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AUC MS2 > Skin/Soft Tissue Micro > Flashcards

Skin/Soft Tissue Micro Flashcards

1
Q

Pus in a skin lesion-purulent

A

Pyoderma

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2
Q

Skin redness

A

Erythema

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3
Q

Severe itching

A

Pruritis

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4
Q

Dried serum residue, pus, or blood on the skin

A

Crust/scab

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5
Q

Material composed of serum that escapes from blood vessels into a superficial lesion or area of inflammation

A

Exudate/transudate

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6
Q

Serum; thin, watery consistency; serous fluid

A

Transudate

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7
Q

Pus; neutrophils, cell debris and bacteria; purulent

A

Exudate

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8
Q

Small number of RBCs mixed with serum

A

Serosanguinous

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9
Q

Accumulation of fluid in tissue

A

Edema

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10
Q

Acute inflammation that involves subcutaneous tissue. Caused by many organisms.
Manifested clinically by rapid spreading areas of edema, redness and heat (24-48hrs). Hematogenous spread can lead to septicemia.

A

Cellulitis

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11
Q

Infection in the dermis with lymphatic involvement. Lesions are raised with clear demarcation of “brilliant red salmon” color. Often unilateral. Fever, chills, pain, leukocytosis. May follow throat infection (->face lesions) in kids or skin infection (->LE ) in adults

A

Erysipelas

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12
Q

Cause(s) of erysipelas

A

Strep. pyogenes

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13
Q

Syndromes that could involve cellulitis (10)

A 
Erysipelas
Pyoderma
Abcesses
Cutaneous mycoses
Toxigenic rashes
Myonecrosis/gangrene
Necrotizing fasciitis
Ulcers/eschars/granulomas
Opportunistic
Osteomyelitis
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14
Q

Types of pyoderma

A

Pustules (Impetigo)
Folliculitis
Pustules

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15
Q

5 general characteristics of Strep. pyogenes

A 
Gm+ cocci in chains
Aerobic (5% CO2)
Catalase -
Lancefield group A
Beta hemolytic- BAP
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16
Q

2 structural virulence factors of Strep. pyogenes (Invasive strains)

A

M proteins 1-3 (serotype)

Hyaluronic acid capsule

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17
Q

4 enzymatic toxins (VFs) of Strep. pyogenes.

3 exotoxins

A

*Streptolysin S (O2 stable hemolysin, breaks cell junctions)
Hyaluronidase (spread)
Streptodornase (DNAse)
Streptokinase (fibrinolysin)

Pyrogenic exotoxin A (SpeA) superantigen
SpeB proteinase
SLO (antigenic, O2 labile, thiol-activated cytolysin (muscle))

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18
Q

Reservoir and transmition for Strep. pyogenes

A

Human throat/skin

Direct contact/ resp. droplets

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19
Q

Consequences/ sequeale of Strep. pyogenes

A

APSG 2-3 wks post skin infection

ARF 2-3 wks post throat infection

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20
Q

Diagnosis process for Strep. pyogenes

A

Rapid strep (detects carb. ag)
Streptozyme (Hydrolytic enzyme assay, ab’s against toxins)
Streptolysin ASO is more sensitive

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21
Q

Treatment for Strep. pyogenes

A

Beta lactams (penams, cephams)

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22
Q

A bacterial skin infection often called school sores. It is highly contagious. Vesicles turn to pustules which rupture and crust a yellow-brown microbe containing fluid. There is NO fever/sepsis.

A

Pyoderma: Impetigo

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23
Q

Cause(s) of pustules (impetigo)

A

Strep. pyogenes

Staph. aureus

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24
Q

4 general characteristic of Staph. aureus

A

Gram + cocci in clusters
Catalase +
Coagulase +
MSA+

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25
Q

5 enzymatic toxins (VFs) of Staph. aureus

A 
Coagulase
Hyaluronidase (invasion thru BM)
Fibrinolysin
Exfoliative toxin (phage/plasmid)
TSST (superantigen, Path. island)
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26
Q

Reservoir and transmition of Staph. aureus

A

Human skin, nose

Direct contact, resp. droplets, fomites/foreign object, opportunistic

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27
Q

MRSA is associated with what gene?

A

PVL

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28
Q

Nasopharyngeal carriage of Staph. aureus is treated with

A

Mupirocin

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29
Q

MRSA is treated with

A

Vancomycin

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30
Q

Non-resistant Staph. aureus is treated with

A

Naficillin, cephalosporin

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31
Q

Infected hair follicle; follicle surrounded by erythematous, edematous area; pus accumulates at the site

A

Pyoderma: folliculitis

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32
Q

3 causes of pyoderma: folliculitis

A

Staph. aureus
Pseudomonas aeruginosa
Candida albicans

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33
Q

5 general characteristics of P. aeruginosa

A 
Gram - bacillus
Aerobe
Capsule
Oxidase +
Lactose -
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34
Q

4 structural characteristics of P aeruginosa

A
  1. Pilli (biofilms)
  2. Capsule
  3. Pyocyanin: generates ROS
  4. Pyochelin: scavenges iron
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35
Q

4 enzymatic toxins (VFs) of P. aeruginosa

A
  1. Exotoxin A: Inhibit protein synthesis via ADP ribosylation of EF-2
    2-4. Exo-enzymes: PLP-C, leukocidins, proteases
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36
Q

Reservoir and transmission of P. aeruginosa

A

Soil, water, rarely human carriers (URT GI in hospitalized pts)

Direct contact,aerosol

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37
Q

Risk groups for P. aeruginosa

A

Anyone for folliculitis,
Burn patients
Chronic disease
Hospital

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38
Q

What causes the ABX resistance seen in P. aeruginosa? (4)

A

Capsule
Porin mutation
Efflux pumps
Beta lactamase

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39
Q

What skin/ST infections can be caused by P. aeruginosa?

A 
Impetigo
Otitis externa
Malignant otitis externa
Nail infection (green)
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40
Q

What is the danger of malignant otitis externa? Who is the risk group?

A

MO can spread to bone/other structures causing exotoxin damage (paralysis, death)
Diabetics/immunocompromised

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41
Q

What diseases can be caused by Candida albicans?

A

Cutaneous: diaper rash, folliculitis
Mucocutaneous/oral: thrush
Erosio interdigitalis blastomycetia
Onychomycosis

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42
Q

General characteristics of C. albicans

A

Yeast producing pseudohyphae, filaments

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43
Q

Virulence factors of C. albicans

A

Enzymes: acid proteases and phospholipases
Structural: pseudohyphae

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44
Q

Culture method and treatment for C. albicans

A

MYC or SDA

Azoles

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45
Q

Cause(s) of pyoderma: pustules

A

Bartonella henselae
Streptobacillus moniliformis
Eikenella corrodens
Yersinia pestis

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46
Q

Diagnose: A small papule develops 5-10 days after bite or scratch. Progresses to pustules at the site and may persist for a few weeks.
Extreme swelling of the axillary or cervical lymph nodes: immune response-limits bacterial growth and causes lymphadenopathy

A

Cat-Scratch Disease

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47
Q

Cat-Scratch Disease is caused by:

A

Bartonella henselae

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48
Q

3 general characteristics of B. henselae

A

Gram - rod
Facultative intracellular
Zoonotic (40% all cats)

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49
Q

Consequence/sequeale of B. henselae infection and risk group

A

Bacillary angiomatosis

Low CD4

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50
Q

Describe bacillary angiomatosis

A

Proliferative, neo-vascular, cutaneous and visceral lesions
Red to purplish, elevated, nodular lesions (satellite lesions common)
May resemble cherry angiomas or Kaposi’s sarcoma lesions. Biopsy shows BV prolif., cuboidal epithelial cells, inflam. infiltrates.

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51
Q

How is B. henselae diagnosed (vs bacillary angiomatosis)?

A

Silver stain
Immunostain
Serology (IgM or IgG pair sera)
PCR

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52
Q

Diagnose: Chills, headache, and migratory arthralgias and myalgias.
2-4 days after fever: nonpruritic rash (maculopapular, petechial or purpuric and pustular - erupts over the palms, soles and extremities
Transient fever profile

A

Rat Bite Fever/ Haverhill Fever

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53
Q

What causes myalgia?

A

Deposition of immune complexes

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54
Q

What causes Rat Bite/ Haverhill Fever?

A

Streptobacillus moniliformis

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55
Q

General characteristics of Streptobacillus moniliformis

A

Gram - pleomorphic rod which forms filaments (tangles)

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56
Q

Consequence/sequeale of Streptobacillus moniliformis

A

Untreated causes endocarditis, myocarditis and degenerative disease of kidneys and liver

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57
Q

Reservoir and transmission of S. moniliformis

A

Nasopharynx/Oropharynx of rats and other small rodents

Bite or scratch from rodents
Transiently by animals who prey on rodents (dogs, cats) if the rodents are infected

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58
Q

Treatment of Streptobacillus moniliformis

A

Penicilllin

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59
Q

Diagnose: Pustules at the site of bite: hand, head, neck.
Some stiffness with limitation of movement: clenched-fist: due to accumulation of microbial gas fermentation
~1 week IP; pustules

A

Human bite, infection with Eikenella corrodens

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60
Q

Consequence/sequeale of Eikenella corrodens

A

Osteomyelitis
Endocarditis
CNS/organ failure

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61
Q

General characteristics of Eikenella corrodens

A

Gram - pleomorphic bacillus
Fastidious
Anaerobic

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62
Q

Describe the colony formation of Eikenella corrodens

A

Small, greyish colonies which corrode agar, leaving a greenish discoloration and hypochlorite (bleach) smell

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63
Q

Risk factors for Eikenella corrodens

A 
Periodontal diseases – cancer
Immunosuppressed
Fight-involving a human bite
IDU who licks the needles
Chronic finger or nail biters
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64
Q

Treatment of Eikenella corrodens

A

Sensitivity d/t high resistance

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65
Q

Diagnose: Sudden onset of fever, weakness and headache
Lymphadenitis – Buboes: groin, axilla, neck
Skin: Papules, vesicles or pustules: site of the bite (commonly found distal of the affected lymph node)

A

Bubonic plague

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66
Q

The bubonic plague is caused by

A

Yersinia pestis

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67
Q

Consequences/sequaele of Yersinia pestis

A

Septicemic plaque

Pneumonic plague

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68
Q

Within what time period can Yersinia pestis cause primary pneumonic plague?

A

24-72 hours

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69
Q

Within what time period can Yersinia pestis cause bubonic plague?

A

48-144 hours

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70
Q

Yersinia pestis can cause secondary pneumonic or septicemic plague after ___ hours and aquiring ____ (disease)

A

168

Bubonic plague

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71
Q

2 general characteristics of Yersinia pestis

A

Gram - rod

Bipolar staining

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72
Q

Reservoir and transmission for Yersinia pestis

A

Zoonotic (mostly rodents)

Flea bite => Bubonic p.
Pneumonic => resp. droplets PtP

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73
Q

4 toxins/VFs of Yersinia pestis

A

Coagulase (transmission)
F1 antigen (high temps, decrease phagocytosis)
Plasminogen activator protease gene (Degrades compliment and fibrin)
Type III secretion of YOPs (trigger macrophage apoptosis, disrupt actin)

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74
Q

A localized collection of pus surrounded by inflamed tissue and a fibrous capsule

A

Abscess

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75
Q

Boil; may progress from infected hair follicle or follow other damage to the hair follicle – deep folliculitis
Alt: Hard, walled-off abscess (marble-like)

A

Furuncle

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76
Q

Coalesced boils/furuncles. Involves subcutaneous tissue. Chills and fever indicate systemic disease: induction of fibrinolysin and hyaluronidase

A

Carbuncle

77
Q

Cause(s) of abscess/furuncle/carbuncle (3)

A 
Pasturella multocida (soft abscess)
Actinomyces israelii (hard abscess)
Staph. aureus (furuncle/carbuncle)
78
Q

Cause of rapid onset cellulitis within 24 hours after domestic animal bite, regional lymphadenopathy, fever in 20%, some have soft abscess and tenosynovitis

A

Pasturella multocida

79
Q

Complications of Pasturella multocida in immune compromised patients may include

A

Systemic infections of bone, heart, CNS, and abdominal abscesses

80
Q

5 general/structural features of Pasturella multocida

A 
Gram - rod
capsule
bipolar staining "safety pins"
fimbrae/pilli
aerobe/ facultative anaerobe
81
Q

2 Enzymatic toxins/VFs of Pasturella multocida

A

PMT (potent mitogen)

ToxA and PMG (Inhibit DC migration)

82
Q

Reservoir and transmission of Pasturella multocida

A

Zoonotic, mouth of domestic animals (cats, dogs, etc.)

Bite/scratch, lick open wound

83
Q

Describe the culture of Pasturella multocida

A

BAP agar- white mucoid colonies with a “mousy odor”

84
Q

Cause (common) of cutaneous oral-cervicofacial abscess with/without sinus tracts
Acute: painful cellulitis
Chronic: dense fibrotic lesions “wooden/lumpy jaw”
Hematogenous spread is possible.

A

Actinomyces israelli

85
Q

Term used to describe a chronic subcutaneous infection by either Actinomyces or fungi causing a granuloma

A

Mycetoma

86
Q

General features for ID and VFs of Actinomyces israelli

A

Gram + rod, filamentous
Anaerobe
Sulfur granules in pus
Molar tooth colonies

No VFs identified

87
Q

Reservoir and transmission of Actinomyces israelli

A

Normal flora

Endogenous

88
Q

Risk factors for infection with Actinomyces israelli

A

Trauma, dental work, immunocompromised

89
Q

Treatment for abscess d/t Actinomyces israelli

A

Penicillin G (high dose for months) and drainage

90
Q

Cause of furuncle/carbuncle

A

Staph. aureus

91
Q

VFs (2) of Staph. aureus involved in carbuncle formation

A

Hyaluronidase

Fibrinolysin

92
Q

Two types of cutaneous mycoses

A

Dermatophytes

Superficial

93
Q

Cause(s) of annular (ring shaped) erythematous scaling lesion usually with raised borders; pruritic; some become vesicular.

A

Dermatophytes:
Microsporum
Trichophyton
Epidermophyton

94
Q

General characteristics, reservoir, and transmission of dermatophytes

A

Monomorphic fungi (as molds), septated hyphae

Soil, animals, humans

Direct contact: arthrospores adhere to keratinocytes, germinate in 2-3 hrs, then invade

95
Q

Which type of dermatophytes fluoresce and can be seen with a wood lamp?

A

Microsporium

96
Q

The disease is a consequence of the host reaction to metabolites from the fungi: Keratin as substrate, epidermis.
Infection range from mild to severe: Depends on host immunological state and fungal species- NO SYSTEMIC MANIFESTATIONS

A

Tineas (ringworm)

97
Q

Produces classic concentric- ring like lesions on skin- ringworm
They can become inflamed.
Two types of lesions: dry or vesicular

A

Tinea corporis

98
Q

Also known as Athlete foot
Soreness and itching of any part of the foot. Most common between the toes
Infection can be
Class I – subclinical: athletes and college students carriers
Class II - clinical
Class III infected with bacteria

A

Tinea pedis

99
Q

Also known as jock itch. Groin
Erythematous scaling lesion; pruritic
Most diseases are transmitted Human-Human: T.pedis

Adolescence - males predominate

A

Tinea cruris

100
Q

Affects scalp, eyebrows and eyelashes
Most common in children: prevalence African American.
Fungus grows into hair follicle:
Ecthotrix infection: arthroconidia around the hair
Endotrix infection: arthroconidia forms in the hair with destruction of cuticle.

A

Tinea capitis

101
Q

hands
classic pattern of erythema and mild scaling on the dorsal aspect of the hands or as a chronic, dry, scaly hyperkeratosis of the palms.
When the palms are infected, the feet are also commonly infected.

A

Tinea manuum

102
Q

Beard hair

Edematous, erythematous lesion

A

Tinea barbae

103
Q

(onychomycosis) - Nail

Nails thickened or crumbling distally; discolored; lusterless

A

Tine unguium

104
Q

Describe the malassezia specied (furfur) which cause superficial mycoses. Name two important products.

A

Dimorphic fungi (yeast on skin; mold pathogenic (mixed forms may appear on skin)-Lipophilic
Mold forms produce:
Azaleic acid this is believed to lead to the depigmentation (blocks tyrosinase which is a key step in melanin synthesis)
Malassezin induces apoptosis of melanocytes

105
Q

Clinical disease caused by Malassezia spp. Involves a chronic mild superficial infection of the stratum corneum: Outer skin layer - no immune response
Hypo pigmented /Hyper pigmented maculae on skin (Chest, upper back, arms, or abdomen)
Scaling, inflammation and irritation minimal: After treatment, it will take months for pigmentation to return to affected areas
Some species implicated in dandruff and seborrhea dermatitis

A

Tinea versicolor

106
Q

KOH-shows clusters of round thick wall yeast
Growth on media markedly enhanced by adding fat (Clinical mycology labs routinely stock olive oil)-Culture not routine. “Spaghetti and meatballs”
Wood’s light: affected area fluoresce yellow
Histology: shows no inflammation

A 
Malassezia species (furfur)
(Pityrosporum ovale)
107
Q

Cause(s) of toxigenic rashes

A

Staph. aureus

Strep. pyogenes

108
Q

Staph. aureus causes which type(s) of toxigenic rash?

A

Scalded skin syndrome

Staphylococcal TSS

109
Q

Strep. pyogenes causes which type(s) of toxigenic rash?

A

Streptococcal TSS

110
Q

Scalded skin syndrome is also called

A

Ritters Disease

111
Q 
The usual sequence of this 
disease is:
1.Cutaneous erythema
2.Development of superficial
vesicles and bullae. Fever.
3.Skin separation in sheets 
and ribbons leaving a moist red
base that dries quickly without scarring (7-10 days)

What is the disease/bacteria/toxin

A

Ritters ds or Scalded Skin Syndrome

Staph. aureus

Exfoliative toxin (binds GM4 on cell membrane, degrades desmoglein 1)

112
Q

Primarily an “endogenous” infection by toxin producing strains. Quorum sensing induces toxin production
(Superantigen) Toxins released into bloodstream
trigger signs and symptoms:
Sudden Fever
Rash: diffuse macular erythematous rash which resembles a sunburn
Capillary leak syndrome with hypotension and multi-organ involvement
Pain rare
Desquamation: 1-2 weeks after onset (palms and soles)

Treat the “infection” and shock; no antitoxin available

A

Staphylococcal Toxic Shock Syndrome

113
Q

Primarily an “exogenous” infection”
Clinical presentation is very similar to Staphylococcal TSS
Initial soft tissue inflammation at site of infection
Septicemia
Toxin produced
Fever, chills, malaise, nausea, vomiting and diarrhea, shock; may lead to organ failure
Localized erythema ~ cellulitis
Severe pain is common

A

Streptococcal Toxic Shock Syndrome

114
Q

Destruction of epidermis, dermis, fascia (+/-muscles)

A

Necrotizing fasciitis

115
Q

Destruction of muscle tissue

A

Myonecrosis

116
Q

Loss/death off a mass of tissue (loss of vascular supply/putrification)

A

Gangrene

117
Q

Cause(s) of necrotizing fasciitis

A

Strep. pyogenes

Vibrio vulnificus

118
Q

Cause(s) of myonecrosis/gangrene

A

Clostridium perfringens

119
Q

Name the disease: Begins with cellulitis-inflammation- area becomes pale to brownish red- painful swelling (splotchy, shades of red/purple)
Gas (from microbial fermentation) accumulates under skin and in tissue resulting in crepitus =crepitant tissue
gas is generated through bacterial fermentation of host cell debris

A

Myonecrosis/gas gangrene/clostridial myonecrosis

120
Q

5 characteristics of C. perfringens

A 
Gram + rod
Spore former
Anaerobe
Double hemolysis on BAP
12 exoenzymes for invasion
Alpha toxin (lecithinase): Nagler rxn

Induces BV occlusion via aggregating platelets/neutrophils (Decreased neutrophils at site)

121
Q

Reservoir, transmission, and risk groups for Clostridium perfringens

A

Soil and human colon

Spores into wounds

DM/ poor peripheral circulation

122
Q

Treatment for C. perfringens/gas gangrene

A

Debribements, penicillin G, hyperbaric

123
Q

Strep. pyogenes and Vibrio vulnificus both can cause:

A

Necrotizing fasciitis

124
Q

____ is a membrane-damaging extracellular toxin produced by hemolytic streptococci. The membrane-damaging activity is measured by hemolysis of red-blood cell. SLO is oxygen-sensitive and is easily inactivated in its presence but can be reactivated by thiol compounds , so it is also called thiol-activated cytolysin

A

Streptolysin O (SLO)

125
Q

Name the disease involving deep tissue infection (fascia),
extensive destruction of muscle and fat.
Initial cellulitis progress rapidly to systemic symptoms.
Fluid filled bullae; NO gas (crepitate) in tissue, Infected tissue is devoid of neutrophils.
May result in failure of multiple organs.

A

Necrotizing fasciitis

126
Q

The protease toxin released by Strep. pyogenes causing necrotizing fasciitis has two functions:

A
  1. prevents migration of neutrophils and degradation of IL-8

2. invades tissue

127
Q

Name the organism:
Open wounds exposed to contaminated water result in infections which may lead to skin breakdown and necrosis
Infected skin lesions occur 24 to 48 hours after exposure
Present with erythema, edema, painful bullous (blood filled, hemorrhagic) lesions, ulcers, and may rapidly progress to necrotizing fasciitis and sepsis.

Patients with underlying liver disease are at higher risk for invasion of the organism into the bloodstream and potentially fatal complications.
life-threatening illness characterized by fever and chills, decreased blood pressure (septic shock), and blistering skin lesions.
Bloodstream infections are fatal about 50% of the time.

A

Vibrio vulnificus

128
Q

4 general characteristics of Vibrio vulnificus

A

Gram - curved rod
Motile
Capsule (stimulates TNFa)
Requires salt

129
Q

Toxin of Vibrio vulnificus

A

RTX toxin (cytolysin) punches holes in plasma membranes

130
Q

Vibrio vulnificus is often consumed in ____, risk factors include ____ (3)

A

Raw oysters

Salt water, liver disease, iron-overload hemachromatosis

131
Q

Areas of diseased tissue characterized by raw, ragged edges, serous exudates

A

Ulcers

132
Q

Areas of active and/or walled-off chronic inflammation (contain T lymphocytes , macrophages)

A

Granulomas

133
Q

Causes (5) of ulcers/malignant pustules (eschars)/granulomas

A 
Francisella tularensis
Leishmania spp.
Micobacterium spp (MOTTS)
Sporothrix schenckii
Bacillus anthracis
134
Q

Name the disease: Papule ulcerates with necrotic center and raised border primarily due to cell mediated immunity
Swelling of regional lymph nodes
Fever, chills, sweating, coughing
Cell mediated response results in granulomatous infiltrate of lymph nodes, liver, lung, spleen and bone marrow

A

Ulceroglandular sx due to Tularemia (“Rabbit Fever”)

135
Q

Tularemia can also occur in the ___(2) systems

A

Respiratory (Pneumonic tularemia, aerosol) and GI (oropharyngeal or gastrointestinal tularemia, meat contamination)

136
Q

4 general characteristics of F. tularensis

A

Gram - rod
Facultative intracellular
Capsule
Cystein requirement

137
Q

What feature allows Francisella tularensis to survive on macrophages?

A

P.I. (17-19 genes): regulation of expression: iron, intracellular growth and acidity of lysosymes.
Most symptoms due to cell mediated immune response/hypersensitivity to an intracellular organism

138
Q

Reservoir and transmission of Francisella tularensis

A

Zoonotic (wildlife like rabbits, deer, rodents)

Direct contact with contaminated animals (Low I.D. of 50-100)

139
Q

Name the disease: producing of a papule, 1-2 weeks (or as long as 1-2 months) after a sandfly bite.
grows to form a relatively painless ulcer surrounded by induration and raised borders.
The ulcer heals in 2-10 months, even if untreated but leaves a disfiguring scar.
Disseminate (multiple lesions): immune compromised (AIDS)
Death from secondary infection
Pathogenesis: reaction to pathogen= CMI (predominant Th1 response)
Vector-borne disease

A

Cutaneous leishmaniasis

140
Q

Two species of Leishmania that cause cutaneous disease

A

donovani and tropica

141
Q

What are the infective and replicative forms of Leishmania spp?

A

Promastigote is injected, transform into amastigotes in macrophages, evading host response (diagnostic stage)

142
Q

Name the disease: Involvement and destruction of mucus membranes.
Very disfiguring.
Infects tissue at mucosal-dermal junctions.
Extensive spreading into mucosal tissues shown to obliterate nasal septum and buccal cavity
It could be sequela (consequence) of cutaneous disease (Latin America). IP- from 1month to 20 years from initial skin infection

PREVENTION: treat the cutaneous infection.

A

Mucocutaneous leishmaniasis (espundia-sponge)

143
Q

Which organism causes the cutaneous leishmaniasis thought to cause mucocutaneous leishmaniasis from the Yucatan peninsula to Central and South America

A

Leishmania brasiliensis

144
Q

In what region is visceral (liver, spleen) leishmaniasis (Kala-azar) found?

A

South Asia

145
Q

Describe characteristics, reservoir, and transmission of Leishmania spp.

A

Flagellated protozoan
Intracellular replication

Humans (accidental in rodents, wild animals)

Bite of sand fly

146
Q

Where should a sample be taken to see leishmania amastigote in a skin lesion?

A

Border

147
Q

What media must be used in order to grow Leishmania promastigotes?

A

Triple N

148
Q

Name the disease-causing organism: Usually begins as a single lump or pustule
Self limiting rough, wart like lesions
Ulcerations, non-caseating (no necrosis) granuloma
Other lumps may occur around the initial lesion, particularly along the lines of lymphatic drainage-Nodular lymphadenitis

A

Mycobacterium spp. MOTTS

149
Q

4 mycobacterium species often involved in skin and soft tissue infections

A

M.marinum
M. abscessus
M. ulcerans
M. chelonae

150
Q

3 characteristics of Mycobacterium spp

A

Acid fast, pleomorphic rod
Facultative intracellular
No enzymes/toxins

151
Q

Reservoir and transmission of MOTTS

A

Environmental sources: water, soil, animals

Direct contact (wound, cut) contaminated fresh and salt water, aquariums and soil (contamination of wounds)

152
Q

Name the disease and organism: Ulcer to granulomatous lesions: fixed ulcerative lesion
May form sinus tracts (draining on to epidermis) and lymphatics become thickened and cord-like with subcutaneous nodules and abscesses
Nodular lymphadenitis

A

Sporotrichosis (“Rose Growers Disease”)

Sporothrix schenckii

153
Q

Thermally dimorphic fungi
Mold at 25*
Cigar shaped yeast at 35-37*
Found on rose thorns, sphagnum moss, timber, soil

A

Sporothrix schenckii

154
Q

On incubation, Sporothrix schenckii mycelium is ____, ____, and very delicate with _____ ____ forming a typical arrangement in groups

A

Branching, septate, pyriform conidia

155
Q 
Name the disease: 
2-5 days after exposure
Progression through:
erythematous papule
Central necrosis progressing to a Purple to Black necrotic eschar
Edematous and may be surrounded by purplish vesicles
Accompanied by:
lymphadenopathy, 
 Massive edema; may progress
        to toxemia

Lesion may be confused with bite
of Brown recluse spider or Orf viral infection

A

Cutaneous anthrax (Bacillus anthracis)

156
Q

5 general characteristics and reservoir of Bacillus anthracis

A 
Gram + rod
Spore former
Capsule
Aerobe
Medusa head colonies
Soil dweller
157
Q

Dehydrated, multi-shelled structure that contains a complete copy of the chromosome, the bare minimum concentrations of essential proteins and ribosomes and a high concentration of calcium bound dipicolinic acid

A

Bacterial endospore

158
Q

Describe the capsule of B. anthracis

A

Polypeptides, repeated D-Glutamic acid, carried by a plasmid

159
Q

Describe the enzymatic toxin of B. anthracis

A

Anthrax exotoxin carried by plasmid with:
Edema factor
Lethal factor
Protective antigen

160
Q

A calmodulin- dependent adenylate cyclase), causes increase in cAMP=reduce phagocytosis. Part of anthrax exotoxin.

A

Edema factor

161
Q

Zinc metalloprotease which inactivates MAPKK) – tissue necrosis; activates macrophages with excessive cytokines production =shock
Part of anthrax exotoxin.

A

Lethal factor

162
Q

Binds to host cell and EF LF=lethal toxin
(antibodies against PA block entry.
Part of anthrax exotoxin.

A

Protective antigen

163
Q

Treatment for cutaneous anthrax

A

Doxyxycline/ciprofloxacin

60-90 days

164
Q

Anthrax vaccine for high-risk populations is made of

A

Antibodies against PA factor

165
Q

Name the disease: Known as malignant pustule-eschar
Characterized by small, painful, reddish, maculopapular, well circumscribed lesion with a margin that begins pink, darkens to purple and finally becomes black and necrotic.
Histology: shows vascular invasion -hemorrhagic vasculitis

A

Ecthyma gangrenosa

166
Q

Organism which causes ecthyma gangrenosa

A

Pseudomonas aeruginosa

167
Q

Risk group for ecthyma gangrenosa

A

Those with weakened immune systems: neutropenic patients/those in poor health: diabetics

168
Q

4 structural characteristics of P. aeruginosa

A
  1. Pilli (biofilms)
  2. Capsule
  3. Pyocyanin: generates ROS
  4. Pyochelin: scavenges iron
169
Q

5 general characteristics of P. aeruginosa

A 
Gram - bacillus
Aerobe
Capsule
Oxidase +
Lactose -
170
Q

Cause(s) of opportunistic soft tissue infections/abscesses

A

Bacteroides fragilis
Acinetobacter baumanii
Staphylococcus aureus
Pseudomonas aeruginosa

171
Q

Diseases caused by Bacteroides fragilis

A

Intra-Abdominal Abscess, peritonitis, genital infections and PID in females (soft abscesses)

172
Q

4 general characteristics of Bacteroides fragilis

A

Gram - rod
Anaerobe
Capsule (^binding)
LPS cell wall (No lipid A)

173
Q

Enzymes on B. fragilis

A 
Succinic acid (inhibits phagocytosis)
Superoxide dismutase (allows survival with small amounts of O2)
174
Q

Reservoir and transmission of Bacteroides fragilis

A

Normal flora UG/GI

Endogenous with perforation of bowel/vagina

175
Q

Risk group of B. fragilis

A

Surgical procedures

176
Q

Media for growth of Bacteroides fragilis

A

Bacteroides Bile Eschulin agar with gentamycin

177
Q

Those with wounds d/t surgery, trauma, or burn are at higher risk for infection with (2)

A

Staph. aureus (implants)

P. aeruginosa

178
Q

Organism causing wound infections:
Surgical-cellulitis and bullae with a visible necrotizing process
Breathing tubes
Complications: pneumonia- high risk of mortality
Military outbreaks infections began to be seen in the US in in American soldiers returning from Iraq-Iraqibacter

A

Acinetobacter baumanii

179
Q

6 general characteristics of Acinetobacter baumanii

A 
Gram - rod
Facultative anaerobe
Oxidase -
Gamma hemolytic
Capsule
Biofilms
180
Q

Special media designed for highly resistant Acinetobacter baumanii

A

CHROM agar

Red = MDR

181
Q

Acinetobacter baumanii reservoir and transmission

A

Soil and water, skin of healthcare workers/others, oro-pharyngeal flora in few people

Direct contact/respiratory droplets

182
Q

Where do most outbreaks of Acinetobacter baumanii occur?

A

ICU/ ill patient housing

183
Q

Name the disease: The signs and symptoms may include:
Swelling, pain and/or tenderness in the infected area
Fever
+/-Drainage of pus through the skin

Additional signs and symptoms include:
Excessive sweating ,Chills
Lower back pain (if the spine is involved)
Swelling of the ankles, feet, and legs
Changes in gait (walking pattern that is a painful, yielding a limp)

A

Osteomyelitis

184
Q

Cause(s) of osteomyelitis

A

Staph. aureus (common)
Pseudomonas spp. (trauma)
Salmonella spp. (Sickle cell pts)

185
Q

Which bones are usually affected by osteomyelitis in adults? kids?

A

Feet, spine, hips in adults

Long bones in kids

186
Q

Risk factors for osteomyelitis

A

open bone injury, seeding of clot from minor trauma, bacteremia, chronic wound.
DM, dialysis, IDU all increase treatment time.

187
Q

Along with increased WBCs and ESR and/or CRP, what IV drug can be injected to diagnose osteomyelitis in a bone scan?

A

Technetium-99 pyrophosphate

188
Q

5 general characteristics of Salmonella

A 
Gram - rod
Lactose -
>2000 serotypes
Hektoen agar shows
H2S production (green colony with black center)
189
Q

Reservoir, transmission, and increased risk groups for Salmonella

A

Animal reservoir, human carriers (gallbladder)

Endogenous/hematogenous (food borne or carrier)

^Risk with sickle cell anemia

AUC MS2 (2 decks)

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