Lower Respiratory Infection = Viral Flashcards

1
Q

What is viral bronchiolitis and how is it related to repsiratory synctial virus?

A

Bronchiolitis – disease restricted to children, mostly <2 yr

  • Bronchioles narrow, inflammation and swelling blocks them, restricting air passage and causing epithelial death
  • 75% of cases due to Respiratory syncytial virus (RSV)
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2
Q

What is the respiratory synctial virus (form of bronchiolitis)? Discuss its viral characteristics, transmission, epidemiology and clinical features

A

Family: Parymxoviruses (ssRNA, enveloped)

  • 2 major strains: group A and B
  • 2 envelope spikes: G and F proteins

G protein – attachment to cell

F (fusion) – initiated entry into cell, also causes fusion of host cells –> syncytia

  • Transmitted through droplets, contaminated hands
  • Outbreaks in winter
  • Virus infects upper and lower respiratory tract
  • Incubation period 4-5 days, clinical signs follow

> Infants – can be particularly severe, peak mortality 3 months

Symptoms: rapid respiratory rate, cough, cyanosis, bronchiolitis and pneumonia

  • Children and adults – less severe, upper respiratory tract only, cold-like illness
  • Treatment – in children, supportive: rehydration, bronchodilators and hospitalisation if needed, oxygen
  • Vaccine – at present none available
  • Prophylaxis with monoclonal antibody (palivizumab) in high risk children <2 yr (passive immunity)
  • Preterm babies, congenital malformations of the heart and airways
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3
Q

What is viral pneumonia

A
  • Many viruses cause pneumonia
  • Healthy individuals are at risk
  • Most of the viruses have surface molecules that attach specifically to epithelium
  • Even if virus doesn’t cause pneumonia, damage to epithelium may result in secondary bacterial pneumonia
  • Look at:  Parainfluenza virus  Influenza virus  Measles virus
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4
Q

What is parainfluenza virus - Pneumonia

A

Family: Paramyxoviruses (ssRNA, enveloped)

Parainfluenza virus – 2 envelope spikes:

> Haemagglutinin-neuraminidase (HN)

> Fusion protein (F)

  • Spread through respiratory droplets and infect respiratory epithelium
  • 4 types based on different antigens (serotypes)
  • Parainfluenza 1-3 – pneumonia, pharyngitis, bronchiolitis and croup Croup – in children <5 yr, acute laryngo-tracheo-bronchiolitis

> Narrow airway, harsh barking cough = croup

  • Parainfluenza 4 – less common, cold-like symptoms –> no vaccine
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5
Q

What is influenza?

A
  • Influenza is an acute respiratory tract infection that usually occurs in epidemics
  • fever, cough, running nose
  • Compare with the common cold which is less severe: no fever, runny nose –> different viruses
  • Family: Orthomyxoviruses, ssRNA, enveloped •
  • 3 types: A, B, C, based on proteins inside capsid

Influenza Virus Strains:

  • Type A - moderate to severe illness: all age groups, humans and other animals, reservoir birds –> causes epidemics, occasional pandemics
  • Type B - milder diseaseprimarily affects children & elderly, humans only –> causes epidemics
  • Type Crarely reported in humansno epidemics • minor respiratory illness
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6
Q

What are the antigenic properties for Influenza?

A

The major surface antigens are the glycoproteins (spikes)

– haemagglutinin (HA)

– neuraminidase (NA)

  • These two surface glycoproteins are important antigens that determine antigenic variation and are targets for host immunity
  • Type A is antigenically highly variable (most epidemics)
  • Type B can show antigenic changes and some epidemics
  • Type C is antigenically stable causing mild illness

Antigenic drift (can occur in all types –> A,B)

  • Minor change in viral antigens
  • Changes occur because of point mutation in genes
  • Same subtype; can cause epidemic

Antigenic Shift (type A only)

  • Major change resulting in new subtype
  • Caused by exchange of gene segments
  • Co-infection of a host with different viral strains from different species (human and animal)
  • Antigen genes recombine –> cause epidemics and pandemic
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7
Q

Influenza A nomenclature? Influenza pathogenesis? Clinical features?

A

Nomenclature

Based on glycoprotein combinations

  • H, Haemagglutinin –> gain entry, attach to sialic acid
  • N, neuraminidase – since new virions take cell membrane, N cleaves sialic acid of virion membranes and infected cells
  • H = 18 (H1-H18)
  • N = 9 (N1-N9)

Pathogenesis

  • Respiratory transmission of virus through droplets
  • Replication in respiratory epithelium with subsequent destruction of cells
  • Viraemia rarely occurs
  • Virus shed in respiratory secretions for 5-10 days

Clinical Features

  • Incubation period 2 days (range 1-4 days)
  • 50% of infected persons develop classic symptoms –> Abrupt onset of fever, myalgia, sore throat, non-productive cough, headache
  • Fever usually lasts 3 days as do systemic symptoms
  • Respiratory symptoms typically last another 3-4 days
  • The cough and weakness may persist for 1-3 weeks
  • Children may have higher fever and higher incidence of GI manifestations such as vomiting

Complications

  • Pneumonia

> secondary bacterial – most common

> primary influenza viral – less common

  • Myocarditis
  • Mortality < 1/1000 cases usually in elderly
  • In pandemics severe disease may occur healthy young adults

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8
Q

What is the epidemiology of Lower respiratory tract infections?

A
  • Epidemiology of influenza is closely associated with antigenic changes – drift and shift
  • Incidence peaks during the winter with periodic outbreaks due to antigenic changes
  • High susceptibility to a particular antigenic change can result in an epidemic
  • Antigenic shift in influenza type A is thought to occur because related influenza A viruses circulate in animal and bird populations
  • Influenza outbreaks occur in waves with the period between epidemic waves of influenza A being 2-3 years
  • Every 10-40 years when a new subtype of influenza A appears a pandemic results
  • H1NI = spanish (severe)
  • H2N2 = asian (Severe)
  • H3N2 = hong kong (moderate_
  • H5N1 is particularly virulent –> avian flu
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9
Q

What is the influenza vaccination?

A
  • Influenza vaccine prevents morbidity and mortality by:

Preventing infection and Attenuating disease

  • Changing antigenic nature of the virus creates a problem in vaccine production

> Vaccine gives protection only against strains in vaccine and also against related strains

>WHO has worldwide surveillance centres to monitor viral antigenic changes

>The southern hemisphere gets a few more months as the epidemics are evident first in the northern winter

Being in the Southern hemisphere has an advantage –> Because of the changing nature of the viruses vaccination is only effective for about 1 year

  • Influenza vaccines in Australia are inactivated virus
  • Prepared from purified influenza virus made in hens eggs (allergy to eggs is contraindicated)
  • Significant market with many different manufacturers
  • Influenza vaccination is broadly recommended in the population there are some groups specifically targeted

>65 year, pregnancy, Indigenous people, those suffering from chronic illness, health care workers, etc (see Immunisation Handbook)

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10
Q

What is measles? Describe it pathogenesis, clinical features and complications

A

Measles virus: ssRNA genome, enveloped,

  • Paramyxoviridae family
  • Highly infectious, with 99% of population infected prior to vaccine - asymptomatic or subclinical infection rare
  • After infection, complete life-long resistance
  • Before a vaccine became available, measles killed 7–8 million children each year worldwide.

Pathogenesis

  • Transmitted by respiratory droplets
  • Virus enters in the upper/lower respiratory tract or conjunctiva and spreads to sub-epithelial and local lymphatic tissues
  • During the next few days, there is a primary viraemia: virus spreads and multiplies in lymphoid tissues (inc. spleen, respiratory tract)
  • Secondary viraemia, ~5 days after the infection, virus disseminates to a variety of epithelial sites including the skin, kidney, and bladder
  • Does not replicate at site of entry
  • Replicates systemetically and then returns in large numbers to entry surface and replicates further and is shed

Clinical features

  • After 9-10 days post infection: acute, respiratory illness with a runny nose, fever and cough, and conjunctivitis
  • Patient is highly infectious with large amoutnt of virus being shed in respiratory infections
  • Koplik spots appear inside cheek and shortly afterwards –> the maculopapular rash is seen, first on the face, then down the body to extremities

Treatment

  • Antiviral Ribavirin may be used; MMR vaccine
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11
Q

What is aspergillosis? What are its causative agents and clinical features?

A

Fungal infection of the respiratory tract is usually associated with immunocompromised individuals

  • Immune suppressive treatment
  • Concomitant disease

​Most medically important: Aspergillosis fumigatus and Aspergillosis flavus

  • Do not form part of the normal flora
  • Spores inhaled and able to cause a range of diseases

Allergic bronchopulmonary aspergillosis

  • allergic irritation to antigens in lungs, in asthma patients

Aspergilloma

  • A fungal ball of growth in lung cavitis, form pre-existing condition, no invasion of tissue but can cause respiratory problems
  • Disseminated disease in immunocompromised patients –> high mortality as limited number and toxicity of antifungal agents
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