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Microbiology > Exam #8: SSTI III > Flashcards

Exam #8: SSTI III Flashcards

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Biology 101 flashcards
1
Q

List the characteristics of Clostridium.

A

Gram (+) rods
Spore-forming

*can last for years & resistant to heat, desiccation, & disinfectants

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2
Q

What SSTIs are caused by C. perfringens? What other diseases are caused by C. perfringens?

A

Gas Gangrene (Clostridial myonecrosis)

Also,

  • Cellulitis
  • Fasciitis
  • Suppurative myositis
  • Myonecrosis i.e. Gas gangrene
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3
Q

What toxins are associated with C. perfringens?

A
  • Alpha-toxin that destroys cell membranes by lysing cells
  • Also, note that C. perfringens growth is accompanied by large amounts of hydrogen and carbon dioxide gas (that can be seen on X-ray)
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4
Q

When is C. perfringens Gas Gangrene most common?

A

Traumatic wound
Surgical post-op

*Note, this is a wound infection accompanied by gas production or “crepitations”

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5
Q

Describe the progression of Gas Gangrene.

A

1) Starts as cellulitis
2) Progresses to suppurative myositis
4) myonecrosis (painful, rapid destruction of muscle tissue)
3) Gas gangrene

*Note that this rapid spread is mediated by Alpha-toxin associated with C. perfringens

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6
Q

How is C. perfringens diagnosed & how is it treated?

A
  • Clinical observations are key!
  • Microscopic detection of gram positive rods WITHOUT leukocytes (killed by the alpha-toxin)
  • Immediate surgical debridement & high dose PCN therapy
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7
Q

List the characteristics of C. tetani.

A

Gram (+) rod
Spore forming
Strict anaerobe*

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8
Q

How is C. tetani introduced into the body?

A
  • Wound puncture

- Umbilical stump infection

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9
Q

How does C. tetani present?

A

“Spastic paralysis” caused by tetanospasmin mediated prevention of the release of inhibitory neurotransmitters (Glycine & GABA)

*vs. Flaccid Paralysis in Botulinsm

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10
Q

What toxins are produced by C. tetani?

A

Tetanospasmin

Heat labile Neurotoxin

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11
Q

What is the mechanism of Tetanospasmin?

A

Inactivates proteins that control the release of inhibitory neurotransmitters and results in spastic paralysis

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12
Q

What is risus sardonicus?

A

Lock jaw

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13
Q

What is opisthotonic posturing?

A

Involvement of the spinal musculature in the newborn infected with Tetanus (omphalitis)

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14
Q

How is C. tetani diagnosed?

A

Clinical presentation
- Cannot be cultured b/c it is a strict anaerobe

*Mostly seen in the elderly population esp. those that have NOT maintained their booster & like to garden

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15
Q

How is C. tetani infection treated?

A
  • Debridement of the primary wound
  • Metronidazole
  • HTIG (Human tetanus immunoglobulin i.e. anti-toxin)
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16
Q

How is C. tetani prevented?

A

Vaccination (Tetanoid toxin)

Boosters

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17
Q

List the characteristics of the mycobacterium.

A
  • Acid fast
  • Lipid-rich cell wall (mycolic acid)
  • Resistant to disinfectants, detergents, antibiotics…etc.
  • Slow-growing

*Weakly Gram (+) but not visualized very well

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18
Q

What diseases are associated with Mycobacterium?

A

TB

Leprosy

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19
Q

How much of the world’s population is infected with MTB?

A

1/3, mostly in Saharan Africa

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20
Q

Describe the pathogenesis of MTB.

A
  • Primary infection is pulmonary

-

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21
Q

What is Pott’s disease?

A

Pott’s Disease is a type of bacterial osteomyelitis that progresses slowly over months

  • Occurs most in undeveloped countries & immunocompromised
  • Occurs via respiratory route & hematogenous spread
  • Most commonly seen in thoracic and lumbar vertebrae
22
Q

What is a gibbus deformity?

A

Abnormal kyphosis of the lower thoracic spine that is associated with Pott’s Disease

23
Q

How is Pott’s Disease diagnosed?

A
  • Hx of travel or recent immigration to the US
  • Slowly progressing back pain
  • “Gibbus deformity”
  • Positive PPD
  • Evidence of Mycobacterium in aspirate or biopsy of spinal lesion (granuloma)
24
Q

How is MTB treated?

A

RIPE (long duration)

  • Rifampin
  • Isonidazole
  • P
  • Ethambutol

*6 months of treatment

25
Q

What organism causes Leprosy?

A

Mycobacterium leprae

26
Q

What are the two reservoirs for Mycobacterium leprae?

A

Humans

Armadillos

27
Q

What cells are targeted by Mycobacterium leprae?

A

Macrophages and Schwann cells

28
Q

What are the two different stages of M. leprae?

A

Tuberculoid (Th1) response

Lepromatous (Th2)= classic

29
Q

What is the difference between Tuberculoid and Lepromatous?

A

Lepromatous= antibody production that is NOT helpful in eradicating the disease–>Hansen’s Disease
- Th2 response & antibody

30
Q

List the characteristics associated with Tuberculoid (Th1) leprosy.

A
  • Few lesions with flat centers
  • Few acid fast rods
  • DTH reaction to lepromin (Th1) like PPD but for leprosy
  • Normal immunoglobulin levels
  • No Erythema nodosum
31
Q

List the characteristics of Lepromatous (Th2) leprosy.

A
  • Many lesions with nodules & nerve involvement
  • Many acid fast rods
  • No reactivity to lepromin (Th2)
  • Hypergammaglobulinemia
  • Erythema nodosum usually present
32
Q

How is Leprosy diagnosed?

A
  • Lepromin test= M. leprae injection similar to PPD
  • Culture is impossible
  • Must take a biopsy and perform acid fast staining
33
Q

Which type of leprosy is NOT associated with a positive skin test?

A

Lepromatous (Th2)

34
Q

What are Nocardiosis and Actinomycosis?

A

Filamentous bacteria that cause skin infection

35
Q

What are the different presentations associated with Nocardia?

A 
Bronchopulmonary Disese
Cutaneous infections 
- Mycetoma 
- Lymphocutaneous infections 
- Chronic ulcerative lesions 
- Subcutaneous abscesses 
- Cellulitis
36
Q

List the characteristics of Nocardia.

A

Gram positive rod
Weakly acid fast*
Filamentous
Forms aerial hyphae in culture (furry stuff that grows off the plate)

*Resembles fungi/ hyphae

37
Q

What is mycetoma?

A
  • Skin infection caused by Nocardia that is usually seen in the lower limb, and painless
  • Wound on the foot gets infected with Nocardia
38
Q

How is Nocardia diagnosed?

A
  • Hx (environment)
  • Direct examination of clinical specimen–>weakly acid fast*

Note that this can be confused with Sporothrix schenckii (fungal infection)

39
Q

How does Actinomycosis differ from Nocordia?

A
  • Not acid fast

- “Molar” appearance on plate, NOT aerial hyphae

40
Q

List the characteristics of Actinomyces.

A
  • Filamentous bacteria that resembles fungi
  • Strict anaerobe
  • Normal flora in respiratory tract
  • Associated with dental work–> lump on the cervicofacial region
41
Q

What is a hallmark of Actinomycoses?

A

Sulfur granules–colonizes of the organism that look like grains of sand

42
Q

How is Actinomycosis diagnosed?

A
  • Direct examination

- Differentiate from Nocordia with the acid fast stain

43
Q

How is Actinomycosis treated?

A

PCN

44
Q

What is Acne vulgaris?

A

Common disorder of the pilosebaceous unit

45
Q

What are the four key elements of acne vulgaris?

A

1) Follicular epidermal hyperproliferation
2) Excess sebum production
3) Inflammation
4) Presence and activity of Propionibacterium acnes

46
Q

What organism is associated with acne vulgaris?

A

Propionibacterium acnes

47
Q

List the characteristics of Propionibacterium acnes.

A
  • Small anaerboic Gram-positive rod
  • Part of the normal flora
  • Stimulates an inflammatory response that some people have
48
Q

How is acne treated?

A

1) Benzoyl peroxide (exfoliation)
2) Topical antibiotics
3) Oral antibiotics (doxycyline)
4) Isotretenoin

49
Q

What is gingivitis?

A

Inflammation of the gums that is reversible

50
Q

What is periodontitis?

A

Chronic inflammatory disease that includes gingivitis along with loss of connective tissue and bone support for the teeth that is irreversible

51
Q

What are the causative organisms of gingivitis and periodontitis?

A

Bacteria in dental plaque primarily by Gram-negative anaerobic flora, including:

  • Poryphyromonas gingivalis
  • Treponema denticola
52
Q

What is the dominant organism that causes dental caries?

A

S. mutans (viridans strep)

-acid from these organisms lead to tooth decay

Microbiology (49 decks)

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