A new cage cover as an aid to laboratory rodent disease control.
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Animals↗
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Results for “RODENT DISEASES”
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Urban rodent-borne disease and rodent distribution in Israel and nighboring countries.
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Animals↗
Respiratory diseases of rodents.
Practitioners may be called on to treat rodents with respiratory diseases or to advise clients concerning the care of these rodents. Respiratory diseases of mice, rats, guinea pigs, and Syrian hamsters are well known because of the use of these species in research, whereas few or no reports of respiratory disease in rodents of other species exist. Features of the respiratory diseases of these four commonly encountered species are reviewed, including causes; clinical signs; diagnostic procedures; preventive measures; and, where appropriate, therapies.
Adenoviridae Infections↗
The assessment of human health risks from rodent-borne diseases by means of ecological studies of rodent reservoirs.
Zoonoses in general, and more specifically rodent-borne diseases, have proven to be of increasing importance in recent decades. The study of vector biology, therefore, is the foundation for understanding the infection mechanisms for humans. Military operations on the European and Asian continent have been substantially affected by Hantavirus infections during World War I and World War II, the Korean War, and the more recent events in Bosnia. The recently discovered Hantavirus serotypes with high mortality may extend the risk for the future to North America. In this article, we focus on the host and ecosystem relationships that might be useful in predicting potential outbreaks in Western Europe.
Age Factors↗
Methylprednisolone retards the progression of inherited polycystic kidney disease in rodents.
Polycystic kidney disease in adult laboratory animals and humans is associated with enlarged kidneys and a progressive decline of renal function, resulting in death from uremia. Interstitial inflammation and fibrosis typically are observed in association with the development of renal insufficiency. To determine whether amelioration of interstitial inflammation and fibrosis may diminish cyst expansion/kidney enlargement and stabilize renal function, we administered methylprednisolone, an anti-inflammatory drug with antifibrogenic effects, to mice and rats with hereditary polycystic kidney disease. The experiment was repeated once for each species. Mice were studied both in America and in Japan. Weanling male and female mice (DBA/FG pcy/pcy [cystic] and +/+ [normal], n = 87 and 20, respectively) and rats (Han:SPRD Cy/+ and +/+, n = 70 and 33, respectively) were administered methylprednisolone (1 to 2 mg/kg/d) in the drinking water for 100 days (mice) or 42 days (rats). Control animals drank distilled water. In normal DBA +/+ mice, methylprednisolone had no effect on serum urea nitrogen (SUN) levels, kidney weight, or kidney/body weight. Untreated male and female mice developed cystic kidneys and azotemia to an equal extent. Methylprednisolone administered in America to mice with renal cystic disease decreased kidney weight, kidney/body weight, SUN levels, volume density of cysts, and severity of interstitial fibrosis. In Japan, methylprednisolone decreased kidney weight and SUN levels of animals with cystic disease, but the effect on kidney/body weight did not reach statistical significance. In contrast to mice, male rats developed more severe renal cystic changes and were more azotemic than female rats. Methylprednisolone administered to male rats with cystic disease decreased SUN levels, kidney weight, kidney/body weight, volume density of cysts, and severity of interstitial fibrosis. Methylprednisolone had no effect on kidney/body weight or SUN levels in female rats with renal cystic disease. In normal Han:SPRD (+/+) rats of both sexes, kidney and body weight were decreased by methylprednisolone, but kidney/body weight and SUN levels were unchanged. On the basis of this study, we conclude that methylprednisolone decreased the extent of renal enlargement, reduced renal interstitial fibrosis, and preserved kidney function in mice and rats with relatively severe forms of inherited polycystic kidney disease.
Animals↗
Development of multiorgan pathology in the wpk rat model of polycystic kidney disease.
Rodent models of polycystic kidney disease (PKD) have provided valuable insight into the cellular changes associated with cystogenesis in humans. The present study characterizes the morphology of renal and extrarenal pathology of autosomal recessive PKD induced by the wpk gene in Wistar rats. In wpk(-/-) rats, proximal tubule and collecting duct cysts develop in utero and eventually consume the kidney. Increased apoptosis, mitosis, and extracellular tenascin deposition parallel cyst development. Extrarenal pathology occurs in the immune system (thymic and splenic hypoplasia) and central nervous system (CNS; hypoplasia to agenesis of the corpus callosum with severe hydrocephalus). Severity of hydrocephalus varied inversely with size of the corpus callosum. In wpk(-/-) rats, the corpus callosum exhibits relatively few axons that cross the midline. This CNS pathology is similar to that described in three human renal cystic syndromes: orofaciodigital, genitopatellar, and cerebrorenal-digital syndromes. Collecting duct and ventricular ependymal cilia appear morphologically normal. To determine if rodent background strain and the presence of modifier genes affect severity of the disease, we crossed the Wistar-wpk rat with Brown Norway (BN) and Long Evan (LE) rats and found the degree of renal and cerebral pathology was diminished as evidenced by lower kidney weight as a percent of body weight and serum urea nitrogen concentration in cystic rats on LE or BN strains as well as less prominent cranial enlargement. Crosses with BN rats allowed us to localize the wpk gene on chromosome 5 very close to the D5Rat73 marker. The wpk gene lies within a chromosomal region known to harbor a PKD modifier locus. In summary, the types of renal and cerebral pathology seen in the Wistar wpk rat are a unique combination seen only in this rodent model.
Agenesis of Corpus Callosum↗
Fungal diseases of laboratory rodents.
Although fungal disease is uncommon in rodents, dermatophytosis is the most common mycosis seen in clinical practice. T. mentagrophytes is the most common etiologic agent, and the guinea pig is the most common species affected, although there are reports in all pet and laboratory rodent species except the gerbil. Despite the low incidence of clinical disease, rodents are common asymptomatic carriers of dermatophytes, and ringworm is the most common zoonotic disease transmitted from rodents to people.
Animals↗
Experimental transmission of Creutzfeldt-Jakob disease and related diseases to rodents.
Sporadic Creutzfeldt-Jakob disease (CJD) with 129M/M, and iatrogenic and familial CJD with E200K and M232R, showed similar clinicopathologic features, a synaptic type deposition of PrPCJD, and high transmission frequencies to mice. Sporadic patients with 129M/V or 129V/V, and mutation cases with V180I, showed slightly different features and low or null transmission frequencies to mice. Hereditary cases with P102L, P105L, A117V, Y145stop, and insertions had different features but all demonstrated a long clinical duration and the presence of PrP plaques. The experimental transmission to mice of these mutant forms was difficult, except for one-third of the cases with P102L. CJD and related diseases, even those that are hereditary, may thus be divided into two different groups, those that are easily transmissible and those that are either difficult to transmit or nontransmissible.
Adult↗
Behavioral models of Parkinson's disease in rodents: a new look at an old problem.
The circuitry important for voluntary movement is influenced by dopamine from the substantia nigra and regulated by the nigrostriatal system. The basal ganglia influence the pyramidal tract and other motor systems, such as the mesopontine nuclei and the rubrospinal tract. Although the neuroanatomical substrates underlying motor control are similar for humans and rodents, the behavioral repertoire mediated by those circuits is not. The principal aim of this review is to evaluate how injury to dopamine-mediated pathways in rodents gives rise to motor dysfunction that mimics human Parkinsonism. We will examine the behavioral tests in common use with rodent models of Parkinson's disease and critically evaluate the appropriateness of each test for detecting motor impairment. We will show how tests of motor performance must be guided by a thorough understanding of the clinical symptoms accompanying the disease, the circuitry mediating dopamine deficits in rodents, and familiarity with the rodent behavioral repertoire. We will explain how investigations in rodents of skilled forepaw actions, including placing, grooming, or foot faults, have clear correlates in Parkinson's disease, and are, therefore, the most sensitive ways of detecting motor impairment following dopamine loss from the basal ganglia of rodents.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
Cyclosporine treatment of high dose and long duration reduces the severity of graft coronary artery disease in rodent cardiac allografts.
BACKGROUND: Graft coronary artery disease (GCAD) limits allograft survival after cardiac transplantation. The objective of this study was to correlate GCAD with the level of immunosuppression in an established allogeneic rodent cardiac chronic rejection model to better understand the mechanisms of GCAD in this system. METHODS: Donor PVG hearts were transplanted into the abdomen of ACI rats. Six recipient groups received either 10, 7.5 or 5 mg/kg/day of oral cyclosporine (CsA), for 90 (10 mg/90 d, 7.5 mg/90 d, 5 mg/90 d) or 10 days (10 mg/10 d, 7.5 mg/10 d, 5 mg/10 d; n = 10 all groups), and grafts procured on Day 90. GCAD was assessed by histology for percent luminal narrowing (%LN), percent affected vessels (%AV) and intima/media ratio (I/M ratio). Sections were stained for ED1-positive macrophages and MHC Class II-positive cells. RESULTS: The 10 mg/90 d treatment group showed significantly reduced GCAD compared with the 5mg/10d treatment group (%LN = 4.3 +/- 3.1% vs 39 +/- 11.9%, p < 0.05). The 7.5 mg/90 d group had a reduced %LN and I/M ratio compared with the 5 mg/10 d group (%LN = 8.0 +/- 3.5% vs 39 +/- 11.9%, p < 0.05; I/M ratio = 0.06 +/- 0.02 vs 0.41 +/- 0.14, p < 0.05). There was a trend toward reduction of GCAD with both increasing the dose of CsA as well as the duration of treatment. Continuous treatment with CsA reduced perivascular macrophage and MHC II cell infiltration. Macrophage infiltrates correlated strongly with GCAD (R(2) > 0.90, p < 0.01), and MHC II infiltrates showed a weak correlation, although not statistically significant (R(2) > 0.56, p = NS). CONCLUSIONS: This study further defines the effect of cyclosporine on GCAD in this cardiac transplantation model. In this system, higher dose and longer duration of treatment with CsA markedly reduces macrophage and MHC II infiltration, correlating with diminished GCAD. However, increasing dose and duration of CsA did not completely eliminate the development of GCAD. Non-immunologic factors could contribute to this occurrence.
Animals↗
Small rodents.
Although rodent pets constitute only a small percentage of pets seen in practice, owners of rodents are as dedicated to those pets as are other owners to the more common dogs and cats. Rodents make excellent pets, with low space, feeding, and economic requirements. Medical care for rodents is based primarily on gross clinical signs, because most standard diagnostic tests done in larger animals cannot be done in small rodents. Even with that disadvantage, however, specific diagnosis of most rodent diseases is possible, and several of those diseases can be treated successfully. Among the common diseases of small rodents are ascariasis, pyoderma, incisor malocclusion and overgrowth, neoplasia and abcessation, nephrosis and amyloidosis, respiratory infection, enteritis, and neurologic disorders. Most drugs used in rodents, including anesthetics, are the same as those used in other species, with the exception of several drugs contraindicated in hamsters.
Animal Husbandry↗
Respiratory diseases of rodents and rabbits.
This article is written to provide differential diagnostic help for the practitioner who suspects respiratory disease in rodents or rabbits. The authors are laboratory animal veterinarians who work with rodents and rabbits on a herd health basis but also have considerable experience dealing with individual mice, rats, guinea pigs, hamsters, gerbils, and rabbits. The article presents descriptions of the presentation, pathology, treatment, and control of the primary respiratory pathogens of these species, along with an explanation of conditions that may confuse the diagnostic efforts. The article also mentions reported pathogens of secondary importance and provides extensive references.
Animals↗
Calorie restriction in obesity: prevention of kidney disease in rodents.
The incidence of end-stage renal disease (ESRD) has risen considerably in the past two decades. This trend is partly due to the alarming rise in the incidence of type 2 diabetes over the same period, which in turn might be linked to the staggering increase in overweight and obesity. If these trends continue, ESRD can be expected not only to cause suffering of ever growing numbers of patients, but also to become an increasing financial as well as logistical burden on the health care system. Therefore, it is imperative not only to gain a better understanding of the molecular, cellular and metabolic mechanisms involved in renal pathology, but also to uncover treatment modalities, including lifestyle changes, that can help prevent and/or slow the progression of kidney pathogenesis. Insights into both of these aspects are provided by animal models of obesity and diabetes. It has long been known that food restriction, more so than restriction of any particular dietary component, can greatly enhance longevity in laboratory rodents. These findings are being extended into a variety of other mammals, including nonhuman primates. These studies have indicated that caloric restriction in nonobese laboratory animals does not primarily affect specific disease processes but rather nonspecifically slows the aging process. In contrast, a growing body of evidence suggests that in genetically obese animals, food restriction can prevent or greatly delay the onset of specific degenerative lesions, in particular glomerulonephritis associated with obesity and diabetes.
Animals↗
Animal models of rheumatoid arthritis and their relevance to human disease.
Rodent models of rheumatoid arthritis (RA) are useful tools to study the pathogenic process of RA. Among the most widely used models of RA are the streptococcal cell wall (SCW) arthritis model and the collagen-induced arthritis (CIA). Both innate and adaptive immune mechanisms are involved in these rodent models. While no models perfectly duplicate the condition of human RA, they are easily reproducible, well defined and have proven useful for development of new therapies for arthritis, as exemplified by cytokine blockade therapies. Besides SCW and CIA models, there are numerous others including transgenic models such as K/BxN, induced models such as adjuvant-induced and pristane models, and spontaneous models in certain mouse strains, that have been used to help understand some of the underlying mechanisms. This review provides an update and analysis of RA models in mice and rats. The array of models has provided rheumatologists and immunologists a means to understand the multifactorial disease in humans, to identify new drug targets, and to test new therapies.
Journal Article↗
Skin diseases of rodents and small exotic mammals.
Small exotic mammals and rodents are becoming popular pets in the United States. Like most other exotics, the popularity of these animals has vastly preceded the accumulation of practical husbandry and veterinary information available about them. Several dermatologic conditions have been described in most rodents and small exotic mammals; however, the practitioner can assume that more exist that have not yet been diagnosed or documented. It is not unreasonable to assume that rodents and small exotic mammals could be affected by many of the same dermatologic conditions well described in other animals. Veterinarians are encouraged always to apply the same diagnostic protocols used to work up skin problems in dogs and cats when presented with an exotic pet with a dermatologic disease.
Animals↗
[Occurrence of the abdominal form of rodent-borne diseases (pseudotuberculous infection) in children].
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Animals↗
Animal models of Parkinson's disease in rodents induced by toxins: an update.
The development of animal models of Parkinson's disease is of great importance in order to test substitutive or neuroprotective strategies for Parkinson's disease. Such models should reproduce the main characteristics of the disease, such as a selective lesion of dopaminergic neurons that evolves over time and the presence of neuronal inclusions known as Lewy bodies. Optimally, such models should also reproduce the lesion of non-dopaminergic neurons observed in a great majority of patients with Parkinson's disease. From a behavioral point of view, a parkinsonian syndrome should be observed, ideally with akinesia, rigidity and rest tremor. These symptoms should be alleviated by dopamine replacement therapy, which may in turn lead to side effects such as dyskinesia. In this review, we analyze the main characteristics of experimental models of Parkinson's disease induced by neurotoxic compounds such as 6-hydroxydopamine, MPTP and rotenone. We show that, whereas MPTP and 6-hydroxydopamine induce a selective loss of catecholaminergic neurons that in most cases evolves over a short period of time, rotenone infusion by osmotic pumps can induce a chronically progressive degeneration of dopaminergic neurons and also of non-dopaminergic neurons in both the basal ganglia and the brainstem.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
Thiol compounds metabolism in mice, rats and humans: comparative study and potential explanation of rodents protection against vascular diseases.
BACKGROUND: Rodents are often used as animal models to dissect mechanisms underlying hyperhomocysteinemia atherogenicity in humans. However, neither wild-type rodents nor cystathionine beta-synthase deficient mice develop spontaneous atherosclerosis. We investigated whether species-specific differences in thiols metabolism may explain the respective sensitivity of rodents and humans to hyperhomocysteinemia. METHODS: Thiols and vitamins B levels were determined in normohomocysteinemic humans and rodents, and in hyperhomocysteinemic mice. RESULTS: In basal status, although plasma homocysteine, cysteine and cysteinylglycine levels were lower, glutathione levels were higher in mice than in humans (4.0+/-1.6 vs. 7.9+/-2.2, P<0.0005; 147.4+/-40.3 vs. 278.5+/-50.0, P<0.0001; 2.3+/-0.7 vs. 36.6+/-7.3, P<0.0001; and 70.9+/-20.1 vs. 4.6+/-1.6, P<0.0001). Serum vitamin B12 and folate levels were 2.5- and 7.7-fold higher in rats than in humans. In wild-type mice, the increase in plasma Hcy levels induced by methionine-enriched diet was accompanied by a proportional increase in GSH levels. CONCLUSION: GSH levels are enough to modulate Hcy effects in normo- and hyperhomocysteinemic mice but not in humans. This rodents characteristic, likely supported by species differences in the relative contribution of remethylation and transsulfuration pathways, may partly explain their protection against atherosclerosis.
Animals↗