Intra-abdominal Infection

Objectives:

  1. Know the different types of infections (parts)
    1. Gut, Biliary, Pancreas, Peritonuem
  2. Case Study of CDI

Our Gut is:

  • GIT home to >100,000 billion micro-organisms of 36,000 spp.
  • Inhibit colonisation by pathogenic spp.
    • Competition for nutrients & receptors
    • Producing bacteriocins & fermentation acids
  • Source of energy (butyrate) & essential vitamins (biotin, folate, vit K)

Common Bacterias found along the GIT

Gastroenteritis

inflammation of the stomach and intestines, typically resulting from bacterial toxins or viral infection and causing vomiting and diarrhoea.

Bacterial causes: Viral Causes Others:
  • Campylobacter; Salmonella; Shigella
  • Pathogenic strains of E.coli (eg. VTEC)
  • Listeria; Vibrio cholerae;
  • Norovirus
  • Rotavirus; adenovirus; etc.
  • Cryptosporidium
  • Giardia lamblia
  • Entamoeba histolytica

[ Gastroenteritis (infection) sometimes → leads to Intra-abdominal Infections ]

Biliary System Infection

Cholecystitis: gallbladder infection

Cholangitis: bile duct infection

Complications

– bacteraemia; liver abscesses; gall bladder perforation; etc.

(image: gallbladder is blocked by gallstones; accumulation of bile causes dilation of bile duct; pathogens from gut can then travel up duct [ascending infection] to infect the gallbladder)

Acute Pancreatitis

Pancreatitis is a condition characterized by inflammation of the pancreas. The pancreas is a large organ behind the stomach that produces digestive enzymes and a number of hormones.

Caused by:

  • Gallstones / Alcohol
  • ERCP (endoscopic retrograde cholangio-pancreatography);
  • Drugs/toxins; infections eg. mumps, Ascaris, etc.

Infective complications:

  • Infected necrosis
  • Pancreatic abscess, pseudocyst, bacteraemia (bacteria in blood), etc.

Peritonitis

inflammation of the peritoneum

 

Primary peritonitis (spontaneous bacterial peritonitis)

  • usually in the presence of ascites

Secondary peritonitis: (indirect)

  • peritonitis following pathology of an intra-abdominal viscus or organ.
  • Abscess, perforation, ischaemia, surgery, etc

Management:

  • Antimicrobial therapy
  • Drainage / debridement / surgical excision

 

Intra-Abdominal Infection

Complicated intra-abdominal infection, which extends into the peritoneal space, is associated with abscess formation and peritonitis

Caused by:

  • Perforated Viscus (hole in the wall of gut)
    • perforated appendix, diverticulum, duodenum
  • Gangrene
    • (eg. appendix); abscess formation (eg. diverticular)
  • Infections complicating GIT ischaemia
    • Necrotic tissue
  • Iatrogenic (elating to illness caused by medical examination or treatment)
    • post-surgery
    • extension of wound infection, anastomotic leak, etc.
CT scan: Abscess

 Perforated “consequence” air under diaphragm

Aetiology

Often polymicrobial (mainly GNB + anaerobes)

Normal flora of gut (asymptomatic) → enters peritoneal cavity (severe)

Skin: Proprionibacterium; Peptostreptococcus
Upper respiratory tract: Variety of anaerobes
GIT: Variety of anaerobes
Vagina: Lactobacillus; Proprionibacterium; Prevotella; Peptostreptococcus; Veillonella.

Types of Anaerobes:

Gram-negative bacilli (facultative)

Enterobacteriaceae: E. coli; Klebsiella; Enterobacter; Proteus; etc.
Anaerobes

Bacteroides fragilis; Clostridium spp.; etc.

  • Gram-positive rods: Clostridium perfringens, Clostridium difficile.
  • Gram-positive cocci: Peptococcus.
  • Gram-negative rods: Bacteroides, Prevotella, Fusobacterium.
  • Gram-negative cocci: Veillonella
Others

Enterococcus, streptococci, yeasts, etc

 

Infections by anaerobes

Often as part of polymicrobial aetiology

  • Intra-abdominal infections
  • Liver abscesses
  • Dental abscesses
  • Brain abscesses
  • Chronic suppurative soft tissue infections

 

Treatment: Antibiotics

(good against anaerobes)

Good:

  • Metronidazole
  • Amoxicillin-clavulanate
  • Piperacillin-tazobactam
  • Carbapenems eg. meropenem
 Maybe:

  • Clindamycin – certain anaerobes
  • Vancomycin – Gram-positive anaerobes only

Clostridium Difficile Infection (CDI)

(Common gut infection)

  • Gram-positive, anaerobic, spore-forming bacillus
  • 1978: identified as the aetiology of pseudomembranous colitis (PMC)
  • Also accounts for 20-30% antibiotic-associated diarrhoea
  • Recurrent infections in 15-30% patient
New Bug Strain

  • Clostridium Difficile, which causes sever diarrhoea, mainly affects elderly people; new strain has also affected younger patients

 

Risk Factors:

  1. Exposure to antibiotics (‘Big 3’: clindamycin, cephalosporins, fluoroquinolones)
  2. Advanced age (>65 yrs)
  3. Duration of hospitalisation (>4 wks 40-50% colonisation)
  4. Proton pump inhibitors / other antacids
  5. GI surgery, NG intubation

 

Antimicrobials associated with C. difficile:

High

Moderate

Rarely Associated
  • Cephalosporins
  • Carbapenems
  • Fluroquinolones
  • Clindamycin
  • Penicillins
  • Trimethroprim
  • Macrolide
  • Trimethoprim
  • Tetracycline
Recent trends in CDI

  • Resurgence in CDI in N. America & Europe in recent years:
    • assoc. with outbreaks by hypervirulent strains (eg. NAP1/027 strain)
    • hyperproduction of toxins (16-23X)
  • Increased severity of CDI
    • Quadrupling of attributable mortality where incd had remained stable
  • Increase in community-acquired CDI
  • Resistant to fluoroquinolones (ciprofloxacin, moxifloxacin, gatifloxacin)
  • Decreased efficacy of metronidazole Rx
    • 96% (vanc) vs 22% (mtz)

 

Pathogenesis

 

Diagnosis

(Clostridium difficile)

  1. Index of clinical suspicion (symptoms)
  2. Laboratory diagnosis:
    1. C. difficile Toxin testing (eg. enzyme-immunoassay)
    2. PCR of toxin-producing genes
    3. Other methods eg. culture
  3. Radiological investigations

 

Treatment

  1. Antibiotics
  2. Fidaxomicin
  3. Intravenous immunoglobulin
  4. Faecal transplantation

 

Infection Control

  • Isolate/cohort CDI pts plus contact precautions & maintain such precautions for the duration of diarrhoea
  • Compliance with hand hygiene
  • Gloves & gowns on entry to room of pt with CDI
  • In a setting of an outbreak or increased CDI rate, to wash hands with soap & water after contact with pt with CDI
  • Scrupulous and regular cleaning of the healthcare environment and patient-use equipment
  • Alcohol cannot kill spores = Soap cannot kill spores
    • Washing/drying hands = Physical removal of spores