Pertussis (whooping cough), Corynebacterium diphtheria, Mycoplasma, and Legionella

Question 1

What is the causative agent of whooping cough?

Answer 1

Bordetella pertussis, a gram-negative coccobacillus.

Question 2

What bacterial structure allows B. pertussis to adhere to the respiratory epithelium?

Answer 2

• Filamentous hemagglutinin (FHA), a surface protein.
• Pertactin, which forms the basis of the acellular pertussis vaccine, promotes B pertussis adherence to the ciliated upper respiratory epithelium. Tracheal cytotoxin subsequently promotes local tissue destruction, resulting in cough.
• Pertussis toxin causes excessive adenylate cyclase activity, which prevents effective phagocytosis and allows the organism to persist in alveolar macrophages and ciliated epithelial cells, leading to a prolonged disease course.
• Lymphocytosis, induced by pertussis toxin, is also common.

Question 3

What toxins are produced by B. pertussis?

Answer 3

Pertussis toxin (exotoxin) is released and activates the adenylate cyclase, which disrupts chemokine receptors, leading to lymphocytosis, however, there is decreased lymphocyte recruitment and and impaired phagocytosis. The tracheal cytotoxin (exotoxin) damages the tracheal epithelium, causing increased mucus production and microaspiration.

Question 4

What is the mechanism of the pertussis toxin?

Answer 4

ADP-ribosylation of Gi proteins, increasing cAMP in host cells.

Pertussis toxin is an AB toxin (also called two-component toxin) with B enabling Binding and triggering uptake (endocytosis) of the Active A component. The A component is an ADP ribosyltransferase that activates adenylate cyclase (increasing cAMP) by inactivating the inhibitory subunit (Gi).

Question 5

What is the function of the adenylate cyclase toxin in B. pertussis?

Answer 5

It elevates cAMP, disrupting ion and water transport in epithelial cells.

The tracheal cytotoxin of Bordetella pertussis specifically targets and damages ciliated respiratory epithelial cells.

Question 6

What are the three clinical stages of whooping cough?

Answer 6

• Catarrhal : 1 to 2 weeks of flu like prodrome (mild cough and rhinitis)
• Paroxysmal (whooping stage) : severe cough with an inspiratory whoop and post-tussive emesis that usually lasts for 2 to 6 weeks.
• Convalescent : eventual resolution of symptoms.
• Usually referenced the 100-day cough.

Question 7

Why do they call it Whooping cough?

Answer 7

Whooping cough:

The coughs occur on expiration and “whoops” occur on inspiration

This is also called the “100-day cough”

Question 8

What are some complications associated with the whooping cough?

Answer 8

Associated with:
- post-tussive emesis
- syncope
- retinal hemorrhage
- fractured ribs
- Severe disease in infants, leading to apnea, seizures, respiratory failure

Question 9

what abnormal, yet severe, complication is associated with whooping cough?

Answer 9

pneumothorax.

Question 10

In which stage of the pertussis infection are patients most contagious?

Answer 10

Catarrhal : 1 to 2 weeks of flu like prodrome (cough/rhinitis)

Question 11

In which stage of the pertussis infection are patients no longer contagious?

Answer 11

Convalescent stage where patients experience an eventual resolution of symptoms.

Question 12

How is whooping cough transmitted?

Answer 12

• Respiratory droplets, therefore patients will require isolation and PPE to prevent droplet exposure.
• Antibiotics given in the first few weeks can reduce transmission by eradicating bacteria in the nasopharynx.

Question 13

What is the full clinical picture of pertussis?

Answer 13

Pertussis is a prolonged illness that typically progresses through 3 stages: catarrhal (mild rhinorrhea or cough), paroxysmal (bouts of severe cough), and convalescent (weeks to months of gradual resolution). Infants are at high risk of complications (eg, cyanosis, apnea, seizure), particularly during the paroxysmal stage. Diagnostic clues include lack of fever, as well as cough associated with turning red in the face, an inspiratory whoop, or posttussive emesis. Lymphocytosis, the degree of which correlates with disease severity, is also a characteristic finding and related to impaired leukocyte chemotaxis caused by pertussis toxin.

Question 14

How is pertussis diagnosed?

Answer 14

Clinically. The symptoms might be mild initially, therefore the diagnosis is often delayed into the Paroxysmal Stage. Confirmation might be needed, particularly if early in the disease course.

Question 15

What is the hallmark laboratory finding in pertussis?

Answer 15

Lymphocytosis (elevated lymphocytes in the bloodstream).

Question 16

What is the recommended treatment for pertussis infection?

Answer 16

• Macrolides are the first-line treatment.
• Recommended to start ASAP prior to the development of cough to mitigate severity of disease and to reduce degree of contagion.
• Ensure patient has an updated Tdap.
• Reduction of transmission occurs if the patient is given antibiotics in the first few weeks of infection.
• Reduction and severity of symptoms occurs if the patient is given antibiotics in the first couple weeks of infection.

Question 17

Why are antibiotics minimally effective during the paroxysmal stage of pertussis infection during the disease course?

Answer 17

Because symptoms are predominantly caused by the exotoxins rather than the bacteria.

Question 18

How can the pertussis infection be confirmed?

Answer 18

Culture, PCR or serology.

Question 19

What vaccines protect against pertussis?

Answer 19

• DTaP and Tdap vaccines provide protection.
• DTaP for child vaccination series (5 doses).
• Tdap for pregnant patients, adolescents, and adults.

Question 20

In what instance could pertussis still affect adolescents and young adults (even if vaccinated)?

Answer 20

Due to waning immunity after vaccination.

Question 21

Does vaccination status matter when providing post-exposure prophylaxis for pertussis?

Answer 21

No. Provide macrolides regardless of vaccine status. Also provide antibiotics to those who are high risk even with limited exposure, such as immunocompromised or pregnancy.

Question 22

What is the post-exposure prophylaxis for contacts of a patient who had a pertussis infection?

Answer 22

Macrolide.

Question 23

What is the treatment for pertussis if the patient is allergic to macrolides?

Answer 23

if allergic use TMP-SMX.

Question 24

What type of bacterium is Corynebacterium diphtheriae?

Answer 24

Corynebacterium diphtheriae is a gram-positive, non-spore-forming bacillus.

Question 25

What is the causative organism of diphtheria?

Answer 25

Corynebacterium diphtheriae — Gram-positive Non-motile Rod-shaped bacterium that produces an exotoxin.

Question 26

Does the bacterium Corynebacterium diphtheriae form spores?

Answer 26

No. Corynebacterium diphtheriae is a non-spore forming bacterium.

Question 27

What is the unique characteristic of Corynebacterium diphtheriae seen on the microscope?

Answer 27

Palisading ("V" and "Y" shapes) Gram ⊕ rods Occur in angular arrangements

Question 28

How does Corynebacterium diphtheriae typically appear under the microscope?

Answer 28

It forms V- or Y-shaped chains due to unique snapping division during replication.

Question 29

What staining characteristic helps identify Corynebacterium diphtheriae?

Answer 29

It contains metachromatic granules that stain red with aniline dyes, while the rest of the bacillus stains blue.

Question 30

What special media is used to culture Corynebacterium diphtheriae?

Answer 30

Tellurite agar (produces black/grey colonies) and Loeffler's medium.

Question 31

What test differentiates toxigenic strains of Corynebacterium diphtheriae?

Answer 31

The Elek test. Elek's test is used for differentiating between toxigenic and nontoxigenic strains of Corynebacterium diphtheriae. This test involves streaking the isolated bacterium on a special agar plate covered with filter paper containing diphtheria antitoxin. If the bacterium produces diphtheria toxin, it diffuses into the filter paper and forms a line of precipitation known as a 'toxigenic line.'

Question 32

What is the pathogenesis of diphtheria?

Answer 32

Causes diphtheria via exotoxin encoded by β-prophage. The diphtheria toxin inhibits elongation factor-2 (EF-2), halting protein synthesis, leading to cell death and formation of a pseudomembrane in the pharynx, cardiac, and CNS tissue. The A-B exotoxin inactivates elongation factor-2 (EF-2) via ADP-ribosylation, leading to inhibition of protein synthesis and cell death.

Question 33

What is the mechanism of the diphtheria toxin?

Answer 33

The toxin uses ADP ribosylation to inhibit elongation factor-2 (EF-2), causing ribosomal dysfunction, halting protein synthesis and causing cell death.

Question 34

What is a hallmark clinical manifestation of diphtheria in the throat?

Answer 34

Formation of a dense, grey pseudomembrane over the tonsils and pharyngeal area.

Question 35

How is diphtheria transmitted?

Answer 35

Respiratory droplets or contact with infected lesions on the skin or fomites.

Question 36

What systemic effects can the diphtheria toxin have?

Answer 36

- nerve damage (demyelination) and paralysis that generally begins at the posterior pharyngeal wall and soft palate. - cardiac toxicity (heart blocks, myocarditis, arrhythmias). - renal injury

Question 37

What are the hallmark clinical features of respiratory diphtheria?

Answer 37

Pseudomembrane (gray-white membrane) on the tonsils, pharynx, or larynx. Bull neck due to severe cervical lymphadenopathy. Sore throat and dysphagia. Low-grade fever and malaise.

Question 38

What is the significance of bull neck in diphtheria?

Answer 38

Bull neck is marked swelling of the neck due to cervical lymphadenopathy and soft tissue edema caused by local toxin effects. It refers to cervical edema and lymphadenopathy, causing a swollen appearance. The most specific symptom of diphtheria is pseudomembranous pharyngitis (grayish-white membrane A ) with lymphadenopathy (“bull’s neck” appearance).

Question 39

What are the potential complications of diphtheria?

Answer 39

Airway obstruction from pseudomembrane. Myocarditis (toxin-induced, potentially fatal). Demyelination and paralysis of cranial and peripheral nerves. Renal failure (due to toxin-induced necrosis).

Question 40

What is the vaccine for diphtheria composed of?

Answer 40

An inactivated exotoxin vaccine (inactivated diphtheria toxin), often combined with tetanus and pertussis vaccines (e.g., DTaP, Tdap).

Question 41

What is the diagnostic method for diphtheria?

Answer 41

Clinical diagnosis: presence of pseudomembrane in the pharynx. Gram stain showing gram ⊕ rods with metachromatic (blue and red) granules and culture of throat swab on Loeffler medium or tellurite agar. Elek test for toxin production.

Question 42

What is the role of the Elek test in diphtheria diagnosis?

Answer 42

The Elek test confirms toxin production by Corynebacterium diphtheriae. It is used to differentiate toxigenic from non-toxigenic strains.

Question 43

How do you differentiate diphtheria from streptococcal pharyngitis?

Answer 43

Diphtheria: Presence of pseudomembrane, bull neck, and history of no vaccination. Streptococcal pharyngitis: Exudative pharyngitis, fever, no pseudomembrane, positive rapid strep test.

Question 44

How is diphtheria acutely managed?

Answer 44

Diphtheria antitoxin (neutralizes unbound toxin). Antibiotics: Penicillin or Erythromycin to eradicate bacteria. Airway support if pseudomembrane causes obstruction.

Question 45

What is the treatment protocol if a patient is exposed to diphtheria but is asymptomatic?

Answer 45

Post-exposure prophylaxis with Erythromycin or Penicillin for close contacts. Check vaccination status and administer a booster dose of DTap or Tdap if needed.

Question 46

How is diphtheria prevented?

Answer 46

DTaP vaccine for children (diphtheria, tetanus, acellular pertussis). Tdap vaccine booster in adolescents and adults.

Question 47

What is the difference between respiratory diphtheria and cutaneous diphtheria?

Answer 47

Respiratory diphtheria: Pseudomembrane in the oropharynx, sore throat, airway obstruction. Cutaneous diphtheria: Chronic, non-healing ulcers with a grayish membrane.

Question 48

Which populations are at the highest risk of diphtheria infection?

Answer 48

Unvaccinated individuals Communities that may have an opposition to government or the healthcare industry. Residents of areas with low vaccination coverage due to barriers to healthcare. Individuals with travel history to endemic areas.

Question 49

What type of bacteria is Legionella pneumophila?

Answer 49

gram-negative bacillus. water-loving bacteria. oxidase-positive.

Question 50

What special stain is required for Legionella pneumophila?

Answer 50

Silver stain.

Question 51

What type of agar does Legionella pneumophila thrive on?

Answer 51

Buffered charcoal yeast extract (BCYE) agar enriched with iron and cysteine.

Question 52

What are the two clinical diseases caused by Legionella pneumophila?

Answer 52

Legionnaires' disease and Pontiac fever.

Question 53

Which population is more susceptible to Legionnaires' disease?

Answer 53

Smokers.

Question 54

Legionnaires' disease causes what extrapulmonary symptoms?

Answer 54

GI symptoms (diarrhea) Nausea and vomiting Fever (usually very high surpassing 102.2) Myalgias Headaches Confusion

Question 55

What distinguishes Legionnaires' disease on a chest X-ray?

Answer 55

Patchy consolidation, predominantly in the mid-to-lower lung zones. Atypical pneumonia

Question 56

What electrolyte abnormality is commonly associated with Legionnaires' disease?

Answer 56

Low sodium. Hyponatremia. Also hypokalemia and hypophosphatemia but resources seem to be more stuck on sodium.

Question 57

What is the characteristic fever presentation in Legionnaires' disease?

Answer 57

High fever, often surpassing 39°C (102.2°F).

Question 58

Pontiac fever typically presents with ... ?

Answer 58

Brief, self-resolving respiratory illness with symptoms resembling a mild flu. Patients might also have a headache, fever, muscle aches due to inhalation of Legionella endotoxin. This disease is self-limited and doesn't require workup.

Question 59

How is Legionnaires' disease typically diagnosed?

Answer 59

Rapid urine antigen test.

Question 60

What are the preferred antibiotics for treating Legionnaires' disease?

Answer 60

Macrolides (e.g., azithromycin) or fluoroquinolones (e.g., levofloxacin or moxifloxacin) are less commonly used.

Question 61

What is unique about the structure of Mycoplasma pneumoniae?

Answer 61

Mycoplasma pneumoniae lacks a cell wall and cannot be visualized using Gram stain. Mycoplasma pneumoniae is a gram-indeterminate pleomorphic bacterium.

Question 62

What adaptation allows Mycoplasma pneumoniae to maintain membrane integrity?

Answer 62

Incorporation of cholesterol molecules into its cell membrane.

Question 63

What clinical condition does Mycoplasma pneumoniae cause, and what is its colloquial name?

Answer 63

It causes atypical pneumonia, also known as "walking pneumonia" due to its mild symptoms that allow patients to remain active. Other symptoms include: pharyngitis, headache, and malaise.

Question 64

What population is most commonly affected by Mycoplasma pneumoniae?

Answer 64

Young adults (younger than 30 and often children), particularly those in close-contact settings like military recruits or dormitories.

Question 65

What does the chest X-ray typically show in Mycoplasma pneumoniae infections?

Answer 65

A reticulonodular or patchy infiltrate, often appearing more severe than the clinical presentation.

Question 66

What laboratory test is used to detect Mycoplasma pneumoniae?

Answer 66

The cold agglutinin test, which detects IgM antibodies that agglutinate red blood cells at low temperatures. IgM cold agglutinins may cause red blood cell agglutination and subsequent hemolysis.

Question 67

What medium is used to culture Mycoplasma pneumoniae?

Answer 67

Eaton's agar is the specialized medium for cultivation.

Question 68

What is the treatment for Mycoplasma pneumoniae infections?

Answer 68

Macrolides (e.g., azithromycin, erythromycin) or respiratory fluoroquinolones.

Question 69

Why is Mycoplasma pneumoniae resistant to beta-lactam antibiotics?

Answer 69

It lacks a peptidoglycan cell wall, which is the target of beta-lactam antibiotics.