Fungal And Parasitic Infections Flashcards
Trichinosis
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
Lice
Insects Transmission through direct contact Reservoir is humans Worldwide Pediculosis- head/pubic/body lice
Bed bugs
Insects Human environment Direct contact Worldwide Itchy welts in a line
Scabies
Mites Reservoir in humans Direct contact Worldwide, nosocomial outbreaks Pruritic, track-like skin lesions
Leishmaniasis
Leishmania spp Protozoan parasite Reservoir- wild animals, humans Transmission- sand fly bites Tropics or subtropics Cutaneous, mucocutaneous, VL, PKDL
Dermatophytes
Molds Human, pets, and soil reservoir Skin breaks/fomites Worldwide Tinea corporis- capitis, pedis, cruris, unguium
Pityriasis versicolor
Malassezia spp Dimorphic yeast Reservoir in skin microbiota Overgrowth Worldwide Pityriasis (tinea) versicolor of skin
Sporotrichosis
Dimorphic mold On plant surfaces, soil Trauma transmission Worldwide Fixed cutaneous, lymphocutaneous infection
Cryptococcosis
Cyrptococcus spp Yeast Pigeon droppings, decaying wood Inhalation transmission Worldwide Pulmonary infection, disseminating to CNS and skin
Trichinosis disease severity
Dose-dependent
Low numbers of ingested cysts= mild,asymptomatic
Large numbers= more severe, more cardiac complications
Trichinosis clinical progression
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
Trichinosis lab confirmation
Anti-parasite antibody
Muscle biopsy
Trichinosis treatment
Minor infection- rest, antipyretics, analgesics
Severe- glucocorticoids, anti-nematode medication like albendazole/mebendazole
What type of parasite is pediculosis?
Lice- ectoparasite, likes to live on the hair itself
Crawls along hair shafts to lay eggs- nits
Lice diagnosis
No labs
Pruritus (hypersensitive to lice saliva), excoriations from scratching
Visible nits
Body lice- important vector for epidemic typhus
Bacterium- rickettsia prowazekii: widespread endothelial damage, vasculiotis, coagulation, petechial rash
Sylvatic cycle with flying squirrels
Pediculosis treatment
Permethrin insecticide- first line OTC lotions/shampoos
Second line prescription
Nits removed with fine tooth comb
Bed bug treatment
Antihistamines, cortisone creams
Not known to transmit disease
Scabies lifecycle
Burrows into the stratum corneum with eggs and feces- cause the itching
Demodex mites
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
Leishmaniasis organism lives as
Protozoan parasites that live extracellularly as promastigotes- flagellated, extracellular form
Macrophages ingest promastigotes,then they proliferate into amastigotes
3 major groupings of leishmaniasis
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)
PKDL
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.
Leishmaniasis diagnosis
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
Leishmaniasis treatment
Pentavalent antimony compounds: mech is unclear, inhibits parasite metabolism
Miltefosine- PL analogue
Amphotericin B (salvage therapy)
3 major genera for dermatophytes
Epidermophyton, microsporum, trichophyton
Dermatophyte pathogenesis
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
Dermatophyte: clinical
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
Dermatophyte diagnosis
Skin/nail scrapings- KOH prep: destroys the tissue but not fungus, microscopy shows septate hyphae
Culture- mold-like colonies with spores
Dermatophytes treatment
Topical antifungals first line- anoles, tolnaftate, terbinafine: inhibit ergosterol synthesis
Oral antifungals- recalcitrant infections: azoles, terbinafine
Nail infections- oral antifungals for 3 months
Cutaneous fungal infection from microbiota dysbiosis
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
Dandruff treatment
Active ingredient in shampoo have antifungal activity and reduce epidermal scaling- zinc pyrithione, selenium sulfide, azole antifungal
Cigar shaped budding yeast on skin biopsy
Sporotrichosis
Chronic subcutaneous infections from other fungi inoculation
Chromoblastomycosis
Mycetoma
Systemic fungal infections have
Cutaneous manifestations- cryptococcosis
Two organisms of cryptococcus
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)
Cryptococcus diagnosis/treatment
Detection of yeasts in skin or CSF
India ink staining of capsule
Serological tests for capsular antigen
Culture
Amphotericin B, azoles
