%0 Journal Article
%T Type IV fimbrial subunit protein ApfA contributes to protection against porcine pleuropneumonia
%A Lenka Sadilkova
%A Jiri Nepereny
%A Vladimir Vrzal
%A Peter Sebo
%A Radim Osicka
%J Veterinary Research
%D 2012
%I BioMed Central
%R 10.1186/1297-9716-43-2
%X Actinobacillus pleuropneumoniae, the etiological agent of porcine pleuropneumonia, is a Gram-negative bacterium colonizing the porcine respiratory tract [1-3]. Pleuropneumonia is a severe contagious and economically significant disease. It can range from acute to chronic, depending on host age, immune status, the bacterial strain causing the infection, or the infective dose [4-6]. The acute stage is characterized by a haemorrhagic necrotizing pneumonia and fibrinous pleuritis and may progress rapidly to death [7,8]. In the chronic stage, localized lung lesions and adhesive pleuritis can be observed and chronically infected animals can become a source of infection for the whole non-infected herd [1,2,9].To control porcine pleuropneumonia, vaccination is useful [10,11], but development of efficient vaccines against the disease appears difficult due to the existence and diversity of 15 serotypes of A. pleuropneumoniae that are differentiated on the basis of surface polysaccharide antigens [12-14]. The first vaccines against A. pleuropneumoniae infection comprised formalin-treated or heat-inactivated bacteria. These whole-cell bacterin vaccines reduce mortality after challenge with the homologous serotypes of A. pleuropneumoniae, but usually do not confer efficient protection against infection with heterologous serotypes [15-17]. The limited protection observed with bacterins might be explained by (i) the absence of secreted immunogenic proteins, such as the ApxA toxins that are the key virulence factors of A. pleuropneumoniae, (ii) the alteration of antigenic potency of certain bacterial antigens due to inactivation treatment, or (iii) the absence of immunogenic antigens that are expressed only within the host [11,18-22]. Indeed, pigs surviving natural or experimental infection with A. pleuropneumoniae were found to be completely protected against homologous serotypes and generally also against heterologous serotype infections [16,23,24]. To overcome the drawbacks of b
%U http://www.veterinaryresearch.org/content/43/1/2