
Hot Topics in Infection and Immunity in Children VII
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Content
2 - Acknowledgments [Seite 5]
3 - Contents [Seite 6]
4 - Contributors [Seite 8]
5 - The Value of Vaccination [Seite 12]
5.1 - 1 Population Health and Economic Well-Being [Seite 12]
5.2 - 2 A New Paradigm for the Value of Vaccination [Seite 16]
5.3 - 3 Applications of the New Approach [Seite 17]
5.4 - 4 Two Calls to Action [Seite 18]
6 - References [Seite 19]
7 - Recent Trends in Global Immunisation [Seite 20]
7.1 - 1 Introduction [Seite 20]
7.2 - 2 Official Development Assistance at the Global Level [Seite 20]
7.3 - 3 Health Progress is Possible [Seite 21]
7.4 - 4 The GAVI Alliance, Formerly the Global Alliance for Vaccines and Immunisation [Seite 22]
7.5 - 5 Polio Eradication Still Somewhat Problematic [Seite 23]
7.6 - 6 Recent Developments in Malaria [Seite 23]
7.7 - 7 HIV/AIDS Vaccine A Long Way to Go [Seite 24]
7.8 - 8 Measles Remains a Threat [Seite 25]
7.9 - 9 Anti-Vaccine Activists are a Real Danger [Seite 25]
7.10 - 10 Conclusion [Seite 26]
8 - References [Seite 27]
9 - New Advances in Typhoid Fever Vaccination Strategies [Seite 28]
9.1 - 1 Introduction [Seite 28]
9.2 - 2 Typhoid Fever Epidemiology [Seite 29]
9.3 - 3 Typhoid Fever: Clinical Presentation and Outcome [Seite 30]
9.3.1 - 3.1 Diagnosis [Seite 31]
9.3.2 - 3.2 Management [Seite 32]
9.4 - 4 Control Strategies [Seite 32]
9.4.1 - 4.1 Antimicrobial Resistance [Seite 33]
9.4.2 - 4.2 Vaccination [Seite 34]
9.4.2.1 - 4.2.1 Ty21a [Seite 36]
9.4.2.2 - 4.2.2 Vi Capsular Polysaccharide [Seite 38]
9.4.2.3 - 4.2.3 New Vaccines in Pipeline [Seite 38]
9.4.3 - 4.3 Perceived Risk of Disease and Vaccination Acceptance [Seite 40]
9.4.4 - 4.4 The Market (Vaccine Demand and Supply) [Seite 40]
9.4.4.1 - 4.4.1 Vaccination Strategies [Seite 41]
9.4.4.2 - 4.4.2 Determining Endemicity [Seite 42]
9.5 - 5 Population Impact [Seite 42]
9.5.1 - 5.1 Guangxi Province, China [Seite 42]
9.5.2 - 5.2 National Immunization Program, Vietnam [Seite 43]
9.5.3 - 5.3 Delhi State, India [Seite 44]
9.5.4 - 5.4 Disease of Most Impoverished (DOMI) Studies in South and SouthEast Asia [Seite 44]
9.6 - 6 Conclusion [Seite 46]
10 - References [Seite 46]
11 - Prevention of Vertical Transmission of HIVin Resource-Limited Countries [Seite 51]
11.1 - 1 Introduction Global Status of Efforts to Prevent Vertical Transmission of HIV [Seite 51]
11.2 - 2 Program Experience [Seite 52]
11.2.1 - 2.1 Thailand and Botswana National Programs [Seite 52]
11.2.1.1 - 2.1.1 Thailand [Seite 52]
11.2.1.2 - 2.1.2 Botswana [Seite 53]
11.2.2 - 2.2 Elizabeth Glaser Pediatric AIDS Foundation Program and Experience [Seite 53]
11.3 - 3 Lessons Learned [Seite 56]
11.3.1 - 3.1 Counseling [Seite 56]
11.3.2 - 3.2 Testing [Seite 56]
11.3.3 - 3.3 ARV Prophylaxis [Seite 56]
11.3.4 - 3.4 Uptake of Maternal and Infant Prophylaxis [Seite 57]
11.3.5 - 3.5 HIV Testing in Labor and Delivery [Seite 58]
11.4 - 4 Modeling Service Coverage [Seite 58]
11.4.1 - 4.1 2000--2002 [Seite 60]
11.4.2 - 4.2 2003--2005 [Seite 60]
11.4.3 - 4.3 2006--2008 [Seite 61]
11.5 - 5 Effectiveness of Prevention of Vertical Transmission Programs: The PEARL Study [Seite 61]
11.6 - 6 Importance of Identifying Pregnant Women Eligible for ART [Seite 62]
11.7 - 7 Prevention of Vertical Transmission During Breastfeeding [Seite 63]
11.8 - 8 Conclusion [Seite 65]
12 - References [Seite 65]
13 - Pneumonia in Children in Developing Countries [Seite 68]
13.1 - 1 Introduction [Seite 68]
13.2 - 2 Aetiology [Seite 68]
13.3 - 3 Standard Management [Seite 69]
13.4 - 4 Which Children Need an Antibiotic [Seite 70]
13.5 - 5 Which Children Need Admission [Seite 71]
13.6 - 6 Which Children Have Very Severe Pneumonia [Seite 71]
13.7 - 7 Which Antibiotic for Outpatients With Non-severe Pneumonia [Seite 72]
13.8 - 8 Which Antibiotics for Severe Pneumonia [Seite 73]
13.9 - 9 Which Antibiotics for Very Severe Pneumonia [Seite 74]
13.10 - 10 Oxygen Therapy [Seite 75]
13.11 - 11 Fluid Therapy [Seite 75]
13.12 - 12 Fever [Seite 75]
13.13 - 13 Neonates, Malnutrition and HIV [Seite 76]
13.14 - 14 Overall Effect of Case Management [Seite 76]
13.15 - 15 Immunisation [Seite 76]
13.16 - 16 Conclusion [Seite 77]
14 - References [Seite 80]
15 - Darwin, Microbes and Evolution by Natural Selection [Seite 85]
15.1 - 1 Darwin, Microbes and Evolution by Natural Selection [Seite 85]
15.2 - Box 1 [Seite 92]
16 - References [Seite 93]
17 - Human Herpesvirus 6 [Seite 95]
18 - References [Seite 98]
19 - Advances in the Diagnosis and Management of Central Venous Access Device Infections in Children [Seite 99]
19.1 - 1 Introduction [Seite 99]
19.2 - 2 Types of Devices Used in Children for Central Venous Access [Seite 100]
19.2.1 - 2.1 Temporary CVAD [Seite 100]
19.2.2 - 2.2 Permanent, Tunnelled CVAD [Seite 100]
19.3 - 3 Pathogenesis [Seite 101]
19.3.1 - 3.1 Common Organisms [Seite 101]
19.4 - 4 Epidemiology [Seite 102]
19.5 - 5 Diagnosis [Seite 103]
19.6 - 6 Prevention [Seite 104]
19.7 - 7 Management [Seite 105]
19.7.1 - 7.1 Antimicrobial Therapy [Seite 105]
19.7.2 - 7.2 New Strategies [Seite 106]
19.8 - 8 Antimicrobial Lock Therapy (ALT) [Seite 106]
19.9 - 9 Ethanol Locks [Seite 107]
19.10 - 10 Hydrochloric Acid Locks [Seite 107]
19.11 - 11 Taurolidine Citrate Locks (TauroLock) [Seite 109]
19.12 - 12 Urokinase Locks and Infusions [Seite 109]
19.13 - 13 Conclusions [Seite 109]
20 - References [Seite 110]
21 - Moraxella catarrhalis -- Pathogen or Commensal? [Seite 115]
21.1 - 1 Introduction [Seite 116]
21.2 - 2 Phylogenetic Evidence for Virulence [Seite 116]
21.3 - 3 Expression of Virulence Factors [Seite 117]
21.3.1 - 3.1 Complement Resistance [Seite 117]
21.3.2 - 3.2 Adherence to Human Epithelial Cells [Seite 117]
21.3.3 - 3.3 Colonization and Immune Response [Seite 118]
21.3.4 - 3.4 Biofilm Formation [Seite 119]
21.3.5 - 3.5 Cellular Invasion [Seite 120]
21.3.6 - 3.6 Proinflammatory Activity of Moraxella catarrhalis [Seite 120]
21.4 - 4 Cold Shock Response of Moraxella catarrhalis [Seite 120]
21.5 - 5 Summary [Seite 122]
22 - References [Seite 122]
23 - Anaerobic Infections in Children [Seite 125]
23.1 - 1 Introduction [Seite 125]
23.2 - 2 Microbiology [Seite 126]
23.2.1 - 2.1 Gram-Positive Spore-Forming Bacilli [Seite 126]
23.2.2 - 2.2 Gram-Positive Non-Spore-Forming Bacilli [Seite 128]
23.2.3 - 2.3 Gram-Negative Bacilli [Seite 129]
23.2.4 - 2.4 Gram-Positive Cocci [Seite 130]
23.2.5 - 2.5 Gram-Negative Cocci [Seite 130]
23.3 - 3 Pathogenicity and Virulence [Seite 130]
23.3.1 - 3.1 Anaerobes as Normal Flora [Seite 130]
23.3.2 - 3.2 Conditions Predisposing to Anaerobic Infection [Seite 132]
23.3.3 - 3.3 Virulence Factors [Seite 134]
23.4 - 4 Diagnostic Microbiology [Seite 134]
23.4.1 - 4.1 Collection of Specimens for Anaerobic Bacteria [Seite 134]
23.4.2 - 4.2 Transportation of Specimens [Seite 136]
23.4.3 - 4.3 Laboratory Diagnosis [Seite 136]
23.4.4 - 4.4 Antimicrobial Susceptibility Testing [Seite 137]
23.5 - 5 Prevention [Seite 137]
23.6 - 6 Clinical Infections [Seite 138]
23.6.1 - 6.1 Central Nervous System Infections [Seite 138]
23.6.2 - 6.2 Head and Neck Infections [Seite 139]
23.6.2.1 - 6.2.1 Sinusitis [Seite 141]
23.6.2.2 - 6.2.2 Parotitis [Seite 141]
23.6.2.3 - 6.2.3 Cervical Lymphadenitis [Seite 141]
23.6.2.4 - 6.2.4 Thyroiditis [Seite 142]
23.6.2.5 - 6.2.5 Infected Cysts [Seite 142]
23.6.2.6 - 6.2.6 Wound Infection After Head and Neck Surgery [Seite 142]
23.6.2.7 - 6.2.7 Tonsillitis [Seite 142]
23.6.3 - 6.3 Pleuropulmonary Infections [Seite 143]
23.6.4 - 6.4 Intra-Abdominal Infections [Seite 145]
23.6.5 - 6.5 Female Genital Tract Infection [Seite 146]
23.6.6 - 6.6 Skin and Soft Tissue Infections [Seite 146]
23.6.7 - 6.7 Osteomyelitis and Septic Arthritis [Seite 147]
23.6.8 - 6.8 Bacteremia [Seite 148]
23.6.9 - 6.9 Neonatal Infection [Seite 148]
23.7 - 7 Management [Seite 149]
23.7.1 - 7.1 Hyperbaric Oxygen [Seite 149]
23.7.2 - 7.2 Surgical Therapy [Seite 149]
23.7.3 - 7.3 Antimicrobial Therapy [Seite 150]
23.7.4 - 7.4 Antimicrobial Agents [Seite 153]
23.7.4.1 - 7.4.1 Penicillins [Seite 153]
23.7.4.2 - 7.4.2 Cephalosporins [Seite 154]
23.7.4.3 - 7.4.3 Carbapenem (imipenem, meropenem) [Seite 154]
23.7.4.4 - 7.4.4 Chloramphenicol [Seite 155]
23.7.4.5 - 7.4.5 Clindamycin and Lincomycin [Seite 155]
23.7.4.6 - 7.4.6 Metronidazole [Seite 155]
23.7.4.7 - 7.4.7 Macrolids (Erythromycin, Azithromycin, Clarithromycin) [Seite 155]
23.7.4.8 - 7.4.8 Glycopeptides (Vancomycin, Teicoplanin) [Seite 155]
23.7.4.9 - 7.4.9 Tetracyclines [Seite 156]
23.7.4.10 - 7.4.10 Quinolones [Seite 156]
23.7.5 - 7.5 Choice of Antimicrobial Agents [Seite 156]
24 - References [Seite 157]
25 - Encephalitis Diagnosis and Management in the Real World [Seite 161]
25.1 - 1 Approach to Focusing Possible Etiologies [Seite 161]
25.1.1 - 1.1 Pathogenesis [Seite 161]
25.1.2 - 1.2 Prioritizing Treatable Etiologies [Seite 163]
25.1.3 - 1.3 Etiologically Focussed Prevention of Acute Encephalitis [Seite 165]
25.1.4 - 1.4 Season, Geography, and Epidemiology of Viral Encephalitis [Seite 166]
25.1.5 - 1.5 Studies of Causes of Acute Encephalitis [Seite 169]
25.1.6 - 1.6 Additional Noteworthy Diagnoses [Seite 172]
25.1.6.1 - 1.6.1 Acute Disseminated Encephalomyelitis (ADEM) [Seite 172]
25.1.6.2 - 1.6.2 Acute Necrotizing Encephalopathy (ANE) [Seite 174]
25.1.7 - 1.7 Additional Noteworthy Pathogens [Seite 175]
25.1.7.1 - 1.7.1 B. burgdorferi [Seite 175]
25.1.7.2 - 1.7.2 Parvovirus B19 [Seite 175]
25.1.7.3 - 1.7.3 Balamuthia mandrillaris [Seite 176]
25.1.8 - 1.8 Specific Clinical Neurologic Syndromes [Seite 176]
25.2 - 2 Approach to Empiric Management [Seite 176]
26 - References [Seite 179]
27 - Toxic Shock Syndrome -- Evolution of an Emerging Disease [Seite 182]
27.1 - 1 Introduction [Seite 182]
27.2 - 2 Epidemiology [Seite 182]
27.3 - 3 Pathogenesis [Seite 182]
27.4 - 4 Clinical Findings [Seite 183]
27.5 - 5 Management [Seite 184]
27.6 - 6 Prognosis [Seite 185]
28 - References [Seite 186]
29 - Dissection of B-Cell Development to Unravel Defectsin Patients with a Primary Antibody Deficiency [Seite 189]
29.1 - 1 Introduction [Seite 189]
29.2 - 2 Generation of Nave Mature B Cells by Stepwise Differentiation in Bone Marrow [Seite 189]
29.3 - 3 Antigen-Dependent B-Cell Maturation in Secondary Lymphoid Organs [Seite 191]
29.4 - 4 Dynamics in the Peripheral B-Cell Compartment During Early Childhood [Seite 194]
29.5 - 5 Antibody Deficiencies [Seite 194]
29.5.1 - 5.1 Agammaglobulinemia [Seite 195]
29.5.2 - 5.2 B-Cell Antigen Receptor Signaling Deficiency [Seite 198]
29.5.3 - 5.3 IgCSR Deficiency [Seite 198]
29.5.4 - 5.4 Common Variable Immunodeficiencies (CVID) [Seite 199]
29.6 - 6 Conclusion [Seite 200]
30 - References [Seite 200]
31 - Mumps is Back: Why is Mumps EradicationNot Working? [Seite 203]
31.1 - 1 Introduction [Seite 203]
31.2 - 2 Mumps: The Clinical Presentation [Seite 204]
31.3 - 3 Mumps: The Virus [Seite 205]
31.4 - 4 Mumps: The Pathogenesis and Transmission [Seite 207]
31.5 - 5 Mumps: The Diagnosis [Seite 207]
31.5.1 - 5.1 Mumps: Laboratory Diagnosis for Mumps Infection [Seite 208]
31.5.1.1 - 5.1.1 Specimen Collection [Seite 208]
31.5.1.2 - 5.1.2 Tissue Culture [Seite 208]
31.5.1.3 - 5.1.3 Molecular Testing [Seite 209]
31.5.1.4 - 5.1.4 IgM Serology [Seite 209]
31.5.1.5 - 5.1.5 IgG Serology [Seite 210]
31.6 - 6 Mumps: The Epidemiology [Seite 211]
31.7 - 7 Mumps: The Vaccines [Seite 212]
31.8 - 8 Mumps: Recent Resurgence [Seite 213]
31.8.1 - 8.1 Vaccine Program: Refusal to Accept Immunization: 2007--2008 Outbreak in the Netherlands [Seite 214]
31.8.2 - 8.2 Vaccine Program: Failure to Immunize an Age Group: --Lost Cohort--: 2004--2006 Outbreak in United Kingdom [Seite 214]
31.8.3 - 8.3 Vaccine Program: Single Dose: Forgotten Cohort 2004--2007 Outbreaks in Canada, 2005--2007 in Australia [Seite 217]
31.8.4 - 8.4 Vaccine Failure: Primary Vaccine Failure: Ineffective Vaccine -- Rubini [Seite 218]
31.8.5 - 8.5 Vaccine Failure: Two-dose Vaccine Failure: Waning Immunity: 2006 Outbreaks in the United States [Seite 219]
31.9 - 9 Mumps Elimination in Finland [Seite 219]
31.10 - 10 Mumps: Public Health Control Strategies in Outbreaks [Seite 220]
31.11 - 11 Mumps Outbreaks: Lessons Learned [Seite 220]
31.12 - 12 Mumps Control: Unanswered Questions [Seite 221]
31.13 - 13 Summary [Seite 222]
32 - References [Seite 222]
33 - Neonatal Herpes Simplex Virus Infections: Where Are We Now [Seite 227]
33.1 - 1 Background [Seite 227]
33.2 - 2 Epidemiology of Neonatal HSV [Seite 228]
33.3 - 3 Clinical Manifestations of Neonatal HSV [Seite 228]
33.4 - 4 Mortality and Morbidity [Seite 228]
33.5 - 5 Antiviral Therapy [Seite 229]
33.6 - 6 Determining Dosage and Duration of Treatment [Seite 230]
33.7 - 7 Polymerase Chain Reaction (PCR)-Guided Therapy [Seite 230]
33.8 - 8 Oral Suppression Therapy [Seite 233]
33.9 - 9 Antiviral Resistance [Seite 234]
33.10 - 10 Conclusion [Seite 235]
34 - References [Seite 235]
35 - Rational Approach to Pediatric Antifungal Therapy [Seite 237]
35.1 - 1 Introduction [Seite 237]
35.2 - 2 Treatment of Pediatric Invasive Aspergillosis [Seite 238]
35.2.1 - 2.1 Voriconazole Dosing in Children [Seite 240]
35.2.2 - 2.2 Combination Therapy for Invasive Aspergillosis [Seite 242]
35.3 - 3 Treatment of Pediatric Invasive Candidiasis [Seite 243]
35.4 - 4 Conclusion [Seite 246]
36 - References [Seite 246]
37 - Antiviral Therapy of CMV Disease in Children [Seite 249]
37.1 - 1 Spectrum of Clinical Disease [Seite 249]
37.1.1 - 1.1 Congenital CMV [Seite 249]
37.1.1.1 - 1.1.1 Clinical Features [Seite 250]
37.1.1.2 - 1.1.2 Predicting Long-Term Neurological Impairment [Seite 251]
37.1.2 - 1.2 PostNatal CMV [Seite 252]
37.1.2.1 - 1.2.1 Clinical Features [Seite 252]
37.1.3 - 1.3 CMV Disease in Older Children [Seite 252]
37.2 - 2 Ganciclovir and Valganciclovir Use in Children [Seite 253]
37.2.1 - 2.1 Pharmacokinetics [Seite 253]
37.2.1.1 - 2.1.1 Ganciclovir [Seite 253]
37.2.1.2 - 2.1.2 Valganciclovir [Seite 254]
37.2.1.3 - 2.1.3 CSF and CNS Penetration [Seite 255]
37.2.2 - 2.2 Pharmacodynamics [Seite 255]
37.2.3 - 2.3 Resistance [Seite 256]
37.2.4 - 2.4 Drug Levels [Seite 257]
37.2.5 - 2.5 Safety [Seite 257]
37.3 - 3 Clinical Studies of GCV in Childhood CMV Infection [Seite 258]
37.3.1 - 3.1 Congenital CMV [Seite 258]
37.3.2 - 3.2 Clinical Use of GCV in Postnatal CMV Infection [Seite 262]
37.3.3 - 3.3 CMV Disease and GCV Treatment in Older Immunocompromised Children [Seite 262]
37.4 - 4 Summary [Seite 263]
38 - References [Seite 263]
39 - Infectious Hazards from Pets and Domestic Animals [Seite 267]
39.1 - 1 Introduction [Seite 267]
39.2 - 2 Global Trends in Emerging Infectious Diseases (EID) [Seite 268]
39.3 - 3 Pets and Domestic Animals as Reservoirs of Antimicrobial Resistance (AMR) [Seite 270]
39.4 - 4 Staphylococcus intermedius in Pets [Seite 271]
39.5 - 5 MRSA in Pets and Domestic Animals [Seite 273]
39.6 - 6 A Call for an Action [Seite 274]
39.7 - 7 Pets and Immunocompromised Hosts [Seite 275]
39.8 - 8 Conclusion [Seite 275]
40 - References [Seite 276]
41 - Novel Technology to Study Co-Evolution of Humans StaphylococcusINTtie [Seite 279]
41.1 - 1 Introduction [Seite 279]
41.2 - 2 The Microorganism [Seite 280]
41.2.1 - 2.1 Detection and Identification [Seite 280]
41.2.2 - 2.2 Habitat and Genome Complexity [Seite 280]
41.3 - 3 The Host [Seite 281]
41.3.1 - 3.1 Human Niches [Seite 281]
41.3.2 - 3.2 Patterns of and Susceptibility to Carriage [Seite 282]
41.4 - 4 Artificial Colonisation Studies [Seite 282]
41.4.1 - 4.1 Setting Up a Nasal Colonisation Study [Seite 283]
41.4.2 - 4.2 Examples of Previous Colonisation Studies [Seite 284]
41.4.3 - 4.3 Ongoing Experiments and Ideas for Future Colonisation Studies [Seite 285]
41.5 - 5 Example Of A Cohort Study [Seite 286]
41.5.1 - 5.1 Relevance of Cohort Studies [Seite 286]
41.5.2 - 5.2 Microbiology in Generation R [Seite 286]
41.5.3 - 5.3 Preliminary Results [Seite 287]
41.6 - 6 Humoral Immunity and S. aureus Carriage and Infection [Seite 288]
41.6.1 - 6.1 Technical Aspects of Multiplex Anti-staphylococcal Antibody Measurements [Seite 288]
41.6.2 - 6.2 Application of the Luminex Technology and Microbiological Implications [Seite 288]
41.7 - 7 Conclusion [Seite 290]
42 - References [Seite 290]
43 - A Practical Approach to Eosinophilia in a Child Arriving orINTtie [Seite 295]
43.1 - 1 Introduction [Seite 295]
43.2 - 2 Why it is Often Difficult to Determine the Parasite Causing Eosinophilia [Seite 295]
43.2.1 - 2.1 Patients with Helminthic Infection may be Asymptomatic [Seite 295]
43.2.2 - 2.2 Patients with Eosinophilia may have a Helminthic Infection that is too Early to Diagnose [Seite 296]
43.2.3 - 2.3 It is Difficult to Distinguish Between Different Helminthic Infections by Either Degree or Persistence of Eosinophilia [Seite 296]
43.2.4 - 2.4 Whether a Child is an Immigrant or Returned Traveller does not help to Distinguish Between Different Helminthic Infections [Seite 297]
43.2.5 - 2.5 Serum IgE Level does not help to Distinguish Between Different Helminthic Infections or Exclude a Non-Parasitic Cause for Eosinophilia [Seite 298]
43.2.6 - 2.6 Patients with Helminthic Infection may not have Eosinophilia [Seite 298]
43.2.7 - 2.7 The Degree of Eosinophilia does not Necessarily Relate to the Burden of Infection [Seite 299]
43.2.8 - 2.8 Negative Investigations for Parasites do not Exclude Helminthic Infection [Seite 299]
43.2.9 - 2.9 Eosinophilia may Worsen Despite Appropriate Treatment [Seite 300]
43.2.10 - 2.10 Patients from a Tropical Country may have an Alternative Explanation Other than Helminthic Infection for Their Eosinophilia [Seite 300]
43.3 - 3 An Approach to Diagnosing and Treating Parasitic Infections in Children with Eosinophilia Returning From Tropical Countries [Seite 300]
43.3.1 - 3.1 History [Seite 301]
43.3.2 - 3.2 Investigations [Seite 302]
43.3.3 - 3.3 Treatment [Seite 304]
44 - References [Seite 304]
45 - Subject Index [Seite 306]
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