Anaerobic Bacteria

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Ananaerobic organism or anaerobe is / background...

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Any organism that does not require oxygen for growth. It may react negatively or even die if oxygen is present.

•Anaerobesare found in Gram positives and Gram negatives

•Widelydistributed in nature

•Commonin soil

•Partof the normal flora; indigenous to human–Mostlyopportunistic pathogens –Diseasesoccur mainly due to trauma

•Injury,or surgery

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•Aerobes-

•Obligateanaerobes-

•Facultativeanaerobes-

•Microaerophilicaerobes (microaerophiles)-•Aero-tolerantorganisms-

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•Aerobes, which require oxygen for growth (by definition, we are aerobes)

•Obligate anaerobes, which are harmed by the presence of oxygen

•Facultative anaerobes, which can grow with or without oxygen but prefer to use oxygen if it is present (brewer’s yeasts and muscle cells of our body are examples)

•Microaerophilic aerobes (microaerophiles) do not grow at all aerobically or grow poorly, but grow better under 10% carbon dioxide or anaerobically. Anaerobic bacteria can be divided into strict anaerobes that can not grow in the presence of more than 0.5% oxygen and moderate anaerobic bacteria that are able of growing between 2 to 8% oxygen

•Aero-tolerant organisms, which cannot use oxygen for growth, but tolerate its presence (also called obligate fermenters)

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•Obligateanaerobes are sensitive to...

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to oxygen

–Lack of ROS (reactive oxygen species) scavenging enzymes

•No peroxidases

•No superoxide dismutases

•No catalases

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Sitesof infectious disease development caused by anaerobes...

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–Intra-abdominal

–Pulmonary

–Pelvic

–Brain abscesses

–Skin and soft tissue

–Oral and dental

–Heart

–Blood (in veins)

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•Classification

–G(+)

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–G(+) Bacilli •Sporulating G(+) Bacilli – Clostridium spp. and Bacillus spp.) •Nonsporulating G(+) Bacilli (mainly Lactobacillus spp. and Propionibacterium spp.)

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•Classification

–G(-)

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–G(-) Bacilli

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•Classification

Anaerobic

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-Anaerobic Cocci

•G(+) Cocci •G(-) Cocci

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•Classification

Clostridia

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•SporulatingG(+) Bacilli

•Genus:Clostridium

•Species:perfringens,tetani, botulinum, difficile• Formendospore

–However,endospores are rarely seen in clinical samples

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•Diseases

Clostridia

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–Tetanus - C.tetani

–Botulism - C.botulinum

–Gasgangrene - C.perfringens

–Pseudomembranouscolitis (PC) – C. difficile

–Foodpoisoning – C. perfringens

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•Distinctive Properties

Clostridia

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•Employbutyric acid fermentation–Oftenproduce a foul odor

•C.perfringens

•C.tetani

•C.botulinum

•C.difficile

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•C. tetani

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–Motile

–Tetanus toxin: neurotoxic exotoxin

•Single antigenic type

•Heat labile

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•C. perfringens

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–Non-motile

–Large rectangular spores

–Associated with polymicrobic wound infections •Produce large amount of CO2 and H2: gas gangrene

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•C.botulinum

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–Motile

–Different strains (A to G) –Botulinum toxin (meaning sausage poison; botulus (Latin)=sausage): 8 exotoxin types

•Highly toxic neurotoxic exotoxins –Lethal dose: less than 1 mg to kill a person (LD50 = 1ng toxin/kg body)

•A strain produces one of 8 toxin types

•Heat labile

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•C. difficile

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–Motile

–Two exotoxin types

•Toxin A: enterotoxin

•Toxin B: cytotoxin

•Act synergistically

•Heat labile

–Antibiotic-associated diarrhea (AAD)

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Pathogenesis- Clostridia

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•C.perfringens

–themost commonbacteriain soil, dust, mud, decaying vegetation, marine sediment, and may be found inintestinal tract of humans and other animals

–Gas Gangrene

–Foodpoisoning

–Anaerobiccellulitis

•C.tetani

•C.botulinum

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–Stepwise progress of Gas gangrene

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1.Anaerobictissue environment caused by poor blood supply (due to injury, surgery, etc)

2.Rapidgrowth followed by spreading along muscle bundles and a-toxin production (a-toxin: lipase eventually causing edemaand tissue necrosis)

–Producelarge quantity of gas3.Increased vascular permeability

–Leadingto gangrene–Increasedsystemic absorption of the toxin: leads to shock

4.Increasedtoxin absorption is the probable cause of fatal cases

–Nosign of bacteremia

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MANIFESTATIONS - Gas Gangrene

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MANIFESTATIONS - Gas GangreneGas gangrene usually begins 1 to 4 daysafter the injury but may start within 10 hours. The earliest symptom is severepain at the site of the wound accompanied by a sense of heaviness or pressure.The disease then progresses rapidly with edema, tenderness, and Pallor(unhealthy pale), followed by discoloration and hemorrhagic sites. Toxic shockwith intravascular hemolysis, hypotension, and renal failure leading to comaand death. Patients are often remarkably alert until the terminal stages.

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Treatmentof Gas Gangrene

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Treatmentof gas gangrene must be initiated immediately because these conditions arealmost always fatal if untreated. Removal of all devitalized tissue is very importance because it preventsanaerobic condition required for bacterium multiplication and toxin production.This often entails wide resection of muscle groups even amputation of limbs.Administration of massive doses of penicillin with cephalosporins isan important adjunctive procedure. Placement of patients in a hyperbaric oxygenchamber, which increases the tissue level of dissolved oxygen. Oxygen will slowthe spread/progress of disease, probably by inhibiting bacterial growth.

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Antibiotic administered for Gas Gangrene

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•Cephalosporins:a class of β-lactam antibiotics originally derived from the fungus Acremonium,which was previously known as "Cephalosporium"

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Preventionof Gas Gangrene

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•Debridement:removal of dead tissue•Devascularizedtissues: tissues with interrupted blood supply

Themost effective method of prevention of gas gangrene is the surgical debridementof traumatic injuries as soon as possible. Thorough cleansing, removal of deadtissue and foreign bodies, and drainage of hematomas limit organismmultiplication and toxin production. Antibiotic prophylaxis is indicated but cannot replace surgicaldebridement, because the antibiotics may fail to reach the organism in devascularizedtissues.

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C. tetani

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1.Introductionof C.tetanispore to the low oxygen environment •deeppenetration of a large splinter•Soilcontamination in the area of necrosis

2.Germinateand reproduce•Locally;no invasion to near by tissues

3.Productionof tetanus toxin

4.Tetanustoxin reaches terminal motor neurons

5.Toxinspread to the central nervous system6.Blocksspinal motor reflexes (causing systemic spasms)

7.Deathdue to respiratory failure

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Tetanustoxin

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Themost important product of C tetani is its neurotoxic exotoxin, tetanospasmin ortetanus toxin, a metalloproteinase that has structural and pharmacologicfeatures similar to those of botulinum toxin. The most important differencefrom botulinum toxin is that the neurotransmitters are the ones that affectinhibitory neurons. The result is unopposed firing of the active motor neurons,generating spasms and spasticparalysis,which are the opposite of the botulinum flaccidparalysis.Thetoxin is heat-labile, antigenic, readily neutralized by antitoxin, and rapidlydestroyed by intestinal proteases. Treatment with formaldehyde yields anontoxic product or toxoid that retains the antigenicity of toxin and thusstimulates production of antitoxin.

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Treatment of tetanus

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Specifictreatment of tetanus involves neutralization of any unbound toxin with largedoses of human tetanus immune globulin (HTIG), which is derived from the bloodof volunteers hyperimmunized withtoxoid. Most important in treatment arenonspecific supportive measures, including maintenance of a quiet darkenvironment, sedation, and provision of an adequate airway. Benzodiazepines arealso used to indirectly antagonize the effects of the toxin. The value ofantibiotics is not clear. Because toxin binding is irreversible, recoveryrequires the generation of new axonal terminals.

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•C.botulinum

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–Food-borne botulism

–Infant botulism

–Woundbotulism

–Botulinumtoxins (Botox)

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Botulism Prevention

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Adequatepressure cooking or autoclaving in the canning process kills spores, andheating food at 100°C for 10 minutes before eating destroys the toxin. Foodfrom damaged cans or those that present evidence of positive inside pressureshould not even be tasted because of the extreme toxicity of the C botulinumtoxin.Inan interesting twist, botulinum toxin as Botox has itself become a therapueuticagent. Originally licensed as a treatment of spasmotic neuromuscular conditions by directinjection into muscle (in other words, a muscle relaxant), it has found a farlarger use for cosmetic applications. For those that can afford it, a temporaryrespite from the wrinkles of aging can be gained from Botox injectionsadministered by dermatologists and plastic surgeons.

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Botulism Treatment

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Theavailability of intensive supportive measures, particularly mechanicalventilation, isthe single most important determinant of clinical outcome. With proper ventilatory support,mortality rate should be less then 10%. The administration of large doses of horsebotulinum antitoxin is thought to be useful in neutralizing the toxin. Frequenthypersensitivity reactions related to the equine origin of this preparationmake it unsuitable for use in infants. Antimicrobial agents are given only to patients with wound botulism.