The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Yersinia pseudotuberculosis is a gram-negative coccobacillus belonging to the family Enterobacteriaceae. Isolated first in 1883 by Malassez and Vignal the organism has received numerous names before being included in the genus Yersinia. The designation pseudotuberculosis derives from the characteristic histopathological aspect found in mesenteric lymph nodes of lymphoid hyperplasia cases which closely resemble those observed during tuberculosis infection.
Yersinia pseudotuberculosis is widely spread in the environment (soil, water, vegetables, etc). This bacterium is a primary pathogen of wild and domestic animals in all continents. Nearly all animal species are potential carriers of Yersinia pseudotuberculosis and asymptomatic carriage can evolve into a fulminating and fatal infection when the animals are subjected to stress (famine, cold temperatures, etc.). The disease is transmitted by the feco-oral route. In humans, Yersinia pseudotuberculosis infections are not frequent although outbreaks associated with consumption of water or food supplies contaminated with animal feces are reported. Humans develop varying degrees of illness, from abdominal pain and fever to septicemia, but a mesenteric adenitis that mimics an acute appendicular syndrome (pseudoappendicitis) is the most common clinical presentation. In most instances, the infection is self-limiting and can be effectively treated with antibiotic therapy.
A striking characteristic of Yersinia pseudotuberculosis is the high degree of sequence identity to Yersinia pestis (the causative agent of plague) which is intriguing given the markedly different epidemiological and clinical features of the two species. In this regards, it should be noted that Yersinia pestis has been proposed to be a recently emerged clone of Yersinia pseudotuberculosis (Achtman et al. 1999). Although the mode of transmission of Yersinia pestis (from rodent to rodent and from rodent to humans by the bite of infected fleas) may be attributed to the acquisition of two plasmids unique to this species, the presence of these plasmids is not sufficient to account for the extraordinary virulence of Yersinia pestis (Kutyrev et al. 1999, Welkos et al. 1995).