Etiology

Mumps virus is in the family Paramyxoviridae and the genus Rubulavirus. It is a single-stranded pleomorphic RNA virus encapsulated in a lipoprotein envelope and possessing 7 structural proteins. Two surface glycoproteins, HN (hemagglutinin-neuraminidase) and F (fusion), mediate absorption of the virus to host cells and penetration into cells, respectively. Both of these proteins stimulate production of protective antibodies. Mumps virus exists as a single immunotype, and humans are the only natural host.

Epidemiology

In the prevaccine era, mumps occurred primarily in young children between the ages of 5 and 9 yr and in epidemics about every 4 yr. Mumps infection occurred more often in the winter and spring months. In 1968, just after the introduction of the mumps vaccine, 185,691 cases were reported in the USA. Following the recommendation for routine use of mumps vaccine in 1977, the incidence of mumps in young children fell dramatically (Fig. 240-1), the disease occurring instead in older children, adolescents, and young adults. Outbreaks continued to occur even in highly vaccinated populations as a result of to vaccine failure and also of undervaccination of susceptible persons. After implementation of the 2-dose recommendation for the measles-mumps-rubella (MMR) vaccine for measles control in 1989, the number of mumps cases declined further. During 2001-2003, <300 mumps cases were reported each year. In 2006, the largest mumps epidemic in the last 20 years occurred in the USA. A total of 6584 cases occurred, 85% of them in 8 Midwestern states. Twenty-nine percent of the cases occurred in patients 18-24 yr old, most of whom were attending college. An analysis of 4039 patients with mumps seen in the first 7 months of the epidemic indicated that 63% had received >2 doses of the MMR vaccine.

Figure 240-1 Number of reported mumps cases by year in the USA from 1980 to 2006 (data for 2005 and 2006 are provisional). Mumps vaccine was first licensed in 1967 and recommended for routine use in 1977. After expanded recommendation for 2 doses of measles-mumps-rubella (MMR) vaccine in 1989 for measles control, mumps incidence further declined. During 2001–2003 there were <300 mumps cases each year, a 99% decline from the 185,691 cases reported in 1968. More than 2,500 cases were reported in the 1st half of 2006 as part of a multistate outbreak, the largest number of cases in the USA since 1991.

(From the Centers for Disease Control and Prevention: Summary of notifiable diseases—United States, 2004, MMWR Morb Mortal Wkly Rep 53:1–79, 2006.).

Mumps is spread from person to person by respiratory droplets. Virus appears in the saliva from up to 7 days before to as long as 7 days after onset of parotid swelling. The period of maximum infectiousness is 1-2 days before to 5 days after onset of parotid swelling. Viral shedding before onset of symptoms and in asymptomatic infected individuals impairs efforts to contain the infection in susceptible populations. The U.S. Centers for Disease Control and Prevention (CDC), the American Academy of Pediatrics, and the Health Infection Control Practices Advisory Committee recommend an isolation period of 5 days after onset of parotitis for patients with mumps in both community and health care settings.

Pathology and Pathogenesis

Mumps virus targets the salivary glands, central nervous system (CNS), pancreas, testes, and, to a lesser extent, thyroid, ovaries, heart, kidneys, liver, and joint synovia.

Following infection, initial viral replication occurs in the epithelium of the upper respiratory tract. Infection spreads to the adjacent lymph nodes by the lymphatic drainage, and viremia ensues, spreading the virus to targeted tissues. Mumps virus causes necrosis of infected cells and is associated with a lymphocytic inflammatory infiltrate. Salivary gland ducts are lined with necrotic epithelium, and the interstitium is infiltrated with lymphocytes. Swelling of tissue within the testes may result in focal ischemic infarcts. The cerebrospinal fluid (CSF) frequently contains mononuclear pleocytosis, even in individuals without clinical signs of meningitis.

Clinical Manifestations

The incubation period for mumps ranges from 12 to 25 days but is usually 16-18 days. Mumps virus infection may result in clinical presentation ranging from asymptomatic or nonspecific symptoms to the typical illness associated with parotitis with or without complications involving several body systems. The typical patient presents with a prodrome lasting 1-2 days and consisting of fever, headache, vomiting, and achiness. Parotitis then appears and may be unilateral initially but becomes bilateral in about 70% of cases (Fig. 240-2). The parotid gland is tender, and parotitis may be preceded or accompanied by ear pain on the ipsilateral side. Ingestion of sour or acidic foods or liquids may enhance pain in the parotid area. As swelling progresses, the angle of the jaw is obscured and the ear lobe may be lifted upward and outward (Figs. 240-2 and 240-3). The opening of Stensen duct may be red and edematous. The parotid swelling peaks in approximately 3 days, then gradually subsides over 7 days. Fever and the other systemic symptoms resolve in 3-5 days. A morbilliform rash is rarely seen. Submandibular salivary glands may also be involved or may be enlarged without parotid swelling. Edema over the sternum due to lymphatic obstruction may also occur.

Figure 240-2 Schematic drawing of a parotid gland infected with mumps (right) compared with a normal gland (left). An imaginary line bisecting the long axis of the ear divides the parotid gland into 2 equal parts. These anatomic relationships are not altered in the enlarged gland. An enlarged cervical lymph node is usually posterior to the imaginary line.

(From Mumps [epidemic parotitis]. In Krugman S, Ward R, Katz SL, editors: Infectious diseases in children, ed 6, St Louis, 1977, Mosby, p 182.)