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HDID 2 > 27/28 Host-Parasite Interactions > Flashcards

27/28 Host-Parasite Interactions Flashcards

1
Q

principal pathogen

A

regularly causes disease in a proportion of susceptible hosts who have normal specific and nonspecific defense mechanisms. Eg streptococcus pneumoniae, neisseria meningitidis, coccidioides immitis

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2
Q

commensal organism

A

lives within or on the surface of the host, almost never perturbing homeostasis. Eg: diphtheroids, lactobacilli

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3
Q

opportunistic pathogen

A

rarely causes disease except in hosts who have defects in specific or nonspecific defense mechanisms. Eg pseudomonas aeruginosa, staphylococcus epidermidis, aspergillis fumigatus

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4
Q

what is virulence?

A

measure of the tendency of an organism to cause disease

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5
Q

what is LD50? ID50?

A

dose of a microorganism that will kill/infect 50% of susceptible population

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6
Q

koch’s postulates?

A
  1. orgnaism must be found in all cases of disease but generally not in healthy animals
  2. organism must be isolated from diseased animals and grown in pure culture
  3. disease must be reproduced when the isolated organism is inoculated into susceptible animals
  4. organism must be isolated in pure culture from the experimentally infected animals

*** beware that these are not universally applicable - most pathogenic microorganisms cause disease in only a subset of infected animals and therefore may be cultured from asymptomatic indivs, or some can’t be cultivated in vitro, or some are host-adapted and don’t cause a similar disease in animals

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7
Q

molecular koch’s postulates are useful to determine what?

A

if a particular phenotype (trait) is required for disease)

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8
Q

what are koch’s molecular postulates?

A
  1. gene(s) encoding the phenotype should be associated with pathogenic strains
  2. inactivation of the gene(s) results in reduction in virulence
  3. restoration of the gene(s) into the avirulent mutant reestablishes virulence
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9
Q

each organism has evolved its own unique survival strategy that enables it to fulfill its primary objective, which is what?

A

proliferation

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10
Q

in the case of infectious agents, survival requires what?

A

both multiplication and transmission to new hosts

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11
Q

for most primary pathogens, what is the most common outcome of infection?

A

asymptomatic (disease results more or less often depending on the details of the survival strategy)

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12
Q

one important distinction between pathogens and non-pathogens may be the degree to which the microbe does what?

A

exposes the host to molecules recognized by pattern recognition receptors of the innate immune system (non-pathogens often occupy niches where such interactions are uncommon or unproductive)

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13
Q

death is a _______ outcome of infection for the microorganism, as well as the host.

A

unfavorable

because it reduces opportunities for the organism to proliferate

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14
Q

infections with high mortality rates often represent what?

A

unstable host-pathogen relationships (insufficient time for co-evolution of host and microbe, When an organism adapted for one host is introduced into a naive population, the result is often devastating)

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15
Q

what are the damaging consequences of most pathogens encountering an intracellular niche?

A

host will detect the organism and innate immune response will be activated

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16
Q

what are the microbial factors involved in the emergence of new infections?

A
  1. short generation time (evolution in response to changing environmental factors)
  2. mutations because of 1 and that bacteria/viruses are haploid
  3. genetic exchange (bacteria evolved several mechs of genetic exchange including conjugatoin, transformation, and transduction…transposons can move genes from one DNA molecule to another)
  4. environmental factors/changes in vector distribution
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17
Q

conjugation

A

DNA transfer through direct contact

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18
Q

transformation

A

DNA uptake from the environment

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19
Q

transduction

A

DNA transfer through bacteriophage infection

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20
Q

host factors involved in the emergence of new infections

A
  1. changes in behavior (new niches for microorganisms, eg super-absorbent tampons leading to toxic-shock syndrome)
  2. expanding populations (into new environments leads to increased contact with other species which have their own pathogens, eg lyme disease)
  3. Increased travel (epidemics can quickly become pandemics like SARS)
  4. opportunities for contamination and distribution of food and water are greater than ever (Listeria, E.coli)
  5. advances in medicine and emergence of immunosuppressive infections has increased the population of susceptible individuals
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21
Q

pathogenic microorganisms generally follow similar themes in their life cycle: what are they?

A

entry into new host, establishment and multiplication, avoidance of host defense mechanisms, tissue damage, and exit

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22
Q

skin as an anatomic barrier?

A

extremely effective - thick, dru, acidic, and constantly being shed

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23
Q

mucosa as an anatomic barrier?

A

mucin, motility, sIgA

24
Q

respiratory tract as an anatomic barrier?

A

nostril hair, mucociliary escalator, lysozyme, cough, sneeze, gag (may be compromised by cigarette smoke, air polution, endotracheal tubes, altered consciousness)

25
Q

alimentary tract as an anatomic barrier?

A

mouth defenses: saliva, swallowing, lysozyme, sIgA

GI defenses: pH, digestive enzymes, mucus, peristalsis, sIgA, shedding

26
Q

GU tract as an anatomic barrier?

A

Urinary tract down to urethra is sterile due to flow, pH, distance of bladder from exterior (UTIs far more common in females than males), may be compromised by mechanical trauma (intercourse) or poor bladder emptying

female GU tract: normally sterile above cervix, vaginal defenses include pH (4.5)

27
Q

ecological barriers to infection?

A

normal flora composed of commensal organisms established within days of birth that is:

  • dense (every surface is covered)
  • dynamic (affected by extrinsic factors like diet, hormones, sanitary conditions, antibiotics)
  • protective (can inhibit est of new microorgs - competition for nutrients, and adherence sites, and secretion of inhibitor substances like toxic metabs)
28
Q

normal flora of skin?

A

diphtheroids, staph epidermidis

29
Q

normal flora of mouth?

A

viridans, streprococci, anaerobes

30
Q

GI tract normal flora?

A

somach - only transient or unculturable bacteria

upper small bowel lots mixed

lower small bowel - even more (coliforms, anaerobes)

colon - even more: anaerobes more than aerobes, bacteroides, fusobacterium, bifidobacterium, peptococcus, peptostreptococcus, clostridium, eshcerichia coli, candida

31
Q

normal flora of female genital tract?

A

lactobacilus, gram positive anaerobes

32
Q

how does salmonella use tetrathionate respiration?

A

to outcompete the normal flora in the colon

lumen of colon is an anaerobic env’t where the normal flora produce H2S, which is detoxified by the mucosa to thiosulfate. Salmonella invade colonic cells, exposing MAMPs and inducing intense inflammation. ROS produced in response to the bacteria oxidise thiosulfate to tetrathionate, which the salmonella are uniquely able to reduce back to thiosulfate and outgrow the anaerobes in the colon

microbiota -> H2S -> S2O3(-2) -> inflammation and S2O3 (-2) -> S4O6(-2) -> S2O3(-2) to help the salmonella grow

33
Q

for most diseases, adherence to host tissues is requisite for pathogenesis. Specific molecular interactions between what mediate binding with high avidity?

A

adhesins and receptors

34
Q

adhesion is often mediated by structures that extend from the microbial surface - why?

A

negative charges on the surface of both host cells and many microbes

35
Q

what happens to a V.cholerae mutatnt that is unable to make fimbriae?

A

it is avirulent, even though it still makes toxin (mutant is unable to establish itself in the human intestine long enough to produce enough CT to cause illness)

36
Q

facts of bacterial pili (fimbriae)?

A
  • different classes, many varieties within each class
  • rod-like structures that protrude from the cell surface
  • composed of repeating subunits in helical arrangement
  • some have tip or local adhesins
  • specific moleclar interaction
  • expression regulated to allow bacteria to adjust to env’t
  • binding to receptors may help to signal bacteria that they are in contact w/host cells
37
Q

receptors on the host surface is critical for adherence to the adhesion of various gram-positive bacteria. The receptors are often what?

A

glycoproteins or glycolipids (globotrioacyl ceramide, a P1 blood group antigen) and related molecules for P fimbriae, uroplakin (surface glycoprotien on bladder cells) for Type-1 Pilli

38
Q

fibronectin is a protein implicated in adhesion of many ____ bacteria.

A

gram positive

39
Q

surface carbs, including blood group antigens, can alter risk of infections, what are two examples?

A

UTI and norovirus

40
Q

pathogen adherence to foreign bodies and biofilms?

A

many org adhere to foreign bodies (catheters, CSF shunts, pacemaker wires). Biofilm composed of bacteria, bacterial polysaccharides, and proteins, and host ECM on a foreign body constitutes a site (*******protected from phagocytes and the action of antibiotics)

41
Q

how do pathogens use complement evasion to avoid host defenses?

A

N. meningitidis specifically binds to and sequesters factor H, resulting in complement avtivation and depletion. Indivs who produce more fH have an increased risk of N. Meningiditis disease. Other pathogens bind, block, or degrade other C’ components.

42
Q

how do pathogens use cellular invasion to avoid host defenses?

A

all viruses and other pathogenic microbes are capable of efficiently entering cells. This ability may allow them to avoid host antibody and complement with competition with extracellular micro-organisms. Comes at a price because the host is likely to detect and respond to invasion

43
Q

zipper method of cellular invasion?

A

tight binding of a microbial ligand to a receptor that is coupled to the cytoskeleton results in recruitment of more receptors that in turn bind to the ligand. Eventually organism is completely surrounded by host membrane

eg:
yersinia pseudotuberculosis and Y. enterocolitica produce an outer membrane potein known as invasin which mimics the binding site of the natural ligand (fibronectin) and binds to members of the B1 family of integrins with high affinity (which are linked to the cytoskeleton)

listeria monocytogens produces a surface protein known as internalin, which binds to E-cadherin. Cadherins are surface molecules that mediate calcium-dependent homophilic interactions important for cell-cell contact. Cadherins are also linked to the actin cytoskeleton.

44
Q

trigger method of cellular invasion?

A

microbe engages host signaling proteins that regulate actin and cause the cell to form ruffles that engulf the organism

eg
salmonella and shigella species each have a type III secretion system that can deliver bacterial proteins into the cytoplasm of host cells. Delivery of these proteins results in activation of Rac and Cdc42, small GTPases that are members of the Rho subfamily of Ras homologues and regulate the actin cytoskeleton. Activaiton of CDC42 results in rapid changes in cell shape and the formation of filopodia. Mutations in the genes that encode the type III secretion system or in the genes that encode teh secreted protein markedly reduce invasion. Salmonella delivers an additional protein that acts as a guanosine exchange facotr, deactivating Rac and cdc42, restoring shape to normal

45
Q

how do pathogens use type III secretion systems to avoid host defenses?

A
  1. one of several systems for exporting proteins to external env’t and into host cells
  2. present in gam-positive pathoges like salmonella, shigella, yersinia, pseudomonas, and some strains of E. coli
  3. allow delivery of viruence factors directly into cytoplasm of host cells
  4. secretion of these factors is triggered by contact w/ host cells
  5. factors mediate diverse functions including invasion, avoidance of phagocytosis, cytotoxicity, innate immune response inhibition, apoptosis)
46
Q

how do pathogens use avoidance of phagocytosis to avoid host defenses?

A
  1. ENCAPSULATION. the most important causative agents of meningitis and pneumonia are all encapsulated. Capsule consists of demarcated external layer (usu polysaccharide)…resistant to phagocytosis by masking internal structures that activate the alternative pathway of C’, by mechanical, by electrostatic interference
  2. OTHER: M protein of strep. pyogenes is a surface protein that prevents interaction b/w streptococcal cell wall and complement components; salmonella dn shigella deliver proteins to host cytoplasm that bind pro-caspase-1, which then cleaves and releases IL-1 and induces an inflammatory form of programmed cell death termed pyroptosis. Yersinia induces apoptosis by blocking antiapoptotic pathways
47
Q

how do pathogens use survival in the phagocyte to avoid host defenses?

A
  1. escape from endocytic vacuole (trypanosoma cruzi, some rickettsiae, shigella, and listeria monocytogenes escape before they can be destroyed.
  2. inhibition of phagolysosomal fusion (toxoplasma gondii and legionella pneumophila are taken into vacuoles that do not acidify and do not fuse with lysosomes. Legionella uses a type IV secretion system to create a unique compartment that does not fuse with lysosome and recruits cellular organelles)
  3. survival in a hostile env’t (leishmania and coxiella burnetii remain within the phagolysosome but resist phagocytic killing by mechanisms under investigation)
48
Q

how do pathogens use antigenic variation to avoid host defenses?

A

means of avoiding immune system by changing surface components recognized by the host. Many mechanisms employed:

  • rapid mutation (HIV)
  • recombination of silent loci into expression loci (gonococcal pili)
  • slip-strand mispairing leading to frameshift silencing and unsilencing of alternative gonococcal opa proteins)
  • invertible elements: promoter for type I pili is within an invertable element. pili are made only when the promoter is facing the rest of the operon.
49
Q

how do pathogens use antibody inactivation to avoid host defenses?

A

bacteria may inactivate antibody, either by binding or degrading

  • staph. aureus makes protein A which binds immunoglobulins, inhibits phagocytosis, causes B cell apoptosis, and inhibits the immune response
  • many mucosal pathogens make IgA proteases, which specifically degrade IgA
50
Q

how do pathogens use iron scavenging to avoid host defenses?

A

Fe is required for pathogen sruvival

host sequesters Fe

bacteria have mechanisms for Fe acquisition:

  • siderophores which compete with host iron-binding proteins for iron, and bind to receptors ton the bacterial membrane, which in turn transport iron across the memrbane
  • some bacteria like N. gonorrhoeae have receptors that bind human transferrin. A mutant that lacks the transferrin receptor is unable to cause urethritis in volunteers.
51
Q

direct host damage

A

exotoxins

can be classified by structure, by activity, or by target

52
Q

diptheria and shiga toxins do what to the host?

A

inhibit protein synthesis

certain endothelial cells, like those of the glomerulus, are especially sensitive to toxin

death of endothelial cells leads to microinfarcts, thrombocytopenia, microangiopathic hemolytic anemia, and HUS

53
Q

membrane damaging toxins?

A

often identified as hemolysins - many have lipid or protein targets

  • phospholipases like Clostridium and Bacillus produce enzymes that hydrolyze phospholipids
  • pore-formers like staph alpha toxin inserts into the membrane and causes leakage
54
Q

are superantigens involved in direct or indirect host damage?

A

indirect

55
Q

endotoxin?

A

lipid A component of LPS associated with outer membrane of Gram (-) bacteria released during growth, by dead bacteria, and by antibiotics

causes fever in nanogram quantities

mammals are programmed to recognize and respond to endotoxin

binds to LPS-binding protein, complex binds to CD14 receptor and TLR4 - leads to IL-1 and TNF txn through NF-kB and thus activation of C’ cascade and release of inflammatory mediators. Can lead to DIC and shock

HDID 2 (32 decks)

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