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Micro > HHD - Microbiology Flashcards - All Micro Videos > Flashcards

HHD - Microbiology Flashcards - All Micro Videos

1
Q

What is the bacterial cell wall material?

A

Peptidoglycan

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2
Q

What is the source and effect of cholera toxin?

A

Cholera toxin disrupts chloride channels such that chloride rushes out of the cell, followed by Na+ and water, which causes severe diarrhea

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3
Q

What is the organization of the Baltimore classification scheme (and the no. of classes)?

A

Viruses are organized by their genome (e.g. ssDNA, dsDNA, ssRNA (+), ssRNA (-), etc.), which tells us how they produce mRNA and protein. There are 7 classes.

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4
Q

Define immune escape.

A

Antigenic variation, or mutation of the antigens that would allow the immune system to recognize the virus, allows the virus to escape detection

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5
Q

Where does VZV hide from the immune system?

A

In the dorsal root ganglion, before traveling down the sensory nerves to the skin to cause a rash, known as shingles

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6
Q

Define virulence.

A

Virulence is the relative capacity to cause damage to the host

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7
Q

What factor of the virus does attenuation decrease?

A

Virulence

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8
Q

Why can most fungi not cause disease in humans?

A

Their optimal growth temperature is much lower than 37°C

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9
Q

Name three components of the fungal cell wall (innermost to outermost).

A

Chitin, β-glucans, galactomannans

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10
Q

What is the major fungal membrane molecule that differentiates fungi from animals?

A

Ergosterol

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11
Q

What are the three main types of pathogenic fungi?

A

Yeasts, molds, and thermally dimorphic fungi

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12
Q

What is the difference between environmental and colonizing fungi?

A

Their “natural” habitat outside of humans; Coccidioides is a soil fungus and Candida is a mucosal colonizer

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13
Q

What are the two main categories of parasites?

A

(1) Protozoa, eukaryotic, single-celled organisms and (2) multicellular eukaryotes such as helminths and ectoparasites

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14
Q

Name four groups disproportionately affected by parasitic infections

A

Agriculture workers, women during pregnancy, children, and poor people living in wealthy countries

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15
Q

What are three different kinds of hosts in a parasitic life cycle?

A

Definitive host: hosts the parasite during reproduction stage; intermediate host: hosts the parasite during larval development; dead-end host: parasite enters the wrong host and dies

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16
Q

What are four bactericidal compounds secreted by epithelial cells?

A

Acid in stomach, bile detergents in intestine (microbes could change LPS to withstand detergents), antimicrobial peptides and enzymes (microbes could change the cell wall to resist lysozymes), IgA (microbes could produce IgA proteases)

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17
Q

What is the biggest clinical concern about bacterial biofilms?

A

Biofilms (interbacterial mucoid adhesions) can act as a barriers, allowing bacteria to avoid the immune system! They allow bacteria to infect catheters. Catheter-related bloodstream infections often require removal of the device

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18
Q

What are the four common mechanisms of antibiotic resistance?

A

(1) Decrease entry by mutating the porin proteins in the cell membrane (gram-negative bacteria specifically), (2) degrade the antibiotic wtih an enzyme (e.g. B-lactamases), (3) remove the antibiotic by producing efflux pumps, (4) alter the target by mutating the ribosome

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19
Q

What percentage of the population is infected by influenza yearly?

A

15-20% of the world’s population

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20
Q

Name influenza’s viral family and its characteristics.

A

Orthomyxovirus; spherical, enveloped, ssRNA, (-) sense, segmented genome that replicates in the nucleus

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21
Q

What are the two key influenza surface molecules and their function? Are antibodies against each neutralizing?

A

Hemagglutinin and neuraminidase; HA binds sialic acid receptors for entry and can clump RBCs; NA degrades mucin (entry) and cleaves sialic acid (exit); antibodies against HA are neutralizing, while antibodies against NA are non-neutralizing

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22
Q

What are the influenza subgroups and who can they infect?

A

A, B, and C. Only A can infect both humans and animals and is responsible for pandemics. B and C infect humans only.

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23
Q

What is the difference between antigenic shift and drift?

A

Drift is small antigenic changes; shift is caused by a major mutation, usually from a zoonotic recombination and causes a pandemic

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24
Q

How is influenza transmitted?

A

Large respiratory droplet transmission over short distances

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25
Q

What is the incubation period for influenza?

A

1-4 days from exposure

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26
Q

What is the illness period of influenza and when are patients infectious?

A

Adults shed virus from 1 day before symptoms to 5-10 days after symptom onset. By 3 to 5 days their infectious ability is greatly decreased; children may be infectious for 10 days or more; immunocompromised people may shed virus for several weeks

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27
Q

Name symptoms of influenza infection.

A

Abrupt onset of fever, myalgias (sore muscles), headache, pharyngitis, rhinorrhea, cough, and fatigue

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28
Q

What is the difference between primary and secondary influenza pneumonia?

A

Primary pneumonia is caused by direct infection of lungs by influenza virus with the resulting immune system-mediated tissue damage; secondary is caused by a bacterial pathogen that enters right afterwards (usually after a period of improvement); S. pneumonia, S. aureus, H. influenza, nosocomial gram (-) rods

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29
Q

What is Reye’s syndrome?

A

Unknown cause, though aspirin is implicated; rare, life-threatening syndrome in children following viral infection with influenza or varicella virus; fever, rash, encephalopathy, liver failure

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30
Q

What are four diagnostic tests for the flu and which is the current gold standard?

A

Viral culture (10 days); immunofluorescence (1-4 hours); PCR (1-6 hours, gold standard); rapid antigen detection (<30 min)

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31
Q

What are the the two common groups of antivirals for flu treatment? Give examples of each.

A

Adamantanes (Ex: amantadine, rimantadine) and NA inhibitors (Ex: oseltamivir, zanamavir)

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32
Q

Name the mechanism, adverse effects, and usage of adamantanes.

A

They block the M2 ion channel to prevent uncoating; have CNS effect, anticholinergic effects, and are teratogenic; used against Influenza A; most viruses are resistant so this is NOT used in clinical practice.

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33
Q

Name the mechanism, adverse effects, and usage of NA inhibitors.

A

(Ex: oseltamivir, zanamivir) Inhibits NA cleavage of sialic acid; well-tolerated; used on Influenza A and B within 48 hours of onset, but effectiveness is debated

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34
Q

Who is at the highest risk for flu infection?

A

Elderly, infants, chronic disease patients, obese patients, pregnant women

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35
Q

What are the two kinds of flu vaccines?

A

Inactivated IM vaccine; LAIV intranasal (best for children 2-8)

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36
Q

Who should be vaccinated against influenza?

A

All those over 6 months of age

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37
Q

What is the morphological difference between Strep and Staph?

A

Streptococci form chains; staphylococci form “grape clusters”

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38
Q

What is the catalase test difference between Strep and Staph?

A

Streptococci are catalase negative (they will NOT bubble); staphylococcus are catalase positive

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39
Q

What is the species of Group A Strep?

A

S. pyogenes

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40
Q

What are the two β-hemolytic Strep species and how do you distinguish them?

A

β-hemolytics show complete hemolysis; the two species are S. pyogenes (Group A) and S. agalactiae (Group B); GAS is bacitracin sensitive, while S. agalactiae is not.

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41
Q

What are the α-hemolytic Strep species and how do you distinguish them?

A

α-hemolytics show partial hemolysis; S. pneumoniae and Viridans, and S. pneumoniae is optochin-sensitive and has pearly colonies due to its capsule and Quellung (+); neither have Lancefield antigens.

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42
Q

What are the γ-hemolytic Strep species and how do you distinguish them?

A

γ-hemolytic means no hemolysis; Enterococcus and non-Enterococcus species (Lancfield group D); both are bile esculin (+) but only Enterococcus grows in salt media.

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43
Q

What does hyalorunate do in S. pyogenes?

A

It forms a protective capsule to help protect it from the immune system

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44
Q

What are the functions of the M-protein?

A

(1) Binds complement, (2) anti-opsonization; autoantibodies can form to M-proteins

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45
Q

What are the two invasion factors of Strep?

A

Hyaluronidase breaks down ECM and Streptokinase activates plasmin, dissolving the blood clots to release bacteria

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46
Q

What are the two major toxins from Strep?

A

(1) Streptolysin O: lyse RBCs and WBCs, cause beta-hemolysis.
(2) Strep pyogenic exotoxins: agents like erythrogenic toxin cause scarlet fever; superantigens overactivate T cells, leading to Toxic Shock Syndrome.

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47
Q

What is a suppurative infection?

A

A pus-producing infection

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48
Q

What are some common suppurative infections caused by GAS?

A

Erysipelas (outermost layer, dermis); cellulitis (middle layer, dermis/sub-cu); necrotizing fasciitis; impetigo (crusty red sores around the nose)

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49
Q

What are some of the classic signs of scarlet fever?

A

Desquamating sandpaper rash, circumoral pallor, strawberry tongue, fever

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50
Q

What are some of the signs and causes of streptococcal toxic shock syndrome?

A

Hypotension, end organ damage; thought to be caused by superantigen activation

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51
Q

What are the organ systems usually affected by acute rheumatic fever?

A

Skin, joints, heart, brain

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52
Q

What are three of the five criteria for ARF?

A

Pancarditis, polyarthritis, subcutaneous nodules, erythema marginatum, Sydenham chorea

53
Q

What is the common renal complication of GAS infection?

A

Post-streptococcal glomerulonephritis (PSGN), which is caused by antibody complex deposition

54
Q

What are the four categories of β-lactams?

A

Penicillins, cephalosporins, carbapenams, and monobactams

55
Q

What is the mechanism of β-lactams?

A

They block the active site of the penicillin binding protein, so the bacterial cell wall cannot form

56
Q

What are the two main paths to β-lactam resistance?

A

β-lactamases and modifications of the PBPs

57
Q

What are the two types of resistance development?

A

Inducible resistance and plasmid transfer

58
Q

What is the most common adverse effect of β-lactam drugs?

A

GI adverse effects

59
Q

How is viral pharyngitis distinguished from bacterial?

A

Viral pharyngitis also has coryza, conjunctivitis, cough, and body aches.

60
Q

What are the two major diagnostic tests for strep?

A

Bacterial culture of pharyngeal swab (24-48 hours); strep rapid antigen detection test (10 min; follow-up culture if negative)

61
Q

What are the Centor criteria for?

List the criteria and explain the scoring system.

A

The Centor criteria help a clinician decide if s/he should use the RADT screen for GAS for a patient with pharyngitis.

Criteria: +1 point for: (1) Fever >38°C, (2) tender anterior cervical LNs, (3) tonsillar swelling, (4) lack of a cough; (5) 3-14.

-1 point for age >45;

Test with RADT for if patient scores 2+

62
Q

What is the treatment for GAS pharyngitis?

A

Penicillin (or azithromycin/clindamycin if allergic)

63
Q

What are two major risk factors for Aspergillus infection?

A

Neutropenia, chronic granulomatous disease, lung dysfunction (asthma, emphysema)

64
Q

Which species of Aspergillus is most commonly pathogenic in humans?

A

A. fumigatus

65
Q

What is the infectious agent of Aspergillus?

A

The spores, or conidia

66
Q

Describe the three steps in the pathogenesis of Aspergillus.

A

(1) Germination of the spores, (2) hyphal extension, (3) tissue and blood vessel destruction

67
Q

What is the presentation and the worst course of invasive aspergillosis?

A

Presents as a primary pulmonary infection w/ fever and lung nodules on CT; disseminates to other organs and shows organ-specific symptoms; worst case scenario is spread to the CNS resulting in ALOC.

68
Q

What sorts of patients usually develop chronic aspergillosis?

A

Patients with altered anatomy (e.g. emphysema patients) but intact immune systems

69
Q

What is an aspergilloma and why can it develop?

A

It is a fungal ball and can develop when patients have lung cavities (sometimes due to past TB)

70
Q

How is allergic bronchopulmonary aspergillosis treated and why is it different from the usual tx? Which patient population is most at risk?

A

Rather than an invasive fungal infection, this is an allergic reaction to fungus on the respiratory mucosa; it is treated with immune suppressives rather than with antifungals; this is typically a problem in asthma patients.

71
Q

What are two crucial antigens in blood/BAL that can indicate Aspergillus?

A

Galactomannan and β-D-glucan

72
Q

What is the appearance of Aspergillus under the microscope?

A

Regular, septate hyphae with acute angle branching

73
Q

What is the radiographic appearance of invasive aspergillosis?

A

“Air crescent” sign of lungs, which forms as dead tissue is expectorated

74
Q

What is the best treatment for aspergillosis?

A

Due to diagnostic challenges, empiric tx for this disease is crucial; mold-active azoles (voriconazole is the best), amphotericin B, echinocandins are less effective; surgical debridement can be indicated

75
Q

What are two morphological characteristics of mucorales or zygomycete fungi?

A

Rapidly growing hyphal molds (grow on bread), broad hyphal diameter, few septa, ribbon-like folding in tissue

76
Q

What is the classic (and most deadly) presentation of mucormycosis?

A

Rhinocerebral infection that spreads from the sinuses into other facial structures and even into the brain

77
Q

What is the critical sign of rhino cerebral mucormycosis?

A

Palatal eschar, a necrotic lesion on the hard palate

78
Q

What are alternate (less common) presentations of mucormycosis?

A

Pulmonary or GI infection

79
Q

What is the most effective diagnostic tool for mucor infection? What is ineffective?

A

Radiography is not effective because it is not specific; culture is a terrible idea because of contamination risk; histopathology is the move because you can see the ribbon-like, aseptate hyphae

80
Q

What is the treatment for mucormycosis?

A

Surgical debridement is really the only effective therapy; most antifungals are not effective, except for ampho; Fe modulation has been approached as a potential therapy

81
Q

What is a major endemic fungus of the Southwest USA?

A

Coccidioides immitis/posadasii

82
Q

Distinguish the primary and chronic infections in coccidiomycosis/“valley fever.”

A

The primary infection is a self-limiting respiratory infection, while the secondary causes chronic pneumonia, skin, or eosinophilic meningeal infections

83
Q

Name the two different structures present in the tissue vs environmental forms of Coccidioides.

A

The tissue form contains spherules, or sacs of yeast cells, while the environmental form has hyphae with many arthroconidia

84
Q

What is a major endemic fungus of the Ohio/Mississippi River valleys?

A

Histoplasma spp.

85
Q

Distinguish the primary and chronic infections in histoplasmosis.

A

The primary infection is a self-limiting respiratory infection, while the secondary causes chronic pneumonia, hiding in macrophages and DCs for years until it emerges, causing infections in AIDS or anti-TNF patients

86
Q

What is a major endemic fungus of the Great Lakes region?

A

Blastomyces spp.

87
Q

Distinguish the primary and chronic infections in blastomycosis.

A

The primary infection is a self-limiting respiratory infection, while the secondary causes chronic pneumonia, skin/bone lesions, and male GU tract issues.

88
Q

What is the defining morphological characteristic of paracoccidiomycosis?

A

The captain’s wheel form in culture

89
Q

Describe the course of Sporothrix infection.

A

Primary skin inoculation followed by proximal spread via lymphatics causing “nodular lymphangitis”

90
Q

What is the mechanism of amphotericin B?

A

It binds ergosterol and forms pores in membrane, which disrupts the structure and causes cell death

91
Q

What are two major adverse effects of amphotericin B?

A

Renal toxicity and electrolyte changes; ototoxicity, altered vestibular function causing hearing loss and ringing in ears

92
Q

Which formulation of amphotericin B minimizes adverse effects?

A

Lipid associated amphotericin B

93
Q

What is the spectrum of amphotericin B?

A

Cryptococcal meningitis (induction phase); systemic mold infections (mucormycosis); serious endemic fungal infections; resistant Candida infections

94
Q

What is the mechanism of triazoles?

A

Inhibit the Erg11 protein in the ergosterol synthesis pathway

95
Q

What are two major adverse effects of triazoles?

A

P450 enzyme inhibition can cause liver and drug metabolism issues; QT prolongation

96
Q

Which azoles are mold-active and which are yeast-active?

A

Fluconazole is yeast-active and voriconazole, itraconazole, and posaconazole are mold-active

97
Q

What is the usage of fluconazole?

A

Candida, Cryptococcus neoformans maintenance-phase therapy, or non-CNS C. neoformans

98
Q

What is the usage of the mold-active azoles?

A

Systemic infections of Aspergillus fumigatus; invasive yeast infections (Candida and cryptococcus); endemic fungal infections

99
Q

What is the mechanism of echinocandins?

A

Inhibit β-glucan synthesis

100
Q

What is the usage of echinocandins?

A

Serious Candida infections like candidemia; second-line therapy for Aspergillus

101
Q

What is the usage of flucytosine?

A

C. neoformans meningitis, induction phase in combination with amphotericin B; never alone

102
Q

What are the most common viruses that cause pharyngitis?

A

Adenoviruses (pharyngoconjunctival fever), influenza, cold viruses (rhinoviruses, coronaviruses)

103
Q

What is the most common bacteria that causes pharyngitis?

A

Streptococcus pyogenes

104
Q

What are the most common viruses that cause otitis media?

A

RSV, rhinoviruses, adenoviruses, influenza

105
Q

What is the most common bacteria that causes otitis media?

A

Streptococcus pneumoniae

106
Q

What is a common infection that is a complication of untreated otitis media? What bacteria causes this infection?

A

Mastoiditis, where the air cells are infected, usually by H. influenzae

107
Q

What are the most common bacteria that cause sinusitis?

A

S. pneumonia, H. influenzae, M. catarrhalis

108
Q

What is one of the most serious common complications of sinusitis?

A

Orbital cellulitis usually caused by Staph. aureus, Strep. pneumonia, and other specieis; the bacteria move through the lamina papyracea (the thin bones separating the sinuses and orbit)

109
Q

What structures make up the URT and the LRT?

A

Division is vocal vords; upper respiratory tract (URT) is the nasal cavity, nasopharynx, oropharynx, larynx; lower respiratory tract (LRT) is the trachea, bronchi, bronchioles, lung

110
Q

Name the syndrome and most common viruses infecting the nasal cavity.

A

Rhinitis (common cold); rhinovirus, coronavirus

111
Q

Name the syndrome and most common viruses infecting the nasopharynx, oropharynx, or larynx.

A

Pharyngitis (sore throat) or laryngitis; adenovirus or parainfluenza virus

112
Q

Name the syndrome and most common viruses infecting the trachea or bronchi.

A

Laryngotracheobronchitis (croup); parainfluenzavirus; common in children, listen for the barking cough

113
Q

Name the syndrome and most common viruses infecting the bronchi.

A

Brochitis; parainfluenza virus, influenza, adenovirus, metapneumovirus, RSV, coronavirus; watch for heavy productive cough with purulent sputum

114
Q

Name the syndrome and most common viruses infecting the bronchioles.

A

Brochiolitis; RSV, influenza, metapneumovirus, adenovirus; very severe in infants because of small bronchiole size

115
Q

Name the syndrome and most common viruses infecting the alveoli.

A

Pneumonia; (all respiratory viruses) influenza, rhinovirus, parainfluenzavirus, metapneumovirus, RSV, SARS, MERS, coronavirus, adenovirus

116
Q

How are bacterial and viral respiratory pneumonias distinguished radiographically?

A

CXR shows viral pneumonias to be diffuse and bilateral while bacterial pneumonias are more focal with demarcated areas of opacity representing filled alveoli

117
Q

Which respiratory viruses are RNA and which are DNA?

A

All are RNA except for adenoviruses

118
Q

Describe the seasonality of respiratory viruses.

A

Most peak in the winter (e.g. RSV, influenza), except for parainfluenzavirus (late fall) and adenovirus (year round)

119
Q

Describe the Baltimore classification, the family, and the structure of the rhinovirus.

A

(+) sense RNA virus; Picornaviridae; naked capsid

120
Q

Describe the Baltimore classification, the family, and the structure of the coronavirus.

A

(+) sense RNA virus; Coronaviridae; enveloped, which makes it susceptible to detergents; includes SARS and MERS

121
Q

Describe the Baltimore classification, the family, and the structure of the adenovirus.

A

dsDNA virus; Adenoviridae; naked capsid, but can survive and invade the GI tract or cause system infections because of globular membrane proteins that can bind tight junctions, allowing epithelial invasion

122
Q

Describe the Baltimore classification, the family, and the structure of the parainfluenzavirus.

A

(-) RNA virus; Paramyxoviridae; 4 serotypes; enveloped; buds out of the apical cell so it doesn’t cause cell lysis, but the increased epithelial turnover causes swelling

123
Q

Describe the Baltimore classification and the family of RSV.

A

(-) RNA virus; Paramyxoviridae;

124
Q

What are the two important surface proteins of RSV?

A

G-protein attaches to host and F-protein fuses the viral envelope to the host cell membrane

125
Q

How does RSV evade the immune system?

A

The glycosylation of G-protein is hard for Ig to bind to, and soluble G-protein consumes Ig; RSV also infects DCs, hampering the immune response

126
Q

What are the common clinical manifestations of adenovirus?

A

Pharyngitis/Laryngitis, including acute febrile pharyngitis and pharyngoconjunctival fever

127
Q

What are the common clinical manifestations of parainfluenzavirus?

A

Laryngotracheobronchitis, croup (look for the steeple sign, or subglottic stenosis on the radiograph)

128
Q

How does RSV cause bronchiolitis?

A

Increased vascular flow, permeability, and mucus production after respiratory epithelial cell infection causes tachypnea, cough, respiratory distress with retractions, and wheezing

129
Q

Which major virus is most similar to metapneumovirus?

A

RSV

Micro (1 decks)

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