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 VIROLOGY LECTURE 
 FOURTEEN  
 MEASLES (RUBEOLA) AND 
 MUMPS VIRUSES  

Virology Lecture 1
BASIC VIROLOGY: DEFINITIONS, CLASSIFICATION, 
MORPHOLOGY AND CHEMISTRY  

Virology Lecture 2
 
 DNA VIRUS REPLICATION 
 STRATEGIES  

 RNA VIRUS REPLICATION
 STRATEGIES  

 ONCOGENIC VIRUSES 
 
 SEVEN  HUMAN  
 IMMUNODEFICIENCY VIRUS  
 AND AIDS  

 PICORNAVIRUSES - 
 PART ONE  
 ENTEROVIRUSES  
Virology Lecture 

 HERPES VIRUSES  

Virology Lecture 9

INFLUENZA VIRUS

Virology Lecture 10

MEASLES (RUBEOLA) 
AND MUMPS VIRUSES  

Virology Lecture 11
RUBELLA (GERMAN 
 MEASLES) VIRUS

Virology Lecture 12
RABIES  




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  VIROLOGY LECTURE FOURTEEN  

  MEASLES (RUBEOLA) AND MUMPS VIRUSES  

Dr. Margaret Hunt

MEDICAL MICROBIOLOGY, MBIM 650/720   LECTURE: 71 
READING: Murray et al., Microbiology, 3rd Ed., Chapter 55

TEACHING OBJECTIVES

Brief review of structure and properties of measles and mumps viruses. Discussion of viral pathogenesis and disease, epidemiology, prevention and treatment.

 

INTRODUCTION

Infections with measles, mumps and rubella viruses are confined to man and occur worldwide. They are all spread primarily via the aerosol route. Each of these viruses exists as a single serotype. MMR  (mumps, measles, rubella) vaccine contains live, attenuated forms of all three of these viruses.

Measles and mumps viruses belong to the Paramyxovirus Family and are enveloped, non-segmented, negative-sense RNA viruses with helical symmetry. (Rubella virus is a member of the Togavirus Family and is an enveloped, non-segmented, positive-sense RNA virus with icosahedral symmetry.)

 

  PARAMYXOVIRUS FAMILY  

MMR1.jpg (65876 bytes) Paramyxovirus structure

GENUS

MEMBERS

  GLYCOPROTEINS

Paramyxovirus

mumps
human parainfluenza viruses (HPIV 1-4)

HN, F

Morbillivirus

measles

H, F

Pneumovirus

respiratory syncytial virus

G, F

 

  MEASLES (RUBEOLA)  

WEB INFORMATION

Mumps, measles and rubella vaccine (CDC)

Measles, Mumps, and Rubella -- Vaccine Use and Strategies for Elimination of Measles, Rubella, and Congenital Rubella Syndrome and Control of Mumps: Recommendations of the Advisory Committee on Immunization Practices (ACIP) (CDC)

PATHOGENESIS AND DISEASE
Infection is via an aerosol route  and the virus is very contagious.
The virus replicates initially in the upper/lower respiratory tract. This is followed by replication in lymphoid tissues leading to viremia and growth in a variety of epithelial sites. The disease develops 1-2 weeks after infection.

measlepath.jpg (92279 bytes)  The pathogenesis of measles. The virus invades the body via blood vessels and reaches surface epithelium first in the respiratory tract where there are only 1-2 layers of epithelial cells then in mucosae (Koplik's spots) and finally in the skin (rash). Adapted from Mims et al. Medical Microbiology, 1993, Mosby

Uncomplicated disease

Fever
Respiratory tract symptoms: running nose (coryza), cough
Conjunctivitis
Koplik's spots on mucosal membranes
- small (1-3mm), irregular, bright red spots, with bluish-white speck at center - may get enormous number, red areas may become confluent (see below). 
Maculopapular rash (extends from face to extremities), seems to be associated with T-cells targeting infected endothelial cells in small blood vessels (see below).
Infection is prostrating.
Recovery is usually rapid, cell mediated response important (patients with agamma-globulinemia recover normally).
Tends to be more severe in adults than children.

Complications of measles

If patient has an impaired cell-mediated immune response, there is continued growth in lungs leading to giant cell pneumonia (such patients may not have a rash). This is rare, but often fatal.

Since virus grows in epithelia of the nasopharynx, middle ear, lung, all of these sites may then be susceptible to secondary bacterial infection. Otitis media and bacterial pneumonia are quite common.

Outcome is affected by the nourishment of the patient and access to medical care. Measles is still a major killer in underdeveloped countries and several studies in areas with severe vitamin A deficiency problems have found that vitamin A treatment of children with measles has resulted in reduction in morbidity and mortality. Pneumonia accounts for 60% of deaths from measles.

1 in 1000 cases may get encephalitis a few days after the rash disappears. Most patients (90%) survive encephalitis but there may be complications - deafness, seizures, mental disorders.

SSPE

Very rarely (7 in 1,000,000 cases) the patient may get subacute sclerosing panencephalitis (SSPE). This develops 1-10 years after initial infection. It is a progressive, fatal disease. Risk factors include acquiring primary measles at an early age. The incidence of SSPE has decreased since vaccination. SSPE is associated with defective forms of the virus in the brain and so it is difficult to isolate infectious virus from such patients. Certain viral proteins are often not expressed,  the M protein being frequently absent.

CLINCAL ASPECTS OF MEASLES

Site of replication of virus

Symptoms in a well nourished child with good medical care

Symptoms in a malnourished child with poor medical care

Lung

Temporary respiratory illness

Pneumonia (life threatening)

Ear

Otitis media is quite common

Otitis media is experienced more often and is more severe

Oral mucosa

meas5.jpg (19608 bytes)  Koplik's spots   WHO/Immunization Action Coalition.

Severe ulcerating lesions

Conjunctiva

meas1.jpg (56558 bytes)   Conjunctivitis Eyes of child with measles. CDC/Barbara Rice ber2@cdc.gov 

Severe corneal lesions. There may be secondary bacterial infections of the eyes and blindness may occur

Skin

meas2.jpg (55251 bytes)  Maculopapular rash  Face of boy with measles. Third day of rash.  CDC 

meas4.jpg (70484 bytes) This child shows a classic day-4 rash with measles. CDC/NIP/Barbara Rice

Possibility of hemorrhagic rashes (black measles)

Intestinal tract

No lesion

Diarrhea which increases malnutrition, halts growth and impairs recovery

Urinary tract

Virus in urine

No further effect

Overall impact

Serious disease in a small proportion of patients

Major cause of infant death (estimates of 1.5 million deaths per year)

Adapted from Mims et al. Medical Microbiology, 1993

 

OTHER CONSEQUENCES OF MEASLES INFECTION

Measles can cause temporary defects in the immune response; for example, tuberculin-positive individuals may temporarily give a negative response. There may be reactivation of herpes or exacerbation of tuberculosis with natural measles, but this does not seem to happen with the vaccine strain.

Measles virus replicates in the cytoplasm, but inclusions containing nucleocapsid protein can accumulate in the nucleus. It is not known if this has any effect on the host cell, but histologically typically giant cells with cytoplasmic and nuclear inclusion bodies are seen.

measle-cell3.jpg (127172 bytes)   measle-cell2.jpg (142452 bytes)   Histopathology of measles pneumonia.  Giant cells.  CDC/Dr. Edwin P. Ewing, Jr.  epe1@cdc.gov 

DIAGNOSIS

Clinical picture is the first part of diagnosis (that is: exposure plus upper respiratory tract symptoms, Koplik's spots and rash (which is usually quite characteristic for physicians familiar with measles)).
This diagnosis is confirmed by serodiagnosis or isolation. Serodiagnosis is simpler but  two samples are needed, one 10-21days post rash, and so takes longer.
It is recommended that all suspect cases in the United States be confirmed by laboratory testing

EPIDEMIOLOGY

Almost all infected individuals show signs of disease. There is only one serotype of measles and a single natural infection gives life-long protection.

The main route of infection is via inhalation. Measles virus is highly contagious. Note the period of maximum contagiousness is the  2-3 day period before onset of rash.

PREVENTION

There is an attenuated virus vaccine. It is currently recommended to give a first dose of  the vaccine at 12-15 months. If given earlier, the recipient does not mount a strong immune response to the vaccine. A second dose is administered at 4-6 yrs of age, before the recipient enters kindergarten or first grade. This reduces the proportion of persons who remain susceptible due to primary vaccine failure. The vaccine gives long term immunity and does not spread from the vaccinee.

Immune serum globulin can be used for at risk patients during an outbreak; that is those less than 1 year old or with impaired cellular immunity.

Measles vaccine can cause problems (e.g. fatal giant cell pneumonia) in those with severely compromised cell-mediated immunity. No inactivated vaccine is available, due to past problems in which subsequent infection with naturally acquired measles was sometimes associated with an atypical, severe form of measles.

TREATMENT

No antiviral therapy available for primary disease. Treat complications appropriately.

 

 

  MUMPS  

British "to mump" - to grimace or grin, from the appearance of the patient as a result of parotid gland swelling. (Note: Other agents can also cause parotitis).

WEB INFORMATION

CDC (requires Acrobat)
Association of State and Territorial Directors of Health Promotion and Public Health Education

 

PATHOGENESIS AND DISEASE

Mumps is very contagious and is probably usually acquired from respiratory secretions and saliva via aerosols or fomites. The virus is secreted in urine and so urine is a possible source of infection.

mumppath.jpg (152968 bytes)  Pathogenesis of mumps  Adapted from Mims et al Medical Microbiology 1993. Mosby, 1993

 

CLINICAL ASPECTS OF MUMPS

Site of replication of virus Symptoms Notes
Salivary glands mumps.jpg (33840 bytes) Inflammation, parotitis, in a child with mumps. CDC/NIP/Barbara Rice 
Virus is shed in saliva from 3 days before to 6 days after symptoms
Salivary gland symptoms are often absent  or may be unilateral
Meninges

Brain

Meningitis

Encephalitis

Up to 7 days after parotitis Meningitis is found in about 10% of cases.
Encephalitis  is less common. Usually there is complete recovery; nerve deafness is a rare complication
Kidney Virus in urine No clinical consequences
Testis, ovary epididymo-orchitis; rigid tunica albuginea around testis makes orchitis more painful, more damaging in male Common in adults (20% in adult males), often unilateral; not a significant cause of sterility
Pancreas Pancreatitis Rare complication (There is a possible role in juvenile diabetes)
Mammary gland Virus detectable in milk; mastitis in 10% post-pubertal females  
Thyroid Thyroiditis Rare
Myocardium Myocarditis Rare
Joints Arthritis Rare
Adapted from Mims et al. Medical Microbiology, Mosby, 1993

 

Virus infects upper/lower respiratory tract leading to local replication. The virus spreads to lymphoid tissue which, in turn, leads to viremia. The virus thus spreads to a variety of sites, including salivary, other glands and other body sites.

The average time to full manifestation of disease is 2-3 wks but there may be fever, anorexia, malaise, myalgia during prodromal phase.

Symptoms of mumps:

Fever

Pain from parotitis swelling persists 7-10 days

Meningitis more common in males, usually mild

Hearing loss, rare, usually unilateral. May not have overt mumps. May improve with time

Orchitis - especially severe in adolescent and adult males, usually unilateral, some degree of testicular atrophy, damage tends to be patchy, rarely causes infertility.

Pancreatitis - occurs, but very little evidence from controlled studies that mumps plays any role in diabetes mellitus.

More severe in adults.

Seems cell-mediated immunity is important in recovery.

 

DIAGNOSIS

Approximately 30% of infections are subclinical. Parotitis is suggestive (30-40% infections). The disease is confirmed by isolating the virus or by serology (HI, CF, enzyme immunoasssay).

Complement fixing antibody to the S (soluble) antigen (nucleocapsid protein) is seen for a few months after infection and is used to diagnose a recent infection. However, one needs to be careful as there is some cross reaction with other human parainfluenza virus nucleocapsid proteins. CF antibody to the viral envelope (V antigen) persists.

EPIDEMIOLOGY

Man is the only known natural host. Many (~30%) infections are subclinical. Single serotype.

Mumps is contagious from ~7 days before infection and  becomes clinically apparent at ~9 days afterwards.

PREVENTION

Attenuated vaccine. The vaccine virus does not spread to contacts and gives long-term immunity. It is given as MMR vaccine (three live, attenuated viruses: mumps, measles and rubella).

Vaccine is contraindicated in immunosuppressed patients and in pregnant women.

TREATMENT

There is no  specific treatment for mumps.


 

 

 


 






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