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MSK Midterm > Microbiology > Flashcards

Microbiology Flashcards

0
Q

How will Staph aureus culture vs. Staph epidermis?

A

Blood agar: S. aureus will culture as yellow beta hemolytic, while S. epidermis will appear as white, non-hemolytic.

Gram stain: both will be purple (Gram postitive) cocci in clusters; both are catalase positive.

Coagulase: S. aureus is coagulase positive, while S. epidermis (and S. saphrophyticus and other species) are coagulase negative.

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1
Q

How does Strep vs Staph appear on a Gram stain?

A

Both will appear as purple (Gram positive) cocci and but Strep colonies will arrange in a line, whereas Staph colonies will cluster.

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2
Q

Describe the catalse test and its applications.

A

Colonies of a particular bacteria are added to a test tube containing hydrogen peroxide. The liquid will bubble if the bacteria are catalase positive (able to break down hydrogen peroxide to water and oxygen). Useful for differentiating Staph (catalase positive) from Strep (catalase negative).

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3
Q

Describe the coagulase test and its applications.

A

Plasma is inoculated with a particular bacteria and left to incubate. If the bacteria contains coagulase, it will react with coagulase-reacting factor in the plasma and thicken until it forms a clot. This is used to differentiate Staph. aureus from other Staph bacteria (which are generally coagulase negative).

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4
Q

What is the hallmark sign of Staph skin infections?

A

The presence of pus (suppurative lesions).

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5
Q

What is the treatment for a furuncle?

A

Heat, drainage, and antibiotics if it invades the subcutaneous layer.

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6
Q

Hydradentis suppurativa

A

Infection of sweat glands. Especially common when hygiene is poor.

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7
Q

What is the treatment for chronic furunculosis?

A

Topical mupirocin to eliminate nasal carriage (spread or recurrence).

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8
Q

Impetigo

A
  • infection of the epidermis
  • presents as erythematous macules that progress to pustules, which result in erosions with dry, crusted, honey colored serum when they erupt
  • Usually due to Group A Strep, but in 30% of cases both Group A Strep and Staph aureus are present
  • Usually seen in kids on the face
  • Highly contagious
  • Climate and hygiene affect incidence
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9
Q

Folliculitis

A
  • inflamed hair follicles
  • may present as scattered individual vesicles or pustules
  • usually caused by an infection of Staphylococci or Pseudomonas aeruginosa
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10
Q

Carbuncles and furuncles

A
  • furuncles are boils, (deep folliculitis) and carbuncles are a larger collection of furuncles
  • both present as painful, swollen areas surrounding the infect hair follicle(s), which is full of pus and dead tissue
  • usually caused by an infection of Staphylococci
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11
Q

Erysipelas

A
  • an acute infection of the upper dermis which usually involves dermal lymphatics
  • presents as a pink patch on the skin which may be slightly raised and swollen
  • usually caused by Streptococci
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12
Q

Cellulitis

A
  • inflamation of the subcutaneous fat layer
  • presents as a swollen, bright red area of skin that feels hot and tender
  • usually caused by Streptococci, staphylococci, Haemophilus influenzae type B (among unimmunized kids)
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13
Q

What causes synergistic cellulitis? (3)

A

Streptococci, enteric bacteria, anaerobes

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14
Q

Gas gangrene

A
  • AKA myonecrosis
  • produces fas in tissues in gangrene
  • causes necrosis specifically to muscle tissue via the release of endotoxins
  • a medical emergency: can lead to shock, require amputation of the affected limb, or be fatal
  • common cause is Clostridia
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15
Q

Necrotizing fasciitis

A
  • characterized by extensive necrosis of the subcutaneous tissue and fascia which usually spares the underlying muscle but may spread to the dermis and epidermis
  • can be caused by Streptococci, enteric bacteria, or anaerobes
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16
Q

What are the clinical features of toxic shock syndrome and who is at risk?

A

Features: sudden onset of fever, chills, diaarrhea, muscle pains and rash, and later development of hypotension, involvement of mucous membranes, multiple membranes, and desquamation.

At risk: menstruating women, women with barrier contraceptive devices, those who have undergone nasal surgery (whenever a moist orifice gets plugged up with something, allowing the normal flora to grow out of control, and sometimes release toxins which are only upregulated when oxygen is limited).

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17
Q

Virulence factors of Staph aureus? (9)

A
  1. Protein A (defend against phagocytes)
  2. Catalase (defend against phagocytes)
  3. Leukocidin (defend against phagocytes)
  4. Ribotechoic and techoic acid (binds fibrogen, induces shock)
  5. Coagulase (initiates conversion of fibrinogen to fibrin)
  6. Capsule (requires greater specificity to be bound for opsonization)
  7. Hyaluronidase (acts on hyaluronic acids in tissues, faciliates dissemination thru subQ tissues
  8. Cytotoxins
  9. Sphingomyelinase C (hydrolyzes membrane)
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18
Q

What are basic lab tools for identifying S. aureus strains?

A
  1. Pulsed field gel electrophoresis (identify bacterial clones)
  2. Bacteriophage typing (tracks antibiotic resistance and food poisoning outbreaks).
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19
Q

Identify 3 sources of skin/soft tissue infections.

A
  1. Exogenous: direct microbe invasion from external environment
  2. Endogenous: microbe invasion from internal source, such as blood or infected organ
  3. Toxin-mediated manifestations: from an infection at a distant site
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20
Q

Resident vs transient skin flora?

A

Resident: not easily removed by clinical skin prep techniques; mostly bacterial and include Staph epidermis, and P. acnes.

Transient: temporary, easily removed; usually Staph. aureus and Strep pyrogenes (Group A Strep)

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21
Q

Generalizations about Streptococci? (3)

A
  1. Gram positive
  2. catalase negative
  3. they are a diverse group of organisms characterized by hemolysis (on blood agar), physiological traits and biochemical rxns, and antigenic composition (e.g. Lancefield antigen)
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22
Q

What is the difference between suppurative and non-suppurative Group A Strep diseases?

A

Suppurative has pus-causing lesions; non-suppurative do not.

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23
Q

What are detection methods for Group A Strep? (3)

A
  1. Rapid-looking for Lancefield (Group A carb antigen on cell wall)
  2. rapid antigen test (swab and dip for enzyme assay; has a control and specimen site on strip)
  3. culture (using blood agar and a bacitrin disk, which inhibits growth in Group A strep)
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24
Q

Characteristics of Group A Strep (5)

A
  1. Gram positive cocci in chains
  2. Beta homolytic
  3. catalase negative
  4. bacitrin sensitive
  5. PYR positive
25
Q

Virulence factors of S. pyrogenes (5)

A
  1. M protein (anti-phagocytic)
  2. Hyaluronic acid capsule (so similar to human equivalent that we can’t make an antibody against it)
  3. pyrogenic exotoxins: can stimulate super antigens, cause Scarlet fever or shock
  4. Steptolysin O (toxin, basis for ASO test)
  5. DNAses (de-polymerize DNA in damaged cells)
26
Q

Common types of Group A suppurative infections (3)

A
  1. pharyngitis
  2. pyoderma
  3. streptococcal toxic shock syndrome
27
Q

Non-suppurative Group A Strep diseases (2)

A
  1. Rheumatic fever

2. Acute glomerunephritis

28
Q

Mechanism of super antigen toxins

A

Super antigens are bound by MHC and T cells just like normal antigen, but successfully bind more often (non-specific) and triggers a much larger expansion of T cells. It leads to skin and mucus membrane changes, fever, myalgias, abdominal pain, weakness, confusion hypotension, headache, vomiting, diarrhea.

30
Q

Difference between alpha and beta hemolytic?

A

Alpha: on a blood agar plate, only partially lyse RBCs, leaving a greenish discoloration of the agar around the bac colony

Beta: completely lyse RBCs, leaving a clear zone of hemolysis around bac colony

31
Q

What are the possible outcomes when the immune system responds to a viral infection? (3)

A
  1. Acute infection, eventual elimination of virus, immune system is ‘primed’ in case of future encounters
  2. Acute infection, virus enters latency (can re-activate later)
  3. Failure to control infection, chronic persistence of viral infection
32
Q

What is the common morphology of all herpes viruses?

A
  • 150-200 nm in diameter
  • linear double-stranded DNA (150-200 kbp)
  • icosahedral capsid (162 capsomeres)
33
Q

What specific strains do alpha-herpesviruses include, and what are the life cycle characteristics?

A
  • HSV-1, HSV-2, VZV
  • variable host-range
  • short replication cycle
  • undergo latency in sensory ganglia/neuron
34
Q

Compare the clinical presentation of HSV-1, HSV-2, and VZV.

A

HSV-1: labial lesions, keratitis, encaphalitis
HSV-2: genital lesions, severe CNS disease in neonates (usually infection passed from mother in utero)
VZV: chicken pox, shingles

35
Q

Infection with which virus is a major cause of blindness?

A

HSV-1

36
Q

Compare the methods of transmission for alpha-herpesviruses.

A

HSV-1 and HSV-2: direct mucosal contact (oral/oral, oral/genital, genital/genital esp for HSV-2)
VZV: respiratory droplets (more contagious)

37
Q

Describe the two possible genetic programs of herpesvirus.

A
  1. Lytic replication: cells are actively replicating DNA, synthesizing proteins, and assembling proteins (leads to host cell death)
  2. Latency: circular viral genome is maintained in neurons without replication, expresses LAT transcript
38
Q

What stimuli will cause reactivation of herpes simplex virus (HSV-1 and -2) after latency? (4)

A
  1. Stress
  2. Sunlight
  3. Trauma
  4. Menstruation
39
Q

What are the processes involved in reactivation of herpes virus?

A

Reactivation involves limited viral replication in neurons, transport of viral capsid to axonal terminals.

40
Q

What stimuli will cause reactivation of VZV after latency?

A
  1. Immune-suppression (e.g., transplant patients, AIDS patients, chemotherapy/leukemia)
  2. Depressed cell-mediated immunity (with age)
41
Q

What clinical differences are seen in a primary infection of alpha-herpes virus vs a recurrence?

A

Primary infection: skin lesions (vesicular lesions that rupture) more spread on surface, accompanied by systemic symptoms like fever and malaise.
Recurrence: skin lesions isolated to site of neuron innervation, accompanied by prodromal pain, numbness, itchiness, tingling.

42
Q

What are the general regions of HSV-1 vs HSV-2?

A

Above the waist –> HSV-1. Below the waist –> HSV-2.

43
Q

Identify Acyclovir and Ganciclovir and their general mode of action.

A

Both are treatments for HSV, activated by viral Thymidine Kinase. They get incorporated into viral DNA and terminate replication. Results in chain termination of DNA elongation and inhibition of viral DNA polymerase.

44
Q

Identify phosphonoacetic acid and its mode of action.

A

Anti-herpes therapy. Prevents virus replication.

45
Q

Identify forscarnet and its mode of action.

A

Used to treat herpes. Targets viral DNA polymerase. Must be given continuously via IV and has serious renal effects.

46
Q

Discuss the VZV vaccine (Varivax), and who should not get it.

A
  • is a live-attenuated vaccine

- not recommended for pregnant women, HIV+, immunosuppressive therapy patients.

47
Q

Describe who most commonly spreads herpes virus.

A

Mild, asymptomatic infections of HSV-1 and -2 most commonly result in transmission, usually due to shedding from infected epithelial surfaces.

48
Q

How does alpha-herpes virus bind to cells it will infect?

A

Viral glycoproteins will bind to heparan sulfate on cell-surface proteoglycans

49
Q

Describe the phases of temporal transcription in alpha-herpes virus.

A
  1. Immediate-early genes: transcriptional regulatory factors; turn on delayed early gene expression
  2. Delayed-early genes: thymidine kinase, ribonucleotide reductase, DNA polymerase, primase/helicase etc. for DNA replication
  3. DNA replication (circular)
  4. Late genes: structural proteins
50
Q

Discuss the characteristic spread of HSV within the body.

A

Herpes simplex virus is fragile, hence the need for direct contact to susceptible (mucosal) skin for spread. After infection/replication within a cell, it will spread to adjacent cells, almost never spreading systemically throughout the body. Diseases induced by HSV are characterized by local spread and progression of lesions.

51
Q

Which of the host’s immune defenses are most effective against HSV and why?

A

Cell-mediated (T cells, but not antibodies) immune defenses are most effective. The local spread of infection gives little opportunity to attack the virus as it circulates systemically (because it doesn’t). This is also the reason babies under 1 month are particularly susceptible.

52
Q

What is the purpose of treating a specimen with 10% KOH?

A

It dissolves tissue so that the fungus can be seen clearly.

53
Q

What is the purpose of using Sabouraud’s agar?

A

This type of agar inhibits bacterial growth, so using it when a fungi is suspected rules out all bacteria if the specimen grows.

54
Q

What are the major characteristics of Sporotrichosis?

A
  • subcutaneous infection caused by Sporothrix schenckii (dimorphic) in an open wound
  • caused by inoculation from soil, moss or decaying vegetation
  • cutaneous ulceration or ulceration nodules that spread proximally along lymphatics
  • diagnosed with culture
  • treated with itraconazole
55
Q

What are the major characteristics of Mycetoma and Chromoblastomyosis?

A
  • subcutaneous infection seen mostly in the tropics (caused by environ fungi getting into open wounds)
  • usually requires surgical excision
56
Q

What are the characteristics of dermatophyte infections?

A
  • caused by the genera Trichophyton, Microsporum, and Epidermophyton
  • cutaneous infection of skin, hair, nails
  • presents as tinea (ring) infections
  • treatment with topical antifungals like azoles for skin
  • hair and nails require systemic oral therapy
57
Q

What are the characteristics of superficial mycoses?

A
  • caused by Malassezia species, normal flora
  • cause tinea versicolor (AKA Pityriasis versicolor) and seborrheic dermatitis
  • treated with topical antifungals (azoles) or selenium sulfide shampoo
58
Q

Describe the mechanism of action of azoles, toxicity concerns, and what they typically treat.

A
  • inhibit ergosterol synthesis
  • all have -azoles as name ending
  • most are topicals
  • some have associated liver problems (fluconazole best, voriconazole worst)
59
Q

Describe the mechanism of action of polyenes, toxicity concerns, and what they typically treat.

A
  • bind ergosterol; leads to a pore and osmotic death
  • e.g. amphotericin (broad spectrum) or nystatin (topical)
  • watch for kidney problems (liposomal amphotericin B –> renal toxicity)
60
Q

Describe the mechanism of action of echinocandins, toxicity concerns, and what they typically treat.

A
  • inhibits synthesis of beta-glucan, blocks cell wall synthesis
  • all have -flungin ending names
  • given by IV, broad spectrum
  • associated GI side effects and flushing (turning red)

MSK Midterm (9 decks)

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