Gram Positive Bacilli

Question 1

Bacillus anthracis

Answer 1

Gram positive rods, non-motile/-fastidious/-hemolysic. Spores are resistant to heat/radiation/ disinfection. Produce medusa head colonies. Firmly adherent colonies. Spores can stay dormant for decades

Question 2

B. Anthracis Epidemiology

Answer 2

1º disease of grazing herbivores. No human to human transmission seen.

Question 3

Virulence of B. Anthracis

Answer 3

2 large plasmids account for all virulence (pXO2, pXO1)

Question 4

Unique characteristic of B. Anthracis

Answer 4

Polyglutamate capsule**

Question 5

Cutaneous Anthrax

Answer 5

Germination of spores occurs at inoculation site. Painful lymphadenopathy and lymphangitis. If becomes bacteremia, very lethal. Black eschar lesions and edema is typically presentation. No pain until later.

Question 6

Inhalational anthrax

Answer 6

aka Woolsorter’s disease. Carry spores to mediastinum lymphnodes. Leads to widening of mediastinum (Dx via chest x-ray), and pulmonary edema. Lung compression/septic shock are major causes of death.

Question 7

Intestinal anthrax

Answer 7

Very rare, but deadly. Ulcer. Acute inflammation and severe GI difficulty.

Question 8

Identification of B. Anthracis

Answer 8

Bicarbonate agar: induce capsule production. Non-hemolytic. Medusa-head colonies. “String of pearls.”

Question 9

Bacillus Cereus Characteristics

Answer 9

Large, facultative Gram positive rods (non-fastidious). Beta hemolytic on blood agar**

Question 10

Heat resistant B. Cereus

Answer 10

Emetic. Rapid onset

Question 11

Heat sensitive B. Cereus

Answer 11

Diarrheal. Slow onset

Question 12

B. Cereus Identification

Answer 12

Hemolysis on blood agar
Positive motility
NO string of pearls
No lysis by gama phage

Question 13

Clostridium

Answer 13

Anaerobic spore-formers. All gram positive. Part of normal colonic flora

Question 14

Most abundant Clostridium in colon

Answer 14

C. Ramosum

Question 15

Most common clostridia in tissue infection/bacteremia

Answer 15

C. Perfringens

Question 16

Characteristics of C. Peerfringens

Answer 16

Gram (+), anaerobic rod. More aero-tolerant. Serotype ‘A’ predominates in human fecal flora/in soil

Question 17

Pathogenesis of C. Perfringens

Answer 17

12 different toxins. Alpha toxin is associated with gas gangrene. Cause leukocyte aggregation at margin of tissue.

Question 18

C. Cellulitis

Answer 18

After surgery/trauma. Damage to arteries. Does NOT involve muscle.

Question 19

C. Myonecrosis

Answer 19

Gas gangrene. Requires emergency surgery and aggressive IV antibiotics. Very rapid growth of cell. More common in agricultural regions.

Question 20

Clinical presentation of C. Myonecrosis

Answer 20

Sudden excruciating pain, and gas bubbles. Crepitus and foul wound smell. Extensive hemolysis/shock/renal failure. Bacteria in tissues but NO inflammatory cells.

Question 21

C. Perfingens and food poisoning

Answer 21

2/3rd most common cause of food poisoning. Most pts recover on their own.

Question 22

C. Perfringens GI diseases

Answer 22

Necrotizing enteritis (ileum) and enteritis necroticans (jejunum). Caused but alpha and beta toxins. Found in Papua New Guinea after a pig feast with sweet potato (trypsin inhibitor).

Question 23

Septicemia and C. Perfringens

Answer 23

Myonecrosis and necrotizing enteritis. Correlate presence in blood with clinical findings**

Question 24

Nagler reaction

Answer 24

Addition of anti alpha toxin to cultures on egg yolk agar prevents visible opacity (lecithinase action of alpha toxin)=positive Nagler test. Indicative of C. Perfringens

Question 25

Clostridium Tetani

Answer 25

Spore forming/ Gram (+) rod. Strict anaerobe**. Immunization by D-Tap vaccine.

Question 26

Virulence of C. Tetani

Answer 26

Tetanospasmin. Plasmid encoded that is responsible for tetanus. Is a neurotransmitter. Blocks the release of GAMA and glycine, which inhibits muscle relaxation, causing muscle spasm.

Question 27

Generalized Tetanus

Answer 27

Most common clinical presentation. Lock jaw. Sardonic smile. Very common in neonates due to dirty umbilical cut.

Question 28

Identification of C. Tetani

Answer 28

Clinical presentation. Wound will have Gram (+) strict anaerobes. Terminal spores “Tennis racquet” (can look like botulinum, but is used for tetani for boards)

Question 29

C. Botulinum

Answer 29

Produces botulinum toxin responsible to botulism.

Question 30

Virulence of C. Botulinum

Answer 30

Toxin prevents ACh release(binds to vesicles), paralyzingly the muscle (flaccid paralysis). Requires regeneration of receptors.

Question 31

4 forms of botulism

Answer 31

Foodborn
Intestinal
Wound
Inhalation (terrorism)

Question 32

Foodborne botulism

Answer 32

Very limited cases. Canned food. Mild to severe symptoms. Blurred vision, constipation, abdominal pain, NO FEVER. Most die from respiratory paralysis

Question 33

Intestinal botulism

Answer 33

Mostly in infants. Spores germinate in GI tract. Symptoms: constipation/weak cry. Flaccid paralysis, respiratory arrest is possible. Honey is most common course.

Question 34

Inhalational botulism

Answer 34

Outbreak with no common source. Bioterrorist source.

Question 35

C Difficile

Answer 35

Gram (+) spore forming rode, strict anaerobe. Nosocomial infections. Almost always after antibiotic use. Elaborate 2 toxins (A:enterotoxin, B:cytotoxin).

Question 36

3 steps for C. Difficile infection

Answer 36

Exposure to antibiotics. Exposure to C. Diff with toxins, Inadequate immune response

Question 37

Pseudomembranous colitis

Answer 37

Punctate dirty yellow pseeudomembranse that may cover entire colon surface. Must use fecal donation for healthy flora