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Block 6: Microbio, ID, Derm, Heme-Onc > Eye, Fungi, Antifungals, Parasites (Week 5) > Flashcards

Eye, Fungi, Antifungals, Parasites (Week 5) Flashcards

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1
Q

Visual parameters

A

Central visual acuity

Contrast sensitivity

Color vision

Visual field

Dark adaptation

Binocularity

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2
Q

What does 20/40 vision mean?

A

What you see at 20 feet, normal person can see at 40 feet

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3
Q

Scotomata

A

Blind spot

Occurs when part of macula not working well

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4
Q

4 things that go wrong to cause vision loss

A

1) Focused light doesn’t reach the retina (common, fix w/glasses!)
2) Retina doesn’t turn it into nerve impulses
3) Optic nerve doesn’t transmit impulses to the brain
4) Brain doesn’t process them correctly

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5
Q

Pre-retinal and retinal mechanisms for vision

A

Pre-retinal: barriers to light, misdirection of light

Retinal: tissue loss, disorganization/dysfunctional tissue

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6
Q

Steropsis

A

Perception of depth

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7
Q

How much refracting of light does the cornea do?

A

Cornea does 2/3 of refracting of light

(more than lens!)

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8
Q

How does the cornea remain so clear?

A

Orderly arrangement of collagen fibers

This arrangement is maintained by relative dehydration of stroma (endothelial cells on inner surface of cornea must continually pump water out of corneal stroma)

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9
Q

Abnormalities of the cornea

A

Epitheliopathies (disruption, edema)

Stromal opacities (scarring, edema)

Irregular shape

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10
Q

Clinical disorders of the cornea

A

Keratitis sicca

Infectious keratitis

Peripheral ulcerative keratitis (RA)

Pseudophakic corneal edema

Keratoconus

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11
Q

Symptoms and pathology of cornea

A

Everything is white = opacities

Colored haloes = edema

Distortion = irregularities

Ghost images = refractive errors, epitheliopathies

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12
Q

Abnormalities of the eyelids

A

Structural defects (tumors)

Entropion/eyelashes hitting eye (trichiasis)

Ectropion/eyelid laxity

Dysfunction (lagophthalmos, ptosis)

Weakness

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13
Q

Anterior segment

A

Lens forward

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14
Q

How much refracting of light does the lens do?

A

Lens does 1/3 refracting of light

Only does focus/fine tuning

Does accommodation (change focus for near vision)

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15
Q

Abnormalities of the lens

A

Dislocation

Opacification (cataract)

Swelling

Hardening with age

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16
Q

Abnormalities of retina

A

Loss of tissue (infection, degeneration)

Edema

Disturbances of normal position (traction = distortion, retinal detachment = distortion)

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17
Q

Symptoms of macular degeneration

A

Problem with part of retina

Blurry spot in center of vision

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18
Q

Onchocerciasis

A

AKA River Blindness

Endemic in equatorial Africa

Transmitted by black fly (filarial nematode)

Tx: Ivermectin (1 x per year for 10 years)

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19
Q

Three serious diseases that cause blindness

A

Leprosy

Onchocerciasis

Trachoma

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20
Q

Conjunctivitis

A

Red eye with no pain and nodecreased vision

Cornea clear with good light reflex

Causes: allergic (itching), bacterial (pus, adenopathy, potential source), viral (acute, hx exposure, mucus, preauricular adenopathy)

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21
Q

What causes epidemic conjunctivitis

A

Adenoviruses

Also could be coxsackie, enterovirus, Strep pneumoniae

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22
Q

Epidemic conjunctivitis

A

Lasts 10 - 14 days

Highly contagious (for 3 weeks)

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23
Q

Hemorrhagic conjunctivitis

A

More severe form of conjunctivitis

Vessels of conjunctiva so inflamed that they burst

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24
Q

Herpetic viral conjunctivitis

A

Due to HSV

Can have recurrences with corneal dendrites

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25
Q

Viral causes of ocular infections

A

Adenovirus

Coxsackie

Herpes simplex

Herpes zoster

Varicella

CMV

RSV

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26
Q

Bacterial causes of ocular infections

A

Strep

Staph

Pseudomonas

Neisseria

Syphilis

Borrelia (Lyme disease)

Chlamydia (trachoma)

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27
Q

Mcobacteria (?) that cause ocular infections

A

Mycobacteria (?) tuberculosis

Leprosy

Atypical forms

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28
Q

Fungal causes of ocular infections

A

Mucormycosis

Candida

Others

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29
Q

Protozoa and nematodes that cause ocular infections

A

Acanthamoeba

Filariasis (elephantiasis)

Toxoplasmosis

Toxocara

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30
Q

Methods of infection and spread of ophthalmic disease

A

1) Direct contact with or without disruption of normal protective barriers (contact lens, trauma, foreign bodies, birth canals, hands; ophthalmia neonatorum)
2) Direct spread (sinus infection spreading into orbit)
3) Hematogenous spread (retinal and choroidal infections, septic embolus from endocarditis, meningitis, fungemia; CMV retinitis)
4) Iatrogenic (post-lasik non-tuberculous mycobacterial infection)

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31
Q

Ophthalmia neonatorum

A

Spread by direct contact

Chemical conjunctivitis within 24 hours of birth

N. gonorrhoeae within 4 days of birth

Chlamydia within 3 weeks of birth

Herpes simplex

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32
Q

Causes of pediatric acute conjunctivitis

A

Bacterial (H. influenzae, S. pneumoniae, M. catarrhalis (same as otitis media!))

Viral infection (adenovirus)

Allergy

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33
Q

Polytrim

A

Good ophthalmic antibiotic

Polymyxin: Gram - coverage

Trimethoprim: Gram + coverage

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34
Q

3 ways to deliver antibiotic therapy for the eye

A

1) Topical
2) Intravitreal injection
3) Systemic

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35
Q

Fungi

A

Eukaryotes (have nuclear membrane, chromosomes, mitochondria)

Cell walls made of complex polysaccharides (chitin, chitosan, glucans, mannans)

Plasma membrane contains ergosterol (rather than cholesterol)

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36
Q

Yeasts

A

Unicellular fungi

Reproduce by budding or fission

Form colonies in culture (similar to bacteria)

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37
Q

Molds

A

Multicellular fungi

Germ tubes grow with extension of hyphae (either septate or non-septate)

Form cottony colony called mycelium

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38
Q

Fungal reproduction

A

Asexual reproduction without propagules (hyphae form new mycelium)

Asexual reproduction by propagules (either conida or sporangia)

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39
Q

Dimorphism

A

In environment, grow as mold

In infected host, grow as yeast

This is temperature dependent

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40
Q

Fungal pathogenesis in human disease

A

Hypersensitivity

Mycotoxicoses (release toxin)

Colonization

Invasive disease (but virulence factors not as well understood)

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41
Q

Hypersensitivity disease

A

Allergic reaction to fungal spores or other components

Can cause pneumonitis, rhinitis, asthma, alveolitis, sinusitis

Can do skin tests with purified antigens to diagnose

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42
Q

Mycotoxicoses

A

Ergot alkaloids: alpha-adrenergic agonist caused vasoconstriction and gangrene, and interaction with dopaminergic and serotinergic receptors caused hallucinations

Aflatoxins (Aspergillus flavus) causes liver disease, and is possible carcinogen (contaminated peanuts)

Psychotropics (psilocybin and psilocin used in rituals and as recreational drugs)

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43
Q

Different layers fungi can colonize

A

1) Superficial: outermost layer of skin and hair, colonization of mucosa
2) Cutaneous: extend into epidermis, invade hair and nail
3) Subcutaneous: invade dermis, subcutaneous tissue, muscle, fascia
4) Systemic: originate in lung, may disseminate to other organs

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44
Q

Superficial mycoses

A

Colonize dead tissue from dying skin cells and lipids

Usually cosmetic problems

Tinea versicolor (M. furfur; pigmented macules, “spaghetti and meatballs” and likes fatty acid)

Tinea nigra (H. werneckii; produces melanin)

White or black piedra (Trichosporon species)

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45
Q

Cutaneous mycoses

A

“Dermatophytes” = Microsporum, Trichophyton, Epidermophyton

In epidermis

Skin, hair, nails

Clinical manifestation called “tinea” or “ringworm”

Named for structure infected: Tinea pedis, capitis, magnus, unguium, cororis, cruris

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46
Q

Different kinds of dermatophytes

A

Geophilic: reservoir in environment, soil

Zoophilic: reservoir in animals

Anthropophilic: like covered areas of skin

All use keratin as nutritional substrate

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47
Q

Subcutaneous mycoses

A

Fungal infections invasive into soft tissue

Sporotrichosis (sporothrix shenkii) is only one in US

Usually at site of trauma

May require surgery and antifungal therapy

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48
Q

Lymphocutaneous sporotrichosis

A

Sporothrix schneckii

Dimorphic

Get from rose thorn scrape –> tracks up lymphatics

Causes ulcerating lesions, nodules, adenitis and rarely pulmonary and disseminated disease

49
Q

Dematiaceous fungi

A

“Black molds”

Chromoblastomycosis

Phaeohyphomycosis (chronic allergic sinusitis)

Eumycotic mycetoma (madura foot)

50
Q

Systemic mycoses

A

Dimorphic: histoplasma, blastomyces, coccidioides (spherules), paracoccidioides

Monomorphic yeast: cryptococcus

Usually enter by inhalation in lung –> short or asymptomatic respiratory infection –> secondary spread or dissemination

51
Q

Coccidioides immitis

A

Coccidioidomycosis = “San Joaquin Valley Fever”

Inhaled from soil in southwest US

Mild respiratory infection

Some may get progressive pulmonary infection

Dissemination to skin, bones, CNS (especially in dark skinned people)

Erythema nodosum or erythema marginatum with associated non-infectious arthritis

Unique yeast form (spherule with tiny coccidioides inside)

Thin walled cavity

Directly infectious to microbiologists because of environment

Complement fixation (IgG to chitinase) correlates with active disease, use to monitor infection

52
Q

Opportunistic mycoses

A

Candida

Aspergillus

Zygomyces

Fusarium

Scedosporium

Penicillium

Pneumocystis

53
Q

3 targets for antifungal drgus

A

1) Fungal cell wall
2) Cell membrane (ergosterol)
3) Nucleotide metabolism

54
Q

Antifungals that disrupt fungal cell wall

A

Echinocandins: capsofungin, anidulafungin, micafungin

55
Q

Antifungals that disrupt fungal cell membrane

A

Allyamine: terbinafine

Azoles: ketoconazole, fluconazole, itraconazole, voriconazole, posaconazole

Polyenes: amphotericin B (including lipid formulations)

56
Q

Antifungals that are antimetabolites

A

Pyrimidine analogue: 5-flucytosine

57
Q

Antifungal that is a microtubule assembly inhibitor

A

Griseofulvin

58
Q

Amphotericin B

A

Polyene antifungal

“Atomic bomb” of fungal infection

Extremely broad spectrum; used for cryptococcus and aspergillus fumigatus

Disrupt fungal cell membrane by binding directly to ergosterol and opening up a channel that lets intracellular cations out

IV for systemic or topical for sinus

Adverse effects: fast infusion can cause fever, chills, nausea; nephrotoxicity

Lipid formulations show better tissue distribution and lower toxicity

59
Q

Ketoconazole

A

Azole

Not as well absorbed

Not great spectrum of activity

60
Q

Antifungal triazoles

A

Inhibit ergosterol synthesis by interfering with lanosterol 14alpha demethylase (fungal CYP450 molecule)

Ex: fluconazole, voriconazole, posaconazole

61
Q

Fluconazole

A

Triazole

IV or PO

Active against cryptococcus, candida (best drug for candida), coccidioimycosis

Gets into CSF

62
Q

Voriconazole

A

Triazole

IV or PO

Treatment of choice for invasive aspergillosis

Active against candida

Gets into CSF

63
Q

Posaconazole

A

Triazole

PO

Active against zygomycosis, candida, aspergillus

64
Q

Terbafine

A

Allylamine

Inhibits squalene epoxidase step to inhibit ergosterol synthesis

Oral or topical

Used for onychomycosis, tinea

Adverse effects: GI upset, hematotoxocity

65
Q

Echinocandins

A

Inhibits beta glucan synthetase activity so cannot synthesize cell wall

IV

Ex: caspofungin, anidulafungin, micafungin

66
Q

Caspofungin

A

Echinocandin

IV

Use to treat invasive candida, invasive aspergillosis (second line or together with voriconazole)

67
Q

5-flucytosine

A

Antimetabolite (prevents DNA and RNA synthesis)

PO

Used to treat candida and cryptococcal meningitis (together with amphotericin B)

68
Q

Topical antifungals

A

Polyenes: amphotericin, nystatin

Azoles: ketoconazole, butoconazole, clotrimazole, econazole, miconazole

Allylamine: terbinafine, naftifine

Antimetabolites: ciclopirox, tolnaftate, others

69
Q

How to treat different dermatophytoses

A

Treat tinea corporis, cruris, pedis with topical antifungal (clotrimazole, econazole; don’t use products containing corticosteroids!)

Treat tinea capitis with systemic therapy (terbinafine, itraconazole, griseofulvin, fluconazole)

Treat onychomycosis (nail infections) with systemic therapy (terbinafine, itraconazole, griseofulvin, fluconazole)

70
Q

Kerion

A

Fungal infection of the hair follicles accompanied by secondary bacterial infection and marked by raised, usually pus-filled and spongy lesions

71
Q

Parasite

A

Free-living, eukaryotic cells (?)

Parasite depends metabolically on host and causes harm to host

Have mouth called cytostome

Reproduce sexually or asexually

Secrete protective coat and become cyst to infect humans; after ingestion can convert back into motile form called trophozoite

72
Q

Protozoa

A

Single celled parasites

Amoebae: entamoeba; have no distinct shape

Apicomplexa: plasmodium, toxoplasma, cryptosporidium; have group of organelles at one end of cell

Flagellates: giardia, leishmania, trypanosoma, trichomonas; have flagella

73
Q

Helminths

A

Multicellular parasites

Nematodes: round worms

Platyhelminths: flat worms (cestodes/tapeworms, trematodes/flukes)

74
Q

Transmission of parasites

A

1) Direct contamination (ingestion/fecal-oral, active penetration, passive transfer)
2) Vector borne (mosquitoes or other insects)

75
Q

Ova and parasite test (O&P)

A

Microscopic observation of stool sample

If do test 3x, is 98% effective

76
Q

Cyst

A

Form the parasite is in when it infects humans (we eat cysts)

To form cyst, the protozoa secrete protective coat and shrink into round armored form

Non-dividing, rigid cell coat, resistant to water and dessication

77
Q

Trophozoite

A

Form the parasite is in when it causes disease (after we eat cyst, it gets into our intestine and converts back into trophozoite)

Motile, dividing (binary fission), labile cell membrane

78
Q

Excystation

A

When trophozoites “hatch” from initial cyst

79
Q

How do you differentiate Entamoeba histolytica from Entamoeba dispar?

A

Have to do PCR assay because they look identical

80
Q

Anthroponosis vs. zoonosis

A

Anthroponosis: only humans

Zoonosis: humans and other animals (reservoir host is animal that maintains parasite in nature)

81
Q

Cyclospora cayetenensis

A

Cyclosporiasis

AKA Cyanobacteria-like Bodies (CLBs)

May cause diarrhea lasting up to 6 weeks

Occurs in immunodeficient adults and travelers

Diagnosis with acid-fast stain (acid-variable cysts in feces)

Fluoresce under UV light

82
Q

Naegleria fowleri

A

Causes Primary Amebic Meningoencephalitis

Acute infection in normal host

Enters through nasal passage when in fresh warm water (hot springs, hot tubs)

“Fowl” play! 95% of people die within 1 week of infection

Exist as cysts, trophozoites, flagellates but amebic/trophozoite form is what infects us

Diagnose by seeing amebic trophozoites in CSF and tissue, or flagellates in tissue

Looks exactly like bacterial meningitis (high neutrophils, high protein, low glucose) but obvi no bacteria when you culture

Treatment: amphotericin B

83
Q

Acanthamoeba

A

Causes Granulomatous Amebic Encephalitis (GAE) by entering lower respiratory tract
or broken skin

Chronic infection in immunocompromised host

Causes Ocular Keratitis (in normal hosts) if contaminates contact lenses!

84
Q

Kinetoplast

A

Part of the flagella of protozoa

85
Q

Terms for flagellated (kinetoplastid) protozoa

A

Trypomastigote: has flagella, is highly motile, is extracellular form of parasite

Amastigote: no flagella, intracellular form of parasite

86
Q

Trypanosoma brucei brucei

A

Does not affect humans, only infects cows

Still carried by tsetse fly

87
Q

Human resistance to T. b. brucei

A

Human HDL component ApoL1 lyses T. b. brucei

However, some people have mutation in ApoL1 that also causes lysis of T. b. rhodesiense, which sounds good but actually correlates with greater incidence of kidney disease

88
Q

Are trypomastigotes detectable in the blood in Chagas Disease?

A

Only during the acute phase

Not in the indeterminate and chronic phases (but do see amastigotes in muscle)

This means that we can do microscopy to see flagellated protozoa in blood during the acute stage but must do serology/PCR/xenodiagnosis in the indeterminate and chronic phase

89
Q

Modes of transmission of Chagas Disease

A

1) Reduviid bug feces (vector-borne)
2) Congenital (vertical transmission)
3) Blood transfusion
4) Ingestion (drink sugar cane juice)

90
Q

Different kinds of leishmaniasis

A

Old world cutaneous: Africa, Middle East (L. major) = oriental sores

New World cutaneous: Latin America (L. mexicana) = Chiclera’s ulcer

New World mucocutaneous: Latin America (L. braziliensis)

Visceral: Africa, India, Brazil (L. donovani)

91
Q

Leishmaniasis infantum

A

In Southern Europe

Infects children and HIV positive people

92
Q

Lifecycle of leishmaniasis

A

1) Promastigote exits sand fly’s mouth and goes into human bloodstream
2) Engulfed by macrophage
3) Amastigotes divide within macrophage
4) Amastigotes released and infect other cells

93
Q

Recurrence of symptoms in malaria

A

Chills –> fever –> sweats

Parasites invade RBCs –> RBCs burst they release lots of foreign material and the immune system responds to those antigens by creating fever (inflammation, cytokines, etc) –> hypothalamus resets and causes profuse sweating to stop fever

94
Q

Plasmodium (malaria) lifecycle

A

1) Sporozoite comes out of mosquito and goes into human blood
2) Sporozoite gets to liver within 30 seconds
3) Sporozoite gets into hepatocyte and turns into merozoite, which replicates
4) Merozoites released into bloodstream and infect RBCs
5) In RBCs, merozoites replicate (by schizogony, NOT binary fission) then turn into trophozoites
6) Trophozoites turn into schizonts which undergo nuclear division but NOT cytoplasmic division so get multinucleated RBC
7) RBC bursts and merozoites spread to other RBCs (?)

95
Q

Different manifestations of P. malariae compared to other plasmodium species

A

P. malariae causes immune complex disease and renal failure

Other Plasmodium species cause splenomegaly, hepatomegaly, immunosuppression

96
Q

Relapse vs. recrudescence

A

P. vivax causes relapsing disease due to reactivation of hypnozoite stage in liver

P. falciparum causes recrudescence due to residual low levels of merozoites in RBCs

97
Q

Hypnozoite

A

Only exists in P. vivax (and P. ovale)

Some sporozoites don’t divide in hepatocytes but form dormant hypnozoites in liver and can cause relapse of malaria months to years later

98
Q

Which receptors do P. vivax and P. falciparum bind to in order to enter RBCs?

A

P. vivax binds duffy antigen receptor on immature RBCs and causes them to enlarge

P. falciparum binds several receptors on immature and mature RBCs (which can’t enlarge)

99
Q

How does P. falciparum cause attachment of RBCs to epithelial cells in brain capillaries?

A

P. falciparum secretes protein that inserts into RBC membrane causing “sticky knobs” on outside of RBC that let RBCs attach to capillary walls

Note: can undergo antigenic variation so host cannot mount successful immune response to clear parasite

100
Q

Malaria treatment

A

Primaquine prevents relapse by P. vivax

Quinine 100% effective but try not to use all the time because P. falciparum resistance is a problem

Chloroquine only works in some regions because lots of resistance now (and toxicity)

Mefloquine (LARIUM) causes GI and CNS disorders, vivid dreams

Atovaquone/proguanil (MALARONE) is a mitochondrial and DHFR inhibitor used for P. falciparum

Pyrimethamine (FANSIDAR) is a DHFR inhibitor

Artemisinin (Qinghaosu) has been used in China for thousands of years but only limited FDA approval in US

101
Q

Why haven’t we developed a good malaria vaccine yet?

A

Need to stimulate cell-mediated immune system and haven’t been able to do that yet

102
Q

Babesia microti

A

Babesiosis (Nantucket Fever)

Worldwide, but in NE and NW states of US

Transmitted via ixodes deer tick, but mouse is reservoir host

Trophozoites asexually bud and divide into 4 merozoites that stick together to form an x-shaped tetrad (“Maltese cross”)

Treat with quinine and clindamycin

103
Q

Toxoplasmosis infection during pregnancy

A

1st trimester: spontaneous abortion, stillbirth

2nd/3rd trimester: chorioretinitis, hydrocephalus

104
Q

Toxoplasma lifecycle

A

Rodent eats spore –> cyst forms in rodent (intermediate host = asexual replication cycle) –> cat eats rodent –> oocysts form in cat (definitive host = sexual replication cycle) –> cat poops out oocysts –> oocysts form spores

105
Q

How do humans get toxoplasma?

A

1) Ingest cyst (oocyst) in cat feces from changing litter box
2) Ingest tissue cyst (pseudocyst) in raw beef
3) Congenital if mother gets initial/active infection during pregnancy

106
Q

Stages of life of helminths

A

1) Egg: dormant, transmission (like cyst of protozoa)
2) Larva: immature, disease
3) Adult: mature, disease

Note: 1 egg –> 1 helminth

107
Q

Definitive vs. intermediate host

A

Definitive host: harbors adult stage

Intermediate host: harbors larval stage

Note: this is different from indeterminate host!

108
Q

When are humans accidental intermediate hosts?

A

Cutaneous larva migrans (dog hookworm)

109
Q

When are humans definitive hosts?

A

Taenia solium, Taenia saginata

110
Q

Schistosoma species

A

S. mansoni: in adult inferior mesenteric venules and near rectum; eggs in feces; fibrosis around eggs trapped in liver and intestinal tract; chronic Salmonella infection

S. japonicum: adult in superior mesenteric venules; eggs in feces

S. haematobium: adult in venules around urinary bladder; eggs in urine; correlation with bladder cancer

111
Q

Trichuris trichura

A

Whipworm

Similar to Pinworm (Enterobius vermicularis) but no perianal itching

Bloody diarrhea, malnutrition, anemia, rectal prolapse

112
Q

Baylisascaris procyon

A

Raccoon roundworm

Possible bioterrorism agent because eggs can be distributed in aerosol

Visceral larva migrans can be asymptomatic but can cause blindness, neurologic damage, death

No treatment

113
Q

Autoinfection

A

The entire lifecycle of the parasite occurs in the host without need for another host

Usually eggs or larvae are ingested, grow into adults and then produce eggs or larvae that must exit the host (to incubate in soil, etc) in order to go infect a new host

With autoinfection, adult produces larvae that can penetrate intestinal wall (etc) and infect the host again right away without leaving!

Ex: Strongyloides stercoralis, Enteroius vermicularis, Taenia solium

114
Q

Classes of protozoa

A

Amoebae: entamoeba

Apicomplexa: plasmodium, toxoplasma, cryptosporidium

Flagellates: giardia, leishmania, trypanosoma, trichomonas

115
Q

Classes of helminths

A

Nematodes (roundworms): Ascaris lumbricoides, Enterobias vermicularis, Trichinella spiralis, Strongyloides stercoralis, Necator americanus, Ancyclostoma duodenale, Onchocerca volvulus, Wuchereria bancrofti

Platyhelminths (flatworms), Cestodes (tapeworms): Taenia saginata, Taenia solium, Echinococcus granulosus

Platyhelminths (flatworms), Trematodes (flukes): Schistosoma

116
Q

Mucormycosis (zygomycosis)

A

Due to fungal infection with Mucor, Rhizopus

Rhinocerebral (sinuses, orbits, brain), pulmonary, cutaneous, GI, often fatal

Diagnosis: necrotic palate, CT imaging of sinus, brain, non-septate hyphae at 45 degree angle (or 90??)

Treatment: surgical debridement, amphotericin B synergy with rifampin, posaconazole

117
Q

Fusarium

A

Mold with banana shaped macroconidia

Skin disease, disseminated disease (hematologic malignancy, bone marrow transplant)

Diagnose by blood culture in dissemination

Use voriconazole, posaconazole (resistant to amphotericin B and caspofungin)

118
Q

Scedosporium

A

S apiospermum, S prolificans

Local disease in immunocompetent hosts: bone, joint, skin, eye

Immunocompromised hosts: pulmonary infection, dissemination, brain

Culture from tissue

Treat with voriconazole, itraconazole, caspofungin (may be resistant to amphotericin B)

119
Q

Penicillium

A

P marnefeii

Dimorphic found in SEA

Immunocompromised hosts: disseminated infection with skin manifestation

Culture from blood or tissue

Treat with amphotericin B, itraconazole, voriconazole, terbinafine

Block 6: Microbio, ID, Derm, Heme-Onc (10 decks)

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