Clostridium PDF

 Bacillus (aerobic) Spore Clostridium (anaerobic) forming Corynebacterium Non-spore Listeria forming  CLOSTRIDIUM SPECIES  The clostridia are spore-forming, anaerobic, Gram- positive, motile rods (peritrichous flagella).  Many form toxins  Th...

 Bacillus (aerobic) Spore Clostridium (anaerobic) forming Corynebacterium Non-spore Listeria forming  CLOSTRIDIUM SPECIES  The clostridia are spore-forming, anaerobic, Gram- positive, motile rods (peritrichous flagella).  Many form toxins  Their natural habitat is the soil, marine sediments, sewage, or the intestinal tract of animals and humans  There are four medically important species:  Clostridium botulinum  Clostridium tetani,  Clostridium perfringens  Clostridium difficile.  Clostridium botulinum C. botulinum, which causes the disease botulism Transmission Spores, widespread in soil, contaminate vegetables and meats. When these foods are canned or vacuum-packed without adequate sterilization, spores survive and germinate in the anaerobic environment. Toxin is produced within the canned food and ingested preformed. The toxin is relatively heat-labile; it is inactivated by boiling for several minutes. Thus, disease can be prevented by sufficient cooking.  Pathogenesis Botulinum toxin (BT) after entry (either ingested, inhaled or produced in the wound) the toxin transported via the blood to peripheral nerve synapses BT binds to acetylcholine receptors on the nerve terminals where it blocks release of acetylcholine causing flaccid paralysis  There are eight immunologic types of toxin; types A, B, and E are the most common in human illness.  Clinical finding Descending weakness and paralysis, including diplopia, dysphagia flaccid paralysis and respiratory muscle failure, are seen. No fever is present.  Clinical finding  Special clinical forms occur  Food-borne botulism consumption of contaminated canned food  Wound botulism, in which spores contaminate a wound, germinate, and produce toxin at the site. (injection drug users)  Infant botulism, the most common type. Ingestion of contaminated food (honey). Affected infants develop weakness or paralysis and may need respiratory support Laboratory Diagnosis  The organism is usually not cultured  Gram staining of smears from suspected food Treatment  Immediately without waiting laboratory result Trivalent antitoxin (types A, B, and E) is given, along with respiratory support. Prevention  Proper sterilization of all canned and vacuum-packed foods is essential. Food must be adequately cooked to inactivate the toxin. Swollen cans must be discarded (clostridial proteolytic enzymes form gas, which swells cans). Disease  Clostridium tetani causes tetanus Transmission  Spores are widespread in soil. The portal of entry is usually a wound site (e.g., where a nail penetrates the foot),  surgery done without proper asepsis  Neonates following abortion/ delivery due to unhygienic practice  Tetanus toxin (tetanospasmin) is an exotoxin produced by vegetative cells at the wound site.  This polypeptide toxin is carried intra-axonally (retrograde) to the central nervous system, where it binds to ganglioside receptors and blocks release of inhibitory mediators, neurotransmitter (e.g., glycine and GABA) at spinal synapses.  The toxin prevents the presynaptic release of inhibitory neurotransmitters (GABA) leads to spastic muscle contraction  Tetanus is characterized by strong muscle spasms or contraction (spastic paralysis, tetany).  Rigid contraction of the jaw muscles, which prevents the mouth from opening ( lockjaw ,trismus).  Pronounced arching of the back due to spasm of the strong extensor muscles of the back (Opisthotonos) is often seen.  Respiratory failure followed. A high mortality rate is associated with this disease.  There is no microbiologic or serologic diagnosis. Organisms are rarely isolated from the wound site.  Clostridium tetani produces a terminal spore (i.e., a spore at the end of the rod). This gives the organism the characteristic appearance of a “tennis racket.” Clostridium tetani produces a terminal spore (i.e., a spore at the end of the rod  Tetanus immunoglobulin (tetanus antitoxin) is used to neutralize the toxin.  Metronidazole or Penicillin G can be given but the role of antibiotics is uncertain.  An adequate airway must be maintained and respiratory support given.  Tetanus is prevented by immunization with tetanus toxoid (formaldehyde-treated toxin) in childhood and every 10 years  Tetanus toxoid is usually given to children in combination with diphtheria toxoid and the acellular pertussis vaccine (DTaP).  When trauma occurs, the wound should be cleaned and debrided, and tetanus toxoid booster should be given.  Clostridium perfringens  Many different toxin-producing clostridia invasive infection (including myonecrosis and gas gangrene) if introduced into damaged tissue  Clostridium perfringens causes two distinct diseases, , depending on the route of entry into the body  Gas gangrene  Food poisoning Spores are located in the soil;. Gas gangrene is associated with war wounds, automobile and motorcycle accidents  Organisms grow in traumatized tissue (especially muscle) and produce a variety of toxins. The most important is (lecithinase), which damages cell membranes, including those of erythrocytes, resulting in hemolysis.  Degradative enzymes produce gas in tissues.  Clinical Findings  Pain  edema  cellulitis  gangrene (necrosis) occur in the wound area  Crepitation indicates the presence of gas in tissues.  Shock and death can ensue. (Mortality rates are high)  Laboratory Diagnosis Specimen: necrotic tissues, muscle fragments from deeper part of the wound Smears of tissue and exudate samples show thick, stubby large gram positive rods.  C. perfringens colonies exhibit a double zone of hemolysis on blood agar. (double zone hemolysis,  On blood agar an inner narrow zone of complete hemolysis (due to θ-toxin), surrounded by a much wider zone of incomplete hemolysis (due to the alpha toxin) Treatment  Early surgical debridement  Combination of Penicillin and clindamycin are recommended for 10=14 days Transmission  Spores are located in soil and can contaminate food.  The heat-resistant spores survive cooking and germinate.  The organisms grow to large numbers in reheated foods, especially meat dishes. Pathogenesis  C. perfringens is a member of the normal flora in the colon but not in the small bowel, where the enterotoxin acts to cause diarrhea. Clinical finding  The disease has an 8- to 16-hour incubation period and is characterized by watery diarrhea with cramps and little vomiting. It resolves in 24 hours. Laboratory Diagnosis  This is not usually done. There is no assay for the toxin. Large numbers of the organisms can be isolated from uneaten food. Treatment  Symptomatic treatment is given; no antimicrobial drugs are administered. Prevention  There are no specific preventive measures. Food should be adequately cooked to kill the organism. Clostridium difficile causes antibiotic-associated pseudomembranous colitis C. difficile is the most common nosocomial (healthcare- associated infection - /hospital-acquired) cause of diarrhea.  The organism is carried in the gastrointestinal tract in approximately 3% of the general population and up to 30% of hospitalized patients.  Most people are not colonized, which explains why most people who take antibiotics do not get pseudomembranous colitis.  The hands of hospital personnel are important intermediaries.  Antibiotics suppress drug-sensitive members of the normal flora, allowing C. difficile to multiply and produce exotoxins A and B.  The main effect of exotoxin in particular is to cause depolymerization of actin, resulting in a loss of integrity, apoptosis, and death of the enterocytes.  Many antibiotics are known to cause this disease. Such as Clindamycin  C. difficile causes diarrhea associated with pseudomembranes (yellow-white plaques) on the colonic mucosa  The diarrhea is usually not bloody  Fever and abdominal cramping often occur.  surgical resection of the colon may be necessary.  The presence of exotoxins in the filtrate of a patient’s stool specimen is the basis of the laboratory diagnosis.  Antigen detection: various methods such as rapid test in stool specimen  PCR assay for the presence of the toxin gene DNA is also used.  The causative antibiotic should be withdrawn.  Oral metronidazole or vancomycin should be given and fluids replaced.  Also in life-threatening cases, surgical removal of the colon may be required