Mid Anaerobes

Front 1

Strict anaerobe

Back 1

Unable to grow in the presence of more than 0.5% oxygen

Front 2

Moderate anaerobe

Back 2

Capable of growing at between 2% to 8% oxygen

Front 3

Facultative anaerobe

Back 3

Can gow both in the presence and absence of air

Front 4

Microaerophilic

Back 4

Grows poorly or not at all in air, but distinctly better in anaerobic condtions

Front 5

Clostridium Perfringes

Back 5

-Gram positive bacilli
-Anaerobic
-Spore producing
-alpha, beta, theta toxin, enteroxin producing

Front 6

Clostridium tetani

Back 6

-Gram positive bacilli
-Anaerobic
-Spore producing
-Botulinum tetanospasmin toxin producing

Front 7

Clostridium botulinum

Back 7

-Gram positive bacilli
-Anaerobic
-Spore producing
-Botulinum toxin producing

Front 8

Clostridium dificile

Back 8

-Gram positive bacilli
-Anaerobic
-Spore producing
-A enterotoxin, B cytotoxin producing

Front 9

Bacteroides fragilis

Back 9

-Gram negative bacilli
-Anaerobic
-Polysaccharide capsule (aids in abscess formation)

Front 10

alpha-toxin

Back 10

-From C perfringes
-Lecithinase (PLC) that lyses erythrocytes, platelets and endothelial cells. Increases vascular permeability, resulting in massive hemolysis and bleeding and tissue destruction (myonecrosis)

Front 11

beta toxin

Back 11

-Formed by C. perfringes
-Necrotizing activity, responsible for lesions in necrotizin enteritis

Front 12

theta toxin

Back 12

-Formed by C. perfringes
-Heat and oxygen labile hemolysis; cytolytic

Front 13

C. perfringes enterotoxin

Back 13

Heat-labile, produced during phase transition from vegetative cells to spores and released when cells are lysed. Binds to the brush border membrane of the small intestine and disrupts transport and membrane permeability

Front 14

Tetanospasmin

Back 14

-From C. tetani
-Heat-labile neurotoxin produced during the stationary phase of growth, which is released when the cell is lysed. Tetanospamin is a metalloproteinase that enzymatically degrades a protein required for docking of neurotransmitter vesicles on presynaptic membranes. Loss of this function blocks the release of neurotransmitters for the inhibitory synapses causing excitatory synaptic activity to be unregulated. Toxin binding is irreversible.

Front 15

Botulinum

Back 15

-Produced by C. botulinum
-Blocks neurotransmission at peripheral cholinergic synapses by preventing release of the neurotransmitter ACh. Binding is irreversible and recovery depends upon regeneration of nerve endings.

Front 16

Toxin A

Back 16

-Produced by C. dificil
-Enterotoxin
-Produces chemotaxis of PMNs, induces cytokine production, hypersecretion of fluid, and hemorrhagic necrosis

Front 17

Toxin B

Back 17

-Produced by C. dificil
-Cytotoxin
-Induces polymerization of actin with loss of cellular cytoskeleton

Front 18

P. acnes

Back 18

-Gram positive bacillus
-Propionibacterium
-Produces propionic acid as a major byproduct of fermentation
-Colonize skin, conjunctiva, external ear, oropharynx, female GU tract
-Causes acne - resides n sebaceous follicles
-Opportunistic infections on prosthetic devices

Front 19

Actinomyces

Back 19

-Gram positive bacillus
-Facultative or strict anaerobe
-Colonizes upper respiratory tract, GI, female GU tract
-Causes actinomycosis

Front 20

Actinomycosis

Back 20

-From Actinomyces
-Endogenous disease, no person-person spread
-Low virulence, development of disease when normal mucosal barriers are disrupted (dental proc)
-Diagnosis made by examination on infected fluid
-Cervicofacial actinomycosis
-Chronic granulomatous lesions that become suppurative and form sinus tracts
-Slowly evolving, painless process
-Treatment: surgical debridement and prolonged penicillin

Front 21

Lactobacillus

Back 21

-Gram positive bacillus
-Facultative or strict anaerobes
-Colonizes GI and GU tract
-Certain strains produce H2O2 which is bactericidal to Gardenella vaginalis
-Clinical disease:
-Transient bacteremia from GU source
-Bacteremia in immunocompromized host
-Endocarditis (rare)

Front 22

Describe the clinical presentation of intra-abdominal infections

Back 22

-Biphasic clinical presentation
-Initially: Generalized peritonitis characterized by fever, diffuse abdominal pain, nausea, vomiting, and a rigid abdomen, followed by signs and symptoms of shock

-Second stage: Characterized by the formation of an intra-abdominal abscess, may be quite variable depending upon modification with antibiotics

-Bacteroides are the most common pathogens

Front 23

How do you treat an intra-abdominal infection?

Back 23

-Drainage of abscess
-Antibiotic therapy (immediately after results of culture)

Front 24

C. difficile colitis

Back 24

-Anlteration of the normal gut flora with antimicrobials favors C. difficile
-Disease occurs if organism proliferates in the colon and produces toxins A and B
-Toxin A causes disruption o f intercellular tight junctions followed by altered membrane permeability and fluid secretion
-Toxin B causes destruction of the cellular cytoskeleton
-Diarrhea begins 5-10 days after antibiotic treatment
-Mild/watery to Bloody and accompanied by abdominal cramping, leukocytosis and fever
-Colonic muscos can develop inflammatoryu plaques that coalesce into a pseudomembrane compoed of fibrin, leukocytes, and necrotic colonic cells

Front 25

How do you diagnose C. diffficile colitis? How do you treat?

Back 25

-Direct detection of toxins in stool
-Discontinue implicated antimicrobial agent and /or treatment with oral metronidazole or vancomycin
-Relapses requiring retreatment occur in 20% of patients because only the vegetative forms of C. difficile (no spores) are killed by antibiotics

Front 26

Clostridial myonecrosis

Back 26

-Gas gangrene
-Develops in traumatic wounds
with muscle damage after contamination with dirt or forming material
-Low oxidation-reduction potential favors spore germination and multiplication resulting in production of alpha and theta toxin
-Promotes vascular permeability and dema
-Intense pain and sense of heaviness and pressure develop at site of injury within 1-4 days
-Rapidly progresses to extensive muscle necrosis and shock (2 days of onset)
-Muscle contains gas from metabolic activity of rapidly dividing bacteria
-Many gram positive bacilli in absence of inflammatory cells
-Mortality: 40-100%

Front 27

How is clostridial myonecrosis treated?

Back 27

Surgical debridement and high dose penicillin

Front 28

Describe Tetanus

Back 28

-C. tetani spores are found in soil and colonize the GI tract of many animals
-Spores can enter wounds or infants if umbillical cord is cut in an unsterile manner
-C. tetani elaborate tetanospasmin
-Neurotoxin enters presynaptic terminal of lower motor neurons and reaches the CNS by retrograde axonal transport system
0Toxin blocks the postsynaptic inhibiton of spinal moror reflees in the anterior horn cells
-Results in spasmodic contraction of both protagonist and antagonist muscles
-Time to onset can be days to weeks

Front 29

What are the clinical manifestations of tetanus? How is diagnosis made? Treatment?

Back 29

-Generalized tetanus
-Sustained contraction of the masseter muscles or facial muscles
-Drooling
-Sweating
-Irritability
-Persistent back spasms

Diagnosis is made on basis of clinical symptoms

Treatment is debridement of primary wound and treatment with metronidazole to eliminate remaining vegetative bacteria, passive immunization with human tetanus immunoglobulin to bind free tetanospasmin and vaccination with tetanus toxoid.

Front 30

Botulism

Back 30

-Human disease is associated with botulinum toxins A, B, E, and F
-Botulinum toxin is very specific for cholinergic nerves
-Blocks neurotransmission at peripheral chloinergic synapses by preventing release of ACh.
-Most common presentations are infant botulism and foodborne botulism

Front 31

Infant botulism

Back 31

-Most common form of botulism in US
-C botulinum can surviv e in the infants GI tract, but not in the adult
-Affects infants less than 1 yo, especially those exposed to honey
-Symptoms are usually nonspecific but progressive disease may develop (flaccid paralysis, respiratory arrest)

Front 32

Food botulism

Back 32

-Starts 12-36 hours after ingestion
-Initial signs:
-Blurred vision
-Dry mouth
-Constipation
-Abdominal pain
-Fever absent
-Bilateral descending weakness of peripheral muscles develops in patients with progressive disease
-Complete reversal is dependent upon regeneration of affected nerve endings and may requires months to years

Front 33

How do you diagnose botulism? How do you treat it?

Back 33

-Diagnnosis confrimed if the organism is isolated or toxin activity is demonstrated
Treatment involves intensive supportive measures, elimination of GI carriage of organism (gastric lavage, metronidazole) and botulinum antitoxin to bind circulating toxin