Investigating Europa's Habitability with the Europa Clipper.

The habitability of Europa is a property within a system, which is driven by a multitude of physical and chemical processes and is defined by many interdependent parameters, so that its full characterization requires collaborative investigation. To explore Europa as an integrated system to yield a complete picture of its habitability, the Europa Clipper mission has three primary science objectives: (1) characterize the ice shell and ocean including their heterogeneity, properties, and the nature of surface-ice-ocean exchange; (2) characterize Europa's composition including any non-ice materials on the surface and in the atmosphere, and any carbon-containing compounds; and (3) characterize Europa's geology including surface features and localities of high science interest. The mission will also address several cross-cutting science topics including the search for any current or recent activity in the form of thermal anomalies and plumes, performing geodetic and radiation measurements, and assessing high-resolution, co-located observations at select sites to provide reconnaissance for a potential future landed mission. Synthesizing the mission's science measurements, as well as incorporating remote observations by Earth-based observatories, the James Webb Space Telescope, and other space-based resources, to constrain Europa's habitability, is a complex task and is guided by the mission's Habitability Assessment Board (HAB).

Exploring the Interior of Europa with the Europa Clipper.

The Galileo mission to Jupiter revealed that Europa is an ocean world. The Galileo magnetometer experiment in particular provided strong evidence for a salty subsurface ocean beneath the ice shell, likely in contact with the rocky core. Within the ice shell and ocean, a number of tectonic and geodynamic processes may operate today or have operated at some point in the past, including solid ice convection, diapirism, subsumption, and interstitial lake formation. The science objectives of the Europa Clipper mission include the characterization of Europa's interior; confirmation of the presence of a subsurface ocean; identification of constraints on the depth to this ocean, and on its salinity and thickness; and determination of processes of material exchange between the surface, ice shell, and ocean. Three broad categories of investigation are planned to interrogate different aspects of the subsurface structure and properties of the ice shell and ocean: magnetic induction, subsurface radar sounding, and tidal deformation. These investigations are supplemented by several auxiliary measurements. Alone, each of these investigations will reveal unique information. Together, the synergy between these investigations will expose the secrets of the Europan interior in unprecedented detail, an essential step in evaluating the habitability of this ocean world.

The Carotid Body "Tripartite Synapse": Role of Gliotransmission.

In mammals, cardiorespiratory reflexes originating in the carotid body (CB) help maintain homeostasis by matching oxygen supply to oxygen demand. CB output to the brainstem is shaped by synaptic interactions at a "tripartite synapse" consisting of chemosensory (type I) cells, abutting glial-like (type II) cells, and sensory (petrosal) nerve terminals. Type I cells are stimulated by several blood-borne metabolic stimuli, including the novel chemoexcitant lactate. During chemotransduction, type I cells depolarize and release a multitude of excitatory and inhibitory neurotransmitters/neuromodulators including ATP, dopamine (DA), histamine, and angiotensin II (ANG II). However, there is a growing appreciation that the type II cells may not be silent partners. Thus, similar to astrocytes at "tripartite synapses" in the CNS, type II cells may contribute to the afferent output by releasing "gliotransmitters" such as ATP. Here, we first consider whether type II cells can also sense lactate. Next, we review and update the evidence supporting the roles of ATP, DA, histamine, and ANG II in cross talk among the three main CB cellular elements. Importantly, we consider how conventional excitatory and inhibitory pathways, together with gliotransmission, help to coordinate activity within this network and thereby modulate afferent firing frequency during chemotransduction.

Lactate sensing by neuroepithelial cells isolated from the gills of killifish (Fundulus heteroclitus).

Lactate is produced in most vertebrate cells as a by-product of anaerobic metabolism. In addition to its role as a fuel for many tissues, circulating lactate can act as a signalling molecule and stimulates ventilation in air- and water-breathing vertebrates. Recent evidence suggests lactate acts on O2- and CO2/H+-sensitive chemoreceptors located in the mammalian carotid body. While analogous receptors (neuroepithelial cells or NECs) in fish gills are presumed to also function as lactate sensors, direct evidence is lacking. Here, using ratiometric Fura-2 Ca2+ imaging, we show that chemosensitive NECs isolated from killifish gills respond to lactate (5-10 mmol l-1; pHe ∼7.8) with intracellular Ca2+ elevations. These responses were inhibited by an L-type Ca2+ channel blocker (nifedipine; 0.5 µmol l-1), a monocarboxylic acid transporter (MCT) blocker (α-cyano-4-hydroxycinnamate; 300 µmol l-1) or a competitive MCT substrate (pyruvate; 5 mmol l-1). These data provide the first direct evidence that gill NECs act as lactate sensors.

The effect of marine dissolved organic carbon on nickel accumulation in early life-stages of the sea urchin, Strongylocentrotus purpuratus.

Dissolved organic carbon (DOC) is known to ameliorate the toxicity of the trace metal nickel (Ni) to aquatic animals. In theory, this effect is mediated by the capacity of DOC to bind Ni, rendering it less bioavailable, with the resulting reduction in accumulation limiting toxicological effects. However, there is a lack of experimental data examining Ni accumulation in marine settings with natural sources of DOC. In the current study, radiolabelled Ni was used to examine the time- and concentration-dependence of Ni accumulation, using naturally sourced DOC, on developing larvae of the sea urchin Strongylocentrotus purpuratus. Contrary to prediction, the two tested natural DOC samples (collected from the eastern United States, DOC 2 (Seaview park, Rhode Island (SVP)) and DOC 7 (Aubudon Coastal Center, Connecticut)) which had previously been shown to protect against Ni toxicity, did not limit accumulation. The control (artificial seawater with no added DOC), and the DOC 2 sample could mostly be described as having saturable Ni uptake, whereas Ni uptake in the presence of DOC 7 was mostly linear. These data provide evidence that DOC modifies the bioavailability of Ni, through either indirect effects (e.g. membrane permeability) or by the absorption of DOC-Ni complexes. There was some evidence for regulation of Ni accumulation in later-stage embryos (96-h) where the bioconcentration factor for Ni declined with increasing Ni exposure concentration. These data have implications for predictive modelling approaches that rely on known relationships between Ni speciation, bioavailability and bioreactivity, by suggesting that these relationships may not hold for natural marine DOC samples in the developing sea urchin model system.

Voltage-gated calcium channels regulate K+ transport in the Malpighian tubules of the larval cabbage looper, Trichoplusia ni.

Transporting epithelia are tissues that specialize in the directional movements of ions and water and are typically either secretory or reabsorptive. Recent work on the Malpighian tubule of larval lepidopterans (caterpillars) demonstrated that the distal ileac plexus segment of this epithelium is capable of rapidly switching between ion secretion and reabsorption. Subsequent transcriptomic studies suggested expression of voltage-gated ion channels in the lepidopteran MTs (which are not contractile and not innervated). The present study shows that isolated MTs of larval Trichoplusia ni express α1, ß2, and α2δ4 subunits of voltage-gated Ca2+ channel CaV1 and that pan-CaVα immunoreactivity is present in the apical and basolateral membranes of the principal cells. Basolateral membrane potential (Vbl) in isolated MTs of larval Trichoplusia ni was influenced by CaV1 functioning; pharmacological inhibition of CaV1 reversed Vbl from inside-negative to inside-positive, and also reduced transepithelial potential (Vte), lowered [Ca2+]i and reversed the direction of K+ transport from secretion to reabsorption. Thus, our findings indicate that a functional CaV1 channel is necessary for constitutive K+ secretion observed in isolated preparations of lepidopteran MTs. Lastly, Vte and Vbl of isolated MTs were influenced by changes in bathing saline [K+]. Our findings suggest that epithelia may rely on CaV channels to enable robust ion secretion and downregulation of CaV channels, together with other transcriptional changes, enables ion reabsorption.

Expanding Role of Dopaminergic Inhibition in Hypercapnic Responses of Cultured Rat Carotid Body Cells: Involvement of Type II Glial Cells.

Dopamine (DA) is a well-studied neurochemical in the mammalian carotid body (CB), a chemosensory organ involved in O2 and CO2/H+ homeostasis. DA released from receptor (type I) cells during chemostimulation is predominantly inhibitory, acting via pre- and post-synaptic dopamine D2 receptors (D2R) on type I cells and afferent (petrosal) terminals respectively. By contrast, co-released ATP is excitatory at postsynaptic P2X2/3R, though paracrine P2Y2R activation of neighboring glial-like type II cells may boost further ATP release. Here, we tested the hypothesis that DA may also inhibit type II cell function. When applied alone, DA (10 µM) had negligible effects on basal [Ca2+]i in isolated rat type II cells. However, DA strongly inhibited [Ca2+]i elevations (Δ[Ca2+]i) evoked by the P2Y2R agonist UTP (100 µM), an effect opposed by the D2/3R antagonist, sulpiride (1-10 µM). As expected, acute hypercapnia (10% CO2; pH 7.4), or high K+ (30 mM) caused Δ[Ca2+]i in type I cells. However, these stimuli sometimes triggered a secondary, delayed Δ[Ca2+]i in nearby type II cells, attributable to crosstalk involving ATP-P2Y2R interactions. Interestingly sulpiride, or DA store-depletion using reserpine, potentiated both the frequency and magnitude of the secondary Δ[Ca2+]i in type II cells. In functional CB-petrosal neuron cocultures, sulpiride potentiated hypercapnia-induced Δ[Ca2+]i in type I cells, type II cells, and petrosal neurons. Moreover, stimulation of type II cells with UTP could directly evoke Δ[Ca2+]i in nearby petrosal neurons. Thus, dopaminergic inhibition of purinergic signalling in type II cells may help control the integrated sensory output of the CB during hypercapnia.

Influence of 96h sub-lethal copper exposure on aerobic scope and recovery from exhaustive exercise in killifish (Fundulus heteroclitus).

Production of industrial effluents have led to increased copper (Cu) pollution of aquatic ecosystems, impacting the physiology of aquatic vertebrates. Past work has shown that Cu exerts its toxicity by disruption ion regulation and/ or increasing oxidative stress. However, it remains unclear how Cu may influence aerobic metabolism and hypoxia tolerance, two possible targets of its toxicity. To address this issue, we exposed freshwater acclimated killifish (F. heteroclitus) to a 96 h Cu exposure at a target concentration of 100 µg L-1. We determined resting oxygen consumption (MO2), MO2max after exhaustive exercise, and followed MO2 for 3 h in post-exercise recovery in water with either no Cu or 100 µg L-1 Cu. We assessed hypoxia tolerance by determining the critical oxygen tension (Pcrit). It was found that killifish exposed to combined 96 h Cu exposure and Cu present during metabolic measurements, showed a significant decrease in MO2max and in aerobic scope (MO2max - MO2rest), compared to control fish. However, changes in blood and muscle lactate and muscle glycogen were not consistent with an upregulation of anaerobic metabolism as compensation for reduced aerobic performance in Cu exposed fish. Hypoxia tolerance was not influenced by the 96 h Cu exposure or by presence or absence of Cu during the Pcrit test. This study suggests that Cu differentially influences responses to changes in oxygen demand and oxygen availability.

Increase in Gonorrhea Incidence Associated With Enhanced Partner Notification Strategy.

OBJECTIVES: Partner notification services for reportable sexually transmitted infections vary based on jurisdiction, resources, type of infection, and whether an outbreak has been reported. The objective of this study was to determine whether case finding increased after implementation of enhanced notification and follow-up activities for contacts of cases of Neisseria gonorrhoeae in Central Zone, the largest health authority in Nova Scotia, Canada. METHODS: Enhanced contact tracing by public health professionals was implemented in May 2015. N. gonorrhoeae multiantigen sequence typing (NG-MAST) was conducted on all positive specimens. Epidemiologic and NG-MAST information for reported gonorrhea cases were captured and analyzed. Case numbers, rates, and NG-MAST results in the preintervention and postintervention periods were compared. Laboratory testing data were extracted and analyzed for association with reported incidence. RESULTS: There was a significant increase in the number of reported gonorrhea cases per month when comparing the preintervention and postintervention periods. The reported gonorrhea rate in 2016 was 2.9 times that in 2014. This increase was not associated with changes in testing rates and was more pronounced among women than men. Larger groups of cases sharing the same NG-MAST profiles were detected postintervention. CONCLUSIONS: The implementation of an enhanced contact tracing program for N. gonorrhoeae resulted in increased case finding and a notable increase in the reported rate of cases per 100,000 population. Owing to these findings, the practice of enhanced partner notification was continued as standard public health practice in Central Zone. An understanding of case finding efforts is required when interpreting observed trends in rates of N. gonorrhoeae, as early infection is highly asymptomatic in women and can be asymptomatic in men.

Evidence for protein kinase involvement in the 5-HT-[Ca2+ ]i -pannexin-1 signalling pathway in type II glial cells of the rat carotid body.

NEW FINDINGS: What is the central question of this study? The mammalian carotid body (CB) is a peripheral chemoreceptor organ involved in O2 and CO2 /H+ homeostasis. Recent studies suggest that 5-HT, released from CB receptor cells, can stimulate adjacent glial-like type II cells, leading to an increase in intracellular Ca2+ (Δ[Ca2+ ]i ) and activation of ATP-permeable pannexin-1 (Panx-1) channels. The aim of this study was to elucidate the role of protein kinases in the 5-HT-[Ca2+ ]i -Panx-1 signalling pathway. What is the main finding and its importance? Src family kinase and protein kinase A, acting downstream from Δ[Ca2+ ]i , played central roles in 5-HT-mediated Panx-1 channel activation. This provides new insight into mechanisms regulating CB excitation, especially in pathophysiological conditions. ABSTRACT: Chemoreceptor (type I) cells of the rodent carotid body (CB) synthesize and release several neurotransmitters/neuromodulators, including 5-hydroxytryptamine (5-HT), implicated in enhanced CB excitation after exposure to chronic intermittent hypoxia, e.g. sleep apnoea. However, recent studies suggest that 5-HT can robustly stimulate adjacent glial-like type II cells via ketanserin-sensitive 5-HT2 receptors, leading to intracellular Ca2+ elevation (Δ[Ca2+ ]i ) and activation of ATP-permeable pannexin-1 (Panx-1) channels. Using dissociated rat CB cultures, we investigated the role of protein kinases in the intracellular signalling pathways in type II cells. In isolated type II cells, 5-HT activated a Panx-1-like inward current (I5-HT ) that was reversibly inhibited by the Src family kinase inhibitor PP2 (1 µm), but not by its inactive analogue, PP3 (1 µm). Moreover, I5-HT was reversibly inhibited (>90%) by H89 (1 µm), a protein kinase A blocker, whereas the protein kinase C blocker GF109203X (2 µm) was largely ineffective. In contrast, the P2Y2R agonist UTP (100 µm) activated Panx-1-like currents that were reversibly inhibited (∼60%) by either H89 or GF109203X. Using fura-2 spectrofluorimetry, the 5-HT-induced Δ[Ca2+ ]i was unaffected by PP2, H89 and GF109293X, suggesting that the kinases acted downstream of the Ca2+ rise. Given that intracellular Ca2+ chelation was previously shown to block receptor-mediated Panx-1 current activation in type II cells, these data suggest that CB neuromodulators use overlapping, but not necessarily identical, signalling pathways to activate Panx-1 channels and release ATP, a CB excitatory neurotransmitter. In conclusion, these studies provide new mechanistic insight into 5-HT signalling in the CB that has pathophysiological relevance.

Characterization of cadmium and calcium fluxes along the gut, malpighian tubules, and anal papillae of the dipteran Chironomus riparius.

Chironomids are often one of the dominant organisms in significantly polluted freshwater. Many invertebrate studies have characterized whole-organism mechanisms of toxicity, for example, assessing cadmium (Cd) uptake via calcium (Ca) channels. However, with the use of the scanning ion-selective electrode technique and an innovative Cd-selective microelectrode, we analyze this relationship at the organ level using a realistic concentration of Cd and Ca in the hemolymph (blood). Generally, Cd fluxes follow the same directional pattern as Ca, although Ca fluxes are approximately 5 times higher than those of Cd. These results correlate well with previous studies indicating that chironomids have a higher affinity for Ca over Cd, which affords them tolerance to Cd toxicity. When saline Ca concentration was increased to 10 times physiological levels, Cd fluxes from the gut lumen into the cells of the midgut regions were reduced by 50 to 80%. Transport of Cd from hemolymph to tissue for the posterior midgut, Malpighian tubule, and proximal ceca was also reduced by approximately 50%. The present results indicate that Cd fluxes into or across the gut and Malpighian tubules are reduced by high Ca, suggesting that Cd may be transported in some cells by similar mechanisms. However, Cd was actively excreted at the anal papillae after a 48-h waterborne exposure to Cd, but this process was independent of Ca and instead may involve a P-glycoprotein-related pump to detoxify Cd. Environ Toxicol Chem 2018;37:2542-2549. © 2018 SETAC.

Sensory Processing and Integration at the Carotid Body Tripartite Synapse: Neurotransmitter Functions and Effects of Chronic Hypoxia.

Maintenance of homeostasis in the respiratory and cardiovascular systems depends on reflexes that are initiated at specialized peripheral chemoreceptors that sense changes in the chemical composition of arterial blood. In mammals, the bilaterally-paired carotid bodies (CBs) are the main peripheral chemoreceptor organs that are richly vascularized and are strategically located at the carotid bifurcation. The CBs contribute to the maintenance of O2, CO2/H+, and glucose homeostasis and have attracted much clinical interest because hyperactivity in these organs is associated with several pathophysiological conditions including sleep apnea, obstructive lung disease, heart failure, hypertension, and diabetes. In response to a decrease in O2 availability (hypoxia) and elevated CO2/H+ (acid hypercapnia), CB receptor type I (glomus) cells depolarize and release neurotransmitters that stimulate apposed chemoafferent nerve fibers. The central projections of those fibers in turn activate cardiorespiratory centers in the brainstem, leading to an increase in ventilation and sympathetic drive that helps restore blood PO2 and protect vital organs, e.g., the brain. Significant progress has been made in understanding how neurochemicals released from type I cells such as ATP, adenosine, dopamine, 5-HT, ACh, and angiotensin II help shape the CB afferent discharge during both normal and pathophysiological conditions. However, type I cells typically occur in clusters and in addition to their sensory innervation are ensheathed by the processes of neighboring glial-like, sustentacular type II cells. This morphological arrangement is reminiscent of a "tripartite synapse" and emerging evidence suggests that paracrine stimulation of type II cells by a variety of CB neurochemicals may trigger the release of "gliotransmitters" such as ATP via pannexin-1 channels. Further, recent data suggest novel mechanisms by which dopamine, acting via D2 receptors (D2R), may inhibit action potential firing at petrosal nerve endings. This review will update current ideas concerning the presynaptic and postsynaptic mechanisms that underlie chemosensory processing in the CB. Paracrine signaling pathways will be highlighted, and particularly those that allow the glial-like type II cells to participate in the integrated sensory response during exposures to chemostimuli, including acute and chronic hypoxia.

Role of glial-like type II cells as paracrine modulators of carotid body chemoreception.

Mammalian carotid bodies (CB) are chemosensory organs that mediate compensatory cardiorespiratory reflexes in response to low blood PO2 (hypoxemia) and elevated CO2/H+ (acid hypercapnia). The chemoreceptors are glomus or type I cells that occur in clusters enveloped by neighboring glial-like type II cells. During chemoexcitation type I cells depolarize, leading to Ca2+-dependent release of several neurotransmitters, some excitatory and others inhibitory, that help shape the afferent carotid sinus nerve (CSN) discharge. Among the predominantly excitatory neurotransmitters are the purines ATP and adenosine, whereas dopamine (DA) is inhibitory in most species. There is a consensus that ATP and adenosine, acting via postsynaptic ionotropic P2X2/3 receptors and pre- and/or postsynaptic A2 receptors respectively, are major contributors to the increased CSN discharge during chemoexcitation. However, it has been proposed that the CB sensory output is also tuned by paracrine signaling pathways, involving glial-like type II cells. Indeed, type II cells express functional receptors for several excitatory neurochemicals released by type I cells including ATP, 5-HT, ACh, angiotensin II, and endothelin-1. Stimulation of the corresponding G protein-coupled receptors increases intracellular Ca2+, leading to the further release of ATP through pannexin-1 channels. Recent evidence suggests that other CB neurochemicals, e.g., histamine and DA, may actually inhibit Ca2+ signaling in subpopulations of type II cells. Here, we review evidence supporting neurotransmitter-mediated crosstalk between type I and type II cells of the rat CB. We also consider the potential contribution of paracrine signaling and purinergic catabolic pathways to the integrated sensory output of the CB during chemotransduction.

Municipal wastewater treatment plant effluent-induced effects on freshwater mussel populations and the role of mussel refugia in recolonizing an extirpated reach.

Global human population and urbanization continually increase the volume of wastewater entering aquatic environments. Despite efforts to treat these effluents, they contribute a diverse suite of substances that enter watersheds at concentrations that have the potential to elicit adverse effects on aquatic organisms. The relationship between wastewater treatment plant (WWTP) effluent exposure and biological responses within aquatic ecosystems remains poorly understood, especially at the population level. To examine the effect of WWTP effluents on sentinel invertebrates, freshwater mussels were assessed in the Grand River, Ontario, in populations associated with the outfall of a major WWTP. This watershed, within the Laurentian Great Lakes basin, has a diverse community of twenty-five species of mussels, including nine Species at Risk, and is representative of many habitats that receive WWTP effluents regionally as well as globally. Surveys were conducted to assess the presence and species richness of freshwater mussels. In total, 55 sites downstream of the WWTP were examined using timed visual searches with one or 2 h of effort spent searching 100 m segments. Although seven species of mussels were found in moderate abundance (mean of 8 mussels per hour of searching across 2 sites) upstream of the WWTP outfall, no live mussels were observed for 7.0 km downstream of the WWTP. Long-term water quality monitoring data indicate that ammonia and nitrite concentrations along with large seasonal declines in diel dissolved oxygen were associated with the extirpation of mussels downstream of the WWTP. The first live mussels found downstream were below the confluence with a major tributary indicating that in addition to an improvement in water quality to a state that enables mussels (and/or their fish hosts) to survive, a nearby mussel refuge may have facilitated the recolonization of the depauperate WWTP-impacted zone.

Mechanisms of nickel toxicity to fish and invertebrates in marine and estuarine waters.

In freshwater settings the toxicity of the trace metal nickel (Ni) is relatively well understood. However, until recently, there was little knowledge regarding Ni toxicity in waters of higher salinity, where factors such as water chemistry and the physiology of estuarine and marine biota would be expected to alter toxicological impact. This review summarizes recent literature investigating Ni toxicity in marine and estuarine invertebrates and fish. As in freshwater, three main mechanisms of Ni toxicity exist: ionoregulatory impairment, inhibition of respiration, and promotion of oxidative stress. However, unlike in freshwater biota, where mechanisms of toxicity are largely Class-specific, the delineation of toxic mechanisms between different species is less defined. In general, despite changes in Ni speciation in marine waters, organism physiology appears to be the main driver of toxic impact, a fact that will need to be accounted for when adapting regulatory tools (such as bioavailability normalization) from freshwater to estuarine and marine environments.

Freshwater mussels in an urban watershed: Impacts of anthropogenic inputs and habitat alterations on populations.

The substantial increase in urbanization worldwide has resulted in higher emissions of wastewater to riverine systems near urban centers, which often impairs aquatic populations and communities. This study examined the effect of urbanization on freshwater mussel populations, including Species at Risk in two rivers receiving wastewater. The influence of anthropogenic activities was assessed in a watershed in the Laurentian Great Lakes basin, one that historically supported one of the most diverse mussel faunas in Canada. In the Grand River (ON), four sites along a 60km reach spanning from an upstream reference site to an urban-impacted downstream area were examined. In the Speed River, mussel populations at six sites along a 10km reach, selected to bracket specific anthropogenic inputs and structures were assessed. A semi-quantitative visual search method revealed that catch per unit effort in the Grand River declined by >60% from the upstream reference site to the area downstream of an urban center. The size (length) frequency distribution of the most abundant species, Lasmigona costata, was significantly (p≤0.008) different upstream of the majority of urban inputs (45-130mm) compared to downstream of the cities (85-115mm). In the Speed River, impoundments and wastewater treatment plants (WWTP) reduced both the diversity and catch per effort. Most striking were 84 and 95% changes in the number of mussels found on either side of two impoundments, and a 98% drop in mussels immediately downstream of a WWTP outfall. These population level effects of decreased abundance and underrepresentation of smaller mussels downstream of the urban area correspond to previously documented impacts at the biochemical and whole organism level of biological organization in wild mussels at this location. Our results demonstrate that poor water quality and physical barriers in urban environments continue to impair susceptible populations and communities of aquatic animals.

Risk factors for carriage of antimicrobial-resistant Salmonella spp and Escherichia coli in pet dogs from volunteer households in Ontario, Canada, in 2005 and 2006.

OBJECTIVE To determine pet-related management factors associated with the carriage of antimicrobial-resistant Salmonella spp and Escherichia coli in a population of pet dogs. SAMPLE 138 dogs from 84 households in Ontario, Canada. PROCEDURES From October 2005 through May 2006, dogs and households in Ontario, Canada, were recruited to participate in a cross-sectional study. Fecal samples were submitted for culture of Salmonella spp and E coli, which provided 515 bacterial isolates for antimicrobial susceptibility testing. Multilevel logistic regression models with random effects for household and dog were created to identify pet-related management factors associated with antimicrobial resistance. RESULTS Bacterial species, feeding a homemade diet or adding homemade food to the diet, feeding a raw diet or adding anything raw to the diet, feeding a homemade raw food diet, and feeding raw chicken in the past week were significant risk factors for antimicrobial resistance in this population of dogs. CONCLUSIONS AND CLINICAL RELEVANCE In this study, several potentially important pet-related risk factors for the carriage of antimicrobial-resistant Salmonella spp and E coli in pet dogs were identified. Further evaluation of risk factors for antimicrobial resistance in dogs may lead to development of evidence-based guidelines for safe and responsible dog ownership and management to protect the public, especially pet owners who are immunocompromised.

The increasing risk of Lyme disease in Canada.

There is an increasing risk of Lyme disease in Canada due to range expansion of the tick vector, Ixodes scapularis. The objectives of this article are to i) raise public awareness with the help of veterinarians on the emerging and expanding risk of Lyme disease across Canada, ii) review the key clinical features of Lyme disease in dogs, and iii) provide recommendations for veterinarians on the management of Lyme disease in dogs.

Risque accru de maladie de Lyme au Canada. Il existe un risque grandissant de maladie de Lyme au Canada en raison d'un élargissement de la portée de la tique vectrice, Ixodes scapularis. Les objectifs du présent article consistent à i) rehausser la sensibilisation du public avec l'aide des vétérinaires quant au risque émergent et grandissant de la maladie de Lyme au Canada, ii) examiner les principales caractéristiques cliniques de la maladie de Lyme chez les chiens et iii) présenter des recommandations aux vétérinaires pour la gestion de la maladie de Lyme chez les chiens.(Traduit par Isabelle Vallières).

Effects of exposure to high concentrations of waterborne Tl on K and Tl concentrations in Chironomus riparius larvae.

Thallium (Tl) is a non-essential metal which is released into the environment primarily as the result of anthropogenic activities such as fossil fuel burning and smelting of ores. The ionic radius of monovalent Tl⁺ is similar to that of K⁺ and Tl⁺ may thus interfere with K⁺-dependent processes. We determined that the acute (48 h) lethal concentration where 50% of the organisms do not survive (LC50) of Tl for 4th instar Chironomus riparius larvae was 723 µmol L⁻¹. Accumulation of Tl by the whole animal was saturable, with a maximum accumulation (Jmax) of 4637 µmol kg⁻¹ wet mass, and K(D) of 670 µmol Tl l⁻¹. Tl accumulation by the gut appeared saturable at the lowest four Tl concentrations, with a Jmax of 2560 µmol kg⁻¹ wet mass and a K(D) of 54.5 µmol Tl l⁻¹. The saturable accumulation at the gut may be indicative of a limited capacity for intracellular detoxification, such as storage in lysosomes or complexation with metal-binding proteins. Tl accumulation by the hemolymph was found to be linear and Tl concentrations in the hemolymph were ~75% of the exposure concentration at Tl exposures >26.9 µmol L⁻¹. There was not a significant decrease in whole animal, gut or hemolymph K during exposure to waterborne Tl at any of the concentrations tested (up to 1500 µmol L⁻¹). The avoidance of hypokalemia by C. riparius larvae may contribute to survival during acute waterborne exposures to Tl.

Chronic nickel bioaccumulation and sub-cellular fractionation in two freshwater teleosts, the round goby and the rainbow trout, exposed simultaneously to waterborne and dietborne nickel.

Rainbow trout and round goby were exposed for 30 days to waterborne and dietary Ni in combination at two waterborne concentration ranges (6.2-12 µmol/L, 68-86 µmol/L), the lower of which is typical of contaminated environments. The prey (black worms; Lumbriculus variegatus) were exposed for 48 h in the effluent of the fish exposure tanks before being fed to the fish (ration=2% body weight/day). Ni in gills, gut, and prey was fractionated into biologically inactive metal [BIM=metal-rich granules (MRG) and metallothionein-like proteins (MT)] and biologically active metal [BAM=organelles (ORG) and heat-denaturable proteins (HDP)]. Gobies were more sensitive than trout to chronic Ni exposure. Possibly, this greater sensitivity may have been due to the goby's pre-exposure to pollutants at their collection site, as evidenced by ∼2-fold greater initial Ni concentrations in both gills and gut relative to trout. However, this was followed by ∼2-16× larger bioaccumulation in both the gills and the gut during the experimental exposure. On a subcellular level, ∼3-40× more Ni was associated with the BAM fraction of goby in comparison to trout. Comparison of the fractional distribution of Ni in the prey versus the gut tissue of the predators suggested that round goby were more efficient than rainbow trout in detoxifying Ni taken up from the diet. Assessing sub-cellular distribution of Ni in the gills and gut of two fish of different habitat and lifestyles revealed two different strategies of Ni bioaccumulation and sub-cellular distribution. On the one hand, trout exhibited an ability to regulate gill Ni bioaccumulation and maintain the majority of the Ni in the MT fraction of the BIM. In contrast goby exhibited large Ni spillovers to both the HDP and ORG fractions of the BAM in the gill. However, the same trend was not observed in the gut, where the potential acclimation of goby to pollutants from their collection site may have aided their ability to regulate Ni spillover to the BAM more so than in trout. Overall, chronic mortality observed in goby may be associated more with Ni bioaccumulation in gills than in gut; the former at either 4-d or 30-d was predictive of chronic Ni toxicity. BIM and BAM fractions of the goby gills were equally predictive of chronic (30-d) mortality. However, critical body residue (CBR50) values of the BIM fraction were ∼2-4× greater than CBR50 values of the BAM fraction, suggesting that goby are more sensitive to Ni bioaccumulation in the BAM fraction. There was insufficient mortality in trout to assess whether Ni bioaccumulation was predictive of chronic mortality.