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Concurrent Session Presentations (Pdf) CONCURRENT SESSION PRESENTATIONS ZINC-ASSOCIATED DERMATOSES OF THE DOG Crow DW1 1Animal Dermatology Referral Clinic, Dallas, TX, USA BACKGROUND Zinc is an essential dietary element and is incorporated into enzymes where it plays a key role in regulating various aspects of cellular metabolism.1 If zinc levels are low due to insufficient dietary intake, decreased dietary absorption, competition between hormones such as estrogen and zinc for serum protein, or an inherent defect of zinc utilization or uptake at the cellular level, a disease state will likely result. 1-2 Four basic groups of zinc-associated dermatoses have been reported to date in the dog. The first (Syndrome I) may occur in any age of dog fed balanced diets and Siberian Huskies appear to be over represented as a breed. 1 The second (Syndrome II) has been reported in young dogs fed unbalanced diets low in zinc or high in plant protein (phytate) or calcium, which binds zinc and prevents absorption. Cereal or soy based diets have also been linked to this syndrome. 2 The third is lethal acrodermatitis in Bull Terriers that appears to be an inherited autosomal recessive trait that produces a lethal syndrome. These patients’ serum zinc levels are low, however, they do not respond to oral or parenteral zinc supplementation. 3 The last group reported was a litter of Pharaoh hound puppies that were severely clinically affected, exhibited low serum zinc levels and did respond favorably to intravenous but not oral zinc supplementation. 4 PHYSICAL FINDINGS The clinical hallmarks of zinc-associated dermatoses in the dog are crusting, alopecia and erythema with variable amounts of focal pruritus. Lesions are often on the face and lip margins and are usually symmetrical, however, asymmetry is not uncommon. Crusted and alopecic lesions have also been reported on the nasal bridge / planum, footpads, perigenital region, distal limbs and the elbows. 1 DIAGNOSIS Skin biopsy is the gold standard for confirmation of suspected zinc-associated dermatoses.1 The hallmark histologic finding is parakeratotic hyperkeratosis, oftentimes extending into the follicles. Orothokeratosis and acanthosis are also common findings and may be present concurrently with the parakeratosis. One must be ceratin that all skin infections (especially Malassezia dermatitis) are cleared prior to biopsy and that surgical scrubbing is NOT performed as these mistakes will readily lead to a misdiagnosis. PROGNOSIS Syndrome I and II patients typically have good to excellent response to therapy with dietary correction (Syndrome II only) and oral zinc supplementation.1 Bull Terriers with lethal acrodermatitis carry a uniformly grave prognosis5 and the Pharaoh hound disease appears to have a prognosis between the other reported diseases as they did respond favorably to intravenous zinc infusions. 4 THERAPY Lifetime supplementation of zinc will likely be required for all patients but the Syndrome II puppies with dietary deficiencies. Oral products such as zinc sulfate, zinc methionine and zinc gluconate are dosed based on the elemental zinc present at dosages between 1.2 and 5.1mg kg-1. Patients appear to have variable zinc absorption and the wide dosage range appears to reflect the need to specifically tailor dose to the patient. Improvement is typically noted within 6 weeks. Intravenous therapy with zinc infusions as previously described using 10-15mg kg-1 of zinc sulfate (basing dose on elemental zinc content) then diluted 1:1 and administered IV very slowly once weekly5 can lead to severe gastrointestinal symptoms of vomiting and bloody diarrhea. If attempting intravenous IV infusion of zinc, this author recommends to start with 3-5 mg kg-1 diluted 1:1 with saline, administer very slowly (over several hours) then gradually increase the dose on subsequent infusions as needed to balance side effects and clinical efficacy. REFERENCES 1. White SD, Bourdeau P, Rosychuk RA, et al. Zinc-responsive dermatosis in dogs: 41 cases and literature review. Vet Dermatol 2001: 12:101-109 2. Scott DW, Miller WH, Griffin CE. Small Animal Dermatology, 6th Edition. Philadelphia: WB Saunders Co; 2001: 1119-1123 3. Smits B, Croft DL, Abrams-Ogg ACG. Lethal acrodermatitis in bull terriers: A problem of defective zinc metabolism. Vet Dermatol 1991: 2:91-95 4. Campbell GA, Crow DW. Severe zinc responsive dermatosis in a litter of Pharaoh Hounds. J Vet Diagn Invest. 2010: 22:663-666. 5. Willemse T. Zinc-related cutaneous disorders of dogs. In Kirk RW, Bonagura JD (eds): Current Veterinary Therapy XI. Philadelphia: WB Saunders Co; 1992: 532-534 NOTES ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ ________________________________________________________ EUROPEAN CANINE LEISHMANIOSIS Carlotti DN Aquivet Clinique Vétérinaire, PA Mermoz, F-33320 Eysines (Bordeaux), France (EU) INTRODUCTION Canine leishmaniosis is a major infectious and zoonotic disease in many parts of the world. European canine leishmaniasis is caused by the diphastic protozoan intracellular parasite Leishmania infantum, transmitted by sandflies of the genus Phlebotomus. It is mainly a Mediterranean disease but it is currently expanding northerly. Surveys based on polymerase chain reaction (PCR) and serology show an infection rate up to 70 % in enzootic areas i.e. much higher than previously thought, with millions of dogs infected. As many companion animals travel all over Europe and beyond, cases can be seen far from the enzootic areas, in Europe but also in North America. AETIOLOGY, PATHOGENESIS AND EPIDEMIOLOGY1-3 The sandflies (phlebotomes) live in adapted biotopes (rocks, dry areas with humid micro-habitats, moderately high temperatures) and their activity is mainly crepuscular. Only the adult females are haematophage, but not the males. The infection of dogs by L. infantum depends on the phagocytosis and transformation of promastigotes (the extracellular and flagellated form in sandflies) into intracellular amastigotes, the latter being much more resistant to cellular defense mechanisms. Transmission other than via sandflies, e.g. in utero4, venereal5 or by blood transfusion has been demonstrated and transmission by contact6, via fleas and ticks7 is likely to be possible but not well documented. They probably do not play an important role. There is a “new paradigm” of canine leishmaniosis (L Ferrer). Some contaminated dogs will develop the clinical disease but not all: some others will develop a persistent asymptomatic infection (and perhaps will develop the disease eventually) and there is a third group of dogs that are resistant to or eliminate the infection without developing clinical signs. In other words, there are “susceptible” vs “clinically resistant” dogs (due to a cellular immune response) that are seronegative or have borderline titers. A study using the polymerase chain reaction (PCR) techniques on different tissues has demonstrated that two thirds of dogs are infected in Mallorca, most of them showing no clinical signs8. Genetic factors are probably involved. For instance, Ibizian hounds, a breed originating from the Balearic Islands show a predominantly cellular response, which is protective9. In contrast, other breeds such as Boxer, Cocker spaniel, Rottweiler and German shepherd seem to be predisposed10. In addition, it has been shown that susceptible dogs in Europe have a mutation in a particular gene (Nramp1 or Slc11c1). This gene controls an ion transport protein involved in the intraphagosomal replication of amastigotes11. However, the genetics of resistance/susceptibility is probably complex and several genes are involved, as demonstrated in human leishmaniosis and in murine models. The prevalence of the clinical disease in enzootic areas is usually below 10% and dogs that develop it have a predominant humoral response and are strongly immunodepressed biologically (poor response in lymphocyte proliferation test, low cytokine production by peripheral blood mononuclear cells after stimulation, low number of circulating CD4+ cells and decreased CD4+/CD8+ ratio). In contrast dogs which develop a cellular immune response (Th 1 type) are more resistant. Alterations in immunological status can trigger the
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