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”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
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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↗
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↗
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↗
Protease inhibition causes some manifestations of aging and Alzheimer's disease in rodent and primate brain.
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Aging↗
The effect of paclitaxel on the progression of polycystic kidney disease in rodents.
Woo et al (Nature 368:750-753) reported that parenteral administration of paclitaxel arrested the striking renal enlargement and prolonged life in C57BL/6J-cpk/cpk mice with a rapidly progressive form of polycystic kidney disease (PKD). In the current study, we sought to determine whether paclitaxel could alter the progression of other forms of hereditary PKD in rodents. Paclitaxel was administered by intraperitoneal injection to C57BL/6J-cpk/cpk mice and Han:SPRD-Cy/Cy rats with rapidly progressive PKD and to DBA/2FG-pcy/pcy mice and Han:SPRD-Cy/+ rats with slowly progressive PKD. Paclitaxel (150 micrograms/wk) prolonged the survival of cpk/cpk mice from 24.5 days to more than 65 days and decreased kidney weight relative to body weight from 16.5% at 21 days of age to 8.2% at more than 65 days of age. Mortality attributable to paclitaxel was 12%. By contrast, the administration of paclitaxel (0.1 to 15 mg/kg/wk) to 7- to 10-day-old Han:SPRD-Cy/Cy rats with rapidly progressive PKD had no effect on the course of the disease; moreover, paclitaxel caused severe side effects and premature death in all the Cy/Cy animals. Heterozygous male Cy/+ rats develop slowly progressive renal enlargement and azotemia. Paclitaxel, administered at 7, 15, or 27 mg/kg/wk to male Cy/+ rats from 4 until 10 weeks of age, reduced body weight gain, had an inconsistent effect on kidney weight relative to body weight, and had no effect on the serum urea nitrogen concentration. Mortality associated with the 7, 15, and 27 mg/kg/wk doses of paclitaxel was 0%, 15.4%, and 28.5%, respectively. DBA/2FG-pcy/pcy mice of either sex developed slowly progressive renal enlargement and azotemia. The administration of paclitaxel (100 to 150 micrograms/wk) from 2 to 10 weeks of age to DBA/2FG-pcy/pcy mice with cystic disease had no effect on the increase in kidney weight or on the level of serum urea nitrogen in comparison to untreated cystic animals. Mortality associated with 100- and 150-micrograms/wk doses of paclitaxel was 0% and 20%, respectively. We conclude that paclitaxel diminished the rate of renal enlargement and increased the life span of cpk/cpk mice but not Cy/Cy rats with rapidly progressive forms of PKD. Paclitaxel had no apparent benefit in Cy/+ rats nor pcy/pcy mice with slowly progressive PKD. On the basis of these studies in rodents, it appears that paclitaxel has limited potential usefulness as a therapeutic agent in the treatment of PKD.
Animals↗
Bovine spongiform encephalopathy in cattle mimics ultrastructurally experimental scrapie and Creutzfeldt-Jakob disease in rodents.
We report a comparison of the ultrastructural pathology of bovine spongiform encephalopathy, experimental scrapie in hamsters and a panencephalopathic model of Creuzfeldt-Jakob disease (CJD) in mice. Vacuoles in dendrites, intramyelinic vacuoles (myelin ballooning), dystrophic axons, phagocytic astrocytes and macrophages, differing in extent, were found in all three models. We conclude, that this axonal and myelin pathology is a phenomenon common to the three models of SSVE studied, and the differences between panencephalophatic CJD and polioencephalopathic BSE and scrapie are only quantitative.
Animal Diseases↗
Hemorrhagic disease in rodents infected with virus associated with Thai hemorrhagic fever.
KLA 16 virus, recovered from a child with Thailand hemorrhagic fever, produces infant mouse, rat, and hamster disease that is characterized by spontaneous bleeding at multiple sites, notably in the gastrointestinal tract, and by marked abnormalities in hemostatic mechanisms. This virus differs in this respect from Chikungunya virus to which it is immunologically similar and from other Thai hemorrhagic fever viruses.
Alphavirus Infections↗