clostridium Flashcards
clostridium characteristics
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
where are clostridium
in the soil, water, sewage and some are members of gastrointestinal microbiota in humans and animals
why can clostridium cause disease easily
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
clostridium perfringens virulence factors
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
clostridium perfringens epidemiology
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
clostridium perfringens pethogensis and diseases
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
suppurative myositis
(c. perfringes) - develops if cellulitis progresses and pus accumulates in the muscle planes; there is no muscle necrosis or systemic symptoms at this point
clostridial myonecrosis (gas gangrene)
(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
clostridial food poisoning
(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
necrotizing enteritis
(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
c. difficile
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
c. difficile virulence factors
enterotoxin; cytotoxin
enterotoxin
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
cytotoxin
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)
c. difficile pathogenesis
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
c. difficile diseases
antibiotic-associated diarrhea
psuedomembranous colitis - inflammation of the colon; can become life-threatening if the colon ruptures
clostridium tetani
although the vegetative cells dies rapidly when exposed to oxygen, endospore formation allows the organism to survive in the most adverse conditions
c. tetani epidemiology
ubiquitous; it is found in fertile soil and colonizes the gastrointestinal tracts of many animals, including humans
c. tetani virulence factors
tetanolysin - hemolysin
tetanospasmin - AB toxin (specifically a neurotoxon); blocks the release of inhibitory neurotransmitters; responsible for the disease symptoms associated with tetanus
c. tetanis pathogenesis
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
generalized tetanus
trismus (lockjaw); persistant back spasms; more severe disease includes cardiac arrhythmias, fluctuations in blood pressure, sweating and dehydration
neonatal tetanus
typically associated with an initial infection of the umbillical stump
c. botulinum epidemiology
commonly isolated in soil and water samples
c. botulinum virulence factors
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
c. botulinum foodborne botulism pathogenesis
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
c. botulinum infant botulism pathogenesis
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
wound botulism
c. botulinum infects and existing wound and produces the neurotoxin; the symptoms are identical to foodborne botulism
foodborne and wound botulism disease symptoms
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
infant botulism symptoms
initial symptoms are nonspecific; progressive disease iwth flaccid paralysis and respiratory arrest can develop
