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BIO 325 - Pathophysiology > Infection - CH. 9 > Flashcards

Infection - CH. 9 Flashcards

1
Q

Commensalism

A

Colonizing bacteria obtain what they need without host body being affected.

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2
Q

Portals of entry

A

Parenteral
Direct Contact
Ingestion
Inhalation

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3
Q

Communicability

A

Ability to spread from one individual to others and cause disease

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4
Q

Infectivity

A

Ability of pathogen to invade and multiply in host.

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5
Q

Virulence

A

Degree to which a microorganism is capable of causing infectious disease

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6
Q

Adhesion

A

Prevents pathogens from being swept from the body

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7
Q

Mechanisms of adhesion

A

Slime layer
Proteins (COVID-19 spike protein)
Pili or fimbriae

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8
Q

Biofilm

A

Community of bacteria that colonize together within a sticky web of extracellular material biofilms

Protects from antibiotics and host elimination

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9
Q

First stage of infection

A

Colonization

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10
Q

Mechanism of action

A

How microorganism damages tissue

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11
Q

Toxigenicity

A

Ability to produce soluble toxins or endotoxins, factors that greatly influence the pathogen’s degree of virulence

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12
Q

Endotoxins

A

LPS contained in the cell walls of gram-negative organisms released during cell destruction that activate the inflammatory response, immune, response, and produce fever (pyrogenic)

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13
Q

Exotoxin

A

Enzymes released during growth of the bacteria, can damage the plasma membranes of host cells or can inactivate enzymes critical to protein synthesis.

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14
Q

Stages of Infection

A

Exposure
Incubation
Prodromal
Acute stage (invasion)
Convalescent
Resolution

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15
Q

Exposure period

A

Host exposed and infected by infective agent

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16
Q

Incubation period

A

Begins active replication - asymptomatic

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17
Q

Prodromal stage

A

Generic symptoms appear and pathogens continue to multiply

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18
Q

Acute Stage (Invasion)

A

Maximum impact of infectious process

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19
Q

Convalescent Stage

A

Containment, repair of tissue
Immune system successfully removes pathogen and symptoms decline

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20
Q

Resolution stage

A

Total elimination of pathogen from body

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21
Q

What happens during acute stage?

A

Proliferation and dissemination of pathogen - invading further w/larger impact
Production of toxic byproducts
Inflammatory and immune responses triggered
SPECIFIC symptoms

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22
Q

Staphylococcus, Streptococcus, TB

A

Toxins alter function for immune system to fight off or resist immune defenses

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23
Q

Bacterial growth phases

A

Initial lag phase
Log phase
Stationary phase
Death/spore formation

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24
Q

Spores

A

Dehydrated structures that represent a formant or nonvegetative state of a bacteria

Formed during nutrient deprivation/harsh condition
Highly resilient, can survive for centuries
Germinate to VEGETATIVE state when water and nutrients are available

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25
Q

Escherichia Coli

A

Causes UTIs

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26
Q

Salmonella

A

Self-limiting gastroenteritis
Enteric typhoid fever

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27
Q

Pyogenic cocci

A

Bacteria that can cause fever and suppurative infections

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28
Q

Spirilla

A

Helicobacter pylori causes most peptic and duodenal ulcers

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29
Q

Pseudamonas

A

Frequent cause of hospital based post-surgical pneumonia and UTIs

30
Q

Staphylococcus aureus

A

Produce systemic infections such as pneumonia, septic arthritis

Can cause: impetigo, furuncles, carbuncles

31
Q

Impetigo

A

Usually appears as red sores on the face. Burst and develop honey-colored crusts

In children, commonly seen on child’s nose and mouth, hands and feet.

32
Q

Furuncles

A

Skin abscesses that involve a hair follicle and surrounding tissue (boils)

33
Q

Carbuncles

A

Red, swollen, and painful cluster of boils that are connected to each other under the skin

34
Q

Streptococcus pyogenes

A

Can cause acute pharyngitis (strep throat)

35
Q

Streptococcus pneumoniae

A

Most common cause of pneumonia and otitis media

36
Q

Gut barrier failure

A

Decreased perfusion of gut -> Flora bacteria escape into outside fluid -> Inflammatory response -> vasodilation -> shock

37
Q

Septicemia

A

Proliferation of bacteria in the blood
Gram - release endotoxin and gram + release exotoxins that cause excess of cytokines (TNF-a, IL-1, IL-6, ROS)

38
Q

Septic shock

A

Most common vasodilatory shock

Symptoms of gram - septic shock produced by endotoxins

39
Q

Symptoms of septic shock

A

Vasodilation, edema, third spacing, fever, increased WBCs, flushed skin, personality changes

40
Q

Multiple organ dysfunction

A

Progressive dysfunction of two or more organ systems from uncontrolled inflammatory response to severe illness or injury

41
Q

Characteristics of a virus

A

Protein coat (capsid) surrounding nucleic acid core
No metabolic enzymes of their own
Insert their genome into a host cell’s DNA
Use that cell’s metabolic machinery to make new viruses

42
Q

Viral Replication – Early phase

A

Viral recognition of host target cell
Attachment to host cell
Penetration of host cell membrane
Release and uncoating of viral genome into a host cell’s cytoplasm

43
Q

Viral replication - Late phase

A

Viral genome transcription
Synthesis of viral structural components
Assembly of new viral particles - capsid
Release of new viruses from the host cell

44
Q

Eclipse period

A

Period of time from viral uncoating to release of new viruses, during which the virus loses its infectivity

45
Q

Latent Period

A

Time during which extracellular viruses cannot be detected; includes eclipse period and ends with release of new virus from infected cells

46
Q

Antigenic drift/shift

A

Viral mutation
Mutations constantly occur due to rapid rate of division.

47
Q

Latent viral state

A

Virus is never eliminated - is harbored in the body in an inactive state but can be reactivated by stressors

48
Q

Measles

A

Enters through oropharynx
Enters blood after 5-7 days and spreads to body surfaces
Virus replicates in tissues causing URI symptoms
End of overt symptoms, person sheds virus and is highly contagious
ABs are produced but absorbed quickly by viral particles

49
Q

Common Cold

A

Most common RI
Rhinovirus: portal is nasal mucosa and conjunctiva
Spread person/person
Incubation: 5 days
Rhinorrhea, sinusitis, pharyngitis, laryngitis, headache

50
Q

Flu/Influenza

A

Orthomyxoviridae family: A, B, and C
Inhalation of droplet nuclei or direct contact
More contagious than bacterial RI
Damages epithelial cells of respiratory tract by undergoing necrosis and ECF leaks out.

51
Q

Influenza symptoms

A

Abrupt onset of symptoms
Severe body aches, fever, anorexia, headache, malaise, and a dry cough

If in lower RT = viral pneumonia

52
Q

Fungi

A

Large microorganisms with rigid chitin- or cellulose-based cells walls

53
Q

Diseases caused by fungi

A

Mycoses (yeasts or molds)

54
Q

Where are most fungal infections located

A

Surface of the body

55
Q

Dermatophytes

A

Fungi, cause athlete’s foot and ringworm

56
Q

Pathogenicity of fungi

A

Adapt to host environment

57
Q

Parasitic microorganism range

A

Unicellular protozoa to large worms

58
Q

Method of infection - parasites

A

Vectors or through contaminated water/food

59
Q

Protozoa

A

Malaria, amoebic dysentery, giardiasis, plasmodium

60
Q

Helminths

A

Roundworms, tapeworms, flukes

61
Q

Arthropods

A

Ticks, mosquitoes, mites, lice, fleas

62
Q

Fever

A

Hallmark of infectious diseases
Reset hypothalamus = body temperature increases
Can be caused by exogenous and endogenous pyrogenes

63
Q

Specific

A

Reflects site of infection

64
Q

Nonspecific

A

Can be shared by a number of diverse infectious diseases

65
Q

Obvious

A

Predictable patterns

66
Q

Covert

A

May require lab testing to detect

67
Q

Serology

A

Detection of characteristic antigens/antibody

68
Q

Bacteriostatic

A

Inhibit growth until the microorganisms are destroyed by the individual’s own protective systems

69
Q

Antibiotic methods

A

Inhibit synthesis of cell wall
Damage cytoplasmic membrane
Alter metabolism of nucleic acid
Inhibit protein synthesis
Modify energy metabolism

70
Q

How do bacteria fight against antibiotics

A

Inactivating antibiotics
Changing antibiotic binding sites
Using different metabolic pathways
Changing their walls to keep antibiotics out

71
Q

Antiviral agents kill viruses by blocking

A

Viral RNA or DNA synthesis
Viral binding to cells
Production of the protein coats (capsids) of new viruses

BIO 325 - Pathophysiology (8 decks)

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