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PubMed2004

Preventive effects of D-004, a lipid extract from Cuban royal palm (Roystonea regia) fruits, on testosterone-induced prostate hyperplasia in intact and castrated rodents.

Benign prostatic hyperplasia (BPH) is the noncancerous, uncontrolled growth of prostate gland cells and stroma that can cause difficulty urinating. Fruit lipid extracts from saw palmetto, a palm from the Arecaceae family, are used for BPH management. The Cuban royal palm, Roystonea regia, is also a member of the Arecaceae family and therefore it was appropriate to investigate the protective effects of Roystonea regia fruit lipid extracts on prostatic hyperplasia. The aim of this study was to investigate whether D-004, a lipid extract from Roystonea regia fruits, prevented testosterone-induced PH in castrated and intact rodents. Two series of experiments were performed. The first one was conducted in castrated and intact rats, distributed into five groups of 10 rats per group. The negative control group was injected with soy oil and treated orally with vehicle, while the four testosterone-injected groups were treated with vehicle (positive control), D-004 100, 200 and 400 mg/kg, respectively. The other experiment was conducted in castrated and intact mice. These were distributed into four groups of 10 mice per group: a negative control group and three testosterone-injected groups, of which one was a positive control, while two received D-004 200 and 400 mg/kg, respectively. At study completion, the rodents were sacrificed and prostates removed and weighed. D-004 at doses of 100, 200 and 400 mg/kg significantly and dose-dependently prevented prostate enlargement in intact and castrated rats and mice. The percentage inhibitions obtained in mice were greater: 77% and 84% for intact and castrated mice, respectively. D-004 therapy did not affect body weight. It is concluded that D-004 administered orally significantly prevented testosterone-induced prostate enlargement in both intact and castrated rodents, indicating that an endogenous supply of testosterone is not necessary to observe such an effect The results of the present investigation support further studies of D-004 on experimental models of prostatic hyperplasia.

Animals↗

PubMed2001

Co-expression of estrogen and thyroid hormone receptors in individual hypothalamic neurons.

Estrogen receptors (ER) and thyroid hormone receptors (TR) are members of the nuclear receptor family of transcription factors that induce or repress the expression of target genes. Previous behavioral studies in female rodents have demonstrated that thyroid hormones can antagonize the effects of estrogen in the central nervous system (CNS), particularly by attenuating estrogen's ability to facilitate reproductive behaviors. Additional molecular studies have suggested a mechanism for this antagonism by showing that ligand-activated ER alpha and TRs have the potential to interact in their transcriptional controls. Although the expression patterns of ER alpha and TRs in the rodent brain appear to overlap in behaviorally relevant areas, it remained to be determined whether these two classes of proteins coexist in vivo at the level of single neurons. To address this possibility, we employed a highly sensitive double-label in situ hybridization technique using digoxigenin and (35)S-labeled cRNA probes to analyze, in detail, the expression of ER alpha mRNA with TR alpha 1 and TR alpha 2 mRNAs in the same neurons of the ovariectomized (OVX) adult mouse brain. Our results demonstrate that a large majority of the ER alpha-positive neurons also expresses TR alpha 1 and TR alpha 2 mRNAs. Quantitative examination of the cellular expression in the ventromedial and arcuate nuclei of the hypothalamus (VMH and Arc) showed that 81.5% and 80.5% of the neurons endowed with ER alpha mRNA also contain TR alpha 1 and TR alpha 2 mRNAs, respectively. In the amygdala, more than 60.5% and 67% of ER alpha-positive cells also contain TR alpha 1 and TR alpha 2 mRNAs, respectively. These findings provide the first anatomical evidence that ER and TR can be found in the same neurons, including hypothalamic neurons. This coexpression of ER alpha and TR provides the cellular basis for a new level of neuronal integration in a brain region where estrogens control female reproductive behaviors.

Amygdala↗

PubMed1996

Exposure of laboratory animals to polychlorinated dibenzodioxins and polychlorinated dibenzofurans from commerical rodent chow.

Polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDDs/PCDFs) are ubiquitous low level environmental contaminants. Present finding of PCDDs and PCDFs in the human food supply suggested that laboratory animals maintained under controlled conditions may also receive unwanted exposure to these compounds from food. In this study, a commercial rodent chow, Prolab-RMH 1000, was analyzed for the toxicologically active 2,3,7,8-substituted PCDDs and PCDFs. The results show that the feed had a total PCDD/F dioxin toxic equivalence (I-TEq) of 0.13 pg/kg (ppt) wet weight. OCDD was the most abundant congener present, followed by 1,2,3,4,6,7,8-HpCDD, with these congeners representing the 5th and 6th greatest contributors to the calculated TEq. Daily ingestion of I-TEqs for the rats is calculated to be 3.9-6.5 pg/kg/day, and 13.0-32.5 pg/kg/day for mice. It is therefore important to consider the potential for background exposure to PCDDs and PCDFs from the diet when conducting studies with laboratory animals. This is particularly important when sensitive responses, such as enzyme induction, immunotoxicity, and developmental/reproductive toxicity are being investigated at very low exposures to this class of compounds.

Animal Feed↗

PubMed2006

The development of hippocampal interneurons in rodents.

Interneurons are GABAergic neurons responsible for inhibitory activity in the adult hippocampus, thereby controlling the activity of principal excitatory cells through the activation of postsynaptic GABAA receptors. Subgroups of GABAergic neurons innervate specific parts of excitatory neurons. This specificity indicates that particular interneuron subgroups are able to recognize molecules segregated on the membrane of the pyramidal neuron. Once these specific connections are established, a quantitative regulation of their strength must be performed to achieve the proper balance of excitation and inhibition. We will review when and where interneurons are generated. We will then detail their migration toward and within the hippocampus, and the maturation of their morphological and neurochemical characteristics. We will finally review potential mechanisms underlying the development of GABAergic interneurons.

Animals↗

PubMedDate not supplied

Preservation of various microsomal drug metabolizing components in tissue preparations from the livers, lungs, and small intestines of rodents.

The livers, lungs, and small intestines of untreated rabbits and the livers of control rats were stored intact, or as microsomal suspensions, under liquid nitrogen at -196 degrees C. Aniline hydroxylase, aminopyrine demethylase, benzpyrene hydroxylase, biphenyl hydroxylase, NADPH-cytochrome c reductase, UDP-glucuronyltransferase activities, the microsomal content of cytochrome P-450, and the aniline- and benzphetamine-induced spectral changes were compared in fresh and stored preparations. Few significant changes in any of the above parameters resulted from storage of rabbit tissue preparations in liquid nitrogen for periods of up to 28 days. Pretreatment of rabbits with phenobarbital did not affect the stability of their stored microsomal preparations. Enzyme activities in the livers of untreated or 3-methylcholanthrene-pretreated rats were less stable to storage than in tissue preparations from rabbits stored under identical conditions. However, when rat hepatic microsomes were resuspended in KCl-HEPES supplemented with 1 mM EDTA before storage, enzyme activities were largely unaffected by freezing in liquid nitrogen.

Aminopyrine N-Demethylase↗

PubMed1995

Stages of intestinal carcinogenesis and their control by host NK cells. Implications to prevention and therapy.

DMH-induced (25mg/kg/wk) rodent intestinal carcinogenesis was re-examined using histometry under various conditions including modulation of host natural killer (NK) cell activity and mutagen administration. Early lesion was enterocyte hyperplasia all along the intestinal tract. Cell kinetic analysis showed that it was caused by a slightly altered but still functional "initiated" enterocyte population added to the normal population which remained unchanged. Primarily, initiated stem (IS) cells were added which then produced their initiated progeny which still renewed normally. NK cells countered the initiated cells selectively, either inhibiting IS cell proliferation or killing them when activated by lymphokines. Evidence was obtained that the IS cells could further transform into preneoplastic stem (PS) and then neoplastic stem (NS) cells under the influence of promoters and mutagens, respectively. Subsequent transformation of normal stem cells into IS, PS, and NS cells apparently is the basis of carcinogenesis. These produce lesions, hyperplastic, preneoplastic, and neoplastic, respectively, only when and where NK activity is inhibited. Under the influence of normal NK cells, they remain dormant (nonproliferative), compatible with normal life.

Animals↗

PubMed2006

The control of UCP1 is dissociated from that of PGC-1alpha or of mitochondriogenesis as revealed by a study using beta-less mouse brown adipocytes in culture.

In rodent brown adipose tissue, the beta-adrenergic signaling is believed, by an action on PGC-1alpha, to control UCP1 expression and mitochondriogenesis. We addressed this hypothesis using beta(1)/beta(2)/beta(3)-adrenoceptor knockout (beta-less) brown adipocytes in primary culture. In these cells: (a) proliferation and differentiation into multilocular cells were normal; (b) UCP1 mRNA expression was dramatically decreased (by 93%), whereas PGC-1alpha and mtTFA mRNA expressions were not; (c) UCP1, PGC-1alpha and COX IV protein expressions were decreased by 97%, 62% and 22%, respectively. Altogether the data show a dissociation between the control of UCP1, which is mostly beta-adrenoceptor-dependent and that of PGC-1alpha and of mitochondriogenesis which are not.

Adipocytes↗

PubMedDate not supplied

Spontaneous neoplasm incidences in Fischer 344 rats and B6C3F1 mice in two-year carcinogenicity studies: a National Toxicology Program update.

Spontaneous neoplasm rates were determined for control Fischer 344 (F344) rats and B6C3F1 mice from 2-yr rodent carcinogenicity studies carried out by the National Toxicology Program (NTP). The most frequently occurring neoplasms in untreated male F344 rats were testicular adenoma (89.1%), mononuclear cell leukemia (50.5%), adrenal gland pheochromocytoma (31.9%), and pituitary gland neoplasms (30.4%). For untreated female F344 rats, the most frequently occurring neoplasms were pituitary gland neoplasms (54.2%), mammary gland fibroadenoma (41.2%), and mononuclear cell leukemia (28.1%). The most frequently occurring neoplasms in untreated male B6C3F1 mice were liver adenoma/carcinoma (42.2%), lung adenoma/carcinoma (20.5%), and malignant lymphoma (8.3%). For untreated female B6C3F1 mice, the most frequently occurring neoplasms were liver adenoma/carcinoma (23.6%), malignant lymphoma (20.9%), and pituitary gland adenoma/carcinoma (14.8%). The tumor rates observed in feeding study (untreated) and inhalation study (chamber) control rats were generally similar. The major exceptions were pituitary gland tumors and testicular adenoma in male F344 rats. The overall incidence of testicular adenoma was much lower in chamber controls (69.4%) than in feeding study controls (89.1%), whereas pituitary gland neoplasm showed the opposite trend (60.7% vs 30.4%). The most likely explanation for this difference is related to the individual housing of chamber controls and the group housing of feeding study controls. Differences in diagnostic criteria may influence reported tumor rates. To ensure consistency and comparability of tumor diagnosis from study to study, the NTP uses rigorous histopathology quality assurance and peer review procedures. Biological factors such as body weight may also affect tumor incidence. For example, increased body weights are associated with increased incidences of certain site-specific neoplasms, especially pituitary gland and mammary gland neoplasms in rats and liver tumors in mice. The presence of Helicobacter hepaticus has been associated with an increased incidence of liver neoplasms in male B6C3F1 mice. Other factors that may produce differences in control tumor rates from study to study include diet, environmental factors, genetic drift, study duration, and survival differences. The NTP database provides historical control data that may be useful in the evaluation of possible chemically related changes in tumor incidence. However, it is essential that the study being evaluated be comparable to those in the NTP database with respect to those factors that are known to influence tumor occurrence.

Animals↗

PubMed1998

Roles of amylin in diabetes and in regulation of nutrient load.

In summary, amylin, via its hormonal actions, may be relevant to the treatment of both forms of diabetes, and, paradoxically, via its amyloidogenic properties, may also be relevant to the pathogenesis of NIDDM. Amylin potently inhibits postprandial glucagon secretion. The absence of this action could contribute to the hyperglucagonemia and subsequently, excessive endogenous glucose production, fasting hyperglycemia, and propensity to ketosis seen in insulinopenic diabetes. Restoration of normal glucagon secretion by amylin replacement therapy could therefore be therapeutically important in treatment of insulin-dependent diabetes mellitus. Amylin potently inhibits gastric emptying. This action is consistent with a physiologic role of amylin to regulate carbohydrate absorption. Of peptides known to be secreted in response to ingested carbohydrate, only amylin and glucagon-like peptide-1 are reported to inhibit gastric emptying at near-physiologic concentrations, and could therefore participate in nutrient-mediated feedback control of carbohydrate release from the stomach. Amylin reduces food intake in rodents. This action, which synergizes with a similar action of CCK, could reflect a role as short-term peripheral satiety agent. Amylin alone or in combination with CCK may be useful in moderating caloric intake in obesity and other metabolic disorders. Although insulin has been extensively studied as a therapy and as a controller of nutrient storage and metabolism, the role of its beta-cell partner, amylin, has been largely unrecognized. In contrast to the nutrient disposal and storage role of insulin, amylin appears to more generally address the opposite side of the energy balance equation, the assimilation of nutrient.

Amyloid↗

PubMed2006

Lack of trophic pancreatic effects in humans with long-term administration of ximelagatran.

OBJECTIVES: Negative feedback regulation of pancreatic proteases controls pancreatic secretion in most species and pancreatic growth in rodents. Its mechanism involves the inhibition of intraluminal proteases, resulting in sustained elevation of plasma cholecystokinin (CCK) concentrations, producing a chronic trophic stimulus to the pancreas that leads to the formation of pancreatic nodules and adenomas. Ximelagatran, whose active form, melagatran, inhibits both thrombin and the serine protease trypsin, is under clinical development as an oral anticoagulant. Recent data indicate species differences in the expression of CCK receptor subtypes in the pancreas. CCK1 receptors are abundant in rat pancreas but are either absent or present at very low levels in human pancreas. As part of the clinical studies, we examined whether long-term ximelagatran administration causes CCK release and exerts possible trophic effects on the pancreas in humans. METHODS: One hundred thirty patients requiring anticoagulation treatment for atrial fibrillation randomly received, in a double-blind fashion, either 36 mg oral ximelagatran twice daily or warfarin dose adjusted to an international normalized ratio of 2.0 to 3.0. Before enrollment and after 12 months of treatment, computed tomography scans of the pancreas were performed, and pancreas volumes were quantified using the summation-of-areas technique. Three months after the initiation of drug treatment, plasma CCK concentrations were measured by radioimmunoassay 120 minutes after the patients drank 240 mL of a mixed liquid meal (Ensure). RESULTS: After 3 months of treatment, plasma CCK concentrations did not differ between the ximelagatran and warfarin groups, 15 +/- 18 and 11 +/- 17 pmol/L (X +/- SD; P = 0.22), respectively. The initial average pancreas volumes were 82 +/- 31 and 88 +/- 28 mL in the ximelagatran and warfarin groups, respectively, and decreased to 70 +/- 25 and 75 +/- 28 mL, respectively, after 12 months of treatment. Although the decrease in pancreas volume with time was significant in each group (P = 0.0001), the magnitude of the volume reduction was similar in the 2 groups. CONCLUSION: In contrast to rats, in which long-term oral administration of ximelagatran stimulates pancreatic growth and adenoma formation, in humans, ximelagatran does not increase plasma CCK concentrations and has no demonstrable trophic effect on the human pancreas.

Aged↗

PubMed2002

Interactions between aromatase (estrogen synthase) and dopamine in the control of male sexual behavior in quail.

In male quail, like in other vertebrates including rodents, testosterone acting especially through its estrogenic metabolites is necessary for the activation of male sexual behavior. Also, the administration of dopamine agonists and antagonists profoundly influences male sexual behavior. How the steroid-sensitive neural network and dopamine interact physiologically, remains largely unknown. It is often implicitly assumed that testosterone or its metabolite estradiol, stimulates male sexual behavior via the modification of dopaminergic transmission. We have now identified in quail two possible ways in which dopamine could potentially affect sexual behavior by modulating the aromatization of testosterone into an estrogen. One is a long-acting mechanism that presumably involves the modification of dopaminergic transmission followed by the alteration of the genomic expression of aromatase. The other is a more rapid mechanism that does not appear to be dopamine receptor-mediated and may involve a direct interaction of dopamine with aromatase (possibly via substrate competition). We review here the experimental data supporting the existence of these controls of aromatase activity by dopamine and discuss the possible contribution of these controls to the activation of male sexual behavior.

Animals↗

PubMed2005

Somatosensory integration controlled by dynamic thalamocortical feed-forward inhibition.

The temporal features of tactile stimuli are faithfully represented by the activity of neurons in the somatosensory cortex. However, the cellular mechanisms that enable cortical neurons to report accurate temporal information are not known. Here, we show that in the rodent barrel cortex, the temporal window for integration of thalamic inputs is under the control of thalamocortical feed-forward inhibition and can vary from 1 to 10 ms. A single thalamic fiber can trigger feed-forward inhibition and contacts both excitatory and inhibitory cortical neurons. The dynamics of feed-forward inhibition exceed those of each individual synapse in the circuit and are captured by a simple disynaptic model of the thalamocortical projection. The variations in the integration window produce changes in the temporal precision of cortical responses to whisker stimulation. Hence, feed-forward inhibitory circuits, classically known to sharpen spatial contrast of tactile inputs, also increase the temporal resolution in the somatosensory cortex.

Animals↗

PubMed1995

Calcium and colorectal epithelial cell proliferation in sporadic adenoma patients: a randomized, double-blinded, placebo-controlled clinical trial.

BACKGROUND: The kinetics of colorectal epithelial cell proliferation is altered in patients at increased risk for colon cancer. Calcium administration ameliorates such proliferative changes in rodents. Findings in preliminary clinical trials have suggested similar effects in humans. PURPOSE: A randomized, double-blind, placebo-controlled, clinical trial was designed to determine whether calcium supplementation will reduce the colorectal epithelial cell proliferation rate and normalize the distribution of proliferating cells within colorectal crypts (i.e., shift the zone of proliferation from the entire crypt to the lower 60% of the crypt, which is thought to be the normal proliferative zone of the crypt) in patients with sporadic adenomas. METHODS: Sporadic adenoma patients (n = 193) were treated with placebo (n = 66), 1.0 g calcium (n = 64), or 2.0 g calcium (n = 63) daily for 6 months. Rectal mucosa biopsy specimens were obtained at base line and at 1-, 2-, and 6-month follow-up. Cell proliferation was measured by detection of S-phase-associated proliferating cell nuclear antigen by immunohistochemical methods. The cell proliferation rate, called labeling index (LI), was calculated as the proportion of labeled cells in the crypts. The deviation of the proliferative zone from the normal location in the lower 60% of the crypt was calculated as the proportion of labeled cells in the upper 40% of the crypt, called distributional index (phi h). The effects of calcium treatment on the LI and phi h were expressed as relative effects--(calcium follow-up/calcium base line)/(placebo follow-up/placebo base line). Calculations and inference testing of the relative effects were accomplished using a repeated-measures mixed model on log-transformed LI and phi h values. All statistical tests were two-sided. RESULTS: Scorable biopsy specimens were obtained on 170 patients at base line, 164 at 1 month, 161 at 2 months, and 163 at 6 months. The difference in the change in the LI between the combined calcium groups and the placebo group was insignificant, with a relative effect of calcium versus placebo of 0.97 (P = .87). However, for the phi h, the relative effect of calcium versus placebo was 0.50 (P = .05) in the combined calcium groups, 0.56 (P = .16) in the 1.0-g calcium group, and 0.44 (P = .05) in the 2.0-g calcium group. CONCLUSIONS: Calcium supplementation normalizes the distribution of proliferating cells without affecting the proliferation rate in the colorectal mucosa of sporadic adenoma patients. IMPLICATIONS: These results support further study of whether alterations in colon cell proliferative kinetics represent true intermediate steps in colon carcinogenesis that can be used to investigate the etiology and prevention of, and whether a higher calcium consumption can reduce the risk of, colon cancer.

Adult↗

PubMed2004

Odor discrimination assessment with an automated olfactometric method in a prosimian primate, Microcebus murinus.

The present study was aimed at adapting an automated olfactometer designed for use with rodents to a nocturnal lemur Microcebus murinus. This apparatus allows rigorous control of odor stimuli. We show that M. murinus could remain quiet and attentive for about 20 min in the test chamber, allowing daily sessions of 40 consecutive trials. This allowed us to train M. murinus subjects to learn a go/no-go discrimination procedure using fruity-odor cues. Each of seven subjects reached or exceeded a criterion of 33 correct responses in a block of 40 trials in a range of 4-14 training sessions. When trained on an odor reversal task, performance initially dropped sharply, followed by rapid acquisition of the new task. These outcomes demonstrate that, like rodents, M. murinus can be trained using operant conditioning in an automated olfactometer. This species should prove useful for investigating cognitive capacities and neurodegenerative disease in a primitive primate model.

Animals↗

PubMed1988

Pathology and glutathione status in 3-methylindole-treated rodents.

Light and electron microscopic studies were performed to assess the pathology induced by 3-methylindole (3MI) in Sprague-Dawley rats and Swiss-Webster mice. Rats have not been established as a susceptible species to 3MI-induced pulmonary damage, whereas mice are known to be a good model for this pneumotoxicity. Therefore, mice were used as a comparison species for pneumotoxicity studies in the rat. Rats were as susceptible to 3MI-mediated toxicity as mice. The loss of Clara cells in the bronchiolar epithelium was the major pulmonary lesion in both species. Alveolar cells in the lungs of either species were not damaged. The only other lesion in the rat was that the nasal epithelium was totally eroded in caudal areas of the sinuses. Glutathione was depleted by 3MI in pulmonary tissues of mice and rats. Maximal depletion (53% of control values) occurred in rat lung. This work demonstrates that both rodent species are susceptible to 3MI-induced pulmonary damage.

Animals↗

PubMed1992

Splicing of two alternative exon pairs in beta-tropomyosin pre-mRNA is independently controlled during myogenesis.

Two known tissue-specific tropomyosin (TM) isoforms are produced from the rodent beta-TM gene. Skeletal muscle beta-TM uses the alternative exons 6b and 9a and the exon 9a-associated poly(A) site. Fibroblast and smooth muscle TM-1 use exons 6a and 9b and the exon-9b associated poly(A) site. We have identified a new skeletal muscle beta-TM isoform, beta-TM2. beta-TM2 contains exon 6b (muscle) and exon 9b (nonmuscle). Full-length beta-TM2 cDNA clones were isolated from a cDNA library of mouse muscle BC3H1 cells. Its mRNA was also found in mouse skeletal muscle tissue but not in other tissues. beta-TM2 mRNA level and protein synthesis are differentiation-dependent, with a transient high level in the early stages of myogenesis both in BC3H1 cells and in mouse embryo limbs. Trace amounts of beta-TM3 mRNA, the other hybrid form (exons 6a + 9a), were found in less differentiated BC3H1 cells, mouse uterus, heart, and 3T3 fibroblasts but not skeletal muscle tissue. Thus, the selection of the two alternative exons appears to be controlled independently. Furthermore, during myogenesis, there is a sequential switch in the internal alternative exon, the terminal exon, and the poly(A) site from the nonmuscle to the muscle type.

Amino Acid Sequence↗

PubMed1990

Response of the ke test to NCI/NTP-screened chemicals. I. Non-genotoxic carcinogens and genotoxic non-carcinogens.

The response of a physico-chemical carcinogen-screening test, the k(e) test, to 46 rodent carcinogens and 20 putative non-carcinogens that had been screened in long-term two-species bioassays by the National Cancer Institute/National Toxicology Program are reported. All of the chemicals screened are those that yield mutagenicity responses in the Ames Salmonella/microsome test that are either equivocal or contrary to the rodent carcinogenicity responses. The electron attachment rate constants, k(e)S, of the test chemicals in cyclohexane at 21 degrees C were measured using a pulse-conductivity technique. The k(e)S of 27 of the 46 rodent carcinogens (59%) are equal or greater than the diffusion-controlled k(e) of carbon tetrachloride, which is regarded as the boundary between a positive and negative response; the k(e)S of 8 of the 20 mutagenic non-carcinogens (40%) are less than diffusion-controlled. If the boundary between positive and negative k(e) responses is decreased to half the diffusion-controlled k(e), six additional carcinogens yield a positive ke response which increases the k(e) test sensitivity to 72% while the specificity to non-carcinogens remains at 40%. Comparison of these k(e)S with measures of the chemicals' electrophilicity that had been inferred from chemical structure indicates that k(e) provides a markedly different measure of electrophilicity and one that complements the Ames Salmonella assay. The use of the k(e) test as an analytical tool to indicate the presence of electron-attaching impurities in solvents such as benzene is discussed, as is the sensitivity of the k(e) test to rodent-liver carcinogens.

Animals↗

PubMed1997

Surveillance and spatiotemporal associations of rabies in rodents and lagomorphs in the United States, 1985-1994.

Between 1985 and 1994, 368 cases of rabies in rodents (95% of reports) and lagomorphs (5%) were reported to the Centers for Disease Control and Prevention, Atlanta, Georgia (USA), from 22 states. This was a 354% increase from the period 1971 to 1984. Most reports were cases of rabies in woodchucks (Marmota monax) (n = 317), primarily from the eastern United States, which has been recently experiencing an epizootic of raccoon (Procyon lotor) rabies. Cases of rabies in woodchucks were temporally and spatially associated with reports of raccoon rabies. Antigenic or genetic characterization of variants of rabies viruses from rodents and woodchucks corresponded to the variants associated with the major terrestrial wildlife reservoir within the geographic region of specimen origin. Although rodents and lagomorphs are infrequently infected with rabies and human contact with these animals rarely requires postexposure treatment, appropriate health authorities need to evaluate individual circumstances surrounding potential exposures.

Animals↗