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Simple Summary: Pig diarrhoea is one of the most frequent health problem in modern production, which can be associated with high mortality, decreased growth rates and an increase in treatment costs. The solution for an enteric disease requires a diagnosis which is based on diagnostic criteria, that must be respected to be reliable. The veterinary practitioner has the responsibility of making a final diagnosis, and based on this to make decisions concerning the management of swine health problems. The veterinary diagnostic laboratory can be an important support providing technical assistance in performing laboratory testing and consultancy activity. The aim of this paper is to focus on the diagnostic approach of enteric disorders in pigs, from sampling to the aetiological diagnosis, taking into consideration the diagnostic criteria for the various diseases and the methods considered to be the best choice for diagnosis. The diagnosis of enteric disorders in pigs is extremely challenging, at any age. Outbreaks of enteric disease in pigs are frequently multifactorial and multiple microorganisms can co-exist and interact. Furthermore, several pathogens, such as Clostridium perfrigens type A, Rotavirus and Lawsonia intracellularis, may be present in the gut in the absence of clinical signs. Thus, diagnosis must be based on a differential approach in order to develop a tailored control strategy, considering that treatment and control programs for enteric diseases are pathogen-specific. Correct sampling for laboratory analyses is fundamental for the diagnostic work-up of enteric disease in pigs. For example, histology is the diagnostic gold standard for several enteric disorders, and sampling must ensure the collection of representative and optimal intestinal samples. The aim of this paper is to focus on the diagnostic approach, from sampling to the aetiological diagnosis, of enteric disorders in pigs due to different pathogens during the different phases of production. [ABSTRACT FROM AUTHOR]

Porcine Circovirus 2 (PCV2) vaccines are based on either inactivated whole virion, or recombinant ORF2 capsid protein assembled into Virus-like Particles (VLPs). No data are available about the immunizing properties of free, non-assembled capsid protein. To investigate this issue, ORF2 of a reference PCV2b strain was expressed in a Baculovirus-based expression system without assembly into VLPs. The free purified protein was formulated into an oil vaccine at three distinct Ag payloads: 10.8/3.6/1.2 micrograms/dose. Each dose was injected intramuscularly into five, 37-day old piglets, carefully matched for maternally-derived antibody. Five control piglets were injected with sterile PBS in oil adjuvant. Twenty-eight days later, all the pigs were challenged intranasally with 105.3 TCID50 of PCV2b strain DV6503. After challenge infection, all the pigs remained in good clinical conditions. The recombinant vaccine did not induce significant antibody and PCV2-specific IFN-γ responses. ELISPOT and lymphocyte proliferation data confirmed poor induction of cell-mediated immunity. In terms of PCV2 viremia, there was no significant difference between vaccinated and control animals. The histological data indicated the absence of a detectable viral load and of PCVAD lesions in both vaccinated and control animals, as well as of histiocytes and multi-nucleated giant cells. We conclude that free, non-assembled ORF2 capsid protein does not induce protective immunity. [ABSTRACT FROM AUTHOR]

• The PCV2-specific, IFN-gamma release assay is a valid tool for assessing the efficacy of whole virion PCV2b vaccines. • The PCV2b-specific, IFN-gamma response is stimulated by vaccination, and not by infection. • Mean antibody titers and T cell responses to PCV2b vaccines are proportional to antigen doses. Porcine Circovirus 2 (PCV2) vaccines are poorly standardized in terms of antigen payload and correlates of protection. Therefore, twenty, 45-day old piglets were divided into four groups of 5 animals each and vaccinated with 800 / 266 / 88 / 0 nanograms, respectively, of an inactivated PCV2b strain formulated in the same oil adjuvant. Twenty-six days later, all the pigs were challenged intranasally with the homologous PCV2b strain. No clinical signs were observed in the pigs under study. Viremia was observed after challenge in all the control pigs, as well as in 3 pigs of the 266 and 88-ng groups (one and two, respectively). No pigs of the 800-ng group developed viremia. On the basis of post challenge viremia, the PCV2b vaccine under study had a titer of 11 Protective Doses (PD) 50 %, and 1 PD 50 amounted to 74 ng of PCV2b Ag. Neutralizing and ELISA Ab titers showed no obvious correlation with protection in the single animals, even though the 800-ng group developed a significantly higher mean Ab response. All the pigs with a PCV2-specific, IFN-gamma response at 3 weeks after vaccination in whole blood samples were protected against viremia. In lymphoid tissues (mainly tonsils and ileum) the presence of sparse reactive histiocytes and multinucleated giant cells was the only PCV2-associated feature and, by immunohistochemistry, only 3 out of 20 subjects showed a low viral load. [ABSTRACT FROM AUTHOR]