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Microbiology > Exam #4: Lower Respiratory Infections III > Flashcards

Exam #4: Lower Respiratory Infections III Flashcards

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1
Q

Describe the characteristics of Mycobacteria tuberculosis.

A
  • Weakly gram (+)
  • Acid fast rods (Ziehl-Neelsen or Kinyou stain)
  • Lipid rich cell wall
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2
Q

Describe the cell wall of Mycobacteria tuberculosis. What is unique about the cell wall?

A

The cell wall of mycobacteria is lipid rich & responsible for acid fast staining. Specifically, the cell wall contains:

1) Arabinogalactan
2) Lipoarabinomannin
3) Mycolic acids
4) Mycolic acid associated glycolipids

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3
Q

What does Mycobacteria tuberculosis cause?

A

TB

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4
Q

What is the #1 bacteria causing infection in the world?

A

Mycobacterium tuberculosis (Mtb)

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5
Q

Globally, where is TB most endemic?

A

Sub-Saharan Africa

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6
Q

What is the reservoir for Mycobacterium tuberculosis (Mtb)?

A

Humans

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7
Q

How is Mycobacterium tuberculosis (Mtb) transmitted?

A

Person to person transmission via respiratory aerosol droplets

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8
Q

How does Mycobacterium tuberculosis (Mtb) cause infection?

A

1) Mycobacteria tuberculosis inhaled & enters alveolus
2) Bacteria is then by alveolar macrophages;
3) Replication occurs in alveolar macrophages & lymphocytes are recruited to the site of infection
4) Incoming macrophages are unable to clear the Mycobacteria tuberculosis infection & consequently the body form a “wall of macrophages” surrounding the bacteria

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9
Q

What is primary TB?

A
  • Mycobacteria tuberculosis enters the lungs & travels to the alveoli
  • Asymptomatic (or maybe minor symptoms) but capable of spread
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10
Q

What is active TB?

A
  • Mycobacteria tuberculosis enters the body & evades killing & granuloma formation
  • Spread of TB to other parts of the lung & systemic spread
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11
Q

What is latent TB?

A
  • Inability of the immune system to kill Mycobacteria tuberculosis
  • CD4+, CD8+, & NK cells surround Mycobacteria tuberculosis & macrophages
  • This becomes necrotic & is referred to as “caseous necrosis” because it is the texture of soft white cheese
  • A granuloma forms and prevents further spread
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12
Q

How is TB reactivated?

A
  • Immunocompromising event leads to “reactivation” of TB

- Aging i.e. senescence of the immune system

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13
Q

Why is CMI considered to be a double-edged sword in TB?

A
  • CMI controls TB infection by leading to granuloma formation
  • However, when granulomas do not prevent the spread of Mycobacteria tuberculosis, or granuloma does not completely wall off TB, then the majority of the pathology that is seen is in response to the immune response to the organism, NOT tissue destruction from a toxin produced by the organism
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14
Q

What is miliary TB?

A

Disseminated or extrapulmonary TB

  • Granuloma formation outside of the lung
  • Looks like “millet seeds,” hence the name “miliary”
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15
Q

What are the symptoms of primary TB?

A

Often asymptomatic

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16
Q

What are the symptoms of active TB?

A
  • Fatigue
  • Weight loss
  • Weakness
  • Fever
  • Night sweats
  • Chest pain
  • Dyspnea
  • Cough
  • Hemoptysis (necrosis of lung is the source of blood)
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17
Q

What are the symptoms of reactivation TB?

A
  • Patients can often be asymptomatic for 2-3 years and be infectious
  • Symptoms are similar to / the same as active TB
  • In reactivation TB, on CXR, the granuloma falls apart & Mycobacteria tuberculosis moves to other parts of the lung–also, it can be aerosolized & transmitted to other people
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18
Q

How is latent TB diagnosed?

A
  • Rapid lab test i.e. PPD
  • CXR

(Ghon Focus= calcified granulmona outside of hilar lymph node
Ghon Complex= calcified granulmona outside of hilar lymph node & in lymph node)

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19
Q

How is active or reactivation TB diagnosed?

A

1) Clinical symptoms
2) Rapid lab tests
3) CXR
- See the granuloma start to fall apart
- See a lobar pneumonia in apical posterior segments of the upper lobes
- Cavitation

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20
Q

What is the difference between a Ghon focus & Ghon complex?

A

Ghon Focus= lesion/ granuloma seen on CXR as is calcifies in the lung

Ghon Complex= lesion seen in lung & affection hilar lymph node

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21
Q

What is a PPD?

A
  • Tuberculin skin test

- Involves an intra-dermal injection of purified protein derivatives (PPD), which come from the TB cell wall

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22
Q

What is the BCG-vaccine?

A

TB vaccine

23
Q

Will people vaccinated with a BCG-vaccine test positive on PPD?

A

Yes–every time

24
Q

What is the IFN-y release assay? What patient population is it best for?

A
  • Better test for vaccinated individuals

- IFN-y release by T-cells is measured in whole blood stimulated with Mycobacteria tuberculosis antigen

25
Q

What other lab techniques are available to test for TB in addition to PPD & IFN-y?

A

1) Ziehl-Neelsen/ Kinyoun stain
- Acid fast staining methods; NOT specific for TB
2) PCR (expensive)
3) Culture

26
Q

What are some of the drawbacks of TB culture?

A
  • Mtb is very slow growing, which leads to contamination issues
  • Preparation with KOH or NaOH treatment improves contamination
27
Q

How is TB treated?

A

2 months of:

  • Isoniazid (INH)
  • ethambutol
  • pyrazinamide
  • rifampin

26 months of:

  • INH
  • rifampin
28
Q

What is INH associated with? What are the compliance issues associated with INH?

A
  • INH is a prodrug that is administered to patients w/ TB
  • Its metabolite inhibits mycolic acid synthesis
  • However, it is hepatotoxic & associated with many adverse effects

*Because it has to be taken for >26 months, there are significant patient compliance issues

29
Q

What is the BCG vaccine?

A
  • Mycobacterium bovis vaccine that is used in endemic countries
  • Cow strain of TB that is slightly infectious to humans
30
Q

Where are people vaccinated against TB? Why?

A

Most of Europe, Asia, Africa, South & Central America because this is where TB is endemic

*Not American & Netherlands because it is not completely protective & vaccinated individuals test positive on test & require v. expensive & complicated INF-y test

31
Q

What is the connection between TB & AIDS?

A
  • Primary infection with TB is more likely in HIV patients
  • Progression to active TB is more likely in HIV infected
  • Reactivation risk is higher in HIV patients
  • Multi- and extended-drug resistant strains of TB have a high incidence in HIV patients

*TB & AIDS are the leading causes of premature death in the world

32
Q

What are nontuberculosis mycobacteria?

A

Atypical mycobacteria including:

  • Mycobacterium avium-intracellulare, which is a complex of several mycobacteria that results in pulmonary infection resembling TB in immunocompromised patients
  • Mycobacterium kanassii, which is more common in the elderly, chronic granulomatous disease, and COPD patients
33
Q

What are the symptoms of laryngitis, tracheitis, & epiglotitis?

A
  • Hoarseness
  • Burning retrosternal pain

Note that the larynx & trachea have non-expandable cartilage rings in the wall; inflammation & swelling of mucous membranes can lead to life-threatening obstruction in children

34
Q

What bacteria cause laryngitis, tracheitis, & epiglotitis?

A
  • GAS
  • Haemophilus influenzae
  • Staphylococcus aureus
35
Q

List the characteristics of haemophilus influenzae sterotype B (HiB).

A
  • Gram (-)
  • Coccobacilli
  • Requires NAD+ & hematin (NAD+= factors V & X= hematin) for growth (chocolate agar)
  • Some capsulated, some not
  • Capsule is composed of polyribosylribitol phosphate (PRP)
  • Type B is the most pathogenic

*Remember when a child has the flu, Mom goes to the five (V) & dime (X) to buy some chocolate (agar),

36
Q

What is PRP?

A
  • Polyribosylribitol phosphate
  • A polysaccharide that forms the capsule of HiB

Important because it is part of the HiB vaccine

37
Q

What diseases can HiB cause?

A 
Remember hAEMOPhilus
A= septic arthritis 
E= epiglotittis 
M= meningitis 
O= OM
P= pneumonia
38
Q

How is HiB transmitted?

A
  • Respiratory droplets or direct contact with respiratory secretions
  • Mostly pediatric (mostly unvaccinated)
39
Q

What are the virulence factors assocaited with HiB?

A
  • PRP
  • LPS
  • IgA protease
40
Q

How is HiB infection diagnosed?

A

Gram staining & culture of:

  • blood
  • nasopharungeal swab
  • sputum
  • spinal fluid
41
Q

How is HiB infection treated?

A

Severe case= Broad-spectrum cephalosporin

Less severe case= amoxicillin

42
Q

What is the HiB vaccine?

A

A conjugate vaccine containing the type B capsular polysaccharide, PRP

43
Q

What is bacterial bronchitis?

A

Inflammation of the tracheobronchial tree

44
Q

What is the most common agent of bacterial bronchitis? What are the virulence factors associated with this causative agent?

A

Mycoplasma pneumoniae

- P1 Adhesin

45
Q

What are the symptoms of bacterial bronchitis?

A

Dry cough that can lead to atypical pneumonia

46
Q

What is pertussis?

A

Whooping cough or paroxysmal cough due to an increase respiratory secretions & decreased mucociliary clearance

47
Q

What causes pertussis?

A

Bordetella pertussis

48
Q

What are the characterstics of Bordetella pertussis?

A
  • Gram (-) coccobacilli
  • Fastidious
  • Adheres to ciliated respiratory mucosa
49
Q

Describe the presentation of pertussis.

A

1) Incubation period of 7-10 days without symptoms

2) Catarrhal= 1-2 weeks (like common cold)
- Rhinorrhea
- Malaise
- Fever
- Sneezing
- Anorexia

3) Paroxysmal= 2-4 weeks
- Repetitive cough with whoops
- Vomiting (post-tussive emesis)
- Leukocytosis

4) Convalescent= 3-4 weeks+
- Secondary complications with lessened cough severity
- Pneumonia, seizures, encephalopathy

50
Q

What are the virulence factors associated with pertussis?

A

Major adhesins=
- Filamentous hemagglutinin, which binds to ciliated epithelial cells

Major toxins=
- Pertussis toxin that causes an increase in respiratory secretions & paroxysmal cough

51
Q

Describe the mechanism of action of the pertussis toxin.

A
  • AB toxin
  • Active portion leads to a gratuitous activation of adenylate cyclase & consequently increased host cell cAMP–>increased respiratory secretions
52
Q

How is pertussis diagnosed?

A

Clinically with lab tests to confirm

  • Culture (Bordet-Gengou agar)
  • PCR*
  • Microscopy
  • Serology
53
Q

How is pertussis treated?

A
  • Supportive therapy

- Macrolides (azithromycin & clarithromycin)

54
Q

How is pertussis prevented?

A

Vaccination with DTaP i.e. acellular pertussis

- Vaccine contains detoxified pertussis toxin

Microbiology (49 decks)

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