Musculoskeletal System: Lec.3 - Anerobes

Front 1

Musculoskeletal System:
Lec.3 - Anerobes

Back 1

Musculoskeletal System:
Lec.3 - Anerobes

Front 2

Q3:

Anerobic growth requires what?

Back 2

- Low oxidation-reduction potential
- absence of oxygen

Front 3

Q3:

a high pH corresponds to a ...redox potential?

Back 3

low

Front 4

Q3:

list the redox potential for the folowing locations
-Oxygen electrode
-hunam cell
-venous blood
-periodontal pocket
-dental plaque
-colon

Back 4

-Oxygen electrode (815mv)
-hunam cell (240)
-venous blood (185)
-periodontal pocket (-50)
-dental plaque (-200)
-colon (-300)

Front 5

Q3:

Most anerobe lack what enzymes?

Back 5

- Superoxide dismutase
- catalase
- perodidase

Front 6

Q3:

what are the most common type of infection?

Back 6

polymicrobic

Front 7

Q3:

anerobic bacteria are generally non- communicable, except what?

Back 7

-CDIFF

Front 8

Q3:

What are some suggestive findings of anaerobic infections?

Back 8

- foul smalling
- necrotic tissue with gas
- black discoloration of blood containing exudate
- organism fails to grow aerobically
- mucosal surfaces
- DM
- Human or animal bites
Severe traumas (from soil infection)

Front 9

Q3:

How are specimines collected?

Back 9

- aspirate pus
- specimines can not be collected from the following locations for anerobes (due to local floura)
- throat swabs
-NG swabs
- Sputum
-Bowel contents
-Vaginal swabs

Front 10

Q3:

Do anerobic organisms require any special media for culturing?

Back 10

- yes, Kanamycin-vancomycin agar
-reduced anaerobic blood agar
- thioglycolate broth
- most are slow growing 48hrs
- require anerobic conditions

Front 11

Q3:

Describe Bacteroides fragalis

Back 11

- lightly staining
- Gram (-) rods
- grow rapidly and are stimulated by bile
- normal habitat in the human gut
- about 75% have a capsule
- frequent infections GI Abscess, PID
(the GI, and pelvis are fragrant)

Front 12

Q3:

Describe,
Prevotella (Bacteriodes) melaninogenicus

Back 12

- Gram (-) coccobacilli
- "brick red" flourescence under woods lamp
- oral flora (low numbers in GI tract)
- frequent infections: Oral and Brain Abscesses, lung abscesses, female genital tract abscesses

Front 13

Q3:

Treatment of bacteroides?

Back 13

- debridement and drainage in cellulitis and severe abscesses
- Drug of choice:
metroidazole or clindamycin
(resistant to tetracyclines)
(Beta lactamase producers)

Front 14

Q3:

Describe
Fusobacterium nucleatum

Back 14

- Gram (-) long slender filaments
- normal habitat: oral and sometimes stool
- infections: Head, neck and chest infections; may synergize with oral spirochetes resulting in ulcerating necrotizing gingivitis known as "vincent's angina" or "trench mouth"
(nuclea...r - slender like a cooling rod, people in the trenches are there to prevent nukes, one of their names is vincent)

Front 15

Q3:

Describe,
Peptostreptococcus and other anerobic streptococci

Back 15

- normal habitat: Mouth or stool
- synergistic infections, brain abscesses, head infections, ect.

Front 16

Q3:

What kinds of infections are most common?

Back 16

mixed infections

Front 17

Q3:

Describe,
Actinomyces israelii

Back 17

- Gram (+) branching rods
- Produce sulfur granules in abscesses and culture
- only pathogenic actinomycete that is anerobic
(Israel is a positive government with lots of branches, there is yellow sand there, and they can cause damage)

Front 18

Q3:

What are the general characteristics of gram (+) spore formers?

Back 18

- Often infection is exogenous
- most pathology is due to toxins
- Toxemia may arise from ingestion of toxins, or from localized infection with release of toxins into the bloodstream
- site must be low redox potential

Front 19

Q3:

Describe,
Clostridium perfringens

Back 19

- Habitat: GI and Soil
- disease: cellulitis and Myonecrosis (gas gangrene), food poisoning
- Virulence factors: Exotoxins (Alpha toxin), some other toxins have hemolytic, cytotoxic, and necrotic effects.

Front 20

Q3:

Gas Gangrene (myonectosis)

Back 20

- Clostridium perfingens infection
- usually following severe trauma
- organism utilized glycogen --> gas, edema, impaired circulatoin --> vascular destruction and lactic acid buildup lowers redox potential --> cellulitis -->myonecrosis --> shock and renal failure (fatal in 30%)

Front 21

Q3:

What are some diagnostic signs of C.perfinges?

Back 21

- gram (+) "box car like" rods
- Culture: distinctive double zone of hemolysis

Front 22

Q3:

What is the treatment for cellulitis and myonecrosis?

Back 22

- debride wound
- DOC: PCN & Clindamycin

Front 23

Q3:

What is the treatment for food poisioning, as a result of C.perfingens?

Back 23

-Self Limiting without treatment

Front 24

Q3:

Describe Clostridium tetani

Back 24

- Gram (+) motile rod w/ terminal spores
- Habitat: Human GI tract
- Clinical disease: tetanus

Front 25

Q3:

Mechanism of tetanospasm?

Back 25

Tetanospasm, suppresses neurotransmitters (GABA) and therefore signals are unopposed and muscles are constantly stimulated to contract

Front 26

Q3:

Treatment for tetanus?

Back 26

- antitoxin
- debride tissue of wound
- DOC: PCN
- Support Pt.
- Tracheostomy
- Quiet dark external environment

Front 27

Q3:

What are some preventative treatments for tetanus?

Back 27

- DTaP
- Tetanus booster every 10yrs

Front 28

Q3:

Describe,
Clostridium botulinum

Back 28

- Gram (+) rod
- It is an anaerobic spore-former, which produces oval, subterminal endospores and is commonly found in soil.
- produces the neurotoxin botulin

Front 29

Q3:

Virulence factors for C. botulinum

Back 29

- Potent neurotoxin (8 antigenic types)
- (types A, B, and E cause human disease)

Front 30

Q3:

Describe Botulism in the adult

Back 30

- Nausea, vomiting, dizziness cranial palsy, double vision, swalling difficulties → respiratory paralysis and death

Front 31

Q3:

Describe Botulism in the child

Back 31

- Ingestion of spores → exotoxin → constipation and generalized weakness (floppy baby syndrome)

Front 32

Q3:

Mechanism of Botulinum toxin?

Back 32

- Toxin prevents the release of acetycholine from the alpha-motor neuron → muscle cannot receive signal → flaccid paralysis

Front 33

Q3:

Describe,
Clostridium Difficile

Back 33

- Clinical Disease: pseudomembraneous colitis
- Virulence factor: Toxin A (enterotoxin), Toxin B (Cytotoxin)
- Diagnosis: CDIFF Toxin assay

Front 34

Q3:

What is the treatment for C. difficile?

Back 34

- DOC: Metronidazole (Vancomycon)

Front 35

Q3:

What is the mechanism of C.diff. infection?

Back 35

- toxin A (enterotoxin) → fluid production and mucosal damage and

- toxin B (cytotoxin) → kills mucosal cells