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الانزيمات
Mumps Virus Infections
المؤلف:
Stefan Riedel, Jeffery A. Hobden, Steve Miller, Stephen A. Morse, Timothy A. Mietzner, Barbara Detrick, Thomas G. Mitchell, Judy A. Sakanari, Peter Hotez, Rojelio Mejia
المصدر:
Jawetz, Melnick, & Adelberg’s Medical Microbiology
الجزء والصفحة:
28e , p605-607
2025-12-31
51
Mumps is an acute contagious disease characterized by non-suppurative enlargement of one or both salivary glands. Mumps virus mostly causes a mild childhood disease, but in adults complications including meningitis and orchitis are fairly common. More than one-third of all mumps infections are asymptomatic.
Pathogenesis and Pathology
Humans are the only natural hosts for mumps virus. Primary replication occurs in nasal or upper respiratory tract epithelial cells. Viremia then disseminates the virus to the salivary glands and other major organ systems. Involvement of the parotid gland is not an obligatory step in the infectious process.
The incubation period may range from 2 to 4 weeks but is typically about 14–18 days. Virus is shed in the saliva from about 3 days before to 9 days after the onset of salivary gland swelling. About one-third of infected individuals do not exhibit obvious symptoms (inapparent infections) but are equally capable of transmitting infection. It is difficult to control transmission of mumps because of the variable incubation periods, the presence of virus in saliva before clinical symptoms develop, and the large number of asymptomatic but infectious cases.
Mumps is a systemic viral disease with a propensity to replicate in epithelial cells in various visceral organs. Virus frequently infects the kidneys and can be detected in the urine of most patients. Viruria may persist for up to 14 days after the onset of clinical symptoms. The central nervous system is also commonly infected and may be involved in the absence of parotitis.
Clinical Findings
The clinical features of mumps reflect the pathogenesis of the infection. At least one-third of all mumps infections are subclinical, including the majority of infections in children younger than 2 years. The most characteristic feature of symptomatic cases is swelling of the salivary glands, which occurs in about 50% of patients.
A prodromal period of malaise and anorexia is followed by rapid enlargement of parotid glands as well as other salivary glands. Swelling may be confined to one parotid gland, or one gland may enlarge several days before the other. Gland enlargement is associated with pain.
Central nervous system involvement is common (10 30% of cases). Mumps causes aseptic meningitis and is more common among males than females. Meningoencephalitis usually occurs 5–7 days after inflammation of the salivary glands, but up to half of patients will not have clinical evidence of parotitis. Meningitis is reported in up to 15% of cases and encephalitis in fewer than 0.3%. Cases of mumps meningitis and meningoencephalitis usually resolve without sequelae, although unilateral deafness occurs in about five in 100,000 cases. The mortality rate from mumps encephalitis is about 1%.
The testes and ovaries may be affected, especially after puberty. Around 20–50% of men who are infected with mumps virus develop orchitis (often unilateral). Because of the lack of elasticity of the tunica albuginea, which does not allow the inflamed testis to swell, the complication is extremely painful. Atrophy of the testis may occur as a result of pressure necrosis but only rarely does sterility result. Mumps oophoritis occurs in about 5% of women. Pancreatitis is reported in about 4% of cases.
Immunity
Immunity is permanent after a single infection. There is only one antigenic type of mumps virus, and it does not exhibit significant antigenic variation.
Antibodies to the HN glycoprotein, the F glycoprotein, and the nucleocapsid protein (NP) develop in serum after natural infection. Antibodies to the NP protein appear earliest (3–7 days after the onset of clinical symptoms) but are transient and are usually gone within 6 months. Antibodies to HN antigen develop more slowly (∼4 weeks after onset) but persist for years.
Antibodies against the HN antigen correlate well with immunity. Even subclinical infections are thought to generate lifelong immunity. A cell-mediated immune response also develops. Interferon is induced early in mumps infection. In immune individuals, IgA antibodies secreted in the nasopharynx exhibit neutralizing activity.
Passive immunity is transferred from mother to off spring; thus, it is rare to see mumps in infants younger than 6 months.
Laboratory Diagnosis
The diagnosis of typical cases usually can be made on the basis of clinical findings. However, other infectious agents, drugs, and conditions can cause similar symptoms. In cases without parotitis, the laboratory can be helpful in establishing the diagnosis. Tests include detection of viral nucleic acid by RT-PCR, isolation of infectious virus, and serology.
A. Nucleic Acid Detection
RT-PCR is a very sensitive method that can detect mumps genome sequences in clinical samples. It can detect the virus in many clinical samples that have negative results in virus isolation attempts. RT-PCR assays can identify virus strains and provide useful information in epidemiologic studies.
B. Isolation and Identification of Virus
The most appropriate clinical samples for viral isolation are saliva, cerebrospinal fluid, and urine collected within a few days after onset of illness. Virus can be recovered from the urine for up to 2 weeks. Monkey kidney cells are preferred for viral isolation. Samples should be inoculated shortly after collection because mumps virus is thermolabile. For rapid diagnosis, immunofluorescence using mumps specific antiserum can detect mumps virus antigens as early as 2–3 days after the inoculation of cell cultures in shell vials.
In traditional culture systems, cytopathic effects typical of mumps virus consist of cell rounding and giant cell formation. Because not all primary isolates show characteristic syncytial formation, the hemadsorption test may be used to demonstrate the presence of a hemadsorbing agent 1 and 2 weeks after inoculation.
C. Serology
Simple detection of mumps antibody is not adequate to diagnose an infection. Rather, an antibody rise can be demonstrated using paired sera: A fourfold or greater rise in antibody titer is evidence of mumps infection. The ELISA or HI test is commonly used. Antibodies against the HN protein are neutralizing.
ELISA can be designed to detect either mumps-specific IgM antibody or mumps-specific IgG antibody. Mumps IgM is uniformly present early in the illness and seldom persists longer than 60 days. Therefore, demonstration of mumps specific IgM in serum drawn early in illness strongly suggests recent infection. Heterotypic antibodies induced by parainfluenza virus infections do not cross-react in the mumps IgM ELISA.
Epidemiology
Mumps occurs endemically worldwide. Cases appear throughout the year in hot climates and peak in the winter and spring in temperate climates. Mumps is primarily an infection of children, with the highest incidence in children ages 5–9 years. Outbreaks occur where crowding favors dis semination of the virus. In children younger than 5 years, mumps may commonly cause upper respiratory tract infection without parotitis.
Mumps is quite contagious; most susceptible individuals in a household will acquire infection from an infected member. The virus is transmitted by direct contact, airborne droplets, or fomites contaminated with saliva or urine. Closer contact is necessary for transmission of mumps than for transmission of measles or varicella.
About one-third of infections with mumps virus are inapparent. During the course of inapparent infection, the patient can transmit the virus to others. Individuals with subclinical mumps acquire immunity.
The overall mortality rate for mumps is low (one death per 10,000 cases in the United States), mostly caused by encephalitis.
The incidence of mumps and associated complications has declined markedly since introduction of the live-virus vaccine. In 1967, the year mumps vaccine was licensed, there were about 200,000 mumps cases (and 900 patients with encephalitis) in the United States. From 2001 to 2003, there were fewer than 300 mumps cases each year.
In 2006, there was an outbreak of mumps in the United States that resulted in more than 5700 cases. Six states in the Midwest reported 84% of the cases. The outbreak started on a college campus among young adults and spread to all age groups. In 2009, a mumps outbreak occurred in the states of New York and New Jersey in which 88% of those affected had been vaccinated. The SH gene of mumps virus is variable and has allowed classification of known virus strains into 12 genotypes. The viruses that caused the 2006 and 2009 outbreaks in the United States were both identified as belonging in genotype G. A massive mumps epidemic occurred in 2004 in the United Kingdom that caused more than 56,000 cases. It also involved closely related genotype G viruses.
Treatment, Prevention, and Control
There is no specific therapy.
Immunization with attenuated live mumps virus vac cine is the best approach to reducing mumps-associated morbidity and mortality rates. Attempts to minimize viral spread during an outbreak by using isolation procedures are not effective because of the high incidence of asymptomatic cases and the degree of viral shedding before clinical symptoms appear; however, students and health care workers who acquire mumps illness should be excluded from school and work until 5 days after the onset of parotitis.
An effective attenuated live-virus vaccine made in chick embryo cell culture was licensed in the United States in 1967. It produces a subclinical, noncommunicable infection. Mumps vaccine is available in combination with measles and rubella (MMR) live-virus vaccines. Combination live-virus vaccines produce antibodies to each of the viruses in about 78–95% of vaccines. There is no increased risk of aseptic meningitis after MMR vaccination. Other live attenuated mumps virus vac cines have been developed in Japan, Russia, and Switzerland.
Two doses of MMR vaccine are recommended for school entry. Because of the 2006 outbreak of mumps, updated vaccination recommendations for prevention of mumps trans mission in settings with high risk for spread of infection were released. Two doses of vaccine should be given to health care workers born before 1957 without evidence of mumps immunity, and a second dose of vaccine should be considered for those who had received only a single dose.
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