Ch. 14 Mechanisms of Infectious Disease Flashcards

1
Q

Host

A

An organism that can support the nutritional and physical growth of another organism

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2
Q

Infection

A

Presence and multiplication within another living organism, causing injury to the host

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3
Q

Colonization

A

Establishing a presence (step of infection)

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4
Q

Microflora

A

Normal and beneficial bacteria in the host

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5
Q

Type of relationship where bacteria get nutritional support from the host, but the host is not negatively affected.

A

Commensalism

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6
Q

Type of relationship where the microorganism and host both benefit from their interaction

A

Mutualism

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7
Q

Type of relationship where the microorganism gains benefits but the host is harmed or gains nothing from the interaction.

A

Parasitic

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8
Q

What occurs if the host sustains injuries in a parasitic relationship with a microorganism?

A

Infectious disease

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9
Q

Virulence

A

The potential of a microorganism to cause infectious disease

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10
Q

What makes a pathogen different from a microorganism?

A

Pathogens are extremely virulent and are rarely found in the absence of infectious disease.

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11
Q

Saprophytes

A

Microorganisms that get nutrients through dead or decaying organic material and are usually harmless

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12
Q

Opportunistic pathogens

A

When any type of microorganism, including microflora and saprophytes, produce infectious disease when the immune system of the host is extremely weak.

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13
Q

Examples of prion diseases

A

CJD
chronic wasting disease (deer/elk)
scrapie (sheep)
bovine spongiform encephalopathy (mad cow)
kuru

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14
Q

What is the collective name for prion diseases and what are their shared characteristics?

A

Transmissible neurodegenerative diseases

slow progression (months-years)
noninflammatory neuronal degeneration
loss of coordination (ataxia)
dementia
death

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15
Q

What does a normal prion protein (PrP) do in the cell?

A

Not well understood!

Exists on the cell surface, maybe involved in cell adhesion, cell binding, copper metabolism, and/or synaptic fx.

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16
Q

What is molecularly different about diseased prions?

A

Misfolded host prion.

Resistant to proteases (apoptosis) and clumps IN the cytoplasm of neurons (amyloid fibrils), whereas it is normally on the cell surface.

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17
Q

How do diseased prions replicate?

A

PrPsc binds to PrPc on the cell surface and changes the normal prion into PrPsc. The complex releases from the cell and forms amyloid plaques in the brain. Cell replenishes PrPc and cycle continues.

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18
Q

Why aren’t there antimicrobial agents for prions?

A

Prions don’t have reproductive or metabolic functions since they are just part of the cell (they don’t have their own genome).

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19
Q

What do viruses consist of?

A
  1. protein coat (capsid)
  2. nucleic acid core (genome of RNA OR DNA)
  3. Some are enclosed in a lipoprotein envelope from the cell membrane of the host cell (ie herpes, paramyxoviruses (flu and poxviruses))
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20
Q

What type of replication do herpesviruses use?

What diseases are included in herpesviruses?

A

Latent - they insert their genome into the host chromosome and wait until a stimulation to undergo active replication and cause disease symptoms months to years later.

  • Chickenpox and zoster (varicella-zoster)
  • cold sores (herpes simplex virus type 1)
  • genital herpes (HSV type 2)
  • infectious mononucleosis (cytomegalovirus or Epstein-Barr virus)
  • Kaposi sarcoma (human herpesvirus 8)
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21
Q

How do retroviruses replicate?

What is an example of a retrovirus?

A
  1. enter the host cell
  2. viral RNA genome translated into DNA by viral enzyme reverse transcriptase
  3. viral DNA copy is integrated into the host chromosome
  4. Latency
  5. reactivation and replication through the reversal of the process and potentially lysis of the host cell

Example: HIV targets immune cells and lyses them during replication = permanent suppression of immune system

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22
Q

What are oncogenic viruses?

A

Viruses can transform normal host cells into malignant cells in the replication process.

Epstein-Barr virus

Hepatitis B virus

Papillomavirus

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23
Q

What characteristics are universal in bacteria?

A
  1. lack a nucleus
  2. contain DNA and RNA
  3. Genome is encoded on one chromosome, with extrachromosomal pieces of circular DNA (plasmids)
  4. Cytoplasm with surrounding cytoplasmic membrane
  5. Cell wall
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24
Q

What is the cell wall of bacteria made of?

A

Peptidoglycan

Produced only by prokaryotes it is a target of antibacterial therapy!

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25
Q

What is the purpose of the capsule in bacteria?

A

It encloses the cell wall and protects the bacteria from immune defenses of the host.

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26
Q

Difference between flagella and pili (or fimbriae)

A

Flagella external microfilaments that propel the bacteria

Pili or fimbriae are hairlike and allow the bacteria to adhere to mucus membranes or other bacteria

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27
Q

How do most bacteria replicate?

A

Asexually by simple cellular divison

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28
Q

What do the following prefixes mean?

Strepto-

Diplo-

Staphylo-

A

chain

pairs

cluster

(how the bacteria look after they divide)

29
Q

What are biofilms and how do they work?

A

Structured bacterial communities that form on environmental surfaces

Chemical signals produced by microorganisms inform the community when the environment requires dormancy and permits proliferation

Polysaccharides in the biofilm protect the bacteria from antimicrobial agents

30
Q

What is the term for bacteria that can adapt to aerobic or anaerobic conditions?

A

Facultatively anaerobic

31
Q

Staining color of gram positive bacteria

A
  • stained purple by crystal violet dye
32
Q

Staining color of gram negative bacteria

A
  • not stained by crystal violet
  • stained red by second dye (safranin)
33
Q

How are Rickettsiaceae, Anaplasmataceae, Chlamydiaceae, and Coxiella similar to viruses and bacteria?

A
  • obligate intracellular pathogens (like viruses)
  • make a rigid peptidoglycan cell wall
  • reproduce asexually
  • contain RNA and DNA
34
Q

Examples of Chlamydiaceae

A
  • chlamydia
  • neonatal and adult conjunctivitis
  • infant pneumonia
35
Q

Characteristics of fungi

A
  • eukaryotic
  • free-living
  • saprophytes
  • yeasts and molds
36
Q

Yeast

A

Single-celled

reproduce by budding

37
Q

Mold

A
  • long, hollow branching filaments (hyphae)
  • Some have septations separating hyphae into compartments
  • asexual and sexual reproduction
38
Q

Why are fungi not often able to grow in the body?

A

Not many types can live and grow at the core body temperature

39
Q

Superficial mycoses

A
  • Infection is limited to cooler cutaneous surfaces
  • ringworm, athlete’s foot, jock itch
40
Q

Systemic mycoses

A
  • serious fungal infections of deep tissues because the fungi are capable of growth at 37oC.
41
Q

Why type of fungus is Candida albicans?

A

commensal! They can grow at a range of temps on the skin, mucous membranes, and GI tract.

41
Q

Why type of fungus is Candida albicans?

A

commensal! They can grow at a range of temps on the skin, mucous membranes, and GI tract.

42
Q

Parasites

A
  • eukaryotes
  • infect or colonize other animals, which transmit the parasite to humans
  • Can sometimes directly infect the human
  • Protozoa, helminths, arthropods
43
Q

Epidemiology

A

Study of factors, events, and circumstances that influence the transmission of disease

44
Q

How can microorganisms enter a host?

A

Direct contact, penetration, ingestion, and inhalation

45
Q

Vertical transmission

A

Transmission from parent to child across the placenta or during childbirth from vaginal secretions

46
Q

An infant is infected with cytomegalovirus during pregnancy. What type of infection is this?

A

Congenital infection

47
Q

Types of sources of infectious disease

A
  1. Endogenous: acquired from the host’s microflora
  2. Exogenous: acquired from sources in the environment like water, food, air, soil
  3. Another human: congenital
  4. Inanimate object: fomite
  5. Animal or biting arthropod: vector
48
Q

Mechanisms of disease production

A
  • toxins
  • adhesion factors
  • evasive factors
  • invasive factors
49
Q

How do bacterial endotoxins affect host cells?

A
  • lipopolysaccharides (LPS) of cell wall in gram-neg bacteria
  • Free LPS attaches to circulating LPS-binding protein, which then binds leukocyte receptors involved in innate immune activation.
  • Induces cytokines and stimulatory molecules to increase leukocytes and T-lymphocyte activation
  • BUT high levels of LPS can cause septic shock, disseminated intravascular coagulation, and ARDS
50
Q

How do exotoxins affect cells?

A
  • proteins released from bacteria during growth
  • Inactivate or modify host cell structure or function, causing cell death or dysfunction
  • example: Shiga toxins produced by E coli causes hemorrhagic colitis and hemolytic uremic syndrome in infants and young children
51
Q

What is the purpose of a slime layer?

A

It is a gelatinous matrix of polysaccharides that anchors the bacteria to host tissues and protects it from the host’s immune defense.

52
Q

What is the purpose of fimbriae?

A

Hairlike projections used by viruses and bacteria to attach to other cells

53
Q

How do microorganisms evade the host’s immune system?

A
  1. Physical: slime, capsules, and mucous discourage engulfment by neutrophils and monocytes
  2. Chemical: excretion of leukocidin C toxins which damage membranes of host neutrophils and macrophages, neutralization of stomach acid (H Pylori)
  3. Adaption: Some bacteria can survive and reproduce WITHIN wbcs after they are ingested (salmonella, listeria, and Legionnaires)
  4. Avoiding host antibodies: produce surface proteins (protein A) that immobilize immunoglobin G and secrete coagulase to form a protective clot. Flu and gonorrhea secrete enzymes that inactivate IgA.
54
Q

How do pathogens use invasive factors?

A

Enzymes that destroy cell membranes, CT, and proteins

55
Q

What is an abscess?

A

A localized pocket of infection composed of devitalized tissue, microorganisms, and phagocytic WBCs

It is a roadblock in the immune response and usually requires surgical drainage.

56
Q

What is the incubation period?

A

The pathogen begins active replication without producing symptoms in the host

57
Q

What is the prodromal stage?

A

The initial appearance of symptoms in the host but they are usually universal inflammation symptoms (fever, headache, fatigue)

58
Q

What is the acute stage?

A

The pathogen is at its peak and combined effects of toxic byproducts of pathogen metabolism, cell lysis, and immune response produce tissue damage and inflammation. Symptoms are more specific.

59
Q

What is the convalescent period?

A

The infection is contained with elimination of the pathogen. Symptoms start to decline and damaged tissue is repaired.

60
Q

What is the resolution stage?

A

total elimination of the pathogen without lasting signs or symptoms of the disease

61
Q

What is a fulminant illness?

A

There is little to no prodromal stage.

62
Q

How is diagnosis of an infectious disease made based on serology?

A

If the antibody level (antibody titer) against a pathogen rises during the acute phase and falls during convalescence (not as good as a culture)

63
Q

How can specific antibody detection be used to detect congenital infections?

A

IgM antibodies don’t cross the placenta but some IgG antibodies are passively transferred from parent to infant during the 3rd trimester.

Elevated serum IgM antibodies in the infant would have originated from the child = congenital infection

64
Q

Direct antigen detection

A

Uses purified antibodies (monoclonal antibodies) to detect antigens of specific infectious agents in diseased host specimens

65
Q

Bactericidal vs bacteriostatic antibiotics

A

Bactericidal = causes irreversible and lethal damage to bacteria pathogen

Bacteriostatic = inhibitory effects on bacterial growth are reversed when the agent is eliminated

66
Q

What are the 4 basic mechanisms of antibiotic action?

A
  1. interference with a step in bacterial cell wall synthesis
  2. inhibition of bacterial protein synthesis
  3. interruption of nucleic acid synthesis
  4. interference with normal metabolism
67
Q

How do antiviral agents generally work?

A

They target DNA or RNA synthesis (inhibits viral DNA polymerase, impairs the synthesis of reverse transcriptase, protease inhibitors)