Measles Lecture Notes
Measles Overview
Definition: Measles is caused by an enveloped RNA-containing virus.
Genetic Relation: It is genetically related to the canine distemper virus.
Virus Classification
Families: Measles virus falls under the Paramyxoviridae family.
Clinical Disease Naming
Rubeola: The clinical disease caused by the measles virus is known as rubeola.
Difference from Rubella: Rubeola should not be confused with rubella, which is also known as German measles.
Pathogenesis of Clinical Disease
Transmission:
Measles virus is transmitted via the respiratory route through respiratory droplets.
These droplets can remain infectious in the air for several hours.
Initial Infection Site:
The initial site of infection occurs within the epithelial cells of the respiratory tract.
Incubation Period:
The incubation period for measles is typically between 9 to 11 days.
Clinical Presentation:
Initial symptoms include:
Sudden onset of sneezing and congestion.
Cough.
Rapidly increasing fever.
Redness of the eyes and photophobia.
Viremia: The virus spreads to local lymph nodes and subsequently enters the bloodstream, where a viremia is established in monocytes/macrophages.
Subsequent Symptoms
Koplik’s Spots:
These are tiny bluish-white spots on a red base that appear within the mouth 2 to 4 days after infection.
Further Spread:
The virus disseminates through the blood (viremia) to the liver, spleen, and skin.
Infection of Endothelial Cells:
The virus infects endothelial cells of small blood vessels in the skin.
The onset of the rash coincides with the appearance of cellular immunity.
The rash is characterized by the action of CD4+ DTH T cells that recognize virus-infected endothelial cells.
The destruction of these cells results in tiny hemorrhages under the skin, presenting as a rash specific to measles (not vesicles as seen in smallpox).
Rash Characteristics
Rash Appearance:
The rash appears first on the forehead and behind the ears.
Within 24 to 48 hours, the rash spreads to the face, neck, trunk, and limbs.
The rash persists for around 10 days.
Immunity:
Following recovery from measles, individuals gain life-long immunity to re-infection.
Mortality and Complications
Mortality Rates:
Deaths due to measles virus infection vary:
0.1% in industrialized countries.
Up to 15% in developing countries.
Neurological Complications:
The measles virus can invade the brain, causing various neurologic complications, including life-threatening acute encephalitis.
Neurologic Diseases Associated with Measles
Complications Overview:
Acute disseminated encephalomyelitis (ADEM).
Measles inclusion body encephalitis (MIBE).
Subacute sclerosing panencephalitis (SSPE).
Summary of Neurologic Complications
Disease | Host | Onset | Incidence | Pathology | Time Course |
|---|---|---|---|---|---|
Acute disseminated encephalomyelitis (ADEM) | Normal > 2 yr | 1:1,000 | Inflammation, demyelination | Monophasic, weeks | |
Measles inclusion body encephalitis (MIBE) | Immunocompromised | Any | 1:10 | Inclusion bodies | Progressive, months |
Subacute sclerosing panencephalitis (SSPE) | Normal < 2 yr | 1:10,000 | Inclusion bodies, inflammation | Progressive, years |
Subacute Sclerosing Panencephalitis (SSPE) Pathogenesis
M Protein: Expression of the M protein is low, with mutations throughout the mRNA encoding the M protein.
Functional Implications: These alterations interfere with the assembly and budding of the virus, contributing to persistent measles virus infection and SSPE.
Clinical Course of SSPE
Age of Onset: The age of onset for neurologic disease is typically around 8 to 10 years, but occurrences have been reported as late as age 35.
Stages of SSPE:
First Stage: Behavioral problems and decline in school performance appear quickly after onset.
Second Stage: Occurrence of intellectual decline, motor function disturbances (myoclonic jerks and seizures), retinitis, optic nerve atrophy, and cerebellar ataxia.
Third Stage: The child may lapse into a stuporous state.
Fourth Stage: Characterized by loss of cortical function, potential mutism, coma, and death.
Immunological Implications of Measles Infection
Impact on Immune Memory: Measles virus infection significantly impairs the immune system’s memory B cells, erasing between 11% to 73% of a person’s protective antibodies to other infections (e.g., influenza, hepatitis, tuberculosis).
Resulting Susceptibility: This immunosuppression following the resolution of acute measles virus viremia increases susceptibility to these other infectious agents.
Immunization and Vaccine Efficacy
Lifelong Immunity: Once a person has had a clinical case of measles, they are immunized for life.
Impact of MMR Vaccine:
The incidence of measles significantly decreased in the United States post-immunization introduction.
Rates of measles-associated encephalitis are significantly lower in vaccinated individuals.
SSPE incidence reduced by a factor of 10 in vaccinated persons.
The measles vaccine helps protect the immune system’s memory from being erased.
Global Eradication Efforts
Vaccination Potential: Measles could potentially be eradicated globally through an aggressive vaccination program.
Public Concerns: Fears that measles vaccination (MMR vaccine) may contribute to autism have led to increased measles incidence, notably in the United Kingdom and more recently in the United States.