Bovine alphaherpesvirus 5 (BoHV5) is responsible for triggering a typical neurological condition, which has a high mortality rate in cattle up to 8 years of age (Barros et al., 2006; Rissi et al., 2006). The most important characteristic of BoHV5 lies in its ability to establish latency in the trigeminal ganglion, allowing the virus to perpetuate itself in the animal organism for a lifetime, being reactivated in periods of decreased immunity (Perez et al., 2002).The main clinical signs associated with the infection caused by this agent include deep prostration, pressure of the head against objects, runny nostrils, involuntary movements, nystagmus, opisthotonus, and staggering, culminating in death between 4 and 10 days (Rissi et al., 2006).BoHV5 has a worldwide distribution, but its occurrence is geographically limited to South America, mainly to Brazil and Argentina (Perez et al., 2002). Although its occurrence is described in Brazil, where it is considered one of the three main causative agents of neurological diseases in cattle (Queiroz et al., 2018;Terra et al., 2018), studies about its occurrence in the Northeast region are lacking, despite evidence of its presence (Galiza et al., 2010). The objective of this study was to report the occurrence of BoHV5 in cattle with neurological signs in the period from 2012 to 2016 in the state of Pernambuco.Samples of the central nervous system (cerebellum, pituitary, rete mirabile, brain stem, telencephalon, medulla, and thalamus) embedded in paraffin from 32 cattle with neurological

A case of a donkey attacked by Africanized honeybee is reported here with clinical signs of agitation, dehydration, congestion of the ocular mucous membranes, tongue edema, tachycardia and inspiratory dyspnea, and progression to death. At necropsy, diffuse, severe subcutaneous edema at face and cervical regions and severe diffuse pulmonary hyperemia with abundant edema without parenchymal collapse were observed. Microscopically, marked, diffuse deep dermis and panniculus carnosus edema and marked diffuse alveolar edema, with moderate population of eosinophils predominantly around larger caliber vessels were noted. The final diagnosis of anaphylactic shock was supported by history, clinical signs, and anatomic pathology findings. This is the first report of a honeybee attack with pulmonary eosinophilic infiltration in a mammal.