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MHD 1 > L28 The Gram Positive Rods and Aerobic Actinomycetes > Flashcards

L28 The Gram Positive Rods and Aerobic Actinomycetes Flashcards

1
Q

What are the major Gram Positive rods?

A
  1. Bacillus
  2. Listeria
  3. Erysipelothrix
  4. Corynebacteria
  5. Arcanobacterium
  6. Lactobacillus
  7. Nocardia
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2
Q

What are the general characteristics of Bacillus?

A
  1. Spore-forming Gram positive rod
  2. Widespread in nature
  3. Prefers aerobic conditions
  4. Motile (Except anthracis)
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3
Q

Bacillus anthracis is a category ___ biothreat agents.

A

A

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4
Q

What disease is caused by B. anthracis?

A

Anthrax

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5
Q

What are the three routes of entry for B. anthracis and which is most common?

A
  1. Inoculation (95%) - contaminated soil or infected animal products
  2. Ingestion
  3. Inhalation - wool sorter’s disease, processing goat hair, biological weapons
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6
Q

Inhalation anthrax has a prolonged ___ period.

A

Latent (2+ months)

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7
Q

What are the initial symptoms of inhalation anthrax?

A

Non-specific fever, shortness of breath, cough, headache, vomiting, chills, chest and abdominal pain

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8
Q

Describe the second stage of inhalation anthrax.

A

Rapidly worsening fever, edema, enlargement of mediastinal lymph nodes

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9
Q

What is a class imaging finding in inhalation anthrax?

A

Widening of the mediastinum

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10
Q

___ symptoms occur in 50% of inhalation anthrax patients.

A

Meningeal

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11
Q

What occurs within 3 days of the second stage of inhalation anthrax if treatment is not initiated?

A

Shock and death

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12
Q

What is caused by inoculation of B. anthracis?

A

Cutaneous anthrax

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13
Q

What are the symptoms of cutaneous anthrax and what is the mortality rate?

A

Painless papules that progress to ulcers surrounded by vesicles, and finally to nectrotic eschar; 20%

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14
Q

What is caused by ingestion of B. anthracis?

A

GI anthrax

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15
Q

What are the symptoms of GI anthrax and what is the mortality rate?

A

Ulcers in mouth and esophagus (upper GI), necrosis of the terminal ileum, nausea, vomiting, malaise, bloody diarrhea (lower GI); 100%

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16
Q

What are the virulence factors associated with anthrax and how do they contribute to the pathogenesis?

A
  1. Capsule: inhibits phagocytosis of replicating cells
  2. Edema toxin: causes fluid accumulation
  3. Lethal toxin: stimulates macrophages to release tumor necrosis factor and IL-1-beta
  4. Protective AG: binds specific cell surface receptors that enable ET and LT to enter the cell.
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17
Q

Both edema factor and lethal factor require translocation into the host cells by ___.

A

The protective antigen

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18
Q

How is anthrax diagnosed?

A 
Culture (skin, blood, sputum, CSF)
Gram + box car-shaped bacilli
Non-motile
Non-hemolytic
Penicillin susceptible
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19
Q

How is anthrax treated?

A

Penicillin, ciprofloxacin, or doxycycline

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20
Q

How is B. anthracis ruled out?

A

Motility (it is non-motile) and hemolysis (it is non-hemolytic)

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21
Q

What diseases are caused by B. cereus?

A

Food poisoning (exotoxins), ocular infections, central line infections, opportunistic infections

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22
Q

What is cultured when B. cereus is suspected?

A
  1. Eye
  2. Wound infection
  3. Implicated food product
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23
Q

What are the general characteristics of Listeria?

A

Non-spore forming, Gram-positive rod

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24
Q

What is the habitat of Listeria?

A

Animals, environment, refrigerated foods

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25
Where is L. monocytogenes found?
Soil, stream water, fecal flora of many animals, contaminated food, undercooked and unpasteurized foods
26
What types of food become contaminated with L. monocytogenes?
Soft cheeses, veggies, cold cuts, ready to eat foods, smoked seafood
27
What is the pathogenesis of Listeria?
Bacteria invade epithelial cells, M cells, and macrophages by an internalin protein. Bacteria are engulfed in a vacuole, where they produce listeriolysin and phospholipases to excape from the phagosome. Host cell actin is utilized to move bacteria into adjacent cells with exposure to the immune system.
28
What encodes the host cell actin utilized by Listeria?
ActA gene
29
Why will patients with defects in cellular immunity but not humoral immunity be susceptible to severe infections by Listeria?
Humoral immunity is relatively unimportant because bacteria move within cells and avoid antibody-mediated clearance
30
What diseases does Listeria cause in neonates?
Early-onset diseases (acquired via placenta in uter): disseminated abscesses and granulomas in multiple organs Late-onset disease (at or shortly after birth): meningitis with septicemia
31
What diseases does Listeria cause in the elderly?
Influenza-like illness with or without gastroenteritis
32
What diseases does Listeria cause in pregnant women or patients with cell-mediated immune defects?
Primary bacteremia or disseminated disease with hypotension and meningitis
33
How long does it take for Listeria to be cultured?
1-2 days
34
What type of hemolysis is seen in Listeria?
Beta
35
Describe the Gram stain of Listeria.
Short Gram-positive rods
36
What biochemical tests can be done to diagnose listeria?
1. Catalase + 2. Tumbling motility/umbrella motility 3. Motile at RT, non-motile at 37 degrees C
37
How is Listeria treated?
Penicillin or ampicillin with or without gentamicin; it is resistant to all cephalosporins
38
Describe the shape of E. rhusiopathiae.
Pleomorphic Gram positive rods that form long filaments
39
What are the lab characteristics of E. rhusiopathiae?
1. Microaerophilic or facultative anaerobe 2. Slow growth (2-3 days) 3. Small, grayish, alpha-hemolytic colonies 4. Catalase negative 5. Non-motile 6. Weakly fermentive 7. Produces hydrogen sulfide on triple sugar iron agar (TSI)
40
What is the habitat of E. rhusiopathiae?
Ubiquitous in soil and groundwater, distributed worldwide
41
Does E. rhusiopathiae occur frequently in animals, humans, or both?
Widely recognized in animals, uncommon in humans
42
Colonization of E. rhusiopathiae is high in what types of animals?
Swines and turkey
43
Human infection with E. rhusiopathiae is acquired from ___ and it is often associated with their occupation.
Animals
44
What diseases are caused by E. rhusiopathiae?
Cutaneous infections (organism is inoculated subcutaneously)
45
What are the two forms of cutaneous infection caused by E. rhusiopathiae?
1. Erysipeloid - localized skin infection on fingers or hands; appears violaceous with a raised edge; spreads slowly peripherally as discoloration fades; suppuration is uncommon. 2. Septicemic - uncommon, presents frequently with endocarditis
46
What distinguishes cutaneous infection with E. rhusiopathiae from streptococcal erysipelas?
E. rhusiopathiae erysipelas does not have suppuration commonly
47
What is the treatment of choice for E. rhusiopathiae?
Penicillin
48
What are the major characteristics of Corynebacterium?
1. Pleomorphic Gram positive rods, clumps 2. Grows aerobic or facultatively anaerobic 3. Small white non-hemolytic colonies
49
What is the habitat of Corynebacterium?
Ubiquitous in plants and animals
50
Where does Corynebacterium colonize?
Skin, upper respiratory tract, GI tract, UG tract
51
How is C. diptheriae transmitted?
Respiratory droplets or direct contact with cutaneous infection
52
What is the primary disease caused by C. diptheriae?
Diptheria
53
Describe the diphtheria vaccination.
Vaccinate with a toxoid (formalin-treated toxin); re-vaccinate every 10 years
54
What is the pathogenesis of C. dipththeriae?
Disease caused by potent exotoxin that inhibits protein synthesis of eukaryotic cells
55
What are the functions of the subunits of the diphtheria toxin?
A: shuts of protein synthesis B: binds to cell receptor
56
Where is the toxin gene for diphtheria found?
Bacteriophage
57
What are the symptoms of diphtheria?
1. Pharyngitis with patchy exudates on tonsils, uvula, soft palate 2. Tough gray pseudomembrane consists of fibrin, white cells, bacteria, debris, which can lead to respiratory obstruction and suffocation 3. Toxin can injure the heart 4. Toxin can circulate to the CNS and cause reversible paralysis
58
How is diphtheria diagnosed?
Clinical evaluation; no rapid lab test; lab looks at throat cultures
59
How is diphtheria treated?
Anti-toxin and penicillin/erythromycin
60
What are the main characteristics of Arcanobacterium hemolyticum?
1. Non-spore forming 2. Gram-positive rod (irregular, club-shaped, curved, or V-formation) 3. Catalase-negative 4. Beta-hemolytic
61
Arcanobacterium hemolyticum is isolated mostly from what population? What sypmtoms do they present with?
Young adults (15-25 y/o); symptomatic pharyngitis, fever, cutaneous rash, some with pseudomembranous pharynx/tonsils, submandibular lymphadenopathy
62
Arcanobacterium hemolyticum is also isolated from...
...wounds, abscesses, and blood of patients with septicemia and endocarditis.
63
What are the major characteristics of Lactobacillus?
1. Non-spore forming 2. Gram positive rod 3. Prefers carbondioxide or anaerobic atmosphere
64
Where is Lactobacillus found?
Normal flora of oral cavity and vaginal tract, yogurt
65
What diseases are caused by Lactobacillus?
Sepsis, endocarditis
66
Describe the major characteristics of aerobic actinomycetes.
1. Aerobic 2. Gram-positive rods 3. Catalase-positive
67
Where are aerobic actinomycetes found?
Soil and decaying vegetation
68
True or false - aerobic actinomycetes = actinomyces species.
False
69
What are the characteristics of Nocardia?
1. Gram-positive rods 2. Partially acid-fast 3. Cell wall with mycolic acid 4. Strict aerobe 5. Grows on most non-selective agars 6. Prolonged incubation (7+ days)
70
What is the habitat of Nocardia?
Worldwide distribtuion in soil
71
How is Nocardia tarnsmitted?
Inhalation or traumatic introduction (cutaneous)
72
Disease caused by Nocardia is most common in what patient populations?
Immunocompetent patients with chronic pulmonary diseases or immunocompromised patients with T-cell deficiencies
73
What diseases are caused by Nocardia?
Bronchopulmonary disease, primary or secondary cutaneous infections, secondary CNS infections like brain abscesses
74
How is Nocardia treated?
Antibiotics (sulfonamides usually) and proper wound care

MHD 1 (58 decks)

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