Kozel: Skin and Soft Tissue Infections II Flashcards

1
Q

Gram positive bacillus
Aerobic and facultative anaerobe
Spore former
200 species

A

Bacillus spp.

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2
Q

What is unique about the capsule of Bacillus spp? What is its role?

A

it is a polypeptide (poly-D-glutamic acid) capsule instead of a polysaccharide capsule;
it is antiphagocytic and induces protective immunity

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3
Q

What type of toxin is associated with Bacillus spp?

A

A-B type toxin

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4
Q

What are the three antigens on the Bacillus toxin?

A

Protective antigen - induces protective immunity
Lethal factor - produces cell death
Edema factor - produces edema

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5
Q

Follows inoculation with spores

Painless papule progresses to ulcer to necrotic black eschar (malignant pustule)

A

cutaneous anthrax

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6
Q

Follows ingestion of spores

Local infection that may spread to systemic disease

A

GI anthrax

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7
Q

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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8
Q

What type of specimen would you obtain for Bacillus infection?

A

blood or material from eschar

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9
Q

What would you see on the blood culture of Bacillus spp?

A

gram-positive rods in chains, capsule can be seen via negative stain

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10
Q

Bacillus infection is primarily a disease of (blank); humans are normally infected by exposure to (blank) or (blank) products

A

herbivores; animals; animal

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11
Q

Is there a human vaccine for anthrax?

A

yes, there is also a live vaccine for animals

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12
Q

What is the treatment for antrax poisoning?

A

ciprofloxacin
there is also a potential for monoclonal antibodies to protective antigen

**can use prophylaxis for exposed individuals or vaccinate with AVA

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13
Q
Gram-positive bacillus
Anaerobic
Spore-formers
Ubiquitous in soil, water, sewage
Normal flora of GI tract of man and animals
Produce numerous toxins
A

Clostridium spp.

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14
Q

What is the major lethal toxin produced by C. perfringens in gas gangrene? What does this toxin do?

A

alpha toxin; lecithinase, lyses numerous host cells and causes massive hemolysis

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15
Q

This is another toxin released by C. perfringens when cells undergo sporulation
Altered membrane permeability – loss of fluids and ions
Superantigen

A

enterotoxin

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16
Q

What 3 diseases can be caused by Clostridium perfringens infection? What are the symptoms of each?

A

Cellulitis and gas gangrene: spores introduced by trauma or surgery, causes intense pain, muscle necrosis, shock and renal failure

Food poisoning: ingestion of contaminated meat leads to ab cramps and watery diarrhea

Necrotizing enteritis: ingestion of contaminated meat leads to necrosis of the small intestine

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17
Q

Where is Clostridium perfringens found?

A

ubiquitous in soil, water, and human GI tract

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18
Q

What is the treatment for C. perfringens?

A

for soft tissue infections: rapid treatment necessary, surgical debridement as needed and high dose penicillin + clindamycin

for food poisoning: antibiotics not effective, symptomatic treatment

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19
Q

Weakly gram-negative, motile, spirochete

Complex nutritional requirements; can be grown in culture

A

Borellia burgdorferi

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20
Q

What occurs during the early localized infection in Lyme disease? Early disseminated disease? Late in infection?

A

early localized infection: incubation period of 3-30 days, characteristic skin lesion (erythema migrans) at site of initial infection

early disseminated disease: days to weeks after onset of erythema migrans, multiple secondary annular skin lesions, fatigue, arthritis, myalgia, cardiac dysfunction

late infection: months after initial infection, more extensive arthritis, chronic skin involvement and neuro symptoms

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21
Q

What occurs with post-Lyme disease syndrome?

A

symptoms similar to chronic fatigue syndrome or fibromyalgia

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22
Q

What is acrodermatitis chronica atrophicans?

A

bluish-red skin lesions

occur in late, disseminated stage of lyme disease

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23
Q

When diagnosing Lyme disease, what do you look for?

A

erythema migrans (5cm)

or

at least one late manifestation (musculoskeletal, CNS, or cardiovascular) + lab confirmation

24
Q

What is the lab test of choice for diagnosing Lyme disease?

A

antibody detection
IgM peak after 6-8 weeks
IgG peak after 4-6 months

25
Q

What is the vector for Lyme disease? What is the reservoir?

A

hard ticks (nymph stage causes >90% of cases); white footed mouse or white-tailed deer

26
Q

Where is Lyme disease seen in the US?

A

NE and mid-Atlantic states, upper midwest and Pacific west

27
Q

What is the drug of choice for Lyme disease?

A

doxycycline for early disease

IV ceftriazone for recurrent arthritis or CNS/PNS disease

28
Q

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

Rickettsia

29
Q

Rickettsia replicates in cytoplasm/nucleus of (blank) cells; causes (blank) due endothelial cell damage and leakage of blood vessels

A

endothelial; vasculitis

30
Q

How does Rickettsia present clinically?

A

7 day incubation after bite
high fever, headache, malaise
macular rash w centripetal spread which becomes petechial
complications include pulmonary, CNS, renal or cardiac abnormalities

31
Q

What are two methods of antibody detection for Rickettsia?

A

Weil-Felix test: detects antibodies that cross-react with a Proteus antigen

Indirect immunofluorescnece: detects ab against outer membrane protein and LPS**

32
Q

What is the principal reservoir and vector for Rickettsia? Where is it found?

A

ticks; throughout the US

33
Q

Treatment for Rickettsia?

A

doxycycline

**early treatment is critical

34
Q

What do the following cause?

Orientia tsutsugamushi?
Rickettsia prowazekii?
Rickettsia typhi?

What symptoms are common to all?

A

scrub typhus *sudden onset
epidemic typhus *sudden onset
murine endemic typhus *gradual onset

**fever, headache, myalgia, maculopapular rash

35
Q

Gram-negative, facultatively anaerobic rod with bipolar staining
Member of Enterobacteriaceae
Zoonotic disease
Enormous historic importance

A

Yersinia pestis

36
Q

How does bubonic plague present clinically? How is it transmitted?

A

incubation period of <7 days after FLEA BITE; high fever, painful inflammatory swelling of lymph nodes; high mortality if untreated

37
Q

How does pneumonic plague present clinically? How is it transmitted?

A

incubation period of 2-3 days after AEROSOL EXPOSURE; initially headache, malaise and pulmonary signs; high mortality in untreated

38
Q

How do you make a lab diagnosis of Yersinia?

A

culture a sample of blood, bubo aspirate, sputum

39
Q

What are the natural hosts for Yersinia pestis? How is it transmitted?

A

rats, squirrels, rabits; flea bite transmission

40
Q

What is the drug of choice for plague?

A

streptomycin

**doxycycline could be used alternatively

41
Q

molds that invade stratum corneum of skin or other keratinized tissues

A

dermatophytes

42
Q

3 major genera of dermatophytes

A

Trichophyton
Microsporum
Epidermophyton

43
Q

What are the following?

Tinea pedis
Tinea cruris
Tinea corporis
Tinea capitis
Onchomycosis
A
Tinea pedis: athletes foot
Tinea cruris: jock itch
Tinea corporis: infection of arm, legs, trunk
Scalp ringworm
infection of nails
44
Q

There are anthrophilic, zoophilic, and geophilic species of dermatophytes. Which species cause chronic, relatively noninflammatory infections and are difficult to cure? Which species cause profound host reaction, high inflammatory lesions, and respond well to therapy

A

anthropophilic; zoophilic/geophilic

45
Q

How do you diagnose dermatophyte infection?

A

take a sample of the scraping or clipping and dissolve the tissue with KOH, examine microscopically for hyphae

you can also culture the scrapings, but it takes weeks

46
Q

What do you use to treat dermatophytes?

A

topicals for locolized infections, azoles or terbinafine

oral agens for more extensive infection, itraconazole, fluconazole, terbinafine

47
Q

What is pityriasis (tinea) versicolor?

A

it is caused by Malassezia furfur (budding yeast like cells) which cause small hypo or hyper-pigmented macules (depending on skin color)

48
Q

What does pityriasis versicolor look like on a KOH mount?

A

spaghetti and meatballs

yeast + hyphal elements

49
Q

How do you treat pityriasis versicolor?

A

topical azoles or selenium sulfide shampoo

oral azoles for widespread infection

50
Q

Classic infection follows traumatic inoculation 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

A

Lymphocutaneous sporotrichosis

51
Q

What is the dimorphic fungus responsible for lymphocutaneous sporotrichosis?

A

Sporothrix schenckii

52
Q

Why is lymphocutaneous sporotrichosis considered “rose gardener’s disease?”

A

because sporothrix schenckii grows on soil, plants, and decaying vegetation

**seen w florists, rose gardener’s, greenhouse workers

53
Q

What do you use to treat sporotrichosis?

A

itraconazole

54
Q

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

55
Q

What causes mycetoma?

A

multiple filamentous fungi: Curvularia, Fusarium, Exophiala, etc

56
Q

What will you see in the exudate of mycetoma?

A

grains or granules

57
Q

What is the only definitive treatment for mycetoma?

A

amputation