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M & D > Chapter 15: Mechanisms of Pathogenicity > Flashcards

Chapter 15: Mechanisms of Pathogenicity Flashcards

1
Q

Disease

A

Any condition in which the normal structure or function of the body is damaged or imparied

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2
Q

Infection

A

A successful colonization of the hoast by a microorganism

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3
Q

Infectious disease

A

Any disease directly caused by the effect of a pathogen

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4
Q

Pathogen

A

May be a bactureium, virus, fungi or yeast, viroid, prion

single celled organisms (not parasites) or a cellular

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5
Q

Fungal infections

A

not in temperate climates

require humid/ moist conditions

if aquaired can be very serious

systemic infeciton with antifungals can still be upwards of 40% mortality

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6
Q

superfical infection

A

skin and mucus layers

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7
Q

systemic infeciton

A

all throughout the body

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8
Q

Viroid

A

tiny virus without a capsid

mainly attack plants and single celled organisms

dont really attack humans

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9
Q

Communicalble disease

A

capable of being spread from person to person

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10
Q

non-communicable disease

A

not capable of being spread from person to person

usually from the environment ot a host

(a bacterium like vibrio vulnificans entering a cut from the soil)

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11
Q

Contagious disease

A

a disease easily spread from person to person

an infectious disease

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12
Q

Zoonotic disease

A

A disease pread between a non-human host to a human host

animal to human

(not usually insects, those are usually refered to as vectors), but his can be the case?

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13
Q

Perioids of disease

A

incubation

prodromal

illness

decline

convalescence

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14
Q

incubation

A

after colonization but not enough pathogens to cause signs and symptoms

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15
Q

prodromal

A

start of signs and symptoms, not definitive or diagnostic

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16
Q

illness

A

signs and symptoms are most severe and obvious or diagnostic

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17
Q

Decline

A

decrease in the number of pathogens in the body, decrease in severity of signs and symptoms

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18
Q

Convalescence

A

return to normal function (health), may be long term or permanent damage

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19
Q

Acute disease

A

fast progression through the periods, hours to days

20
Q

Chronic disease

A

slow progression through the periods, weeks to months

21
Q

Latent disease

A

pathogen becomes dormant, ro replication, usually no cultavatable pathogens in blood or other samples

may be life long

22
Q

Molecular kochs postulates

A

revision of kochs postualtes to demonstrate that a single gene is responsible for pathogenicity

virulence factors???

the pathogenic phenotype should be associated only with pathogenic strains

Inactive (mutate, delete) the gene suspected of encoding the virulence factor, this should reduce pathogenicity

replace the inactivated gene with a functional copy, this should restore pathogenicity

23
Q

Why are some strains for a species pathogenic while others are not

A

Molecular kochs postulates

In Gram-negative bacteria, this is often due to the presence of a gene in pathogenic staisn abstent in non-pathogenic strains

virulence factors???

24
Q

Pathogenicity

A

the ability of a microorganism to cause disease

should be a yes/ no definition

25
Q

Virulence

A

The degree to which a microorganism can cause disease

variable from avirulent (not pathogenic) to hihghly virulent

26
Q

Infectious does (median) ID50

A

the number of pathogens required to cause infection in 50% of test subjects

27
Q

Lethal dose (median) LD50

A

the number of pathogens required to kill 50% of test subjects

fig 15.5 x-axis (dose) is in a logarithmic scale

28
Q

Primary pathogen

A

a pathogen which can cause disease regardless of the state of the immune system of the host

29
Q

Opportunistic pathogen

A

can only infect a damaged or immuno-compromised host

30
Q

5 stages of pathogenesis

A

exposure

adhesion

invasion

infeciton

transmission

31
Q

Exposure

A

some type of physical contact with the pathogen, not necessarily the start on an infection

not every exposure results in infection, but every infection comes from exposure

32
Q

Adhesion

A

some mechanism by which the pathogen sticks to cells of the body or to mucosal membranes

portals of entry
skin (damaged)
mucosal membranes
parenteral - through the skin or mucosus membbranes
adhesins on pathogen stick to receptors on host cells

33
Q

Invasion

A

pathogen spreads throughout tissue locally or throughout the whole body, usually through the bloodstream

can produce factors whcih aid in invasion (proteaases, lipases, toxins)
=> morphology = membrane ruffling to induce its self to be phagocytosed

salmonella and lysteria

some bacteral and all viral pathogens enter inside cells by endocytosis, some bacteria are ingested by host phagocytes and reproduce inside these cells

34
Q

Infection

A

pathogens reproduces in or on the host

local infection is in a small part of the host

pretty much the same thing for a fungal infection

systemic infection is when the pathogen spreads throughout the body (blood stream)

secondary infection is when a second different pathogen infects a host after disease caused by the first pathogen
= example = influenza increases the risk of streptococcus pneumonia secondary infections which cause death

35
Q

Transmission

A

for a disease to reamin in a host population it must spread from the infected host to a new one

may leave by the original portal on entry or a new route
= fecal oral route or really the oral fecal route
= most airborne diseases enter and leave through the respiratory tract

36
Q

Virulence factors of bacteria and viruses

A

virulence factors are individual properties or mechanisms which allow pathogenicity and increase virulence

a product of a single or a couple of genes
sometimes, cumulative effect of bacteria leads to virulence.

best example is a toxin is produced that causes the symptoms of a disease

37
Q

adhesion

A

pathogens need a mechanism to stick to hosts

A virulence factor

often is specific to a host species or type of cell = trophism = species specificity, is also tissue specificity

mediated by specific molecules both on the host and the pathogen

38
Q

Exozymes

A

Type of virulence factor

are soluable, not toxins, are protiens

are SECREATED enzymes which damage the host, increase the spread of the pathogen or increase it’s survival

proteses hydrolyse the protein which connect cells into tissue, destroy antibodies, kill cells

killing cells allows an entry point, also releases nutrients (like the iron from haemolysis)

(phospho)lipases damage membranes and kill cells

nucleases breakdown DNA which can trap cells (puss) (NETosis)

39
Q

Toxins

A

type of virulence factors

protiens or not

often enzymes, sometimes not

compounds which damage the host and usually kill host cells

the production of toxins is called toxigenicity

40
Q

Portal of entry

A

how the pathogen gets into you

nose, mouth, cuts or abbression

skin is only a portal of entry unless it is damaged (except fungi)

mucosal membranes are the major point on entry

disease symtpoms and outcomes depend on the portal of entry

41
Q

Parenteral

A

going through the skin

(or sometimes a mucus membrane)

usually from injetions, Or insect bites

skin damage

42
Q

Adhesions

A

used by the pathogen to stick to receptors on host cells

sometimes just refered to as a receptor? but more specific?

43
Q

endotoxins

A

not enzymes

ex= LPS, lipid A which is very toxin
= induction of fever, and septic shock

ex= fragmented peptidoglycan induces fever and inflammation (not as toxic as lipid a)

44
Q

Exotoxins

A

are protein toxins with enzymatic activity

may cause all the symptoms of the disease such as tetanus toxin in tetanus

(see table 15.10)

AB toxins have two different proteins, A for binding to a host receptor and B which is the actual toxin

(See enzymology notes)

45
Q

superantigen

A

are proteins which cause an excessive stimulaiton of immune system cells which can damage the host

causes toxic shock syndrome = low blood pressure, shock, organ failure death

lots of cytokines

46
Q

Virulence factors for immune evasion

A

in mammals the immune system detects and kills or removes pathogens

many bacterial and viral pathogens have evolved mostly protiens (exozymes) whihc interfere or suppress the immune system

capsules inhibit phagocytosis by mactophages (polysaccharides) = streptococcus pneumonia
=> these interfere or suppress the immune system

produce catalase to break down hydrogen peroxide

protein A and G bind antibodies (non-catalytic inactivaiton of antibodies)

M protiens prevents complement activaiton (and thus the complement cascade, MAC attack)

many viruses down regulate interferon production

antigenic variation many many O antigens in salmonella and e. coli. Or phase variatiohn in lyseria

M & D (18 decks)

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