Intra-Abdominal Infections Flashcards
In hospital, a blood culture was taken, and antibiotics were empirically started. At 48 hours, the culture was negative, but after 72 hours, the blood culture flagged positive for:
• BCx + “Clostridium septicum” in ½ bottles @ 3d
Q: Where did this bacteria come from?
Q: Also – why does that detail matter?
livies in colon specifically
can tell where the problem is
source control important for intrab infection
A drain is
placed directly into the common bile duct to drain
excess bile and fluids that have backed up. This tube is
draining into a bag that is hanging at the bedside
The Microbiota of the Gastrointestinal Tract
• Unlike many other sites of human infection, the gastrointestinal tract (below the stomach) is NOT considered a sterile site. In fact, most of our microbiome lives and thrives in our intestinal tract, which is home to billions of bacteria (and yeast
select for certain kinds of bacteria with specific properties (e.g., the ability to live in an environment without much oxygen such as anaerobes or facultative anaerobes, or those able to survive the acidity of the stomach such as H. pylori and Streptococcus)
Memorizing The Microbiome: Critically Important!
stomach
SI
LI
Sinuses / Upper Respiratory Tract
• Streptococcus pneumonia
Lower Respiratory Tract (Lungs)
• If organisms present, drip down from
upper respiratory tract! (same as above)
Genitourinary Tract (Urinary Tract)
• If any organisms living there normally,
ascending route from GI tract
organisms!
Skin / Cutaneous
• Staphylococcus aureus (MSSA or MRSA)
• Coagulase –ve Staphylococcu
Brain / Central Nervous System
Should be STERILE (no bacteria)
Mouth / Oropharynx
• Streptococci (VGS, S. anginosus > betahemolytic, but GAS present)
• Oral anaerobes
• Candida spp
Stomach / Small-Intestine / Biliary Tree
• Stomach (mostly H. pylori, Streptococci)
• SI / Biliary Tree (they are conducted): Enterobacteriales (E. coli, Klebsiella, Proteus), Enterococcus, Streptococcus (GI > beta-hemolytic)
• Candida spp, fungus, yeast
Large Intestine / Colon - losing oxygen (anaerobes present)
• Enterobacteriales, Entero/Streptococcus
• Enteric Anaerobes
• The peritoneum (cavity surround intraabdominal organisms) should be STERILE (no bacteria)
• Candida spp
reminder
which are G+ coci?
Staphylococcus MSSA MRSA CoNS (e.g., S. epidermidis, S. haemolyticus)
Streptococcus Beta-hemolytic (Group A>G) “GI-Strep” (VGS, S. milleri group) S. pneumonia
Enterococcus:
E. Faecalis
E. Faecium
Others, rare
G+ bacilli (rods)
Predominantly anaerobes (e.g., Clostridia, Lactobacillus)
But also, some common
contaminants or uncommon pathogens like Corynebacteria, Cutibacterium (acne), and
Bacillus. Listeria is a GPB
reminder G-
enterobacterales
E. Coli Klebsiella Proteus Can produce ESBL enzymes over years (often not inducible
misc
Haemophilus Neisseria Moraxella Salmonella Generally, predictable resistance patterns
Anaerobic (G+/-)
colon/gi anaerobes
Bacteroides fragilis (B. frag), Clostridia/Clostridioides, Lactobacillus Usually managed by metronidazole, sometimes by extended BL-BLIs (e.g., Amox-Clav, Pip-Taz)
When Do Good Bacteria Go Bad?
• Under normal circumstances, our microbiota is in a state of homeostasis and infection/overgrowth of a certain bacterial species is thwarted by our immune system and bacterial antagonism
• Infection therefore occurs under abnormal circumstances:
1. Obstruction
o Blockage (i.e., stricture, gallstones, dysmotility) causing
loss of physiologic flow and nidus formation
2. Translocation/Perforation
o Inflammation/membrane permeability leading to
bacterial penetration into the blood OR sterile sites
3. Opportunistic or Exogenous
o Exogenous bacterial inoculation (e.g., food poisoning) or
idus – (noun): “a place in which bacteria have multiplied OR may multiply. A focus of infectiloss of bacterial antagonism/immunity (e.g., C. difficile)
Mouth
stomach
Site Normal Microbiota / Most Likely Pathogens
- Streptococci (GI Strep > Beta-Hemolytic)
- Oral Anaerobes (e.g., Fusobacterium, Peptostreptococcus)
- Not very many true pathogens in the stomach!
- H. pylori induced PUD
SI
biliary tree
LI
Normal Microbiota / Most Likely Pathogens
SI
Enterobacteriales (E. coli, Klebsiella, Proteus spp)
• Streptococci (GI Strep > Beta-Hemolytic)
• Enterococcus spp. (faecalis > faecium)
bil tree
• Same as small intestine! (contiguous)
LI
• Enterobacteriales (E. coli, Klebsiella, Proteus spp)
• Streptococci & Enterococci
• Colonic Anaerobic Bacteria (e.g., B. fragilis, Clostridium spp.)
But Do We Need To Empirically Treat For Drug Resistance?
Some places in the world have higher endemic rates of drug-resistant GNs. Consider this when deciding!
Previous samples from our patient are
positive for drug-resistant gram-negatives
(i.e., most recent isolates are ESBL+ in recent
few years); prolonged hospital (pressure on Gitract to stay and
++antibiotic use
Reasonable to treat empirically as if likely
drug-resistant until culture data is available if
feasible
Most recent isolates non-resistant OR nil
past isolates whatsoever, acquired infection
in the community-setting, nil prolonged
antibiotic or hospital exposure
No added benefit in treating as if drugresistant, assume local susceptibility rates
apply; adjust with treatment
Infections of the Biliary Tree (Accessory Tract)
Gallstones can cause obstruction WITHOUT infection – look for FEVER to prompt/justify antibiotic use!
Cholecystitis (“gall-bladder” – “inflammation”)
• Obstruction of the cystic duct (draining the gall bladder),
trapping organisms in the gall bladder which can grow,
proliferate, cause inflammation
• Usually obstructed by gallstones but could be by another anatomical stricture/problem
• Sx: RUQ pain, fever, abdominal tenderness, but lack of
‘jaundice
• Dx: clinical, ultrasound for obstruction
*Ascending Cholangitis (“biliary-tree” – “inflammation”)
• Obstruction of the common bile duct (draining the liver & GB), trapping organisms in the whole biliary tree, causing backup of bile into the liver
• Usually obstructed by gallstones but could be by another anatomical stricture/problem (e.g., sclerosing cholangitis)
• Sx: RUQ pain, fever, abdominal tenderness, +jaundice
(backup of bile into the liver > into the blood)
• Dx: clinical, ultrasound for obstruction, blood cultures
Beta-Lactams (CRITICALLY IMPORTANT)
prefer ceftriaxone
45M with choledocholithiasis (gall-stones which have fallen and are obstructing the common-bile duct but NOT causing infection) undergoes an ERCP procedure (endoscopic retrograde cholangiopancreatography) for stone retrieval.
The next day, the patient complains of sharp abdominal pain (RUQ), develops a temperature of 38.5*C and is tachycardic.
Q: What is the problem, and what pathogens could be at play with this problem?
- Problem: Post-ERCP Cholangitis - irritated their bile duct
- Most Likely Pathogens: typical organisms causing cholangitis!
- Other possible pathogens: Pseudomonas aeruginosa, possibly even others if contaminating the endoscope
need to think critically about the case, we normally wouldnt think abt pseudomonas from tertiary reosurces
Pancreatitis
n inflammatory condition with multiple
causes that ultimately leads to pancreatic enzyme autodigestion of the pancreas and substantial inflammation.
• Sx: can include fever, tachycardia, hypotension and a
systemic leukocytosis (++WBC!), commonly confused
for acute infection
None of the causes of acute pancreatitis are bacterial in nature (some are viral). However: after an episode of
acute pancreatitis – patients may develop complications (whcih cab be bacteriak):
• E.g., a pancreatic pseudocyst
• E.g., necrotizing pancreatitis
These foci CAN become infected but are incredibly
difficult to manage. Consulting ID expertise is justified.
Infections of the Liver
Liver Abscess
• Problem: trapping of bacteria in the hepatic ducts leading to growth and formation of an abscess that pushes on the liver, can also be from organisms that infect the liver VIA the bloodstream (rarely)
• Pathogens: most commonly E. coli, Klebsiella pneumoniae, and Streptococcus anginosus (3 most dominant), if from contaminated water ingestion can get an Entamoeba histolytica liver abscess
• Sx: indolent course, subacute presentation of fevers, chills, eventually some abdominal pain +/- jaundice, can have elevated liver enzymes
• Dx: CT-scan of the abdomen for abscess, drainage, if possible, for culture & sensitivity, can do serology for Entamoeba
Liver abscesses need drainage to resolve – but if cannot obtain, prolonged antibiotics with imaging follow-up.
