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micro orgamisims Flashcards

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1
Q

microrganisims

A

essential for decomposition/ recycle nutrients

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2
Q

prokaryote vs eukaryote

A

pro- lack nucleus/ have free floating DNA, undergo asexual reproduction ( binary fusion )/ unicellular

euk- multicelluar, membrane bound organells, nucleus, sexual reproduction ( mitosis )

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3
Q

virus

A

not living
no cellular strucute
protein coat around the DNA or RNA
can mutate
antibiotics are innefective antivirals required

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4
Q

bacteria

A

prokaryotic
unicellular
have a cell wall

e.coli
gastrointestianal tract bacteria
syphylisis

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5
Q

protazoa

A

eukaryotic
no cell wall
drugs are usually more toxic b/c damaging same cells as human\
motoz- move around
malaria

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6
Q

fungi

A

eukaryotic
antifungals
have a cell wall
produce spores- how they reproduce
ringworm tinea

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7
Q

helminths

A

eukaryotic
multicellular
eggs, larva, then develop into adult
don’t proliferate the host

tapeworm

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8
Q

bacteria optimum temperature

A

37 degrees

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9
Q

bacteria optimum PH

A

7

exceptions- bacteria in stomachs

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10
Q

3 types of bacteria

A

oligate arobes- oxygen only grow in presence in oxygen

oligate anerobes- can only grow in prsence of no oxygen

faculative anerobes - both conditions

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11
Q

gram positive bacteria

A

thick layer of peptidoglycan
can form spores- survive harsh conditions so will cause
reinfection

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12
Q

gran negative bacteria

A

reinforced with second membrane
more difficult to kill
produce endotoxins

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13
Q

microbiota

A

normal flora

work in symbiotic relationship with the human body to help the body

prevent bad bacteria from gorwing, take up space, nutrients
reduce PH, outcompete other pathogens, syntehsise important nutrients
could prevent normal cells from growing
could transfer antibiotice resistance to bad bacteria
use gloves to prevent

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14
Q

mode of transmission

A

contact= contact between 2 people by touch

vichele- using air, water, food

vector- transfer of pathogen via an animal

fomite- born= by air or inanimate object

vertical- through the placenta so mum to child

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15
Q

chain of infection

A

infectious agent- reservoir ( population that the infectious agent sits ) - portal of entry ( how it enters )- mode of transmision ( how it transmits to each patient ) - point of exit ( how it leaves )- suseptible host ( contract disease, people with low immune systems )

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16
Q

enviroment control

A

steralisation

disinfection

sanitation

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17
Q

steralisation

A

destrcution/ elimination of all microbes

heat - glass wear
radiation - heat sensitive matirial
filitration- protein solutions
chemical - bleach- metal implements

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18
Q

disinfection

A

elimination of most pathogens from inanimate object

chemical- alcohol
gas-

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19
Q

sanitation

A

safe disposial of human waste- e.g urine, blood

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20
Q

requirements for disease

A

Pathogenicity – the ability of a microbial agent to cause disease

Virulence – the degree to which an organism is pathogenic- ability to cause

Sufficient dose
Portal of entry and exit: breach host defences

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21
Q

pathogenic properties

A

Adherence
Adhesion is the capability of pathogenic microbes to attach to the cells of the body using adhesion factors

Invasion is the ability of a pathogen to enter host cells or tissues, spread and cause disease.

Toxins
In addition to enzymes, certain pathogens are able to produce toxins, biological poisons that assist in their ability to invade and cause damage to tissues

Evasion

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22
Q

Adherance

A

Adhesins are found on the surface of certain pathogens and bind to specific receptors on host cells, for example on;

fimbriae and flagella of bacteria
cilia of protozoa
capsids or membranes of viruses

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23
Q

invasion

A

Glycohydrolases- Degrades hyaluronic acid that cements cells together to promote spreading through tissues

nucleases- Degrades DNA released by dying cells

Phospholipase- Degrades phospholipid bilayer of host cells

protease- Degrades collagen in connective tissue to promote spread

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24
Q

toxins

A

endotoxins- gram negative bacteria- resulting in the disintegration of the membrane

exotoxins- gram positive bacteria and gram negative
Exotoxin targets specific receptors on specific cells and damages those cells through unique molecular mechanisms.

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25
Q

antigen

A

can initiate an immune response

identified as foreign

26
Q

inate immune response

A

non-specific

react same to every pathogen

inborn

1st and 2nd line of defense

27
Q

adaptive/ aquired

A

specific

against one specific pathogen

developed over time

require exsposure

3rd line of defense

28
Q

first line of defense

A

inate/ non specific

protect portal of entry
keep every invader out and prevent infection
Barriers ( physical, chemical )

physical- intact barrier/ structure- skin,

chemical- mucous membrane/ hair and cilia

fluids- tears, saliva, acid

defaction/ vommiting

29
Q

second line of defense

A

inate/ non specific

antimicrobial chemicals

phagocytes

natural killer cells

inflamtion

fever

30
Q

antimicrobial second line of defesne

A

interferon= inteferes with viral infection and activates immune cells… will flag for destruction

complement proteins- will bind to anything forigen= so will highlight it and will flag pagocytes to destroy it.

31
Q

phagocytes second line of defense

A

chemotaxins will flag phagocytes

phagocytosis occurs,

  1. phagocyte will recognise pathogen as forign
  2. pahgocyte will engulg the pathogen and form a phaosome
  3. lysosome in the cell will then merge and bind with phagosome forming a phagolysosome
  4. lysomome contains digestive enzymes which will break down pathogen
  5. exocytosis will occur
32
Q

natural killer cells second line of defense

A

target abnormal cells

will attack pre cancerous cells

33
Q

inflamation second line of defense

A

to limit chances of infections at this wound

damaged cells will see MAST cells release histamine and causes pahgocytes to come to the site.
increased blood flow// increased leakage
traps the pathogen from entering the blood stream
remove dead tissue because it will stop healing

  1. redness- increase blood flow for phagocytosis
  2. heat- increase blood flow
  3. swelling- capilary permability increase fluid leakage- increase phagocytosis
  4. pain
  5. loss of function in this site
34
Q

fever 2nd line of defense

A

systemic response

increase temp to increase immune cell functions
decrease the pathogen functions

higher metabolic rate to increase healing

35
Q

two adaptive immune responses

A

cell-mediated

antibody- mediated

specific/ versatile/ memory/ tolerance/ memory

36
Q

cell mediated response

third line of defense

A

T cell
kill directly and don’t make antibodies

T CELL activation= MHC marker on the surface of T cell- the antigen will bind to this

CD4- prsented on T helper cell

CD8 - T killer cells

37
Q

MHC 1

A

For a T cell to recognize an antigen, the antigen must be bound to
Major Histocompatibility Complex (MHC) in the PM of another cell

so will display the non-self antigen on MHC 1 marker to have it destroyed

thus activate cytoxic T cells to destroy by releaseing toxins

38
Q

MHC 2

A

Antigen presenting cell (APC): Macrophage, Lymphocyte B or
dendritic cells, express MHC 2

Helper T cell (via CD4 receptor) recognise
foreign II MHC
7. Helper T cells secrete cytokines
A. Attract and stimulate macrophages
B. Attract and stimulate cytotoxic T cells
C. Promote activation of B cells → make
antibodies

39
Q

helper T cells

A

ACTIVATED by pathogens

actract macrophages or activate B cells

40
Q

antibody

A

plasma cells secrete antibodies

long protein chain- heavy and a light chain

constant region- Ige antibodies have the same
variable region changes depending on the shape of the antigen binding site

41
Q

types of antibody

A

IgA- on muscosa/ blood
IgE- activate in allergies
IgD- B cell surface
IgG- memory
IgM- first made

42
Q

antibody - mediated response

A

Defend against antigens and pathogens
* B cell doesn’t directly touch antigen
* Produce antibodies (immunoglobulin)
* Provides immunological memory
* React instantly next time it sees the same enemy

43
Q

antibodies

A

Activation of complement
2. Attraction of phagocytes
3. Stimulation of inflammation
4. Prevention viral/bacterial adhesion
5. Precipitation and agglutination
6. Neutralisation
7. Opsonisation

44
Q

4 types of immunity

A

active or passive
(memory)

natural or artificial

45
Q

natural

A

come into contact with the disease

46
Q

artificial

A

immunisation- given a vaccine/ the disease

47
Q

immunisation

A

body will make antibdies against antigen

memory cells made

destroy if re-exsposed

secondary response- quicker/ more rapid and a greater concentration of antibodies are produced because of the B cells already being present

48
Q

vaccine pros/ cons

A

pros= Protective for relevant disease
* Safe
* No adverse effects
* Sustained
* Long-term protection
* Generate antibodies (B cells) or protective T cells
* Practical
* Use and stability

cons=
Adverse reactions
* Redness and swelling
* Allergic reactions
* Consider
* Prevalance of disease
* Severity of disease
* Morbidity and mortality

49
Q

herd immunity

A

85 percent of immunity will protect the entire population

decreases the number of hosts able to pass on disease

50
Q

nosocomial infection

A

an infection that you get in a hospital

51
Q

acute inflamation

A

remove injuury agents
remove infectious agent
clear damaged cells

innate

52
Q

chronic inflammation

A

if acute goes on for a long time

auto-immune

53
Q

purpose of inflammation

A

destroys, dilutes, neutralises disease agents

stimmulate immune response

enable healing

54
Q

chemical inflammation

A

cells that are damaged will release histamine

histamine will increase capilary permability

prostaglandis- vasodilation

thromboxanes- clotting

leukotrines- attract wbc

55
Q

two types of inflamtion

A

vascular phase

cellular phase

56
Q

vascular phase of inflammation

A

vasodilation

increased blood flow to site of injury
redness and heat

increased vascular permability
- swelling
protein rich plasma leaves the blood vessels

57
Q

exudate vs transudate

A

rich in protein
fibrin present
increased vascular permability

58
Q

cellular phase

A

Margination and adhesion.
2. Transmigration or Diapedesis.
3. Chemotaxis.
4. Activation of leukocytes  phagocytosis

59
Q

inflammation signs cardinal

A

redness
warmth
pain
swelling
loss of function

60
Q

systemic effects of inflammation

A

fever
aneorexia
leukocytosis
malasise

61
Q

aged effects to inflammation

A

longer onset

less dendritic cells

NK cells less toxic

decline in phagocytosis

Biology (19 decks)

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