Detection of antibodies against tick-borne encephalitis flaviviruses in breeding and sport horses from Spain.

Tick-borne encephalitis virus (TBEV) and louping-ill virus (LIV) are two closely related zoonotic flaviviruses leading to neurological diseases and belonging to the tick-borne encephalitis (TBE) serocomplex. Both viruses are transmitted by the same ixodid tick vector, Ixodes ricinus. Due to global warming affecting vector biology and pathogen transmission, the viruses pose an emerging threat for public health in Europe and Asia. These flaviviruses share some hosts, like sheep, goats and humans, although the main hosts for LIV and TBEV are sheep and small rodents, respectively. Whereas LIV has been detected in Spanish sheep and goat herds, circulating antibodies against TBEV have only been reported in dogs and horses from particular regions in this country. The limited available information about the prevalence of these viruses in Spain led us to investigate the serological evidence of TBE flaviviruses in horses from Spain. Serum neutralization tests (SNT) were performed using sera from 495 breeding and sport horses collected during two periods (2011-2013 and 2015-2016). A seroprevalence of 3.1 % (95 % CI 1.5-4.6) was found and cross-reactivity with West Nile virus was excluded in the positive samples. Sport horses showed a significantly higher TBE serocomplex seropositivity compared to breeding horses. An increased seroprevalence was observed in the second sampling period (2015-2016). Our results demonstrate for the first time the presence of antibodies against TBE flaviviruses in horses residing in mainland Spain; further epidemiological surveys are necessary in order to understand and monitor the active transmission of TBE flaviviruses in this country and rule out the presence of other flaviviruses co-circulating in Spain.

[New etiopathogenic, diagnostic and therapeutic aspects in primary pulmonary hypertension]. / Nuevos aspectos etiopatogénicos, diagnósticos y terapéuticos en la hipertensión pulmonar primaria.

Primary Pulmonary Hypertension (PPH) is a rare disease of unknown aetiology that is diagnosed only when the underlying causing factors are undetermined. Usually is discovered in its late stage, when pulmonary vascular resistances are severely compromised and the pathologic changes already well developed, resulting in right heart failure and death within several years of the onset of symptoms. The data published in the last years have provided new insights into the disease knowledge. In this article currents concepts about aetiology, pathogenesis and open lung biopsy value are reviewed; clinical manifestations and diagnostic methods are described; the usefulness of medical treatment to improve quality of life in these patients, mainly anticoagulation and vasodilator therapy with high-dose nifedipine, and how lung transplantation has increasingly become an option for selected patients with PPH, is also analysed.

[Adverse reactions to trimethoprim-sulfamethoxazole in AIDS patients]. / Reacciones adversas a trimetoprima-sulfametoxazol en pacientes con SIDA.

BACKGROUND: The aim of the present was to evaluate the incidence of side effects to Trimethoprim-sulphamethoxazole (TMP-SMX) in 32 patients with AIDS and pneumonia by Pneumocystis carinii. METHODS: A retrospective study was carried out following a protocol which included all items related with the drug used. RESULTS: Side effects to TMP-SMX were seen in 75% of the patients treated with the most important and severe being at a cutaneous level. These severe reactions require withdrawal of the drug and its substitution by pentamidine in half of the cases, while in the remaining 25% the reactions were mild. To date none of the 9 patients prophylactically treated with TMP-SMX have relapsed over 3 years of follow up while 4 out of the 9 treated with pentamidine have had relapsed. CONCLUSIONS: Trimethoprim-sulphamethoxazole is the ideal prophylactic drug for those who are able to tolerate it. Following review of the literature 2 schedules of tolerance induction were proposed for use in patients who have had previous reactions with this drug, including a rapid schedule and another slow schedule.

The effects of gaboon viper (Bitis gabonica) venom on voltage-clamped single heart cells.

The effects of crude B. gabonica venom on single ventricular myocytes from guinea-pig hearts were studied using the patch clamp technique in the 'whole cell' mode. Irreversible effects on the membrane currents, which became prominent within 15 min of venom application, were: (1) a decrease in the time invariant current (associated with the inward rectifying K+ current), most clearly seen over a voltage range negative to the resting membrane potential; and (2) a decrease in the peak inward current (associated with the Ca2+ current) elicited by steplike depolarizations from a holding potential of -40 mV. A transient increase in the peak inward current, which preceded its eventual decline, was also noticed; it peaked 6-10 min after the venom was applied. Application of the venom to unclamped, stimulated cells resulted in a shortening of the plateau phase and disturbances of the repolarization phase of action potentials. An early transient prolongation and elevation of the plateau was observed, occurring with the same time course of the transient increase in the peak inward current. No signs of damage to the cell membrane integrity, neither electrical (appearance of a leakage current) nor morphological (surface blebs, loss of striation pattern and of rodlike shape in the isolated myocytes), accompanied the effects observed on ionic currents and action potential activity, supporting the hypothesis of a selective cardiotoxic action of B. gabonica venom.

The effects of Gaboon viper (Bitis gabonica) venom on the electrical and mechanical activity of the guinea-pig myocardium.

The effects of Bitis gabonica venom were tested on guinea-pig heart, using both Langendorff preparations and isolated atrial strips or papillary muscles. In the self-paced whole heart, a single passage of 50 micrograms of venom per ml produced in sequence: irregularities of the A-V conduction and decrease of the contractile strength, progressive failure to relax and systolic arrest of the heart. Pretreatment with atropine reduced but did not abolish these effects. Venom recycled through the heart was effective at a much lower dose. The relationship between resting membrane potential and [K+]o was unaffected by envenomation, suggesting that the action of the venom cannot be ascribed to a loss of ionic selectivity of the cell membrane. The peak amplitude of action potentials declined in papillary muscle exposed to venom at physiological [K+]o, while in atrial cells it was affected only at higher [K+]o. Maximum upstroke rate of the action potential vs. resting potential at different [K+]o gave a sigmoid relationship, characterized by a higher upper asymptote as compared to controls, and by a shift of the curve towards more negative voltage values. A marked shortening of the action potential duration, paralleled by a decrease in time to peak tension, was recorded as well. 'Slow' action potentials, elicited in 20 mM K+ solution, were completely abolished within 10 min of perfusion with venom. These results are consistent with the hypothesis that the venom interacts with both transmembrane Ca2+ inflow and Ca2+ binding at the external side of the cell membrane. A transient positive inotropic effect induced by the venom was observed in papillary muscle and in atropinized atrium. This effect was abolished by previous administration of reserpine to the animal or by addition of propranolol to the perfusing solution, suggesting a venom-induced release of both adrenergic and cholinergic transmitters from nerve endings within the cardiac tissue.

Contraction features in normal and hypodynamic lizard ventricle.

Isometric twitches and intra- and extracellular electrical activity were recorded at various driving rates from lizard ventricles, either in the normal inotropic state, or in a hypodynamic state induced by perfusing at a high flow rate for a long time. Electron micrographs were obtained from hearts fixed immediately after dissection and from preparations perfused in vitro for various periods. It was found that the peak of the steady-state strength-interval relationship shifts towards higher stimulation rates with the development of hypodynamia. Such a change is similar to that induced in normal preparations by perfusing with calcium-poor solutions. The normal strength-interval relationship can be restored in hypodynamic preparations by perfusion with a calcium-rich solution. Also, in the hypodynamic state, the action potential duration is increased and (+ dP/dt)max is decreased, while the shape of the staircases at various stimulation rates is modified. These changes occur in the presence of well-preserved ultrastructural features of the preparation. The results suggest that the twitch tension results from the contribution of two Ca ions fluxes: an early one from a cellular store, and a late one related to the action potential duration. The ultrastructural findings are consistent with the hypothesis that a store, from which a rapid release of calcium occurs, exists in the lizard ventricle. A hypodynamic state would be caused by a reduced calcium affinity of such store, and by a decreased Ca++ influx during the action potential plateau.