Internal Medicine_Infectious Diseases_7 Flashcards

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

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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

Why do they call it Whooping cough?

A

Whooping cough
child coughs on expiration and “whoops” on inspiration
can cause “100-day cough” in adults
associated with posttussive emesis

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7
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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8
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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9
Q

How is whooping cough transmitted?

A

Respiratory droplets.

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10
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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11
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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12
Q

what severe, yet abnormal clinical sign is associated with whooping cough?

A

rib fracture or even pneumothorax.

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13
Q

How can the pertussis infection be diagnosed?

A

Culture, PCR or serology.

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14
Q

What is the treatment for pertussis infection?

A

Macrolides and ensure patient has an updated Tdap.

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15
Q

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

A

if allergic use TMP-SMX.

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16
Q

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

A

Macrolide.

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17
Q

What type of bacterium is Corynebacterium diphtheriae?

A

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

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18
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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19
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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20
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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21
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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22
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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23
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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24
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.

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25
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.

26
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.

27
Q

How is diphtheria transmitted?

A

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

28
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
29
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.

30
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).

31
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).

32
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).

33
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.

34
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.

35
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.

36
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.

37
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.

38
Q

How is diphtheria prevented?

A

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

Tdap vaccine booster in adolescents and adults.

39
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.

40
Q

Which populations are at the highest risk of diphtheria infection?

A

Unvaccinated individuals
(the “woke” community).

Residents of areas with low vaccination coverage (the “broke” community).

Individuals with travel history to endemic areas. (the “float” community).

41
Q

What type of bacteria is Legionella pneumophila?

A

gram-negative bacillus.

water-loving bacteria.

oxidase-positive.

42
Q

What special stain is required for Legionella pneumophila?

A

Silver stain.

43
Q

What type of agar does Legionella pneumophila thrive on?

A

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

44
Q

What are the two clinical diseases caused by Legionella pneumophila?

A

Legionnaires’ disease and Pontiac fever.

45
Q

Which population is more susceptible to Legionnaires’ disease?

A

Smokers.

46
Q

Legionnaires’ disease causes what extrapulmonary symptoms?

A

GI symptoms (diarrhea)

Nausea and vomiting

Fever (usually very high surpassing 102.2)

Myalgias

Headaches

Confusion

47
Q

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

A

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

Atypical pneumonia

48
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.

49
Q

What is the characteristic fever presentation in Legionnaires’ disease?

A

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

50
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.

51
Q

How is Legionnaires’ disease typically diagnosed?

A

Rapid urine antigen test.

52
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.

53
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.

54
Q

What adaptation allows Mycoplasma pneumoniae to maintain membrane integrity?

A

Incorporation of cholesterol molecules into its cell membrane.

55
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.

56
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.

57
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.

58
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.

59
Q

What medium is used to culture Mycoplasma pneumoniae?

A

Eaton’s agar is the specialized medium for cultivation.

60
Q

What is the treatment for Mycoplasma pneumoniae infections?

A

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

61
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.