Lecture 6: Anaerobic Bacteria

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Anaerobic organism

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any organism that does not require oxygen for growth, it may react negatively or even die if oxygen is present.

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Aerobes

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require oxygen for growth

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Obligate anaerobes

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are harmed by the presence of oxygen

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Facilitative anaerobes

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can grow with or without oxygen but prefer to use oxygen if it is present

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What are two examples of facilitative anaerobes?

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Brewer's Yeast and Muscle cells

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Microphilic aerobes or microphiles

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do no grow at all aerobically or grow poorly, but grow better under 10% carbon dioxide or anaerobically.

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Aerotoleratant organisms or obligate fermenters

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cannot use oxygen for growth, but tolerate its presence

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Anaerobes are often what gram type

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can be either

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Where are anaerobes found in nature?

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Widely distrubuted; common in soil, part of the normal flora, indigenous to humans

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What is the nature of anaerobic bacteria?

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mostly oppurtunititc pathogens

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Disease from anaerobic pathogens usually occurs due to

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trauma which includes injury or surgery

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Why are obligate anaerobes sensitive to oxygen?

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Lack ROS scavenging enzymes (peroxidases, superoxide dismutases, catalases)

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sites of infectious disease development caused by anaerobes

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intraabdominal, Pulmonary, Pelvic, Brain abscesses, skin and soft tissue, oral and dental, heart, blood ( in vein)

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Alcoholics are more susceptible to infectious disease development due to anaerobes at which site?

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Pulmonary because more abundant anaerobic pockets

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What are the specific classifications that include anaerobic bacteria?

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G+ bacilli sporulating and non-sporulating, G- Bacilli, SOME G+ cocci, G- cocci

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Clostridium genus

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G+ Bacilli; forms endospores but rarely seen in clinical examples

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Important species of Clostridium genus

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Perfringens, tetani, botulinum, difficile

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Diseases caused by Clostridium genus

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Tetanus, Botulism, Gas gangrene, pseudo-membrane colitis, food poisoning

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Distinctive property (ies) of all clostridia

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Employ butyric acid fermentation which often produces a foul odor

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Distinctive property (ies) of C.Perfringens

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-non-motile, large rectangular spores, associated with polymicorbic wound infections, produce a lot of CO2 and H2 which leads to gas gangrene

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Distinctive property (ies) of C.tetani

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Motlie with peritrcus flagella, tetanus toxin which is a neurotoxin endotoxin and heat liable, and single antigenic type

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Distinctive property(ies) C.Botulinum

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Motile, strains A to G, botulism toxin which has 8 exotoxin types

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Botulinum Toxin

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Highly toxic neurotoxins and exotoxins; less than one microgram can kill a person, one strain produces one type, heat liable

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Distinctive property (ies) C.difficile

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motile, 2 exotoxin types, antibiotic associated diarrhea

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C difficile toxin

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two exotoxin types; toxin A: enterotoxin, Toxin B: cytotoxin, act synergestically, heat liable

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What about C.difficile causes major inflammation or colitis

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the two toxins working synergistically

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The most common bacteria is soil, dust, mud, decaying vegetation, marine sediment, and may be found in intestinal tract of humans and other animals

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C.Perfringens

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C. perfringens causes

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gas gangrene

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Step-wise process of gas gangrene

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1.anaerobic tissue environment cause by poor blood supply 2. rapid growth followed by spreading along muscle bundles and alpha toxin production 3. increased vascular permeability 4. increased toxin absorption is the probable cause of fatal cases

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alpha toxin of C.perfringens

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lipase; eventually causing edema and tissue necrosis

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During C.perfringens rapid growth

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they produce a lot of gas because they are fermenters

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During gas gangrene process, increased vascular permeability leads to

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gangrene and increased systemic absorption of toxin which leads to shock

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Does bacterimea occur in gas gangrene?

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No; only absorption of toxin

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Gas gangrene usually begins

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1 to 4 days after an injury but may start withing 10 hours. `

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The earliest sx of gas gangrene

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severe pain at the site of the wound accompanied by a sense of heaviness or pressure.

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LAter sx of gas gangrene

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progresses rapidly with edema, tenderness, pallor followed by discoloration and hemorrhagic sites. Toxic shock with intravascular hemolysis, hypotension, and renal failure leading to coma and death. Pt are often remarkably alert until the terminal staged

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Gas gangrene is the number one cause of

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amputation

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Why is a very large dose of abx given for the tx of gas gangrene?

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It is very important to lower the ID ASAP

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Treatment for gas gangrene

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must be immediate due to possible fatality, removal of devitalized tissue, administration of massive doses of penicillin with cephlosporins, placement of pt in hyperbaric oxygen chamber

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Why is removal of devitalized tissue in the treatment of gas gangrene important?

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prevents anaerobic condition for the bacteria multiplication and toxin production; often entails wide resection of muscle groups and even amputation of limbs.

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What is the purpose of a hyperbaric oxygen chamber in the tx of gas gangrene?

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increases the tissue levels of dissolved oxygen which will slow the spread and progress of the disease probably by inhibiting bacterial growth

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Cephlosporins

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a class of b lactam antibiotics originally derived from fungus Acremonium which was preciously known as cephalasporium

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Prevention of Gas gangrene

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surgical debridement of traumatic injuries asap, thorough cleansing, removal of dead tissue, and fb, and drainage of hematoma limit organisms multiplication and toxin production. Antibiotic prophylaxis is indicated but cannot replace surgical debridement because abx may fail to reach the organism in devascularized tissues.

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C.Perfringens causes

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gas gangrene, food poisoning, and anaerobic cellulitis

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3rd most common cause of food poisoning, caused by poorly cooked meat plus long incubation time, exotoxin mediated

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c.perfringens

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sx of c perfringens foof posioning

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severe diarrhea, abd pain, no fever though

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Anaerobic cellulitis

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c.perfringens, similar to gas gangrene but no toxin production

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Species that cause food poisoning

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Campylobacter jejuni, samonella spp, Clostridium perfringens (AKA cafeteria germ)

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Steps of infection and disease caused by C.Tetani

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introduction of clostridium tetani spore to the low oxygen environment 2. germinate and reproduce 3.production of tetanus toxin 4. Tetanus toxin reaches terminal motor neurons 5. toxin spreads to CNS 6. block spinal motor reflexes 7. death due to respiratory failure

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How can clostridium tetani be introduce to a host low oxygen environment?

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deep penetration of large splinter or soil contamination in the area of necrosis

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Tetanus toxin

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extotoxin, neurotoxin, tetanospasmin, a metalloproteinase that is structurally and pharmacologically similar to the botulinum toxin, heat liable, antigenic, rapidly destroy by intestinal proteases, useful toxiod created by tx with foremaldehyde

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What is the major difference between the tetanus toxin and the botulinum toxin

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neurotransmitters are the ones that effect inhibitory neurons. which results in unopposed firing of active motor neurons generating spasms and spastic paralysis

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Spastic paralysis

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caused by tetanus toxin

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Falccid paralysis

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caused by botulinum toxin

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Treatment of tetanus

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neutralization of any unbound neurotoxin with large doses of human tetanus immuno globulin (HTIG), non-specific supportive measures, benzodiazapoenes,

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What are the non-specific supportive measures for tx of Tetanus?

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maintenance of quite dark environment, sedation, provision of adequate airway

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Why are Benxodiazapenes used in tx of tetanus?

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indirectly antagonize the direct effect of the toxins

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Recovery from tetanus requires

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The generation of new neuron axons due to irreversible binding of the tetanus toxin

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Food borne botulism is caused by (or requires)

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canned food, ineffective sterilization, anaerobic environment, then ingestion of the toxin,

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When does intoxication sx of botulism onset?

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12-36 hours after ingestion

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ingestion of botulinum toxin eventually leads to

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respiratory failure

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Infant botulism

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3 weeks - 8 months, honey, virtually impossible to sterilize, spores germinate in the colon due to lack of acidity, toxin production

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sx of infant botulism

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initially: constipation, poor muscle tone, feeding problems; in some cases could be responsible for SIDS

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Wound botulism

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Very rare, mainly associated with intranasal cocaine users, due to ingestion of Botulism spores, disease progression similar to infant

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Botulinum Toxins (BOtox)

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8 stereo types, important ones are A, C1, D, and E, most powerful neurotoxin ever discovered, LD is 1 ng/kg of body weight

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Mechanism of botulinum toxins

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absorbed in intestinal tract, reaches neuromuscular junction via blood stream, blocks acetlycholine an neuronal synapses causing muscle paralysis, eventually leads to cardiac arrest and or respiratory failure

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What is the single most important determinate clinical factor in tx of botulism?

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availability of intensive supportive measures particularly mechanical ventilation which decreases mortality to less than 10%

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antimicrobial treatment for what kind of botulism

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wound

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Administration of horse botulism anti-toxin

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used to be thought to be useful in neutralizing the toxin. Frequent hypersensitivity reactions related to the origin make it unsuitable for infants.

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Prevention of Botulism

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adequate pressure cooking, autoclaving in the canning process kills spores, heating food at 100C for 10 minuets destroys the toxin, DON'T EVEN TASTE CONTAMINATED OR SUSPECTED FOOD

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anaerobic gram + cocci significant species

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peptosteptococcus

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peptosteptococcus

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gram + cocci, anaerobic, commensals living in mainly the mouth and intestine, pathogenic uner immunocompromised ot traumatic contions, often clinical infectins, combined with poor blood supply to the infections sies, no known toxins,

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peptosteptococcus can cause

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abscessed in the brain, liver, breasts, lungs and general tissue necrosis

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Gram - cocci significant species

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Velionella

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Velionella

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Gram - cocci, anaerobes, commensals mainly living in the intestines, rarely pathogenic, recent increases of cases

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Velionella causes

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Osteomyelitis, endocarditis, abscesses of internal organs`

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Gram - Bacilli significant species

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Bacteroides fragilis

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Bacteroides fragilis

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gram - bacilli, encapsulated, anaerobic, enterotoxin, produces superoxide dismutases, LPS endotoxin

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Enterotoxin of Bacteroides fragilis

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stimulates abscess formation even without the live bacteria, unique to the capsule

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What is the signifcance of Bacteroides fragilisproducing superoxide dismutases?

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They are able to tolerate atmospheric oxygen

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Bacteroides fragilis causes

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mostly self limiting watery diarrhea in children, effects