anaerobic bacteria Flashcards
List normal anaerobic flora in oral cavity, colon, female genital tract and skin
Oral cavity: Bacteroides. Colon: Bacteroides, Peptostreptococcus, Fusobacterium, Clostridium, Lactobacillus. Female genital tract: Lactobacillus. Skin: Propionibacterium
features of anaerobic gram-negative rods/ anaerobic cocci infections
Organisms are members of normal flora and rarely cause disease without predisposing condition. Autoinfection- normal flora transgresses epithelial barrier. typically “polymicrobial”, or “mixed infections”, containing both anaerobic and facultative or aerobic organisms. biphasic pattern- aerobes and facultative organisms predominate at first, then create an anaerobic environment for anaerobes.
Chronic abscess formation
The later stage of anaerobe infection - The abscess is conducive to maintaining a low oxygen tension environment and provides protection from host defenses and antimicrobial agents
treatment of anaerobic infections
frequently requires surgical drainage of abscesses and debridement of devitalized tissue, along with appropriate antimicrobial agents
Bacteroides fragilis structure
anaerobic, aerotolerant. Gram-negative rods that appear pleomorphic and stain irregularly. Positive catalase test, tolerant to bile, resistant to kanamycin, vancomycin and colistin.
B. fragilis virulence factors
a. Fimbrae (pili) mediate adherence to epithelial cells.b. Extracellular enzymes such as phospholipase A, collagenase, heparinase result in tissue damage. c. Superoxide dismutase (plus catalase) enhances the ability of the organism to survive under less than stringent anaerobic conditions in the host. d. Polysaccharide capsule- abscess formation.
Host responses to B. fragilis
a. Antibodies to capsular polysaccharide enhance killing but do not protect against abscess formation. b. Specific T-cell immunity is induced by capsular polysaccharide and protects against abscess. c. B. fragilis LPS lacks the lipid A (endotoxin) moiety. Thus, septic shock is not commonly associated with B. fragilis bacteremias.
List the causes of tetanus, botulism and food poisoning/ gas gangrene
tetanus: Clostridium tetani. Botulism: C. botulinum. Food poisoning/ gas gangrene: C. perfringens
C. tetani and botulinum toxins
Both are “typical” two subunit AB toxins; one subunit promotes specific host-cell binding and uptake, and the second subunit is a specific protease that mediates the toxic activity. The mechanism of action is cleavage of specific proteins at the synaptic cleft, thereby blocking release of neurotransmitters
Clostridium tetani structure
Gram-positive, spore-forming rods. Sporulating cells have a characteristic “tennis racquet” shape. Organisms are difficult to isolate and lesions are often inconspicuous, so diagnosis is on the basis of clinical criteria.
Clostridium tetani pathogenesis
C. tetani spores are usually introduced into wounds by environment. Locally produced tetanus toxin (tetanospasmin) is transported to by retrograde axonal transport along peripheral motor neurons. Toxin binds to gangliosides on presynaptic internucial cells of the spinal cord (Renshaw cells). There, the toxin interferes with release of the inhibitory neurotransmitters (GABA, glycine). This results in unopposed motor excitation and generalized spasticity (spastic paralysis). Toxin binding is irreversible; recovery requires formation of new axonal terminals.
C. tetani transmission
C. tetani is widespread in feces of domestic animals and man; its spores are abundant in soil and the environment
Tetanus clinical
Incubation period ranges from a few days to 3 weeks. Generalized tetanus is characterized by trismus (lockjaw), neck stiffness, difficulty swallowing, rigidity of abdominal and back muscles and fever. The highest mortality is in newborns where disease progression in rapid
tetanus prevention/ treatment
i) debridement of the wound ii) treatment with an antimicrobial such as metranidazole iii) passive immunization with human tetanus immunoglobulin, iv) vaccination with tetanus toxoid. Antitoxin antibodies work by neutralizing free toxin. However, toxin that is already bound to nerve endings cannot be neutralized with antibody. Tetanus is preventable by immunization with tetanus toxoid.
neonatal tetanus
illness caused by infection with Clostridium tetani, usually of the umbilical stump. The case-fatality ratio for this infection is greater than 80%; it is preventable with maternal vaccination, hygienic birth practices to ensure infection is not contracted by mother or newborn during the birth process and proper cord care to ensure that contamination of cord does not put the newborn at risk.
Clostridium botulinum structure
Anaerobic, Gram-positive, spore-forming rod. Pressure sterilization is required to kill the spores. Seven antigenically distinct forms of botulism toxin (A-G) are described; A, B, E and F are associated with human disease. The toxins are phage-encoded (e.g., lysogenic conversion); each strain produces a single toxin type.
C. botulinum pathogenesis
Botulinum neurotoxin is one of the most potent toxins known. It is released during growth or sporulation of C. botulinum. Although C. botulinum spores remain viable for several hours at 100°C, preformed botulinum toxin is rather heat labile and is destroyed by boiling for 10 minutes or heating to 80°C for 30 minutes.
Botulism is similar in structure and function to tetanus toxin, except that botulinum is very specific for cholinergic nerves. The toxin blocks release of the neurotransmitter acetylcholine at the neuromuscular junction. Botulinum neurotoxin is one of the most potent toxins known. It is released during growth or sporulation of C. botulinum. Although C. botulinum spores remain viable for several hours at 100°C, preformed botulinum toxin is rather heat labile and is destroyed by boiling for 10 minutes or heating to 80°C for 30 minutes.
Botulism is similar in structure and function to tetanus toxin, except that botulinum is very specific for cholinergic nerves. The toxin blocks release of the neurotransmitter acetylcholine at the neuromuscular junction.
foodborne botulism
Preformed toxin resists digestion in the GI tract and is absorbed. Symptoms generally begin 18 to 36 hours after eating a contaminated food, but they can occur as early as 6 hours or as late as 10 days
infant botulism
consumption of certain foods (esp. raw honey) by infants. Ingested spores germinate and produce toxin in the GI tract.
wound botulism
toxin production by organisms contaminating traumatic wounds.
botulism sx
Typical symptoms begin with blurred vision with fixed dilated pupils, dry mouth, constipation and abdominal pain. . Flaccid paralysis develops with bilateral descending weakness of the peripheral muscles; death is attributed to respiratory paralysis.
botulism treatment
Diagnosis is confirmed by demonstrating: i) botulinum toxin in the blood; ii) toxin and/or C. botulinum organisms in the stool or the implicated food source.
botulism treatment and prevention
Treatment includes i) support ventilation, and ii) polyvalent antitoxin. Antitoxin neutralizes circulating toxin, but cannot reverse effects of toxin already bound to neurons. Recovery requires regeneration of affected nerve endings, and may take weeks to months. Botulism can be prevented by proper canning
transmission of botulism as bioterrorism
inhalation botulism- absorption of inhaled, aerosolized toxin across the mucosal surface of the lung
Clostridium perfringens structure/ growth
Gram-positive spore-forming rods, although spores are seldom seen in clinical specimens. Gram-stain of wound exudates are notable for the absence of PMN’s due to the cytotoxic effects of alpha toxin. C. perfringens has an exceptionally fast growth rate, with a generation time of 8 minutes. The organism is relatively aerotolerant.
C. perfringens virulence factors
12 toxisn that are active on tissues, plus an enterotoxin. The most important is alpha toxin, a phospholipase C (lecithinase) that cleaves phosphatidyl choline, a major lipid component of eukaryotic cell membranes. It is lyses a variety of cell types, including RBC’s, platelets, leukocytes and endothelial cells; resulting in destruction of vital tissue and widespread capillary damage
C. perfringens transmission
common component of the normal intestinal flora of humans and animals, and is very commonly isolated from soil and water. Spores may survive for extended periods.
C. perfringens diseases
- food poisoning- enterotoxin produced during sporulation in large intestine causing cramps and watery diarrhea. Self limited. 2. soft tissue infections: cellulitis, fasciitis and myonecrosis (gas gangrene).
describe gas gangrene
clostridial myonecrosis is a life-threatening, progressively destructive infection of a contaminated wound. Sudden onset of pain around the wound, followed rapidly by discoloration, swelling, and the appearance of foul-sweet smelling watery exudate. There is crepetis (gas bubbles in tissue) and general toxemia. Infection extends deep into tissue to involve muscle, which is devitalized and has the appearance of cooked meat. The usual setting is that of a crushing-type traumatic wound (gunshot, industrial and automobile accidents) in which there is considerable tissue damage and impaired bloodflow to the area (i.e. creation of an anaerobic environment). Nearly half of incidents occur following bowel surgery.
c. perfringens treatment
Surgical debridement to remove dead tissue and antibiotic therapy. Hyperbaric oxygen may be useful since high oxygen tension inhibits growth and toxin production
C. difficile disease
normal flora of some. Disease typically develops in hospitalized patients during broad-spectrum antibiotic treatment of an unrelated condition. In these patients, antibiotic treatment alters the normal enteric flora, allowing either 1) overgrowth by endogenous C. difficile, or 2) makes the patient more susceptible to colonization and infection by exogenous organisms.
C. difficile transmission
This is perhaps the only clostridial disease in which there is significant risk of person-to-person spread. Spread of the organism is facilitated by the ability of C. difficile to readily sporulate, and spores are resistant to alcohol-based hand sanitizer
C. difficile pathogenesis
toxin A (an enterotoxin) and toxin B (a cytotoxin). Toxins are phage encoded, and only certain strains of C. difficile are lysogenized, produce toxin and capable of causing disease.
C. difficile diagnosis
Diagnosis is made by detecting C. difficile toxin in patient stool by a cytotoxicity assay or ELISA, or by isolation of toxin-producing C. difficile from patient stool. Rapid PCR-based methods are being developed.
C. difficile treatment
metronidazole (first line drug) and oral vancomycin (second-line drug). Prolonged treatment is indicated and recurrence of disease is not uncommon
list the sources of infectin for the 4 types of clostridium
botulinum: soil and water. Tetani: man, animals, soil and water. Perfringens: man, animals, soil and water. Difficile: man, fomites
