Test 2 Bugs 1 Part 2/2

Question 1

Define Endospores:

Answer 1

• Metabolically inert and antibiotic resistant.
  
  • Allows survival in adverse conditions.
• Calcium dipicolinate dehydrates nucleic acids.
• Keratin coat protects.
• Need an autoclave to kill spores.
• Limited carbon or nitrogen triggers sporulation.

Question 2

Bacillus anthracis traits

Answer 2

• Aerobes & facultative anaerobes
• Catalase: Positive

Question 3

Three types of Bacillus anthracis infections?

Answer 3

• Cutaneous
• Gastrointestinal
• Inhalation

Question 4

Cutaneous anthrax details

Answer 4

• Most human cases
• Hazard for work with hooved animals, their skins or wools.
• Process:
  
  • Traumatic Spore impantation
  • Papule
  • Raised red lesion
  • Painless, black, necrotic eschar with a red, rolled edge.
• Edema + Lymphadenopathy.

Question 5

Gastrointestinal anthrax details.

Answer 5

• Rare
• Spores in contaminated meat
  
  • GI ulcers + edema.
• Nausea, fever, abdominal pain, vomiting blood, and diarrhea.

Question 6

Inhalation anthrax details:

Answer 6

• Woolsorter’s disease
• Rapid, hemorrhagic lymphadenitis and pneumonia.
• Exotoxin ⇢ lymph node hemorrhage and edema, hemorrhagic mediastinitis, pulmonary edema, and hemorrhagic pleural effusions. A widened mediastinum is a critical diagnostic feature.

Question 7

How does Bacillus anthracis to inhibit phagocytosis?

Answer 7

Poly-D-glutamate capsule

Question 8

Anthrax toxin:

Protective antigen (PA)

Answer 8

Binds to cells and facilitates entry of lethal factor and/or edema factor.

Question 9

Anthrax toxin:

Lethal factor (LF)

Answer 9

Metalloprotease of MAP kinase (needed of cell signaling, cell division and differentiation) → cell death.

Question 10

Anthrax toxin:

Edema Factor (EF)

Answer 10

• Calmodulin-activated adenylate cyclase that increases cAMP (changing membrane permeability).
• Cell water loss → pulmonary/other edema.

Question 11

Anthrax Toxin details

Answer 11

• Three types:
  
  • Protective antigen (PA)
  • Lethal factor (LF)
  • Edema factor (EF)
• Non-toxic individually but form important toxin when combined.
  
  • PA+LF = Lethal Toxin
  • PA+EF = Edema Toxin

Question 12

Treatment and prevention of B. anthracis

Answer 12

• Prevention:
  
  • Vaccination of animal proper disposal of infected.
  • Human Vaccination is limited to those at risk.
• Treatment
  
  • Prompt treatment with amoxicillin if penicillin sensitive.
    
    • Otherwise use Ciprofloxacin

Question 13

Bacillus cereus natural environment

Answer 13

Ubiquitous soil organism found in grains, vegetables, and dairy products.

Question 14

Bacillus cereus details:

Answer 14

• Most common pathogenic bacilli
• B. cereus food poisoning
  
  • Emetic form
    
    • heat-stable enterotoxin ingested in reheated foods.
    • Rapid onset: 1 to 5 hours after eating toxin-contaminated food.
  • Diarrheal form
    
    • Heat-labile enterotoxin produced by bacteria multiplying in the GI tract following ingestion of contaminated food.
    • Slow onset: 10 to 15 hours

Question 15

Listeria: Listeria monocytogenes traits

Answer 15

• Tumbling motility
• Facultative anaerobes
  
  • Grow in:
    
    • Acid
    • High salt
    • Cold temps
• Grow in cell lining of GI or inside macrophages.
  
  • Poor CMI (Cell mediated immunity)

Question 16

Listeria

In adults:

Answer 16

Often from contaminated food (undercooked meat, unwashed vegetables, un-pasteurized milk.

Question 17

Listeria

In neonates:

Answer 17

Transplacental or vaginal transmission.

Question 18

Treatment for listeria?

Answer 18

Ampicillin

Question 19

Two results of Listeria infection in adults?

Answer 19

• Mild gastroenteritis in the summer.
  
  • Some people remain fecal carriers
• Meningitis in immunocompromised (Most common)
  
  • Renal transplant
  • Newborns
  • Pregnant women
  • those >65 yrs.

Question 20

Two forms of Neonatal listeriosis?

Answer 20

• Granulomatosis infantiseptica: severe in utero infection from Listeria
  
  • Most babies are stillborn or die soon after birth.
• Late-onset disease: Acquired at or soon after birth by contact with contaminated body fluids of infected mother.

Question 21

Listeria monocytogenes

Immune avoidance:

Answer 21

• Ingest L. monocytogenes → intestines → uptake into epithelial cells.
• Listeriolysin forms pores and escapes phagosome before fusion occurs.
• Multiplies in cells with poor CMI.

Question 22

What are the 4 types of Clostridium and their associated toxins?

Answer 22

1. C. tetani (tetanus)
   
   1. Tetanus toxin (tetanospasmin)
2. C. perfringens (wound infection, food poisoning)
   
   1. Alpha toxin
3. C. botulinum (botulism)
   
   1. Botulinum toxin
4. C. difficile (diarrhea after antibiotic use)
   
   1. Toxin A = an enterotoxin
   2. Toxin B = a cytotoxin that induces depolymerization of actin & cell cytoskeleton loss.

Question 23

Effect of Tetanus toxin

Answer 23

Blocks the release glycine + GABA, which inhibit motor nerve impulses, resulting in spastic paralysis.

Question 24

Effect of Alpha Toxin

Answer 24

Fermentation of muscle carbohydrates which produces gas.

Question 25

Effect of **Botulinum toxin**

Answer 25

Acts on myoneural junctions, blocking the release of acetylcholine → **flaccid paralysis.**

Question 26

Effect of Toxin A and B.

Answer 26

* Toxin A: Mucosal injury and hemorrhagic necrosis. * **Toxin B**: Cytotoxin, that induces depolymerization of actin and cytoskeleton loss.

Question 27

C. tetani Infection

Answer 27

* Paralysis begins in jaw (trismus/lock-jaw, risus sardonicus) and descends into large muscle groups (back arching). * Death from paralysis of throat & respiratory muscles.

Question 28

C. tetani Prevention and treatment

Answer 28

* **Vaccines:** Tetanus toxoid vaccines DTaP, Tdap, DT, Td. * **Treatment:** Wound debridement * Metronidazole; tetanus immune globulin * Benzos or neuromuscular blockers until toxin wears off.

Question 29

C. perfringens Infections

Answer 29

* Wound infection: results in **Gas gangrene** (anaerobic cellulitis), clostridial myonecrosis. * **Food poisoning**: watery diarrhea, **late onset 8-24 hrs** after ingestion. No vomiting. Resolves in 24h. * Since toxin is not preformed such as in S. aureus/ B. cereus, onset is delayed.

Question 30

C. botulinum Infection

Answer 30

* **Foodborne botulism**: * Produced in poorly canned vegetables. * 12-48hrs after meal. * **Neurological**, not GI * **Infant botulism** * **Spores ingested** in dust or **honey.** * Results in **Floppy baby syndrome**. * **Wound botulism**: similar to food botulism. * **Treatment:** * Antitoxin blocks circulating toxin, but cannot effect that already in the nerves.

Question 31

C. difficile Infection

Answer 31

* Environmental - spores transferred to patients. * Endogenous ~5% of adults carry it. * Anti-biotics allow it to overgrow other bacteria. * Pseudomembrane formation (white-yellow plaques). * **Treatment:** Metronidazole; oral vancomycin * Stool transplant or surgery in severe cases.

Question 32

Corynebacterium diphtheriae Details

Answer 32

* Catalase: positive * aerobic * Human is reservoir host. * Can be grown on **Loeffler coagulated serum medium; tellurite medium.** * Spread: Respiratory droplets or skin contact.

Question 33

Cornebacterium diphtheria: explain how while normally present can turn pathogenic.

Answer 33

C. diphtheria only creates toxin (A-B toxin) when the bacteria is infected by **corynephage beta** through lysogenic conversion (transduction). No phage = no toxin = no disease.

Question 34

Describe Respiratory Diphtheria:

Answer 34

* 2-6 days incubation * Toxin absorbed and disseminated → **myocarditis, cardiac dysfunction, and laryngeal nerve palsy.** * Death from **respiratory obstruction or cardiac failure.**

Question 35

Describe Cutaneous diphtheria:

Answer 35

Acquired by skin contact, forming nonhealing ulcer, toxin can cause systemic effects.

Question 36

Corynebacterium diphtheria Vaccines

Answer 36

Diphtheria toxoid vaccines: DTaP, Tdap, DT, Td.

Question 37

**Gardenerlla: Gardnerella vaginalis** Details:

Answer 37

* Main organism in bacterial **vaginosis**. * Disease is the most common **vaginal infection.** * Occurs due to disruption of normal flora. * **Lactobacillus** maintains **acidic environment.** * Tested by **positive amine test** * **Fishy smell** * “clue cells” help differentiate it from **Trichomonas vaginalis**. * Due to low inflammatory changes, it is a **vaginosis** rather than a **vaginitis.** * Treatment of choice is metronidazole.

Question 38

**Cutibacterium** (**Propionibacterium) acnes** Details:

Answer 38

* Gram+ and normally found on **skin.** * Lives on **glycerol** from sebum. * **Acne** * **Cutibacterium** produce **lipases** which digest sebum but also release **proinflammatory fatty acids,** results in **pustule or nodule** formation (comedones). * Treatment: Benzoyl peroxide and vitamin a (to reduce keratin production)

Question 39

**Actinomyces: Actinomyces israelii**

Answer 39

* **Anaerobe** * Bacilli, to **branched, filamentous** forms (looks like fungi). * Normal mucosal flora in **gingival crevices**, the female **genital tract** and **gastrointestinal tract.** * Endogenous infection from trauma that compromises tissue **blood flow** allows penetration. * **Cervicofacial** ("lumpy jaw" from tooth extraction), thoracic, abdominal, or pelvic abscesses (**interuterine device**) * Can result in hard **yellow microcolonies (sulfur granules).** Brain abscesses occur. Often misdiagnosed as neoplasms.

Question 40

Nocardia Details:

Answer 40

* Obligate aerobe * Partially **acid-fast** (have mycolic acid in cell wall) * Catalase: Positive * Urease: Positive

Question 41

3 types of Nocardia infection and details:

Answer 41

* **Pulmonary nocardiosis** * Inhalation * In patients with low WBC or CD4+ * Not contagious * **Immunocompetent patients: Cutaneous or subcutaneous infections** * Ulcers & Cellulitis. * **Rare other infections** * **Brain abscesses** * **Bacteremia**