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GER Unit 2 > Microbio 2 > Flashcards

Microbio 2 Flashcards

1
Q

definitive host

A

harbors the adult/sexually mature stages of parasite (or in whom sexual reproduction occurs)

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2
Q

intermediate host

A

harbors the larval/sexually immature stages of parasite (or in whom asexual reproduction occurs)

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3
Q

permanent parasite

A

lives in (endo) or on (ecto) host without leaving (e.g., lice)

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4
Q

opportunistic parasite

A

capable of producing disease in an immunodeficient host, found in latent form or causes a self-limiting disease (i.e., cysts remain dormant until immunosuppressed, then travel and cross blood-brain barrier to form in brain)

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5
Q

what are 5 types of parasitic transmission?

A
  • direct ingestion of infective larvae, eggs, or cysts
  • ingestion of intermediate host
  • penetration of the principle host
  • maternal transmission
  • vector borne
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6
Q

what is IgE and what is it’s role in parasitic diseases

A
  • immunity to parasites (helminths)
  • IgE antibody levels are often high in people with allergies, may be increased in autoimmune diseases
  • total IgE test sometimes used as screening test if a parasitic infection is suspected
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7
Q

helminthic therapy

A

using worms to treat immune-mediated disease; epidemiological studies suggest that people who carry helminths have less immune-mediated disease
-reduce disease activity in patients with ulcerative colitis or crohn’s disease

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8
Q

what are some of the strategies used by parasites to evade host defenses?

A
  • complicated lifecycle: affective immune response difficult because host may be harboring several different stages of parasite
  • antigenic concealment: intracellular survival within macrophage
  • antigenic variation: gene switching
  • antigenic shedding: shedding of surface antigens or components
  • antigenic mimicry: incorporation of host “self” antigens into parasite surface
  • immunological subversion
  • immunological diversion
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9
Q

sCJD

A
  • usually white geriatrics, mostly sporadic infection
  • NOT transmitted p2p
  • complete dimension by 6th mo., death in a year
  • brain biopsy: spongiform change, neuronal loss without inflammation, accumulation of PrPsc
  • PrPsc deposition is diffuse
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10
Q

vCJD

A
  • mad cow; median age is 29
  • type 4 PrPsc
  • bovine to human and p2p by blood or food contaminated with BSE (NOT milk or muscle)
  • slower progression of dementia
  • peripheral pathogenesis in lymphoid organism
  • florid PrPsc plaques consisting of round amyloid core surrounded by ring of spongiform vacuoles
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11
Q

what is a virion vs. virus?

A
  • virion: virus particles, inert carriers of the genome that are assembled inside cells from virus-specified components; they do not grow and form by division
  • virus: capsid-encoding organism; infected cell
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12
Q

what is the structure of a virion?

A

genome + capsid +/- envelope

  • modular genome: encodes for capsid proteins, replicon, and host cell interacting factors
  • capsid: can be icosahedral, helical, or complex in symmetry; shape independent of genome
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13
Q

cytopathic effects

A

visible effect of viral infection; cells breakdown/morph

-not all viruses cause CPE but it can be used to study replication and infectivity

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14
Q

what are the requirements for viral replication?

A
  • right host (trophism)
  • susceptible cell (right receptors)
  • permissive cell (appropriate intracellular environment
  • biosynthesis machinery
  • abundant building blocks
  • time to finish
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15
Q

what are the general steps of virus replication?

A
  • recognition
  • attachent
  • entry
  • uncoating
  • transcription of mRNA (RDRP or RT)
  • protein synthesis by host machinery
  • replication of genome (RDRP, viral DNA pol, or host DNA pol or RNA pol II)
  • assembly of visions
  • egress
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16
Q

describe the single step viral growth curve

A
  • eclipse: no virus recovered during the replication and assembly phase
  • maturation and release: virus particles are made and can infect cells
  • burst size: # of infectious progeny from a single round of replication; difference between what you put in and what you get out, distinctive for that virus
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17
Q

general scheme of RNA virus replication

A
  • recognition and unpacking
  • transcription
  • replication with RNA-dependent RNA pol (all RNA viruses have, either package in virion or encoded)
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18
Q

RNA-dependent RNA Pol

A

highly efficient, low fidelity enzyme that catalyzes the replication of RNA from an RNA template
-functions in cytoplasm (except influenza)

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19
Q

Polio

A

+ssRNA genome, linear mRNA molecule

  • enterovirus, adapts in vivo to affect muscles and nerves (flaccid paralysis)
  • fecal-oral transmission
  • vaccination with live or attenuated virus
  • entry: changes shape after binding to receptor, capsid proteins become hydrophobic and form pore through membrane
  • RDRP copies + and - strands
  • translation happens first when RDRP is scarce
  • collisions occur between RDRP and ribosomes
  • RNA synthesis occurs later when RDRP is abundant
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20
Q

Rotavirus

A

dsRNA, reovirus, segmented, naked isocahedron

  • severe gastroenteritis
  • RDRP in virion first transcribes mRNA
  • egress via exocytosis (membrane vesicles) or cell lysis
  • virions mature in gut lumen and infect more enterocytes or are shed in profuse diarrhea
  • ORS
  • live attenuated vaccines
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21
Q

Influenza

A
  • ssRNA, segmented, primarily in lung
  • sements traffic to nucleus for transcription and translation
  • egress by budding
  • Neuraminidase (N antigen) releases virions from sialic acid on cell surface
  • antivirals: tamiflu and relenza (sialic acid analogs; virions remain attached to cell which stops spread)
  • vaccines: trivalent inactivated vaccine
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22
Q

HIV

A

+ssRNA

  • virion fuses with plasma membrane, reverse transcriptase converts +ssRNA into dsDNA which integrates into host chromosome for life
  • host RNA pol II transcribes mRNA from integrated genome
  • viral proteins bud from plasma membrane
  • virion maturation occurs outside cell
  • serologic assays for antibodies, CD4 T cell counts, nucleic acid assays for viral load
  • treatment to suppress viral load, restore immune function, prevent drug resistance, and improve QALY
  • meds: AZT (thymidine analog; chain terminator); stribild (4 drug combo; includes cobiscistat: targets host cell enzyme in liver that breaks drugs down)
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23
Q

general scheme of DNA virus replication

A
  • transcription and translation in nucleus (except pox)
  • host RNA pol transcribes mRNA (except pox)
  • both cellular and viral TFs regulate
  • viral or host DNA pol replicates genome
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24
Q

Adenovirus

A
  • linear dsDNA
  • respiratory
  • fecal-oral and aerosol transmission
  • susceptible populations: kids and military
  • capsid–>NPC–>DNA uncoats through nuclear pore–>host RNA pol II makes mRNA, (TFs first, then amplification)–>genome replication by viral DNA pol–>virions egress by lysis
  • treat with cidofivir (just dire cases, nephrotoxicity)
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25
Q

Papillomavirus

A
  • circular dsDNA
  • most commonly diagnosed STI
  • host RNA pol transcribes viral mRNA
  • host DNA pol synthesizes viral genomes
  • viral factors E6 and E7 are oncogenes
  • vaccines with virus-like particles
  • diagnose with DNA tests, treat with oncotherapy or excision
26
Q

Herpesvirus

A

-linear dsDNA
-envelop and tegument; dense body = only tegument, no capsid
-big genome (5x bigger than adeno)
-tegument into cytoplasm to modify host cell
capid–>NPC–>DNA uncoats through nuclear pore
-immediate early genes (TFs)–>early gene (replication)–> late proteins (structure proteins)
-capsids assemble in nucleus and bud through nuclear pore
-latency in genome for the life of infected person
-treatment: acyclovir (guanosine analog; chain terminator)

27
Q

HSV1

A
  • primary: gingibostomatitis
  • recurrent: prodrome precedes lesions
  • latency in dorsal root ganglia
  • infection can cause meningitis
  • PCR to distinguish between HSV1 and HSV2
28
Q

HSV2

A
  • contagious vesicular lesion below waist; asymptomatic shedding
  • latency in dorsal root ganglia
  • PCR to distinguish between HSV1 and HSV2
  • infection can cause meningitis
  • chemoprophylax with valtrex or famvir
29
Q

VZV

A
  • primary: chicken pox
  • recurrance: zoster/shingles
  • latency in dorsal root ganglia
  • aerosol transmission
  • outbreak out of 1 neuron (single dermatome)
  • vaccine: live attenuated virus
30
Q

EBV

A
  • mono (severe sore throat)
  • latency in B cells
  • transmission through saliva
  • recurrance is rare: lymphoma (e.g. burkitt’s)
  • diagnose based on serology and blood smear
31
Q

CMV

A
  • primary: asymptomatic or diagnosed (splenomegaly, rash, jaundice); mono like but no spore throat
  • latent in bone marrow
  • frequent cause of transplant failure
  • congenital CMV causes hearing loss and developmental disabilities
  • treatment: ganciclovir (guanosine analog; recognized by host DNA pol, highly toxic)
32
Q

HHV6, HHV7

A
  • roseola infantum; 3 day high fever followed by noncontagious rash on trunk
  • transmission through saliva
  • peak incidence 7-13 mo
33
Q

HHV8

A
  • kaposi sarcoma
  • primary: inapparent
  • infectious cancer associated with age and immunosuppression (treat immunosuppression and cancer goes away)
  • highly vascularized tumors
34
Q

characteristics of viral genomes

A
  • eukaryotic (all genes are single units)
  • TFs bind to enhancer/promoter and regulate
  • reading frames can overlap on the same strand (express 2 different proteins at once)
  • ribosomal frame shifting changes amino acid sequence
  • alternative splicing of RNA changes amino acid sequence
  • expression of polyproteins: create multiple proteins from 1 promoter by cutting big mRNA with viral protease
  • frequency of mutation is high
35
Q

types of virus interactions

A
  • interference: blocks receptors, competes for resources, produces interferon or other anti-viral genes
  • complementation: gene function of one virus replaces mutated or missing gene of another
  • phenotypic mixing: similar viruses can exchange cupids, pseudo type created can’t replicate or grow
  • recombination: viruses with similar genomes can exchange genes by crossing over at homology; new hybrids can grow and replicate
  • reassortment: rearrangement of segments to form new ones; very rapidly changes the virus (antigenic shift)
36
Q

gene therapy

A
  • delete essential gene from virus and insert that gene into complementing cell, clone therapeutic human gene into complemented cell line, and grow
  • monogenic disorders might be abled to be treated (ex. retinoblastoma, hemophilia)
  • problems associated: short duration of expression, low efficiency of gene transfer means high dose of virus, inflammatory response to virus vector
37
Q

primary viremia

A

viruses spread from surface of body to lymph node and blood stream

38
Q

secondary viremia

A

second time virus is detectable in the blood, disseminates virus to organs where it is shed

39
Q

pathogenesis of chicken pox/shingles

A
  • primary viremia: respiratory route to lymph node
  • secondary viremia infects epithelial cells and causes lesions
  • latency established simultaneously in dorsal root ganglion
40
Q

modes of viral transmission

A
  • respiratory
  • fecal-oral
  • contact
  • zoonoses
  • blood
  • sexual
  • maternal-neonatal
  • genetic (prions and retroviruses)
41
Q

patterns of viral disease

A
  • acute: disease occurs and resolves (ex. common cold)
  • latent: acute episode then virus is undetectable/noninfectious then second disease episode (ex. varicella/zoster)
  • chronic: virus acquired, potential acute episode, then virus maintains detectable level with shedding throughout life course (ex. hep B and C)
42
Q

how do viruses injure host?

A
  • directly: any virus that gets out of the cell by lysis (ex. norwalk and respiratory syncytial virus)
  • indirectly: host response to infection (interferon response)
  • successful virus will avoid destruction by immune system and avoid destroying host before replication is finished
43
Q

Hep A

A
  • picornavirus: RNA, no envelope
  • transmission: fecal-oral
  • vaccination: raises IgG response, protective against reinfection
  • virus itself is not hepatotoxic, symptoms are largely immunogenic (worse in adult than child)
  • diagnosis: elevated ALT, IgM (acute), IgG (recovered/vaccinated)
44
Q

Hep B

A
  • hepadnavirus: DNA, envelope
  • transmission: sex/birth/bood
  • virus itself is not hepatotoxic; produces immunological decoys (viral protein) that ties up antibodies
  • antibody-antigen complexes in blood try to pass through capillaries (cause joint pain because of deposition)
  • carries RT and replicates through RNA intermediate
  • vaccination
  • diagnosis: biopsy (“ground glass”), serology of viral surface antigen (acute), IgG against viral surface antigen (recovered/vaccinated)
  • most hepB resolves, can cause chronic hepatitis and/or hepatocellular carcinoma
  • treatment: tenofovir: designed for HCV and HIV (targets RT); pegylated interferon; entecavir (guanosine analog)
45
Q

Hep C

A
  • flavavirus: RNA, envelope
  • transmission: sex/birth/blood
  • highly mutagenic
  • acute infection similar to HepB but no decoys (less likely to raise a strong immune response)
  • higher rate of chronic hepatitis leading to cirrhosis and/or cancer
  • diagnosis: elevated ALT, EIA (real or false positive, follow up with RIBA); screen for HIV, hepB, and drug abuse
  • no vaccine (IgG not protective)
  • treatment: pegylated interferon, sofosbuvir: uridine analog (inhibits RDRP), telaprevir (inhibits NS3.4A protein in replication complex)
46
Q

antiviral methods of action

A
  • nucleoside analogs: genome replication
  • non-nucleoside analogs: genome replication
  • protease inhibitors: assembly and release
  • entry inhibitors
  • many drugs are competitive inhibitors (reversible); rebound can occur
47
Q

potential resistance to antivirals

A
  • mutations often exist in patient before drug is administered (drug treatment selects for resistant virus strands)
  • resistance occurs because of high rate of virus replication, high mutation rate, high selective drug pressure, immunosuppressed host
  • counteract by combining drugs with different targets; targeting host functions (beware of toxicity), and alleviating immunosuppression to antivirals
48
Q

broad spectrum DNA antivirals

A

foscarnet and cidofavir (both are toxic to kidneys)

49
Q

broad spectrum RNA antivirals

A

ribavirin (guanosine analog): targets RDRP enzyme, can immunomodulate (change T cell profile), lowers GTP in cell

50
Q

properties of fungi

A
  • eukaryotes
  • chitin and ß-glucan cell wall
  • cell membrane has ergosterol (not cholesterol)
  • no endotoxins, mycotoxicosis: fungal poisoning after ingestion
  • aflatoxins: mutates p53, linked to hepatic carcinoma
  • fungal allergies
  • yeasts (single cell; budding) or mold (multicellular; hyphae form mycelium; most are asexual–5 types of conidia: spores with distinctive microscopic appearance)
  • thermal dimorphism: mold in environment, yeast in body
  • immune response: granulomatous and/or supporative
51
Q

diagnosis of fungi

A
  • PPD
  • direct microscopy: KOH mount microscopy with final stains
  • culture on sabouraud’s agar
  • PCR available for dangerous systemics
  • serology for epidemiology
52
Q

fungal treatments

A
  • polyenes: binds ergosterol; broad spectrum disrupts cell membranes (ex. amphotericin B: systemic and nephrotoxic, only antiviral safe for pregnancy)
  • azoles: inhibit ergosterol synthesis (ex. fluconazole/diflucan for candidiasis and cryptoccosis)
  • echinocandins: inhibis ß-glucan synthesis (effective against candida and aspergillus)
53
Q

four major categories of fungal infections

A
  • superficial
  • subcutaneous
  • systemic
  • opportunistic
54
Q

superficial fungal infection

A
  • minor infections or overgrowth on superficial skin layer
  • does not require thermal dimorphism
  • symptoms: itch or discoloration
  • treatment: topical azoles or oral griseofulvin if necessary
  • ex. dermatophytosis
55
Q

subcutaneous fungal infection

A
  • granulomatous infection of low dermal layers
  • requires thermal dimorphism
  • trauma exposes subcutaneous tissue to soil or vegetation
  • treatment: oral azoles, amphotericin B and local surgery
  • ex. sporotrichosis
56
Q

dermatophyosis

A
  • transmitted by fomites or auto inoculation
  • very common; minor symptoms (called tinea)
  • infect only superficial keratinized structures
  • diagnosis: KOH mount, culture
  • treat: affected body sites simultaneously with topical antifungal
57
Q

sporotrichosis

A
  • caused by sporothrix spp; thermally dimorphic fungi
  • enters through thorns
  • painless ulcer spreads through lymphatics over the years
  • if immunocompromised there can be disseminated symptoms or meningitis
  • diagnosis: biopsy and culture at room temp from pus
  • treat: oral azoles, amphotericin B for more serious forms
58
Q

systemic fungal infection

A
  • infection spreading from inhaled spores
  • thermal dimorphism, NO p2p
  • range of severity
  • most common is coccidioides/histoplasma/blastomyces (mimic TB but source is American dirt)
59
Q

coccidioides

A
  • thermally dimorphic (mold/spherule) endemic to US southwest
  • mold grows in wet weather, releases arthrospores in drug weather
  • 60% mild (asymptomatic or flulike; clearance by CMI), moderate (valley fever/desert rheumatism; pulmonary and EN), severe: major pneumonia or dissemination
  • diagnosis: exam, history, ppd, biopsy for spherules, culture, serology
  • treatment: if predisposed to complications (oral azoles), meningitis (fluconazole), pregnant/disseminated (ampho. B)
60
Q

opportunistic fungal infection

A
  • diseases and severity are widely varied, predicated on patients’ pre-existing conditions
  • optimal treatment addresses infection and underlying problem
  • ex. cryptococcosis
61
Q

cryptococcosis

A
  • enabled by reduced CMI, blunted inflammatory response complicates diagnosis
  • dimorphic BUT NOT thermally dimorphic
  • presents late in disease with meningitis (subacute) and skin nodules or pulmonary symptoms
  • No p2p except organ transplantation
  • steroids, AIDS, and survival with malignancy have increased caseload
  • diagnosis: biopsy, CSF, crag (crytococcal antigen in blood and CSF)
  • treatment: pulmonary may not need treatment, meningitis or cryptococcoma (localized, solid, tumor-like masses) require combo of azoles and ampho. B

GER Unit 2 (2 decks)

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