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MicroBio > Module 6 chapter 15 > Flashcards

Module 6 chapter 15 Flashcards

1
Q

What are the signs of a disease?

A
  • Are objective and measurable
  • Can be directly observed by a clinician
  • Ex. having a high fever (body temp a lot higher than 37) is a sign of a disease because it can measured
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2
Q

What are vital signs?

A
  • used to measure the body’s basic functions
  • Include body temp (37), heart rate (60-100 beats per min), breathing rate (12-18 breaths per min), blood pressure (between 90/60 and 120/80 mm Hg)
  • Changes in vital signs may be indicative of disease
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3
Q

What are other observable conditions other than vital signs that are a sign of disease?

A
  • Presence of antibodies in a patient’s serum (liquid portion of blood that lacks clotting factors) can be observed and measures through blood test so it is a sign
  • Antibodies not always a sign of disease as they can remain in the body after an infection has been resolved; also may develop in response to a pathogen that is in the body but not currently causing disease
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4
Q

What are symptoms of a disease

A
  • They are subjective
  • Are felt or experienced by the patient, but cannot be clinically confirmed or objectively measured
  • Important when diagnosing disease, but are subject to memory bias and are difficult to measure precisely
  • Some clinicians attempt to quantify symptoms by asking patients to assign a numerical value to their symptoms
    • ex: Wong-Baker Faces pain-rating scale (0-10)
    • ex: Skin conductance fluctuations: reflect sweating due to skin sympathetic nerve activity resulting from the stressor of pain
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5
Q

What are some examples of symptoms

A
  • Nausea
  • Loss of appetite
  • Pain
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6
Q

What is a syndrome?

A

A specific group of signs and symptoms characteristic of a particular disease

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7
Q

What does it mean if a disease is asymptomatic or subclinical

A
  • They do not present any noticeable signs or symptoms
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8
Q

What is an infectious disease?

A
  • Any disease caused by the direct effect of a pathogen
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9
Q

What does it mean for a disease to be communicable?

A
  • They are able to be spread from person to person through either direct or indirect mechanisms
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10
Q

What does it mean for an infectious communicable disease to be contagious

A
  • It is easily spread from person to person
  • Degree to which a disease is contagious usually depends on how the pathogen is transmitted
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11
Q

What is a iatrogenic disease (communicable)

A
  • Diseases that are contracted as the result of a medical procedure
  • Ex:
  • After procedures involving wound treatments
  • Catheterization
  • Surgery, if the wound or surgical site becomes contaminated
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12
Q

What is a nosocomial disease (communicable)?

A
  • Diseases acquired in hospital settings
  • Sick patients bring in pathogens
  • Hospital patients have weakened immune systems, making them more susceptible to infections
  • Prevalence of antibiotics in hospital settings can select for drug-resistant bacteria that can cause very serious infections that are difficult to treat
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13
Q

What is a zoonotic disease (or zoonosis) (communicable)?

A
  • Infectious diseases that are transmitted from animals to humans
  • WHO says its when a pathogen is transferred from a vertebrate animal to a human, but sometimes used more broadly to include diseases spread from all animals (including invertebrates)
  • Ex. rabies
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14
Q

What is a noncommunicable disease?

A
  • Infections disease that is not spread from one person to another
  • ex. tetanus
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15
Q

What is a noninfectious disease?

A
  • Not caused by a pathogen
  • Noncommunicable infectious disease
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16
Q

What are the 5 periods of disease

A
  • Incubation
  • Prodromal
  • Illness
  • Decline
  • Convalescence
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17
Q

Incubation period

A
  • Occurs in an acute disease after the initial entry of the pathogen into the host
  • Pathogen beings multiplying in host
  • Insufficient numbers of pathogen particles present to cause signs and symptoms of disease
  • Can vary from a day or two (acute) or months or year (in chronic)
  • Patient unaware that a disease is beginning to develop
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18
Q

What factors are involved in determining the lentgth of the incubation period

A
  • Strength of pathogen
  • Strength of the host immune defenses
  • Site of infection
  • Type of infection
  • Size infectious dose received
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19
Q

Prodromal period

A
  • After incubate period
  • Pathogen continues to multiply and host beings to experience general signs and symptoms of illness, which typically result from activation of the immune system
  • Ex: fever, pain, soreness, swelling, or inflammation
  • Signs and symptoms too general to indicate a particular disease
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20
Q

Period of illness

A
  • Happens after prodromal period
  • Signs and symptoms of disease are most obvious and severe
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21
Q

Period of decline

A
  • After period of illness
  • Number of pathogen particles begins to decrease
  • Signs and symptoms of illness being to decline
  • Patients may become susceptible to developing secondary infections because their immune systems have been weakened by the primary infection
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22
Q

Period of convalescence

A
  • Final period
  • Patient generally returns to normal functions
  • Some diseases may inflict permanent damage that the body cannot fully repair
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22
Q

Period of convalescence

A
  • Final period
  • Patient generally returns to normal functions
  • Some diseases may inflict permanent damage that the body cannot fully repair
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23
Q

Summarize the classical version of Koch’s postulates and compare and contrast them with molecular Koch’s postulates

A
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24
Q

Describe virulence in terms of infectious dose and lethal dose

A
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25
Q

Use examples to explain primary pathogens versus opportunistic pathogens

A
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26
Q

Summarize the stages of pathogenicity

A
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27
Q

Use examples to describe the roles of portals of entry and exit in the transmission of disease

A
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28
Q

What do each of Koch’s postulates represent?

A

A criterion that must be met before a disease can be positively linked with a pathogen

  • On order to determine this, tests are performed on laboratory animals and cultures from healthy and diseased animals are compared
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29
Q

What are Koch’s postulates?

A
  1. The suspected pathogen must be found in every case of disease and not be found in healthy individuals
  2. The suspected pathogen can be isolated and grown in pure culture
  3. A healthy test subject infected with the suspected pathogen must develop the same signs and symptoms of disease as seen in postulate 1.
  4. The pathogen must be re-isolated from the new host and must be identical from postulate 2.
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30
Q

What was found wrong with Koch’s postulate 1

A
  • Pathogens are not only found in diseased individuals
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31
Q

What was wrong with Koch’s postulate 2?

A
  • All healthy test subjects are not equally susceptible to disease
  • Individuals are unique in terms of microbiota and the state of their immune system at any given time
  • Not all pathogens are microorganisms that can be grown in pure culture and animals cannot always serve as reliable models for human disease
  • Can’t ethically test diseases in humans (postulate 3)
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32
Q

What is the premise for molecular Koch’s postulates?

A
  • Not the ability to isolate a particular pathogen, but rather to identify a gene that may cause the organism to be pathogenic
  • Not only explain infections caused by intracellular pathogens but also the existence of pathogenic strains of organisms that are usually nonpathogenic
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33
Q

What are the molecular Koch’s Postulates

A
  1. The phenotypes (sign or symptom of disease) should be associated only with pathogenic strains of a species
  2. Inactivation of the suspected gene(s) associated with pathogenicity should result in a measurable loss of pathogenicity
  3. Reversion of the inactive gene should restore the disease phenotype
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34
Q

What are some limitations of the molecular Koch’s postulates

A
  • Genetic manipulation of some pathogens is not possible using current methods of molecular genetics
  • Some diseases do not have suitable animals models, which limits the utility of both the original and molecular postulates
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35
Q

What is pathogenicity

A

The ability of a microbial agent to cause disease

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36
Q

What is virulence?

A

The degree to which an organism is pathogenic

  • On a continuum
  • On one end of the spectrum organisms are avirulent (not harmful) and on other end organisms are highly virulent
  • Can be quantified using controlled experiments with laboratory animals
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37
Q

What are two important indicators of virulence?

A
  • The median infectious dose (ID50)
  • The median lethal dose (LD50)
  • Both are typically determined experimentally using animals models
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38
Q

What is the median infectious dose?

A

The number of pathogen cells or virions required to cause active infection in 50% of inoculated animals

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39
Q

What is the median lethal dose

A

The number of pathogenic cells, virions, or amount of toxin required to kill 50% of infected animals

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40
Q

How do you calculate the ID50 and LD50?

A
  • Each group of animals is inoculated with one of a range of known numbers of pathogen cells or virions
  • The percentage of animals that have been infected or killed is plotted against the concentration of pathogen inoculated
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41
Q

What are two ways that pathogens can be classified?

A

As either primary pathogens or opportunistic pathogens

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42
Q

What is a primary pathogen?

A

Can cause disease in a host regardless of the host’s resident microbiota or immune system

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43
Q

What is an opportunistic pathogen?

A
  • Can only cause disease in situations that compromise the host’s defenses, such as the body’s protective barriers, immune system, or normal microbiota
44
Q

What individuals are susceptible to opportunistic infections?

A
  • Very young
  • Elderly
  • Women who are pregnant
  • Patients undergoing chemotherapy
  • People with immunodeficiencies
  • Patients who are recovering from surgery
  • Those who have had a breach of protective barriers (such as severe wound or burn)
45
Q

Give an example of a primary pathogen

A
  • Enterohemorrhagic E.coli (EHEC)
  • Produces virulence factor known as Shiga toxin
  • This toxin inhibits protein synthesis, leading to severe and bloody diarrhea, inflammation, and renal failure, even in patients with healthy immune systems
46
Q

Give an example of an opportunistic pathogen

A
  • Staphylococcus epidermis
  • Among the most frequent causes of nosocomial disease
  • Member of normal microbiota of the skin, where it is generally avirulent
  • In hospitals it can also grow in biofilms that form on catheters, implants, or other devices that are inserted into the body during surgical procedures
  • Once inside body, S. epidermidis can cause serious infections such as endocarditis, and it produces virulence factors that promote the persistence of such infections

Other members of the normal microbiota can also cause opportunistic infections under certain conditions. This often occurs when microbes that reside harmlessly in one body location end up in a different body system, where they cause disease. For example, E. coli normally found in the large intestine can cause a urinary tract infection if it enters the bladder. This is the leading cause of urinary tract infections among women.

47
Q

What is pathogenesis?

A
  • The 4 steps a pathogen must successfully achieve to cause a disease
48
Q

What are the stages of pathogenesis?

A
  1. Exposure (contact)
  2. Adhesion (colonization)
  3. Invasion
  4. Infection
49
Q

Exposure stage

A
  • Encounter with a potential pathogen
  • Ex: food we eat, objects we handle
  • For a pathogen to cause disease it needs to be able to gain access into host tissue
  • An anatomic site through which pathogens can pass into host tissue is called a portal of entry: location where the host cells are in direct contact with the external environment
50
Q

What are the most important portals of entry for microbes?

A

Mucosal surfaces
- Mucous membranes of the respiratory tract
- Gastrointestinal tract
Genitourinary tract

51
Q

What does it mean is a pathogen enters the body through the parenteral route?

A
  • Entered through a break in the protective barriers of the skin
52
Q

Adhesion stage

A
  • Following initial exposure, the pathogen adheres at the portal of entry
  • Adhesion refers to the capability of pathogenic microbes to attach to the cells of the body using adhesion factors, and different pathogens use various mechanisms to adhere to the cells of host tissues
53
Q

What are adhesions?

A
  • Molecules (either proteins or carbohydrates) found on the surface of certain pathogens and bind to specific receptors (glycoproteins) on host cells
  • Are present on the fimbriae and flagella of bacteria, the cilia of protozoa, and the capsids or membranes of viruses
  • Protozoans can also use hooks and barbs for adhesion; spike proteins on viruses also enhance viral adhesion
  • The production of glycocalyces (slime layers and capsules) with their sugar and protein content can also allow certain bacterial pathogens to attach to cells
  • Biofilm growth can also act as an adhesion factor
54
Q

Invasion phase

A
  • Once adhesion is successful, invasion can proceed
  • Involves the dissemination of a pathogen throughout local tissues or the body
  • Pathogens may produce exoenzymes or toxins which serve as virulence factors that allow them to colonize and damage host tissues as they spread deeper in to the body
  • Pathogens may also produce virulence factors that protect them against the immune system defenses
  • A pathogens specific virulence factors determine the degree of tissue damage that occurs
55
Q

Infection phase

A
  • Following invasion, successful multiplication of the pathogen leads to infection
  • Can be described as local, focal, or systemic
56
Q

What is a local infection?

A
  • Confined to a small area of the body, typically near the portal of entry
57
Q

What is a focal infection?

A

A localized pathogen, or the toxins it produces, can spread to a secondary location

58
Q

What is a systemic infection?

A

When an infection becomes disseminated throughout the body

59
Q

Primary infection vs secondary infection

A

Sometimes a primary infection, the initial infection caused by one pathogen, can lead to a secondary infection by another pathogen.

60
Q

For a pathogen to persist what must it do?

A
  • Put itself in a position to be transmitted to a new host, leaving the infected host through a portal of exit
61
Q

Most common portals of exit

A
  • Skin, respiratory, urogenital, and gastrointestinal tracts
62
Q

What can expel pathogens from the respiratory tract?

A

Coughing and sneezing

63
Q

What can transport pathogens out of other portals of exits?

A
  • Secretions
  • Excretions
  • Feces
  • Urine
  • Semen
  • Vaginal secretions
  • Tears
  • Sweat
  • Shed skin cells
64
Q

How do pathogens that reply on insect vectors for transmission exit the body?

A
  • In the blood extracted by a biting insect
  • By blood extracted by needles
65
Q

portal of entry

A
  • location where the host cells are in direct contact with the external environment
  • An anatomic site through which pathogens can pass into host tissue
66
Q

Give some examples of portal’s of entry:

A
  • Eye (conjunctiva)
  • nose
  • mouth
  • broken skin
  • Insect bite
  • Needle
  • Urethra
  • Anus
  • Vagina
  • Ear
  • Placenta (portal of entry for fetus)
67
Q

Give some examples of portals of exits:

A
  • Earwax
  • Nose (secretions)
  • Eye (tears)
  • Mammary glands (milk, secretions)
  • Placenta (transmission to fetus)
  • Skin (flakes)
  • Vagina (secretions, blood)
  • Urethra (urine, semen (males), secretions(males))
  • Anus (feces)
  • Mouth Saliva, sputum)
  • Broken skin (blood)
  • Insect bite
  • Needle (blood)
68
Q

Describe how virulence factors may affect signs and symptoms of disease

A
69
Q

Differentiate between endotoxins and exotoxins, and provide examples of each

A
70
Q

Use examples to explain viral adhesion and how antigenic variation helps viruses evade the immune system

A
71
Q

What are virulence factors?

A

They are factors produced by individual pathogens, which determine the extent of disease they may cause

72
Q

What happens if the genes encoding the virulence factors are inactivated?

A
  • Virulence in the pathogen is diminished
73
Q

What is an adehsion

A
  • A protein or glycoprotein found on the surface of a pathogen that attaches to receptors on the host cell
74
Q

Type 1 fimbrial adhesion

A
  • Bacterial adhesion
  • A molecule found on the tips of fimbriae of enterotoxigenic E. coli (ETEC)
  • Fimbriae: hairlike protein bristles on the cell surface
  • Allows the fimbriae of ETEC cells to attach to the mannose glycans expressed on intestinal epithelial cells
75
Q

What are toxins?

A

Biological poisons produced by certain pathogens that assist in their ability to invade and cause damage to tissues

76
Q

What is toxigenicity?

A

The ability of a pathogen to produce toxins to cause damage to host cells

77
Q

Endotoxin

A

The lipopolysaccharide (LPS) found on the outer membrane of gram-negative bacteria

78
Q

What happens during infection with an endotoxin

A

During infection and disease, gram-negative bacterial pathogens release endotoxin either when the cell dies, resulting in the disintegration of the membrane, or when the bacterium undergoes binary fission

79
Q

What lipid is responsible for the toxic properties of the LPS molecule

A
  • Lipid A
  • Relatively conserved across different genera of the gram-negative pathogen.
80
Q

What does lipid A do?

A

Lipid A triggers the immune system’s inflammatory response

81
Q

What happens if the concentration of endotoxin in the body is low?

A
  • The inflammatory response may provide the host an effective defense against infection
82
Q

What happens if the concentration of endotoxin in the blood is high?

A

It can cause an excessive inflammatory response, leading to a severe drop in blood pressure, multi-organ failure, and death

83
Q

What are exotoxins?

A

Protein molecules that are produced by a wide variety of living pathogenic bacteria

84
Q

What kind of pathogens produce exotoxins?

A

Some gram-negative, but mainly gram-positive pathogens

85
Q

What do exotoxins do?

A
  • Target specific receptors on specific cells and damages those cells through unique molecular mechanisms
86
Q

Source Endotoxin vs. Exotxin

A

Endotoxin: Gram-negative bacteria
Exotoxin: Gram-positive (primarily) and gram-negative

87
Q

Composition Endotoxin vs. Exotoxin

A

Endotoxin: Lipid A component of lipopolysaccharide
Exotoxin: Protein

88
Q

Effect on host Endotoxin vs Exotoxin

A

Endotoxin: General systemic symptoms of inflammation and fever
Exotoxin: Specific damage to cells dependent upon receptor-mediated targeting of cells and specific mechanisms of action

89
Q

Heat stability Endotoxin vs Exotoxin

A

Endotoxin: Heat stable
Exotoxin: Most are heat labile (think denaturation of proteins in heat), but some are heat stable

90
Q

LD50 Endotoxin vs Exotoxin

A

Endotoxin: High
Exotoxin: Low

91
Q

What is antigenic variation and what does it allow pathogens to do?

A

It allowed pathogens to protect themselves against the immune system by altering the surface proteins so that a pathogen is no longer recognized by the host’s immune system.

92
Q

Viral adhesions

A
  • Adhesion of the virus to specific receptors on the surface of cells
  • Process is mediated by adhesions that are part of the viral capsid or membrane envelope
  • Interaction of viral adhesins with specific cell receptors defines the tropism (preferential targeting) of viruses for specific cells, tissues, and organs in the body
93
Q

Spike protein hemagglutinin

A
  • Found on Influenzavirus
  • An example of a viral adhesin
  • Allows virus to bind to the sialic acid on the membrane of host respiratory and intestinal cells
94
Q

What type of viruses does antigenic variation occur in?

A

Enveloped viruses

95
Q

What are the two forms of antigenic variation for influenza viruses

A
  • Antigenic drift
  • Antigenic shift
96
Q

What is antigenic drift

A

The result of point mutations causing slight changes in the spike proteins hemagglutin (H) and neuraminidase (N).

97
Q

What is antigenic shift?

A

A major change in spike proteins due to gene assortment. Occurs typically when two different influenza viruses infect the same host

98
Q

Why is it difficult for the immune system to recognize the many different strains of influenzavirus?

A
  • The rate of antigenic variation in influenza is very high
  • Body may develop immunity to one strain through through natural exposure or vaccinations, antigenic variation results in the continual emergence of new strains that the immune system will not recognize.
99
Q

Describe unique Eukaryotic virulence factors, and compare and contrast them with bacterial virulence factors

A
100
Q

Provide examples of how eukaryotic pathogens can evade the immune system

A
101
Q

Candida albicans

A
  • Opportunistic fungal pathogen and causative agent of oral thrush, vaginal yeast infections, and cutaneous candidiasis
  • Produces adhesins (surface glycoproteins) that bind to the phospholipids of epithelian and endothelian cells.
  • To assist in spread and tissue invasion, it produces proteases and phopholipases
  • exoenzymes). One of these proteases degrades keratin, a structural protein found on epithelial cells, enhancing the ability of the fungus to invade host tissue. In animal studies, it has been shown that the addition of a protease inhibitor led to attenuation of Candida infection.9 Similarly, the phospholipases can affect the integrity of host cell membranes to facilitate invasion.
102
Q

What are mycotoxins?

A

Fungal toxins

103
Q

What kind of toxins do fungi produce?

A

Exotoxins

104
Q

Are protozoans capable of antigenic variation?

A
  • some are
105
Q

Example of antigenic variation in protozoans

A
  • Obligate intracellular pathogen Plasmodium falciparum
  • A causative agents of malaria
  • Resides inside red blood cells, where it produces an adhesin membrane protein knwon as PfEMP1
  • This protein is expressed on the surface of the infected erythrocytes, causeing blood cells to stick to each other and to the walls of blood vessels
  • The process impedes blood flow sometimes leading to organ failure, anemia, jaundice, and death
  • Although PfEMP1 can be recognized by the host’s immune system, antigenic variations in the structure of the protein over time prevent it from being easily recognized and eliminated. This allows malaria to persist as a chronic infection in many individuals.
106
Q

What are exoenzymes?

A

Produced by pathogens, also known as extracellular enzymes, enable them to invade hose cell and deeper tissues
- have a wide variety of targets

107
Q

Virulence factors Eukaryotic vs Prokaryotic

A

Eukaryotic:
- Adhesions
- Toxins (fungal toxins, mycotoxins)
- Antigenic variation (protozoan)
- Exoenzymes (helminths)
- Ability to survive inside phagocytic vesicles
Prokaryotic:
- Adhesions
- Toxins
- Antigenic variation
- Exoenzymes

108
Q

Trypanosoma (Protozoan)

A

The virulence factors of Trypanosoma brucei, the causative agent of African sleeping sickness, include the abilities to form capsules and undergo antigenic variation. T. brucei evades phagocytosis by producing a dense glycoprotein coat that resembles a bacterial capsule. Over time, host antibodies are produced that recognize this coat, but T. brucei is able to alter the structure of the glycoprotein to evade recognition.

MicroBio (8 decks)

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