Bacilus

Question 1

Bacilus gram stain

Answer 1

Gram positive

Question 2

Bacilus oxygen requirements

Answer 2

Aerobic or facultatively anaerobic

Question 3

Bacilus spore formation

Answer 3

Form endospores

Question 4

Bacilus location

Answer 4

Ubiquitous: soil, water, airborne dust

Question 5

Bacilus transmission

Answer 5

Inhalation of spores, zoonotic (infected animals and human contact)

Question 6

Bacilus motility

Answer 6

No motility (no flagella)

Question 7

Bacilus anthraxis capsule

Answer 7

Capsule made of glutamic acid (polypeptide)—> typically only seen in cultured organism in specific media/ under very specific conditions

Question 8

Bacilus anthraxis hemolysis

Answer 8

NONhemolytic

Question 9

Bacilus anthraxis morphology

Answer 9

Long, smaller chains

Question 10

Bacilus anthraxis virulence factors (2)

Answer 10

Capsule and 3 exotoxins
— edema factor
— protective antigen
— lethal factor

Question 11

Bacilus anthraxis capsule

Answer 11

Made of glutamic acid, anti-phagocytic, antibodies to capsule are not protective to host

Question 12

Bacilus anthraxis exotoxins

Answer 12

1. Edema factor 2. Protective antigen 3. Lethal factor. Mediated by temperature sensitive plasmid: individually nontoxic but lethal when combined
   Protective antigen + edema factor= edema toxin
   Protective antigen + lethal factor= lethal toxin

Question 13

Bacilus anthraxis protective antigen

Answer 13

Reacts with host cell tissue receptors where it is cleaved (leaves small fragment) multiple PA fragments associated to form a pre-pore. LF or EF bind then, and can enter the cell (LF binds= triggers cell death. EF binds= increases cAMP levels to cause edema (^^ cytosolic fluid content)

Question 14

Bacilus anthraxis epidemiology quick facts

Answer 14

Rare in US, spores can be dormant/ infectious for decades

Primarily a disease for herbivorous animals

Question 15

Bacilus anthraxis— how do humans acquire?

Answer 15

Direct contact with animal products (wool/hair)

Inhalation and/ or ingestion of spires (increased mortality with these forms of entry)

Question 16

3 types of Bacilus anthracis diseases

Answer 16

1. Pulmonary anthrax (Woolsorter’s disease)
2. Intestinal anthrax (ingestion of spores)
3. Cutaneous anthrax

Question 17

Pulmonary anthrax (woolsorter’s disease)

Answer 17

Inhalation of spores— virtually 100% fatality. Spores germinate, bacteria multiplies and causes fatal septicemia or meningitis
May have prolonged latent period (>2months) followed by rapid onset
— sepsis with a fever, edema, swollen lymph nodes, but NOT pneumonia

Question 18

Intestinal anthrax

Answer 18

Very rare, but Virtually 100% fatal- causes abdominal pain, ulcers at site of invasion, swelling of lymph nodes, edema, sepsis, nausea and vomiting. Hemorrhagic ascites (fluid in abdominal cavity). Testing this fluid (paracentesis) may reveal gram+ rods

Question 19

Cutaneous anthrax

Answer 19

95% of human cases. Symptoms 1-5 days after contact. Small itchy (pruritic), non-painful papule at inoculation site. Develops into hemorrhagic vehicle and ruptures. Slow healing painless ulcer covered with black Escher (piece of dead tissue cast off from surface of the skin) 20% mortality if left untreated (septicemia if spread to lymph)

Question 20

Bacilus anthraxis vaccine?

Answer 20

Yes, but only available to military and important people. Unpleasant to be administered…

Question 21

Bacilus anthraxis diagnosis:

Answer 21

Morphology (microscope): large, nonmotile gram+ bacilli in samples. PCR can confirm. Colony morphology: gray-white colonies w/ irregular margins and coarse texture.

Question 22

Bacilus cereus spores

Answer 22

Yes, spore forming

Question 23

Bacilus cereus oxygen requirements

Answer 23

Facultative anaerobe

Question 24

Bacilus cereus hemolysis

Answer 24

Most strains are betahemolytic

Question 25

Bacilus cereus epidemiology

Answer 25

Ubiquitous soil bacterium- usually arise from contact with contaminated soil (or hospital acquired)

Question 26

Bacilus cereus virulence factors (4)

Answer 26

1. Heat stable enterotoxin
2. Heat labile enterotoxin (necrotic toxin)
3. Cerolysin/ hemolysin
4. Phospholipids C- cleaves phospholipids (lecithinase) frees itself from phospholipid-membrane bound vesicles/ cells

Question 27

Bacilus cereus emetic GI disease

Answer 27

(Nausea, vomiting, abdominal cramps) caused by heat STABLE enterotoxin (intoxication- no bacteria present/required)
— acute onset (1 to 6 hours) and short duration (<24 hours)
— common source is contaminated rice

Question 28

Bacilus cereus diarrheal GI disease

Answer 28

Diarrhea, nausea, abdominal cramps. Caused by heat LABILE enterotoxin. True infection (bacteria present/ associated) delayed onset (>6hrs) and longer duration (>1day)
— contaminated meats, vegetables and sauces

Question 29

Bacilus cereus ocular disease

Answer 29

Infection resulting from trauma (penetration) to the eye
— keratitis, and tissue damage due to cereolysin and phospholipase C
— inflammatory response causes further damage

Question 30

Other Bacilus cereus infections:

Answer 30

1. Infections associated with indwelling units
2. Rare/extreme case of endocarditis
3. Pneumonitis, bacteremia, meningitis, anthrax-like-pneumonia (all in severely immunocompromised patients)

Question 31

Bacilus cereus diagnosis

Answer 31

Isolation of colonies from wound or food substance
Gram stain (gram positive)

Question 32

Bacilus cereus treatment

Answer 32

GI: relief of symptoms (hydration)
Ocular: vacomycin, clindamycin or ciprofloxacin and romval of foreign object if present