Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (507 page)

BOOK: Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis
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   Laboratory Findings

Culture
: Detection of rubella virus in cell culture is slow and technically challenging. There is little CPE in cell lines. Rubella infection can be inferred by interference assays, such as inhibition of enterovirus superinfection of cell lines infected by rubella virus from a specimen. Rubella-specific neutralization or immunostaining techniques are used for confirmation.

Serology
: Serologic diagnosis is most commonly used to document rubella infection. See Rubella Serology Screen (Rubella IgG and IgM) in Chapter
17
, Infectious Disease Assays.

   Infection is confirmed by demonstration of a positive reaction for rubella IgM (acute primary infection) or by change in rubella IgG titers in acute (7–10 days) and convalescent (14–21 days) serum specimens. IgM antibodies are detected and peak within several days after appearance of rash and then rapidly fall below detectable levels after approximately 8 weeks. IgG usually appears around 2 weeks after onset of rash and usually remain detectable, at lower levels, for life.
   In congenital infection, IgM can be detected at birth and persists for ≤6 months in >90% of infants. During the first 6 months of life, IgM is the best test for congenital or recent infection. After age 7 months, assess persistence of IgG. IgG appears 15–25 days after infection and >25 to 50 days after vaccination; <33% of persons may show no detectable IgG after 10 years. Absence of IgG in infant excludes congenital infection.
RUBEOLA (MEASLES)
   Definition

Measles is caused by the measles virus in the family
Paramyxoviridae
, genus
Morbillivirus
. It is a single-stranded RNA virus. The virus is transmitted by respiratory droplets and infects epithelial cells of the respiratory tract of exposed individuals. Measles is highly contagious, and outbreaks are well documented. The disease is preventable by vaccination. Imported infections are transmitted to nonimmune individuals in regions with a low endemic rate.

   Who Should Be Suspected?
   Clinical disease develops after an incubation period of 10–14 days. In typical measles, the characteristic morbilliform rash appears after 4–5 days of prodromal symptoms, which include cough, coryza, and conjunctivitis, with fever and malaise. Local lymphadenopathy may develop. Koplik spots, the characteristic enanthem, appear on the buccal mucosa 1 day or 2 before the appearance of the rash. The blanching rash first appears behind the ears and forehead and spreads over the trunk and limbs over the ensuing several days. Otitis media, diarrhea, and pneumonitis occur relatively frequently in uncomplicated measles.
   Pregnant women are at risk for more severe measles-associated pneumonia. Although not associated with congenital anomalies, measles may be transmitted to the fetus, and neonates may develop mild to severe clinical infection. Patients with defects of cell-mediated immunity are susceptible to severe measles virus pneumonia and progressive encephalitis demonstrating typical inclusion bodies in neurons and glial cells.
   Neurologic complications are uncommon in patients with normal immunity, but acute postinfectious measles encephalomyelitis and subacute sclerosing panencephalitis (SSPE) are rare complications of measles infections.
   Acute postinfectious encephalomyelitis, an autoimmune reaction, usually occurs in the week following onset of rash. Patients present with headache, irritability, and change in mental status progressing to seizures, obtundation, and coma. CSF lymphocytic pleocytosis and protein elevation are seen. Mortality is as high as 20%, and many survivors have neurologic sequelae.
   SSPE is a progressive neurologic complication with a high mortality rate. It usually occurs 5–10 years after primary measles. SSPE is more common when primary infection occurred before 2 years of age. The onset is subtle with personality changes, declining intellectual function and loss of coordination, which usually progress relentlessly. Death usually occurs within several years of onset. There are characteristic EEG changes (Rodermacker complexes). CSF analysis shows oligoclonal bands and intrathecal production of antimeasles antibodies.

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