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microb - bacteria > Gram Positive Rods - Anaerobic > Flashcards

Gram Positive Rods - Anaerobic Flashcards

1
Q

Classification of anaerobic GPRs

A

Sporing anaerobic GPRs

  1. Clostridium perfringens
  2. Clostridium tetani
  3. Clostridium botulinum
  4. Clostridium difficile

Non-sporing anaerobic GPRs

  • exceptions to generalisations
    1. Actinomyces israelii
    2. Fusobacterium necrophorum
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2
Q

Virulence factors of C. perfringens

A

Freq present in human faeces, may colonize skin esp below waist

  1. Alpha toxin (lecithinase) - destroys cell membranes, kill cells
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3
Q

Clinical presentations of C. perfringens (5)

A
  1. Gas gangrene (clostridial myonecrosis)
    - spores introduced into anaerobic area of tissue germinate - toxins damage surrounding tissue - inf spreads rapidly
    - gas is usually produced - detected by pressing on tissue (crepitus) or xrays
    - systemically unwell, febrile/hypothermic, shock leading to drowsiness/LOC
    - local signs: severe pain, swelling, skin discolouration, fluid filled blebs, thin smelly discharge
    - predisposing factors: bullet wounds & accidents (trauma forces spores deep into tissues + damage blood supply), vascular disease (?amputation), surgery on bowel/biliary tract, adrenaline injection
    - can cause septic abortion, can enter tissue via blood (rare)
    - also caused by C. novyi & C. septicum (assoc w malignancy)
  2. Food poisoning
    - spores survive cooking, can germinate in anaerobic areas eg depths of stew
    - after consumption, sporulation & toxin release occurs in gut
    - abdominal cramps, diarrhea (12-24h after consumption)
  3. Diarrhea in elderly patients
  4. Pigbel: necrotising enteritis in New Guinea after pork feasts
    - risk factors: protein deprivation - inadequate synth of trypsin protease to which toxin is sensitive, episodic meat feasting, poor food hygiene, staple diets eg sweet potatoes with trypsin inhibitors, parasite inf
  5. Cellulitis
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4
Q

Diagnosis of C. perfringens

A
  1. Histology, culture (blood, discharge, tissue)
    - lecithinase (alpha toxin) detected using Nagler plate (agar with egg yolk) - lipids broken down by toxin to produce insoluble fat droplets seen as an opaque zone around the streak of bacterial growth
    - half plate precoated with antitoxin - shows that lipase activity is specifically due to alpha toxin
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5
Q

Treatment of C. perfringens (3+1)

A

Gas gangrene

  1. Early surgery - remove dead/damaged tissue
  2. Benzylpenicillin + clindamycin
  3. Hyperbaric oxygen (poor efficacy)

Food poisoning
1. Rehydration, antibiotics not indicated

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6
Q

Prevention of C. perfringens (2+1)

A

Gas gangrene

  1. Good surgical technique, avoid damaging tissues, careful debridement of traumatized tissue
  2. At risk patients - prophylaxis
    - benzylpenicillin for 5 days (short courses are inadequate)
    - penicillin allergic - metronidazole

Food poisoning
1. Good food handling practices, reheat pre cooked dishes

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7
Q

Virulence factors of C. tetani

A

Found in faeces of large farm animals, human guy, soil, spores widespread in envt

  1. Tetanospasmin - potent neurotoxin, blocks inhibitory stimuli to LMN cell body, nerve cell fires continuously, muscle goes into tetanic spasm
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8
Q

Clinical presentations of C. tetani (4)

A

Tetanus (spastic paralysis)

  1. Local pain & stiffness (no site of infection - cryptogenic tetanus)
  2. Tetanus neonatorum (umbilical stump dressed with dung in LDCs)
  3. Lockjaw (stiffness of jaw) & facial spasms producing risus sardonicus (sardonic grin)
  4. Sever symptoms - opisthotonus (back muscles contract)
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9
Q

Diagnosis of C. tetani

A
  1. Histology - long thin rod-shaped, with large terminal spores (drumsticks)
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10
Q

Treatment of C. tetani (5)

A
  1. Wounds explored & debrided (dead & unhealthy tissue removed)
  2. Human tetanus immunoglobulin (HTIG) neutralize free toxin
  3. Antibiotics given to kill remaining clostridia in tissues
  4. Paralysis & ventilation in breathing diff due to spasms, until the bound toxin is broken down
  5. Immunization of patients that have recovered (infection does not confer immunity)
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11
Q

Prevention of C. tetani

A
  1. Toxoid vaccine
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12
Q

Virulence factors of C. botulinum

A

Direct wound infection, ingestion of food with preformed toxin (badly preserved foods)

  1. Botulinum toxin
    - blocks ACh release at neuromuscular junction - prevents transmission of impulsess - flaccid paralysis
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13
Q

Clinical presentation of C. botulinum (3)

A

Botulism (flaccid paralysis)

  1. Early signs: diplopia, ptosis, N/V, no fever
  2. Severe: paralysis of resp muscles, req mechanical ventilation
  3. Young children <6 months: floppy child syndrome
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14
Q

Diagnosis of C. botulinum

A
  1. Culture (patient sample, food)

2. Toxin detected by mouse inoculation

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15
Q

Treatment of C. botulinum (2)

A
  1. Purge remaining unabsorbed toxin from gut

2. Antiserum (neutralize free toxin) & ventilation if necessary

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16
Q

Prevention of C. botulinum (2)

A
  1. Safe food prep

2. Antiserum for those who consumed contaminant

17
Q

Virulence factors of C. difficile

A
  • found in faeces of a minority of the population, higher carriage rates in hospitalised patients
    1. Exotoxin
18
Q

Clinical presentations of C. difficile (3)

A
  1. CDAD - C. diff associated diarrhea - mild diarrheal illness
  2. overgrowth of bacteria + toxin release - Pseudomembrane colitis +/- toxic megacolon (may perforate)
  3. precipitated by antibiotics (alters balance of normal flora) - esp clindamycin, cephalosporins, quinolones
19
Q

Diagnosis of C. difficile (3)

A
  1. Clinical suspicion, in PMC - pseudomembranes can be seen on colon surface (sigmoidoscopy)
  2. Stool culture & toxin detection (immunoassays/cell culture assays)
  3. Nucleic acid tests (Expensive), GDH assays, PCR
20
Q

Treatment of C. difficile (3)

A
  1. stop antibiotics if possible
  2. Oral metronidazole/vancomycin
  3. Recolonisation of gut with normal flora has been attempted - isolate patient & infection control, faecal transplant
21
Q

Features of non-sporing anaerobic GPRs

A
  • infections usually involve several species of bacteria (aerobic & anaerobic)
  • mixed infections commonly involves precipitating causes eg surgery, malignancy, gut perforation, diabetes
  • usually endogenous, from own normal flora (except bites)
  • produce disgusting smells
22
Q

Clinical presentations of non-sporing anaerobic GPRs (10)

A
  1. Head & Neck infections (5)
    - Vincent’s infection: acute necrotising ulcerative gingivitis - painful ulceration of gums w bleeding, may spread to tonsils (stain shows a mix of fusiform/cigar-shaped & spiral bacteria) causing painful swallowing (Vincent’s angina)
    - Dental sepsis (incl periodontal disease)
    - Abscess/cellulitis - submandibular infection = Ludwig’s angina
    - Chronic ENT infection - sinusitis, otitis media, mastoiditis, poor drainage due to inflamm & blockage
    - Brain abscess - often caused by spread of infection
  2. Pleuropulmonary infections
    - usually following aspiration of oral flora (due to pneumonia, lung abscess, empyema), may also infect diseased lung tissues in bronchiectasis & lung cancer (sputum culture usually not helpful, get deeper samples)
  3. Abdominal infections - peritonitis, abscess, wound inf, secondary to appendicitis, diverticulitis, abdominal surgery, cancer
  4. SSTI - infections of diabetic foot ulcers, decubitus ulcers, sebaceous cysts, chronic paronychia, acne, anaerobic cellulitis
  5. Female genital tract - bacterial vaginosis, endometritis, tubo-ovarian sepsis, Bartholin’s abscess, septic abortion, IUD associated inf, chronic PID, neonatal pneumonitis
  6. Male genital tract - incl scrotal abscesses & prostate infections
  7. UTI - rare, look for fistula
  8. Bone & Joint infections - bites, diabetic foot - polymicrobial inf
  9. Bacteremia - commonly Bacteroides fragilis
  10. Synergistic infections
    - Necrotising fasciitis
    - Meleney’s synergistic gangrene
    - Fournier’s gangrene
23
Q

Treatment of non-sporing anaerobic GPRs (2)

A
  1. almost all sensitive to Metronidazole, most to penicillin (except B. fragilis, has beta lactamase)
  2. Drainage of pus & removal of dead tissue
24
Q

Clinical presentations of Actinomyces israelii

A

part of normal mucosal flora

  • Invasive infections following disease/trauma, or spontaneously
  • spreads slowly crossing tissue planes - causes fibrosis - hard swelling forms & pus drains from sinus tracks, appearing at the skin as “sulphur granules”
  • affects cervicofacial (tooth extraction, dental caries), thoracic (lung inf), abdominal, pelvic (assoc w IUD)
25
Q

Diagnosis of Actinomyces israelii

A

Culture - gram pos branching filaments, slow growing

26
Q

Treatment of Actinomyces israelii (2)

A
  1. Penicillin/amoxicillin, IV benzylpenicillin when serious, long course (2-3m)
  2. Resistant to metronidazole
27
Q

Clinical presentations of Fusobacterium necrophorum

A

Necrobacillosis (septicemia) - Lemierre’s disease

  • Sore throat leading to septicemia - seeds to many internal organs - forms multiple abscesses
  • May locally invade jugular vein - septic jugular thrombophlebitis, & further invade carotid artery - life threatening
28
Q

Diagnosis of Fusobacterium necrophorum

A

Culture (blood, abscess fluid)

29
Q

Treatment of Fusobacterium necrophorum (2)

A
  1. Benzylpenicillin

2. Drain collections of pus in abscesses

microb - bacteria (11 decks)

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