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Flashcards in Anaerobic bacteria Deck (54):
1

C tetani are what? How can it be introduced?

environmental, gram positive, and spore-forming; Think soil contamination of wounds like splinters, IV drugs, septic surgery, thorns

2

C tetani releases what? What are the four types of disease?

Exotoxin tetanospasmin;
1. neonatal
2. cephalic
3. local
4. generalized

3

Neonatal tetanus involves

contamination of umbilical cord and lack of materal immunization

4

Cephalic and local tetanus

both have low mortality so long as they remain local

5

In generalized tetanus, what happens to the exotoxin? What can lead to >50% untreated mortality?

It ENTERS THE BLOODSTREAM;
respiratory failure

6

In C tetani, the two subunits are

B and A, with B delivering A to end of motor neuron and A moves retrograde to CNS

7

The A subunit acts as what?

a protease, cleaving synaptobrevin in inhibitory motor nerves of the CNS

8

On C tetani exam, what are some hallmark features? Test that can demonstrate C tetani?

1. Local rigidity, difficulty swallowing
2. Strong muscle spasms/paralysis
3. Trismus (lockjaw)
4. Grimace (risus sardonicus)
5. Look for the STRONG ARCHING OF THE BACK!;
Spatula test: they bite down

9

Lab tests for C tetani include:

1. Microscopy with tennis racket appearance
2. Bloodwork can confirm vaccination and rule out STRYCHNINE POISONING

10

For C tetani treatment, this includes

tetanus antitoxin to neutralize the toxin;
could use antibiotics like metronidazole, but wound often clear on presentation;
maybe benzo!!

11

Prevention of C tetani includes

vaccination, with tetanus toxoid, while adults get boosters every 10 years; unvaccinated adults can get vaccine at any time

12

C botulinum is a; presents as; most common sources of C botulinum?

gram +, spore-forming, environmental bacteria; foodborne botulism;
alkaline vegetables like home-canned beans or if the spores survive inadequate sterilization of pre-prepped foods

13

C bot: Germinating cells infected by ____ phage release what?

lysogenic; botulinum toxins, with A and B being most common

14

For C botulinum, what happens to germinating bacteria and the bot exotoxin? How do bot and tetani differ once they arrive at a neuromuscular junction?

The germinating bacteria typically die;
bot tetani will stay in periphery and affect ACh release!!

15

A consequence of Bot pathogenesis is

flaccid paralysis and could affect respiratory system

16

Two less common presentations of Bot include

Infant botulism (kid is floppy and has uncooked honey) and wound botulism (wound contaminated in IV drug user)

17

On exam for bot, you would see in foodborne botulism

descending weakness and paralysis, and patient has history of suspect foods

18

For treatment of C botulinum what are you worried about? What is needed in wound botulism?

Horse-sourced antitoxin can inactivate toxin in bloodstream, which could lead to SERUM SICKNESS;
debride and high-dose IV penicillin

19

How to prevent C botulinum?

Cook adequately, sterilize the canned foods and vacuum-packed foods, and discard swollen cans!!

20

What can botulinum toxin A be useful for?

Cosmetics and blepharospasm (eyelid), writer's cramp, anal fissures and torticollis

21

C perfigrens is a

gram pos spore-forming rod that can lead to necrotizing fasciitis/myonecrosis

22

How does C perfringens enter? What can be seen on histology?

Serious wounds like war, car accident, septic abortion, where you disrupt blood flow;
Gas production!!!

23

C perfrigens can produce

alpha toxin with enzymes that break down tissue

24

On exam, C perfringens can show

1. Bronze skin color, then blue-black
2. maybe develops at site of malignancy
3. could see crepitation and tachy
4. Then ARDS, renal failure, shock!!

25

In C perfringens, what do you see on radiography, and what is needed to confirm myonecrosis?

Feathering pattern of gas in soft tissue;
SURGICAL EXPLORATION FIRST!!

26

To treat C perfrigens and prevent it?

Can give antibiotics like penicillin G and clindamycin, or clindamycin with metronidazole;
clean and debride the wounds!!

27

In C perfringens, besides gas gangrene, what can happen?

Food poisoning: inadqueate cooking fails to kill the bacteria and the spores grow up

28

For C perfringens poisoning, what area is affected?

Type A enterotoxin can destroy tight junctions between epi cells in gut

29

Tests, treatment and prevention for C perfringens food poisoning?

None required; DON'T STOP THE DIARRHEA;
Thorough cooking!!

30

C difficile is a ____ that causes what? How can it emerge?

Gram positive, spore-forming rod; pseudomembranous colitis;
fecal-oral or can come up in normal gut flora and spike in hospitalized pop (maybe antibiotic use)

31

What two toxins of C diff can cause issues?

Exotoxin A: disrupts tight junctions and causes intestinal swelling and inflammation
Exotoxin B: MAJOR TOXIN, disrupting cytoskeleton by depolymerizing acting, killing surrounding cells

32

On C diff exam, what could be seen?

Nonbloody cramping diarrhea; antibiotic use, chemo, or immunsuppressants in history;
patches of dead cells on sigmoidoscopy, maybe toxic megaolon or colonic perforation

33

Treatment of C diff?

1. Withdraw initial antibiotics
2. Unless disease is very mild, give oral metronidazole or vanco
3. LET TOXINS FLUSH
4. Maybe removal/surgical resection of colon

34

Bacteroides and prevotella are

gram-negative bacilli that are NON-SPORE forming; these guys are opportunistic pathogens that are in normal flora of mucous membranes

35

Treatment of B and P complicated by

1. slow growth (potential antibiotic resistance)
2. polymicrobial, so if one secretes beta-lactamase, whole abscess/colony protected from penicillin!!

36

Abscesses for B and P start off as ___ which use up the O2, followed by?

Facultative anaerobes; anaerobes

37

Diagnosis of B and P includes in the history:

Painful abscess that could move to meningitis (neck)

38

B and P are usually found

below the diaphragm if B, above if P

39

B and P can be diagnozed lab-wise via

needle aspiration (bypass normal flora and maintain anaerobic condition); MAKE SURE YOU CULTURE ON ANAEROBIC BLOOD AGAR; identify by sugar fermentation and gas chromatograpohy

40

Treatment and prevention of B and P includes

metronidazole primarily, and combine with aminoglycides to kills facultatives in abcesses, REQUIRES SURGICAL CARE;
perioperative cephalosporin

41

Actinomyces are

gram+ filmaentous rods, non spore-forming; anaerobitc to microaerophilic and normal flora of mouth, vag

42

Actinomyces pathology includes

bacteria escaping proper compartment during trauma; non-comm, with good prognosis

43

Presentations of actinomyces include:

1. Head/neck: pus drainage and hard, non-tender swelling in face, neck, chest; history of dental work, poor dental hygiene
2. Abdomen: slow-growing tumor and usually diagnozed on EXPLORATORY SURGERY

44

For actinomyces: you'll see on lab; treatment could include

branching Gram+ rods with sulfur granules; can be anaerobically cultured;
penicillin G with possible surgical drainage

45

SS: Anaerobic infections usually follow

deep-tissue trauma: accidents, cancer, surgery, immunosuppression, IV drug use

46

SS: For what is there a vaccine available?

ONLY TETANUS

47

SS: All of the anaerobes here are? What is gram pos and neg?

RODS;
Clostridia and actinomyces are gram pos, B and P are gram neg

48

SS: of the bacteria in this lecture, which are environmental, normal flora, both?

Environmental: C tetani, botulinum;
normal: C difficile, B and P, and actinomyces;
Both: C perfringens

49

SS: C tetani and botulinum produce

neurotoxins with same protease activity butopposite clinical effects because of nerves affected: tetanospasmin inhibitor CNS leads to spasms, botulinum toxin stimulatory on periphery, leading to flaccid paralysis

50

SS: Diagnosis of C tetani and botulinum includes; infection is usually; how do you treat? who is affected?

exam; the infection is usually transiet; treatment is primarily with ANTITOXIN to bind and inactivate neurotoxin; you would see this in neonates, IV drug users, infected wounds, botulism in contaminated food

51

SS: C perfringes in gas gangrene, B and P produce; how do you identify and treat? What's special about gas gangrene?

tissue-degrading enzymes;
identify by anaerobic culture and gas chromatography, treat with antibiotics plus surgical care; resolved ASAP: lethal exotoxemia

52

SS: C perfringens in food poisoning produces

enterotoxin: symptomatic treatment

53

SS: C difficile causes ____ after what? How to treat?

pseudomembranous colitis; antibiotic use;
often nosocomial, change antibiotic and intervene SURGICALLY as necessary

54

SS: Actinomyces produces ____ containing what? Where is it found and how do you treat?

nodules; pus with sulfur granules;
mouth or colon and treat with penicillin with surgical care as necessary