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Y Microbiology > Week 2 Lecture - Host and Parasite > Flashcards

Week 2 Lecture - Host and Parasite Flashcards

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Biology 101 flashcards
1
Q

Characteristics of a Host:

A
  • Macroorganism, usually multicellular
  • Phylogenetically a higher level
  • Eukaryote normally, but could be prokaryote
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2
Q

Characteristics of a Parasite:

A
  • Living on/in the host -> damage -> possibly disease
  • Obtains necessities of life from the host
  • No sharp distinction between normal and pathogenic, but parasitism has a unilateral benefit
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3
Q

Types of parasites, broadly:

A
  • Non-living: unique proteins (prions), nucleic acids (viroid)
  • Non-living/living?: virus
  • Prokaryotes: bacteria
  • Eukaryotes: microscopic fungi, protozoa, helmiths (worms which may be non-microscopic)
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4
Q

What is commensalism?

What is mutualism?

A

Commensalism is a relationship between a microorganism and host that is altogether neutral (no damage to each other)

Mutualism is a relationship that is beneficial for both the microorganism and the host

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5
Q

What is the ratio of host cells : microbe cell number?

A

1 host cell : 10 microbe cells

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6
Q

What percent of the human genome are human endogenous retroviruses (HERVs) accountable for?

A

HERV’s have contributed ~ 8% of the human genome without any serious problems and even encoding for some vital functions (i.e. the placenta development is encoded by viral-origin DNA)

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7
Q

Which microorganisms are considered a normal part of the microbe flora? Which are NOT normal?

A
  • Normal: bacteria, microscopic fungi
  • Not normal: viruses, protozoa, helminths
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8
Q

What are some benefits to microorganisms for commensalism/mutualism?

And benefits for the host?

A
  • Microorganism Benefits: shelter and food, colonisation on the tissues. Rarely, they will enter the tissue and cause disease
  • Host Benefits: prevent colonization of harmful microbes, often producing antimicrobial compounds (e.g. lactic acid in the vagina). Also GI bacteria process/degrade food components, producing Vitamin K and B12
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9
Q

How many species of parasitic/pathogenic microorganisms are there?

A

>1400

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10
Q

What are 4 ways that parasites can damage humans?

(the answers are kind of stupid but directly from the slide)

A
  • Entry/penetration form surface into tissues (invasivity)
  • Passively enter through wounds (damaged tissue integrity)
  • Actively via enzymes
  • Multiplication/replication in tissue -> pathogenic effects
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11
Q

What is the difference between obligate, facultative, and opportunistic parasites?

A
  • Obligate: always pathogenic, never found in normal flora
  • Facultative: conditionally, based on risk factors, a parasite may be either part of the normal flora or pathogenic. they don’t need a host to live, so may also be free living organisms and not parasitic
  • Opportunistic: members of the environment normally, not pathogenic at all for healthy people, but take advantage in disorders - especially immunosuppression
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12
Q

What are 3 risk factors for facultative pathogen infection?

A
  • Physical/mental stress
  • Acute diseases, wounds, burns
  • Chronic debilitating conditions (like diabetes, alcoholism, nutritional defects, leukemia + immunosuppression, etc.)
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13
Q

What are some examples of infection that have iatrogenic origins?

A

These are caused by medical diagnosis and/or therapy

  • Antibiotics and other drugs can cause changes in normal flora
  • Surgery, especially oral surgery
  • Prosthetics, catheters
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14
Q

What is a nosocomial infection?

A

An infection that results from time in a hospital or other health care facility. Infection could come from anyone, including patients, staff, or visitors

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15
Q

What are 4 viruses that replicate in immune cells, causing immunodeficiency?

A
  • HHV-6 (human herpes virus)
  • HHV-7
  • HIV
  • EBV (Epstein-Barr Virus aka HHV-4, infects B cells, causes mono)
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16
Q

What is the difference between pathogenicity and virulence?

A
  • Pathogenicity: ability of the whole population of a given microbe species to elicit disease in their hosts
    • simpler def’n: “ability to cause disease”
    • pathogenicity is determined by virulence factors
  • Virulence: ability to elicit a disease by a smaller population of the species.
    • simpler def’n: “degree of damage caused by a pathogen”
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17
Q

What are the 4 Koch Postulates?

A

Criteria to identify the causative agent of a particular disease

  1. Microorganism/pathogen must be present in all cases of the disease
  2. Pathogen can be isolated from the disease host and grown in pure culture
  3. Pathogen from the pure culture must cause the disease when inoculated into a healthy, susceptible laboratory animal
  4. Pathogen must be reisolated from the new host and shown to be the same as the originally inoculated pathogen
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18
Q

What might increase or decrease virulence? What is it called when virulence is lost?

A
  • Increasing virulence: mutations, GMO, bioterrorism
  • Decreasing virulence: mutations, attenuation
  • Microorganism loses virulence -> avirulent
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19
Q

How can virulence be measured?

A
  • Measured by number of germs
  • How many microbe(s) defined among standard circumstances induces pathological conditions = dose
    • ID50 = infective dose inducing disease in 50% of hosts
    • DL50 = lethal dose causing death in 50% of hosts
      • can also be measured as DL90, DL100 etc
    • TCID50 = tissue culture infecting dose - damaging 50% of cultures
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20
Q

What would be considered a small number of germs that -> disease and are thus highly virulent?

And as a large number of germs/low virulence?

A
  • Small # of germs that are highly virulent: 1-102
  • Large number of germs that have low virulence: >105
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21
Q

How would a bacterial endotoxin work to be poisonous to a host and what is a major example of one?

A

Because bacteria replicate and die quickly, their endotoxins are released into the host during bacterial infections.

Major example is LPS (liposaccharide) in Gram negative bacteria

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22
Q

What are some non-toxic virulence roles of the bacteria capsule?

A
  1. Protection - including the anti-phagocytic activity involving masking/hiding antigens
  2. Adhesion to host cells
  3. Antigen variations in one species - helping evade the immune system
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23
Q

What are 4 “non-toxic” (according to slide but they sound pretty toxic to me) extracellular enzymes secreted by bacteria that have an antiphagocytic effect?

(again might be a bit more than we need to know)

A
  • Leukocidines - pore-forming chemicals that kill leukocytes, helping the bacteria evade the immune system
  • Coagulase - reacts with prothrombin to make an active form that converts fibrinogen to fibrin. Apparently fibrin helps certain types of bacteria evade phagocytosis
  • Hemolysins - by definition they lyse red blood cells, but some can also lyse WBC’s
  • Proteases (pretty broad)
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24
Q

What are some virulence factors in which bacteria use enzymes to facilitate invasion?

A
  • Solubilizing cells and tissues of the host
  • Streptokinase (fibrinolysin)
  • Collagenase
  • Hyaluronidase
25
Q

What are two ways that bacterial exotoxins can damage the host cell surface?

A
  • Membrane damage / pore formation
  • Superantigens: APC MHCII + TCR binding -> cytokine production -> toxic shock
    • staphylococcus aureus: toxic shock syndrome toxin, TSST
26
Q

What are 4 ways that bacterial exotoxins can damage a cell with intracellular mechanisms?

A
  • A + B toxin (two protein component complexes - A: “active,” toxic effect; B: binding to cell surface)
  • Inhibition of protein synthesis (diptheria)
  • Overproduction of mediators, neurotransmitters (acetylcholine release -> tetanus)
  • Hypersecretion (cholera toxin causes severe electrolyte loss/diarrhea)
27
Q

What can be beneficial about the bacterial endotoxin LPS?

A

A small amount of it is an immunostimulant, essential for strong innate immunity.

28
Q

What is the structure of LPS?

A

Have to know it, sajnos

29
Q

What is a “reservoir” in terms of sources of infection

A

Animals or humans or other vehicles that permanently carry pathogenic microbes

30
Q

How might someone get an infection from an “endogenous” source?

A

From the normal flora, or by activation of latent/persistent microbes

31
Q

What the fuck does “vertical spread” mean in terms of transmission of infection?

A

Spreading to the next generation, as in through the placenta

32
Q

What is incubation time?

A

Symptomless period between the moment of infection and the onset of symptoms/disease outbreak

May take a few hours to months, years, even decades

33
Q

What is the difference between bacterial colonization and dissemination?

A
  • Colonization is irreversible, occurs at/near the site of entry. Microbes multiple and cause local infections
  • Dissemination is the spreading of the bacteria into the body, causing a generalized infection.
34
Q

What are the symptoms of Systemic Inflammatory Response System (SIRS)?

A
  • generalized weakness, malaise, warm skin, rash
  • high (>38°C) or low (<36°C) body temperature
  • tachycardia (>90/min)
  • tachypnea (>20/min)
  • WBC count increase (10-12x10 9 /L)
35
Q

What are some consequences of sepsis?

A
  • Systemic Inflammatory Response Syndrome
  • Aggravation: organ hypoperfusion
  • Septic shock: hypotension
  • Resistance to medications
  • Death (multiorgan dysfunction syndrome, MODS)
36
Q

What might be the results of symptomless infections in childhood?

(labeled as very important on the slide)

A
  • Lifelong immunity (i.e. toxoplasma)
  • Cross immunity (HSV-1/HSV-2)
37
Q

What is a latent infection?

A

One where the pathogen remains symptomless in the body until it is activated upon intrinsic/extrinsic factors

38
Q

What is a persistent infection?

A

The pathogen is activated regularly, sometimes symptomless but can still infect others

39
Q

When is a person a carrier of infection?

A

When they can spread it continuously w/o having symptoms

40
Q

What is the reason to take antibiotics even after your symptoms have disappeared?

A

Because the times of microbial and clinical recovery are different

41
Q

What are some unspecific ways that the body inhibits attachment, entry, and facilitates removal of microbes?

A
  • skin integrity
  • cilia movement in respiratory tract
  • pH variable on skin (from sebum), in the vagina and stomach, etc.
  • Enzymes: tears have lysozymes, mouth and GI tract have other antimicrobial enzymes
  • Osmolality in urine
  • Accelerated peristaltic movement, vomiting
42
Q

What are some Cell Surface Receptors on phagocytotic cells?

A

C type lectin

Toll-Like Receptor (TLR) 1,2,4,5,6

43
Q

What are some Endosomal Receptors on phagocytotic cells?

A

C-type Lectin

Toll-Like Receptor (TLR) 3,7,8,9

44
Q

What two types of molecules do the non-specific immune system phagocytes detect?

A
  • PAMPs: pathogen-associated molecular pattern. i.e. LPS, gram pos bacterial cell wall peptidoglycan, lipoteichoic acid, flagellin, N-formylmethionin, hypomethylated CpG-DNA, ss/dsDNA, ss/dsRNA
  • DAMPs: damage associated molecular pattern. Intracellular components of lysed cells. May be nuclear polypeptides, mitochondrial DNA, ROS, matrix proteins, heat shock proteins
45
Q

What are 5 aspects in the cascade of events in the activation of innate immunity?

A
  1. ​Activation of Interferon Regulatory Factors (IRF) - produce interferons, activate IFN-stimulated genes in immune and adjacent cells
  2. Formation of intracellular inflammasomes and stress granules
  3. Protein Kinase R (PKR) activation -> RNAaseL activation -> degradation of foreign RNA
  4. Caspase activation -> apoptosis of infected cells
  5. Release of pro-inflammatory mediators like IL-1,-2,-8 and TNF alpha, etc
46
Q

How do bacteria induce the complement system with part of their cell wall?

A

With mannose binding lectin (MBL) -> MASP1/MASp2 protease activation -> C4/C2 split -> C3 convertase -> production of C3a and C3b fragments

47
Q

What is the C3b fragment responsible for?

A

Opsonization, help phagocytes eat bacteria

48
Q

What type of antibodies are produced early in primary infection?

A

IgM - rapid but transient effect

49
Q

When are IgG antibodies produced?

A

Later in the course of primary infections (“seroconversion”), then rapidly and in high level during secondary infections.

50
Q

Which antibody is on the surface of mucous membranes, responsible for mucosal immunity (MALT, GALT)

A

IgA

Inhibits binding of microbes to mucosal cell receptors

Forms a dimer

51
Q

What are some ways that tuberculosis evades the immune system?

A
  • Damages macrophages
  • Inhibitions activation of IFN-gamma
  • Inhibits fusion between phagosome-lysosome
52
Q

What do shigella, listeria, and rickettsia do to evade the immune system?

A

Damage the lysosomal membrane

53
Q

What do salmonella and coxiella do to evade the immune system?

A

Inhibit lysozomal enzymes

54
Q

What do neisseria and enteric bacteria do to evade the immune system?

A

Inhibit activation of the complement system (“serum resistance”) - inhibit opsonization

55
Q

What does Neisseria meningitidis B do to evade the immune system?

A

self antigen mimicry (?)

56
Q

What type of cells destroy virus-infected cells?

A
  • NK cells activated by IL-12
  • Cytotoxic T cells
  • Other phagocytes based on MHC-II antigen presentation
57
Q

What are some ways that viruses evade the immune system?

A
  • Replicating in immune cells (like HIV, HHV)
  • Persistence
  • Cell-to-cell spreading, avoiding antibodies
  • Antigen variations (how the cold and flu virus always changes)
  • Inhibition of MHC synthesis (adenoviruses)
  • Interleukin mimicry (EBV)
  • Complement fragment neutralization (HSV-1 - C3b)
58
Q

There’s a lot of other crap in here that’s better covered in immunology so I’m not putting it here. Take a look at the lecture slides though.

A

Stop this now, no more cards

Y Microbiology (9 decks)

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