block 4- toxaemia Flashcards
(29 cards)
diphtheria
-respiratory transmission
-ore throat and fever
-difficulty swallowing, irregular heartbeat,coma
-characteristic = pseudomembranes in throat(greyish in the throat= combination of dead cells)
the causative agent of Diphtheria
-actinobacteria= same phylum as mycobacterium
-bacteria is only found in the throat but damage occurs to the heart and kidney this is because it secretes a toxic protein that circulates in the blood
-injection of the toxin can cause the disease
-blood of an immunized animal can cure disease
diphtheria toxin and vaccination
- because the disease is mainly caused by the toxin and antibody against the toxin is enough to prevent disease
-since the toxin is a protein it can be made safe by denaturing it to make a (toxoid)= denatured protein
-
treating diphtheria in unvaccinated patients
- an antibiotic (penicillin or erythromycin) will kill the bacteria in the throat so prevents transmission and cures infection
-antitoxin (antibody that blocks toxin is needed to protect the heart and other organs
-both are needed
bacterial exotoxins
-proteins made/secreted by bacteria that have toxic effects on other cells
dipheria toxin
-an enzyme that modifies elongation Factor Tu,blocking translation
- example of a A-B toxin
-
mechanism of dipheria toxin
-receptor binding
-endocytosis
-
finish in a sc
what advantages does bacteria have by producing a toxin
-many toxins are virulence factors so may kill cells e.g. immune cells and release nutrients
Clostridium tetani
-gram-positive, rod-shaped bacteria
-opportunistic pathogens
- causes muscle paralysis
-can infect wounds
-produces toxin gthnat targets neuron es = muscle spasms
- toxin targets cental nerves
treatment of c.tetani(tetanus
)
-antitoxin antibody (stops more damage)
-antimicrobial e.g. penicillin
-breathing support while nerve endings regrow
-sometimes surgery on the wound
c. botulium
spores germinate in food and bacteria produces the toxin
-if the person eats the food with the toxin without heating it up properly as heat kills the toxin then they would absorb the toxin via the intestine and targbetsz neurones
-causes flaccid paralysis (kind of like flimsy limbs)
-toxin targets periphetal nerves
toxamia
- a disease where symptoms are entirely due to the toxin
bordetella pertussis
- an obligate human pathogen (must infect host to survive and reproduce)
-does not produce acid for sugars
-produces 4 toxins
filamentous haemagglutinin (FHA)
-a virulence factor
-. Processing
Starts as a 367 kDa precursor protein.
Processed into a 230 kDa mature protein.
Functional part is 60% of the precursor (N-terminal).
2. Structure
Filamentous: 2 nm wide, 50 nm long.
3. Function
Key for B. pertussis adherence to respiratory cells.
Helps bacteria attach to ciliated cells in the trachea.
4. Binding Targets
Recognizes glycolipids, proteoglycans, and integrins on host cells.
FHA structure
Binding to Sulfated Sugars
Spanning residues bind to sulfated sugars on mucus-secreting epithelial cells.
RGD Tripeptide
The Arg-Gly-Asp (RGD) sequence binds to CR3 integrins on macrophages and ciliated cells.
Carbohydrate Recognition Domain (CRD)
The CRD binds to lactosyl ceramides on macrophages and ciliated cells.
pertussis toxin
-it catalyses ADP-ribosylation of heterotrimeric G proteins= blocks several signalling mechanisms
-has two types of subunits
-A= enzymatic activity
-B- receptor binding part
-its important for colonization and establishment of infections
what does pertussin toxin do?
- causes lymphocytosis (increased number of lymphocytes) increased release of insulin = less glucose=hypoglycemia
-impairs neutrophil chemptaxis,phagocytosis and enhances respiratory tract
-prevents movement of cilla
colinisation = cells cannot kill pathogen or impaired function to kill pathogen
tracheal cytotoxin
-fragment of peptioglycan
-lytic transglycoylases= cleaves peptioglycan= releases the toxin
-it causes stasis and death of cilliated epithelial cell
are exotoxins always proteins
-mostly but no e.g. tracheal cytotoxin
adenylate cyclase toxin
-converts Atp to cAMP and increases cAMP levels=inhibits immune effec tor cells by intoxicating macrophages and neutophils therefore cAMP = virulence factor
-secreted by bacteria and oftem remains attched
-inserts into cell membranes of eukaryotic cells
-can cause histamine sensitisation
dermonecrotic toxin
-cell differecfauses modification of GTP-ases receptors e.g. polyamination or deamidation
-results in distruption of cytokinesis,cell differintation, gene expression etc…
-results in damage of tissues
BvgAS two component system
- BvgS: Sensor protein (histidine kinase), detects Mg²⁺ and SO₄²⁻.
BvgA: Response regulator, turns specific genes on/off. via phosphorlation hence why its a kinase
Function: Helps bacteria adapt to the environment by regulating virulence genes.