LEGIONELLA - World Health Organization

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Typing Helbig et al. (1995) suggested that differences in the virulence of Legionella species or serogroups are associated with different epitopes within the bacterial cell wall (epitopes are parts of a foreign organism or its proteins that are recognized by the immune system and targeted by antibodies, cytotoxic T cells or both). Tests using monoclonal subtyping show that the strains of L. pneumophila serogroup 1 most commonly associated with disease in humans share a common epitope (Watkins et al., 1985; Ehret, von Specht & Ruckdeschel, 1986; Dournon et al., 1988). Depending on the typing scheme used, these strains may be referred to as Pontiac (Watkins et al., 1985); monoclonal antibody (MAb) 2-reactive (Joly et al., 1986) or MAb 3/1-positive (Dresden Panel, 2002; Helbig et al., 2002). In a European-wide study of L. pneumophila, 1335 cases of Legionnaires’ disease were serotyped, and monoclonal types of serogroup 1 were grouped according to the presence of the epitope recognized by MAb 3/1 (Dresden Panel, 2002). Approximately 66.8% of cases were MAb 3/1-positive, and 11.7% of the overall isolates belonged to the MAb 3/1-negative serogroup 1 subgroups. Monoclonal subtype Philadelphia was the most frequently recognized. Most of the MAb 3/1-negative strains were from nosocomial infections (53.5%), with 27.3% from community-acquired cases and 14.2% from travel-associated cases (Helbig et al., 2002). The proportion of MAb 3/1-negative strains was significantly higher in the Scandinavian region than in Mediterranean countries or the United Kingdom, for both community-acquired and nosocomial cases. 1.5 Virulence and pathogenicity Various studies have shown that the pathogenesis and ecology of Legionella are inherently related. Rowbotham first demonstrated that L. pneumophila could infect amoeba, and characterized the life cycle of Legionella in amoeba (Rowbotham, 1980). Horwitz’s classical experiments demonstrated that L. pneumophila multiplied intracellularly in human macrophages by avoiding phagosome–lysosome fusion (Horwitz, 1983). There are striking similarities in the processes by which legionella infect protozoa and mammalian phagocytic cells (Bozue & Johnson 1996; Horwitz 1984, Garduno et al., 2002). The abilities of Legionella to infect mammalian and protozoan cells are related, using common genes and gene products. 1.5.1 Overview and life-cycle The virulence mechanisms of L. pneumophila are complex and not fully understood. Virulence is an important factor in the ability of L. pneumophila to infect and subsequently multiply within amoebae (Fields et al., 1986; Moffat & Tompkins, 1992). However, some strains with low virulence can multiply within certain host cells (Tully, Williams & Fitzgeorge, 1992). Studies contrasting the role that different virulence factors play in host populations may help to show how the bacteria develop an ability to infect humans, without the need for a protozoan host. <strong>LEGIONELLA</strong> AND THE PREVENTION OF LEGIONELLOSIS
The interaction of virulent legionellae with phagocytic cells can be divided into several steps: • binding of microorganisms to receptors on the surface of eukaryotic cells • penetration of microorganisms into phagocytes • escape from bactericidal attack • formation of a replicative vacuole (a compartment within the cell where bacterial replication occurs) • intracellular multiplication and killing of the host cell. Legionellae have a similar life-cycle within protozoa and human macrophages; however, there are differences in the mechanisms used to enter and exit from the respective host cell types. These differences are summarized in Figure 1.1. Not all of the species of Legionella that have been studied are able to infect macrophages. However, L. pneumophila that possess the relevant virulence factors can infect and replicate within various protozoa found in soil and in water; and by replicating in this way they may become more virulent (Cianciotto, 2001). F gure . L fe-cycle of Legionella pneumophila n protozoa and human macrophages Entry in amoebae: Receptor mediated uptake Requires dot/icm Gal/GalNAc receptor Entry in macrophages: Actin dependent Requires dot/icm Replicative form Fusion with endoplasmic reticulum Source: Fields, Benson & Besser (2002) (Reproduced with permission of authors) <strong>LEGIONELLA</strong> AND THE PREVENTION OF LEGIONELLOSIS Amimo acid depletion ppGpp buildup Stationary phase Gene expression Intracellular motility Release from amoebae: Necrosis – pore formation Release from macrophages: Apoptosis Necrosis – pore formation
Page 1 and 2: LEGIONELLA AND THE PREVENTION OF LE
Page 3 and 4: LEGIONELLA AND THE PREVENTION OF LE
Page 5 and 6: Foreword Legionellosis is a collect
Page 7 and 8: Contents Foreword . . . . . . . . .
Page 9 and 10: Chapter 5 Cooling towers and evapor
Page 11 and 12: Chapter 9 Disease surveillance and
Page 13 and 14: Tables Table 1.1 Main characteristi
Page 15 and 16: Figure 8.1 Visible biofilm on inter
Page 17 and 18: Acknowledgements The World Health O
Page 19 and 20: • John Newbold, Health and Safety
Page 21 and 22: Executive summary Legionellosis is
Page 23 and 24: • Health-care facilities — Chap
Page 25 and 26: Chapter 1 Legionellosis Britt Horne
Page 27 and 28: Legionnaires’ disease is often in
Page 29 and 30: 1.1.2 Pontiac fever Symptoms Pontia
Page 31 and 32: Table . Extrapulmonary nfect ons ca
Page 33 and 34: Proteins produced by the body’s i
Page 35 and 36: Aspiration may occur in patients wi
Page 37 and 38: Table . R sk factors for Legionella
Page 39 and 40: In the outbreak of Legionnaires’
Page 41 and 42: Table . Potent al treatments for d
Page 43 and 44: 1.4.2 Species and serogroups associ
Page 45: Other causes of infection In Europe
Page 49 and 50: 1.5.2 Surface structures involved i
Page 51 and 52: 1.5.4 Host defence The host defence
Page 53 and 54: Chapter 2 Ecology and environmental
Page 55 and 56: L. pneumophila is thermotolerant an
Page 57 and 58: 2.2.3 Environmental factors and vir
Page 59 and 60: Figure 2.1 Biofilm formation Biofil
Page 61 and 62: 2.4 Sources of Legionella infection
Page 63 and 64: Chapter 3 Approaches to risk manage
Page 65 and 66: Table . Cool ng tower outbreaks Fac
Page 67 and 68: Even when a source reaches a state
Page 69 and 70: The WSP should be prepared in conju
Page 71 and 72: Identify control measures Control m
Page 73 and 74: F gure . Dec mal reduct on t mes fo
Page 75 and 76: Method Advantages D sadvantages Dos
Page 77 and 78: Validate effectiveness of water saf
Page 79 and 80: • clear statements of responsibil
Page 81 and 82: Chapter 4 Potable water and in-buil
Page 83 and 84: The remainder of this chapter provi
Page 85 and 86: 4.3.1 Document and describe the sys
Page 87 and 88: Construction materials — risk fac
Page 89 and 90: Where temperature controls (discuss
Page 91 and 92: 4.4.2 Monitor control measures This
Page 93 and 94: Chapter 5 Cooling towers and evapor
Page 95 and 96: 5.1.1 Cross-flow cooling towers As
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water treatments (including chemica
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5.3 System assessment This section
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Spray drift — risk factors Even w
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The section on control measures for
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• periodic or continuous bleed-of
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Box . Po nts to be noted when clean
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In certain circumstances, samples m
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Table . Example documentat on for m
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Chapter 6 Health-care facilities Ma
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For 1999 and 2000, a total of 384 c
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6.3 System assessment This section
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Table . Type of colon zat on of wat
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6.4.1 Identify control measures Thi
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6.5.1 Prepare management procedures
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Until the situation is under contro
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Chapter 7 Hotels and ships Roisin R
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F gure . Detected and reported case
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Table . Rev ew of outbreaks (more t
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7.2 Water safety plan overview WSPs
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The risk of legionellosis is increa
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Kingdom to 66% in Spain (Starlinger
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Agency, Legionella Section, United
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Given the complexity of distributio
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Chapter 8 Natural spas, hot tubs an
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Spas “Natural spa”, denotes fac
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Rare cases of Legionnaires’ disea
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Process step P pework Water n hot t
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Hosepipes may sometimes be used to
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Hot tubs that are not effectively d
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Nutrients — control measures Bath
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Various additives may also be used
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• descriptions of any significant
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Table . Examples of m crob olog cal
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Chapter 9 Disease surveillance and
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Exposure histories allow cases to b
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F gure . Invest gat ng a s ngle cas
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Box . (cont nued) Since the incepti
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Country United Kingdom All reported
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F gure . Annual reported cases, - 0
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Training opportunities Trainees in
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Box . Example of terms of reference
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ecause doing anything more could un
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9.4 Case studies This section descr
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9.4.4 Concrete batcher process on a
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Chapter 10 Regulatory aspects David
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• validation of the effectiveness
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• operating conditions, such as t
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10.4.6 Outbreak investigation and n
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hot water (e.g. health-care facilit
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General prevent on Country DW Wp SB
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Country General prevent on DW Wp SB
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Chapter 11 Laboratory aspects of Le
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• detection of the bacterium in t
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Method Sens t v ty (%) PCR • Rapi
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11.2.2 Detecting Legionella antigen
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DFA has been used successfully with
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• Serologic testing can be used f
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Although not all strains can be rel
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Generally, any water source that ma
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During outbreak investigations, swa
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• other Legionella species that d
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Appendix 1 Example of a water syste
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Weekly water system check list Week
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Appendix 2 Example of a 2-week foll
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Travel Work/travel in the UK: ❑ Y
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Checklist of local places Health/sp
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Appendix 3 Example of a national su
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Strictly Confidential 2 Hospital Ac
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Glossary aerobic bacteria Bacteria
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health-care acquired Legionellosis
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surveillance The process of systema
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References Abu KY, Eisenstein BI, E
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Barbaree JM et al. (1987). Protocol
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Blatt SP et al. (1994). Legionnaire
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Byrne B, Swanson MS (1998). Express
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Crespi S (1993). Legionella y legio
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Edelstein PH (1982b). Comparative s
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Falguera M et al. (2001). Nonsevere
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Gaia V et al. (2003). Sequence-base
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Hayden RT et al. (2001). Direct det
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Ingram JG, Plouffe JF (1994). Dange
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Ko KS et al. (2003). Molecular evol
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Loret JF et al. (2003). Comparison
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McEvoy M et al. (2000). A cluster o
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Olaechea PM et al. (1996). A predic
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Regan CM et al. (2003). Outbreak of
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Schulze-Robbecke R, Rodder M, Exner
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Surman SB, Morton LHG, Keevil CW (1
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Tully M, Williams A, Fitzgeorge RB
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Welti M et al. (2003). Development
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LEGIONELLA - World Health Organization

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