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MSK Assessment 3 > Fungal And Parasitic Infections > Flashcards

Fungal And Parasitic Infections Flashcards

1
Q

Trichinosis

A

Trichinella spirosis- helminth parasite (roundworm nematode)
Reservoir: carnivores (pigs, bears, others)
Transmission: ingestion of raw or undercooked meat containing trichinella cysts- mature/mate in GI and released by gastric digestion into muscles via circulation
Worldwide endemicity
Invades muscles, fever, diarrhea, myalgia, facial/periorbital edema, eosinophilia

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2
Q

Lice

A 
Insects
Transmission through direct contact
Reservoir is humans
Worldwide
Pediculosis- head/pubic/body lice
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3
Q

Bed bugs

A 
Insects
Human environment
Direct contact
Worldwide
Itchy welts in a line
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4
Q

Scabies

A 
Mites
Reservoir in humans
Direct contact
Worldwide, nosocomial outbreaks
Pruritic, track-like skin lesions
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5
Q

Leishmaniasis

A 
Leishmania spp 
Protozoan parasite
Reservoir- wild animals, humans
Transmission- sand fly bites
Tropics or subtropics
Cutaneous, mucocutaneous, VL, PKDL
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6
Q

Dermatophytes

A 
Molds
Human, pets, and soil reservoir
Skin breaks/fomites
Worldwide
Tinea corporis- capitis, pedis, cruris, unguium
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7
Q

Pityriasis versicolor

A 
Malassezia spp
Dimorphic yeast
Reservoir in skin microbiota
Overgrowth
Worldwide
Pityriasis (tinea) versicolor of skin
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8
Q

Sporotrichosis

A 
Dimorphic mold
On plant surfaces, soil
Trauma transmission
Worldwide
Fixed cutaneous, lymphocutaneous infection
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9
Q

Cryptococcosis

A 
Cyrptococcus spp
Yeast
Pigeon droppings, decaying wood
Inhalation transmission
Worldwide
Pulmonary infection, disseminating to CNS and skin
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10
Q

Trichinosis disease severity

A

Dose-dependent
Low numbers of ingested cysts= mild,asymptomatic
Large numbers= more severe, more cardiac complications

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11
Q

Trichinosis clinical progression

A

Week 1- gut invasion: diarrhea, nausea, vomitting
Week 2- muscle invasion: myalgia, blood eosinophilia, periorbital and facial edema
Weeks 3-6- larval encystment in muscle (infected cell becomes nurse cell, viable for years), provokes inflammation (extra ocular muscles, biceps, jaw, neck, lower back, diaphragm, heart), myalgia and weakness

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12
Q

Trichinosis lab confirmation

A

Anti-parasite antibody

Muscle biopsy

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13
Q

Trichinosis treatment

A

Minor infection- rest, antipyretics, analgesics

Severe- glucocorticoids, anti-nematode medication like albendazole/mebendazole

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14
Q

What type of parasite is pediculosis?

A

Lice- ectoparasite, likes to live on the hair itself

Crawls along hair shafts to lay eggs- nits

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15
Q

Lice diagnosis

A

No labs
Pruritus (hypersensitive to lice saliva), excoriations from scratching
Visible nits

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16
Q

Body lice- important vector for epidemic typhus

A

Bacterium- rickettsia prowazekii: widespread endothelial damage, vasculiotis, coagulation, petechial rash
Sylvatic cycle with flying squirrels

17
Q

Pediculosis treatment

A

Permethrin insecticide- first line OTC lotions/shampoos
Second line prescription
Nits removed with fine tooth comb

18
Q

Bed bug treatment

A

Antihistamines, cortisone creams

Not known to transmit disease

19
Q

Scabies lifecycle

A

Burrows into the stratum corneum with eggs and feces- cause the itching

20
Q

Demodex mites

A

Normal skin microbiota- live in hair follicles
Dysbiosis may contribute to disease: Rosacea (higher density of mites) antibiotics and anti-mice creams have shown efficacy. And chronic blepharitis (eyelid)
Mites bring in more bacteria with them

21
Q

Leishmaniasis organism lives as

A

Protozoan parasites that live extracellularly as promastigotes- flagellated, extracellular form
Macrophages ingest promastigotes,then they proliferate into amastigotes

22
Q

3 major groupings of leishmaniasis

A

Localized cutaneous- majority, resolves spontaneously (others systemic therapy indicated)
Mucocutaneous- mucosal spread to nasopharyngeal mucosa from initial cutaneous infection. Associated with new world species in Brazil: L.brasiliensis: parasite is infected with mRNA virus to trigger inflammatory, destroys nasal septum and surrounding tissue
Visceral leishmaniasis (Kala-azar)- internal spread months to years after infection to liver, spleen, bone marrow, lymph nodes. Fever, weight loss, hepatosplenomegaly, pancytopenia (all of the blood components are lowered)

23
Q

PKDL

A

Post-kala-azar dermal leishmaniasis- cutaneous sequela of VL up to 20 years after treatment for VL
Facial skin lesions gradually increase in size and spread over the body
Lesions coalesce to form disfiguring, swollen structures resembling leprosy.

24
Q

Leishmaniasis diagnosis

A

Relevant travel history even in distant past
Tissue biopsy of amastigotes in macrophages in skin or BM or liver
Biopsy culture- promastigotes
Serology- systemic disease

25
Q

Leishmaniasis treatment

A

Pentavalent antimony compounds: mech is unclear, inhibits parasite metabolism
Miltefosine- PL analogue
Amphotericin B (salvage therapy)

26
Q

3 major genera for dermatophytes

A

Epidermophyton, microsporum, trichophyton

27
Q

Dermatophyte pathogenesis

A

Specialized to grow on keratin-containing structures and digest it
Inflammation promotes desquamation and aids spontaneous healing
Weak inflammatory response= chronic infection
Corticosteroids reduce shedding and exacerbate infection
Not invasive infections- superificial

28
Q

Dermatophyte: clinical

A

Ringworm fungus
‘Tinea’ applied to various forms
Tinea corporis- skin infection, expanding erthematous borders
Tinea pedis- most common, itching/scaling/fissures (secondary bacterial infections)
Tinea cruris- groin and adjacent skin, intensely pruritic, fomites/autoinoculation from athlete’s foot transmission, obesity predisposes
Tinea capitis- scalp/hair, hair loss in ring like shape
Tinea unguium- nail infection, hyperkeratosis and distortion of nail plate

29
Q

Dermatophyte diagnosis

A

Skin/nail scrapings- KOH prep: destroys the tissue but not fungus, microscopy shows septate hyphae
Culture- mold-like colonies with spores

30
Q

Dermatophytes treatment

A

Topical antifungals first line- anoles, tolnaftate, terbinafine: inhibit ergosterol synthesis
Oral antifungals- recalcitrant infections: azoles, terbinafine
Nail infections- oral antifungals for 3 months

31
Q

Cutaneous fungal infection from microbiota dysbiosis

A

Malasezzia furfur- dimorphic yeast can switch to mold form
Dandruff or pityriasis versicolor
Overgrowth of superficial layer, forms hyphae that invade corneum
Inflammation damages melanocytes, triggers redness, scaling
Yeast is lipid dependent- affects seborrheic areas
Predisposing factors- genetics, warmth, oily skin

32
Q

Dandruff treatment

A

Active ingredient in shampoo have antifungal activity and reduce epidermal scaling- zinc pyrithione, selenium sulfide, azole antifungal

33
Q

Cigar shaped budding yeast on skin biopsy

A

Sporotrichosis

34
Q

Chronic subcutaneous infections from other fungi inoculation

A

Chromoblastomycosis

Mycetoma

35
Q

Systemic fungal infections have

A

Cutaneous manifestations- cryptococcosis

36
Q

Two organisms of cryptococcus

A

C. Neoformans- soil contaminated with bird excreta, primarily infects immunocompromised
C. Gatti- trees in Brazil, Australia, pacific NW, can infect immunocompetent as well
Fever, headache, fatigue, blurred vision
Lungs, CNS (meningoencephalitis), skin (may be first indication of disseminated infection)

37
Q

Cryptococcus diagnosis/treatment

A

Detection of yeasts in skin or CSF
India ink staining of capsule
Serological tests for capsular antigen
Culture

Amphotericin B, azoles

MSK Assessment 3 (13 decks)

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