935 resultados para Rabbits - Diseases


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First edition published in 1926 under title: Diseases and treatment of the rabbit.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Rabbit Haemorrhagic Disease Virus (RHDV) was introduced to Australia in 1995 for the control of wild rabbits. Initial outbreaks greatly reduced rabbit numbers and the virus has continued to control rabbits to varying degrees in different parts of Australia. However, recent field evidence suggests that the virus may be becoming less effective in those areas that have previously experienced repeated epizootics causing high mortality. There are also reports of rabbits returning to pre-1995 density levels, Virus and host can be expected to co-evolve. The host will develop resistance to the virus with the virus subsequently changing to overcome that resistance. It has been 12 years since the release of RHDV and it is an opportune time to examine where the dynamic currently stands between RHDV and rabbits. Laboratory challenge tests have indicated that resistance to RHDV has developed to different degrees in populations throughout Australia. In one population a low dose (1:25 dilution) of Czech strain RHDV failed to infect a single susceptible rabbit, yet infected a low to high (up to 73%) percentage across other populations tested. Different selection pressures are present in these populations and will be driving the level of resistance being seen. The mechanisms and genetics behind the development of resistance are also important as the on-going use of RHDV as a control tool in the management of rabbits relies on our understanding of factors influencing the efficacy of the virus. Understanding how resistance has developed may provide clues on how best to use the virus to circumvent these mechanisms. Similarly, it will help in managing populations that have yet to develop high levels of resistance.

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Rabbit haemorrhagic disease is a major tool for the management of introduced, wild rabbits in Australia. However, new evidence suggests that rabbits may be developing resistance to the disease. Rabbits sourced from wild populations in central and southeastern Australia, and domestic rabbits for comparison, were experimentally challenged with a low 60 ID50 oral dose of commercially available Czech CAPM 351 virus - the original strain released in Australia. Levels of resistance to infection were generally higher than for unselected domestic rabbits and also differed (0-73% infection rates) between wild populations. Resistance was lower in populations from cooler, wetter regions and also low in arid regions with the highest resistance seen within zones of moderate rainfall. These findings suggest the external influences of non-pathogenic calicivirus in cooler, wetter areas and poor recruitment in arid populations may influence the development rate of resistance in Australia.

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The release of myxoma virus (MYXV) and Rabbit Haemorrhagic Disease Virus (RHDV) in Australia with the aim of controlling overabundant rabbits has provided a unique opportunity to study the initial spread and establishment of emerging pathogens, as well as their co-evolution with their mammalian hosts. In contrast to MYXV, which attenuated shortly after its introduction, rapid attenuation of RHDV has not been observed. By studying the change in virulence of recent field isolates at a single field site we show, for the first time, that RHDV virulence has increased through time, likely because of selection to overcome developing genetic resistance in Australian wild rabbits. High virulence also appears to be favoured as rabbit carcasses, rather than diseased animals, are the likely source of mechanical insect transmission. These findings not only help elucidate the co-evolutionary interaction between rabbits and RHDV, but reveal some of the key factors shaping virulence evolution.

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Hyperlipidemia is well recognized as an important risk factor in the development of atherosclerosis. Low-density lipoproteins (LDL) are components of cholesterol that are highly associated to an increased risk of cardiovascular diseases. Hypercholesterolemia induces proteolytic and oxidative changes in vasculature, leading to a local inflammatory response. Since dietary antioxidants have attracted considerable attention as preventive and therapeutic agents, the polyphenolic compound resveratrol seems to play an important role in prevention of human atherosclerosis. Researches show that resveratrol inhibits LDL oxidation and platelet aggregation, as well as vascular prolifer ation of smooth muscle cells. However, recent findings in animal models reveal conflicting results regarding its effects on plasma lipid levels. The aim of the present study was to evaluate the effect of resveratrol on plasma biochemistry profile in New Zealand white rabbits submitted to a hypercholesterolemic diet. Twenty healthy, male, adult New Zealand white rabbits were fed with ordinary diet for one week before being divided into four treatment groups, containing five animals each. Group CT received maintenance diet; group R received maintenance diet and resveratrol (3mg/kg/day) given orally; group CL received maintenance diet enriched with 1.5% cholesterol; and group CR received maintenance diet enriched with 1.5% cholesterol and resveratrol (3mg/kg/day) given orally. During the experiment, from each animal, samples of 3mL venous blood were collected in heparin twice monthly for measurements of total cholesterol, triglycerides, and low- and high-density lipoproteins. The data analysis revealed that resveratrol did not have a hypolipidemic effect in experimentally induced hypercholesterolemic New Zealand white rabbits.

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Ticks are hematophagous ectoparasites which can transmit several diseases to the host during their feeding process. When ticks mechanically damage the tissue, they eventually induce inflammatory responses on the skin spot where they are fixed. One of the alternatives to control these ectoparasites is the use of chemical substances like selamectin - the active principle of Pfizer's antiparasitic Revolution® - a macrocyclic lactone capable of doing neurotoxic damage to the tick and eventually eliminating infestation in dogs and cats. The purpose of this study was to analyze, using histological and histochemical techniques, the occurrence of morphophysiological alterations in the skin of the host rabbits exposed to selamectin and infested with Rhipicephalus sanguineus (Acari: Ixodidae). Histologically, the exposed and infested rabbits showed a partial and/or total decrease in the stratum corneum and the epithelium decreased in the number of cell layers, consequently reducing the stratification (thinning) and quite pronounced formations of sub-epidermal edemas with consequent disorganization of collagen fibers in the dermal layer's connective tissue. Histochemical tests showed strong periodic acid-Schiff-positive reaction in the hair follicle and some regions of the dermis, besides resynthesis of collagen fibers detected by Mallory's trichrome technique. The obtained results showed that selamectin acts like a toxicant agent when in contact with the skin of the rabbit infested with ticks, inducing morphophysiological alterations in the acute inflammatory process in the animal's tegument. Selamectin is a chemical substance which has a dose-dependent action since higher concentrations cause greater morphophysiological damage in the skin of rabbits. © 2013 Springer-Verlag Berlin Heidelberg.

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Objective: Develop a model that allowed the study of bone regeneration in infection conditions. Method: A 15 mm defect was surgically created in the rabbit ulna and inoculated with 5x10(8) colony-forming units (CFU) of S. aureus. Surgical debridement was performed two weeks after and systemic gentamicin was administered for four weeks. Animals were followed up to 12 weeks to evaluate infection control and bone regeneration. Result: Bone regeneration was inferior to 25% of the defect in radiological and histological analysis. Conclusion: Infected bone defect of 15 mm in the rabbit ulna was unable to achieve full regeneration without further treatment. Level of Evidence V, Experimental Study.

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Pasteurella multocida is responsible for a wide range of diseases in domestic animals. In rabbits, the agent is related to nasal discharge, pneumonia, otitis media, pyometra, orchitis, abscess, and septicemia. One hundred and forty rabbits with respiratory diseases from four rabbitries in Sao Paulo State, Brazil were evaluated for the detection of P. multocida in their nasal cavities. A total of twenty-nine animals were positive to P. multocida isolation, and 46 strains were selected and characterized by means of biochemical tests and PCR. P. multocida strains were tested for capsular type, virulence genes, and resistance profile. A total of 45.6% (21/46) of isolates belonged to capsular type A, and 54.34% (25/46) of the isolates were untypeable. None of the strains harboured toxA or pfhA genes. The frequency of the other twenty genes tested was variable, and the data generated was used to build a dendrogram, showing the relatedness of strains, which were clustered according to origin. Resistance revealed to be more common against sulfonamides and cotrimoxazole, followed by erythromycin, penicillin, and amoxicillin.

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The effects of indomethacin on central nervous system abnormalities in rabbits with experimental pneumococcal meningitis were studied. As expected, prostaglandin E2 levels in cerebrospinal fluid were significantly lower in the indomethacin-treated group, indicating that the drug effectively reduced prostaglandin synthesis. Brain edema was markedly attenuated in the indomethacin-treated group; however, cerebrospinal fluid white blood cell counts, lactate and protein concentrations, and intracisternal pressure were not significantly different between groups. It seems that indomethacin, while effective in reducing brain edema, does not significantly affect other important pathophysiologic alterations in experimental pneumococcal meningitis.

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We investigated the effect of cefotaxime and chloramphenicol on endotoxin concentrations in cerebrospinal fluid (CSF) and on the development of brain edema in rabbits with Escherichia coli meningitis. Both antibiotics were similarly effective in reducing bacterial titers. Cefotaxime, but not chloramphenicol, induced a marked increase of endotoxin in CSF, from log10 1.5 +/- 0.8 to log10 2.8 +/- 0.7 ng/ml (P less than .01). This result was associated with an increase in brain water content (405 +/- 12 g of water/100 g of dry weight compared with 389 +/- 8 g in untreated controls; P less than .01), whereas in animals treated with chloramphenicol, brain water content was identical to controls. The cefotaxime-induced increase in endotoxin concentration and brain edema were both neutralized by polymyxin B, which binds to the lipid A moiety of endotoxin, or by a monoclonal antibody to lipid A. These results indicate that treating gram-negative bacillary meningitis with selected antibiotics induces increased endotoxin concentrations in CSF that are associated with brain edema.

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The relevance of a postantibiotic effect in the treatment of pneumococcal meningitis was evaluated in a rabbit model. After administration of a single intravenous bolus of ampicillin at various dosages, such an effect was observed in all animals. The duration of this effect in vivo (2.5-18 hr) was consistently longer than that in vitro (1-4.3 hr); however, in rabbits the postantibiotic effect was eliminated by the administration of intravenous plus intracisternal beta-lactamase. In an assessment of the potential therapeutic benefit of the postantibiotic effect, the efficacy to two regimens of treatment with different intervals between doses was compared. One group of animals received ampicillin every 4 hr and another every 12 hr. With sufficiently high doses, drug concentrations in cerebrospinal fluid exceeded the minimal bactericidal concentration for most of the 4-hr interval but for only about one-third of the 12-hr interval. The rate of cure was similar for the two regimens and approximated 100% when peak drug concentrations in cerebrospinal fluid exceeded the minimal bactericidal concentration by at least 10-fold.