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38 Cards in this Set

  • Front
  • Back
Common features of Anaerobic Infections:
1) Origin
2) Characteristics
3) Predisposing conditions
4) Location
5) Redox potential
6) Species
1) Many abscesses originate from native flora (anaerobes are a large part of native flora)
2) Foul-smelling discharge, gas, necrotic tissue
3) pulm aspiration, bowel surg, poor dental hygiene, bites, trauma, malignancy
4) Most in deep or necrotic tissues (low O2 and high access to endogenous bacteria)
5) Healthy tissues have high oxid-red potential due to presence of O2, can't support anaerobe growth. Oxidation-reduction potential may decrease due to - Wound, impaired blood supply, necrosis
6) All are "mixed" : >1 offending organism with 1 or more anaerobe or microaerophilic (fac anaerobe) organism

Side note: most aerobic infections involve a single species
Predicting anaerobic species involved:

Knowledge of flora influences therapy b/c:
1) by normal flora found in mucous membranes near infection site
2) Bacteroides fragilis is found in infections below the waist (penicillin resistant) - disting upper and lower GI

Oral infections: penicillin sensitive, G+ cocci, mixed anaerobic infections

Intraabdominal: penicillin resistant, G- rods, mixed anaerobic infections
How to ID clinically important Anaerobic Bact:
Correct Specimen sampling and inject directly into culture tubes or bottles (v. little air exposure!)
Anticipate mixed infection (aerobic and anaerobic)
Gram stain
Morphology (colonies, spores)
Unusual FA production (analyze with gas chromatography)
Other Metabolic characteristics

Don't submit oral or fecal cultures for anaerobes (have been subjected to air)

Antibiotic sensitivity assays aren't as reliable as for aerobes
Common anaerobic media:
Thioglycollate broth: chemical reducing agent, removes oxygen from liquid media
Anaerobic G+ Rods:
Bacteriodes fragilis
Prevotella (Bacteroides) melaninogenicus
Non-Spore Forming Anaerobic G+ Rods:

Spore forming G+ rods:
Propionobacterium (diptheroid)

Anaerobic G+ cocci:

Anaerobic G- cocci:

Bacteroides fragilis:
growth conditions
common infections
E. coli
pleiomorphic, most common
anaerobic G- rod

Large #s in small intestine

Resistant to bile bactericidal activity, and *Penicillin resistant*

In clinical specimens - DOESN'T require strict anaerobic conditions to survive
During growth - may tolerate traces of O2, but definitely anaerobic

causes septicemia via extraintest invasion, almost as common as Clostridia perfringens (these both cause ~80% anaerobic septicemias -> only 10% bacteremias caused by anaerobes -> these both cause 8% of all septicemias)

common in intraabdominal (bowel rupture) and female genital infections - foul smell, gas production, necrotic

Capsule = MAJOR virulence factor (only strains with capsule produce abscess in animal models)

Infections in comb with E. coli are more severe

Don't use penicillin (below the diaphragm), Use clindamycin, cefotoxin, metronidazole, aminoglycoside antibiotics (like gentamicin)
Prevotella (Bacteroides) melaninogenicus:

infection location
disease caused
Named for
more common in oral infections, and occasionally in genital infect

serious cause of periodontal disease

Many strains penicillin resistant, more sensitive to O2 than B fragilis

Named for black pigment formed in colonies on blood agar plates and infected tissue = Hemin

Hemin = precursor for cytochrome synthesis, required for growth

infections caused
tapered ends (needle shape), thin

sensitive to penicillin and oxygen (more than B. fragilis)

oral and abdominalinfections, lung and liver abscesses, other pleuropulmonary infections, peritonitis
Propionibacterium (diptheroid):

oxygen requirements
pleomorphic rod

aerotolerant (will grow in presence of low O2)

normal skin inhabitant, often a contaminant in blood cultures

doesn't usually cause infect
rarely -> endocarditis in immunocompromised patients

NOT pleomorphic

Normally *lots* in intestine and vagina
Used to make yogurt, sour milk, saurkraut

NON PATHOGEN, but often associated with GU and GI tract

Prevent growth of pathogens in vagina and intestine by maintaining low pH
Converts Lactic acid to sugar

oxygen requirements
G+ branching rods
Lesions contain microcolonies of actinomyces and cell debris with *Yellow sulfur granules*

some strains aerotolerant

oral pharynx and GI

Usually mixed infections
cervico-facial infections (oral or dental infections/abscesses), abdominal infections and sinus tract

oxygen requirements
G+ cocci, in chains

obligate anaerobe

mouth, GU and GI tracts

widely involved in infect, often in assoc with other anaerobes

Found in pure culture or pleuro-pulmonary, OG-GYN infections, and brain abscesses

G- cocci

a commensual, not important pathogen
Anaerobic infection treatment:
1) Penicillin - EXCEPT B. fragilis (*thus not used for infections below diaphragm*)
2)Newer Cephalosporins (cefoxitin) *more effective for B. fragilis*
3) Clindamycin
4) Chloramphenicol (bacteriostatic)
5)Metronidazole (trade name Flagyl)
6) For mixed aerobe-anaerobe: aminoglycosides plus antibiotic for anaerobes (ex - gentamycin and cefoxitin and clindamycin)
7) Surgically drain any abscesses (antibiotics can't kill bact in abscess)
Normal flora vs Carrier state:
natural flora of body sites vs. carriage of pathogen in body sites
Importance of normal flora:
1) interfere with pathogen colonization
2) can cause disease if immunocompromised (ex suppression of part of normal flora with antibiotic)
3) Nutritional - ex intestinal bact produce vitB12 and K
4) *Overgrowth of sm intest bacteria can lead to obstruction or decreased motilit, fat malabsorption and vit B12 deficiency*
5) Each lesion has its own flora - knowing local flora will assist in choosing antibiotic when barrier is violated (wound)
Normal Mouth/Saliva Flora:

S. viridans
aerobes or facultative Bact:
1) Streptococcus viridans:
predominant mouth microorg (10^6/ml saliva)
G+ cocci, may be in chains
Most common cause of subacute bacterial endocarditis
Highly adherent to dental tissue (plaque) and cardiac valves in bacteremia
Thrive on sugar, some turn sucrose -> polysacch Dextran (component of plaque) with lactic acid byproduct
G- diplococci, coffee bean shape

second most predominant

Non-path species as well as pathogenic (N. meningitidis which causes meningitis and can colonize in throat or nasopharynx)
common name for non-pathogenic Corynebacterium species (except for C. diptheria which is pathogenic)

Pleomorphic, G+ rods

most common contaminant in blood cultures along with S. epidermidis

colonize the skin

RARE infection cases reported in absence of foreign bodies
S. epidermidis:
Major oral coagulase-negative staph species

G+ cocci, grape-like clusters

most common blood culture contaminant along with diptheroids

May be pathogens in the presence of foreign bodies (catheters, travasc artificial devices)
Eikenella corrodens:
facultative, G- rod

part of normal oral flora

causes skin and soft tissue infections assoc with human bites and clenched-fist injuries (bite wound on the hand, caused when a person's closed fist strikes the teeth of another person)
Role of Normal aerobic throat flora in disease:
1) NTF eliminated by antibiotics may be replaced by more resistant G- rods or yeast -> drug resistant infections in pt's with malignancy or chemo

2) 5-40% of healthy individuals have low #s of potential pathogens in oral cavity (ex pneumococcus or staph aureus)

3) Hospitalization and antibiotics can allow G- rods to colonize (E. coli or Klebsiella
Oral Cavity Anaerobes:
present in small #s in gums and throat

grow in close assoc with mucous membranes (gum/teeth interface)

Common ones:
1)Fusobacterium (G- rod, cigar-shape) penicillin sens
2) Prevotella (G- rod), usually penicillin sens
3) Anaerobic streptococci (peptostreptococcus G+ cocci in chains, 15% bacteria in saliva) usually penicillin sensitive
4) Others (ex anaerobic spirochetes)
Lower Trachea:
bacteria free in healthy individuals
Diseases related to aerobes or anaerobes in the oral cavity:

Aspiration pneumonia: caused by aspiration of own oral secretion, offending pathogens are mix of normal flora

may not be helpful to determine causative organism because many are involved

many NFT aerobes and anaerobes sensitive to penicillin
Normal Stomach Flora:
few organisms because of high acidity

Exceptions: in gastric achlorhydria (no stomach acid), Gastric obstruction (bact can proliferate)
Upper Sm Intestine Flora:

role of upper small intestine microflora in disease:
Sterile in normal fasting subjects

If present, some G+ aerobes, few anaerobes, normally low #s and transported from mouth and resp tract

Sterility due to rapid peristalsis and antibact properties of unconjugated bile acids

Disease: Bacterial counts may increase in anatomical alterations cause stasis (ex post gastric bypass)
Normal flora of Terminal Ileum:

Stasis occurs here and allows for increase in bact #s

Usually 10^6/ml or less, species and #s closely resemble bact in feces

Coliforms = E. coli, enterobacter, and other G-

Anaerobes: ex B. fragilis, found mostly in lower intestine, not part of mouth flora, RESISTANT to penicillin
Normal flora of Large Intestine and Feces:

amount of bact
marked bact proliferation b/c of stasis

bact is probably 1/3 - 1/4 weight of feces
10^10-10^12 bact per g wet feces
Normal flora of Large Intestine and Feces:

Bacteroides: G- anaerobic rods, non spore forming, pleomorphic

Metabolic generation of ammonia (*formed by splitting urea and proteins), acid, gas

Bacteroides Fragilis:
most common (see above)


Bifidobacterium: non spore forming, G+, penicillin sensitive, in 2/3 fecal samples, 10^9 bact/gm

Lactobacilli: see above

Clostridial species: esp C. perfringens found in 1/3 samples at 10^6 per gram

Coliforms and Enterococcus (faecalis and faecium) = enteric G- rods, present at 10^7 CFU (colony forming unit) per gram, aerobic flora, common cause of UTIs

Other Anaerobes: present sporadically @ low #s, >400 species reported in normal feces
important factors in intestine =redox potential, pH, flow
gases produced = methane and hydrogen

Less frequent aerobes = S. aureus, Pseudomonas, Proteus, Klebsiella
Establishing Intestinal Flora:
Fetal Intestine is sterile -> at birth contains a few bacteria, colonized within hours -> breast fed infants mostly have Bifidobacterium -> upon weaning, resembles adult flora
Intestinal Flora Maintenance:
ability of bact (path or non path) to proliferate depends on:

Redox Potential (low O2 level) and pH

Synerg and Antag of competing microbes:

Anaerobes -> reducing conditions

Growth factor production used by other bact (vit K)

Acid (dec. pH), organic acid (prevent bact growth), and bacteriocin (antibact factors) produced and secreted by intest flora

Antibiotic administration can allow growth of pathogens (ex salmonella or shigella)
Physiological implications of normal flora metabolic activities:
1) Bile Acid deconjugation: convert to free bile acids by large intest flora, important for fat absorption
*this is why overgrowth in sm intest can cause overprod of free bile acids and fat malabsorption

2) Source of ammonia via degrad of nitrogenous substances (proteins) in COLON
impaired liver function can increase blood ammonia
Hepatic Coma - treatment aims to dec normal intest flora with broad spectrum antibiotics, cathartics, enemas
3) convert bile pigments (bilirubin) to urobilin and stercobilin
4) Carbs not absorbed by host are fermented -> decreased pH (helps maintain local flora)
Normal skin flora:
10^3 - 10^4 CFU/cm2

Staphylococcus epidermidis:
predominant microorg
generally nonpath, except in foreign body presence
catheter-related bacteremia is common

S. aureus: found in skin and nares, opportunistic

Anaerobes (ex Proprionibacterium and Peptococcus)located in deeper dermis follicles
(P. acnes implicated in acne)

Upper Resp Tract Flora:
Nose: S. aureus - in 25% healthy individuals
Throat: viridan strep, Neisseria, S. epidermidis
Anaerobes: Bacteroides, Fusobacterium, Clostridium, Peptostreptococcus (anaerobic oral strep)
Normal GU Flora:
Vaginal in adult women:
Lactobacillus (for acid pH, antibiotic suppression -> candida albicans overgrowth, not dominant before puberty and after menopause)

Vagina can be colonized by fecal flora due to location, can find E. coli and Enterobacter in the introitus (opening), these are pathogens implicated in UTIs and occasional sepsis

15-20% childbearing age women carry group B strep in vagina, important source of newborn sepsis during birth