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Yersinia PDF Print E-mail
Tuesday, 17 February 2009 00:00
Andreas Nocker

Deise P. Falcão

Juliana P. Falcão

  • pathogenic species comprise Y. enterocolitica, Y. pseudotuberculosis, and Y. pestis
  • pathogenicity typically associated with the presence of a virulence plasmid
  • preference for colder waters
  • can grow at very low temperatures (4°C and lower) in oligotrophic environments
  • susceptible to disinfectants, but increased resistance when ingested by protozoa
Most of the Yersinia species in the environment are considered non-pathogenic ( Fredriksson-Ahomaa and Korkeala 2003). Among Yersinia species causing human disease, Yersinia enterocolitica is the most well known species, besides Y. pseudotuberculosis and Y. pestis. This chapter mainly focuses on Y. enterocolitica as it is the only one out of the three pathogenic species which is primarily an excreted pathogen and is considered a pathogen of growing importance ( Feachem et al. 1983; Sharma et al. 2003). Pathogenicity is typically associated with different biotypes and serogroups and the presence of a 40-50 MDa virulence plasmid (70 kb-virulence plasmid in the case of Y. enterocolitica). This plasmid has been found in all pathogenic strains and encodes some immune suppression factors and a number of virulence genes required to induce disease and to survive and replicate in human lymphoid tissue ( Fredriksson-Ahomaa and Korkeala 2003). In addition to plasmid-borne genes, other virulence factors are chromosomally encoded ( Aarts et al. 2001). In summary, in order to cause disease, pathogenic Yersinia needs a group of virulence factors of plasmid and chromosomal origin that enable the microorganism to colonize the host and escape its specific and nonspecific immune response ( Robins-Browne RM 2001). In the example of Y. enterocolitica, which is a very heterogeneous species, only some serogroups like O:3, O: 5,27, O:5, O:8, and O:9 are responsible for almost all registered cases of yersiniosis in humans ( Langeland G 1983; Robins-Browne RM 2001). Serogroups are further differentiated in different biotypes with biotypes 1B, 2, 3, 4, and 5 being pathogenic. Biotype 1A, which was not considered pathogenic, can possibly cause disease by some novel mechanisms different from the ones the pathogenic biotypes mentioned before ( Sharma et al. 2003; Tennant et al. 2003).

Pathogenic Y. enterocolitica strains can cause a variety of intestinal and extra-intestinal clinical symptoms. Upon uptake, Y. enterocolitica passes the stomach, colonizes and invades epithelial cells, causes diarrhea and inflammatory reactions, and can finally cause ulceration and enter lymph nodes and the blood stream. Detailed epidemiological information has been presented ( Bottone EJ 1999; Sulakvelidze A 2000; Robins-Browne RM 2001; Falcão et al. 2008).

Disease is typically caused by ingestion of contaminated food or water via the fecal-oral route. A mass outbreak occurred in Big Sky Montana in the winter 1974/5, where about 750 resort guests showed symptoms of gastrointestinal illness ( Highsmith et al. 1977). A significant correlation between the amount of consumed unchlorinated well water and illness was observed (U.S. Department of Health, Education, and Welfare 1975). Y. enterocolitica was isolated from the well water that served as the resorts water supply ( Highsmith et al. 1977). Also foodborne outbreaks can originate from contaminated water: A small outbreak in 1995 in Vermont and New Hampshire was probably associated with consumption of pasteurized bottled milk. Contamination of milk bottles might have occurred when rinsing empty bottles with untreated well water prior to filling ( Ackers et al. 2000).

Y. enterocolitica and other Yersinia species are ubiquitous in the environment, but the vast majority lacks the classical virulence factors. Y. enterocolitica has been widely isolated from many natural waters including stream and lake water, wastewater, river water, ocean and estuary water ( Shayegani et al. 1981; Meadows and Snudden 1982; Gönül and Karanapir 1991; Brennhovd et al. 1992; Arvanitidou et al. 1994; Sandery et al. 1996; Schaffer and Parriaux 2002; Belt et al. 2007; Harvey et al. 1976; Falcão et al. 2004; Falcão et al. 2008; Cheyne et al. 2009). Higher prevalence rates of Y. enterocolitica have been reported especially in sewage and wastewater although most strains belonged to non-pathogenic serotypes ( Langeland G 1983; Weagant and Kaysner 1983; Aleksic and Bockemühl 1988). Quantitative data, i.e. number of Yersinia spp. per water volume, is very rare, most studies report isolation frequencies from water samples.

Although rare, isolation of pathogenic Y. enterocolitica and Y. pseudotuberculosis strains from drinking water and fresh water has been reported ( Schindler PR 1984; Fukushima H 1992; Sandery et. 1996; Falcão et al. 2004; Falcão et al. 2008). Pathogenic Y. enterocolitica of biotype 4 and serogroup O:5 (4/O:5) was also isolated from ice made of artesian well water used for general refrigeration ( Falcão et al. 2002). Other Yersinia species frequently isolated from water include Y. intermedia, Y. frederiksenii, and Y. kristensenii ( Marinelli et al. 1985; Sulakvelidze A 2000; Falcão et al. 2004; Falcão et al. 2008). They belong to the Y. enterocolitica-like group and are non-pathogenic (or are at the most opportunistic human pathogens). Y. ruckeri receives attention as an important fish pathogen in fish farms ( Coquet L 2002).

The presence of Yersinia tends to be poorly correlated with levels of coliforms and HPC bacteria ( Health Canada 2006; Arvanitidou M 1995; Langeland G 1983; Gönül and Karanapir 1991; Falcão et al. 2002). This might to a large extent be due to the different temperature preference of these bacteria: Whereas fecal coliform counts are lower in winter, the occurrence of Y. enterocolitica is more frequent in colder months ( Meadows and Snudden 1982; Massa et al. 1988). The preference for colder waters is also reflected by the fact that the majority of yersiniosis cases are reported from cooler regions in Europe and North America.

Selected studies about occurrence in water are summarized in the following.

  • Falcão et al studied the biotypes, serogroups, drug resistance profiles and phenotypic virulence markers characteristics of different Yersinia spp. strains isolated from fresh and salt water sources and from sewage in Brazil. Among the total of 144 Yersinia spp. environmental isolates, Y. enterocolitica was the most prominent species with 67 isolates. Those strains were found in fresh water, sewage, ocean water, waterfalls, and polluted rivers. Fifty seven percent of Y. enterocolitica isolates belonged to biotypes and serogroups with some degree of clinical and epidemiological significance. Also Y. intermedia was a prominent species (64 isolates) and was found in a wide variety of water sources. Fifty percent of a total of 144 isolated strains showed resistance to three or more drugs used in human therapy with almost 24% among Y. enterocolitica isolates ( Falcão et al. 2004).

  • A study of Y. ruckeri in a French rainbow trout farm revealed that this species could mainly be isolated from algae and sediment samples rather than from the water. Y. ruckeri can cause a serious infectious disease in fish farms. Isolated strains were able to adhere to solid supports (like wood). Killing experiments with oxolinic acid showed that sessile cells in biofilms were more resistant than their planktonic counterparts ( Coquet L 2002).

  • Y. pseudotuberculosis was recovered from 21% of 500 freshwater samples from 40 rivers in Japan. The incidence of isolation from mountain rivers was significantly higher in cooler months (September to May: 102 isolates from 380 samples) compared to warmer months (June to August: 1 isolate from 120 samples) ( Fukushima H 1992). An earlier study reported the isolation of Y. pseudotuberculosis serotype 4b from a Japanese mountain stream. Water consumption from this stream very likely caused the death of a 3-year-old boy whose feces contained 106 cells of this serotype per gram. The same serotype was also found in a rat from the upper part of this stream ( Fukushima et al. 1988). Y. pseudotuberculosis has also been isolated from nonchlorinated drinking water at a considerable rate in Japan ( Tsubokura et al. 1989). The study lists examples of outbreaks by this organism between 1977 and 1986. Suspected sources of contamination comprise food and water. 

  • A German study identified Yersinia spp. after cold enrichment in 90.6% of 32 raw wastewater samples from two WWTPs. Of a total of 118 isolated Yersinia strains, 8 belonged to serotype O:3 and harboured a 48 MDa plasmid associated with disease. Yersinia strains were also isolated from 3 out of 6 effluent samples ( Ziegert and Diesterweg 1990).

  • A total of 416 Yersinia strains isolated between 1982 and 1987 from well water and drinking water in Germany were analyzed with 82% being Y. enterocolitica, 11% Y. intermedia, 5.8% Y. frederiksenii, and 1.2% Y. kristensenii. Serogroups O:3, O:9, or O:5 were not isolated. The majority of strains cultured from drinking water plants were reported to be markedly different from strains isolated from patients. Virulence tests were negative suggesting lack of pathogenic importance ( Aleksic and Bockemühl 1988).

  • Y. enterocolitica was isolated from 60% of water samples taken from the Aterno River near the town of L’Aquila, Italy ( Marinelli et al. 1985).

  • Meadows et al. examined the presence of Y. enterocolitica in the lower Chippewa River drainage basin in Wisconsin over a 14-month period. From 303 water samples, 25 (8.25%) were positive for Y. enterocolitica by cultivation. 22 of the positive samples came from rural areas, only 3 from urban areas. A pronounced seasonality was observed with isolations being most frequent in winter months. Only one isolation was recorded outside of the period from November through April. The authors pointed out the ability of Y. enterocolitica to withstand low temperatures ( Meadows and Snudden 1982).  

  • Y. enterocolitica was isolated from unchlorinated well water during a large waterborne outbreak in a winter ski resort.  Growth of selected isolates was observed in sterile distilled water without added nutrients at 4, 25, and 37°C during the first 40 hours ( Highsmith et al. 1977).

  • Harvey et al. studied the presence of Y. enterocolitica in stream and mountain lake water from the Mammoth Lakes region in California during the summer months. Y. enterocolitica isolates could be biochemically identified in 10 of 34 sites examined. The majority of the strains, however, could not be typed. The degree of pathogenicity of the isolates for humans remained unknown ( Harvey et al. 1976).
Conventional water treatment and chlorination are likely to destroy Yersinia ( Health Canada 2006). Results from studies on the susceptibility to disinfection, however, have been found to depend on antecedent growth conditions. This was observed when studying the susceptibilities of Yersinia enterocolitica (and Klebsiella pneumoniae) to chlorine dioxide ( Harakeh et al. 1985). Bacterial populations grown under conditions that more closely resemble natural aquatic environments (i.e. low temperatures and nutrient limitation) showed increased resistance. Indeed, Yersinia spp. strains have been found in chlorinated drinking water supplies, particularly in Europe where chlorine levels are lower. Another factor to consider when testing susceptibility to disinfection is that a great number of bacterial pathogens, including Y. enterocolitica, were shown to reveal significantly increased resistance to disinfection when ingested by protozoa ( King et al. 1988).

Selected studies on susceptibility to disinfection are summarized in the following:

  • Ozone was reported to be an effective disinfectant against Y. enterocolitica. A 1 min treatment with ozone (1.4 and 1.9 ppm) was reported to decrease the Y. enterocolitica population in water by 4.6 and 6.2 log10 units per ml, respectively. Ozone also proved efficient for killing Y. enterocolitica on fresh produce surfaces ( Selma et al. 2006).

  • When comparing inactivation of Y. enterocolitica in distilled water and 0.015% tryptic soy broth (TSB), the presence of the organic material strongly increased chlorine resistance. The increased resistance in TSB was not only due to the chlorine demand by the TSB components (as sufficient chlorine was added to compensate for the chlorine demand of the TSB components), but was in part explained with a protective coat formed by amino acids and proteins in the TSB medium. The survival curves in the two systems showed a great difference: In distilled water inactivation was exponential (with a tailing to a zero slope), whereas in the presence of organic matter survival curves were concave downward. In both systems, inactivation was enhanced by increasing the temperature ( Virto et al. 2005).

  • The contact time required to achieve a 99% loss of culturability (CT99) for Y. enterocolitica was reported to be 0.5 min with concentrations of free chlorine between 0.25 and 1 mg per liter (pH 7.0, 25°C). When ingested by the protozoan Tetrahymena pyriformis, the CT99 value increased to over 90 min at free chlorine concentrations of 0.5 or 1.0 mg per liter suggesting an increase in resistance of more than 180 fold. Similar data was obtained for other waterborne pathogens ( King et al. 1988).

  • Aqueous chlorine dioxide was found to efficiently inactivate Y. enterocolitica on food surfaces. Treatment with ClO2 at a concentration of 3 ppm for 2 hours resulted in a reduction of 2.88 log10 CFU per gram blueberries. At this concentration, Y. enterocolitica was more susceptible than L. monocytogenes, P. aeruginosa, Salmonella enterica serovar Typhimurium and S. aureus ( Wu and Kim 2007). When studying susceptibility of Y. enterocolitica to 0.25 mg ClO2 in PBS, Harakeh et al. found an decrease of culturability of ≥ 5 log10 units after 15 min contact time (at pH 7.0, 23°C) ( Harakeh et al. 1985).
Yersinia spp. have the important feature to be able to grow at very low temperatures (4°C and lower) in oligotrophic environments and are mostly isolated during cold months ( Bitton G 2005; Karapinar and Gönül 1991). The minimum temperature for growth was reported to be -2°C ( Stern and Pierson 1979). An extended survival of Yersinia enterocolitica was observed in stream water at reduced temperatures, with the pathogen surviving for at least 14 days at 16°C ( Terzieva and McFeters 1991). Long time survival in cold water for many months was also reported by Karapinar and Gönül 1991. However, Yersinia survives (and in some cases grows) also in warmer waters with temperatures up to 25°C reaching levels as high as 103 CFU per ml ( AWWA 2006). Some strains survive in sewage sludge for more than 1 year ( AWWA 2006). Like for other bacterial waterborne pathogens, conclusions on survival are complicated by the fact that Yersinia spp. can become non-culturable ( Alexandrino et al. 2004). Furthermore, it has been demonstrated that environmental factors like pH or the presence of other organisms in the same habitat can influence the survival and growth rate of Y. enterocolitica in water ( Chao et al. 1988; Adams and Easter 1991; Kot et al. 2005). Interestingly, in a study performed with bottled mineral water artificially contaminated with Y. enterocolitica, it was shown that factors like darkness and light conditions and the ‘age’ of water influenced the survival of the pathogen ( Ramalho et al. 2001).

Examples of selected studies on survival are given in the following:

  • Liao and Shollenberger reported the survival of two Y. enterocolitica strains for at least 5 years in sterile distilled water or phosphate buffered saline ( Liao and Shollenberger 2003). Recovery was successful by plating the preserved culture on rich medium. Bacteria were collected from rich agar media and were transferred into 10 ml of sterile water or PBS, sealed with parafilm and stored in the dark at room temperature (20-25°C).

  • Results by Thorson et al. suggested that the fish pathogen Y. ruckeri can survive for prolonged periods in freshwater and brackish water. Survival was measured by using plate counts. The bacterium survived starvation in lake water or mixtures of aged seawater and distilled water or  for at least 4 months. Flasks with seeded water (inoculum app. 107 CFU per ml) were stored in the dark at 8 to 10°C. During starvation, cells tended to acquire a coccoid morphology. At salinities of 0 to 20%, CFU numbers did not change within the first 3 days of starvation and decreased only slightly (less than 2 orders of magnitude) during the following 4 months. Survival was significantly reduced, however, in the presence of 35% salinity. Direct viable count method (measured by epifluorescece microscopy and flow cytometry) showed for strain S2 at 10% salinity an app. 1 log10 unit reduction of viable cells in about 70 days ( Thorsen et al. 1992).

  • Schillinger and McFeters reported a reduction in culturability of 2 log10 units within 2 weeks for Y. enterocolitica submerged in diffusion chambers in stream water at 5 to 8.5°C. E. coli, in comparison, showed a greater die-off with a 3-5 log10 reduction under the same conditions. Time periods in which 50% of the population was inactivated (t50 values) were 63 hours for Y. enterocolitica and 25 hours for E. coli. Survival of the two organisms in tap water was, however, comparable with a t50 value of 0.5 hours for E. coli and 0.4 hours for Y. enterocolitica (Schillinger and McFeters 1987).

  • Karapinar and Gönül studied the survival of Y. enterocolitica in comparison with E. coli in sterile spring water stored at 4°C. This temperature still supported growth of Yersinia, but not of E. coli. When inoculated with a dose of app. 105 cells per ml, E. coli culturability gradually declined and culturable cells were no longer detectable after about 13 weeks. Yersinia seeded in the water at the same concentration replicated and showed an increase of app. 3 log10 units within the first 7 weeks of storage. After this time plate counts gradually decreased. However, after 64 weeks Yersinia concentrations were still above the initial spike level. When Yersinia was spiked together with E. coli in spring water, the survival behaviors of the two species were similar although growth of Yersinia did not reach the same level as in the pure culture ( Karapinar and Gönül 1991). These results correlated with an earlier report that Y. enterocolitica survived in sterile distilled water at 4°C for more than 18 months. Growth was observed at 4°C, 25°C, and 37°C, but not at 42°C ( Highsmith et al. 1977).

  • In contrast to long-term survival in clean water, Jamieson et al. reported a rapid loss of culturability of Y. enterocolitica in sterilized saline water with salinities of 0.5, 2.0, and 3.5% at different temperatures (4, 25, and 37°C). Starting with an inoculum concentration of 1.5 x 107 cells per ml, a 6 log10 reduction in culturability was observed after 24 hours. No culturable cells were found after 4 days ( Jamieson et al. 1976).
The infectious dose of pathogenic Yersinia spp. is not well known. For Y. enterocolitica and Y. pseudotuberculosis, a dose of around 106 cells was reported (http://www.phac-aspc.gc.ca/msds-ftss/msds168e-eng.php). However, in individuals with gastric hypoacidity, the infectious dose may be lower as the gastric acid appears to be a significant barrier to infection ( Robins-Browne RM 2001).
The major obstacle in obtaining epidemiologically meaningful data is the differentiation between pathogenic and non-pathogenic Yersinia species and serotypes. This requirement together with growth inhibition by other bacteria are especially challenging for culture techniques. Growth inhibition was suggested to explain the common failure of traditional cultivation to isolate pathogenic Yersinia spp. from contaminated water ( Waage et al. 1999). Also in food samples, difficulties in the isolation of pathogenic Y. enterocolitica have been related to the small number of pathogenic strains and the large numbers of other organisms in the background flora ( Fredriksson-Ahomaa and Korkeala 2003). A method comparison has shown that culture-based methods tend to underestimate the number of occurrence of pathogenic Y. enterocolitica in environmental samples compared to PCR assays ( Sandery et al. 1996; Fredriksson-Ahomaa et al. 2000; Fredriksson-Ahomaa and Korkeala 2003). A survey of environmental waters in Victoria, Australia, for example showed that 10% of samples tested positive using PCR compared to only 1% of samples using culture-based methods ( Sandery et al. 1996). However, it has to be considered that PCR-based detection methods without a viability component also detect dead cells, which consequently can lead to an overestimation of viable pathogenic Y. enterocolitica ( Wolffs et al. 2005).

Molecular methods to assess the prevalence of pathogenic Y. enterocolitica are often based on the detection of the yadA and virF genes, which are located on the 70 to 75-kb virulence plasmid, and on the chromosomal ail and yst genes, which (among other virulence genes) play a critical role in the pathogenesis of Y. enterocolitica ( Fredriksson-Ahomaa and Korkeala 2003). Although the ail gene is located on the chromosome, it has only been found in pathogenic Y. enterocolitica strains.

Selected molecular detection methods are listed in the following: 

  • PCR: A large number of PCR assays for a variety of samples has been developed targeting genes like virF, yadA, yopN, yopT, ail, 16S rRNA. A detailed list with gene targets, sample preparation methods, and detection systems can be found in a review by Fredriksson-Ahomaa and Korkeala ( Fredriksson-Ahomaa and Korkeala 2003). Example: An assay developed to detect Y. enterocolitica serogroup 0:3 targets a 16S rRNA gene fragment (specific for Yersinia spp.) and a yadA gene fragment (the yadA gene is located on the virulence plasmid). The assay was optimized for wastewater. Detection thresholds were reported to depend on the water type. For wastewater from constructed wetlands, five cells of Y. enterocolitica could be detected in 100 ml treated water, and 200 cells in settled wastewater. For municipal wastewater with higher loads of potential PCR inhibitors, 200 cells could be detected in treated wastewater and 2,500 cells in settled wastewater (in 100 ml each) ( Alexandrino et al. 2004).
  • Multiplex PCR: Y. enterocolitica was detected together with other common waterborne pathogens (Aeromonas hydrophila, Shigella flexneri, Salmonella typhimurium, Vibrio cholerae, and Vibrio parehaemolyticus) in a multiplex PCR reaction. The target gene for Y. enterocolitica detection was the attachment invasion locus (ail) gene. The detection limit for the bacterial targets was estimated to be between 1-100 CFU per reaction ( Kong et al. 2002).

  • IMS – nested PCR – colorimetric detection: Y. enterocolitica O:3 cells were concentrated using immunomagnetic beads coated with antibodies specific for this serogroup. Extracted DNA was amplified with primers targeting the virulence plasmid-borne yadA gene. Amplification products were either visualized on an agarose gel or with a colorimetric method (DIANA) with identical results. For seeded foods a detection limit 10-30 cfu/g meat (2 cfu/g after preenrichment) was reported. With seeded surface water samples (containing a background flora of 25-60 CFU coliforms per 100 ml and 22-25 fecal coliforms per 100 ml) the assay was able to detect 10 to 30 CFU of Y. enterocolitica O:3 per 100 ml water after a 3 hour non-specific enrichment. A negative PCR result was obtained with 1 to 3 CFU per 100 ml. The time demand was in the range of few hours ( Kapperud et al. 1993).

  • Preenrichment and nested PCR: This assay targeting the virulence plasmid-borne yadA gene was developed for detection of low numbers of Y. enterocolitica from natural waters with variable background flora, ranging from oligotrophic water to sewage. Samples were filtered and pre-enriched overnight in a non-selective medium. A detection limit of at least 8–17 cfu 100 ml-1 water with background levels of up to 8,700 heterotrophic organism’s ml-1 and 10,000 CFU coliforms per ml was reported with a time demand 2-3 days. Analysis of water samples containing < 8 CFU per 100 ml was not attempted (Waage et al. 1999). An alternative semi-nested PCR assay (targeting the chromosomally encoded ail gene) with prior enrichment was reported by Sandery et al. ( Sandery et al. 1996). A sensitivity of 5-175 CFU in 500 ml water was reported.

  • qPCR: There have been limited studies using qPCR to monitor bacterial pathogens in water samples ( Böckelmann et al. 2009). The presence of Y. enterocolitica among two others human pathogens with long-time survival capacity in water by real-time quantitative PCR assays targeting the 16S rRNA gene were adapted or developed for water samples differing in pollutant content ( Böckelmann et al. 2009). Although, a number of different assays were developed they were not validated specifically with water samples. Some of those studies are briefly described bellow. A TaqMan qPCR assay was developed for food samples based on the detection of the chromosomal ail gene. A threshold cycle value over 40 was interpreted as a negative result ( Fredriksson-Ahomaa et al. 2007). The ail gene was also targeted in a TaqMan assay presented by Jourdan et al. ( Jourdan et al. 2000). Three different primer and probe sets were tested amplifying different gene regions. The assay was able to detect ≤4 CFU per ml pure culture and 10 CFU per ml in the presence of 108 CFU of bacterial background flora. Another TaqMan assay developed to detect pathogenic Y. enterocolitica in food targeted the chromosomal yst gene with a sensitivity of app. 10 CFU per PCR reaction, ≥ 102 CFU per ml pure culture and ≥103 CFU per g spiked ground pork ( Vishnubhatla et al. 2000). A TaqMan assay targeting the 16S rRNA gene was developed for detecting Y. enterocolitica in blood ( Sen K 2000). As few as six Y. enterocolitica cells in 200 μl of blood could be detected. A SYBR Green-based qPCR assay was developed based on amplification of enterobacterial repetititive intergenic consensus (ERIC) sequences. The assay could selectively detect pathogenic Y. enterocolitica strains. No detection limit was determined ( Aarts et al. 2001).

Picture 1 is part of the Public Health Image Library (PHIL) from the Centers for Disease Control and Prevention (CDC) and picture 4 is  part of the NIH photo collection (credit: Rocky Mountains Laboratories, NIAID, NIH). The photos are in the public domain and thus free of copyright restrictions. We would like to express our appreciation for providing these images.

Figure 1:

                                                   Yersinia_Photo 1                                 

This image depicts a Petri dish containing a sheep’s blood agar (SBA) medium, which had been inoculated with Gram-negative Yersinia pestis bacteria. Y. pestis is the pathogen responsible for causing human plague. This was the appearance of the colonial growth after 96 hours of incubation at 25º C.

Please consider thatYersinia pestis is not a waterborne pathogen. However, it has the same morphology as Y. entercolitica and other waterborne Yersinia spp.

Source: http://phil.cdc.gov/phil/home.asp
Photo ID: 11774
Content provider(s): Centers for Disease Control/ Megan Mathias and J. Todd Parker

Figure 2:

                                                     Yersinia_Photo 2                                            

Optical microscopy of mice spleen infected with Yersinia spp. The staining was done using Methylene Blue according to Loeffer.

Credit: The picture was kindly provided by Dra. Alzira Almeida, Centro de Pesquisas Aggeu Magalhães – Fundação Oswaldo Cruz (CpqAm-Fiocruz)

Figure 3:

                                                     Yersinia_Photo 3                                                                                     

Optical microscopy of blood infected with Yersinia spp.

Credit: The picture was kindly provided by Dra. Alzira Almeida, Centro de Pesquisas Aggeu Magalhães – Fundação Oswaldo Cruz (CpqAm-Fiocruz)

Figure 4:

                                                            Yersinia pestis

Scanning electron micrograph depicting a mass of Yersinia pestis bacteria (the cause of bubonic plague) in the foregut of the flea vector.

Please consider thatYersinia pestis is not a waterborne pathogen. However, it has the same morphology as Y. entercolitica and other waterborne Yersinia spp.

Source: http://www3.niaid.nih.gov/topics/BiodefenseRelated/Biodefense/PublicMedia/image_library.htm
Credit (photo and description): Rocky Mountain Laboratories, NIAID, NIH

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New Zealand Food Safety Authority:

Virtual Museum of Bacteria:



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