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MICROBIOLOGY II > Lecture 3- C.tetani > Flashcards

Lecture 3- C.tetani Flashcards

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1
Q

What family does c.tetani belong to

A

Coostridiaceae

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2
Q

Clostridium genus obligate or facûltative anaerobic sporeformer

A

OBLIGATE ANAEROBIC

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3
Q

Clostridium genus gram+/-?

A

Gram positive

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4
Q

Size of Clostridium genus

A

1um x 20um (BIG)

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5
Q

Specific base frequent in Clostridium genus

A

Low G/c content

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6
Q

Where are Clostridium genus found

A

Ubiquitous

Gut, soil

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7
Q

What does Clostridium genus use as fińal electron acceptor in obtaining energy

A

Sulfate to get ATP

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8
Q

Clostridium genus are generally saprophytes but which are pathogenic

A

Botulinum, tetani, perf

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9
Q

What two routes do Clostridium genus obtain ATP

A

Fermentation or anaerobic respiration.

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10
Q

What occurs in anaerobic respiration for c genus

A

Electron accepter is exogenous and reduce sulfate to sulphite. Sulfate is less oxidising than oxygen so less ATP produced

Take 2-3 days to grow

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11
Q

What occurs in fermentation route for c genus

A

ELECTRON ACCEPTOR ENDOGENOUS (opposite to anaerobic respiration)

Don’t use electron transport chain.
Glucose get oxidised to first intermediate and oyrvate act as a final electron acceptor. Energy produce substrate level phosphorylation

Pyruvate further reduced to get more fermentation products

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12
Q

What are Other fermentation products produced via c genus

A

Lactate, ethanol, propionic acid, acetic acid etc

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13
Q

Clostridia utilise a fermentation pathway to obtain an acid from pyruvate. What is the pathway and the acid called

A

Butyric fermentation produce butyric acid from pyruvate

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14
Q

What unfavourable condition for c. Would form endospore

A

OXYGEN

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15
Q

What location of spores are present for c genus and name examples

A

C diff subterminal
Central spores
Tetani - terminal spores - chicken drumstick

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16
Q

What are the distinct components of the endospore for c genus

A

Exosporium - attach loosely to environment
Spore coat - huge chunk of protein
Cortex - huge layer of peptidoglycan
Core - DNA , ribosomes. LOW H2O, small acid soluble spore proteins (SASP) and DPA-Ca2+

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17
Q

Name function of two key components of spore core ; SASPS and DPA- ca2+

A

SAPS- saturates DNA so protection from wet/dry heat

DPA- ca2+ bind free H20 leading to dehydration so protection against wet heat

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18
Q

Describe the process of spore formation

A

1- dna condenses and in centre of cell (become mother cell)
2- dna divide in two.
3- mother cell invaginates and become forespore
4- mother cell membrane grow and engulf spore so two layers of membrane
5- layer of peptidoglycan form between two membranes to make cortex
6- DPA in core and then calcium move into cell and lead to water removal
7- protein coat may make it mature. May form exosporium.
8- lytic enzymes destroy mother cell and spore released

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19
Q

Clostridium sp. germination of spores process

A

1- exposure to specific GERMINANT and activation (irreversible)
2- partial rehydration. DPA- ca2+ release. Loss of some resistance
3- cortex hydrolysis. Full core rehydration and expansion
4- (outgrowth). SASP degradation, metabolism can divide via binary fission, escape from spore coat and divide

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20
Q

Once germinant has bound to receptor is this process of germination reversible

A

NO - irrevsible once started

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21
Q

Name historical derivation, spore structure, disease caused and frequency of disease for c. Botulinum

A

HD- sausage
SS - oval, subterminal
DC- Botulism (foodborne, infant, wound)
FOD- Uncommon

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22
Q

Name historical derivation, spore structure, disease caused and frequency of disease for c diff

A

HD - difficult - hard to grow
Ss- oval, subterminal
Dc- AAD (antibiotic associated diahorrea and PMC
FOD - very common

23
Q

Name historical derivation, spore structure, disease caused and frequency of disease for c perf

A

HD- breaking through
SS- large rectangular
DC- Gi infection
FOD - Common

24
Q

Name historical derivation, spore structure, disease caused and frequency of disease for c tetani

A

HD - tension
SS - round terminal (drumstick)
DC- tetanus
FOD - uncommon

25
Q

Who studied a man with a dart wound which led to spastic paralysis in face and back

A

Hippocrates

26
Q

Who discovered clostridium tetani in 1884 by injecting soil into mice to get paralysis?

A

Arthur Nicolaier

27
Q

Who discovered that soldiers were getting ill on the waterloo battlefield in 1832 and drew the symptoms?

A

Sir charles bell

28
Q

Who first isolated c tetani from a soil sample and described them as obligate anaerobes?

A

Shibasaburo kitasato

29
Q

Displacement activity: when is a chair not a chair

A

Who knows. If you’re smart enough to answer you’re probably a genius

30
Q

Where are the spores for c tetani?`

A

Round terminal spores drumstick

31
Q

What virulence factors does c tetani have?

A

A)spore former which can contaminate wounds

B)exotoxins TETANOLYSIN and TETANOSPASMIN (which causes spasmic paralysis)

32
Q

Name 7 counties where c tetani is highly prevalent?

A

India, china,Africa (ghana,egypt,zaire,mali)

33
Q

How many cases are theee worldwide?

A

50 million

34
Q

How many deaths are there worldwide and how many are in neonates?

A

Half a million deaths. 60 thousand in neonates

35
Q

Where does 80 percent of the cases occur

A

Africa/south east asia

36
Q

How many cases were there in the uk in 2014 and generally in USA?

A

UK: 3-5 CASES PER ANNUM
USA:50-100 CASES PER ANNUM

37
Q

Name some key risk factors for c tetani infection

A

Lack of immunisation
Age over 60 years (Age 60-65 need to get a booster vaccination ideally)
Open wounds contaminated with soil/manure
Skin/tissues puncture eg. Rusty metals, thorns and ear piercings
Childbirth especially in africa and india - rural african communities use cow dung and soil put on umbilical cords of youngsters to help heal but the spores get in and cause neonatal tetanus

38
Q

Why does the location of c tetani spore germination suggest it is an anaerobic organism?

A

Germinates in deep areas of tissue

39
Q

How does c tetani adhere to host cells?

A

Fibronectin binding proteins
S-layer surface proteins (also help evade phagocytosis)
Peritrichous flagella - movement and attach

40
Q

What four things are used by c tetani to increase its damage?

A

Haemolysin III - pore forming
Tetanolysin - pore forming
Collagenase spread through deeper tissue
Tetanospasmin yassss

41
Q

Describe key characteristics of tetanospasmin

A

It is a type lll toxin. Has alpha beta sub units (KDa).

42
Q

What the lethal dose of this neurotoxin tetanospasmin?

A

2.5 nanograms per kilogram. Eg. 175ng will kill a 70 kg human. OMG RIGHT.
Second most potent toxin

43
Q

Describe the mechanism of action of tetanospasmin

A

Prevents inhibitory neurotransmitters gamma-aminobutyric acid (GABA) and glycine from being releases( spastic paralysis).
Organism release tetanospasmin in stationary phase, transport to CNS, peripheral NS via vasculature

44
Q

Describe the molecular weight and function of both the light and heavy chain of tetanospasmin

A

Heavy chain - carboxyl and amino group 100kda combined carry toxin to neurones. Carboxyl bind to the cell and amino group help the toxin get into the cell across membrane

Light chain - active part. Has activity in neurones. Destroy component synaptobrevin (proteolytic activity). Contain one zinc atom

45
Q

What happens to disulphides bridges inside neurones

A

Link heavy and light chain together. Inside neurone get refuge which frees light chain

46
Q

Describe normal MOA for muscle contractions before tetanospasmin

A

Neuron; vesicles dock via snare protein complexes (v-snare/T -share) and release Ach - muscle contract

Inhibitory interneuron - vesicles containing GABA/glycine dock via snare complex and release inhibitory neurotransmitters by exocytosis

47
Q

What is the vsnare

A

Synaptobrevin

48
Q

Describe tetanospasmin MOA

A

A subunit (light chain) cleaves synaptobrevin (v snare) and prevents DOCKING of INHIBITORY neurotransmitters vesicle to presynaptic membrane

V snare form snare complex with T snare on pre synaptic terminal
Permentant contraction

49
Q

What are two main symptoms of generalised tetanus (80% of cases) and what are other types (20%)

A

Lockjaw - trismus
Spascity in head and spinal column (opisthotonus)

20% - cephalic tetanus, localised tetanus, neonatal

50
Q

What is first symptom of general tetanus

A

Lockjaw or trismus.
Incubation period 8-12 days post puncture

Cannot eat, to swallow or speak
Result in risus sardonicus - sardonic smile

51
Q

Describe sardonic smile

A

Abnormal sustained spasm of facial muscle - appear lie grinning - raised eyebrows and open ‘grin’ - appear scary

52
Q

How is tetanus diagnoses

A

CLINICAL PRESENTATION and combo of below

  • PATIENT HISTORY - recent injury - 70% cases identify injury. Or incomplete tetanus immunization
  • specific symptoms progressive muscle spasms ( starting in facial region, especially lockjaw and progressing outward from the face to include all muscles of the body
  • non specific - fever, high BP, irregular heartbeat
53
Q

What is the 3 fold treatment objectives

A

1- limit growth via antibiotics - penicillin, metranidizol, gentomyocin to kill it
2- neutralise circulating toxin. : TIG - tetanus immunoglobulin
3- supportive measures - wound cleaning, valium, ventilator support

54
Q

How is tetanus prevented

A

VACCINE -toxoid (formaldehyde inactivated) given as part of childhood immunisation programme (DTaP); diphtheria, tetanus, pertussis (whooping cough) in 5 doses.

Primary course - given in arm or thigh to children aged 2,3,4 months
Fourth dose - 3 years and 4 months
Fifth dose - 13- 18 years

Booster - international travel e.g africa, asia to areas

MICROBIOLOGY II (9 decks)

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