# Current Challenges in _Yersinia_ Diagnosis and Treatment
## 7 _Yersinia_ Transmission  
Both _Y. enterocolitica_ and _Y. pseudotuberculosis_ are characterized by psychrophilicity--the ability to multiply and accumulate in the environment in low and variable temperatures (4-12 \({}^{\circ}\)C) while maintaining or increasing their virulence [3]. Adapting to low temperatures allows bacteria to initiate an infectious process. As a result, their increased motility, chemotaxis, adhesion, invasion, resistance to phagocytosis, and toxin formation are observed. All of them are key factors necessary for the development of an outbreak or an epidemic [3]. _Yersinia_ species possess type II and type III secretion systems (T2 SS and T3 SS), which are involved in initiating host infection. The T2 SS is present in all _Yersinia_ species, both pathogenic (e.g., the T2 SS of the human pathogenic _Y. enterocolitica_ strain 1b called Yts1) and nonpathogenic [90]. The T3 SS is a hallmark of infection with pathogenic _Yersinia_ species and induces Ysc (which forms a multimeric integral membrane complex in the membrane of eukaryotic cells to help Yop translocation) and the Ysa system (which controls Yop secretion in the early stages of infection and invasion of the epithelial M-cells in the Peyer's patches) [91; 92] (Table 2). System T3 SSs are contact-activated secretion systems that allow bacteria to inject effector proteins across eukaryotic cell membranes. Upon contact, the secretion apparatus, called the injection complex, exports two types of hydrophobic proteins called translocators (YopB and YopD in _Y. enterocolitica_) and effectors [91]. A crucial role in the pathogenicity of _Y. enterocolitica_ is played by chromosomally transferred virulence genes, including _Ail_ (attachment invasion locus), _Inv_ (invasin), and _Yet_ (_Yersinia_ stable toxin) [93; 94; 95]. The adhesin of _Y. enterocolitica_ with pleiotropic virulence effects predominantly expressed by _Y. enterocolitica_ is _Yersinia_ adhesin A (YadA). This protein enables bacterial attachment to host cells and the extracellular matrix (YadA mediates cell adhesion and bacterial translocation to M cells and the colonization of Peyer's patches) [94]. The major invasion factor of _Y. enterocolitica_ is the invasion protein InvA, which induces proinflammatory host cell responses. InvA induces IL-8 synthesis in epithelial cells by engaging beta1 integrins. Inv-induced beta1 integrin signaling involves the small GTPase Rac; the activation of MAP kinases such as p38, MEK1, and JNK; and activation of the transcription factor NF-kB [95]. The attachment and invasion locus (Ail) cooperates with YadA to ensure high serum resistance to _Y. enterocolitica_[93]. _Y. enterocolitica_ is divided into six biotypes. Biotype 1A is nonpathogenic, while five other biotypes (1B, 2-5) cause infections in humans and/or animals. Pigs are the main reservoir of bio-serotype 4/O:3 strains. Biotype 4 is most frequently responsible for human infections worldwide. It is usually associated with the serotype O:3 (4/O:3), occurring in pigs that are asymptomatic carriers. The contamination of pork meat often occurs during the evisceration of pigs at slaughter [96]. Most reported cases of yersiniosis in Poland are caused by serotypes 4/O:3, 2/O:9, and 1B/O:8 [69]. \begin{table}
\begin{tabular}{c c l} \hline \hline
**Human Activity** & \multicolumn{2}{c}{**Animal and Plant Sources of _Yersinia_ spp.**} \\ \hline \multirow{6}{*}{Outbreaks} & \(\bullet\) & Japan [42]; \\  & \(\bullet\) & Canada [43]; \\  & \(\bullet\) & Europe [6]; \\  & \(\bullet\) & Russia [3]; \\  & \(\bullet\) & New Zealand [4]; \\  & \(\bullet\) & Iceberg lettuce [72]; \\  & \(\bullet\) & Carrots [73]; \\  & \(\bullet\) & Raw milk [74]. \\ \hline \hline \end{tabular}
\end{table} 
Table 1: _Cont._Lipopolysaccharide (LPS) is the major component of the outer leaflet of the outer membrane of Gram-negative bacteria, including the genus _Yersinia_. It is responsible for the activation of the host's innate immune system.