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Microbiology > L28-30: Bacterial Infections of the Respiratory Tract > Flashcards

L28-30: Bacterial Infections of the Respiratory Tract Flashcards

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1
Q

Characteristics of lower respiratory tract infections (LRTI)

A

Less common than URTI but more severe, includes pertussis, bronchitis, and pneumonia

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2
Q

Airway defenses

A

Ciliated epithelium and mucociliary escalator

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3
Q

General features of bacterial pneumonia

A

Inflammation of the lung as a result of bacterial infection, causes fever, malaise, cough and crackles, pleuritic chest pain, dyspnea, and potentially sputum production

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4
Q

Those at increased risk to pneumonia

A

Comorbidities (heart disease, diabetes, lung disease/cancer, immunosuppression), age extremes, smoking/alcohol/narcotics

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5
Q

Pathogenesis of bacterial pneumonia

A

Bacteria enter small airways or alveoli and grow in rich lung environment; local effects are due to inflammatory immune response to bacteria; can cause accumulation of fluid, bacteria, neutrophils, and fibrin

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6
Q

Typical/lobar pattern of CXR and what causes it

A

Alveoli are full of bacteria (consolidation occurs in one lung), associated with S. pneumo, S. aureus, H. influenzae, and most G- bacteria

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7
Q

Atypical/patchy pattern of CXR and what causes it

A

Mostly all of the lobes of the lung are involved, not entire lung is full, associated with M. pneumoniae, C. pneumoniae, and L. pneumophila (special pattern)

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8
Q

Characteristics of typical (“lobar”) pneumonia

A

Sudden onset, patient looks sick, productive cough, bloody sputum, fever of 103-104 oF, consolidation and pleurisy, WBC count elevated (typically neutrophils), most commonly caused by S. pneumoniae

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9
Q

Characteristics of atypical (“patchy”) pneumonia

A

Onset is gradual, patient looks well, nonproductive cough, scant/watery sputum, no fever (usually), normal WBC count, most commonly caused by M. pneumoniae

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10
Q

Complications of pneumonia

A
  • -Pleural effusion (excess fluid buildup in pleural space)
  • -Anemia (with chronic) or thromboxytopenia
  • -With chronic: decrease in oxygen arterial pressure, weight loss/muscle atrophy, and bronchiectasis
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11
Q

Aspiration pneumonia

A

Introduction of foreign material into the bronchial tree (usually fluid with bacteria); associated with alcoholics, coma/stroke patients

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12
Q

Community acquired pneumonia (CAP)

A

Any pneumonia not acquired in a healthcare setting

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13
Q

Hospital acquired pneumonia (HAP)

A

Acquired in a healthcare setting, occurs more often in immunocompromised patients and associated with ventilator use (VAP) – frequently caused by MDR Gram- bacteria

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14
Q

Importance of labs with pneumonia

A

Elevated WBC count (“left shift”), blood culture (positive = severe disease), sputum analysis (>25 PMNS and <10 epithelial cells)

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15
Q

Streptococcus pneumoniae

A

Normal colonizer of URT but causes pneumococcal pneumonia, Gram+ diplococci, alpha-hemolytic, catalase-, many serotypes

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16
Q

Pneumococcal virulence factors

A
  • -Surface adhesins (colonize pharynx)
  • -IgA protease (cleaves IgA, prevents clearance)
  • -Pneumolysin*** (pore-forming toxin, colonization, invasion, inflammation, complement activation, etc.)
  • -Teichoic acid and peptidoglycan (inflammation)
  • -Thick polysaccharide capsule (antiphagocytic)
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17
Q

Lab diagnosis of S. pneumoniae

A

Gram+ sputum, alpha-hemolysis on blood agar, catalase-, bile solubility positive, optochin sensitive

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18
Q

Treatment for S. pneumoniae pneumonia

A

Empiric therapy of penicillin, azithromycin, or azithromycin + cephalosporin

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19
Q

Prevention of S. pneumoniae pneumonia

A

Vaccination with 23-valent pneumococcal polysaccharide vaccine or 13-valent conjugated-pneumococcal vaccine

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20
Q

Staphylococcus aureus

A

Normal microbiota in some, Gram+ cocci clusters, catalase+, coagulase+, protein A binds Fc portion of antibody

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21
Q

Panton-Valentine leukocidin (PVL)

A

Virulence factor of S. aureus; cyotoxin that causes severe necrosis of tissue that is irreversible

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22
Q

MRSA (methicillin resistant S. aureus)

A

Resistant to all beta-lactam antibiotics, harder to treat (more dangerous because less options for treatment)

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23
Q

1 causes of Gram- bacterial pneumonia

A

Klebsiella pneumoniae (facultative anaerobe), Pseudomonas aeruginosa (aerobe)

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24
Q

Gram- pneumonia characteristics

A

Generally an underlying disease, anaerobic bacterial etiology includes foul-smelling sputum, antibiotic resistance is HUGE

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25
Q

Gram- pneumonia diagnosis and treatment

A

Can diagnose with sputum culture and Gram-staining, sometimes blood culture; treat with broad spectrum antibiotics and multiple drug therapy

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26
Q

Klebsiella pneumoniae

A

Gram- rod, non-motile, mucoid colonies, oxidase-, present in respiratory tract and occasionally feces

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27
Q

How does Klebsiella pneumoniae present?

A

Classic lobar pneumonia with bloody sputum

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28
Q

Virulence factors of Klebsiella pneumoniae

A

LPS and capsule

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29
Q

Pseudomonas aeruginosa

A

Gram- rod, flagellated, obligate aerobe (sugar fermentation-), oxidase+, smells like grapes

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30
Q

Where does Psuedomonas aeruginosa grow?

A

Water, hand soaps (soap containers), dilute antiseptics (like at restaurants), humidifiers – forms biofilms

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31
Q

Pseudomonas aeruginosa virulence factors

A
  • -Toxin A (ribosylates EF-2)
  • -Leukocidin (targets leukocytes)
  • -Phospholipase C (membrane disruption)
  • -Capsule (anti-phagocytic)
  • -Pyocyanin
  • -Pyoverdin
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32
Q

Treatment for Pseudomonas aeruginosa

A

Antipseudomonal penicillin (ticarcillin or piperacillin) + aminoglycoside (gentamycin, tobramycin, amikacin)

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33
Q

Correlation between Psuedomonas aeruginosa and CF

A

Most common cause of death in this population – cystic fibrosis patients have a significantly impaired mucociliary escalator, so when strains convert from non-mucoid to mucoid there are significant effects and it is almost impossible to eradicate

34
Q

Causes of walking pneumonia

A

Mycoplasma pneumoniae, Chlamydophila pneumoniae, Chlamydophila psittaci, Coxiella burnetti

35
Q

Cause of toxic pneumonia

A

Legionella pneumophila

36
Q

Symptoms of atypical pneumonia

A

Bronchopneumonia with gradual onset (fever, headache, fatigue, muscle ache, dry cough, scant/watery sputum)

37
Q

Treatment of atypical pneumonia

A

Tetracycline and erythromycin (empiric therapy for atypical pneumonia)

38
Q

Mycoplasma pneumoniae

A

One of the smallest bacteria, pleomorphic, no peptidoglycan, membrane contains sterols, restricted to humans, low infectious dose transmission by respiratory droplets

39
Q

Virulence factor of Mycoplasma pneumoniae

A

P1 adhesin (binds to base of cilia to cause ciliostasis –> epithelial cell damage/death –> defect in mucociliary clearance)

40
Q

Diagnosis of Mycoplasma pneumoniae

A

Cold agglutinin test (when RBCs agglutinate at 4 oC), PCR, serology, culture and microscopy not recommended

41
Q

Treatment for Mycoplasma pneumoniae and Chlamydophila pneumoniae

A

Tetracycline and macrolide (erythromycin), NOT beta-lactams!

42
Q

Chlamydophila pneumoniae

A

Gram-, obligate intracellular, causes atypical pneumonia

43
Q

Diagnosis of Chlamydia pneumoniae

A

Microimmunofluorescence and PCR

44
Q

Life cycle of Chlamydophila pneumoniae

A

Elementary body (EB) attaches and enters cytoplasm, then forms reticulate body (RB) which undergoes binary fission and divides, then releases EBs from cell

45
Q

2 types of disease caused by Legionella pneumophila

A
  1. Legionnaires’ disease (rare, requires antibiotics)

2. Pontiac fever (not much known)

46
Q

Legionella pneumophila

A

Gram-, coccobacilli inside cells and pleomorphic outside, difficult to culture, grows outside in water sources (parasites of amoebas)

47
Q

Transmission of Legionella pneumophila

A

Aerosols from man-made water supplies – outbreaks are associated with cooling towers/air conditioning and old buildings

48
Q

Virulence/pathogenesis of Legionella pneumophila

A
  1. Target and attach to alveolar macrophage using pili, flagella, and other proteins
  2. Enter macrophage in endocytic vacuole (coiling phenomenon)
  3. Hijacks cell and replicates
49
Q

Clinical manifestation of Legionella pneumophila

A

Severe toxic pneumonia, causes myalgia, headache, rapidly rising fever, dry cough, etc. – patchy infiltrates on CXR and elevated WBC count – patient becomes progressively ill over 3-6 days

50
Q

Diagnosis of Legionella pneumophila

A

Culture, direct fluorescent antibody (DFA), nucleic acid amplification test (NAAT)

51
Q

Treatment of Legionella pneumophila

A

NOT beta-lactams, macrolide or fluoroquinolone is best

52
Q

Mycobacteria cell wall

A

Recognize these terms: membrane, peptidoglycan, arabinogalactan, lipoarabinomannin, mycolic acids, mycolic acid-associated glycopipids

53
Q

What causes tuberculosis?

A

Mycobacterium tuberculosis

54
Q

Transmission of TB

A

Only in humans, person-to-person transmission via respiratory aerosol droplets (coughs, sneezes, speaking, singing)

55
Q

Process of infection with TB

A
  • -Mtb is inhaled into lungs and enters alveoli
  • -Mtb is taken up and multiplies within alveolar macrophages; lymphocytes are recruited
  • -Mtb can’t be killed so granulomas form around it
56
Q

How does latent TB infection occur?

A

The immune system is unable to kill Mtb and surrounds Mtb-infected macrophage to form a granuloma – necrotic

57
Q

What occurs with primary TB infection?

A

Usually asymptomatic and can lead to clearance, active TB (in immunosuppressed individuals), or latent TB (most individuals) that can reactivate

58
Q

Cell-mediated immunity in TB

A

Causes most of the damage/pathology from TB but also can control it

59
Q

Disseminated TB infection

A

Granuloma formation, also called miliary or extrapulmonary TB

60
Q

Active TB symptoms

A

Gradual onset, variable manifestations including fatigue, weight loss, weakness, fever, night sweats, chest pain and dyspnea – cough*

61
Q

Reactivation TB symptoms

A

Similar to/same as active TB

62
Q

Diagnosis of TB

A
  • -CXR (Ghon focus: lung lesion seen on CXR as granuloma calcifies, Ghon complex: lung lesion and calcification seen together in hilar lymph)
  • -Rapid lab tests
  • -Must be reported immediately
63
Q

Lab diagnosis of TB

A
  • -Tuberculin skin test: ID injection of PPDs from Mtb cell wall looking for immune reaction (BCG vaccine = positive test)
  • -IFN-y release assay: blood sample tested for IFN-y release with Mtb
  • -Microscopy: acid-fast stains (not definitive), nucleic acid amplification tests, culture – less useful
64
Q

Treatment of TB

A

Drug cocktail including isonaizid

65
Q

Vaccine for TB

A

BCG vaccine (Mycobacterium bovis), not common in US and not completely protective

66
Q

TB and AIDS

A

TB infection risk, progression to active TB, and reactivation risk all much greater in HIV+ individuals; drug-resistant strains common – leading causes of premature death in the world

67
Q

Nontuberculous Mycobacteria

A
  • -Mycobacterium avium-intracellulare (like TB, immunocompromised or those with lung disease)
  • -Mycobacterium kansasii (common in elderly)
68
Q

Laryngitis, tracheitis, and epiglottitis basic info

A

Symptoms: hoarseness, burning retrosternal pain
Causes: most likely viral, less common are GAS, Haemophilus influenzae, and S. aureus

69
Q

Characteristics of Haemophilus influenzae serotype B (HiB)

A

Gram- coccobacilli, requires NAD and hemin, typed strains based on capsule and nontypeable but B has polysaccharide capsule of PRP (important)

70
Q

Transmission of HiB and most susceptible population

A

Transmitted by respiratory droplets or direct contact; mostly pediatric

71
Q

Virulence factors of HiB

A

LPS, IgA protease, PRP

72
Q

Diagnosis of HiB

A

Gram staining and culture of blood, nasopharyngeal swab, sputum, etc.

73
Q

Treatment of HiB

A

Broad-spectrum cephalosporin if severe, amoxicillin if less severe (also there is vaccine)

74
Q

Common cause of acute bacterial bronchitis

A

Mycoplasma pneumoniae – adhesin/receptor combo, can also cause pneumonia

75
Q

Common cause of pertussis/whooping cough

A

Bordetella pertussis

76
Q

Characteristics of Bordetella pertussis

A

Gram- coccobacilli, highly susceptible to toxic metabolites, adheres to ciliated respiratory mucosa and produces toxic factors, makes it hard to breathe due to paroxysmal cough and patients can become cyanotic

77
Q

Progression of symptoms of pertussis

A

7-10 days = no symptoms
1-2 weeks = rhinorrhea, malaise, fever, sneezing (like common cold) – MOST COMMUNICABLE
2-4 weeks = repetitive cough with whoops, vomiting, leukocytosis
3-4 weeks+ = diminished cough, secondary complications

78
Q

Major adhesins in pertussis

A

B. pertussis mainly binds to ciliated epithelial cells using these: filamentous hemagglutinin***, peractin, fimbrae

79
Q

Major toxins in pertussis

A

Activation of adenylate cyclase –> increase cAMP –> increase in respiratory secretions –> paroxysmal cough: pertussis toxin*** (AB toxin), adenylate cyclase/hemolysin toxin, LPS

80
Q

Diagnosis of pertussis

A

Culture, nucleic acid amplification test, microscopy

81
Q

Treatment of pertussis

A

Supportive therapy and macrolides (Z-packs and clarithromycin)

82
Q

Vaccine for pertussis

A

DTap (contains detoxified pertussis toxin)

Microbiology (20 decks)

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