Bats and zoonotic viruses: can we confidently link bats with emerging deadly viruses?

An increasingly asked question is 'can we confidently link bats with emerging viruses?'. No, or not yet, is the qualified answer based on the evidence available. Although more than 200 viruses - some of them deadly zoonotic viruses - have been isolated from or otherwise detected in bats, the supposed connections between bats, bat viruses and human diseases have been raised more on speculation than on evidence supporting their direct or indirect roles in the epidemiology of diseases (except for rabies). However, we are convinced that the evidence points in that direction and that at some point it will be proved that bats are competent hosts for at least a few zoonotic viruses. In this review, we cover aspects of bat biology, ecology and evolution that might be relevant in medical investigations and we provide a historical synthesis of some disease outbreaks causally linked to bats. We provide evolutionary-based hypotheses to tentatively explain the viral transmission route through mammalian intermediate hosts and to explain the geographic concentration of most outbreaks, but both are no more than speculations that still require formal assessment.

Metabolic evaluation of dairy cows submitted to three different strategies to decrease the effects of negative energy balance in early postpartum / Avaliação metabólica de vacas leiteiras submetidas a três estratégias para diminuir os efeitos do balanço energético negativo no pós-parto inicial

In early lactation dairy cattle suffer metabolic alterations caused by negative energy balance, which predisposes to fatty liver and ketosis. The aim of this study was to evaluate the metabolic condition of high yielding dairy cows subjected to three treatments for preventing severe lipomobilization and ketosis in early lactation. Fifty four multiparous Holstein cows yielding >30 L/day were divided into four groups: control (CN= no treatment), glucose precursor (PG= propylene-glycol), hepatic protector (Mp= Mercepton®), and energy supplement with salts of linolenic and linoleic faty acids (Mg-E= Megalac-E®). Treatments were administrated randomly at moment of calving until 8 weeks postpartum. Blood samples were collected on days 1, 7, 14, 21, 28, 35, 42 and 49 postpartum. Body condition score (BCS) was evaluated at the same periods and milk yield was recorded at 2nd, 4th, 5th, 6th, 7th, and 8th weeks of lactation. Concentrations of non-esterified fatty acids (NEFA), albumin, AST, ß-hydroxybutyrate (BHBA), cholesterol, glucose, total protein, urea and triglycerides were analyzed in blood samples. Cut-off points for subclinical ketosis were defined when BHBA >1.4 mmol/L and NEFA >0.7 mmol/L. General occurrence of subclinical ketosis was 24 percent during the period. An ascendant curve of cholesterol and glucose was observed from the 1st to the 8th week of lactation, while any tendency was observed with BHBA and NEFA, although differences among treatments were detected (p<0.05). BCS decreased from a mean of 3.85 at 1st week to 2.53 at 8th week of lactation (p=0.001). Milk yield was higher in the Mg-E group compared with the other treatment groups (p<0.05) Compared with the CN group, the treatments with Mp and PG did not show significant differences in blood biochemistry and milk yield. Cows receiving PG and Mg-E showed higher values of BHBA and NEFA (P<0.05), indicating accentuated lipomobilization. Supplementation with Mg-E also resulted in significant higher concentrations of cholesterol, BHBA, urea, AST and lower values of glycemia. This performance may be explained by the highest milk yield observed with this treatment. Treatments with PG and Mp did not improve milk yield, compared with control cows, but did not show metabolic evidence of ketosis, fat mobilization or fatty liver. These results suggest that treatment with Mg-E improves milk production but induces a higher negative energy balance leading to moderated lipomobilization and ketone bodies production, increasing the risk of fatty liver.

Durante o início da lactação as vacas leiteiras sofrem transtornos metabólicos causados pelo balanço energético negativo, o que predispõe a infiltração gordurosa hepática e cetose. O objetivo deste estudo foi avaliar o status metabólico de vacas leiteiras de alta produção submetidas a três tratamentos para prevenir severa lipomobilização e cetose no início da lactação. Cinquenta e quatro vacas de raça Holandesa multíparas produzindo >30 L/dia foram divididas em quatro grupos: controle (CN= sem tratamento), precursor de glicose (PG= propileno-glicol), protetor hepático (Mp= Mercepton®) e suplementação com sais de ácidos linolênico e linoléico (Mg-E= Megalac-E®). Amostras de sangue foram coletadas nos dias 1, 7, 14, 21, 28, 35, 42 e 49 do pós-parto. A condição corporal foi avaliada nos mesmos períodos e a produção de leite foi registrada nas semanas 2, 4, 5, 6, 7 e 8 de lactação. As concentrações de ácidos graxos não esterificados (AGNE), albumina, AST, ß-hidroxibutirato (BHB), colesterol, glicose, proteína total, uréia e triglicerídeos foram determinadas nas amostras de sangue. Pontos de corte para diagnosticar cetose subclínica foram definidos quando BHB >1,4mmol/L e AGNE >0,7mmol/L. A ocorrência geral de cetose subclínica foi de 24 por cento durante o período. Uma curva ascendente de colesterol e de glicose foi observada desde a 1ª até a 8ª semana de lactação, enquanto que nenhuma tendência foi observada com BHB e AGNE, embora diferenças entre os tratamentos foram detectadas (p<0,05). A condição corporal diminuiu de uma media de 3,85 na 1ª semana até 2,53 na 8ª semana de lactação (p=0,001). A produção de leite foi superior no grupo de Mg-E comparado com os demais tratamentos. Comparado com o grupo CN, os tratamentos de Mp e PG não mostraram diferenças significativas na bioquímica sanguínea nem na produção de leite (p<0,05) As vacas que receberam PG e Mg-E mostraram maiores valores de AGNE, indicando uma acentuada lipomobilização. A suplementação com Mg-E também resultou em maiores concentrações de colesterol, BHB, uréia, AST e menores valores de glicemia. Este resultado pode ser explicado pela maior produção de leite observada com este tratamento. Os tratamentos com PG e Mp não melhoraram a produção de leite, comparados ao grupo CN, mas também não mostraram evidências metabólicas de cetose, alta lipomobilização nem infiltração gordurosa hepática. Os resultados sugerem que o tratamento com Mg-E melhora a produção de leite, mas induz um balance energético negativo maior levando a moderada lipomobilização e produção de corpos cetônicos, aumentando o risco de fígado gorduroso.

Obesidad y diabetes mellitus tipo 2 / Obesity and type 2 diabetes mellitus

The mechanism by which obesity leads to type 2 diabetes mellitus is unknown. It is generally agreed that insulin resistance is an invariable accompaniment of obesity but that normoglycemia is maintained by compensatory hiperinsulinemia until the pancreatic B cells become unable to meet the increased demand for insulin, at which point type 2 diabetes mellitus begins. The precise cause of insulin resistance is yet to be determined, but is association with obesity has long been established. Recent data has implied free fatty acids tumoral necrosis factor - alfa, muscle fiber type II b and leptin, as a link resistance and obesity