BSCI 424 — PATHOGENIC MICROBIOLOGY — Fall 2000


Bacteroides Summary


  Bacteroides fragilis is prototype endogenous anaerobic pathogen 

Morphology & Physiology:

  Pleomorphic group of non-spore forming anaerobic Gram-negative (some weakly or variable staining) bacilli (see WebLinked image)

  Genus Bacteroides formerly included the genera Porphyromonas and Prevotella

Taxonomy:

  Bacteroides fragilis group

  Major opportunistic pathogen
  Most important member of genus

  Non-fragilis Bacteroides (many species)

Clinical Syndromes:

  Abscess formation in normally sterile sites

  Bacteremia

  Intraabdominal infections: more than 80% caused by B. fragilis

  Gynecological infections: polymicrobial anaerobic infections with B. fragilis frequently causing abscesses

  Skin and soft tissue infections: most commonly associated with B. fragilis; Gram-negative anaerobes gain access to these sites via bites or trauma

  Respiratory tract: polymicrobial infections including non-fragilis Bacteroides

Epidemiology:

  Normal flora of upper respiratory and gastrointestinal tract which are colonized in large numbers

  Endogenous spread to normally sterile sites

  Although Bacteroides fragilis is relatively minor member of the normal flora of the gastrointestinal tract, more than 80% of all intraabdominal infections are associated with B. fragilis

  Surgical and trauma patients

  Patients with spontaneous peritonitis

Pathogenesis & Immunity:

  Virulence factors can be organized into three broad categories:

   Adherence to tissues
   Protection from host immune response (oxygen toxicity and phagocytosis)
   Destruction of tissues

  Fimbriae and agglutinins function as adhesins

  Polysaccharide capsule

  Antiphagocytic
  Responsible for abscess formation (see table below)

  Lipopolysaccharide

   Antiphagocytic
   Stimulates leukocyte chemotaxis and migration

  Oxygen tolerance

   Superoxide dismutase
   Catalase

  Wide array of enzymes:

   Histolytic (tissue destruction)
   Inactivation of immunoglobulins (IgA, IgM, IgG proteases)
   Hydrolysis of antibiotics (beta-lactamase)

Laboratory Identification:

  Specimen collection to avoid contamination with normal flora

  Oxygen-free transport medium system

  Avoid drying

  Bacteroides spp. grow rapidly (within two days) but most other anaerobes are slow growers on selective media

  B. fragilis are resistant to kanamycin, vancomycin and colistin

  B. fragilis growth is stimulated in the presence of 20% bile

Treatment, Prevention & Control:

  Surgical drainage of abscess(es) and removal of necrotic tissue(s)

  Long-term course of antibiotics

  Prophylatic use of antibiotics

  Prior to invasive surgical procedures that disrupt mucosal barriers
  Immediately following trauma that disrupts mucosal barriers

 

Virulence of Polysaccharide Capsule of Bacteroides fragilis
as Demonstrated by Kasper, et al.

DESCRIPTION
BIOLOGICAL
MATERIAL
INFECTION
METHOD
DISEASE
OBSERVED
ORGANISMS
ISOLATED
MIXED
Fecal Pellet
Intraperitoneal
Injection
(Simulates
intraabdominal
infection
)
Peritonitis
or
E. coli,
Enterococcus
,
Bacteremia
Intraabdominal
Abscess
B. fragilis
MIXED
Nonencapsulated
B. fragilis
+
Enterococcus
IP Injection
Intraabdominal
Abscess
B. fragilis
+
Enterococcus
MIXED
Encapsulated
B. fragilis
+
Enterococcus
IP Injection
Intraabdominal
Abscess
B. fragilis
LIVE
Encapsulated
B. fragilis
IP Injection
Intraabdominal
Abscess
B. fragilis
LIVE
CONTROL
Encapsulated
Streptococcus
pneumoniae
IP Injection
No Disease
---
LIVE
CONTROL
Enterococcus
IP Injection
No Disease
---
LIVE
Nonencapsulated
B. fragilis
IP Injection
No Disease
---
DEAD
Heat-killed
Encapsulated
B. fragilis
IP Injection
Intraabdominal
Abscess
Sterile
SUBUNIT
Purified
B. fragilis
Capsule
IP Injection
Intraabdominal
Abscess
Sterile
SUBUNIT
CONTROL
Purified
E. coli
Capsule
IP Injection
No Disease
---

   Go to Pathogen List

 

 

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Designed & Maintained by David M. Rollins
Copyright © 2000, D.M. Rollins and S.W. Joseph
Revised: August 2000
URL: http://life.umd.edu/classroom/bsci424