Measles, Causes, Signs and Symptoms, Diagnosis and Treatment.

Measles, Causes, Signs and Symptoms, Diagnosis and Treatment.

Clinical manifestations, diagnosis, treatment, and prevention

Syndrome and incubation period − Measles is a highly contagious viral illness that occurs worldwide. The infection is characterized by fever, malaise, cough, coryza, and conjunctivitis, followed by exanthem. Following exposure, approximately 90 percent of susceptible individuals develop measles. The period of contagiousness is estimated to be from five days before the appearance of the rash to four days afterward. The illness may be transmitted in public spaces, even in the absence of person-to-person contact. Patients being evaluated for measles should be isolated.

Stages of infection − Classic measles infection in immunocompetent patients consists of the following clinical stages: incubation, prodrome, exanthem, and recovery.

Incubation – The incubation is 6 to 21 days (median 13 days).

Prodrome – A two- to four-day prodrome phase is characterized by fever, malaise, and anorexia, followed by conjunctivitis, coryza, and cough. If present, Koplik spots, an enanthem considered pathognomonic for measles infection, typically occurs approximately 48 hours prior to the exanthem.

Exanthem – The characteristic exanthem arises approximately two to four day after onset of fever; it consists of a red maculopapular rash, which classically begins on the face and head and spreads downward. Early on, the lesions are blanching; in later stages, they are not. The rash resolves in five to six days, fading in the order it appeared.

Recovery – Cough may persist for one two weeks after measles. The occurrence of fever beyond the third to fourth day of rash suggests a measles-associated complication.

Clinical variants − Clinical variants include modified measles and atypical measles. Modified measles occurs in patients with preexisting but incompletely protective anti-measles antibody. Atypical measles occurs in patients immunized with the killed virus vaccine administered between 1963 and 1967 in the United States who are subsequently exposed to wild-type measles virus. 

Diagnosis − The diagnosis of measles should be considered in a patient presenting with a febrile rash illness and clinically compatible symptoms. The approach to diagnosis differs depending on the regional prevalence of measles. 

In regions of low measles prevalence, cases of suspected or confirmed measles should be reported to the local health authorities, who provide guidance on specimen collection for diagnosis as well as infection control interventions. In general, it is useful to obtain three samples from patients with suspected measles infection: a serum sample for measles immunoglobulin (Ig)M, a throat or nasopharyngeal swab for viral culture, and a urine sample for viral culture. In the setting of diagnostic uncertainty, the diagnosis may be confirmed by evaluation of paired acute and convalescent sera for anti-measles virus IgG; at least fourfold increase in anti-measles antibody titer is indicative of infection.

In countries with high measles prevalence, the World Health Organization uses serum IgM as the standard test to confirm the diagnosis of measles. However, the anti-measles IgM assay should be interpreted with caution as false-positive and false-negative results have been reported.

Complications

Complications of measles include secondary infections such as diarrhea and pneumonia. Complications of measles among immunocompromised individuals include giant cell pneumonia and measles inclusion body encephalitis. Groups at increased risk for complications of measles include immunocompromised hosts, pregnant women, individuals with vitamin A deficiency or poor nutritional status, and individuals at the extremes of age. 

Neurologic syndromes following measles virus infection include acute disseminated encephalomyelitis (ADEM) and subacute sclerosing panencephalitis (SSPE). ADEM is a demyelinating disease that presents during the recovery phase of measles infection and is thought to be caused by a postinfectious autoimmune response. SSPE is a progressive degenerative disease of the central nervous system that generally occurs 7 to 10 years after natural measles infection; its pathogenesis may involve persistent infection with a genetic variant of measles virus within the central nervous system.

Treatment − The treatment of measles is largely supportive; in some cases, vitamin A and/or ribavirin may be beneficial.

Supportive care − Supportive therapy includes antipyretics, fluids, and treatment of bacterial superinfections and other complications.

Role of vitamin A − For children with severe measles, we suggest administration of vitamin A (Grade 2C). In addition, for children in resource-limited settings with measles (regardless of severity), we suggest administration of vitamin A (Grade 2C). Dosing is summarized above.

Role of ribavirin − For patients <12 months with measles pneumonia, patients ≥12 months with measles pneumonia requiring ventilatory support, and immunosuppressed patients with measles, we suggest treatment with ribavirin (Grade 2C). Dosing is summarized above.

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