Principles and Practice of Clinical Bacteriology Second Edition - Free

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10 β-HAEMOLYTIC STREPTOCOCCI Table 1.5 Clinical syndrome of STSS (from Working Group on Severe Streptococcal Infections 1993) Symptoms Renal impairment (raised creatinine) Coagulopathy or low platelets Liver dysfunction (raised transaminases) Respiratory failure/hypoxaemia Erythematous rash (which desquamates) Soft-tissue necrosis Identification of a GAS from a normally sterile site (definite case) or Identification of a GAS from a nonsterile site (probable case) and Systolic blood pressure
LABORATORY DIAGNOSIS AND IDENTIFICATION 11 childbearing age, adult and childhood infection is more common in males than females (HPA 2003b). Immunologically Mediated Disease: Nonsuppurative Sequelae of β-Haemolytic Streptococcal Disease In addition to toxin-mediated complications, such as scarlet fever and STSS, GAS infection can also be complicated by defined postinfectious sequelae. Although the aetiology of these heterogeneous conditions is poorly understood, it is likely that some, if not all, result from cross-reactive T- and B-cell epitopes shared by streptococcal cell wall and human matrix protein antigens. It is also possible that bacterial superantigens drive some of these conditions in susceptible individuals. A full description of all these conditions is beyond the scope of this chapter. The references in Table 1.6 provide good overviews of each subject. Rheumatic Fever RF affects 1–4% of children with untreated streptococcal pharyngitis and is a major cause worldwide of acquired cardiovascular disease, with an incidence of 100–200 per 100 000 children in countries where RF is endemic (Guilherme et al. 2000; Olivier 2000). Although the incidence of RF in developed countries is usually low (1–2 per 100 000), the disease occurs with marked frequency amongst the economically deprived native communities of New Zealand and Australia. RF can also cause outbreaks in affluent communities: an eightfold increase in RF incidence occurred across Utah and other states within the United States in the late 1980s, leading to carditis in over 90% of cases (Veasy et al. 1987; Bisno 1991). Rheumatic heart disease follows acute RF in 30–50% of cases (Majeed et al. 1992; Guilherme et al. 2000). The so-called rheumatogenic S. pyogenes serotypes have been associated with outbreaks of RF (M1 and M18 in the United States and M1, M3 and M5 in the United Kingdom), although RF can be associated with a broad range of strains. Epidemiological study is hampered because isolates are rarely available for typing (Veasy et al. 1987; Colman et al. 1993). Study of the pathogenesis of RF has focused on the role of streptococcal M protein. Cases with arthritis not meeting the acknowledged criteria for RF are often designated as poststreptococcal reactive arthritis. Here, the risk of cardiac involvement appears low (Shulman and Ayoub 2002). The diagnosis of RF requires clinical recognition of a collection of signs coupled with laboratory evidence of recent streptococcal infection (Table 1.7). Although numerous cases suggest that acute RF follows GAS infection of the skin, best-documented cases and outbreaks have followed episodes of pharyngitis. Table 1.6 Spectrum of poststreptococcal immunologically mediated disease Recognised poststreptococcal sequelae Rheumatic fever Sydenham’s chorea Poststreptococcal reactive arthritis Glomerulonephritis Guttate psoriasis Proposed poststreptococcal sequelae PANDAS Kawasaki disease PANDAS, paediatric autoimmune disorders associated with streptococcal infections, overlap with chorea and tic disorders. For reviews on Sydenham’s chorea and PANDAS, see Snider and Swedo (2003), Simckes and Spitzer (1995) and Shulman and Ayoub (2002). For reviews on guttate psoriasis, see Valdimarsson et al. (1995). For reviews on Kawasaki disease, see Curtis et al. (1995). Table 1.7 Revised Jones Criteria for diagnosing acute rheumatic fever (Adapted from American Heart Association 1992) Major Carditis Polyarthritis Erythema marginatum Chorea Subcutaneous nodules Minor Arthralgia Fever Prolonged PR interval Raised C-reactive protein/erythrocyte sedimentation rate Evidence of recent streptococcal throat infection plus One major and two minor criteria or Two major criteria It is difficult to predict how RF may evolve in the coming years. It is not clear whether the epidemic outbreaks or the observed rare cases are aberrations in the generally declining profile currently observed in developed countries or whether there is a true risk of resurgence of the disease. Consequently, accurate identification of GAS pharyngitis and follow-up of rheumatogenic strains with their appropriate treatment are still important (Olivier 2000). LABORATORY DIAGNOSIS AND IDENTIFICATION Serological grouping provides the first precise method for identifying the β-haemolytic streptococci, in particular the human pathogens of Lancefield groups A, B, C and G. The main characteristics of these β-haemolytic streptococci are summarised in Table 1.8. Isolates from primary culture are traditionally identified by colony morphology, Gram stain, catalase test and Lancefield grouping. If Lancefield grouping does not provide sufficient identification, full biochemical identification may be obtained usually using a commercial identification system. Streptococcus pyogenes is identified in a diagnostic laboratory from its polysaccharide group A antigen, using commercial grouping systems. Presumptive identification is usually made by bacitracin susceptibility or pyrrolidonylarylamidase activity. Streptococcus pyogenes is the only species within the genus that is positive for both tests (Facklam 2002). Streptococcus agalactiae is the most common cause of neonatal sepsis and is the only species that carries the Lancefield group B antigen. Lancefield grouping usually identifies the organism, but the organism can also be identified presumptively by the CAMP test and hippurate hydrolysis. Streptococcus dysgalactiae subsp. equisimilis is the revised taxonomic species for the human streptococci of Lancefield group C (S. equisimilis) and group G (nameless). Detection of the group antigen in combination with the phenotypic characteristics will subdivide these organisms into the appropriate species (Table 1.8). Studies have also revealed that strains of Lancefield group L should also be included within this species. To complicate this even further some strains of S. dysgalactiae subsp. equisimilis possess the group A antigen. Therefore, the group antigen can only be used as an aid in species identification. The phenotypic tests listed in Table 1.8 should be used, together with the haemolytic reaction and group antigen, to identify the species. Streptococcus equi subsp. equi is the classic cause of strangles in horses. Identification of the species is again based upon the phenotypic test reactions and demonstration of the group C antigen. Streptococcus equi subsp. zooepidemicus is usually identified according to Lancefield group and phenotypic profile. The animal pathogen S. canis carries
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: CLINICAL ASPECTS OF β-HAEMOLYTIC S
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 and 44: LABORATORY DIAGNOSIS 31 Figure 2.4
Page 45 and 46: LABORATORY DIAGNOSIS 33 Table 2.8 D
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
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CLINICAL INFECTIONS 61 Another fact
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LABORATORY DIAGNOSIS 63 Table 4.2 T
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MECHANISMS OF RESISTANCE TO ANTIMIC
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MANAGEMENT OF ENTEROCOCCAL INFECTIO
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REFERENCES 69 VRE-positive patients
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REFERENCES 71 Paulsen, I. T., Baner
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74 STAPHYLOCOCCUS AUREUS gentamicin
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76 STAPHYLOCOCCUS AUREUS Table 5.2
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78 Table 5.3 Antibiotic resistance
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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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