anaerobic bacteria – Flashcards
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| what are obligate, (strict), anaerobes? |
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| O2 is toxic |
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| what are aerotolerant anaerobes? |
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| do not use O2, but can tolerate low levels of it |
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| what are facultative anaerobes? |
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| grow in the presence or absence of O2 |
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| what are microaerophilic organisms? |
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| these utilize O2, but only grow in the presence of low O2 |
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| what gram+ anaerobic cocci should we know? |
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| peptostreptococcus |
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| what spore-forming gram+ anaerobic bacilli should we know? |
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| clostridium |
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| what nonspore-forming gram+ anaerobic bacilli should we know? |
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| actinomyces, lactobacillus, mobiluncus, and propionibacterium |
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| what are anerobic gram- bacilli we should know? |
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| bacteroides, fusobacterium, porphyromonas, prevotella |
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| what are anerobic gram- cocci we should know? |
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| veillonella |
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| of the anaerobes, what are the most common pathogens? |
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| clostridium, bacteroides, fusobacterium, and peptostreptococcus |
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| of the anaerobes, which are potential pathogens? |
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| prevotella, veillonella, porphyromomas, actinomyces |
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| of the anaerobes, which are opportunistic pathogens? |
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| bifidobacterium, eubacterium, lactobacillus, mobiluncus, (can be associated with bacterial vaginosis), proprionibacterium, (can be associated with acne) |
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| what are sites colonized by aneaerobic bacteria? |
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| mucosal surfaces (colon, urogenital tract, oral cavity: gingival crevices, tonsillar crypts, tooth surfaces) and hair follicles |
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| is anaerobic bacterial growth facilitated by other bacteria? what about aerotolerant bacteria? |
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| anaerobic bacterial growth can be facilitated by facultative organisms. aerotolerant bacteria can also co-colonize with facultative organisms. in both instances the facultative organisms use up the O2, creating a microenvironment. in many places in the body such as the oral cavity and colon, anaerobes outnumber aerobes >1000:1 |
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| what are the predominant anaerobic bacteria in the oral cavity, upper respiratory tract? |
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| peptostreptococcus, actinomyces, porphyromonas, prevotella, fusobacterium, veillonella |
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| what are the predominant anaerobic bacteria in the gastrointestinal tract? |
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| peptostreptococcus, bacteroides, fusobacterium |
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| what are the predominant anaerobic bacteria in the skin? |
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| propionibacterium |
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| what are the predominant anaerobic bacteria in the genitourinary tract? |
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| mobiluncus, prevotella, lactobacillus |
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| how are most anerobic infections acquired? are there any exceptions? |
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| most infections are endogenously acquired from the normal flora, except for clostridium which is a spore that can be picked up from the environment |
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| are there more than one kind of anaerobic bacteria often involved in an infection? |
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| yes, infections are often polymicrobial consisting of a mixture of several different kinds of anaerobes and facultative organisms |
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| can anaerobic organisms form abscesses? |
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| yes infections with anaerobic bacteria often involve abscesses |
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| what are some tell-tale signs of anaerobic bacterial infection? |
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| foul odor and gas |
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| how do anaerobic flora cause pathogenesis in the same body? what are some examples with the lungs or peritoneal cavity? |
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| normal anaerobic flora can become pathogenic at a sterile site, such as with pneumonia, (caused by aspiration of oral flora), infection of the peritoneal cavity, (after abdominal sx), or tissue infections due to trauma or tissue damage, (impaired blood flow increases anaerobic infection risk) |
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| what is a common way to get an anaerobic bacterial infection intra-abdominally? |
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| bowel perforations, (due to sx or injury), can cause abcesses, wound infections, or peritonitis via bacteroides, peptostreptococcus, fusobacterium, + facultative organisms |
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| how do pulmonary anaerobic infections occur? |
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| peptostreptococcus, fusobacterium nucleatum, actinomyces and prevotella melaninogenica can be aspirated from the oropharynx causing abcesses, necrotizing pneumonia, and aspiration pneumonia |
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| how can anaerobic bacteria cause pelvic infections? |
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| gynecologic sx or malignancies can lead to infection by prevotella bivia and prevotella disiens, fusobacterium, and bacteroides, leading to tubo-ovarian abscesses or salpingitis |
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| how can brain abcesses be caused by anaerobic bacteria? |
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| peptostreptococcus, fusobacterium and prevotella from the oral cavity, (often associated with a hx of chronic sinusitis/otitis), can disseminate from the blood across the BBB |
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| what kinds of anaerobic bacteria cause skin+soft tissue infections, what are they characterized by? what kinds of infections affect the skin and tissue? |
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| clostridium perfringens alone or in a mixed infection with peptostreptococcus, bacteroides, S. aureus, Str. pyogenes or gram - aerobic/facultative organisms can cause necrotic tissue, foul smell and gas. gas gangrene, myonecrosis, necrotizing fascitis, crepitant cellulitis and bite wounds are all examples of these infections |
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| what kinds of anaerobic bacteria can cause oral and dental infections? what kinds of infections can they cause? what is an associated risk with these infections? |
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| porphyromonas are associated with periodontal infections as well as actinomyces, prevotella, fusobacterium, peptostreptococcus, and veillonella. these can cause dental abscesses, gingivitis, chronic sinusitis, and chronic otitis. these can disseminate into the blood or CNS from this area, causing even worse problems |
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| what anaerobic bacteria can cause bacteremia and endocarditis? |
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| bacteroides fragilis is the most common anaerobe associated with bacteremia |
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| how do actinomyces react to O2? what is their gram stain? what is their shape? where are they found? what kinds of infections are they associated with? |
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| actinomyces are gram + aerotolerant anaerobes. they are filamentous bacteria and are endogenously found in the mouth. they can cause cervivofacial infections, (face, neck, jaw), following injury or dental work, and aspiration of actinomyces can cause thoractic infection |
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| where can actinomyces cause abcesses? what do the lesions resemble? |
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| actinomyces can cause abcesses in the lung, chest wall, abdominal cavitiy, pelvic area and brain. these lesions resemble subcutaneous mycoses and are chronic and slow developing with pus and draining sinuses. the pus contains colonies of the organism, called sulfur granules. |
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| what genus of bacteria is responsible for the most common cause of serious anaerobic infection? where does the most common form infect? what is its virulence factor? how does its LPS affect hosts? where is it found? |
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| bacteroides, the most important pathogen of which is B. fragilis. bacteroides fragilis is the most important pathogen of the genus, a common cause of abdominal infection due to it's polysaccharide capsule, however its LPS has little endotoxin activity due to an atypical lipid A. bacteroides is very prevalent in the colon, called the "E. coli" of anaerobic bacteria |
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| what is the relationship between bacteroides, polyphyromonas, and prevotella? |
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| many bacteroides species have been re-classified as porphyromonas or prevotella |
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| what does prevotella melaninogenica usualy infect? does it have a capsule? |
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| prevotella melaninogenica typically infects above the diaphragm and it does make a capsule |
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| what are both prevotella bivia and disiens both associated with? |
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| gynecologic infections |
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| what kind of infection is porphyromonas associated with? |
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| dental abcesses and gingivitis |
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| what shape are fusobacterium? gram stain? where do they normally inhabit? what infections are they associated with? which is the most common species? |
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| fusobacterium are gram - rods w/pointed ends. they are normal flora of the mouth, colon and female genital tract. they can cause oral, brain, pulmonary, intra-abdominal, or pelvic abscesss, (usually mixed infections, but this or bacteriodes are usually dominant). fusobacterium nucleatum is the most common species |
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| what kind of metabolism do lactobacillus have? where are they found and what useful function to they perform? what kind of pathogen are they? can they cause UTIs? |
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| lactobacillus can be facultative or obligate anaerobes. they colonize the female genital tract, fermenting and keeping the pH low via lactic acid, which protects against bacterial vaginosis. they are opportunistic pathogens, but cannot grow in urine, so rarely does lactobacillus cause UTIs. (if lactobacillus is found in a urine cx, the conclusion will be that it was contaminated) |
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| how is mobiluncus considered in terms of gram staining? what kinds of infection is it associated with? what kind of pathogen is it? |
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| mobiluncus appears gram -/+ variable, but is classifies gram + b/c of its cell wall composition. it is associated with bacterial vaginosis along with the facultative organism, gardnerella vaginalis. mobiluncus is an opportunisitc pathogen |
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| what is peptostreptococcus an anaerobic version of? where is it found? what kinds of infection can it cause? what does it often participate in mixed infections with? |
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| peptostreptococcus is an anaerobic version of streptococci. it is a part of normal flora in the mouth & colon. it can cause periodontal disease, peritontis, intra-abdominal abscesses, pulmonary, skin & genital infections. it is also a part of mixed infections with bacteriodes or facultative organisms |
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| where is proprionibacterim found, what species is associated with acne? |
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| proprionibacterium is found on the skin and GI tract, and proprionibacterium acnes is an opportunistic contributor to acne |
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| where is veillonella found? shape/gram stain? what kinds of infections is it associated with? |
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| veillonella is gram - cocci (only one), part of normal flora in the mouth, it is an opportunistic pathogen associated with mixed infections. it is found in abscesses of the sinuses, tonsils, and brain, and may be associated with human bites |
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| what is different about clostridium? gram stain? where is it found? what toxins can it produce? |
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| clostridium is a gram + spore former, (only anaerobe that does this). they are usually obligate anaerobes, though some are aerotolerant. they are ubiquitous in the soil, water, and sewage - thus are usually exogenous infectors, but sometimes are seen in human/animal GI tracts. they produce neurotoxins, enterotoxins, hemolysins, and a variety of tissue-damaging enzymes |
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| what are the 4 clostridium pathogens we should know? |
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| clostridium botulinum (botulism), difficile (antibiotic-associated diarrhea, pseudomembranous colitis), perfringes (food poisoning, nectrotizng enteritis, cellulitis, gas gangrene, septicemia), and tetani, (tetanus) |
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| what do you often not see in tissue or cx's of clostridium perfringens? how do they hemolyse? |
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| spores are not usually seen. clostridium perfringes create double zones of hemolysis when cultured, (immediate beta, and surrounding alpha zones) |
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| what clinical diseases are associated with clostridium perfringes? |
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| cellulitis, (only connective tissue, no muscle), suppurative myositis, (fascitis, pus, but no muscle necrosis), myonecrosis, (gas gangrene, necrosis of muscle), food poisoning, (enterotoxin), enteritis necroticans, (toxin-dependent, severe food poisoning w/tissue damage in colon) |
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| what is the most common type of clostridium perfringens? how are the types classified? where are B-E found? |
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| type of clostridium perfringens is dependent on combination of 4 lethal toxins, w/type A being the most common, (present in the environment). types B-E colonize the GI tract of animals, sometimes humans |
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| what is the alpha toxin produced by clostridium perfringens? how does it act? what cells can it affect? |
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| the alpha toxin is a lethal phospholipase C, (lecthinase), that degrades lecithin in cell membranes, lysing endothelial cells, erythrocytes, leukocytes and platelets |
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| what is the beta toxin produced by clostridium perfringens? how does it act? what disease can it cause? |
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| the beta toxin can cause necrotizing activity in the intestinal mucosa, it is responsible for enteritis necroticans via type C clostridium perfringens, (lethal toxin) |
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| how does the epson toxin of clostridium perfringens affect the GI wall? |
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| it can increase the vascular permeability, contributing to a type of diarrhea. (lethal toxin) |
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| what are the 2 toxins produced by clostridium perfringens? what kinds of infections does it cause? is enterotoxin a lethal toxin? what does it cause? how does it act? |
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| group A clostridium perfringens is responsible for most human infections, producing both alpha toxin and enterotoxin. enterotoxin causes food poisonin, but is not lethal like the alpha toxin. it is a heat labile protein that binds to epithelial cells in the small intestine and disrupts ion transport, leading to fluid loss and watery diarrhea. |
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| how does clostrium perfringens cause gas gangrene/myonecrosis? |
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| spores enter the tissue from soil and toxins damage/kill the cells. enzymes, (collagenase, hyalurnidase), facilitate spread and metabolic activity of the organisms leads to creptitation, (gas formation). copious and foul smelling exudates are seen and dissemination of the toxins can lead to shock, renal failure and death. |
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| how does clostridium perfringens from a wound, (as opposed to a cx), respond to gram staining? |
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| a gram stain of clostridium perfringens will show some positive, some not, (doesn't maintain stain well). the exudate will also not show many neutrophils, b/c the alpha toxin lyses them |
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| what is the appearance of clostridium tetani? where does it infect? what toxin does it produce? can it be vaccinated against? |
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| clostridium tetani appear as terminal spores, (drumsticks). this organism remains localized in wounds, but produces a neurotoxin called tetanospasm. tetanospasm is a heat-labile neurotoxin, but a toxiod is made in the US that can vaccinate pts |
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| what kind of toxin is tetanospasm? where does it travel to? what do the AB subunits do? how does it affect the CNS? |
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| tetanospasm is an A-B toxin that travels to inhibitory neurons via blood or retrograde neuronal transport. the B chain binds to neurons and the A chain blocks the release of inhibitory neurotransmitters, (GABA), leading to unregulated excitation and spastic paralysis, (constant contraction) |
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| what is the incubation period for tetanus? what muscles are affected? what happens if these muscles are affected? |
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| the incubation period for tetanus is 4 days->several weeks. spastic paralysis can affect the jaw muscles, causing trismus/lockjaw or risus sardonicus, a "smile" resulting from contraction of facial muscles. if the back muscles are affected, opisthotonos (severe arching) occurs. if chest muscles are affected, respiratory failure leading to death can occur. |
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| what is the shape of clostridium botulinum? |
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| with a drumstick shape, clostridium botulinum can be foodborne, (consuming home-canned goods, ingestion of the toxins, not the organism is sufficient), infant, (ingestion of spores in honey), or wound, (rare contaimination of wound with spores) |
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| is the neurotoxin produced by clostridium botulinum heat-labile? what is it similar to? is it complexed with anything? what nerves its it specific for? where does the B subunit bind? what is its main action? |
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| the toxin of clostridium botulinum is a heat-labile neurotoxin, similar in structure/function to the tetanus toxin. it is complexed with non-toxic proteins which protect it in the GI tract. the B subunit binds to the receptors on motor neurons, remaining at the neuromuscular junction. it is very specific for cholinergic nerves and prevents release of ACh at these neuromuscular junctions. it prevents contractions, causing a flaccid paralysis. |
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| what is the main difference between the tetanus and botulism toxins? |
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| tetanus produces spastic contraction, where botulism prevents contraction |
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| what are symptoms of botulism? is there fever/sepsis? |
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| symptoms of foodborne botulism include blurrd vision, dry mouth, constipation, abdominal pain 1-3 days after ingestin contaminated food beginning with bilateral descending weakness of peripheral muscles, progressing to respiratory paralysis. there is no fever or sepsis associated. |
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| why is recovery from foodborne botulism prolonged? what is diagnosis based on? what is the mortality rate in the US? |
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| the neurotoxin is irreversibly found the neurons, so recovery consists of regrowth of nerve endings. diagnosis is based on demonstrating toxin activity, rather than organism presence. mortality in the US is low due to supportive care |
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| what is floppy baby syndrome? how is botulism poisoning different in infants? what are symptoms? how is it detected? |
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| infant botulism, due to consumption of food contaminated with botulism toxin, (honey, formula). clostridium botulism colonizes the GI tract of infants, (normal flora in adults prevents this), leading to constipation, feeding problems, lethargy, and poor muscle tone. toxin or organism can be detected in stool |
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| where are the spores located in clostridium difficle? |
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| in the center of the organism. clostridium difficle is a minor component of normal intestinal flora, but it can infect pts on antibiotic therapy, (such as clindamycin, cephalosporins, fluroquinolones). it is responsible for antibiotic-dependent GI disease which ranges from mild diarrhea to severe pseudomembranous colitis |
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| how is c. difficle different from other clostridium? |
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| it can be endogenous |
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| when do clostridium difficle infections start to appear? how are they transmitted in the hospital? what is treatment for it? how is it diagnosed? |
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| c. difficle infections typically occur 5-10 days after starting antibiotic tx, (though can take up to 10 wks). the spores are present in hospital settings, leading to nosocomial outbreaks of c. difficile GI disease. tx includes discontinuing the implicated antibiotic, metroconidazole or vancomycin, which kills vegetative forms, but not spores. it is diganosed by detecting toxins in stool, (ELISA) |
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| what are the toxins produced by c. difficle? |
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| enterotoxin, (toxin A), which is chemotactic for neutrophils, inducing cytokine production and increasing permeability of the intestinal wall with hypersecretion of fluid. cytotoxin, (toxin B), induces depolymerization of actin with loss of cellular cytoskeleton |
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| where are c. difficle cx's best performed? can swabs be used? |
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| absecesses via needle/syringe, CSF, pleural, or synovial fluid, or material from sx or deep wound, none of which can be exposed to O2. swabs are not acceptable due to possibility of contamination with normal anaerobic flora |
