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DEN 7102 Micro & Immuno Concepts > Exam 2 Gram Positive Bacilli > Flashcards

Exam 2 Gram Positive Bacilli Flashcards

1
Q

Gram positive spore forming bacilli

A
  1. Clostridium
  2. Bacillus
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2
Q

Gram positive branching bacteria

A
  1. Nocardia
  2. Actinomyces
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3
Q

Anaerobic non-spore forming rods: example?

A

Lactobacillus

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4
Q

Sporulation is common in ______ bacteria

A

gram positive

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5
Q

Prior to forming spores, bacteria are found in ____ state

A

Vegetative (non-spore, growing)

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6
Q

Bacteria will form spores in response to:

A

Adverse conditions

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7
Q

To form spore, what happens in bacteria?

A
  1. asymmetric cell division
  2. partitioning of chromosome into an internal spore (endospore)
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8
Q

How many endospores can a bacterium create?

A

1 per bacterium

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9
Q

Spore can germinate under what conditions?

A

Anaerobic

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10
Q

True or false: spore is contained within cell’s plasma membrane

A

False - they become “free” because rest of cell dies off, leaving behind the spore by itself

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11
Q
A

Clostridia (spoons)
- Spores form at the end of the cell

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12
Q

Clostridia is found deep in the soil, which means they are:

A

Obligate anaerobes

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13
Q

Clostridium will form spores in what kind of conditions?

A

Nutrient-limiting conditions

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14
Q

Clostridium spores are resistant to:

A
  • dryness
  • heat (boiling)
  • many chemical disinfectants
    “indestructable”
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15
Q

Clostridium spores germinate and may produce toxins under what conditions?

A

Anaerobic conditions (deep in soil; human tissues)

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16
Q

Clostridium contains a ____ toxin, which enters into cells by:

A

AB toxin; either endocytosis to bring in whole complex or only A enters through cytoplasmic membrane

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17
Q

What does A stand for in AB toxin?

A

Active

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18
Q

What does B stand for in AB toxin?

A

Binding

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19
Q

What bacteria causes tetanus?

A

Clostridium tetani

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20
Q

Where are Clostridium tetani spores found?

A

Ubiquitous in soil, animals/human feces

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21
Q

How does Clostridium tetani colonize tissue?

A

Wounds contaminated with feces or soil, usually by penetrating trauma (ex. nail puncturing through skin/deep tissues)

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22
Q

Neonatal tetanus can occur via:

A

unclean deliveries and cord care practices that can infect the umbilical cord

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23
Q

Clostridium tetani incubation time

A

3-21 days

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24
Q

What toxin does Clostridium tetani produce?

A

Tetanospasmin (potent neurotoxin)

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25
Q

True or false: many toxins are responsible for tetanus symptoms

A

False - only tetanospasmin is responsible for all symptoms

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26
Q

Tetanus toxin structure

A

AB structure

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27
Q

How does tetanus toxin travel to the CNS?

A

Via bloodstream or along nerves toward the spine

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28
Q

What does tetanospasmin do?

A
  • Destroys proteins that regulate release of inhibitory neurotransmitters
  • Enhanced and continuous involuntary muscle contraction
  • Unregulated excitatory activity leads to spastic paralysis
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29
Q

Trismus

A

Lockjaw

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30
Q

Risus sardonicus

A

Sardonic smile, causes difficulty swallowing

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31
Q

Opisthotonos

A

Muscle rigidity and spasms

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32
Q

Spastic paralysis can lead to:

A
  • trismus
  • risus sardonicus
  • opisthotonos
  • seizures
  • arrhythmias
  • respiratory arrest –> death
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33
Q

How to prevent and treat Clostridium tetani

A
  • vaccination
  • debridement, clean wound
  • antitoxin
  • supportive care, sedation
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34
Q

True or false: Tetanus has no immunity

A

True - so toxic that not much bacteria is needed to produce symptoms, but is not enough to produce antibodies. Cannot build immunity to it or you’d already be dead

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35
Q

What is found in the tetanus vaccine?

A

Inactivated tetanus toxin; given with diphtheria and pertussis vaccines (DTaP/Tdap)

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36
Q

DTaP is given to:

A

Young children (high dose of everything)

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37
Q

Tdap is given to:

A

preteens (11-12 years old) and adults (every 10 years)

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38
Q

_____ is always given as a high dose in vaccines

A

Tetanus

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39
Q

Clostridium botulinum causes:

A
  • botulism
  • infant botulism
  • wound botulism
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40
Q

What is botulism?

A

Life threatening paralytic illness - muscles become relaxed and don’t work

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41
Q

C. botulinum spores are:

A

Ubiquitous - on surface of vegetables used for home canning, preserves, fermented food

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42
Q

True or false: C. botulinum spores can survive boiling but are killed by autoclaving

A

True

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43
Q

How many toxins does C. botulinum have?

A

7 (A-G)

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44
Q

C. botulinum toxin structure

A

AB structure

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45
Q

C. botulinum toxin is a:

A

Neurotoxin

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46
Q

What does C. botulinum toxin do?

A

Prevents release of acetyl choline from motor neuron, stops muscle contraction - leads to flaccid paralysis

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47
Q

True or false: C. botulinum can be inactivated by boiling for 10 min

A

True but may not kill spores

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48
Q

_____ has potential for bioterrorism

A

C. botulinum (1g of toxin can kill 1 million people)

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49
Q

Foodborne botulism is caused by which toxins?

A

Toxins A and B

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50
Q

Foodborne botulism onset

A

18-38 hours; ranges 2 hours - 8 days

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51
Q

Symptoms reported for foodborne botulism

A

Headaches, dizziness, descending flaccid paralysis

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52
Q

Descending flaccid paralysis symptoms

A
  1. diplopia (double vision)
  2. difficulty swallowing and speaking, unable to move lips or tongue
  3. progressive difficulty breathing –> death

Also bilateral descending muscle weakness

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53
Q

Diagnosis for foodborne botulism

A

Toxin in feces or contaminated food

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54
Q

True or false: foodborne botulism is an acute illness

A

False - long lasting, takes months or years to recover

55
Q

Ptosis

A

Drooping eyelid

56
Q

If someone has botulism, what signs can you see from their eyes?

A

Ptosis, fixed dilated pupils

57
Q

What is the most common botulism in the US

A

Infant botulism

58
Q

Infant botulism affects infants ____ weeks of age

A

3-20

59
Q

How is infant botulism acquired?

A

Spores may be ingested with food, honey is the only known risk factor

60
Q

Wound botulism occurs in:

A

Almost exclusively injection drug users associated with black tar heroin

61
Q

Treatment of botulism

A

- antitoxin to bound remaining circulating toxin (has to be done before symptoms appear)
- supportive therapy (ventilation)

62
Q

Where is antitoxin available for botulism

A

Health department has to contact CDC - it is so rare, not on hand at hospital

63
Q

Botulism prevention

A
  • proper sterilization in canning (home canning major disease source)
  • toxin can be deactivated by heat
64
Q

Where is botox derived from

A

C. botulinum toxin (BoTox)
Diluted VERY well

65
Q

What is botox used for

A

Rid frown lines, crow’s feet, etc.; can treat migraines, muscular, bowel, gland disorders
Temporarily paralyzes the muscle. Toxicity is due to overdosing

66
Q

____ may administer botox in a majority of US states

A

Dentists - can treat TMD or for cosmetic purposes

67
Q

C. perfringens causes what kind of infections?

A

Soft tissue or intestinal infections

68
Q

C. perfringens soft tissue infections

A
  1. gas gangrene and myonecrosis
  2. anaerobic cellulitis
69
Q

C. perfringens example of intestinal infection

A

Food poisoning

70
Q

There are several types of gangrene, which are:

A
  • dry gangrene
  • wet gangrene
  • gas gangrene
71
Q

Dry gangrene is caused by:

A

Ischemia (inadequate blood supply to organs) as a result of atherosclerosis, diabetes, frost bite

72
Q

Wet gangrene is caused by:

A

Ischemia and infection (by many bacteria types)
Low blood supply but infection on top of that (lots of pus)

73
Q

Gas gangrene is caused by:

A

C. perfringens - infection deep in tissues, causes gas buildup

74
Q

Which C. perfringens toxins cause gas gangrene

A
  • Alpha
  • Epsilon
75
Q

C. perfringens alpha toxin causes:

A
  • Phospholipid destruction
  • lyses RBC, WBC, platelets
  • tissue destruction
  • renal failure
76
Q

C. perfringens Epsilon toxin causes formation of ____ and is implicated in ___

A

membrane pore; multiple sclerosis

77
Q

What does Gas gangrene look like in histology

A

Large gas bubbles in muscle tissue (fermentation)

78
Q

Gas gangrene treatment

A
  • debridement
  • high dose penicillin can sometimes work
  • hyperbaric oxygen (because the bacteria is anaerobic)
79
Q

True or false: Anti-toxin is ineffective in C. perfringens

A

True - toxin is already bound/inside cell

80
Q

C. perfringens enterotoxin causes:

A

food poisoning - alters membrane permeability of small intestine epithelium

81
Q

C. perfringens enterotoxin may act like

A

Superantigen

82
Q

C. perfringens enterotoxin is inactivated by:

A

Heat (heat labile)

83
Q

C. perfringens food poisoning is commonly associated with:

A

chicken/poultry (improper cooling of cooked meat)

84
Q

C. perfringens food poisoning symptoms

A

Watery diarrhea, abdominal pain

85
Q

True or false: C. perfringens food poisoning is self limiting, meaning you don’t generally die from it or require treatment

A

True

86
Q

Antibiotic-associated colitis is associated with what bacteria?

A

Clostridium difficile

87
Q

C. difficile causes what disease?

A

Antimicrobial-induced (pseudomembranous)
enterocolitis

88
Q

C. difficile infection is associated with:

A

Broad spectrum antibiotics - normal flora is decreased and allows opportunistic infection

89
Q

What toxins does C. difficile produce?

A

Enterotoxin, cytotoxin

toxic to cells, necrosis of villi

90
Q

In C. difficile infection, ____ forms on the large intestine

A

Pseudomembrane

91
Q

C. difficile associated pseudomembrane is made up of:

A

inflammatory cells, fibrin, bacteria

92
Q

C. difficile enterocolitis symptoms

A

Watery diarrhea, leukocytosis, fever, abdominal pain

93
Q

Diagnosis of C. difficile enterocolitis

A

stool culture, toxin in feces by PCR

94
Q

Treatment for C. difficile enterocolitis

A
  • discontinue current antimicrobial therapy
  • fecal microbiota transplantation (poorly regulated but high success rate 90%)
  • preventative measure: take probiotics
95
Q

Bacillus anthracis classification

A

gram positive, spore-forming rods

96
Q

B. anthracis metabolism

A

Obligate aerobes

97
Q

Anthrax toxin structure

A

AB toxin with 2 alternate A subunits
- Edema factor (EF)
- lethal factor (LF)

Has Protective antigen (PA) that binds to cell, is equivalent to B subunit

98
Q

Anthrax edema factor causes:

A

swelling, trapping of fluids

99
Q

Anthrax lethal factor causes:

A

cell death, hypoxia

100
Q

B. anthracis forms of infection

A
  1. cutaneous anthrax
  2. Gastrointestinal anthrax
  3. pulmonary anthrax
101
Q

Symptoms of cutaneous anthrax

A

Ulceration, eschar formation, lymphadenopathy

102
Q

GI anthrax symptoms

A

Ulceration of oropharynx, esophagus, intestine; severe gastroenteritis

103
Q

Pulmonary anthrax is also known as

A

Cattle and sheep “wool sorter’s disease”

104
Q

Symptoms of pulmonary anthrax

A

Severe/fatal pneumonia, fever, lymphadenopathy of mediastinal lymph nodes

105
Q

Bacteremia, meningitis, shock, and death can result from which form of anthrax?

A

Pulmonary anthrax

106
Q

Eschar definition

A

dark scab, dead tissue sloughs off

107
Q

Oropharyngeal anthrax is marked by formation of:

A

Pseudomembrane overlying ulcers

108
Q

Telltale sign of inhalation anthrax

A

Widening mediastinum (membrane separating the lungs)

109
Q

From inhalation anthrax, dissemination of ____ can be seen in blood

A

Gram positive rods

110
Q

Bacillus anthracis treatment

A

Ciprofloxacin - military grade anthrax is resistant to penicillin and other antibiotics so cannot use those

111
Q

B. anthracis has potential for ______

A

bioterrorism

112
Q

What event occurred in 2011 regarding anthrax?

A

Biowarfare - 22 people infected, all got some kind of disease (half inhalation, half cutaneous) - 5 died, making it a 45% death rate
33,000 people given prophylactic abx

113
Q

Nocardia is a ______

A

pulmonary opportunist (infect those that are immune deficient)

114
Q

Which bacteria stains weakly gram positive and also has mycolic acid in its cell wall?

A

Nocardia

115
Q

Nocardia causes what kinds of infection?

A

Traumatic skin lesion infection, abscess formation (can occur in mouth), hematogenous dissemination to the brain

116
Q

Actinomyces is found where?

A

Normal oral flora on teeth/tonsillar crypts

117
Q

____ is associated with root surface caries

A

Actinomyces

118
Q

Which bacteria forms slow growing, “molar” colonies?

A

Actinomyces

119
Q

Actinomycosis is primarily caused by:

A

A. israelii and A. viscosus

120
Q

Actinomycosis disease symptoms

A
  • acute or chronic abscesses
  • draining sinuses with sulfur granules
  • cervicofacial (lumpy jaw) in over half of all infections
121
Q

Actinomycosis treatment

A

Surgery, penicillin

122
Q

Cervicofacial actinomycosis commonly occurs at:

A

Angle of mandible

123
Q

Trauma in the form of injury, perio pocket, nonvital tooth, extraction socket, and an infected tonsil increase the risk of aquiring:

A

Cervicofacial actinomycosis

124
Q

Which teeth are often involved in cervicofacial actinomycosis?

A

Mandibular first molars and anterior maxillary teeth

125
Q

True or false: cervicofacial actinomycosis is reported to be very painful

A

False - pain often minimal

126
Q

Sulfur granules are associated with:

A

Actinomycosis (colonies look like tiny molars)

127
Q

Which gram positive bacilli species does not form spores?

A

Lactobacillus

128
Q

Where is lactobacilli found?

A

Normal flora of the mouth, GI tract, vagina

129
Q

Lactobacilli produces _____ and is tolerant of ____

A

Lactic acid; acid

130
Q

Lactobacilli is involved in _____ progression

A

Caries

131
Q

True or false: lactobacilli can be ingested via fermented foods and food supplements

A

True

132
Q

Normal vaginal smear should show some lactobacilli - why is this important?

A

Keeps vaginal environment slightly acidic to prevent other infections (like yeast infection)

133
Q

Bacillus anthracis major virulence factors

A

toxin and capsule

DEN 7102 Micro & Immuno Concepts (26 decks)

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