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21 Cards in this Set

  • Front
  • Back
Bacteroides, Prevotella, Porphyromonas & Fusobacterium sp.
Prevalent members of the normal flora of all mucosal surfaces; they are opportunistic pathogens

Many conditions may predispose to infection, eg open wounds, diabetes, leukopenia, corticosteroids, immunosuppression, some cancers, etc.

These organisms often benefit from co-infecting, e.g. P. melaninogenica + Fusobacterium cause more serious disease in rabbits than P. melaninogenica alone

Many of these species form biofilms
Gm- anaerobes in oral disease
16-20% of the cultivable flora of the gingival crevice area; 8-17% of cultivable flora of dental plaque

Clinical characteristics: foul-smelling discharge, infection near mucosal surface, tissue necrosis, gas in tissue, often seen in patients on aminoglycoside antibiotics, infection may follow human bite, etc

Diagnosis requires isolation or demonstration by direct staining or immunofluorescence (IFA)
Common virulence factors
Anti-phagocytic capsule
Also promotes abscess formation
Tissue destructive enzymes
Lipases, proteases, collagenases that destroy tissue and promote abscess formation
Beta-lactamase production
Protects self and other species in mixed infections
Superoxide dismutase production
Protects bacteria from toxic O2 radicals as they move out of usual niche
Bacteroides fragilis
1.5-4.5 um long
Encapsulated
Gut normal flora
Drug resistance plasmids
Bacteroides fragilis - Pathogenesis
Fimbriae and agglutinins function as adhesins
Polysaccharide capsule
Antiphagocytic
Responsible for abscess formation
Lipopolysaccharide
Antiphagocytic
Stimulates leukocyte chemotaxis and migration
Contains little lipid A -> weak endotoxin activity
Oxygen tolerance
Superoxide dismutase
Catalase
Degradative enzymes, eg neuraminidase, hyaluronidase, DNAses, proteases
Histolytic (tissue destruction)
Inactivation of immunoglobulins (IgA, IgM, IgG proteases)
Some drug resistance plasmids
Bacteroides fragilis 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; Gm- anaerobes gain access to sites via bites or trauma
Respiratory tract: polymicrobial infections including non-fragilis Bacteroides
Prevotella melaninogenica
Short coccoid rods
Produces black pigment
Requires vitamin K
Weak endotoxin
Other sp.: P. oralis
Porphyromonas gingivalis
Gram negative, short, rod-shaped, pleiomorphic, anaerobic bacteria
Porphyromonas gingivalis
virulence factors and pathogenesis
Virulence factors
Fimbriae (adherence)
Capsule (antiphagocytic)
Many degradative enzymes (proteases, collagenase, hemolysin)
Pathogenesis
Aggressive periodontal pathogen in humans and animals
Found almost exclusively at subgingival sites
Fusobacterium nucleatum
Gram-negative anaerobe
Spindle shape, with sharp ends
Similar to Bacteroides
5-10um long
Butyric acid fermenters
Fusobacterium nucleatum Symptoms and diseases
Gut normal flora
Pleuropulmonary infections
Tropical skin ulcers
Gingivitis
Cause of trench mouth (common during WWI)
Ulcerative disease of the gums associated with poor oral hygiene, fatigue, malnutrition, heavy smoking, etc.
F. nucleatum + Treponema vincentii -> Vincent’s Angina
Necrotizing infection of the pharynx
Unilateral with same side earache
Bleeding ulcer on one tonsil
Antibiotics and debridement recommended
Fusobacterium necrophorum
Normal throat flora
Lemierre’s syndrome
very rare today but common before penicillin
Rising incidence in children may result from encouraged reduced use of antibiotics
starts with sore throat, viral cause usually is suspected, hence rarely treated with antibiotics
Potentially leads to severe disease: high fever spikes, septicemia, abscesses on organs
Predisposition to abscess formation, in liver, spleen and muscles
Pulmonary lesions
Leptotrichia sp.
Gm- thin, filamentous,
non-motile bacteria
Related to Fusobacterium sp.
Aerotolerant anaerobes, fastidious slow-growers
Several species cause disease in humans:
L. amnionii
L. trevisanii
L. sanguinegens
L. buccalis
Associated disease: periodontal disease, bacteremia, serious systemic disease in immunocompromised patients, disease of reproductive tract, etc
Campylobacter
Microaerophilic
grows best at reduced O2 and CO2 concentrations of 10%
Non-fermenting
Motile curved rods
Single polar flagellum
Small: will pass through .65 uM filters that filter out most enteric bacteria
Many serotypes based on O (LPS O-side chain) and H (surface proteins) antigens
Five different species of Campylobacter may be isolated from clinical specimens
Campy - Epidemiology
commensal flora of birds
many other animals serve as vehicles for human infection
usually through the consumption of contaminated food
the major cause of food-borne bacterial infection of humans
campy virulence factors
Virulence factors
Enterotoxin
Endotoxin
Adhesins
Ability to penetrate cells
Intracellular survival
campy clinical significance
Gastroenteritis
Caused mainly by C. jejuni and C. coli
Systemic infections
Usually due to C. fetus ssp. fetus
Occurs in debilitated or immunocompromised individuals
campy pathogenesis
invades epithelium of lower small intestine

provokes inflammatory response that may be responsible for many of the symptoms

Symptoms start 1-10 days after ingestion with crampy abdominal pain, bloody diarrhea, fever

Untreated patients may excrete Campy for months
C. jejuni pathogenesis
Antecedent to Guillain-Barré syndrome
ascending paralysis immune in etiology
Stems from autoimmune cross-reactivity with Campylobacter antigens
campy control (treatment)
No vaccine

Treatment
macrolides and quinolones
antibiotic resistance is common