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ANAEROBIC INFECTIONS

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 Bidobacterium spp.) Gram-negative cocci (mainly Veillonella spp.)

ANAEROBES OF CLINICAL IMPORTANCE: CLOSTRIDIA C tetani; C perfringens; C difficile; C botulinum BACTEROIDES B fragilis; 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, contaminaton with foreign bodies (dirt), tissue damage Germination of spores Toxin release Binding of toxin to receptor Resulting effect produces symptom(s) of disease.

Clostridium perfringens:
Large rectangular Gram positive bacillus Spores seldom seen in vivo or in vitro non motile Produces several toxins alpha (lecithinase), beta, epsilon ...... enterotoxin Causes a spectrum of human diseases -- Gas gangrene Bacteraemia Myonecrosis food poisoning enteritis necrotica (pig bel)

Gas gangrene:
As capillary permeability increases, the accumulation of fluid increases, and venous return eventually is curtailed.

As more tissue becomes involved, the clostridia multiply within the increasing area of dead tissue, releasing more toxins into the local tissue and the systemic circulation.

Diagnosis Myonecrosis clinical Gram stain of exudate - typical organisms no pus cells Culture -growth of C perfringens (and/or other clostridia associated with this clinical condition) Food poisoning abdominal pain, diarrhoea and vomiting 8-18 hours after a suspect meal. Self limiting Enteritis necroticans severe abdominal pain, bloody diarrhoea , shock and peritonitis (C perfringens type C)

Treatment and prevention: Myonecrosis Proper wound debridement and ensure adequate blood supply Penicillin antitoxin and hyperbaric oxygen - 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

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-1970s Found in human GIT in small numbers With antibiotic use, increase in number in GIT Clindamycin, ampicillin, cephalosporins. Produces 2 entero toxins Toxin A -enterotoxin & Toxin B cytotoxin Diagnosis: Detection of toxins in stools, culture of organism Clinical Pseudomembranous colitis Treatment omit antibiotic if possible oral vancomycin or metronidazole Pseudomembranous colitis

Clostridium botulinum:
Fastidious spore forming anaerobic gram positive bacillus Produces 8 antigenically distinct toxins Human disease described with types A, B & E Heavy chain binds to ganglioside receptor Toxin internalized and prevents release of acetyl choline from vesicles Clinical Food borne botulism (weakness, dizziness, ocular palsy and progressive flaccid paralysis) infant botulism (floppy baby) wound botulism ANAEROBIC GRAM NEGATIVE BACILLI Bacteroides, Prevotolla, Porphyromonas and Fusobacterium Present in GI tract -form large component of normal flora >80% of human infections associated with B fragilis virulence factors - capsule, LPS, agglutinins and enzymes Clinical - 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, GI tract and female genital tract. 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.

Clinical -cervicofacial, abdominal and thoracic. Diagnosis:

Gram stain of sulpher granules Culture - surgery and long term penicillin.

Treatment

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