clostridium

Question 1

clostridium characteristics

Answer 1

a genus of gram-positive bacilli; capable of producing endospores; anaerobes - vegetative cells of the strictly anaerobic species are killed by exposure to oxygen but the endospores can exist in an oxygen-rich environment

Question 2

where are clostridium

Answer 2

in the soil, water, sewage and some are members of gastrointestinal microbiota in humans and animals

Question 3

why can clostridium cause disease easily

Answer 3

their ability to form endospores enables them to survive adverse environmental conditions; most grow rapidly in nutritionally, oxygen-free environments; each pathogenic species is capable of producing toxins

Question 4

clostridium perfringens virulence factors

Answer 4

Type A toxin is responsible for most human infections and produces the largest quantities of alpha toxin

alpha toxin - lethal toxin; lecithinase; increases vascular permeability; hemolysin; necrotizing activity

beta toxin - lethal toxin; necrotizing activity

enterotoxin - alters membrane permeability

Question 5

clostridium perfringens epidemiology

Answer 5

C. perfringens type A commonly inhabits the intestinal tract of humans and animals and is widely distributed in nature, particularly in soil and water contaminated with feces.

disease follows exogenous or endogenous exposure

Question 6

clostridium perfringens pethogensis and diseases

Answer 6

soft tissue infections occur if the bacteria are introduced into the tissue during surgery or through traumatic injury

simple wound contamination

cellulitis - bacterial invade the fascial planes but not invade muscle tissue

Question 7

suppurative myositis

Answer 7

(c. perfringes) - develops if cellulitis progresses and pus accumulates in the muscle planes; there is no muscle necrosis or systemic symptoms at this point

Question 8

clostridial myonecrosis (gas gangrene)

Answer 8

(c. perfringes) - life-threatening disease - due to abundant toxin production; extensive muscle necrosis; gas build up in the tissue is caused by the metabolic activity of the rapidly dividing bacteria

Question 9

clostridial food poisoning

Answer 9

(c. perfringens) - clostridial food poisoning; ingesting meat products contaminated with large numbers of C. perfringens type A producing enterotoxin; abdominal cramps, watery diarrhea, but no fever, nausea or vomiting, lasts less than 24 hrs

Question 10

necrotizing enteritis

Answer 10

(c. perfringes) - rare, actue disease causes by C. perfringens type C, which produces the beta toxin; the disease is characterized by a necrotizing jejunum causing abdominal pain, bloody diarrhea, shock, and peritonitis

Question 11

c. difficile

Answer 11

ubiquitous; colonizes the intestines of a small proportion of healthy individual (<5%); exposure to antibiotics, which eliminate many of the other bacterial species in the intestines, is associated with the overgrowth of C. difficile and subsequent disease in these previously healthy carriers; hospital rooms and bathrooms of infected patients contain endospores, which were shed in the feces; people may acquire an infection by becoming infected with an endospore (these tend to be people currently taking antibiotics

Question 12

c. difficile virulence factors

Answer 12

enterotoxin; cytotoxin

Question 13

enterotoxin

Answer 13

also referred to as clostridium difficile toxin A (TcdA); chemotactic for neutrophils, which release cytokines that cause hypersecretion of fluid and the development of hemorrhagic necrosis

Question 14

cytotoxin

Answer 14

also referred to as clostridium difficile toxin B (TcdB); causes cellular actin to depolymerize resulting in destruction of the cellular cytoskeleton (loss of structural integrity)

Question 15

c. difficile pathogenesis

Answer 15

the endospores are either acquired exogenously from an environmental reservoir such as a hospital room or were already carried endogenously; disease develops when the composition and numbers of the normal enteric microbiota are altered from antibiotic usage; at this point C. difficile has the opportunity to overgrow and produce toxins in the colon

does not invade the colonic mucosa and it does not cause disease if toxins are not produced; even when toxins are produced, the disease level varies from no disease (carrier state) to mild, self-limited diarrhea to severe colitis

Question 16

c. difficile diseases

Answer 16

antibiotic-associated diarrhea

psuedomembranous colitis - inflammation of the colon; can become life-threatening if the colon ruptures

Question 17

clostridium tetani

Answer 17

although the vegetative cells dies rapidly when exposed to oxygen, endospore formation allows the organism to survive in the most adverse conditions

Question 18

c. tetani epidemiology

Answer 18

ubiquitous; it is found in fertile soil and colonizes the gastrointestinal tracts of many animals, including humans

Question 19

c. tetani virulence factors

Answer 19

tetanolysin - hemolysin
tetanospasmin - AB toxin (specifically a neurotoxon); blocks the release of inhibitory neurotransmitters; responsible for the disease symptoms associated with tetanus

Question 20

c. tetanis pathogenesis

Answer 20

the bacteria gain access to the body through broken skin; tetanospasmin is produced during stationary phase of growth and is released when the bacterial cells die and lyse

the B subunit binds to a receptor on neuronal membranes; the AB toxin is endocytosed; the A subunit moves up the axon to an inhibitory neuron of the central nervous system; in an inhibitory neuron, the toxin cleaves proteins required for exocytosis of vesicles containing inhibitory neurotransmitters; in the absence of inhibitor signals, excitatory signals that stimulate muscle contraction prevail

Question 21

generalized tetanus

Answer 21

trismus (lockjaw); persistant back spasms; more severe disease includes cardiac arrhythmias, fluctuations in blood pressure, sweating and dehydration

Question 22

neonatal tetanus

Answer 22

typically associated with an initial infection of the umbillical stump

Question 23

c. botulinum epidemiology

Answer 23

commonly isolated in soil and water samples

Question 24

c. botulinum virulence factors

Answer 24

botulism toxin - AB toxin (specifically a neurotoxin); blocks the release of excitatory signals (acetylcholine); responsible for the disease symptoms associated with botulism; B subunits protect A from being inactivated by stomach acids

Question 25

c. botulinum foodborne botulism pathogenesis

Answer 25

foodborne botulism ovcurs when someone consumes food contaminate with botulism toxin; food containing C. botulinum endospores is improperly canned (endospores are not killed); the endospores germinate. as the vegetative cells grow in the nutritionally-rich, anaerobic environment, they produce botulism toxin; the toxin is extremely potent therefore consuming even a small amount will lead to disease

Question 26

c. botulinum infant botulism pathogenesis

Answer 26

infant botulism occurs when an infant consumes C. botulinum endospores; if an adult consumes endospores, the competitive microbiota of the gastrointestinal tract prevent colonization; in infants a c. botulinum infection becomes established and the bacteria produce the neurotoxin within the host

Question 27

wound botulism

Answer 27

c. botulinum infects and existing wound and produces the neurotoxin; the symptoms are identical to foodborne botulism

Question 28

foodborne and wound botulism disease symptoms

Answer 28

patients feel weak and dizzy 1-2 days after cosnuming the neurotoxin; initial symptoms are blurred vision, dry mouth, constipation, and abdominal pain; flaccid paralysis

Question 29

infant botulism symptoms

Answer 29

initial symptoms are nonspecific; progressive disease iwth flaccid paralysis and respiratory arrest can develop