Fungi (1/28) Flashcards

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1
Q

What are fungi?

A

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)

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2
Q

What is a dimorph?

A

Dimorphs can be either yeast or mold depending on the environment

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3
Q

How do fungi cause disease?

A

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

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4
Q

What are the three main locations for fungal infections?

A

Superficial (cutaneous– hair, skin, nails)

Subcutaneous

Systemic: dimorphs infect everyone, opportunists i.e. pathogenic yeasts and molds affect immunocompromised

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5
Q

Dermatophytes?

Which diseases does it include?

A

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)

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6
Q

Who can get dermatophytes?

A

Anyone!!

Except it’s always worse in the immunocompromised

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7
Q

What are diagnostic characteristics of dermatophyte infections?

A

“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

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8
Q

What are malassezia furfur?

A

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

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9
Q

How do you get subcutaneous fungal infections?

A

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

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10
Q

What is mycetoma of feet?

A

Note that it doesn’t extend past the ankle = localized infection

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11
Q

What is Sporptrichosis?

A

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

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12
Q

Which dimorphs cause systemic fungal infections?

What are their characteristics?

A

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

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13
Q

What is histoplasmosis?

Where is it?

What disease does it cause?

A

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

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14
Q

What is coccidiodomycosis?

Where?

What diseases?

A

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

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15
Q

What is blastomycosis?

A

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

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16
Q

How ar the opportunitsts different from the “true” pathogesn?

A

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

17
Q

What is cryptococcosis?

A

Cryptococcus neoformans: yeast with thick polysaccharide capsule

Lives worldwide

Pathogenesis: inhalation of yeasts, bioterrorism via pigeons

18
Q

What is the pathophysiology/ clinical presenation of cyptococcosis?

A

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

19
Q

What is Candidiasis?

A

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

20
Q

What host defenses protect against candida?

A

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

21
Q

Where can you get candida infection

A

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

22
Q

What is the pathogenesis of invasive Candida infections?

A

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

23
Q

What’s the symptoms of invasive candidiasis?

A

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

24
Q

What is aspergillosis?

A

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

25
Q

What’s the pathophysiology/clinical presentation of aspergillosis?

A

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

26
Q

What is mucormycosis?

A

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

27
Q

What’s the pathophysiology for mucormycosis?

A

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