RABIES VIRUS SEROSURVEY OF THE SMALL INDIAN MONGOOSE (URVA AUROPUNCTATA) ACROSS MULTIPLE HABITATS IN PUERTO RICO, 2014-21.

The small Indian mongoose (Urva auropuncata) is a rabies reservoir in Puerto Rico and accounts for over 70% of reported animal rabies cases annually. The presence of rabies virus-neutralizing antibodies (RVNA) is often used as a tool to measure exposure to rabies virus in wildlife populations. We conducted a serosurvey of mongooses at 11 sites representing six habitat types across Puerto Rico. We collected a serum sample from 464 individual mongooses during 2014-21. Overall, 80/464 (17.0%; 95% confidence interval, 14.1-20.9%; 55 male, 23 female, and two sexes not recorded) of individual mongooses sampled across all habitats were RVNA positive. The geometric mean (SD) RVNA titer for 80 unique seropositive animals was 0.58 (2.92) IU/mL. Our models indicated that the probability of mongooses being RVNA seropositive mostly varied by habitat, with some influence of sex in the individual-level analyses. Population-level RVNA seroprevalence is dynamic in mongoose populations, but these data may shed light on rabies virus transmission across regions to help inform rabies management activities in Puerto Rico.

[Purpura due to Strongyloides stercoralis in an immunocompetent patient]. / Púrpura por Strongyloides stercoralis en un paciente inmunocompetente.

Infection with Strongyloides stercoralis is a common parasitic infection in tropical and subtropical regions, including the Peruvian Amazon. The clinical manifestations are varied in patients with immunocompromised disease, and the systemic spread of the disease is frequent, compromising different organs and systems. Cutaneous manifestations are infrequent, being described in patients with some degree of immunosuppression. We present the case of an immunocompetent patient who developed a reactive purpura due to chronic Strongyloides stercoralis infection. Thus, skin involvement is possible in immunocompetent patients with systemic exacerbation due to this parasite.

Púrpura por Strongyloides stercoralis en un paciente inmunocompetente / Purpura due to Strongyloides stercoralis in an immunocompetent patient

Resumen La infección por Strongyloides stercoralis es una parasitosis frecuente en las regiones tropicales y subtropicales, incluyendo la Amazonía peruana. En pacientes con inmunocompromiso, las manifestaciones clínicas son variadas y es frecuente la diseminación sistémica de la enfermedad, con compromiso de diversos órganos. Las manifestaciones cutáneas son infrecuentes y se describen en pacientes con algún grado de inmunosupresión. Se presenta el caso de un paciente inmunocompetente que desarrolló una púrpura reactiva por una infección por Strongyloides stercoralis crónica. Ante ello, es posible el compromiso cutáneo en pacientes inmunocompetentes con reagudización sistémica por este parásito.

Infection with Strongyloides stercoralis is a common parasitic infection in tropical and subtropical regions, including the Peruvian Amazon. The clinical manifestations are varied in patients with immunocompromised disease, and the systemic spread of the disease is frequent, compromising different organs and systems. Cutaneous manifestations are infrequent, being described in patients with some degree of immunosuppression. We present the case of an immunocompetent patient who developed a reactive purpura due to chronic Strongyloides stercoralis infection. Thus, skin involvement is possible in immunocompetent patients with systemic exacerbation due to this parasite.

Impairment on sperm quality and fertility of adult rats after antiandrogen exposure during prepuberty.

This study evaluated the effects of antiandrogen exposure during the prepubertal period on reproductive development and reproductive competence in adults. Male rats were divided into two groups: flutamide, receiving 25 mg/kg/day of flutamide by oral gavage and control, receiving vehicle daily. Dosing continued from PND 21 to 44, and animals were killed on PND 50 or PND 75-80. The epididymis, prostate, vas deferens and seminal vesicle weights were lower in Flutamide group on PND 50, while on PND 80 only seminal vesicle weight was reduced. Fertility assessed by IUI revealed a decrease in the fertility potential in the flutamide-treated adults. Flutamide accelerated sperm transit time through the epididymis, impairing sperm motility and storage. A quantitative analysis of the cauda sperm membrane proteome revealed a few significant changes in protein expression. Thus, exposure to flutamide during the prepubertal period compromises the function of the epididymis along with epididymal sperm quality at adulthood.

Paternal treatment with cisplatin impairs reproduction of adult male offspring in rats.

This study evaluated the acute and persistent effects of paternal cisplatin-treatment on progeny. Wistar male rats (45 days old) were assigned into 2 groups. Control and cisplatin (CP: 1mg/kg-d, 5 days/week, for 3 weeks, ip.). Male rats at 66 (end of treatment, acute effects evaluation) and 140 days old (after recovery period, persistent effects evaluation) were mated with females. Fetal and post-natal developments of the offspring sired by treated-male mated in both ages were evaluated, including fertility of adult male offspring. No adverse effects in fetal development or puberty onset were seen in CP offspring. However, testicular descent was delayed and postnatal growth was impaired in these animals (acute effect). Moreover, seminal vesicle weight and epididymal sperm count from adult progeny were affected (acute effects) by paternal CP-exposure. The only persistent effect found was alterations in the spermatogenesis. We conclude that paternal CP-administration during peri-puberty affects reproductive endpoints of the progeny.

In utero and lactational exposure to fenvalerate disrupts reproductive function in female rats.

Fenvalerate is a synthetic pyrethroid insecticide used in agriculture and domestic insect control. Some studies have proposed that it may act as an environmental estrogen; other studies suggest possible genotoxicity in germ cells. This study aimed to evaluate the effects of fenvalerate on the female reproduction in rats whose mothers were exposed during gestation and lactation. Pregnant Wistar rats were exposed to fenvalerate (40 mg/kg) or corn oil (vehicle) orally from gestational day 12 until the end of lactation. The dose selection was based on previous studies, whereas this was considered an effective dose. Results showed decreases in ovarian weight, pre-antral follicles and corpora lutea at PND 75 and an increase in the resorption number, when fertility test was performed at PND 80. Under some experimental conditions, fenvalerate may impair reproductive development of female offspring, manifested as reduced fecundity and ovulation number, resulting from the impairment in corpora lutea counting.

Assessment of female reproductive endpoints in Sprague-Dawley rats developmentally exposed to Diuron: potential ovary toxicity.

BACKGROUND: Diuron is widely used in agriculture but its deleterious effects on the reproductive system and mammary gland are still poorly understood. This study evaluated whether early-life-stage exposure to Diuron alters puberty onset or susceptibility to mammary carcinogenesis in female Sprague-Dawley rats. METHODS AND RESULTS: Pregnant rats received basal diet or diet containing Diuron at 500, 750, and 1,250 ppm, from gestational day 12 to the end of lactation (postnatal day 21 [PND21]). After weaning, female offspring continued receiving basal diet or diet containing Diuron until PND 51. At PND 51, female Sprague-Dawley offspring received a single dose of 50 mg/kg b.w. of 7,12-dimethylbenz(a)anthracene (DMBA) for initiation of mammary carcinogenesis. The animals were sacrificed on PND 51, 75, and 226 to 233 (week 25) for mammary gland morphology, reproductive organs and tumor analysis, respectively. There were no significant differences among groups on vaginal opening, estrous cycle, mammary morphology, or carcinogenesis. However, reductions in ovary weight and corpora lutea were observed at PND 75 in the group treated with Diuron at 1,250 ppm. CONCLUSIONS: The findings suggesting that Diuron exposure (1,250 ppm) may have been potentially toxic to the ovaries.

In utero protein restriction causes growth delay and alters sperm parameters in adult male rats.

BACKGROUND: Recent studies have supported the concept of "fetal programming" which suggests that during the intrauterine development the fetus may be programmed to develop diseases in adulthood. The possible effects of in utero protein restriction on sexual development of rat male offspring were evaluated in the present study. METHODS: Pregnant Wistar rats were divided into two experimental groups: one group treated with standard chow (SC, n = 8, 17% protein) and the other group treated with hypoproteic chow (HC, n = 10, 6% protein) throughout gestation. After gestation the two experimental groups received standard chow. To evaluate the possible late reproductive effects of in utero protein restriction, the male offspring of both groups were assessed at different phases of sexual development: prepubertal (30 days old); peripubertal (60 days old); adult (90 days old). Student's t-test and Mann-Whitney test were utilized. Differences were considered significant when p < 0.05. RESULTS: We found that in utero protein restriction reduced the body weight of male pups on the first postnatal day and during the different sexual development phases (prepubertal, peripubertal and adult). During adulthood, Sertoli cell number, sperm motility and sperm counts in the testis and epididymal cauda were also reduced in HC. Furthermore, the numbers of sperm presenting morphological abnormalities and cytoplasmic drop retention were higher in HC. CONCLUSIONS: In conclusion, in utero protein restriction, under these experimental conditions, causes growth delay and alters male reproductive-system programming in rats, suggesting impairment of sperm quality in adulthood.

Effects of gestational and lactational fenvalerate exposure on immune and reproductive systems of male rats.

The aim of this study was to determine the consequent reproductive developmental and immunotoxic effects due to exposure to fenvalerate during pregnancy and lactation in male offspring of maternal-treated rats. Pregnant rats were treated daily by oral gavage with 40 or 80 mg/kg of fenvalerate or corn oil (vehicle, control), from d 12 of pregnancy to d 21 of lactation. Immune and reproductive developmental effects were assessed in male offspring at postnatal days (PND) 40 (peripuberty), 60 (postpuberty), and 90 (sexual maturity). Treatment with the higher dose (80 mg/kg) resulted in convulsive behavior, hyperexcitability, and mortality in 45% of the dams. Fenvalerate was detected in the fetus due to placental transfer, as well as in pups due to breast-milk ingestion, persisting in male offspring until PND 40 even though pesticide treatment was terminated on PND 20. However, fenvalerate did not produce marked alterations in age of testicular descent to the scrotum and prepucial separation, parameters indicative of puberty initiation. In contrast, at puberty, there was a reduction in testicular weight and sperm production in male offspring of maternal-treated rats. At adulthood, the sperm counts and fertility did not differ between control and treated groups. Testosterone levels were not changed at any time during reproductive development. Similarly, no apparent exposure-related effects were detected in the histological structures of the lymphohematopoietic system. Data indicate that fenvalerate, in this experimental model, interfered with initial development of the male reproductive system, but that these effects on sperm production or fertility did not persist into adulthood. There was no apparent evidence that fenvalerate altered testosterone levels or produced a disruption in male endocrine functions.

Functional and morphological reproductive aspects in male rats exposed to di-n-butyl phthalate (DBP) in utero and during lactation.

The potential adverse reproductive effects, with emphasis on the epididymis, of in utero and lactational exposure to 100 mg/kg/d di-n-butyl phthalate (DBP) in adult male rat offspring were investigated. The fetal testis histopathology was also determined. The selected endpoints included reproductive organ weights, sperm motility and morphology, sperm epididymal transit time, sperm quantity in the testis and epididymis, hormonal status, fetal testis and epididymal histopathology and stereology, and androgen receptor (AR), aquaporin 9 (AQP9), and Ki-67 immunoreactivities. Pregnant females were divided into two groups: control (C) and treated (T). The treated females received DBP (100 mg/kg/d, by gavage) from gestation day (GD) 12 to postnatal day (PND) 21, while control dams received the vehicle. Some pregnant dams were killed by decapitation on GD20, and testes from male fetuses were collected for histopathogy. Male rats from other dams were killed at PND 90. Fetal testes from treated group showed Leydig-cell clusters, presence of multinucleated germinative cells, and increase of the interstitial component. Testosterone levels and reproductive organ weights were similar between the treated and control adult groups. DBP treatment did not markedly affect relative proportions of epithelial, stromal, or luminal compartments in the epididymis; sperm counts in the testis and epididymis; sperm transit time; or sperm morphology and motility in adult rats. The AR and AQP9 immunoreactivities and proliferation index were similar for the two groups. These results showed that fetal testes were affected by DBP as evidenced by testicular histopathologic alterations, but reproductive parameters and epididymal structure/function were not significantly altered in the adult animals exposed to 100 mg/kg DBP in utero and during lactation.

Reproductive development and function of female rats exposed to di-eta-butyl-phthalate (DBP) in utero and during lactation.

Phthalates are environmental contaminants used in the production of plastics, cosmetics and medical devices. Studies on the effects of phthalates on female reproductive health are particularly sparse and mostly restricted to high-dose exposure in rats. In the present study, pregnant rats were treated with 100mg/kg-d of di-eta-butyl-phthalate (DBP) or only the vehicle (control group), from GD 12 to GD 20 for evaluation of reproductive outcomes and fetal gonads analysis (F0), and from GD 12 to PND 21 to evaluate reproductive development and function on F1 female offspring. Results showed that all parameters were comparable between groups, although there was a significant increase in the fetal weight after DBP exposure. However, the body weight at birth was normal. Based on these data we can conclude that, in these experimental conditions, DBP did not disturb the reproductive development or function of female rats.

Long-term effects of developmental exposure to di-n-butyl-phthalate (DBP) on rat prostate: proliferative and inflammatory disorders and a possible role of androgens.

In the present study we evaluated the toxic effects on the male adult rat prostate of DBP exposure during fetal and lactational periods, because although many studies have addressed the influence of phthalates on the male reproductive system, only a few have discussed their possible effects on prostate development. Pregnant females were distributed into two experimental groups: Control (C) and Treated (T). The females of the T group received DBP (100mg/kg, by gavage) from gestation day 12 to postnatal day 21, while C rats received the vehicle (corn oil). In adulthood (90 days old), the animals were euthanized. The serum and testicular testosterone levels were measured. Ventral prostate was removed and weighed. Distal segment fragments of the ventral prostate were fixed and processed for histochemistry and immunohistochemistry to detect androgen receptor (AR) and Ki67 antigens. Protein extraction from ventral prostate fragments was performed for AR immunoblotting and Gelatin zymography for MMP-2 and MMP-9 (MMP, metalloproteinase). Stereological and histopathological analyses were also performed. Serum and testicular testosterone levels and prostate weight were comparable between groups. In the T group the relative proportions (%) of epithelial (C=32.86; T=42.04*) and stromal (C=21.61; T=27.88*) compartments were increased, while the luminal compartment was decreased (C=45.54; T=30.08*), *p<0.05. InT, disseminated inflammatory infiltrate in the stroma, associated or not with epithelial dysplasia and PIN (Prostatic Intraepithelial Neoplasia), was observed. Increases in AR expression, proliferation index and metalloproteinase 9 (MMP-9) activity were noted in T animals. In some T animals, collagen fibrils accumulated adjacent to the epithelium. As far as we are aware, this is the first report in the literature showing that phthalates could play a role in proliferative and inflammatory disorders of the rat prostate.