Micro - Skin, Blood, Muscle Flashcards

1
Q

S. aureus Alpha-toxin

A

Cause mammalian cell membranes to leak through pores formed by toxin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

S. aureus exfoliatins

A

Split epidermis between the stratum spinosum and stratum granulosum by disruption of intercellular junctions -> scalded skin syndrome

Toxin is absorbed in blood stream, w/erythema and intraepidermal desquamation at remote sites -> no S. aureus can be isolated from desquamation sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

S. aureus - coagulase

A

Coagulase is not a toxin, but plays role in pathogenesis -> fibrin coat makes Staph resistant to phagocytosis. Fibrin deposition in area of staph infxn helps localize the lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

TSST-1 sx’s

A

High fever, vomiting, diarrhea, sore throat, muscle pain. Shock w/in 48 hours. Renal and hepatic dmg. Skin rash (followed by desquamatio at deeper level than toxic shock syndrome) and strawberry tongue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Coagulase negative Staph

A

Normal commensals. Non-beta-hemolytic (lack major virulence factors of S. aureus).

S. lugdunensis - primary pathogen like S. aureus. Occasional very serious infxns. Abscess formation. Can cause prosthetic joint infxn. Emerging pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Staph. epidermidis

A

EPS or biofilm -> adhesion to catheters, artificial heart valves, etc. Biofilm -> protected from phagocytosis and abx, yet still obtain nutrients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Grp A Strep pyogenes

A

Pyrogenic exotoxin (SPE) -> cytokine release ->

  • Red rash on skin (scarlet fever) cheeks, temples, buccal mucosa, strawberry tongue, punctate hemorrhages on palate, sandpaper rash on trunk, arms legs
  • Pharyngitis (spread by direct contact or aerosols)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Poststreptococcal sequelae

A

Acute rheumatic fever ->

  • Inflammatory dz -> fever, carditis, subcutaneous nodules, migratory polyarthritis
  • Heart valve dmg -> murmurs, cardiac enlargement, repeat infxns -> progressive dmg
  • Acute glomerulonephritis (children) -> 10 days after infxn, occasional renal failure, type III hypersensitivity
  • Impetigo - starts at insect bite or minor abrasion. Small vesicles w/erythema become pustular and later crusted. Ecthyma
  • Erysipelas - skin and subcut tissues. Spreading area of erythema and edema, often on face -> pain, fever, lymphadenopathy
  • Strep pyogenes cellulitis, necrotizing fasciitis, TS-like S
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Grp B Strep (GBS) - Strep agalactiae

A
  • Neonate can acquire GBS during passage through birth canal unless preventative measures are taken
  • Neonatal dz - lethargy, fever, sepsis, meningitis, resp distress
  • Older children and adults - puerperal fever at delivery, gyn surgery infxns, skin and soft tissue infxns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Beta strep, NOT grps A or B

A

Grps C and G can cause pharyngitis -> no post infxn sequelae. Skin and soft tissue infxns, infxns of wounds, occasional bacteremias. Same txt as for grps A and B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Viridans strep (all other alpha strep once Strep pneumoniae has been ruled out)

A

Alpha hemolytic.

  • S. milleri grp - deep tissue abscesses
  • Species that cause subacute bacterial endocarditis - S. mutans (dental caries), S. mitis, S. salivarius. Detect w/blood cultures. Tx w/PCN for weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Strep Abiotrophia sp

A

Nutritionally-deficient Strep.

  • Will not grown on ordinary blood agar -> needs spec vitamin or nutrient. Colony resembles viridans or non-hemolytic strep species
  • Causes bacterial endocarditis -> sometimes difficult to detect by culture unless lab thinks to add “feeder colony” or special nutrients to media
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Enterococcus

A

Naturally in gut. Non-hemolytic strep. Grp D. Strep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

E. faecalis and E. faecium

A
  • IS SUSCEPTIBLE (to ampicillin). Most common clinical isolate.
  • UM (ultra mean) - resistant to ampicillin. More likely to be resistant to vancomycin than E. faecalis (VRE). Ctrl w/std precautions and reduced use of vancomycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Enterococcus dzs

A
  • Opportunistic infxns (wound and soft tissue, bacteremia related to indwelling lines).
  • Endocarditis
  • UTIs
  • Wound infxns in intensive care units “Me too”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Opportunistic Corynebacterium pathogens

A
  • Corynebacterium ulcerans - skin infxns

- Corynebacterum jeikeium - nosocomial bloodstream and wound infxns (automatically resistant to ampicillins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Erysipelothrix rhusiopathiae

A

Coryneform. Gram positive diphtheroid-like rod. Found in animals, meat, and seafood

Disease: Erysipeloid – Painful slowly spreading skin infection.
• Follows traumatic inoculation of skin –Fishermen, butchers, veterinarians

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Clostridium perfringens features

A

Gram positive spore forming rod. No spores in tissue stains.
– Fast growing anaerobic fermenter - generates large amounts of H2 & CO2
– Found in colon and soil.
– Encapbsulated and non-motile.

Culture characteristics: 1) double zone of hemolysis on blood agar. 2) Litmus milk stormy fermentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clostridium perfringens toxins

A
  • Alpha - main pathogenic factor!!! Diffuses through tissue, killing cells and producing more necrotic growth
  • Theta toxin - toxic for heart mm and caps. Similar to Streptolysin O in beta strep
  • Enterotoxin - causes food poisoning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Clostridium perfringens - other destructive mechs

A
  • Fermentation of mm carbs -> crepitation, palpable gas -> gas gangrene. Contam w/dirt, feces. Rapidly life-threatening! -> can’t wait for cultures -> clinical dx needed! Remove infected tissues immediately, surgical debridement, drain wound. Hyperbaric O2 chamber, tx w/PCN. Culture and gram stain -> boxcar.
  • Destructive EC enzs - collagenase, DNAse, hyaluronidase, protease
  • Anaerobic cellulitis -> mixed anaerobic flora including Clostridium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Lactobacillus

A

Resemble alpha strep. Nml vaginal flora. If replaced with Mobiluncus, vaginitis results. Can cause blood infxn in big doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Actinomyces

A

Pathogenic anaerobe! Long, Gram pos rods. Often BRANCHING. No spores, not acid-fast

Can cause serious chronic infxn. IUDs, aspiration pneumonia, abscesses in neck or head. May see pus w/granules in infxn (sulphur granules)

  • A. israelii - most common pathogen in serious infxn. “Molar tooth” colony morphology. (A. naeslundii, A. meyeri)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Propionibacterium

A

Anaerobic, “coryneform,” Gram pos, non-sporeforming rod. Nml skin flora -> opportunistic pathogen, common blood culture contam.

Infxns - acne, opportunistic infection of prosthetic devices. Part of mixed anaerobic infxns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Bacteroides fragilis

A

Most common Gram neg anaerobic infxn. PCN RESISTANT.

#1 member - B. fragilis - capsule w/antiphagocytic fxn
#2 - Fusobacterium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Rickettsia

A

Gram neg bacilli. Fevers w/a rash. Infect vascular endothelium -> RBCs leak from breaks in BVs -> rash and petechial lesions. Systemic sx’s.

Gen sx’s: fever, HA, external rash and internal focus lesions, endotoxin-like shock may occur

Difficult to culture (not routine testing!), need PH labs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Rickettsia rickettsii

A

D/t bite from Dermacentor variabilis. Sim dz as R. conorii.

Rash is main feature -> wrists, ankles, trunk. RASH ON PALMS AND SOLES IS KEY

  • Need clinical dx -> tx w/abx immediately!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Rickettsia akari

A

Rickettsialpox. Transmit via house mouse mite bite. Benign, self-limiting illness. Papulovesicle -> fever w/rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Rickettsia tsutsugamushi

A

Scrub typhus. Rodent mites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Rickettsia prowazekii

A

Pediculus humanus (louse, defecates when it feeds -> ctrl pops!)

Typhus fever sx’s: fever, HA, malaise, myalgia. Rash on trunk to extremities (can get gangrene). Complications: CNS and heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Rickettsia prowazekii relapse

A

Brill’s Dz. Relapse of louse-borne typhus. 10-40 years after first infxn.

Rickettsiae remain dormant in reticuloendothelial cells. Decreased immunity of old age enables attack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Borrelia burgdorferi

A

Large spirochète. Stains weakly w/ordinary stains -> culture is difficult -> use EIA for AB plus Wetern blot for confirmation. Long doubling time: 8-24 hours. Has toxic LPS. Transmitted by Ixodes tick. Deer, white-footed mouse.

Dz stages: - Primary lesion -> erythema chronicum migrans (ECM rash). Slowly expanding red ring, biopsy of leading edge -> organism in leading edge

  • Secondary stage -> Spirochetemia and systemic sx’s - fever, mm and jt pains, meningeal irritation
  • Late stage -> few organisms in diverse organs w/immunological-mediated dmg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Measles/Rubeola virus

A

Paramyxovirus (G: Morbivilivirus). ssRNA. Imp prots: hemagglutinin prot, fusion prot, matrix prot

Resp spread. Prodroma fever plus 3 C’s (cough, coryza [runny nose - like a head cold], conjunctivitis). Koplik’s spots (oral mucosa), maculopapular rash, lymphadenopathy, photophobia. Rep at mucosal epi, spread to skin, lymphoid tissues, other organs

Deaths d/t failure to have at least one dose

33
Q

Measles complications

A
  • Postinfectious encephalitis
  • Interstitial pneumonia
  • Bacterial superinfxns - pneumonia, otitis media
  • Subacute sclerosing panencephalitis
34
Q

Measles dx and tx

A

Dx: urine or pharyngeal cell sample. PCR, culture w/monkey kidney cells, 4-fold rise in Ab (both IgG and IgM) between acute and convalescent titers

Best immunization is live attenuated vaccine. Need 2 doses. May cause fever and rash

35
Q

Rubella virus

A

Togavirus. ssRNA. Humans only. Low-grade fever, catarrhal upper resp sx’s, lymphadenopathy, rash. Mild dz in adults -> usually ignored bc it lasts few days

Rubella palatial spots, rubella exanthem (macular rash after onset of prodromal fever)

Rare complications: transient arthralgia/arthritis, encephalitis

36
Q

Rubella congenital infxn

A

High risk in first trimester. No major threat to fetus after 5th month.

Transplacental spread to fetus -> chronic fetal infxn, compromised fetal oxygenation, disruption of nml organogenesis.

Cintinued postnatal dmg -> shed virus for years, Ab-immune complex, continuing tissue dmg

If titer drops over 3-4 mos, baby was probably NOT infected

If mother is seroneg, immunize, but no preg for months. Monitor titer, stay away from unimmunized children

37
Q

Parvovirus B19

A

ssDNA. Replicates in nuc of immature RBCs and synovial fluid cells. Resp drop inhalation

Fifth dz/erythema infectiousum: fever, malaise, HA, myalgia, slapped-cheek rash on face (spreads to extremities), itching, lymphadenopathy, leukopenia, anemia, arthralgia/arthritis

  • Rep in RBC precursors -> arrest of erythropoiesis -> aplastic crisis in SCD, Thalassemia
  • Chronic anemia w/chronic infxn - fetus w/immat immune system, adult w/deficient immune system

Can cause congenital infxn -> hydrops fetalis!

38
Q

Hand, Foot, and Mouth dz

A

Coxsackie virus A16 (enterovirus). Fever and blister-like eruptions around mouth and/or a skin rash. No treatment, children recover from xanthems with little effect

39
Q

West Nile Virus dz

A

Mild sx’s include fever, HA, myalgia, arthralgia, lymphadenopathy, and rash on trunk and extremities. Occasionally, pancreatitis, hepatitis, and myocarditis

Serious WNV dz - meningitis-like.

No txt, simply tx sx’s

Dx: clinical suspicion, immunoassay for WNV AB (IgM and 4-fold rise in IgG Ab). PCR

40
Q

Herpesvirus varicellae

A

DNA virus. NOT A TRUE POX VIRUS!!! Belongs to Herpes grp. Not as resistant to drying and survival outside the body as true pox viruses

41
Q

Chickenpox pathogenesis

A

Enters through upper respiratory tract, direct contact, and aerosol. Carried by phagocytic cells to local LNs for primary replication (can also happen in resp tract)

  • Lesions: macular -> papular -> vesicular (fluid in cellular interspaces lifts superficial corneal layer to form delicate vesicle) -> scab
  • Highest risk of death is in susceptible children with leukemia
41
Q

Chickenpox in pregnancy

A

Infxn during 1st trimester of preg. Fetal abnormalities occur in up to 3%. Infant fatality up to 50%

Infxn of baby 5 days or less before delivery - high infant mortality risk

Vaccinate susceptible women after their pregnancy

42
Q

Roseola infantum syndrome

A

Sixth dz. In infants up to 4 yrs of age. Herpesvirus 6B (HHV-6B) (resembles adenovirus, enterovirus infxn). HHV-6A infects adults -> virus in LNs of HIV-1 infected persons progressing to AIDS

Initial sx’s 3-5 days: abrupt onset, high fever, sometimes brief convulsions, leukopenia.

Later sx’s: (after 3-5 days): fever subsides -> macular rash (faint and transient)

No tx for severe HHV6 infxn. Very rare complications: CNS, liver, or lungs

43
Q

HHV-7

A

Isolated from CD4 T cells of healthy individuals. Closely related to HHV-6. 97% of all adults are serologically positive. Often children >2 yo become infected. Clinical relevance unknown

44
Q

EBV (HHV-4)

A

Large atypical lymphocytes (Downy cells). New assays use quantitative PCR to detect level of EBV in whole blood. Self-limiting dz -> supportive measures.

For serious infxns (transplants) - antivirals may be used.

45
Q

HHV-8

A

Kaposi’s sarcoma. Affects CTs such as cartilage, bone, fat, mm, and BVs. Assoc w/HIV infxn and AIDS.

Skin lesions can resemble other skin d/os -> inflam, bacterial/fungal infxn, non-Hodgkin lymphoma, or hemangioma. -> punch biopsy sent to surgical path lab.

Antiviral therapy against AIDs can shrink lesions. Radiation or cryotherapy used for lesions in some areas.

46
Q

Family Poxviridae

A

dsDNA virus. Brick shape, lipid envelope, reps in cytoplasm.

47
Q

Human papilloma virus

A

Small DNA tumor viruses, family Papovaviridae. Certain HPV types target squamous epithelium on hands, feet, lips, and GUTs.

Skin warts in various body sites. Common warts, freq found on soles of feet, on hands, and around knuckles. Flat warts (verruca plana), plantar warts, genital warts (condylomata acuminata)

48
Q

Tanapox group

A

Africa along Tana river in Kenya and Zaire. Infxn of lower primates. Dz in man: 3-4 day fever w/body aches. 1-2 lesions appear on skin. Lesions develop slowly and become large, heal in 2-7 wks.

49
Q

Parapoxvirus

A

ORF pox. Less brick-shaped than Orthopox. Cylinder w/rounded ends. At risk: dz of sheepherders, vets, and others working with sheep. Transmitted through abraded skin. Most common pox virus spread to man in the US bc of sheep and goats

Lesions (never many in number), develop from maculopapular rash that becomes elevated and eventually nodular. Crust and sheds several scabs and heals after 35+ days.

Dx: scrape lesion and send for EM -> virus particles are shaped like cylinder with rounded ends wrapped with rope.

50
Q

Monkey pox

A

Endemic in monkeys. Africa, middle America (prairie dogs). Spread at 1/4 the rate of smallpox, 16% mortality.

51
Q

Black piedra

A

Asymptomatic. Ascomycete genus Piedraia spp. Restricted to humid tropical areas. Nodules CANNOT be pulled off hair shaft. Difficult to tx: topical azole antifungals.

52
Q

Molluscum contagiosum

A

Unclassified pox. dsDNA. Affects in all age grps throughout the world. Virus causes benign tumor or the skin. 1-20 lesioins lasting up to 2 yrs w/second crop occasionally lasting longer. localized proliferation of eli to form lobulated and umbilicated papules 2-8 mm in diameter. Water warts. Pore in center of papule. Below is crater filled with loosely adherent partially keratinized epi cells -> white, curd-like material called “molluscum body.” Spread by scratching. Spont resolution.

Children get dz during play or sports. Predisposing factors: crowded living conditions, poor hygiene. May be spread sexually. Tx: uninflamed lesions, few in number are best treated with curettage or other forms of removal.

Opportunistic infxn in AIDS pts -> more generalized lesions on face and upper body as well as genital lesions. May become large and atypical

53
Q

White piedra

A

Caused by several species of Trichosporon. Asymptomatic growth on outside of hair shaft. Soft, white/green/yellow nodules that can easily be pulled off the hair (compacted fungal elements). Hairs are not invaded, but may break if fungi has been there for long periods. Warm, moist conditions predisposes.

Ctrl: shaving and local application of antifungal agents.

54
Q

Pityriasis versicolor

A

Malassezia furfur. Infects outer layers of stratum corneum. Superficial, chronic, asx’s. Macular rash or fine scaling of upper trunk and shoulders -> lesions appear lighter or darker than surrounding skin.

Lab dx confirmed by microscopy -> spaghetti and meatballs.

Tx: topical antifungals clear infxn. Condition frequently recurs.

55
Q

Tinea nigra

A

Don’t confuse with black piedra on hair! Caused by Hortae werneckii. Smooth colonies with oily, glistening, olive-black color. Aged colonies velvety d/t aerial hyphae. Hyphae darken w/age. Somewhat halophilic

Superficial infxn of skin: stratum corneum. Brown to black lesions. Mainly on palm, sometimes on sole of foot. Only outer, dead layers of skin involved, no invasion of living tissue.

56
Q

Other infxns with Malassezia spp

A

Lipid nutirents through CVCs -> colonization of catheters. Deep-line cather-assoc sepsis in neonates - M. fur fur or M. pachydermatis

May cause seborrheic dermatitis and dandruff. Old name: Pityrosporum oval

Lab dx: isolation of the yeast using lipid containing media. Can also see yeast in tissues

57
Q

Microsporum spp

A

Attack skin and hair, not nails. Macroconidia with rough walls are more numerous than microconidia.

58
Q

Epidermophyton floccosum

A

Attacks skin and nails, not hair. Macroconidia with large smooth walls. Born singly or in banana-like clusters. NO MICROCONIDIA

59
Q

Cutaneous mycoses: dermatophytes

A

Use keratin as nutrient source, colonize stratum corneum. Annular ring, scaly patch w/raised margin -> ring worm/jock itch. Hair - hair loss w/dry scaly patch of skin. Nails -> yellow, thickened, crack

60
Q

Tinea corporis

A

Ringworm of upper parts of covered body. Trunk, shoulders, etc. Areas with relatively less hair. Lesions are well-marginated with raised erythematous, vesicular borders. Infn may be mild to severe. Most serious chronic infxn often d/t T. rubrum.

61
Q

Tinea cruris

A

Jock itch. Frequently caused in adults by T. rubrum or E. floccosum. Lesions are erythematous, scaly, raised inflamed borders, often w/vesicles. Usually bilaterally extending down the sides of inner thighs, waist area, and buttocks. Sx’s: itching and burning.

62
Q

Trichophyton spp

A

Attack skin, hair, and nails. “Lifelong” nail infxns. Microconidia are more numerous than smooth pencil-shaped macroconidia.

T. rubrum - colony surface is white, velvety to fluffy. Colony reverse is wine red. Urease negative.

T. tonsurans - major cause of ringworm in skin

63
Q

Tinea pedis

A

Common agents: T. mentagrophytes, T. rubrum, E. floccosum

Scaling, fissuring, erythema, itching, burning. Less clinical form is infxn of soles and heeles extending up sides of foot (moccasin foot).

Acute condition - vesicles, inflam, and pustules

64
Q

Tinea capitis

A

Infxn of scalp, eye brows, eye lashes.

Ectothrix invasion when fungus forms sheath of hyphae and arthroconidia around shafts of hair

Ectothrix invasion when hyphae invades hair follicle and shaft and form many spores within. Infected grayish-white hairs break off easily at the scalp giving ‘black dot’ appearance.

Common agents: ectothrix ringworm of the scalp: M. audouiniii, M. canis, and M. gypseum

Endothrix ringworm of the scalp in US is T. tonsurans

65
Q

Tinea barbae

A

Often caused by zoophilic dermatophytes: T. verrucosum (cattle), T. mentagrophytes (mice, rodents)

More severe form w/pustumar lesions

66
Q

Candidiasis of skin

A

Lesions - erythematous papules or as confluent areas of tenderness and redness of skin.

Tx: decrease moisture and chronic trauma. Disposable diapers.

67
Q

Fungal eye infxn

A

Fusarium (hyalohyphomycosis) commonly infects d/t its pointy curved shape.

Scratches, contact lenses predispose. Caused by various fungi

68
Q

Tinea unguium

A

Causes: T. rubrum, T. mentagrophytes, E. floccosum

Invasion of nail plate by a dermatophyte. Nail invasion involves nail bed and skin on underside of nail -> lifting off nail plate and detachment from nail bed.

69
Q

Subcutaneous mycoses (mycetomas)

A

Hyalohyphomycosis. Chronic subcutaneous infxns caused by fungi or certain bacteria (actinomycetes). Traumatically implanted into deep tissue. No systematic spread, seldom fatal. Abscesses may discharge to surface through draining sinuses, may extend to bone -> chronic osteomyelitis

70
Q

Chromoblastomycosis (chromomycosis)

A

Phaeohypomycosis. Aka verrucous dermatitis. Caused by Phialophora and Cladosporium.

Traumatic inoculation of skin -> cause wart-like nodules. Infxn remains localized. Slow, painless infxn.

71
Q

External otitis

A

Hyalohyphomycosis. Several common molds. Most common includes Aspergillus spp. Often occur together w/mixed pops of bacteria and yeasts, so establishing their role in otitis can be difficult

72
Q

Sporotrichosis

A

Phaeohypomycosis. Sporothrix schenckii. Fungus of soil, plants, wood, and moss -> gardening. Flower-like sporulation.

73
Q

Eumycetoma - madura foot

A

Pseudoallescheria (Petriellidium) boydii. Usual infxn assoc w/trauma to feet, lower extremities, and hands -> local swelling w/suppuration and abscess formation -> formation of granulomas and draining sinuses

74
Q

Wood’s light exam

A

Tinea versicolor - subtle gold

Tinea capitis - caused by Microsporum canis and Microsporum audouinii -> light bright green. Most tinea capitis infxns are Trichophyton species - no fluorescence

75
Q

Mycobacterium marinum

A

Acid fast photochromogen. Lab media -> light -> yellow pigment. 28-30C for optimal growth, does not grow at 37C.

Traumatic inoculation. Working in or around sea water or aquarium water -> need clinical suspicion. Chronic non-healing lesions on hands, arms, or feet. Lesions that did not respond to nml outpt abx

76
Q

Mycobacterium ulcerans

A

Aka Buruli ulcer. Story similar to M. marinum, EXCEPT: Scotochromogen -> non-pigmented

77
Q

Mycobacterium chelonae

A

AFB. Causes soft tissue abscesses and chronic cutaneous lesions. Traumatic inoculation into skin. Can be difficult to tx.