Campylobacter jejuni/ coli Infection: Is It Still a Concern?

Abstract

Campylobacteriosis is a leading cause of infectious diarrhea and foodborne illness worldwide. Campylobacter infection is primarily transmitted through the consumption of contaminated food, especially uncooked meat, or untreated water; contact with infected animals or contaminated environments; poultry is the primary reservoir and source of human transmission. The clinical spectrum of Campylobacter jejuni/coli infection can be classified into two distinct categories: gastrointestinal and extraintestinal manifestations. Late complications are reactive arthritis, Guillain-Barré syndrome, and Miller Fisher syndrome. In the pediatric population, the 0-4 age group has the highest incidence of campylobacteriosis. Regarding the use of specific antimicrobial therapy, international guidelines agree in recommending it for severe intestinal infections. Host factors, including malnutrition, immunodeficiency, and malignancy, can also influence the decision to treat. The Centers for Disease Control and Prevention (CDC) has identified antibiotic resistance in Campylobacter as a 'significant public health threat' due to increasing resistance to FQs or macrolides. Although numerous vaccines have been proposed in recent years to reduce the intestinal colonization of poultry, none have shown sufficient efficacy to provide a definitive solution.

Keywords: Campylobacter; antibiotic resistance; foodborne illness; pediatric population.

Figure 1

Transmission, environmental reservoirs, and risk factors for human Campylobacteriosis. As a zoonotic disease, poultry is the primary reservoir for Campylobacter. In non-endemic regions, consuming raw or undercooked poultry meat and direct contact with animals are the primary risk factors. However, in endemic areas, environmental contamination, including water sources, along with poultry contact, increased meat consumption, and inadequate hygienic practices contribute to the widespread persistence of the bacterium.

Figure 2

Campylobacter jejuni/coli virulence factors. The main pathogenic factors of Campylobacter have been categorized into four broad groups in this image: motility and chemotaxis, adhesion and translocation, invasion and evasion of the host immune system, and survival and biofilm formation. The flagellar apparatus, encoded by the FlgA gene, is the factor that confers motility to the bacterium, counteracting peristaltic movements. Additionally, it is involved in the secretion of effector molecules (Campylobacter invasion antigens, Cia), in the evasion of TLR5-mediated immunity, and in the biofilm formation. CiaB, CiaC, and CiaD facilitate bacterial uptake by and invasion of host cells. The type 3 secretion system (T3SS), a key virulence factor in many Gram-negative pathogens, is primarily responsible for the secretion of Cia effectors. Despite T4SS presence in Campylobacter remaining unclear, T6SS plays a clear role in host invasion, mediating both invasion and adhesion to colon cells. During invasion, Campylobacter jejuni cytolethal distending toxin (Cj-CDT). Capsular polysaccharide (CPS) and Campylobacter-containing vacuoles (CCVs) act as an immune shield, allowing the bacterium to persist within the host.

Figure 3

Clinical manifestations and late complications of Campylobacter infection. While uncommon, bacteremia is a key factor in the systemic spread of the bacteria following intestinal infection, leading to potential complications in distant organs. Molecular mimicry underlies the pathogenesis of late complications.