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FM 2 > Anaerobes > Flashcards

Anaerobes Flashcards

1
Q

Name the major genera and (where applicable) the principal species of each microbe responsible for most human anaerobic bacterial infections

A 
Gram-negative rods:
Bacteroides fragilis group 
•	#1 most commonly isolated anaerobe found in lab
•	Many species in GI tract
•	Hallmark: abscess formation 
•	Increasing drug resistance to clindamycin and beta-lactams
Bacteroides spp
•	Live in mouth and GU tract
Fusobacterium spp
•	Long, thin, fusiform (pointed ends)
•	In mouth and gingivae
•	Produce exotoxin
Prevotella spp
Porphyromonas spp

Gram-positive cocci:
Peptostreptococcus spp
• #2 most commonly isolated anaerobe in lab
• Found in mixed flora infections

Gram-positive rods (spore forming):
o Clostridia spp

Gram-positive rods (non-spore forming)
o Actinomyces spp
o Propionibacterium

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2
Q

Oral cavity infections: normal flora

A

Aerobes: Streptococci, lactobacilli, staphylococci, cornybacteria

Anaerobes: bacteroides, fusobacterium, prevotella, peptostreptococcus, porphyromonas, actinomyces

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3
Q

Oral cavity infections: types

A

Lead to infections in CNS, mouth, head & neck, lungs & pleural space

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4
Q

Mouth, head & neck infections from oral cavity bacteria

A

Periodontal disease and gingivitis

Necrotizing gingivitis
o Associated with ulcerations and bleeding
o More common in immunocompromised

Ludwig’s Angina
o Soft tissue infection in floor of mouth (submandibular and sublingual spaces)
o Mixed infection
o Can result in respiratory compromise (tongue blocks airway)

Lemierre’s syndrome
o Soft tissue infection of lateral pharyngeal space
o Fusobacterium necrophorum
o Jugular vein thrombosis and septic emboli, bacteremia

Chronic sinusitis (>3 months duration)
Chronic otitis media
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5
Q

Brain abscess from oral cavity bacteria

A
  • Direct extension from sinus, middle ear, dental infection
  • Mouth flora anaerobes and aerobes
  • Treatment: prolonged IV antibiotics, may need drainage
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6
Q

Lung infections from oral cavity bacteria

A
  • Oral anaerobes mixed with aerobes: Prevotella, fusobacterium, peptostreptococci, bacteroides
  • Often bad teeth and gingival disease
  • Commonly misdiagnosed as malignancy or TB

Lung abscess
o Constitutional symptoms: weight loss, anorexia, night sweats
o Thick, foul smelling “fetid” sputum
o Treatment: weeks to months of antibiotics

Empyema (infection of pleural space)
o	70% are complications from pneumonia
o	Anaerobes present about 40% of time
Pleural fluid: 
•	Positive culture or Gram stain
•	Low pH: less than 7.2
•	High LDH: greater than 60
Treatment: drainage + antibiotics; decortication (strip out infected pleura)
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7
Q

GI tract infections: normal flora

A

o Anaerobes: B. Fragilis group, prevotella, fusobacterium, peptostreptococcus, clostridia

o Aerobes: E. coli, Klebsiella, enterobacter, staphylococci, streptocossi, enterococci

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8
Q

GI tract infections: associated diseases

A

o Associated with peritonitis, intra-abdominal abscess, liver abscess, and biliary tract infections

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9
Q

Female GU tract infections: normal flora

A

o Anaerobes: prevotella, peptostreptococcus, bacteroides fragilis group, clostridia

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10
Q

Female GU tract infections: associated infections

A

Endometritis:
• Infection of uterine lining
• Often from Clostridium perfringens infection

Tuboovarian abscesses and PID
• Usually mixed infections
• May need surgical drainage
• Can lead to reproductive system scarring, infertility

Bacterial vaginosis
• Decline in acid-producing Lactobacilli (normal flora)
• Increase in anaerobic bacteria → vaginal discharge

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11
Q

Skin and soft tissue infections: common anaerobes

A

o Common anaerobes: Bacteroides, Peptostreptococci, Clostridia

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12
Q

Skin and soft tissue infections: types of infections

A

Diabetic foot ulcers
• Characteristically polymicrobial infection

Pressure ulcers

Necrotizing fasciits
• Ex: Founier’s gangrene of male perineum

Bite bounds

Contiguous osteomyelitis
• Via direct extension from soft tissue infection

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13
Q

Clostridium tetani: Characteristics

A
  • Terminal spore = tennis racket appearance
  • Extremely hardy
  • Found in soil, animal intestinal tracts
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14
Q

Clostridium tetani: pathogenesis

A

o Spore enters via wound
o Incubation 3-21 days (average of 8)
o Germinates under low O2 conditions
o Produces toxin → disseminates through blood and lymphatics

Tetanospasmin (tetanus toxin)
o Exotoxin made at wound site
o Extremely potent
o Enters nervous system via presynaptic terminals of lower motor neurons
o Carried via retrograde axonal transport to CNS → diffuses to terminals of inhibitory cells
o Prevents NT release from inhibitory cells → motor neurons have no inhibition
o Result: sustained muscle rigidity

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15
Q

Clostridium tetani: clinical infection/complications

A 
Generalized tetanus:
Descending pattern:
•	Trismus (lockjaw)
•	Neck stiffness
•	Swallowing problems
•	Abdominal muscle rigidity
•	Generalized
o	Spasms can last several minutes and go on for months
o	Increased body temperature, sweating, increased BP
Complications:
o	Laryngospasms
o	Fractures
o	Autonomic hyperactivity 
o	Pulmonary embolism
o	Aspiration pneumonia
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16
Q

Clostridium tetani: diagnosis

A

o Clinical = not based on bacteria identification

17
Q

Clostridium tetani: treatment

A 
o	Supportive
o	Muscle relaxants (benzodiazepines)
o	HTIG (Human tetanus immune globulin)
o	Antibiotics against C. tetani
o	Wound debridement
18
Q

Clostridium tetani: prevention

A

Immunize:
• Tetanus toxoid vaccine (DTaP) in childhood
• Td or Tdap boosters for adults

o HTIG when indicated
o Wound assessment → tetanus prone or not?

Prone if:
Wound > 6 hours old
Stellate or avulsion type wound
> 1 cm depth
Injury by missile, crush, burn, or frostbite
If contaminants (dirt, saliva, etc.) present
If devitalized tissue present

19
Q

Clostridium botulinum: Characteristics

A

Gram-positive rod
• Worldwide prevalence: soil, marine
• Subterminal spore, heat stable
• Different groups (4) and toxin types (A-G) [Most human diseases from types A, B, E, and F]
• Potent neurotoxin = Prevents pre-synaptic release of acetylcholine

20
Q

Clostridium botulinum: clinical features

A 
Acute, bilateral cranial nerve dysfunction 
•	Blurred vision
•	Diplopia
•	Dysphagia
•	Facial and tongue weakness
•	Drooping eyelids
•	Slurred speech

Descending motor weakness (upper extremities → trunk → lower extremities)
Alert, afebrile

21
Q

Clostridium botulinum: sources

A 
Foodborne: (15%)
•	Ingest preformed toxin
•	Onset within 36 hours
•	Home canned foods, fruits, fish products
•	Outbreaks

Infant (65%)
• Ingest spores
• From honey or soil

Wound (20%)
• Spores germinate in wound
• Onset within 4-14 days

Inhalational
• From toxin, bioterrorism
• 1 g/1.5 million people

22
Q

Clostridium botulinum: diagnosis

A

o Clinical

o Stool, serum, food for toxin identification

23
Q

Clostridium botulinum: prevention

A

o Food handling and preparation
o No honey < 1 year old
o Pressure cookers to kill spores

24
Q

Clostridium botulinum: treatment

A

o Supportive
o Trivalent antitoxin (A, B, and E) from CDC
o BIG (botulinum immune globin) for infant botulism
o Wound debridement and antibiotics

25
Q

Clostridium difficile

A

Most common cause of nosocomial diarrhea
• 80% of cases = onset during antibiotic therapy
o Spores can germinate → form vegatations
o Proliferate → produce exotoxins → mucosal damage and diarrhea
o Can result in life-threatening Pseuodmembranous colitis

Diagnose from toxin in stool

Treatment:
• Stop unnecessary antibiotics
• Antibiotics agains C. difficile: oral metronidazole, oral vancomycin
• Other: IV metronidazole, IVIG, colectomy
o Problem with recurrence:
• 15-30% relapse within 1 month

26
Q

Clostridium perfringens

A

o Occurs with improper temperature control of foods prepared ahead of time
o Organisms multiply in food, ingested, multiply in GI tract
o Produce a toxin in vivo
o Onset 8-16 hours = abdominal cramps, diarrhea, usually no vomiting
o Typically ends within 24 hours

27
Q

Explain the concept of the anaerobic microenvironment and cite examples.

A

• Some sites relatively protected from oxygen:
• Generated by metabolism of aerobes and facultative bacteria = consume oxygen
o Synergism between aerobic and anaerobic bacteria
o Most infections are mixed or polymicrobial

Examples:
o Mucosal surfaces
o Oral cavity, GI tract, female GU tract

28
Q

Discuss the mechanisms by which anaerobic bacteria cause human illness.

A

Mucosal barrier disruption → flora leaks into sterile site
Devitalized tissue
o Aerobic bacteria start infection → create anaerobic microenvironment
Toxin mediated
o Ex: Clostridia
o Exotoxin mediated disease: tetanus, botulism, pseudomembranous colitis

Predisposing factors (to barrier disruption or ischemic tissues)
o Malignancy
o Occlusion (airway or vascular)
o Vascular disease = ischemia
o Diabetes (vascular disease, neuropathy)
o Trauma
o Immune compromise
o Foreign bodies
o Antibiotics (because select out anaerobes)

29
Q

Discuss the general principles of diagnosis and treatment of anaerobic bacterial infections.

A

Diagnose: difficult due to fastidious growth
o Need proper transport and growth media
o Specialized lab procedures

Treatment:
o Source control and debridement; drain abscesses
Antibiotics with activity against anaerobes:
• Metronidazole
• Carbapenems
• Beta-lactamase inhibitor combinations
• Tigecycline
• Moxifloxacin
• Clindymycine = best for anaerobes “above the diaphragm” (derived from oral flora)
• Vancomycin and Penicillin = Gram-positives only
• Cefoxitin = moderately active
o Active or passive immunization for some toxin mediated diseases

30
Q

Recognize the clinical scenarios that should prompt the clinician to consider anaerobes as

A 
Syndrome recognition = some diseases have high likelihood of anaerobic infection 
o	Intra-abdominal abscesses
o	Brain abscess
o	Liver abscess
o	Severe diabetic foot ulcers
  • Sites close to mucosal surfaces (GI, GU, oral)
  • Clostridia toxin-mediated diseases
  • Failure to respond to antibiotics not covering anaerobes
  • “Sterile pus” = purulence, Gram stain showing different morphologies, but nothing grows on culture
  • Reported by micro lab

FM 2 (7 decks)

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