4. Morphology
• Coccobacilli
• Pleomorphic
• Bipolar metachromatic
granules by toluidine blue
staining
• Sometimes, a poorly
defined capsule (from fresh
strains)
• In culture smears, bacilli are
arranged in loose clumps
with clear spaces between
the clumps- thumb print
appearance
5. Culture
• Strict aerobe
• Fastidious- grow on
Bordet-Gengou agar
• Bisected pearls or
mercury drop colonies
• Confluent growth as
aluminium paint
appearance
7. Pathogenesis
• Non-invasive
• Colonizes cilia of respiratory tract
• Initially, it causes local tissue damage.
• Then it releases toxins resulting in toxemia,
and damage at distant sites
8. Virulence factors
• Filamentous haemagglutinin (FHA)
• Pertussis toxin
• Invasive adenylate cyclase
• Lethal toxin
• Tracheal cytotoxin
• Unusual lipopolysaccharide (LPS): two distinct
types of LPS with lipid A or lipid X
• Pertactin or outer membrane protein (OMP)
9. Filamentous haemagglutinin (FHA)
• Most important virulence factor
• Helps in the attachment of bacilli to the
ciliated epithelium
• Antibodies against FHA are protective
10. Pertussis toxin
• Secreted extracellularly, and also bound to cell wall
• Consists of two subunits A and B
• B helps in binding to cells, whereas A is responsible for
the action of toxin
• Responsible for profound lymphcytosis (lymphocytosis
producing factor, LPF)
• Histamine sensitising factor (HSF) and Islet activating
protein (IAP) in experimental animals
• Antibodies against toxin are protective
• Pertussis toxin can be toxoided
14. Pertactin or outer membrane protein
(OMP)
• Probably, also helps in binding to respiratory
epithelium
• Antibodies against pertactin are protective
16. Catarrhal stage
• Mild cough and cold
• Mild fever may be present
• Lasts 1-2 weeks
• Highly infectious stage
• Disease can be arrested by antibiotic
treatment
17. Paroxysmal stage
• Consists of paroxysms of intense coughing
followed by inrush of air into the empty lungs
giving a characteristic inspiratory whoop
• Paroxyms may end with vomiting and
exhaustion
• Lasts 1-10 weeks
18. Complications
1. subconjunctival hemorrhage or
subcutaneous emphysema (due to pressure
effects),
2. bronchopneumonia and lung collapse,
3. neurological (like convulsions, coma) due to
anoxia
20. Epidemiology
• Humans are the only reservoir
• Source: infectious patient, especially during
catarrhal stage
• Transmission: droplet route
• 75% cases are seen in children
• 25% cases are seen in adults due to waning
immunity after vaccination
21. Laboratory diagnosis
• Specimen collection:
1. Cough plate method
2. Pernasal swab:
nasopharyngeal wall
3. West post-nasal/peroral
swab: posterior pharyngeal
wall
( Calcium alginate or Dacron
swabs should be used only)
• Swabs should be
immediately inoculated, or
else should be transported in
modified Stuart or Regan-
Lowe transport medium
22. • Diagnosis can be made by
direct fluorescent
antibody (DFA) technique
OR
• Culture and biochemical
properties OR
• Serology (IgG and IgA
antibodies against FHA or
IgG against pertussis
toxin) OR
• Molecular techniques
(PCR)
24. Prophylaxis
• An attack of whooping
cough gives life long
immunity
• Vaccines:
1. Whole cell killed
vaccine
2. Acellular vaccine
25. Whole cell vaccine
• Killed cell vaccine
• Given along with diphtheria and tetanus toxoid
(triple vaccine). Here B. pertussis also acts as an
adjuvant
• 80-85% effective
• Complication include encephalopathy, especially
in children more than 7 years of age
• Immunity lasts around 12 years
• Even fully immunized individuals can develop
pertussis, but a mild one
26. Acellular vaccine
• Contains FHA, pertussis toxin, and pertactin
• Much safer than cellular vaccine
• Almost same efficacy as cellular vaccine