Brucellosis is a zoonotic disease caused by a number of Brucella species and is characterized by chronic macrophage infection. However, genes that may contribute to intracellular survival of the Brucella species are not well studied. This review presents, first, genomic islands that are present or absent in various Brucella species that may help establish Brucella infection and survival strategies. Second, the alteration in macrophage transcription by Brucella to permit its long-term survival within this hostile intracellular environment. A large number of macrophage gene transcripts are altered following Brucella infection indicating that Brucella is not a silent invader of host cells. Macrophage transcript levels associated with inflammation, apoptosis, signal transduction and vesicular intracellular trafficking are altered during Brucella infection, and likely contribute to intracellular survival of Brucella. Lastly, the host–pathogen interaction events associated with Brucella infection in living mice visualized in real-time using biophotonic imaging. Mice are often used to evaluate Brucella infections; however, Brucella dissemination and pathogenesis is poorly understood in mice. Biophotonic imaging of Brucella infections revealed sites of bacterial localization similar to human infections and different patterns of infection by attenuated or virulent Brucella.

Pasteurella multocida has been recognized as a contributor to debilitating and fatal porcine pneumonia for at least 120 years and there continues to be sustained, unabated high prevalence of the organism in cases submitted for diagnostic work up. Understanding of its role in disease has been limited, in part because of difficulty in reproducing the disease experimentally with capsular type A strains of P. multocida, the predominant type associated with porcine pneumonia. This limitation has stymied the development of improved methods for disease control. In this review, the reports of efforts to reproduce the disease are compared. Reports have indicated induction of pneumonia in combined infections with agents such as hog cholera virus, pseudorabies virus and Mycoplasma hyopneumoniae. Pneumonia has been induced with intratracheal or endobronchial inoculation of anesthetized swine using capsular type A strains. Substantial recent progress in understanding the putative virulence attributes and molecular genetics of P. multocida will likely lead to better understanding of the host–parasite and parasite–parasite interactions in porcine pneumonia associated with this organism. In particular, it seems important to consider the role of biofilm formation in the pathogenesis of this disease. Ultimately, this understanding should provide a foundation for better methods for induction of the experimental disease, development of improved diagnostics, development of better therapeutic/prophylactic pharmaceutical approaches and development of immunoprophylactic products.

Adequate blood calcium (Ca) concentrations are a prerequisite to maintain several physiological functions of mammals such as pig and ruminants. Thus, blood Ca levels have to be regulated within very close limits. This is basically ensured through the coordinated effects of the calcitropic hormones parathyroid hormone (PTH) and calcitriol (1,25-dihydroxyvitamin D3). If plasma Ca decreases, one main effect of subsequently secreted PTH is the stimulation of renal reabsorption of Ca from the glomerular filtrate to reduce urinary Ca loss. Another important action of PTH is the induction of the renal enzyme 1[@@@]\rmalpha [@@@]-hydroxylase, which is responsible for the production of calcitriol. In most monogastric species, so far investigated, one of the most important effects of calcitriol is to stimulate active absorption of Ca from the gastrointestinal tract, particularly the upper small intestines, via a vitamin D-receptor-mediated genomic action. Whether this concept can be transferred without any constrictions to ruminants is still under discussion. Marked interspecies differences have to be recognized with respect to ruminant or non-ruminant animals, particularly with respect to individual segments along the gastrointestinal axis and with respect to vitamin D sensitivity of Ca transport mechanisms. This review will elucidate some of the current concepts related to the mechanisms and sites of Ca absorption in pigs and ruminants with special emphasis on dairy cows where Ca homeostasis is occasionally compromised at the time of parturition.

The transport of nitrogen across the rumen epithelium is characterized by absorption of ammonia from the rumen and by an influx of urea into the rumen. The transport rates of both compounds are large and exhibit wide variation. The transport of ammonia occurs in two forms: in the lipophilic form as NH3, the magnitude of which is linearly related to the pH in the ruminal fluid at pH values above 7, while at a physiological pH of 6.5 or lower, ammonia is predominantly absorbed as NH4+ via putative potassium channels in the apical membrane. The uptake of NH4+ depends on the potential difference of the apical membrane, Pda, and shows competition with K uptake. The pathway for basolateral exit of NH4+ is unknown. Hence, the relative transport rates of NH3 or NH4+ are determined by the ruminal pH according to the Henderson–Hasselbalch equation. Transport of ammonia interacts with the transport of Na and Mg mainly via changes of the intracellular pH. Urea recycling into the rumen has been known for many years and the transport across the rumen epithelium is mediated via urea transporters in the luminal and basolateral membrane of the epithelium. Transport of urea occurs by simple diffusion, but is highly variable. A significant increase of urea influx is caused by the fermentation products CO2 and short-chain fatty acids. Conversely, there is some evidence of inhibition of urea influx by ruminal ammonia. The underlying mechanisms of this modulation of urea transport are unknown, but of considerable nutritional importance, and future research should be directed to this aspect of ruminal transport.

The immune system is not always successful in recognizing and destroying pathogens it may encounter. Host immunity to mycobacteria is characterized by a very complex series of events, designed to clear the infection. The first line of defense is uptake and processing of the pathogen by macrophages, followed by the initiation of cell-mediated immunity. The secretion of pro-inflammatory cytokines such as IFN-γ is credited with containment of mycobacterial infections. Yet it is clear that activated T-cells may contain but fail to clear the infection in some hosts. Further, it is recognized that if infection progresses to a more clinical state, the production of pro-inflammatory cytokines is suppressed and expression of anti-inflammatory cytokines is increased. It is unclear what defines a host that can successfully contain the infection versus one that succumbs to severe immunopathologic disease. This review will address some of the key elements in host immunity to mycobacterial pathogens, with an emphasis on Mycobacterium avium subsp. paratuberculosis (M. paratuberculosis), in an attempt to understand the dialogue between immune cells and their mediators during infection and what causes this discourse to go awry.

In the past few decades, vector-borne diseases have been spreading into countries previously free of these agents. It is necessary for a surveillance method to be tailored to the biology of these agents in order to detect their incursion. Using a sentinel herd system, it is possible to target high-risk areas where occurrence is most probably due to vector presence. Since the 1970s, diseases such as Akabane, vesicular stomatitis and Bluetongue disease have successfully been monitored using cattle herds as sentinels in many countries such as Saudi Arabia, Australia, China, Indonesia, Sultanate of Oman and most recently in countries in Western Europe. This paper reviews the strengths and weaknesses of sentinel herd surveillance systems in general. In order to determine their efficacy, the following criteria were found to be essential: the choice of sentinel locations, sentinel animal, seasonality of sampling and diagnostic testing methods. We conclude that due to its ability to focus on a specific disease, sentinel herd systems have been successful in the early detection of the spread of a targeted agent. This review is used as a basis for recommendations for the development of future sentinel herd systems.

The present review concentrates on the biological aspects of porcine T lymphocytes. Their ontogeny, subpopulations, localization and trafficking, and responses to pathogens are reviewed. The development of porcine T cells begins in the liver during the first trimester of fetal life and continues in the thymus from the second trimester until after birth. Porcine T cells are divided into two lineages, based on their possession of the [@@@]\rmalpha [@@@]β or γδ T-cell receptor. Porcine [@@@]\rmalpha [@@@]β T cells recognize antigens in a major histocompatibility complex (MHC)-restricted manner, whereas the γδ T cells recognize antigens in a MHC non-restricted fashion. The CD4+CD8− and CD4+CD8lo T cell subsets of [@@@]\rmalpha [@@@]β T cells recognize antigens presented in MHC class II molecules, while the CD4−CD8+ T cell subset recognizes antigens presented in MHC class I molecules. Porcine [@@@]\rmalpha [@@@]β T cells localize mainly in lymphoid tissues, whereas γδ T cells predominate in the blood and intestinal epithelium of pigs. Porcine CD8+ [@@@]\rmalpha [@@@]β T cells are a prominent T-cell subset during antiviral responses, while porcine CD4+ [@@@]\rmalpha [@@@]β T cell responses predominantly occur in bacterial and parasitic infections. Porcine γδ T cell responses have been reported in only a few infections. Porcine T cell responses are suppressed by some viruses and bacteria. The mechanisms of T cell suppression are not entirely known but reportedly include the killing of T cells, the inhibition of T cell activation and proliferation, the inhibition of antiviral cytokine production, and the induction of immunosuppressive cytokines.

Transmissible spongiform encephalopathies (TSEs) are a family of neurodegenerative diseases characterized by their long incubation periods, progressive neurological changes, and spongiform appearance in the brain. There is much evidence to show that TSEs are caused by an isoform of the normal cellular surface prion protein PrPC. The normal function of PrPC is still unknown, but it exhibits properties of a cupro-protein, capable of binding up to six copper ions. There are two differing views on copper's role in prion diseases. While one view looks at the PrPC copper-binding as the trigger for conversion to PrPSc, the opposing viewpoint sees a lack of PrPC copper-binding resulting in the conformational change into the disease causing isoform. Manganese and zinc have been shown to interact with PrPC as well and have been found in abnormal levels in prion diseases. This review addresses the interaction between select trace elements and the PrPC.

Small ruminants represent an important component of the Ethiopian livestock production system, providing 12% of the value of livestock products consumed at the farm level and 48% of the cash income generated. Ethiopia is second in Africa and sixth in the world in terms of sheep population. The country has, however, benefited little from this enormous resource owing to a multitude of problems, disease being the most important. Disease alone accounts for mortalities of 30% in lambs and 20% in adults. Productivity losses attributable to helminth parasites are often substantial. A loss of US[dollar] 81.8 million is reported annually due to helminth parasites. In a country confronted with challenges of an ever-rising human population and food shortage, such enormous losses caused by helminth parasites, ‘the silent predators’, are intolerable. Therefore, helminth control should receive special attention in poverty reduction strategies through improved productivity of livestock if the present and future challenges of food shortage are to be addressed. Productivity loss due to helminth infections can be substantially reduced through implementation of effective disease control strategies, which require an understanding of the epidemiology and ecology of parasites and parasitic infections under local conditions. This paper reviews extensive evidence demonstrating that helminthosis is a major constraint to productivity of sheep in Ethiopia. It also discusses epidemiology and ecology of major helminth parasites in the country and suggests strategies for improved control in various agro-ecological zones and production systems.

The objective of the study was to evaluate treatments for infectious bovine keratoconjunctivitis (IBK), based on a systematic review of the published literature. A search was conducted to identify all manuscripts relating to antibiotic treatment of cattle with IBK. Relevant studies involved naturally occurring IBK and reported the resolution of lesions as a study outcome. Studies which failed to use methods such as blinding, blocking or randomization to minimize bias were excluded from the review. The initial search yielded 196 manuscripts, of which nine described high-quality, randomized clinical trials. These manuscripts reported antibiotic treatment of IBK with florfenicol, ceftiofur, oxytetracycline, procaine penicillin G, procaine penicillin G and dexamethasone, tilmicosin, or benzathine cloxacillin compared to either a placebo control or a non-medicated control. Overall, the studies suggest that antibiotic treatment is successful in reducing healing times of IBK-associated corneal lesions. Very few manuscripts reported a direct comparison of different antibiotic classes, so it was not possible to make comparative evaluations of efficacy. This review demonstrates the need for further randomized controlled trials that evaluate the efficacy of antibiotic treatment for IBK, including direct comparisons of two or more antibiotics.