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Block 7 Week 2 > Skin and Soft Tissue infections II > Flashcards

Skin and Soft Tissue infections II Flashcards

1
Q

What is this;

  • gram positive BACILLUS
  • spore former
  • Aerobic and facultative anaerobe
  • 200 species
A

Bacillus spp.

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2
Q

What are the major 2 types of bacillus spp?

A

B. anthracis -anthrax

B. cereus- misc. infections

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3
Q

What does the bacillus spp capsule do?

A
  • antiphagocytic

- induces protective immunity

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4
Q

What is the capsule of bacillus spp. made of?

A

poly Y D glutamic acid

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5
Q

What are the toxins produced in bacillus spp?

A

toxins- AB type toxin

  • Protective antigen
  • lethal factor
  • edema factor
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6
Q

What does this:
binds cellular receptors and facilitates uptake of LF or EF
Induces protective immunity

A

Protective antigen

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7
Q

What does this:
releases proteases
produces cell death

A

lethal factor (LF)

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8
Q

What does this:
release adenylate cyclase
produces edema

A

Edema factor (EF)

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9
Q

What is this:
Follows inoculation with spores
Painless papule progresses to ulcer to necrotic black eschar (malignant pustule)

A

Cutaneous anthrax

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10
Q

What is this:
Follows ingestion of spores
Local infection that may spread to systemic disease

A

GI anthrax

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11
Q

What is this:
Follows inhalation of spores
Lungs → regional lymph nodes → systemic spread
Hypotension, pulmonary edema, massive bacteremia, acute fatal toxic shock
May have prolonged incubation period
Fatal if untreated

A

inhalation anthrax

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12
Q

What specimen do you collect to diagnose bacillus anthrax?

A

blood, material from eschar

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13
Q

What does a direct examination show if you are looking at bacillus anthrax?

A

gram stain of blood often positive

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14
Q

How will you culture bacillus anthrax?

A

blood agar

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15
Q

What will the lab identify on bacillus anthrax?

A

Gram-positive bacillus in chains
Capsule by negative stain
Identification by PCR and other specialized tests
Key role for the Laboratory Response Network

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16
Q

anthrax is primarily a disease of (blank)

A

herbivores

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17
Q

Is anthrax communicable?

A

no (ie not contagious)

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18
Q

How are humans normally infected with anthrax?

A

by exposure to animals or animal products e.g. woolsorters disease

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19
Q

What is the vaccine for humans with anthrax?

A

AVA (acelluar vaccine adsorbed)

Efficacy is shown in woolsorters disease, many problems

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20
Q

How do you vaccinate animals with anthrax?

A

live vaccine

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21
Q

How do you treat anthrax?

A

Ciprofloxacin

potential for mAbs to PA

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22
Q

How can you prophylacticly treat exposed individuals?

A

ciprofloxacin or doxycycine for 40 days

vaccination with AVA

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23
Q 
What is this:
gram positive bacillus
anaerobic
spore-formers
ubiquitous in soil, water sewage
normal flora of GI tract of man and animals
prodcue numerous toxins
A

clostridium spp.

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24
Q

Does C. perfrigens grow slow or fast?

A

fast in tissue

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25
Q

What is the pathogenesis of c. perfringens?

A

Alpha toxin

entertoxins

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26
Q

What all does the alpha toxin of C. perfringens do?

A

major lethal toxin of gas gangrene

  • lecithinase
  • lyses numerous host cells
  • massive hemolysis
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27
Q

What does C. perfrings release when undergoing sporulation?

A

enterotoxins

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28
Q

What do the enterotoxins of C. perfringins do?

A

alter membrane permeability-loss of fluids and ions

superantigen

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29
Q

What are the clinical diseases associated with C. perfringins?

A 
Soft tissue infection
Food poisoning (relatively common)
Necrotizing enteritis (rare)
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30
Q

What are the 2 soft tissue infections associated with C. perfringins?

A

Myonecrosis (gas gangrene)

cellulitis

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31
Q

What is this:
Spores or vegetative cells introduced by trauma or surgery
Intense pain
Muscle necrosis, shock, renal failure

A

myonecrosis (gas gangrene) caused by C perfringins

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32
Q

What is this:
Follows ingestion of contaminated meat
Abdominal cramps, watery diarrhea
Due to enterotoxin production in intestine

A

Food poisoning-relatively common

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33
Q

What is this:
Follows ingestion of contaminated pork with sweet potatoes
Necrotizing destruction of jejunum
Due to beta toxin

A

necrotizing enteritis

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34
Q

where do you get the specimens to diagnose C perfringens?

A

fluids from site

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35
Q

Can you directly exam c perfringins and how?

A

yes-gram positive rods

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36
Q

How can you culture C perfringins?

A

rapid anaerobic growth on agar or blood culture broth

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37
Q

If you have food poisoning, how can you tell if it was caused by c. perfringins?

A

distinguish infection from colonization

immunoassay fro enterotoxin in stool

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38
Q

Where do you find C. perfringins?

A
  • ubiquitous in soil, water, and human GI tract

- traumatic injury followed by contamination with spores

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39
Q

How do you treat soft tissue infections caused by c perfringins?

A

rapid treatment s critical to outcome-treated mortality is 40-100%
surgical debridement as needed
High dose penicillin and clindamycin
prevent by proper wound care

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40
Q

How do you treat food poisoning caused by c. perfrinigns

A

antibiotics not effective, symptomatic treatment

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41
Q

What is this:
weakly gram negative, motile, spirochete.
Complex nutritional requirements; can be grown in culture. Several species can cause disease.

A

B. burgdorferi (only species in north america)

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42
Q

Describe the early localized infection phase of lyme disease

A

incubation period 3-30 days after bite of hard shelled tick. Characteristic skin lesion (erythema migrans) at site of initia infection -80% of patients

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43
Q

Describe the early disseminated disease?

A

days to weeks after onset of erythema migrans
multiple secondary annular skin lesions
fatigue, arthritis (60%), myalgia, cardiac dysfunction (20%), neurologic signs (10-15%)

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44
Q

Describe the late infection

A

Months after initial infection
Untreated or inadequately treated patients
More extensive arthritis, chronic skin involvement (seen more in Europe), chronic neurological symptoms

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45
Q

What is this:

symptoms similar to chronic fatigue syndrome or fibromyalgia

A

post-lyme disease syndrome

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46
Q

Found in lyme disease,
3-30 day incubation after infection
Most patients with chronic disease never remember lesion

What am I talking about?

A

erythema migrans

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47
Q

What is this:
Bluish-red skin lesions
Late, disseminated disease
More common in Europe

A

Acrodermatitis chronica atrophicans (also found in lyme disease)

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48
Q

What is the pathogenesis of the clinical features of lyme disease?

A

direct consequence of microbial growth and immune response

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49
Q

What is the clinical case definition of lyme disease?

A 
Erythema migrans (~5 cm)
At least one late manifestation (musculoskeletal, CNS or cardiovascular) plus laboratory confirmation
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50
Q

How should you lab test for lyme disease?

A

antibody detection (elisa first then western blot)

51
Q

When does IgM peak for lyme disease?

A

after 6-8 weeks

52
Q

When does IgG peak for lyme disease?

A

after 4-6 months and persists during late disease

53
Q

What is the vector for lyme disease?

A

hard ticks (Ixodes)- species varies with location

54
Q

What is the most common vector-borne disease in U.S and europe?

A

hard ticks

55
Q

(blank) stage of hard ticks causes greater than 90% of cases

A

nymph

56
Q

When do you most commonly get lyme disease?

A

May-September (when nymph stage is most active)

57
Q

What are the resevoir hosts for lyme disease?

A

white footed mouse (host larval and nymph forms)

White-tailed deer-host of adult ticks

58
Q

What are the regional foci for lyme disease?

A

Northeast and mid-atlantic states, upper midwest and pacific west

59
Q

How do you control lyme disease?

A

avoid bites

control resevoir hosts

60
Q

How do you treat early disease form of lyme disease?

A

doxycycine is drug of choice; alternatives-amoxicillin, cefuroxime or erythromycin

61
Q

How do you treat recurrent arthritis or central or peripheral nervous system disease caused by lyme disease?

A

IV ceftriaxone; alternatives-cefotaxime or doxycycline

62
Q

How do you treat chronic or post-lyme disease syndrome

A

no treatment, just treat symptoms

63
Q

What is this:
Gram-negative rods
Aerobic
Obligate intracellular parasites – grow only in cytoplasm of eukaryotic cells
Maintained in animal and arthropod reservoirs and transmitted by arthropod vectors
Humans are accidental hosts

A

Ricketssia

64
Q

What is the pathogenesis of RMSF?

A

-replicates in cytoplasma and nucleus of endothelial cells, -vasculitis due to endothelial cell damage and leakage of blood vessels

65
Q

What are the clinical manifestations of the disease?

A

7-day incubation period after tick bite
-high fever, headache, malaise
-macular rash, centripetal spread, evolve to “spotted” or petechial form
-

66
Q

What are complications that can occur with RMSF?

A

pulmonary, CNS, renal or cardiac abnormalities

67
Q

Death may occur in RMSF within (blank) days- this is a potentially serious infection.

A

7-15

68
Q

How do you lab diagnose RMSF?

A

immunofluorescence staining of biopsy tissue
Culture-done in tissue culture or embryonated eggs
antibody detection

69
Q

What are the antibody detection RMSF laboratory tests?

A

Weil-Felix test

indirect immunoflourescence

70
Q

What is this:
Detects antibodies that cross-react with a Proteus antigen
No longer recommended – lacks sensitivity and specificity

A

Weil-Felix test

71
Q

What is this:
Detects antibodies against outer membrane protein and LPS
LPS shared across rickettsial species

A

Indirect immunofluorescence

72
Q

(blank) are the principle resevoir and vector for RMSF

A

ticks

73
Q

When do most RMSF infections occur?

A

april to september when ticks are most active

74
Q

Where do you find RMSF?

A

throughout US

mostly south and east

75
Q

What is the treatment for RMSF?

A

doxycycline is drug of choice

EARLY TREATMENT is critical. should start treatment if RMSF is even just suspected

76
Q

What are three other rickettsial infections other than ricketssia ricketssi?

A

Orientia tsutsugamushi
Rickettsia prowazekii
Rickettsia typhi

77
Q

What is this:
Reservoir – mites (chiggers) and wild rodents; vector – mites
Japan, eastern Asia, northern Australia
Abrupt onset, fever, headache, myalgias, maculopapular rash

A

Orientia tsuttugamushi-scrub typhus

78
Q

What is this:
Reservoir – humans; vector – human body louse
Worldwide distribution; crowded, unsanitary conditions; war, famine
100,000 cases during civil war in 1997 in Burundi
Killed 700,000 of Napoleon’s troops during Russian campaign
Abrupt onset, fever headache, myalgias, macular rash

A

Ricketssia prowazekki-edemic typhus

79
Q

What is this:
Reservoir – wild rodents; vector – flea
Worldwide distribution
Gradual onset, fever, headache, myalgias, maculopapular rash

A

Rickettsia typhi (murine endemic typhus)

80
Q 
What is this:
Gram-negative, facultatively anaerobic rod with bipolar staining
Member of Enterobacteriaceae
Zoonotic disease
Enormous historic importance
A

Y. pestis

81
Q

What is this:
Follows bite by flea; incubation period ≤ 7 days
High fever; painful bubo (inflammatory swelling of lymph nodes)
High mortality if untreated (75%)

A

Bubonic plague

82
Q

What is this:
Follows aerosol exposure; short incubation period (2-3 days)
Initially, headache, malaise and pulmonary signs
Highly infectious; rapidly fatal if untreated

A

Pneumonic plague

83
Q

What specimens do you grab for lab diagnosis of Y. pestis?

A

blood, bubo aspirate, sputum, others

84
Q

How do you diagnose the plague via lab?

A

lab identification by standard microbiological techniques (easily misidentified by automated ID systems)

85
Q

the plague is (blank) in the US

A

rare

86
Q

What are the natural hosts for Y. pestis?

A

rats, squirrels, rabbits, etc.

87
Q

What is the transmission of Y. pestis?

A
  • Flea bite
  • direct contact w/ infected tissues
  • person to person (pneumonic)
88
Q

How do you prevent plague?

A

reservoir and vector control

potential biothreat

89
Q

How do you treat plague?

A

streptomycin is drug of choice

doxycycline is best alternative

90
Q

what are these:

dermatophytosis, sporotrichosis and mycetoma

A

fungal infections of skin and subcutaneous tissue

91
Q

(blank) are molds that invade stratum corneum of skin or other keratinized tissues

A

dermatophytes

92
Q

What are the major genera of dermatophytosis?

A

Trichophyton, microsporum and epidermophyton

93
Q

What are the major genera of dermatophytosis?

A

trichophyton
microsporum
epidermophyton

94
Q

What is this:
itching, cracked skin, scaling between toes
T. rubrum, T. interdigitale, sometimes E. floccosum

A

Tinea pedis (athletes foot)

95
Q

What is this:
jock itch-groin infection
T. rubrum most common

A

Tinea cruris

96
Q

What is this:
Infection of arms, legs or trunk
Differential diagnosis – eczema, psoriasis
T. rubrum, M. canis, M. gypseum

A

Tinea corpis

97
Q

What is this:

  • scalp ringworm
  • scaling of scalp, itching, hair loss
  • numerous species of trichopyton and microsporum
A

Onchomycosis

98
Q

What is the natural habitat for dermophytosis?

A

anthropophilic species
zoophilic species
geophilic species

99
Q

Which species of dermatophytes cause this:

chronic, relatively noninflammatory infections; difficult to cure

A

anthropophilic

100
Q

What species of dermatophytes cause this:

profound host reaction, highly inflammatory lesions, respond well to therapy

A

zoophilic and geographic species

101
Q

How do you diagnose dermatophytes?

A

direct examianation of scraping or clippings

102
Q

How do you do a scrapings or clippings to diagnose dermatophytes?

A

take samples from edge of skin lesions or nails or hair

  • dissolve tissue with KOH
  • examine microscopically for hyphae
103
Q

What do you do with the scrapings of dermatopytes?

A

culture on mycologic media and it takes 7-28 days

104
Q

How do you treat dermatophytes?

A
  • topicals for localized infection

- oral agents for more extensive infection or infection of hair or nails

105
Q

What are the topics used for localized infection for dermatophytes?

A

azoles or terbinafine

106
Q

What are the oral agents used for extensive infection or infection of hair or nails for dermatophytes?

A

itraconazole, fluconazole, terbinafine, griseofulvin

107
Q

What is the etiology of pityriasis (tinea) versicolor?

A

Malassezia furfur, budding yeast like cells

108
Q

What are the clinical syndromes associated with pityriasis (tinea) versicolor?

A

small hypo or hyperpigemented macules
hypo-pigmented in dark skinned individuals; blocks melanin production
light-skinned indivuduals (pale to pale brown)

109
Q

how do you use the lab to diagnose Pityriasis (tinea) versicolor?

A

KOH mount of skin scrapings

spaghetti and meatballs appeaerance-yeasts plus hyphal elements

110
Q

What is the epidemiology of pityriasis (tinea) vesicolor?

A

worldwide

Most prevalent in tropical or subtropical regions ( may infect up to 60% of population)

111
Q

How do you transmit Pityriasis (tinea) versicolor?

A

man to man transmission

112
Q

What is the treatment for pityriasis (tinea) versicolor?

A
  • topical azoles or selenium sulfide shampoo

- oral azoles for more widespread infection

113
Q

What is the fungus that causes lymphocutaneous sporotrichosis?

A

sporothrix schenckii (dimorphic fungus)

114
Q

What are the clinical features of lymphocutaneous sporotrichosis?

A

classic infection follows traumatic incoulation of soil or vegetable matter; termed “rose gardener’s disease”

  • small nodule at site of inoculation; may ulcerate
  • secondary nodules along lymphatics that drain primary lesion
115
Q

What is the epidemiology of lymphocutaneous sporotrichosis?

A
  • worldwide distribution
  • grows on soil, plants and decaying vegetation
  • considered an occupational disease; florists, rose gardeneres, greenhouse workers
116
Q

How do you use the lab to diagnose sporotrichosis?

A
  • culture of infected pus or tissue

- budding yeast at 35 degrees celcius, mold at 25 degrees celcius

117
Q

How do you treat sporotrichosis?

A

itraconazole

118
Q

What is the etiology of eumycetoma?

A

multiple filamentous fungi (curvularia, fusarium, exophiala)

119
Q

What is this:
Localized, chronic, granulomatous process involving cutaneous and subcutaneous tissues
Multiple granulomas and abscesses containing masses of hyphae
Abscesses drain through skin; may extrude granules of hyphae
May destroy muscle and bone locally

A

Mycetoma

120
Q

How do you use the lab to diagnose mycetoma?

A

microscopy (demonstrates grains or granules in exudate) and culture

121
Q

What is the epidemiology of mycetoma?

A
  • Tropical areas with low rainfall
  • Implantation of fungi from environmental sources
  • Specific agents vary by region
122
Q

What is the treatmet for mycetoma?

A
  • poor response to antifungals

- amputation is only definitive treatment

123
Q

A patient has been exposed to spores of Bacillus anthracis following a deliberate terrorism attack. The patient presents with a “flu-like” illness characterized by low-grade fever, malaise, fatigue and myalgias. What would be the best specimen to confirm a diagnosis of inhalational anthrax?
A) Throat swab
B) Nasopharyngeal swab
C) Blood culture
D) Stool sample and rectal swab
E) Environmental sample at the site of spore release

A

C) Blood culture

Block 7 Week 2 (10 decks)

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