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Microbiology > Gram Positive Rods > Flashcards

Gram Positive Rods Flashcards

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Biology 101 flashcards
1
Q

Non-Spore Formers

A
  • Listeria
    ^ L. monocytogenes
  • Corynebacterium
    ^ C. diptheriae
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2
Q

Spore Formers

A 
- Bacillus AEROBIC
     ^ B. anthracis
     ^ B. cereus
- Clostridium ANAEROBIC
     ^ C. perfringens
     ^ C. botulinum
     ^ C. tetani
     ^ C. difficile
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3
Q

Branching Gram + Rods

A
  • Actinomyces ANAEROBIC

- Nocardia AEROBIC

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4
Q

Lysteria

A 
Non-Spore Former
Gram + Rod
- short slender rods
- intracellular parasites
- tumbling motility
- small B-hemolytic colonies
- found in livestock
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5
Q

Listeria monocyogenes

A

Gram + Rod
Only species pathogenic to humans
- infections usually food borne
- grows at 4C - REFRIGERATION DOES NOT HINDER GROWTH
- found in those with suppressed immune systems
- pregnant women, babies, old people

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6
Q

Listeria monocytogenes

Disease

A
  • Septicemia
  • Gastroenteritis
  • Meningitis
  • Fetus-spontaneous abortions
  • Neonatal meningitis
    • common cause; transferred during birth

Disease type dependent on where the infection occurs

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7
Q

L. Monocytogenes Pathogenesis

A
  • Phagocytosed
  • Grows in cytoplasm
  • Reorganizes cellular actin for locomotion
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8
Q

L. Monocytogenes

Treatment and Prevention

A
  • Antibiotics
  • Proper food handling
  • Expiration Dates
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9
Q

Corynebacterium

A
  • Widely distributed in nature
  • Pleomorphic: many sizes and shapes
  • Palisading (arranged parallel)
  • Irregular staining
  • Non-motile
  • Unencapsulated
  • Facultative anaerobes
  • Growth on standard media (blood agar)
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10
Q

Corynebacterium diphtheria

A
  • Infection of URT
    • grey PSEUDOMEMBRANE forms covering throat and nose
  • Pathogenic strains have exotoxins
    • cause CNS and cardiac problems
    • inhibits protein synthesis (EF-2)
    • On phage: must integrate into chromosome
  • Small grey colonies on blood agar
  • childhood vaccination
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11
Q

C. Diphtheria

Clinical Significance

A 
Respiratory
- localized in throat; spread via droplets
- Toxin inhibits protein synthesis
     - Heart and CNS issues
- PSEUDOMEMBRANE
Cutaneous
- from puncture or deep cut
- grey membrane
- rare: exotoxins causing tissue necrosis
Asymptomatic carriers
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12
Q

C. Diphtheria

Identification

A 
Clinical Observation
- pharyngitis
- fever
- swelling of neck
- GREY PSEUDOMEMBRANE
Definitive
- culture
     - TINSDALE AGAR (Potassium TELLURITE)
Assay for toxin
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13
Q

C. Diphtheria

Treatment and Prevention

A 
Treatment
- antibiotics
- neutralize toxin
Prevention
- Toxoid immunization (antigenic)
- childhood immunizations
- DTaP
     - Diptheria, Tetanus, Pertussis
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14
Q

Bacillus

A

Large Gram + Rod

  • aerobic
  • ubiquitous in soil or water
  • can have airborne spread
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15
Q

B. cereus & B. anthrax

A

Cereus - food poisoning
Anthraces - anthrax from livestock

Closely related; differ in virulence factor toxin

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16
Q

Bacillus cereus

A
  • MEDIAL Spore (middle of bacteria)
  • Found in GI tract and nature
  • Virulence Factors:
    • Enterotoxins
    • Spores
  • Food poisoning
  • Large and feathery colony
  • B-hemolytic
  • Motile
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17
Q

B. Cereus

A 
FRIED RICE SYNDROME: spores not killed by boiling
-germinate if not refrigerated properly
- produce ENTEROTOXINS
     - food poisoning
     - 2 types enterotoxins
          ^ Heat Stable: Vomiting
          ^ Heat Liable: diarrhea
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18
Q

B. Anthracis

A
  • Widely distributed in nature
    • primarily in livestock; humans infected through contact
  • Virulence factors:
    • Capsule
    • Spores: medial spores
    • Exotoxins that allows cell and tissue destruction
  • EXTREMELY VIRULENT
  • Bamboo sticks
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19
Q

Anthrax Disease

A
  • Cutaneous: spores enter through cuts
  • PAINLESS ulcer with a black center (ESCHAR)
  • Systemic
  • INHALATION: PULMONARY
    • inhale; presents with fever, chest pain, shortness of breath
    • 100% mortality if not treated
  • GI
    • infected meat; GI symptoms
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20
Q

B. Anthracis

Pathogenesis

A
  • Capsule
    -PROTEIN; poly-D-glutamic acid
  • Two Exotoxins
    • EDEMA FACTOR: elevates intracellular cAMP = severe edema
    • LETHAL FACTOR: kill signal transduction; apoptosis of macrophages
      ^ necrosis
  • PROTECTIVE ANTIGEN: delivers exotoxins
    • needed for toxin factor effects!
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21
Q

B. Anthracis

Growth and Identification

A
  • Medial oval spores
  • Non-hemolytic
  • Irregular borders
  • Non-motile
  • Encapsulated
  • Detection biz immunofluorescence assay
22
Q

B. Anthracis

Treatment and Prevention

A

Treatment: antibiotics
Prevention: vaccine if high risk; prophylaxis antibiotics if exposed

ONLY KILL SPORES WITH AUTOCLEAVING

23
Q

B. Anthracis

Bioterrorism

A

Why?

- ease- very hard to detect

24
Q

Clostridium

A

TERMINAL SPORES

  • found in nature
  • obligate anaerobes
  • motile
  • Virulence Factors
    • capsules
    • potent exotoxins
25
Q

Gram Positive Rods

A 
Non-Spore Formers
- Corynebacterium
- Listeria
- Lactobacillus
- Actinmyces
- Nocardia
Spore Formers
-  Bacillus
- Clostridium
26
Q

Spore Forming Gram Positive Rods

A 
Aerobic
- Bacillus
     - anthracis
     - cereus
Strict Anaerobes 
- Clostridium
     - perfringens
     - tetani
     - botulinum
27
Q

Non-Spore Forming Gram Positive Rods

A
  • Coryenbacterium
  • Listeria
  • Lactobacillus
  • Actinomyces
  • Nocardia
28
Q

Clostridia Species

A
  • C. Perfringens
  • C. botulinum
  • C. tetani
  • C. Difficile
29
Q

C. perfringens

A
  • Histotoxin: tissue destruction
  • Gas gangrene, food poisoning
  • normal flora of vaginal and GI tract
  • cause gas gangrene (NECROSIS)
    • high mortality
30
Q

Clostridium perfringens

Disease

A 
CRUSHING INJURY
GAS GANGRENE 
- tissues and muscles 
- spores enter body; toxins cause death
- fermentation of tissue produces gas (gas=virulence factor)
- more dangerous; fatal in days
CELLULITIS
- tissue only
-similar but no muscle damage
FOOD POISONING
31
Q

C. Perfringens

Pathogenesis

A
  • Secretes exotoxins
    • Alpha Toxin REQUIRED for virulence; degrades cell membranes & lyses cells
  • Hydrologic enzyme facilitate necrosis
  • Enterotoxins: GI illness
32
Q

C. Perfringens

Identification

A
  • clinical presentation
  • anaerobic culture on blood agar
  • double zone of hemolysis in blood agar
33
Q

C. Perfringens

Treatment and Prevention

A
  • immediate removal of foreign matter
  • debride and remove tissue
  • EXPOSE WOUND TO O2
  • amputate
  • high doses antibiotics
34
Q

Clostridium botulinum

A
  • Ubiquitous spores
  • Produces strong neurotoxin
    • muscles unable to flex or tense
    • FLACCID paralysis
    • progressive paralysis leads to respiratory failure
35
Q

C. Botulinum

Clinical Significance

A
  • Foodborne (classic) botulism: most common
    • eat toxin
  • Wound botulism
    • wound contaminated with cells or spores and produces toxins
  • Infant botulism: FLAPPY BABY SYNDROME
    • immature microbial flora (aka immature immune system) makes kiddos susceptible
36
Q

C. Botulinum

Treatment and Prevention

A

Treatment: Antitoxin and Antibiotics
Prevention: Toxin inactivated by boiling; AUTOCLEAVING of SPORES

37
Q

Clostridium tetani

Tetanus

A

OPPOSITE TO BOTULISM

  • found ubiquitously in soil
  • spores enter via puncture wounds/trauma
  • produces neurotoxin which prevents muscle relaxation
    • SPASTIC paralysis
  • Rare
    • immunization
    • extremely anaerobic
38
Q

Tetnus

A
  • initial spasms at site of infection
  • lockjaw syndrome
  • spreads elsewhere
  • 50-60% mortality due to respiratory failure
39
Q

Tetanus

Treatment and Prevention

A 
Treatment:
- start immediately
- antitoxin
- hyper immune immunoglobulin
- antibiotics
Prevention:
- toxoid vaccine
- DTaP with booster 
Post Exposure Prophylaxis
40
Q

Clostridium difficile

A
  • minor component of normal colon flora
  • opportunistic
  • found often in hospitals
    • because spores = hard to eradicate
41
Q

C. Difficile

Disease

A
  • aggressive healthcare pathogen
    • majority of infections involve healthcare
  • antibiotics increase risk by disrupting normal colonic flora
  • opportunistic pathogen
  • PSEUDOMEMBRANOUS COLITIS
  • GI symptoms that can progress to toxic megacolon, sepsis, and death
42
Q

C. Diff

Treatment and Prevention

A

Treatment: stop predisposing drug (antibiotics); reconstitute normal gut flora

Prevention: reduce use of associated antibiotics

43
Q

Actinomyces

A
  • Ubiquitous in environment and body (normal flora)
  • Branching
  • Grows anaerobically
  • Pathogenic in immunocompromised individuals
44
Q

Actinomyces

Epidemiology

A
  • chronic, slow developing infections
  • no person to person spread
  • low virulence; only causes disease if mucosal barrier is disrupted
45
Q

Actinomyces

Clinical Significance

A

Yellow pus and abscesses

46
Q

Actinomyces

Identification

A
  • “sulfur granules” in pus
  • grow in rich media anaerobically
  • slow growth
47
Q

Actinomyces

Treatment and Prevention

A
  • antibiotics
  • lasting months
  • surgical debridement and drainage
48
Q

Nocardia

A
  • breathe in/breaks in skin
  • strictly Aerobic
  • low virulence; no person to person spread
    • effects mostly immunocompromised
  • opportunistic organism
49
Q

Nocardia

Clinical Significance

A
  • Pneumonia in immunosuppresed patients
  • Abscesses and necrosis but NO YELLOW PUS!
  • Avoids phagocytosis via secreted enzymes
  • Can live in macrophage
  • Can spread to BRAIN and KIDNEYS
50
Q

Norcardia

Identification

A
  • Poorly stained with Gram stain
  • Irregular staining
  • No sulfur granules
  • Gram +

Microbiology (7 decks)

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