Gram Positive Anaerobes

Question 1

Which gram positive anaerobes form spores?

Answer 1

Clostridium Species (Perfringens, Tetani, Botulinum, Difficile)

Question 2

What diseases can C.Perfringens cause?

Answer 2

Gas Gangrene
Intraabdominal infections
Food poisoning

Question 3

Describe the structural features of C.Perfringens

Answer 3

Gram Positive
Non Motile
Encapsulated
Spore Forming
Double zone hemolysis

Question 4

How does gas gangrene arise?

Answer 4

Requires injury/trauma -> spores and C.Perfringens get int and germinate -> effects via toxins

Question 5

What are the toxins of C.Perfringens?/

Answer 5

a-toxin: lecithinase ; PLC; lyses inflammatory cells and tissues

B-toxin: enteritis necroticans
i toxin: necrosis and vascular permeability
e-toxin: systemic vascular permeability

Question 6

What characteristic lesions are found in gas gangrene?

Answer 6

Bullae -> full of liquid -> will find gram positive box-car organisms but NO WBCs

Question 7

What is the clinical presentation of gas gangrene?

Answer 7

Rapid onset 
Necrosis of skin and muscle
Tense edema
Bullae
Gas formation => CREPITUS

Can lead to shock

Question 8

How is gas gangrene diagnosed?

Answer 8

Clinical setting and history

Gram stain/culture

Question 9

How is gas gangrene treated?

Answer 9

DEBRIDEMENT + Abx (Penicillin, B-lactam inhibitor)

Can also add Clindamycin to shut down toxin production while treatment given

Question 10

What causes C.Perfringens food poisoning?

Answer 10

Heat resistant spores survive -> produce enterotoxin after germination -> nausea, abd pain, diarrhea within 24 hours after ingestion

Question 11

How is C.Perfringens associated food poisoning treated?

Answer 11

Diagnosed clinically, no culture needed

Tx: Self limiting, just supportive therapy

Question 12

How are C.Tetani and C.Perfringens different?

Answer 12

C.Tetani:NO Gas gangrene

local germination without necroses

Question 13

What is the main toxin produced by C.Tetani and what does it do?

Answer 13

Tetanospamin- neurotoxin

Blocks post synpatic inhibition of spinal motor reflexes leading to uninhibited spasmotic contractions

Question 14

What do C.Tetani look like in culture and stain?

Answer 14

they LOOK gram neg but are GRAM POSITIVE

Look like mini tennis raquets

Question 15

What is the general clinical presentation of C.Tetani infection?

Answer 15

Trismus- lockjaw
Risus Sardonicus- inc tone of orbicularis oris
Opisthotonus: arm/leg flexion/extension
Respiratory- obstructioin due to diaphragm spasms

Question 16

How do we take care of pts with spastic contractions in C.Tetani infecitons?

Answer 16

Support with respiratory help and monitoring until synapses reform (it is a permanent inhibition) -> takes weeks to months

Question 17

How is tetanus diagnosed?

Answer 17

Clinical presentation

Question 18

How is tetanus treated?

Answer 18

Human tetanus Ig
Control spasms
Supportive airway

Question 19

How can tetanus be prevented?

Answer 19

3 doses of DPT for prophylaxis every 10 years

Passive immunity for people without previous vaccination

Question 20

Where is C.Botulinum commonly found?

Answer 20

Home canned foods

Question 21

How is botulism different from tetanus?

Answer 21

Botulism: we have paralysis (flaccid) rather than overstimulation/spasm

Question 22

What causes botulinum in adults?

Answer 22

Preformed toxin in contaminated foods

Question 23

What causes botulinum in children/infants?

Answer 23

Spores in honey that germinate once inside the baby

Question 24

What are the characteristics of the C.Boutlinum toxin?

Answer 24

Bacteriophage born
Blocks release of Ach at synapse - permanent damage!
Descending Paralysis
Heat labile

Question 25

How is the paralysis seen in botulinum different from that in Guillen Barre?

Answer 25

Botulinum: descending paralysis | Guillen Barre: Ascending paralysis

Question 26

What is the clinical presentaiton of botulism?

Answer 26

GI: nausea, dry mouth, diarrhea Flaccid Descending paralysis Wound Botulism: local paralysis

Question 27

How is botulism diagnosed?

Answer 27

Clinical history and presentation | Toxin Assay from serum, stool, food

Question 28

What is in the DDx of botulism?

Answer 28

``` Botulism Myasthenia Gravis Eaton Lambert Tick PAralysis Guillen Barre ```

Question 29

How can botulism be prevented./treated?

Answer 29

Avoid contaminated food Adequate heating of food Antitoxin Supportive

Question 30

Where is C.Diff infections mostly found?

Answer 30

Spores are acquierd in hospital

Question 31

What precedes C.Diff infections usually?

Answer 31

Antibiotic therapy | Just ingestion is not enough-> abx kills off normal flora-> C.Diff proliferates then

Question 32

What does Toxin A of C.Diff cause?

Answer 32

Enterotoxin: inflammatory response -> diarrhea

Question 33

What does Toxin B of C.Diff cause?

Answer 33

Cytotoxic effects

Question 34

What else can C.Diff cause besides diarrhea?

Answer 34

Diffuse hemorrhagic colitis | Pseudomembrane formation

Question 35

How is C.Diff clinically presented?

Answer 35

``` Diarrhea Pseudomembrane colitis Abd Pain Leukocytosis Fever Toxic Megacolon ```

Question 36

Why do we see leukocytosis with C.Diff?

Answer 36

Inflmmatory reaction in gut -> high white count

Question 37

What can happen with C.diff associated toxic megaocolon?

Answer 37

Dilation-> can lead to perforation and pt can die without intervention

Question 38

Which strain of C.Diff is associated with higher mortality and increased Toxin A production?

Answer 38

BI/NAP1 Strain: dominant strian in US

Question 39

How is C.Diff diagnosed?

Answer 39

ELISA: Detect toxin A in stool PCR: standard Sigmoidoscopy/Colonoscopy

Question 40

How is C.Diff treated?

Answer 40

Mild: Oral Metroinidazole, oral vancomycin Relapsing C.Diff: Fidaxemicin Fecal Transplat? Colon resection

Question 41

What are 2 other pathogenic clostridium species besides perfringens, tetani, botulinum, and difficile?

Answer 41

C.Septicum | C.Sordelli

Question 42

Describe Actinomyces

Answer 42

``` Non spore forming Gram positive rod Filamentous hyphae Forms sulfur granules Neg Acid Fast Slow growing ```

Question 43

How are actinomyces and nocardia different?

Answer 43

Nocardia: Acid fast positive, aerobic Actinomyces: Acid fast negative, anaerobic

Question 44

How are actinomyces presented clinically?

Answer 44

``` Orally associated (LOCK JAW) Cervicofacial ```

Question 45

How is actinomyces treated?

Answer 45

Penicllin: Clindamycin or Erythromycin

Question 46

What is propionobacterium acnes?

Answer 46

Slow growing anaerobe Opportunistic infections Found on prosthetic device or hardware Commonly contaminant in blood cultures

Question 47

What is the treatment for Propionobacterium acnes?

Answer 47

Penicillin NO METRONIDAZOLE

Question 48

Which species of bacteria are anaerobic gram positive cocci?

Answer 48

Peptostreptococcus

Question 49

Where is peptostreptococcus found?

Answer 49

Normal flora of mouth, GI, pelvis

Question 50

What can peptostreptococcal infections cause?

Answer 50

Brain abscess

Question 51

How is peptostreptococcal infections treated?

Answer 51

Debridement and penicillin