Lower respiratory tract bacteria 3ish Flashcards

1
Q

describe the physiology and structure of Mycobacteria

A
  • Weakly gram positive, acid-fast rods
  • Lipid rich cell wall which is responsible for acid-fast staining
  • Humans are the only reservoir
  • person to person transmission via respiratory aerosol droplets (coughs, sneezes, speaking, singing)
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2
Q

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A

Alveolar macrophage engulf Mtb
- Mtb evades killing
- recrutiement of T and NK cells
- Some alveolar macrophage migrate to hilar lymph nodes leads to systemic dissemination of Mtb
Latent TB infection:
- inability of immune system to kill Mtb
- CD4+, CD8+ and NK cells surround necrotic mass of Mtb infectied macrophage and form a Caseous necrosis

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3
Q

define Latent TB

A
  • inability of immune system to kill Mtb
  • CD4+, CD8+ and NK cells surround necrotic mass of Mtb infected macrophage causing caseous necrosis
  • forming a Granuloma which prevents further spread
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4
Q

Define Primary TB

A

Usually asymptomatic

  • leads to:
    1) Clearance
    2) active TB in immunocompromised patients
    3) latent TB in most individuals
  • reactivation upon some immuno-comprimising event or immunosenescence.
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5
Q

Describe CMI’s effect on TB

A

Control of TB infection:

  • Adequate control = granuloma
  • inadequate control = active TB/reactivation TB –> dissemination
  • Most of the pathology/disease is a direct consequence of CMI response
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6
Q

Define the pathology of Active and Reactivation TB

A

Active TB and reactivation TB

1) Rapidly dividing Mtb
2) increase CMI activation
3) more caseous necrotic lesions, inflammation
4) tissue damage

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7
Q

Describe the symptoms associated with Active TB

A
  • Gradual onset, variable manifestations
  • Fatigue, WEIGHT LOSS, weakness, fever, NIGHT SWEATS, chest pain, and dyspnea
  • COUGH - absent or mild with SCANT SPUTUM (severe productive cough with yellow/yellow-green/blood-streaked sputum)
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8
Q

Describe the symtpoms associated with Reactivation TB

A

Patients can often be asymptomatic for 2-3 years and be infectious

  • -> granulomas fall apart, Mtb can move to other parts of the lung, can be expectorated/aerosolized and transmitted to other individuals, can spread systemically
  • -> symptoms similar to/same as active TV
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9
Q

How do you diagnose latent TB

A
  • Ghon focus = lung lesion (granuloma seen on chest x-ray as it calcifies)
  • Ghon complex = lung lesion and calcification seen in an affected hilar lymph
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10
Q

How do you diagnose active or reactivation TB

A
  • Clinical symtpoms
  • Rapid lab tests
  • Chest x-ray = focal infiltration with cavitation (often in the apical posterior segment of the upper lobes of both lungs)
  • Consider TB in immunosuppressed patients with other diagnosis
  • Report known or suspected cases of TB to Health department
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11
Q

Describe the immuno-diagnosis labs for the diagnosis of TB

A

Tuberculin skin test = intradermal injection of purified protein derivatives (PPD’s)
- BCG-vaccinated people will test positive
IFN-gamma release assay
- measure IFN-gamma release by T-cells in whole blood stimulated with Mtb antigen
- ideal for patients that have been BCG-vacinated

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12
Q

describe the microscopy labs for the diagnosis of TB

A
  • Ziehl Neelsen or Kinyoun stains = acid-fast staining due to lipid rich cell wall
  • -> confirms mycobacterial disease but not specific for Mtb
  • Nucleic Acid Amplification test
  • Culture = Mtb slow growing, contamination issues (10-21 days)
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13
Q

Describe the Treatment of TB

A

Treatment:

  • Isoniazid (INH), ethambutol, pyrazinamide, and rifampin (4 drugs) for 2 months followed by 26 months of INH and rifampin or an alternative drug combination
  • -> Isonaizid = prodrug, inhibits mycolic acid synthesis, heptatoxicity
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14
Q

Describe the Prevention of TB

A

Vaccination:

  • BCG-vaccine = mycobacterium bovis
  • -> not completely protective
  • -> vaccinated individuals test positive in TB skin test
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15
Q

describe TB’s relationship with AIDS

A
  • Primary TB infection risk much greater in HIV infected individuals
  • progression to active TB much more likely in HIV infected individuals
  • Much greater reactivation risk
  • disseminated TB
  • Multi- and extended drug resistant strains are prevalent in populations with a high incidence of HIV infection
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16
Q

describe Mycobacterium avium-intracellulare

A
  • Atypical mycobactera
  • Nontuberculous mycobacteria
  • complex of several mycobacteria
  • Pulmonary infection resembling TB in immunocompromised patients or with lung disease
17
Q

Describe Mycobacterium kansasii

A
  • Atypical mycobacteria
  • Nontuberculous mycobacteria
  • More common in elderly
  • Chronic gradulomatous pulmonary disease
  • Seen in COPD patients
18
Q

Describe Laryngitis, Tracheitis, and Epiglotitis

A
  • Symptoms = Hoarseness, burning retrosternal pain
  • Larynx/Trachea have non-expandable cartilage rings in the wall (inflammation, swelling of mucous membranes can lead to obstruction in children)
19
Q

What are the cause of Laryngitis, tracheitis, and epiglotitis

A
  • Most likely viral
  • Less common causes:
    GAS, Haemophilus influenzae and Staphylococcus aureus
20
Q

Describe Haemophilus influenzae serotype B (HiB)

A
  • Gram-negative, coccobacilli
  • Fastidious - requires NAD and hemin for growth
  • Typed strains = capsule
  • Nontypeable = no capsule\
    Transmission = via respiratory droplets or direct contact with respiratory secretions
21
Q

Effects of Haemophilus influenzae serotype B (HiB)

A
  • Conjunctivitis
  • Meningitis
  • epiglotitis
  • purpuric fever
  • pneumonia
  • Otitis media/sinusitis
22
Q

describe the virulence factors of Haemophilus influenzae serotype B

A

LPS
IgA protease
TYPED STRAINS –> polysaccharide capusle polyribosylribitol phosphate (PRP)

23
Q

Describe the diagnosis and treatment of HiB

A
  • Gram staining and culture of blood, nasopharyngeal swab, sputum, spinal fluid
  • Treatment = (high mortality rate)
  • -> severe cases = broad-spectrum cephalosporin
  • -> less severe cases = amoxicillin (if sensitive)
  • Vaccination: Conjugate vaccine = PRP capsule linked to protein carrier
24
Q

Describe Acute bronchitis

A

Inflammation of the tracheobronchial tree

  • Commonly caused by Mycoplasma pneumoniae
  • Symptoms = dry cough, treatment of symptoms
  • Sequelae = pneumonia
25
Describe the bacterial bronchitis: Pertussis
Caused by Bordetella Pertussis - Gram negative coccobacilli - Fastidious (highly susceptible to toxic metabolites) - adhere to cilitated respiratory mucosa, multiple, produce toxic factors - Causes whooping cough --> paroxysmal cough (increased respiratory secretions; decreased mucociliary clearance
26
Describe the epidemiology of Pertussis
restricted to humans - infection risk high for people greater than 1 yo or unvaccinated - person to person spread via AEROSOLS
27
describe the Virulence factors of Pertussis
Major adhesins: - Filamentous hemagglutinin (binds to ciliated epithelial cells - peractin, fimbrae Major Toxins: - Pertussis toxin, Adenylate cyclase/hemolysin toxin
28
Describe the effects of Pertussis toxin and Adenylate cyclase/hemolysin toxin
- gratuitous activation of adenylate cyclase causes increased levels of hos cell cAMP - leads to increase in respiratory secretions leading to PAROXYSMAL COUGH
29
Describe the diagnosis of Pertussis
Diagnosis: - Pertussis is a clinical diagnosis - laboratory tests to confirm - -> culture, bordet-gengou agar - -> nucleic acid amplification test
30
Describe the treatment and prevention of Pertussis
Treatment: - supportive therapy - Macrolides (azithromycin, clarithromycin) Prevention: - vaccination with DTaP (aP = acellular pertussis) --> vaccine contains a detoxified pertussis toxin, peractin, filamentous hemagglutinin