Yersiniosis is a zoonosis caused by the Yersinia bacterium. The route of infection is most commonly oral and is caused by consumption of Yersinia-contaminated food. The clinical presentations of chronic yersiniosis are abdominal pain, diarrhea, relapsing arthritis, and skin lesions, that is, nodular erythema. The diagnosis is based on culture-dependent identification of Yersinia in stool, positive serologic test results, or molecular techniques. The treatment of choice is combination antibiotic therapy. Mild forms of the disease do not usually require treatment. Yersiniosis frequently mimics or confounds other chronic intestinal and extraintestinal inflammatory conditions, particularly Crohn’s disease. Therefore, diagnosis of yersiniosis may be a challenge for medical practitioners. Not including Yersinia infection in the differential diagnosis of abdominal symptoms can lead to an incorrect diagnosis and inappropriate treatment. This review summarises the current knowledge of Yersinia enterocolitica and pseudotuberculosis infection, with special focus on differential diagnosis between this infection and Crohn’s disease.
Yersinia is a facultative anaerobe and gut-derived Gram-negative bacterium of the genus Enterobacteriaceae. Three species of Yersinia are pathogenic to humans: Yersinia (Y.) enterocolitica, a disease of increasing medical concern with plenty of diagnostic and therapeutic challenges; Y. pseudotuberculosis, the cause of rodenciosis (a zoonosis); and Y. pestis, the cause of plague, also known as the Black Death [1, 2]. According to the WHO classification, yersiniosis is defined as a disease caused by either Y. enterocolitica or Y. pseudotuberculosis.
Aleksander Yersin first described the Y. pestis bacterium in 1944. Since then, other researchers have undertaken investigations, particularly at times of epidemics, which led to establishment of a new Yersinia genus with subdivisions of species. This classification was based on molecular DNA hybridization techniques and finalized by Brenner et al. in 1976 .
Seventy serologic groups of Y. enterocolitica species have been identified so far . In Poland, the predominant pathogenic serotype is 0:3 . Yersinia contains the DNA genetic code and virulence plasmid pYV responsible for synthesis of YadA protein, which has adhesive and invasive properties, secretory Yersinia outer proteins (Yops), and the effector protein Ysc [6, 7]. The high-pathogenicity island 1 protein is involved in synthesis of the siderophores responsible for rapid bacterial growth and virulence . Yersinia has developed several self-defense mechanisms. First, the bacterium is resistant to high temperatures, including boiling point. Therefore, cooked meat, for example, remains an infectious reservoir of bacteria. Second, Yersinia is resistant to low pH, so can survive in the acidic environment of the stomach and pass through to infect the lower parts of the gastrointestinal tract. Of note, Yersinia secretes A and B beta-lactamases, so is resistant to penicillin and first-generation cephalosporins . Moreover, Yersinia thrives at temperatures between 0°C and 45°C. Therefore, the bacterium can survive and reproduce in household refrigerators. However, the optimal temperature to support the life cycle of Yersinia is 22–29°C [10, 11].
Y. enterocolitica and Y. pseudotuberculosis can exist in all climates but are most abundant in temperate regions. Yersinia spp. are natural habitants of soil, water, plants, and, most frequently, the digestive tracts of animals. The most important and largest natural reservoir are pigs, cattle, goats, and geese, followed by foxes, dogs, and birds.
The infection in humans is triggered by consumption of contaminated food or water. Yersinia bacteria are often found in household appliances, particularly refrigerators, which are a common source of contamination [10, 11, 12, 13]. At low temperatures, Yersinia produces a heat-stable enterotoxin that is resistant to high or boiling temperatures. Humans are frequently found to be carriers and to present with asymptomatic bacteraemia. Some authors have reported cross-infection between humans via blood transfusion or dialysis [1, 10, 14].
Yersinia enters the digestive tract in food and releases lipopolysaccharide, which acts as a heat-stable enterotoxin. Once in the digestive tract, the bacteria interact with gut-associated lymphoid tissue via expression of surface adhesion and virulence proteins and enter Peyer’s patches. Intracellular bacteria then proliferate and trigger colitis and/or translocate to lymph nodes, causing reactive lymphadenitis. The rate and scope of these processes depend on the species of Yersinia and its serotype. Yersinia is rarely a cause of sepsis [2, 7, 15, 16, 17].
The clinical picture depends on the bacterial serotype and the age, comorbidities, and immune status of the patient. Yersinia enterocolitica can manifest as acute or subacute, and less frequently as chronic infection. There have been some reports of sporadic familial or endemic infections [9, 10]. The incubation period is several days (usually 3–7). Patients with acute infection present with diarrhea, abdominal pain, and fever but rarely with vomiting. There is usually a short history of symptoms and infected individuals are often initially diagnosed to have viral gastroenteritis, food poisoning, or Crohn’s disease [9, 10, 18, 19].
On physical examination, there is palpable abdominal tenderness and a palpable mass in the right lower abdomen with loud and vivid peristalsis on auscultation. On occasions, Y. enterocolitica, like Crohn’s disease, can mimic acute appendicitis with the presence of a positive Blumberg sign [20, 21, 22]. Extraintestinal disease involves the joints, with signs of redness, edema, warmth, and limitation of joint movement because of stiffness. The large joints are most frequently involved but not symmetrically. Rarely, inflammation of the palmar interdigital and sacroiliac joints is observed .
In young children (aged 5–7 years), the disease manifests as gastroenteritis. Watery diarrhea, abdominal pain, and fever (up to 39°C) are common [21, 23]. These symptoms are self-limiting and do not require medical attention. Dehydration due to severe diarrhea might require hospital admission . However, death from Yersinia infection is rare and reported mostly in neonates . The disease can also lead to hepatosplenomegaly and lymphadenopathy and mimic neoplastic disease .
Teenagers and adults develop more complex disease and present with a range of symptoms. Watery bloody diarrhea might complicate the disease, along with diffuse abdominal pain located in the middle and right abdomen and a fever of 40°C. Ileocecal involvement may manifest as lymphadenopathy with positive peritoneal signs. Lower right abdominal pain without diarrhea might guide physicians towards a diagnosis of acute appendicitis (the peri-appendiceal sign). Patients with similar symptoms are often referred acutely for surgery with a diagnosis of acute and purulent appendicitis with associated abdominal lymphadenitis and peritoneal fluid [9, 10, 20, 21, 22, 23, 24]. Disease with ileocecal involvement frequently mimics Crohn’s disease. The presence of gastrointestinal and extraintestinal symptoms accompanied by endoscopic findings similar to those found typically in Crohn’s disease frequently mislead physicians in their diagnosis. An incorrect choice of treatment in these situations could have serious consequences for patients.
Untreated yersiniosis can result in chronic infection, which most frequently manifests as seronegative peripheral arthritis with no other symptoms . Approximately 20% of Y. enterocolitica infections are associated with skin lesions manifesting as gangrenous pyoderma or nodular erythema. Other lesions involving skin and connective tissue could also be present. There are case reports of pharyngitis, pneumonia, meningitis, liver and spleen abscesses, inflammation of bone marrow, osteitis, and urinary tract infections [10, 11, 27].
The most severe form of Y. enterocolitica infection is sepsis . Asymptomatic carriers are a potential source of infection. In cases of bacteremia, the course of the disease is sudden with formation of metastatic abscesses, frequently requiring admission to hospital and broad-spectrum antibiotic therapy. Despite intensive care, approximately 20% of patients with severe infection will die .
Pathogenic strains of Y. pseudotuberculosis cause symptoms that resemble those of Y. enterocolitica [1, 10]. However, there are some differences. Unlike adults, children and teenagers (aged 6–18 years) may develop mesenteric lymphadenopathy . Colitis is of mild intensity. Extraintestinal manifestations, such as purulent arthritis, osteitis, spleen and liver abscesses, and pneumonia, occur infrequently. Sepsis and other generalized infections are rare in patients with chronic comorbidities, such as liver cirrhosis, diabetes mellitus, and hematologic disorders. A lymphoma-like appearance has also been reported. The most common source of Y. pseudotuberculosis infection is iatrogenic spread via blood transfusion or dialysis. Of note, patients infected with Y. pseudotuberculosis can develop a scarlet fever-like rash and gastrointestinal symptoms with polyarthritis and high fever [1, 10, 11, 28].
Symptomatic disease is more common in individuals with the HLA B27 haplotype. Approximately 10–30% of patients with arthritis are HLA B27-positive.
A number of biological samples, including blood, urine, stool, cerebrospinal fluid, pus, periarticular fluid, and pharyngeal swab, can be used for detection of Yersinia infection [1, 10, 11]. The diagnostic test of choice is stool analysis, which is performed using cefsulodin-irgasan-novobiocin agar [9, 11, 29]. Yersinia is difficult to detect using simple or routine microbiological medium. In practice, microbiological diagnostic tests are performed at 37°C, the threshold at which other microorganisms thrive and overgrow Yersinia, which confounds the diagnosis . In order to preserve the biological material for correct diagnosis, it should be kept at 4–8°C immediately after drawing. The incubation period is 48 hours at 22°C, after which the bacteria are seeded on MacConkey agar to identify the pathogenic strain. Identification is based on detection of pYV Yersinia plasmid on Congo red-magnesium oxalate agar [30, 31]. The pathogenic strains can be identified as tiny red colonies. Nonpathogenic strains form beige-colored large colonies. The mean time required for the diagnostic procedure should not be longer than 7–10 days [1, 10], but depends on the type of test used.
Following infection, IgM, IgA, and IgG antibodies form in the plasma. Serologic tests and immunoassays (enzyme-linked immunoassay and immunoblot) are the methods of choice. Presence of Yersinia outer proteins (Yops) (less frequently, lipopolysaccharide as a source of somatic antigen O) are used as a diagnostic target. Yop is present only on the surface of pathogenic strains and its detection reflects present or past infection. False-positive tests are possible because of antigenic cross-reactivity with other bacteria (other Yersinia spp., Escherichia coli, Salmonella spp, Brucella spp, Morganella spp). The presence of IgM antibodies is a sign of recent infection; these are replaced in time by IgG antibodies. Patients with chronic disease and extraintestinal manifestations (arthritis) should be investigated for the presence of IgA and/or IgA plus IgG [1, 10, 11, 32, 33].
The length of time over which plasma levels of immunoglobulins are measurable depends on the type of Yersinia and the patient’s age and immune status. When the clinical manifestations are mild, plasma IgM levels could be low or under the threshold of detection; however, in severe cases, IgM levels could be high for up to several months. Other IgG and IgA plasma antibodies circulate over a longer time. The presence of plasma IgA is most frequently associated with additional symptoms, such as migratory arthritis or pyoderma gangrenosum. Dynamic serologic tests should be repeated after 14 days to assess the disease. The rationale for the diagnosis is a rapid rise or fall in plasma antibodies (minimum 4× of the basic levels) [9, 10, 11].
Another technique now frequently used is MALDI-TOF mass spectrometry, which has been introduced as a rapid, accurate, and inexpensive method for diagnosis of bacteria according to specific protein profiles. It is currently replacing standard biochemical characterization in an increasing number of clinical microbiology centers [33, 34].
Molecular techniques based on DNA hybridization, polymerase chain reaction (PCR), and sequencing are available for detection of Y. enterocolitica and Y. pseudotuberculosis species, targeting the yadA or virF gene located on the pYV plasmid. Nevertheless, current reports indicate that molecular tests may soon outcompete standard diagnostic tests. For example, Leli et al. successfully developed a multiplex gastrointestinal polymerase chain reaction (PCR) panel for diagnosis of Y. enterocolitica in patients with infectious diarrhea . Valledor et al. documented the importance of implementing a real-time PCR technique in a clinical algorithm because it allowed for better accuracy and a shortened time to diagnosis in comparison with routine clinical methods .
A full blood count could reveal leucocytosis or microcytic anemia, and laboratory investigations could show other biochemical abnormalities (elevated C-reactive protein and erythrocyte sedimentation rate, iron deficiency). Moreover, the patient could have manifestations of malabsorption, and stool examination might reveal the presence of blood and leucocytes.
Imaging Studies and Endoscopy
Imaging studies are useful for clinical diagnostic purposes. An ultrasound examination of the abdomen may detect enlarged mesenteric lymph nodes and signs of intestinal inflammation, such as wall thickening, in the ileocecal region . Ultrasound findings should be confirmed by colonoscopy. The differential diagnosis includes Crohn’s disease, other infectious diseases such as tuberculosis or salmonellosis, and autoimmune disorders leading to terminal ileitis, such as Behcet’s disease .
The endoscopic picture resembles that of Crohn’s disease, namely edema of the granular mucosa, aphthous and ulcerative lesions, and sometimes strictures and narrowing of the colonic lumen. However, there are some differences. In a case series of patients with yersiniosis, Matsumoto et al. found that the lesions were most commonly located in the terminal ileum, ileocecal valve, and cecum (similar to Crohn’s disease) and that the most typical findings were round or oval mucosal elevations with or without small ulcerations . This is in contrast with the typical manifestations of Crohn’s disease, in which longitudinal and serpiginous ulcerations forming a cobblestone pattern can be found . There are also some rare case reports in which yersiniosis manifested as a tumor (with liver metastases), a perianal ulcer, or massive rectal bleeding [38, 39, 40]. Histopathological examination rarely adds anything of diagnostic value. The presence of a variety of inflammatory cells could be microscopically identified as giant cell granuloma in both Crohn’s disease and yersiniosis. Microscopic analysis of a postsurgical specimen is helpful in differentiation; unlike in Crohn’s disease, Yersinia infiltrates are detected mainly at the mucosal surfaces. Figures 1 and 2 show the endoscopic findings in Crohn’s disease and Figures 4 and 5 present an endoscopic picture of Y. enterocolitica infection. The differential diagnosis of both diseases is presented in Table 1.
Differential diagnosis of Yersinia enterocolitica and Crohn’s disease
Fever (+++)Abdominal pain (++)Diarrhea (++/+++)Weight loss (−)
Abdominal pain (+++)Diarrhea (++)Weight loss (++)Fever (+)
Multifactorial: genetic, environmental, immune
Acute or subacute (few days/weeks)
Lifelong with periods of aggravation and/or remissions
Serpiginous and longitudinal ulcers forming a cobblestone pattern, fistula, perianal lesions, intestinal stricture
Nonspecific infiltration with dominance of mononuclear cells
Multiple granulomas with abscesses present in bowel wall and follicles
Treatment of Y. enterocolitica depends on the clinical picture, including severity of infection and presence of extraintestinal manifestations. Mild forms of the disease manifesting with diarrhea and abdominal pain of short duration are most frequently self-limiting and do not require treatment. Dehydration complicating the course of the disease might require rehydration and admission to the hospital. The presence of bacteremia associated with high fever might require antipyretic drugs, rehydration, and broad-spectrum antibiotics . Given that Yersinia secrete A and B beta-lactamases, a combination of antibiotics should be prescribed, for example a fluoroquinolone plus an aminoglycoside, a fluoroquinolone plus a third-generation cephalosporin, or a third-generation cephalosporin plus an aminoglycoside [5, 41, 42]. The duration of antibiotic treatment should be 10–14 days. Treatment of mild forms of yersiniosis is controversial, with the statement of no treatment to fluoroquinolones alone [1, 10]. Treatment of yersiniosis caused by Y. pseudotuberculosis is more efficacious and straightforward because this bacterium does not produce beta-lactamases. Therefore, treatment with ampicillin (or one of its derivatives), an aminoglycoside, a fluoroquinolone, and a tetracycline is advocated . Surgery is reserved for complicated cases.
Diagnosis of Yersinia infection is not straightforward but should be included in the differential diagnosis in patients with abdominal symptoms and extraintestinal manifestations. Misdiagnosis of yersiniosis as Crohn’s disease can result in incorrect or delayed treatment followed by debilitating complications. It is important to note that the differential diagnosis is not simple because Yersinia is frequently found in inflammatory and non-inflammatory areas of the ileum in patients with Crohn’s disease . Several medical aspects need to be considered, including when to reassess the patient after antibiotic therapy, when to repeat diagnostic tests including colonoscopy, and when to introduce immunosuppressive therapy in relation to ongoing or completed antimicrobial treatment. These medical uncertainties are heightened by the concept that Y. enterocolitica may induce inflammatory bowel disease, given that approximately 11% of patients with new-onset Crohn’s disease also had Y. enterocolitica infection . Therefore, medical practitioners should always be aware of Y. enterocolitica infection and keep it in mind in patients with new onset or aggravation of abdominal symptoms who have been diagnosed or are suspected to have Crohn’s disease.
Aleksic S, Bockemühl J. Yersinia and other Enterobacteriaceae. In: Manual of Clinical Microbiology, ed. P.R. Murray. American Society for Microbiology, Washington 1999, 483–491.AleksicSBockemühlJYersinia and other EnterobacteriaceaeIn:ed.MurrayP.R.American Society for MicrobiologyWashington1999483491Search in Google Scholar
Butler T. Yersinia infections: Centennial of the discovery of the plague bacillus. Clin Infect Dis. 1994; 19: 655–661.ButlerTYersinia infections: Centennial of the discovery of the plague bacillus19941965566110.1093/clinids/19.4.655Search in Google Scholar
Brenner DJ, Ursing J, Bercovier H, Steigerwalt AG, Fanning GR, Alonso JM, Mollaret HH. Deoxyribonucleic acid relatedness in Yersinia enterocolitica and Yersinia enterocolitica-like organisms. Curr Microbiol. 1980; 4: 195–200.BrennerDJUrsingJBercovierHSteigerwaltAGFanningGRAlonsoJMMollaretHHDeoxyribonucleic acid relatedness in Yersinia enterocolitica and Yersinia enterocolitica-like organisms1980419520010.1007/BF02605856Search in Google Scholar
Tao J, Liu W, Ding W, Han R, Shen Q, Xia Y, Zhang Y, Sun W. A multiplex PCR assay with a common primer for the detection of eleven food-borne pathogens. J Food Sci. 2020; 85: 744–754.TaoJLiuWDingWHanRShenQXiaYZhangYSunWA multiplex PCR assay with a common primer for the detection of eleven food-borne pathogens20208574475410.1111/1750-3841.15033Search in Google Scholar
Rastawicki W, Gierczyński R, Jagielski M, Kałużewski S, Jeljaszewicz J. Wrażliwość na wybrane antybiotyki pałeczek Yersinia enterocolitica grupy O3 posiadających i nieposiadających plazmidu pYV. Med Dośw Mikrobiol. 1999; 51: 331–337.RastawickiWGierczyńskiRJagielskiMKałużewskiSJeljaszewiczJWrażliwość na wybrane antybiotyki pałeczek Yersinia enterocolitica grupy O3 posiadających i nieposiadających plazmidu pYV199951331337Search in Google Scholar
Górska A, Brzostek K, Hrebenda J. Białka Yop rodzaju Yersinia – mechanizm sekrecji i translokacji. Post Mikrobiol. 1999; 38: 141–162.GórskaABrzostekKHrebendaJBiałka Yop rodzaju Yersinia – mechanizm sekrecji i translokacji199938141162Search in Google Scholar
Wiśniewski J, Bielecki J. Mechanizmy wirulencji bakterii z rodzaju Yersinia. Post Mikrobiol. 1996; 35: 213–241.WiśniewskiJBieleckiJMechanizmy wirulencji bakterii z rodzaju Yersinia199635213241Search in Google Scholar
Czerkies M, Raczkowska A, Brzostek K. Quo vadis Yersinia pestis? Ewolucja patogennych gatunków z rodzaju Yersinia. Post Mikrobiol. 2009; 48: 181–196.CzerkiesMRaczkowskaABrzostekKQuo vadis Yersinia pestis? Ewolucja patogennych gatunków z rodzaju Yersinia200948181196Search in Google Scholar
Mielczarek P, Bagłaj M. Jersinioza – rzadko rozpoznawana choroba układu pokarmowego. Gastroenterol Pol. 2004; 11: 69–74.MielczarekPBagłajMJersinioza – rzadko rozpoznawana choroba układu pokarmowego2004116974Search in Google Scholar
Jagielski M, Rastwicki W, Kałużweski S. Gierczyński R. Jersinioza - niedoceniana choroba zakaźna. Przegl Epidemiol. 2002; 56: 57–64.JagielskiMRastwickiWKałużweskiSGierczyńskiRJersinioza - niedoceniana choroba zakaźna2002565764Search in Google Scholar
Janowska M, Jędrzejewska B, Janowska J. Jersinioza - nowe wyzwanie współczesnej medycyny. Med. Og Nauk Zdr, 2012; 18: 257–260.JanowskaMJędrzejewskaBJanowskaJJersinioza - nowe wyzwanie współczesnej medycyny201218257260Search in Google Scholar
Clarke M, Dabke G, Strakova L, Jenkins C, Saavedra-Campos M, Mc-Manus O, Paranthaman K. Introduction of PCR testing reveals a previously unrecognized burden of yersiniosis in Hampshire, UK. J Med Microbiol. 2020; 69: 419–426.ClarkeMDabkeGStrakovaLJenkinsCSaavedra-CamposMMc-ManusOParanthamanKIntroduction of PCR testing reveals a previously unrecognized burden of yersiniosis in Hampshire, UK20206941942610.1099/jmm.0.001125Search in Google Scholar
Czernomysy-Furowicz D, Furowicz AJ. Zakażenia pokarmowe wywołane przez Yersinia enterocolitica i Yersinia pseudotuberculosis. In: Choroby odzwierzęce przenoszone drogą pokarmową. ed. A. Boroń-Kaczmarska, A.J. Furowicz; Wydawnictwo Lekarskie PZWL, Warszawa 1999: 64–78.Czernomysy-FurowiczDFurowiczAJZakażenia pokarmowe wywołane przez Yersinia enterocolitica i Yersinia pseudotuberculosisIn:ed.Boroń-KaczmarskaA.FurowiczA.J.Wydawnictwo Lekarskie PZWLWarszawa19996478Search in Google Scholar
Centers for Disease Control and Prevention (CDC). Red blood cell transfusions contaminated with Yersinia enterocolitica – United States, 1991–1996, and initiation of a national study to detect bacteria-associated transfusion reactions. JAMA. 1997; 278: 196–197.Centers for Disease Control and Prevention (CDC)Red blood cell transfusions contaminated with Yersinia enterocolitica – United States, 1991–1996, and initiation of a national study to detect bacteria-associated transfusion reactions199727819619710.1001/jama.1997.03550030036016Search in Google Scholar
Brzostek K. Mechanizmy regulacji czynników wirulencji Yersinia enterocolitica. Post Mikrobiol. 2004; 43: 7–38.BrzostekKMechanizmy regulacji czynników wirulencji Yersinia enterocolitica200443738Search in Google Scholar
Guinet F, Carniel E, Leclercq A. Transfusion-transmitted Yersinia enterocolitica sepsis. Clin Infect Dis. 2011; 53: 583–591.GuinetFCarnielELeclercqATransfusion-transmitted Yersinia enterocolitica sepsis20115358359110.1093/cid/cir452Search in Google Scholar
Revell PA, Miller VL. Yersinia virulence: More than a plasmid. FEMS Microbiol Lett. 2001; 205: 159–164.RevellPAMillerVLYersinia virulence: More than a plasmid200120515916410.1111/j.1574-6968.2001.tb10941.xSearch in Google Scholar
Franczak P, Witzling M, Siczewski W. Yersiniosis or Leśniowski-Crohn’s disease. Pol Przegl Chir. 2018; 90: 52–54.FranczakPWitzlingMSiczewskiWYersiniosis or Leśniowski-Crohn’s disease201890525410.5604/01.3001.0011.5966Search in Google Scholar
Piaścik M, Pawlik M, Rydzewska G. Infekcyjne zapalenia jelita a choroba Leśniowskiego-Crohna – problemy diagnostyczne i terapeutyczne. Przegl Gastroenterol. 2006; 1: 88–91.PiaścikMPawlikMRydzewskaGInfekcyjne zapalenia jelita a choroba Leśniowskiego-Crohna – problemy diagnostyczne i terapeutyczne200618891Search in Google Scholar
Lamps LW, Madhusudhan KT, Greenson JK, Pierce RH, Massoll NA, Chiles MC, Dean PJ, Scott MA. The role of Yersinia enterocolitica and Yersinia pseudotuberculosis in granulomatous appendicitis: A histologic and molecular study. Am. J. Surg. Pathol. 2001; 25: 508–515.LampsLWMadhusudhanKTGreensonJKPierceRHMassollNAChilesMCDeanPJScottMAThe role of Yersinia enterocolitica and Yersinia pseudotuberculosis in granulomatous appendicitis: A histologic and molecular study20012550851510.1097/00000478-200104000-00011Search in Google Scholar
Rowicka G. Bóle brzucha sugerujące zapalenie wyrostka robaczkowego spowodowane zakażeniem bakterią Yersinia u pięciorga dzieci – opis przypadków. Pediatr Współcz Gastroenterol Hepatol Żyw Dziecka. 2005; 7: 235–237.RowickaGBóle brzucha sugerujące zapalenie wyrostka robaczkowego spowodowane zakażeniem bakterią Yersinia u pięciorga dzieci – opis przypadków20057235237Search in Google Scholar
Talarek M, Rastawicki A, Marczyńska M. Obraz kliniczny i trudności diagnostyczne jersiniozy u dzieci. Pediatr Współcz Gastroenterol Hepatol Żyw Dziecka. 2009; 11: 9–12.TalarekMRastawickiAMarczyńskaMObraz kliniczny i trudności diagnostyczne jersiniozy u dzieci200911912Search in Google Scholar
Kay B, Black R. Francisella, Pasteurella, Yersinia. In: Infectious diseases, ed.: SL Gorbach, JG Bartlett, NR Blacklow, WB Saunders Comp., Philadelphia. 1992: 1496–1500.KayBBlackRFrancisella, Pasteurella, YersiniaIn:ed.:GorbachSLBartlettJGBlacklowNRWB Saunders Comp.Philadelphia199214961500Search in Google Scholar
Yoshino K, Takao T, Huang X, Murata H, Nakao H, Takeda T, Shimonishi Y. Characterization of a highly toxic, large molecular size, heat-stable enterotoxin produced by a clinical isolate of Yersinia enterocolitica. FEBS Lett. 1995; 362: 319–322.YoshinoKTakaoTHuangXMurataHNakaoHTakedaTShimonishiYCharacterization of a highly toxic, large molecular size, heat-stable enterotoxin produced by a clinical isolate of Yersinia enterocolitica199536231932210.1016/0014-5793(95)00267-DSearch in Google Scholar
Wacławowicz W, Czernik J, Bagłaj M. Zakażenia pałeczkami Yersinia enterocolitica jako przyczyna „ostrego brzucha” u dzieci. Pol Przegl Chirurg. 1995; 67: 720–725.WacławowiczWCzernikJBagłajMZakażenia pałeczkami Yersinia enterocolitica jako przyczyna „ostrego brzucha” u dzieci199567720725Search in Google Scholar
Garwolińska H. Reaktywne zapalenie stawów – diagnostyka i obraz kliniczny. Alergia Astma Immunologia. 1999; 4: 114–115.GarwolińskaHReaktywne zapalenie stawów – diagnostyka i obraz kliniczny19994114115Search in Google Scholar
Thwaites PA, Woods ML. Sepsis and siderosis, Yersinia entercolitica and hereditary haemochromatosis. BMJ Case Rep. 2017; 2017: bcr2016218185.ThwaitesPAWoodsMLSepsis and siderosis, Yersinia entercolitica and hereditary haemochromatosis20172017bcr201621818510.1136/bcr-2016-218185Search in Google Scholar
Noworyta J, Brasse-Rumin M, Ząbek J. Ocena wartości serodiagnostyki bakteriologicznej u chorych na niesklasyfikowane zapalenie stawów. Reumatologia. 2008; 46: 115–124.NoworytaJBrasse-RuminMZąbekJOcena wartości serodiagnostyki bakteriologicznej u chorych na niesklasyfikowane zapalenie stawów200846115124Search in Google Scholar
Schiemann D. Synthesis of a selective agar medium for Yersinia enterocolitica. Can J Microbiol. 1979; 25: 1298–1304.SchiemannDSynthesis of a selective agar medium for Yersinia enterocolitica1979251298130410.1139/m79-205Search in Google Scholar
Rastawicki W, Kowaleska-Kontecka B, Karney A. Obraz kliniczny i metody diagnozowania zakażeń wywoływanych przez pałeczki z rodzaju Yersinia. Przegl Pediatr (Suplement 1). 2000; 30: 17.RastawickiWKowaleska-KonteckaBKarneyAObraz kliniczny i metody diagnozowania zakażeń wywoływanych przez pałeczki z rodzaju Yersinia20003017Search in Google Scholar
Riley G, Toma S. Detection of pathogenic Yersinia enterocolitica by using Congo red magnesium oxylate agar medium. J Clin Microbiol. 1989; 27: 213–314.RileyGTomaSDetection of pathogenic Yersinia enterocolitica by using Congo red magnesium oxylate agar medium19892721331410.1128/jcm.27.1.213-214.1989Search in Google Scholar
Granfors K, Viljanen M, Tiilikainen A, Toivanen A. Persistence of IgM, IgG and IgA antibodies to Yersinia in Yersinia arthritis. J Infect Dis. 1980; 141: 424–429.GranforsKViljanenMTiilikainenAToivanenAPersistence of IgM, IgG and IgA antibodies to Yersinia in Yersinia arthritis198014142442910.1093/infdis/141.4.424Search in Google Scholar
Stephan R, Cernela N, Ziegler D, Pflüger V, Tonolla M, Ravasi D, Fredriksson-Ahomaa M, Hächler H. Rapid species specific identification and subtyping of Yersinia enterocolitica by MALDI-TOF mass spectrometry. J Microbiol Methods. 2011; 87: 150–153.StephanRCernelaNZieglerDPflügerVTonollaMRavasiDFredriksson-AhomaaMHächlerHRapid species specific identification and subtyping of Yersinia enterocolitica by MALDI-TOF mass spectrometry20118715015310.1016/j.mimet.2011.08.016Search in Google Scholar
Leli C, Di Matteo L, Gotta F, Vay D, Cavallo V, Mazzeo R, Busso S, Carrabba L, Rocchetti A. Evaluation of a multiplex gastrointestinal PCR panel for the aetiological diagnosis of infectious diarrhoea. Infect Dis. 2020; 52: 114–120.LeliCDi MatteoLGottaFVayDCavalloVMazzeoRBussoSCarrabbaLRocchettiAEvaluation of a multiplex gastrointestinal PCR panel for the aetiological diagnosis of infectious diarrhoea20205211412010.1080/23744235.2019.1688861Search in Google Scholar
Valledor S, Valledor I, Gil-Rodriguez MC, Seral C, Castillo J. Comparison of several real-time PCR kits versus a culture-dependent algorithm to identify enteropathogens in stool samples. Sci Rep. 2020; 10: 4301.ValledorSValledorIGil-RodriguezMCSeralCCastilloJComparison of several real-time PCR kits versus a culture-dependent algorithm to identify enteropathogens in stool samples202010430110.1038/s41598-020-61202-zSearch in Google Scholar
Matsumoto T, Iida M, Sakai T, Kimura Y, Fujishima M. Yersinia terminal ileitis: Sonographic findings in eight patients. Am J Roentgenol. 1991; 156: 965–967.MatsumotoTIidaMSakaiTKimuraYFujishimaMYersinia terminal ileitis: Sonographic findings in eight patients199115696596710.2214/ajr.156.5.2017961Search in Google Scholar
Matsumoto T, Iida M, Matsui T, Sakamoto K, Fuchigami T, Haraguchi Y, Fujishima M. Endoscopic findings in Yersinia enterocolitica enterocolitis. Gastrointest Endosc. 1990; 36: 583–587.MatsumotoTIidaMMatsuiTSakamotoKFuchigamiTHaraguchiYFujishimaMEndoscopic findings in Yersinia enterocolitica enterocolitis19903658358710.1016/S0016-5107(90)71169-8Search in Google Scholar
Azghari I, Bargach A, Billah NM, Essaoudi MA, Jahid A, Kabbaj N. Ileocecal resection for massive rectal bleeding due to Yersinia enterocolitica: A case report and review of the literature. J Med Case Rep. 2016; 10: 6.AzghariIBargachABillahNMEssaoudiMAJahidAKabbajNIleocecal resection for massive rectal bleeding due to Yersinia enterocolitica: A case report and review of the literature201610610.1186/s13256-015-0786-2471755826781434Search in Google Scholar
Manookian P, Yavrouian R, Mahmoud A. An unusual case of Yersinia enterocolitica infection manifesting as perianal and colonic ulcers. Am Surg. 2013; 79: E271–E272.ManookianPYavrouianRMahmoudAAn unusual case of Yersinia enterocolitica infection manifesting as perianal and colonic ulcers201379E271E27210.1177/000313481307900807Search in Google Scholar
Sue K, Nishimi T, Yamada T, Kamimura T, Matsuo Y, Tanaka N. A right lower abdominal mass due to Yersinia mesenteric lymphadenitis. Pediatr Radiol. 1994; 24: 70–71.SueKNishimiTYamadaTKamimuraTMatsuoYTanakaNA right lower abdominal mass due to Yersinia mesenteric lymphadenitis199424707110.1007/BF020176698008505Search in Google Scholar
Le Baut G, O’Brien C, Pavli P, Roy M, Seksik P, Tréton X, Nancey S, Barnich N, Bezault M, Auzolle C, et al. Prevalence of Yersinia species in the ileum of Crohn’s disease patients and controls. Front Cell Infect Microbiol. 2018; 8: 336.Le BautGO’BrienCPavliPRoyMSeksikPTrétonXNanceySBarnichNBezaultMAuzolleCPrevalence of Yersinia species in the ileum of Crohn’s disease patients and controls2018833610.3389/fcimb.2018.00336616074130298122Search in Google Scholar
Lemaitre BC, Mazigh DA, Scavizzi MR. Failure of beta-lactam antibiotics and marked efficacy of fluoroquinolones in treatment of murine Yersinia pseudotuberculosis infection. Antimicrob. Agents Chemother. 1991; 35: 1785–1790.LemaitreBCMazighDAScavizziMRFailure of beta-lactam antibiotics and marked efficacy of fluoroquinolones in treatment of murine Yersinia pseudotuberculosis infection1991351785179010.1128/AAC.35.9.17852452691952849Search in Google Scholar
Saebo A, Vik E, Lange OJ, Matuszkiewicz L. Inflammatory bowel disease associated with Yersinia enterocolitica O:3 infection. Eur J Intern Med. 2005; 16: 176–182.SaeboAVikELangeOJMatuszkiewiczLInflammatory bowel disease associated with Yersinia enterocolitica O:3 infection20051617618210.1016/j.ejim.2004.11.00815967332Search in Google Scholar
Mantle M, Atkins E, Kelly J, Thakore E, Buret A, Gall D.G. Effects of Yersinia enterocolitica infection on rabbit intestinal and colonic goblet cells and mucin: Morphometrics, histochemistry, and biochemistry. Gut, 1991; 32: 1131–1138.MantleMAtkinsEKellyJThakoreEBuretAGallD.G.Effects of Yersinia enterocolitica infection on rabbit intestinal and colonic goblet cells and mucin: Morphometrics, histochemistry, and biochemistry1991321131113810.1136/gut.32.10.113113793731955167Search in Google Scholar
Bartnik W, Wejmana J. Atlas kliniczno-patologiczny nieswoistych chorób zapalnych jelit. Termedia, Poznań 2011.BartnikWWejmanaJTermediaPoznań2011Search in Google Scholar