Lecture 25: GI Infections

HoyaDocs — GI Block | USMLE Step 1 Preparation

Lecture 25 — Overview

GI Infections · HoyaDocs GI Block

Page Summaries

🦠 Pathogens of Infectious Diarrhea
Covers LO 1
Viral (Rota, Noro) · Bacterial (invasive vs. toxigenic) · Campylobacter, Salmonella, Shigella · E. coli pathotypes · Vibrio · Listeria · Preformed-toxin food poisoning · Protozoa
Practice Qs: 1–4
🧖 Clinical Syndromes of Diarrhea
Covers LO 2
Syndromic framework (secretory / invasive / osmotic) · Watery diarrhea · Dysentery · Preformed-toxin food poisoning · Traveler’s diarrhea · C. difficile colitis
Practice Qs: 5–8
🏥 Intraabdominal Infections
Covers LO 3
Normal flora & empiric coverage · H. pylori · Liver abscess (pyogenic vs. amebic) · Intraperitoneal abscess · Peritonitis (SBP, secondary, CAPD) · Site-by-site recap
Practice Qs: 9–12

Official Learning Objectives Map

1 Describe the epidemiology, pathogenesis, clinical presentation, diagnosis, and treatment of the major infectious causes of diarrhea (viral, bacterial, and parasitic) Diarrhea Pathogens ▼
2 Differentiate among the clinical syndromes of infectious diarrhea (watery, dysentery, food poisoning, traveler’s diarrhea, and C. difficile colitis) and identify the most likely causative agents Clinical Syndromes ▼
3 Identify the most common intraabdominal infections (including H. pylori, liver abscess, intraperitoneal abscess, and peritonitis), their typical pathogens, and principles of management Intraabdominal ▼

LO 1 — Pathogens That Cause Infectious Diarrhea

Viruses, Bacteria (invasive + toxigenic), Preformed Toxins · HoyaDocs GI Block

Learning Objective Covered
  • LO 1: Review the different pathogens that cause infectious diarrhea
On This Page
  1. Defining Diarrhea & Big-Picture Pathogen Classes
  2. Viral Pathogens
  3.   ↳ Rotavirus
  4.   ↳ Norovirus
  5. Bacterial Pathogens — Frequency & Overview
  6.   ↳ Campylobacter
  7.   ↳ Salmonella (non-typhoidal + typhoid)
  8.   ↳ Shigella
  9.   ↳ Pathogenic E. coli (5 types)
  10.   ↳ Yersinia
  11.   ↳ Vibrio species
  12.   ↳ Listeria
  13. Preformed Toxin (“Food Poisoning”) Bugs
  14. Protozoa — At-a-Glance

🧠 Testing Your Understanding!

Testing Your Understanding — LO 1, Question 1

A 7-year-old presents with 2 days of bloody diarrhea after eating at a backyard cookout. Stool culture on sorbitol-MacConkey agar shows colorless (non-fermenting) colonies. She develops anemia, thrombocytopenia, and an acute rise in creatinine. Why would antibiotics be the wrong treatment here, and what pathogen is responsible?

Consider: SMAC sorbitol-negative, Shiga-like toxin, HUS triad, SOS response

✓ Answer: EHEC (E. coli O157:H7). Antibiotics increase toxin release via the SOS response and worsen HUS risk.

EHEC is the only Shiga-toxin-producing E. coli you’ll see on Step 1 in the US context. It’s sorbitol-negative on SMAC (colorless colonies), whereas normal stool E. coli ferments sorbitol to pink colonies. The Shiga-like toxin (Stx) inhibits the 28S rRNA of the 60S ribosomal subunit on endothelial cells, damaging renal and cerebral microvasculature and producing the HUS triad: microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. Antibiotics that induce the bacterial SOS response (especially TMP-SMX and fluoroquinolones) up-regulate the lambdoid prophage carrying the stx gene and can paradoxically increase toxin release. Management is supportive hydration and dialysis as needed; eculizumab may be considered in severe atypical cases.

Testing Your Understanding — LO 1, Question 2

Two pregnant women are in clinic. One ate a salad with queso fresco two weeks ago and now has fever, myalgias, and mild diarrhea. The other ate raw oysters at a seafood bar; she has cirrhosis and now presents with fever and hemorrhagic skin bullae. Identify each organism and explain why each host population is uniquely vulnerable.

Consider: Gram-positive cold grower, transplacental transmission, iron/cirrhosis susceptibility

✓ Answer: (1) Listeria monocytogenes in pregnancy; (2) Vibrio vulnificus in cirrhosis.

Listeria is a Gram-positive rod that uniquely grows at refrigeration temperatures — soft cheeses and deli meats are the classic vectors. It invades intracellularly and is controlled by cell-mediated immunity, which is physiologically blunted in pregnancy. Transplacental spread causes granulomatosis infantiseptica or neonatal meningitis/sepsis. Treat with ampicillin (± gentamicin).

Vibrio vulnificus is a Gram-negative comma-shaped rod acquired from raw oysters or salt-water wounds. Cirrhotics and patients with iron overload (hemochromatosis, thalassemia) are strikingly susceptible because free iron fuels the organism’s virulence. It produces a characteristic hemorrhagic bullous skin lesion and can progress rapidly to septic shock with >50% mortality. Treat with doxycycline + a third-generation cephalosporin; aggressive debridement may be needed.

LO 2 — Clinical Syndromes of Infectious Diarrhea

Watery, Dysentery, Food Poisoning, Traveler’s, C. difficile · HoyaDocs GI Block

Learning Objective Covered
  • LO 2: Understand the different clinical manifestations of and pathogens that cause watery diarrhea, dysentery, food poisoning, traveler’s diarrhea, and C. difficile
On This Page
  1. The 5-Syndrome Framework
  2. Watery (Secretory / Non-Inflammatory) Diarrhea
  3. Dysentery (Inflammatory Bloody Diarrhea)
  4. Food Poisoning (Preformed Toxin)
  5. Traveler’s Diarrhea
  6. Clostridioides difficile Infection

🧠 Testing Your Understanding!

Testing Your Understanding — LO 2, Question 1

A church potluck features rice, creamed chicken, and potato salad left on the table for several hours. Three attendees are ill within 3 hours with vomiting and cramps. A fourth attendee becomes ill 10 hours later with watery diarrhea but no vomiting. Assuming two distinct pathogens are involved, name each, the toxin mechanism, and predict the stool WBCs.

Consider: preformed toxin incubation, emetic vs. diarrheal bugs, fecal leukocytes

✓ Answer: (1) S. aureus (preformed enterotoxin) in the first cohort; (2) C. perfringens (late incubation, diarrhea-dominant, no vomiting) in the fourth attendee. Both are non-inflammatory — stool WBCs should be absent.

S. aureus produces a heat-stable enterotoxin that acts as a superantigen on vagal afferents → intense vomiting within 1–8 hours (mean 4 hours). Potato salad and custard pastries are classic vectors. C. perfringens type A produces an enterotoxin in the gut after ingestion of spores; the 8–24 hour incubation and predominance of diarrhea without vomiting are the tells. Reheated meats/gravy are classic. Both mechanisms are toxin-mediated and non-inflammatory, so stool fecal leukocytes are negative and no colonic invasion occurs. Management is supportive rehydration — no antibiotics.

Testing Your Understanding — LO 2, Question 2

A 72-year-old inpatient finishes a 5-day course of ceftriaxone for pneumonia and develops frequent watery diarrhea, fever, and a WBC of 22,000. Stool NAAT is positive for tcdB. Flexible sigmoidoscopy shows yellow-white adherent plaques on the colon. What drug should be started, what drug should be avoided, and what mechanism underlies pseudomembrane formation?

Consider: toxins A & B, actin disruption, vanc/fidaxo/metro, loperamide risks

✓ Answer: Start oral vancomycin (or fidaxomicin). Avoid antimotility agents like loperamide. Pseudomembranes form when toxins A and B glucosylate Rho-family GTPases, disrupting the actin cytoskeleton → enterocyte death, fibrin/mucin/neutrophil plaques.

C. difficile toxin B (and to a lesser extent toxin A) inactivates Rho/Rac GTPases by monoglucosylation, collapsing actin filaments and tight junctions — cells round up and slough off, and the resulting inflammatory exudate forms the classic yellow-white pseudomembrane. In a patient with severe features (WBC >15,000, creatinine rise, hypotension), you can add IV metronidazole to oral vancomycin. Loperamide prolongs toxin contact time and can precipitate toxic megacolon. Recurrence is common (10–25%) — fidaxomicin has lower recurrence rates; refractory/recurrent cases often get fecal microbiota transplantation.

LO 3 — Intraabdominal Infections

H. pylori, Liver & Intraperitoneal Abscess, Peritonitis, Normal Flora · HoyaDocs GI Block

Learning Objective Covered
  • LO 3: Review the clinical manifestations of common intraabdominal infections
On This Page
  1. Mouth-to-Anus: Normal Flora & Potential Pathogens
  2. Helicobacter pylori
  3. Pyogenic Liver Abscess
  4. Intraperitoneal Abscess
  5. Peritonitis (Secondary, SBP, CAPD)
  6. Other Intraabdominal Infections

🧠 Testing Your Understanding!

Testing Your Understanding — LO 3, Question 1

A 58-year-old man with alcoholic cirrhosis and chronic ascites presents with two days of diffuse abdominal pain, low-grade fever, and new confusion. Paracentesis shows ascitic PMNs of 750 cells/mm3, glucose 95 mg/dL, protein 0.8 g/dL, and a monomicrobial E. coli culture. Explain the most likely diagnosis, empiric therapy, and a key secondary-prevention strategy.

Consider: SBP criteria, gut translocation, ceftriaxone, norfloxacin prophylaxis

✓ Answer: Spontaneous bacterial peritonitis (SBP). Empiric ceftriaxone (or cefotaxime) × 5 days. Long-term oral fluoroquinolone (norfloxacin) prophylaxis is indicated after the first episode.

SBP is diagnosed by ascitic fluid PMNs ≥250/mm3 in a cirrhotic with ascites; the fluid is typically low-protein (impaired opsonin delivery) and monomicrobial. E. coli is the #1 organism because translocation of gut flora across a leaky intestinal barrier is the pathogenesis. Third-generation cephalosporins are standard empiric therapy. Add IV albumin (1.5 g/kg day 1, 1 g/kg day 3) in patients with creatinine >1 mg/dL, BUN >30, or bilirubin >4 — this reduces the risk of hepatorenal syndrome and improves survival. Recurrence exceeds 50% in the year after a first episode, so long-term norfloxacin (or TMP-SMX or ciprofloxacin) prophylaxis is indicated. Polymicrobial growth or very high ascitic protein should prompt evaluation for secondary (surgical) peritonitis.

Testing Your Understanding — LO 3, Question 2

A 54-year-old woman with 6 months of epigastric pain develops melena. EGD reveals a clean-based duodenal ulcer. A rapid urease test on antral biopsy is positive. Six weeks after completing bismuth quadruple therapy, you are deciding how to confirm eradication. Why is simple repeat serology useless, what is the preferred non-invasive test, and what is the theoretical downside of treating her?

Consider: IgG persistence, urea breath/stool antigen, H. pylori protective effects

✓ Answer: Serology stays positive for years after cure (IgG persistence). Confirm eradication with a urea breath test or stool antigen, holding PPIs/antibiotics/bismuth beforehand. Downside: eradicating H. pylori may raise her risk of GERD and lower esophageal/gastric cardia adenocarcinoma.

H. pylori serology (IgG) reflects past or present infection and cannot discriminate active colonization from eradicated disease; it remains positive long after successful treatment. Urea breath test relies on labeled-CO2 generation by active urease in the stomach and is rapidly accurate once treatment works. Stool antigen is a similarly reliable alternative. Hold PPIs for 2 weeks and antibiotics/bismuth for 4 weeks before either test to prevent false-negatives. The “H. pylori dilemma” is that colonization protects against GERD, Barrett’s, and gastric-cardia adenocarcinoma by lowering acid output (atrophic body gastritis) — this is why we don’t screen asymptomatic patients. In patients with PUD, MALT lymphoma, early gastric cancer, or unexplained iron-deficiency anemia, though, the benefits of eradication clearly outweigh the risks.

Practice Questions

Lecture 25 — GI Infections · HoyaDocs GI Block

LO 1 — Pathogens of Infectious Diarrhea (Q1–Q4)

Question 1

A 22-year-old returns from a backpacking trip in Thailand with 3 days of watery, non-bloody diarrhea, abdominal cramps, and a low-grade fever. No vomiting. Stool culture is negative on routine media. Which toxin is most likely responsible?

A. Shiga toxin

B. Heat-labile and heat-stable enterotoxins

C. Cholera toxin

D. Toxin B (TcdB)

E. Botulinum toxin

✓ Correct: B — ETEC produces heat-labile (↑cAMP) and heat-stable (↑cGMP) enterotoxins; it is the #1 cause of traveler’s diarrhea.

ETEC is not routinely identifiable on standard stool cultures, explaining the “culture-negative” clue. Cholera toxin (C) causes profuse rice-water diarrhea in endemic outbreaks, not this self-limited traveler picture. Shiga toxin (A) produces bloody diarrhea and risks HUS. Toxin B (D) implies C. difficile, which is antibiotic-associated. Botulinum toxin (E) causes flaccid paralysis, not diarrhea.

Question 2

A 4-year-old unvaccinated child is hospitalized with vomiting, non-bloody watery diarrhea, fever, and respiratory symptoms. Stool EIA is positive. What is the structural feature of the causative organism?

A. Segmented double-stranded RNA virus

B. Non-enveloped single-stranded RNA virus (Caliciviridae)

C. Gram-positive rod that grows at 3°C

D. Gram-negative curved rod that grows at 42°C

E. Protozoan acid-fast oocyst

✓ Correct: A — Rotavirus is a segmented double-stranded RNA virus (Reoviridae).

The unvaccinated young child with winter viral gastroenteritis ±respiratory symptoms is classic Rotavirus; 30–50% have respiratory findings. (B) describes Norovirus, which causes cruise-ship/adult outbreaks. (C) is Listeria, (D) is Campylobacter, (E) is Cryptosporidium — all wrong demographics/presentations.

Question 3

A 25-year-old develops bloody diarrhea, fever, and crampy abdominal pain 3 days after eating undercooked chicken at a cookout. Stool culture at 42°C on selective medium grows a curved Gram-negative rod. Three weeks later he develops ascending flaccid paralysis. The most likely organism also causes which additional complication?

A. Hemolytic uremic syndrome

B. Ascending cholangitis

C. Reactive arthritis (Reiter’s)

D. Typhoid fever

E. Pseudoappendicitis

✓ Correct: C — Campylobacter jejuni is classically linked to Guillain-Barré syndrome AND reactive arthritis.

Campylobacter (curved Gram-negative rod, 42°C selective culture, chicken source) is the most common US bacterial diarrhea and the most common worldwide antecedent of Guillain-Barré. It is also a member of the “SSCY(C)” reactive arthritis group (Salmonella, Shigella, Campylobacter, Yersinia, Chlamydia). HUS (A) is EHEC/Shigella. Cholangitis (B) is biliary obstruction with gut flora. Typhoid (D) is S. typhi. Pseudoappendicitis (E) is Yersinia.

Question 4

A 6-year-old child with sickle cell disease presents with fever and right femur pain. Blood cultures grow a Gram-negative H2S-producing rod. Which of the following best explains why this organism is particularly problematic in this patient population?

A. Production of IgA protease

B. Splenic autoinfarction impairs clearance of encapsulated and invasive organisms

C. Low inoculum transmissibility from person to person

D. Direct invasion via iron scavenging

E. Preformed enterotoxin in contaminated food

✓ Correct: B — Functional asplenia in sickle cell disease predisposes to invasive Salmonella infections, classically osteomyelitis.

Non-typhoidal Salmonella species cause osteomyelitis in sickle-cell patients because splenic microinfarcts eliminate clearance of bacteremia, and Salmonella has a tropism for infarcted bone. In the general population, S. aureus is the top cause of osteomyelitis; Salmonella is the outlier for sickle cell. IgA protease (A) is a feature of S. pneumoniae, H. influenzae, and Neisseria. Low-inoculum transmission (C) is Shigella. Iron scavenging (D) describes Yersinia in iron-overloaded hosts. Preformed toxin (E) is not the mechanism.

LO 2 — Clinical Syndromes (Q5–Q8)

Question 5

A 29-year-old eats leftover fried rice from dinner the night before. Two hours later he develops severe vomiting and cramping; no fever. He feels better within 10 hours. What is the causative organism?

A. Staphylococcus aureus

B. Bacillus cereus (emetic form)

C. Clostridium perfringens

D. Norovirus

E. Salmonella enteritidis

✓ Correct: B — The reheated-fried-rice + short-incubation emetic picture is classic Bacillus cereus (cereulide toxin).

Cereulide is a heat-stable preformed toxin; re-heating does not destroy it. S. aureus food poisoning (A) also has a short incubation and vomiting, but the classic foods are custard pastries, mayo salads, and processed meats. C. perfringens (C) has an 8–24 hr incubation and is diarrhea-predominant. Norovirus (D) can also produce vomiting but with a longer 12–48 hr incubation and typically an outbreak context. Salmonella (E) is invasive, fever-positive, and has a 6–48 hr incubation.

Question 6

A 4-year-old previously healthy girl presents after 4 days of watery diarrhea that turned bloody. She has abdominal pain but no fever. Labs show Hb 8 g/dL with schistocytes, platelets 55,000, BUN 65, creatinine 2.2. Which of the following is the most appropriate initial management?

A. Empiric ciprofloxacin

B. Oral metronidazole

C. IV fluids and supportive care

D. Loperamide and oral rehydration

E. TMP-SMX and bismuth

✓ Correct: C — EHEC with HUS is treated with supportive care; antibiotics and antimotility agents worsen toxin release and HUS severity.

The triad of microangiopathic hemolytic anemia, thrombocytopenia, and AKI in a child with preceding bloody diarrhea is hemolytic uremic syndrome, classically post-EHEC (O157:H7). Antibiotics (especially fluoroquinolones, TMP-SMX) induce the bacterial SOS response → up-regulate the lambdoid prophage carrying stx → increased toxin release → worse HUS. Loperamide increases toxin contact time and is contraindicated. Provide aggressive IV fluid resuscitation, monitor renal function, transfuse judiciously, and consider dialysis as needed.

Question 7

A 68-year-old nursing home resident on day 5 of ceftriaxone for pneumonia develops 8 watery stools per day and a WBC of 24,000. Stool toxin EIA is positive. Sigmoidoscopy reveals adherent yellow-white plaques. Which agent is first-line?

A. IV metronidazole alone

B. Oral ciprofloxacin

C. Oral vancomycin

D. Rifaximin

E. IV vancomycin

✓ Correct: C — Oral vancomycin (or fidaxomicin) is first-line for CDI, per updated IDSA/ACG guidance.

Oral vancomycin reaches therapeutic luminal concentrations (it is not systemically absorbed), exactly where C. difficile resides. IV vancomycin (E) does NOT reach the colonic lumen and is inappropriate. Metronidazole (A) is no longer preferred for initial CDI but may be added IV in severe/fulminant disease with ileus. Fluoroquinolones (B) are often causative, not therapeutic. Rifaximin (D) is used for hepatic encephalopathy and traveler’s diarrhea, not CDI.

Question 8

A 52-year-old relief worker returns from Haiti with a single day of “rice-water” diarrhea exceeding 10 L and now has hypotension, hypokalemia, and metabolic acidosis. The toxin responsible acts by which mechanism?

A. Activates guanylate cyclase via heat-stable enterotoxin

B. ADP-ribosylates Gs, leading to persistent ↑cAMP and Cl– secretion

C. Inactivates EF-2 via ADP-ribosylation

D. Cleaves SNARE proteins at the neuromuscular junction

E. Glucosylates Rho GTPases, disrupting actin cytoskeleton

✓ Correct: B — Cholera toxin ADP-ribosylates Gs → locked-on adenylate cyclase → ↑cAMP → CFTR-mediated Cl– and water secretion.

This drives the massive “rice-water” stool. Treat with aggressive oral rehydration salts (the glucose-Na+ SGLT1 cotransporter remains functional) + doxycycline. (A) is ETEC heat-stable toxin. (C) is diphtheria toxin and Pseudomonas exotoxin A. (D) is botulinum/tetanus toxin. (E) is C. difficile toxins A and B.

LO 3 — Intraabdominal Infections (Q9–Q12)

Question 9

A 64-year-old with Child-Pugh B cirrhosis presents with low-grade fever, diffuse abdominal pain, and new encephalopathy. Paracentesis shows 500 PMNs/mm3 and grows a single organism on culture. Which empiric antibiotic is most appropriate?

A. Vancomycin + aztreonam

B. Ceftriaxone

C. Oral vancomycin

D. Piperacillin/tazobactam + vancomycin

E. TMP-SMX

✓ Correct: B — Ceftriaxone (or cefotaxime) is standard empiric therapy for SBP.

SBP (primary peritonitis) is defined by ascitic PMN ≥250/mm3 in a cirrhotic; monomicrobial growth (usually E. coli) supports the diagnosis. Third-generation cephalosporins cover the typical enteric Gram-negatives. Add IV albumin to reduce risk of hepatorenal syndrome. Oral vancomycin (C) is for CDI. Broader coverage (A, D) is reserved for nosocomial or healthcare-associated peritonitis. TMP-SMX (E) is a prophylactic option, not primary therapy.

Question 10

A 48-year-old man is referred for dyspepsia. Endoscopy shows a duodenal ulcer; rapid urease test is positive. He is treated with bismuth quadruple therapy. Why should clarithromycin-based triple therapy have been avoided as empiric first-line today in many US regions?

A. Clarithromycin is ineffective in achlorhydric stomachs

B. Rising clarithromycin resistance (>15%) has compromised cure rates

C. Clarithromycin does not reach therapeutic levels in gastric mucus

D. Clarithromycin is known to eradicate protective Lactobacillus species

E. Clarithromycin accelerates bismuth metabolism

✓ Correct: B — Regional clarithromycin resistance >15% has dropped cure rates below acceptable thresholds; current guidelines favor bismuth or non-bismuth quadruple therapy empirically.

Triple therapy (PPI + clarithromycin + amoxicillin) was once standard but is now reserved for patients without prior macrolide exposure in low-resistance regions. Quadruple regimens (PPI + bismuth + metronidazole + tetracycline, or PPI + clarithromycin + amoxicillin + metronidazole) achieve higher eradication rates × 14 days. Confirm eradication with urea breath test or stool antigen 4 weeks post-treatment (off PPI).

Question 11

A 34-year-old man returned from Mexico 2 months ago. He now presents with RUQ pain, low-grade fever, and an 8-cm right-hepatic-lobe fluid collection on ultrasound. Percutaneous drainage yields thick reddish-brown fluid with no organisms on Gram stain. What is the best therapy?

A. Ceftriaxone + metronidazole

B. Oral vancomycin

C. Metronidazole + paromomycin

D. Amphotericin B

E. Praziquantel

✓ Correct: C — Amebic liver abscess (Entamoeba histolytica): metronidazole clears tissue forms, then paromomycin (or iodoquinol) eliminates luminal cysts.

The right-lobe single abscess with reddish-brown (“anchovy paste”) sterile fluid in a returned traveler is pathognomonic. Serology (antibodies to E. histolytica) confirms. Antibiotics like ceftriaxone + metronidazole (A) would fit a pyogenic abscess — but pyogenic collections are usually polymicrobial with gut flora on Gram stain, not sterile. Paromomycin is essential to eradicate luminal cysts and prevent recurrence/transmission.

Question 12

A 71-year-old man with a perforated sigmoid diverticulum is taken to the OR. Peritoneal fluid grows E. coli + Bacteroides fragilis + Enterococcus faecalis. What is the key mechanistic principle explaining the empirical antibiotic choice?

A. Cover only Gram-negative organisms because anaerobes rarely matter

B. Cover anaerobes empirically even if cultures are negative, since gut flora from the colon reliably seed these infections

C. Antibiotics alone are adequate if they cover all three organisms

D. Use narrow-spectrum therapy to preserve microbiome

E. Prophylactic antifungals are always required

✓ Correct: B — Secondary peritonitis from a colonic perforation is polymicrobial with reliable anaerobic involvement; empiric anaerobic coverage (metronidazole, pip-tazo, carbapenems) is essential regardless of culture results.

Anaerobes, especially Bacteroides fragilis, are notoriously hard to culture but nearly always present in colonic perforations. “Give anaerobic coverage even if anaerobes don’t grow” is a core teaching point. Surgical or percutaneous source control is also required — antibiotics alone cannot cure a walled-off abscess or fix a perforation. Narrow-spectrum therapy (D) is inappropriate at initial empiric coverage. Enterococcal coverage (ampicillin, vancomycin) is added for healthcare-associated or severe disease. Antifungals (E) are not routine unless risk factors (TPN, prolonged ICU, immunosuppression) are present.