Measles Virus Infection
Measles is another example of acute respiratory but systemic viral disease. It is caused by specific virus of a single serotype that pertains to morbillivirus genus.
Measles is extremely contagious – its transmission rate in unvaccinated persons is almost absolute – 95-100%. It is solely human anthroponotic illness.
Measles virus usually gives outbreaks of the disease among children.
Pathogenesis, clinical findings and immunity in measles
Disease transmission is promoted by the airborne mechanism. Incubation period lasts from 9 to 18 days.
Virus replicates in respiratory tract epithelium and moves to regional lymphatic nodes (primary viremia). After second propagation in the lymphoid tissue it spreads throughout the body and penetrates into epithelial cells in skin, conjunctiva, endothelium of vessels, respiratory tract, etc.
Virus persists within circulating immune cells that facilitates viremia.
Giant cells appearance and symplast formation is observed in tissue epithelial cells. Measles virus F-protein activates intercellular fusion. It permits direct viral spread across the epithelial layer and prevents virions against antibody neutralization.
Prodromal phase lasts several days and it is shown to be highly contagious. Virus is excreted with biological fluids (urine, nasal secretion) and appears in blood. Filatov’s-Koplik’s spots are developed on the buccal epithelium in oral cavity of patients. The spots are the sites of intensive viral replication. This finding is proven to be the pathognomonic symptom of measles.
Fever and maculopapular rash are the other main clinical findings of the disease. Eruptive phase lasts about five days. Rash development results from T cell cytotoxic activity, directed against virus-infected capillary endothelial cells. Rash descends from the face to the body and legs and dampens gradually within 1-2 weeks.
The main complications in measles are secondary bacterial pneumonia, otitis, and disorders of CNS (e.g., encephalitis).
The extremely rare but potentially lethal late post-measles complication is subacute sclerosing panencephalitis. It may appear in many years after the infection regress because of immune system incapability to eliminate measles agent. The virus persists within CNS, causing gradual damage of neuronal structures with fatal consequences.
Humoral immunity against measles develops in 10-14 days after the disease onset. It is maintained by circulating antibodies. The immunity is lifelong and stable that ensues from single antigenic type of virus.
Maternal anti-measles antibodies passively protect newborns for 6 months. They may develop modified mild clinical forms of measles.