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Anaerobic Infections

Anaerobic Infections

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Published by: dilawarj_2 on Dec 26, 2012
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• • • • • • • • • • • • • • • • • • • • • • • • LEARNING OBJECTIVES: At the end of the lecture, students should be able to: Describe about the anaerobic bacteria. Describe the classification of anaerobes. Describe the pathogenesis of anaerobic infections. ANAEROBIC INFECTIONS: Anaerobic infections are caused by anaerobic bacteria. ANAEROBIC BACTERIA: Anaerobic bacteria do not grow on solid media in room air (10% carbon dioxide and 18% oxygen). OBLIGATE ANAEROBE – Lack superoxide dismutase and/or catalase – toxic radicals formed by oxidative enzymes kill organisms AERO-TOLERANT ANAEROBES – survive in presence of oxygen – Do not use oxygen for energy requirements FACULTATIVE ANAEROBES can grow in the presence as well as in the absence of air. ANAEROBIC BACTERIA: Gram-negative rods: Bacteroides Prevotella Porphyromonas Fusobacterium Bilophila and Sutterella spp. Gram-positive cocci (primarily Peptostreptococcus spp.) Gram-positive spore-forming (Clostridium spp.) and nonspore-forming bacilli (Actinomyces, Propionibacterium, Eubacterium, Lactobacillus and Bifidobacterium spp.) Gram-negative cocci (mainly Veillonella spp.)

.• • • ANAEROBES OF CLINICAL IMPORTANCE: CLOSTRIDIA – C tetani. C botulinum BACTEROIDES – B fragilis. • • • • • • • • • • • • • • • • Clostridium perfringens: Large rectangular Gram positive bacillus Spores seldom seen in vivo or in vitro non motile Produces several toxins – alpha (lecithinase). epsilon . C difficile. . – enterotoxin Causes a spectrum of human diseases -.. contaminaton with foreign bodies (dirt). and venous return eventually is curtailed. – Prevotella – Porphyromonas ACTINOMYCES FUSOBACTERIUM ANAEROBIC STREPTOCOCCI: Pathogenesis of anaerobic infections: Contamination of site with spores Factors which promote anaerobiasis – ‘crush’ injuries with interruption of blood supply.Gas gangrene – Bacteraemia – Myonecrosis – food poisoning – enteritis necrotica (pig bel) • • Gas gangrene: As capillary permeability increases... tissue damage Germination of spores Toxin release Binding of toxin to receptor Resulting effect produces symptom(s) of disease. C perfringens.. the accumulation of fluid increases. beta.

the clostridia multiply within the increasing area of dead tissue.typical organisms no pus cells – Culture -growth of C perfringens (and/or other clostridia associated with this clinical condition) Food poisoning – abdominal pain. releasing more toxins into the local tissue and the systemic circulation. • • • • Diagnosis Myonecrosis – clinical – Gram stain of exudate . diarrhoea and vomiting 8-18 hours after a suspect meal.• As more tissue becomes involved. bloody diarrhoea . shock and peritonitis (C perfringens type C) . Self limiting Enteritis necroticans – severe abdominal pain.

no proven value Food poisoning – Proper preparation and storage of food – self limiting disease -antibiotics not indicated Enteritis necroticans – Proper cooking of food – immunization of susceptible population • • • • • • Clostridium tetani: Small motile spore forming gram positive bacillus with round terminal spores Causes tetanus Pathogenesis: – produces tetanospasmin during stationary phase which is released when cell lysis occurs – heavy chain binds to ganglioside on neuronal membranes – toxin internalized and moves from peripheral to central nervous system by retrograde axonal transport – crosses synapse and localized within vesicles – acts by blocking release of inhibitory neurotransmittors (eg GABA) – TETANUS Clinical syndromes due to unregulated excitatory synaptic activity resulting in spastic paralysis – – – Generalised tetanus Neonatal tetanus localized tetanus • • .• • Treatment and prevention: Myonecrosis – Proper wound debridement and ensure adequate blood supply – Penicillin – antitoxin and hyperbaric oxygen .

• • • Prevention and treatment: Active immunization with tetanus toxoid Wound toilet and active/passive immunization of ‘risk’ injuries – management of wound – tetanus toxoid – Anti-tetanus serum (ARS -horse serum) or Human Tetanus ImmunoGlobulin (HTIG) – Penicillin or Metronidazole Management of patient with tetanus – reduce stimuli – respiratory and CVS support • • • • • • • • • Clostridium difficile: Associated with human disease in mid-1970’s Found in human GIT in small numbers With antibiotic use. increase in number in GIT – Clindamycin. ampicillin. culture of organism Clinical Pseudomembranous colitis Treatment – omit antibiotic if possible – oral vancomycin or metronidazole Pseudomembranous colitis • . cephalosporins. Produces 2 entero toxins – Toxin A -enterotoxin & Toxin B –cytotoxin Diagnosis: – Detection of toxins in stools.

• • • • • • • • • • • . Prevotolla.Endogenous infections – Intra-abdominal pyogenic infections – pleuro-pulmonary infctions – genital infection ACTINOMYCES: Strict anaerobic Gram positive bacilli typically arranged in hyphae which fragment into short bacilli Normal flora of upper respiratory tract. Porphyromonas and Fusobacterium Present in GI tract -form large component of normal flora >80% of human infections associated with B fragilis – virulence factors .capsule. GI tract and female genital tract. agglutinins and enzymes Clinical . ocular palsy and progressive flaccid paralysis) – infant botulism (floppy baby) – wound botulism ANAEROBIC GRAM NEGATIVE BACILLI Bacteroides. B & E Heavy chain binds to ganglioside receptor Toxin internalized and prevents release of acetyl choline from vesicles Clinical – Food borne botulism (weakness. dizziness. Low virulence produce disease when mucosal barrier is breached (eg: following dental trauma or surgery) ENDOGENOUS Establishes chronic infection that spreads through normal anatomical barriers. LPS.• • • • • • • Clostridium botulinum: Fastidious spore forming anaerobic gram positive bacillus Produces 8 antigenically distinct toxins Human disease described with types A.

surgery and long term penicillin. abdominal and thoracic.• • Clinical -cervicofacial. Treatment ------------------------xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx------------------------------- . Diagnosis: – – • Gram stain of ‘sulpher’ granules Culture .

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