## 1 Introduction  
_Campylobacter_ infection in humans (campylobacteriosis) is a major cause of foodborne illness and is the most frequently isolated foodborne bacterial pathogen from clinical samples in the US [1]. The number of campylobacteriosis cases in the US has been estimated at between 0.9 and 1.5 million per year, with greater than 8000 hospitalizations [2]. The monetary cost of _Campylobacter_ infections in the US has been estimated at USD 1.75 billion per year [3, 4]. _Campylobacter_ infections commonly cause symptoms such as diarrhea and fever that resolve after about one week [5]. Although most cases of _Campylobacterinfection are not life-threatening, complications such as bacteremia, arthritis, and [PERSON] syndrome, a potentially life-threatening neurological condition, are known to occur, especially in patients with an immune deficiency or liver disease [5; 6]. Enteritis caused by _Campylobacter_ is a common risk factor for the development of irritable bowel syndrome (IBS). Infectious enteritis (IE) patients are four times more likely to develop IBS compared to those without IE [7]. Treatments for human campylobacteriosis include fluoroquinoline, macrolide, and aminoglycoso antibiotics, but resistance to all three has been reported [8]. Beta-lactam resistance in _Campylobacter_ is common, with the addition of clavulanic acid and sulbactam as beta-lactamase inhibitors improving susceptibility but not completely eliminating it from foodborne isolates [9]. _Campylobacter_ was previously thought to be strictly a commensal microbe of food animals but has more recently been implicated in animal disease as well as human disease. The experimental infection of broiler chickens with _C. jejuni_ has been shown to elevate pro-inflammatory chemokine expression in the ceca and ileum and has been linked to intestinal villus damage [10]. In addition, _Campylobacter jejuni_ and _C. fetus_ subsp. _fetus_ cause abortion in sheep [11], and _C. hepatitis_ causes spotty liver disease in layer hens [12]. Treatments for _Campylobacter_ in food animals include whole-cell attenuated vaccines in sheep, but these need to be species-specific to _Campylobacter_, and antibody titers are short-lived [11]. Other treatments in animals include chlorotetracycline and tulathromycin [13], although _Campylobacter_ resistance to chlorotetracycline has occurred [14]. The consumption of poultry products is a major risk factor for campylobacteriosis, mainly in developed countries [15; 16; 17; 18]. _Campylobacter_ colonizes the poultry GI tract and is commonly present there in large numbers in broilers at slaughter age, ranging from log 6 to log 7 CFU/g of cecal content [10; 19]. During evisceration, the contents of the ceca and other organs are released, contaminating equipment, working surfaces, water that is part of the process, and air, as well as contaminating the skin of the poultry carcass [20]. Although the subsequent washing and chilling of the carcass reduces bacteria counts, _Campylobacter_ is often still present in a large proportion (85-91%) of carcass after packaging [20]. A strong correlation exists between _Campylobacter_ concentrations in the poultry intestinal tract and the concentration of _Campylobacter_ on carcass [21]. Thus, any interventions that reduce _Campylobacter_ in the intestinal tract before the carcass is processed could reduce the spread of _Campylobacter_ to carcass surfaces and parts and in turn reduce the incidence of campylobacteriosis. There are three main pre-harvest intervention measures for the control of _Campylobacter_ in poultry currently under development: vaccination, breeding for genetic resistance, and competitive exclusion [22]. Vaccination studies have demonstrated both mucosal and systemic humoral responses in _Campylobacter_-colonized poultry and anti-_Campylobacter_ maternal antibodies [23], along with the development of subunit vaccines [24; 25].