Measles

Question 1

1. What does “non-segmented ssRNA” mean?

• ssRNA = single-stranded RNA genome.
• Non-segmented = the entire genome is one continuous strand of RNA.
  • Some viruses (like Influenza) have segmented RNA (multiple pieces like chromosomes).
  • Measles, Rabies, Ebola, Lassa, etc. all have non-segmented ssRNA genomes.

2. What’s the difference between +ssRNA and –ssRNA?

This is key to understanding viral replication:

+ssRNA (positive-sense RNA):

• Acts like mRNA.
• Host ribosomes can directly translate it into viral proteins.
• E.g. Flaviviruses (Yellow fever, Dengue)

–ssRNA (negative-sense RNA):

• NOT readable by host ribosomes.
• It must be converted into +ssRNA first.
• Needs to carry RNA-dependent RNA polymerase in its virion.
• E.g. Measles, Rabies, Ebola, Lassa, Marburg

3. Why is this distinction important clinically?

a. Replication & Immune Evasion

• –ssRNA viruses must replicate in the cytoplasm using their own polymerase.
• This makes them less dependent on the host nucleus, but also highly error-prone ⏩rapid mutation ⏩ evasion of immune response.

b. Infection Control

• –ssRNA viruses often cause acute, systemic infections (e.g. VHF, rabies).
• Because they bring their polymerase, they replicate fast and spread quickly before the immune system catches up.

c. Vaccine Development

• RNA structure influences how stable the virus is, how it mutates, and what kind of vaccine (live, killed, subunit) might work.

d. Lab Diagnosis

• Knowing whether it’s + or – helps choose the right PCR primers and detection methods.

Summary Table:

Feature | +ssRNA | –ssRNA |
| ———————— | ———————— | ————————— |
| Acts as mRNA? | Yes | No |
| Requires RNA polymerase? | No (host ribosome-ready) | Yes (brings its own) |
| Examples | Dengue, Yellow fever | Measles, Rabies, Ebola |
| Clinical implication | Often milder, chronic | Often severe, acute disease |

Question 2

Measles Overview

• Cause: Measles virus (Paramyxoviridae family)
• Host: Only humans (no animal reservoir in nature)
• Type: Acute, highly contagious viral illness

What are the hallmarks of measles

Answer 2

• Hallmarks: Fever, cough, coryza, conjunctivitis, and maculopapular rash

Question 3

What’s the Structure & Antigenic Properties of measles

Answer 3

• Genome: Non-segmented ssRNA, helical nucleocapsid
• Envelope spikes:
  • Hemagglutinin (H): Responsible for viral attachment; neutralizing antibody targets this
  • Fusion protein (F): Causes cell fusion (syncytia) and entry
• These help the virus evade immune responses and spread from cell to cell

Question 4

What’s the mode of Transmission

Answer 4

• Mode: Respiratory droplets (coughing, sneezing)
• Contagious period:
  • 4 days before to 4 days after rash appears
• Airborne spread also possible due to aerosolized droplets

Question 5

Epidemiology

• Endemic and epidemic in unvaccinated populations
• Occurs in 2–3 year cycles when herd immunity drops
• 30 million cases/year globally (WHO)
• High mortality in:
  • Malnourished children
  • Immunosuppressed (e.g. HIV/AIDS)

Question 6

What are the Risk factors for the dxs becoming severe

Answer 6

• Vitamin A deficiency
• Young age (<5 years)
• High population density
• Poor vaccination coverage

Question 7

Clinical Significance

• High mortality (up to 25%) in poor-resource settings
• Can cause severe complications: such as?

Answer 7

• Pneumonia
  
  • Encephalitis
  • Subacute sclerosing panencephalitis (SSPE)

Question 8

Explain the Replicative Cycle – Key Clinical Points

Answer 8

After exposure

1. Attachment:
   • Hemagglutinin on measles virus binds to host cell receptors (CD150/SLAM on lymphocytes).
   • Why important? ➡️ Explains early lymphoid involvement and immune suppression.
2. Penetration & Uncoating:
   • Virus enters the host cell and releases its –ssRNA genome.
3. Transcription:
   • RNA-dependent RNA polymerase (carried by virus) transcribes viral mRNAs.
   • Why? –ssRNA isn’t readable directly by host ribosomes.
4. Translation & Assembly:
   • Viral proteins are made, and the nucleocapsid is formed.
   • Matrix protein helps package everything as the virus buds off.

Question 9

Whats the Pathogenesis – Step-by-Step (With “Why”)

Answer 9

1. Entry via respiratory tract ➡️ local replication.
   • Why? Explains respiratory symptoms early in the prodrome.
2. Spread to local lymph nodes ➡️ primary viremia.
   • Why? Causes systemic symptoms (fever, malaise).
3. Replication in RES (e.g., liver, spleen) ➡️ secondary viremia.
   • Why? Amplifies viral load, spreads virus body-wide.
4. Seeding of epithelial surfaces (skin, conjunctiva, trachea).
   • Why? Explains rash, cough, conjunctivitis.
5. Infection of lymphocytes (especially CD4+).
   • Why? Leads to transient immune suppression, raising risk of secondary infections.

Question 10

Pathology
Whats the Hallmark of measles-induced tissue damage?
The Rash is caused by?

Answer 10

• Giant cells with intranuclear inclusions in lymphoid tissue:
  • Why? Hallmark of measles-induced tissue damage (seen in tonsils, nodes, appendix).
• Rash is immunologic, not viral damage.
  • Caused by cytotoxic T cells attacking infected endothelial cells in the skin.
  • Why important? Rash appears with antibody production and signals immune response.
• CNS involvement (rare):
  • Likely autoimmune (e.g., acute disseminated encephalomyelitis).
  • Why? Could explain rare complications like subacute sclerosing panencephalitis (SSPE).

Question 11

Wha are the Clinical Features – Timeline and Significance
Incubation period is?

Answer 11

Stage | Features Clinical Importance
Incubation (10–14 days) Asymptomatic Virus spreads systemically

| Koplik spots | Grayish ulcers near molars | Pathognomonic – early diagnostic clue |

| Rash | Starts on face, spreads downward | T-cell response to infected vessels |

| Resolution | Rash fades with desquamation | Coincides with antibody appearance

Prodrome | Fever, cough, coryza, conjunctivitis | Highly contagious phase |

Question 12

Modified Measles (Why It Matters)

• Occurs in partially immune individuals (killed vaccine or maternal antibodies).
• Atypical: less intense or prolonged symptoms, may confuse diagnosis.
• Why important? Delayed or misdiagnosed cases ⏩ more spread in community.

Question 13

What are the Immunities in Measles – How It Works & Why It Matters

Answer 13

1. Lifelong immunity after infection
   • Why? The immune system develops strong memory responses (B and T cells) against the virus.
2. Humoral (antibody-mediated) immunity is protective
   • Especially neutralizing antibodies against the hemagglutinin spike.
   • Why? These antibodies prevent reinfection.
3. Maternal IgG crosses the placenta
   • Protects newborns during the first 6 months.
   • Why? Explains why measles is rare in infants <6 months in areas with high maternal immunity.
4. Cell-mediated immunity (CMI) clears the virus
   • Why? Necessary because measles infects and spreads via immune and epithelial cells.
5. Transient suppression of CMI
   • Why important? Measles causes temporary immunosuppression, increasing susceptibility to infections like tuberculosis and bacterial pneumonia

Question 14

What are the Complications of Measles – What Can Go Wrong (And Why)

Answer 14

• Otitis Media
  Occurs in about 5–9% of measles cases.
  Why? The virus impairs mucosal immunity and causes Eustachian tube dysfunction, predisposing to middle ear infections.
• Pneumonia
  Seen in up to 10% of cases in developed countries and as high as 80% in developing ones.
  Why? Can be due to secondary bacterial infection or direct viral damage. It’s the leading cause of measles-related deaths, accounting for up to 90%.
• Giant Cell Pneumonia
  Occurs in patients with impaired cell-mediated immunity, such as those with HIV.
  Why? Caused by the measles virus itself, not bacteria, and often fatal without strong immune defenses.
• Stillbirth in Pregnant Women
  Measles increases the risk of fetal loss during pregnancy.
  Why? Immune activation and systemic viral spread may compromise the placenta or fetal development.
• Acute Encephalitis
  Develops during the early recovery phase.
  Why? Due to direct viral invasion of brain tissue, leading to seizures, confusion, or coma.
• Postinfectious Encephalomyelitis
  Occurs about 2 weeks after rash resolution.
  Why? An autoimmune reaction causes demyelination of CNS tissue, similar to ADEM.
• Subacute Sclerosing Panencephalitis (SSPE)
  A rare, fatal complication occurring 5–15 years after measles, especially if infection happened early in life.
  Why? Caused by persistent, defective measles virus in the CNS, leading to progressive cognitive and motor decline, seizures, rigidity, and eventual coma.

Question 15

SSPE Snapshot:

• Rare (1 in 10,000–100,000 cases)
• Early measles (especially <2 years) increases risk
• Symptoms: personality change, myoclonus, dementia, rigidity, coma
• Why important? Emphasizes need for early vaccination to prevent early childhood infection

Question 16

**

Answer 16

At Birth:

• BCG Vaccine: Protects against tuberculosis.
• OPV0 (Oral Polio Vaccine, dose 0): Provides initial protection against poliomyelitis.
• Hepatitis B Vaccine (Birth dose): Prevents hepatitis B infection.

At 6 Weeks:

• Pentavalent Vaccine (DPT-HepB-Hib) – Dose 1: Protects against diphtheria, pertussis (whooping cough), tetanus, hepatitis B, and Haemophilus influenzae type b.
• OPV1: Second dose of oral polio vaccine.
• PCV1 (Pneumococcal Conjugate Vaccine) – Dose 1: Prevents pneumococcal diseases.
• Rotavirus Vaccine – Dose 1: Protects against rotavirus infections.([Smart Parenting In Nigeria][2])

At 10 Weeks:

• Pentavalent Vaccine – Dose 2
• OPV2
• PCV2 – Dose 2
• Rotavirus Vaccine – Dose 2

At 14 Weeks:

• Pentavalent Vaccine – Dose 3
• OPV3
• PCV3 – Dose 3
• Inactivated Polio Vaccine (IPV) – Single dose

At 9 Months:

• Measles Vaccine: Protects against measles infection.
• Yellow Fever Vaccine: Prevents yellow fever.

At 12 Months:

• Meningitis A Vaccine: Protects against meningococcal meningitis.

It’s important to adhere to this schedule to ensure children receive timely protection against these diseases. The measles vaccine, administered at 9 months, is particularly crucial in preventing measles outbreaks.

Note: While the measles vaccine is typically administered alone at 9 months in Nigeria, in some countries, it is given as part of the combined MMR (measles, mumps, and rubella) vaccine. However, the MMR vaccine is not currently part of Nigeria’s routine immunization schedule.

Question 17

What are the Laboratory Diagnosis of Measles?

What how’s the clinical diagnosis made?

Answer 17

• Clinical Diagnosis
  Diagnosis is primarily clinical, based on the triad of fever, cough, conjunctivitis, and Koplik’s spots followed by rash.
• Serology (ELISA)
  Detects a 4-fold rise in IgG antibodies between acute and convalescent sera.
  Why? Confirms recent infection and is useful for retrospective diagnosis or in atypical cases.
• Molecular Testing (RT-PCR)
  Detects measles RNA in throat swabs, urine, or blood.
  Why? Highly sensitive and specific, especially useful during outbreaks or in vaccinated individuals.
• Virus Isolation
  Grown in monkey or human kidney cells or lymphoblastoid cell lines.
  Why? Mainly used in research or for epidemiologic surveillance, not routine diagnosis.
• Electron Microscopy
  Shows pleomorphic enveloped particles with surface projections.
  Why? Confirms viral morphology, especially in specialized labs.

Question 18

What are the Treatments for Measles

Answer 18

• Supportive Therapy
  Includes hydration, fever management, and nutritional support.
  Why? There is no antiviral treatment for measles; management focuses on preventing complications.
• Vitamin A Supplementation
  Given especially to children in low-resource settings.
  Why? Reduces severity and mortality by enhancing epithelial integrity and immune response.

Question 19

Prevention and Control of Measles

Answer 19

• Live Attenuated Vaccine (MMR)
  Given subcutaneously at 15 months, with a booster before school entry.
  Why? Induces long-lasting immunity and has dramatically reduced global measles incidence.
• Booster Dose
  Ensures adequate immunity in case of primary vaccine failure or waning immunity.
• Contraindications
  Not given to immunocompromised individuals or pregnant women.
  Why? Risk of uncontrolled viral replication due to live vaccine.

Question 20

What’s the Immunization Schedule for Children in Nigeria?

It’s incomplete check slide

Answer 20

At Birth:

• BCG Vaccine: Protects against tuberculosis.
• OPV0 (Oral Polio Vaccine, dose 0): Provides initial protection against poliomyelitis.
• Hepatitis B Vaccine (Birth dose): Prevents hepatitis B infection.

At 6 Weeks:

• Pentavalent Vaccine (DPT-HepB-Hib) – Dose 1: Protects against diphtheria, pertussis (whooping cough), tetanus, hepatitis B, and Haemophilus influenzae type b.
• OPV1: Second dose of oral polio vaccine.
• PCV1 (Pneumococcal Conjugate Vaccine) – Dose 1: Prevents pneumococcal diseases.
• Rotavirus Vaccine – Dose 1: Protects against rotavirus infections.([Smart Parenting In Nigeria][2])

At 10 Weeks:

• Pentavalent Vaccine – Dose 2
• OPV2
• PCV2 – Dose 2
• Rotavirus Vaccine – Dose 2

At 14 Weeks:

• Pentavalent Vaccine – Dose 3
• OPV3
• PCV3 – Dose 3
• Inactivated Polio Vaccine (IPV) – Single dose

At 9 Months:

• Measles Vaccine: Protects against measles infection.
• Yellow Fever Vaccine: Prevents yellow fever.

At 12 Months:

• Meningitis A Vaccine: Protects against meningococcal meningitis.

It’s important to adhere to this schedule to ensure children receive timely protection against these diseases. The measles vaccine, administered at 9 months, is particularly crucial in preventing measles outbreaks.

Note: While the measles vaccine is typically administered alone at 9 months in Nigeria, in some countries, it is given as part of the combined MMR (measles, mumps, and rubella) vaccine. However, the MMR vaccine is not currently part of Nigeria’s routine immunization schedule.