Fungi (1/28) Flashcards
What are fungi?
Eukaryotic, non motile, aerobic, cell wall contains glucan and chitin
Includes yeasts (which grow by budding off) and molds (which have a long, thin morphology)
What is a dimorph?
Dimorphs can be either yeast or mold depending on the environment
How do fungi cause disease?
Some make toxins but none of the medically important ones do this!
Cause disease because they are big – gum up capillaries, CSF drainage
Disease from our immune response to their presence
What are the three main locations for fungal infections?
Superficial (cutaneous– hair, skin, nails)
Subcutaneous
Systemic: dimorphs infect everyone, opportunists i.e. pathogenic yeasts and molds affect immunocompromised
Dermatophytes?
Which diseases does it include?
Molds that produce keratinase
Trivial, common, grow on skin/nails, cause inflammation below
Includes tinea corporis (ringworm), tinea pedis (athletes foot), tinea capitis (on scalp), tinea cruris (crotch), tinea unguum (gross nails)
Who can get dermatophytes?
Anyone!!
Except it’s always worse in the immunocompromised
What are diagnostic characteristics of dermatophyte infections?
“active border” as opposed to psoriasis
no mucosal involvement because tehre’s no keratin there (vs. candidasis)
You can look at it under a microscope with KOH prep
UV fluorescence: makes the fungi fluoresce
Rarely biopsy/culture
What are malassezia furfur?
A lipophilic yeast, also causes superficial fungal infections; they eat skin lipids
Lives on the skin, causes pigment changes and itch underneath
Diseases include: tinea versicolor (kids don’t get it, because they don’t have enough lipids on the skin)
Rarely you’ll see fungemia (fungus in the blood) with lipid infusion
Treat with topical creams
How do you get subcutaneous fungal infections?
When the fungus is introduced through skin by foreign body; grow in subcut. tissue & spread through lymph
Usually cause local disease but can disseminate to bones, joints via lymph
Most common in nonindustrialized world
What is mycetoma of feet?
Note that it doesn’t extend past the ankle = localized infection
What is Sporptrichosis?
Sporothrix schenkii = a dimorphic soil fungus (mold in environment, yeast in body)
Once it’s introduced in the body via splinters or thorns, it inoculates into subcutaneous tissues, yeast can travel along lymphatics, elicit mixed pyogenic-granulomatous reaction
This disease is seen in the US: gardeners, outdoors people
Forms ulcerating nodules along the lymphatics; can also cause bone and joint destruction; dissemination is rare
In an immunocompromised patient, it will be less localized i.e. spots all over the body- skin, lungs
Diagnose it by biopsy
Which dimorphs cause systemic fungal infections?
What are their characteristics?
Histoplasmosis, coccidiodomycosis, blastomycosis
“true” pathogens bc can cause disease in normal people
All are dimorphics (mold become yeast in body), respiratory acquisition- spores, disease reminiscent of TB, restricted geographic distribution)
Once you’re infected, you’re immune to reinfection
What is histoplasmosis?
Where is it?
What disease does it cause?
Histoplasma capsulatum: soil dimorph
Lives in Ohio-Mississipi valley, caribbean, central and s. america including DR and puerto rico
Guano of bats, birds, poultry
Inhalation of spores –> pathogenesis
Ellicits cellular immunity just like TB does: organism is ingested, T cells are activated, the organism goes all over the body inside macrophages which leads to granuloma formation
Skin test is positive like in TB: useful tool for public health, not individual diagnoses
Usually latent disease but may cause acute/chronic cavitary lung disease, may disseminate after infection, may reactivate years later i.e. if you get HIV
What is coccidiodomycosis?
Where?
What diseases?
Coccidioides immites: dimorph = mold in soil, becomes spherules with endospores in host (like pommegranates)
Habitat = desert, lower Sonoran life zone i.e. Southwest US, Mexico, Central/S. America
Pathogenesis is due to inhalation of spores –> transform into spherules in lung, ellicite cellular immunity like TB, hematogenous dissemination, skni test reactivity, walled off granulomas
Clinically: cute, self-limited flu-like seroconversion syndrome “valley fever”, acute or chronic lung disease, dissemination (pregnent women, dark skin, immunocompromised) to skin, bone, CNS
What is blastomycosis?
Blastomyces dermatiditis: causes skin infection from the inside out; dimorph: mold to yeast
Habitat: midatlantic coast, beaver dams, peanut farms, organic debris
Pathogenesis is due to inhalation of spores –> dissemination, disease similar to TB
Has a broad base to the bud: characteristic
Can cause acute or chronic lung infection, disseminate to skin, bone, urinary tract in men
How ar the opportunitsts different from the “true” pathogesn?
Histo, Blasto, Cocci
• Geographic
distribution
• Dimorphic
• Infection by inhalation
• Pyogenic/granulomatous
host response
• Similar to TB
• Infection =~ immunity
Opportunists
• Omnipresent
• Yeasts or molds
• Various routes of
infection
• Host response varies
• Clinical syndromes
vary
• No lasting immunity
What is cryptococcosis?
Cryptococcus neoformans: yeast with thick polysaccharide capsule
Lives worldwide
Pathogenesis: inhalation of yeasts, bioterrorism via pigeons
What is the pathophysiology/ clinical presenation of cyptococcosis?
Inhalation leads to transient colonizatoin or acute/chronic lung disease, sometimes CNS invasion
Presents with acute or chronic meningoencephalitis – presents with fever, headache, stiff neck, fever, delerium, communicating hydrocephalus
You’re infected wtih the yeast but what you get is a polysaccharide capsule– all over your brain
Pneumonia also possible but more rare
It’s the most common infection seen in AIDS patients in Africa
What is Candidiasis?
Candida albicans et al (yeast with hyphal forms)
Normal human flora i.e. genitalia, perineum, GI tract, skin
Pathogenesis is due to change in environment –> overgrowth/local infection, also change in immunity can lead to invasion
What host defenses protect against candida?
Intact skin, intact mucosa with normal pH and normal flora, functioning lymphocytes, functioning neutrophils
A change in any of these can leave you susceptible!
Lymphocyte dysfunction i.e. immaturity, destruction (HIV) makes you susceptible to skin infection
If you don’t have good neutrophils, this is when you get invasion
Environmental changes i.e. wet skin, chagnes in local flora, hormones, foreign bodies also leaves you susceptible
Where can you get candida infection
Skin: i.e. in baby who’s always wearing wet diaper
Nail bed
Genitalia i.e. in woman with UTI’s that takes antibiotics
Pharynx “oral thrush” i.e. in HIV patient
Esophagous - extenuaton of oral thrush, diagnostic of AIDS
What is the pathogenesis of invasive Candida infections?
Elimination of normal flora
Breach in anatomic integrity (often biofilm
on catheter)
Defective PML function (first line of
defense)
Perfect storm: critically ill patients with
multiple risks (hospitalized, on antibiotics,
many catheters, neutropenic)
It’s not “virulent” but there are things that make it a good pathogen: tolerats lots of environmental conditions, has hydrolases, beta proteases, phospholipases, adheres to plastic, can invade GI, renal epithelium, hyphae protect against phagocytosis
What’s the symptoms of invasive candidiasis?
Fever, leukocytosis, organ dysfunction, microabscesses in kidney, liver, skin, eye, lung, heart (can cause endocarditis with large vegetations and significant emboli)
It’s difficult to distinguish infection and colonization
Best treatment restores missing defense
What is aspergillosis?
Aspergillus fumigatus: a mold (no yeast phase)
Everywhere worldwide
Pathogensis due to inhalation of spores
Acute angle branching: looks like malevolent fingers, can extend through any tissue
What’s the pathophysiology/clinical presentation of aspergillosis?
Spores in lung can ellicit allergy & cause allergic bronchopulmonary aspergillosis
Can grow in preexisting cavity, invade vasculature, disseminate with local and distant disease –> Aspergilloma = mass in lung, invasive aspergillosis with pneumonia/other end organ disease
Neutrophils are the prime defenders
What is mucormycosis?
Very non virulent but causes awful disease! Paradox
Mucorales genera - Rhizopus and Mucor (zygomycetes)
Mold, no yeast phase
Everywhere worldwide
Less malevolant looking than aspergillosis
What’s the pathophysiology for mucormycosis?
When the environment changes to make it a happy place for mucor to grow i.e. acid, warm
Alveolar MPH/PML clear organisms, BUT:
• Metabolic acidosis
• Diabetes
• Neutrophil dysfunction
• Iron overload
May enable relentless growth: impossible to treat once it starts to grow
Clinical presentation:
Acute, fulminant, often fatal
Lower airways: pneumonia progressing to infarction
Upper airways: sinusitis progressing to brain abscess
