Chapter 10: Host–Microbe Interactions and Pathogenesis Flashcards

1
Q

Host Microbe Interactions

A

dynamic give and take

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2
Q

Normal Microbiota

A

colonize our skin, areas of the digestive, genital, urinary and respiratory systems; can help manufacture vitamins for us, compete with potential pathogens, promote immune system maturation; have mutualistic relations with us; disrupting it can compromise patients helath

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3
Q

Pathogens

A

disease causing microbes; have adaptations that allow them to interact with certain host tissues which are dangerous to the host

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4
Q

Dysbiosis

A

microbiota disruption; such as course of antibiotics kill off normal microbiota in gut which could allow C. Diff to fluorish and cause disease (bc it is normally present in small amts in the intestines)

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5
Q

Immune system recognizes our normal microbiota presence…

A

and it mounts a moderate response to it and normally balanced communication between the two that keep it from mounting a full blow immune response

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6
Q

Opportunistic Pathogens

A

agents of disease under certain circumstances; such as a weakened immune sys allows yeast infections

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7
Q

Tropism

A

preferences of a pathogen for a specific host and even a specific tissue within the host; can change over time; most emerging pathogens expanded host or tissue range to become able to infect humans

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8
Q

Pathogenicity

A

ability of a microbe to cause disease

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9
Q

Virulence

A

describes the degree or extent of disease that a pathogen causes

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10
Q

Virulence Factors

A

mechanisms pathogens overcome our defenses; such as features that help microbes adhere to host cells, invade host tissues etc

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11
Q

Virulence factors damage host cells by…

A

directly damaging host cells; provoking dangerious immune response (such as shock)

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12
Q

Virulence Factors are often linked to…

A

transmission; if you learn how a pathogen is transmittied you can often deduce the pathogens virulence factors; pathogens that are more easily transmitted from one host to a new host become more prevalent in populations

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13
Q

Basic Reproduction Number

A

or R-naught; is a measure of a pathogens transmissibility or contagiousness; if R0 is 2, then one infected person is expected to infect an average of 2 other people;

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14
Q

Effective Reproduction Number

A

more appropriate in epidemics and pandemics; Re values can change as host pathogen interactions change

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15
Q

Pathogens evolve new virulence factors…

A

through interacting with their environment and responding to the selective pressures

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16
Q

Attenuated

A

pathogen is still infectious but weakened; pathogens often become attenuated when grown in cell culture; lose virulence factors needed to cause disease; still infectious but reakened; do not cause disease in an immunocompetent host; sometimes used in vaccines

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17
Q

Infectious Dose- 50

A

ID50; number of cells or virions needed to establish an infection in 50% of exposed hosts; most infectious pathogens have a lower ID50; just because a pathogen is highly infectious do not mean it is dangerous/lethal

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18
Q

Lethal Dose- 50

A

LD50; amount of toxin needed to kill 50% of affected hosts that are not treated

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19
Q

ID50 and LD50 can change based on…

A

species affected, hosts immune fitness and route of exposure

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20
Q

Toxins

A

molecules that generate a range of adverse host effects such as tissue damage and suppressed immune response; NOT a cell or actual pathogen

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21
Q

Toxigenic

A

microbes that make toxins

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22
Q

Toxemia

A

toxins in the bloodstream

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23
Q

Endotoxins

A

are a part of the cells; such as structure; produced when the cell is living and when dead (bc it breaks down); ex) LPS in gram negative bacteria is an endotoxin; if present in suffiecient quataties can cause septic shock

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24
Q

Endotoxemia

A

endotoxin in the blood stream

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25
Endotoxins enter from...
localized infections, systemic infections, gram-negative microbiota being introduced where they do not belong, surgery complications
26
Treating Lipid Based Endotoxins
not readily neutralized' no vaccines to protect against them; so it is necessay to ensure endotoxins are not spread in patient care
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Exotoxins
toxic; soluble proteins; affect wide range of cells; made by both gram positive and gram negative bacteria
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Exotoxins are named...
based on the organism that makes it or the type of cells it targets
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Neurotoxins
affect the nervous system
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Enterotoxins
target the GI tract
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Hepatotoxins
affect the liver
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Nephrotoxins
damage the kidneys
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Exotoxins are classified based on...
their mode of action; 3 types
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Type I Exotoxin
membrane acting extracellular toxins; bind to target via receptors on the surface; propagate a signaling cascade via the receptor; evokes changes in gene expression; leads to diverse outcomes which can range from temporary altered cell physiology to cell death
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Type I Exotoxin Example
superantigens such as pyrogens (cause fever) and overstimulate the immune sys to cause massive inflammation that harms the host
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Type II Exotoxins
membrane damaging toxins; disrupt the host cell plasma membrane; forms pores or removes phosphate head groups from phospholipids; destabilizes the membrane; cause cell lysis
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Type III Exotoxin
intracellular toxin; bind to a receptor and enter the cell; most exotoxins in this group are AB toxins--- B part binds it to the region and the A part actually causes the effect insides
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5 Steps of Infection
1) enter the host, 2) adhere to host tissues, 3) invade tissues and obtain nutrients, 4) replicate while warding off immune defenses, 5) transmit to a new host
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Portal of Entry
any site that a pathogen uses to enter the host; mucous membranes are most common portal; site where disease develops (but not necessarily the only or main site); some pathogens have more than 1 portal
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Integumentary System
largest body sys; blocks most microbes; pathogens have developed virulence factors that penetrate the inegumentary sys
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Respiratory Tract Entry
most common portal of entry; coughing and sneezing suspends pathogens in the air as respiratory droplets; infectious agents stirred up from dust or soil;
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GI Tract Entry
digestive sys pathogens frequently have a fecal-oral transmission; invade the mucosal surfaces of the GI tract;
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Urogential Tract and Transplacentral Entry
most STI enter through the mucosal lining of the vagina or cervix in women or the urethra in men; certain STI invade through the skin of the genitalia; pathogens that cause UTI invade urethra of men and women; some exhibit vertical transmission by transplacental entry
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Pathogen Must Adhere to a Host Tissue
initial adhesion is often nonspecific, such as through hydrophobic interactions; after nonspecific anchoring, the agent may target an exact surface molecule on the host cell;
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Adhesins
virulence factors used to stick to host cells in a specific or nonspecific manner; bacterial adhesins include cell wall components, capsules, fimbria and pili, a variety of plasma membrane associated molecules
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Third: a Pathogen must invade tissues and obtain nutrients
it can stay on the surface of the host cell; pass through cells to invade deeper tissues; enter cells to reside as an intracellular pathogen; tend to damage host tissues and generate cytopathic effects
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Invasins
allow pathogens to invade host tissues; local acting factors; extracellular enzymes that pathogens secrete; mechanism of action: break down host tissues, form blood clots, induce the host to uptake the pathogen
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Motility
important invasion strategy that helps a pathogen spread
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Siderophores
snatch iron from transferrin (what humans use to bind to the iron and shuttle it)
50
Extracellular Enzymes
break down nutrients in the local environment; allow pathogens to scavenge nutrients as they damage host tissues; ex) lipases ad proteases
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Cytocidal
kill the clel
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Noncytocidal
damage the cell
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Intracellular Pathogens
include all viruses, many protozoans, and some bacterial pathogens; spend a majority of their time inside host cells (hiding mechanism)
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Latency
hiding tactic; ability of a pathogen to quietly exist inside a host; usually causes persitent or recurrent disease; such as herpes viruses, HIV; latent stage protects pathogen from imm sys
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Antigenic Masking
upon entering the host, the pathogen may conceal antigenic features; coats itself with host molecules
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Antigenic Mimicry
emulating host molecules; capsules can resemble host carbohydrates
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Antigenic Variation
periodically altering the surface molecule; prevents a rapid immune response; causes include mutations in the genome, change in protein expression; causes the immune sys to lag behind with each new variation
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Interference of Phagocytosis
by making a capsule, bursting free of the phagosome, blocking fusion of the pahgosome with the lysosome, neutralizing enzymes of the phagocytes, damaging phagocytic cells using toxins, evolving to survive the harsh conditions
59
Pathogens suppress immune function by...
directly targeting immune system cells, making proteases that break down host antibodies, interfering with transcprition of interleukins, interfering with the molecular signaling that activates parts of the immune system
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Transmission to a New Host
could occur through itching, sneezing, coughing, diarrhea
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Portal of Exit
any route a pathogen uses to exit its host; often the same as the portal of entry
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Biosafety Level 1 Agents
well characterized agents; rarely cause disease in healthy people; pose limited risk; Bacillus subtilis, E.Coli (k-12), staphylococcus epidermidis
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Biosafety Level 2 Agents
infectious agents; not airborne; human bodily fluids treated as BSL 2; ex- S. aureus, herpes simplex, most flu strains, C. tentani, salmonella species
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Biosafety Level 2 + Agents
dangerous and incurable; not vaccine preventable; such as HIV; require additional safety practices but managed in BSL2 because they are not airborne
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Biosafety Level 3 Agents
serious or lethal human disease; many have airborne transmission; some are treatable, but high severity; ~2000 faciliites in the US; restricted access to area; requires PPE; ex- SARS-CoV-2; TB
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Biosafety Level 4 Agents
dangerous and exotix pathogens; tend to be lethal to humans; no cures or treatments; ~15 BSL4 facicilites in US; ex- ebola, marburh
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Standard Precautions
limit transmission of bloodborne pathogens; all patients are treated as potential sources of bloodborne or other infectious agents; handling precautions exist for all bodily fluids
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Universal and Standard Precautions include..
handwashing before and after each patient; change gloves between tasks or procedures; barrier clothing and face shields or masks; proper management of biosharps waste; disinfection of surfaces, laundry and garment
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Transmission Precautions
prevent direct contact, droplet, and airborne disease transmission; apply when a specific infectious agent is suspected or known to be present; signage is posted to informa healthcare providers and visitors of necessary precautions
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Contact Precautions
minimize transmission of infectious agents spread by fomites and healthcare workers; barrier gowns and gloves worn; disinfection practices increase; patient transport is limited; noncritical equipment dedicated for single patients use; MRSA C. Diff
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Droplet Precautions
procedural mask when in the patients room; limit patient transport; during transport the patient wears a mask; ex- rubella, flu, pertussis
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Airborne Precautions
airborne infection isolation room (AIIR); specialized pressure systems; ex- tuberculosis, chicken pox, measles
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