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MMR Flashcards

1
Q

Measles virus is DNA or RNA virus?

A 
•	RNA virus 
–	1 serotype
–	a member of the genus Morbillivirus
•	Humans are the only natural host 
•	Measles infection is a multisystem disease
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2
Q

Measles also affects animals. True/False

A

False

Humans are the only natural host

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3
Q

how measles is transmitted?

A

direct contact with or inhalation of virus-containing droplets

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4
Q

what is the seasonal pattern of measles?

A

late winter and spring

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5
Q

what is the incubation period of measles?

A

∼ 2 weeks after infection

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6
Q

how long measles is communicable?

A

Infectivity: ∼ 90%; highly contagious 5 days before and up to 4 days after the onset of exanthem.

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7
Q

why measles is highly contagious?

A
  • A very large number of viral particles is shed from the infected respiratory tract = a large inoculum for an exposed person
  • Measles infection can follow brief exposure = low infecting dose
  • This combination of factors may facilitate spread of infection, especially in a crowded and poorly ventilated environment
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8
Q

what are the virulence factors of the measles virus?

A

Two Membrane envelope proteins are important in the pathogenesis
• H (haemagglutinin) protein – adsorption of virus to cells
• F (fusion) protein – a fusion of virus and host cell membrane, viral penetration and hemolysis
binding and invasion

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9
Q

what is the portal of entry of the measles virus?

A 
Droplet inhalation (Large and/or small droplets)
or deposition on conjunctiva, mouth or in nose
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10
Q

to what cells attach measles virus?

A
  • Bind to Dendritic cells in the alveolar
    spaces/in the submucosa of the RT, and specific CD cells in the lumen of the RT (and/or DCs/lymphoid cells in the conjunctiva)
  • Migration to BALT and draining lymph
    nodes – massive replication in T and B cells
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11
Q

in what cells measles virus replicate?

A

massive replication in T and B cells

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12
Q

how the measles virus spread throughout the body?

A

Systemic spread - infection of lymphocytes and DCs in the skin and epithelial submucosa → mucosal cells

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13
Q

when primary viremia occurs?

A

Two to three days after invasion and replication in the respiratory tract and regional lymph nodes, a primary viremia occurs followed by infection of the reticuloendothelial system

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14
Q

when secondary viremia occurs?

A

Further viral replication occurs in regional and distal reticuloendothelial sites, and a secondary viremia occurs 5–7 days after the initial infection; during this viremia, there may be infection of the respiratory tract and other organs

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15
Q

what are the main clinical features of measles?

A

• After the primary viraemia, other organs are affected
• Acute illness
– Fever - Stepwise increase in fever to 39oC or higher
– Cough, coryza, conjunctivitis, Koplik’s spots &maculopapular rash

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16
Q

what are the koplik spots?

A

An enanthem of the buccal mucosa characterized by tiny white or bluish-gray spots on an irregular erythematous background. The spots are pathognomonic for measles infection and appear during the prodromal stage.
• Appear towards the end of the prodrome – 2 or 3 days before the appearance of the rash, disappear with onset of rash

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17
Q

describe the rash of measles

A
  • Rash appears 2 - 4 days after the prodrome, 14 days after exposure
  • Maculopapular initially, becomes confluent
  • Begins at the hairline and spreads to face & head, then all over
  • Lesions blanches initially; most lesions are non-blanching by day 3-4
  • Persists for 5-6 days
  • Fades in the order of its appearance
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18
Q

how measles rash spreads

A

Usually begin in the face, frequently behind the ears along the hairline
Disseminates to the rest of the body towards the feet (palm and sole involvement is rare)
Recovery phase

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19
Q

is measles rash confluent?

A

Confluent on face and trunk, less so on extremities.

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20
Q

how long does measles rash persist?

A

Persists for 5-6 days

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21
Q

what is the post-measles staining?

A

During the healing phase a transient brownish staining may be apparent on the skin caused by capillary leakage

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22
Q

what are the complications of measles?

A

1) Bacterial superinfection: otitis media, pneumonia, laryngotracheitis
2) Gastroenteritis
3) (Viral) giant-cell pneumonia
4) Acute encephalitis, often with permanent neurological deficits
- -Frequency: ∼ 1:1000
- -Develops within days of infection
- -Acute disseminated encephalomyelitis may develop within weeks
5) Subacute sclerosing panencephalitis (SSPE): a lethal, generalized, demyelinating inflammation of the brain caused by persistent measles virus infection
- -Epidemiology: very rare
- -Primarily affects males between 8 and 11 years old
- -Usually develops at least 7 years after measles

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23
Q

what are the most common causes of death in measles?

A

pneumonia
diarrhea and dehydration
encephalitis

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24
Q

measles is more severe in what children

A

• High attack rate in children <12 months
• Most severe in malnourished children especially those who are deficient in Vitamin A, with severe diarrhea a major manifestation
• Measles is a leading cause of blindness in children in Africa
–Temporary (sometimes permanent) blindness may occur because of retinitis
–In malnourished individuals, especially those who are deficient in vitamin A, corneal ulceration may develop, followed by scarring and blindness

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25
Q

Reactivation of Herpes simplex infection with severe stomatitis & rhinitis can be caused by measles. True/False

A

True

26
Q

what is the acute disseminated encephalomyelitis?

A

– Thought to be a post-infectious autoimmune response (May be triggered by a number of infectious causes)
– 10 to 20 percent mortality
– Presents during the recovery phase of measles, typically within two weeks of the exanthem

27
Q

what is the Subacute sclerosing panencephalitis (SSPE)

A

– A RARE degenerative CNS disease believed to be caused by persistent measles virus infection in the brain
– Onset 7 years (on average) after measles (range 1 month – 27 years)
– Insidious onset with progressive deterioration in behavior and intellect, followed by ataxia, myoclonic seizures, and ultimately, death
– Diagnosed by detection of IgM to measles in CSF
– Prevention of SSPE is NOT the reason why measles vaccine is administered

28
Q

how SSPE is diagnosed?

A

Diagnosed by detection of IgM to measles in CSF

29
Q

what are the 3 clinical stages of SSPER?

A
  • Dementia
  • Epilepsy and myoclonus
  • Decerebration (increased tone, vegetative state, coma)
30
Q

how measles is clinically diagnosed?

A
  • Fever
  • “Sore eyes” and coryza (runny nose)
  • “Miserable child”
  • Koplik’s spots
  • Rash
  • Anorexia, diarrhoea and generalised lymphadenopathy - especially in infants
31
Q

how measles laboratory is diagnosed?

A

1) Serology
- -Gold standard: detection of Measles-specific immunoglobulin M (IgM) antibodies
- -IgG antibodies: the 4-fold rise of tier
2) Identification of pathogen
- -Direct virus detection via reverse-transcriptase polymerase chain reaction (RT-PCR) possible

32
Q

how measles is treated

A

• Single room isolation in hospitals / airborne precautions
• Management of contacts
– Vaccine if within 72 hours of exposure
– Immunoglobulin (HNIG) (where available) if the vaccine is contraindicated or > 72 hours following exposure
-in developing countries, the fatality rate of measles has drastically reduced following the administration of vitamin A. There is an inverse correlation between vitamin A levels and the severity of measles infection. Vitamin A enhances the barrier function and immunity of the ocular, respiratory, and gastrointestinal epithelium. The WHO recommends the administration of vitamin A to all children with acute measles.

33
Q

how measles is prevented?

A 
•	Measles vaccine included in MMR vaccine 
•	A live vaccine
•	Childhood immunisation programme
–	12 months
–	Booster 4 - 5 years
•	Also given to contacts
34
Q

what is the post-exposure prophylaxis of measles?

A

–Active immunization :
Immunocompetent patients after direct exposure
–Passive immunization
Vulnerable, chronically ill, and immunocompromised patients

35
Q

Mumps virus belongs to what genus?

A

The virus is an RNA Paramyxovirus; there is one antigenic type

36
Q

how mumps is transmitted?

A

Airborne droplets
Direct contact with contaminated saliva or respiratory secretions
Contaminated fomites

37
Q

what is the pathophysiology of mumps?

A
  • Respiratory transmission – acquired via respiratory droplets
  • Replication in nasopharynx & regional lymph nodes
  • At the end of the incubation period (12-25 days after exposure), viremia occurs, with spread to multiple tissues, including the meninges, and glandular tissue such as the salivary glands, pancreas, testes/ovaries
  • Parotitis typically appears 16-18 days after exposure
  • Following replication in the target sites, a secondary viremia occurs
38
Q

when viremia occurs in mumps?

A

Viraemia, 12-25 days after exposure with spread to tissues

39
Q

animals are the reservoir for mumps?

A

no only humans

40
Q

how many days is the incubation period of measles?

A

14-18 days

41
Q

what are the clinical features of mumps?

A
  • Nonspecific prodrome of low-grade fever, headache, malaise, myalgias
  • Parotitis in 30%-40%; may be unilateral
  • Up to 20% of infections are asymptomatic
  • May present as lower respiratory illness, particularly in pre-school children
  • It is easy to remember that MUMPS causes LUMPS (facial swelling due to parotid gland inflammation, and testicular swelling due to orchitis) and NOT a rash
42
Q

Prior to the introduction of the mumps vaccine, infection with mumps virus was one of the most common causes of “aseptic meningitis” and acquired sensorineural deafness in childhood. True/False

A

True

43
Q

what are the complications of mumps?

A

1) Orchitis (< 10% of cases; most common complication in post-pubertal males)
- -Primarily unilateral, although bilateral in ∼ 15% of cases
- -Sudden onset of fever, nausea, vomiting
- -On examination: swollen and tender affected testicle(s)
- -May lead to atrophy and, in rare cases, infertility
2) Aseptic meningitis (1–10% of cases): predominantly mild course; usually no permanent sequelae
3) Encephalitis (< 1% of cases)
- -Reduced consciousness, seizures
- -Neurological deficits: cranial nerve palsy, hemiplegia, sensorineural hearing loss (rare)
4) Acute pancreatitis (< 1% of cases)
- -Vomiting, nausea, upper abdominal pain
- -↑ Lipase in addition to ↑ amylase
- -Diabetes mellitus type I (delayed complication)

44
Q

what is the laboratory diagnosis of mumps?

A

• Oral fluid – IgM detection and PCR for mumps virus
• PCR
– throat swabs, urine, CSF
• Serology
– acute IgM or fourfold rise in titre in blood
– oral fluid
• Isolation (culture) of mumps virus (not routine)
– Oral fluid, throat swabs, urine, CSF

45
Q

how mumps is prevented?

A

• MMR: Childhood immunization programme
– 12 months
– Booster 4 – 5 years
• If hospitalised (rare) – droplet precautions

46
Q

what type of virus is the rubella virus?

A

RNA virus , Togavirus, with one antigenic type

47
Q

how rubella is transmitted?

A

Airborne droplets or transplacental
Infectivity: 7 days prior to and 7 days following the appearance of an exanthem
Low infectivity and virulence

48
Q

how the rubella virus spreads inside the body?

A

– Replication in the nasopharynx & regional lymph nodes
– Viraemia 5-7 days after exposure with spread to tissues
• In a pregnant woman, the placenta & fetus become infected during the viraemic phase; damage to the fetus occurs due to destruction of cells and also arrest of mitosis

49
Q

what are the virulence features of rubella?

A
  • Attachment to cells of respiratory tract following inhalation of droplets
  • In a pregnant woman, the placenta & fetus become infected during the viraemic phase; damage to the fetus occurs due to destruction of cells and also arrest of mitosis – in this setting rubella is a teratogenic virus
50
Q

what are the clinical features of rubella?

A
  • Prodrome of low grade fever mainly in adults; rubella prodrome is rare in children
  • Lymphadenopathy in the second week (before the appearance of the rash); may last several weeks; post-auricular, posterior cervical and suboccipital nodes are most commonly involved
  • Maculopapular rash14-17 days after exposure, initially on the face, and spreads from head to foot; non-blanching fainter than the measles rash and does not coalesce
51
Q

what lymph nodes are specifically affected during rubella?

A

Post-auricular and suboccipital lymphadenopathy and occasionally splenomegaly

52
Q

describe the rash or rubella

A

Non-confluent, pink maculopapular rash
Begins at the head, primarily behind the ears → extends to the trunk and extremities sparing palms and soles
Rash may be itchy in adults

53
Q

70% of teenagers and adult females with rubella present with

A

polyarthritis

54
Q

what is the laboratory diagnosis of rubella?

A

• PCR for rubella virus
– Respiratory secretions, oral fluid, urine, blood
• Serology
– acute IgM or fourfold rise
– blood, oral fluid
• Isolation (culture)
– Respiratory secretions, oral fluid, urine

55
Q

what is the incubation period of rubella?

A

2-3 weeks

56
Q

how long is the infectivity of rubella?

A

7 days prior to and 7 days following the appearance of an exanthem

57
Q

what are the complications of rubella?

A

1)Congenital rubella syndrome
2)Arthralgia and arthritis
– May last for up to 1 month; rarely becomes chronic
– Occurs frequently in adult females (up to 70%)
– Rare in adult males and children.
3)Post-infectious encephalitis
– 1 in 6,000 cases, more often in adult females.

4)Haemorrhagic manifestations
– 1 in 3,000 cases, more commonly in children
– Due to thrombocytopenia or vascular damage.
– Cerebral, GIT or renal haemorrhage may result.
– Conjunctivitis
5)Orchitis
6)VERY RARE: A LATE syndrome of progressive panencephalitis

58
Q

what is the congenital rubella syndrome?

A

A neonatal rubella infection as a result of intrauterine transmission during the first trimester. Classic triad of defects is sensorineural hearing loss, cataracts, and cardiac defects (e.g., patent ductus arteriosus). Additional features include low birth weight, purpura/petechiae, a blueberry muffin rash, hepatosplenomegaly, osteitis, microcephaly, and other ocular manifestations (e.g., salt and pepper retinopathy, microphthalmos, congenital glaucoma).

59
Q

The severity of the damage to the fetus depends on congenital rubella depends on…

A

the gestational age
– Up to 85% of infants will be affected if infected during the first trimester
– No documented risk after 20 weeks

60
Q

how rubella is prevented?

A

• Rubella immunisation
– routine schedule of infant immunisations
– non-immune adolescents/adults
– healthcare workers
• Antenatal screening – to detect women who are non-immune and administer rubella vaccine postpartum in order to protect subsequent pregnancies

61
Q

what are the Contraindications & Precautions

A
  • LIVE vaccine
  • Severe allergic reaction to prior dose or vaccine component
  • Pregnancy
  • Immunosuppression
  • Moderate or severe acute illness
  • Recent blood product

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