Internal Medicine_Infectious Diseases_7 Flashcards

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

1
Q

What is the causative agent of whooping cough?

A

Bordetella pertussis, a gram-negative coccobacillus.

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2
Q

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

A

Filamentous hemagglutinin (FHA), a surface protein.

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3
Q

What toxin produced by B. pertussis disrupts chemokine receptor signaling on lymphocytes?

A

Pertussis toxin disrupts chemokine receptors, leading to lymphocytosis.

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4
Q

What is the mechanism of the pertussis toxin?

A

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).

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5
Q

What is the hallmark laboratory finding in pertussis?

A

Lymphocytosis (elevated lymphocytes in the bloodstream).

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6
Q

What are the three clinical stages of whooping cough?

A

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

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7
Q

Why do they call it Whooping cough?

A

Whooping cough:

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

This is also called the “100-day cough”

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8
Q

What are some complications associated with the whooping cough?

A

associated with:

  • post-tussive emesis
  • syncope
  • retinal hemorrhage
  • fractured ribs
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9
Q

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

A

pneumothorax.

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10
Q

What is the recommended treatment for pertussis infection?

A

Macrolides are the first-line treatment.

Recommended to start ASAP prior to the development of cough to mitigate severity of disease.

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11
Q

How is whooping cough transmitted?

A

Respiratory droplets.

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12
Q

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

A

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.

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13
Q

What vaccines protect against pertussis?

A

DTaP and Tdap vaccines provide protection.

DTaP for child vaccination series (5 doses).
Tdap for older children and adults.

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14
Q

How can the pertussis infection be diagnosed?

A

Culture, PCR or serology.

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15
Q

What is the treatment for pertussis infection?

A

Macrolides and ensure patient has an updated Tdap.

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16
Q

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

A

if allergic use TMP-SMX.

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17
Q

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

A

Macrolide.

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18
Q

What type of bacterium is Corynebacterium diphtheriae?

A

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

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19
Q

What is the causative organism of diphtheria?

A

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

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20
Q

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

A

Palisading

Gram ⊕ rods

Occur in angular arrangements

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21
Q

How does Corynebacterium diphtheriae typically appear under the microscope?

A

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

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22
Q

What staining characteristic helps identify Corynebacterium diphtheriae?

A

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

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23
Q

What special media is used to culture Corynebacterium diphtheriae?

A

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

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24
Q

What test differentiates toxigenic strains of Corynebacterium diphtheriae?

A

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.’

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25
Q

What is the pathogenesis of diphtheria?

A

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.

26
Q

What is the mechanism of the diphtheria toxin?

A

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

27
Q

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

A

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

28
Q

How is diphtheria transmitted?

A

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

29
Q

What systemic effects can the diphtheria toxin have?

A
  • nerve damage (demyelination) and paralysis that generally beings at the posterior pharyngeal wall and soft palate.
  • cardiac toxicity (heart blocks, myocarditis, arrhythmias).
  • renal injury
30
Q

What are the hallmark clinical features of respiratory diphtheria?

A

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.

31
Q

What is the significance of bull neck in diphtheria?

A

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).

32
Q

What are the potential complications of diphtheria?

A

Airway obstruction from pseudomembrane.

Myocarditis (toxin-induced, potentially fatal).

Demyelination and paralysis of cranial and peripheral nerves.

Renal failure (due to toxin-induced necrosis).

33
Q

What is the vaccine for diphtheria composed of?

A

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

34
Q

What is the diagnostic method for diphtheria?

A

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.

35
Q

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

A

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

36
Q

How do you differentiate diphtheria from streptococcal pharyngitis?

A

Diphtheria:
Presence of pseudomembrane, bull neck, and history of no vaccination.

Streptococcal pharyngitis: Exudative pharyngitis, fever, no pseudomembrane, positive rapid strep test.

37
Q

How is diphtheria acutely managed?

A

Diphtheria antitoxin (neutralizes unbound toxin).

Antibiotics: Penicillin or Erythromycin to eradicate bacteria.

Airway support if pseudomembrane causes obstruction.

38
Q

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

A

Post-exposure prophylaxis with Erythromycin or Penicillin for close contacts.

Check vaccination status and administer a booster dose of DTap or Tdap if needed.

39
Q

How is diphtheria prevented?

A

DTaP vaccine for children (diphtheria, tetanus, acellular pertussis).

Tdap vaccine booster in adolescents and adults.

40
Q

What is the difference between respiratory diphtheria and cutaneous diphtheria?

A

Respiratory diphtheria:
Pseudomembrane in the oropharynx, sore throat, airway obstruction.

Cutaneous diphtheria:
Chronic, non-healing ulcers with a grayish membrane.

41
Q

Which populations are at the highest risk of diphtheria infection?

A

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.

42
Q

What type of bacteria is Legionella pneumophila?

A

gram-negative bacillus.

water-loving bacteria.

oxidase-positive.

43
Q

What special stain is required for Legionella pneumophila?

A

Silver stain.

44
Q

What type of agar does Legionella pneumophila thrive on?

A

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

45
Q

What are the two clinical diseases caused by Legionella pneumophila?

A

Legionnaires’ disease and Pontiac fever.

46
Q

Which population is more susceptible to Legionnaires’ disease?

A

Smokers.

47
Q

Legionnaires’ disease causes what extrapulmonary symptoms?

A

GI symptoms (diarrhea)

Nausea and vomiting

Fever (usually very high surpassing 102.2)

Myalgias

Headaches

Confusion

48
Q

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

A

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

Atypical pneumonia

49
Q

What electrolyte abnormality is commonly associated with Legionnaires’ disease?

A

Low sodium.

Hyponatremia.

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

50
Q

What is the characteristic fever presentation in Legionnaires’ disease?

A

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

51
Q

Pontiac fever typically presents with … ?

A

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.

52
Q

How is Legionnaires’ disease typically diagnosed?

A

Rapid urine antigen test.

53
Q

What are the preferred antibiotics for treating Legionnaires’ disease?

A

Macrolides (e.g., azithromycin)

or

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

54
Q

What is unique about the structure of Mycoplasma pneumoniae?

A

Mycoplasma pneumoniae lacks a cell wall and cannot be visualized using Gram stain.

Mycoplasma pneumoniae is a gram-indeterminate pleomorphic bacterium.

55
Q

What adaptation allows Mycoplasma pneumoniae to maintain membrane integrity?

A

Incorporation of cholesterol molecules into its cell membrane.

56
Q

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

A

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.

57
Q

What population is most commonly affected by Mycoplasma pneumoniae?

A

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

58
Q

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

A

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

59
Q

What laboratory test is used to detect Mycoplasma pneumoniae?

A

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.

60
Q

What medium is used to culture Mycoplasma pneumoniae?

A

Eaton’s agar is the specialized medium for cultivation.

61
Q

What is the treatment for Mycoplasma pneumoniae infections?

A

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

62
Q

Why is Mycoplasma pneumoniae resistant to beta-lactam antibiotics?

A

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