Yersinia pseudotuberculosis is a Gram-negative bacterium that causes Far East scarlet-like fever in humans, who occasionally get infected zoonotically, most often through the food-borne route.
In animals, Y. pseudotuberculosis can cause tuberculosis-like symptoms, including localized tissue necrosis and granulomas in the spleen, liver, and lymph nodes.
Y. pseudotuberculosis infections can mimic appendicitis, especially in children and younger adults, and, in rare cases, the disease may cause skin complaints (erythema nodosum), joint stiffness and pain (reactive arthritis), or spread of bacteria to the blood (bacteremia).
[2] The symptoms of fever and abdominal pain mimicking appendicitis (actually from mesenteric lymphadenitis) [3][4][5] associated with Y. pseudotuberculosis infection are not typical of the diarrhea and vomiting from classical food poisoning incidents.
Although Y. pseudotuberculosis is usually only able to colonize hosts by peripheral routes and cause serious disease in immunocompromised individuals, if this bacterium gains access to the blood stream, it has an LD50 comparable to Y. pestis at only 10 CFU.
[8] These modern estimates differ dramatically from earlier suggestions in popular scientific literature which claimed that Y. pestis evolved in rodents "millions of years ago.
[5] For example, YopN and TyeA are positioned as a plug on the apparatus so only their conformational change, induced by their interaction with certain host cell membrane proteins, will cause the unblocking of the secretory pathway.
[5] The combined function of these effector Yops permits the bacteria to resist internalization by immune and intestinal cells and to evade the bactericidal actions of neutrophils and macrophages.
[4][5][12] LcrV inhibits neutrophil chemotaxis and cytokine production, allowing Y. pseudotuberculosis to form large colonies without inducing systemic failure[12] and, with YopQ, contributes to the translocation process by bringing YopB and YopD to the eukaryotic cell membrane for pore-formation.
[4] In addition, YopJ inhibits TNF-α release from many cell types, possibly through an inhibitory action on NF-κB, suppressing inflammation and the immune response.
[32] Since administering anti-TNF-α and anti-IFN-γ monoclonal antibodies neutralizes YPM toxicity in vivo,[30] these cytokines are largely responsible for the damage caused indirectly by the exotoxin.
[34] Although the superantigen poses the greatest threat to host health, all virulence factors contribute to Y. pseudotuberculosis viability in vivo and define the bacterium’s pathogenic characteristics.
Y. pseudotuberculosis can live extracellularly due to its formidable mechanisms of phagocytosis and opsonisation resistance through the expression of Yops and the type III pathway;[11] yet, by limited pYV action, it can populate host cells, especially macrophages, intracellularly to further evade immune responses and be disseminated throughout the body.
Members of this family of Yersinia pseudotuberculosis mitogens adopt a sandwich structure consisting of 9 strands in two beta sheets, in a jelly roll fold topology.