Micro-Anaerobes

Front 1

What are the two board categories of anaerobic bacteria?

Back 1

1) Clostridum (genus) – in soil and also in gut
2) anaerobic members normal flora which escaped from usual location and invaded parts that are normally sterile.

There is some overlap between these two categories.

Front 2

Obligate anaerobes

Back 2

Bacteria which will not grow and cannot survive for very long in the presence of oxygen. Must be cultured in the absence of oxygen & must obtain their energy from fermentation instead of respiration.

Front 3

What bacteria are usually found on skin?

Back 3

Dry areas of the skin: the Staphylococcus epidermidis (facultative) predominant
& Propionibacterium (obligate anaerobes)
Oily areas of the skin - the Propionibacteria outnumber the Staph

Front 4

How can obligate anaerobes survive and grow on the skin?

Back 4

Growing in the skin, not on the skin, down in sweat & sebaceous glands, hair follicles, beneath the dead cells of the stratum corneum, in environments that are shielded from oxygen. Also, facultative bacteria growing in these same sites will consume oxygen there to lower local oxygen concentration.

Front 5

Why oxygen is detrimental to obligate anaerobes?

Back 5

May generate toxic derivatives of oxygen, which may then damage the cells (called "autoassassination").
Ex.- during metabolism H2O2 can be produced through the action of oxidases. This is toxic unless eliminated by enzymes such as catalase or peroxidase. Flavoprotein oxidase or dehydrogenases can cause the univalent (partial) reduction of oxygen, producing the very reactive and toxic superoxide anion.

Front 6

An alternate theory of why oxygen is detrimental to obligate anaerobes?

Back 6

Oxygen itself may react directly with sensitive targets in the cell, (ie iron-sulfur centers in the active sites of certain enzymes) oxidizing them to non-functional form & causing cell death. Obligate anaerobes may have more of these oxygen-sensitive targets than facultative or aerobic bacteria do.

Front 7

What reaction does superoide dismutase (SOD) catylze? Catalase?

Back 7

SOD: superoxide anion to oxygen plus hydrogen peroxide

Catalase turns H2O2 to O2 and H2O

Front 8

How are Anaerobic Bacteria cultured on solid media without being in anaerobic chambers ?

Back 8

Compressed anaerobic gas or gas-generated packets that are H20 activated (H reacts with O2 to eliminate most of it). Methylene blue indicator (colorless = anaerobic)

Front 9

How are Anaerobic Bacteria cultured in liquid media without being in anaerobic chambers ?

Back 9

Pre-reduced liquid medium must contain a reducing agent such as thioglycollate, beta-mercaptoethanol, or dithiothreitol to maintain anaerobic conditions. Methylene blue as indicator & agar to prevent convection

Front 10

General characteristics of Bacteroides?

Back 10

Anaerobic Gram-negative rods
Resistant to the aminoglycoside antibiotics, such as gentamicin and kanamycin

Front 11

3 most important pathogens in genus Bacteroides?

Back 11

B. fragilis, B. thetaiotaomicron, and B. melaninogenicus.

Front 12

General characteristics of B. fragilis?

Back 12

*The most important anaerobic pathogen in humans

obligately anaerobic, non-sporeforming, non-motile, Gram-negative, small pleomorphic rod, sometimes coccobacillus, has polysaccharide capsule

Front 13

B. fragilis pathogenesis?

Back 13

Polysaccharide capsule promotes abcess formation, LPS is weak endotoxin, produces superoxidase dismutase, catalase, neuraminidase, lipase and protease

Front 14

B. fragilis infections?

Back 14

Associated with intra-abdominal, lung, brain, and pelvic abscesses; also peritonitis, and septicemia. Also endocarditis (uncommon).

Front 15

What are the two bacteria that produce black-pigment on blood culture? Used to be considered part of which genus?

Back 15

PORPHYROMONAS AND PREVOTELLA

Bacteroides

Front 16

PORPHYROMONAS AND PREVOTELLA are found where? Cause what kind of infections?

Back 16

Commonly isolated from oral cavity (both) or vagina (Prevotella)

Cause infections of the head, neck, and respiratory tract, chronic periodontitis. Also pelvic or abdominal infections

Front 17

Characteristics of Fusobacterium?

Back 17

Anaerobic, G-, spindle-shaped bacilli normally found in the mouth. Have normal endotoxin & can produce septic shock/vascular collapse

Front 18

Peptococcus and Peptostreptococcus

Back 18

Anaerobic Gram-positive cocci, normal flora, ofter found in mixed anaerobic infections

Front 19

Propionibacterium acnes

Back 19

Gram positive anaerobic rod in normal skin flora, associated with inflammatory process of acne lesions

Front 20

CHARACTERISTICS OF ENDOGENOUS ANAEROBIC INFECTIONS

Back 20

1.Proximity to colonized mucosal surfaces.
2.Abscesses frequently seen.
3.Foul-smelling discharge
4.Presence of gas in tissues
5.Necrotic tissue.
6.Frequently are mixed obligate anaerobes and facultative
7.Not responsive to aminoglycosides; responsive to clindamycin or metronidazole.

Front 21

General Characteristics of Clostridium tetani

Back 21

Round terminal spores in long, narrow, pleomorphic rods
Motile (peritrichous flagella)
Colonies with "ground-glass" appearance, hemolytic, thin, spreading growth.

Front 22

Pathogenesis of Clostridium tetani (not specifics of toxin)&

Back 22

Spores enter wound, germinate, organisms multiply, produce toxin
Result is convulsive contraction of voluntary muscles; initially at site of injury, then jaw muscles ("lockjaw") and other voluntary muscles may become involved; death is due to respiratory failure

Front 23

Pathogenesis of Clostridium tetani TOXIN

Back 23

Intracellular protein released from bacterial cell by autolysis, not secretion
Toxin is split into two fragments of increased toxicity
Initially binds to peripheral nerve endings, then internalized & transported up axon to cell body of the neuron, in the spinal cord.

Then transported to inhibitory interneurons & binds to gangliosides in synaptic membranes. Inhibits the release of an inhibitory neurotransmitter.

Front 24

Treatment for Clostridium tetani TOXIN

Back 24

Antitoxin - use before toxin becomes fixed to nerve tissue.
Surgical debridement of wound site.
Antibiotic
"Booster" injection of tetanus toxoid (formalin-inactivated toxin)

Front 25

General Characteristics of Clostridium botulinum

Back 25

Oval, subterminal spores
Large, grayish colonies, hemolysis usually present

Front 26

3 forms of botulism are:

Back 26

classical form, recognized for many years;
wound botulism;
infant botulism, recognized for less than 20 years

Front 27

Pathogenesis of Classical botulism

Back 27

aka food-borne botulism
Flaccid paralysis and respiratory failure. Mortality rate formerly 70%, now reduced to about 10%. Fewer than 50 cases per year in the US.

Front 28

Pathogenesis of Wound botulism

Back 28

Rarest form of the disease in the US.
Wound is infected with C. botulinum spores, and toxin is produced in vivo. Can be seen in IV drug users

Front 29

Pathogenesis of Infant botulism

Back 29

C. botulinum infects GI tract of newborns and produces toxin in vivo. The source is frequently honey with viable spores. Mortality rate (1 to 2% lower than food-borne botulism. Affected infants may need respiratory support, but usually recover spontaneously. Infant botulism is 10x more frequent than food-borne

Front 30

Pathogenesis of C. botulinum toxin

Back 30

Highly neurotoxic. Inhibits the release of Ach at neuromuscular synapses. Result: flaccid paralysis. Most potent of all toxins found in nature; 1-2 ug will kill a human. Toxin genes are located on genome of lysogenic bacteriophage. Eight antigenic variants (A-H) of the toxin are known

Front 31

Treatment for C. botulinum toxin

Back 31

Trivalent antitoxin (against A,B,E toxin variants)
Maintain ventilation via mechanical respirator, if needed.
No antibiotics needed for foodborne; may be used in other two forms of botulism

Front 32

General Characteristics of Clostridium perfringens

Back 32

Very large rods, encapsulated within tissue, nonmotile
Spores are rare (oval, subterminal, not bulging)
Rapid growth, double zone of hemolysis on anaerobic blood agar plate.
Ferment carbohydrate in muscles with gas production.
Many varied toxins (cytolytic, histolytic enzymes) are produced (up to 12 reported).

Front 33

Pathogenesis of Clostridium perfringens - Wound infection

Back 33

Spores germinate, bacteria multiply, ferment carbohydrates & produce gas (distends tissue and interferes with blood supply), necrotizing toxins produced. Tissue necrosis extends, providing increased anaerobic opportunity for bacterial growth, hemolytic anemia, and ultimately severe toxemia and death

Front 34

Other types of Clostridium perfringens besides Wound infection

Back 34

Uterine infection. Septic abortion.
Septicemia
Food poisoning. Enterotoxin-producing strains, preformed toxin in food. Mild/common form of food poisoning. 3rd most common after S. aureus and Salmonella.
Enteritis necroticans. Rare. Acute infection of small intestine causing Necrosis and perforation. Mortality is 50%.

Front 35

Treatment for Clostridium perfringens infections

Back 35

Surgical debridement
Massive antibiotic therapy
Hyperbaric oxygen treatment.

Front 36

General characteristics of Clostridium difficile

Back 36

gram-positive anaerobic bacterium that induces iatrogenic infection - Pseudomembranous colitis; (caused by medical treatment)

Front 37

Pathogenesis of Clostridium difficile

Back 37

Antibiotic disrupts the normal bowel flora and allows overgrowth of antibiotic-resistant bowel flora, such as C. difficile. Produces a potent cytotoxin (causes diarrhea and kills colon epithelial cells) and results in the formation of necrotic plaques on the bowel mucosa. Leads to bowel perforation, peritonitis and death

Front 38

Diagnosis and treatment of Clostridium difficile

Back 38

Diagnosis is by detection of cytotoxin in stool. Treatment is to stop giving the antibiotic which caused the problem, start fluid replacement therapy, and start giving (orally) a different antibiotic which is effective against C. difficile, such as vancomycin