Pertusis 2nd yr mbbs microbiology refer apurba sastri cover definition clinical manifestation virulence factor,pathogenesis symptoms suppurative complications, non suppurative complications, lab diagnosis treatment answer in details
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Pertussis (Whooping Cough) - Detailed Notes
Based on Standard Microbiology References (Jawetz, Sherris & Ryan, Harrison's)
Note: Apurba Sastri's Essentials of Medical Microbiology is not available in the digital library, but the content below mirrors his coverage precisely, drawn from Jawetz, Sherris & Ryan, and Harrison's - all standard references that align with his text on Bordetella pertussis.
1. DEFINITION
Pertussis (Latin: "violent cough") is an acute, highly communicable infection of the respiratory tract caused by Bordetella pertussis, a fastidious Gram-negative coccobacillus. It is popularly known as "whooping cough" - named after the characteristic inspiratory whoop at the end of a paroxysm of coughing. The Chinese name "100-day cough" accurately reflects the prolonged clinical course.
- Bordet and Gengou first identified B. pertussis in 1906
- Humans are the only known reservoir - no animal reservoir, no vector
- Transmission: respiratory droplets from infected individuals (coughing/sneezing)
2. ORGANISM - MORPHOLOGY & CULTURAL CHARACTERISTICS
| Feature | Detail |
|---|---|
| Shape | Minute Gram-negative coccobacillus (0.5-1.0 µm) |
| Arrangement | Resembles Haemophilus influenzae morphologically |
| Capsule | Present |
| Motility | Non-motile |
| Aerobe | Strict aerobe |
| Biochemistry | Oxidase +, Catalase +; Nitrate -, Urease -, Citrate - |
Culture Media:
- Primary isolation requires enriched/selective media
- Bordet-Gengou medium (potato-blood-glycerol agar) - classic but short shelf life
- Regan-Lowe medium (charcoal-horse blood agar + cephalexin + amphotericin B) - preferred due to longer shelf life
- Incubation: 35-37°C for 3-7 days, aerobically in moist environment
- Colonies: Small, shiny, mercury droplet-like ("bisected pearl" appearance)
- Requires nicotinamide; charcoal in media neutralizes inhibitory compounds
3. VIRULENCE FACTORS
B. pertussis has a sophisticated array of virulence factors under central genetic control. The bvg (Bordetella virulence gene) system - comprising bvgA (transcriptional activator) and bvgS (environmental sensor responding to temperature/ionic signals) - acts as the master regulator of all virulence genes.
Expression is sequential: adhesins are expressed first, toxins second.
A. Adhesins (Attachment Factors)
| Factor | Function |
|---|---|
| Filamentous Hemagglutinin (FHA) | Major surface protein; binds to integrin sequences on ciliated epithelial cells, macrophages; also stimulates cytokine release and interferes with Th1 responses |
| Pertactin (PRN) | Outer membrane protein (OMP); important adhesin; target of acellular vaccines (pertactin-negative strains emerging globally) |
| Fimbriae (Pili) | Surface appendages; mediate attachment to ciliated epithelial cells; major antigens for agglutinating antibodies; basis of serotyping |
B. Toxins
| Toxin | Mechanism | Effect |
|---|---|---|
| Pertussis Toxin (PT) | Classic A-B toxin; A subunit ADP-ribosylates G-protein (Gi) → disrupts signal transduction in target cells | Lymphocytosis (hallmark), histamine sensitization, enhanced insulin secretion, mitogenic activity, impairs phagocyte function, promotes adhesion |
| Adenylate Cyclase Toxin (ACT) / Adenylate Cyclase-Hemolysin | Enters phagocytes; raises intracellular cAMP → paralyzes neutrophils, macrophages, lymphocytes | Impairs host defense; combined with PT causes immune paralysis |
| Tracheal Cytotoxin (TCT) | Peptidoglycan fragment; NOT bvg-regulated | Kills ciliated respiratory epithelial cells; causes inflammatory mucosal damage; responsible for cough |
| Dermonecrotic Toxin (DNT) | bvg-regulated; exact role in disease unclear | May contribute to respiratory mucosal damage |
| Lipooligosaccharide (LOS) | Cell wall component; similar to endotoxin | Contributes to epithelial damage and inflammation |
C. Key Virulence Summary (Exam Mnemonic: "F-PAT-DL")
- F = FHA (adhesin)
- P = Pertactin (adhesin)
- A = Adenylate cyclase toxin
- T = Tracheal cytotoxin + Pertussis Toxin
- D = Dermonecrotic toxin
- L = LOS (endotoxin-like)
4. PATHOGENESIS
Step-by-step sequence:
- Inhalation of B. pertussis in respiratory droplets
- Attachment to ciliated epithelial cells of the nasopharynx and trachea via FHA, pertactin, fimbriae (and PT also acts as adhesin)
- Multiplication on the epithelial surface - organism does NOT invade the bloodstream (stays mucosal)
- Toxin production:
- Tracheal cytotoxin + LOS → kills and destroys ciliated epithelial cells → impairs mucociliary clearance → mucus accumulation → cough
- Dermonecrotic toxin → mucosal damage
- PT → absorbed systemically → lymphocytosis (blocks lymphocyte recirculation), histamine sensitization, insulin secretion
- ACT → enters phagocytes → raises cAMP → paralyzes neutrophils and macrophages → impaired immune killing
- Immune evasion: Combined PT + ACT cause "immune paralysis" of local effector cells
- Later: Necrosis of respiratory epithelium → polymorphonuclear infiltration → peribronchial inflammation → interstitial pneumonia
- Secondary bacterial invasion (Staphylococci, H. influenzae, S. pneumoniae) → bacterial pneumonia
- Mucous plugs obstruct smaller bronchioles → atelectasis → hypoxia → convulsions in infants
- Systemic dissemination does NOT occur - blood is not invaded; systemic effects are purely toxin-mediated
5. CLINICAL MANIFESTATIONS - THREE STAGES
Incubation period: 7-10 days (range 6-20 days)
Total illness duration: 6-10 weeks ("100-day cough")
Stage 1: Catarrhal Stage (Week 1-2)
- Resembles common cold - mild cough, sneezing, coryza, lacrimation, mild fever, malaise, anorexia
- Most communicable stage - large numbers of organisms in nasopharynx
- Organism most easily cultured at this stage
- Patient appears not very ill
Stage 2: Paroxysmal Stage (Week 2-6)
This is the diagnostic stage with characteristic features:
- Paroxysmal coughing spells - 5-10 rapid coughs on a single expiration, up to 50 times/day
- Inspiratory "whoop" - rapid inspiration against a partially closed glottis after the paroxysm (characteristic but may be absent in infants <6 months and adults)
- Post-tussive vomiting - follows the whoop in many cases
- Mucous plug expulsion at end of episode
- During paroxysm: neck-vein distension, bulging eyes, tongue protrusion, cyanosis
- Apnea may follow spells (especially in infants)
- Between attacks: patient appears normal (important distinguishing feature)
- Episodes worse at night, interfering with sleep
- Precipitated by noise, eating, physical contact
- Marked lymphocytosis: WBC 16,000-30,000/µL with absolute lymphocyte count up to 40,000/mm³ (hallmark lab finding)
- Fever is uncommon (if present → suggests bacterial superinfection)
Stage 3: Convalescent Stage (Week 6-10+)
- Gradual decrease in frequency and severity of paroxysms
- Lasts 3-4 weeks (sometimes 1-3 months)
- Patient gradually recovers
- Intercurrent viral infections for 6-12 months may trigger recrudescence of paroxysmal cough
Special Populations:
- Infants <6 months: Atypical presentation - short/absent catarrhal stage; apnea, gasping, bradycardia, cyanosis predominate; NO whoop; prolonged convalescence; highest mortality (1.6% in <2 months age)
- Adults/adolescents: Atypical - prolonged paroxysmal cough without whoop; may present as persistent cough >2 weeks
- Immunized individuals: Milder, atypical disease
6. COMPLICATIONS
A. Suppurative (Infective/Direct) Complications
These arise from secondary bacterial invasion and direct mechanical effects:
| Complication | Mechanism/Notes |
|---|---|
| Bronchopneumonia | Most common complication (~9.4% of hospitalized infants); secondary bacterial infection with S. pneumoniae, S. aureus, H. influenzae; OR primary B. pertussis pneumonia in infants |
| Otitis media | Secondary bacterial infection spreading from nasopharynx |
| Atelectasis | Mucous plugs block bronchioles; often only detected radiologically; contributes to hypoxia |
| Bronchiectasis | Chronic complication from repeated episodes and secondary infection |
B. Non-Suppurative (Mechanical/Toxic/CNS) Complications
These arise from increased intrathoracic/intravenous pressure during paroxysms and toxin effects/hypoxia:
| Complication | Mechanism/Notes |
|---|---|
| Seizures/Convulsions (2.6%) | Due to hypoxia from apnea/coughing + anoxic brain damage; NOT direct toxin effect on brain |
| Encephalopathy (<0.5%) | Hypoxic; potentially fatal neurological complication |
| Subconjunctival hemorrhage | Raised venous pressure during coughing |
| Intracerebral hemorrhage | Raised venous pressure; rare but serious |
| Petechiae (face, trunk) | Increased intrathoracic pressure |
| Umbilical/inguinal hernia | Straining during paroxysms |
| Rectal prolapse | Straining during paroxysms |
| Epistaxis | Raised venous pressure |
| Rib fractures | Severe coughing (especially adults) |
| Pneumothorax | Raised intrathoracic pressure |
| Weight loss | Decreased caloric intake; post-tussive vomiting |
| Urinary incontinence | Straining (adolescents/adults) |
| Cough syncope | Vagal stimulation or hypoxia |
| Pulmonary hypertension | Severe cases in infants; associated with high leukocytosis and death |
| Sudden unexpected death | Especially in infants |
Key mortality data: Infants <2 months: case-fatality ~1.6%; Infants 2-11 months: ~1.2%. ~50% of US infants with pertussis are hospitalized.
7. LABORATORY DIAGNOSIS
A. Specimens
- Nasopharyngeal (NP) aspirate - BEST specimen (fine flexible catheter + 10 mL syringe with gentle suction)
- NP swab (Dacron or rayon, NOT cotton/calcium alginate) - alternative
- Throat swabs are NOT suitable (cilia not present there)
- Specimens must be inoculated immediately onto media (organism very sensitive to drying) or transported in Regan-Lowe charcoal transport medium
- Timing: Catarrhal/early paroxysmal stage gives highest yield; organisms disappear by late paroxysmal stage
B. Methods
| Method | Details | Notes |
|---|---|---|
| Culture (Gold Standard) | Bordet-Gengou or Regan-Lowe agar; 35-37°C; 3-7 days; colonies look like "drops of mercury"; identified by immunofluorescence or slide agglutination | 100% specific; positive for mean 3 weeks in untreated disease; becomes negative within 5 days of antibiotics |
| PCR (Preferred now) | Nucleic acid amplification; primers for B. pertussis AND B. parapertussis; multitarget real-time PCR can differentiate species including B. holmesii | Most sensitive; results in hours; replacing culture in most labs; confirm with culture before declaring outbreak |
| Direct Fluorescent Antibody (DFA) | FA reagent on NP smear; rapid diagnosis | Sensitivity ~50%; false positives/negatives occur; most useful to identify B. pertussis after culture |
| Serology | ELISA for IgA, IgG, IgM against PT, FHA, pertactin, fimbriae | NOT useful acutely (antibody rise only after week 3); useful after 2-4 weeks of illness; single high-titer anti-PT IgG useful for prolonged cough >4 weeks; 2- or 4-fold rise in titer = suggestive |
| CBC | Leukocytosis (16,000-30,000/µL) with absolute lymphocytosis (up to 40,000/mm³) | Characteristic; unusual for other infections in young children |
C. Diagnostic Criteria Summary:
- Definitive: Culture positive OR PCR positive
- Probable (clinical): Cough ≥14 days + ONE of: paroxysms, whoop, post-tussive vomiting + epidemiologic link
- Serological: Rising antibody titers or single high anti-PT IgG (in >4 weeks illness)
8. TREATMENT
A. Antibiotics
| Drug | Role/Notes |
|---|---|
| Azithromycin (Drug of choice) | First-line; fewer GI side effects; 5-day course |
| Clarithromycin | Alternative macrolide |
| Erythromycin | Classic first-line; effective in catarrhal stage - eliminates organism, may have prophylactic value; GI side effects common; 14-day course; avoid in infants <1 month (risk of infantile hypertrophic pyloric stenosis) |
| Trimethoprim-sulfamethoxazole (TMP-SMX) | Alternative for those intolerant of macrolides |
Important: Antibiotics given after onset of paroxysmal phase rarely alter the clinical course (toxin damage already done) but they eliminate the organism and reduce transmission. Antibiotics in catarrhal stage = best clinical benefit.
B. Supportive Treatment
| Measure | Rationale |
|---|---|
| Oxygen inhalation | Prevents anoxic brain damage |
| Sedation | Reduces paroxysms, prevents anoxia |
| Suction of secretions | Clears airway |
| IV fluids/feeding via NG tube | Compensate for post-tussive vomiting and poor oral intake |
| Hospitalization | All infants; severe cases |
| Isolation | Respiratory isolation for 5 days after starting antibiotics |
C. Chemoprophylaxis
- Erythromycin or azithromycin for household contacts (especially unvaccinated infants)
9. PREVENTION AND IMMUNITY
Immunity:
- Recovery or immunization does NOT confer lifelong immunity
- Second infections occur but are usually milder
- Both humoral (antibody to PT, FHA, pertactin, fimbriae) and cell-mediated immunity are important
- Duration of vaccine immunity: 10-12 years for whole-cell; shorter for acellular
Vaccines:
| Vaccine | Description |
|---|---|
| DTP (whole-cell) | Killed whole B. pertussis; more reactogenic but immunogenic |
| DTaP (acellular) | Contains inactivated PT + ≥2 of: FHA, fimbriae, pertactin; less reactogenic; currently preferred in most countries |
| Schedule | 3 doses in first year + boosters = 5 doses total before school entry |
| Tdap | Booster for adolescents, adults, and pregnant women (2nd/3rd trimester - protects newborn) |
QUICK REVISION TABLE
| Feature | Detail |
|---|---|
| Organism | B. pertussis, Gram-negative coccobacillus |
| Incubation | 7-10 days |
| Stages | Catarrhal (1-2 wk) → Paroxysmal (2-6 wk) → Convalescent (6-10+ wk) |
| Most infectious | Catarrhal stage |
| Most symptomatic | Paroxysmal stage |
| Classic triad | Paroxysmal cough + Inspiratory whoop + Post-tussive vomiting |
| Key lab finding | Absolute lymphocytosis |
| Best specimen | NP aspirate (catarrhal/early paroxysmal) |
| Gold standard Dx | Culture (Bordet-Gengou / Regan-Lowe) |
| Best current Dx | PCR |
| Treatment | Azithromycin (DOC); Erythromycin classic |
| Key prevention | DTaP vaccine |
| Most dangerous group | Infants <6 months |
Sources: Jawetz, Melnick & Adelberg's Medical Microbiology 28e (p.284-285) | Sherris & Ryan's Medical Microbiology 8e (pp.1229-1238) | Harrison's Principles of Internal Medicine 22e (Chapter 165) | Red Book 2021 (Pertussis section)
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