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Flashcards in Anaerobes Deck (42):
1

Spore-forming: rod, Gram (+) anaerobe?

Clostridium

2

Non spore forming Rod Gram neg that we talked about?

Bacteroides
Campylobacter (gullian barre)

3

The clostridia are opportunistic pathogens. Nonetheless, they are responsible for some of the deadliest diseases including?5

gas gangrene, tetanus and botulism, pseudomembranous colitis (c. difficile) and food poisoning.

4

HOw do the clostridium spieces cause disease primarily?

What are the 4 main subtypes?

cause disease primarily through the production of numerous exotoxins.

Subtypes include
perfringens, tetani, botulinum, difficile

5

What are the two places of C. tetani found?

Are the spore forming?

Ubiquitous in soil, it is occasionally found in intestinal flora of humans and animals

Spore forming

6

Morphology of C. tetani?

Culture?

Biochemical activity?

Resistance?

Classification?

long and slender; flagella, no capsule, terminal located round spore(drum-stick appearance).

Culture: obligate anaerobic; Gram(+); swarming occurrs on blood agar, faint hemolysis.
Biochemical activities: does not ferment any carbohydrate and proteins.
Resistance: tolerate boiling for 60 min. Live for several years in the soil.
Classification and Antigenic Types: C. tetani is the only species. There are no serotypes

7

C. tetani produces two exotoxins. What are they?

tetanolysin, and tetanospasmin(a kind of neurotoxin, toxicity strong)

8

The actions of tetanospasmin are complex and involve three components of the nervous system?

central motor control, autonomic function, and the neuromuscular junction.

9

How does tetani transport to the CNS?

How long do symtpoms last?

retrograde transport to (CNS)

a few days to several weeks

10

Tetanospasmin, a toxin of Clostridium tetani, binds to ganglioside receptors which are what?

This prevents the release of what?

This all together causes what?

inhibitory neurons in the CNS (keeps sending signal to contract)

the neurotransmitter glycine
(inhibitory neurotransmitter)

spastic paralysis
-severe muscle contractions and spasms
-can be fatal
CONTINUOUS STIMULATION

11

WHat are the initial symtpms of tetanus? 3


What wont the patient have?

1. ramping and twitching of muscles around a wound. The patient usually has no fever but
2. sweats profusely and begins to experience
3. pain, especially in the area of the wound and around the neck and jaw muscles (trismus).

12

What is a spasm in which the head and heels are bent backward and the body bowed forward?

opisthotonos

13

Comlpications from tetanus?
5

1. fractures,
2. bowel impaction,
3. intramuscular hematoma, 4. muscle ruptures, and
5. pulmonary, renal, and cardiac problems

14

Where does neonatal tetanus often originate from?

umbilical stump;very poor prognosis in infants whose mothers are nonimmune

Cutting the umbilical cord with dirty instruments

15

HOw do we diagnose tetani?

What else should we consider in the diagnosis?
2

the clinical symptoms. The wound may not be obvious.


rabies
menigitis

16

How should we control the symptoms and spread of a pt with tetanus?
4

1. Debridement of the wounded area
2. Antibody
3. Metronidazole
4. booster or vaccine

17

What does C. perfringens cause?

gas gangrene
-swelling of tissues
-gas release
*fermentation products

18

Where do you acquire C. perfringens?

soil or fecal contamination

19

Pathogenesis of C. perfringens?
5

1. Tissue degrading enzymes
2. Destruction of blood vessels
3. Tissue necrosis
4. Anaerobic environment created
5. Organism spreads

20

What are the tissue degrading enzymes that C. perfrongens produces?

What do these do?
2

lecithinase [ toxin]
proteolytic enzymes
saccharolytic enzymes

Toxin necrotizes tissue
Then enzymes ferment carbs that results in the release of gas (bubbling).

21

Which treatment how quickly does death occur in gas gangrene?

How should we treat gas gangrene?
3

2 days

1. effective antibiotic therapy
2. debridement
3. anti-toxin
amputation & death is rare

22

C. perfringens is an anaeriobe. What allows it to infect the human body?

Initial trauma to host tissue damages muscle and impairs blood supply----lack of oxygenation

The anaerobe then grows there and continues to spread through the toxin and gas release.

23

IN gas gangrene, as capillary permeability increases, the accumulation of fluid does what?

increases, and venous return eventually is curtailed.

24

C. Botulism:
Aerobic or Anerobic?
Gram + or -?
Shape?
Spore former or not?

What does it produce?

Where is it found?
2

Anaerobic
Gram-positive
rod-shaped
sporeformer


produces a protein neurotoxin

1. soil, sediments of lakes, ponds, decaying vegetation
2. intestinal tracts of birds, mammals and fish

25

How is botulism transmitted?

Why are the spores so dangerous?

Whats the usual cause of death with botulism?
2

Canning
Eating uncooked foods

Heat resistant, not easily killed


Respiratory paralysis
Second is cardiac failure

26

Pathogenesis of botulism?
2

1. binds peripheral nerve receptors
--acetylcholine neurotransmitter
2. inhibits nerve impulses resulting in flaccid paralysis

27

Clinical syndromes
of botulism:
Onset?
Symptoms?4

18-36 hours:

--weakness, dizziness,
--dryness of the mouth.
---Nausea,vomiting.
---Neurologic features

28

What are the neurological features of botulism?
5

1. blurred vision,
2. inability to swallow,
3. difficulty in speech,
4. descending weakness of skeletal muscles,
5. respiratory paralysis.

29

What is the most common kind of botulism and what is it caused by?

Neonatal botulism
-no normal flora to compete
Causes of spores being in fresh honey

30

How do we diagnose botulism?

Whats the most direct and effective test used for botulism?

by clinical symptoms alone

serum or feces tests

31

Treatment for botulism?
2

1. Individuals known to have ingested food with botulism should be treated immediately with antiserum.
2. If a wound infection, treat with anitbiotics. (not in found bourne kind)

32

Describe the path of infection for C. difficile?
5

1. After antibiotic use
2. Intestinal normal flora --greatly decreased
3. Colonization occurs
4. Enterotoxin secreted
5. Pseudomembanous colitis

33

Pseudomembranous colitis (PC) results predominantly as a consequence of what?

What do symtpoms include? 3

What can be observed by colonoscopy?

elimination of normal intestinal flora through antibiotic therapy.

abdominal pain with a watery diarrhea and leukocytosis.

"Pseudomembranes" consisting of fibrin, mucus and leukocytes can be observed by colonoscopy.

34

Therapy for C. Difficle?
2

Discontinuation of initial antibiotic (e.g. clindamycin)

Specific antibiotic therapy (e.g. vancomycin)

35

Problems in identification of
anaerobic infections?
3

1. air in sample (sampling, transportation)
no growth

2. identification takes several days or longer
limiting usefulness

3. often derived from normal flora
--sample contamination can confuse

36

Most pathogenic anaerobes are usually what kind of bacteria?

1. commensals
Originate from our own flora

37

Predisposing conditions from for anaerobic infections?
4

1. Breeches in the mucocutaneous barrier
→ displace normal flora
2. Compromised vascular supply
3. Trauma with tissue destruction
4. Antecedent infection

38

Synergistic Mixture of Aerobes & Anaerobes usually in anaerobic infections. Give an example

E. coli → Consume O2
Allow growth of anaerobes

39

What do anaerobes promote the growth of other bacteria by being what?2

1. being antiphagocytic and 2. producing B-lactamases

40

Clues to Anaerobic Infection
6

1. Infections in continuity to mucosal surfaces
2. Infections with tissue necrosis and abscess formation
3. Putrid odor
4. Gas in tissues
5. Polymicrobial flora
6. Failure to grow in the lab

41

Major disease causing strict anaerobic growth after abdominal surgery?

Bacteroides fragilis

42

What is different about Bacteroides fragilis compared to other species of anaerobes?

What makes it really virulent?3

non-spore-former

- Prominent capsule
- anti-phagocytic
- abscess formation