Peritonitis and inta-abdominal infection - enterobacteriaceae and anaerobes

Question 1

Patient presentation: peritonitis

Answer 1

Fever 
Ince HR (>90bpm) 
Nausea and vomiting 
Diffuse abdo pain, may become more localised 
Rebound tenderness 
Abdominal wall rigidity 
Increased blood leukocytes 
CT/US: fluid accumulation, inflammation

Question 2

What is peritonitis?

Answer 2

Inflammation of the peritoneum / serial membrane lining abdominal cavity

• May be generalised/diffuse infection
• May be localised/abscess infection

Question 3

What is primary (spontaneous) peritonitis

Answer 3

Diffuse bacterial infection without loss of GI tract integrity, Rare
- Liver disease, portal vein hypertension and ascites

Question 4

Secondary

Answer 4

Acute infection resulting from loss of GI tract integrity or from infected viscera. Most common
Visceral pathology (appendicitis, diverticulitis, ulcers etc)  or post surgical infection

Question 5

Tertiary

Answer 5

Recurrent infection of peritoneal cavity following adequate initial therapy. Often due to defective immunity
Pervious primary or secondary peritonitis

Question 6

Microbial causative agents: Poly microbial infection

Answer 6

More than one species involved
Synergistic infection
Reflective of the source
Hospital acquired infections may be one species

Question 7

Microbial causative agents

Answer 7

Enterobacteriaceae (E coli etc) 
Anaerobes 
GNB: Bactericides fragilis 
GPC: peptostreptococcus 
GBP: Clostridium 
Enterococci

Question 8

Sources of bacteria

Answer 8

Increasing as you go down the tract 
Stomach / duodenum: 
- aerobes and facultative anaerobes 
Jejunum / ileum 
- Transition form aerobes and facultative anaerobes to more anaerobes 
Colon 
- Anaerobes and facultative anaerobes

Question 9

Route of transmission from the GI tract to the peritoneum?

Answer 9

via a perforation 
Appendicitis (ruptured appendix) 
Diverticulitis (rupture of inflamed diverticulum) 
Stomach / duodenal ulcer 
Infection / access of other visceral organ 
Pelvic inflammatory disease 
Tubo ovarian infection 
Necrotising enterocolitis (neonates) 
Surgery/trauma

Question 10

Bacteria gain entry, bacteria not cleared?

Answer 10

Normally there will be phagocytosis (macrophage)
Normally bacteria quickly contained in a fibrin clot
Clearance not effective in presence of nutrients (e.g. haemoglobin) and necrotic tissue
All depends on the relative speeds of the immune system vs inflammation

Question 11

Inflammation

Answer 11

Fluid exudate in the peritoneal cavity
Dilution of antibacterial factors (e.g. opsonins)
May lead to hypovolemia

Question 12

Abscess formation

Answer 12

Fibrin deposited traps bacteria
- Bacteroides fragilis capsule promotes fibrin deposition to hide bacteria underneath
May prevent phagocytosis and other antimicrobial access
Microbial growth continues
protease etc damage to tissue - may lead to bacterial dissemination

Question 13

Diagnostic microbiology

Answer 13

Aspirate pus 
- Foul smelling 
Grams stain of pus from the bless 
- Gram negative rods 
- Possibly gram positive cocci 
- Probably more than one type 
anaerobic and aerobic cultures 
- Culture from pus 
- Anerobic transport swabs

Question 14

Anaerobes and bacteriodes

Answer 14

Because of their fastidiousness, bactericides are difficult to isolate and often overlooked
Often present in mixed infections - E coli cultured on macconkey agar
Isolation requires appropriate methods of collection - aseptic aspiration, transportation (rapid in the appropriate medium - they’re anaerobes) and cultivation of specimens
Gram negative rod
Gas-liquid chromatography can be used to detect volatile fatty acids produced by anaerobic bacteria
PCR

Question 15

Synergy example of bactericides fragile and Escheria coli

Answer 15

B. Fragilis
- Antiphagocytic capsule and LPS (O-antigen)
- Capsule elicits deposition of fibrin (access formation)
Complement degradation by proteases
reduced oxygen toxicity - SOD, Catalase (both are iron containing proteins)
E.coli
- In mixed infections - Ecoli Haem binding protein, HBP can be intercepted by B. fragalis

Question 16

Clinical consequences of polymicrobial infections

Answer 16

Therapy needs to target all possible organisms and so will be of broader spectrum

Question 17

Treatment of peritonitis

Answer 17

1. of symptoms
   - fluids, pain relief
   - Removal / drainage of pus guided by US/CT
2. Of source
   - Establish the cause and control the origin of sepsis
   - Removal and drainage of pus guided by US/CT
   - Removal of dead tissue
   - Corrective surgery to repair leak
3. OF the microbial cause
   - empiric antimicrobial therapy
   - Broad spectrum

Question 18

Empiric antimicrobial treatment

Answer 18

Is medical emergency, can't wait for culture to grow before you start antibiotics 
Triple therapy 
Enterobacteriaceae (E.coli) 
- Amnioglycoside 
- Fluoroquinolone 
- 4th gen cephalsoporin 
Anaerobes (B. fragalis) 
- Cindamycin 
- Metronidazole 
Enteroccus 
- Ampicillin 
Single therapy 
- Less toxic for patients with liver/kidney disease concerns

Question 19

Time length of treatment

Answer 19

Shouldn’t be longer than a weeks course although some of the recommendations go for longer, this can cause increasing damage to the microbiota and increases the chances of something like a C. difficile infection with longer broad spectrum treatment regimes

Question 20

metronidazole

Answer 20

Bactericidal, amoebicidal and trichomoncidal 
Exact MOA not fully known 
Stops bacteria replicating 
Get to: 
- Anaerobic gram negative bacilli 
- Anaerobic gram positive cocci 
- Wide range of pathogenic protozoa 
BUT is ineffective against both erobic and facultatively anaerobic bacteria

Question 21

Prevention of peritonitis

Answer 21

Prompt diagnosis and treatment of predisposing conditions

Question 22

What tests to confirm acute appendicitis and peritonitis?

Answer 22

ultrasound or CT to look for area offload accumulation