Exam 3: Infection and Epidemiology Part 2 Flashcards

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1
Q

How can a contamination lead to an infection, and how can an infection lead to disease?

A

A person can become contaminated with a pathogen. The pathogen may overcome the body’s external defenses and invade the body establishing an infection. The infection may succumb to the body defenses (most do) however some infections evade the body’s defenses, multiply, and adversely affect the body function. Thus a disease is caused.

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2
Q

What is a disease?

A

Any harmful deviation from the normal structural or functional state of an organism, generally associated with certain signs and symptoms and differing in nature from physical injury. Normally a result of an infection that evades the body’s defenses.

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3
Q

Do all diseases result from infection? Explain.

A

No, diseases may be hereditary, congenital, some fall into multiple categories.

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4
Q

Symptoms

A

are subjective characteristics of a disease that can be felt by the patient alone. E.g pain, headache, disness, fatigue, nausea, etc.

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5
Q

Signs

A

objective manifestation of disease that can be observed or measured by others. Swelling, vomiting, fever, rash ,redness, etc.

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6
Q

Difference between symptoms and signs?

A

Symptoms=subjective
Signs=objective

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7
Q

What is a syndrome? Give at least one specific example.

A

A group of symptoms and signs that collectively characterize a particular disease or condition. AIDS/HIV characterized by low T-cell count, weight loss, increased susceptibility to and prevalence of opportunistic infections, etc.

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8
Q

What is a subclinical infection? Is there another term for such an infection?

A

Also called “asymptomatic”, infections that lack symptoms and goes unnoticed. Certain signs my still be detected with proper testing.

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9
Q

What is etiology?

A

The study of the cause of disease.

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10
Q

What is the germ theory of disease? When and by whom was it proposed?

A

Theory states “Microorganisms are the causes of many diseases”. Proposed during the golden age of microbiology 1800-1900s. Proposed by Louis Pasteur and Robert Koch.

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11
Q

How did Robert Koch propose that we establish that a particular pathogen is the cause of a particular disease?

A

Koch’s postulate: series of criteria used to establish a specific infectious agent is the cause of a specific disease.

Koch established Bacillus anthracis as the cause of anthrax and Mycobacterium tuberculosis as the cause of tuberculosis.
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12
Q

List Koch’s postulates

A
  1. The suspected agent must be present in every case of the disease.
  2. The suspected agent must be isolated and grown in pure culture.

3.The cultured agent must cause the disease when it is inoculated into a healthy susceptible host.

  1. The same agent must be recovered from the diseased experimental host.

*All of these criteria must be satisfied to establish the microbe as the causative agent of the disease in question. *

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13
Q

Can Koch’s postulates always be satisfied? Explain, giving at least two specific examples.

A

No, sometimes it’s not ethically appropriate to inoculate a healthy individual with a disease for example smallpox.

Many microbes cannot be grown in pure culture, for example viruses are obligate intracellular parasites requiring a living host.

Some infected individuals do not exhibit disease, human carriers of avirulent strains.

Some diseases are polymicrobial, caused by a combination of pathogens or the combination of a pathogen and an environmental genetic factor. e.g. Hepatitis B and D virus together cause liver cancer.

Same condition can be caused by multiple pathogens. E.g. Common cold is caused by rhinoviruses or coronaviruses, but can also be caused by respiratory syncytial viruses and many others. E.G Pneumonia can be caused by a variety of bacteria, viruses, and or fungi.

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14
Q

List the molecular Koch’s postulates and compare them to Koch’s initial postulates. How might they be an improvement?

A

Similar to Koch’s Postulates but relies on molecular techniques to study a microbe. Especially relevant to pathogenic species of E.Coli and Streptococcus pyogens which can cause several diseases depending upon which virulence factors are produced by a given strain.

  1. The virulence factor gene or its products should be found in pathogenic strains of the organism.
  2. Mutating the virulence gene to disrupt its function should reduce the virulence of the pathogen.
  3. Reversion of the mutated virulence gene or replacement with a wild-type version should restore virulence to the strain.
  • Still not always possible to apply all these criteria, but at least provides an approach to study. *
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15
Q

What is an adhesion factor?

A

Specialized structures or attachment proteins that facilitate the adhesion of pathogens to cells.

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16
Q

Ligands

A

Type of adhesion factor.

Viruses and many bacteria have ligands that bind to complementary receptors on host cells. Ligands are glycoproteins or lipoproteins. Receptors on host cells are generally glycoproteins. Termed “adhesions” in bacteria. Termed “attachment proteins” or “spike proteins” in viruses.

Ligand-receptor binding often determines pathogen-host specificity.

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17
Q

Give at least one example of a bacterial adhesion factor.

A

Adhesion fimbriae of neisseria gonorrhoeae adhere to cells lining the human urethra and vagina.

Ligands

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18
Q

Give at least one example of a viral adhesion factor.

A

Ligands, specifically known as “attachment proteins” or “spike proteins”.

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19
Q

Give at least one example of an adhesion factor possessed by a protozoan.

A

adhesion disks

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20
Q

Give at least one example of an adhesion factor possessed by a helminth.

A

Suckers and hooks in some parasitic worms

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21
Q

Can adhesins vary within an individual or a population? Could this be beneficial? Explain.

A

Yes. variations in adhesions can be advantageous to the pathogens. Some bacteria possess multiple types of adhesions each binding to a different type of receptor. Some pathogens change their adhesions over time, helping pathogens evade the immune system and or each binds to a different type of receptor.

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22
Q

Is it possible that a bacterium or virus might lose its ability to make a ligand? What is the result?

A

Yes, due to mutations, chemical exposure, radiation, etc. These microbes become harmless and “avirulent”. Commonly used in vaccines.

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23
Q

What is a biofilm? Do you currently possess any biofilms? Explain.

A

Sticky web of bacteria and polysaccharides that adhere to a host surface. Complex synergistic relationships between numerous microorganisms.

Yes, dental plaque on teeth.

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24
Q

Pathogenicity

A

ability of a microorganism to cause disease. It either can CAN or CANNOT cause disease.

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25
Q

Virulenece

Not the factors.

A

degree of pathogenicity, relative ability to cause disease. High virulent organisms almost always cause disease while less virulent organisms cause disease only in weakened hosts. Does not describe the severity of the disease.

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26
Q

Can an infectious agent with low virulence cause a serious disease? Can a highly virulent infectious agent routinely cause a mild disease? Explain.

A

Yes, virulence does not describe the severity of the disease.

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27
Q

What are virulence factors? By what general means to they act?

A

Traits or molecules of pathogens that facilitate pathogenicity.

Enable the pathogen to enter a host, adhere to host cells, gain access to nutrients, escape detection or removal by the immune system.

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28
Q

Types of virulence factors

A

Adhesion factors
biofilm formation
extracellular enzymes
toxins
antiphagocytic factors.

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29
Q

Describe the role of adhesion factors in the facilitation of pathogenicity, giving at least three different examples

A

Facilitate adhesion to the host. Protozoa have adhesion discs, some parasitic worms have suckers and hooks, and bacteria possess surface ligands.

30
Q

Describe the role of extracellular enzymes in the facilitation of pathogenicity.

A

Enzymes are secreted by many pathogens that enable them to dissolve host structural chemicals. Helps maintain infection, invade further, and avoid body defenses. E.g hyaluronidase, collagenase, coagulase, kinases.

31
Q

Hyaluronidase

A

Extracellular enzyme that breaks down hyaluronic acid (a glycosaminoglycan), key molecule of extracellular matrix. Hyaluronic acid makes the extracellular matrix vicious, impending microorganism movement, and acts as a layer of protection. When it breaks down the viscosity is decreased making microbe movement easier.

32
Q

Collagenase

A

Extracellular enzyme that breaks down collagen which is a key structural protein in animal connective tissue. Imparts strength and flexibility to tissues. Breakdowns allow pathogens to penetrate deeper into the host.

33
Q

Coagulase

A

Extracellular enzyme that converts the plasma protein fibrinogen into fibrin. Result sin formation of blood clots, normally beneficial to the body. Coagulase causes blood clots and the clots stick to bacteria and “hides” them from phagocytosis.

34
Q

Streptokinase or staphylokinase

A

Extracellular enzyme. Kinases produce blood clots that are formed in response to injury or infection, seal wounds to reduce blood loss, act as microbe barrier, and isolate bacteria present. The enzymes digest the fibrin clots promoting invasion of damaged tissues.

35
Q

Hemolysins

A

Extracellular enzyme. Red blood cells are filled with hemoglobin. The enzyme combined with RBC membrane and lyse cells, gives pathogens access to iron required for metabolism.

36
Q

Keratinase:

A

Extracellular enzyme. Keratin is a key structural protein in hair, nails, and outer layers of skin. Enzyme digests keratin proteins producing food for the microbes and allowing them to go deeper. e.g ringworm.

37
Q

Mucinase

Entamoeba histolytica

A

Extracellular enzyme. Produced and secreted by eukaryote Entamoeba histolytica. Digests the mucus lining of the intestinal tract, allows the amoeba to enter underlying tissue, results in amoebic densentery.

38
Q

Exotoxin

A

Heat sensitive protein molecules, central to pathogenicity of the microbe, destroy host cells or interfere with host metabolic.

39
Q

Types of Exotoxins

A

Cyotoxins
Neurotoxins
Enterotoxins

40
Q

Cytotoxins, define and give example.

A

Type of endotoxin that kills host cells or affects their function.

Example: Corynebacterium diphtheriae produces cytotoxin that causes diphtheria. Interferes with protein synthesis in epithelial cells of the upper respiratory tract. Damaged cells, mucous, white blood cells, etc, accumulate causing a life threatening blockage.

41
Q

Neurotoxins, define and give examples.

A

Type of endotoxins that specifically interfere with nerve cell function.

Example, clostridium botulinum, produces neurotoxin that’s among the most lethal toxins known. Inhibits release of acetylcholine at synaptic junction which disrupts communication between nerve cells and muscle cells. Results in paralysis typical of botulism. Found in soil, major risk of at home canning.

Example, Clostridium tetani, produces neurotoxin that blocks the relaxation pathway that should follow the contraction of a muscle. Permits volleys of spontaneous nerve impulses. Results in uncontrolled muscular contractions typical of tetanus.

42
Q

Enterotoxins, define and example.

A

Affect cell lining the gastrointestinal tract.

Example, Vibrio cholerae, produces enterotoxin, “colera toxin”. Causes release of ions and water into intestinal lumen, watery diarrhea characteristic of cholera. Homologous toxin is produced and secreted by some strains of E.Coli.

Example, shigella dysenteriae, produces enterotoxin that causes dysentery. Inhibits protein synthesis by irreversibly altering a rRNA. Homologous toxins are produced and secreted by some virulent strains of E.Coli.

43
Q

Toxins

A

Are chemicals that damage host tissues. May harm tissue directly or trigger host response that damages tissues. Overalls with extracellular enzymes.

44
Q

Toxemia

A

Toxins that enter the bloodstream and are carried to other body parts.

45
Q

Anitoxins

A

Antibodies produced by the host against toxins. Bind and neutralize specific toxin.

46
Q

Toxoid

A

Production of antitoxin stimulated by immunization. Inactivated toxins that elicit immune response.

47
Q

What is an endotoxin and where is it found? Describe the role of endotoxins in the facilitation of pathogenicity.

A

Present in the outer membrane of Gram-negative bacteria. lipid A component of the LPS molecules in the outer leaflet in the toxic part. Released into the host under certain conditions like bacterial cell division, bacterial death, and when bacteria is digested by macrophages. Stimulates the body to release chemical messengers termed “cytokines” that cause immune response.

48
Q

Cytokines

A

Chemical messengers released by the body when stimulated by an endotoxin. Causes fever, inflammation, low BP, shock. Particularly damaging when released in large amounts.

49
Q

Describe the role of antiphagocytic factors in the facilitation of pathogenicity. Do all of them prevent phagocytosis? Explain.

A

Role of antiphagocytic factors is to actively remove invading pathogens. Engulfed and destroyed by phagocytic cells such as macrophages (a type of white blood cell). Some virulence factors are related to the evasion of phagocytosis. Includes capsules and antiphagocytic chemicals. Some prevent the fusion between lysosomes and phagocytic vesicles. Some inhibit phagocytosis but not all. Some destroy phagocytic white blood cells.

50
Q

Describe the various virulence factors possessed by the bacterium Yersinia pestis, and how they may interact with each other.

A

Yersinia pestis is the causative agent of pneumonia, septicemic, and bubonic plague. Produces an assortment of virulence factors. Adhesion promote attachment and invasion of the epithelial cells. Type II secretion system injects (yersinia outer proteins)YOPs into immune cells. Multiple YOPs lead to cytolysis, prevention of phagocytosis, and reduced immune system signaling. Anit-phagocytic “Fraction 1” and “LerV” proteins.

51
Q

What is epidemiology? Why is it useful?

A

Study of the effects of pathogens on populations. Its goal and usefulness forms from the ability to learn how to reduce the number of cases and improve the health of people within a community.

52
Q

Define the terms incidence and prevalence, showing the relationship between them.

A

Incidence: number of new cases.

Prevalence: total number of cases. This number is increased by incidence.

53
Q

Endemic

A

Disease occurs normally at a relatively stable incidence in a particular area. Think seasonal influenza, relatively similar number of cases every year.

54
Q

Sporadic

A

When only a few scattered cases occur within an area.

55
Q

Epidemic

A

Disease occuring at a greater than usual frequency in a specific area. No specific number of cases required just that the number of cases must be more than expected when compared to the historical data.

56
Q

Pandemic

A

An epidemic simultaneously occurring on multiple continents.

57
Q

In epidemiology tabulated data is analyzed to determine?

A

Probable cause of the disease, mode of transmission, possible means of prevention. These analyses are often retrospective, occurring after an outbreak has occurred.

58
Q

Epidemiology involves the testing of what hypothesis?

A

Cause of disease, efficacy of preventative measure, and efficacy of a treatment.

59
Q

Nosocomial infections definition and other name.

A

Infections acquired by patients or health care workers while in health care facilities. About 10% of american acquire 1 each year. Also called Healthcare-associated infections (HAIs).

60
Q

4 main types of nosocomial infections

A

1) Exogenous HAIs
2) Endogenous HAIs
3) Iatogenic infections
4) Superinfections

61
Q

Exogenous HAIs

A

Caused by pathogens acquired from the healthcare environment.

62
Q

Endogenous HAIs

A

arise from normal microbiota within the patient that have become pathogenic (opportunistic infections).

63
Q

Iatrogenic Infections

A

direct result of medical procedures such as cauterization

64
Q

Superinfections

A

Result from the use of antimicrobial drugs that inhibit resident microbiota and reduce competition.

E.g. The transient microbe C.diffcile can grow excessively in the digestive system. Occurs when antibiotics kill microbes around the body. This specific one has the ability to form endospores and hide out from the antibiotics. When they generate and start growing they have an environment with very low competition as all the other microbes have been killed off.

65
Q

What key factors make acquiring nosocomial infections very likely?

A

Exposure to numerous pathogens- lots of sick people.

Weakened immune system of ill patients- sick or old people.

Pathogen transmission between individuals- patient, staff, visitors.

66
Q

What key procedures can greatly reduce the prevalence of nosocomial infections?

A

Disinfection
Medical asepsis
Surgical asepsis and sterile procedures
Use of sterile gloves, gowns, cas, and masks.
Isolation of particularly contagious or susceptible patients
Continuous surveillance.

67
Q

In what specific ways is the sharing of public health data helpful in combating infectious disease?

A

Physicians learn of current disease trends
Physicians can be provided with lab and diagnostic assistance.
Focus research on etiology and prevention.
Revise recommendations on immunization schedules.
Coordination of global efforts at disease education, control, and eradication.

68
Q

List at least three specific methods/initiatives by which disease transmission is reduced.

A

Enforce food and water safety standards.
Work to reduce disease vectors and reservoirs.
Establish and enforce immunization schedules
Locate and treat individuals exposed to pathogens.
Establish isolation and quarantine procedures.

69
Q

Define and contrast contamination, infection, and disease.

A

Contamination is a foreign pathogen that comes in contact with the body. Infection is a foreign pathogen that overcomes the body’s defenses. While a disease is an infection and succumbs to the body’s defenses, multiplies, and adversely affects body function.

70
Q

Key difference between endotoxin and exotoxin?

A

Endotoxins are specific to Gram-negative bacteria while exotoxins are not.