anaerobic bacteria

Question 1

List normal anaerobic flora in oral cavity, colon, female genital tract and skin

Answer 1

Oral cavity: Bacteroides. Colon: Bacteroides, Peptostreptococcus, Fusobacterium, Clostridium, Lactobacillus. Female genital tract: Lactobacillus. Skin: Propionibacterium

Question 2

features of anaerobic gram-negative rods/ anaerobic cocci infections

Answer 2

Organisms are members of normal flora and rarely cause disease without predisposing condition. Autoinfection- normal flora transgresses epithelial barrier. typically “polymicrobial”, or “mixed infections”, containing both anaerobic and facultative or aerobic organisms. biphasic pattern- aerobes and facultative organisms predominate at first, then create an anaerobic environment for anaerobes.

Question 3

Chronic abscess formation

Answer 3

The later stage of anaerobe infection - The abscess is conducive to maintaining a low oxygen tension environment and provides protection from host defenses and antimicrobial agents

Question 4

treatment of anaerobic infections

Answer 4

frequently requires surgical drainage of abscesses and debridement of devitalized tissue, along with appropriate antimicrobial agents

Question 5

Bacteroides fragilis structure

Answer 5

anaerobic, aerotolerant. Gram-negative rods that appear pleomorphic and stain irregularly. Positive catalase test, tolerant to bile, resistant to kanamycin, vancomycin and colistin.

Question 6

B. fragilis virulence factors

Answer 6

a. Fimbrae (pili) mediate adherence to epithelial cells.b. Extracellular enzymes such as phospholipase A, collagenase, heparinase result in tissue damage. c. Superoxide dismutase (plus catalase) enhances the ability of the organism to survive under less than stringent anaerobic conditions in the host. d. Polysaccharide capsule- abscess formation.

Question 7

Host responses to B. fragilis

Answer 7

a. Antibodies to capsular polysaccharide enhance killing but do not protect against abscess formation. b. Specific T-cell immunity is induced by capsular polysaccharide and protects against abscess. c. B. fragilis LPS lacks the lipid A (endotoxin) moiety. Thus, septic shock is not commonly associated with B. fragilis bacteremias.

Question 8

List the causes of tetanus, botulism and food poisoning/ gas gangrene

Answer 8

tetanus: Clostridium tetani. Botulism: C. botulinum. Food poisoning/ gas gangrene: C. perfringens

Question 9

C. tetani and botulinum toxins

Answer 9

Both are “typical” two subunit AB toxins; one subunit promotes specific host-cell binding and uptake, and the second subunit is a specific protease that mediates the toxic activity. The mechanism of action is cleavage of specific proteins at the synaptic cleft, thereby blocking release of neurotransmitters

Question 10

Clostridium tetani structure

Answer 10

Gram-positive, spore-forming rods. Sporulating cells have a characteristic “tennis racquet” shape. Organisms are difficult to isolate and lesions are often inconspicuous, so diagnosis is on the basis of clinical criteria.

Question 11

Clostridium tetani pathogenesis

Answer 11

C. tetani spores are usually introduced into wounds by environment. Locally produced tetanus toxin (tetanospasmin) is transported to by retrograde axonal transport along peripheral motor neurons. Toxin binds to gangliosides on presynaptic internucial cells of the spinal cord (Renshaw cells). There, the toxin interferes with release of the inhibitory neurotransmitters (GABA, glycine). This results in unopposed motor excitation and generalized spasticity (spastic paralysis). Toxin binding is irreversible; recovery requires formation of new axonal terminals.

Question 12

C. tetani transmission

Answer 12

C. tetani is widespread in feces of domestic animals and man; its spores are abundant in soil and the environment

Question 13

Tetanus clinical

Answer 13

Incubation period ranges from a few days to 3 weeks. Generalized tetanus is characterized by trismus (lockjaw), neck stiffness, difficulty swallowing, rigidity of abdominal and back muscles and fever. The highest mortality is in newborns where disease progression in rapid

Question 14

tetanus prevention/ treatment

Answer 14

i) debridement of the wound ii) treatment with an antimicrobial such as metranidazole iii) passive immunization with human tetanus immunoglobulin, iv) vaccination with tetanus toxoid. Antitoxin antibodies work by neutralizing free toxin. However, toxin that is already bound to nerve endings cannot be neutralized with antibody. Tetanus is preventable by immunization with tetanus toxoid.

Question 15

neonatal tetanus

Answer 15

illness caused by infection with Clostridium tetani, usually of the umbilical stump. The case-fatality ratio for this infection is greater than 80%; it is preventable with maternal vaccination, hygienic birth practices to ensure infection is not contracted by mother or newborn during the birth process and proper cord care to ensure that contamination of cord does not put the newborn at risk.

Question 16

Clostridium botulinum structure

Answer 16

Anaerobic, Gram-positive, spore-forming rod. Pressure sterilization is required to kill the spores. Seven antigenically distinct forms of botulism toxin (A-G) are described; A, B, E and F are associated with human disease. The toxins are phage-encoded (e.g., lysogenic conversion); each strain produces a single toxin type.

Question 17

C. botulinum pathogenesis

Answer 17

Botulinum neurotoxin is one of the most potent toxins known. It is released during growth or sporulation of C. botulinum. Although C. botulinum spores remain viable for several hours at 100°C, preformed botulinum toxin is rather heat labile and is destroyed by boiling for 10 minutes or heating to 80°C for 30 minutes.
Botulism is similar in structure and function to tetanus toxin, except that botulinum is very specific for cholinergic nerves. The toxin blocks release of the neurotransmitter acetylcholine at the neuromuscular junction. Botulinum neurotoxin is one of the most potent toxins known. It is released during growth or sporulation of C. botulinum. Although C. botulinum spores remain viable for several hours at 100°C, preformed botulinum toxin is rather heat labile and is destroyed by boiling for 10 minutes or heating to 80°C for 30 minutes.
Botulism is similar in structure and function to tetanus toxin, except that botulinum is very specific for cholinergic nerves. The toxin blocks release of the neurotransmitter acetylcholine at the neuromuscular junction.

Question 18

foodborne botulism

Answer 18

Preformed toxin resists digestion in the GI tract and is absorbed. Symptoms generally begin 18 to 36 hours after eating a contaminated food, but they can occur as early as 6 hours or as late as 10 days

Question 19

infant botulism

Answer 19

consumption of certain foods (esp. raw honey) by infants. Ingested spores germinate and produce toxin in the GI tract.

Question 20

wound botulism

Answer 20

toxin production by organisms contaminating traumatic wounds.

Question 21

botulism sx

Answer 21

Typical symptoms begin with blurred vision with fixed dilated pupils, dry mouth, constipation and abdominal pain. . Flaccid paralysis develops with bilateral descending weakness of the peripheral muscles; death is attributed to respiratory paralysis.

Question 22

botulism treatment

Answer 22

Diagnosis is confirmed by demonstrating: i) botulinum toxin in the blood; ii) toxin and/or C. botulinum organisms in the stool or the implicated food source.

Question 23

botulism treatment and prevention

Answer 23

Treatment includes i) support ventilation, and ii) polyvalent antitoxin. Antitoxin neutralizes circulating toxin, but cannot reverse effects of toxin already bound to neurons. Recovery requires regeneration of affected nerve endings, and may take weeks to months. Botulism can be prevented by proper canning

Question 24

transmission of botulism as bioterrorism

Answer 24

inhalation botulism- absorption of inhaled, aerosolized toxin across the mucosal surface of the lung

Question 25

Clostridium perfringens structure/ growth

Answer 25

Gram-positive spore-forming rods, although spores are seldom seen in clinical specimens. Gram-stain of wound exudates are notable for the absence of PMN’s due to the cytotoxic effects of alpha toxin. C. perfringens has an exceptionally fast growth rate, with a generation time of 8 minutes. The organism is relatively aerotolerant.

Question 26

C. perfringens virulence factors

Answer 26

12 toxisn that are active on tissues, plus an enterotoxin. The most important is alpha toxin, a phospholipase C (lecithinase) that cleaves phosphatidyl choline, a major lipid component of eukaryotic cell membranes. It is lyses a variety of cell types, including RBC’s, platelets, leukocytes and endothelial cells; resulting in destruction of vital tissue and widespread capillary damage

Question 27

C. perfringens transmission

Answer 27

common component of the normal intestinal flora of humans and animals, and is very commonly isolated from soil and water. Spores may survive for extended periods.

Question 28

C. perfringens diseases

Answer 28

1. food poisoning- enterotoxin produced during sporulation in large intestine causing cramps and watery diarrhea. Self limited. 2. soft tissue infections: cellulitis, fasciitis and myonecrosis (gas gangrene).

Question 29

describe gas gangrene

Answer 29

clostridial myonecrosis is a life-threatening, progressively destructive infection of a contaminated wound. Sudden onset of pain around the wound, followed rapidly by discoloration, swelling, and the appearance of foul-sweet smelling watery exudate. There is crepetis (gas bubbles in tissue) and general toxemia. Infection extends deep into tissue to involve muscle, which is devitalized and has the appearance of cooked meat. The usual setting is that of a crushing-type traumatic wound (gunshot, industrial and automobile accidents) in which there is considerable tissue damage and impaired bloodflow to the area (i.e. creation of an anaerobic environment). Nearly half of incidents occur following bowel surgery.

Question 30

c. perfringens treatment

Answer 30

Surgical debridement to remove dead tissue and antibiotic therapy. Hyperbaric oxygen may be useful since high oxygen tension inhibits growth and toxin production

Question 31

C. difficile disease

Answer 31

normal flora of some. Disease typically develops in hospitalized patients during broad-spectrum antibiotic treatment of an unrelated condition. In these patients, antibiotic treatment alters the normal enteric flora, allowing either 1) overgrowth by endogenous C. difficile, or 2) makes the patient more susceptible to colonization and infection by exogenous organisms.

Question 32

C. difficile transmission

Answer 32

This is perhaps the only clostridial disease in which there is significant risk of person-to-person spread. Spread of the organism is facilitated by the ability of C. difficile to readily sporulate, and spores are resistant to alcohol-based hand sanitizer

Question 33

C. difficile pathogenesis

Answer 33

toxin A (an enterotoxin) and toxin B (a cytotoxin). Toxins are phage encoded, and only certain strains of C. difficile are lysogenized, produce toxin and capable of causing disease.

Question 34

C. difficile diagnosis

Answer 34

Diagnosis is made by detecting C. difficile toxin in patient stool by a cytotoxicity assay or ELISA, or by isolation of toxin-producing C. difficile from patient stool. Rapid PCR-based methods are being developed.

Question 35

C. difficile treatment

Answer 35

metronidazole (first line drug) and oral vancomycin (second-line drug). Prolonged treatment is indicated and recurrence of disease is not uncommon

Question 36

list the sources of infectin for the 4 types of clostridium

Answer 36

botulinum: soil and water. Tetani: man, animals, soil and water. Perfringens: man, animals, soil and water. Difficile: man, fomites