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CELL MICRO S1 > Endospore > Flashcards

Endospore Flashcards

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1
Q

which two are the main types of spore forming bacteria?

A

Clostridium and Bacillus

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2
Q

Bacillus oxygen requirements?

A

aerobic or facultative anaerobes

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3
Q

Clostridium oxygen requirements?

A

anaerobic

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4
Q

endspores are formed when?

what are the characteristics of endospores?

A
  • when NUTRIENT LIMITATION is reached
  • DORMANT
  • resistant to UV, HEAT, TOXIC CHEMICALS, IONISING RADIATION
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5
Q

what is the heat resistance of endospores used for?

A

selection

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6
Q

how do endospores stain?

A

variably

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7
Q

where do endospore formers generally live/habitat?

A

soil

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8
Q

in a spore what is the exosporium like?

A

thin delicate layer, mostly protein

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9
Q

in a spore what is the spore coat like?

A

multiple layers of spore specific proteins

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10
Q

in a spore what is the cortex like?

A

loosely packed peptidoglycan

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11
Q

in a spore what is the spore protoplast/ core composed of ?

A

normal cell wall
plasma membrane
cytoplasm and nucleoid

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12
Q

what are the properties of the core?

A
  • dipicolinate
  • dehydrated (10-30% of total water content of a vegetative cell)—> heat and stress resistance
  • cont Small Acid-Soluble Spore Proteins (SASPs)—> dry heat, dessication, UV resistance. also C source during outgrowth
  • more ACIDIC pH than vegetative cell
  • low metabolic activity (low O2 uptake)
  • no macromolecular synthesis
  • low enzymatic activity
  • low/absent mRNA synthesis
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13
Q

how are spores ACTIVATED (taken out of dormancy)?

A

1) heat shock-hours at 65°C

2) storage at low temp (4°C)

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14
Q

what happens when spores are activated and placed in favourable conditions?

A

GERMINATION

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15
Q

what are the 3 main stages of a spore?

A

1) ACTIVATION
2) GERMINATION
3) OUTGROWTH

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16
Q

Bacillus habitat?

A
  • mainly soil

- some parasites and pathogens

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17
Q

what disease does Bacillus anthracis cause?

A

agent of ANTHRAX

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18
Q

who does Bacillus anthracis cause disease of?

A

sheep, goats, cattle, transmissable to humans

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19
Q 
describe cutaneous anthrax 
who does it affect
where do spores germinate 
appearance
treatment
A
  • most common form
  • animal workers
  • spores germinate in akin abrasions
  • skin ulcer- BLACK eschar (can become systemic)
  • AB treatment, if no treatment 20% mortality
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20
Q

describe GI anthrax
cause
types

A
  • cause: undercooked contaminated meat

- types: abdominal (rare) & oral-pharyngeal (v rare)

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21
Q

describe pathogenesis of abdominal anthrax

A
  • spored germinate in lower GI tract

- causes PRIMARY INTESTINAL LESION

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22
Q

what are the symptoms of abdominal anthrax?
how does it cause death?
high/low mortality?

A
  • nausea
  • severe abdominal pain
  • vomiting
  • bloody diarrhoea
    DEATH: caused by ANTHRAX TOXEMIA (HIGH mortality)
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23
Q

what is the pathogenesis of pulmonary anthrax

A
  • spores inhaled
  • some spores mopped up by macrophages
  • others trafficked to the lymph nodes
  • GERMINATION in lymph (up to 60 days)
  • anthrax REPLICATE in lymph, causing disease (hemorrage, edema, necrosis caused by exotoxins released during replication)
  • CAPSULE inhibits phagocytosis
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24
Q

what are the symptoms of pulmonary anthrax?

A
  • flu like
  • fever
  • myalgia
  • cough
  • headache
  • vomiting
    -chills
  • abdominal pain
  • chest pain
    CYANOSIS and HYPOTENSION—> DEATH
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25
why is anthrax used in biological warfare?
80% MORTALITY (2-4 days) if ABs/no ABs | inhalational anthrax= 99% lethal in unvaccinated individuals
26
what virulence factors does Bacillus anthracis use?
``` CAPSULE - made of poly-D-glutamate polypeptide - smooth mucoid colonies - pX02 plasmid TOXIN- encoded on plasmid pX01 - consists of 1) PA (binding domain) 2) EF (Edema factor) 3) LF (Lethal factor) ```
27
how is Bacillus anthracis inf diagnosed?
- blood, skin lesions, respiratory secretions or by measuring specific antibodies in blood - G+ve rod, sometimes in chains - central (non- staining) spore occurs in soil and culture but not clinical samples
28
how is Bacillus anthracis inf treated?
penicillin, doxycycline, fluoroquinolones started early
29
how is Bacillus anthracis inf prevented? what are side effect rates like? who uses prevetative measures?
VACCINE- 3 types: Russian, UK, US. (Russian= inoculation with live spores= high side effects, UK/US=dead cell free prep of bacterial filtrates) - used for those at occupational exposure - from strain that lacks plasmid pX02 (capsule) - wool sterilisation from areas where anthrax is endemic
30
how predominant is Bacillus cereus?
one of the most abundant aerobic sporeformers in soil
31
what is the shape of Bacillus cereus colonies?
loosely spreading, may resemble fungi
32
what can Bacillus cereus cause? what is the short type type? symptoms? cause?
food poisoning 1) short incubation/emetic - 1-6 hrs after eating - nausea, vomiting, abdomina, pain - caused by heat stable enterotoxin (cannot be destroyed by cooking--->rice kept warm)
33
what can Bacillus cereus cause (long-type)? symptoms? cause? who does it affect?
2) long incubation/diarrheal - 6-18 hours after eating - diarrhoea - caused by enterotoxin that CAN be destroyed by cooking - toxin activates INTESTINAL ADENYLATE CYCLASE that causes intestinal fluid secretion - Bacilli found in stools - immunocompetent and compromised
34
oxygen requirements of Clostridia?
mostly onligate anaerobes, some aerotolerant
35
how do Clostridia metabolise?
fermentation
36
where are Clostridia found?
ub in nature, soil, water, intestinal tract of animals
37
how does Clostridia obtain nutrition?
they are SAPROPHYTES, involved in protein decomposition
38
how pathogenic are Clostridia? what is disease caused by in Clostridia?
- some pathogenic species | - disease caused by: production of highly toxic proteins
39
what is the shape of Clostridium barkeri spore? postioning?
oval, terminal
40
what is the shape of Clostridium botulinum spore? postioning?
oval, between centre and end
41
what is the shape of Clostridium tetani spore? postioning?
spherical, terminal
42
how does Clostridia obtain ENERGY (ATP)?
sub level phosporylation (no cytochrome system) - use wide variety of fermentable substrates - some ferment sugar producing end products (butyric acid, butanol, acetone)
43
describe the range of pathogenic Clostridia?
can REMAIN at site of inoculation: Tetanus not enter tissue at all: Botulism some use destructive enzymes to invade necrotic tissue HIGHLY powerful poisons
44
what does C.Botulinum cause?
Botulism
45
where is C.Botulinum found?
soil, water, decaying vegetation
46
how can C.Botulinum cause fatalities?
- ingest preformed toxin from food | - fatal food poisoning
47
who is commonly affected by C.Botulinum?
animals- from their feeds
48
which conditions cause toxin production in C.Botulinum ?
ANAEROBIC conditions may germinate spores---> vegetative cells---> prod toxin
49
where does C.Botulinum infect?
sometimes wounds - INFANT botulism from ingestion of spores in soil/dust (& germination in anaerobic intestine) - HONEY added to formula feed may contain spores
50
how is C.Botulinum diagnosed?
ELISA for toxin in suspected food injected into mice, culture attempted
51
how is C.Botulinum infection prevented?
as C.Botulinum produces a toxin and not a spore, toxin is HEAT LABILE O cooking inactivates is suspected case: ANTITOXIN es
52
which type of botox is used? what is botox used for?
Botulinum toxin type A | - treat patients with overactive muscles
53
C.tetani causes which disease?
tetanus
54
where is C.tetani found?
soil and intestines of animals | transiently in humans
55
what is the shape of the terminal spore of C.tetani?
drumstick shape (like the stick part of a lollipop?)
56
how does C.tetani enter the body? | how does this cause disease?
via a wound | wound prod necrotic cells, allows anaerobic conditions to develop, spores germinate and toxin produced
57
``` what are the 2 types of tetanus? describe cause source fatality rate ```
1) generalised 2) neonatal - if umbilical stump is infected (via soil or bindings containing spores) - lack of passive immunity from mother - high fatality (>200,000 deaths p/a)
58
describe the pathogenesis of tetanus
- toxin migrates via peripheral nerve axons to CNS (site of action) - symptoms take 3-21 days to develop, last 3-4 weeks - SPASTIC PARALYSIS- convulsive contractions of voluntary muscles (inc neck and jaw--->lockjaw) - DEATH: caused by respiratory muscle spasms 50% mortality
59
how does tetanus toxin cause uncontrolled muscle spasms?
- tetanus toxin binds to inhibitory neurones - inhibitory neurones fire but DON'T RELEASE GLYCINE O excitatory neurones have no opposition - causes muscle spasms
60
how is tetanus diagnosed?
usually by clinical picture BUT organism can be isolated: - look for G+ve, drumstick shape OR half spread agar plate with ANTITOXIN, will show HAEMOLYTIC TOXIN PRODUCTION
61
how is tetanus prevented? | what about following injury?
vaccination- DPT cont formalin-inactivated toxin has 100% efficacy following injury: given tetanus IMMUNOGLOBINS but mortality is 20-30%
62
what disease does C.perfringens cause? | how?
gas gangrene | -caused by contamination of wounds w/ Clostridia spores
63
where is C.perfringens found normally?
GI and vagina flora
64
C.perfringens can grow in which conditions?
anaerobic (deep necrotic wounds w/ reduced blood supply)
65
what happens to C.perfringens after germination?
- secrete exotoxin (causes tissue damage & spread of organism) - carbohydrate may be fermented---> large quantities of gas(smell)--->constriction of blood vessels
66
what kinds of things can cause gas gangrene?
- surgery - battlefield casualties - motor vehicle crashes - farm injuries - post-abortal sepsis
67
how is gas gangrene diagnosed? on which media? what do we look for?
1) clinical picture---> smell 2) X-ray---> gas but to be DEFINITIVE: need 3) ISOLATION AND IDENTIFICATION - Robertsons meat media - blood agar (incubate anaerobically) look for LARGE G+ve rods, RANCID smell on meat media
68
how can egg yolk medium be used to test for C. Perfringens?
LECITHIN in egg yolk medium is HYDROLYSED if ALPHA TOXIN is produced ---> opaque area around colony - can be neutralised by ANTITOXIN ANTIBODY---> Nagler reaction
69
how is gas gangrene prevented?
proper cleaning of wounds
70
how is gas gangrene treated?
ABs have little effect on necrotic areas | SURGERY may be required to remove affected parts
71
other than gas gangrene, what else can C.perfringens cause?
food poisoning | ENTEROTOXINS are produced
72
which disease does C.difficile cause?
Pseudomembraneous colitis
73
how is a C.difficile infection diagnosed?
ELISA test for toxins A and B in stools
74
how is C.difficile infection treated?
stop the causative AB therapy - anti diarrhoea drugs - Metronidazole and Vancomycin
75
what causes Pseudomembrane Colitis?
after AB therapy
76
what does Psudeomembranous Colitis cause?
diarrhoea
77
how common is C.difficile infection?
most common nosocomial GI infection
78
what are the 2 major types of toxin in C.difficile?
toxin A- 308kD ENTEROtoxin toxin B- 269kDa CYTOtoxin both stimulate the production of PROINFLAMMATORY CYTOKINES--->imp in pathogenesis of pseudomembranous colitis

CELL MICRO S1 (16 decks)

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