Principles and Practice of Clinical Bacteriology Second Edition - Free

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32 ORAL AND OTHER NON-β-HAEMOLYTIC STREPTOCOCCI Figure 2.4 (Continued). Identification to Species Level The identification of isolates to species level may be carried out using either laboratory-based biochemical test schemes or commercial identification kits with accompanying databases. Although species-level identification of non-β-haemolytic streptococci is not routinely carried out in many clinical laboratories, this may be deemed necessary for suspected pneumococcal infection, isolates obtained from deep-seated abscesses, specimens from endocarditis or where pure cultures have been grown. Differential tests for the identification of non-β-haemolytic streptococci are summarized in Tables 2.9–2.13.
LABORATORY DIAGNOSIS 33 Table 2.8 Differential characteristics of Streptococcus and other Gram-positive, catalase-negative, facultatively anaerobic coccus genera that grow in pairs or chains Genus Pyrrolidonyl arylamidase Leucine aminopeptidase production 6.5% NaCl BE Growth at Susceptibility to vancomycin 10 °C 45°C Haemolysis Streptococcus a − + − b − c − V S α, β, γ Enterococcus d + + + + + + S e α, β, γ Lactococcus + + V + + − f S α, γ Vagococcus d + + + + + − S α, γ Globicatella + − + − − − S α Leuconostoc g − − V V + V R α, γ BE, reaction on bile–aesculin medium. +, ≥95% of strains are positive; –, ≥5% of strains are negative; V, variable reaction; R, resistant; S, susceptible. a Abiotrophia and Granulicatella (formerly nutritionally variant streptococci strains) are weakly pyrrolidonyl arylamidase and leucine aminopeptidase production positive and grow in 6.5% NaCl broth. Some group A streptococci are pyrrolidonyl arylamidase positive. b Some β-haemolytic streptococci grow in 6.5% NaCl broth. c 5–10% of viridans streptococci are bile–aesculin positive. d Some enterococci are motile; Vagococcus is motile (formerly called group N streptococci). e Some strains are vancomycin resistant. f Some strains grow very slowly at 45 °C. g Gas is produced by Leuconostoc from glucose in Mann, Rogosa, Sharpe (MRS) Lactobacillus broth. Table 2.9 Differential biochemical characteristics of the anginosus group We do not have permission to reproduce the table electronically The rapid and extensive taxonomic revision of the genus Streptococcus, including the demonstration of several new species and amended descriptions of others, has, to some extent, outpaced the availability of comprehensive schemes for routine identification. However, significant improvements to this situation have come about through the incorporation of fluorogenic and chromogenic substrates into identification schemes for the rapid detection of preformed enzyme activities. These test schemes combine tests for the detection of glycosidase and arylamidase reactions with more traditional tests that detect carbohydrate fermentation, arginine dihydrolase and acetone production. A further development has been the inclusion of these tests in a more standardized format in some commercially available test kits, which helps reduce the degree of discrepancy between biochemical test results from different laboratories. Currently, a 32 Test Kit for identifying streptococci is available, which takes into account most of the currently recognized species (Rapid ID32 Strep system; bioMérieux Vitek, bioMérieux, Durham, NC, USA). In an independent evaluation the kit gave correct identification for 95.3% (413/433) of strains examined, including 109 strains that required some additional tests for complete identification. Sixteen strains remained unidentified and four were misidentified (Freney et al., 1992). In another study the test kit gave correct identification for 87% of strains examined. However, S. mitis and S. oralis were not easily differentiated using this method (Kikuchi et al., 1995). Other phenotypic markers that have been reported to be potentially useful, particularly for the oral streptococci, include acid and alkaline phosphatases, neuraminidase (sialidase), IgA1 protease production, salivary amylase binding, extracellular polysaccharide production and the detection of hyaluronidase and chondroitin sulphate depolymerase activities. Several other approaches to species identification have been investigated such as pyrolysis–mass spectrometry, whole-cell–derived polypeptide patterns by sodium dodecyl sulphate–polyacrylamide gel electrophoresis (SDS-PAGE) or other electrophoretic separation techniques and the analyses of long-chain fatty acids and cell-wall components. However, these strategies have not been widely adopted and remain a part of the repertoire of the specialist research laboratory. Significant progress has been already made in developing geneticbased approaches to species identification. DNA probes for this purpose have been described that utilize whole chromosomal preparations or cloned DNA fragments. However, as with most other groups of bacteria, by far the greatest promise for a genetically based identification approach lies in the analysis of nucleotide sequence data derived from the 16S rRNA gene. Published studies have provided 16S rRNA gene sequence data for most, but not all, non-β-haemolytic streptococci, which have been found to be distinct for each of the species so far examined (Bentley, Leigh and Collins, 1991; Kawamura etal., 1995a). Other approaches have been described including restriction fragment length polymorphism (RFLP) analysis of amplicons of 16S–23S rDNA and intergenic spacer regions (Rudney and Larson, 1993; Schlegel et al., 2003b) or tDNA intergenic spacer regions (De Gheldre etal., 1999) and PCR amplification and sequence analysis of the gene encoding manganese-dependent superoxide dismutase (Poyart, Quesne and Trieu-Cuot, 1998). Serology The success obtained in producing a serological classification for the pyogenic streptococci was not extended to the non-β-haemolytic species. Several early attempts to this end were unsatisfactory and failed to produce an all-encompassing scheme for these streptococci.
Page 1: Principles and Practice of Clinical
Page 5 and 6: Principles and Practice of Clinical
Page 7 and 8: Contents List of Contributors Prefa
Page 9 and 10: List of Contributors Dlawer A. A. A
Page 11: Preface Change is inevitable and no
Page 15 and 16: 1 β-Haemolytic Streptococci Androu
Page 17 and 18: PATHOGENESIS AND VIRULENCE FACTORS
Page 19 and 20: EPIDEMIOLOGY OF β-HAEMOLYTIC STREP
Page 21 and 22: CLINICAL ASPECTS OF β-HAEMOLYTIC S
Page 23 and 24: LABORATORY DIAGNOSIS AND IDENTIFICA
Page 25 and 26: LABORATORY DIAGNOSIS AND IDENTIFICA
Page 27 and 28: PREVENTION AND CONTROL 15 and nonin
Page 29 and 30: REFERENCES 17 Courvalin PM, Carlier
Page 31 and 32: REFERENCES 19 Nelson D, Loomis L, F
Page 33 and 34: 2 Oral and Other Non-b-Haemolytic S
Page 35 and 36: INFECTIONS CAUSED BY NON-β-HAEMOLY
Page 43: LABORATORY DIAGNOSIS 31 Figure 2.4
Page 47 and 48: ANTIBIOTIC SUSCEPTIBILITY 35 Table
Page 49 and 50: REFERENCES 37 Billington, S.J., Jos
Page 51: REFERENCES 39 Streptococcus bovis b
Page 54 and 55: 42 STREPTOCOCCUS PNEUMONIAE infecti
Page 56 and 57: 44 STREPTOCOCCUS PNEUMONIAE virulen
Page 58 and 59: 46 STREPTOCOCCUS PNEUMONIAE togethe
Page 60 and 61: 48 STREPTOCOCCUS PNEUMONIAE and it
Page 62 and 63: 50 STREPTOCOCCUS PNEUMONIAE of resi
Page 64 and 65: 52 STREPTOCOCCUS PNEUMONIAE more se
Page 66 and 67: 54 STREPTOCOCCUS PNEUMONIAE Contrai
Page 68 and 69: 56 STREPTOCOCCUS PNEUMONIAE Nuermbe
Page 71 and 72: 4 Enterococcus spp. Esteban C. Nann
Page 73 and 74: CLINICAL INFECTIONS 61 Another fact
Page 75 and 76: LABORATORY DIAGNOSIS 63 Table 4.2 T
Page 77 and 78: MECHANISMS OF RESISTANCE TO ANTIMIC
Page 79 and 80: MANAGEMENT OF ENTEROCOCCAL INFECTIO
Page 81 and 82: REFERENCES 69 VRE-positive patients
Page 83: REFERENCES 71 Paulsen, I. T., Baner
Page 86 and 87: 74 STAPHYLOCOCCUS AUREUS gentamicin
Page 88 and 89: 76 STAPHYLOCOCCUS AUREUS Table 5.2
Page 90 and 91: 78 Table 5.3 Antibiotic resistance
Page 92 and 93: 80 STAPHYLOCOCCUS AUREUS of peptido
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82 STAPHYLOCOCCUS AUREUS newborn in
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84 STAPHYLOCOCCUS AUREUS Bone and J
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86 STAPHYLOCOCCUS AUREUS A wide ran
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88 STAPHYLOCOCCUS AUREUS guidelines
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90 STAPHYLOCOCCUS AUREUS Boelaert,
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92 STAPHYLOCOCCUS AUREUS Haggar, A.
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94 STAPHYLOCOCCUS AUREUS Massey, R.
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96 STAPHYLOCOCCUS AUREUS Ross, J.I.
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98 STAPHYLOCOCCUS AUREUS Weisblum,
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100 Table 6.2 Laboratory characteri
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102 COAGULASE-NEGATIVE STAPHYLOCOCC
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Section Two Gram-Positive Bacilli
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116 CORYNEBACTERIUM SPP. The genus
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% DTP3 coverage 118 CORYNEBACTERIUM
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120 CORYNEBACTERIUM SPP. the absenc
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122 CORYNEBACTERIUM SPP. Table 7.2
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124 CORYNEBACTERIUM SPP. yellowish
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126 CORYNEBACTERIUM SPP. Colman, G.
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128 CORYNEBACTERIUM SPP. Schmitt, M
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130 LISTERIA AND ERYSIPELOTHRIX SPP
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140 BACILLUS SPP. AND RELATED GENER
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160 MYCOBACTERIUM TUBERCULOSIS they
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162 MYCOBACTERIUM TUBERCULOSIS The
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164 MYCOBACTERIUM TUBERCULOSIS An i
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166 MYCOBACTERIUM TUBERCULOSIS trea
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168 MYCOBACTERIUM TUBERCULOSIS Hobb
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11 Non-Tuberculosis Mycobacteria St
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MYCOBACTERIUM AVIUM-INTRACELLULARE
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MYCOBACTERIUM XENOPI 175 et al. 198
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RAPID GROWING MYCOBACTERIA 177 laye
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REFERENCES 179 OTHER NON-TUBERCULOS
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REFERENCES 181 Tunkel, D. E. and Ro
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184 AEROBIC ACTINOMYCETES and treha
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186 AEROBIC ACTINOMYCETES Sabouraud
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188 AEROBIC ACTINOMYCETES Georghiou
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13 Moraxella catarrhalis and Kingel
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KINGELLA KINGAE-MEDIATED DISEASES I
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ANTIMICROBIAL SUSCEPTIBILITY 195 la
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IMMUNITY 197 VIRULENCE In general,
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REFERENCES 199 Ahmed, K., Rikitomi,
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REFERENCES 201 Hager, H., Verghese,
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REFERENCES 203 Samukawa, T., Yamana
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14 Neisseria meningitidis Dlawer A.
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THE CELL ENVELOPE: ANATOMY, HETEROG
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PATHOGENESIS 209 a sialyl donor. LO
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CLINICAL MANIFESTATIONS 211 The Sou
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LABORATORY DIAGNOSIS 213 poor progn
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MANAGEMENT 215 recommended for empi
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PREVENTION AND CONTROL 217 incorpor
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REFERENCES 219 Caugant, D.A., Froho
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15 Neisseria gonorrhoeae Catherine
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LABORATORY DIAGNOSIS 223 predominan
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LABORATORY DIAGNOSIS 225 In an atte
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MANAGEMENT OF INFECTION 227 region
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REFERENCES 229 Fenton, K.A., Ison,
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16 Acinetobacter spp. Peter Hawkey
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ACINETOBACTER 233 have identified m
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CLINICAL FEATURES OF ACINETOBACTER
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TREATMENT 237 reported in the medic
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CHRYSEOBACTERIUM (PREVIOUSLY FLAVOB
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REFERENCES 241 ofloxacin) (Mensah,
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REFERENCES 243 Husni RN, Goldstein
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17 Haemophilus spp. Derrick W. Croo
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EPIDEMIOLOGY 247 routinely used in
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PREVENTION AND CONTROL 249 flaring
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REFERENCES 251 Peltola, H. (2000) W
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254 BORDETELLA SPP. Table 18.2 Viru
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256 BORDETELLA SPP. superfamily and
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258 BORDETELLA SPP. diagnosis of pe
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260 BORDETELLA SPP. vaccines (Edwar
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262 BORDETELLA SPP. Gordon, J.E. an
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264 BORDETELLA SPP. Schaeffer, L.M.
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266 BRUCELLA SPP. Table 19.2 Charac
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268 BRUCELLA SPP. Periplasmic Prote
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270 BRUCELLA SPP. Although no singl
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20 Actinobacillus actinomycetemcomi
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PATHOGENICITY 275 flp-1 flp-2 orfB
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TREATMENT AND MANAGEMENT 277 presen
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REFERENCES 279 Lepine, G., Caudry,
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282 FRANCISELLA TULARENSIS similar
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284 FRANCISELLA TULARENSIS Saslaw,
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286 RICKETTSIA SPP. that manifest t
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288 RICKETTSIA SPP. develop into sh
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290 RICKETTSIA SPP. onto sheep or h
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292 RICKETTSIA SPP. the specific de
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294 RICKETTSIA SPP. Olson, J. G., B
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296 BARTONELLA SPP. Table 23.1 Spec
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298 BARTONELLA SPP. The term quinta
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300 BARTONELLA SPP. study showing t
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302 BARTONELLA SPP. Fournier PE, Ma
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304 BARTONELLA SPP. Spaulding WB, H
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306 MYCOPLASMA SPP. described rarel
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308 MYCOPLASMA SPP. Genital Mycopla
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310 MYCOPLASMA SPP. Specimens Speci
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312 MYCOPLASMA SPP. antigens in com
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314 MYCOPLASMA SPP. Macrolides are
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25 Chlamydia spp. and Related Organ
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DESCRIPTION OF THE ORGANISM 319 C.
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CLINICAL FEATURES 321 leave shallow
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LABORATORY DIAGNOSIS 323 aetiologic
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MANAGEMENT 325 some merit in screen
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REFERENCES 327 Chlamydia trachomati
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26 Tropheryma whipplei F. Fenollar
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DESCRIPTION OF THE ORGANISM 331 81
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IMMUNOLOGY AND PATHOLOGY 333 EPIDEM
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DIAGNOSIS 335 The manifestations co
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REFERENCES 337 Serology The recent
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REFERENCES 339 Lepidi, H., Costedoa
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27 Identification of Enterobacteria
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343 Table 27.3 Biochemical reaction
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REFERENCES 345 Bacterial identifica
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348 ESCHERICHIA COLI AND SHIGELLA S
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29 Salmonella spp. Claire Jenkins 1
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EPIDEMIOLOGY 369 Lab reports (1000s
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LABORATORY DIAGNOSIS 371 complicati
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PREVENTION AND CONTROL 373 two prob
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REFERENCES 375 Duthie, R. and Frenc
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30 Klebsiella, Citrobacter, Enterob
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PATHOGENICITY 379 Capsule A key cha
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PATHOGENESIS 381 Pneumonia due to K
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EPIDEMIOLOGY AND INFECTIONS 383 pro
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REFERENCES 385 Cooke, E.M., Sazegar
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31 Donovanosis and Klebsiella spp.
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REFERENCES 389 Kharsany, A.B., Hoos
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392 PROTEUS, PROVIDENCIA AND MORGAN
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398 YERSINIA SPP. infected. Yersini
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400 YERSINIA SPP. Figure 33.2 The n
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402 YERSINIA SPP. fever is a childh
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404 YERSINIA SPP. REFERENCES Abdel-
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406 YERSINIA SPP. Wauters, G., Kand
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408 VIBRIO SPP. Genus Definition Th
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410 VIBRIO SPP. Heat-shock reaction
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412 VIBRIO SPP. It has long been as
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414 VIBRIO SPP. Most of the strains
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416 VIBRIO SPP. produced by the met
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35 Aeromonas and Plesiomonas spp. A
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CLINICAL FEATURES 421 O-antigen LPS
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LABORATORY DIAGNOSIS 423 spp., have
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REFERENCES 425 can also produce chr
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36 Pseudomonas and Burkholderia spp
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PATHOGENICITY 429 organism from the
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INFECTIONS DUE TO P. AERUGINOSA 431
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ANTIBIOTIC RESISTANCE AND THERAPY 4
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EPIDEMIOLOGY 435 P. aeruginosa. Var
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PATHOGENESIS AND INFECTION 437 type
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ANTIBIOTIC SUSCEPTIBILITY AND TREAT
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REFERENCES 441 specimens from CF pa
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REFERENCES 443 therapy for sepsis i
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446 LEGIONELLA SPP. Table 37.1 Legi
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448 LEGIONELLA SPP. numerous other
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450 LEGIONELLA SPP. DIAGNOSTIC METH
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452 LEGIONELLA SPP. antigens such a
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454 LEGIONELLA SPP. Dournon, E. (19
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456 LEGIONELLA SPP. Petitjean, F.,
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458 COXIELLA BURNETII been reported
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460 COXIELLA BURNETII Laughlin, T.,
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39 Leptospira spp. P. N. Levett Sas
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CLINICAL FEATURES 465 only the most
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MANAGEMENT 467 Molecular Typing Pul
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REFERENCES 469 CONTROL Control and
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REFERENCES 471 World Health Organiz
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474 HELICOBACTER SPP. AND RELATED O
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41 Campylobacter and Arcobacter spp
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PROPERTIES OF THE FAMILY CAMPYLOBAC
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ANIMAL PATHOGENS AND COMMENSAL CAMP
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THE GENUS ARCOBACTER 495 Table 41.4
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REFERENCES 497 at the CDC it was co
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REFERENCES 499 Karmali, M.A., Skirr
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REFERENCES 501 conservative re-trea
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42 Treponemes Andrew J. L. Turner M
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EPIDEMIOLOGY 505 thought to be a su
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LABORATORY DIAGNOSIS 507 Oral Trepo
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REFERENCES 509 provision of accessi
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43 Borrelia spp. Sudha Pabbatireddy
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CLINICAL MANIFESTATIONS 513 The inf
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CLINICAL MANIFESTATIONS 515 IgM ant
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DIAGNOSIS 517 and myalgias (Asch et
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TREATMENT 519 et al., 1993). Agger
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REFERENCES 521 Agger WA and Case KL
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REFERENCES 523 Kristoferitsch W, Sl
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REFERENCES 525 van der Linde MR (19
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44 Anaerobic Cocci D. A. Murdoch De
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GRAM-POSITIVE ANAEROBIC COCCI (GPAC
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GRAM-NEGATIVE ANAEROBIC COCCI 537 m
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REFERENCES 539 Genovese A, Bouvet J
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45 Non-Sporing Gram-Negative Anaero
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DESCRIPTION OF THE ORGANISMS 543 ar
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NORMAL HUMAN MICROBIOTA 545 host’
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CLINICAL FEATURES OF ANAEROBIC INFE
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LABORATORY DIAGNOSES 549 Epstein-Ba
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551 Table 45.6 Identification of Ba
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MANAGEMENT OF ANAEROBIC INFECTIONS
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REFERENCES 555 Curtis MA, Aduse-Opo
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46 Clostridium difficile Mark H. Wi
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EPIDEMIOLOGY 559 carriers, and yet
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LABORATORY DIAGNOSIS 561 C. diffici
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PREVENTION AND CONTROL 563 boulardi
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REFERENCES 565 Johnson S, Gerding D
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47 Other Clostridium spp. Ian R. Po
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CLOSTRIDIUM PERFRINGENS 569 GENERAL
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NEUROTOXIC CLOSTRIDIA 571 Laborator
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REFERENCES 573 reported in IDUs in
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48 Anaerobic Actinomycetes and Rela
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PATHOGENESIS 577 develop very slowl
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LABORATORY DIAGNOSIS 579 The most c
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LABORATORY DIAGNOSIS 581 However, o
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LABORATORY DIAGNOSIS 583 Commercial
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REFERENCES 585 REFERENCES Barsotti
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Index Abiotrophia 60 Abiotrophia ad
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INDEX 589 natural epidemics 147 nor
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INDEX 591 Cefoxitin in GPAC 536 in
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INDEX 593 Coxiella burnetii 457-9 a
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INDEX 595 modifications 534 musculo
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INDEX 597 direct detection in clini
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INDEX 599 natural immunity 216 Opa
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INDEX 605 histological diagnosis 33
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602 INDEX Sexually transmitted infe
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604 INDEX Toxin-coregulated pilus (
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