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Pathogenicity Islands

Kelly N. Hallstrom, Beth A. McCormick, in Molecular Medical Microbiology (Second Edition), năm ngoái

Tóm lược đại ý quan trọng trong bài

  • Pathogenicity Islands
  • Listeria spp.
  • LISTERIA | Introduction
  • Characteristics of the Species
  • Listeria and Related Gram-Positive Bacteria
  • Respiratory Diphtheria
  • Clinical Bacteriology
  • Immunity to Listeria Monocytogenes
  • 2.2 Escape from the vacuole
  • Placental Pathologies Intrauterine Infections
  • Listeria monocytogenes

Listeria spp.

Listeria spp. include Listeria monocytogenes, a cause of foodborne illness. The infection (listeriosis) typically causes gastroenteritis, but can spread beyond the intestines. Most healthy people who are exposed to L. monocytogenes will only present with mild symptoms; however, listeriosis can become a serious infection in the young, elderly and immunocompromised. Further, pregnant women who become infected are at risk of miscarriage, stillbirth and premature labour.

Listeria spp. contain the Listeria pathogenicity island 1 (LIPI-1), a PAI of about 9kb that contains several genes that promote pathogenesis. These genes include plcA and prfA, which together form an operon. prfA is a transcription activator that regulates the expression of various Listeria virulence genes, and plcA is a phospholipase C with phosphatidylinositol activity. LIPI-1 also contains the lecithinase operon, which contains mpl, actA and plcB. actA encodes an actin-polymerizing protein that recruits and polymerizes actin filaments to Listeria once it is inside the cell to promote its intracellular motility [67,68]. plcB encodes a phospholipase C with lecithinase activity, and mpl encodes a metalloprotease that processes PlcB into a mature form. PlcB assists with Listeria escape from phagosomes, thus promoting the spread of Listeria to other cells [69].

LIPI-1 also contains Hly, which encodes listeriolysin O (LLO), which lyses erythrocytes and other cells, but also lysis vacuoles of eukaryotic cells allowing Listeria to spread through the cytoplasm. Deletion of hly leads to avirulence, demonstrating the importance of LLO in Listeria pathogenesis.

Listeria ivanovii (a pathogen of ruminating animals) also contains LIPI-2 and the inlCD gene cluster. Both of these PAIs encode small internalins, which contribute to internalization and host cell specificity.

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LISTERIA | Introduction

C.A. Batt, in Encyclopedia of Food Microbiology (Second Edition), năm trước

Characteristics of the Species

Listeria is a Gram-positive rod that is typically of 0.52 μm in length. It is non-spore-forming and is not encapsulated. Listeria can appear coccoid and motile depending upon the growth temperature. They have an optimum growth temperature of 3037 °C, and some species, most notably Listeria monocytogenes, can grow at temperatures as low as 4 °C. As such, these species are a particular foodborne hazard because of their ability to replicate, albeit slowly, at refrigerated temperatures. At 2025 °C, they form flagella (and other antigens as well as virulence factors) and are therefore motile, whereas at 37 °C they are not. Listeria is a facultative anaerobe and grows vigorously on a variety of complex truyền thông.

The genus Listeria is characterized by its catalase activity, its lack of hydrogen sulfide production, and its production of acid from glucose. It has a positive methyl red reaction and a positive VogesProskauer reaction. It does not produce indole, utilize citrate, or possess urease activity. At one time, there was only a single species, L. monocytogenes in the genus Listeria. Subsequently, Listeria denitrificans, Listeria grayi, Listeria murrayi, Listeria innocua, Listeria ivanovii, Listeria welshimeri, and finally Listeria seeligeri were added. Listeria denitrificans subsequently was reclassified as Jonesia denitrificans. Finally, it has been suggested based on rRNA sequences that L. murrayi and L. grayi are a single species. Multilocus enzyme electrophoresis (MEE) reveals that L. monocytogenes, L. ivanovii, L. welshimeri, and L. seeligeri all form distinct clusters with no overlap. 16S rRNA sequences help to form two groups: one consists of L. grayi and the other consists of L. monocytogenes, L. ivanovii, L. innocua, L. welshimeri, and L. seeligeri. From this latter group, a further division that clusters L. monocytogenes and L. innocua appears distinct from L. ivanovii, L. seeligeri, and L. welshimeri. This next stage of distinction is curious as only L. monocytogenes and to a lesser extent L. ivanovii are considered to be virulent. Among the various Listeria species, the most studied is L. monocytogenes. Listeria monocytogenes is covered in detail elsewhere. Among the other Listeria species, none are considered to be highly virulent, and apart from L. monocytogenes, only L. ivanovii has been associated with disease in animals. There are rare reports of human disease caused by L. ivanovii, but these may be compromised by difficulty in accurately identifying the organism to the species level.

Virulence in Listeria is mediated by a number of factors, some of which are unique to L. monocytogenes, whereas a number also are shared by the non-L. monocytogenes species, including L. ivanovii and L. welshimeri. Table 1 presents a list of a selected group of virulence factors. Most of these virulence genes, including prfA, plcA, hlyA, and actaA, are clustered into a single operon.

Table 1. Selected virulence genes found in Listeria

ProteinGeneCommentsPrfAprfARegulatory protein for operonPI-PLCplcAPhospholipaseLLOhylAHemolysisActAactAActin polymerizationInlAInlAInternalin needed for cell entryA Positive Test Result

Listeria spp. may be an indicator of the presence of L. monocytogenes. Surveys of foods, processing plants, and other environments document that non-L. monocytogenes often are found in samples that contain L. monocytogenes. For example, whereas a total of 12.5% of fresh chicken wings tested positive for L. monocytogenes, more than 42% tested positive for all Listeria species. Testing for Listeria spp. in environmental samples of food production environments has been recognized widely as an effective control for the pathogen. It serves as an indicator whose presence is correlated to the presence of L. monocytogenes. Although the ecology of Listeria species is not completely understood nor is the overlap in the ecology of non-L. monocytogenes versus L. monocytogenes known, surveys for all Listeria might be a useful indicator of the presence of L. monocytogenes.

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Patrick R. Murray PhD, F(AAM), F(IDSA), in Medical Microbiology, 2021

Respiratory Diphtheria

The symptoms of diphtheria involving the respiratory tract develop after a 2- to 4-day incubation period (Clinical Case 21.3). Organisms multiply locally on epithelial cells in the pharynx or adjacent surfaces and initially cause localized damage as a result of exotoxin activity. The onset is sudden, with malaise, sore throat,exudative pharyngitis, and a low-grade fever. The exudate evolves into a thickpseudomembrane composed of bacteria, lymphocytes, plasma cells, fibrin, and dead cells that can cover the tonsils, uvula, and palate and can extend up into the nasopharynx or down into the larynx (Fig. 21.4). The pseudomembrane firmly adheres to the underlying tissue and is difficult to dislodge without making the tissue bleed (unique to diphtheria). As the patient recovers after the approximately 1-week course of the disease, the membrane dislodges and is expectorated. Systemic complications in patients with severe disease primarily involve the heart and nervous system. Evidence ofmyocarditis can be detected in the majority of patients with diphtheria, typically developing 1 to 2 weeks into the illness and at a time when the pharyngeal symptoms are improving. Symptoms can present acutely or gradually, progressing in severe disease to congestive heart failure, cardiac arrhythmias, and death.Neurotoxicity is proportional to the severity of the primary disease, which is influenced by the patients immunity. The majority of patients with severe primary disease develop neuropathy, initially localized to the soft palate and pharynx, later involving oculomotor and ciliary paralysis, with progression to peripheral neuritis.

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Clinical Bacteriology

Jeffrey K. Actor PhD, in Elsevier’s Integrated Review Immunology and Microbiology (Second Edition), 2012

Listeria

Listeria is a gram-positive, catalase-positive rod (diphtheroid) that is not capable of forming endospores. Two species are of human pathogenic significance: L. monocytogenes and L. ivanovii. In particular, L. monocytogenes causes meningitis and sepsis in newborns and accounts for 10% of community-acquired bacterial meningitis in adults. While host monocytes are critical for control and containment of Listeria, they also are involved in disseminating infection to other areas of the body toàn thân. Listeria is also diarrheagenic in humans, with those infected having vomiting, nausea, and diarrhea. Ingestion of Listeria from unpasteurized milk products can lead to bacteremia and septicemia with meningoencephalitis. When transmitted across the placenta to the fetus, infection can lead to placentitis, neonatal septicemia, and possible abortion. Individuals at particular risk for listeriosis include newborns, pregnant women and their fetuses, the elderly, and persons lacking a healthy immune system. The bacterium usually causes septicemia and meningitis in patients with suppressed immune function. Antibiotics are recommended for treatment of infection because most strains of Listeria are sensitive to ampicillin plus an aminoglycoside. Identification uses β-hemolysis on blood agar plates.

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Immunity to Listeria Monocytogenes

Serge Mostowy, Pascale Cossart, in Advances in Immunology, 2012

2.2 Escape from the vacuole

Listeria survives intracellularly by modifying and escaping from phagosomes using a combination of effectors (Hamon et al., 2006). This step is mainly mediated by the pore-forming and cholesterol-dependent toxin listeriolysin O (LLO) (Schnupf and Portnoy, 2007). LLO inhibits the maturation of phagosomes by creating pores in the phagosomal membrane which inhibit lysosome fusion by altering pH and calcium (Shaughnessy et al., 2006). The contribution of host factors to Listeria phagosomal escape is incompletely defined. LLO needs to be activated by acidification and/or by the host enzyme GILT (IFNγ-inducible lysosomal thiol reductase) that is found inside the phagosome (Singh et al., 2008). A recent report has shown that CFTR (cystic fibrosis transmembrane conductance regulator) increases chloride concentration inside the phagosome and potentiates LLO-mediated pore formation (Radtke et al., 2011). In addition to LLO, Listeria expresses two membrane-active phospholipase C enzymes (i.e., PI-PLC and PC-PLC) that contribute to rupture the Listeria-containing phagosome and help bacteria escape to the cytosol (Smith et al., 1995; Vazquez-Boland et al., 1992).

Although thought to reside primarily in the cytosol, L. monocytogenes can replicate under some circumstances inside macrophage vacuoles called SLAPs (spacious Listeria-containing phagosomes) (Birmingham et al., 2008). The formation of SLAPs only occurs upon impaired LLO production. The rate of bacterial replication inside SLAPs is reduced compared with bacterial replication in the cytosol, yet it could contribute to the development of chronic Listeria infection.

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Placental Pathologies Intrauterine Infections

I. Ariel, D.B. Singer, in Pathobiology of Human Disease, năm trước

Listeria monocytogenes

Listeria is a ubiquitous organism that is found in soil and is generally of low pathogenic virulence. However, the organism is often lethal to the fetus or newborn, and intrauterine infection is a result of vulnerability of the immunocompromised state of the pregnant woman and fetus. Listeria monocytogenes infections produce acute villitis and/or villous abscesses and intervillositis. Often, grossly visible correlation of these histopathologic features is the presence of necrotic yellow-white abscesses in cross sections of an infected placenta. If such foci are seen, cultures should be taken, since the infection is usually acquired from infected meat, contaminated vegetables, or unpasteurized cheese and dairy products. Moreover, Listeria is quite hardy, even surviving and replicating at refrigerated temperatures. Culture allows the organism to be typed and for health officials to track its origin, since even a single case is a reportable incident for public health surveillance. While other bacterial species, especially enteric organisms, can produce acute villitis, Listeria does this most consistently. Chorioamnionitis is less prominent (Figure 5). Histopathology with Gram and silver stains is useful in making the diagnosis. If villitis is found, the mother should be cultured and tested for both aerobes and anaerobes to rule out Listeria. The laboratory can miss Listeria, which resembles Streptococcus on the culture plate and on early Gram stains, but it is catalase positive. Listeria may recur in subsequent pregnancies with reinfection.

Figure 5. Chorioamnionitis with visible Listeria organisms. (a) Note the karyorrhexis and coccobacillus forms. (b) Funisitis with Listeria organisms in Whartons jelly (specimen kindly provided by Scott Hyde, PhD, Tulsa, Oklahoma).

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