This document provides an overview of pertussis (whooping cough) including its epidemiology, clinical presentation, diagnosis, treatment and post-exposure prophylaxis. Pertussis is caused by Bordetella pertussis and presents in three stages - catarrhal, paroxysmal and convalescent. It is highly contagious and vaccination is the primary prevention. For treatment, supportive care and macrolide antibiotics are recommended to reduce infectivity. Post-exposure prophylaxis with antibiotics may be considered for at-risk contacts.

1. Dr. Sayan Misra
Emergency Department
Peerless Hospital
PERTUSSIS

2. Perspective
Background –
 An acute respiratory disease that was first described in
1578 when an epidemic swept through Paris.
 Name was first used by Sydenham in 1670 when he
described the illness in infants.
 It literally means “violent cough,” which is the hallmark of
the disease.
 In China it is known as “the cough of 100 days.”

3. Perspective
 It is also called whooping cough because the severe
episodes of coughing are followed by forceful inspiration,
which creates the characteristic whooping sound.
 Caused by the aerobic gram-negative rod which was
identified in 1906 by Bordet and Gengou.

4. Perspective
Epidemiology –
 Pertussis is a localized respiratory illness transmitted by
aerosolized droplets.
 Highly contagious  Attack rates >50% in adults
exposed more than 12 years after completion of a
vaccination series and up to 90% in susceptible
individuals with a household exposure.
 Average incubation period is 7 to 10 days, may range
from <1 week to 3 weeks.
 Neither vaccination nor prior infection confers lifelong

5. Perspective
 Although pertussis can occur at any age, it is
predominantly a pediatric and adolescent illness.
 The age-specific attack rates are highest in children
younger than 1 year who have not yet received the entire
vaccine series.

6. Principles of Disease
Etiology –
 Caused by organisms of the Bordetella genus  small,
aerobic, gram-negative coccobacilli that occur singly or in
pairs.
 Bordetella pertussis and Bordetella parapertussis 
primarily responsible for disease in humans.
 Bordetella bronchiseptica, a flagellated, motile
organism, causes illness in animals, including kennel
cough  rarely cause respiratory infection in

7. Principles of Disease
Pathophysiology –
 Bordetella organism adheres to ciliated respiratory
epithelial cells.
 B. pertussis does not invade beyond the submucosal
layer in the respiratory tract.
 Elaborates several toxins that act locally and systemically
 pertussis toxin, dermonecrotic toxin, adenylate cyclase
toxin, and tracheal cytotoxin.

8. Clinical Features
Pertussis arises in three distinct sequential clinical stages:
 Catarrhal or Prodromal phase
 Paroxysmal phase
 Convalescent phase

9. Catarrhal or Prodromal phase
 Begins after an incubation period of approximately 7
to 10 days and lasts approximately 1 to 2 weeks.
 Infectivity is greatest during the catarrhal phase.
 Signs and symptoms  rhinorrhea, low-grade fever,
malaise, and conjunctival injection, which are
clinically indistinguishable from a common upper
respiratory tract infection.
 Dry cough usually begins at the end of the catarrhal

10. Paroxysmal phase
 Begins as fever subsides and cough increases and lasts 2
to 4 weeks. Paroxysms of staccato coughing occur 40 to
50 times per day.
 Patient coughs repeatedly in short exhalations, followed
by a single, sudden, forceful inhalation that produces the
characteristic “whoop.”
 Only one third of adults with pertussis develop this whoop,
and it is rare in young infants.
 More frequently at night, or be precipitated by noise or

11. Paroxysmal phase
During the paroxysm, the patient may exhibit –
 Cyanosis
 Diaphoresis
 Protrusion of the tongue
 Salivation
 Lacrimation
 Post-tussive vomiting, syncope, and brief episodes
of apnea may occur.

12. Convalescent phase
 Characterized by a residual cough  lasts several
weeks to months.
 Paroxysms of coughing may be triggered by an
unrelated upper respiratory infection or by exposure to a
respiratory irritant.

13. Physical examination findings
 Tachypnea
 Low-grade fever is common during the catarrhal phase.
Presence of fever during other stages of illness suggests
secondary infection.
 Conjunctival injection
 Rhinorrhea
 Petechiae above the nipple line, Subconjunctival
hemorrhages, Pneumothorax and Epistaxis may occur
because of increased intrathoracic pressure during

14.  Consider pertussis in situations of chronic cough >2
weeks in duration.
 Highly communicable, with an attack rate of about 20%
even in the immunized, suspect pertussis if there is
contact with other individuals with prolonged cough.

15. Complications
 Pneumonia superinfection  complicating pertussis is a
leading cause of death
 Otitis media
 Complications related to the paroxysm of coughing
 Aspiration of gastric contents and respiratory secretions
may occur during the paroxysm of coughing, whooping,
and vomiting

16. Complications
 Bacterial – 1.Streptococcus pneumoniae
2.Streptococcus pyogenes
3.Haemophilus
influenzae
4.Staphylococcus aureus
 Viral - 1.Respiratory syncytial virus
2.Cytomegalovirus
3.Adenovirus
 Superinfections can complicate pertussis infections.

17. Complications
 Central nervous system (CNS) sequelae - seizures and
encephalopathy in about 1%. Causes are unclear, may
include –
1.hypoxia
2.hypoglycemia
3.cerebral petechia
4.effects of a toxin
5.secondary infection by
neurotropic
viruses or bacteria
 Hemorrhages may occur as a consequence of the

18. Complications
In short –
 Periorbital edema
 Subconjunctival hemorrhage
 Petechiae
 Epistaxis
 Hemoptysis
 Subcutaneous emphysema
 Pneumothorax
 Pneumomediastinum
 Diaphragmatic rupture
 Umbilical and inguinal hernias
 Rectal prolapse

19. Diagnostic Strategies
 Diagnosis of pertussis should be entertained in any
patient with prolonged cough with paroxysms, whoops,
or post-tussive emesis, regardless of previous
vaccination status.
 Late catarrhal and early paroxysmal phases -
Leukocytosis and a characteristic Lymphocytosis. WBC
count  25,000 to 50,000/mL (not uncommon), may
exceed 100,000/mL in infants.

20. Diagnostic Strategies
 Chest radiograph may show peribronchial thickening,
atelectasis, or pulmonary consolidation
 Laboratory confirmation  Nasopharyngeal culture and
PCR. Sputum and throat swabs are inadequate.
 The sensitivity of pertussis cultures is only 15 to 80%,
drops to only 1 to 3% three weeks after the onset of
cough.

21. Diagnostic Strategies
 Definitive diagnosis  PCR of nasopharyngeal
secretions Or Serologic detection of antibodies.
 PCR  More likely to identify the organism but has a
high false-positive rate.
 Most laboratories use ELISA, which rises 2 to 3 weeks
after infection or primary immunization.
 Paired serologic tests showing a Two-Fold increase are
the “Gold standard” for diagnosis.

22. Differential Diagnoses
 Acute viral upper respiratory tract infection
 Pneumonia
 Bronchiolitis
 Cystic fibrosis
 Tuberculosis
 Exacerbation of chronic obstructive pulmonary
disease
 Foreign body aspiration
 The marked leukocytosis may suggest the diagnosis
of leukemia

23. Treatment
Immunization –
 Two types of vaccines - Whole-cell vaccine (DPT)
Acellular vaccine (DTaP)
Distributed in combination with diphtheria and tetanus
toxoids.
 Whole-cell pertussis vaccination is effective for about 10
years and is used in developing nations.
 Acellular pertussis vaccine (DTaP), developed to remove
toxins from the cell membrane, does not protect as long
as the whole-cell vaccine. Used in the developed world

24. Immunization –
 Immunization schedule  2, 4, 6, and 18 months of
age and a booster at age 5. Adolescents should
receive a DTaP booster.
 Pregnant women should receive a booster of DTaP
to protect neonates and infants and to prevent
infection in the mother.
 In Unimmunized elderly(>65 years old), one dose of
DTaP is recommended.
 There is no lifelong immunity after a clinical episode

25. Treatment
Acute Treatment –
 Primarily – A,B,C approach. Supportive, includes Oxygen,
Frequent suctioning, Appropriate hydration, Parenteral
nutrition if necessary, and avoidance of respiratory
irritants.
 Associated  Pneumonia, hypoxia, CNS complications or
those experiencing severe paroxysms should be
hospitalized.
 Children younger than 1 year  admit because they are
not yet fully immunized  greatest risk for morbidity and

26. Acute Treatment –
 Neonates with pertussis should be admitted to NICU .
 Primary goal of antibiotic therapy is to decrease infectivity
and carriage.
 Does not reduce the severity or duration of illness when it
is started in the Paroxysmal phase. Best if started early, in
the first week.

27. Acute Treatment –
 Erythromycin is the antibiotic of choice  40 to 50
mg/kg/day (maximum 2 g/day) in two or three divided
doses for 14 days.
 Azithromycin  10 mg/kg i.e. 500 milligrams on day 1,
then, 5 mg/kg i.e. 250 milligrams on days 2 to 5.
 Clarithromycin 15 mg/kg/day in two divided doses, and,
a 7-day course of erythromycin are effective alternatives
for patients who do not tolerate 14 days of erythromycin

28. Acute Treatment –
 Trimethoprim-sulfamethoxazole  8 mg/kg/day i.e. 160
milligrams/800 milligrams twice a day for 14 days 
alternative for macrolide-allergic patients, but efficacy is
unproven.
 Corticosteroids may reduce the severity and course of
illness, but effectiveness is not well established.
 Beta2-adrenergic agonists  do not reduce the frequency
or severity of paroxysmal coughing episodes  may be
helpful in patients with reactive airway disease.

29.  Patients should be considered infectious for 3 weeks after
the onset of the paroxysmal phase or until at least 5 days
after antibiotics are started.
 Strict droplet isolation is recommended during this period.

30. Postexposure prophylaxis –
 Chemoprophylaxis is typically given for household
contacts, although the evidence base for such treatment
is weak.
 Erythromycin is considered for infants younger than 6
months, any unimmunized/partially immunized person.