Book contents
- Frontmatter
- Dedication
- Contents
- List of Contributors
- Preface
- Part I Clinical syndromes: general
- Part II Clinical syndromes: head and neck
- Part III Clinical syndromes: eye
- Part IV Clinical syndromes: skin and lymph nodes
- Part V Clinical syndromes: respiratory tract
- Part VI Clinical syndromes: heart and blood vessels
- Part VII Clinical syndromes: gastrointestinal tract, liver, and abdomen
- Part VIII Clinical syndromes: genitourinary tract
- Part IX Clinical syndromes: musculoskeletal system
- Part X Clinical syndromes: neurologic system
- Part XI The susceptible host
- Part XII HIV
- Part XIII Nosocomial infection
- Part XIV Infections related to surgery and trauma
- Part XV Prevention of infection
- Part XVI Travel and recreation
- Part XVII Bioterrorism
- Part XVIII Specific organisms: bacteria
- Part XIX Specific organisms: spirochetes
- Part XX Specific organisms: Mycoplasma and Chlamydia
- Part XXI Specific organisms: Rickettsia, Ehrlichia, and Anaplasma
- Part XXII Specific organisms: fungi
- Part XXIII Specific organisms: viruses
- 182 Cytomegalovirus
- 183 Dengue
- 184 Enteroviruses
- 185 Epstein–Barr virus and other causes of the mononucleosis syndrome
- 186 Hantavirus cardiopulmonary syndrome in the Americas
- 187 Herpes simplex viruses 1 and 2
- 188 Human herpesviruses 6, 7, 8
- 189 Influenza
- 190 Papillomavirus in oro-genital infection
- 191 Acute and chronic parvovirus infection
- 192 Rabies
- 193 Varicella-zoster virus
- 194 Viral hemorrhagic fevers
- Part XXIV Specific organisms: parasites
- Part XXV Antimicrobial therapy: general considerations
- Index
- References
182 - Cytomegalovirus
from Part XXIII - Specific organisms: viruses
Published online by Cambridge University Press: 05 April 2015
- Frontmatter
- Dedication
- Contents
- List of Contributors
- Preface
- Part I Clinical syndromes: general
- Part II Clinical syndromes: head and neck
- Part III Clinical syndromes: eye
- Part IV Clinical syndromes: skin and lymph nodes
- Part V Clinical syndromes: respiratory tract
- Part VI Clinical syndromes: heart and blood vessels
- Part VII Clinical syndromes: gastrointestinal tract, liver, and abdomen
- Part VIII Clinical syndromes: genitourinary tract
- Part IX Clinical syndromes: musculoskeletal system
- Part X Clinical syndromes: neurologic system
- Part XI The susceptible host
- Part XII HIV
- Part XIII Nosocomial infection
- Part XIV Infections related to surgery and trauma
- Part XV Prevention of infection
- Part XVI Travel and recreation
- Part XVII Bioterrorism
- Part XVIII Specific organisms: bacteria
- Part XIX Specific organisms: spirochetes
- Part XX Specific organisms: Mycoplasma and Chlamydia
- Part XXI Specific organisms: Rickettsia, Ehrlichia, and Anaplasma
- Part XXII Specific organisms: fungi
- Part XXIII Specific organisms: viruses
- 182 Cytomegalovirus
- 183 Dengue
- 184 Enteroviruses
- 185 Epstein–Barr virus and other causes of the mononucleosis syndrome
- 186 Hantavirus cardiopulmonary syndrome in the Americas
- 187 Herpes simplex viruses 1 and 2
- 188 Human herpesviruses 6, 7, 8
- 189 Influenza
- 190 Papillomavirus in oro-genital infection
- 191 Acute and chronic parvovirus infection
- 192 Rabies
- 193 Varicella-zoster virus
- 194 Viral hemorrhagic fevers
- Part XXIV Specific organisms: parasites
- Part XXV Antimicrobial therapy: general considerations
- Index
- References
Summary
Cytomegalovirus (CMV) permanently resides in its human-restricted host by toggling between productive and latent states of infection. CMV infection is serologically marked by immunoglobulin (Ig) G antibody against CMV. CMV seroprevalence varies widely by geographic region, ranging from 45% to 100% for women of reproductive age. In the US population, CMV seroprevalence is 50% overall and varies by age, socioeconomic status, sexual activity/practice, and race/ethnicity. Over 90% of all persons are CMV seropositive by age 80, 55% of women are seropositive by age 30, and the annual CMV seroconversion (primary infection) rate is ~2% for women of reproductive age. Congenital CMV infection afflicts ~1% of all babies born in the United States, is the leading infectious cause of birth defects, and the most common non-genetic cause of sensorineural hearing loss.
CMV is transmitted through close mucosal contact with body fluids bearing infectious CMV particles, i.e., saliva, urine, breast milk, semen, and cervical secretions. Infants and young children experiencing a primary (acute) CMV infection often continue to shed CMV in urine and, sometimes, saliva for several weeks to months. Immunosuppression or underlying illness may bring about viral shedding in body fluids at any stage of the infection. CMV persists in virtually all tissues and resides latently in monocytes, dendritic cells, and myeloid precursors. Viable tissue or leukocytes of CMV-seropositive donors are a source of CMV infection in seronegative persons. Risk for intrauterine CMV transmission is greatest for maternal primary CMV infection and less for reinfection with another CMV strain or CMV reactivation.
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- Information
- Clinical Infectious Disease , pp. 1161 - 1167Publisher: Cambridge University PressPrint publication year: 2015