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Foundations Week 3 > Principles of Infectious Disease II > Flashcards

Principles of Infectious Disease II Flashcards

1
Q

<p>What are the most &quot;successful&quot; pathogens?</p>

A

<p>Often those pathogens that limit host damage = balanced pathogenocity</p>

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2
Q

Whate are “Normal Flora”?

A
  • microbial flora that inhabit various body sites of healthy individuals
  • profoundly affect metabolism and host physiology, including immune system development and homeostasis - “prime” the immune system
  • help exclude dangerous microbes (this balance can be upset by antibiotic treatment or hygiene practices)
  • some normal flora represent a potential reservoir for disease

Fun fact: there are more bacteria in your colon than cells in your body!

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3
Q

Ebola virus vs. Human Cytomegalovirus - which is a more “successful” pathogen?

A

Human Cytomegalovirus (HCMP, type of herpesvirus) because it infects over 90% of some populations, once you have it it stays. It does not cause much disease, but can be passed on readily.

Rapidly fatal infections tend to be self-limiting in a population (ex: Ebola virus).

Side note: HIV has a long phase with little disease but plenty of virus production. Also “successful.” Good host-pathogen balance.

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3
Q

<p>Steps of scientific proof to identify pathogenicity</p>

A

<p>1 - ASSOCIATE
2 - ISOLATE
3 - INOCULATE
4 - RE-ISOLATE: the agent must be recoverable from the susceptible host</p>

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5
Q

Whate are the four steps of scientific proof to identify pathogenicity (Koch’s Postulates)?

A

1 - ASSOCIATE: the infectious agent must be present in every disease case
2 - ISOLATE: the agent must be isolated from the disease case and grown in pure culture (when appropriate)
3 - INOCULATE: the specific disease must be reproduced from pure culture in a healthy susceptible host inoculated with the agent
4 - RE-ISOLATE: the agent must be recoverable from the susceptible host

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6
Q

What are the general features of infection?

A 
Pathogens must:
1 - gain ENTRY into the host
2 - PERSIST in the host
3 - CAUSE DISEASE
4 - DISSEMINATE
  • each of these steps require the pathogen to overcome the host defenses
  • *collectively - factors that facilitate these steps are called VIRULENCE FACTORS
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7
Q

For host entry, a pathogen must…

A

Pathogen must colonize host through portal of entry, which are heavily defended:
skin, conjunctiva, oropharynx, URI, lower respiratory tract, stomach, intestinal tract, urinary tract

*in some cases, pathogen may enter tissues directly (ex. blood, mosquito)

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8
Q

Host Entry (Infection-Step 1)

A

ADHERENCE (of bacteria, viruses) to host cells

  • bacteria adhere to host cells or extracellular matrix via adhesins
  • viruses use receptors (ex: gp102 binding to CD4 receptor on CD4 T cell, or to macrophage)
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8
Q

<p>Once within the body, what defenses does the invader encounter?
(What are the barriers to persistence of the microbe?)</p>

A

<p>-macrophages

- phagocytes
- neutrophils
- complement
- type 1 interferon response (for viral infection)
- fever (harder for microbes to replicate?)</p>

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9
Q

Invasion (Infection-Step 2)

A
  • pathogens can invade beyond epithelial surfaces, they can move through or between cells
  • can involve initial replication in epithelial cells, followed by release of progeny into circulation to infect other cell types
  • “Trojan horse” - transport by immune cells. Macrophages and dendritic cells can become infected and migrate to other sites (such as lymph nodes) to spread infection

Bacteria:
-many bacteria encode INVASINS that promote uptake and survival
-this allows bacteria to live and replicate within host cells, though bacteria are free-living
Ex: molecules that
-cause host cell endocytosis
-prevent phagosome acidification
-cause phagosome rupture for escape to cytosol
-degrade cell-to-cell junctions
*some bacteria inject factors into host cell to make it more permissive to infection

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11
Q

What are methods of persistence (during infection-step 3) against host defenses by pathogen within host?

A
  • anti-phagocytic activity
  • antigenic variation
  • hideout
  • induction or inhibition of apoptosis
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12
Q

What is anti-phagocytic activity?

A
  • bacteria are readily engulfed by neutrophils and macrophages
  • many pathogens resist uptake due to the production of the POLYSACCHARIDE CAPSULE
  • may also inhibit killing activity of the phagocytes (Mycobacterium)
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13
Q

What is antigenic variation?

A
  • some bacteria (such as N. gonorrhea) have elaborate mechanisms to alter their surface proteins to avoid antibodies
  • viruses are masters of antigenic variation through simple natural selection during the course of infection
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14
Q

What is hideout (method of persistence)?

A

agent may occupy niche to avoid detection and/or elimination (ex: herpesvirus becomes latent - quiescent state with limited replication; HSV latent in neurons)

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15
Q

What is induction or inhibition of apoptosis (method of persistence)?

A
  • some agents may induce host cell apoptosis to prevent killing (macrophages killed by Salmonella, for example)
  • for some host cell types, apoptosis is a defensive response, and pathogens actively block it (epithelial cells and N. gonorrhea)
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16
Q

What are bacterial biofilms?

A
  • mechanism for bacteria to adhere to a surface
  • typically involves the elaboration of a viscous extracellular polysaccharide layer
  • permits tenacious adherence (close adherence) to host tissues or medical devices (catheters, artificial joints and heart valves)
  • –>increases virulence by rendering the bacteria less accessible to clearance by the immune system
  • –>serves as a focus for persistence/recurrence
17
Q

Define “tropism”

A

Different viruses have different cell/tissue preferences

**tropism can also refer to the host range (some viruses can infect many species)

17
Q

Define “virulence”

A

the relative ability of a pathogen to cause host damage/disease

18
Q

What effects tropism?

A
  • determined by expression of cell surface RECEPTORSfor virus
  • –>ex: HIV gp120 binds to CD4 molecule on T cells
  • ANATOMICAL LOCATION
  • –>depending on site of entry, virus is exposed to different cell types
  • –>enteroviruses can survive low pH of digestive system to infect gut epithelia; many other viruses cannot
  • INTRACELLULAR ENVIRONMENT
  • ->some viruses can only replicate in certain cell types that have the right transcription factors to turn on viral genes or required host genes
19
Q

Define “commensal organisms”

A

“normal flora” of the host

  • largely benign or even beneficial
  • some commensals can cause disease when one or more host defense mechanisms is compromised in some way:
  • ->immune-compromised individuals
  • ->through wounds/surgery
  • ->antibiotic treatments altering microbial balance
  • ->acquisition of new virulence genes by commensals
  • *these are referred to as “opportunistic pathogens”
20
Q

Define “carrier state”

A

colonization with a potential pathogen in the absence of disease

**not always easy to differentiate between commensal and carrier state

21
Q

Define “true” or “primary” pathogens

A

almost always cause disease when present

22
Q

What can increase pathogen dissemination (spread)?

A

Coughing, and other symptoms

23
Q

What are the mechanisms in which infection causes disease?

A
  • DIRECT CELL DEATH or cell dysregulation by pathogen
  • ->HIV depletes T cells
  • ->poliovirus can kill neurons
  • production of TOXINS that can act systemically
  • ->exotoxins (many bacteria produce potent toxins that affect host cells and processes to somehow benefit the pathogen)
  • ->endotoxin [lipopolysaccharide (LPS) found in Gr- membrane is a potent stimulator of cytokine secretion by many immune cells]
  • IMMUNE PATHOLOGY
  • ->inflammatory response can be very damaging, even lethal. A major cause of symptoms in many infections
24
Q

What are exotoxins?

A

Proteins released from bacterial cells that may act at tissue sites distant from the site of bacterial growth.

25
Q

What factors can result in a commensal organism becoming a pathogen?

A

Some commensals can cause disease when one or more host defense mechanisms is compromised in some way:

  • ->immune-compromised individuals
  • ->through wounds/surgery
  • ->antibiotic treatments altering microbial balance
  • ->acquisition of new virulence genes by commensals
  • *these are referred to as “opportunistic pathogens”
26
Q

An example of an exotoxin is a “superantigen.” Describe “superantigens”

A
  • produced by some staph. and strep.
  • bring together MHC-II and T cell receptor molecules in an antigen-independent way. This leads to massive T cell activation, causing systemic inflammatory response that may include (toxic) shock.
27
Q

What are endotoxins?

A

-structural component of the outer membrane of Gr- bacteria (lipopolysaccharide; LPS)

  • potent immune stimulant - binds to Toll-like Receptor 4, mainly on macrophages, dendritic cells, and B cells
  • ->results in cytokine release, producing disease symptoms
  • can cause “septic shock” as a result of a severe infection either at one location or systemically
  • ->LPS can be released form bacterial cells as they die, and this may be the result of effect host defense or treatment (antibiotics)

*note that some Gr+ cell wall components can produce a similar response from immune cells, but these components are not “officially” referred to as endotoxin

28
Q

What are the viral mechanisms of host damage/disease?

A
  • direct cell damage
  • host response
  • transformation
29
Q

Describe DIRECT CELL DAMAGE as a viral mechanism of host damage/disease

A

Virus infection can damage or kill cells through alterations in key pathways (ex: protein synthesis). In some cases, infected cells may undergo apoptosis as a way to stop the infectious cycle. Cytopathic effects (CPE) can be observed microscopically.

30
Q

Describe HOST RESPONSE as a viral mechanism of host damage/disease

A
  • for many viral infections, the inflammatory response causes the majority of symptoms (such as influenza)
  • note: this is the major cause of damage during most fungal infections
31
Q

Describe TRANSFORMATION as a viral mechanism of host damage/disease

A

Some viruses keep infected cells alive by altering survival pathways, and this can lead to transformation and tumorigenesis (Human Papilomavirus and cervical cancer, The Human T-lymphotropic virus and leukemia/lymphoma)

32
Q

Difference between pathogenic vs non-pathogenic strain is, in many cases…

A

Difference between pathogenic vs non-pathogenic strain is, in many cases…the presence of a set of virulence genes encoding proteins that confer pathogenic properties.
Ex: toxins, adhesins, antibiotic-resistance proteins, iron acquisition pathways, etc.

33
Q

Define “pathogenicity islands”

A

Virulence genes frequently found grouped together in clusters on the bacterial chromosome

-these DNA sequences can be transferred horizontally to other bacteria (including different species) giving the recipient new properties. (these are “mobile” genetic elements)
-virulence genes can be encoded on:
1 - small “mini-chromosomes” called plasmids, which can also be transferred
2 - bacteriophages (bacterial viruses) which can introduce virulence genes into new bacteria

34
Q

Viruses: “standard” natural selection shapes the pathogeneic properties of viruses.
Is there horizontal transfer of genes in viruses?

A

Unlike bacteria, there is LITTLE horizontal transfer of genetic information between viruses.

There is strong evidence that most/all virus genes ultimately came from the host - virus genes are homologous to cellular genes. (Would this mean viral DNA encodes for a little portion of the translated viral DNA which then incorporates a lot of the host genes?)
–>viruses encoded polymerases, proteases, oncogenes, cytokines, etc. that resemble host versions

35
Q

What is meant by adaptation of viruses?

A

Viruses often adapt during the course of a single infection.
For example, HIV viral polymerase that copies viral genome is error-prone which produces substantial sequence diversity. Antibody responses may be made by the host, but mutants arise that are not ‘seen’ by the antibodies. These mutants quickly expand. Mutations can arise that evade the CD8 T cell response

Foundations Week 3 (12 decks)

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