Pertussis A Clinical Description

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PertussisA Clinical Description

• Susan Chandler, R.N., MPH
• P. H. Nurse Consultant
• N. C. Immunization Branch

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Bug Hunt
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The Bug

• Bordetella Pertussis
• Natural history of the bacteria
• Clinical description of disease

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What Difference Does it Make?

• To heighten your Index of Suspicion
• You cant find it unless you know what it looks
  like
• For better investigation and better application
  of control measures

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What Difference Does it Make?

• Encourages you to put the pieces together as you
• follow the clues...

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Puzzle Pieces
Agent
Host
Environment
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Agent
Bordetella pertussis
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Agent- Bordetella pertussis

• Gram negative rod bacteria
• Disease described since 1500s
• Bacteria isolated 1906

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Agent- Bordetella pertussis

• Barbed surface
• Adheres to cilia of respiratory epithelium
• Causes paralysis and necrosis of cells

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Components of Bacteria

• Pertussis Toxin- facilitates attachment to
  respiratory cilia causing mucosal damage
• Filamentous hemagglutinin- an antigen that
  induces clumping of red blood cells helping
  attachment to cilia
• Cellular Enzyme- disrupts host cell metabolism
  helping w/ cilia destruction
• Tracheal cytotoxin- causes cell damage

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Host
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Who Gets the Disease

• Disease wide spread before vaccine available
• Availability of vaccine brought about a 98
  decrease in incidence
• At turn of century, 5 of 1000 infants born alive
  died of pertussis before their fifth birthday
• Today in unvaccinated world gt300,000 deaths occur
  per year

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Who Gets the Disease

• Infants susceptible w/in first few weeks of life
  when mortality is highest

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Who Gets the Disease

• No maternal transplacental immunity, so infants
  highly vulnerable
• Nearly all non-immune household contacts will
  contract the disease if exposed
• Approximately 50 of susceptible contacts at
  school will contract the disease

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Who Gets the Disease

• Girls have higher incidence than boys
• Girls have higher mortality than boys
• Seasonal pattern to disease is difficult to
  interpret-seems highest earliest part of calendar
  year
• Incidence highest in children lt1 year
• Increasing cases among adolescents and adults

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Environment
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Environment- Transmission

• Person to Person by aerosolized droplets from
  cough or sneeze or direct contact w/ secretions
  from respiratory tract
• Intimate respiratory contact
• Contact w/ Contaminated Articles-rare if at all

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Puzzle Pieces
Agent
Host
Environment
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Disease-description

• Toxin mediated
• Bacteria attaches to respiratory cilia and
  releases toxins
• Toxins paralyze cilia and inflame
  respiratory track
• Result is inability to clear secretion-
  possible pneumonia

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Disease-description

• Pertussis antigen allows bacteria to evade bodys
  defenses by lymphocytosis (? lymph cells)
• Impairs ability of body to move white blood cells
  to areas of inflammation to fight infection
• Bacteria can invade tissue-has been found in
  alveolar macrophages

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Disease-description

• Respiratory cilia damage and destruction-edema w/
  accumulation of mucoid secretions
• Bronchiolar obstruction
• Atelectasis (collapsed lung)
• Bronchopneumonia
• Secondary findings in brain-edema and anoxia

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Stages of Disease

• There are three and they relate directly to our
  ability to intervene..

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Stages of Disease

• Stage I
• Catarrhal
• First 1-2or 3 weeks of illness
• Insidious on-set of runny nose, sneezing,
  low-grade fever, mild occasional cough
• Easily cultured while colonizing

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Stages of Disease

• Stage II
• Paroxysmal
• Lasting several weeks
• Enough Sx to suspect paroxysmal cough
  because of thick mucous and unable to expel
  mucous
• Possible cyanosis, vomiting, exhaustion,
  appears toxically ill

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Stages of Disease

• Stage II- continued
• Paroxysmal
• Appears normal between attacks
• Cough can last up to 10 weeks
• Infants lt6 months may not have strength
  to whoop but do have paroxysms
• Rarely recover bacteria

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Stages of Disease

• Stage III
• Convalescent
• Last 2-3 weeks (can be as long as 3 months)
• Gradual recovery
• Coughing but less paroxysms and disappears
  gradually
• With other respiratory infections, paroxysms may
  recur

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Investigation
 

• Incubation Period
• Period of Communicability

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Incubation Period

• Interval between exposure and first symptoms
• Average 9-10 days (range 6-20 days)

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• Incubation Period9 to 10 Days Average
• Range 6 to 20 Days

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Period of Communicability

• The period of time the disease can be transmitted
• Highly communicable in early catarrhal stage and
  at the beginning of paroxysmal stage (first 2-3
  weeks).
• Thereafter, communicability gradually
  decreases-becoming negligible in 3 weeks

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