ANAEROBIC BACTERIA Flashcards
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
superoxide dismutase and catalase,
anaerobes lack
Lack superoxide dismutase and catalase,
(enzymes for oxygen tolerance)
catalase
Obligate anaerobic prokaryotes
may live by
fermentation, anaerobicrespiration, bacterial photosynthesis, or the novel process of
methanogenesis
Survive some oxygen exposure but will not be able to
perform metabolic function
Obligate anaerobes
exampleof obligate anaerobe
o Many belong to this type
o Include Archaea such as methanogens and bacteria
(e.g., ABC – Actinomyces, Bacteroides, and
Clostridium)
o Cannot use O2
o Not damaged by O2
- Aerotolerant anaerobes
what type of metabolism does aerotolerant anaerobes have
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
- Aerotolerant anaerobes
o E.g., Lactobacillus, Proprionibacterium,
Clostridium.
Most strains of
streptococci,
o Can use O2
o Can survive without O2
- Facultative anaerobes (facultative aerobes)
Require the oxygen concentration to be reduced to 5%
or less
Microaerophile
Microaerophile
o E.g., Campylobacter, Helicobacter1
Grow best when the concentration of carbon dioxide is
increased to the range of 5% to 10% in a CO2 incubator
Capnophilic
Capnophilic
o E.g., Some anaerobes, Neisseria
Facultative
anaerobe
Enterobacteriaceae,
most staphylococci
Obligate aerobe
Mycobacteria, fungi
Obligate anaerobes
- 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
Strict anaerobic
environment (0%
O2)
Obligate
anaerobe
Reduced
concentrations of O2 (anaerobic
system and
microaerophilic
environments)
Aerotolerant
anaerobe
Multiplies well in
the presence or
absence of O2
Facultative
anaerobe
5% O2
Microaerophile
5%–10% CO2
Capnophile
15%–21% O2
(as found in a
CO2 incubator
or air)
Obligate aerobe
During oxidation-reduction reactions that occur during
normal cellular metabolism, molecular oxygen is reduced to
superoxide anion (O2−
) and hydrogen peroxide (H2O2) in a
stepwise manner
superoxide anion reacts with hydrogen peroxide in the presence of iron (Fe3+/Fe2+) to generate the
to generate the hydroxyl
radical (·OH) the most potent biological oxidant known
- Most can survive in 3-5% O2
anaerobes
Where are Anaerobes found?
- 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
exogenous vs endogenous
- Endogenous – intestinal tract of animals; oral
cavity of animals - Exogenous – exist outside the bodies of animals
- Most anaerobic infections are endogenous
Non-spore forming, gram-positive bacilli are divided into
two phyla:
o Actinobacteria – Actinomyces, Bifidobacterium,
Mobiluncus, Eggerthella and Proprionibacterium
o Firmicutes – Lactobacillus
Former Peptostreptococcus is now re-classified into at
least 5 different genera
o Peptostreptococcu
o Anaerococcus
o Finegoldia
o Parvimonas
o Peptophilus
Gram-positive,
endosporeforming bacilli
Clostridium
diseases caused by clostridium
- perfringens Gas gangrene
-tetanus Tetanus
-botulinum Botulism
Gram positive,
non-sporing
bacilli
Actinomyces
Eubacterium
Bifidobacterium
Proprionibacterium,
Mobiluncus,
Lactobacillus
Eubacterium
disease
Infections of
female genital
tract, intraabdominal
infections,
endocarditis
Propionibacterium
disease
Difficult to assess;
had clinical
significance in
cultures of blood,
bone marrow,
and spinal fluid
Bifidobacterium
disease
Occasionally
isolated from
blood;
significance not
established
Gram-negative,
non-sporing
Bacteroides
Fusobacterium and
Prevotella
Poryphromonas
Leptotrichia
Bacteroides
disease
nfections of
female genital
tract,
intraabdominal
and
pleuropulmonary
infections, wellestablished as a
pathogen
Fusobacterium and
Prevotella
disease
Same as
Bacteroides but
less frequent
Infections of
female genital
tract,
intraabdominal
and
pleuropulmonary
infections, wellestablished as a
pathogen
Leptotrichia
disease
Found in mixed
infections in oral
cavity or
urogenital areas;
significance not
established
Gram-positive
cocci
Peptococcus
Peptostreptococcus
(anaerobic
Streptococci)
Veilonella
Peptostreptococcus
(anaerobic
Streptococci)
disease
Infections of
female genital
tract,
intraabdominal
and
pleuropulmonary
infections, often
found with
Bacteroides;
established
pathogen
Veilonella
disease
Found in mixed
anaerobic oral
and
pleuropulmonary
infections,
significance not
established
disease
Factors that Predispose Patients to Anaerobic
Infections
- 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
Clinical Manifestation Suggestive of Anaerobic
Infection
- 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
Indications of Involvement of Anaerobes in
Infectious Processes
- 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
Promotes
abscess
formation;
antiphagocytic
function
Polysaccharide
capsules
Fimbriae, fibrils
enable organisms
to adhere to cell
surfaces
Adherence
factors
Catalyze the
degradation of
collagen
Collagenases
Toxic to specific
types of cells
Cytotoxins
Destroy DNA
DNases
Certain
Clostridium spp
Toxic to cells of
the intestinal
mucosa
EnterotoxinsC. difficile
Lyse red blood
cells liberating
hemoglobin
Hemolysins
Certain
Clostridium spp
Catalyzes the
hydrolysis of
hyaluronic acid,
the cement
substance
of tissues
Hyaluronidase
Certain
Clostridium spp
Catalyze the
hydrolysis of ester
linkages between
fatty acids and
glycerol of
triglycerides and
phospholipids
Lipases
Destroy or disrupt
nerve tissue
Neurotoxins
(e.g., botulinum
toxin,
tetanospasmin)
C. botulinum, C.
tetani
Catalyze the
splitting of host phospholipids
(lecithinase)
Phospholipases
Certain
Clostridium spp.
Split host proteins
by hydrolysis of
peptide bonds
Proteases
Certain
Clostridium spp.
Diameter of the spore is larger than the cell, resembling a
spindle
Clostridium
clostridium Spore location – terminal end
- Spore location – terminal end
- Classification of clostridium based on the type of disease produced
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
Gas gangrene (myonecrosis)
– 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
Food sources involved commonly in
botulism include
home-canned vegetables,
home-cured meat such as ham, fermented
fish, and other preserved foods
- Caused by pre-formed toxins
clostridium A, B and E
Botulism
enterotoxin of clostidium A-G enterotoxins cause
flaccid type of
paralysis
Toxin attached to the neuromuscular
junction of nerved and prevents
transmission of Acetylcholine
Botulism
when present is a marker of GI
malignancy
C. septicum
o Affect CNS of the host
- Tetanus (Lock-jaw)
- Antibiotic-Associated Colitis (C. difficile)
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
Dead tissue, blood clots, foreign matter, aerobic
organisms develop anaerobic condition in an
injury
d. Lecithinase C (α-toxin)
At birth under unhygienic conditions babies can get –
tetanus neonatorum
o Neuromuscular disease
- Clostridium tetani
Entrance of spores through accidental puncture
wounds (e.g., burns, umbilical stumps, frostbite,
crushed body parts)
- Clostridium tetani
o Drumstick appearance
- Clostridium tetani
o Grow on Robertson’s cooked medium
Clostridium
loc of c tetani
o Soil/intestine/vagina
o Motile with peritrichous flagella
- Clostridium tetani
toxins of c tetani
- tetanokysin
- tetanoplasmin
-spore germinate
-ascending tetanus
-descending tetanus
heat and oxygen labile/lyse RBC
Tetanolysin
– heat and oxygen stable/ highly
lethal; dies within 1-2 days; gets easily neutralized
with antitoxin
Tetanospasmin
Act at the synaptic junction, preventing the
synthesis of acetylcholine, preventing synaptic
transmission
Toxins of c tetani
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)
Spores germinate –
when toxins spreads
upwards along the spinal cord towards CNS; gives
generalized spasms
Ascending tetanus
– when toxin is given IV,
spasms will appear in the musscles of the head,
neck and spreads downwards
Descending tetanus
spasms of
the masseter muscle
Early symptom is trismus (lock jaw)
– the semblance of a grin
caused by facial spasm especially in tetanus at the
angle of the mouth
Risus sardonicus
back is slightly curved
Opisthonotus
c tetani treatment
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)
disease caused by c tetani
- trismus or lock jaw or tetanus
- risus sardonicus
-opithosnotus
o Prevention and Control
- 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
Food poisoning:
type of clostridium and severity
Type A, a relatively mild and selflimited GI illness, and type C, a more serious but rarely
seen disease
usually follows the
ingestion of large numbers of enterotoxin-producing
strains in contaminated food
C. perfringens foodborne disease
Lacks the ability to produce a number of essential
amino acids
Clostridium perfringens
type of food implicated in c perfringens
meats and gravies are commonly
implicated in outbreaks
Food poisoning caused by C. perfringens type A is
caused by a
C. perfringens enterotoxin linked to
sporulation
what happens after an 8-30hour incubation period of c perfringens
After an 8-30-hour incubation period, the patient
experiences diarrhea and cramping abdominal pain
for about 24 hours.
Other than fluid replacement, therapy is usually
unnecessary.
- Clostridium perfringens
what happens after incubation period of 5-6hours in c perfringens
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.
Early symptoms are followed by necrotic inflammation
of the small intestines, at times leading to
bowel
perforation
fatality rate is 15% to 25%
c perfringens
Most common cause of bacteremia and
myonecrosis
c perfringens
- from the ingestion of preformed botulinum
toxins A, B, and E, produced in food
Botulism
revents the release of acetylcholine
(a neurotransmitter), which results in flaccid
paralysis and death
Botulinum toxin
is also used medically
to treat strabismus (wandering and chronic migraines,
and as a beauty enhancer by temporarily improving
facial wrinkles
Botulinum toxin type A (Botox)
wandering and chronic migraines,
and as a beauty enhancer by temporarily improving
facial wrinkles.
strabismus
potential bioterrorism agents
- Clostridium botulinum
diagnosis of c botulism
a. Isolation or organism in food/feces
b. Detection of toxin in feces/serum
Incubation period of c botulism
Incubation period 12-36 hours
Diplopia, dysphagia and dysphonia
c botulism
difficulty in swallowing
Dysphagia
difficulty in speaking due to physical
disorder of the mouth, throat or vocal cords
Dysphonia
double vision
Diplopia
- Mortality rate is 65-70%
- Clostridium botulinum
- Paralysis of muscles and respiratory system
c botulinum
▪ Weak-sucking response
▪ Weakness and cachexia
▪ Generalized loss of tone
▪ Flaccid paralysis
- Infant botulism
spores in infant botulism
▪ Spores are common in dust and soil
▪ Spores germinate in the intestine and give off
neurotoxin
The spores enter a wound or puncture much
as in tetanus
- Wound botulism
he symptoms are similar to those of foodborne
- Wound botulism
▪ More common in drug abusers
wound botulism
- Treatment and Prevention
c botulinum
▪ 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
found in soil and occasionally in animal feces
- Clostridium botulinum
Spores of c botulinum
Spores are highly heat-resistant, withstands
100°C for 3-5 hours (120°C to 5-10 minutes)
Heat resistance is reduced by acidic pH or high
salt concentrations
c botulinum
toxins of c botulinum
▪ 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
Most common but not the sole cause of antibiotic
associated diarrhea and pseudomembranous
colitis
- Clostridium difficile
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
- Clostridium difficile
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:
- Clostridium difficile
toxin A, an enterotoxin, and toxin B, a
cytotoxin
Bloody diarrhea with associated necrosis of
colonic mucosa is seen in patients with
pseudomembranous colitis
- Clostridium difficile
toxin of c difficile
two
toxins: toxin A, an enterotoxin, and toxin B, a
cytotoxin
myonecrosis occurs when
Usually occurs when organisms contaminate
wounds, through trauma or surgery
what causes myonecrosis
C. perfringens, C. histolyticum, C. septicum, C.
novyi, and C. bifermentans
Myonecrosis clinical manifestation
- Pain and swelling in the affected area
- Bullae (fluid-filled blisters)
- Serous discharge
- Discoloration
- Tissue necrosis
extensive surgical debridement of the necrotic
tissue is often required.
If treatment is delayed, amputation of the affected
limb is not uncommon
myonecrosis of c difficile
most common cause of myonecrosis
c perfringens
Gram-Positive, Non–Spore-Forming Anaerobic
Bacilli
Actinobacteria and the
Firmicutes
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
bacterial vaginosis
Diagnosed based on critical appearance and a gram
stain of vaginal secretions
- Bacterial vaginosis
diagnosing bv
Wet mounts may show Trichomonas, but if negative, a
Gram stain should be done to rule out Gardnerella
Important clinical genera of actinobacteria
Important clinical genera: Actinomyces, Bifidobacterium,
Eggerthella, Mobiluncus, and Propionibacterium
Actinomycosis is due to
Caused by Actinomyces israelii, Proprionibacterium
and Bifidobacterium
o Chronic granulomatous infectious disease
Actinobacteria
Characterized by the development of sinus tracts and
fistulae which erupt to the surface and drain pus that
may contain “sulfur granules”
Actinomycosis
actinobacteria
– dense clumps of bacteria that
may be colored
Sulfur granules
Most common site of actinomycosis
Most common site is the maxillary region and the
female genital tract
Firmicutes
Lactobacillus
o Appear as coccoid or spiral-shaped organisms
Lactobacillus
o Widely distributes in nature and foods
Lactobacillus
o Normal biota in the mouth, GIT, and female genital tract
Lactobacillus
Help protect the health of female genital tract by
producing lactic acid from glycogen
Lactobacillus
Lactobacilli lowers vaginal pH which suppresses
overgrowth of
Mobiluncus, Prevotella, and Gardnerella
anaerobe o Associated with endocarditis, the most common clinical
disease it can cause
lactobacillus
Pinpoint α-hemolytic colonies on SBA, medium
size, gray color and rough on other media
o Lactobacillus acidophilus
o Lactobacillus acidophilus
treatment
- Frequently resistant to cephalosporins
- Treatment is usually P with an aminoglycoside
Anaerobic Gram-Negative Bacilli
Most commonly encountered in clinical specimens include
members of the B. fragilis group and the genera
Porphyromonas, Prevotella, and Fusobacterium
More virulent and antimicrobial resistant than many other
anaerobic bacteria
Anaerobic Gram-Negative Bacilli
- Predominant members of the GI biota
Anaerobic Gram-Negative Bacilli
*` – commonly isolated in blood cultures
B. fragilis
Anaerobic Gram-Negative Bacilli
- Clinical Infections
o Peritoneal infections
o Septicemia
o Abcesses such as diabetic foot ulcers, decubitus
pressure sores
o Lemierre disease -
o Brain abscesses -
a syndrome of thrombophlebitis of
the jugular vein that occurs rarely
Lemierre disease
Lemierre disease
F. necrophorum
Anaerobic Cocci
Veilonella and Finegoldia
most pathogenic anaerobic cocci
and most often isolated in pure culture
Finegoldia magna
Seen in brain abscesses, lung abscess, gingivitis,
periodontal diseases
Anaerobic Cocci
- Often associated with polymicrobic infections
- Occasionally recovered from blood cultures or following
orthopedic surgery - inhabits oral cavity
Anaerobic Cocci
4 GENERA OF ANEROBIC COCCI
4 genera: Peptostreptococcus, Anaerococcus, Finegoldia,
Peptoniphilus
- Formerly Peptostreptococcus
Anaerobic Cocci
Should be used only when aspiration of material is not
possible and a biopsy specimen is not available
Swabs
