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Micro Exam 1 > Jackson: Host-Parasite Relationships > Flashcards

Jackson: Host-Parasite Relationships Flashcards

1
Q

Portals of Entry:
• Skin:

Arthropod vectors:

Strep and staph bind to:

A

Primary barrier to infection but some pathogens can traverse it

Arthropod vectors inject pathogens into humans

Strep and staph bind to fibronectin in wounds and indwelling devices

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2
Q

Portals of Entry:
• Lungs:

How do pathogens overcome ciliary action? (2)

A

o Adapt Strong Adhesins:

o Paralyze Ciliary Action:

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3
Q

Adapt Strong Adhesins:
Rhinovirus:
Mycoplasma:

A

Adapt Strong Adhesins:
• Rhinovirus uses capsid protein for attachment to ICAM-1-type molecule
• Mycoplasma pneumonia attaches to neuramic acid on host respiratory epithelium

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4
Q

Paralyze Ciliary Action:
Bordetella pertussis:
Influzena virus infection:

A

Paralyze Ciliary Action:
• Bordetella pertussis produces tracheal cytotoxin
• Influzena virus infection causes ciliated cell dysfunction

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5
Q

Gastrointestinal Tract:

Intestinal pathogens express:

Receptor specificity dictates:

Where are adhesins typically located? Why?

  • Some microbes enter through what type of cells of Peyer’s patches?
A

Gastrointestinal Tract:

  • Intestinal pathogens express receptor-specific adhesins

o Receptor specificity dictates colonization site and pathogenesis

o Adhesins typically located on the tip of bacterial pili to overcome cell-cell repulsion

  • Some microbes enter through antigen sampling cells of Peyer’s patches
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6
Q

What are the best defense for the GI tract?
Disruption leads to:
What causes enterocolitis?

A

Resident microflora are the best defense for GI tract:
o Disruption can lead to opportunistic infections
o Antibiotic-associated enterocolitis is caused by overgrowth of resident opportunist

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7
Q

Urogenital Tract:

Vaginal pathogens:

Urethral Pathogens:
Primary defense (3):
Why are females more susceptible to UTIs?

A

Vaginal Pathogens: must colonize mucosa or take advantage of localized injuries

Urethral Pathogens: primary defense is flushing action of urine; mucus lining of the bladder and sIgA also provide defense against UTIs
o Female more susceptible to UTIs because of shorter urethra

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8
Q

Urogenital Tract:

What do UTI pathogens (E.coli) have that permits ascending infections?

A

UTI pathogens (E.coli) have adhesins that permit ascending infections

  • Adhesins specialized for urinary epithelium
  • Inflammatory response to UTI causes pathology
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9
Q

Different Mechanisms of Transmission (5):

A
  • Respiratory
  • Fecal-oral
  • Sexual contact
  • Vector-borne (malaria), person-person, or animal-person (rabies)
  • Vertebrate reservoir (plague)
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10
Q

Routes of Infection:

Some pathogens transiently infect at a primary layer and rapidly shed (2):

Some pathogens invade deeper tissues and may be shed from secondary site (1):

A

Routes of Infection:

Some pathogens transiently infect at a primary layer and rapidly shed (influenza and Shigella)

Some pathogens invade deeper tissues and may be shed from secondary site (Varicella)

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11
Q

Vertical vs. Horizontal Transmission:

A

Vertical: from parent to offspring, via placenta, sperm, ovum, blood or milk

Horizontal: from person to person

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12
Q 
Infectious Dose (ID50):
Variance:
A

ID can vary: can range from very small (ie. only 10 cells) to very large (ie. 10,000,000 cells)

10: Shigella
10,000,000: Vibrio cholerae

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13
Q

Route of Infection Important:

What is the most effective means of person-to-person transmission?

A

Aerosol is the most effective means of person-to-person transmission
o Successful infections depend on receptors and localized defenses

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14
Q

Rhinovirus Route of Entry: Nasal vs. pharynx

A

A single rhinovirus particle in the nasal cavity causes successful infection

200 rhinovirus particles are required for infection if inoculation occurs in the pharynx

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15
Q

Stability of Organism in Environment: another factor involved in transmission.

Spore producing vs respiratory and STDs

A

Respiratory and sexually transmitted pathogens are unstable: need person-to-person contact

Spore producing organisms: spores can persist in the environment for years

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16
Q

Microbe Replication Rates:

E. coli vs Mycobacteria

A
  • Can take minutes (E.coli) or days (Mycobacteria spp.) to double
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17
Q

Susceptibility to Infection is Influenced by Genetic Determinants in the Host:

Host Specificity (measles, Shigella vs rabies):

A

Some pathogens only infect humans or closely related primates (measles, Shigella)

Others are capable of infecting a wide range of hosts (rabies)

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18
Q

Intraspecies Genetic Determinants Dictate Susceptibility:

Sickle cell: heterozygous vs aa:

Effect to Plasmodium falciparum parasite:

A

Individuals heterozygous for sickle cell trait are less susceptible to malaria

Sickle cell trait due to aa substitution in Hb (HbS)

Result is Plasmodium falciparum parasite (causes malaria) is unable to utilize the altered Hb

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19
Q

Why are individuals homozygous for sickle cell trait susceptible to other infections?

What are they susceptible to?

A

Individuals homozygous for sickle cell trait are susceptible to other infections (due to functional asplenia)

Susceptible to infection with encapsulated bacteria, which are usually filtered by the spleen
- Positive selection for sickle cell trait occurs amongst populations in endemic areas

20
Q

Regulon definition:

A

A regulon is a collection of genes or operons under regulation by the same regulatory protein. This term is generally used for prokaryotic systems.

21
Q

Virulence Factor Genes for Various Bacteria:

Uropathogenic E.coli

Shigella spp.

S.pyogenes

Cholera toxin production

Neisseria

A

o Adhesins (uropathogenic E.coli)
o Invasion attributes (Shigella spp.)
o Antigenic drift of M protein (S.pyogenes)
o Environmentally responsive regulon (cholera toxin production)
o Antigenic variation of pili (Neisseria)

22
Q

Streptococcus pyogenes

Gene or gene product

Effect on virulence

A

Gene or gene product: M protein, a cell wall component

Effect on virulence: Antiphagocytic, autoimmune complications

23
Q

Yersinia enterocolitica

Gene or gene product

Effect on virulence

A

Gene or gene product: Invasion surface protein

Effect on virulence: Uptake into epithelial cells and phagocytes

24
Q

Shigella spp

Gene or gene product

Effect on virulence

A

Gene or gene product: Invasion plasmid antigens

Effect on virulence: Escape from vacuole and cell-cell spread

25
Q

Neisseria gonorrhoeae

Gene or gene product

Effect on virulence

A

Gene or gene product: Pili and outer membrane proteins

Effect on virulence: Attachment and antigenic variation

26
Q

Herpes simplex virus

Gene or gene product

Effect on virulence

A

Gene or gene product: Envelope glycoprotein C

Effect on virulence: C3b binding, blockage of classical complement pathway

27
Q

Mechanisms Bacteria and Protozoa Use to Resist Complement Mediated Killing:

S.pneumoniae:

Salmonella typhi:

S.aureus and S.pyogenes:

What can degrade complement?

A

Capsule (S.pneumoniae)

Long LPS O antigen (Salmonella typhi)

Coating with immunoglobulins (S.aureus and S.pyogenes)

Membrane-bound enzymes can degrade complement

28
Q

Mechanisms Bacteria and Protozoa Use to Resist Phagocytosis (5)

A
  1. Release toxins that kill phagocytes
  2. Catalase to resist oxidative killing
  3. Prevent phagosome fusion with lysosome; still taken up by phagocyte
  4. Escape from phagolysosome and live in cytoplasm; still taken up by phagocyte
  5. Defenses against cytokines:
    - Secretion of IL-2 receptors that prevent T cell activation during malaria
    - Secretion of enzymes that cleave IL-2 and IFN-gamma
29
Q

Mechanisms Bacteria and Protozoa Use to Resist Phagocytosis:

A. S.aureus and S.pyogenes

B. S.aureus

C. Mycobacterium tuberculosis

D. Trypanosoma cruzi

E.1 Plasmodia spp.

E.2 Pseudomonas aeruginosa

A

A. Staph. aureus and Strep. pyogenes release toxins that kill phagocytes
B. Staph. aureus produces catalase to resist oxidative killing
C. Mycobacterium tuberculosis prevents phagosome and lysosome fusion
D. Trypanosoma cruzi escapes from phagolysosome and lives in the cytoplasm of macrophage
E. Pathogenic microbes have evolved defenses against cytokines
1. Plasmodia spp. secrete IL-2 receptors that prevent T-cell activation during malaria
2. Pseudomonas aeruginosa secretes enzymes that cleave IL-2 and IFNγ

30
Q

Highly adapted parasites can live in host for long periods (years). Shed of persistent microbes into the environment may be (2):

A

Continuous (ie. shed of Hepatitis B virus into the blood)

Intermittent (ie. tubercle bacillus)

31
Q

Viruses are well adapted to persistent infections (can silently infect host)
Herpesvirus:

A

Herpesvirus may latently infect DRG becoming re-activated later

Herpesvirus may be shed in saliva secretions and infect others

32
Q

Persistant infection:
Microorganism, site of persistence, consequence

Herpes virus 1
Hepatitis B virus
HIV
Chlamydia trachomatis
Salmonella typhi
Mycobacterium tuberculosis
Treponema pallidum
Plasmodium vivax
A

Herpes virus 1 Trigeminal ganglia Activation, cold sore

Hepatitis B virus Liver Hepatitis, cancer

HIV T cells Chronic disease

Chlamydia trachomatis Conjunctiva Blindness

Salmonella typhi Gall bladder Shedding in feces, urine

Mycobacterium tuberculosis Lung Activation tuberculosis

Treponema pallidum Disseminated Progressive disease

Plasmodium vivax Liver Clinical malaria

33
Q

Strategies Microbes Use to Evade Host Immune Response (3)

A
  • Concealment of Antigens
  • Antigenic Variation
  • Immunosuppression
34
Q

Concealment of Antigens:

Some viruses interfere with the display of:

What do skin or secretory duct colonizers do that make them less susceptible to circulating lymphocytes?

A

Some viruses interfere with the display of Ags on the surface of infected cells (HIV)

Skin or secretory duct colonizers readily shed, making them less susceptible to circulating lymphocytes

35
Q

What mechanism do CMV and strep pyogenes use to conceal antigen? What does it cause?

What does S.aureus cover itself with? What can viruses secrete?

How does CMV avoid inducing an immune response? Coccidiodes immitis induces anergy by:

A

Molecular Mimcry (CMV, strep pyogenes):

  • Bacteria and protozoa synthesize molecules that cross react with human proteins
  • Basis for autoimmune disease following infection

Pathogens can coat themselves with host proteins

  • S.aureus covers itself with Fc receptors to bind Ig molecules
  • Viruses can secrete Fc receptors to bind Igs on the surface of infected cells

Induction of tolerance or anergy

  • CMV avoids inducing an immune response by infecting during embryonic life
  • Coccidiodes immitis induces anergy by producing large quantities of Ag
36
Q

Antigenic Variation def:

Antigenic drift and shift in influenza virus:

A

Variation of surface components during infection (confounds immune response to pathogen):

a. Antigenic drift: repeated point mutations in hemagglutinin and neuraminidase genes
b. Antigenic shift: Recombination of different strains → new strain, can lead to pandemics

37
Q

What are some parasites that carry a repertoire of unexpressed surface protein genes

A

Neisseria and the African Trypanosomes

38
Q

Parasites may carry repertoire of unexpressed surface protein genes (3):

A
  • Movement of gene 3’ to promoter permits its expression (cassette mechanism)
  • Sequential recombination permits the expression of different Ags during the life cycle
  • Antigenic switching may lead to relapses during infection
39
Q

Immunosuppression:

Can be caused by infection of:

How do bacterial toxins disrupt normal immune response?

Herpesvirus encodes:

A

Can be caused by infection of T cells, B cells and macrophages by viruses

Bacterial toxins disrupt normal immune response

  • Some toxins lyse lymphocytes, cleave Ig, and inactivate complement
  • Staph and strep superantigens disrupt normal immune response

Herpesvirus encodes a cytokine homologue that interferes with the immune system

40
Q

What are bacterial Exotoxins?

A

Hydrolytic enzymes that degrade DNA or connective tissue, promoting spread

41
Q

Cytolysins:

A

Disrupt cell membrane and cause it to lyse

42
Q

Cytotoxins:

Subunits:

Most cytotoxins transfer:

A
  • Cytotoxins: classic bacterial toxins with AB subunit structure. Disrupt mammalian cellular physiology by modifying some substate.
  • B subunit binds receptor on a cell (gets A into the cell)
  • A subunit is an enzyme that does something to your cell

Most transfer ADP-ribose group from NAD to a substrate

43
Q

Cytotoxins

Effects (3 examples):

A

Inhibit protein synthesis (diphtheria toxin)

Increases cytosolic cAMP levels (cholera toxin)

Disrupt nerve transmission (tetanus and botulinum toxin)

44
Q

Bacterial Endotoxins:

Gram +/-?

Effects:
-Primarily due to:

Superantigens:

A

Bacterial Endotoxins: Gram (-) LPS

Effects: induces fever and vascular collapse (shock); primarily due to action of cytokines (IL-1 and TNF)

Note: staph and strep superantigens induce similar physiological responses

45
Q

Damage Response:

A

You do not want the host response to be too weak or too strong (results in extensive microbial-induced cell damage at both of these extremes)

Want a response of moderate intensity to have minimal host damage

Micro Exam 1 (18 decks)

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