Anaerobes Clostridium, Peptostreptococcus, Bacteroides Flashcards
1
Q
What are anaerobes?
A
- defined as failure to grow in presence of 10% oxygen or more.
- some anaerobes will die in the presence of as little as 0.5% O2
- oxygen tolerance - the ability for an organism to survive the presence of O2 for brief periods of time
- many produce catalase and/or superioxide dismutase or other enzymes to help neutralize ROS created by phagocytes to help destroy bacterial cell
- generate energy solely by fermentation
- don’t have electron transport to use O2 to use as energy
2
Q
How can anaerobes be classified?
A
- there are every morphotypes and hundreds of species
- biochemical and culture tests are used but can be difficult
- can characterize by cellular fatty acids and metabolic products
3
Q
What are anaerobic infections?
A
- colonize deeper parts of body
- aerobics help with colonization of anaerobics by taking up all of the O2
- we are heavily colonized by anaerobic bacteria
- sebaceous glands
- gingival crevices
- lymphoid tissue in throat
- intestinal and urogenital lumens
- most infections originate from our commensal (reside in us naturally and grow more readily) microbiota
- many anaerobes are also present in the environment
4
Q
What’s clostridia?
A
-genus: clostridium
-gram-positive bacilli
large, spore-forming (so can be difficult to get rid of, aka endospores)
* when environmental conditions aren’t ideal, use energy to create spores which survive everything
-some produce exotoxins which cause disease
* hemolysin: lyse cells
* neurotoxins: affect nerves and toxin are made by bacteria and are released out
* enterotoxin: afferent enterocytes in GI tract that can cause gas or food poisoning
5
Q
What’s clostridium perfringens?
A
- gram +, non-motile rods = no flagella, not move
- produces hemolytic colonies on blood agar
- yellow is the clost. perfringens and that halo around it is the toxin secrete to lyse RBC
- when it is given fermentable carbs it will produce large amounts of hydrogen and carbon dioxide gas which can lead to:
- gas gangrene
6
Q
What clostridium perfringens toxins form pores
A
- theta toxin: similar to streptolyin O (pore-former). Leads to altered capillary permeability. Toxic to heart muscle. forms pores in cells which leads to leakage and leads to release of toxin. is present in gas gangrene.
- enterotoxin: form pores in enterocyte membranes leading to changes in permeability, alterations of tight junctions and eventual fluid loss
- forms pores in GI tract epithelial cells - so fluid loss means diarrhea because of food poisoning.
7
Q
What is the disease gas gangrene caused by clostridium perfringens?
A
- is called clostridial myonecrosis aka muscle death
- develops in traumatic wounds when contaminated with C. perfringens or other histotoxic clostridia (a different clostridia species)
- is caused by any trauma in which the time between injury and intervention is significantly delayed because the longer you wait to get this fixed, the longer clostridium has time to multiply and grow
- compound fracture
- bullet wounds
- wartime traumas
8
Q
What is food poisoning in clostridium perfringens?
A
- over a million cases/yr in US
- love growing in meat dishes, especially at buffets
- enterotoxin-producing strains
- ileum is most affected by toxin
- incubation period is 8-24 hours
- nausea, abdominal pain, diarrhea because it affects ileum which is low in GI tract
- no fever, vomiting is rare
- spontaneous recovery within 24 hours
- spores stay in food and when ingested, it will germinate and grow as clostridium and produce enterotoxins
9
Q
What’s the diagnosis and treatment of clostridium perfringens?
A
- clostridium is usually already in the body but not the bad type
- diagnosis is usually based on clinical observations
- culture isolation is usually not sufficient for diagnosis
- treat gas gangrene by amputation to get rid of the affected tissue and then lots of penicillin (Ab)
- if food poisoning doesn’t resolve on it’s own in 24 hours, then will use Ab
10
Q
What’s clostridium botulinum?
A
- is the most common disease
- already eating a spore that has germinated
- large rod + rod
- very heat resistance –> the spores are
- produce botulinum toxin (human lethal dose <1 microgram)
- neurotoxin
- blocks acetylcholine release into the neuromuscular junction leading to a flaccid paralysis
- damage to the synapse is permanent
- symptoms begin 12-36 hours after ingestion
- nausea, dry mouth, blurred vision
- respiratory paralysis is more severe
- botulinum goes into synapse and blocks release of Acetylcholine so it can’t act on muscle cells
- spores are found in the environment
- prefer to grow in alkaline condition (like in cans - vegetables, mushrooms, fish, and honey)
- often no change in food taste, odor, or color
- toxin is heat-labile -> toxin and bacteria will break down if you heat it up, but not the spore
- outbreaks are usually small and within families
11
Q
What’s clostridium botulinum?
A
- is the most common disease
- already eating a spore that has germinated
- large rod + rod
- very heat resistance –> the spores are
- produce botulinum toxin (human lethal dose <1 microgram)
- neurotoxin
- blocks acetylcholine release into the neuromuscular junction leading to a flaccid paralysis
- damage to the synapse is permanent
- symptoms begin 12-36 hours after ingestion
- nausea, dry mouth, blurred vision
- respiratory paralysis is more severe
- botulinum goes into synapse and blocks release of Acetylcholine so it can’t act on muscle cells
- spores are found in the environment
- prefer to grow in alkaline condition (like in cans - vegetables, mushrooms, fish, and honey)
- often no change in food taste, odor, or color
- toxin is heat-labile -> toxin and bacteria will break down if you heat it up, but not the spore
- outbreaks are usually small and within families
- foodborne botulism is considered an intoxication, not an infection
- when toxin is growing, you need low amount of it
- once get it to stomach, it will not survive
12
Q
What’s clostridium tetani?
A
- toxin is more spastic and irreversible
- slim, gram + rod
- requires strict anaerobic conditions
- found in the environment
- spores can last for years in soil and once it gains access to host, the spores will germinate and produce a neurotoxin
- produces a potent neurotoxin
- tetanospasmin
13
Q
What is the tetanus toxin tetanospasmin?
A
- is an irreversible neurotoxin
- causes a spastic paralysis (stops uncontrollable muscle contraction - lock jaw)
- prevents the release of glycine and gamma aminobutyric acid (GABA) from presynaptic neurons
- GABA is an inhibitory neurotransmitter (so it stops a response)
- toxin is heat-labile, antigenic (can’t create Ab), rapidly destroyed by intestinal proteases and readily neutralized by antitoxin
- so if block GABA, you won’t stop contracting mm and have lock jaw.
14
Q
What’s tetanus?
A
- spores usually enter through a deep, penetrating wound
- stepping on a nail
- surgery with non sterile instruments
- C. tetani multiplies locally and doesn’t invade tissue but secretes toxin which travels around everywhere
- toxin is produced and can travel to the CNS via retrograde axonal transport –> closer it is to CNS, the faster the symptoms will occur
- tetanus shot kills toxins
- incubation period is 4 days (depends on how close it is to CNS) - several weeks
- shorter incubation usually means a more severe diseases
- masseter muscles are usually affected first
- then respiratory, swallowing, and back muscles
- diagnosis is clinical
- don’t need to culture wound to find out what this is
15
Q
What’s the treatment for tetanus?
A
- neutralize free toxin with human tetanus immune globulin (HTIG)
- nonspecific supportive measures
- dark environment, sedation, ensuring adequate airway
- benzodiazepines can antagonize the effects of toxin
- also work on GABA receptors, act on GABA receptors by mimicking it
- preventative vaccine against tetanus toxoid (inactive toxin)
