Gaussian noise the equal energy hypothesis for noise-induced hearing loss is an acceptable unifying principle.

Indigenous health research: a critical review of outputs over time.

OBJECTIVE: To determine the number and nature of publications on Indigenous health in Australia, Canada, New Zealand and the United States) in 1987-1988, 1997-1998 and 2001-2003. DATA SOURCES: MEDLINE and PsychLit databases were searched using the following terms: Aborigines or Aboriginal; Torres Strait Islander; Maori; American Indian; North American Indian, or Indian, North American; Alaska/an Native; Native Hawaiian; Native American; American Samoan; Eskimos or Inuit; Eskimos or Aleut; Metis; Indigenous. STUDY SELECTION: Publications were included if they were concerned with the health of Indigenous people of the relevant countries. 1763 Indigenous health publications were selected. DATA EXTRACTION: Publications were classified as either: original research; reviews; program descriptions; discussion papers or commentaries; or case reports. Research publications were further classified as either measurement, descriptive, or intervention. Intervention studies were then classified as either experimental or non-experimental. DATA SYNTHESIS: The total number of publications was highest in 1997-1998 for most countries. The most common type of publication across all time periods for all countries was research publications. In Australia only, the number of research publications was slightly higher in 2001-2003 compared with other time periods. For each country and at each time, research was predominantly descriptive (75%-92%), with very little measurement (0-11%) and intervention research (0-18%). Overall, of the 1131 research publications, 983 were descriptive, 72 measurement and 76 intervention research. CONCLUSIONS: The dominance of descriptive research in Indigenous health is not ideal, and our findings should be carefully considered by research organisations and researchers when developing research policies.

The kurtosis metric as an adjunct to energy in the prediction of trauma from continuous, nonGaussian noise exposures.

Data from an earlier study [Hamernik et al. (2003). J. Acoust. Soc. Am. 114, 386-395] were consistent in showing that, for equivalent energy [Leq= 100 dB(A)] and spectra, exposure to a continuous, nonGaussian (nonG) noise could produce substantially greater hearing and sensory cell loss in the chinchilla model than a Gaussian (G) noise exposure and that the statistical metric, kurtosis, computed on the amplitude distribution of the noise could order the extent of the trauma. This paper extends these results to Leq= 90 and 110 dB(A), and to nonG noises that are generated using broadband noise bursts, and band limited impacts within a continuous G background noise. Data from nine new experimental groups with 11 or 12 chinchillas/group is presented. Evoked response audiometry established hearing thresholds and surface preparation histology quantified sensory cell loss. At the lowest level [Leq=90 dB(A)] there were no differences in the trauma produced by G and nonG exposures. For Leq >90 dB(A) nonG exposures produced increased trauma relative to equivalent G exposures. Removing energy from the impacts by limiting their bandwidth reduced trauma. The use of noise bursts to produce the nonG noise instead of impacts also reduced the amount of trauma.

Sensitivity of distortion product otoacoustic emissions in noise-exposed chinchillas.

The present study investigates the effect of small amounts of outer hair cell (OHC) loss on distortion product otoacoustic emission (DPOAE) levels and evoked potential permanent threshold shifts (PTS) in a population of 12 noise-exposed chinchillas. The group mean DPOAE level, which decreased by up to approximately 15 dB in the presence of less than 8 dB PTS and 15% OHC loss, indicates that DPOAEs can detect an underlying cochlear pathology (i,e., OHC damage/loss) despite the presence of normal to near normal thresholds. The sensitivity of DPOAEs in detecting OHC loss makes this test measure suited for diagnosing sensorineural hearing impairment, particularly when abnormal auditory symptoms (i.e., speech discrimination problems) are associated with a normal audiogram in the clinical setting and as part of a hearing conservation program.

The use of distortion product otoacoustic emissions in the estimation of hearing and sensory cell loss in noise-damaged cochleas.

Distortion product otoacoustic emissions (DPOAE), permanent threshold shifts (PTS) and outer hair cell (OHC) losses were analyzed in a population of 187 noise-exposed chinchillas to determine the predictive accuracy (sensitivity and specificity) of the DPOAE for PTS and OHC loss. Auditory evoked potentials (AEP) recorded from the inferior colliculus of the brainstem were used to estimate hearing thresholds and surface preparation histology was used to determine sensory cell loss. The overlapping cumulative distributions and high variability in emission responses for both PTS and OHC loss made it difficult to predict AEP threshold and OHC loss from DPOAE level measurements alone. Using a strict criterion (i.e. emissions better than the 5th percentile of the preexposure DPOAE level, and PTS< or = 5 dB or OHC loss< or = 5%), it was found that the postexposure DPOAE level could be used with reasonable confidence to determine if the status of peripheral auditory system was either normal (i.e. PTS< or = 5 dB) or abnormal (PTS>30 dB or OHC loss>40%). However, the high variability of individual DPOAE responses resulted in a broad region of 'uncertainty' (i.e. 5 or = 50%) or PTS (> or = 35 dB) in noise-exposed chinchillas. Based on an exponential regression analysis of individual subjects, correlations were higher for PTS/DPOAE than for OHC loss/DPOAE.

The effects of the amplitude distribution of equal energy exposures on noise-induced hearing loss: the kurtosis metric.

Seventeen groups of chinchillas with 11 to 16 animals/group (sigmaN = 207) were exposed for 5 days to either a Gaussian (G) noise or 1 of 16 different non-Gaussian (non-G) noises at 100 dB(A) SPL. All exposures had the same total energy and approximately the same flat spectrum but their statistical properties were varied to yield a series of exposure conditions that varied across a continuum from G through various non-G conditions to pure impact noise exposures. The non-G character of the noise was produced by inserting high level transients (impacts or noise bursts) into the otherwise G noise. The peak SPL of the transients, their bandwidth, and the intertransient intervals were varied, as was the rms level of the G noise. The statistical metric, kurtosis (beta), computed on the unfiltered noise beta(t), was varied 3 < or = beta(t) < or = 105. Brainstem auditory evoked responses were used to estimate hearing thresholds and surface preparation histology was used to determine sensory cell loss. Trauma, as measured by asymptotic and permanent threshold shifts (ATS, PTS) and by sensory cell loss, was greater for all of the non-G exposure conditions. Permanent effects of the exposures increased as beta(t) increased and reached an asymptote at beta(t) approximately 40. For beta(t) > 40 varying the interval or peak histograms did not alter the level of trauma, suggesting that, in the chinchilla model, for beta(t) > 40 an energy metric may be effective in evaluating the potential of non-G noise environments to produce hearing loss. Reducing the probability of a transient occurring could reduce the permanent effects of the non-G exposures. These results lend support to those standards documents that use an energy metric for gauging the hazard of exposure but only after applying a "correction factor" when high level transients are present. Computing beta on the filtered noise signal [beta(f)] provides a frequency specific metric for the non-G noises that is correlated with the additional frequency specific outer hair cell loss produced by the non-G noise. The data from the abundant and varied exposure conditions show that the kurtosis of the amplitude distribution of a noise environment is an important variable in determining the hazards to hearing posed by non-Gaussian noise environments.

Cochlear toughening, protection, and potentiation of noise-induced trauma by non-Gaussian noise.

An interrupted noise exposure of sufficient intensity, presented on a daily repeating cycle, produces a threshold shift (TS) following the first day of exposure. TSs measured on subsequent days of the exposure sequence have been shown to decrease relative to the initial TS. This reduction of TS, despite the continuing daily exposure regime, has been called a cochlear toughening effect and the exposures referred to as toughening exposures. Four groups of chinchillas were exposed to one of four different noises presented on an interrupted (6 h/day for 20 days) or noninterrupted (24 h/day for 5 days) schedule. The exposures had equivalent total energy, an overall level of 100 dB(A) SPL, and approximately the same flat, broadband long-term spectrum. The noises differed primarily in their temporal structures; two were Gaussian and two were non-Gausssian, nonstationary. Brainstem auditory evoked potentials were used to estimate hearing thresholds and surface preparation histology was used to determine sensory cell loss. The experimental results presented here show that: (1) Exposures to interrupted high-level, non-Gaussian signals produce a toughening effect comparable to that produced by an equivalent interrupted Gaussian noise. (2) Toughening, whether produced by Gaussian or non-Gaussian noise, results in reduced trauma compared to the equivalent uninterrupted noise, and (3) that both continuous and interrupted non-Gaussian exposures produce more trauma than do energy and spectrally equivalent Gaussian noises. Over the course of the 20-day exposure, the pattern of TS following each day's exposure could exhibit a variety of configurations. These results do not support the equal energy hypothesis as a unifying principal for estimating the potential of a noise exposure to produce hearing loss.