Canine sino-nasal aspergillosis: parallels with human disease

Day, Michael

doi:10.1080/13693780802056038

Cited by 37 publications

(25 citation statements)

References 44 publications

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“…Cribriform plate lysis, a relative contraindication for topical antifungal treatment in canine SNA (Day, 2009), was detected in 25% of cases highlighting the importance of CT evaluation in treatment planning. Some CT features were associated with infecting species and/or anatomic form.…”

Section: Discussionmentioning

confidence: 99%

Computed tomographic features of feline sino-nasal and sino-orbital aspergillosis

Barrs

Beatty

Dhand

et al. 2014

The Veterinary Journal

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Makara, M. (2014). Computed tomographic features of feline sino-nasal and sino-orbital aspergillosis. Vet J. 201(2):215-22. DOI:10.1016DOI:10. /j.tvjl.2014 Computed tomographic features of feline sino-nasal and sino-orbital aspergillosis AbstractFeline upper respiratory tract aspergillosis (URTA) occurs as two distinct anatomic forms, sinonasal aspergillosis (SNA) and sino-orbital aspergillosis (SOA). An emerging pathogen, Aspergillus felis is frequently involved. The pathogenesis of URTA, in particular, the relationship between the infecting isolate and outcome, is poorly understood. Computed tomography was used to investigate the route of fungal infection and extension in 16 cases (SNA n=7, SOA n=9) where the infecting isolate had been identified by molecular testing.All cases had nasal cavity involvement except one cat with SNA that had unilateral frontal sinus changes. A strong association between the infecting species and anatomic form was identified. A. fumigatus infections remained within the sino-nasal cavity. Cryptic species infections were associated 2 | P a g e with orbital and paranasal soft-tissue involvement and with orbital lysis. These species were further associated with a mass in the nasal cavity, paranasal sinuses or nasopharynx. Orbital masses showed heterogeneous contrast enhancement, with central coalescing hypoattenuating foci and peripheral rim enhancement. Severe, cavitated turbinate lysis, typical of canine SNA, was present only in cats with SNA.These findings support that the nasal cavity is the portal of entry for fungal spores in feline URTA and that the route of extension to involve the orbit is via direct naso-orbital communication from bone lysis. Additionally, a pathogenic role for A. wyomingensis and a sinolith in a cat with A. udagawae infection are reported for the first time.

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Section: Discussionmentioning

confidence: 99%

Computed tomographic features of feline sino-nasal and sino-orbital aspergillosis

Barrs

Beatty

Dhand

et al. 2014

The Veterinary Journal

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“…The clinicopathological features of SNA are similar to those of human chronic erosive non-invasive fungal sinusitis [14]. Although TLRs have not been studied in this type of sinusitis in people, they have been better characterized in chronic rhinosinusitis (CRS) including fungal CRS, and some forms of aspergillosis.…”

Section: Introductionmentioning

confidence: 99%

Assessment of Toll-like receptor 2, 4 and 9 SNP genotypes in canine sino-nasal aspergillosis

et al. 2014

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BackgroundThe exact aetiology of canine sino-nasal aspergillosis (SNA) is unknown. In man, dysfunction in innate immunity, particularly in the function of pattern recognition receptors, is implicated in the pathogenesis of inflammatory sino-nasal disease and in fungal diseases. Associations between single nucleotide polymorphisms (SNPs) in Toll-like receptors (TLRs) and these diseases have been identified. Similarly, in dogs SNPs in genes encoding TLRs may be important in the pathogenesis of SNA. The aims of the present study were (1) to identify the presence of non-synonymous SNPs in the coding regions of the TLR2, 4 and 9 genes in dogs suffering from SNA, and (2) to investigate the SNP genotypes in dogs with SNA compared with a control population.ResultsDirect sequencing of nine dogs of various breeds with SNA revealed two non-synonymous SNPs in the coding region of TLR2, eight in TLR4 and four in TLR9. These non-synonymous SNPs were further evaluated in a case-control study of affected Golden Retrievers, Labrador Retrievers, Rottweilers and Beaucerons. Genotyping was performed using a combination of allele-specific primers and hydrolysis probe assays in 31 dogs with SNA and 31controls. No significant difference in minor allele frequency was identified between these groups, for all studied SNPs, in any of the four breeds.ConclusionsThese findings do not support a role for non-synonymous SNPs in the TLR 2, 4 and 9 coding regions in the pathogenesis of canine SNA, but do not exclude a role for innate immunity in the pathogenesis of the disease.

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“…The Th17 response has been associated with experimental autoimmune encephalitis in mice [116] and inflammatory diseases such as multiple sclerosis [117]. As in humans, dogs Th17 responses may relate to immunotherapy [118]. All these similarities between aging in humans and dogs full-fill the objectives mentioned above and make the aged canine a good model for investigating the safety and efficacy of human Aβ immunotherapy.…”

Section: Aβ Immunotherapymentioning

confidence: 94%

Dogs with Cognitive Dysfunction Syndrome: A Natural Model of Alzheimer’s Disease

Bosch¹,

Pugliese²,

Gimeno-Bayón³

et al. 2012

CAR

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In the search for appropriate models for Alzheimer's disease (AD) involving animals other than rodents, several laboratories are working with animals that naturally develop cognitive dysfunction. Among the animals tested, dogs are quite unique in helping to elucidate the cascade of events that take place in brain amyloid-beta (Aβ) deposition aging, and cognitive deficit. Recent innovative research has validated human methods and tools for the analysis of canine neuropathology and has allowed the development of two different approaches to investigate dogs as natural models of AD. The first approach relates AD-like neuropathy with the decline in memory and learning ability in aged housed dogs in a highly controlled laboratory environment. The second approach involves research in family-owned animals with cognitive dysfunction syndrome. In this review, we compare the strengths and limitations of housed and family-owned canine models, and appraise their usefulness for deciphering the early mechanisms of AD and developing innovative therapies.KEYWORDS: aging, Amyloid-beta, animal model, canine cognitive dysfunction syndrome, family dog, therapies. 6 Why a canine model of AD?For years, the search for appropriate animal models for Alzheimer's disease (AD) has focused on a variety of manipulations to reproduce the disease in various species, such as yeast, Drosophyla melanogaster, Caenorabditis elegans, rodents, and rabbits, with a particular interest in obtaining knockout and transgenic animals (for a review, see [1]research is currently performed in the mouse because its brain structure is somewhat similar to that of humans, and it is amenable to highly sophisticated genetic engineering. Because age-related cognitive decline is a common feature of most mammals, other laboratories have focused on the few species that naturally develop cognitive dysfunction with various Alzheimer-like characteristics. These animals include the monkey, polar bear, cat and dog [2][3][4][5]. Canine models are currently considered a useful intermediate between genetically modified mouse models and humans [6,7]. Although many of the transgenic AD models have provided insights into the molecular mechanisms of the pathology, none of them encompass all the cognitive deficits observed in AD (see Table 1). One of the first transgenic mouse AD models was the amyloid precursor protein transgenic mouse, PDAPP mouse, which develops age-dependent amyloid beta accumulation and deposition in both diffuse and fibrillar neuritic plaques in the hippocampus, cerebral cortex, and corpus callosum [8]. Other models with AD-like pathology are apolipoprotein E (ApoE) or Tau transgenic mice, and also mice in which other genes have been modified. In more sophisticated approaches, important information has been gained from crossing PDAPP and ApoE models and with mice lacking or over-expressing genes for beta-secretase, alpha-secretase, or the insulin-degrading enzyme [9,10].All these models have provided valuable information on AD pathology and on the poss...

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Canine sino-nasal aspergillosis: parallels with human disease

Cited by 37 publications

References 44 publications

Computed tomographic features of feline sino-nasal and sino-orbital aspergillosis

Computed tomographic features of feline sino-nasal and sino-orbital aspergillosis

Assessment of Toll-like receptor 2, 4 and 9 SNP genotypes in canine sino-nasal aspergillosis

Dogs with Cognitive Dysfunction Syndrome: A Natural Model of Alzheimer’s Disease

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