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FTCM > L26, L29, L31, L33, L35, L37- Skin, Bone, Muscle Infections > Flashcards

L26, L29, L31, L33, L35, L37- Skin, Bone, Muscle Infections Flashcards

1
Q

what are the 4 ways to classify skin infections

A
  • Etiology: virus, bacteria, fungi, parasite
  • Type: primary, secondary, systemic, scarlet fever syndrome
  • Depth: (sub-)cutaneous
  • Location: keratinized epi., epidermis, hair follicles, dermis, sebaceous glands, muscle, bone
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2
Q

list the 4 categories of medical mycoses

A

1) cutaneous fungi
2) subcutaneous fungi
3) systemic fungi
4) opportunistic fungi

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3
Q

cutaneous fungi are transmitted via (1) and the most relevant examples include (2)

A

1- contact, trauma

2- dematophytes, (other) tineas

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4
Q

subcutaneous fungi are transmitted via (1) and the most relevant examples include (2)

A

1- contact, trauma

2- Sporothrix schenckii, Dematiaceous fungi

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5
Q

systemic fungi are transmitted via (1) and the most relevant examples include (2)

A

1- respiratory

2- blastomyces dermatitidis, coccidiodes immitis, histoplasma capsulatum, paracoccidiodes brasiliensis

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6
Q

opportunistic fungi are transmitted via (1) and the most relevant examples include (2)

A

1- variable

2- aspergillus, candida, cryptococcus neoformans

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7
Q

the most common of the (1) dematophytes is (2)

A

1- anthrophophilic

2- trichophyton rubrum

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8
Q

(T/F) Epidermophyton is only found as a microconidia

A

F- only found as macroconidia (‘club-like’ or ‘beaver tail’ organization)

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9
Q

compare macro-/micro-condidia

A

-asexual, non-motile spores
-Micro: small, single cell, ‘bird on a wire’ organization
-Macro: large, single/multiple cells, ‘pencil shaft’ organization
(Note- a bit different appearance with Microsporum fungi)

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10
Q

Dermatophytic fungi utilize (1) in the (2) skin layers for energy/nutrition and the hyphae will slowly extend (3). Classical presentation of this fungal infection is as follows: (4).

A

1- keratin
2- keratinized layers of skin
3- outwards (central clearance, appears as ring shape = ‘ringworm’)
4- gradual enlarging. pink/red, annular (O-shape) patches/plaques + raised scaly borders extending peripherally with clear center

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11
Q

name the term for tinea (dermatophyte or ‘ringworm’ infections) of the following areas:

(1) head
(2) body
(3) groin
(4) feet
(5) nails

A 
Tinea...
1- capitis
2- corporis
3- cruris ('jock-itch)
4- pedis
5- unguium
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12
Q

Dermatophytic fungi are transmitted via (1), especially in (2) type of areas. It is (highly/poorly) transmissible and the best place to sample the lesion is from its (center/periphery) because of (5).

A

1- direct contact (soil, animal, human, fomite)
2- warm, damp conditions
3- highly transmissible
4- periphery
5- centrifugal expansion as mycelia extend (center –> peripheral expansion)

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13
Q

describe the 3 terms used to explain the origin of dermatophytic fungi

A
  • geophilic, contaminated soil
  • zoophilic, animals
  • anthropophilic, humans (direct contact or fomites)
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14
Q

to culture dermatophytic fungi, (1) samples are taken and placed on (2) agar

A

1- hair/skin/nail scrapings

2- Mycosel agar

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15
Q

list the 3 steps of dermatophytic fungi pathogenesis

A

1) initial infection
2) expansion of virulence factors
3) contribution of host immune response

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16
Q

describe the initial infection of dermatophytic fungi pathogenesis

A

(step 1)

  • exposure via contact / implantation
  • fungal attachment
  • dimorphic switch (some)
  • hyphae extension (enzymes ready for release)
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17
Q

describe how dermatophytic fungi enable expression of virulence factors

A

(step 2 of its pathogenesis)

  • attachment
  • utilization of nutrients –> keratinases, proteinases (melanin in fungal cell walls => specific color)
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18
Q

why are nails susceptible to / favor chronic infections

A

they lack defenses

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19
Q

describe how dermatophytic fungi contribute to host immune response

A

(step 3 of its pathogenesis)

  • response to metabolic by-products
  • affected by host (age, co-morbidities, etc.)
  • affected by source of fungus (where is it from)
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20
Q

____ is the generic name for darkly pigmented fungi associated with skin infections

A

dematiaceous

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21
Q

list the 3 common non-dermatophytic cutaneous fungal infections

A
  • tinea versicolor
  • tinea nigra
  • white/black piedra
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22
Q

tinea versicolor is caused by (1) and presents as (2)

A

(non-dermatophytic fungal infection)

  • malassezia spp.
  • hyper-/hypo-chromatic plaques
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23
Q

tinea nigra is caused by (1) and presents as (2)

A

(non-dermatophytic fungal infection)

  • hortaea werneckii
  • palms with dark plaques
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24
Q

___ is fungal infections of scalp hairs

A

(non-dermatophytic fungal infection)

white or black piedra: forms concretions on hair shaft (colored)

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25
Q

Malassezia furfur causes (1). It comes in the (2- include description) form or (3) form.

  • (4) is one possible classifying symptom with (5) as its mechanism
  • (6) is the other possible classifying symptom with (7) as its mechanism
  • Note, (5)/(7) are proposed mechanisms
A

(non-dermatophytic fungal infection)
1- tinea versicolor
2- lipophilic yeast: on skin flora in areas higher in lipids (ant. back and chest)
3- yeast / hyphal form
4/5- hypopigementation: malassezia induces melanocyte apoptosis
6/7- hyperpigmentation: stratum corneum thickening, melanocyte enlargement, inflammation

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26
Q

Malassezia furfur is found in (1) climates as (2) and (3) are key environmental factors. It mainly affects people of (4) age.

A

1- hot, humid
2/3- temperature, humidity (among others)
4- all ages, people in 20s/30s the most

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27
Q

describe clinical presentation of tinea versicolor (malassezia furfur)

A
  • affects seborrheic areas: trunk, back, proximal limbs
  • confluent (merging) plaques
  • covered by fine scales
  • well-demarcated
  • non-pruritic
  • hypo-/hyper-pigmented plaques (both can be present simultaneously)
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28
Q

describe diagnosis of tinea versicolor (malessezia furfur)

A
  • it requires lipids for growth (mostly – whys its associated with trunk/back/proximal limb body parts)
  • KOH preparation => short hyphae + thick-walled round spores (‘spaghetti (hyphae) and meatballs (spores)’ appearance)
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29
Q

Hortaea werneckii causes (1) by infecting (2). It is usually found in (3) geographic areas. Clinical presentation includes (4). Diagnosis requires (5).

A

(non-dermatophytic fungal infection)
1- tinea nigra
2- superficial infection of stratum corneum via direct inoculation
3- southern USA, topics, subtropics
4- flat, brown to black darkenings (melanin-like pigment in hyphae) with irregular contours usually on palms and occasionally on soles
5- skin scraping culture + microscopic examination

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30
Q

Symptoms of fungal nail infections are (1).

  • when caused by dermatophytes, it is termed (2)
  • when caused by non-dermatophytes, it is termed (3) [include fungi]
A

1- cracked, brittle, discolored nails pulling away from nail bed

2- tinea unguium (majority of nail infections, tinea pedis if feet are involved and extend to nails)
3- onychomycosis: aspergillus spp, cephalosporium spp, fusarium oxysporum, scopulariopsis brevicaulis

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31
Q

Erythrasma is caused by (1) causing (2)

A
  • corynebacterium minutissimum

- scaly plaques (coral-red under UV light)

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32
Q

Corynebacterium minutissimum causes (1). It is a Gram(+/-) (bacillus/cocci), and mainly affects (4) people.

A

1- erythrasma
2/3- Gram+ bacillus
4- adults: diabetics and or those living in tropics

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33
Q

describe the pathogenesis and requirements for diagnosis of Erythrasma (corynebacterium minutissimum)

A
  • bacterial invasion of upper third of stratum corneum
  • favors heat and humid conditions: armpit, foot, groin, skinfolds

Dx: glows coral-red under UV light — secondary to porphyrin production (heme metabolism)

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34
Q

Cutaneous Anthrax is caused by (1) causing (2). (3) and (4) are other types of anthrax infection.

A

1- bacillus anthracis
2- coal-black eschar (black patch of dead tissue)
3/4- GI anthrax, inhalation/pulmonary anthrax

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35
Q

Bacillus anthracis causes (1). It is a Gram(+/-) bacteria that can take up the (3) form. It usually infects (4), but accidental exposure can cause human infections. Skin is affected by (5).

A

1- anthrax: cutaneous (most common), GI, inhalational/pulmonary
2- Gram+
3- endospore
4- sheep, cattle
5- endospores enter thru minor cut => ‘coal-black’ eschar

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36
Q

Bacillus anthracis (anthrax) is most dangerous when it enters through (1). In (1) it produces (2) causing (3) and it produces (4) which affects (5) directly. It has (6) and (7) as resistant / virulence factors. The end result is death by (8).

A

1- lungs (inhalation; also enter skin and ingested)
2- edema toxin (EF- edema factor)
3- vascular leakage + pulmonary/peripheral edema => hypovolumia
4- lethal toxin
5- heart => dec SV –> dec CO
6/7- PA- protective Ag (to activate EF/LF), capsule (glutamic acid - antiphagocytic)
8- hypotension + dec CO => hypotension ——> death

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37
Q

(1) are the parasites that cause cutaneous (epidermal) infections. (2) is the most common species causing (3). They are usually found in (4) locations.

A

1- hookworms / nematodes (roundworms)
2- ancylostoma
3- cutaneous larva migrans
4- sandy beaches, sandboxes, under buildings – warm/moist soils/climates (L3 larvae can survive 3-4 wks)

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38
Q

Cutaneous Larva Migrans is caused by (1) with (2) as symptoms

A

1- ancylostoma (most commonly, otherwise just hookwork species - nematodes)
2- serpiginous erythematous track w/ intense itching, mild swelling

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39
Q

describe life cycle of hookworms

A

(nematodes)

1) eggs in feces (via cats/dogs)
2) rhabditiform larva hatches
3) develops into filariform larva (in environment, L3 stage)

4) ingested by cats/dogs
5) adult form GI intestine –> eggs into feces (1)
OR
6) human contact with filariform (L3) in environment (3) [note dead end infection, die w/in 5-6 wks]

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40
Q

describe the clinical presentation of cutaneous larva migrans (hookworms / ancylostoma)

A
  • 1-5 days after skin penetration (via hyaluronidase) => creeping eruption
  • incubation period >1 mo
  • Serpiginous, Erythematous track
  • associated mild swelling (inflammatory rxn), intense itching
  • > 70% cases affect feet / lower extremities (walking barefoot)
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41
Q

list the general categories that define the risk factors of skin and soft tissue infections

A
  • Host Factors: diseases (DM) or immune status (immunocompromised)
  • Specific Exposure Types: animals, bites, insects
  • Water/Outdoor exposure
  • Drug use
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42
Q

S. Aureus is a Gram(+/-) (non-/motile) (bacillus/cocci). It is special because it is also (4) positive. It is apart of the normal flora on the (5) and can cause (6) type of infections. It has the following three patterns in healthy people: (7).

A

1/2/3- Gram+, nonmotile cocci
4- catalase+
5- anterior nares
6- superficial to life-threatening infections
7- i) persistent carriers (20%), ii) intermediate carriers (60%), iii) never colonized (20%)
[grape-like arrangement on microscopy]

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43
Q

what are the 2 predominant fungi present on normal skin flora

A
  • malassezia spp.

- candida albicans

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44
Q

_______ is the key differentiating feature of S. aureus from other Staph. spp.

A

coagulase+ (also Gram+ cocci, catalase+, nonmotile)

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45
Q

Staph. infections are either (1)-mediated or (2)-mediated

A
  • inflammatory-mediated

- toxin-mediated

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46
Q

list the 4 complications of inflammatory-mediated Staph. infections

A
  • infective endocarditis (acute): due to fibrin-platelet mesh
  • abscesses / mastitis: due to coagulase
  • impetigo**: due to the range of virulence factors and immune response
  • osteomyelitis
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47
Q

list the 3 complications of toxin-mediated Staph. infections

A
  • scalded skin syndrome*: due to exfoliative toxin
  • toxic shock syndrome*: caused by TSST-1
  • food poisoning: ingested of pre-formed enterotoxins A-E
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48
Q

list the virulence factors of S. aureus and the two general divisions

A

Secreted factors: i) enzymes- coagulase, staphlokinase; ii) toxins: TSST-1, enterotoxins, α-hemolysin; iii) invasins: panton-valentine leukocicdin

Membrane Bound factors: Adhesins- collagen binding protein, fibronectin binding protein, elastin binding protein

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49
Q

adhesins (used for bacterial attachment) and (1) are membrane bound virulence factors of S. aureus, and (1) has a (2) function

A

Protein A: binds Fc of IgG, blocks Fc binding to phagocytes – interferes with opsonophagocytic killing

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50
Q

(S. aureus virulence factor) ______ is a pore-forming protein that lyses cell membrane of neutrophils

A

Panton-Valentin Leukocidin- note overall role is unclear

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51
Q

(S. aureus virulence factor) ______ is a pore-forming toxin that causes cell death and is responsible for β-hemolysis on blood agar

A

α-hemolysin/α-toxin

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52
Q

(S. aureus virulence factor) ______ is a superantigen toxin secreted in food

A

enterotoxins A-E (they cause food poisoning upon ingestion)

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53
Q

(S. aureus virulence factor) (1) and (2) are toxins responsible for SSS/TSS (indicate the superantigen)

A

Exfoliative toxin: scalded skin syndrome

TSST-1: toxic shock syndrome (superantigen)

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54
Q

(S. aureus virulence factor) ______ is an enzyme that converts plasminogen to plasmin –> cleavage of fibrin blood clots –> dissemination

A

staphylokinase

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55
Q

(S. aureus virulence factor) ______ is an enzyme that affect plasma and it a general differentiating factor for Staph. species

A

coagulase- note overall role is unclear

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56
Q

Impetigo is a (inflammatory/toxin) mediated S. aureus infection. It comes in two types, (2), and two different (symptomatic) forms, (3). It mainly affects (4) people.

A

1- Both (inflammatory- nonbullous, toxin- bullous)
2- primary (direct skin invasion) or secondary (infection at minor trauma site)
3- bullous, non-bullous (70%)
4- children (highly infectious- overcrowding, schools, daycares)

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57
Q

______ is a less common cause of impetigo (than S. aureus)

A

Group A β-hemolytic Strep., S. pyogenes (GAS) — associated with post-streptococcal glmerulonephritis
(more likely to cause Ecthyma, a deeper penetrating form of non-bullous impetigo)

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58
Q

Bullous impetigo is a (primary/secondary) infection that commonly affects (2). It has the following symptoms: (3). (4) is a risk with extended infection.

A

1- primary (toxin mediated S. aureus, form of localized SSS)
2- neonates
3- flaccid bullae (fluid filled), sharp margins, non-erythematous, brownish crust
4- SSS (toxin-mediated scalded skin syndrome)

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59
Q

Deeper impetigo is called (1) and is defined with the following features: (2). (3) is a risk with extended infection. It is more commonly caused by (4).

A

1- ecthyma- deeper non-bullous impetigo form (inflammatory mediated, penetrate dermis)
2- hard, crusted sores with underlying ulcer (‘punched-out’); 0.5-3 cm diameter
3- SSS (toxin-mediated scalded skin syndrome)
4- GAS (»> S. aureus)

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60
Q

SSS is a (inflammatory/toxin) mediated S. aureus infection. It has the following clinical manifestation and progression: (2). It mainly affects (3) people. Therefore most people develop (4).

A

(scalded skin syndrome)
1- toxin (exfoliated toxin)
2- fever + widespread skin redness –> fluid filled blisters (24-48 hrs) –> easily ruptured blisters => burn like area
3- children < 5 y/o (neonates)
4- Abs protective against Staph. exotoxins (SSS, TSST-1 lifelong protection since early childhood exposure)

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61
Q

list the steps to pathogenesis of SSS

A

(scalded skin syndrome)

1) S. aureus adheres to living epidermis via desmoglein-1 (Dsg1 of desomosomes, external side of skin)
2) neutrophilic recruitment (internal side of skin)
3) penetration of S. aureus thru neutrophil-created intracellular gap
4) blister expansion by Exfoliative toxin cleavage of Dsg1 in superficial epidermis

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62
Q

describe the people susceptible to TSS and the risk factors

A

-men, children, postmenopausal women
-skin wounds / surgery
-desquamation in 1-2 wks
(used to be associated with superabsorbant tampons)

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63
Q

list the Sxs of TSS

A

(superantigen => toxic shock syndrome- triggers T cell activation/proliferation)

  • sudden high fever
  • hypotension
  • n/v
  • ‘sunburn-like’ rash in palms/soles
  • confusion
  • muscle aches
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64
Q

MRSA is resistant to (1). It is divided into the following two types, (2).

A

(methicillin resistant S. aureus)
1- all penicillins and other β-lactams (cephalosporins)
2- HA and CA (hospital or community acquired)

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65
Q

nosocomial definition

A

hospital related or hospital acquired

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66
Q

CA-MRSA:

  • (1) Sxs
  • (2) SCCmec type
  • (3) PVL (Panton-Valentine Leukocidin) toxin present?
  • (4) risk factors
A

1- SSTI (skin or skin structure infection) + necrotizing pneumonia, sepsis (less common than SSTI)
2- IV, occasionally V
3- >80%
4- contact sports*, crowded/unsanitary conditions, MSM, IV drug use

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67
Q

HA-MRSA:

  • (1) Sxs
  • (2) SCCmec type
  • (3) PVL (Panton-Valentine Leukocidin) toxin present?
  • (4) risk factor
A

1- pneumonia, catheter associated UTIs, bacteremia, SSTI (skin or skin structure infection)
2- I, II, III
3- no
4- hospitalization*, invasive medical device. long-term care facility

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68
Q

list the 4 types of folliculitis (include associated species)

A
  • bacterial folliculitis (S. aureus)
  • hot tub folliculitis (P. aeruginosa)
  • razor bumps
  • malasszia folliculitis
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69
Q

what are the risk factors for folliculitis

A
  • DM, HIV/AIDS (+ other medical conditions??)

- acne/dermatitis

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70
Q

(bacterial) folliculitis is caused by the following: (1)

Its clinical manifestations are (2)

Most affected areas are (3)

A

1- S. aureus (mostly), P. aerugosa (hot tubs), Candida / dermatophytes (malassezia - rarely)
2- thin walled papules / pustules, margin of erythema / inflammation, central hair*, mild discomfort + pruritis = pain
3- posterior neck, occipital scalp, axilla

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71
Q

Psedomonas aeruginosa is a Gram(+/-) (bacillus/cocci), (an-/aerobic), (non-/lactose) fermenting, (non-motile) bacteria. Other distinguishing tests include being positive for (6). They have characteristic (7) pigment and (8) smell.

A

Gram- bacillus (rod), aerobic, non-lactose fermenting, nonmotile, catalase+, oxidase+ bacteria

7- pyocyanin (blue/green) pigment
8- grape-like smell

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72
Q

P. aeruguinosa causes (1), It is found (2) in the environment and has a (3)% mortality rate. It is associated (5) and (6) patients. The major virulence factor is (7). It is has (high/low) antibiotic resistance.

A 
1- folliculitis (bacterial, hot-tub)
2- widespread, although important nosocomial pathogen (immunocomprimised)
3- 40-60%
4- burn wound infections
5- CF or other chronic lung diseases
6- capacity to form biofilms
7- highly
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73
Q

Chromoblastomycosis is caused by (1) causing (2)

A

dematiaceous fungi- slow growing granulomatous infection of the dermis / wart-like lesions with crusting abscesses extending along lymphatics

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74
Q

Dematiaceous fungi are characterized by (1) and cause (2). (2) is described as (3). It is usually found in (4). It progresses by stimulating (5). It is diagnosed by (6) under microscopic observation.

A

1- dark gray or black pigmented conidia / hyphae
2- chromoblastomycosis
3- wart-like lesions w/ crusting abscesses extending along lymphatics
4- tropics, due to bare feet/legs
5- slow fibrotic / granulomatous reaction
6- dark-brown, round fungal cells in leukocytes / giant cells (Muriform cells- yeasts that have stopped budding)

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75
Q

Loa Loa is a (1) microbe that infects people in the (2- include Dx form) form and causes (3). It is transmitted via (4) in (5) areas.

A

1- parasite
2- filiarial larvae form (Dx form is *sheathed microfilarae)
3- loiasis (in dermis/subcutaneous skin)
4- fly vectors (humans are only natural resevoir)
5- wet forested areas of west/central africa

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76
Q

describe the clinical presentation of loiasis

A

(caused by Loa Loa)

  • up to several yrs after infection
  • red itchy (Calabar) swellings on forearms, wrists (maybe face, breasts, legs)
  • fever, irritability

-migrating worm is visible under skin and frequently reaches eyes(subconjunctiva)

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77
Q

River Blindness is caused by (1) causing (2)

A

1- onchocerca volvulus

2- sever sight impairment, maculopapular rash with hyperpigmentation and thinning/wrinkling of the skin

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78
Q

Onchocerca volvulus is a (1) microbe that infects people in the (2- include Dx form) form and causes (3). It is transmitted via (4) in (5) areas.

A

1- parasite
2- filiarial larvae (Dx form is *unsheathed microfilariae)
3- river blindness + skin infection
4- blackfly vector
5- sub-saharan africa, S. america, middle east

79
Q

describe the clinical manifestations of Onchocerca volvulus infection and its diagnostic requirements

A

Sxs: mild maculopapular prutitic rash to chronic form with severe itching, skin hyperpigmentation with thinning and wrinkling, severe vision impairment (river blindness)

Dx: microfilariae seen in skin samples immersed in saline + excised nodules show adult worms

80
Q

Streptococcus are Gram(+/-) (bacillus/cocci) that are classified through (3).

A
  • Gram+ cocci

- Lancefield classification: teichoic acid (cell wall carbohydrate)

81
Q

Relevant groups of Streptococcus species include the following….

A

-GAS: group A, S. pyogenes
-GBS: group B, S. agalactiae
-Non-Lancefield group: S. pneumoniae
(hemolysis on blood agar helps in distinguishing factors)

82
Q

list the 3 types of cellulitis (and their associated microbe)

A
  • GAS cellulitis
  • Erysipelas (superficial): also GAS, young children and elderly
  • Erysipeloid: associated with saltwater fish, shellfish, meat, poultry (non-GAS)
83
Q

list some risk factors for cellulitis

A
  • middle-aged and the elderly
  • obesity
  • leg swelling
  • previous Hx
  • immunosuppression
  • lymphedema
84
Q

list the catalase positive Staph. spp., and how are they differentiated from S. aureus

A
  • Staph epidermidis
  • Staph saprophyticus

-both are Coagulase-, S. aureus is coagulase+

85
Q

list the Strep. spp. by blood agar results

A

-α-hemolytic: GBO / Strep. pneumoniae (Optochin sensitive), viridans Strep (Optochin resistant)
β-hemolytic: GAS / Strep. pyogenes (Bacitracin sensitive), GBS / Strep. agalactiae (Bacitracin resistant)
γ-hemolytic: enterococcus sp.

86
Q

Cellulitis is caused by (1) causing (2)

A

1- Strep pyogenes

2- local warmth, erythema, edema, pain with poorly defined borders (usually local extremities)

87
Q

Erysipelas is caused by (1) causing (2)

A

1- Strep pyogenes

2- local warmth, erythema, edema, pain with well-defined borders (usually local extremities)

88
Q

describe how to determine if a culture is Strep. pyogenes

A

1) Gram+
2) catalase-
3) β-hemolytic (blood agar)
4) Bacitracin sensitive

89
Q

GAS can cause (1) and (2) dermal infections, which both share the following symptoms, (3). They differ in (4), (5), (6).

A

(GAS- group A strep / S. pyogenes)
1/2- cellulitis, erysipelas (occasionally due to S. aureus)
3- local warmth, erythema, edema, pain (usually lower extremities)

4- anatomic features (regarding skin layers): erysipelas is more distinctive
5- skin layers involved: i) erysipelas: upper dermis, superficial lymphatics (better boundaries); ii) cellulitis: deeper dermis SQ fat
6- onset: i) erysipelas is acute, systemic, ii) cellulitis is more indolent (slow)

90
Q

describe clinical presentation of cellulitis

A

(GAS- group A strep / S. pyogenes)

  • tender, erythematous, poorly-defined borders* expanding rapidly
  • usually lympangitis (streaking), lymphadenopathy
  • occasionally bacteremia
  • usually on legs
  • involves deeper dermis and subcutaneous fat
  • w/ or w/o fever
  • indolent onset (slow progression)
91
Q

describe clinical presentation of Erysipelas (St. Anthony’s fire)

A

-tender, erythematous, raised, indurated (hard) plaques with well-defined borders*

-usually on face or legs (associated with nasopharyngeal infection)
-involves upper dermis and superficial lymphatics
-w/ or w/o fever
-Systemic Sxs: fever/chills
(includes Peau d’orange- dimpled appearance)

92
Q

list the virulence factors for Streptococci

A
  • Secreted: streptokinase, SPEs (streptococcal pyrogenic exotoxins), SLO (streptolysin O), hyaluronidase
  • Membrane/Cell-bound: M protein, Protein F
93
Q

(Streptococci virulence factor) _____ converts plasminogen to plasmin to cleave fibrin clots (enables dissemination)

A

streptokinase

94
Q

(Streptococci virulence factor) _____ is a superantigen toxin that induces fever and contributes to shock

A

SPEs (streptococcal pyrogenic exotoxins)

95
Q

(Streptococci virulence factor) _____ activates range of cell types; like platelets, endothelial cell –> perfusion deficits

A

SLO (streptolysin, a cytolysin)

Note- Anti-SLO titiers useful in Dx

96
Q

(Streptococci virulence factor) _____ is key to the dissemination of bacteria into tissues

A

hyaluronidase- hydrolyze hyaluronic acid

97
Q

(Streptococci virulence factor) _____ limits phagocytosis by disrupting complement involved in adhesion

A

M Protein (>200 types)

98
Q

(Streptococci virulence factor) _____ responsible for binding to epithelial surfaces

A

Protein F

99
Q

Erysipleoid is caused by (1) causing (2)

A

1- erysipelothrix rhusiopathiae

2- slow developing cellulitis

100
Q

describe identifiable features of erysipelothrix rhusiopathiae and how it is usually exposed to humans

A
  • Gram+, catalase-, non-motile, H2S+, pleomorphic, encapsulated
  • Exposure: handling raw meat/fish; present in soil, animals, and fish; direct inoculation
101
Q

erysipelothrix rhusiopathiae causes (1) with the following clinical presentation, (2)

A

Erysipeloid:

  • either localized (most common), generalized cutaneous, bacteremic (endocarditis)
  • painful: throbbing, burning
  • lesion is violaceous (violet color), slightly elevated, well-defined borders
  • lymphadenopathy, lymphangitis (20% of time)
  • low grade fevers
102
Q

Paronychia is an infection of (1) to cause (2) described as (3). It has a (4) type caused by (5) and a (6) type caused by (7).

A 
1- fingernail
2- cellulitis --> definite abscess
3- painful, red, swollen, visible pus
4/5- Acute, Staph. (painful, purulent)
6/7- Chronic, Candida spp.
(Note- excessive moisture/hand soaking (possibly due to occupation), biting nails increases risk)
103
Q

define skin abscess, furuncles, carbuncles and the most common associated microbe

A
  • infection of the dermis and deeper layers of skin that contains purulent material (visible pus)
  • usually S. aureus (>75%)
  • single follicle: furuncle / boil
  • multiple follicle: carbuncle
104
Q

describe the risk factors for abscesses/furuncles/carbuncles and their involvement in its pathogenesis

A
  • Risks: IV drug users, poor hygiene, friction/abrasion (ex. men’s collars on back of neck)
  • pathogens enter thru skin trauma or spread from folliculitis
  • results from a inflammatory response
  • single follicle = furuncle/boil, multiple = carbuncle
105
Q

describe the clinical manifestations of furuncles and carbuncles, include its treatment plan

A
  • Furuncle: deep follicilitis with surrounding erythema, warmth, tenderness
  • Carbuncle: clustered furuncles (many times on neck where collar rubs - poor hygiene), high fever, chills
  • Tx: drainage, antibiotics
106
Q

Actinomyces israelii:

  • (1) microscopic features
  • (2) where most infections occur and why
  • (3) risk factors for infection
A

1- Gram+, pleomorphic, anaerobic, bacillus, filamentous
2- normal flora of the mouth, 70% of infections
3- poor oral hygiene, invasive dental procedures

107
Q

list the 3 types of Actinomycosis and the clinical presentation

A

(actinomyces israelii)

  • orocervicofacial (lumpy jaw), thoracic, abdominopelvic
  • abscess formation; sinus tracts: drains purulent material containing ‘sulfur granules’ = hard granules of mineralized (Ca++) aggregated bacteria (appears yellow)
108
Q

Sporothrix schneckii:

  • (1) main microbial feature as its virulence factor
  • (2) methods of trasmission
  • (3) what it infects
A

(fungi)
1- thermally dimorphic: yeast (tissues) + branching, septate hyphae (ambient Temp - environment)
2- penetrating trauma: splinters, thorn, moss, mulch, hay due to gardening, carpentry, etc (also zoonotic transmission)
3- Sporotrichosis: ‘rose gardener’s disease; subcutaneous, lymphocutaneous infection

109
Q

Sporothrix schneckii:

(1) clinical features
(2) Dx requirements

A

(sporotrichosis)
1- small red pustule –> spreads along lymphatics –> distal lesions ulcerate and drain –> secondary bacterial infection is common
2- KOH prep: i) cigar-shaped yeast; ii) flowerette arranged conidia in mold phase

110
Q

(1) bacteria is the mainly infects sebaceous glands causing (2). List the key features of (1) microscopically, (3). It produces (4), which is key to its pathogenesis.

A

1- propionibacterium acnes
2- inflammatory, moderate acne
3- Gram+, aerotolerant anaerobe, slow growing, bacillus/branched
4- lactic acid, propionic acid, acetic acid (=> inflammation)

111
Q

list the 3 types of acne

A
  • comedonal, mild
  • inflammatory, moderate (propionibacterium acnes)
  • nodular cystic, severe
112
Q

(1) is a chronic infection of the pilosebaceous unit. (2) is triggered by released mediators, followed by altered (3), increased (4) production, and then (5) and (6) formation.

A 
(propionibacterium acnes)
1- acne vulgaris
2- inflammation
3- keratinization
4- sebum
5- colonization (anaerobic, lipid rich environment)
6- biofilm formation
113
Q

(1) is defined as an infection of deep structures of the skin including underlying fascia, and it includes (2). It comes in the following types, (3), and mainly affects (4) areas of the body.

A 
1- necrotizing fascitis
2- myonecrosis (muscle necrosis)
3- Type I polymicrobial, Type II single organism
4- lower extremities, abdomen, perineum
(25% mortality rate, 70% with sepsis)
114
Q

Type I necrotizing fascitis is caused by the following: (1). Risk factors include (2). Infection of the male perineum is called (3).

A

1- i) anaerobe: bacteroides, peprostreptococcus; ii) facultative anaerobe: enterobacteriaceae, non-GAS
2- intra-abdominal surgery, DM, IV drug use (traumatic or nontraumatic cutaneous lesion)
3- Fournier’s gangrene

115
Q

Type II necrotizing fascitis is caused by the following….

A
  • GAS (S. pyogenes)

- S. aureus

116
Q

(1) and (2) are less common causes of necrotizing fascitis

A
  • Trauma in water: vibrio vulnificus, aeromonas spp.

- Soil-contaminated wounds: clostridium perfringens

117
Q

Describe the early and late symptoms of necrotizing fascitis

A
  • Early Sxs: <24hrs, erythema, warmth, tenderness, pain, fever
  • Late Sxs: 3-5 days, hypoperfusion (blue-gray coloring), bullae, anesthesia + crepitus (gas bubbles, joint crackling), systemic infection, rapid onset
118
Q

describe the pathogenesis and diagnostic requirements for necrotizing fascitis

A

(risk factor- traumatic/non-traumatic skin lesion)

  • thrombosis of vascular supply and adjacent nerve tissue causes infection
  • Dx by clinical presentation + CT/MRI, skin biopsy (culture of fluid from bullae, tissue, blood + gram stain)
119
Q

describe the key features to Clostridium perfringes and where it is normally found

A
  • Gram+ bacilli anaerobe (aerotolerant), non-motile
  • forms endospores
  • found in environment: soil, dust
120
Q

tetanus is caused by….

A

clostridium tetani

121
Q

botulism is caused by….

A

clostridium botulium (caused food poisoning)

122
Q

C. perfringes causes….

A

wound infections:

  • clostridial cellulitis
  • clostridial myonecrosis (gas gangrene)

-difference is whether the strain can produce a specific toxin allowing it to infect into the muscle

123
Q

list the predisposing factors for clostridium spp. wound infections

A
  • surgical incisions
  • compound fractures
  • diabetic ulcers
  • septic abortions
  • puncture wounds
  • GSW
124
Q

describe the pathogenesis of C. perfringes

A

1) Trauma –> suitable environment for anaerobic bacteria: damaged/dead tissue has low/no O2
2) endospores geminate –> bacteria produces toxins + other virulence factors
3) rapid onset, spreads to deeper tissues

Fermentative metabolism => gas bubbles / crepitus (gas gangrene), Medical Emergency

125
Q

describe mechanism of the clinically important exotoxin of C. perfringes

A

α-toxin (CPA- clostridium perfringes α-toxin):
-phospholipase (lecithinase)
-targets membranes of WBCs, thrombocytes, endothelial, muscle cells
-reduces blood supply (and O2) to tissues –> promotes infection (C. perfringes in anaerobic)
(-AB toxin: active enzymatic site, membrane binding site)
[β, ε, ι toxins also present]

126
Q

briefly describe the mechanism and symptoms caused by C. tetani

A
  • tetanus toxin inhibit neurotransmitter release –> muscle relaxation blocked –> rigid muscle paralysis
  • Sxs: lock jaw (trismus), muscle stiffness/spasms, dysphagia, HA, jerking or staring
127
Q

(1) is common (2) type parasite that infects muscle. It is acquired through (3) in the (4) stage. It causes (5).

A

1- trichinella spiralis
2- nematode (roundworm)
3- eating raw meat of infected animal (commonly bear)
4- encysted larval stage (goes into muscle)
5- trichinosis: (usually asymptomatic) myalgia, diarrhea, fever, facial edema, HAs

128
Q

Trichinella spiralis causes (1) causing (2)

A

1- trichinosis (muscle infection)

2- myalgia, diarrhea, fever, facial edema, HAs [Note- mostly asymptomatic]

129
Q

Primary infections of the bone are either (1) or (2). They are caused by (3) species.

A

1- osteomyelitis
2- infectious arthritis
3- bacteria, fungi
(acute or chronic)

130
Q

Immune mediated bone infections can be caused by the following…..

A
  • immune reactions to bacteria or viruses not in the joint
  • Immune complex arthritis
  • reactive arthritis
  • rheumatic fever
131
Q

Acute Osteomyelitis:

1) duration
(2) sequestra present? (pieces of necrotic bone separate from viable bone
(3) associated disorder
(4) Sxs

A

1- days-wks
2- No
3- pyogenic skin infections
4- gradual onset, i) Local: dull pain with tenderness, warmth, erythema, swelling; ii) Systemic: fever, etc

132
Q

Chronic Osteomyelitis:

1) duration
(2) sequestra present? (pieces of necrotic bone separate from viable bone
(3) associated disorder
(4) Sxs

A

1- mos-yrs
2- Yes
3- vascular insufficiency
4- pain, erythema, swelling –> possible draining sinus tract (usually no fever)

133
Q

most osteomyelitis in adults and children are caused by….

A

S. aureus

134
Q

osteomyelitis in patients with hip or knee prostheses are caused by….

A

Staph. epidermidis

135
Q

osteomyelitis related to patients with recent cat bite is caused by….

A 
pasteurella multocida (Gram-, coccobacillus)
[usually involves bite to distal joint- fingers]
136
Q

briefly describe the pathogenesis of pasteurella multocida

A

1) apart of the oral flora of cats
2a) deep bite penetrates periosteum
2b) local extension of infection to bone
3) osteomyelitis
[usually involves bite to distal joint- fingers]

137
Q

list the 3 common causes of osteomyelitis

A
  • S. aureus
  • CoNS (coagulase negative staph. spp.: epidermidis, saprophyticus)
  • aerobic Gram- bacilli
138
Q

describe the 2 classifications of osteomyelitis

A

Hematogenous: monomicrobial (usually) resulting from bacteremia

Non-hematogenous / contiguous:

i) from spread of local infection
ii) direct inoculation into bone
- poly-/mono-microbial

139
Q

describe the diagnosing of osteomyelitis

A

Bone biopsy and culture:
1) Gram stain + culture
2) histopathology
(cultures are positive ~50% of cases)

-Imaging (clearish spot in bone margins)

140
Q

Infectious arthritis (septic) is defined as (1). It is mostly due to (non-/hematogenous) spread of infections that induces a (3) response in bone. It is mostly commonly caused by (4) and infects (5) joints.

A 
1- 1 or more acutely painful joints
2- hematogenous (via bacteremia)
3- synovial membrane inflammatory response
4- S. aureus, MRSA
5- knees (>50% cases)
141
Q

define DGI (in terms of bone infection)

A

disseminated gonococcal infection –> gonococcal arthritis

142
Q
  • M. tuberculosis is transmitted via (1)
  • NTM or RGM are transmitted via (2)
  • M. leprae is transmitted via (3)
A

1- inhalation
2- environment (non-tuberculous or rapidly growing mycobacteria)
3- close contact: nasal droplets

143
Q

list the clinically relevant endorspore forming bacteria

A
  • Clostridium spp.

- Baccilus

144
Q

Mycobacterium marinum is found in (1) and targets people who are the following: (2). It usually found in (1) and affects (3) body parts due to its (4) feature.

A

(aka fish tank granuloma)
1- fresh and salt water (Gulf of Mexico, Atlantic ocean)
2- immunocompromised, fish handlers, swimmers
3- limbs
4- optimal growth at low T, 30-32C

145
Q

what is the key feature of mycobacterium

A

Acid Fast Bacilli (poor Gram staining) due to presence of mycolic acids in its thick waxy cell wall

146
Q

describe the clinical features of M. marinum

A

(fish tank granuloma)
-dormant for 2-6 mos
-affects elbows, knees, feet, knuckles/fingers
-single lump/pustule –> crusty sore / abscess
-sometimes red, swollen, tender joints
(more lesions and more widespread in immunocompromised people)

147
Q

describe the clinical features of M. ulcerans

A

(central/west Africa in swampy areas)

1) slow growing painless itchy lesion
2) 7-14 days: 1-2 cm nodule after infection breaks thru skin
3) 1-2 mos: nodule breaks –> shallow ulcer, spreading rapidly to cover 15% of skin (Buruli ulcer)
- severe infections can destroy BVs, nerves, bone

148
Q

describe the clinical features of M. chelonae

A

(found in water)

  • lung disease, joint infection, eye disease, + other organ infections
  • Skin: non-healing wound, subcutaneous nodule, or abscess (tattoo related)
  • immunocompromised => dissemination
  • rapid grower (5 days on medium)
  • inc in CF patients
149
Q

describe the clinical features of M. foruitum

A

(found in water and dirt)

  • Follows Trauma –> local cutaneous disease, osteomyelitis, joint infections, occular disease
  • immunocompromised –> dissemination skin and soft tissue lesions
  • often cause of wound / surgical site infection
  • Skin: non-healing ulcerative skin lesion / subcutaneous nodules
150
Q

Leprosy, aka (1), is caused by (2) that specifically infects and multiplies in (3) cells. It is transmitted via (4) has an incubation period that can last (5).

A

1- Hansen’s disease
2- Mycobacterium leprae
3- macrophages, schwann cells (infects skin / peripheral nerves)
4- inhalation (infectious aerosols), skin contact with respiratory secretions or wound exudates

151
Q

compare the clinical presentation of both types of leprosy

A

Both: anesthesia of skin lesions, peripheral nerve thickening, tenderness, pigmentation change

Tuberculoid: large single red path, well-defined borders OR large hypo-pigmented macula (asymmetrical)

Leprosy: many erythematous macula, papules, nodules (extensive disfiguring skin lesions)

152
Q

compare both types of leprosy in terms of:

  • (1) bacilli number
  • (2) immunity response
  • (3) communicability
A

Tuberculoid: i) paucibacillary, few bacilli; ii) Th1, strong, cell-mediated immunity; iii) not communicable

Leprosy: i) multibacillary, abundant bacilli; ii) Th2 humoral immunity; iii) communicable

153
Q

list the 4 types of skin rashes or pathologies caused by viruses

A
  • vesicular or pustular rash
  • maculopapular rash
  • maculopapular or vesicular
  • warts and papillomas
154
Q

list the viruses responsible for vesicular/pustular rashes

A
  • chickenpox (VZV, HHV3)
  • shingles (VZV, HHV3)
  • smallpox
  • HSV (1, 2)
155
Q

list the viruses responsible for maculopapluar rashes

A
  • measles
  • rubella
  • sixth disease
  • fifth disease
  • roseola
156
Q

list the viral disease responsible for maculopapular or vesicular rashes

A
  • HFMD (hand, foot, mouth disease)

- herpangina

157
Q

describe the features of VZV (HHV-3)

A

-large 80-120 nm, linear dsDNA, enveloped
-humans are natural host
-cytopathic effect = syncytia
-targets epithelial cells, fibroblasts, T cells, neurons
(alphaherpesvirinae)

158
Q

VZV is transmitted via (1) and can occur (2) days before rash and (3) days after rash. It is considered a (primary/secondary) infection,

A

1- respiratory droplets, direct contact
2- 2 days
3- 7 days
4- primary

159
Q

Variola virus causes (1). It is a (2) type virus, with (3) as features.

A

1- smallpox (+ molluscum contagiosum)
2- poxvirus
3- dsDNA, enveloped, cytoplasmic replication

160
Q

Smallpox is evident by (1) clinical presentation. It is associated with (2)% mortality. It is diagnosed by (3) and treated with (4).

A

1- synchronous diffuse vesicles/pustules
2- 30%
3- clinical Sxs, lab confirmation
4- N/A

161
Q

describe the features of HSV-1/2

A
  • enveloped, dsDNA

- latent viruses in dorsal root ganglia

162
Q

compare the three HSV-1 clinical presentations

A
  • herpes labialis: cold sores/fever blisters, itching/tingling before vesicular development, lesions get crusted over
  • herpetic gingivostomatitis- oropharynx infection (young children): fever, sore throat, lymphadenopathy
  • herpetic keratitis- ocular herpes, inflammation of eye with ‘gritty feeling’ unilaterally, conjunctivitis, sharp pain, photophobia
163
Q

Measles, aka (1) virus, is apart of the (2) virus family with (3) as viral features. It contains two key envelope proteins, (4) and (5) [include function].

A

1- rubeola
2- paramyoxvirus (morbillivirus genus)
3- large, ssRNA(-), enveloped
4- F (fusion) protein: fuses with host cell membrane –> viral penetration –> hemolysis
5- H (hemagglutinin) protein: adsorption of virus to cells (viral replication, no neuraminidase activity)

164
Q

Measles is transmitted via (1), it is more prevalent in the (2) season, and affects (3) people the most

A

1- aerosol (fomites); highly infectous, exposure => 90% symptomatolgy
2- winter, spring
3- children <2 y/o

165
Q

describe MMR vaccine

A

(measles, mumps, rubella)
live attenuated vaccine, 2 doses needed- 100% effective
(MMRV is + varicella)

166
Q

describe clinical presentation of measles

A
  • 3 C’s: cough, coryza (rhinitis), conjunctivitis with photophobia
  • fever
  • Koplik’s spots (enanthem): red spots w/ blue-white center on buccal mucosa
  • K-spots disappear –> maculopapular rash: face (hairline), lateral neck, behind ears –> trunk, extremities, palms/soles (coalesed rash) [disappears in same order it appears]
  • generalized lymphadenopathy
  • possible lifelong disabilities: brain damage, blindness, deafness
  • immunosuppression –> secondary infection
167
Q

CDC requirements for measles Dx

A
  • generalized rash for 3 or mote days
  • Temp. >101F (38.3C)
  • 3 C’s: cough, coryza (nasal mucosa inflammation, conjunctivitis with photophobia)
168
Q

measles causes rash by infecting (1) cells, which are then damaged by (2) cells

A

1- endothelial cells

2- Tc cells

169
Q

HHV-6 causes (1), and has the following viral features, (2). It mainly infects (3) cells in mostly (4) people

A

1- sixth disease (exanthem, subitum/roseola- infantum)
2- 200nm diameter, dsDNA, enveloped (herpes B family)
3- T cells, macrophages, NK cells
4- children <2 y/o (most likely transmission is from saliva of mother)33333

170
Q

clinical presentation of HHV-6

A

(sixth disease / roseola)

1) high fever for 3-7 days; febrile seizures in 10-15% of Pts
2) fever resolution –> nonpruritic maculopapular rash (sudden rash) starting neck/trunk –> face/extremities lasting hrs-days
3) pink macules and papules surrounded by white halos

171
Q

chickenpox rash is described as (1), it starts on (2) and spreads to (3)

A

1- asynchronous (combination of macules, papules, vesicles, pustules, crusts)
2- trunk (upper chest)
3- head and extremities

172
Q

Measles virus is inhaled through the respiratory system and is spread into (1) via (2). It infects (3) cells to cause the exhibited rash, but can target any cell that expresses (4).

A

1- blood (viremia) => dissemination
2- respiratory lymphatics
3- Tc cell damage to endothelial cells
4- CD46

173
Q

Rubella is apart of the (1) family and has the following viral features, (2). (3) are the main reservoir and it is transmitted via (4).

A

1- togaviridae
2- enveloped, ssRNA(+), icosahedral
3- humans
4- air droplets

174
Q

describe clinical presentation of Rubella infection

A
  • 3 days worth of Sxs: flu-like, rarely low grade fever, HA, sore throat, cough, rhinorrhea, conjunctivits, postauricular and posterior cervical lymphadenopathy
  • Maculopapular rash: forehead –> face –> extremities in 24 hrs, no coalescence, Petechial lesion on soft palate / uvula (Forchheimer’s sign)
  • Arthralgia in adult women
175
Q

Rubella bind to (1) receptor for entry and dissemination into a systemic infection. Its most clinically significant feature is its ability to (2) and cause (3).

A

1- myelin oligodendrocyte glycoprotein
2- cross placenta and damage fetus (congenital rubella syndrome)
3- caratacts, deafness, cardiac abnormalities

176
Q

Parvovirus B19 has (1) viral features and causes (2). It is spread through (3) and mainly affects (4) people during the (5) season.

A

1- linear ssDNA, smallest DNA virus (26 nm), icosahedral
2- 5th disease (mild febrile exanthematous infection)
3- respiratory droplets
4- children (school), 4-10 y/o
5- late winter, spring

177
Q

describe clinical presentation of parvovirus B19 / 5th disease

A

(usually asymptomatic)

  • low fever, cold Sxs, ‘slapped cheek’ confluent plaques on face and lacy red rash on trunks and limbs (possibly itchy)
  • joint pains and swelling with adults
178
Q

parvovirus B19 is life-threatening to (1) people and serious in (2) and (3) patients

A

1- people with chronic hemolytic anemia (sickle cell)
2- pregnant women: severe anemia in newborn or miscarriage (crosses placenta)
3- caner Pts or immunocompromised

179
Q

parvovirus B19 enters lungs and binds (1) receptors in (2)

A

erythrocyte precursor via P Ag usually in bone marrow

180
Q

HFMD is caused by (1) virus in the (2) family with (3) as viral features

A

1- enterovirus (A)
2- picornaviridae
3- ssRNA(+), nonenveloped, small (30nm), iscosahedral

181
Q

describe the spread of enterovirus causing HFMD

A
  • oral ingestion
  • replication in GI
  • spreads to lymph nodes (regional)
  • spreads to reticuloendothelial tissue and multiple organs
  • Sxs depend of the infected SITE – HFMD has enterovirus A binding to skin
182
Q

HFMD definition and clinical presentation

A

Dfn: oral enanthem + macular, maculopapular, or vesicular exanthem affecting mouth, hands, feet
-Initial: fatigue, sore throat, fever
-1-2 days: painful sores or blisters in/on mouth and on hands/feet
(rash may appear before blisters, also can be asymptomatic)

183
Q

HFMD usually affects (1) people mostly and sometimes (2) groups, usually in the (3) season

A

1- children <10 y/o
2- colleges (or similar situations)
3- spring, summer, early fall

184
Q

Coxsackievirus causes…..

A

HFMD- A16, A6
Herpangina- A serotypes
(apart of the enterovirus family)

185
Q

herpangina is defined as (1) and can presents clinically with the following: (2)

A

1- painful papulo-vesiculo-ulcerative oral enanthem

2- fever, malaise, sore throat, dysphagia // vesicles in soft palate, erythematous pharyngitis

186
Q

herpangina usually affect (1) people and occasionally (2) people, worse in the (3) season

A

1- children, 3-10 y/o
2- newborns, adolescents, young adults
3- summer

187
Q

describe the viral features of HPV

A

dsDNA, small, non-enveloped

188
Q

HPV usually causes the following cutaneous infections….

A

1) verrucae vulgaris (common warts)

2) verrucae plantaris (plantar warts)

189
Q

Molluscum contagiosum virus (MCV) is apart of the (1) family with (2) as viral features. It is usually spread by (3) affecting (4) people most.

A

1- poxvirus
2- dsDNA, enveloped
3- person to person, fomites, or sexually
4- children, 1-11 y/o (or adults if in STI form)

190
Q

describe MCV clinical presentation

A

(molluscum contagiosum virus)

  • 1-5 mm lesions, dome-shaped with dimpled center
  • described as ‘pearly’
  • usually on face, arms, legs, torso, armpits (genital in STI form)
  • usually painless
  • lasts up to 4 yrs if untreated
191
Q

describe Dx on MCV

A

(molluscum contagiosum virus)

  • clinical appearance, virus cannot be cultured
  • biopsy: histology has molluscum bodies in epidermis = large cells w/ abundant granular eosinophilic and small peripheral nucleus
192
Q

HHV-8 = (1) and causes the following four infections, (2)

A

1- Kaposi’s sarcoma virus
2- i) classic (cutaneous proliferative disease); ii) endemic (equitorial Africa); iii) organ-transplant associated; iv) epidemic/AIDS-related

193
Q

describe the clinical presentation of HHV-8 / KSHV

A
  • painless, purplish cutaneous lesions on legs, face (oral), feet
  • soft-tissue carcinoma / vascular tumor
  • angiogenesis, inflammation, cell proliferation

FTCM (16 decks)

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