block 4- toxaemia Flashcards

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1
Q

diphtheria

A

-respiratory transmission
-ore throat and fever
-difficulty swallowing, irregular heartbeat,coma
-characteristic = pseudomembranes in throat(greyish in the throat= combination of dead cells)

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2
Q

the causative agent of Diphtheria

A

-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

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3
Q

diphtheria toxin and vaccination

A
  • 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
    -
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4
Q

treating diphtheria in unvaccinated patients

A
  • 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
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5
Q

bacterial exotoxins

A

-proteins made/secreted by bacteria that have toxic effects on other cells

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6
Q

dipheria toxin

A

-an enzyme that modifies elongation Factor Tu,blocking translation
- example of a A-B toxin
-

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7
Q

mechanism of dipheria toxin

A

-receptor binding
-endocytosis
-
finish in a sc

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8
Q

what advantages does bacteria have by producing a toxin

A

-many toxins are virulence factors so may kill cells e.g. immune cells and release nutrients

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9
Q

Clostridium tetani

A

-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

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10
Q

treatment of c.tetani(tetanus
)

A

-antitoxin antibody (stops more damage)
-antimicrobial e.g. penicillin
-breathing support while nerve endings regrow
-sometimes surgery on the wound

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11
Q

c. botulium

A

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

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12
Q

toxamia

A
  • a disease where symptoms are entirely due to the toxin
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13
Q
A
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14
Q

bordetella pertussis

A
  • an obligate human pathogen (must infect host to survive and reproduce)
    -does not produce acid for sugars
    -produces 4 toxins
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15
Q

filamentous haemagglutinin (FHA)

A

-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.

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16
Q

FHA structure

A

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.

17
Q

pertussis toxin

A

-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

18
Q

what does pertussin toxin do?

A
  • 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
19
Q

tracheal cytotoxin

A

-fragment of peptioglycan
-lytic transglycoylases= cleaves peptioglycan= releases the toxin
-it causes stasis and death of cilliated epithelial cell

20
Q

are exotoxins always proteins

A

-mostly but no e.g. tracheal cytotoxin

21
Q
A
21
Q

adenylate cyclase toxin

A

-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

22
Q

dermonecrotic toxin

A

-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

23
Q

BvgAS two component system

A
  • 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.
24
Q

whooping cough-pertussis

A

Stage 1 - Colonization: Bacteria present; treatable with antibiotics; key virulence factors are FHA and pertussis toxin.
Stage 2 - Toxemic Phase: No bacteria, symptoms from toxins; antibiotics ineffective; key virulence factors are tracheal cytotoxin, adenylate cyclase toxin, dermonecrotic toxin.

25
Q

whooping cough- symptomatic stages

A

Stage 1: Catarrhal
Symptoms: Nonspecific, similar to a cold or viral infection.
Duration: Lasts 1-2 weeks.
Communicability: Highly contagious during this stage.
Stage 2: Paroxysmal
Symptoms: Severe, repetitive coughing with a characteristic “whoop” sound.
Duration: Lasts 1-4 weeks.
Stage 3: Convalescent
Symptoms: Reduced frequency and severity of coughing spells.
Duration: Complete recovery may take weeks to months.

26
Q

diagnosis of bordetella infections

A

-characteristic cough and clinical pictures
-cultured-based methods= Regar lowe agar containing nicotinic acid(because the bacteria can not make this)
-PCR or serology

27
Q

trasmission of whooping cough disease

A

-highly infectious with 90% efficiency
-infants a\nd young children especially those who haven’t been immunised
-major cause of childhood mortality

28
Q

prevention of whopping cough

A

-pertussis vaccines to everyone
-especially in pregnant women