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by Peter H. Wald, Gregg M. Stave
Physical and Biological Hazards of the Workplace, 3rd Edition
COVER
TITLE PAGE
ABOUT THE EDITORS
LIST OF CONTRIBUTORS
FOREWORD TO THE FIRST EDITION
PREFACE
ACGIH POLICY STATEMENT
ACGIH STATEMENT OF POSITION
Part I: PHYSICAL HAZARDS
Chapter 1: INTRODUCTION to PHYSICAL HAZARDS
MECHANICS
ELECTROMAGNETIC RADIATION
WORKER PROTECTION
Further Reading
I: Worker–Material Interfaces
Chapter 2: ERGONOMICS and UPPER EXTREMITY MUSCULOSKELETAL DISORDERS
OCCUPATIONAL SETTING
MEASUREMENT—ASSESSMENT
EXPOSURE GUIDELINES
NORMAL PHYSIOLOGY AND ANATOMY
PATHOPHYSIOLOGY AND PATHOGENESIS
DIAGNOSIS AND TREATMENT
SURVEILLANCE
PREVENTION
References
Chapter 3: MANUAL MATERIALS HANDLING
OCCUPATIONAL SETTING
NORMAL ANATOMY AND PHYSIOLOGY OF THE SPINE
PATHOPHYSIOLOGY OF INJURY AND RISK FACTORS
MEASUREMENT ISSUES
GUIDELINES AND STANDARDS
DIAGNOSIS AND TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
SUMMARY
References
Chapter 4: OCCUPATIONAL VIBRATION EXPOSURE
OCCUPATIONAL SETTING
OCCUPATIONAL VIBRATION MEASUREMENTS
OCCUPATIONAL VIBRATION GUIDELINES USED IN THE UNITED STATES
WHOLE‐BODY VIBRATION AND LOW BACK PROBLEMS
PREVENTION
HAND–ARM VIBRATION MEDICAL EFFECTS
DIAGNOSIS
PATHOPHYSIOLOGY
TREATMENT AND MANAGEMENT
HAND–ARM VIBRATION CONTROL
References
Chapter 5: MECHANICAL ENERGY
OCCUPATIONAL SETTING
MEASUREMENT ISSUES
EXPOSURE GUIDELINES
PATHOPHYSIOLOGY OF INJURY
TREATMENT
SURVEILLANCE PROGRAMS
PREVENTION
SUMMARY
References
II: The Physical Work Environment
Chapter 6: HOT ENVIRONMENTS
OCCUPATIONAL SETTING
MEASUREMENT ISSUES
EXPOSURE GUIDELINES
ACGIH GUIDELINES
NIOSH GUIDELINES
NORMAL PHYSIOLOGY
PATHOPHYSIOLOGY OF ILLNESS AND TREATMENT
MEDICAL SURVEILLANCE
HEAT EXPOSURE AND REPRODUCTION
PREVENTION
References
Chapter 7: COLD ENVIRONMENTS
OCCUPATIONAL SETTING
MEASUREMENT ISSUES
EXPOSURE GUIDELINES
NORMAL PHYSIOLOGY
PATHOPHYSIOLOGY OF INJURY
DIAGNOSIS
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 8: HIGH-PRESSURE ENVIRONMENTS
OCCUPATIONAL SETTING
MEASUREMENT ISSUES AND PHYSICS OF PRESSURE
EXPOSURE GUIDELINES
SPECIAL UNDERWATER STRESSORS
OTHER HAZARDS IN THE DIVING ENVIRONMENT
PATHOPHYSIOLOGY OF DIRECT PRESSURE INJURY
LONG-TERM HEALTH EFFECTS
TREATMENT OF BUBBLE-RELATED DISEASE
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 9: LOW-PRESSURE and HIGH-ALTITUDE ENVIRONMENTS
OCCUPATIONAL SETTING
LOW-PRESSURE ENVIRONMENTS
HYPOXIA
HIGH-ALTITUDE ACCLIMATIZATION AND ILLNESS
OTHER ALTITUDE-RELATED CONDITIONS
References
Chapter 10: SHIFT WORK
OCCUPATIONAL SETTING
MEASUREMENT GUIDELINES
EXPOSURE GUIDELINES (SCHEDULE DESIGN)
NORMAL PHYSIOLOGY
PATHOBIOLOGY (CIRCADIAN RHYTHMS AND SHIFT WORK)
DIAGNOSIS
TREATMENT (COUNTERMEASURES)
MEDICAL SURVEILLANCE
PREVENTION AND ADMINISTRATIVE CONTROLS
References
III: Energy and Electromagnetic Radiation
Chapter 11: IONIZING RADIATION
BACKGROUND RADIATION
OCCUPATIONAL EXPOSURES
DIAGNOSTIC MEDICAL EXPOSURES
MEASUREMENT ISSUES AND THE PHYSICS OF IONIZING RADIATION
EXPOSURE GUIDELINES
PATHOPHYSIOLOGY AND HEALTH EFFECTS
DIAGNOSIS AND TREATMENT
PREVENTION
EMERGENCY INFORMATION AND EXPERT ADVICE
References
Chapter 12: ULTRAVIOLET RADIATION
OCCUPATIONAL SETTING
MEASUREMENT ISSUES
EXPOSURE GUIDELINES
NORMAL PHYSIOLOGY
PATHOPHYSIOLOGY OF INJURY
DIAGNOSIS AND TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 13: VISIBLE LIGHT and INFRARED RADIATION
OCCUPATIONAL SETTING
MEASUREMENT ISSUES
EXPOSURE GUIDELINES
NORMAL PHYSIOLOGY
PATHOPHYSIOLOGY OF INJURY
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 14: LASER RADIATION
OCCUPATIONAL SETTING
MEASUREMENT ISSUES AND CLASSIFICATION OF LASER POWER
EXPOSURE GUIDELINES
PATHOPHYSIOLOGY OF INJURY
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 15: MICROWAVE, RADIOFREQUENCY, and EXTREMELY LOW-FREQUENCY ENERGY
MICROWAVE AND RADIOFREQUENCY RADIATION
EXTREMELY LOW-FREQUENCY ELECTROMAGNETIC RADIATION: MAGNETIC FIELDS
References
Chapter 16: NOISE
OCCUPATIONAL SETTING
MEASUREMENT ISSUES
EXPOSURE GUIDELINES
NORMAL PHYSIOLOGY
PATHOPHYSIOLOGY OF NOISE-INDUCED HEARING LOSS
DIAGNOSIS
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 17: ELECTRICAL POWER and ELECTRICAL INJURIES
OCCUPATIONAL SETTING
LIGHTNING INJURIES
References
Part II: BIOLOGICAL HAZARDS
Chapter 18: GENERAL PRINCIPLES of MICROBIOLOGY and INFECTIOUS DISEASE
ETIOLOGY OF DISEASE
TRANSMISSIBILITY OF DISEASE
INFECTIVITY OF DISEASE
CLASSIFICATION OF MICROORGANISMS FOR LABORATORY WORK
Chapter 19: CLINICAL RECOGNITION of OCCUPATIONAL EXPOSURE and HEALTH CONSEQUENCES
INFECTION
SPECIFIC CLINICAL DISEASES
IMMUNE MECHANISMS AND HYPERSENSITIVITY DISORDERS
SPECIFIC CLINICAL SYNDROMES
LABORATORY CONFIRMATION OF INFECTIOUS AND HYPERSENSITIVITY DISEASES
CLINICAL TESTING FOR HYPERSENSITIVITY
WHEN TO SUSPECT OCCUPATIONAL ILLNESS OF BIOLOGICAL ORIGIN
EVALUATION OF SUSPECTED OCCUPATIONAL ILLNESS
Chapter 20: PREVENTION of ILLNESS from BIOLOGICAL HAZARDS
OCCUPATIONS WITH POTENTIAL BIOLOGICAL HAZARDS
THE OSHA BLOODBORNE PATHOGENS STANDARD
THE HISTORY OF OSHA GUIDELINES FOR TUBERCULOSIS
PROPOSED OSHA INFECTIOUS DISEASE STANDARD
PREVENTION OF EXPOSURE TO BIOLOGICAL AGENTS
SURVEILLANCE
VACCINATION
SPECIAL SITUATIONS
Chapter 21: VIRUSES
ARBOVIRUSES (Yellow fever, Dengue fever, Chikungunya, Zika fever, Japanese encephalitis, St Louis encephalitis, West Nile encephalitis, Eastern equine encephalitis, Western equine encephalitis, La Cro
References
ARENAVIRUSES
References
CORONAVIRUS
References
CYTOMEGALOVIRUS (CMV)
References
FILOVIRUSES (EBOLA AND MARBURG VIRUSES)
References
HANTAVIRUSES
References
HEPATITIS A VIRUS (HAV)
References
HEPATITIS B VIRUS (HBV)
References
HEPATITIS C VIRUS (HCV)
References
HERPES B VIRUS
References
HERPES SIMPLEX VIRUS (HSV)
References
HUMAN IMMUNODEFICIENCY VIRUS (HIV-1)
References
HUMAN T-CELL LYMPHOTROPHIC VIRUS
References
INFLUENZA VIRUS
References
MEASLES VIRUS
References
MUMPS VIRUS
References
NOROVIRUS (FORMERLY NORWALK VIRUS) AND OTHER ENTERIC VIRUSES
References
PARVOVIRUS B19
References
RABIES VIRUS
References
RESPIRATORY SYNCYTIAL VIRUS (RSV)
References
RUBELLA VIRUS
References
SIMIAN RETROVIRUSES
References
VACCINIA
References
VARICELLA ZOSTER VIRUS (VZV)
References
Chapter 22: BACTERIA
ACINETOBACTER SPECIES
BACILLUS SPECIES
BORRELIA SPECIES
BRUCELLA SPECIES
CAMPYLOBACTER SPECIES
CLOSTRIDIUM BOTULINUM (INCLUDING C. ARGENTINENSE, C. BARATII, AND C. BUTYRICUM)
CLOSTRIDIUM DIFFICILE
CLOSTRIDIUM PERFRINGENS (also C. SEPTICUM, C. NOVI)
CLOSTRIDIUM TETANI
CORYNEBACTERIUM SPECIES
ERYSIPELOTHRIX RHUSIOPATHIAE
ESCHERICHIA COLI
FRANCISELLA TULARENSIS (INCLUDING F. NOVOCIDA)
HAEMOPHILUS DUCREYI
HAEMOPHILUS INFLUENZA
HELICOBACTER PYLORI
LEGIONELLA SPECIES (LEGIONELLA PNEUMOPHILA, LEGIONELLA LONGBEACHAE)
LEPTOSPIRA INTERROGANS
LISTERIA MONOCYTOGENES
MYCOPLASMA PNEUMONIAE
NEISSERIA GONORRHOEAE
NEISSERIA MENINGITIDIS
PASTEURELLA MULTOCIDA
PSEUDOMONAS AND BURKHOLDERIA SPECIES
RAT-BITE FEVER: STREPTOBACILLUS MONILIFORMIS AND SPIRILLUM MINOR
RELAPSING FEVER: BORRELIA SPECIES (other than B. burgdorferi)
SALMONELLA SPECIES
SHIGELLA SPECIES
STAPHYLOCOCCUS SPECIES
STREPTOCOCCUS SPECIES
TREPONEMA PALLIDUM
VIBRIO CHOLERAE
VIBRIO SPECIES OTHER THAN V. CHOLERAE (V. PARAHEMOLYTICUS, V. VULNIFICUS)
YERSINIA PESTIS
YERSINIA PSEUDOTUBERCULOSIS AND ENTEROCOLITICA
Chapter 23: MYCOBACTERIA
MYCOBACTERIUM TUBERCULOSIS (M. tb.)
MYCOBACTERIA OTHER THAN MYCOBACTERIUM TUBERCULOSIS
Chapter 24: FUNGI
ALTERNARIA SPECIES
References
ASPERGILLUS SPECIES
References
BASIDIOMYCETES (INCLUDING MERULIUS LACRYMANS, LYCOPERDON, AND MUSHROOMS)
References
BLASTOMYCES DERMATITIDIS
References
CANDIDA SPECIES
References
CLADOSPORIUM SPECIES
References
COCCIDIOIDES IMMITIS
References
CRYPTOCOCCUS NEOFORMANS AND CRYPTOCOCCUS GATTII
References
CRYPTOSTROMA CORTICALE
References
FONSECAEA AND OTHER AGENTS OF CHROMOMYCOSIS
References
HISTOPLASMA CAPSULATUM
References
MADURELLA SPECIES AND OTHER AGENTS OF MYCETOMA
References
PARACOCCIDIOIDES BRASILIENSIS
References
PENICILLIUM SPECIES
References
SPOROTHRIX SCHENCKII
References
STACHYBOTRYS CHARTARUM
References
TRICHOPHYTON AND OTHER DERMATOPHYTES
References
ZYGOMYCETES
References
Chapter 25: ANAPLASMA, CHLAMYDOPHILA, COXIELLA, EHRLICHIA, and RICKETTSIA
ANAPLASMA
References
CHLAMYDOPHILA PSITTACI
References
COXIELLA BURNETII
References
EHRLICHIA SPECIES
References
RICKETTSIA RICKETTSII
References
Chapter 26: PARASITES
CRYPTOSPORIDIUM PARVUM
References
CYCLOSPORIASIS
References
CUTANEOUS, MUCOCUTANEOUS, AND VISCERAL LEISHMANIASIS
References
NANOPHYETUS
References
PFIESTERIA PISCICIDA
References
PLASMODIUM SPECIES
References
TOXOPLASMA GONDII
References
Chapter 27: ENVENOMATIONS
ARTHROPOD ENVENOMATIONS
HYMENOPTERA
References
LATRODECTUS SPECIES
References
LOXOSCELES SPECIES
References
SCORPIONIDA (SCORPIONS)
References
MARINE ENVENOMATIONS
CATFISH
References
COELENTERATE: ANTHOZOA
References
COELENTERATE: HYDROZOA
References
COELENTERATA: SCYPHOZOA
References
DASYATIS (STINGRAY)
References
ECHINODERMATA
References
MOLLUSCA
References
PORIFERA
References
SCORPAENIDAE
References
SNAKE ENVENOMATIONS
COLUBRIDAE
References
CROTALIDAE
References
ELAPIDAE
References
HYDROPHIDAE
References
Chapter 28: ALLERGENS
ENZYMES
References
FARM ANIMALS
References
GRAIN DUST
References
INSECTS
References
LABORATORY ANIMALS
References
MITES
References
PLANTS
References
SHELLFISH AND OTHER MARINE INVERTEBRATES
References
WHEAT FLOUR AND EGG
References
Chapter 29: LATEX
OCCUPATIONAL SETTING
EXPOSURE (ROUTE)
PATHOBIOLOGY
DIAGNOSIS
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 30: MALIGNANT CELLS
OCCUPATIONAL SETTING
EXPOSURE (ROUTE)
PATHOBIOLOGY
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 31: RECOMBINANT ORGANISMS
OCCUPATIONAL SETTING
EXPOSURE (ROUTE)
PATHOBIOLOGY
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 32: PRIONS
OCCUPATIONAL SETTING
EXPOSURE (ROUTE)
PATHOBIOLOGY
DIAGNOSIS
TREATMENT
PREVENTION
References
Chapter 33: ENDOTOXINS
OCCUPATIONAL SETTING
EXPOSURE (ROUTE)
PATHOBIOLOGY
ACUTE EXPOSURES
CHRONIC EXPOSURE
DIAGNOSIS
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 34: WOOD DUST
OCCUPATIONAL SETTING
EXPOSURE (ROUTE)
PATHOBIOLOGY
DIAGNOSIS
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
INDEX
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COVER
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TITLE PAGE
Table of Contents
COVER
TITLE PAGE
ABOUT THE EDITORS
LIST OF CONTRIBUTORS
FOREWORD TO THE FIRST EDITION
PREFACE
ACGIH POLICY STATEMENT
ACGIH STATEMENT OF POSITION
Part I: PHYSICAL HAZARDS
Chapter 1: INTRODUCTION to PHYSICAL HAZARDS
MECHANICS
ELECTROMAGNETIC RADIATION
WORKER PROTECTION
Further Reading
I: Worker–Material Interfaces
Chapter 2: ERGONOMICS and UPPER EXTREMITY MUSCULOSKELETAL DISORDERS
OCCUPATIONAL SETTING
MEASUREMENT—ASSESSMENT
EXPOSURE GUIDELINES
NORMAL PHYSIOLOGY AND ANATOMY
PATHOPHYSIOLOGY AND PATHOGENESIS
DIAGNOSIS AND TREATMENT
SURVEILLANCE
PREVENTION
References
Chapter 3: MANUAL MATERIALS HANDLING
OCCUPATIONAL SETTING
NORMAL ANATOMY AND PHYSIOLOGY OF THE SPINE
PATHOPHYSIOLOGY OF INJURY AND RISK FACTORS
MEASUREMENT ISSUES
GUIDELINES AND STANDARDS
DIAGNOSIS AND TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
SUMMARY
References
Chapter 4: OCCUPATIONAL VIBRATION EXPOSURE
OCCUPATIONAL SETTING
OCCUPATIONAL VIBRATION MEASUREMENTS
OCCUPATIONAL VIBRATION GUIDELINES USED IN THE UNITED STATES
WHOLE‐BODY VIBRATION AND LOW BACK PROBLEMS
PREVENTION
HAND–ARM VIBRATION MEDICAL EFFECTS
DIAGNOSIS
PATHOPHYSIOLOGY
TREATMENT AND MANAGEMENT
HAND–ARM VIBRATION CONTROL
References
Chapter 5: MECHANICAL ENERGY
OCCUPATIONAL SETTING
MEASUREMENT ISSUES
EXPOSURE GUIDELINES
PATHOPHYSIOLOGY OF INJURY
TREATMENT
SURVEILLANCE PROGRAMS
PREVENTION
SUMMARY
References
II: The Physical Work Environment
Chapter 6: HOT ENVIRONMENTS
OCCUPATIONAL SETTING
MEASUREMENT ISSUES
EXPOSURE GUIDELINES
ACGIH GUIDELINES
NIOSH GUIDELINES
NORMAL PHYSIOLOGY
PATHOPHYSIOLOGY OF ILLNESS AND TREATMENT
MEDICAL SURVEILLANCE
HEAT EXPOSURE AND REPRODUCTION
PREVENTION
References
Chapter 7: COLD ENVIRONMENTS
OCCUPATIONAL SETTING
MEASUREMENT ISSUES
EXPOSURE GUIDELINES
NORMAL PHYSIOLOGY
PATHOPHYSIOLOGY OF INJURY
DIAGNOSIS
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 8: HIGH-PRESSURE ENVIRONMENTS
OCCUPATIONAL SETTING
MEASUREMENT ISSUES AND PHYSICS OF PRESSURE
EXPOSURE GUIDELINES
SPECIAL UNDERWATER STRESSORS
OTHER HAZARDS IN THE DIVING ENVIRONMENT
PATHOPHYSIOLOGY OF DIRECT PRESSURE INJURY
LONG-TERM HEALTH EFFECTS
TREATMENT OF BUBBLE-RELATED DISEASE
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 9: LOW-PRESSURE and HIGH-ALTITUDE ENVIRONMENTS
OCCUPATIONAL SETTING
LOW-PRESSURE ENVIRONMENTS
HYPOXIA
HIGH-ALTITUDE ACCLIMATIZATION AND ILLNESS
OTHER ALTITUDE-RELATED CONDITIONS
References
Chapter 10: SHIFT WORK
OCCUPATIONAL SETTING
MEASUREMENT GUIDELINES
EXPOSURE GUIDELINES (SCHEDULE DESIGN)
NORMAL PHYSIOLOGY
PATHOBIOLOGY (CIRCADIAN RHYTHMS AND SHIFT WORK)
DIAGNOSIS
TREATMENT (COUNTERMEASURES)
MEDICAL SURVEILLANCE
PREVENTION AND ADMINISTRATIVE CONTROLS
References
III: Energy and Electromagnetic Radiation
Chapter 11: IONIZING RADIATION
BACKGROUND RADIATION
OCCUPATIONAL EXPOSURES
DIAGNOSTIC MEDICAL EXPOSURES
MEASUREMENT ISSUES AND THE PHYSICS OF IONIZING RADIATION
EXPOSURE GUIDELINES
PATHOPHYSIOLOGY AND HEALTH EFFECTS
DIAGNOSIS AND TREATMENT
PREVENTION
EMERGENCY INFORMATION AND EXPERT ADVICE
References
Chapter 12: ULTRAVIOLET RADIATION
OCCUPATIONAL SETTING
MEASUREMENT ISSUES
EXPOSURE GUIDELINES
NORMAL PHYSIOLOGY
PATHOPHYSIOLOGY OF INJURY
DIAGNOSIS AND TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 13: VISIBLE LIGHT and INFRARED RADIATION
OCCUPATIONAL SETTING
MEASUREMENT ISSUES
EXPOSURE GUIDELINES
NORMAL PHYSIOLOGY
PATHOPHYSIOLOGY OF INJURY
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 14: LASER RADIATION
OCCUPATIONAL SETTING
MEASUREMENT ISSUES AND CLASSIFICATION OF LASER POWER
EXPOSURE GUIDELINES
PATHOPHYSIOLOGY OF INJURY
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 15: MICROWAVE, RADIOFREQUENCY, and EXTREMELY LOW-FREQUENCY ENERGY
MICROWAVE AND RADIOFREQUENCY RADIATION
EXTREMELY LOW-FREQUENCY ELECTROMAGNETIC RADIATION: MAGNETIC FIELDS
References
Chapter 16: NOISE
OCCUPATIONAL SETTING
MEASUREMENT ISSUES
EXPOSURE GUIDELINES
NORMAL PHYSIOLOGY
PATHOPHYSIOLOGY OF NOISE-INDUCED HEARING LOSS
DIAGNOSIS
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 17: ELECTRICAL POWER and ELECTRICAL INJURIES
OCCUPATIONAL SETTING
LIGHTNING INJURIES
References
Part II: BIOLOGICAL HAZARDS
Chapter 18: GENERAL PRINCIPLES of MICROBIOLOGY and INFECTIOUS DISEASE
ETIOLOGY OF DISEASE
TRANSMISSIBILITY OF DISEASE
INFECTIVITY OF DISEASE
CLASSIFICATION OF MICROORGANISMS FOR LABORATORY WORK
Chapter 19: CLINICAL RECOGNITION of OCCUPATIONAL EXPOSURE and HEALTH CONSEQUENCES
INFECTION
SPECIFIC CLINICAL DISEASES
IMMUNE MECHANISMS AND HYPERSENSITIVITY DISORDERS
SPECIFIC CLINICAL SYNDROMES
LABORATORY CONFIRMATION OF INFECTIOUS AND HYPERSENSITIVITY DISEASES
CLINICAL TESTING FOR HYPERSENSITIVITY
WHEN TO SUSPECT OCCUPATIONAL ILLNESS OF BIOLOGICAL ORIGIN
EVALUATION OF SUSPECTED OCCUPATIONAL ILLNESS
Chapter 20: PREVENTION of ILLNESS from BIOLOGICAL HAZARDS
OCCUPATIONS WITH POTENTIAL BIOLOGICAL HAZARDS
THE OSHA BLOODBORNE PATHOGENS STANDARD
THE HISTORY OF OSHA GUIDELINES FOR TUBERCULOSIS
PROPOSED OSHA INFECTIOUS DISEASE STANDARD
PREVENTION OF EXPOSURE TO BIOLOGICAL AGENTS
SURVEILLANCE
VACCINATION
SPECIAL SITUATIONS
Chapter 21: VIRUSES
ARBOVIRUSES (Yellow fever, Dengue fever, Chikungunya, Zika fever, Japanese encephalitis, St Louis encephalitis, West Nile encephalitis, Eastern equine encephalitis, Western equine encephalitis, La Crosse encephalitis, Colorado tick fever)
References
ARENAVIRUSES
References
CORONAVIRUS
References
CYTOMEGALOVIRUS (CMV)
References
FILOVIRUSES (EBOLA AND MARBURG VIRUSES)
References
HANTAVIRUSES
References
HEPATITIS A VIRUS (HAV)
References
HEPATITIS B VIRUS (HBV)
References
HEPATITIS C VIRUS (HCV)
References
HERPES B VIRUS
References
HERPES SIMPLEX VIRUS (HSV)
References
HUMAN IMMUNODEFICIENCY VIRUS (HIV-1)
References
HUMAN T-CELL LYMPHOTROPHIC VIRUS
References
INFLUENZA VIRUS
References
MEASLES VIRUS
References
MUMPS VIRUS
References
NOROVIRUS (FORMERLY NORWALK VIRUS) AND OTHER ENTERIC VIRUSES
References
PARVOVIRUS B19
References
RABIES VIRUS
References
RESPIRATORY SYNCYTIAL VIRUS (RSV)
References
RUBELLA VIRUS
References
SIMIAN RETROVIRUSES
References
VACCINIA
References
VARICELLA ZOSTER VIRUS (VZV)
References
Chapter 22: BACTERIA
ACINETOBACTER SPECIES
BACILLUS SPECIES
BORRELIA SPECIES
BRUCELLA SPECIES
CAMPYLOBACTER SPECIES
CLOSTRIDIUM BOTULINUM
(INCLUDING
C. ARGENTINENSE, C. BARATII
, AND
C. BUTYRICUM
)
CLOSTRIDIUM DIFFICILE
CLOSTRIDIUM PERFRINGENS
(also
C. SEPTICUM, C. NOVI
)
CLOSTRIDIUM TETANI
CORYNEBACTERIUM SPECIES
ERYSIPELOTHRIX RHUSIOPATHIAE
ESCHERICHIA COLI
FRANCISELLA TULARENSIS
(INCLUDING
F. NOVOCIDA
)
HAEMOPHILUS DUCREYI
HAEMOPHILUS INFLUENZA
HELICOBACTER PYLORI
LEGIONELLA SPECIES (
LEGIONELLA PNEUMOPHILA, LEGIONELLA LONGBEACHAE
)
LEPTOSPIRA INTERROGANS
LISTERIA MONOCYTOGENES
MYCOPLASMA PNEUMONIAE
NEISSERIA GONORRHOEAE
NEISSERIA MENINGITIDIS
PASTEURELLA MULTOCIDA
PSEUDOMONAS AND BURKHOLDERIA SPECIES
RAT-BITE FEVER:
STREPTOBACILLUS MONILIFORMIS
AND SPIRILLUM MINOR
RELAPSING FEVER: BORRELIA SPECIES (other than
B. burgdorferi
)
SALMONELLA SPECIES
SHIGELLA SPECIES
STAPHYLOCOCCUS SPECIES
STREPTOCOCCUS SPECIES
TREPONEMA PALLIDUM
VIBRIO CHOLERAE
VIBRIO SPECIES OTHER THAN
V. CHOLERAE
(
V. PARAHEMOLYTICUS
,
V. VULNIFICUS
)
YERSINIA PESTIS
YERSINIA PSEUDOTUBERCULOSIS
AND
ENTEROCOLITICA
Chapter 23: MYCOBACTERIA
MYCOBACTERIUM TUBERCULOSIS (M. tb.)
MYCOBACTERIA OTHER THAN
MYCOBACTERIUM TUBERCULOSIS
Chapter 24: FUNGI
ALTERNARIA SPECIES
References
ASPERGILLUS SPECIES
References
BASIDIOMYCETES (INCLUDING MERULIUS LACRYMANS, LYCOPERDON, AND MUSHROOMS)
References
BLASTOMYCES DERMATITIDIS
References
CANDIDA SPECIES
References
CLADOSPORIUM SPECIES
References
COCCIDIOIDES IMMITIS
References
CRYPTOCOCCUS NEOFORMANS AND CRYPTOCOCCUS GATTII
References
CRYPTOSTROMA CORTICALE
References
FONSECAEA AND OTHER AGENTS OF CHROMOMYCOSIS
References
HISTOPLASMA CAPSULATUM
References
MADURELLA SPECIES AND OTHER AGENTS OF MYCETOMA
References
PARACOCCIDIOIDES BRASILIENSIS
References
PENICILLIUM SPECIES
References
SPOROTHRIX SCHENCKII
References
STACHYBOTRYS CHARTARUM
References
TRICHOPHYTON AND OTHER DERMATOPHYTES
References
ZYGOMYCETES
References
Chapter 25: ANAPLASMA, CHLAMYDOPHILA, COXIELLA, EHRLICHIA, and RICKETTSIA
ANAPLASMA
References
CHLAMYDOPHILA PSITTACI
References
COXIELLA BURNETII
References
EHRLICHIA SPECIES
References
RICKETTSIA RICKETTSII
References
Chapter 26: PARASITES
CRYPTOSPORIDIUM PARVUM
References
CYCLOSPORIASIS
References
CUTANEOUS, MUCOCUTANEOUS, AND VISCERAL LEISHMANIASIS
References
NANOPHYETUS
References
PFIESTERIA PISCICIDA
References
PLASMODIUM SPECIES
References
TOXOPLASMA GONDII
References
Chapter 27: ENVENOMATIONS
ARTHROPOD ENVENOMATIONS
HYMENOPTERA
References
LATRODECTUS
SPECIES
References
LOXOSCELES
SPECIES
References
SCORPIONIDA (SCORPIONS)
References
MARINE ENVENOMATIONS
CATFISH
References
COELENTERATE: ANTHOZOA
References
COELENTERATE: HYDROZOA
References
COELENTERATA: SCYPHOZOA
References
DASYATIS
(STINGRAY)
References
ECHINODERMATA
References
MOLLUSCA
References
PORIFERA
References
SCORPAENIDAE
References
SNAKE ENVENOMATIONS
COLUBRIDAE
References
CROTALIDAE
References
ELAPIDAE
References
HYDROPHIDAE
References
Chapter 28: ALLERGENS
ENZYMES
References
FARM ANIMALS
References
GRAIN DUST
References
INSECTS
References
LABORATORY ANIMALS
References
MITES
References
PLANTS
References
SHELLFISH AND OTHER MARINE INVERTEBRATES
References
WHEAT FLOUR AND EGG
References
Chapter 29: LATEX
OCCUPATIONAL SETTING
EXPOSURE (ROUTE)
PATHOBIOLOGY
DIAGNOSIS
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 30: MALIGNANT CELLS
OCCUPATIONAL SETTING
EXPOSURE (ROUTE)
PATHOBIOLOGY
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 31: RECOMBINANT ORGANISMS
OCCUPATIONAL SETTING
EXPOSURE (ROUTE)
PATHOBIOLOGY
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 32: PRIONS
OCCUPATIONAL SETTING
EXPOSURE (ROUTE)
PATHOBIOLOGY
DIAGNOSIS
TREATMENT
PREVENTION
References
Chapter 33: ENDOTOXINS
OCCUPATIONAL SETTING
EXPOSURE (ROUTE)
PATHOBIOLOGY
ACUTE EXPOSURES
CHRONIC EXPOSURE
DIAGNOSIS
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
Chapter 34: WOOD DUST
OCCUPATIONAL SETTING
EXPOSURE (ROUTE)
PATHOBIOLOGY
DIAGNOSIS
TREATMENT
MEDICAL SURVEILLANCE
PREVENTION
References
INDEX
END USER LICENSE AGREEMENT
List of Tables
Chapter 01
TABLE 1.1 Mathematical unit prefixes.
TABLE 1.2 The disciplines of mechanics.
TABLE 1.3 Mathematical expressions of Galileo’s description of kinematics.
TABLE 1.4 Newton’s laws of motion.
TABLE 1.5 Mathematical expressions of force, work, and energy.
TABLE 1.6 Mathematical equations for electromagnetic radiation.
TABLE 1.7 Major characteristics of the physical hazards.
TABLE 1.8 Engineering and administrative controls for physical hazards.
TABLE 1.9 Commonly used personal protective equipment for physical hazards.
Chapter 02
TABLE 2.1 Work-related MSD named by occupation.
TABLE 2.2 Evidence for causal relationship between physical work factors and upper extremity musculoskeletal disorders.
TABLE 2.3 Physical stressors checklist.
TABLE 2.4 Hand activity level (0–10) is related to exertion, frequency, and duty cycle (% of work cycle where force is greater than 5% of maximum).
TABLE 2.5 Common upper extremity musculoskeletal disorders by ICD-10 codes.
TABLE 2.6 Interventions used by physiotherapists to treat upper extremity musculoskeletal disorders.
Chapter 03
TABLE 3.1 Risk factors associated with manual material handling injuries.
TABLE 3.2 Ergonomic assessment tools.
TABLE 3.3 Portion of a Psychophysical Table for maximum acceptable Push Force.
TABLE 3.4 Guidelines for recording work activities on videotape.
TABLE 3.5 Formulas for individual multipliers.
TABLE 3.6 Frequency multiplier (FM).
TABLE 3.7 Coupling multiplier (CM).
Chapter 04
TABLE 4.1 The Stockholm Workshop Scale for the classification of cold‐induced Raynaud’s phenomenon in the Hand‐arm Vibration Syndrome [vascular].
TABLE 4.2 The Stockholm Workshop Scale for the classification of sensorineural affects of the Hand‐arm Vibration Syndrome.
Chapter 05
TABLE 5.1 Types of direct injuries and their causes.
TABLE 5.2 Table of contents for 29 CFR Part 1910 occupational safety and health standards (https://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=9696).
TABLE 5.3 OSHA log-based safety performance metrics.
TABLE 5.4 Indicators of a need for further assessment.
TABLE 5.5 Identifying pertinent equipment, operations, and procedures.
TABLE 5.6 Examples of machines that usually require point of operation guarding.
TABLE 5.7 Definitions for machine guarding.
TABLE 5.8 OSHA required openings in inches to guard a power punch press (CFR 1910.217(g)).
TABLE 5.9 Definitions for lockout/tagout.
TABLE 5.10 Training and communication for lockout/tagout as a paradigm for hazards control training.
Chapter 06
TABLE 6.1 Work sites with heat exposure.
TABLE 6.2 Measures of external heat.
TABLE 6.3 Metabolic rate categories and example activities.
TABLE 6.4 Examples of permissible heat exposure threshold limit values: screening criteria for TLV and action limit for heat stress exposure.
TABLE 6.5 Heat balance equation.
TABLE 6.6 Risk factors predisposing to heat disorders.
TABLE 6.7 NIOSH recommended medical surveillance for heat-exposed workers.
TABLE 6.8 Heat strain/heat-related illness prevention.
Chapter 07
TABLE 7.1 Cooling power of the wind on exposed flesh expressed as equivalent temperature (under calm conditions).
TABLE 7.2 Threshold limit values® for work/warm-up schedule for 4-h shift.
TABLE 7.3 Survival times in cold water.
Chapter 08
TABLE 8.1 High-pressure and diving environments.
TABLE 8.2 Units of pressure used in hyperbaric environments.
TABLE 8.3 Toxic effects of gases on divers.
TABLE 8.4 General industrial hazards that may be encountered in the underwater work environment.
TABLE 8.5 Human health effects of environmental pressure change.
TABLE 8.6 A matrix for describing decompression illness.
TABLE 8.7 US Navy Treatment Table 6: Oxygen Treatment of Type II Decompression Sickness.
Chapter 09
TABLE 9.1 Altitude–pessure–temperature relationships.
TABLE 9.2 Atmospheric pressure and oxygen levels at altitude.
TABLE 9.3 Oxyhemoglobin saturation at selected altitudes.
TABLE 9.4 Duration of useful consciousness.
Chapter 10
TABLE 10.1 Potential contraindications for working night or rotating shifts.
Chapter 11
TABLE 11.1 Examples of potential occupational exposure to ionizing radiation beyond US EPA 1 mSv limit set for general public.
TABLE 11.2 Estimates of Effective Dose from Common Single X-rays.
TABLE 11.3 Estimates of Effective Dose from Complete X-ray Procedures.
TABLE 11.4 Types of ionizing radiation important to radiologic health.
TABLE 11.5 Units of radiation and radioactivity.
TABLE 11.6 Ionizing radiation exposure guidelines for the United States.
TABLE 11.7 US federal OSHA radiation exposure limits under 29 CFR 1910.1096.
TABLE 11.8 Signs and Symptoms of Acute Radiation Syndrome in the Three Phases after Exposure. Adapted from Diagnosis and treatment of radiation injuries. Safety series no. 2. Vienna/International Atomic Energy Agency 1998. Reprinted with Permission.
TABLE 11.9 Stages of Cutaneous Radiation Injury.
TABLE 11.10 Examples of decorporation therapies for internal contamination.
TABLE 11.11 Thyroid prophylaxis doses in radiation incident involving radioiodine.
Chapter 15
TABLE 15.1 Radiofrequency and microwave radiation standards.
TABLE 15.2 Electrical and magnetic field strengths at ground level near high-tension transmission lines.
TABLE 15.3 Typical electric and magnetic fields.
TABLE 15.4 Biological effects reported with ELF EMF fields.
Chapter 16
TABLE 16.1 Some industries with risks of hazardous noise exposure.
TABLE 16.2 Sound pressure level versus A-scale.
TABLE 16.3 Time–intensity trading.
Chapter 17
TABLE 17.1 Factors in the Physical Examination and Work-Up Suggesting a High-Risk Electric Injury.
TABLE 17.2 Lightning versus high-voltage electrical injury.
TABLE 17.3 Neurological Sequelae of Lightning Strike.
TABLE 17.4 Recommendations for preventing injuries from lightning strike.
Chapter 20
TABLE 20.1 Disinfectants and their uses.
TABLE 20.2 Vaccines and immunobiologicals commonly administered in occupational settings.
TABLE 20.3 Vaccines and immunobiologicals commonly administered for international travel.
TABLE 20.4 Immunocompromising conditions with potential occupational significance.
TABLE 20.5 Potential Biological Warfare Agents
Chapter 21
TABLE 21.1 Hepatitis B Serologic Patterns.
TABLE 21.2 Post-exposure management of healthcare personnel after occupational percutaneous and mucosal exposure to blood and body fluids, by healthcare personnel Hepatitis B vaccination and response status.
TABLE 21.3 Number of confirmed or possible cases of occupationally acquired HIV infection among health care workers reported to CDC — United States, 1985–2013.
TABLE 21.4 Preferred HIV PEP Regimen.
TABLE 21.5 Currently available rabies biologics.
TABLE 21.6 Rabies post-exposure prophylaxis guide.
TABLE 21.7 Rabies post-exposure prophylaxis (PEP) schedule.
TABLE 21.8 Rabies pre-exposure prophylaxis schedule.
TABLE 21.9 Rabies pre-exposure prophylaxis guide — United States, 2008.
Chapter 22
TABLE 22.1 ACIP recommendations for anthrax vaccination.
TABLE 22.2 Host animals for Brucella species causing disease in humans (adapted from CDC: http://www.cdc.gov/brucellosis/veterinarians/host-animals.html)
TABLE 22.3 CDC recommendations for tetanus wound management.
Chapter 23
TABLE 23.1 Criteria for positive Mantoux test.
TABLE 23.2 Courses of action for typical scenarios when occupational tuberculosis surveillance is conducted.
TABLE 23.3 Risk classifications for various health-care settings and recommended frequency of screening for
Mycobacterium tuberculosis
infection among health-care workers (HCWs).
Chapter 24
TABLE 24.1 Common fungi associated with hypersensitivity diseases.
TABLE 24.2 Common toxigenic fungi.
TABLE 24.3 Occupational fungal infections.
Chapter 29
TABLE 29.1 Prevalence of latex hypersensitivity according to exposure group.
TABLE 29.2 Major food allergies associated with latex hypersensitivity and their prevalence among latex-hypersensitive patients. Adapted from Kim and Hussain.
TABLE 29.3 Common items containing latex.
TABLE 29.4 Recommendations for healthcare workers with latex hypersensitivity.
Chapter 31
TABLE 31.1 Selected products from recombinant organisms.
List of Illustrations
Chapter 01
FIGURE 1.1 Stylized representation of an electromagnetic wave.
FIGURE 1.2 The electromagnetic spectrum.
FIGURE 1.3 Interactions of electromagnetic radiation and biological tissue.
Chapter 02
FIGURE 2.1 Number and incident rate of musculoskeletal disorders involving days away from work, 2008–2014.
FIGURE 2.2 Incidence rate of musculoskeletal disorders involving days away from work by age group, 2014. FTW, full-time workers.
FIGURE 2.3 Musculoskeletal disorder incidence rates for selected private sector industries, 2013–2014.
FIGURE 2.4 Visual analog scale for rating hand activity level (0–10) with verbal anchors.
FIGURE 2.5 The TLV® for reduction of work related musculo-skeletal disorders based on “hand activity” or “HAL” and peak hand force. The top line depicts the TLV®. The bottom line is an Action Limit for which general controls are recommended. .
FIGURE 2.6 Explanatory model of the impact of psychosocial work environmental factors on the onset of musculoskeletal disorders.
Chapter 03
FIGURE 3.1 Manual material handling checklist.
Chapter 04
FIGURE 4.1 Hand‐arm and whole‐body biodynamic coordinate systems for human measurements.
FIGURE 4.2 Biodynamic and basicentric coordinate systems for hand‐arm vibration and power tool measurements.
FIGURE 4.3
a
z
acceleration limits as a function of vibration frequency and exposure time .
FIGURE 4.4
a
x
and
a
y
acceleration limits as a function of vibration frequency and exposure time .
FIGURE 4.5 Nominal gain characteristics of the filter network used to frequency‐weight acceleration components (continuous line). The dashed lines suggest filter tolerances. This is the basis of the ACGIH HAV TLV
®
(1984‐present), ISO 5349‐1 (2001‐present), ANSI S3.34 (1986–2006), and ANSI S2.70 (2006‐present).
FIGURE 4.6 Typical trailer hook in a coupler ring on a dolly to allow a tractor‐trailer set to pull a second trailer. The constraining latch is raised and the compression pad is retracted for visualization purposes. Without the compression pad in place, the space between the pin and tongue ring would be a potential source of slack‐action impact.
FIGURE 4.7 Typical train car couplers. The space provides a source for potential slack‐action impact. Couplers attached to their cars using a spring tend to reduce the impact from slack action at the coupler. (Insight based on personal communication with Robert Hitson) .
FIGURE 4.8 Side view of a style of train‐car coupler that has a design that tends to reduce slack‐action impact at the coupler. (Insight based on personal communication with Robert Hitson) .
Chapter 05
FIGURE 5.1 OSHA 300 and 301 forms (US Department of Labor—Occupational Safety and Health Administration). Fillable PDF files are available at https://www.osha.gov/recordkeeping/ppt1/RK1exempttable.html
FIGURE 5.2 The OSHA 301 form is used to complete the OSHA 300 Log. It must be kept on file for 5 years with the OSHA 300 record (US Department of Labor—Occupational Safety and Health Administration). Fillable PDF files are available at https://www.osha.gov/recordkeeping/RKforms.html
Chapter 06
FIGURE 6.1 Manual, analog WBGT monitor; automated WBGT monitors are available from a variety of manufacturers.
FIGURE 6.2 Heat stress decision tree.
FIGURE 6.3 Recommended heat stress alert limits for heat-unacclimatized workers. C = ceiling limit; RAL = Recommended Alert Limit. Calculations are for a standard worker of 70 kg (154 lb) body weight and 1.8 m (19.4 ft) body surface.
FIGURE 6.4 Recommended heat stress exposure limit for heat-acclimatized workers. C = ceiling limit; REL = Recommended Exposure Limit. Calculations are for a standard worker of 70 kg (154 lb) body weight and 1.8 m (19.4 ft) body surface.
Chapter 08
FIGURE 8.1 A saturation system diving bell.
FIGURE 8.2 SCUBA equipment.
FIGURE 8.3 Diver using Draeger LAR V closed-circuit SCUBA equipment.
FIGURE 8.4 Deep sea diving equipment
FIGURE 8.5 Surface-supplied diving: Diver using a grinding tool.
FIGURE 8.6 Surface-supplied diving: Diver water gouging.
FIGURE 8.7 Surface-supplied diving: Diver welding.
FIGURE 8.8 Surface-supplied diving: Diver working on Habitat with Bell.
FIGURE 8.9 Hyperbaric recompression chamber.
FIGURE 8.10 U.S. Navy Treatment Table 6.
Chapter 10
FIGURE 10.1 Model of interrelated pathways from shift work “circadian stress” to cardiovascular disease outcomes.
Chapter 11
FIGURE 11.1 Sources of Natural and Manmade Background Radiation.
FIGURE 11.2 Interior of a thermoluminescent dosimeter (TLD), showing areas for beta, gamma, and neutron detection.
FIGURE 11.3 Different conceptual models for cancer risk from ionizing radiation dose. The National Research Council Biological Effects of Ionizing Radiation VII Phase 2 report adopts the Linear No-Threshold model (noted above for high and low dose rates) as more scientifically plausible than the threshold model. The linear quadratic model was adopted for leukemias.
FIGURE 11.4 EPA Map of Radon Zones.
FIGURE 11.5 Cytogenetic Assay for Dicentric Chromosomes.
Chapter 16
FIGURE 16.1 Median audiograms for noise-exposed and control subjects.
FIGURE 16.2 Noise-induced permanent threshold shift as a function of time for different frequencies and exposure levels.
FIGURE 16.3 Speech frequency age-related permanent threshold shift as a function of age and gender.
FIGURE 16.4 Speech frequency noise-induced permanent threshold shift as a function of time for different exposure levels.
Chapter 21
FIGURE 21.1 West Nile Virus Incidence per 100 000 of reported cases of neuroinvasive disease — United States and U.S. territories, 2013. Data from the Division of Vector-Borne Diseases (DVBD), National Center for Emerging and Zoonotic Infectious Diseases (ArboNET Surveillance). In 2013, eight states reported an incidence of West Nile virus (WNV) neuroinvasive disease >1 case per 100,000; the four states with the highest reported incidence were North Dakota (8.9), South Dakota (6.8), Nebraska (2.9), and Wyoming (2.8). Six states reported approximately half of the WNV neuroinvasive disease cases: California (237 cases), Texas (113), Colorado (90), Illinois (86), North Dakota (64), and Oklahoma (60).
FIGURE 21.2 Approximate geographic distribution of
Dermacentor andersoni
ticks and counties of residence for confirmed and probable Colorado tick fever (CTF) virus disease cases, United States, 2002–2012. *All cases were acquired in states where local transmission of CTF virus has been reported previously. Two additional cases were reported from Colorado with unknown county of residence. **Derived from James AM, Freier JE, Keirans JE, Durden LA, et al. Distribution, seasonality, and hosts of the Rocky Mountain wood tick in the United States.
J Med Entomol
2006; 43:17–24.
FIGURE 21.3 Dengue fever and dengue hemorrhagic fever. Number of reported cases, by location of residence — United States and U.S. territories, 2013. Number of Dengue fever cases/number of Dengue Hemmorrhagic fever. Data from the Division of Vector-Borne Diseases (DVBD), National Center for Emerging and Zoonotic Infectious Diseases (ArboNET Surveillance).
†
New York City reported cases 131/1.
§
Puerto Rico locally acquired cases 9 557/153.
¶
Virgin Islands reported cases 169/5. .
FIGURE 21.4 Confirmed global cases of MERS-CoV.
FIGURE 21.5 Total reported suspected, probable, and confirmed cases in Guinea, Liberia, and Sierra Leone beginning March 25, 2014 through November 8, 2015.
FIGURE 21.6 Viral Hepatitis Incidence per 100 000 population by year — United States, 1983–2013.
†
Hepatitis A vaccine was first licensed in 1995.
§
Hepatitis B vaccine was first licensed in June 1982.
¶
An anti-hepatitis C virus (HCV) antibody test first became available in May 1990. Hepatitis A incidence declined during 1998–2011 and increased in 2012 and 2013. The hepatitis A vaccine became available in 1995, the last year a peak in incidence of acute, symptomatic hepatitis A was observed. Coinciding with the implementation of the national vaccination strategy to eliminate hepatitis B infections, the incidence of acute hepatitis B has declined since 1987. Acute hepatitis B incidence has remained stable since 2008. The incidence of acute hepatitis C remained fairly stable during 1992–2000, declined in 2001 and 2002, remained stable during 2003–2005, and increased in 2011, 2012, and 2013. Recent investigations suggest this increase is largely driven by acute infections in nonurban young persons who start injecting drugs after habituation to oral prescription opioid drugs such as “OxyContin” and oxycodone. .
FIGURE 21.7 Hepatitis A Incidence by county — United States, 2013. Although effective vaccines to prevent Hepatitis A virus infections have been available in the United States since 1995, cases still occur in almost every state. In 2013, a total of 1,781 cases were reported and 17 counties in 13 states reported incidence rates of >10 cases per 100,000 population. Two of these counties in one state reported incidence rates of >20 cases. .
FIGURE 21.8 Number of confirmed cases (N = 58) of occupationally acquired HIV infection among health care workers reported to CDC — United States, 1985–2013. .
FIGURE 21.9 HIV Diagnoses Per 100 000 population – United States and U.S. territories, 2013. .
FIGURE 21.10 Measles Incidence per 100 000 by year — United States, 1978–2013.
†
In the inset figure, the
Y
axis is a log scale. Measles vaccine was licensed in 1963. Endemic measles was declared eliminated from the United States in 2000. .
FIGURE 21.11 MUMPS Incidence per 100 000 by year — United States, 1988–2013.
†
In the inset figure, the
Y
axis is a log scale. The widespread use of a second dose of mumps vaccine beginning in 1989 was followed by historically low morbidity until 2006, when the United States experienced the largest mumps outbreak in two decades. The 2006 outbreak of approximately 6,000 cases primarily affected college students aged 18–24 years in the Midwest. A second large outbreak occurred during 2009–2010 and affected Orthodox Jewish communities in the Northeast. .
FIGURE 21.12 Animal Rabies reported cases, by county
*
— United States, 2013.
*
Data from the National Center for Emerging and Zoonotic Infectious Diseases, Division of High-consequence Pathogens and Pathology. Several rabies virus variants associated with distinct reservoir species have been identified in the United States. The circulation of rabies virus variants associated with raccoons (eastern United States), skunks (central United States and California), and foxes (Texas, Arizona, and Alaska) occur over defined geographic areas. Several distinct rabies virus variants associated with different bat species are broadly distributed across the contiguous United States. Hawaii is the only state considered free of rabies. .
FIGURE 21.13 Varicella (Chickenpox). Number
*
of reported cases — Illinois, Michigan, Texas, and West Virginia, 1991–2013.
*
In thousands. Varicella was not nationally notifiable in 1996, when the first dose of the varicella vaccine was recommended in the United States. However, four states (Michigan, Illinois, Texas, and Virginia) were reporting varicella cases to CDC before the varicella vaccine was recommended and have continued reporting, providing consistent data to allow for monitoring of trends in varicella disease. In these four states, the number of cases reported in 2013 was 23% lower than 2012, 74% lower than the average annual number reported during the mature 1-dose varicella vaccination era of 2000–2006, and 96% lower than the average annual number reported during the prevaccine years of 1993–1995. .
Chapter 22
FIGURE 22.1 Reported cases of Lyme disease in USA, 2014.
FIGURE 22.2 CDC diagnostic testing algorithm for Lyme disease.
FIGURE 22.3 Number of reported cases of brucellosis – United States and U.S. territories, 2010.
FIGURE 22.4 Tetanus – number of reported cases and deaths, United States, 1900–2010.
FIGURE 22.5
E. coli
O157 outbreaks in the United States, 1982–2002 (
N
= 350).
FIGURE 22.6 Reported cases of tularemia — United States, 2001–2010.
FIGURE 22.7 Meningococcal disease – reported cases per 100 000 population, by year, United States, 1970–2011.
FIGURE 22.8 Salmonellosis and Shigellosis – reported cases per 100 000 population by year, United States, 1982–2012.
FIGURE 22.9 Typhoid fever – reported cases by year, United States, 1982–2012.
FIGURE 22.10 Plague – reported cases among humans, United States, 1970–2012.
Chapter 23
FIGURE 23.1 Incidence of tuberculosis (TB) cases, by state and national average, during 2014. The national TB incidence in 2014 was 3.0 cases per 100 000 persons, ranging by state from 0.3 in Vermont to 9.6 in Hawaii (median = 2.0).
FIGURE 23.2 Number and rate per 100 000 of tuberculosis (TB) cases among U.S.-born and foreign-born persons, by year reported — United States, 2000–2014.
FIGURE 23.3 Rate of new diagnoses of Hansen’s disease, by U.S. birth status — United States, 1994–2011.
Chapter 24
FIGURE 24.1 Photomicrograph showing Alternaria spores.
FIGURE 24.2 Tissue sample hematoxylin and eosin stain revealing Aspergillus hyphae in tissue.
FIGURE 24.3 Bronchoalveolar lavage sample demonstrating typical yeast forms of Blastomycosis.
FIGURE 24.4 Grocott’s methenamine silver stain showing Candida yeast forms.
FIGURE 24.5 Photomicrograph of Cladosporium conidia.
FIGURE 24.6 Tissue sample hematoxylin and eosin stain revealing a typical spherule of Coccidioidomycosis.
FIGURE 24.7 Gram stain of fluid obtained from lumbar puncture demonstrating encapsulated
Cryptococcus
yeast forms.
FIGURE 24.8 Tissue sample hematoxylin and eosin stain revealing a cluster of brown thick walled cells of
Fonsecaea
.
FIGURE 24.9 Grocott’s methenamine silver stain showing Histoplasma yeast forms.
FIGURE 24.10 Tissue sample hematoxylin and eosin stain revealing a fungal mycetoma from Madurella.
FIGURE 24.11 Photomicrograph of Penicillium conidia.
FIGURE 24.12 Lactophenol cotton blue wet mount revealing Trichophyton tonsurans.
FIGURE 24.13 Tissue sample hematoxylin and eosin stain showing Zygomycetes hyphae.
Chapter 25
FIGURE 25.1 Map of the United States showing the number of
Anaplasma phagocytophilum
cases by county in 2012. Cases are reported primarily from the upper Midwest and coastal New England, reflecting both the range of the primary tick vector species, Ixodes scapularis—also known to transmit Lyme disease and babesiosis—and the range of preferred animal hosts for tick feeding.
FIGURE 25.2 Morulae detected in a granulocyte on a peripheral blood smear, associated with
A. phagocytophilum
infection. .
FIGURE 25.3 Map of the United States and U.S. territories showing the number of acute and chronic Q fever cases in each state and territory in 2013. Q fever, caused by
Coxiella burnetii
, is reported throughout the United States. Human cases of Q fever most often result from contact with infected livestock, especially sheep, goats, and cattle.
*
Number of Q fever acute cases/number of Q fever chronic cases.
FIGURE 25.4 Map of the United States showing the number of Ehrlichiosis (
Ehrlichia chaffeensis
) cases by county in 2013.
E. chaffeensis
is the most common type of ehrlichiosis infection in the United States. This tick-borne pathogen is transmitted by
Amblyomma americanum
, the lonestar tick, whose geographic range extends from the Southeast into parts of the Northeast and Midwest. The majority of cases of
E. chaffeensis
are reported from the Midwest, South, and Northeast regions. .
FIGURE 25.5 Map of the United States that presents the number of Ehrlichiosis (
Ehrlichia ewingii
) cases in by county in 2013.
Ehrlichiosis ewingii
is the least common cause of ehrlichiosis.
E. ewingii
is carried by
Amblyomma americanum
, the lonestar tick, which is the same vector that transmits
E. chaffeensis
. Currently, no serologic tests are used to distinguish between the two species, and differentiation can only be made by molecular genotyping. .
FIGURE 25.6 Morulae detected in a monocyte on a peripheral blood smear, associated with
E. chaffeensis
infection.
FIGURE 25.7 Map showing the number of spotted fever rickettsiosis cases by county in the United States in 2012. In the United States, the majority of cases of spotted fever rickettsiosis are attributed to infection with
Rickettsia rickettsii
, the causative agent of Rocky Mountain spotted fever (RMSF), but might also be from other agents such as
Rickettsia parkeri
and
Rickettsia
species 364D. RMSF is ubiquitous across the United States, which represents the widespread nature of the three tick vectors known to transmit RMSF:
Dermacentor variabilis
in the East,
Dermacentor andersoni
in the West, and
Rhipicephalus sanguineus
, recently recognized as a new tick vector in parts of Arizona. Historically, much of the incidence of RMSF has been in the Central Atlantic region and parts of the Midwest; however, endemic transmission of RMSF in Arizona communities has led to a substantial reported incidence rate. .
Chapter 26
FIGURE 26.1
Cryptosporidium
Life Cycle. Sporulated oocysts, containing 4 sporozoites, are excreted by the infected host through feces and possibly other routes such as respiratory secretions
. Transmission of
Cryptosporidium parvum
and
C. hominis
occurs mainly through contact with contaminated water (e.g., drinking or recreational water). Occasionally food sources, such as chicken salad, may serve as vehicles for transmission. Many outbreaks in the United States have occurred in waterparks, community swimming pools, and day care centers. Zoonotic and anthroponotic transmission of
C. parvum
and anthroponotic transmission of
C. hominis
occur through exposure to infected animals or exposure to water contaminated by feces of infected animals
. Following ingestion (and possibly inhalation) by a suitable host
, excystation
occurs. The sporozoites are released and parasitize epithelial cells (
,
) of the gastrointestinal tract or other tissues such as the respiratory tract. In these cells, the parasites undergo asexual multiplication (schizogony or merogony) (
,
,
) and then sexual multiplication (gametogony) producing microgamonts (male)
and macrogamonts (female)
. Upon fertilization of the macrogamonts by the microgametes (
), oocysts (
,
) develop that sporulate in the infected host. Two different types of oocysts are produced, the thick-walled, which is commonly excreted from the host
, and the thin-walled oocyst
, which is primarily involved in autoinfection. Oocysts are infective upon excretion, thus permitting direct and immediate fecal-oral transmission. Centers for Disease Control and Prevention. Parasites –
Cryptosporidium
.
FIGURE 26.2
Cyclospora
Life Cycle. Some of elements of this figure were created based on an illustration by Ortega et al.
Cyclospora cayetanensis
. In: Advances in Parasitology: opportunistic protozoa in humans. San Diego: Academic Press; 1998. p. 399–418. When freshly passed in stools, the oocyst is not infective
(thus, direct fecal-oral transmission cannot occur; this differentiates
Cyclospora
from another important coccidian parasite,
Cryptosporidium
). In the environment
, sporulation occurs after days or weeks at temperatures between 22°C to 32°C, resulting in division of the sporont into two sporocysts, each containing two elongate sporozoites
. Fresh produce and water can serve as vehicles for transmission
and the sporulated oocysts are ingested (in contaminated food or water)
. The oocysts excyst in the gastrointestinal tract, freeing the sporozoites which invade the epithelial cells of the small intestine
. Inside the cells they undergo asexual multiplication and sexual development to mature into oocysts, which will be shed in stools
. The potential mechanisms of contamination of food and water are still under investigation.
FIGURE 26.3 Cutaneous leishmaniasis. Geographical distribution of Old World cutaneous leishmaniasis due to
L. tropica
and related species and
L. aethiopica
. Geographical distribution of Old World cutaneous leishmaniasis due to
L. major
.
FIGURE 26.4 Geographical distribution of cutaneous and mucocutaneous leishmaniasis in the New World.
FIGURE 26.5 Geographical distribution of visceral leishmaniasis in the Old and New world.
FIGURE 26.6 Leishmaniasis Life Cycle: Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies. The sandflies inject the infective stage (i.e., promastigotes) from their proboscis during blood meals
. Promastigotes that reach the puncture wound are phagocytized by macrophages
and other types of mononuclear phagocytic cells. Progmastigotes transform in these cells into the tissue stage of the parasite (i.e., amastigotes)
, which multiply by simple division and proceed to infect other mononuclear phagocytic cells
. Parasite, host, and other factors affect whether the infection becomes symptomatic and whether cutaneous or visceral leishmaniasis results. Sandflies become infected by ingesting infected cells during blood meals (
,
). In sandflies, amastigotes transform into promastigotes, develop in the gut
(in the hindgut for leishmanial organisms in the
Viannia
subgenus; in the midgut for organisms in the
Leishmania
subgenus), and migrate to the proboscis
.
FIGURE 26.7 Number of malaria cases by state or territory in which case was diagnosed—United States, 2011. Number of malaria cases (
N
= 1925) by state or territory in which case was diagnosed—United States, 2011. Nearly all of these cases are imported, though there are rare instances of transmission due to blood transfusion or organ transplantation, congenital transmission, or mosquito-borne cases. Approximately 3–5 malaria deaths occur annually in the U.S. Most of these deaths are due to delayed diagnosis and treatment.
FIGURE 26.8 Malaria parasite life cycle. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female
Anopheles
mosquito inoculates sporozoites into the human host
. Sporozoites infect liver cells
and mature into schizonts
, which rupture and release merozoites
. (Of note, in
P. vivax
and
P. ovale
a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks, or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony
), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony
). Merozoites infect red blood cells
. The ring stage trophozoites mature into schizonts, which rupture releasing merozoites
. Some parasites differentiate into sexual erythrocytic stages (gametocytes)
. Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an
Anopheles
mosquito during a blood meal
. The parasites’ multiplication in the mosquito is known as the sporogonic cycle
. While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes
. The zygotes in turn become motile and elongated (ookinetes)
which invade the midgut wall of the mosquito where they develop into oocysts
. The oocysts grow, rupture, and release sporozoites
, which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites
into a new human host perpetuates the malaria life cycle.
FIGURE 26.9 How travelers can protect themselves against malaria. This picture shows some things that travelers can use to protect themselves against malaria: malaria pills, insect repellent, long-sleeved clothing, bed net, and flying insect spray. (Not shown, but also protective: air conditioned or screened quarters.) Based on the risk assessment, specific malaria prevention interventions should be used by the traveler. Often this includes avoiding mosquito bites through the use of repellents or insecticide treated bed nets, and specific medicines to prevent malaria.
FIGURE 26.10
Toxoplasma gondii
Life Cycle: The only known definitive hosts for
Toxoplasma gondii
are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces
. Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water or plant material contaminated with oocysts
. Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites
. Cats become infected after consuming intermediate hosts harboring tissue cysts
. Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment
. Humans can become infected by any of several routes:
eating undercooked meat of animals harboring tissue cysts
.
consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat)
.
blood transfusion or organ transplantation
.
transplacentally from mother to fetus
.
In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens
. Diagnosis of congenital infections can be achieved by detecting
T. gondii
DNA in amniotic fluid using molecular methods such as PCR
.
In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens
. Diagnosis of congenital infections can be achieved by detecting
T. gondii
DNA in amniotic fluid using molecular methods such as PCR
.
Guide
Cover
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