Anaerobic Infections Flashcards
1
Q
Skin Infections
A
Result from 3 mechanisms:
- Primary infection of healthy tissue
- Primary infection of devitalized, traumatized tissue (wound infections)
- Infection secondary to systemic disease
2
Q
Soft Tissue Infections
A
- Non-necrotizing infections of fascia and muscle
- Can involve subcutaneous CT, fascia and/or muscles
- Fasciitis ⇒ most cases are caused by β-hemolytic Strep
- Pyomyositis ⇒ usu. caused by S. aureus, occasionally Group A Strep
- Tissue necrosis is a prominent feature of progressive soft tissue infections
3
Q
Intra-Abdominal Infections
A
Abscesses and Peritonitis
- Primary peritonitis rarely involves anaerobes
- Secondary peritonitis and intra-abdominal abscess ⇒ involve bacteria found in the GI tract
-
Infections are usu. mixed ⇒ contains both non-anaerobes and anaerobes
- ~ 90% of infections involve anaerobes
- ~ 10-35% show anaerobes only
4
Q
Intra-Abdominal Infections
Pathogens
A
-
Non-Anaerobes
- E. coli (dominant)
- Other Enterobacteriaceae, Strep, Enterococci, S. aureus and Pseudomonas
-
Anaerobes
- Bacteroides fragilis group (dominant)
- Bacteroides, Fusobacterium, Clostridium, Peptostreptococci
- Gram-⊕ non-spore forming rods
- Eubacterium, Lactobacillus, Bifidobacterium, Actinomyces
5
Q
Infections of Bone
A
Osteomyelitis
- Most commonly affect long bones and vertebrae
- Result from hematogenous or contiguous spread
-
Staph causes 50-60% of osteomyelitis
- Majority (90%) occurring in children
-
Neonates (1 month)
- Staph. aureus, group b Strep (S. epidermidis)
- E. Coli, Klebsiella, Proteus, Pseudomonas
-
Older infants, children, adults
- Staph. aureus
- Pseudomonas aeruginosa
- Sickle cell pts ⇒ often due to Strep. pneumoniae and non-typhoidal salmonella
- Other special settings favorable for osteomyelitis are cat or dog bites (pasteurella multocida), human bites, periodontal infections and cutaneous ulcers
6
Q
Anaerobic Infections
A
-
Predominant bacteria primarily responsible for the clinical symptoms are anaerobic
- Are often mixed
- May contain a variety of aerobic types
- Excellent example of opportunism
-
Compromising factors strongly favor the establishment of anaerobic infection
- Trauma, surgery, immunosuppressive drugs, vascular insufficiency and diabetes
-
Tissue hypoxia due to lack of blood supply and/or presence of contaminating aerobes (utilize O2)
- Aids in creating conditions
- Contributes to the rapid development of anaerobic infections
-
Compromising factors strongly favor the establishment of anaerobic infection
7
Q
Spore-Forming Anaerobes
A
- Organisms of medical importance all belong to the genus clostridium
- Clostridium tetani
- Clostridium botulinum
- Clostridium perfringens
- Clostridium difficile
- All are obligate anaerobic, large gram-⊕ rods, saprophytic
- Usu. found in soil or air and intestinal tract of various animals
- Source of clostridium involved in anaerobic infections is usu. exogenous
- Can be endogenous
8
Q
Clostridium perfringens
Skin and Soft Tissue Infections
A
- Infection - mixed infections common
- Exogenous - infections of wound from soil, water, sewage etc.
- Endogenous - C. perfringens may be normal flora of GI tract and female genital tract
- Infections secondary to abdominal surgery or trauma
9
Q
Clostridium perfringens
Disease
A
- Organisms grow in traumatized tissue, especially muscle
- Occurs in contaminated deep wounds / membranes
- Produce a variety of exotoxins
- Pain, edema and cellulitis occur in the wound area
- Crepitation due to gas in tissue
-
Manifestation include:
- Localized cellulitis ⇒ amputations
- Suppurative infections and abscesses ⇒ abdomen, gall bladder, uterus, fallopian tubes
- Severe necrotizing disease of the intestines
-
Gas gangrene/myonecrosis
- Most serious
- Characterized by rapidly progressive, extensive necrosis, gas, foul smell
- Fever, hemolysis, toxemia, jaundice
- Can lead to shock and death
10
Q
Clostridium perfringens
Virulence
A
-
Alpha toxin
-
Lecithinase is the primary exotoxin
- Hydrolyzes lecithin and sphingomyelin
- Disrupts cell and mitochondrial
-
Lecithinase is the primary exotoxin
-
Tissue degrading enzymes
- Collagenase
- Hyaluronidase
- DNase
11
Q
Clostridium perfringens
Diagnosis and Treatment
A
- Culture, isolation, identification by biochemical tests
- Tissue debridement, PCN, hyperbaric oxygen
12
Q
Clostridium tetani
Morphology and General Characteristics
A
- Slim, gram-⊕ rod, motile
-
Forms round terminal spores (drumstick shape)
- Spores remain viable in soil for many years
- Prevalent in manure treated soil
- Organism sometimes found in lower intestinal tract of man and animals
13
Q
Clostridium tetani
Virulence
A
-
Tetanospasmin neurotoxic exotoxin
- Causes spastic paralysis
- Encoded by plasmid
-
Zinc-endopeptidase specific for synaptobrevins of the neuro-exocytosis machinery
- Inhibits release of inhibitory neurotransmitters
14
Q
Clostridium tetani
Pathogenesis and Clinical Considerations
A
- Spores introduced into wounds contaminated by soil or foreign bodies
- Incubation is 4 days to several weeks
- Area of low O2 tension allows spores to germinate
- Bacilli multiply locally
-
Tetanospasmin is produced
- Reaches CNS by retrograde axonal transport or via the bloodstream
- Blocks postsynaptic inhibition of spinal motor reflexes ⇒ spasmodic contractions, hyperreflexia and seizures
- Masseter muscles usu. first affected trismus (lockjaw)
- Untreated spasms can become generalized and extremely painful
-
Death results from respiratory failure when muscles affected
- Untreated, mortality ranges from 15-60%
- Highest seen in the elderly and infants
15
Q
Neonatal Tetanus
A
- Results from contamination of umbilicus by unclean severing implement or bandages
- More common in developing countries
16
Q
Clostridium tetani
Laboratory Diagnosis
A
-
Dx by clinical presentation and history of injury
- Rabies and strychnine poisoning are differential diagnoses
- Anaerobic culture on blood agar w/ material isolated from contaminated wounds may yield C. tetani
- Infection remains localized, disease is entirely a toxemia
- Treatment should never be withheld pending lab confirmation
17
Q
Clostridium tetani
Immunity
A
- No immunity to natural infection w/ tetanus
- Survivors do not demonstrate circulating antibody to the toxin
- Lethal dose < immunogenic dose
18
Q
Clostridium tetani
Treatment
A
-
Tetanus immune globulin (TIG)
- Pooled plasma containing tetanus anti-toxin
- Can neutralize the toxin but only before it binds nervous tissue
-
Surgical debridement to remove necrotic tissue
- Eliminates the environment essential for growth of the organism
-
Abx
- Metronidazole is the current drug of choice
- Historically penicillin was used as it does inhibit growth and production of toxin
- Recent work suggests it may enhance the activity of the toxin
-
Supportive therapy ⇒ for pts who develop symptoms
- Muscle relaxants
- Sedation
- Assisted ventilation
19
Q
Clostridium tetani
Prevention and Control
A
- Tetanus is a preventable disease
-
Universal immunization w/ tetanus toxoid (DTap, Tdap)
- Initial series is 3 shots given during 1st year of life
- Booster shot before entry into school
- Additional boosters every 10 years
- Previously immunized w/ potentially dangerous wound w/o boost in past 10 yrs ⇒ tetanus toxoid
- Immunized w/ heavily contaminated wounds w/o boost in past 5 yrs ⇒ tetanus toxoid
- Unimmunized or incompletely immunized w/ serious wounds ⇒ anti-toxin (TIG) & tetanus toxoid
20
Q
Non-Spore Forming Anaerobes
Pathogens
A
- Organisms belong to diverse variety of gram-⊖ and gram-⊕ rods and cocci
- Normally inhabit mucous membranes and less commonly skin
-
Genera of major clinical importance are:
- Bacteroides
- Prevotella
- Porphyromonas
- Fusobacterium
- Actinomyces
21
Q
Non-Spore Forming Anaerobes
Infections
A
- Source of non-spore forming anaerobes involved in anaerobic infections is endogenous
- Little evidence of person to person spread or exogenous infection
-
Majority of infections of oral cavity and maxiofacial regions are basically anaerobic
- Actinomycosis
- Acute necrotizing ulcerative stomatitis
- Root canal infections
- Periodontal diseases
- Severe dental caries
22
Q
Bacteroides
Overview
A
- Anaerobic, non-spore forming gram-⊖ rods
-
Most common cause of serious anaerobic infections
- Sepsis, peritonitis, and abscesses
-
B. fragilis is the most frequent pathogenic species
- Also predominant in the normal colonic and vaginal flora
23
Q
Bacteroides
Disease
A
-
Infections are endogenous and include intra-abdominal infections
- Peritonitis or local abscesses
- Metastatic abscesses may arise due to hematogenous spread to distant organs
- Lung abscesses due to aspiration of organisms
- Predisposing factors: surgery, trauma, chronic disease
- Contributes to infection: local tissue necrosis, impaired blood supply, growth of facultative anaerobes (E. coli) at the site
24
Q
Bacteroides
Virulence Factors
A
- Polysaccharide capsule ⇒ antiphagocytic, abscess promoting
- Endotoxin ⇒ less biologically active compared to classic endotoxin due to lack of lipid A
25
Q
Actinomyces
Overview
A
- Opportunists that produce indolent, slowly progressive diseases
- Heterogenous group of filamentous bacteria
- Superficially resemble fungi
- Grow as branching organisms
- Tend to fragment into bacteria-like pieces
- Most are free living, particularly in soil
- Many are part of the normal flora of the mouth or GI tract
- Several pathogenic species
- Actinomyces israelii most important medically
26
Q
Actinomyces
Morphology and General Characteristics
A
- Irregular staining gram ⊕, non-spore forming rods
- Grow in a branching filamentous pattern
- Facultative intracellular pathogens
- Facultative or obligate anaerobes
27
Q
Actinomycosis
Overview
A
Chronic suppurative, destructive disease of connective tissues
- Formation of granulomas, pyogenic lesions, or abscess
- Infections are opportunistic
- Actinomyces found as nl flora of mouth and GI tract
- Gain access to CT usu. following trauma of mucosal or epithelial surfaces
- Spread via formation of interconnecting sinuses, granulomatous and pyogenic lesions
28
Q
Actinomycosis
Clinical Subtypes
A
4 clinical forms of the diseases are recognized:
-
Cervicofacial actinomycosis ⇒ 30-60% of cases
- Usu. follows dental surgery or dental disease (poor oral hygiene)
- ± Bone involvement
-
Abdominal actinomycosis ⇒ 20-30% of cases
- Usu. follows rupture of appendix or cecum
- ± Involvement of various abdominal organs
-
Thoracic actinomycosis ⇒ 20-30% of cases
- May develop by extension from cervicofacial disease or by aspiration of sputum causing lung infection
- Pelvic actinomycosis ⇒ associated w/ intrauterine devices
29
Q
Actinomyces
Diagnosis
A
- In vitro: branching filaments, fragment in 24 hrs into bacillary, short chains and coccobacillary forms, stain gram ⊕
-
In vivo: microcolonies formed in infections called sulfur granules
- When crushed, organisms appear as gram ⊕, bacillary and diphtheroid forms
- Presence of sulfur granules in sputum, pus from draining sinuses, or exudates is diagnostic
- Yellow color of granules d/t presence of large numbers of MΦ
- Actinomycotic infections are almost always mixed infections
- Material from sulfur granules
- Inoculated into thioglycollate broth or brain heart infusion blood agar
- Incubated anaerobically
- Growth is slow, may take up to 2 weeks
30
Q
Actinomyces
Treatment
A
- Prolonged tx w/ PCN (or erythromycin as an alternative)
- Surgical excision and drainage often necessary
- Most species are resistant to metronidazole
- Tetracyclines have variable activity
