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Infectious Disease > Anaerobes > Flashcards

Anaerobes Flashcards

1
Q

2 categories of anaerobes

A
  • spore forming: rod, gram +: clostridium
  • nonspore-forming: gm +rod -> propionibacterium, bifidobacterium, lactobacillus, eubacterium, actinomyces

nonspore-forming gm - rod –> bacteroides, fusobacterium, camplyobacter

nonspore-forming gm + cocci -> peptococcus, peptostreptococcus

nonspore forming gm - cocci -> veillonella

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2
Q

Clostridium species

A
  • clostridia are opportunistic pathogens, but they are responsible for some of the deadliest diseases including gas gangrene, tetanus and botulism. Less life threatening diseases include pseudomembranous colitis (c. difficile) and food poisoning.
  • cause disease primarily through the production of numerous exotoxins
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3
Q

Subtypes of clostridium species

A

perfringens, tetani, botulinum, difficile

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4
Q

Pathogenesis of C. Tetani?

A
  1. entry through wound (rusty nail)
  2. spread of toxin
  3. disease: rigid paralysis ex: lockjaw, cardiac failure, respiratory failure
  4. no exit
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5
Q

Where is C. tetani found?

A

worldwide, ubiquitous in the soil, it is occasionally found in intestinal flora of humans and animals

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6
Q

What does C. tetani cause

A

tetanus or lockjaw. When spores are introduced into wounds by contaminated soil or foreign objects such as nails or glass splinters (no inhibition of ACh (in constant contraction –> tetany)

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7
Q

Morphology of C. tetani, culture, biochem. activities, resistance, and classification

A

Morphology: long and slender, flagella no capsule, terminal located round spore (drum stick appearance)

Culture: obligate anaerobic, gram +, swarming occurs on blood agar, faint hemolysis

Biochem activities: doesn’t ferment any carbohydrate and proteins

resistance: tolerate boiling for 60 min. Live for several years in the soil.

classification and antigenic types: C. tetani is only species, no serotypes

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8
Q

Pathogenicity of C. tetani

A
  • produces 2 exotoxins: tetanolysin, and tetanospasmin (type of neurotoxin, toxicity strong) - taken up at neuromuscular junction
  • Actions of tetanospasmin are complex and involve 3 components of the nervous system: central motor control, autonomic fxn, and neuromusc. junction.
  • retrograde transport to CNS
  • delitescence (latency): few days to several weeks
  • the 2 animal species most susceptible to toxemia are horses and humans
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9
Q

Tetanospasmin (exotoxin of c. tetani)

A

disseminates systemically

  • binds to ganglioside receptors, inhibitory neurons in CNS
  • glycine: neurotransmitter
  • spastic paralysis
  • severe muscle contractions and spasms
  • can be fatal
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10
Q

signs and sxs of tetanus

A
  • initial sx: cramping and twitching of muscles around a wound, pt usually has no fever but sweats profusely and begins to experience pain, especially in area of the wound and around the neck and jaw muscles (trismus -> lock jaw)
  • portions of the body may become extremely rigid, and opisthotonos (a spasm in which the head and heels are bent backward and body bowed forward) is common
  • complications: fractures, bowel impaction, intramuscular hematoma, muscle ruptures, and pulmonary, renal, and cardiac problems
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11
Q

generalized disease of C. tetani clinical manifestations

A

involvement of bulbar and paraspinal muscles (truisms, rises sardonicus (creepy smile), difficulty swallowing, irritability, opisthotonos), involvement of autonomic nervous system (sweating, hyperthermia, cardiac arrhythmias, fluctuations in BP

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12
Q

cephalic disease of C. tetani clinical manifestations

A
  • primary infection in head, particularly in the ear, isolated or combined involvement of CNs, particularly the 7th, very poor prognosis
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13
Q

Localized disease of C. tetani clinical manifestations

A

involvement of muscles in area of primary injury, infection may precede generalized disease, favorable prognosis

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14
Q

Neonatal disease of C. tetani clinical manifestations

A

generalized disease in neonates, infection typically originates from umbilical stump; very poor prognosis in infants whose mothers are nonimmune

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15
Q

Epidemiology of Tetanus

A
  • 1 mill. cases occur annually in the world -> mortality rate ranging from 20-50%, rare in most developed countries
  • in developing countries, tetanus is still one of the ten leading causes of death, and neonatal tetanus accounts for 1/2 of these cases
  • in less developed countries -> mortality: 85% neonatal tetanus and 50% non-neonatal tetanus
  • in U.S. -> IV drug users victim to this
  • in untx tetanus, fatality rate is 90% for newborn and 40% for adults
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16
Q

Immunity to C. tetani

A 
humoral immunity (antitoxin), there is little, if any, innate immunity and the disease doesn't produce immunity in the patient
- active immunity follows vaccination with tetanus toxoid
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17
Q

Dx of tetanus

A

dx is primarily by clinical sxs, the wound may not be obvious

  • C. tetani can be recovered from the wound in only about 1/3 of the cases
  • it is imp. for the clinician to be aware that toxigenic strains of C. tetani can grow actively in the wound of an immunized person
  • numerous syndromes, including rabies, and meningitis, have sxs similar to those of tetanus and must be considered in d. dx
18
Q

vaccination for tetanus

A
  • infant: get DTap - (diphtheria, pertussis, tetanus)

- tetanus toxoid: antigenic, no exotoxic activity

19
Q

Control of tetanus

A
  • offending organism must be removed by local debridement
  • toxoid
  • TAT (tetanus antitoxin; metronidazole (for more serious wounds
  • AIDS patients may not respond to prophylactic injections for tetanus toxoid
20
Q

C. perfringens where does it come from and what does it cause?

A
  • found in soil, fecal contamination
  • causes gas gangrene: swelling of tissues, gas release from fermentation products (spores in anaerobic environment: release exotoxins)
  • wound contamination
21
Q

Pathogenesis of C. perfringens

A
  • tissue degrading enzymes: lecithinase (toxin), proteolytic enzymes, saccharolytic enzymes –> spongy, crackling noise made when palpated, gas is produced by enzymes and is a waste product from toxins
  • destruction of blood vessels
  • tissue necrosis
  • anaerobic enviro created
  • organism spreads
22
Q

What will happen in gas gangrene without tx

what is tx?

A

DEATH occurs within 2 days

  • effective abx therapy
  • debridement: get rid of necrotic tissue
  • anti-toxin
  • amputation & death is rare
23
Q

Symptoms of gas gangrene and severity

A
  • life threatening disease w/ poor prognosis and often fatal outcome
  • initial trauma to host tissue damages muscle and impairs blood supply -> lack of oxygenation
  • initial sxs: fever & pain in infected tissue, more local tissue necrosis and systemic toxemia. Infected muscle is discolored (purple mottling) and edematous and produces a foul-smelling exudate; gas bubbles form from the products of anaerobic fermentation
24
Q

progression of gas gangrene

A
  • as capillary permeability increases, the accumulation of fluid increases, and venous return eventually is curtailed
  • as more tissue becomes involved, the clostridia multiply w/in the increasing area of dead tissue, releasing more toxins into the local tissue and the systemic circulation
25
Q

Biologic features of C. botulinum

A
  • anaerobic
  • gram +
  • rod shaped
  • spore former
  • produces a protein neurotoxin
  • soil, sediments of lakes, ponds, decaying vegetation
  • intestinal tracts of birds, mammals, fish
  • found in honey, natural spores (don’t give to infants less than 1 -> don’t have immunity)
  • found in improperly canned foods
26
Q

Transmission of botulism

A
  • spores that are heat resistant, canning, anaerobic environment
  • botulism: eating uncooked foods, spores
  • GI, duodenum, blood stream, neuromuscular synapses
  • Binds to peripheral nerve receptors and block ACh neurotransmitter,
  • inhibits nerve impulses
  • leads to flacci paralysis
  • death b/c of respiratory and cardiac failure
27
Q

Why would the botulinum toxin be considered for bioterrorism?

A
  • not an infection
  • resembles a chemical attack
  • 10 ng can kill a normal adult
28
Q

Clinical syndromes of botulism

A
  • 18-36 hours
  • weakness, dizziness, dryness of the mouth
  • N/V
  • neuro features: blurred vision, inability to swallow, difficulty in speech, descending weakness of skeletal muscles, respiratory paralysis
29
Q

How can you get botulism?

A
  • food poisoning: rare but fatal
  • comes from germination of spore
  • inadequately sterilized canned food -> from home
  • not an infection
30
Q

neonatal botulism (infection with C. botulinum)

A
  • uncommon, the predominant form of botulism
  • colonization occurs
  • no normal flora to compete
  • unlike adult botulism
  • don’t give babies honey until 1 yo
31
Q

Dx of botulism

A
  • by clinical sxs alone
  • differentiation difficult
  • most direct and effective: serum or feces
  • most sensitive and widely used: mouse neutralization test 48 h
  • culturing of specimens 5-7 days
32
Q

Tx of botulism

A
  • individuals known to have ingested food w/ botulism should be tx immediately w/ antiserum
  • abx therapy if infection
  • vaccination will not protect hosts from botulism, however passive immunization w/ ab is the tx of choice for cases of botulism
  • need supp. care: respiratory support
33
Q

Prevention of botulism

A
  • proper food handling and preparation
  • spores surviving boling (100 degrees at 1 atm) 1 hr
  • toxin heat-labile, boiling or intense heating, inactivate the toxin
  • bulge, gas -> spoiled
34
Q

When does C. difficile occur?

A

after abx use

  • intestinal normal flora -> greatly decreased
  • colonization occurs
  • enterotoxin secreted
  • pseudomembranous colitis
35
Q

Pseudomembranous colitis?

A

results predominantly as consequence of elimination of normal intestinal flora through abx therapy

  • sxs include abdominal pain w/ watery diarrhea and leukocytosis
  • pseudomembranous consisting of fibrin, mucus, and leukocytes can be observed by colonoscopy
  • untx pseudomembranous colitis can be fatal in about 27-44%
36
Q

Therapy for pseudomembranous colitis?

A

1st: discontinue initial abx (usually clindamycin)
2nd: specific abx therapy (doc: vanco , resistance to flagyl increasing)

37
Q

Where will you see anaerobe infections?

A

throughout the body, in the muscle, cutaneous/sub-cutaneous necrosis

  • abscesses
  • deep: ex -> liver infections
  • wound will be foul smelling
  • also see dental and sinus infections
38
Q

Why is it so hard to ID anaerobic infections?

A
  • air in sampling -> no growth b/c of O2
  • ID takes several days at least -> limiting usefulness
  • often derived from normal flora: sample contamination can confuse
39
Q

Characteristics of anaerobic infections

A
  1. most pathogenic anaerobes are usually commensals -> originate from our own flora
  2. predisposing conditions: breeches in mucocutaneous barrier so normal flora gets displaced, compromised vascular supply, trauma with tissue destruction
    - antecedent infection
40
Q

Characteristics of anaerobic infections

A

complex flora: multiple species, less complex than normal flora, fecal flora: 400 diff species, species uniquely suited to cause infection predominate
- synergistic mixture of aerobes and anaerobes: e. coli consumes O2 so anaerobes are allowed to grow and anaerobes promote the growth of other bacteria by being antiphagocytic and producing B-lactamases

41
Q

Clues to anaerobic infection

A
  1. infections in continuity to mucosal surfaces
  2. infections with tissue necrosis, and abscess formation
  3. putrid odor
  4. gas in tissues
  5. polymicrobial flora
  6. failure to grow in the lab
42
Q

Bacteroides fragilis

A

Major disease causing strict anaerobic after abdominal surgery, non-spore-former

  • prominent capsule: anti-phagocytic, abscess formation
  • endotoxin: low toxicity, structure different than other lipopolysaccharide

Infectious Disease (27 decks)

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