CRISBERT I. CUALTEROS, M.D. - Measles (rubeola)
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CRISBERT I. CUALTEROS, M.D. Family and Medicine

Measles (rubeola) is an important childhood disease that was widespread in the United States but is now very infrequent. However, in developing countries, measles is still an important cause of childhood morbidity and mortality. It is an acute viral infection characterized by a final stage with a maculopapular rash erupting successively over the neck and face, trunk, arms, and legs, and accompanied by a high fever.
Measles virus, the cause of measles, is an RNA virus of the genus Morbillivirus in the family Paramyxoviridae. Only one serotype is known. During the prodromal period and for a short time after the rash appears, virus is shed in nasopharyngeal secretions, blood, and urine. Virus can remain viable for at least 34?hr at room temperature.
Measles is endemic throughout the world. In the past, epidemics tended to occur irregularly, appearing in the spring in large cities at 2–4-yr intervals as new groups of susceptible children were exposed. It is rarely subclinical. Prior to the use of measles vaccine, the peak incidence was among children 5–10 yr of age. Individuals born before 1957 are considered to have had natural infection and to be immune.

During the 1980s the incidence of measles in the United States rose, probably due to inadequate vaccination as well as vaccine failure. The reported numbers of measles cases dropped from 894,134 cases in 1941 by more than 99.7% to an all-time low of 80 cases in 2000, probably as a result of intensified efforts to ensure appropriate vaccination. Measles now occurs most often among unimmunized preschool-aged children, as occasional epidemics in high schools and colleges, and as imported cases. Because measles is still a common disease in many countries, infective persons entering this country may infect United States residents, and Americans traveling abroad risk exposure there. More than half of the 108 cases reported in 2001 in the United States were imported or due to exposure to imported cases.
The Pan American Health Organization had established the goal of eliminating measles from the Western hemisphere by the year 2000. Although that goal has not been met, efforts have achieved interruption of indigenous measles transmission. During 1990–2000, measles cases in the Western Hemisphere declined 99.3%, from approximately 250,000 to 1,754 cases annually ( Fig. 225–1 ). The many similarities among the biologic features of measles and smallpox suggest the possibility that measles might be eradicated. These features are (1) a distinctive rash as a sentinel marker; (2) no animal reservoir; (3) no vector; (4) seasonal occurrence with disease-free periods; (5) no transmissible latent virus; (6) one serotype; and (7) an effective vaccine. A prevalence of greater than 90% immunization of infants has been shown to produce disease-free zones.
Measles is highly contagious; approximately 90% of susceptible household contacts acquire the disease. Maximal dissemination of virus occurs by droplet spray during the prodromal period (catarrhal stage). Transmission to susceptible contacts often occurs prior to diagnosis of the index case.
Infants acquire immunity transplacentally from mothers who have had measles or measles immunization. This immunity is usually complete for the first 4–6 mo of life and wanes at a variable rate. Although maternal antibody levels are generally undetectable in infants after 9 mo of age by the usual antibody tests performed, some protection persists that may interfere with immunization administered before 12 mo of age. Most women of childbearing age in the United States now have measles immunity by means of immunization rather than disease, and studies suggest that infants of mothers with measles vaccine–induced immunity lose passive antibody at a younger age than infants of mothers who had measles infection. Infants of mothers who are susceptible to measles have no measles

 Figure 225-1 Reported cases of measles and percentage of routine measles vaccination coverage among infants in North, Central, and South America (combined) from 1990 to 2001. (From Centers for Disease Control and Prevention: Progress toward interrupting indigenous measles transmission—Region of the Americas, January–November 2001. MMWR 2001; 50:1133–7.)
immunity and may contract the disease simultaneously with the mother before or after delivery.
The essential lesion of measles is found in the skin, conjunctivae, and the mucous membranes of the nasopharynx, bronchi, and intestinal tract. Serous exudate and proliferation of mononuclear cells and a few polymorphonuclear cells occur around the capillaries. Hyperplasia of lymphoid tissue usually occurs, particularly in the appendix, where multinucleated giant cells of up to 100?µm in diameter (Warthin-Finkeldey reticuloendothelial giant cells) may be found. In the skin, the reaction is particularly notable about the sebaceous glands and hair follicles. Koplik spots consist of serous exudate and proliferation of endothelial cells similar to those in the skin lesions. A general inflammatory reaction of the buccal and pharyngeal mucosa extends into the lymphoid tissue and the tracheobronchial mucous membrane. Interstitial pneumonitis resulting from measles virus takes the form of Hecht giant cell pneumonia. Bronchopneumonia may occur from secondary bacterial infection. In fatal cases of encephalomyelitis, perivascular demyelinization occurs in areas of the brain and spinal cord. In subacute sclerosing panencephalitis (SSPE), there may be degeneration of the cortex and white matter with intranuclear and intracytoplasmic inclusion bodies (see Chapter 225.1 ).
Clinical Manifestations.
Measles has three clinical stages: an incubation stage, a prodromal stage with an enanthem (Koplik spots) and mild symptoms, and a final stage with a maculopapular rash accompanied by high fever. The incubation period lasts approximately 10–12 days to the first prodromal symptoms and another 2–4 days to the appearance of the rash; rarely, it may be as short as 6–10 days. Body temperature may increase slightly 9–10 days from the date of infection and then subside for 24?hr or so. The patient may transmit the virus by the 9th–10th day after exposure and occasionally as early as the 7th day, before the illness can be diagnosed.
The prodromal phase usually lasts 3–5 days and is characterized by a low-grade to moderate fever, a dry cough, coryza, and conjunctivitis. These symptoms nearly always precede the appearance of Koplik spots, the pathognomonic sign of measles, by 2–3 days. An enanthem or red mottling is usually present on the hard and soft palates. Koplik spots are grayish white dots, usually as small as grains of sand, that have slight, reddish areolae; occasionally they are hemorrhagic. They tend to occur opposite the lower molars but may spread irregularly over the rest of the buccal mucosa. Rarely they are found within the midportion of the lower lip, on the palate, and on the lacrimal caruncle. They appear and disappear rapidly, usually within

12–18?hr. As they fade, a red, spotty discoloration of the mucosa may remain. The conjunctival inflammation and photophobia may suggest measles before Koplik spots appear. In particular, a transverse line of conjunctival inflammation, sharply demarcated along the eyelid margin, may be of diagnostic assistance in the prodromal stage. As the entire conjunctiva becomes involved, the line disappears.
Occasionally, the prodromal phase may be severe, being ushered in by a sudden high fever, sometimes with convulsions and even pneumonia. Usually the coryza, fever, and cough are increasingly severe up to the time the rash has covered the body.
The temperature rises abruptly as the rash appears and often reaches 40°C (104°F) or higher. In uncomplicated cases, as the rash appears on the legs and feet, the symptoms subside rapidly within about 2 days, usually with an abrupt drop in temperature to normal. Patients up to this point may appear desperately ill, but within 24?hr after the temperature drops, they appear well.
The rash usually starts as faint macules on the upper lateral parts of the neck, behind the ears, along the hairline, and on the posterior parts of the cheek. The individual lesions become increasingly maculopapular as the rash spreads rapidly over the entire face, neck, upper arms, and upper part of the chest within approximately the first 24?hr ( Fig. 225–2 ). During the succeeding 24?hr the rash spreads over the back, abdomen, entire arm, and thighs. As it finally reaches the feet on the 2nd–3rd day, it begins to fade on the face. The rash fades downward in the same sequence in which it appeared. The severity of the disease is directly related to the extent and confluence of the rash. In mild measles the rash tends not to be confluent, and in very mild cases there are few, if any, lesions on the legs. In severe cases the rash is confluent, the skin is completely covered, including the palms and soles, and the face is swollen and disfigured.
The rash is often slightly hemorrhagic; in severe cases with a confluent rash, petechiae may be present in large numbers, and there may be extensive ecchymoses. Itching is generally slight. As the rash fades, branny desquamation and brownish discoloration occur and then disappear within 7–10 days.
The appearance of the rash may vary markedly. Infrequently a slight urticarial, faint macular, or scarlatiniform rash may appear during the early prodromal stage, disappearing in advance of the typical rash. Complete absence of rash is rare except in patients who have received immunoglobulin (Ig) during the incubation period, in some patients with HIV infection, and occasionally in infants younger than 9 mo of age who have appreciable levels of maternal antibody. In the hemorrhagic type of measles (black measles), bleeding may occur from the mouth, nose, or bowel. In mild cases the rash may be less macular and more nearly pinpoint, somewhat resembling that of scarlet fever or rubella.
Lymph nodes at the angle of the jaw and in the posterior cervical region are usually enlarged, and slight splenomegaly may be noted. Mesenteric lymphadenopathy may cause abdominal pain. Characteristic pathologic changes of measles in the mucosa of the appendix may cause obliteration of the lumen

 Figure 225-2 Maculopapular rash of measles. (From Korting GW: Hautkrankheiten bei Kindern und Jugendlichen, 3rd ed. Stuttgart, FK Schattauer Verlag, 1982.)
and symptoms of appendicitis. Changes of this type tend to subside as the Koplik spots disappear. Otitis media, bronchopneumonia, and gastrointestinal symptoms such as diarrhea and vomiting are more common in infants and small children (especially if they are malnourished) than in older children.


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