micro orgamisims Flashcards
microrganisims
essential for decomposition/ recycle nutrients
prokaryote vs eukaryote
pro- lack nucleus/ have free floating DNA, undergo asexual reproduction ( binary fusion )/ unicellular
euk- multicelluar, membrane bound organells, nucleus, sexual reproduction ( mitosis )
virus
not living
no cellular strucute
protein coat around the DNA or RNA
can mutate
antibiotics are innefective antivirals required
bacteria
prokaryotic
unicellular
have a cell wall
e.coli
gastrointestianal tract bacteria
syphylisis
protazoa
eukaryotic
no cell wall
drugs are usually more toxic b/c damaging same cells as human\
motoz- move around
malaria
fungi
eukaryotic
antifungals
have a cell wall
produce spores- how they reproduce
ringworm tinea
helminths
eukaryotic
multicellular
eggs, larva, then develop into adult
don’t proliferate the host
tapeworm
bacteria optimum temperature
37 degrees
bacteria optimum PH
7
exceptions- bacteria in stomachs
3 types of bacteria
oligate arobes- oxygen only grow in presence in oxygen
oligate anerobes- can only grow in prsence of no oxygen
faculative anerobes - both conditions
gram positive bacteria
thick layer of peptidoglycan
can form spores- survive harsh conditions so will cause
reinfection
gran negative bacteria
reinforced with second membrane
more difficult to kill
produce endotoxins
microbiota
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
mode of transmission
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
chain of infection
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 )
enviroment control
steralisation
disinfection
sanitation
steralisation
destrcution/ elimination of all microbes
heat - glass wear
radiation - heat sensitive matirial
filitration- protein solutions
chemical - bleach- metal implements
disinfection
elimination of most pathogens from inanimate object
chemical- alcohol
gas-
sanitation
safe disposial of human waste- e.g urine, blood
requirements for disease
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
pathogenic properties
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
Adherance
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
invasion
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
toxins
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.
antigen
can initiate an immune response
identified as foreign
inate immune response
non-specific
react same to every pathogen
inborn
1st and 2nd line of defense
adaptive/ aquired
specific
against one specific pathogen
developed over time
require exsposure
3rd line of defense
first line of defense
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
second line of defense
inate/ non specific
antimicrobial chemicals
phagocytes
natural killer cells
inflamtion
fever
antimicrobial second line of defesne
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.
phagocytes second line of defense
chemotaxins will flag phagocytes
phagocytosis occurs,
- phagocyte will recognise pathogen as forign
- pahgocyte will engulg the pathogen and form a phaosome
- lysosome in the cell will then merge and bind with phagosome forming a phagolysosome
- lysomome contains digestive enzymes which will break down pathogen
- exocytosis will occur
natural killer cells second line of defense
target abnormal cells
will attack pre cancerous cells
inflamation second line of defense
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
- redness- increase blood flow for phagocytosis
- heat- increase blood flow
- swelling- capilary permability increase fluid leakage- increase phagocytosis
- pain
- loss of function in this site
fever 2nd line of defense
systemic response
increase temp to increase immune cell functions
decrease the pathogen functions
higher metabolic rate to increase healing
two adaptive immune responses
cell-mediated
antibody- mediated
specific/ versatile/ memory/ tolerance/ memory
cell mediated response
third line of defense
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
MHC 1
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
MHC 2
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
helper T cells
ACTIVATED by pathogens
actract macrophages or activate B cells
antibody
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
types of antibody
IgA- on muscosa/ blood
IgE- activate in allergies
IgD- B cell surface
IgG- memory
IgM- first made
antibody - mediated response
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
antibodies
Activation of complement
2. Attraction of phagocytes
3. Stimulation of inflammation
4. Prevention viral/bacterial adhesion
5. Precipitation and agglutination
6. Neutralisation
7. Opsonisation
4 types of immunity
active or passive
(memory)
natural or artificial
natural
come into contact with the disease
artificial
immunisation- given a vaccine/ the disease
immunisation
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
vaccine pros/ cons
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
herd immunity
85 percent of immunity will protect the entire population
decreases the number of hosts able to pass on disease
nosocomial infection
an infection that you get in a hospital
acute inflamation
remove injuury agents
remove infectious agent
clear damaged cells
innate
chronic inflammation
if acute goes on for a long time
auto-immune
purpose of inflammation
destroys, dilutes, neutralises disease agents
stimmulate immune response
enable healing
chemical inflammation
cells that are damaged will release histamine
histamine will increase capilary permability
prostaglandis- vasodilation
thromboxanes- clotting
leukotrines- attract wbc
two types of inflamtion
vascular phase
cellular phase
vascular phase of inflammation
vasodilation
increased blood flow to site of injury
redness and heat
increased vascular permability
- swelling
protein rich plasma leaves the blood vessels
exudate vs transudate
rich in protein
fibrin present
increased vascular permability
cellular phase
Margination and adhesion.
2. Transmigration or Diapedesis.
3. Chemotaxis.
4. Activation of leukocytes phagocytosis
inflammation signs cardinal
redness
warmth
pain
swelling
loss of function
systemic effects of inflammation
fever
aneorexia
leukocytosis
malasise
aged effects to inflammation
longer onset
less dendritic cells
NK cells less toxic
decline in phagocytosis
