ANAEROBIC BACTERIA Flashcards

1
Q

the enzymes
required to breakdown reactive oxygen species produced
during respiration or aerobic metabolismDifficult to assess;
had clinical
significance in
cultures of blood,
bone marrow,
and spinal fluid

A

superoxide dismutase and catalase,

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2
Q

anaerobes lack

A

Lack superoxide dismutase and catalase,

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3
Q

(enzymes for oxygen tolerance)

A

catalase

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4
Q

Obligate anaerobic prokaryotes

A

may live by
fermentation, anaerobicrespiration, bacterial photosynthesis, or the novel process of
methanogenesis

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5
Q

Survive some oxygen exposure but will not be able to
perform metabolic function

A

Obligate anaerobes

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6
Q

exampleof obligate anaerobe

A

o Many belong to this type
o Include Archaea such as methanogens and bacteria
(e.g., ABC – Actinomyces, Bacteroides, and
Clostridium)

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7
Q

o Cannot use O2
o Not damaged by O2

A
  • Aerotolerant anaerobes
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8
Q

what type of metabolism does aerotolerant anaerobes have

A

o Exclusively anaerobic (fermentative) type of
metabolism but they are insensitive to the presence of
O21
o Live by fermentation alone whether or not O2 is present
in their environment

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9
Q
  • Aerotolerant anaerobes
A

o E.g., Lactobacillus, Proprionibacterium,
Clostridium.

Most strains of
streptococci,

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10
Q

o Can use O2
o Can survive without O2

A
  • Facultative anaerobes (facultative aerobes)
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11
Q

Require the oxygen concentration to be reduced to 5%
or less

A

Microaerophile

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12
Q

Microaerophile

A

o E.g., Campylobacter, Helicobacter1

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13
Q

Grow best when the concentration of carbon dioxide is
increased to the range of 5% to 10% in a CO2 incubator

A

Capnophilic

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14
Q

Capnophilic

A

o E.g., Some anaerobes, Neisseria

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15
Q

Facultative
anaerobe

A

Enterobacteriaceae,
most staphylococci

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16
Q

Obligate aerobe

A

Mycobacteria, fungi

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17
Q

Obligate anaerobes

A
  • Include Archaea such as methanogens and bacteria (e.g., ABC – Actinomyces, Bacteroides, and Clostridium)
  • Most Bacteroides
    spp., many species
    of Clostridium, Eubacterium,
    Fusobacterium,
    Peptostreptococcus,
    Porphyromona
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18
Q

Strict anaerobic
environment (0%
O2)

A

Obligate
anaerobe

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19
Q

Reduced
concentrations of O2 (anaerobic
system and
microaerophilic
environments)

A

Aerotolerant
anaerobe

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20
Q

Multiplies well in
the presence or
absence of O2

A

Facultative
anaerobe

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21
Q

5% O2

A

Microaerophile

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22
Q

5%–10% CO2

A

Capnophile

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23
Q

15%–21% O2
(as found in a
CO2 incubator
or air)

A

Obligate aerobe

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24
Q

During oxidation-reduction reactions that occur during
normal cellular metabolism, molecular oxygen is reduced to

A

superoxide anion (O2−
) and hydrogen peroxide (H2O2) in a
stepwise manner

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25
Q

superoxide anion reacts with hydrogen peroxide in the presence of iron (Fe3+/Fe2+) to generate the

A

to generate the hydroxyl
radical (·OH) the most potent biological oxidant known

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26
Q
  • Most can survive in 3-5% O2
A

anaerobes

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27
Q

Where are Anaerobes found?

A
  • Anaerobic environments (low reduction potential) include:

o Sediments of lakes, rivers and oceans: bogs, marshes,
flooded soils, deep underground areas (e.g., oil packets
and some aquifers)
o Components of microbiota of humans and other
animals

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28
Q

exogenous vs endogenous

A
  • Endogenous – intestinal tract of animals; oral
    cavity of animals
  • Exogenous – exist outside the bodies of animals
  • Most anaerobic infections are endogenous
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29
Q

Non-spore forming, gram-positive bacilli are divided into
two phyla:

A

o Actinobacteria – Actinomyces, Bifidobacterium,
Mobiluncus, Eggerthella and Proprionibacterium
o Firmicutes – Lactobacillus

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30
Q

Former Peptostreptococcus is now re-classified into at
least 5 different genera

A

o Peptostreptococcu
o Anaerococcus
o Finegoldia
o Parvimonas
o Peptophilus

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31
Q

Gram-positive,
endosporeforming bacilli

A

Clostridium

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32
Q

diseases caused by clostridium

A
  • perfringens Gas gangrene
    -tetanus Tetanus
    -botulinum Botulism
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33
Q

Gram positive,
non-sporing
bacilli

A

Actinomyces
Eubacterium
Bifidobacterium

Proprionibacterium,
Mobiluncus,
Lactobacillus

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34
Q

Eubacterium

disease

A

Infections of
female genital
tract, intraabdominal
infections,
endocarditis

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35
Q

Propionibacterium

disease

A

Difficult to assess;
had clinical
significance in
cultures of blood,
bone marrow,
and spinal fluid

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36
Q

Bifidobacterium

disease

A

Occasionally
isolated from
blood;
significance not
established

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37
Q

Gram-negative,
non-sporing

A

Bacteroides

Fusobacterium and
Prevotella
Poryphromonas
Leptotrichia

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38
Q

Bacteroides

disease

A

nfections of
female genital
tract,
intraabdominal
and
pleuropulmonary
infections, wellestablished as a
pathogen

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39
Q

Fusobacterium and
Prevotella

disease

A

Same as
Bacteroides but
less frequent

Infections of
female genital
tract,
intraabdominal
and
pleuropulmonary
infections, wellestablished as a
pathogen

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40
Q

Leptotrichia

disease

A

Found in mixed
infections in oral
cavity or
urogenital areas;
significance not
established

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41
Q

Gram-positive
cocci

A

Peptococcus
Peptostreptococcus
(anaerobic
Streptococci)

Veilonella

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42
Q

Peptostreptococcus
(anaerobic
Streptococci)

disease

A

Infections of
female genital
tract,
intraabdominal
and
pleuropulmonary
infections, often
found with
Bacteroides;
established
pathogen

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43
Q

Veilonella

disease

A

Found in mixed
anaerobic oral
and
pleuropulmonary
infections,
significance not
established

disease

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44
Q

Factors that Predispose Patients to Anaerobic
Infections

A
  • Trauma to mucous membranes or skin – trauma allows
    anaerobes to gain access at deeper tissues
  • Vascular stasis
  • Decreased oxygenation of tissue leading to tissue necrosis
    and decrease of redox potential of tissue
  • Human or animal bite wounds
  • Aspiration of oral contents into the lungs after vomiting
  • Tooth extraction, oral surgery, or traumatic puncture of the
    oral cavity
  • Gastrointestinal tract surgery or traumatic puncture of the
    bowel
  • Genital tract surgery or traumatic puncture of the genital
    tract
  • Introduction of soil into a wound
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45
Q

Clinical Manifestation Suggestive of Anaerobic
Infection

A
  • Odor
  • Tissue
  • Location
  • Necrotic tissue
  • Endocarditis with negative blood culture
  • Infection associated with malignancy
  • Black discoloration
  • Blood containing exudates
  • Associated with sulfur granules
  • Bacteremic feature with jaundice
  • Human bites
  • Infection in close proximity to a mucosal surface
  • Presence of foul odor
  • Presence of large quantity of gas
  • Presence of black color or brick red fluorescence
  • Presence of sulfur granules
    Potential Virulence Factors of Anaerobic Bacteria
    Potential
    Virulence Factor Possible Role
    Anaerobes
    Known or
    Thought to
    Possess
    Polysaccharide
    capsules
    Promotes
    abscess
    formation;
    antiphagocytic
    function
    Bacteroides
    fragilis,
    Porphyromonas
    gingivalis
    Adherence
    factors
    Fimbriae, fibrils
    enable organisms
    to adhere to cell
    surfaces
    B. fragilis, P.
    gingivalis
    Clostridial
    toxins,
    exoenzymes
    Collagenases
    Catalyze the
    degradation of
    collagen
    Certain
    Clostridium spp.
    Cytotoxins Toxic to specific
    types of cells C. difficile
    DNases Destroy DNA Certain
    Clostridium spp.
    Enterotoxins
    Toxic to cells of
    the intestinal
    mucosa
    C. difficile
    Hemolysins
    Lyse red blood
    cells liberating
    hemoglobin
    Certain
    Clostridium spp.
    Hyaluronidase
    Catalyzes the
    hydrolysis of
    hyaluronic acid,
    the cement
    substance
    of tissues
    Certain
    Clostridium spp.
    Lipases
    Catalyze the
    hydrolysis of ester
    linkages between
    fatty acids and
    glycerol of
    triglycerides and
    phospholipids
    Certain
    Clostridium spp.
    Neurotoxins
    (e.g., botulinum
    toxin,
    tetanospasmin)
    Destroy or disrupt
    nerve tissue
    C. botulinum, C.
    tetani
    Phospholipases Catalyze the
    splitting of host
    Certain
    Clostridium spp.
    Factors that Predispose Patients to Anaerobic
    Infections
    Clinical Manifestation Suggestive of Anaerobic
    Infection
    Indications of I
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46
Q

Indications of Involvement of Anaerobes in
Infectious Processes

A
  • Infection in close proximity to a mucosal surface
  • Presence of foul odor
  • Presence of large quantity of gas
  • Presence of black color or brick red fluorescence
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47
Q

Promotes
abscess
formation;
antiphagocytic
function

A

Polysaccharide
capsules

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48
Q

Fimbriae, fibrils
enable organisms
to adhere to cell
surfaces

A

Adherence
factors

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49
Q

Catalyze the
degradation of
collagen

A

Collagenases

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50
Q

Toxic to specific
types of cells

A

Cytotoxins

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51
Q

Destroy DNA

A

DNases

Certain
Clostridium spp

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52
Q

Toxic to cells of
the intestinal
mucosa

A

EnterotoxinsC. difficile

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53
Q

Lyse red blood
cells liberating
hemoglobin

A

Hemolysins

Certain
Clostridium spp

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54
Q

Catalyzes the
hydrolysis of
hyaluronic acid,
the cement
substance
of tissues

A

Hyaluronidase

Certain
Clostridium spp

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55
Q

Catalyze the
hydrolysis of ester
linkages between
fatty acids and
glycerol of
triglycerides and
phospholipids

A

Lipases

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56
Q

Destroy or disrupt
nerve tissue

A

Neurotoxins

(e.g., botulinum
toxin,
tetanospasmin)

C. botulinum, C.
tetani

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57
Q

Catalyze the
splitting of host phospholipids
(lecithinase)

A

Phospholipases

Certain
Clostridium spp.

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58
Q

Split host proteins
by hydrolysis of
peptide bonds

A

Proteases

Certain
Clostridium spp.

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59
Q

Diameter of the spore is larger than the cell, resembling a
spindle

A

Clostridium

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60
Q

clostridium Spore location – terminal end

A
  • Spore location – terminal end
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61
Q
  • Classification of clostridium based on the type of disease produced
A

a. Tetanus – C. tetani

b. Gas gangrene (myonecrosis) – C. perfringens

c. Food poisoning
c.1. Gastroenteritis – C. perfringens,
c.2. Botulism – C. botulinum

d. Acute colitis – C. difficile,

e. Bacteremia - C. perfringens, C. septicum

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62
Q

Gas gangrene (myonecrosis)

A

– produces exotoxin (αtoxin) which is a lecithinase (phopholipase C) produced
by all strains of C. perfringens
o Established
- C. perfringens, gut organism
- C. septicum
- C. noryi
o Less pathogenic
- C. histolyticum
- C. fallax
o Doubtful
- C. bifermentans
- C. sporogenes

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63
Q

Food sources involved commonly in
botulism include

A

home-canned vegetables,
home-cured meat such as ham, fermented
fish, and other preserved foods

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64
Q
  • Caused by pre-formed toxins
    clostridium A, B and E
A

Botulism

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65
Q

enterotoxin of clostidium A-G enterotoxins cause

A

flaccid type of
paralysis

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66
Q

Toxin attached to the neuromuscular
junction of nerved and prevents
transmission of Acetylcholine

A

Botulism

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67
Q

when present is a marker of GI
malignancy

A

C. septicum

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68
Q

o Affect CNS of the host

A
  • Tetanus (Lock-jaw)
69
Q
  • Antibiotic-Associated Colitis (C. difficile)
A

o Part of the GI biota in about 5% of individuals
o A more virulent strain B1/NAP1/027 which produces
larger amount of toxins A & B plus a third binary toxin
and has a high level resistance to fluoroquinolones

70
Q

Dead tissue, blood clots, foreign matter, aerobic
organisms develop anaerobic condition in an
injury

A

d. Lecithinase C (α-toxin)

71
Q

At birth under unhygienic conditions babies can get –

A

tetanus neonatorum

72
Q

o Neuromuscular disease

A
  • Clostridium tetani
73
Q

Entrance of spores through accidental puncture
wounds (e.g., burns, umbilical stumps, frostbite,
crushed body parts)

A
  • Clostridium tetani
74
Q

o Drumstick appearance

A
  • Clostridium tetani
75
Q

o Grow on Robertson’s cooked medium

A

Clostridium

76
Q

loc of c tetani

A

o Soil/intestine/vagina

77
Q

o Motile with peritrichous flagella

A
  • Clostridium tetani
78
Q

toxins of c tetani

A
  • tetanokysin
  • tetanoplasmin
    -spore germinate
    -ascending tetanus
    -descending tetanus
79
Q

heat and oxygen labile/lyse RBC

A

Tetanolysin

80
Q

– heat and oxygen stable/ highly
lethal; dies within 1-2 days; gets easily neutralized
with antitoxin

A

Tetanospasmin

81
Q

Act at the synaptic junction, preventing the
synthesis of acetylcholine, preventing synaptic
transmission

A

Toxins of c tetani

82
Q

toxin, motor nerve endings –
along the motor neurons of the peripheral nerve to
the anterior horn cells – local tetanus (in the
proximity of the wound)

A

Spores germinate –

83
Q

when toxins spreads
upwards along the spinal cord towards CNS; gives
generalized spasms

A

Ascending tetanus

84
Q

– when toxin is given IV,
spasms will appear in the musscles of the head,
neck and spreads downwards

A

Descending tetanus

85
Q

spasms of
the masseter muscle

A

Early symptom is trismus (lock jaw)

86
Q

– the semblance of a grin
caused by facial spasm especially in tetanus at the
angle of the mouth

A

Risus sardonicus

87
Q

back is slightly curved

A

Opisthonotus

88
Q

c tetani treatment

A

Symptomatic treatment
a. Cleansing and removing the affected tissue
b. Penicillin or tetracycline
c. Muscle relaxants
d. Assistance of respiration (sometimes
tracheostomy)
- 10,000 units of human tetanus immunoglobulin
(HTIG)

89
Q

disease caused by c tetani

A
  • trismus or lock jaw or tetanus
  • risus sardonicus
    -opithosnotus
90
Q

o Prevention and Control

A
  • Immunization – HTIG 250-500 units (to immune
    patients only)
  • To non-immune toxoid followed by HTIG
  • The recommended vaccination series for 1–3-
    month-old babies – 3 injections given 2 months
    apart; booster doses about 1-4 years later
  • Protection against neonatal tetanus – vaccination
    of pregnant women
91
Q

Food poisoning:

type of clostridium and severity

A

Type A, a relatively mild and selflimited GI illness, and type C, a more serious but rarely
seen disease

92
Q

usually follows the
ingestion of large numbers of enterotoxin-producing
strains in contaminated food

A

C. perfringens foodborne disease

93
Q

Lacks the ability to produce a number of essential
amino acids

A

Clostridium perfringens

94
Q

type of food implicated in c perfringens

A

meats and gravies are commonly
implicated in outbreaks

95
Q

Food poisoning caused by C. perfringens type A is
caused by a

A

C. perfringens enterotoxin linked to
sporulation

96
Q

what happens after an 8-30hour incubation period of c perfringens

A

After an 8-30-hour incubation period, the patient
experiences diarrhea and cramping abdominal pain
for about 24 hours.

97
Q

Other than fluid replacement, therapy is usually
unnecessary.

A
  • Clostridium perfringens
98
Q

what happens after incubation period of 5-6hours in c perfringens

A

After an incubation period of at least 5 to 6 hours,
symptoms begin as an acute onset of severe abdominal
pain and diarrhea, which is often bloody, and may be
accompanied by vomiting.

99
Q

Early symptoms are followed by necrotic inflammation
of the small intestines, at times leading to

A

bowel
perforation

100
Q

fatality rate is 15% to 25%

A

c perfringens

101
Q

Most common cause of bacteremia and
myonecrosis

A

c perfringens

102
Q
  • from the ingestion of preformed botulinum
    toxins A, B, and E, produced in food
A

Botulism

103
Q

revents the release of acetylcholine
(a neurotransmitter), which results in flaccid
paralysis and death

A

Botulinum toxin

104
Q

is also used medically
to treat strabismus (wandering and chronic migraines,
and as a beauty enhancer by temporarily improving
facial wrinkles

A

Botulinum toxin type A (Botox)

105
Q

wandering and chronic migraines,
and as a beauty enhancer by temporarily improving
facial wrinkles.

A

strabismus

106
Q

potential bioterrorism agents

A
  • Clostridium botulinum
107
Q

diagnosis of c botulism

A

a. Isolation or organism in food/feces
b. Detection of toxin in feces/serum

108
Q

Incubation period of c botulism

A

Incubation period 12-36 hours

109
Q

Diplopia, dysphagia and dysphonia

A

c botulism

110
Q

difficulty in swallowing

A

Dysphagia

110
Q

difficulty in speaking due to physical
disorder of the mouth, throat or vocal cords

A

Dysphonia

111
Q

double vision

A

Diplopia

112
Q
  • Mortality rate is 65-70%
A
  • Clostridium botulinum
113
Q
  • Paralysis of muscles and respiratory system
A

c botulinum

114
Q

▪ Weak-sucking response
▪ Weakness and cachexia
▪ Generalized loss of tone
▪ Flaccid paralysis

A
  • Infant botulism
115
Q

spores in infant botulism

A

▪ Spores are common in dust and soil
▪ Spores germinate in the intestine and give off
neurotoxin

116
Q

The spores enter a wound or puncture much
as in tetanus

A
  • Wound botulism
117
Q

he symptoms are similar to those of foodborne

A
  • Wound botulism
118
Q

▪ More common in drug abusers

A

wound botulism

119
Q
  • Treatment and Prevention
    c botulinum
A

▪ The CDC provides a source of Type A, B, and
E trivalent antitoxins
▪ Respiratory and cardiac support
▪ Penicillin
▪ Attention to home-preserved food
▪ Addition of preservatices (sodium nitrate, salt,
and vinegar)
▪ Toxin is sensitive to 100°C

120
Q

found in soil and occasionally in animal feces

A
  • Clostridium botulinum
121
Q

Spores of c botulinum

A

Spores are highly heat-resistant, withstands
100°C for 3-5 hours (120°C to 5-10 minutes)

122
Q

Heat resistance is reduced by acidic pH or high
salt concentrations

A

c botulinum

123
Q

toxins of c botulinum

A

▪ Released during growth and autolysis of
bacteria
▪ It is found in 8 antigenic varieties A-G
▪ The principle cause for human disease A, B,
E, F

124
Q

Most common but not the sole cause of antibiotic
associated diarrhea and pseudomembranous
colitis

A
  • Clostridium difficile
125
Q

Part of the GI biota in about 5% of individuals,
although the colonization rate in patients
associated with long-term care facilities, such
as nursing homes and rehabilitation facilities, can
reach 20% of the population

A
  • Clostridium difficile
126
Q

Following antimicrobial therapy, many bowel biota
organisms other than C. difficile are killed, thus
allowing C. difficile to multiply with less
competition and produce high levels of two
toxins:

A
  • Clostridium difficile

toxin A, an enterotoxin, and toxin B, a
cytotoxin

127
Q

Bloody diarrhea with associated necrosis of
colonic mucosa is seen in patients with
pseudomembranous colitis

A
  • Clostridium difficile
128
Q

toxin of c difficile

A

two
toxins: toxin A, an enterotoxin, and toxin B, a
cytotoxin

129
Q

myonecrosis occurs when

A

Usually occurs when organisms contaminate
wounds, through trauma or surgery

130
Q

what causes myonecrosis

A

C. perfringens, C. histolyticum, C. septicum, C.
novyi, and C. bifermentans

131
Q

Myonecrosis clinical manifestation

A
  • Pain and swelling in the affected area
  • Bullae (fluid-filled blisters)
  • Serous discharge
  • Discoloration
  • Tissue necrosis
132
Q

extensive surgical debridement of the necrotic
tissue is often required.

If treatment is delayed, amputation of the affected
limb is not uncommon

A

myonecrosis of c difficile

133
Q

most common cause of myonecrosis

A

c perfringens

134
Q

Gram-Positive, Non–Spore-Forming Anaerobic
Bacilli

A

Actinobacteria and the
Firmicutes

135
Q

Result of shift in vaginal biota resulting in the
overgrowth of other endogenous anaerobes such as
Mobiluncus spp., Bacteroides spp., Prevotella spp.,
anaerobic gram-positive cocci, Gardnerella vaginalis

A

bacterial vaginosis

136
Q

Diagnosed based on critical appearance and a gram
stain of vaginal secretions

A
  • Bacterial vaginosis
137
Q

diagnosing bv

A

Wet mounts may show Trichomonas, but if negative, a
Gram stain should be done to rule out Gardnerella

138
Q

Important clinical genera of actinobacteria

A

Important clinical genera: Actinomyces, Bifidobacterium,
Eggerthella, Mobiluncus, and Propionibacterium

139
Q

Actinomycosis is due to

A

Caused by Actinomyces israelii, Proprionibacterium
and Bifidobacterium

140
Q

o Chronic granulomatous infectious disease

A

Actinobacteria

141
Q

Characterized by the development of sinus tracts and
fistulae which erupt to the surface and drain pus that
may contain “sulfur granules”

A

Actinomycosis

actinobacteria

142
Q

– dense clumps of bacteria that
may be colored

A

Sulfur granules

143
Q

Most common site of actinomycosis

A

Most common site is the maxillary region and the
female genital tract

144
Q

Firmicutes

A

Lactobacillus

145
Q

o Appear as coccoid or spiral-shaped organisms

A

Lactobacillus

146
Q

o Widely distributes in nature and foods

A

Lactobacillus

147
Q

o Normal biota in the mouth, GIT, and female genital tract

A

Lactobacillus

148
Q

Help protect the health of female genital tract by
producing lactic acid from glycogen

A

Lactobacillus

149
Q

Lactobacilli lowers vaginal pH which suppresses
overgrowth of

A

Mobiluncus, Prevotella, and Gardnerella

150
Q

anaerobe o Associated with endocarditis, the most common clinical
disease it can cause

A

lactobacillus

151
Q

Pinpoint α-hemolytic colonies on SBA, medium
size, gray color and rough on other media

A

o Lactobacillus acidophilus

152
Q

o Lactobacillus acidophilus

treatment

A
  • Frequently resistant to cephalosporins
  • Treatment is usually P with an aminoglycoside
153
Q

Anaerobic Gram-Negative Bacilli

A

Most commonly encountered in clinical specimens include
members of the B. fragilis group and the genera
Porphyromonas, Prevotella, and Fusobacterium

154
Q

More virulent and antimicrobial resistant than many other
anaerobic bacteria

A

Anaerobic Gram-Negative Bacilli

155
Q
  • Predominant members of the GI biota
A

Anaerobic Gram-Negative Bacilli

156
Q

*` – commonly isolated in blood cultures

A

B. fragilis

157
Q

Anaerobic Gram-Negative Bacilli

  • Clinical Infections
A

o Peritoneal infections
o Septicemia
o Abcesses such as diabetic foot ulcers, decubitus
pressure sores
o Lemierre disease -
o Brain abscesses -

158
Q

a syndrome of thrombophlebitis of
the jugular vein that occurs rarely

A

Lemierre disease

159
Q

Lemierre disease

A

F. necrophorum

160
Q

Anaerobic Cocci

A

Veilonella and Finegoldia

161
Q

most pathogenic anaerobic cocci
and most often isolated in pure culture

A

Finegoldia magna

162
Q

Seen in brain abscesses, lung abscess, gingivitis,
periodontal diseases

A

Anaerobic Cocci

163
Q
  • Often associated with polymicrobic infections
  • Occasionally recovered from blood cultures or following
    orthopedic surgery
  • inhabits oral cavity
A

Anaerobic Cocci

164
Q

4 GENERA OF ANEROBIC COCCI

A

4 genera: Peptostreptococcus, Anaerococcus, Finegoldia,
Peptoniphilus

165
Q
  • Formerly Peptostreptococcus
A

Anaerobic Cocci

166
Q

Should be used only when aspiration of material is not
possible and a biopsy specimen is not available

A

Swabs

167
Q
A