Gram (-) rods

Vibrio cholerae (cholera) presents as “liters and liters” of rice-water stool in someone who went traveling to, e.g., Mexico. Acquired fecal-oral (i.e., fecal-contaminated food/water).

MOA of toxin is same as ETEC heat-labile toxin causing traveler’s diarrhea, which is ADP-ribosylation of adenylyl cyclase (increases cAMP). The way you can differentiate this from ETEC traveler’s diarrhea is that cholera is notably profusely high-volume.

Both ETEC and cholera vignettes can tell you the patient has 8-12 stools daily, so it’s not the # of stools that matters; it’s the emphasis on volume. Cholera causes death via severe dehydration and electrolyte disturbance.

Tx is oral rehydration on USMLE; if patient has low BP or altered mental status (i.e., confusion/coma), IV hydration is done.

Pseudomonas produces a toxin that inhibits Elongation Factor 2 (EF2), same as Diphtheria.

Perforated duodenal ulcer will present as sudden-onset rigid abdomen (involuntary guarding). Patient will often have SIRS, with abnormal vitals due to sympathetic activation. USMLE wants “X-rays of the chest and abdomen” to look for air under the diaphragm (HY finding that indicates ruptured viscus).

E. coli EHEC O157:H7 and Shigella.

Causes bloody diarrhea + either appendicitis-like (i.e., RLQ) pain or arthritis.

The RLQ pain is from mesenteric adenitis or terminal ileitis.

Toxin has same MOA as ETEC heat-stabile toxin (i.e., ­ ADP-ribosylates guanylyl cylase, thereby increasing cGMP).

There is an NBME Q where they tell you a patient was on antibiotics for a week + has bloody stool + LLQ pain, and the answer is C. diff, not Yersinia. C. diff can cause either watery or bloody stool, and sometimes pain. Pseudo-appendicitis due to Yersinia will be RLQ; it will not be LLQ.

Enterotoxigenic E. coli (ETEC) causes traveler’s diarrhea, which is self-limiting watery or brown-green diarrhea following trips overseas to, e.g., Mexico or the Middle East.

Classically acquired via water or lettuce contaminated with human feces.

The mechanism for ETEC diarrhea is heat-labile toxin that ADP-ribosylates adenylyl cyclase, increasing cAMP, as well as heat-stabile toxin that ADP-ribosylates guanylyl cylase, increasing cGMP.

In other words, HL toxin increases cAMP; HS toxin increases cGMP.

The HL toxin increasing cAMP is the same mechanism as cholera toxin (Vibrio cholerae); the difference is cholera causes profuse, high-volume stool, with liters and liters of rice-water stool, wheres traveler’s diarrhea, even if it is described as occurring 8-12 times daily (I’ve seen this on NBME), they will not describe it as profusely high-volume the way cholera presents.

The HS toxin increasing cGMP is the same mechanism as Yersinia enterocolitica toxin. The difference is the latter causes bloody diarrhea and pseudo-appendicitis (RLQ pain) or arthritis, whereas traveler’s diarrhea is not bloody.

E. coli EHEC O157:H7 and Shigella.

HUS presents as triad of: 1) thrombocytopenia; 2) hemolytic anemia with schistocytes; and 3) renal insufficiency with or without hematuria.

The combination of thrombocytopenia + schistocytosis = microangiopathic hemolytic anemia (MAHA).

The mechanism for HUS is: E. coli EHEC O157:H7 (and Shigella) both secrete toxins (Shiga-like toxin and Shiga toxin, respectively) that cause inflammation of renal microvasculature –> ADAMTS13 protein inactivation –> failure of cleavage of vWF multimers –> platelet adherence to vascular endothelium cannot be as readily reversed –> platelet aggregations protrude into vascular lumen causing shearing of RBCs flying past –> fragmentation of RBCs (schistocytes, aka helmet cells).

Shiga-like and Shiga toxins cleave the eukaryotic 60S ribosomal subunit, thereby interfering with protein translation.

Pseudomonas is very important cause of nosocomial pneumonia (i.e., hospital- and ventilator-acquired pneumonia). If a patient has a nosocomial pneumonia (which is defined as a pneumonia starting >48 hours following becoming an in-patient), he or she must receive coverage for both MRSA as well as Psuedomonas. This is accomplished by giving vancomycin (covers MRSA) PLUS either ceftazidime (a 3rd-gen ceph) or cefepime (a 4th-gen ceph).

Ceftriaxone (a 3rd-gen ceph) does not cover Pseumonas, so the combo of vanc + ceftriaxone is wrong for nosocomial infections. This combo is used for community-acquired sepsis or meningitis. For community-acquired pneumonias where there is not sepsis, we give simple azithromycin to treat.

There are other agents that cover Pseudomonas, such as carbapenems, pipericillin/tazobactam, amikacin (an aminoglycoside), etc., but I have not seen NBME assess these. What I have seen that is incredibly HY on forms is the vancomycin + cephalosporin combos as I mentioned above.

Bloody diarrhea 1-3 days after consumption of poultry.

Can cause Guillain-Barre syndrome (ascending paralysis + decreased tendon reflexes + albuminocytologic dissociation in the CSF –> Tx with IVIG + plasmapheresis).

I would say only about 1/4 of GBS Qs will mention any type of preceding infection. So don’t rely on the dude going to some BBQ or getting diarrhea beforehand as a crutch for GBS Qs.

Grows best at high temperatures (42 degrees).

Enterotoxigenic E. coli (ETEC) causes traveler’s diarrhea, which is self-limiting watery or brown-green diarrhea following trips overseas to, e.g., Mexico or the Middle East.

Classically acquired via water or lettuce contaminated with human feces.

The mechanism for ETEC diarrhea is heat-labile toxin that ADP-ribosylates adenylyl cyclase, increasing cAMP, as well as heat-stabile toxin that ADP-ribosylates guanylyl cylase, increasing cGMP.

In other words, HL toxin increases cAMP; HS toxin increases cGMP.

The HL toxin increasing cAMP is the same mechanism as cholera toxin (Vibrio cholerae); the difference is cholera causes profuse, high-volume stool, with liters and liters of rice-water stool, wheres traveler’s diarrhea, even if it is described as occurring 8-12 times daily (I’ve seen this on NBME), they will not describe it as profusely high-volume the way cholera presents.

The HS toxin increasing cGMP is the same mechanism as Yersinia enterocolitica toxin. The difference is the latter causes bloody diarrhea and pseudo-appendicitis (RLQ pain) or arthritis, whereas traveler’s diarrhea is not bloody.

Vibrio parahemolyticus doesn’t cause profuse, watery diarrhea the same way cholera does. I’ve seen this organism asked once in an NBME vignette where the patient ate sushi (can be acquired from sushi and shellfish).

Vibrio vulnificus causes severe sepsis in half of patients. This is asked on offline NBME 19 where a dude went running on a beach and got sepsis, with no mention of consumption of food. But it’s apparently acquired from shellfish.

Normal GI flora for mouth to anus. Most important detail is that it is strictly anaerobic.

Anaerobic infections on USMLE can present as “foul-smelling sputum” or “foul-smelling discharge.”

Causes pulmonary abscess and aspiration pneumonia.

USMLE wants “aspiration of oropharyngeal normal flora,” or “aspiration of oropharyngeal anaerobes” as the cause of pulmonary abscess.

Oropharyngeal normal flora = Bacteroides (strictly anaerobic gram-negative rods); as well as Peptostreptococcus and Mobiluncus. The latter two are not HY, but Bacteroides is. I mention all three, however, because the Q can say sputum sample shows “gram-negative rods, gram-positive cocci, and gram-positive rods,” which refers to all three. But the bigger picture concept is, this = mixed normal flora.

Q will give aspiration risk factor, such as alcoholism, dementia (can cause loss of gag reflex), Hx of stroke (leading to dysphagia), or epilepsy. Q can also mention broken or missing teeth (hypodontia) as risk factor. Pulmonary abscess is often described on NBME as pulmonary lesion with an air-fluid level. This is buzzy, but not a mandatory descriptor. This refers to the top half of the circle being air, and the bottom being pus, the latter settling due to gravity.

Tx for pulmonary abscess = clindamycin. Clindamycin is used for “anaerobes above the diaphragm” (metronidazole for “anaerobes below the diaphragm”). Some students have asked about potentially updated/alternative pharm for pulmonary abscess, but I can tell you clindamycin is all over 2CK NBMEs.

Additionally, USMLE can give some sort of abdominal infection (e.g., after surgery), where the site drains “foul-smelling sputum.” You know right away they’re talking about anaerobes, specifically Bacteroides.

Diagnose H. pylori with urease breath test or stool antigen. Endoscopy + biopsy can be performed to confirm diagnosis in some cases via visualization of the spiral-shaped organisms.

Urease (+), so can cause struvite stones.

Can cause cavitary pneumonia with currant jelly (thick, dark red) sputum; classically seen in alcoholics or those with aspiration risk.

Treat H. pylori with CAP – i.e., clarithromycin, amoxicillin, PPI (e.g., omeprazole).

USMLE really doesn’t give a fuck about the treatment, but CAP is safe to know. Metronidazole, tetracycline, bismuth, and PPI tetrad is used if CAP fails (students ask about those other drugs).

Anaerobic infections on USMLE can present as “foul-smelling sputum” or “foul-smelling discharge.”

This can refer to pulmonary abscess or aspiration pneumonia caused by Bacteroides.

USMLE wants “aspiration of oropharyngeal normal flora,” or “aspiration of oropharyngeal anaerobes” as the cause of pulmonary abscess.

Additionally, USMLE can give some sort of abdominal infection (e.g., after surgery), where the site drains “foul-smelling sputum.” You know right away they’re talking about anaerobes, specifically Bacteroides.

Acquired from beef.

Can cause shigellosis, which is isolated bloody diarrhea (dysentery), or can cause full-blown hemolytic uremic syndrome (same as EHEC).

Shiga-toxin cleaves the eukaryotic 60S ribosome (same as EHEC), but its main virulence factor is its ability to invade GI mucosa. If Shigella loses its ability to invade, it is severely impeded in its ability to cause infection. EHEC does not invade.

Most common cause of UTIs, cystitis, and pyelonephritis. USMLE wants you to know fimbriae or P-pilus are virulence factors that enable adhesion to urothelium.

Helicobacter pylori.

Can cause antral/pyloric ulcers leading to gastric outlet obstruction. They will mention this on NBME as a “succussion splash.”

Increased­ risk of MALT lymphoma, a type of B-cell lymphoma; can be obstructive at the pylorus, as well as at the cardia of the stomach adjacent the lower esophageal sphincter.

Pseudomonas is most important cause of pneumonia in cystic fibrosis patients. I’ve talked about in prior content that S. aureus exceeds Pseudomonas prior to age 10 and that Pseudomonas exceeds S. aureus after age 10. But I’m not convinced that USMLE gives a fuck. I’m not going to go fish for and remove that detail about age from my prior content, however.

Diabetic patients have increased general infection risk due to Pseudomonas. This notably is in reference to osteomyelitis and foot ulcers. However, a caveat is that a new NBME Q for 2CK has “polymicrobial” as the answer for the most likely cause of diabetic foot ulcer, where both Pseudomonas and S. aureus are wrong answers. I mention this because resources over the years have pushed Pseudomonas for foot ulcers. So I just want you to be aware “polymicrobial” is correct if it’s listed alongside Pseudomonas.

Can cause infections on burns. Appears blue-green due to a pigment it produces called pyocyanin. If a burn has a yellow color, in contrast, this is likely S. aureus (“golden Staph), not Pseudomonas.

Patients with nosocomial UTIs. Since Serratia is urease-positive, it can lead to struvite (ammonium magnesium phosphate; staghorn) calculi, since these form at higher pH.

Serratia sepsis can be mentioned on USMLE in patients with NADPH oxidase deficiency (chronic granulomatous disease), since these patients have susceptibility to catalase-positive organisms (Big SPACES –> Burkholderia, S. aureus, Pseudomonas, Aspergillus, E. coli, Serratia).

Pseudomonas can cause otitis externa (swimmer’s ear).

Treat otitis externa with topical ciprofloxacin + hydrocortisone drops.

Prophylaxis for otitis externa (e.g., in someone who does crew who can’t avoid water exposure) is topic alcohol-acetic acid drops. Answers such as ear plugs are wrong. Carbamide peroxide drops are for earwax buildup (distractor on NBME).

E. coli.

NBME gives male who’s 45 with prostatitis where E. coli is correct and Chlamydia is wrong. The latter is presumably younger patients, or if they mention overt sexual activity with new partners.

Salmonella typhi causes typhoid fever, which is high fever + prostration (patient is lying down ill / in pain) + rose spots on the abdomen + either constipation or diarrhea.

Humans are the reservoir for Salmonella typhi, and it is acquired via fecal contaminated food/water. It can remain latent in the gall bladder.

Don’t confuse with Salmonella enteritidis and typhimurium, which cause food poisoning resulting in bloody diarrhea. Acquired from consumption of poultry or eggs, as well as from interaction with reptiles (i.e., pet lizards, snakes, etc.).

Helicobacter pylori.

Spiral-shaped gram-negative rod.

Responsible for almost all duodenal ulcers (>95%), whereas it causes a lower % (only >60%) of gastric ulcers. This is merely because the latter are caused by many other things as well, so we simply have decreased  fraction caused by H. pylori. In other words, there’s no special tropism of H. pylori toward duodenal over gastric mucosa.

Mechanism for ulcers that shows up on USMLE is: “secretes proteinaceous substrates that damage mucosal lining.” This is correct over “­increases gastric acid secretion” if both are listed side-by-side, even though H. pylori does ­ gastrin levels, which ­increases acid secretion.

Produces urease, which causes ­increased ammonia production around the organism, allowing it to survive in the decreased pH of the stomach.

Enterohemorrhagic E. coli (EHEC)  causes bloody diarrhea (dysentery) in isolation, or can also cause full-blown hemolytic uremic syndrome (HUS). Classically acquired from beef.

HUS presents as triad of: 1) thrombocytopenia; 2) hemolytic anemia with schistocytes; and 3) renal insufficiency with or without hematuria.

The combination of thrombocytopenia + schistocytosis = microangiopathic hemolytic anemia (MAHA).

The mechanism for HUS is: E. coli EHEC O157:H7 (and Shigella) both secrete toxins (Shiga-like toxin and Shiga toxin, respectively) that cause inflammation of renal microvasculature –> ADAMTS13 protein inactivation –> failure of cleavage of vWF multimers –> platelet adherence to vascular endothelium cannot be as readily reversed –> platelet aggregations protrude into vascular lumen causing shearing of RBCs flying past –> fragmentation of RBCs (schistocytes, aka helmet cells).

Shiga-like and Shiga toxins cleave the eukaryotic 60S ribosomal subunit, thereby interfering with protein translation.

Urease (+); can cause UTIs leading to struvite stones, same Klebsiella and Serratia.

Salmonella enteritidis and typhimurium cause food poisoning, resulting in bloody diarrhea. Acquired from consumption of poultry or eggs, as well as from interaction with reptiles (i.e., pet lizards, snakes, etc.).

Salmonella typhi causes typhoid fever, which is high fever + prostration (patient is lying down ill / in pain) + rose spots on the abdomen + either constipation or diarrhea. Humans are the reservoir for Salmonella typhi, and it is acquired via fecal contaminated food/water. It can remain latent in the gall bladder.

Pseudomonas

The mechanism for E. coli ETEC traveler’s diarrhea is heat-labile toxin that ADP-ribosylates adenylyl cyclase, increasing cAMP, as well as heat-stabile toxin that ADP-ribosylates guanylyl cylase, increasing cGMP.

In other words, HL toxin increases cAMP; HS toxin increases cGMP.

The HL toxin increasing cAMP is the same mechanism as cholera toxin (Vibrio cholerae); the difference is cholera causes profuse, high-volume stool, with liters and liters of rice-water stool, wheres traveler’s diarrhea, even if it is described as occurring 8-12 times daily (I’ve seen this on NBME), they will not describe it as profusely high-volume the way cholera presents.

The HS toxin increasing cGMP is the same mechanism as Yersinia enterocolitica toxin. The difference is the latter causes bloody diarrhea and pseudo-appendicitis (RLQ pain) or arthritis, whereas traveler’s diarrhea is not bloody.

Yersinia enterocolitica causes bloody diarrhea + either appendicitis-like (i.e., RLQ) pain or arthritis.

The RLQ pain is from mesenteric adenitis or terminal ileitis.

Toxin has same MOA as ETEC heat-stabile toxin (i.e., ­ ADP-ribosylates guanylyl cylase, thereby increasing cGMP).

There is an NBME Q where they tell you a patient was on antibiotics for a week + has bloody stool + LLQ pain, and the answer is C. diff, not Yersinia. C. diff can cause either watery or bloody stool, and sometimes pain. Pseudo-appendicitis due to Yersinia will be RLQ; it will not be LLQ.

Vibrio cholerae (cholera) presents as “liters and liters” of rice-water stool in someone who went traveling to, e.g., Mexico. Acquired fecal-oral (i.e., fecal-contaminated food/water).

MOA of toxin is same as ETEC heat-labile toxin causing traveler’s diarrhea, which is ADP-ribosylation of adenylyl cyclase (increases cAMP). The way you can differentiate this from ETEC traveler’s diarrhea is that cholera is notably profusely high-volume.

Both ETEC and cholera vignettes can tell you the patient has 8-12 stools daily, so it’s not the # of stools that matters; it’s the emphasis on volume. Cholera causes death via severe dehydration and electrolyte disturbance.

Tx is oral rehydration on USMLE; if patient has low BP or altered mental status (i.e., confusion/coma), IV hydration is done.

Tx for pulmonary abscess = clindamycin. Clindamycin is used for “anaerobes above the diaphragm” (metronidazole for “anaerobes below the diaphragm”). Some students have asked about potentially updated/alternative pharm for pulmonary abscess, but I can tell you clindamycin is all over 2CK NBMEs.