Yersinia entercolitica

A presentation about the microorganism yersinia entercolitica, including intro, history, types, cause of pathogenicity, health problems it causes, outbreaks, control measures etc

1. Yersinia Enterocolitica Harjot Singh(21FET207)

2. INTRODUCTION 2 Domain Bacteria Phylum Proteobacteria Class Gammaproteobacteria Order Enterobacterales Family Yersiniaceae Genus Yersinia Species Y. enterocolitica SCIENTIFIC CLASSIFICATION

3. INTRODUCTION 3 HISTORY In 1934, McIver and Pike identified a novel bacterium from the skin of a farm worker and named this bacterium “ Flavobacterium pseudomallei Whitmore ” but in retrospect it is likely to be Y. enterocolitica . The study of yersiniosis – named after the French bacteriologist Alexandre Yersin , who is credited along with Kitasato for first describing the plague bacillus In 1939, Schleifstein and Coleman recorded the similarity between McIver and Pike’s microbe and few they found and they proposed the name “Bacterium enterocoliticum ” for this organism. In 1944, Van Loghen proposed the name Yersinia after Alexandre Yersin , who first described the plague bacillus and had named it in honor of Louis Pasteur.

4. INTRODUCTION 4 PHENOTYPIC CHARACTERSTICS Gram negative, o xidase negative, rod-shaped Non-spore former Facultative anaerobes that ferment glucose Optimum temperature for growth 28-30 degree Celsius Doubling time at optimum temperature is approx. 34 mins Psychrophilic, hence can withstand refrigeration temperatures Less Survival rate at intermediate temperatures Optimum pH for growth is 7.6 Can tolerate alkaline conditions but is not good acid - tolerant

5. INTRODUCTION 5 CHARACTERSTICS Susceptible to heat Readily inactivated by pasteurization at 71.8 degree Celsius for 18s Also susceptible to: Ionizing and UV radiation High pressure homogenization Sodium nitrate and nitrite when added to food Chlorine

6. CLASSIFICATION 6 BIOTYPES Based on the ability of Y. enterocolitica to metabolize selected organic substrates Divided into biotypes 1A, 1B , 2, 3, 4, and 5 Most frequent biotype associated with human disease worldwide is biotype 4 Y. enterocolitica is divided into 3 broad categories: B iotype 1B (the most virulent ) B iotypes 2 to 5 (intermediate virulence) B iotype 1A (the least virulent ) Y. enterocolitica being divided into two subspecies : Y. enterocolitica subsp. Enterocolitica Y. enterocolitica subsp. palearctica, comprising biotype 1B strains and biotype 2 to 5 strains

7. CLASSIFICATION 7 SEROTYPES Serotyping of Y. enterocolitica is based on LPS surface O antigens Serotype O:3 is most common and all are isolates of biotype 4 Other serotypes commonly obtained from humans, include O:9 (biotype 2) and O:5,27 (biotype 2 or 3) Majority of human infections are due to strains of serotype O:3

8. CHARACTERSTICS OF INFECTION 8 Infection with the enteropathogenic yersiniae typically manifests as nonspecific, self-limiting diarrhea but may produce a variety of suppurative and autoimmune complications ACUTE INFECTION It enter the gastrointestinal tract after ingestion in contaminated food or water Median infective dose for humans is not known but is approx. more than CFU Most symptomatic infections occur in children less than 5 years old Diarrhea accompanied by low-grade fever, headache and abdominal pain are common symptoms of yersiniosis in children Lasts from a few days to 3 weeks, but some patients may develop chronic enterocolitis , which may persist for several months Ileocolic intussusception, toxic megacolon , mesenteric vein thrombosis are present in acute form of infection  

9. CHARACTERSTICS OF INFECTION 9 In adolescents , acute yersiniosis is present as a pseudoappendicular syndrome due to acute inflammation of the terminal ileum or the mesenteric lymph nodes Features of this syndrome are abdominal pain and tenderness localized to the right lower quadrant and is similar to appendicitis Focal disease may be present as cellulitis, suppurative lymphadenitis, septic arthritis, osteomyelitis, urinary tract infection, renal abscess, sinusitis , pneumonia, lung abscess, or empyema Bacteremia is a rare complication of infection It is  the presence of bacteria in the bloodstream and Y. enterocolitica is one of the most important causes of fatal bacteremia I mmunosuppression , blood dyscrasias , malnutrition, chronic renal failure, cirrhosis, alcoholism, diabetes mellitus favours bacteremia occurrence Bacteremia also result from direct inoculation of Y. enterocolitica into the circulation during blood transfusion The probable sources of these infections are blood donors with low-grade, subclinical bacteremia.

10. CHARACTERSTICS OF INFECTION 10 AUTOIMMUNE COMPLICATIONS Yersiniosis can lead to a variety of immunological complications, such as reactive arthritis, erythema nodosum, uveitis, glomerulonephritis, carditis , and thyroiditis Most prevalent in Scandinavian countries, where serotype O:3 strains are especially prevalent Men and women are affected equally Arthritis typically follows the onset of diarrhea or the pseudoappendicular syndrome by 1 to 2 weeks and its duration is approx. 3 months Yersinia-induced erythema nodosum occurs predominantly in women Yersiniosis has also been linked to various thyroid disorders , including Graves’ disease hyperthyroidism, non-toxic goiter, and Hashimoto’s thyroiditis

11. RESERVOIRS 11 Intestinal tract of many different mammalian species as well as from birds, frogs, fish, flies, fleas, crabs, and oysters Foods like pork , beef, lamb, poultry, and dairy products such as milk, cream, and ice cream Commonly found in a variety of terrestrial and freshwater ecosystems, including soil, vegetation, lakes, rivers, wells, and streams , and can persist for extended periods in these, especially at low environmental temperatures Some wild animals like wild rodents etc and domesticated animals like sheep and pigs are also significant reservoirs

12. INCIDENCE OF INFECTIONS AND FOODBORNE OUTBREAKS 12 In US, cases of yersiniosis from 1996 to 2007 determined that the annual average incidences of Y. enterocolitica were 0.35 per 1000 and these are very low. For comparison, in 2007, the incidences of infections with Campylobacter, Salmonella, Shigella, Shiga toxin producing E. coli, and Yersinia were 12.79, 14.92, 6.26, 1.77, and 0.36 per 100,000, respectively OUTBREAKS During the mid-1970s , yersiniosis caused by Y. enterocolitica O:5,27 occurred among 138 Canadian schoolchildren who had consumed raw milk , but the organism was not recovered from the suspected source In 1976 , Y. enterocolitica serotype O:8 biotype 1B was responsible for an outbreak in New York State that affected 217 people, 38 of whom were culture positive. The source of infection was chocolate flavored milk , which evidently became contaminated after pasteurization . In 1981 , an outbreak of Y. enterocolitica O:8 infection affected 35% of 455 individuals at a diet camp in New York State . Seven patients were hospitalized as a result of infection, five of whom underwent appendectomies . The source of the infection was reconstituted powdered milk and/or chow mein .

13. INCIDENCE OF INFECTIONS AND FOODBORNE OUTBREAKS 13 In 1982, 172 cases of infection with Y. enterocolitica O:13a,13b occurred in an area that included parts of Tennessee, Arkansas, and Mississippi. The suspected source was pasteurized milk that may have become contaminated with pig manure during transport. More recently, three unrelated outbreaks of infection with Y. enterocolitica O:3 affecting infants and children in Atlanta, Chicago, and the state of Tennessee between 1989 and 2002 were attributed to the transmission of yersiniae from raw chitterlings on the hands of food handlers to affected children

14. MECHANISMS OF PATHOGENICITY 14 Virulent biotypes 1B , 2, 3, 4, and 5 possess a panoply of virulence determinants, including a chromosomally encoded invasin and a ca. 70-kb virulence plasmid, termed pYV (acronym for plasmid for Yersinia virulence ) All pYV-bearing clones of Y. enterocolitica have the capacity to invade epithelial cells in large numbers. Infection is transferred predominantly through the fecal-oral route . After oral inoculation of mice with a virulent strain, most bacteria remain within the intestinal lumen, whereas a small number adhere to the mucosal epithelium. However, invasion of the epithelium occurs almost exclusively through M cells (microfold cells ) Microfold cells are specialized epithelial cells that overlie Peyer’s patches.

15. MECHANISMS OF PATHOGENICITY 15 After penetrating the epithelium, Y. enterocolitica traverses the basement membrane to reach the gut-associated lymphoid tissue , where it causes localized tissue destruction and the formation of microabscesses Y . enterocolitica often spreads via the lymph to the draining mesenteric lymph nodes, where it may also lead to microabscess formation If the bacteria enter the bloodstream, they can disseminate to any organ but continue to show a tropism for lymphoid tissue. Y. enterocolitica is often regarded as a facultative intracellular pathogen because of its innate resistance to killing by macrophages. Highly virulent (biotype 1B) strains of Y. enterocolitica can bypass the Peyer’s patches and disseminate via the bloodstream directly I nvasin, Ail, Myf fibrillae, ureases etc are main Chromosomal Determinants of Virulence

16. VIRULENCE DETERMINANTS 16 Invasin Strains of Y. enterocolitica that carry pYV also produce a 91-kDa surface-expressed protein termed invasin. It imbues the recipient with the ability to penetrate mammalian cells , including epithelial cells and macrophages. The amino terminus of invasin is inserted in the bacterial outer membrane, while the carboxyl terminus is exposed on the surface, where it mediates binding to host cell integrins . Integrins are transmembrane proteins that communicate extracellular signals to the cytoskeleton . Invasin plays a key role in virulence.

17. VIRULENCE DETERMINANTS 17 Ail Pathogenic strains of Y. enterocolitica produce an outer membrane protein unrelated to invasin, which also confers invasive ability on E. coli. This 17-kDa peptide is specified by a chromosomal ail ( attachment-invasion ) locus, so called because it mediates bacterial attachment to some cultured epithelial cell lines and invasion of others . Ail may also enable yersiniae to persist extracellularly by protecting them from complement-mediated killing. It is optimally expressed at 37°C (unlike invasin, which is optimally expressed at 25°C Ail mutants fail to adhere to or invade cultured cells when the inv gene is not expressed. An Ail-negative mutant of Y. enterocolitica showed no reduction in virulence.

18. VIRULENCE DETERMINANTS 18 Myf Fibrillae There are some distinctive colonization factors on the surface, which mediate their adherence to the intestinal epithelium These factors take the form of surface fimbriae , which allow the bacteria to deliver their toxins close to epithelial cells while resisting removal by peristalsis. Eg : Invasin Some strains of Y. enterocolitica produce a fimbrial adhesin, named Myf (acronym for mucoid Yersinia fibrillae), because it bestows a mucoid appearance on bacterial colonies that express it. Its main role in virulence may relate to its ability to mediate binding of bacteria to intestinal mucus before the bacteria make contact with epithelial cells.

19. VIRULENCE DETERMINANTS 19 LPS Y. enterocolitica can be classified as smooth or rough depending on the amount of O-side chain polysaccharide attached to the inner core region of the cell wall LPS. O-antigen- ­negative mutants of a Y. enterocolitica serotype O:8 strain have impaired ability to colonize Peyer’s patches, spleen, and liver of mice infected via different routes. These mutants also alter expression or function of other virulence-associated determinants. The outer core region of LPS plays a role in maintaining outer membrane integrity and may contribute to the resistance of Y. enterocolitica to bactericidal peptides in host tissues and macrophages. Smooth LPS may also enhance virulence by increasing bacterial hydrophilicity and thus facilitate their passage through the mucous secretions that line the intestinal epithelium.

20. VIRULENCE DETERMINANTS 20 Phospholipase Some isolates of Y. enterocolitica are hemolytic due to the production of phospholipase A ( YplA ). Strains in which Y plA gene encoding this enzyme is not present show diminished virulence. Phospholipase contributes to microabscess formation by Y. enterocolitica. YplA is secreted by Y. enterocolitica via the same type III export apparatus as that used for flagellar proteins

21. VIRULENCE DETERMINANTS 21 Urease In Y. enterocolitica , acid tolerance relies on the production of urease , which catalyzes the release of ammonia from urea and allows the bacteria to resist pH as low as 2.5 Acid tolerance is necessary to cause disease. Urease also contributes to the survival of Y. enterocolitica in host tissues Other virulence determinants include Heat stable enterotoxins, Iron acquisition and the high-pathogenicity island (HPI), The YSA pathogenicity island, T2SS

22. The Virulence Plasmid( pYV ) 22 Virulent strains of Y. enterocolitica biotypes 1B to 5 carry pYV , a ca. 70-kb plasmid. pYV has functions that interfere with innate immune response, such as phagocytosis, complement activation, and the production of proinflammatory cytokines Some factors encoded by pYV may act on T and B cells directly to modify adaptive immune responses . Yersiniae that carry pYV exhibit a distinctive phenotype , known as “calcium dependency” or “the low calcium response” because it manifests when the bacteria are grown in media containing low concentrations of Ca2 + The principal features of this response are the cessation of bacterial growth after one or two generations and the appearance of at least 12 new proteins ( Yops ) on the bacterial surface or in the culture medium

23. The Virulence Plasmid( pYV ) 23 Yops are characterized by their common mode of secretion and their regulation by a pYV -encoded DNA-binding protein, known as VirF The expression of pYV -encoded proteins in vitro imbues Y. enterocolitica with novel properties, such as autoagglutination , resistance to killing by human serum, and an ability to bind Congo red and crystal violet

24. CONTROL MEASURES 24 Don't serve or eat raw or undercooked meat . Drink and serve only pasteurized milk and milk products. Wash hands  with soap and water before eating and preparing food; before touching infants or their toys, bottles, or pacifiers; and after contact with animals or handling raw meat. Use separate cutting boards for meat and other foods. Clean all cutting boards , countertops, and utensils with soap and hot water after preparing raw meat. Or run them through the dishwasher. Always cook meat thoroughly before you eat it, especially pork products. Clean up animal poop and clean any area that the poop touched . The drugs of choice are the aminoglycosides or trimethoprim-sulfamethoxazole . Other effective agents include tetracycline (not in children), quinolones and cephalosporins

25. CONTROL MEASURES 25 Sometimes surgery is required to drain an abdominal abscess, and surgical exploration is warranted if appendicitis cannot be ruled out.  Antibiotics should be used only in selected patients such as the elderly, immunocompromised individuals or patients with diabetes . 

26. REFERENC ES 26 Food Microbiology: Fundamentals and frontiers by Michael P. Doyle and Robert L. Buchanan Muhammad Aziz,  Varun S. Yelamanchili (2021). Yersinia Enterocolitica. National Center for Biotechnology Information BAM Chapter 8: Yersinia enterocolitica Edward J Bottone (1999). Yersinia enterocolitica : overview and epidemiologic correlates. Microbes and Infection Volume 1, Issue 4, April 1999, Pages 323-333 Preventing Yersiniosis - Minnesota Dept. of Health (state.mn.us)

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