ANAEROBESDEFINITIONS OBLIGAETE ANAEROBE Lack superoxide dismutase and/or catalse

ANAEROBES

DEFINITIONS OBLIGAETE ANAEROBE Lack superoxide dismutase and/or catalse 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

ANAEROBES OF CLINICAL IMPORTANCE CLOSTRIDIA C tetani; C perfringens; C difficile; C botulinum BACTEROIDES B fragilis; Prevotella Porphyromonas ACTINOMYCES FUSOBACTERIUM ANAEROBIC STREPTOCOCCI

CLOSTRIDIA Gram positive spore forming bacilli ubiquitous intestines of manand animals animal and human faeces contaminated soil and water Several species associated with human disease

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 Bacteraemia Myonecrosis food poisoning enteritis necrotica (pig bel)

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-1970’s 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 - AAC Pseudomembranous colitis Treatment omit antibiotic if possible oral vancomycin (125mg qds or metronidazole

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 Treatment - surgery and long term penicillin