Circadian Disruption and the Molecular Clock in Atherosclerosis and Hypertension.

Circadian rhythms are crucial for maintaining vascular function and disruption of these rhythms are associated with negative health outcomes including cardiovascular disease and hypertension. Circadian rhythms are regulated by the central clock within the suprachiasmatic nucleus of the hypothalamus and peripheral clocks located in nearly every cell type in the body, including cells within the heart and vasculature. In this review, we summarize the most recent preclinical and clinical research linking circadian disruption, with a focus on molecular circadian clock mechanisms, in atherosclerosis and hypertension. Furthermore, we provide insight into potential future chronotherapeutics for hypertension and vascular disease. A better understanding of the influence of daily rhythms in behaviour, such as sleep/wake cycles, feeding, and physical activity, as well as the endogenous circadian system on cardiovascular risk will help pave the way for targeted approaches in atherosclerosis and hypertension treatment/prevention.

Involvement of lysyl oxidase in the pathogenesis of arterial stiffness in chronic kidney disease.

Patients with chronic kidney disease (CKD) are at increased risk for adverse cardiovascular events. CKD is associated with increases in arterial stiffness, whereas improvements in arterial stiffness correlate with better survival. However, arterial stiffness is increased early in CKD, suggesting that there might be additional factors, unique to kidney disease, that increase arterial stiffness. Lysyl oxidase (LOX) is a key mediator of collagen cross linking and matrix remodeling. LOX is predominantly expressed in the cardiovascular system, and its upregulation has been associated with increased tissue stiffening and extracellular matrix remodeling. Thus, this study was designed to evaluate the role of increased LOX activity in inducing aortic stiffness in CKD and whether ß-aminopropionitrile (BAPN), a LOX inhibitor, could prevent aortic stiffness by reducing collagen cross linking. Eight-week-old male C57BL/6 mice were subjected to 5/6 nephrectomy (Nx) or sham surgery. Two weeks after surgery, mice were randomized to BAPN (300 mg/kg/day in water) or vehicle treatment for 4 wk. Aortic stiffness was assessed by pulse wave velocity (PWV) using Doppler ultrasound. Aortic levels of LOX were assessed by ELISA, and cross-linked total collagen levels were analyzed by mass spectrometry and Sircol assay. Nx mice showed increased PWV and aortic wall remodeling compared with control mice. Collagen cross linking was increased in parallel with the increases in total collagen in the aorta of Nx mice. In contrast, Nx mice that received BAPN treatment showed decreased cross-linked collagens and PWV compared with that received vehicle treatment. Our results indicated that LOX might be an early and key mediator of aortic stiffness in CKD.NEW & NOTEWORTHY Arterial stiffness in CKD is associated with adverse cardiovascular outcomes. However, the mechanisms underlying increased aortic stiffness in CKD are unclear. Herein, we demonstrated that 1) increased aortic stiffness in CKD is independent of hypertension and calcification and 2) LOX-mediated changes in extracellular matrix are at least in part responsible for increased aortic stiffness in CKD. Prevention of excess LOX may have therapeutic potential in alleviating increased aortic stiffness and improving cardiovascular disease in CKD.

KUB-UNet: Segmentation of Organs of Urinary System from a KUB X-ray Image.

PURPOSE: The alarming increase in diseases of urinary system is a cause of concern for the populace and health experts. The traditional techniques used for the diagnosis of these diseases are inconvenient for patients, require high cost, and additional waiting time for generating the reports. The objective of this research is to utilize the proven potential of Artificial Intelligence for organ segmentation. Correct identification and segmentation of the region of interest in a medical image are important to enhance the accuracy of disease diagnosis. Also, it improves the reliability of the system by ensuring the extraction of features only from the region of interest. METHOD: A lot of research works are proposed in the literature for the segmentation of organs using MRI, CT scans, and ultrasound images. But, the segmentation of kidneys, ureters, and bladder from KUB X-ray images is found under explored. Also, there is a lack of validated datasets comprising KUB X-ray images. These challenges motivated the authors to tie up with the team of radiologists and gather the anonymous and validated dataset that can be used to automate the diagnosis of diseases of the urinary system. Further, they proposed a KUB-UNet model for semantic segmentation of the urinary system. RESULTS: The proposed KUB-UNet model reported the highest accuracy of 99.18% for segmentation of organs of urinary system. CONCLUSION: The comparative analysis of its performance with state-of-the-art models and validation of results by radiology experts prove its reliability, robustness, and supremacy. This segmentation phase may prove useful in extracting the features only from the region of interest and improve the accuracy diagnosis.

Fecal matter transplant from Ace2 overexpressing mice counteracts chronic hypoxia-induced pulmonary hypertension.

Recent evidence suggests pulmonary hypertension (PH), a disease of the pulmonary vasculature actually has multiorgan pathophysiology and perhaps etiology. Herein, we demonstrated that fecal matter transplantation from angiotensin-converting enzyme 2 overexpressing mice counteracted the effects of chronic hypoxia to prevent pulmonary hypertension, neuroinflammation, and gut dysbiosis in wild type recipients.

SARS-CoV-2 (COVID-19) as a possible risk factor for neurodevelopmental disorders.

Pregnant women constitute one of the most vulnerable populations to be affected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, the cause of coronavirus disease 2019. SARS-CoV-2 infection during pregnancy could negatively impact fetal brain development via multiple mechanisms. Accumulating evidence indicates that mother to fetus transmission of SARS-CoV-2 does occur, albeit rarely. When it does occur, there is a potential for neuroinvasion via immune cells, retrograde axonal transport, and olfactory bulb and lymphatic pathways. In the absence of maternal to fetal transmission, there is still the potential for negative neurodevelopmental outcomes as a consequence of disrupted placental development and function leading to preeclampsia, preterm birth, and intrauterine growth restriction. In addition, maternal immune activation may lead to hypomyelination, microglial activation, white matter damage, and reduced neurogenesis in the developing fetus. Moreover, maternal immune activation can disrupt the maternal or fetal hypothalamic-pituitary-adrenal (HPA) axis leading to altered neurodevelopment. Finally, pro-inflammatory cytokines can potentially alter epigenetic processes within the developing brain. In this review, we address each of these potential mechanisms. We propose that SARS-CoV-2 could lead to neurodevelopmental disorders in a subset of pregnant women and that long-term studies are warranted.

Central Administration of Hydrogen Sulfide Donor NaHS Reduces Iba1-Positive Cells in the PVN and Attenuates Rodent Angiotensin II Hypertension.

Hydrogen sulfide (H2S) is a gaseous signaling molecule with neuromodulatory, anti-inflammatory, and anti-hypertensive effects. Here, we investigate whether chronic intracerebroventricular (ICV) infusion of sodium hydrosulfide (NaHS), an H2S donor, can alleviate angiotensin II (Ang II)-induced hypertension (HTN), improve autonomic function, and impact microglia in the paraventricular nucleus (PVN) of the hypothalamus, a brain region associated with autonomic control of blood pressure (BP) and neuroinflammation in HTN. Chronic delivery of Ang II (200 ng/kg/min, subcutaneous) for 4 weeks produced a typical increase in BP and sympathetic drive and elevated the number of ionized calcium binding adaptor molecule 1-positive (Iba1+) cells in the PVN of male, Sprague-Dawley rats. ICV co-infusion of NaHS (at 30 and/or 60 nmol/h) significantly attenuated these effects of Ang II. Ang II also increased the abundance of cecal Deltaproteobacteria and Desulfovibrionales, among others, which was prevented by ICV NaHS co-infusion at 30 and 60 nmol/h. We observed no differences in circulating H2S between the groups. Our results suggest that central H2S may alleviate rodent HTN independently from circulating H2S via effects on autonomic nervous system and PVN microglia.

Angiotensin-converting enzyme 2 and COVID-19 in cardiorenal diseases.

The rapid spread of the novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has brought into focus the key role of angiotensin-converting enzyme 2 (ACE2), which serves as a cell surface receptor required for the virus to enter cells. SARS-CoV-2 can decrease cell surface ACE2 directly by internalization of ACE2 bound to the virus and indirectly by increased ADAM17 (a disintegrin and metalloproteinase 17)-mediated shedding of ACE2. ACE2 is widely expressed in the heart, lungs, vasculature, kidney and the gastrointestinal (GI) tract, where it counteracts the deleterious effects of angiotensin II (AngII) by catalyzing the conversion of AngII into the vasodilator peptide angiotensin-(1-7) (Ang-(1-7)). The down-regulation of ACE2 by SARS-CoV-2 can be detrimental to the cardiovascular system and kidneys. Further, decreased ACE2 can cause gut dysbiosis, inflammation and potentially worsen the systemic inflammatory response and coagulopathy associated with SARS-CoV-2. This review aims to elucidate the crucial role of ACE2 both as a regulator of the renin-angiotensin system and a receptor for SARS-CoV-2 as well as the implications for Coronavirus disease 19 and its associated cardiovascular and renal complications.

Development of miniaturized trigatron switch and experimental investigation of its switching performance.

There is an increasing interest in synchronization of multiple spark gap switches while maintaining compact geometry, less-complex circuit, and low jitter switching performances. A study of the effect of electrical parameters on switching performances is necessary for the operation of a large number of simultaneous switches. A miniaturized trigatron switch assembly (Outer diameter: 35 mm and thickness: 5 mm) is developed and experimentally investigated for switching performance. A polyether ether ketone insulator and brass conductor electrodes are utilized due to their high insulation and solderable properties, respectively. Important switching parameters, delay time, switch time delay, jitter in delay time, discharging peak current, trigger break down time, and trigger break down voltage, are studied under four typical conditions. These four conditions are: (a) a fast trigger (FT) with normal circuit inductance (10 ns, 20 nH); (b) a fast trigger with higher circuit inductance (10 ns and 500 nH); (c) a slow trigger (ST) with normal circuit inductance (250 ns and 20 nH) and (d) a slow trigger with higher circuit inductance (250 ns and 500 nH). Subsequently, three trigatron spark gaps (4 kV, 5 kA, >100 shots, 4 nH, and 20 mΩ) are simultaneously switched within 5 ns time. Many experimental results are the first of their kind in terms of compact switch development, switching performance, and single electrical trigger based synchronization. This paper will also add a good value to presently available knowledge through systematically implementing the simultaneous switching condition for the generation of 5 kA, 50 ns current pulses. These low cost (US$40) trigatron switches can be utilized in low energy, compact pulsed power applications.

ACE2 (Angiotensin-Converting Enzyme 2) in Cardiopulmonary Diseases: Ramifications for the Control of SARS-CoV-2.

Discovery of ACE2 (angiotensin-converting enzyme 2) revealed that the renin-angiotensin system has 2 counterbalancing arms. ACE2 is a major player in the protective arm, highly expressed in lungs and gut with the ability to mitigate cardiopulmonary diseases such as inflammatory lung disease. ACE2 also exhibits activities involving gut microbiome, nutrition, and as a chaperone stabilizing the neutral amino acid transporter, B0AT1, in gut. But the current interest in ACE2 arises because it is the cell surface receptor for the novel coronavirus, severe acute respiratory syndrome coronavirus-2, to infect host cells, similar to severe acute respiratory syndrome coronavirus-2. This suggests that ACE2 be considered harmful, however, because of its important other roles, it is paradoxically a potential therapeutic target for cardiopulmonary diseases, including coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2. This review describes the discovery of ACE2, its physiological functions, and its place in the renin-angiotensin system. It illustrates new analyses of the structure of ACE2 that provides better understanding of its actions particularly in lung and gut, shedding of ACE2 by ADAM17 (a disintegrin and metallopeptidase domain 17 protein), and role of TMPRSS2 (transmembrane serine proteases 2) in severe acute respiratory syndrome coronavirus-2 entry into host cells. Cardiopulmonary diseases are associated with decreased ACE2 activity and the mitigation by increasing ACE2 activity along with its therapeutic relevance are addressed. Finally, the potential use of ACE2 as a treatment target in COVID-19, despite its role to allow viral entry into host cells, is suggested.

Pulmonary arterial hypertension-associated changes in gut pathology and microbiota.

Emerging evidence implicates an interplay among multiple organs such as brain, vasculature, gut and lung in the development of established pulmonary arterial hypertension (PAH). This has led us to propose that activated microglia mediated-enhanced sympathetic activation contributes to PAH pathophysiology. Since enhanced sympathetic activity is observed in human PAH and the gut is highly innervated by sympathetic nerves that regulate its physiological functions, we hypothesized that PAH would be associated with gut pathophysiology. A monocrotaline rat model of PAH was utilized to investigate the link between gut pathology and PAH. Haemodynamics, histology, immunocytochemistry and 16S RNA gene sequencing were used to assess cardiopulmonary functions, gut pathology and gut microbial communities respectively. Monocrotaline treatment caused increased right ventricular systolic pressure, haemodynamics and pathological changes associated with PAH. PAH animals also showed profound gut pathology that included increased intestinal permeability, increased muscularis layer, decreased villi length and goblet cells. These changes in gut pathology were associated with alterations in microbial communities, some unique to PAH animals. Furthermore, enhanced gut-neural communication involving the paraventricular nucleus of the hypothalamus and increased sympathetic drive were observed. In conclusion, our data show the presence of gut pathology and distinct changes in gut microbiota and increased sympathetic activity in PAH. They suggest that dysfunctional gut-brain crosstalk could be critical in PAH and considered a future therapeutic target for PAH.

Gastrointestinal parasitic nematodes in pet red-footed tortoises (Chelonoidis carbonaria) from Grenada, West Indies.

This study identifies the endoparasites in Red-footed tortoises (Chelonoidis carbonaria) during March 2018 to March 2019 from Grenada, West Indies. Fecal samples from a total of 103 tortoises were collected and examined by simple fecal floatation techniques for parasitic eggs and oocysts. Adult parasites found in the feces were examined under the microscope for identification based on their morphology. Fecal samples for this research were collected from four parishes; St. Andrew, St George, St. John and St. Patrick. The overall prevalence of intestinal parasites among tortoises was 14.6%. The internal parasites consisted of nematodes belonging to three genera: Atractis, Labiduris and Proatractis. The most prevalent nematodes were Atractis spp. (86.7%), which included two species: A. thapari (7.7%) and A. marquezi (15.4%) followed by Labiduris gulosa (20%) and Proatractis parvicapiticaronata (13.3%). All nematodes of three genera found in red-footed tortoises in Grenada are reported for the first time. They are not zoonotic but are serious pathogens for tortoises.

Gut Pathology and Its Rescue by ACE2 (Angiotensin-Converting Enzyme 2) in Hypoxia-Induced Pulmonary Hypertension.

Therapeutic advances for pulmonary hypertension (PH) have been incremental because of the focus on the pulmonary vasculature in PH pathology. Here, we evaluate the concept that PH is, rather, a systemic disorder involving interplay among multiorgan systems, including brain, gut, and lungs. Therefore, the objective of this study was to evaluate the hypothesis that PH is associated with a dysfunctional brain-gut-lung axis and that global overexpression of ACE2 (angiotensin-converting enzyme 2) rebalances this axis and protects against PH. ACE2 knockin and wild-type (WT; C57BL/6) mice were subjected to chronic hypoxia (10% FIO2) or room air for 4 weeks. Cardiopulmonary hemodynamics, histology, immunohistochemistry, and fecal 16S rRNA microbial gene analyses were evaluated. Hypoxia significantly increased right ventricular systolic pressure, sympathetic activity as well as the number and activation of microglia in the paraventricular nucleus of the hypothalamus in WT mice. This was associated with a significant increase in muscularis layer thickening and decreases in both villi length and goblet cells and altered gut microbiota. Global overexpression of ACE2 prevented changes in hypoxia-induced pulmonary and gut pathophysiology and established distinct microbial communities from WT hypoxia mice. Furthermore, WT mice subjected to fecal matter transfer from ACE2 knockin mice were resistant to hypoxia-induced PH compared with their controls receiving WT fecal matter transfer. These observations demonstrate that ACE2 ameliorates these hypoxia-induced pathologies and attenuates PH. The data implicate dysfunctional brain-gut-lung communication in PH and provide novel avenues for therapeutic interventions.

Molecular detection and genetic characterization of Arcobacter butzleri isolated from red-footed pet tortoises suspected for Campylobacter spp. from Grenada, West Indies.

The aim of the study was to detect and genetically characterize Arcobacter butzleri in pet red-footed tortoises suspected for Campylobacter spp., using molecular techniques. A written consent from tortoise owners was obtained, after explaining the advantages of the research to tortoise owners of Grenada. Fecal samples were collected from 114 tortoises from five parishes of the country and cultured for Campylobacter spp. using selective culture techniques. A. butzleri was isolated from 4.39% of pet tortoises. Total thirteen isolates were obtained; all identified as A. butzleri by a universal and a species-specific Polymerase Chain Reaction (PCR) and direct sequencing. Genetic characterization of these isolates was performed based on Enterobacterial repetitive intergenic consensus PCR (ERIC-PCR) that generated eight different genetic fingerprints with a discriminatory power of 0.91. Campylobacter species were not detected molecularly in any of the culture-positive samples. This is the first report of infection of pet tortoises in Grenada, West Indies with A. butzleri. This study emphasizes on the risk of zoonotic transmission of A. butzleri by exotic pets, which is a serious concern for public health.

Transcriptome-wide analysis associates ID2 expression with combined pre- and post-capillary pulmonary hypertension.

Heart failure with preserved ejection fraction (HFpEF) patients who develop pulmonary hypertension (PH) have an increased risk of death, with combined pre- and post-capillary PH (CpcPH) having the highest risk. However, the mechanism behind PH development in HFpEF is poorly understood. We aimed to identify transcriptomic associations with PH development in HFpEF. Blood was collected from 30 HFpEF patients: 10 without PH, 10 with isolated post-capillary PH, and 10 with CpcPH. Gene expression measurements were completed using transcriptome-wide RNA sequencing. Gene expression differences were compared using a quasi-likelihood method adjusting for age, sex, race, and smoking-status. Biological pathways were compared using global gene expression differences. A replication in 34 additional heart failure patients and a validation in lung tissue from a representative mouse model were completed using quantitative PCR. Six differentially expressed genes were identified when comparing transcriptomics between subjects with CpcPH and those without PH. When tested in additional subjects, only the association with ID2 replicated. Consistent with clinical findings, Id2 expression was also upregulated in mice with HFpEF and PH. Pathway analysis identified proliferative and mitochondrial pathways associated with CpcPH. Thus, these patients may possess systemic pathophysiological differences similar to those observed in pulmonary arterial hypertension patients.

Ectoparasites of brown rats (Rattus norvegicus) in Grenada, West Indies.

BACKGROUND AND AIM: Arthropod ectoparasites (mites, lice, ticks, and fleas) on common house rats or brown rats (Rattus norvegicus) are known to transmit zoonotic pathogens and diminish rat health. To the best of our knowledge, there is no published information regarding the prevalence of ectoparasites on R. norvegicus in Grenada. This study aimed to determine the prevalence and types of ectoparasites present on brown rats from Grenada. MATERIALS AND METHODS: One hundred sixty-eight rats were collected live from the parishes of St. George and St. David, Grenada, from May to July 2017. Following euthanasia, external parasites were collected using fine combs, thumb forceps, and paper tape. Tape samples and free specimens were placed in containers with 70% ethanol. External parasites were evaluated using dissection microscopy. RESULTS: Over 2000 ectoparasites were collected from 149 of the 168 trapped rats (88.7%). Ectoparasites identified included mesostigmatid mites (found on 84.6% of infested rats), fur mites in the families Atopomelidae and Listrophoridae (67.1%), Polyplax spp. lice (6.7%), fleas (3.4%), an unidentified larval tick (0.7%), and a mite in the family Myobiidae (0.7%). Infestation rates were higher in St. David Parish (86/89; 96.6%) than in St. George Parish (63/79; 79.7%) (p=0.001). When comparing sex and age, males had a marginal increase in infestation rate (83/89; 93.3%) compared to females (66/79; 83.5%) (p=0.054), and adults had an infestation rate of 90.7% (97/107) compared to juvenile rats who had a 66.7% (14/21) infestation rate. CONCLUSION: Brown rats in Grenada are heavily infested with ectoparasites, including known vectors of pathogens. Future studies will examine the prevalence of zoonotic pathogens in these arthropods.

Detection of serum antibodies against Leptospira spp. in brown rats (Rattus norvegicus) from Grenada, West Indies.

BACKGROUND AND AIM: Leptospirosis is an emerging disease of animals and humans. Among rodents brown rats (Rattus norvegicus) are an important reservoir of bacteria Leptospira. There is a paucity of information on reservoirs of Leptospira in Grenada. This study was conducted to estimate the prevalence of antibodies against Leptospira spp. in brown rats in a densely human populated area of Grenada. MATERIALS AND METHODS: Blood samples from 169 brown rats were collected and sera screened for antibodies against Leptospira spp. using enzyme-linked immunosorbent assay. RESULTS: Among a total of 169 brown rats trapped in two parishes in Grenada, 77/169 (45.5%) were positive for Leptospira spp. antibodies. A significant difference in seropositive population of brown rats between two collection sites was observed. No differences were found between sex and age of seropositive rats. CONCLUSION: Due to the close contact of brown rats with humans in Grenada, rats should be considered a high-risk factor in transmission of Leptospira to humans. Appropriate preventive measures should be instituted to prevent the transmission of Leptospira infection to humans.

Microglial Cells Impact Gut Microbiota and Gut Pathology in Angiotensin II-Induced Hypertension.

RATIONALE: Increased microglial activation and neuroinflammation within autonomic brain regions have been implicated in sustained hypertension, and their inhibition by minocycline-an anti-inflammatory antibiotic-produces beneficial effects. These observations led us to propose a dysfunctional brain-gut communication hypothesis for hypertension. However, it has been difficult to reconcile whether an anti-inflammatory or antimicrobial action is the primary beneficial effect of minocycline in hypertension. Accordingly, we utilized chemically modified tetracycline-3 (CMT-3)-a derivative of tetracycline that has potent anti-inflammatory activity-to address this question. OBJECTIVE: Test the hypothesis that central administration of CMT-3 would inhibit microglial activation, attenuate neuroinflammation, alter selective gut microbial communities, protect the gut wall from developing hypertension-associated pathology, and attenuate hypertension. METHODS AND RESULTS: Rats were implanted with radiotelemetry devices for recording mean arterial pressure. Ang II (angiotensin II) was infused subcutaneously using osmotic mini-pumps to induce hypertension. Another osmotic mini-pump was surgically implanted to infuse CMT-3 intracerebroventricularly. Intracerebroventricular CMT- 3 infusion was also investigated in SHR (spontaneously hypertensive rats). Physiological, pathological, immunohistological parameters, and fecal microbiota were analyzed. Intracerebroventricular CMT-3 significantly inhibited Ang II-induced increases in number of microglia, their activation, and proinflammatory cytokines in the paraventricular nucleus of hypothalamus. Further, intracerebroventricular CMT-3 attenuated increased mean arterial pressure, normalized sympathetic activity, and left ventricular hypertrophy in Ang II rats, as well as in the SHR. Finally, CMT-3 beneficially restored certain gut microbial communities altered by Ang II and attenuated pathological alterations in gut wall. CONCLUSIONS: These observations demonstrate that inhibition of microglial activation alone was sufficient to induce significant antihypertensive effects. This was associated with unique changes in gut microbial communities and profound attenuation of gut pathology. They suggest, for the first time, a link between microglia and certain microbial communities that may have implications for treatment of hypertension.

Antimicrobial resistance patterns of commensal Escherichia coli isolated from feces of non-diarrheic dogs in Grenada, West Indies.

BACKGROUND AND AIM: There is currently no published information on the prevalence and antimicrobial susceptibility patterns of commensal Escherichia coli in dogs of Grenada origin. Monitoring antimicrobial resistance helps in the empirical selection of antibiotics. This study determined the occurrence of E. coli including the O157:H7 serotype in feces of non-diarrheic dogs of Grenada origin and the antibiotic resistance pattern of the E. coli isolates. MATERIALS AND METHODS: Fecal samples from 142 of the 144 (98.6%) dogs were culture positive for E. coli. Selection of up to three colonies from each of the 142 E. coli-positive samples yielded a total of 402 E. coli isolates, which were analyzed for the presence of non-sorbitol fermenting colonies, and O157-agglutination. RESULTS: Of the 402 E. coli isolates, 30 (7.5%) were non-sorbitol fermenters. However, none of the 402 isolates gave a positive reaction (O157:H7) to the E. coli O157:H7 latex kit. Antimicrobial susceptibility tests against 12 antibiotics revealed low resistance rates to all the tested antibiotics except for tetracycline (Te) (23.4%), cephalothin (CF) (13.2%), and ampicillin (AM) (7.7%). Thirty-nine out of the 402 (9.7%), E. coli isolates were resistant to two or more antibiotics of different classes. CONCLUSION: This is the first report of isolation and antimicrobial susceptibilities of commensal E. coli from non-diarrheic dogs in Grenada. Some of the isolates (39/402 isolates, 9.7%) were resistant to multiple antibiotics. This study showed that presently, dogs in Grenada should not be considered a reservoir for the E. coli O157:H7 serotype and for multiple antibiotic-resistant E. coli strains. Among the 402 E. coli isolates, the resistance rate to drugs other than Te, CF, and AM was very low.

Prevalence of antibodies against visceralizing Leishmania spp. in brown rats from Grenada, West Indies.

BACKGROUND AND AIM: Leishmania spp. are known to cause disease in man and animals. Rats are considered important reservoir hosts and transmission takes place through the bite of female sand fly, Phlebotomus spp. To the best of our knowledge, there is no published information on Leishmania infection in rats in Grenada. This study was conducted to estimate the antibodies for visceralizing Leishmania spp. (VL) in rats (Rattus norvegicus) from Grenada. MATERIALS AND METHODS: A total of 146 brown rats (R. norvegicus) were trapped live from two parishes (St. George and St. David) in Grenada. Following anesthesia, blood was collected from the heart through thoracic puncture. The serum was collected after the centrifugation of blood. Serum was tested for antibodies to VL. with a commercially available immunochromatographic dipstick test which is licensed for use in animals and humans. RESULTS: The seroprevalence of antibodies against Leishmania spp. was found in 34 of 146 rats (23.3%; CI 95% from 16.70 to 30.99). No significant differences were found between sexes and young or adults. The prevalence between parishes (St. George and St. David) was also not significant. CONCLUSION: The results show that rats (R. norvegicus) in Grenada are exposed to Leishmania spp. The rats could play an important role in the transmission of leishmaniasis to humans and other animals in Grenada.