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 Bifidobacterium 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-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 - 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

• Treatment - surgery and long term penicillin.

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