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CPR Final > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Common pathogens affecting the nasopharynx?

A

Mostly viral: rhinovirus, coronavirus

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2
Q

Common pathogens affecting the oropharynx?

A

Mostly bacterial: Group A Strep (S. pyogenes), Diptheriae, EBV, Adenovirus, Enterovirus, HIV (initial infection)

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3
Q

Common pathogens affecting the epiglottis?

A

Mostly bacterial: Haemophilus influenzae type B

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4
Q

Common pathogens affecting the middle ear and parasinuses?

A

Mostly bacterial: Step pneumoniae, Haemophilus influenzae (non-typeable)

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5
Q

Contrast the clinical features of viral vs bacterial pharyngitis.

A

Viral (more common cause):

  • conjunctivitis, cough, rhinorrhea (more nasal discharge)
  • fever less common in adults
  • discomfort more than true malaise (not “sick”)

Bacterial (usually Group A Strep): appear sicker

  • more erythema, swelling, white-ish exudate
  • high fever (>101)
  • tender anterior cervical lymph nodes
  • NO conjunctivitis, cough, rhinorrhea
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6
Q

Pharyngitis can rarely be associated with what more serious disease?

A

Scarlet fever

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7
Q

What are petechiae, and what are they associated with?

A

Small red spots on the soft palate. Associated with inflammation of the oropharynx

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8
Q

What is the major virulence factor of Group A Strep?

A

M protein (M for mimicry)

  • it’s a helical anti-phagocytic protein on the outer surface of the protein
  • mimics our own surface proteins, to avoid phagocytosis; if an anti-body is made, it causes autoimmune problems
  • e.g., causes the anti-cardiac antibody that causes valve deposits in rheumatic heart disease
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9
Q

Major characteristics of Haemophilus influenzae?

A

Gram negative coccobacilli

  • Oxidase positive
  • requires X (hemin) and V (NAD or NADP) growth factors to culture; AKA grows on chocolate agar
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10
Q

H. influenzae type B (encapsulated) can cause what diseases in children?

A
  • Meningitis*
  • Epiglottitis*
  • Pneumonia*
  • Bacteremia
  • Cellulitis
  • Septic arthritis
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11
Q

Non-typeable H. influenzae (non-ecapsulated) can causes what infections?

A
  • acute otitis media
  • sinusitis
  • conjuctivitis (outbreaks common in daycares)
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12
Q

Mode of action of diptheria toxin?

A

inhibits protein synthesis

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13
Q

Cells in what organs have receptors that make them susceptible to diptheria toxin?

A

Heart and nerve cells

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14
Q

What are the characteristics of Cornyebacteria diptheriae?

A
  • Gram positive rods
  • form Chinese letters on culture
  • non-motile, non-spore forming
  • catalase positive
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15
Q

What is the hallmark clinical feature of diptheria toxicity?

A

Pseudomembrane visible at the back of the throat

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16
Q

What virus is usually responsible for the common cold?

A

Rhinovirus

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17
Q

Why does the rhinovirus usually stay isolated to the nasopharynx?

A

It’s temperature sensitive - grows optimally at 88-90 degrees (further into the body gets too hot)

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18
Q

What is the primary receptor rhinovirus uses to infect the body?

A

ICAM-1

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19
Q

Who has more difficulty fighting off a rhinovirus?

A

Asthmatics and immune compromised

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20
Q

Treatment for rhinovirus infection?

A

Symptomatic

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21
Q

Viruses that cause upper respiratory infections?

A
  • Rhinovirus
  • Respiratory Syncytial Virus
  • Adenovirus
  • EBV
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22
Q

Common causes of acute, TYPICAL community acquired pneumonia?

A
  • Strep pneumoniae*
  • Staph aureus
  • H. influenzae (esp with COPD)
  • Gram-negative enterics (hospital acquired)
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23
Q

Clinical presentation of TYPICAL community acquired pneumonia?

A
  • high fever
  • shaking chills
  • chest pain
  • lobar consolidation (X-ray)
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24
Q

Common causes of acute, ATYPICAL community acquired pneumonia?

A
  • Mycoplasma pneumoniae*
  • Chlamydia pneumoniae, psittaci
  • Legionella pneumophila
  • influenza and other viruses
  • Coxiella burnetii
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25
Q

Clinical presentation of ATYPICAL community acquired pneumonia?

A

Less severe illness than typical.

  • insidious onset
  • low grade fever
  • dry cough
  • headache
  • diffuse pattern on X-ray (looks worse)
  • more constitutional symptoms than respiratory
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26
Q

Characteristics of Strep pneumoniae?

A
  • G+, lancet shaped cocci
  • catalase negative
  • alpha-hemolytic
  • mucoid colonies (bc of capsule)
  • bile soluble
  • susceptible to optochin* (growth inhibition test, separates it from other Streps)
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27
Q

What is the major virulence factor of Strep pneumoniae?

A

anti-phagocytic capsule (difficult for C3b to opsonize)

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28
Q

When is there an elevated risk of a bacterial upper respiratory tract infection?

A
  • After a viral infection (esp influenza)
  • compromised pulmonary function (asthma)
  • alcoholism
  • general anesthesia
  • immunity impaired
  • very young (<2) or very old
  • blacks, American Indians, Alaskan Natives
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29
Q

Clinical presentation of pneumococcal pneumonia?

A
  • lobar pneumonia on x-ray
  • sudden onset
  • fever
  • pleuritic pain
  • rusty sputum
  • positive blood cultures in 30%
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30
Q

Characteristics of mycoplasmas?

A
  • Smallest bacteria (that cause human disease) –> filterable
  • lack a cell wall (no peptidoglycan)
  • cell membrane resembles ours (don’t gram stain)
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31
Q

Treatment for M. pneumoniae infection?

A

Antibiotics (usually beta-lactam resistant)

  • Tetracycline
  • Erythromycin
  • Azithromycin
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32
Q

Characteristics of Chlamydiaceae?

A
  • obligate intracellular bacteria

- cell envelope similar to G- bacteria (no detectable peptidoglycan)

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33
Q

2 developmental forms of Chlamydia?

A

Elementary body: infectious form

  • small, dense
  • extracellular
  • metabolically inactive
  • disulfide cross-linked outer membrane proteins

Reticulate body: replicative form

  • large
  • intracellular
  • metabolically active
  • osmotically fragile
  • replicate inside vacuoles in the cell until they burst
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34
Q

Clinical features of Pssittatosis?

A
  • caused by chlamydia psittaci, transmitted via birds
  • abprupt onset
  • fever, headache, myalgia, mild cough
  • abnormal chest exam
  • confusion/altered consciousness
  • can culture
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35
Q

Organism responsible for whooping cough?

A

Bordetella pertussis

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36
Q

Characteristics of Bordetella pertussis?

A
  • G+ rod (short)

- viruence factors: pertussis toxin and special adhesion molecules

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37
Q

What distinguishes Legionella infection other respiratory infections?

A

GI involvement. Presentation will include nausea/vomiting while most other pneumonias won’t.

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38
Q

Risk factors for Legionnaire’s disease?

A
  • immunosuppression (requires cell-mediated immunity to fight off)
  • cigarette smoking
  • renal failure
  • > 50
  • AIDS
  • hematologic malignancies
  • lung cancer
  • males
  • alcohol abuse
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39
Q

Characteristics of Legionella?

A

facultative intracellular pathogen

  • G- slender bacilli (but don’t Gram stain)
  • multiplies inside macrophage phagosomes, taken up by coiling phagocytosis
  • pearly appearance on charcoal culture
  • typically grow in water sources
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40
Q

What is the Legionella species that most often causes human disease?

A

Legionella pneumophila

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41
Q

Characteristics of Pseudomonas aeruginosa?

A
  • G- rods
  • flagellated
  • strict aerobes
  • oxidase positive
  • produce Pyocyanin (green pigment)
  • Lactase negative
  • artificial grape odor
  • found everywhere (esp fruits and vegetables)
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42
Q

Virulence factors of Pseudomonas aeruginosa? (7)

A
  • LPS: cytokine agonist
  • Alginate capsule: avoid opsonization (stretchy culture appearance)
  • Pili: adherence
  • Flagella: motility
  • Exotoxin A: inactivation of proteins
  • Exoenzyme S and T: inactivation of proteins
    Alakline protease elastase: protein breakdown
    Phospholipase C: hydrolysis of cell membrane
  • forms biofilms, particularly in CF patients
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43
Q

Common diseases of P. aeruginosa?

A
  • folliculitis
  • swimmer’s ear
  • pneumonia in cystic fibrosis patients
  • burn infections
  • hospital acquired infections
  • cellulitis
  • UTIs
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44
Q

Common ESBL producers?

A

Enterobacteriaceae:

  • E. coli
  • Serratia marsescens
  • Enterobacter cloacae
  • Klebsiella pneumoniae
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45
Q

ESBL?

A

Extended spectrum beta-lactamases

- inactivate the newest generation of beta-lactam antibiotics (cephalosporins, carbepenems)

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46
Q

3 most common causes of fungal infections?

A
  • Histoplasmosis (most common)
  • Blastomycosis
  • Coccidioidomycosis
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47
Q

General method of transmission of fungal infections?

A
  1. In soil (as a multicellular mold), esp with bird or bat droppings
  2. Gets disturbed and aerosolized (construction, person kicking through it)
  3. Spores get inhaled
  4. Mold germinates into single-celled yeast
  5. Yeast cells get taken up by macrophages, which can’t kill them, and multiply by budding
  6. Travel to lymph nodes
  7. Starts respiratory (bc inhaled) –> goes systemic
48
Q

Who is at risk for fungal infections?

A

Everyone - don’t have to be immunocompromised

49
Q

What geographical location is associated with Histoplasmosis var capsulatum?

A

Mississippi river valley

50
Q

Body’s healing response to fugal infection?

A

Cell-mediated

  • macrophages become fungicidal 2-3 weeks after infection
  • form granulomas (fibrosis), esp in spleen
  • granulomas become calcified within a few years (yeast cells in granulomas can relapse later)
51
Q

Complications of Histoplasmosis infection?

A
  • Mediastinitis (from body’s inflammatory response); can lead to acute pericarditis and cardiac tamponade
  • progressive disseminated histoplasmosis (in immunocompromised or patients on TNF-alpha inhibitors
52
Q

What should always be considered whenever Histoplasmosis is on a differential (and vice-versa)?

A

tuberculosis (similar method of transmission and presentation)

53
Q

What geographic location is associated with Blastomycosis?

A

Southern Mississippi river valley

54
Q

Where does Histoplasmosis typically disseminate to?

A

Anywhere

55
Q

Where does Blastomycosis typically disseminate to?

A
  • skin (causes warty outgrowths)
  • bone
  • genitourinary tract (chronic prostatitis)
56
Q

Treatment for fungal infections?

A

Primary: self-limiting
Moderate: Itraconazole
Severe: Amphotericin B

57
Q

Geographical location associated with Coccidiodes immitis?

A

San Joaquin Valley (in California), Arizona and northern Mexico; AKA Valley Fever

58
Q

Unique features of Coccidioidomycosis lifecycle?

A
  • Inhaled as an arthroconidia (barrel-shaped collection of spores separated by disjunctor cells)
  • arhroconidia become spherules (sphere-shaped) in the lung
  • spherules rupture to produce endospores, which can disseminated and form new spherules
59
Q

Clinical presentation of Coccidioidomycosis infection?

A

Fever, cough, chest pain, fatigue, SOB, chills, myalgias, night sweats, weight loss, lymphadenopathy.

Almost always has a pulmonary component, even when it disseminates

Eosinophilia in 25% of patients (big exam giveaway)

60
Q

Most common dissemination locations for Coccidioidomycosis?

A

Skin, bone, meninges (usually only disseminates in immunocompromised)

61
Q

Geographical association of Paracoccidioidomycosis?

A

tropical and subtropical Central and South America

  • patients may have recently traveled or immigrated
  • disease can re-activate years later
62
Q

Unique characteristics of Paracoccidioidomycosis life cycle?

A

yeast form: multiple buds in pilot wheel shape

63
Q

Clinical hallmark of Paracoccidioidomycosis?

A

chronic mucocutaneous ulcers of the mouth

64
Q

Dissemination location of Paracoccidioidomycosis?

A

lymphadenopathy, organomegaly, and bone marrow involvement

65
Q

Clinical presentation of infleunza infection?

A

abrupt onset, headache, high fever, chills, myalgias, malaise, sore throat, non-productive cough, rhinorrhea

66
Q

Complications of influenza?

A
  • Secondary bacterial pneumonia (S. pneumonia, S. aureus, H. influenzae): more common, less severe
  • viral pneumonia: rare, more severe
  • myositis and cardiac involvement
  • neurologic symptoms (Guillain-Barre, encephalopathy, encephalitis, Reye’s)
67
Q

Complications are more common in which patients?

A
  • older (>65)
  • ppl in nursing homes or chronic care facilities
  • underlying CV or pulmonary problems (e.g. asthma)
  • hospitalized
  • kids on aspirin therapy
  • women in 2nd-3rd trimester of pregnancy
68
Q

Characteristics of influenza virus?

A
  • enveloped RNA virus
  • A and B types cause human disease
  • virulence factors: hemagglutinin (viral attachment & membrane fusion in low pH) and neuraminidase (virus release & deaggregation)
69
Q

Who is recommended to get flu vaccine?

A

pregnant women, child caregivers, healthcare personnel, kids 6 mo to 24 yrs, adults up to 64 at risk for complications

70
Q

What antivirals inhibit Neuraminidase?

A

Oseltamivir (Tamiflu) and Zanamivir (Relenza)

  • neuraminidase releases the flu virus from the cell surface for spread
  • good for both Type A and B
71
Q

What antivirals inihibit the M2 ion channel?

A

Amantadine and Rimantadine

  • M2 ion channel facilitates flu virus dissembly and HA maturation
  • only good for Type A flu
  • reduces severity if given early
72
Q

Clinical presentation of tuberculosis?

A

Cough, weight loss/anorexia, fever, night sweats, hemoptysis, chest pain, fatigue

73
Q

Method of transmission/infection of TB?

A
  1. inhalation of droplet nuclei
  2. bacilli implant and multiply in alveoli
  3. inflammation –> caseous necrosis
  4. bacilli transmitted to lymph nodes –> dissemination (usually controlled, cell-mediated immunity)
  5. Ghon complex heals (fibrosis and/or calcification); may contain virulent bacteria
  6. Can reactivate later
74
Q

What is the Ghon complex and where is it seen?

A

Ghon complex = primary TB lesion + infected adjoining lymph node. Usually seen around the hilum of the infected lung

75
Q

Where in the lung will TB typically gravitate?

A

Upper lobes (more O2)

76
Q

Common triggers for TB reactivation?

A
  • Diminished immune response
  • malnutrition
  • aging
77
Q

Miliary TB?

A

TB lesion spread throughout - Lymphadenitis from M. bovis (unpasteurized milk) can become miliary TB

78
Q

Disseminating locations of TB?

A
  • reticuloendothelial system: lympthatics, liver, spleen, bone marrow –> Miliary TB (can also result from Lymphadenitis from M. bovis)
  • brain/spinal cord –> meningitis
  • bone/muscle –> Pott’s Disease
79
Q

Who gets an Interferon gamma release assay?

A

Used on ppl who have been vaccinated for TB and would have a positive PPD. IFN-gamma test is more specific to the human disease.

80
Q

How to distinguish active from latent TB

A
  • imaging (x-ray)

- culture and smear for acid fast bacilli (gold standard): don’t stain, and waxy membrane doesn’t hold the dyes

81
Q

Virulence factors of Mycobacterium species (TB)?

A

Phenolic Glycolipid I: binds complement

Lipoarabinomannan: toxic to macrophages

82
Q

Treatment for TB?

A

Infection w/o symptoms: 9 months of isoniazid therapy (blocks synthesis of mycolic acids)

Infection w symtoms: RIPE (rifampin, isoniazid, pyrazinamide, ethambutol)

83
Q

How to diagnose Group A Strep infection?

A

Throat swab for antigen against Group A Strep

84
Q

How to diagnose rhinovirus?

A

Clinically (symptoms)

85
Q

How to diagnose respiratory syncytial virus?

A
  • Antigen detection by ELISA IFA
  • virus culture
  • RT PCR
86
Q

How to diagnose adenovirus?

A
  • antigen detection by ELISA, IFA
  • CFT
  • virus culture
  • PCR
87
Q

How to diagnose EBV?

A
  • Heterophile antibody
  • atypical lymphocytes
  • EBV antibody ELISA
  • PCR
88
Q

How to diagnose M. pneumoniae?

A
  • difficult to culture
  • Serology: 4x increase in IgM antibody specific to M. pneumoniae
  • test for cold agglutinins (not specific)
89
Q

How to diagnose C. pneumoniae?

A
  • difficult to culture
  • serology: IgM to 1:64, 4x increase in IgG
  • variations in NAATs
90
Q

How to diagnose C. psittaci?

A
  • Culture from respiratory secretions
  • Serology: 4x increase in antibody titer, IgM > 1:16, microimmunofluoresence
  • NAATs
91
Q

How to diagnose Legionella genus?

A
  • Specific LPS antigen in urine
  • Culture: bronchoalveolar lavage
  • nucleic acid probes
  • serology (no Gram stain)
92
Q

How to diagnose Pseudomonas aeruginosa?

A
  • Culture: lactose non-ferment ring
  • oxidase positive
  • green pigment-producing (pyocyanin)
  • grape-like odor
93
Q

How to diagnose Histoplasmosis?

A
  • Culture is gold standard (but takes 2-4 weeks)
  • fungal stain (not sensitive)
  • serology (more sens, but may flag a prior infxn)
  • antigen: not sensitive for mediastinal or pulmonary
94
Q

How to diagnose Blastomycosis?

A
  • culture

- serology not helpful

95
Q

How to diagnose Coccidioidomycosis?

A
  • sputum or tissue eval
  • culture (dangerous)
  • serology: rising titers are a bad prognostic sign
96
Q

How to diagnose Paracoccidioidomycosis?

A
  • direct microscopy
  • tissue biopsy
  • culture
97
Q

How to diagnose TB?

A
  • PPD
  • Biopsy of ghon complex (not desired bc infectious)
  • Sputum smear (acid fast stains)
98
Q

How to diagnose UTI?

A

urine collection, analysis, and culture:

  • uncomplicated: single species > 10^5 bacteria/ml
  • complicated: 10^2-10^4 bacteria/ml (could be multiple species)
  • catheter associated: multiple species common, biofilms
99
Q

Innate defenses against UTI?

A
  • Low pH
  • Urea
  • organic acids
  • Tamm-Horsfall protein
  • Lactoferrin
  • Lipocalin
  • Antimicrobial peptides
  • *Unidirectional flow
100
Q

Risk factors for UTI?

A
  • Female (higher incidence)
  • Sexual intercourse
  • Elderly
  • Pregnant
101
Q

Presentation of cystitis?

A

Dysuria, frequent urination, suprapubic pain

102
Q

Presentation of pyelonephritis?

A 
Flank pain 
fever
nausea, vomiting, chills
inceased C-reactive protein
Bacteremia (30%)
103
Q

Major causes of uncomplicated UTI?

A
  1. E. coli (normal gut flora)

2. Staph saprophyticus

104
Q

Virulence factors of E. coli?

A
  • Type I fimbrae: adherence to uroepithelial cells and exfoliation of bladder walls
  • Pap pili: adhere to digalactoside-receptors to colonize kidney
  • Hemolysin: damages cell membranes
  • Cytonecrotizing factor (CNF toxin): inhibit Rho GTPaes in cytoskeleton
105
Q

Virulence factors of Staph saphrophyticus?

A
  • Adhesins

- Urease: breaks down urea to ammonia and carbamate (raises urine pH)

106
Q

Characteristics of E. coli?

A 
Enterobacteriaceae family
G- straight rods
facultative anaerobe
glucose fermenters
oxidase negative
107
Q

Characteristics of Staph saphrophyticus?

A
  • G+ cocci in clusters
  • coagulase negative
  • novabiocin resistant (distinguishes it from Staph epidermidis)
108
Q

Associations for complicated UTIs?

A
  • metabolic disorders

- kidney stones

109
Q

Presentation of catheter-associated UTIs?

A

often nonspecific

  • fever
  • leukocyotisis
  • pyuria (>50 WBC/hpf)
110
Q

Common causes of complicated UTIs?

A

Proteus mirabilis
Staph aureus
Staph epidermidis
Enterococcus faecalis

111
Q

Characteristics of Proteus mirabilis?

A
  • Enterobacteriaceae family
  • G- straight rods
  • glucose fermenters
  • oxidase negative
  • swarming motility on solid agar (ripple pattern)
  • produces urease (virulence factor to raise urine pH)
  • usually invades upper urinary tract
112
Q

Risk factors for Pseudomoas aeruginosa infections?

A

catheterization and kidney stones (can result in UTIs)

113
Q

Virulence factors of Staph epidermidis?

A 
antibiotic resistance
biofilm formation (can form on indwelling foreign devices like catheters or pacemakers)
114
Q

Virulence factors of enterococcus faecalis and E. faecium?

A
  • can become blood-borne

- antibiotic resistance

115
Q

What causes croup?

A

Parainfluenza virus AKA paramyxovirus

CPR Final (9 decks)

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