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  1. May 2017
    1. Editorial Note Editorial Note: In this investigation pasteurized milk was epidemiologically implicated as the vehicle of transmission of Y. enterocolitica. The temporal and geographic clustering of cases and the negative cultures of subsequent lots of milk are consistent with contamination of a single lot. The mechanism of contamination is unknown. Y. enterocolitica may be found in raw milk (1,2); contaminated raw milk was responsible for an outbreak of yersiniosis among children in Montreal (3). The organism has also been found in pasteurized milk (1,4) although not associated with illness. Y. enterocolitica generally does not survive standard pasteurization (5); however, if present in large enough numbers, viable Yersinia may persist after pasteurization (4-6). Once present in a pasteurized product, the organism grows well at refrigeration temperature (7). Therefore, pasteurization and proper handling of pasteurized milk may not ensure against enteric disease due to Y. enterocolitica. Only two other well documented food-borne outbreaks of Y. enterocolitica enteritis have been reported in the United States: one in New York state in 1976 caused by contaminated chocolate milk (8) and one in Washington state in 1982 caused by tofu (9). Food-borne transmission of yersiniosis has also been suspected in other outbreaks (10-12). This is the largest outbreak of yersiniosis ever reported in the United States.

      historical cases

    1. 9 of 10 fecal cultures containing the organism when inoculated to CAL agar and incubated for 40 h at 25 degrees C.


    1. fourth most commonly reported cause of bacterial diarrhoeal disease

      common infection

    1. Yersinia adhesin A (YadA)


    2. usually raw or inadequately cooked pork
    3. Virulence Factors of pYV-Bearing Strains of Y. enterocolitica [33]


    4. he ability to penetrate the intestinal wall, which is thought to be controlled by plasmid genes, and the production of heat-stable enterotoxin, which is controlled by chromosomal genes.

      major factors

    5. attributed to the presence of a highly conserved 70-kb virulence plasmid, termed pYV/pCD and certain chromosomal genes.


    1. virulence plasmid in Y. enterocolitica. In addition, the lower temperature favors the growth of

      incubation recommendation

    2. 4–6 days (range, 1–14 days)

      incubation period

    3. Colonial growth pattern displayed by Yersinia enterocolitica bacteria

      growth, blood agar

    4. CDC recommends the use of cefsulodin-irgasan-novobiocin (CIN) agar for isolation of Yersinia spp. from nonsterile sites.   Incubation at 25° C is recommended to prevent loss of the virulence plasmid in Y. enterocolitica. In addition, the lower temperature favors the growth of Yersinia over some other members of the Enterobacteriaceae family that can grow on CIN agar.  


    5. virulence plasmid


    6. . They can also be transmitted by direct or indirect contact with animals.


    7. The incidence of yersiniosis in FoodNet(https://www.cdc.gov/foodnet/index.html) sites in 2014 was 0.28 cases per 100,000 population. This met the U.S. Healthy People 2020 target for yersiniosis of 0.30 or fewer cases per 100,000.


    8. Antibiotics should be given for severe cases. Y. enterocolitica isolates are usually susceptible to trimethoprim-sulfamethoxazole, aminoglycosides, third-generation cephalosporins, fluoroquinolones, and tetracyclines; they are typically resistant to first-generation cephalosporins and most penicillins. They are typically resistant to first-generation cephalosporins and most penicillins. Antimicrobial therapy has no effect on postinfectious sequelae.

      antibiotics and resistance

    9. culture on cefsulodin-irgasan-novobiocin (CIN) or other specific for growing it.


    10. Yersiniosis is caused by a facultative anaerobic gram-negative coccobacilli

      gram, morphology

    1. Such symptoms are followed by watery, mucoid diarrhea (78-96%); fever (43-47%); colicky abdominal pain (22-84%); bloody stools (< 10%); and white blood cells (WBCs) in the stool (25%).


    1. As control measures, the distributor improved hygiene measures, and the military bases thoroughly cleaned the bathrooms and kitchens, and increased awareness on hand hygiene among the soldiers. From Week 21, the kitchens in all three bases in Troms voluntarily elected to close the salad bar and refrain from serving pork products until the outbreak was resolved.

      public health interventions

    2. Transmission most frequently occurs through eating contaminated food


    1. Cephalosporins disrupt the synthesis of the peptidoglycan layer of bacterial cell walls, which causes the walls to break down and eventually the bacteria die.

      anitbiotics mechanism

    1. work by binding to the bacterial 30S ribosomal subunit (some work by binding to the 50s subunit), inhibiting the translocation of the peptidyl-tRNA from the A-site to the P-site and also causing misreading of mRNA, leaving the bacterium unable to synthesize proteins vital to its growth


    1. The combination antibiotic TMP-SMZ inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid.

      mechanism for anitbiotics

    1. National outbreak of Yersinia enterocolitica infections in military and civilian populations associated with consumption of mixed salad, Norway, 2014.
    2. National outbreak of Yersinia enterocolitica infections in military and civilian populations associated with consumption of mixed salad, Norway, 2014.
    1. Occasionally Y. enterocolitica infection occurs after contact with infected animals.

      tagging for the picture - virulence

    1. Metabolism Y enterocolitica is non–lactose-fermenting, glucose-fermenting, and oxidase-negative facultative anaerobe that is motile at 25°C and nonmotile at 37°C. Most, but not all, Y enterocolitica isolates reduce nitrates. The presence of bile salts in the medium prevents the organism from fermenting lactose. Colonies of Y enterocolitica do not produce hy


    2. of Y enterocolitica infection typically include the following: Diarrhea - The most common clinical manifestation of this infection; diarrhea may be bloody in severe cases Low-grade fever Abdominal pain - May localize to the right lower quadrant Vomiting - Present in app


    3. if it spreads systemically, can also result in fatal sepsis


    1. .7. Establishment of Yersiniosis Infection


    2. e small conserved RNA chaperone protein, Hfq is required for full virulence of a variety of pathogenic bacteria, including both YE and YPT [90]. Hfq is required for expression of the heat-stable enterotoxin Yst in YE [91]


    3. YE pathogenicity depends on the presence of the 70-kb plasmid associated with Yersinia virulence, pYV [67, 77–79]. The pYV plasmid differentiates pathogenic from non-pathogenic strains, because it is essential for virulence [79]. The highly pathogenic Y. enterocolitica biotype 1B also harbors the chromosomal high-pathogenicity island (HPI), as do almost all European strains of Y. pseudotuberculosis serotype O1 [69]. HPI encodes proteins that are involved in the biosynthesis, regulation, and transport of the siderophore yersiniabactin [80, 81] and has thus been referred to as an “iron capture island” [63, 69]. There are five main genes within this island (psn, irp1, irp2, ybtP, and ybtQ) that are involved in the yersiniabactin system [80, 82, 83]. This system is positively regulated by YtbA, which is, itself, negatively regulated by the iron-responsive regulator F


    4. For instance, strain 1B/O:8 has been the predominant version of pathogenic YE in the United States

      most common in US

    5. Subsequently, YE bacilli replicate in Peyer’s patches and can sometimes spread to more distant lymphoid tissues, such as the mesenteric lymph nodes [16–18]. Dissemination from the distal ileum to the spleen and liver is relatively common, followed by extracellular replication and formation of monoclonal microabscesses [19]


    6. The most common infection is acute gastroenteritis, mainly observed in children and infants on account of being somewhat immunocompromised due to an immature immune system


    7. nfection is usually characterized by a self-limiting acute infection beginning in the intestine and spreading to the mesenteric lymph nodes. However, more serious infections and chronic conditions can also occur, particularly in immunocomp


    1. The fluoroquinolones are the only direct inhibitors of DNA synthesis; by binding to the enzyme-DNA complex, they stabilize DNA strand breaks created by DNA gyrase and topoisomerase IV. Ternary complexes of drug, enzyme, and DNA block progress of the replication fork. Cytotoxicity of fluoroquinolones is likely a 2-step process involving (1) conversion of the topoisomerase-quinolone-DNA complex to an irreversible form and (2) generation of a double-strand break by denaturation of the topoisomerase. The molecular factors necessary for the transition from step 1 to step 2 remain unclear, but downstream pathways for cell death may overlap with those used by other bactericidal antimicrobials. Studies of fluoroquinolone-resistant mutants and purified topoisomerases indicate that many quinolones have differing activities against the two targets. Drugs with similar activities against both targets may prove less likely to select de novo res

      fluoroquinolone mechanism

    1. entration-dependent bactericidal activity (see Effectiveness) by inhibiting the activity of DNA gyrase and topoisomerase, enzymes essential for bacterial DNA replication.


    1. Table 1. Biochemical Characteristics(a) of Yersinia species (2, 9 ,10 ,52)

      table of features

    2. Yersinia are oxidase-negative, Gram-negative rods. Use Tables 1 and 2 to identify species and biotype of Yersinia isolates. Currently only strains of Y. enterocolitica biotypes 1B, 2, 3, 4, and 5 are known to be pathogenic. These biotypes and Y. enterocolitica biotype 6 and Y. kristensenii do not rapidly (within 24 h) hydrolyze esculin or ferment salicin (Tables 1 and 2). However, Y. enterocolitica biotype 6 and Y. kristensenii are relatively rare; they can be distinguished by failure to ferment sucrose, and they are pyrazinamidase-positive (28). Hold Y. enterocolitica isolates which are within biotypes 1B, 2, 3, 4, and 5 for further pathogenicity tests.


    3. e Esculin agar

      bile esculin

    4. ensen's Urea agar


    5. . enterocolitica on YSA (CIN) a


    6. MacConkey agar plates


    7. nvasion of host cells (ail for Y. enterocolitica and inv for Y. pseudotuberculosis), iron complexing and uptake proteins (irps), and heat-stable enterotoxin (ystA). Factors carried on the 70 kb virulence plasmid (pYV for Y. enterocolitica and pIB1 for Y. pseudotuberculosis) include: the Yersinia outer proteins (yops), low calcium response (lcr), Yersinia adherence protein (yadA), and the temperature dependent transcriptional regulator of many of the other plasmid genes (virF) (38).


    8. m may survive and grow during refrigerated

      can grow at cold temp

    1. Yst, included on the genes ystA and ystB, is a membrane-acting virulence factor. It is a heat-stable enterotoxin that is important in causing diarrhea in the host


    2. These plasmids include an outer membrane protein, YadA, that is used for adhesion and can resist phagocytosis by host cell with the help of Yops proteins


    3. Although host gastric acid act as a substantial barrier to prevent infection from the pathogen, Y. enterocolitica utilizes plasmids


    1. Yersiniosis usually goes away on its own without antibiotic treatment. However, antibiotics may be used to treat more severe or complicated infections.


    2. Yersiniosis usually is diagnosed by detecting the organism in the stool of an infected person. Many laboratories do not routinely test for Yersinia, so it is important to notify laboratory personnel when yersiniosis is suspected so that special tests can be done. The organism can also be recovered from other sites, including the throat, lymph nodes, joint fluid, urine, bile, and blood.


    1. Complications are rare and can include skin rash, joint pains, or spread of bacteria to the bloodstream

      rare complications

    1. ersiniosis usually goes away on its own without antibiotic tre


    2. etecting the bacteria in the stool of an infected person


    3. eople occasionally become infected after drinking contaminated milk or untreated water, or after contact with infected animals or their feces. On rare occasions, people become infected through person-


    4. Common symptoms in children are fever, abdominal pain, and diarrhea, which is often bloody. Symptoms typically develop 4 to 7 days after exposure and may last 1 to 3 weeks or longer. In older children and adults, right-sided abdominal pain and fever may be the predominant symptoms and may be confused with appendicitis. Complications are rare, and may include skin rash, joint pains, or spread of bacteria to the bloodstream.


    5. Pigs are the major animal reservoir for the few strains of Y. enterocolitica that cause human illness, but rodents, rabbits, sheep, cattle, horses, dogs, and cats also can carry strains that cause human illness.