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

Infection - CH. 9 Flashcards

(71 cards)

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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
Escherichia Coli
Causes UTIs
26
Salmonella
Self-limiting gastroenteritis Enteric typhoid fever
27
Pyogenic cocci
Bacteria that can cause fever and suppurative infections
28
Spirilla
Helicobacter pylori causes most peptic and duodenal ulcers
29
Pseudamonas
Frequent cause of hospital based post-surgical pneumonia and UTIs
30
Staphylococcus aureus
Produce systemic infections such as pneumonia, septic arthritis Can cause: impetigo, furuncles, carbuncles
31
Impetigo
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
Furuncles
Skin abscesses that involve a hair follicle and surrounding tissue (boils)
33
Carbuncles
Red, swollen, and painful cluster of boils that are connected to each other under the skin
34
Streptococcus pyogenes
Can cause acute pharyngitis (strep throat)
35
Streptococcus pneumoniae
Most common cause of pneumonia and otitis media
36
Gut barrier failure
Decreased perfusion of gut -> Flora bacteria escape into outside fluid -> Inflammatory response -> vasodilation -> shock
37
Septicemia
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
Septic shock
Most common vasodilatory shock Symptoms of gram - septic shock produced by endotoxins
39
Symptoms of septic shock
Vasodilation, edema, third spacing, fever, increased WBCs, flushed skin, personality changes
40
Multiple organ dysfunction
Progressive dysfunction of two or more organ systems from uncontrolled inflammatory response to severe illness or injury
41
Characteristics of a virus
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
Viral Replication -- Early phase
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
Viral replication - Late phase
Viral genome transcription Synthesis of viral structural components Assembly of new viral particles - capsid Release of new viruses from the host cell
44
Eclipse period
Period of time from viral uncoating to release of new viruses, during which the virus loses its infectivity
45
Latent Period
Time during which extracellular viruses cannot be detected; includes eclipse period and ends with release of new virus from infected cells
46
Antigenic drift/shift
Viral mutation Mutations constantly occur due to rapid rate of division.
47
Latent viral state
Virus is never eliminated - is harbored in the body in an inactive state but can be reactivated by stressors
48
Measles
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
Common Cold
Most common RI Rhinovirus: portal is nasal mucosa and conjunctiva Spread person/person Incubation: 5 days Rhinorrhea, sinusitis, pharyngitis, laryngitis, headache
50
Flu/Influenza
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
Influenza symptoms
Abrupt onset of symptoms Severe body aches, fever, anorexia, headache, malaise, and a dry cough If in lower RT = viral pneumonia
52
Fungi
Large microorganisms with rigid chitin- or cellulose-based cells walls
53
Diseases caused by fungi
Mycoses (yeasts or molds)
54
Where are most fungal infections located
Surface of the body
55
Dermatophytes
Fungi, cause athlete's foot and ringworm
56
Pathogenicity of fungi
Adapt to host environment
57
Parasitic microorganism range
Unicellular protozoa to large worms
58
Method of infection - parasites
Vectors or through contaminated water/food
59
Protozoa
Malaria, amoebic dysentery, giardiasis, plasmodium
60
Helminths
Roundworms, tapeworms, flukes
61
Arthropods
Ticks, mosquitoes, mites, lice, fleas
62
Fever
Hallmark of infectious diseases Reset hypothalamus = body temperature increases Can be caused by exogenous and endogenous pyrogenes
63
Specific
Reflects site of infection
64
Nonspecific
Can be shared by a number of diverse infectious diseases
65
Obvious
Predictable patterns
66
Covert
May require lab testing to detect
67
Serology
Detection of characteristic antigens/antibody
68
Bacteriostatic
Inhibit growth until the microorganisms are destroyed by the individual's own protective systems
69
Antibiotic methods
Inhibit synthesis of cell wall Damage cytoplasmic membrane Alter metabolism of nucleic acid Inhibit protein synthesis Modify energy metabolism
70
How do bacteria fight against antibiotics
Inactivating antibiotics Changing antibiotic binding sites Using different metabolic pathways Changing their walls to keep antibiotics out
71
Antiviral agents kill viruses by blocking
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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