België ontsnapt niet aan het 'rabbit hemorrhagic disease virus-2'

Since 2016, an extensive spread of RHDV2, a virus variant of the classical rabbit hemorrhagic disease virus (RHDV) is ongoing in the Belgian rabbit population. Both variants of the virus usually cause acute death without prior symptoms. Vaccination against both variants of the virus is possible. In Belgium, only a vaccine protecting against the classical RHDV has been registered. On their own responsibility, veterinarians are allowed to import a vaccine protecting against RHDV2 that is registered in another EU member state, in accordance with the so-called legislative waterfall-system. The current epidemiological situation warrants preventive vaccination of rabbits against RHD. It should be noted that myxomatosis is currently rather neglected in view of the increased attention for the RHDV2 spread. Myxomatosis also still causes a high mortality in both wild and domesticated rabbits. Veterinarians should correctly inform the public about the two important viral diseases in rabbits and the possibilities for prevention

Poultry as a host for the zoonotic pathogen Campylobacter jejuni

Campylobacteriosis is the most reported foodborne gastroenteritic disease and poses a serious health burden in industrialized countries. Disease in humans is mainly caused by the zoonotic pathogen Campylobacter jejuni. Due to its wide-spread occurrence in the environment, the epidemiology of Campylobacter remains poorly understood. It is generally accepted, however, that chickens are a natural host for Campylobacter jejuni, and for Campylobacter spp. in general, and that colonized broiler chicks are the primary vector for transmitting this pathogen to humans. Several potential sources and vectors for transmitting C. jejuni to broiler flocks have been identified. Initially, one or a few broilers can become colonized at an age of >2 weeks until the end of rearing, after which the infection will rapidly spread throughout the entire flock. Such a flock is generally colonized until slaughter and infected birds carry a very high C. jejuni load in their gastrointestinal tract, especially the ceca. This eventually results in contaminated carcasses during processing, which can transmit this pathogen to humans. Recent genetic typing studies showed that chicken isolates can frequently be linked to human clinical cases of Campylobacter enteritis. However, despite the increasing evidence that the chicken reservoir is the number one risk factor for disease in humans, no effective strategy exists to reduce Campylobachter prevalence in poultry flocks, which can in part be explained by the incomplete understanding of the epidemiology of C. jejuni in broiler flocks. As a result, the number of human campylobacteriosis cases associated with the chicken vector remains strikingly high

Campylobacter control in poultry by current intervention measures ineffective: urgent need for intensified fundamental research

International audienceCampylobacter-contaminated poultry meat is an important source of foodborne gastroenteritis and poses a serious health burden in industrialized countries. Broiler chickens are commonly regarded as a natural host for this pathogen and infected birds carry a very high Campylobacter load in their gastrointestinal tract, especially the ceca. This results in contaminated carcasses during processing. While hygienic measures at the farm and control measures during carcass processing can have some effect on the reduction of Campylobacter numbers on the retail product, intervention at the farm level by reducing colonization of the ceca should be taken into account in the overall control policy. This review gives an up-to-date overview of suggested on-farm control measures to reduce the prevalence and colonization of Campylobacter in poultry

Medium-chain fatty acids and plant-derived antimicrobials to prevent Campylobacter colonization in broiler chickens

Campylobacter jejuni is the most common cause of bacterial-mediated diarrhoeal disease worldwide. Because poultry products are a major source of C. jejuni infections in humans, efforts should be taken to develop strategies to decrease Campylobacter colonization of poultry during primary production. Organic acids and plant-derived antimicrobial compounds possess marked bactericidal activity toward C. jejuni in vitro and might therefore have potential as feed additives to control C. jejuni colonization in broiler chickens. In vitro screening of several plant-derived compounds revealed strong anti-Campylobacter activity for trans-cinnamaldehyde in particular, while medium-chain fatty acids (caproic, caprylic and especially capric acid) were shown to be the most potent organic acids. However, supplementing these promising additives to the feed of broiler chickens before (prophylaxis) or after (therapeutic) oral inoculation with C. jejuni, did not result in a reduction of the cecal Campylobacter load in these animals. In a cecal loop experiment, neither sodium caprate nor trans-cinnamaldehyde were capable of killing or inhibiting growth of C. jejuni, despite direct injection into the ceca at concentrations of several times their respective minimal inhibitory concentration. When incubated in chicken intestinal mucus, C. jejuni was less susceptible to the antimicrobial effect of capric acid, indicating a protective role for the intestinal mucus layer. Thus, despite the marked bactericidal effect of organic acids and trans-cinnamaldehyde in vitro, neither supplementing these compounds to the feed, nor direct injection in the ceca was able to reduce cecal Campylobacter colonization in broiler chickens. Probably, the mucus layer forms a protective niche rendering the bacterium unresponsive to the bactericidal effects of these compounds observed in vitro, making their potential use as feed additives for controlling Campylobacter in poultry doubtful

A tolerogenic mucosal immune response leads to persistent Campylobacter jejuni colonization in the chicken gut

Campylobacter enteritis is the most reported zoonotic disease in many developed countries where it imposes a serious health burden. Campylobacter transmission to humans occurs primarily through the chicken vector. Chicks are regarded as a natural host for Campylobacter species and are colonized with C. jejuni in particular. But despite carrying a very high bacterial load in their gastrointestinal tract, these birds, in contrast to humans, do not develop pathological signs. It seems that in chickens C. jejuni principally harbors in the cecal mucosal crypts, where an inefficient inflammatory response fails to clear the bacterium from the gut. Recent intensive research resulted in an increased insight into the cross talk between C. jejuni and its avian host. This review discusses the chicken intestinal mucosal immune response upon C. jejuni entrance, leading to tolerance and persistent cecal colonization. It might in addition provide a solid base for further research regarding this topic aiming to fully understand the host-bacterium dynamics of C. jejuni in chicks and to develop effective control measures to clear this zoonotic pathogen from poultry lines

The Effect of Counterconditioning on Evaluative Responses and Harm Expectancy in a Fear Conditioning Paradigm

In fear conditioning, extinction targets harm expectancy as well as the fear response, but it often fails to eradicate the negative affective value that is associated with the conditioned stimulus. In the present study, we examined whether counterconditioning can serve to reduce evaluative responses within fear conditioning. The sample consisted of 70 nonselected students, 12 of whom were men. All participants received acquisition with human face stimuli as the conditioned stimuli and an unpleasant white noise as the unconditioned stimulus. After acquisition, one third of the sample was allocated to an extinction procedure. The other participants received counterconditioning with either a neutral stimulus (neutral tone) or a positive stimulus (baby laugh). Results showed that counterconditioning (with both neutral and positive stimuli), in contrast to extinction, successfully reduced evaluative responses. This effect was found on an indirect measure (affective priming task), but not on self-report. Counterconditioning with a positive stimulus also tended to enhance the reduction of conditioned skin conductance reactivity. The present data suggest that counterconditioning procedures might be a promising approach in diminishing evaluative learning and even expectancy learning in the context of fear conditioning

Colonization factors of Campylobacter jejuni in the chicken gut

Campylobacter contaminated broiler chicken meat is an important source of foodborne gastroenteritis and poses a serious health burden in industrialized countries. Broiler chickens are commonly regarded as a natural host for this zoonotic pathogen and infected birds carry a very high C. jejuni load in their gastrointestinal tract, especially the ceca. This eventually results in contaminated carcasses during processing. Current intervention methods fail to reduce the colonization of broiler chicks by C. jejuni due to an incomplete understanding on the interaction between C. jejuni and its avian host. Clearly, C. jejuni developed several survival and colonization mechanisms which are responsible for its highly adapted nature to the chicken host. But how these mechanisms interact with one another, leading to persistent, high-level cecal colonization remains largely obscure. A plethora of mutagenesis studies in the past few years resulted in the identification of several of the genes and proteins of C. jejuni involved in different aspects of the cellular response of this bacterium in the chicken gut. In this review, a thorough, up-to-date overview will be given of the survival mechanisms and colonization factors of C. jejuni identified to date. These factors may contribute to our understanding on how C. jejuni survival and colonization in chicks is mediated, as well as provide potential targets for effective subunit vaccine development

Panton-Valentine Leukocidin Does Play a Role in the Early Stage of Staphylococcus aureus Skin Infections: A Rabbit Model

Despite epidemiological data linking necrotizing skin infections with the production of Panton-Valentine leukocidin (PVL), the contribution of this toxin to the virulence of S. aureus has been highly discussed as a result of inconclusive results of in vivo studies. However, the majority of these results originate from experiments using mice, an animal species which neutrophils - the major target cells for PVL - are highly insensitive to the action of this leukocidin. In contrast, the rabbit neutrophils have been shown to be as sensitive to PVL action as human cells, making the rabbit a better experimental animal to explore the PVL role. In this study we examined whether PVL contributes to S. aureus pathogenicity by means of a rabbit skin infection model. The rabbits were injected intradermally with 108 cfu of either a PVL positive community-associated methicillin-resistant S. aureus isolate, its isogenic PVL knockout or a PVL complemented knockout strain, and the development of skin lesions was observed. While all strains induced skin infection, the wild type strain produced larger lesions and a higher degree of skin necrosis compared to the PVL knockout strain in the first week after the infection. The PVL expression in the rabbits was indirectly confirmed by a raise in the serum titer of anti-LukS-PV antibodies observed only in the rabbits infected with PVL positive strains. These results indicate that the rabbit model is more suitable for studying the role of PVL in staphylococcal diseases than other animal models. Further, they support the epidemiological link between PVL producing S. aureus strains and necrotizing skin infections

Prognostic implications of cellular senescence in resected non-small cell lung cancer

Background: Cure and long-term survival for non-small cell lung cancer (NSCLC) remains hard to achieve. Cellular senescence, an emerging hallmark of cancer, is considered as an endogenous tumor suppressor mechanism. However, senescent cancer cells can paradoxically affect the surrounding tumor microenvironment (TME), ultimately leading to cancer relapse and metastasis. As such, the role of cellular senescence in cancer is highly controversial. Methods: In 155 formalin-fixed paraffin-embedded (FFPE) samples from surgically resected NSCLC patients with pathological tumor-node-metastasis (pTNM) stages I-IV (8th edition), cellular senescence was assessed using a combination of four immunohistochemical senescence markers, i.e., lipofuscin, p16INK4a, p21WAF1/Cip1 and Ki67, and correlated to clinicopathological parameters and outcomes, including overall survival (OS) and disease-free survival (DFS). Results: A tumoral senescence signature (SS) was present in 48 out of 155 NSCLC patients, but did not correlate to any clinicopathological parameter, except for p53 mutation status. In a histologically homogenous patient cohort of 100 patients who fulfilled the following criteria: (I) one type of histology, i.e., adenocarcinoma, (II) without known epidermal growth factor receptor (EGFR) mutation, (III) curative (R0) resection and (IV) no neoadjuvant systemic therapy or radiotherapy, the median OS and DFS for patients with a tumoral SS (n=30, 30.0%) compared to patients without a tumoral SS (n=70, 70.0%) was 53 versus 141 months (P=0.005) and 45 versus 55 months (P=0.25), respectively. In multiple Cox proportional hazards (Cox PH) model analysis correcting for age, pTNM stage I-III and adjuvant therapy, a tumoral SS remained a significant prognostic factor for OS (HR =2.03; P=0.014). Conclusions: The presence of a tumoral SS particularly based on high p16INK4a expression significantly affects OS in NSCLC adenocarcinoma. In this light, adjuvant senolytic therapy could be an interesting strategy for NSCLC patients harboring a tumoral SS, ultimately to improve survival of these patients