Special precautions to take when handling anaerobes
Keep them protected from oxygen when taking them to diagnostics, otherwise they’ll die
Characteristics of anaerobes
Can’t use O2 as final e- acceptor, unable to break down H2O2 because they lack catalase, in the presence of O2 (except bacteroides), superoxide accumulates because they lack superoxide dismutase (except bacteroides)
Toxin-mediated anaerobic infections
Clostridia: C. botulinum (food-borne, infant, infection) is preformed. C. difficile, C. perfringens (gas gangrene and food poisoning) and C. tetani are formed in vivo.
More common source of anaerobic infection? Where else can anaerobic infections come from?
Normal flora, although most infections are mixed. Regions of the body most susceptible have low O2, warm, moisture and substrate (like mucous membranes)Less common sources are exogenous where spores are kicked up in dirt or on contaminated foreign bodies that germinate on infection.
What things create an opportunity for anaerobic infection?
Injury and poor perfusion (like in a dog bite)
Why are anaerobic infections difficult to treat?
They are often mixed infections
Areas in the body with high concentrations of anaerobes
Clinical characteristics of anaerobic infections
Aspiration, brain abscesses, foul-smelling pus, anaerobic sinusitis
Anaerobic infections above the waist (like sinusitis)
Typically related to poor dentition and are more susceptible to antibiotics.
Why is sinusitis commonly associated with anaerobic infection after a URI?
URI results in blockage of the sinuses from inflammation, decreases O2 content and allows for anaerobic growth.
Anaerobic infections below the waist
Typically related to GI and GI. Less susceptible to antibiotics. Use metronidazole, clindamycin, augmentin.
Which species of clostridia are shown below?
Left) Tetani Middle) Perfringens Right) Botulinum. Note that they are all gram + rods.
Most common cause of invasive clostridial infections
C. perfringens (myonecrosis and gas gangrene). Often mixed with facultative organisms like E. coli that use up the oxygen in the environment that allow anaerobes to proliferate.
C. perfringens virulence factors
Lecithinase: phospholipase that kills cells and hemolyzes RBCs (hemolytic and blood agar and egg yolk). This leads to muscle necrosis (reddish blue-black tissue) with ABSENT PMNs.
What happens when you incubate C. perfringens with milk?
Stormy fermentation with lots of gas production.
Pathogenesis of C. perfringens infection.
Contaminated wound -> Spores germinate where O2 is low -> Exotoxins (lecithinase) made -> Tissue necrosis and deeper penetration -> Rapid spread across fascial planes
Anaerobe found in the oral flora that are gram-positive non-spore forming rods that grow in chains and in a molar formation.
Macro colonies that resemble grains of sand that are frequently seen in abscesses and sinus tracts. Associated with actinomyces.
What microbe most likely caused this?
Note the suppurative and granulomatous inflammation of the cervico-facial region. This is most often due to poor oral hygiene after invasive dental surgery by actinomyces.
Gram-positive, non-spore former that causes acne and infection of prosthetic devices
Most common gram-negative non-spore forming rods
Bacteroides and fusobacterium. Bacteroides are commonly pathogenic after GI surgery because it is very prevalent in the colon and urogenital tract, causes intra-abdominal abscesses (below the waist!)
Virulence factors of bacteroides fragilis
Polysaccharide capsule is anti-phagocytic.
How do you treat bacteroides?
Not with penicillins because most below the waist anaerobes make beta lactamase
Lab diagnosis of bacteroides
Grow in bile and turn bile black when they grow on it
What bacteria played a role in periodontal disease?
Fusobacterium nucleatum. Note the long, thin gram-negative rods.
What cancer is fusobacterium linked to?
Colorectal cancer. This is because it can be swallowed in the mouth an infect the GI tract.
Major clinically significant non-spore-forming anaerobes
GRAM NEGATIVES RODS: Bacteroides (intra-abdominal), fusobacterium (oral). GRAM POSITIVE RODS: actinomyces (lumpy jaw), propionibacterium (prosthesis & acne).
The usual antibiotics prescribed for above the waist anaerobic infections?
Penicillin + beta-lactamase inhibitor (amp/sulbactam, amox/clavulanate). Most normal flora are susceptible to normal beta-lactams.
Good antibiotic for coverage of anaerobes mixed with enterococci and gram negatives like E. coli.
Antibiotic to give if you really need to get rid of toxin production
Antibiotic commonly used in deep abdominal infections
Metronidazole. Note that it will be combined to cover gram positives.
A 3 year old presents with a neck abscess and was put on augmentin for 10 days with no resolution. He was later put on clarithromycin, it drained and he felt better. The drainage was cultured and positive for propionibacterium acnes and s. epidermidis. A month later he presents with inflammation on the other side and has torticollis. WBC is 17,000. CT is shown below. On culture small grey colonies grew out that smelled like bleach/locker room (Eikenella). Strep intermedius and prevotella oralis (bacteroides) also grew out. How do you treat him?
Note the vesicle overlying the abscess. The same infection happening 3x recently makes you suspicious for an anatomical cause. His culture shows mixed facultative aerobes and anaerobes. Prevotella is a beta-lactamase producer, so you treat with augmentin and clean out the branchial cleft cyst.
Causes of adult deep neck infections
Dental, tonsils, trauma, foreign bodies
Causes of pediatric deep neck infections
Dental, tonsils and congenital abnormality
Facultative gram - bacillus that is commonly seen in bite wounds and boxers.
What syndrome is a kid at risk for if he grows fusobacterium from a branchial cyst?
Lemierre’s syndrome: bacterial spread to lateral pharyngeal space and progresses to internal jugular vein, leading to vasculitis, septic emboli, metastatic infection and death.
An 11 year old presents with abdominal pain, no bowel movements for the last 2 days, nausea, fever and the pain has migrated to the RLQ. CT shows thickening and fluid around the appendix. WBC is 11,200. Her appendix was removed and brown serous fluid was seen in the abdomen. How would you treat this patient?
E. coli, enterococcus faecalis, bacteroides fragilis, multiple anaerobic streptococci etc. are present in secondary peritonitis. Treatment is not culture based, you empirically treat with PCN + Beta-lactamase inhibitor, cefoxitin, carbapenems, 3rd generation cephalosporins or clindamycin.
An 18 year old man presents with left sided neck swelling that was non-tender, not red, not warm, not boggy and it was nodular, firm and immobile. It started as a small nodule and has grown over the past 10 days. He reports having problems with the gums previously and hasn’t been to the dentist in a while. CT shows an expanding mass crossing fascial planes. All labs WNL. It started draining on its own and culture showed PMNs but no bacteria. What would you expect to see on culture? How would you treat?
Note how grainy the abscess is, this is typical of actinomyces. Treat with PCN + beta-lactamase inhibitor for 6 months to 1 year. On culture you would see filamentous organisms and sulphur granules, gram-positive, anaerobic bacteria.
4 clinical forms of actinomyces
1) Cervicofacial (poor dentition) 2) Thoracic 3) Abdominopelvic (IUDs) 4) CNS (bacteremia, extension from oral cavity)