Exploring local knowledge and perceptions on zoonoses among pastoralists in northern and eastern Tanzania

Background: Zoonoses account for the most commonly reported emerging and re-emerging infectious diseases in Sub-Saharan Africa. However, there is limited knowledge on how pastoral communities perceive zoonoses in relation to their livelihoods, culture and their wider ecology. This study was carried out to explore local knowledge and perceptions on zoonoses among pastoralists in Tanzania. Methodology and principal findings: This study involved pastoralists in Ngorongoro district in northern Tanzania and Kibaha and Bagamoyo districts in eastern Tanzania. Qualitative methods of focus group discussions, participatory epidemiology and interviews were used. A total of 223 people were involved in the study. Among the pastoralists, there was no specific term in their local language that describes zoonosis. Pastoralists from northern Tanzania possessed a higher understanding on the existence of a number of zoonoses than their eastern districts' counterparts. Understanding of zoonoses could be categorized into two broad groups: a local syndromic framework, whereby specific symptoms of a particular illness in humans concurred with symptoms in animals, and the biomedical framework, where a case definition is supported by diagnostic tests. Some pastoralists understand the possibility of some infections that could cross over to humans from animals but harm from these are generally tolerated and are not considered as threats. A number of social and cultural practices aimed at maintaining specific cultural functions including social cohesion and rites of passage involve animal products, which present zoonotic risk. Conclusions: These findings show how zoonoses are locally understood, and how epidemiology and biomedicine are shaping pastoralists perceptions to zoonoses. Evidence is needed to understand better the true burden and impact of zoonoses in these communities. More studies are needed that seek to clarify the common understanding of zoonoses that could be used to guide effective and locally relevant interventions. Such studies should consider in their approaches the pastoralists' wider social, cultural and economic set up

Aponeurosis Disinsertion in Congenital Entropion

• Lower lid retractor aponeurosis disinsertion is a well-recognized etiologic factor in many involutional entropion cases, but to our knowledge it has not previously been reported as a cause of congenital entropion. Four congenitally entropic lower eyelids in three patients with no history of birth trauma were all found to have retractor disinsertion during exploratory procedures. All four eyelids were surgically corrected by reinserting the retractors to the inferior tarsal margin. Detailed histologic studies of orbicularis oculi muscle fibers in two cases showed no evidence of fiber hypertrophy. This finding refutes the commonly accepted concept of orbicularis muscle hypertrophy as an etiologic mechanism of congenital entropion

Effects of UV Inactivated West Nile Particles on Astrocytic Morphology and Expression of Marker Proteins

West Nile virus (WNV) infection results in a spectrum of neurological symptoms ranging from a bening fever to severe West Nile neuroinvasive disease (WNND). The paralytic form of WNND has a poor prognosis, yet potential causes of neuronal death are not well understood. Significantly high levels of reactive astroglial marker proteins have been reported in the serum and cerebrospinal fluid of WNV patients. The spinal cord postmortem tissue shows areas of swollen axons, hypertrophied neuronal cell bodies, and a marked increase in astroglial reactivity. Thus, we hypothesized that factors secreted by astrocytes during or after acute WNV infection trigger neurodegeneration that contributes to WNND. To test this, astrocytic cell lines and dissociated astrocytic primary cultures from mouse brain were treated with UV inactivated WNV particles. We found significantly increased astrocyte specific factors in WNV treated astroglial cells compared with the mock controls. Real-Time PCR showed upregulated mRNA expression of some of those factors. The results suggest that higher levels of astrocytic proteins within the brain or circulating in the CSF or blood may stimulate secondary pathways leading to neurodegeneration. More studies are needed to detertmine whether these changes are associated with severe and prolonged WNV neuroinvasive disease

Does Astroglial Protein S100B Contribute to West Nile Neuro-Invasive Syndrome?

The clinical spectrum of West Nile Virus (WNV) infection ranges from a flu-like febrile condition to a more severe neuro-invasive disease that can cause death. The exact mechanism of neurodegeneration in neuro-invasive form of WNV infection has not been elucidated; however, a destructive role played by glial cells in promoting WNV mediated neurotoxicity has widely been speculated. The clinical studies revealed that the astroglial protein S100B is significantly elevated in the blood and CSF of patients with WNV infection, even in the absence of neuro-invasive disease. Therefore, the present study was designed to explore the potential role of S100B in the pathophysiology of WNV infection. The overarching hypothesis was that WNV primes astroglia to release S100B protein, which leads to a cascade of events that may have deleterious effects in both acute and chronic stages of WNV disease. To justify our hypothesis, we first ascertained increased levels of S100B in post-mortem tissue samples from WNV patients. Next, we looked at the effects of UV-inactivated WNV particles on astroglia using astroglial cell lines or primary cultures. Astroglial activation was measured as an increase in the expression of S100B and was analyzed by immunofluorescence and real-time PCR. Further, the in vitro effects of purified S100B protein on neutrophil migration and glutamate uptake were also determined in astroglial cell lines or primary cultures. We found that incubation of cultured astroglial cells with UV-inactivated WNV particles caused induction of S100B both at the mRNA and protein levels. Varying concentrations of S100B stimulated neutrophil migration in vitro. In addition, varying amounts of S100B caused inhibition of glutamate uptake in astroglia in a dose-dependent manner. Our data suggest that inactivated WNV particles are capable of inducing S100B synthesis in astroglia in vitro. We speculate that S100B release by activated astroglia may have multiple roles in the pathophysiology of WNV neuro-invasive disease, including induction of neutrophil migration to the sites where blood brain barrier is disrupted as well as glutamate neurotoxicity. To further elucidate the WNV-S100B neurotoxic pathway, in vivo studies using mouse models are warranted