Roseola pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Roseola has two phases, the febrile and the rash phase. During the first phase, HHV6 replicates in salivary glands and is secreted as primary source of infection. After completes resolution of the febrile phase, due to the latency of the virus in the lymphocytes and monocytes, the rash phase begins. | |||
==Pathophysiology== | ==Pathophysiology== | ||
Roseola has two phases: | |||
#The febrile phase | #The febrile phase | ||
#The rash phase | #The rash phase |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Roseola has two phases, the febrile and the rash phase. During the first phase, HHV6 replicates in salivary glands and is secreted as primary source of infection. After completes resolution of the febrile phase, due to the latency of the virus in the lymphocytes and monocytes, the rash phase begins.
Pathophysiology
Roseola has two phases:
- The febrile phase
- The rash phase
Transmission of infection
The febrile phase
- HHV 6 virus is replicated in the salivary glands and secreted in saliva in the primary infection.
- Intrauterine transmission was suggested by polymerase chain reaction (PCR) positivity of uncultured cord blood mononuclear cells.
- CNS invasion is believed to occur in rare cases accounting for some of the CNS manifestations such as febrile seizures.
The rash phase
- In the second phase of the disease, the HHV 6 virus is found to remain latent in lymphocytes and monocytes and found in low levels in some tissues. CD4 positive T cells have been found to support the growth of roseola.
Pathogenesis
- The pathogenesis of roseola is unknown. However, in a prospective study of 38 children with roseola, human herpesvirus 6 (HHV-6) was detected in a blood sample in all of the children during the period of high fever [1].
- The human herpes virus infects the T cells, monocytes-macrophages, epithelial cells, and central nervous system cells resulting in a chronic infection.
- HHV-6 has tropism towards CD4 T cells and replicates in the T cells inducing a lifelong latent infection in humans.
- The pathogenicity of HHV-7 is not well understood.
Genetics
- Chromosomal integration of HHV-6A and HHV-6B is responsible for transmission of infection from the parents to the newborn and is observed in 1% of the population.
Associated conditions
A more serious form of HHV 6 is seen in older children, imnmunocompromised adults and organ transplant patients.
Gross pathology
There are no gross pathologic findings associated with roseola.
Microscopic pathology
There are no microscopic findings associated with roseola.
References
- ↑ Asano Y, Yoshikawa T, Suga S, Yazaki T, Hata T, Nagai T; et al. (1989). "Viremia and neutralizing antibody response in infants with exanthem subitum". J Pediatr. 114 (4 Pt 1): 535–9. PMID 2647944.