Bordetella pertussis (Whooping cough)

Last updated: February 23, 2023

Bordetella pertussis (Whooping cough)

Block 2 PHEENT

Block 2 PHEENT

Lung volumes and capacities
Pressure-volume loops
Changes in pressure-volume loops
Obstructive lung diseases: Pathology review
Chronic bronchitis
Alpha-1 antitrypsin deficiency: Year of the Zebra 2024
Emphysema
Chronic obstructive pulmonary disease: Clinical sciences
Bronchiectasis
Cor pulmonale
Asthma: Clinical sciences
Asthma
Asthma: Information for patients and families (The Primary School)
Restrictive lung diseases
Restrictive lung diseases: Pathology review
Approach to interstitial lung disease (diffuse parenchymal lung disease): Clinical sciences
Compliance of lungs and chest wall
Idiopathic pulmonary fibrosis
Approach to pneumoconiosis: Clinical sciences
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Pulmonary corticosteroids and mast cell inhibitors
Bronchodilators: Leukotriene antagonists and methylxanthines
Sarcoidosis
Hypersensitivity pneumonitis
Acute respiratory distress syndrome
Acute respiratory distress syndrome: Clinical sciences
Pulmonary hypertension
Pulmonary arterial hypertension (NORD)
Pulmonary edema
Atelectasis: Clinical sciences
Pneumonia
Pneumonia: Pathology review
Community-acquired pneumonia: Clinical sciences
Aspiration pneumonia and pneumonitis: Clinical sciences
Mycobacterium tuberculosis (Tuberculosis)
Tuberculosis: Pathology review
Tuberculosis (pulmonary): Clinical sciences
Oral candidiasis
Plaque-induced periodontal disease diagnoses
Gingivitis and periodontitis
Risk factors for periodontitis
Diagnosis of periodontitis
Upper respiratory tract infection
Upper respiratory tract infections: Clinical sciences
Cytomegalovirus
Epstein-Barr virus (Infectious mononucleosis)
Streptococcus pyogenes (Group A Strep)
Mumps virus
Otitis media
Sinusitis
Bacterial epiglottitis
Croup and epiglottitis: Clinical sciences
Bordetella pertussis (Whooping cough)
Bronchiolitis: Clinical sciences
Respiratory syncytial virus
Antihistamines for allergies
Streptococcus pneumoniae
Hospital-acquired and ventilator-associated pneumonia: Clinical sciences
Klebsiella pneumoniae
Mycoplasma pneumoniae
Legionella pneumophila (Legionnaires disease and Pontiac fever)
Coronaviruses
COVID-19: Clinical sciences
Hantavirus
Mycobacterium avium complex (NORD)
Pseudomonas aeruginosa
Aspergillus fumigatus
Histoplasmosis
Coccidioidomycosis and paracoccidioidomycosis
Pneumocystis jirovecii (Pneumocystis pneumonia)
Influenza virus
Influenza: Clinical sciences
The flu vaccine: Information for patients and families
Respiratory distress syndrome: Pathology review
Sepsis
Sepsis: Clinical sciences
Lung cancer
Lung cancer: Clinical sciences
Lung cancer and mesothelioma: Pathology review
Pancoast tumor
Mesothelioma
Nasopharyngeal carcinoma
Thyroglossal duct cyst
Cleft lip and palate
Pierre Robin sequence: Year of the Zebra
Gorlin syndrome: Year of the Zebra
Gorlin syndrome (Gorlin Syndrome Alliance)
Periapical lesions
Aphthous ulcers
Oral cancer
Glaucoma
Warthin tumor
Nasal, oral and pharyngeal diseases: Pathology review
Human herpesvirus 8 (Kaposi sarcoma)
Uveitis
Anatomy clinical correlates: Eye
Approach to a red eye: Clinical sciences
Eye conditions: Inflammation, infections and trauma: Pathology review
Age-related macular degeneration
Eye conditions: Retinal disorders: Pathology review
Retinoblastoma
Sialadenitis
Laryngomalacia
Conductive hearing loss
Anatomy clinical correlates: Ear
Tympanic membrane perforation
Muscarinic antagonists
Eye conditions: Refractive errors, lens disorders and glaucoma: Pathology review
Carbonic anhydrase inhibitors
Thyroid cancer
Hordeolum (stye)
Keratitis
Onchocerca volvulus (River blindness)
Acanthamoeba
Otitis media and externa (pediatrics): Clinical sciences
Acoustic neuroma (schwannoma)
Labyrinthitis
Meniere disease
Vertigo
Otitis externa
Neurofibromatosis
Eustachian tube dysfunction
Acute group A streptococcal infections and sequelae (pediatrics): Clinical sciences
Pharyngitis, peritonsillar abscess, and retropharyngeal abscess (pediatrics): Clinical sciences
Cataract

Transcript

Watch video only

Content Reviewers

Pertussis is a contagious infection caused by the bacteria Bordetella pertussis, which causes violent coughing spells, called paroxysms, which make it difficult to breathe.

When it is finally possible to breathe in, air is drawn in through partially closed, swollen airways and that creates a whooping noise which gives pertussis its other name, whooping cough.

Bordetella pertussis is a gram negative coccobacilli - meaning that it looks like a short pink rod on a gram stain.

It transmits from one person to another through a sneeze or cough, when that happens thousands of bacteria-filled droplets spray out about two meters or six feet away.

These droplets can land in the mouths or noses of nearby people, or get directly inhaled into the lungs.

The bacteria can also survive for several days on dry surfaces, so it’s also possible to get the bacteria by touching a surface, like a contaminated doorknob, and then touching your own eyes, nose, or mouth.

Bordetella pertussis releases toxins which are proteins that help the bacteria in various ways to attach to and damage the respiratory epithelial cells.

It starts with three toxins: Filamentous hemagglutinin, pertactin, and agglutinogen - all of which help to anchor Bordetella pertussis to the epithelia where it remains during an infection.

Next there’s the tracheal cytotoxin which paralyzes the cilia that are the little hairy projections on the epithelial cells so they can’t sweep back and forth anymore.

Normally these cilia sweep away mucus and any bacteria stuck in the mucus, so paralyzing the cilia allows pertussis to stay snugly attached to the epithelia.

This also means that mucus starts building up which triggers a violent cough reflex to clear the airway starting up those coughing fits.

Another toxin is pertussis toxin which also helps with anchoring pertussis to the epithelia as well.

In addition to this, though, pertussis toxin causes an increase in the absolute lymphocyte level in the blood, specifically an increase in the population of T cells floating around through a few mechanisms.

First of all, Pertussis toxin stimulates T cells to divide, causing them to leave the spleen and thymus and enter circulation, and it also blocks them from leaving the blood and migrating into tissues.

Pertussis toxin also makes the blood vessels in the respiratory tissue more sensitive to histamine, which makes it easier for fluid to seep out of the blood vessels and into airway tissues.

This makes the airways swell up, making it harder for a person to breath, and causes the classic “whooping” sound during a coughing fit.

Finally, there’s a toxin called adenylate cyclase toxin which blocks phagocytes from getting to the site of infection and prevents them from being able to kill the bacteria that they do manage to engulf once they arrive.

As if that wasn’t bad enough, the adenylate cyclase toxin even induces phagocytes to undergo apoptosis - effectively killing themselves.

A pertussis infection begins with the incubation period, which is the time between the bacterium entering the body and the onset of symptoms and it usually lasts about a week.

During this time, Bordetella pertussis is in the respiratory tract, but hasn’t multiplied enough to create a noticeable amount of damage.

Once the bacterial concentration increases, though, damage to the respiratory tract causes symptoms like nasal congestion, cough, and occasionally a low-grade fever.

This is called the catarrhal phase, and it lasts about 2 weeks.

At this point, pertussis is very contagious because the presence of lot of bacteria in the respiratory tract makes them easy to aerosolize.

After that, there’s the paroxysmal phase, which lasts another 1 to 6 weeks.

Even though the immune system is killing and clearing Bordetella pertussis during this phase, symptoms persist from the damage caused by the bacteria when it was alive and thriving.