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BIIC > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Toxins

A

Made by bacteria and cause damage

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2
Q

Exotoxins

A

Not integral part of bacteria
1. Secreted by bacteria
2. Can act locally or systemically
3. Membrane active: changes stability of membrane
4. Hydrolytic enzymes
5. Superantigen exotoxins
6. Subunits
A. A subunit: toxic activity
B. B subunit
1. Mediates adherence of toxin complex to host cell
2. AIDS entrance of exotoxin into host cell
C. Subunits can be synthesized by same or separate genes

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3
Q

Membrane-active exotoxins

A

Changes stability of host cell membrane

  1. Often pore-forming
  2. Staph aureus
  3. C. Perfringens
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4
Q

Hydrolytic enzymes as exotoxins

A

Cleave host cellular proteins

1. Different effects depending on protein

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5
Q

Superantigen exotoxins

A

Inappropriately activate immune system -> cytokine storm -> shock

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6
Q

Endotoxins

A

Infections caused by gram (-) bacteria

  1. LPS endotoxins of outer membrane
  2. Lipid A portion
  3. Dec platelet count
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7
Q

LPS endotoxin

A
  1. Significant component of disease process
  2. Cause local injury
  3. Major effected when bacteria enter bloodstream
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8
Q

Lipid A portion of endotoxin

A

Causes fever

  1. Release IL-1 and TNF-alpha from macrophages
  2. Inflammation
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9
Q

Bacillus anthracis

A
  1. Gram (+)
  2. Non motile
  3. Facultative anaerobes
  4. Spore-forming rod
  5. Etiological agent = anthrax
  6. Plasmid encode primary virulence factors
    A. Toxin production
    B. Capsule formation: helps resist phagocytosis
  7. Toxins
    A. Protecting antigen (PA): B subunit
    B. Lethal factor (LF): A subunit
    C. Edema factor (EF): A subunit
    D. Can just immunize against PA
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10
Q

Bordetella pertussis

A
  1. Gram (-) aerobics coccobacillus
  2. Whooping cough
  3. Toxins
    A. Pertussis toxin (PT): hydrolyzes cellular NAD and transfers ADP-ribose -> alpha subunit of G-proteins
    B. Adenylate Cyclase toxin (ACT)
    1. Amino terminal adenylate cyclase (AC) domain
    2. Pore-forming repeat in toxin (RTX) hemolysin domain
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11
Q

Corynebacterium diptheriae

A
  1. Gram (+) rod
  2. Mucous membrane uppers resp tract
  3. Diphtheria
  4. Diphtheria toxin: encoded in lysogenic, temperate bacteriophage
    A. Virus in bacteria encoded into bacteria DNA- needs Fc to replicate
    B. Availability of inorganic Fe limits bacterial growth rate -> max toxin production
    C. Inhibits peptide chain elongation factor EF-2
    1. Attaches adenosine diphosphate-ribosyl group
      D. A-B subunits held together by disulfide bonds
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12
Q

Clostridium tetani

A
  1. Anaerobic gram (+) rod
    A. Spores don’t stain
  2. Tetanus
  3. In environment
    A. Contaminates wounds
    B. Spores germinate in anaerobic environment of devitalized tissue
  4. Tetanospasm toxin
    A. Binds to receptors on presynaptic membrane motor neurons
    B. Retrograde transport system -> cell bodies in spinal cord and brainstem
    C. Toxin -> terminal inhibitory cells
    D. Degrades synaptobrevin: required for docking of neurotransmitter vesicles on presynaptic membranes
  5. Spastic paralysis
  6. Extremely small amounts of toxin lethal to humans
  7. Prevention = immunization w/ tetanus toxoid
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13
Q

Clostridium botulinum

A
  1. Anaerobic gram (+) spore forming
  2. Soil, water, canned food
  3. Botulinum toxin: most potent toxin known
    A. Heat labile
    B. Similar to tetanus
    C. Absorbed from gut
    1. Binds presynaptic receptors on motor neuron PNS and cranial n.
    2. Proteolysis of target proteins in neurons
      A. Inhibits release ACh at synapse -I muscle contraction and flaccid paralysis
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14
Q

Clostridium perfringens

A
  1. Assoc w/ war wounds
  2. Anaerobic gram (+) spore-forming
  3. Spores -> wounds via soil/feces
  4. Vegetative cells -> several toxins
    A. Necrotizing and hemolytic
    B. Gas gangrene
  5. Toxins
    A. Alpha (CPA)
    1. Lecithinase: damages cell membrane by splitting lecithin -> diglyceride and phosphorylcholine
    2. Main virulence factor in gas gangrene
      B. Beta (CPB) -> necrotizing enteritis and enterotoxemia (neonates)
      C. Epsilon (ETX)
      D. Iota (ITX)
      E. Enterotoxin (CPE): human food-poisoning
      F. Necrotic B-like (NetB) toxins
      G. Collagenases
      H. DNAses
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15
Q

Staph aureus virulence factors

A
  1. Panton-valentine leukocidin (PVL) -> WBC lysis
  2. Alpha-hemolysin (alpha toxin) -> pore-forming -> cell lysis
  3. Phenol-soluble modeling (PSMs): small, amphipathic proteins -> lyes neutrophils and erythrocytes
  4. Arginine catabolic mobile element (ACME)
  5. Qar regulatory locus: controls expression of toxins
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16
Q

Staph aureus toxins

A
  1. Related to some disease
  2. Damage cell membrane
  3. Enterotoxins
  4. Pore-forming
  5. Exfoliating toxins
  6. Superantigen toxins
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17
Q

S. Aureus toxins related to disease

A
  1. Toxic shock syndrome (TSS)
  2. Staph scalded sin syndrome (SSSS)
  3. Necrotizing pneumonia
  4. Deep-seated skin infections
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18
Q

Staph aureus toxins that damage cell membrane

A
  1. Degrade inter-cellular connections
  2. Modulate immune response
    A. Toxic shock syndrome
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19
Q

Staph aureus enterotoxins

A
  1. Often in food not properly refrigerated
  2. Absorbed in gut
  3. Stimulate vagus receptors -> vomiting center
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20
Q

Staph aureus pore-forming toxins

A
  1. Hemolysin alpha
  2. Hemolysin beta (sphingomyelinase C)
  3. Leukotoxins
  4. Phenol-soluble modulins
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21
Q

Hemolysin- alpha

A

Staph aureus pore-forming toxin

  1. Lysis
  2. Alteration cell-signaling pathways
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22
Q

Hemolysin-beta (sphingomyelinase C)

A

Staph aureus pore-forming toxins

1. Cytotoxic to keratinocytes, polymorphonuclear leukocytes, monocytes, and T lymphocytes

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23
Q

Leukotoxins

A

Staph aureus pore-forming toxins

  1. Panton-Valentine leukocidin (PVL)
  2. Gamma-hemolysin (HIgA, HIgC, HIgB)
  3. Leukotoxins ED (LukE, LukD)
  4. Leukotoxins AB/GH (LukAB/LukGH)
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24
Q

Phenol-soluble modulins (PSMs)

A

Staph aureus pore-forming toxins

1. Attach cytoplasmic membrane in non-specific way -> membrane disintegration

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25
Q

Staph aureus exfoliating toxins

A
  1. Epidermolytic toxins
  2. Specific serine proteases
  3. Hydrolyses desmosome cadherins
  4. Assoc w/ cleavage of keratinocytes junctions and cell-cell adhesion
  5. Deep skin peeling and blisters
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26
Q

Staph aureus superantigen toxins

A
  1. > 23 known
  2. Includes TSST
    A. Shock
    B. High fever
    C. Diffuse red rash
    D. Stimulate T cells by binding MHC-II and TCRs -> IL-2, IFN-gamma, and TNF
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27
Q

Streptococcus toxins

A
  1. Group A beta-hemolytic strep
    A. Pyrogens exotoxins A and C: superantigen act like TSST-1
  2. Rapidly progressive soft tissue infection
  3. Superantigen
    A. Pyrogenic exotoxins (Spe)A,C,G-M
    B. Streptococcal superantigen (SSA)
    C. Streptococcal mitogen exotoxin Z (SmeZ)
  4. Group A strep pore-forming
  5. Streptococcal pyrogenic exotoxin B
  6. Immunoglobulin degrading enzyme
  7. 2 major substilisin-like serine proteases
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28
Q

Group A strep pore-forming toxin

A
  1. Hemolysin
    A. Streptolysin S (SLS): targets RBCs, platelets, subcellular organelles, and leukocytes
    B. Streptolysin O (SLO)
    1. Choloesterol-dependent cytolysin
    2. Targets macrophages, neutrophils, epithelial cells, and endothelial cells
    3. Contributes to impaired phagocytes clearance
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29
Q

Streptococcal pyrogenic exotoxin B (SpeB)

A
  1. Cysteine protease
  2. Cleaves IgG into Fc and Fab fragments and degrades IgA, IgM, IgD, and IgE
  3. Cleaves components of complement activation pathway
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30
Q

Enterotoxins

A
  1. Bacillus cereus
  2. Vibrio cholera
  3. Salmonella
  4. Shigella
  5. Escherichia
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31
Q

Bacillus cereus

A

Enterotoxin

  1. Cerulide
  2. Hemolysin BL (HbL), nonhemolytic enterotoxin (Nhe) and cytotoxic K (CytK)
32
Q

Vibrio cholera

A

Enterotoxin

  1. Toxin -> inc adenylate cyclase activity and inc cAMP
  2. Lead to rapid secretion of electrolytes -> small bowel lumen a/ dec absorption Na+ and CL- and bicarbonate loss
33
Q

Viral hemorrhagic fever

A
  1. Affect many organs
  2. Damage blood vessels
  3. Affect body’s ability to regulate itself
34
Q

Arenaviridae

A 
1. Transmission: rodents
  A. Humans accidental hosts
  B. No obvious illness in rodents
  C. She’s in urine feces rodents 
2. RNA genome, enveloped 
3. Human infection
  A. Incidental to natural viral cycle
  B. Eat contaminate food
  C. Direct contact abraded/broken skin w/ rodent excrement
  D. Inhalation contaminated particles 
4. Tacaribe complex viruses
  A. Assoc w/ new world rates and mice
5. Lassa fever virus/LCM
  A.  Assoc w/ old world rats and mice
35
Q

Acute viral hemorrhagic illness

A 
Arenaviridae: Lassa fever virus
1. 2-21 days duration
2. Occurs in west Africa 
  A. Endemic
    1. Benin
    2. Ghana
    3. Guinea
    4. Liberia
    5. Mali
    6. Sierra Leone
    7. Nigeria 
3. Transmission
  A. Contact food/household items contaminated rodent urine/feces
  B. Person to person infections 
  C. Lab transmission
4. Overall case-fatality = 1%
5. Early supportive care w/ rehydration and symptom tax
36
Q

Bunyavirdae

A
  1. Large family of viruses
  2. SsRNA, enveloped
  3. Transmitted by Arthropods and rodents
  4. Occasionally infect humans
  5. Rift Valley fever
  6. Crimean-Congo hemorrhagic fever
  7. Hantaviruses
37
Q

Rift Valley fever

A 
Bunyavirdae
1. Isolated in 1930
  A. Large outbreak in sheep in East Africa
2. Transmitted by mosquitoes
  A. Blood/organs infected animals
3. Endemic sub-Saharan Africa
4. Primarily zoonotic
5. Incubation period: 2-6 days
6. Prevention: animal vaccination
38
Q

Crimean-Congo hemorrhagic fever

A 
Bunyavirdae
1. Recognized Crimean peninsula
2. Isolated 1956 from single pt Democratic Republic of Congo
3. Transmitted by tick
  A. Person to person characteristic
39
Q

Hantaviruses

A 
Bunyavirdae
1. Observed 1950s in troops in Korea
2. Sin Nombre virus
  A. Cause severe hantavirus pulmonary syndrome (pneumonia)
  B. American SW 1993: more rodents
40
Q

Filoviridae

A
  1. Severe hemorrhagic fever in humans and non-human primates
  2. Virions in several shapes
    A. Long, sometimes branched filaments
    B. Shorter filaments shaped like “6”, “u”, or a circle
    C. Enveloped
  3. (-) sense ssRNA
  4. Marburg virus
  5. Ebola virus
41
Q

Marburg virus

A 
Filoviridae
1. Recognized 1967
  A. Lab workers Germany and Yugoslavia handling tissues from infected green monkeys
2. Re-emerges 1975
  A. Traveler exposed in Zimbabwe sick in Johannesburg, South Africa 
3. Severe, often fatal in humans
  A. Severe viral hemorrhagic fever
4. Transmitted from fruit bats
  A. People to people from there
5. Avg MVD case fatality rate 50%
6. Early supportive care inc survival
42
Q

Ebola virus

A 
Filoviridae
1. Identified 1976
  A. 2 outbreaks Ebola hemorrhagic fever
    1. N. Zaire (Congo)
    2. Southern Sudan
  B. Highly lethal
    1. 90% Zaire cases
    2. 50% Sudan cases
2. Spread
  A. Initially: direct contact w/ blood, body fluids, and tissues of animals 
  B. Then: direct contact body fluids sick/dead people
    1. Some cultures prepare own dead
3. Survivors
  A. Lasting side effects: don’t know why
    1. Tiredness
    2. Muscle aches
    3. Eye/vision probs
    4. Stomach pain
4. Risk of infection: inc risk health worker who don’t use proper PPE
  A. Little risk to travelers/general public who haven’t cared for a been in close contact (w/in 3 ft) of pt
43
Q

Ebola persistence

A
  1. Can remain in immunologically privileged organs
    A. Testes
    B. Interior of eyes
    C. Placenta
    D. CNS
  2. Survives on dry surfaces several hrs
  3. Survives body fluids at room temp for several days
44
Q

Ebola tx and prevention

A
  1. Investigational tx
    A. Regeneron (REGN-EB3) and mAB114
    1. Greatly inc overall survival
    2. Two antivirals used to treat Ebola pts
  2. Vaccines
    A. Ervebo: Ebola Zaire vaccine (rVSVdelta-ZEBOV-GP live)
    1. Has glycoprotein and subunit of virus
45
Q

Flaviviridae

A
  1. Family of viruses
  2. (+) sense ssRNA
  3. Enveloped
  4. Occasionally infect humans
    A. Widespread morbidity and mortality throughout world
  5. Transmission
    A. Mosquitoes
    1. Yellow fever
    2. Dengue fever
    3. Japanese encephalitis
    4. West Nile virus
    5. Zika virus
      B. Ticks
    6. Tick-Bourne encephalitis
    7. Omsk hemorrhagic fever
46
Q

Yellow fever virus

A

Flaviviridae
1. Tropical/subtropical Africa and South America
2. Transmission: mosquitoes
A. Cycles
1. Jungle (sylvatic): non-human primates -> mosquitoes in forest canopy
2. Intermediate (Savannah): mosquitoes -> humans living/working in jungle border areas
3. Urban: humans and urban mosquitoes (Aedes aegypt)
3. Rare in US
A. 1793 epidemic in PA (5000 people dead)
4. Diease
A. Jaundice -> vomiting and bleeding every day
B. Range: can be just fever and aches
5. Dx:
A. Labs
B. Symptoms
C. Travel hx
6. No specific tx

47
Q

Yellow fever prevention

A
  1. Bug spray
  2. Cover skin
  3. Vaccine
    A. Available >80 yrs
    B. Single dose -> lifelong protection
    C. Attenuated
    D. For people 9+ months traveling to inc risk areas
    E. Required to enter certain countries
48
Q

Yellow fever presentation

A
  1. Most asymptomatic
  2. Initial: sudden onset
    A. Fever
    B. Chills
    C. Severe headache
    D. Myalgia
    E. Nausea
    F. Vomiting
    G. Fatigue
    H. Weakness
  3. Severe
    A. High fever
    B. Jaundice
    C. Bleeding
    D. Shock
    E. Organ failure
    F. Fatality 30-60%
49
Q

Dengue fever

A 
Flaviviridae
1. Dengue virus serotypes
  A. DENV1-4
2. Transmission: female mosquitoes
  A. Mostly Aedes aegypti
  B. Less Ae albopictus
3. 1/2 world at risk
4. 390 million infections/year
5. Tropical/subtropical climates worldwide
  A. Urban and semi urban
6. Vector control
50
Q

Dengue fever disease spectrum

A
  1. Sub-clinical
  2. Severe flu-like
    A. Symptoms last 2-7 days
    B. Incubation: 4-10 days
  3. Dengue
    A. Fever (40/104) + 2 others
    1. Severe headache
    2. Pain behind eyes
    3. Muscle and joint pains
    4. Nausea
    5. Vomiting
    6. Swollen glands
    7. Rash
  4. Severe dengue
    A. Critical phase
    1. 3-7 days after onset
    2. Dec fever (38/100)
    3. Dev severe dengue
      A. Plasma leaking
      B. Fluid accumulation
      C. Resp distress
      D. Severe bleeding
      E. Organ impairment
      B. Warning signs
    4. Severe abdominal pain
    5. Persistent vomiting
    6. Rapid breathing
    7. Bleeding gums
    8. Fatigue
    9. Restlessness
    10. Blood in vomit
51
Q

Dengue fever tx and vaccination

A 
1. Tx 
  A. No specific tx 
  B. NSAIDS avoided
  C. Severe: maintaining fluid volume dec mortality from 20% to 1%
2. Vaccine
  A. Live attenuated
  B. Effective and safe in seropositive 
  C. Inc risk severe dengue if given to seronegative people
  D. Should screen before vaccinating
52
Q

HIV-1

A

US

53
Q

HIV-2

A

Africa

54
Q

HTLV

A

Human T cell leukemia virus

55
Q

Retroviruses

A

RNA genome: (+) ssRNA

  1. Diploid = 2 identical copies
  2. Copied into dsDNA
  3. Integrated into host genome
56
Q

HIV accessory (regulatory) proteins

A
  1. Tat = transcription activator
    A. Inc viral RNA synthesis
  2. Rev: transport full length RNA from nucleus -> cytoplasm for packaging
  3. Nef: perturb cell signaling
    A. Enhances infectivity
  4. Vif, Vpr, Vpu: control cellular restriction factors
57
Q

HIV replication cycle

A 
1. Attachment
  A. Mediated by glycoproteins
    1. Gp120: hypervariable because RT can’t fix mistakes
    2. Gp41: brings viral envelope closer for fusion
  B. CD4 molecule 
  C. Chemokine coreceptor: on target cells and macrophages
     1. CCR5
     2. CD4
2. Entry
3. RT
4. Integration
5. Translation
6. Assembly, budding, and maturing
  A. P55 cleaved by protease -> mature
58
Q

HIV gag proteins

A 
Core structural proteins
1. Gag -> pr55 (precursor)
2. Pr55 cleaved by protease ->
  A. P18
  B. P24
  C. P15
59
Q

HIV polymerase gene

A
  1. Pol -> p160 (precursor) ->
    A. P10 = protease
    B. Pp66/65 = RT
    C. P32 = integrase
60
Q

HIV infections

A
  1. Acute retroviral syndrome
  2. Acquired immunodeficiency syndrome (AIDS)
  3. Transmission
    A. Unprotected sex
    B. Anal intercourse
    C. Occupational needlestick/body fluid splash (<0.3% transmission)
    D. Contaminated blood products
    1. Now screened
61
Q

Acute (primary) HIV infection

A
  1. 90% infections
  2. Mononucleosis (flu-like symptoms)
    A. Fever
    B. Lymphadenopathy
    C. Malaise
    D. Pharyngitis
62
Q

HIV infection Dx

A
  1. Won’t see AB before 45 days
  2. P24 core antigen test
  3. RNA detection = viral load
  4. CD4+ cell count
    A. Important to monitor in infected people
  5. Test for othe STIs in HIV+ people
    A. N. Gonorrhoeae
    B. Chlamydia trachomatis
63
Q

HIV screening

A
  1. 13-64 y/o: should screen at least once as routine healthcare
  2. Risk factors: screen annually
  3. Men who have sex w/ other men
    A. Asymptomatic: annually
    B. Inc risk: every 3-6 mo
64
Q

AIDS symptoms

A
  1. Chronic fever
  2. Wt loss
  3. Persistent diarrhea
  4. Lymphadenopathy
  5. Oral lesions
  6. Fatigue
  7. Pneumonia
  8. Other opportunistic infections
65
Q

HIV opportunistic infections

A
  1. CD4 count <200 cells/mm^3
  2. Not taking prophylactic drugs
  3. Pneumocystis jirovecii: rare pneumonia
  4. Cryptosporidium
  5. Cryptococcus
  6. Candida
  7. Cytomegalovirus: encephalitis
  8. HHV-8
  9. Treatment
    A. CMV: foscarnet and gangiclovir
    B. Yeast (and other fungi): fluconazole
    C. Pneumocystis jirovecii:
    1. TMP/SMX
    2. Pentamidine
66
Q

HIV associated malignancies

A
  1. Kaposis sarcoma
  2. Nonhodgkins lymphoma
  3. Lymphocytic leukemia
  4. Hodgkin disease
  5. Burkitt lymphoma
  6. Liver cancer
  7. Mouth/throat cancer
67
Q

HIV therapeutics

A
  1. Nucleoside RT inhibitors
  2. Non-nucleoside RT inhibitor
  3. Protease inhibitors
  4. Fusion inhibitors
  5. CCR5 antagonists
  6. Integrate inhibitors
  7. Pharmacokinetic enhancers
68
Q

NRTIs

A

HIV tx

  1. Abacavir
  2. Emtricitabine
  3. Lamivudine
  4. Tenofovir disproxil fumarate
  5. Zidovudine
69
Q

NNRTIs

A

HIV tx

  1. Doravirine
  2. Efavirenz
  3. Etravirine
  4. Nevirapine
  5. Rilpivirine
70
Q

Protease inhibitors

A

HIV tx

  1. Atazanavir
  2. Darunavir
  3. Fosamprenavir
  4. Ritonavir
  5. Saquinavir
  6. Tripranavir
71
Q

Fusion inhibitors

A

HIV tx

1. Enfuvirtide

72
Q

CCR5 antagonists

A

HIV tx

1. Mararviroc

73
Q

Integrase inhibitors

A

HIV tx

  1. Dolutegravir
  2. Raltegravir
74
Q

Post-attachment inhibitors

A

HIV tx

1. Ibalizumab

75
Q

Pharmacokinetics enhancers

A

HIV tx booster

1. Cobicistat

76
Q

HIV Pre-exposure prophylaxis (PrEP)

A

Oral tenofovir and emtricitabine

  1. Fixed-dose combo tablet
  2. Daily dose
  3. Follow-up every 3 mo
77
Q

HIV post-exposure prophylaxis (PEP)

A

Use ARTs for people HIV (-) after single high-risk exposure

  1. Start ASAP (w/in 72 hrs)
  2. Course 4 weeks
  3. Only for infrequent exposures

BIIC (7 decks)

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