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Anaerobic bacteria ?
Before 1978 : A group of bacteria which cannot grow in the presence of oxygen Why ? Some anaerobic bacteria can grow on mucosal surfaces Anaerobic bacteria can caused brain infection or caused bacteremia After 1978 : Bacteria which can grow in a negative / low oxidation-reduction (redox) potential (Eh)
Aerobic Bacteria
A. Obligate Aerobic Bacteria Require molecular oxygen as a terminal electron acceptor and cannot grow without it. They generate energy oxidatively and are unable to generate sufficient energy for growth by fermentation reactions. Examples include Micrococcus lutea and Nocardia asteroides. B. Microaerophilic Bacteria Require oxygen as a terminal electron acceptor for growth but cannot grow on the surface of solid media in an aerobic incubator. They grow minimally, if at all, under anaerobic conditions.
Anaerobic Bacteria
A.
CLOSTRIDIAL GROUP
Normal flora in Mouth cavity Respiratory tract Intestinal tract Urogenital tract Skin
ANAEROBIC BACTERIA
will grow in a negative / low redox potential (Eh) most of the anaerobic bacteria that cause infections in human are also part of normal flora other pathogenic anaerobes are soil and environmental inhabitans are not considered part of human flora e.g Cl. tetani and Cl. botulinum the majority of anaerobic infections occur when a normal flora of the patient gains access to a sterile site as a result of disruption of some anatomic barrier
Infections in continuity to mucosal surfaces Infections with tissue necrosis and abscess formation Putrid odor Gas in tissues Polymicrobial flora Failure to grow in the laboratory
fragilis group Prevotella and Porphyromonas Fusobacterium nucleatum Peptostreptococcus Clostridium perfringens
Pathogenic
species have virulence factors that allow survival outside their niche and to cause disease
PATHOGENESIS
The type of infections and diseases are caused by anaerobic bacteria span a wide spectrum : Produce some of the most potent toxins e.g Cl. tetani and Cl. botulinum Specific virulence factors e.g B. fragilis group, Cl. difficile Most anaerobic infections involved a mixture of anaerobic and facultatively anaerobic organisms
Virulence Factors
1.
Anti-phagocytic capsule
Also promote abscess formation
1.
1.
Beta-lactamase production
B. fragilis protect themselves and other species in mixed infections
1.
are
Originate from our own flora Breeches in the mucocutaneous barrier displace normal flora Compromised vascular supply Decrease Trauma with tissue destruction Redox Antecedent infection Potential
2.
Predisposing Conditions
1. 1. 2. 3.
Infection Average of 5 species 3 anaerobic 2 aerobic Less complex then nl flora Fecal flora 400 different species Those predominant in stool are not infecting species Veillonella, Bifidobacterium rarely pathogenic Species uniquely suited to cause infection predominate
E. coli Consume O 2
growth of anaerobes Anaerobes promote growth of other bacteria by being antiphagocytic and producing B-lactamases
Allow
Serum, stool and tissue biopsy : Wound botulism Feces : for C. difficile culture Liquid or unformed solid stool : for toxin assay Formed stool or rectal swabs : to detect carriers Stool should be placed in anaerobic transport container
- A crucial factor in the final success of anaerobic cultures is the transport of the specimen, the lethal effect of atmospheric oxygen must be prevented until the specimen can be processed in the laboratory - Recapping a syringe and transporting the needle and syringe to the laboratory is no longer acceptable because of safety concerns involving needle stick injuries Therefore, even aspirates must be injected into some of type of oxygen free transport tube or vial.
rubber stoppered collection vial an oxygen free atmosphere an anaerobic pouch (Gas-Pak Pouch)
SPECIMENS PROCESSING
may be processed on the open bench-top with incubation in anaerobic jars or pouches or in an anaerobic chamber Anaerobic conditions can be setup by two different methods : The easiest method uses a commercially available hydrogen or CO2 generator envelope or the evacuation replacement method can be used
Virulence factor
several exotoxin, alfa toxin is important (11 other toxins) enterotoxin
C. tetani
respiratory failure C. botulinum
Gas-gangrene, destruction of muscle and other tissues Food poisoning, abdominal cramps, diarrhea, vomiting tetanospasmin, neurotoxic (disrupts Tetanus (lockjaw), muscle spasms, nerve impulses to muscles Botulism, paralysis of respiratory and other essential muscle groups Wound botulism Antibiotic Associated Diarrhea diarrhea Pseudomembranous Colitis (PMC) Pseudomembran Associated with inflammatory process in acne Most commonly encountered in anaerobic infections, often mixed with other anaerobic or facultatively anaerobic organisms Most often found mixed with other anaerobic or facultatively anaerobic organisms Mixed infection
C. difficile (AAD), Propionibacterium spp. Bacteroides fragilis groups Fusobacterium spp. Peptostreptococcus Fusobacterium spp. Veillonella spp.
No definitive virulence factors known capsules, endotoxin, succinic acid, various enzymes No definitive virulence factors known No definitive virulence factors known
CLOSTRIDIUM TETANI
)
General characteristics : is a Gram positive, spore forming anaerobe possesses a terminal spore, resulting in a characteristic tennis racquet or drum stick morphologic appearance spores are ubiquitous in soil
Pathogenicity Toxigenicity is mediated by a large plasmid The organism secretes an exotoxin tetanospasmin
Clinical disease : - Infection follows minor trauma (laceration or puncture) or occurs as umbilical cord stump infection in a neonate (Tetanus neonatorum) - Manifestations include muscle stiffness, tetanospasms of lockjaw and back arching, and short, frequent spasms of voluntary muscles - Death occurs after several weeks from exhaustion and respiratory failure - Intrauterine infection : Septic abortion, Post abortal tetanus, Tetanus post partum
Treatment :
o
o o o
The patient should be hospitalized and treatment begun without waiting for definitive diagnosis Antitoxins are effective only if toxins have not yet bound to tissues Antitoxin and penicillin should be given, tissue should be debrided, a quiet and dark environment should be provided to minimize external stimuli that can induce spasms
Prevention : - DTP vaccine A booster should be given every 10 years, for major trauma a booster should be given if the patient has not had one within the last 5 years - Booster should be given to pregnant women to stimulate maternal antibodies That will protect the newborn
CLOSTRIDIUM BOTULINUM
General characteristics : is a Gram positive, spore forming anaerobic rod requires a low redox potential within tissues spores are ubiquitous in soil and are highly resistant to environmental conditions
Pathogenicity :
produces
a potent exotoxin that act at the myoneural junction to produce flaccid muscle paralysis due to suppression of acethylcholine release from the axon terminals of peripheral nerves
Clinical manifestations :
1.Food poisoning
Clinical findings include : nausea, vomiting, dizziness, cranial palsy, double vision, swallowing and speech problems, muscle weakness, respiratory paralysis, and death (in 20 % of cases)
2. Intestinal (infant) botulism - The exotoxin disseminates, causing constipation, generalized weakness, and loss of head and limb control (resulting in a floppy appearance) This type of infection rarely is fatal 3. Wound infection, manifestations similar to those of soft tissue wound
Laboratory Diagnosis : The presence of the toxin in food, stool, blood and vomitus Treatment : - for food poisoning : give antitoxin and supportive measures for respiratory control, stomach lavage and enemas Antibiotics should not be given and the caregiver should act rapidly - for intestinal botulism in infant only supportive care is needed
Prevention :
give
antitoxin to all person who are contaminated food, even if symptoms have not developed heat food to 80 o C - 100 o C for 10 minutes to inactivate the toxin (but not the spores) use proper sterilization techniques for home canning
Pathogenicity -produces alpha toxin -produces 11 other toxins or enzymes that damage eukaryotic cells -Produces an enterotoxin associated with food poisoning
Clinical manifestation :
C. perfringens causes two types of infection : 1. Soft tissue (muscle) wound infection, with two consequences : a. Anaerobic cellulitis, causing destruction of traumatized tissue only b. Myonecrosis (gas gangrene)
Other clostridia may be associated with gas gangrene are : C. septicum , C. novyi , C. histolyticum , C. sordellii 2. Food poisoning following ingestion of contaminated food
Treatment
- For anaerobic cellulitis
Penicillin and additional antibiotics are given to prevent secondary bacterial infections, Necrotic tissue should be debrided - For myonecrosis Penicillin and antitoxin are given Necrotic tissue is debrided. Surgery is likely - For food poisoning Treatment usually is not necessary because the infection is self limiting
CLOSTRIDIUM DIFFICILE
General characteristics : - is a Gram positive, spore forming, anaerobic rod - the normal intestinal flora of infants and some adults Pathogenicity : - has many strains that are resistant to antibiotics - antibiotic treatment kills organisms normally restricting growth of C. difficile resulting in overgrowth of the latter produce two toxins : an enterotoxin and a cytotoxin
Treatment : is with vancomycin or metronidazole Fluid and electrolyte status should monitored be
NON CLOSTRIDIAL GROUP - Endogenous - Chronic - Secondary infection - Non severe toxemia - Normal flora - Mixed infection
BACTEROIDES GROUP
B. fragilis s.s s.s s.s
s.s B. fragilis B. thetaiotaiomicron B. ovatus B. vulgatus
Prevotella ( Bacteroides ) melaninogenicus s.s melaninogenicus intermedius sacharolyticus B. corrodens B. oralis B. capillosum
BACTEROIDES FRAGILIS
General characteristics :
- is a Gram negative, anaerobic rod, usually pleomorphic - grows rapidly under anaerobic conditions and is stimulated by bile - contains level of superoxide dismutase & catalase - is found in the female genital tract but rarely in the oral cavity - usually causes polymicrobic infections - possess a beta-lactamase that destroys penicillins and cephalosporins
Pathogenicity :
- possesses a capsules that inhibits phagocytosis - has a weak endotoxin and no exotoxin - possesses a collagenase and hyaluronidase, which aids its spread
Clinical manifestation
-Gastrointestinal abscesses after damage mucosal barriers - Pelvic inflammatory disease - Brain abscesses and cellulitis - are not communicable or transmissible to
Treatment :
Tetracyclines
is generally ineffective Metronidazole, clindamycin, kanamycin and chloramphenicol are also suggested as therapeutic agents
PREVOTELLA MELANINOGENICUS
(formerly Bacteroides melaninogenicus)
General characteristics
- a small Gram negative coccobacillus, occasional long forms - has a distinctive black colonial appearance on agar - the normal flora of the mouth - low numbers in the gastrointestinal and genitoyrinary tracts
Pathogenicity
possesses a potent endotoxin and a collagenase
Clinical manifestation - causes lung abscesses - causes infections of the female genital tract Treatment - Metronidazole and Clindamycin - Carbapenems are the most potent betalactam
FUSOBACTERIUM SPP.
General characteristics : - Gram negative, anaerobic, non sporeforming, non motile, long filamentous rod - produce copious amounts of butytic acid and lower levels of acetic and propionic acids - as commensals of the upper respiratory and gastrointestinal tracts
Manifestation of infections
Infections of the oral cavity ( F. nucleatum , F. periodonticum , F. naviforme , F. simiae ) Mixed infection of the head and neck region ( F. nucleatum ), including : dental abscesses infection of the central nervous system Intra abdominal infections, perirectal abscesses, osteomyelitis, decubituts (F . mortiferum , F. necrogene , F. varium , together with F. nucleatum )
Treatment
Acidaminococcus
Pathogenic
role-??
Part
- as part of the normal flora of the gastrointestinal tract - mixed anaerobic infections
Species :
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