lecture 33-36 disease stuff AI (gyatt dayum)

What type of virus causes gastroenteritis (rotavirus)?

dsRNA virus; naked (no envelope); looks like wheels

How does rotavirus enter and exit cells?

Enters by direct penetration; exits by cell lysis (no envelope = no budding needed)

What is the transmission route of rotavirus?

Fecal-oral

What is the incubation period of rotavirus?

2–3 days

What are the symptoms of rotavirus gastroenteritis?

Nausea, vomiting, diarrhea (NVD); serious dehydration; not bloody

How long can rotavirus survive on surfaces?

Weeks to months

How concentrated is rotavirus in feces?

Up to 100 trillion viruses per gram of poop

What is the infectious dose of rotavirus?

Only 10–100 virions

What toxin does rotavirus produce and what does it do?

NSP4 — causes loss of water and salts from host cell; similar to cholera toxin

Does rotavirus lead to a carrier state?

No

What happens to intestinal epithelial cells during rotavirus infection?

Cell lysis occurs → inflammation

What is the treatment for rotavirus?

Wait 3–7 days; rehydration therapy

What vaccine exists for rotavirus and what type is it?

RotaTeq — live attenuated virus vaccine; induces B cell (antibody) and cytotoxic T cell response

What type of virus is HIV?

Retrovirus — RNA genome used to make DNA; enveloped virus

How does HIV leave cells?

By budding (enveloped virus)

What soluble proteins does HIV carry?

Reverse transcriptase and integrase (used early in infection)

What is the genome of HIV?

Single-stranded RNA (ssRNA)

What body fluids transmit HIV and at what concentrations?

Blood: >1000 viruses/mL;

semen or vaginal fluid: ~50 viruses/mL

What are routes of HIV transmission?

Anal sex, vaginal sex, blood transfusion, mother's milk, dirty needles; tears in epithelium facilitate entry

What is NOT a reliable transmission route for HIV?

Saliva — too low concentration of virus

What is the HIV life cycle in order?

Attach (enveloped) → enter by fusion → reverse transcription (RNA→dsDNA) → dsDNA integrated into chromosomes → expression of viral genes → assembly of RNA genome and capsid → bud off plasma membrane

What receptor does HIV's gp120 bind to on T helper cells?

CD4 and CCR5 receptors

What cells does HIV mainly infect?

T helper cells (CD4+ T cells)

What enzyme converts HIV's RNA genome to dsDNA?

Reverse transcriptase — produces many missense mutations (very sloppy)

What enzyme integrates HIV's dsDNA into the host genome?

Integrase

What does HIV protease do?

Chops fusion proteins into active viral proteins

Why do HIV-infected cells die?

Overwork, syncytia formation, or cytotoxic T cell killing

What is syncytia formation in HIV?

gp41 on infected cell's membrane causes fusion with neighboring cells — virus spreads without leaving the cell

What other pathogens also cause syncytia formation?

HSV and tuberculosis

What happens in HIV Phase 1 (acute infection)?

HIV enters blood; flu-like symptoms that pass; almost all HIV eliminated; gp120 binds CD4/CCR5 → infection of T helpers

What happens in HIV Phase 2 (chronic latency)?

Starts ~8 weeks post-infection; HIV goes latent as provirus in T helpers; sporadic activation; asymptomatic 5–10 years; T helpers slowly die off

Why can't antibodies and cytotoxic T cells fully eliminate HIV in the acute phase?

Reverse transcriptase errors → missense mutations → high antigenic variation → immune system always one step behind

What is the big problem caused by T helper cell death in HIV?

T helpers are needed to make cytotoxic T cells → eventually no new cytotoxic T cells can be made

What happens in HIV Phase 3 (AIDS / profound immunodeficiency)?

5–10+ years post-infection; T helper count drops below threshold → fewer/weaker B cells, no new cytotoxic T cells, no memory cells

Why can AIDS patients be reinfected by the same pathogen?

Only T-independent response possible → no memory cells created

Why do people die from AIDS?

Unable to fight multiple opportunistic infections; latent infections reactivate (TB, herpes); increased cancer risk

What drugs are used in HIV treatment?

Reverse transcriptase inhibitors, base analogs, protease inhibitors, integrase inhibitors — no cure

Why is there no HIV vaccine?

High mutation rate prevents effective vaccine development

What is Truvada and how does it work for HIV prevention?

Pre-exposure prophylaxis; base analogs targeting reverse transcriptase → premature DNA chain termination

What are dermatophytoses?

Fungal diseases that infect only epidermis, hair, and nails (e.g., ringworm, athlete's foot, jock itch)

What fungi cause dermatophytoses?

Trichophyton, Epidermophyton, Microsporum

What environment do dermatophyte fungi need to thrive?

Moist environment (sweat)

How are dermatophytes spread?

Contact or fomites (exercise equipment, towels, etc.)

What is keratin and why is it relevant to dermatophytes?

Keratin normally can't be digested by most microbes (non-specific host defense); dermatophytes produce keratinase to break it down

How do dermatophytes cause disease?

Keratinase cuts through dead cells → attacks living cells → inflammation

What are the treatments for dermatophytoses?

Topical azoles or allylamines; athlete's foot powder contains: basic agent (fungi like acid), drying agent (fungi like moisture), and azole

What causes candidiasis?

Overgrowth of Candida albicans — normal flora of mouth, gut, skin, and vagina

What type of fungus is Candida albicans?

Dimorphic — mostly yeast phase; other phase is mold

What keeps Candida albicans in check normally?

Other normal flora and nonspecific immune system (phagocytes)

What triggers Candida albicans overgrowth?

Excessive antibiotics, hormone imbalance, disruption of normal flora, or weakened immune system

What are the 5 manifestations of candidiasis?

1. Vaginal yeast infection 2. Intestinal yeast infection 3. Thrush (oral) 4. Cutaneous disease 5. Fungemia

How does vaginal yeast infection develop?

Lack of estrogen → less glycogen → less lactobacilli → less competition for C. albicans → higher pH → overgrowth

What do lactobacilli do in the vagina?

Ferment glycogen → produce acid → keep Candida in check

How does intestinal candidiasis develop?

Antibiotic overuse → normal flora destroyed → yeast survives and overgrows → intestinal upset and inflammation

What is thrush?

Oral candidiasis — small white flecks from C. albicans overgrowth in mouth; common in AIDS patients and with antibiotic overuse

What causes cutaneous candidiasis?

Skin is too moist → C. albicans overgrows → rash and inflammation

What is fungemia?

Fungi entering the bloodstream

What triggers Candida's switch from yeast to mold form?

Environmental change — pH shift from 6 to 7

What are the "big three" exotoxins of fungi (Candida)?

Hyaluronidase, proteases, keratinase

What is thigmotropism in Candida?

Mold hyphae can "feel" surfaces and grow into host cells — directional movement based on touch

How does Candida biofilm form?

Uses capsule to adhere to host cells and gain protection from immune cells — regulated by quorum sensing

What is the treatment for candidiasis?

Topical azoles (vaginal or skin); IV amphotericin B or echinocandin for severe cases

What causes cryptococcosis?

Yeast Cryptococcus neoformans — opportunistic pathogen

What is the reservoir for Cryptococcus?

Pigeon guts — excreted in poop → enters air → inhaled by people

Is there person-to-person transmission of Cryptococcus?

No

How does cryptococcosis become systemic?

Yeast inhaled into lungs → alveoli → spreads via blood → attacks meninges and brain → cryptococcal meningitis

Why is Cryptococcus dangerous in immunocompromised hosts?

Yeast capsule makes it hard to phagocytose and destroy

What are the symptoms of systemic cryptococcosis?

Stiff neck, headache, loss of consciousness, coma, death

What is the treatment for cryptococcosis?

Amphotericin B followed by fluconazole over several months

What causes valley fever (coccidioidomycosis)?

Coccidioides immitis — dimorphic fungus; mold in dry dirt, yeast/endospore in body

Where is valley fever endemic?

San Joaquin Valley

What percentage of valley fever cases are asymptomatic?

60% asymptomatic; 40% develop symptoms; very small percent become chronic

What is the incubation time for valley fever?

1–4 weeks

How is valley fever transmitted?

Arthrospores blown from dry soil → inhaled into lungs; common in outdoor workers; no person-to-person transmission

Why can't a person give valley fever to another person?

Only the arthrospore from soil is infectious; endospores coughed out won't cause infection in others

What happens to arthrospores in lung tissue?

Grow into spherules filled with endospores → spherules burst → endospores infect new areas of lung → inflammation, flu-like symptoms

What happens to immunocompromised patients with valley fever?

Endospores enter blood → rash, meningitis, bone disease, chronic disease

What is the treatment for valley fever?

Amphotericin B plus internal triazoles (IV and oral)

What is ergotism and what causes it?

Fungal intoxication caused by alkaloid toxins from Claviceps purpurea mold growing on rye or other grains

What makes ergot toxin dangerous in food?

Heat resistant — survives cooking; gets into bread

What is the incubation time for ergotism?

2–3 hours

What are the two types of ergotism?

CNS type: convulsive ergotism (hot/cold sensations, convulsions, hallucinations); Cardiovascular type: extreme vasoconstriction → gangrene

What is the treatment for ergotism?

No treatment — wait it out

What causes aflatoxin poisoning?

Metabolite produced by Aspergillus species growing on rotting nuts, corn, and grain in humid conditions

How are aflatoxins consumed?

Directly through contaminated products, or via milk/eggs from livestock fed contaminated feed

How does aflatoxin cause disease?

Reacts with DNA → mutations in human cells, especially liver cells → cancer (p53 mutations)

What is the treatment for aflatoxin poisoning?

None

What is a prion?

A protein infectious particle — a misfolded protein that causes other proteins to fold incorrectly

What is PrPsc?

Prion protein of scrapies — found in food, enters brain cells; causes misfolding of normal PrPc proteins

How tough are prions?

Can survive cooking, radiation exposure, and some proteases

What is the incubation time for prion disease (mad cow)?

8–12 years from consumption to symptoms

How is mad cow disease transmitted?

Eating food containing infected nerve tissue (e.g., head cheese, monkey brain)

What is the pathogenicity of prion disease?

Travel in nerves from gut to brain → PrPsc converts PrPc to PrPsc → clump in brain cells → slow disruption of brain function

What are the symptoms of prion disease?

Loss of coordination, dementia — incurable, always fatal

What causes giardiasis?

Giardia lamblia — a flagellate protozoan

What are the two forms of Giardia?

Trophozoite (reproduces in gut) and cyst (exits in feces, hardy form)

What is the primary reservoir for Giardia?

Beavers (and other mammals)

How is Giardiasis transmitted?

Fecal-oral route; incubation 6–20 days; infectious dose as low as 10 cysts; common in children in daycare

Why are Giardia cysts especially dangerous?

Tough — survive in chlorinated water

How does Giardia cause disease?

Trophozoites emerge in small intestine, attach via sucker discs, asexually reproduce, interfere with digestion/absorption like wallpaper