Strongyloides stercoralis in Swiss dogs - a retrospective study suggests an increasing occurrence of this potentially zoonotic parasite as a consequence of dog imports.

INTRODUCTION: Strongyloides stercoralis is a worldwide occurring nematode infecting canids and primates (including humans), responsible for a largely underestimated zoonotic disease. We here present 18 cases including overall 20 dogs affected by S. stercoralis, diagnosed in Switzerland between 2010 and 2020. The Baermann examination was positive for S. stercoralis larvae in 10, suspicious in 4, negative in one and not performed in 2 dogs. In 3 dogs the infection was identified only at necropsy by histology or by direct faecal or mucosal smears from intestinal tissue. Confirmation of suspected, necropsied and Baermann-negative dogs relied on genetic analyses. Twelve dogs had a history of import from Eastern Europe (n=4), the Mediterranean basin (n=5) or Germany (n=3). They were 7 weeks to 9,5 months old, and also the dogs supposedly born in Switzerland were younger than one year (except two, aged 15 months and 14 years). Thirteen dogs were males and 6 females (1 unknown). The most represented breeds were Chihuahuas (n=5), French Bulldogs (n=4) and Pomeranians (n=3). The most frequent clinical sign and reason for presentation was diarrhoea, occurring in 11/20 animals. Further gastrointestinal symptoms were vomiting, anorexia/hyporexia, adipsia, dehydration, tense abdomen and tenesmus. Respiratory symptoms were the second most frequent, with coughing in 7/20 animals, followed by tachypnoea/dyspnoea in 5 and (reverse) sneezing in 3 dogs. Treatment with 50 mg/kg BW fenbendazole p.o. over 5 days was successful in 4 cases in which a follow-up examination was performed 3-6 weeks later; prolonged treatment over 21 days was also effective. Ivermectin off-label protocols described in the literature, e.g. 0,8 mg/kg BW s.c. or 0,5 mg/kg BW i.m. repeated after 2 weeks, were successful based on control examinations performed 3-10 weeks later. Strongyloides stercoralis infections are clinically relevant, potentially zoonotic and need to be included in differential diagnoses in case of canine gastrointestinal and respiratory disorders, especially in young and imported dogs.

INTRODUCTION: Strongyloides stercoralis est un nématode présent dans le monde entier et infectant les canidés et les primates (y compris les humains), responsable d'une zoonose largement sous-estimée. Nous présentons ici 18 cas incluant au total 20 chiens atteints de S. stercoralis, diagnostiqués en Suisse entre 2010 et 2020. L'examen de Baermann était positif pour les larves de S. stercoralis chez 10, suspect chez 4, négatif chez un et non réalisé chez 2 chiens. Chez 3 chiens, l'infection n'a été identifiée qu'à l'autopsie par histologie ou par frottis fécal ou muqueux de tissu intestinal. La confirmation des chiens suspects, autopsiés et Baermann-négatifs reposait sur des analyses génétiques. Douze chiens avaient des antécédents d'importation d'Europe de l'Est (n=4), du bassin méditerranéen (n=5) ou d'Allemagne (n=3). Ils étaient âgés de 7 semaines à 9,5 mois, et les chiens supposément nés en Suisse avaient moins d'un an (sauf deux, âgés de 15 mois et 14 ans). Treize chiens étaient des mâles et six des femelles (1 inconnu). Les races les plus représentées étaient les Chihuahuas (n=5), les Bouledogues français (n=4) et les Poméraniens (n=3). Le signe clinique et le motif de présentation les plus fréquents étaient la diarrhée, survenant chez 11/20 animaux. D'autres symptômes gastro-intestinaux étaient des vomissements, anorexie/hyporexie, adipsie, déshydratation, tension abdominale et ténesme. Les symptômes respiratoires étaient les seconds plus fréquents, avec une toux chez 7/20 animaux, suivie d'une tachypnée/dyspnée chez 5 et d'éternuements (inverses) chez 3 chiens. Un traitement avec 50 mg/kg de poids corporel de fenbendazole p.o. durant 5 jours a réussi dans les 4 cas dans lesquels un examen de suivi a été effectué 3 à 6 semaines plus tard ; un traitement prolongé sur 21 jours a également été efficace. Les protocoles hors AMM avec de l'ivermectine décrits dans la littérature, par ex. 0,8 mg/kg de poids corporel s.c. ou 0,5 mg/kg de poids corporel i.m. répétés après 2 semaines, ont été couronnés de succès sur la base de contrôles effectués 3 à 10 semaines plus tard. Les infections à Strongyloides stercoralis sont cliniquement pertinentes, potentiellement zoonotiques et doivent être incluses dans les diagnostics différentiels en cas de troubles gastro-intestinaux et respiratoires canins, en particulier chez les jeunes chiens et les chiens importés.

Prognostic Markers in Acute Babesia canis Infections.

BACKGROUND: Canine babesiosis, caused by Babesia canis, is a prevalent and clinically relevant disease in Europe. Severe acute babesiosis is characterized by a high mortality but prognosis is not always correlated with clinical signs nor with the level of parasitemia. OBJECTIVE: This study evaluated prognostic markers associated with poor outcomes in acute Babesia canis infections. ANIMALS AND METHODS: We compared the results of routine laboratory profiles, hand-held lactate and glucose analyzer, and the acute phase response in 2 groups of naturally infected dogs (7 survivors and 8 nonsurvivors). Samples were collected at the time of first admission and before any treatment. Subsequently, the course of prognostic markers was followed in 3 dogs experimentally inoculated with B. canis. RESULTS: Nonsurvivors showed significantly higher concentrations of lactate, triglycerides and phosphate and lower hematocrit, leukocyte counts, total serum protein concentrations, and thrombocyte counts when compared to survivors. All nonsurvivors (8/8) had hyperlactatemia, whereas most survivors (6/7) had values within the reference range. All survivors had leucocyte counts within the reference range, unlike the nonsurvivors, which showed leukopenia. During the course of acute babesiosis, the variables serum lactate, triglyceride, and phosphate concentrations, and thrombocyte count only exceeded a prognostic threshold during acute crisis. CONCLUSIONS AND CLINICAL IMPORTANCE: Poor outcome in acute B. canis infection is indicated by changes in the laboratory profile. Intensive care should be considered for dogs presenting with moderate anemia, severe thrombocytopenia, mild to moderate leukopenia, hyperlactatemia, moderately increased serum phosphate, and triglyceride concentrations, and moderately decreased total serum protein concentrations.

Fasting and meal-suppressed ghrelin levels before and after intragastric balloons and balloon-induced weight loss.

BACKGROUND: Intragastric balloons may be an option for obese patients with weight loss failure. Its mode of action remains enigmatic. We hypothesised depressed fasting ghrelin concentrations and enhanced meal suppression of ghrelin secretion by the gastric fundus through balloon contact and balloon-induced delayed gastric emptying. METHODS: Patients were randomised to a 13-week period of sham or balloon treatment, followed by a 13-week period of balloon treatment in everyone. Blood samples for ghrelin measurement were taken in the fasting state and every 15 min for 1 h after a breakfast meal at the start, after 13 weeks and after 26 weeks. Patients filled out scales to assess satiety and kept a food diary. RESULTS: Forty obese patients (BMI 43.1 kg/m(2)) participated. At the start, fasting ghrelin values were low with a blunted ghrelin response to a test meal. The presence of a balloon had no influence on fasting or meal-suppressed ghrelin concentrations. Despite a weight loss of 10 % after 13 weeks and 15 % after 26 weeks, fasting ghrelin concentrations did not change; neither did the ghrelin response to a meal. No relation was found between ghrelin and insulin, satiety, intermeal interval, the number of meals or subsequent energy intake. Ghrelin concentrations were more suppressed with greater weight loss or with balloons located in the fundus. CONCLUSIONS: Ghrelin concentrations did not change by balloon treatment after 13 and 26 weeks and, unexpectedly, did not rise despite substantial weight loss and negative energy balance. This suppression might be of benefit in the maintenance of weight loss but could not be ascribed to the balloon treatment.

Multi-test analysis and model-based estimation of the prevalence of Taenia saginata cysticercus infection in naturally infected dairy cows in the absence of a 'gold standard' reference test.

The diagnostic values of seven serological tests (ELISAs) and of the obligatory European Union-approved routine visual meat inspection for the detection of Taenia saginata cysticercosis were investigated. A total of 793 slaughtered dairy cows were selected in three European Union approved abattoirs in Switzerland, an endemic area (apparent prevalence by enhanced meat inspection up to 4.5%) with typically low parasite burdens. ELISAs based on a somatic larval antigen, isoelectric focused somatic larval antigen, larval excretory/secretory antigens, peptide HP6-2, peptide Ts45S-10, pooled peptide solution and a monoclonal antibody antigen capture assay were initially screened. As there is no perfect diagnostic 'gold standard' reference test, the obligatory meat inspection and four selected serological tests were further analysed using Bayesian inference to estimate the "true" prevalence and the diagnostic test sensitivities and specificities. The ELISA for specific antibody detection based on excretory/secretory antigens showed highest sensitivity and specificity with 81.6% (95% credible interval: 70-92) and 96.3% (95% credible interval: 94-99), respectively. The Bayesian model estimated the specificity of the ELISA, based on the synthetic peptide Ts45S-10 as 55.2% (95% credible interval: 46-65) and sensitivity as 84.7% (95% credible interval: 82-88). The sensitivity of the ELISA based on mAbs, detecting circulating antigen, was 14.3% (95% credible interval: 9-23) with a specificity of 93.7% (95% credible interval: 92-96). The diagnostic sensitivity of the obligatory standard European Union meat inspection procedure for the detection of T. saginata cysticercus infection at the abattoir was estimated to be 15.6% (95% credible interval: 10-23). Based on these data, the modelled prevalence of cysticercosis in dairy cows presented at abattoirs in Switzerland was estimated to be 16.5% (95% credible interval: 13-21). These cattle also had a high prevalence of infection with Dicrocoelium dendriticum (60.8%) and Fasciola hepatica (13.5%).

CYP 450 enzyme induction by chronic oral musk xylene in adult and developing rats.

Developmental and adult toxicity of musk xylene was studied in Long Evans (LE) rats fed with chow containing musk xylene (MX) in food pellets in concentrations of 1 mg, 10 mg, 33 mg, 100 mg and 1000 mg MX per 1 kg chow corresponding to a daily intake of 0.07-0.08 mg MX/kg up to 70-80 mg MX/kg body weight. Adult male and female rats were MX exposed for a minimum of 10 weeks before mating. Exposure continued throughout pregnancy, birth and lactation. The effects of MX on CYP1A1/1A2 were studied in liver microsomes by EROD (7-ethoxyresorufin-rosomes deethylase) for CYP1A1 and by MROD (methoxyresorufin-o-demethylase) for CYP1A2 activity and by Western blotting. MX induced these enzymes dose dependently in adult and developing rats at PN (postnatal day) 1 and 14. The lowest effective maternal dose was 2-3 mg MX/kg/day. Western blot data of CYP2B and CYP3A indicated the induction of both P450 enzyme proteins in developing rats at PN 14 at the higher dose of 70-80 mg MX/kg/day. In contrast, upon high MX exposure CYP2B but not CYP3A was found to be induced in adult first generation male and female rats, indicating differential sensitivity to MX in development.

The public health care of Central Americans in Houston.

In recent years, Americans have witnessed a marked change in the source of immigrant groups. Current immigrants are more likely to be former residents of the less developed world (nations such as Guatemala, Nigeria, India, and Viet Nam) than were earlier immigrants. In urban Texas, the influx of peoples from Central America is particularly striking and is largely a consequence of homeland political and economic instability. The new immigrants tend to be young and sexually active. We analyzed utilization patterns of Central Americans at our district health care facilities over 18 months and compared results with those of our non-Central American health care recipients. The 30,000 annual visits by Central Americans accounted for 4% of all visits. Disproportionately large amounts of care were given for sexually transmitted diseases and obstetric problems; conversely, small amounts were given for chronic illnesses, infectious diseases, acquired immunodeficiency syndrome, mental health problems, and adverse fetal outcomes. Few exotic tropical diseases were recognized or treated.

CYP 450 enzyme induction by chronic oral musk xylene in adult and developing rats.

Developmental and adult toxicity of musk xylene was studied in Long Evans (LE) rats fed with chow containing musk xylene (MX) in food pellets in concentrations of 1 mg, 10 mg, 33 mg, 100 mg and 1000 mg MX per 1 kg chow corresponding to a daily intake of 0.07-0.08 mg MX/kg up to 70-80 mg MX/kg body weight. Adult male and female rats were MX exposed for a minimum of 10 weeks before mating. Exposure continued throughout pregnancy, birth and lactation. The effects of MX on CYP1A1/1A2 were studied in liver microsomes by EROD (7-ethoxyresorufin-o-deethylase) for CYP1A1 and by MROD (methoxyresorufin-o-demethylase) for CYP1A2 activity and by Western blotting. MX induced these enzymes dose dependently in adult and developing rats at PN (postnatal day) 1 and 14. The lowest effective maternal dose was 2-3 mg MX/kg/day. Western blot data of CYP2B and CYP3A indicated the induction of both P450 enzyme proteins in developing rats at PN 14 at the higher dose of 70-80 mg MX/kg/day. In contrast, upon high MX exposure CYP2B but not CYP3A was found to be induced in adult first generation male and female rats, indicating differential sensitivity to MX in development.

A new assay for the determination of factor XII in plasma using a chromogenic substrate and a selective inhibitor of plasma kallikrein.

A new chromogenic assay for factor XII in plasma was designed by the use of the soluble activator Kalliplastin, the substrate H-D-HHT-Gly-Arg-pNA and a synthetic inhibitor of plasma kallikrein (Pefabloc PK). The assay was carried out in one and the same cuvette and did not require factor XII-deficient plasma. There was a good correlation between F XII coagulant and amidolytic assays.

A new highly selective physicochemical assay to measure NAD+ in intact cells.

A simple, fast, and highly specific chromatographic method for measuring the content of NAD+ in intact cells has been developed. This procedure involves the separation of NAD+ from the bulk of acid-soluble nucleosides, nucleotides, and other pyridine containing molecules by affinity chromatography on dihydroxyboronyl-Bio-Rex. The boronate purified preparations were utilized for the quantification of NAD+ by strong anion exchange high-pressure liquid chromatography under isocratic conditions using a low salt buffer system. The overall recovery of the method exceeded 80%. This new method was applied to determine the extent of NAD+ consumption in intact hepatocytes following treatment with two different DNA damaging agents. A major advantage of this method is that it allows for the simultaneous determination of poly(ADP-ribose) in the acid-insoluble fraction of the same sample.

Poly(ADP-ribose) biosynthesis and suicidal NAD+ depletion following carcinogen exposure of mammalian cells.

Hepatocytes were found to be remarkably resistant to suicidal NAD+ depletion due to consumption for chromatin-associated poly(ADP-ribose) biosynthesis, which normally follows infliction of DNA damage in mammalian cells. N-methyl-N'-nitro-N-nitrosoguanidine treatment, which depleted NAD+ levels of confluent fibroblasts to about 40% of controls, did not reduce hepatocellular NAD+ pools, although poly(ADP-ribose) concentrations were concomitantly elevated by 21-fold. This differential behavior, demonstrable also with other carcinogens, can be attributed to the different NAD+ biosynthetic capacities of these cells.

Tumor-promoting barbiturates act on DNA repair of cultured hepatocytes.

We have observed that two promoters of liver carcinogenesis, i.e. phenobarbital and barbital, markedly increase DNA-repair synthesis of cultured hepatocytes following treatment with the ultimate carcinogens methyl methanesulfonate, N-methyl-N'-nitro-N-nitrosoguanidine, N-acetoxy-2-acetylaminofluorene, and UV light of 254 nm. Phenobarbital also increased the incorporation rates of deoxynucleoside triphosphates into nuclear DNA of permeabilized hepatocytes following carcinogen treatment. The action of these barbiturates apparently correlates with their potential to promote hepatocarcinogenesis in vivo, since the non-promoting agent barbituric acid did not modify carcinogen-induced repair synthesis. Moreover, the mechanisms of action of tumor-promoting barbiturates is different from the known enhancing action on repair synthesis of inhibitors of nuclear poly(ADP-ribose) biosynthesis.