African swine fever virus (ASFV) is the only known DNA arbovirus and the sole member of the family Asfarviridae. It causes a lethal, hemorrhagic disease in domestic pigs. ASFV is enzootic in sub-Saharan Africa and is maintained in a sylvatic cycle by infecting both wild members of the Suidae (e.g. warthogs) and the argasid tick Ornithodoros porcinus porcinus. The pathogenesis of ASFV in O. porcinus porcinus ticks is characterized by a low infectious dose, lifelong infection, efficient transmission to both pigs and ticks, and low mortality until after the first oviposition. ASFV pathogenesis in warthogs is characterized by an inapparent infection with transient, low viremic titers. Thus O. porcinus porcinus ticks probably constitute the most important natural vector of ASFV, although both the mammalian and tick hosts are probably required for the maintenance of ASFV in the sylvatic cycle. The mechanism of ASFV transmission from the sylvatic cycle to domestic pigs is probably through infected ticks feeding on pigs. In addition to O. porcinus porcinus, a number of North American, Central American and Caribbean species of Ornithodoroshave been shown to be potential vectors of ASFV.

The pathogenic strains of Escherichia coli recovered from the intestinal tract of animals fall into categories called enterotoxigenic, enteropathogenic, enterohemorrhagic and necrotoxigenic. The other two categories, enteroinvasive and enteroaggregative, have not been reported in animals. The pathogenicity of these strains is determined by the presence of certain genes that encode adhesins and toxins, are generally organized in large blocks in chromosomes, large plasmids or phages, and are often transmitted horizontally between strains. In this review, we summarize current knowledge of the virulence attributes that determine the pathogenic potential of E. coli strains and the methods available to assess the virulence of the strains. We also discuss the clinical symptoms, the gross and histological lesions, and the molecular diagnostic methods our laboratories have implemented for detecting pathogenic strains of E. coli that are isolated from the gastrointestinal tract of animals.

Mycobacterium avium subspecies paratuberculosis (M. paratuberculosis) is the causative agent of Johne’s disease, a deadly intestinal ailment of ruminants. Johne’s disease is of tremendous economic importance to the worldwide dairy industry, causing major losses due to reduced production and early culling of animals. A highly controversial but developing link between exposure to M. paratuberculosis and human Crohn’s disease in some individuals has led to the suggestion that M. paratuberculosis is also a potential food safety concern. As with many other mycobacteria, M. paratuberculosis is exquisitely adapted to survival in the host, despite aggressive immune reactions to these organisms. One hallmark of mycobacteria, including M. paratuberculosis, is their propensity to infect macrophages. Inside the macrophage, M. paratuberculosisinterferes with the maturation of the phagosome by an unknown mechanism, thereby evading the host’s normal first line of defense against bacterial pathogens. The host immune system begins a series of attacks against M. paratuberculosis-infected macrophages, including the rapid deployment of activated γδ T cells, CD4+T cells and cytolytic CD8+ T cells. These cells interact with the persistently infected macrophage and with each other through a complex network of cytokines and receptors. Despite these aggressive efforts to clear the infection, M. paratuberculosis persists and the constant struggle of the immune system leads to pronounced damage to the intestinal epithelial cells. Enhancing our ability to control this important and tenacious pathogen will require a deeper understanding of how M. paratuberculosis interferes with macrophage action, the cell types involved in the immune response, the cytokines these cells use to communicate, and the host genetic factors that control the response to infection.

The major surface protein (MSP) 1a of the ehrlichial cattle pathogen Anaplasma marginale, encoded by the single-copy gene msp1α, has been shown to have a neutralization-sensitive epitope and to be an adhesin for bovine erythrocytes and tick cells. msp1α has been found to be a stable genetic marker for the identification of geographic isolates of A. marginale throughout development in acutely and persistently infected cattle and in ticks. The molecular weight of MSP1a varies among geographic isolates of A. marginale because of a varying number of tandemly repeated peptides of 28–29 amino acids. Variation in the sequence of the tandem repeats occurs within and among isolates, and may have resulted from evolutionary pressures exerted by ligand–receptor and host–parasite interactions. These repeated sequences include markers for tick transmissibility that may be important in the identification of ehrlichial pathogens because they may influence control strategies and the design of subunit vaccines.