Cytomegalovirus infection pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]
Overview
Pathophysiology
Transmission
- Transmission of CMV occurs from person to person.
- Seroprevalence is age-dependent: 58.9% of individuals aged 6 and over are infected with CMV while 90.8% of individuals aged 80 and over are positive for CMV.[1]
- Infection requires close, intimate contact with a person excreting the virus in their saliva, urine, blood, tears, and semen.
- The shedding of virus may take place intermittently, without any detectable signs, and without causing symptoms.
- CMV can be sexually transmitted and can also be transmitted via breast milk, transplanted organs, and rarely from blood transfusions.
- Although CMV is not highly contagious, it has been shown to spread in households and among young children in day care centers.[2]
Pathogenesis
- Primary CMV infection causes activation of the immune system and results in a mononucleosis like presentation with hepatitis in immunocompromised individuals and few immunocompetent individuals.[3][4][5][6][7]
- In majority of immunocompetent people, primary CMV infection is sub clinical and asymptomatic.
- Following primary infection the virus persists in a latent form in the host tissues invading the immune system.
- Reactivation can occur in response to inflammatory stimuli, physiologic stress and immunosuppression releasing new virions that can infect new cells causing cmv end organ infection.
- T-cells play a role in controlling the replication of the virus.
- In patients with T-cell deficiency the viral replication is uncontrolled and results in excessive shedding of the virus.
- Reactivation of the virus results in the release of cytokines such as TNF-α and IFN-γ resulting in inflammation.
Genetics
There are no genetic factors predisposing individuals for cytomegalovirus infection.
Associated Conditions
- Symptomatic cytomegalovirus is associated with HIV infection in majority of patients.
Microscopic Pathology
- Microscopically, CMV infection can be demonstrated by the presence of intranuclear inclusion bodies. These inclusion bodies stain dark pink on an H&E stain, and are also called "Owl's Eye" inclusion bodies.
References
- ↑ Staras SAS, Dollard SC, Radford KW; et al. (2006). "Seroprevalence of cytomegalovirus infection in the United States, 1988–1994". Clin Infect Dis. 43: 1143&ndash, 51. PMID 17029132.
- ↑ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. pp. pp. 556, 566–9. ISBN 0838585299.
- ↑ Staras SAS, Dollard SC, Radford KW; et al. (2006). "Seroprevalence of cytomegalovirus infection in the United States, 1988–1994". Clin Infect Dis. 43: 1143&ndash, 51. PMID 17029132.
- ↑ Goodman AL, Murray CD, Watkins J, Griffiths PD, Webster DP (2015). "CMV in the gut: a critical review of CMV detection in the immunocompetent host with colitis". Eur J Clin Microbiol Infect Dis. 34 (1): 13–8. doi:10.1007/s10096-014-2212-x. PMC 4281362. PMID 25097085.
- ↑ Rafailidis PI, Mourtzoukou EG, Varbobitis IC, Falagas ME (2008). "Severe cytomegalovirus infection in apparently immunocompetent patients: a systematic review". Virol J. 5: 47. doi:10.1186/1743-422X-5-47. PMC 2289809. PMID 18371229.
- ↑ Khan TV, Toms C (2016). "Cytomegalovirus Colitis and Subsequent New Diagnosis of Inflammatory Bowel Disease in an Immunocompetent Host: A Case Study and Literature Review". Am J Case Rep. 17: 538–43. PMC 4968430. PMID 27460032.
- ↑ Einbinder Y, Wolf DG, Pappo O, Migdal A, Tsvang E, Ackerman Z (2008). "The clinical spectrum of cytomegalovirus colitis in adults". Aliment Pharmacol Ther. 27 (7): 578–87. doi:10.1111/j.1365-2036.2008.03595.x. PMID 18194509.