Curr Top Microbiol
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New and emerging infectious diseases affect humans, domestic animals, livestock and wildlife and can have a significant impact on health, trade and biodiversity. Of the emerging infectious diseases of humans, 75% are zoonotic, with wildlife being an increasingly important source of inter-species transmission. Recent animal health emergencies have highlighted the vulnerability of the livestock sector to the impact of infectious diseases and the associated risks to human health. ⋯ National animal disease emergencies, especially those that spill over to affect human health, require a whole-of-government approach for effective disease containment. As it is highly likely that zoonoses and animal diseases with the potential to affect human health will continue to emerge, surveillance and response systems for emerging zoonotic diseases will need to be strengthened and maintained at national and international levels. Applied research, linked across the human, livestock and wildlife sectors, is needed to inform preparedness planning and the development of evidence-based approaches to zoonotic disease prevention and control.
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Complex interactions involving humans, domestic animals, and wildlife create environments favorable to the emergence of new diseases. Today, reservoirs of Mycobacterium bovis, the causative agent of tuberculosis in animals and a serious zoonosis, exist in wildlife. ⋯ It will not be possible to eradicate M. bovis from livestock until transmission between wildlife and domestic animals is halted. Such an endeavor will require a collaborative effort between agricultural, wildlife, environmental and political interests.
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The seminal work of Le Douarin and colleagues (Ohki et al. 1987; Ohki et al. 1988; Salaun et al. 1990; Coutinho et al. 1993) first demonstrated that peripheral tissue-specific tolerance is centrally established in the thymus, by epithelial stromal cells (TEC). Subsequent experiments have shown that TEC-tolerance is dominant and mediated by CD4 regulatory T cells (Treg) that are generated intrathymically by recognition of antigens expressed on TECs (Modigliani et al. 1995; Modigliani et al. 1996a). From these and other observations, in 1996 Modigliani and colleagues derived a general model for the establishment and maintenance of natural tolerance (MM96) (Modigliani et al. 1996b), with two central propositions: (1) T cell receptor (TCR)-dependent sorting of emergent repertoires generates TEC-specific Treg displaying the highest TCR self-affinities below deletion thresholds, thus isolating repertoires undergoing positive and negative selection; (2) Treg are intrathymically committed (and activated) for a unique differentiative pathway with regulatory effector functions. ⋯ In contrast again, it would now seem that both processes of self-tolerance and microbial defense (self/non-self discrimination) also operate on the basis of evolutionarily ancient, germ-line-encoded innate, nonspecific receptors (Medzhitov and Janeway 2000) capable of a coarse level of self/non-self discrimination (Coutinho 1975). It could thus be interesting to revisit notions of cooperativity between V-regions and such mitogen receptors, both in single cell functions (Coutinho et al. 1974) and in the system's evolution (Coutinho 1975, 1980) as well. After all, major transitions in evolution were cooperative (Maynard-Smith and Szathmary 1995).
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Australian bat lyssavirus (ABLV), first identified in 1996, has been associated with two human fatalities. ABLV is genetically and serologically distinct from, but is closely related to, classical rabies. It has a bullet-shaped morphology by electron microscopy. ⋯ Due to demonstrated cross-protection in mice, rabies vaccine is used to prevent infection. Rabies post-exposure prophylaxis (PEP) protocols have been adopted for when a human is scratched or bitten by a suspect bat. A long-term commitment to public health programs that test bats that have been involved in scratch or bite incidents, followed by PEP if appropriate, will be necessary to minimise further human infection.
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The neuropathological features of human prion diseases are spongiform change, neuronal loss, astrocytic proliferation and the accumulation of PrP(Sc), the abnormal isoform of prion protein (PrP). The pattern of brain involvement is remarkably variable and is substantially influenced by the host PrP genotype and PrP(Sc) isotype. Variant Creutzfeldt-Jakob disease (vCJD) is a novel human prion disease which results from exposure to the bovine spongiform encephalopathy (BSE) agent. ⋯ All cases of vCJD are methionine homozygotes at codon 129 of the prion protein gene (PRNP). Continued surveillance is required to investigate cases of vCJD in the UK and other countries where BSE has been reported, particularly as cases of 'human BSE' in individuals who are MV or VV at codon 129 of the PrP gene have not yet been identified. Histological, genetic and biochemical techniques are essential tools for the adequate diagnosis and investigation of human prion diseases.