Chiefs’ Inquiry Corner- 3/7/22

 Guidelines from the American College of Gastroenterology suggest holding proton pump inhibitors (PPIs) for at least 2 weeks prior to H. pylori noninvasive testing, as the medication is thought to directly suppress bacterial proliferation – note, the sensitivity is affected for the fecal antigen test as well as the urease based breath tests. Multiple studies examining sequential days of testing found increased rates of false negatives among patients until they were 14 days post-PPI.  The question of H2 receptor antagonist (H2RA) use peri-testing is controversial, and guidelines cite conflicting data regarding H. Pylori testing error while taking a high dose H2RA.  Nevertheless, it is suggested to hold H2RAs at least 24-48 prior to a urea breath test as the medicine has been shown to reduce urease activity.  For symptomatic patients awaiting H. pylori testing, consider utilizing antacids, like aluminum hydroxide, as they are considered to have no impact on results.

References: ACG Guidelines

 The Infectious Disease Society of America (IDSA) defines a recurrent case of C. diff infection (CDI) as an episode of symptom onset and positive assay result following a previously confirmed episode in the previous 2-8 weeks. CDI testing in general is quite complicated with conflicting approaches as to how to utilize the toxin testing in conjunction with PCR NAAT. One study at a single-center compared the need for treatment in patients who were toxin +/PCR + versus toxin -/PCR+, and they found that the toxin + patients had more CDI-related complications and diarrhea. The toxin -/PCR + patients actually had similar rates of GI complications to toxin -/PCR – patients. They concluded that the toxin testing alone may be sufficient for diagnosis. On the other hand, another group reported that the absence of toxin in the stool did not correlate with CDI, and they recommended that the NAAT should be used as the primary diagnostic method. They found no difference in toxin positivity in patients with mild vs. severe disease, ahd they also noted that toxin detection is limited by a relatively low sensitivity limit of detection. More recently, another group found that toxin A and B concentrations were not significantly different in patients who had active CDI vs those who were carriers (all with a + NAAT). The C diff toxin is also quite unstable – it can degrade at room temperature within hours of stool specimen collection, so false negatives can occur if the sample is not processed immediately or refrigerated until testing is completed. As with many other diagnostic decisions in medicine, it seems the best choice is to use a combination of clinical context and supportive laboratory data. 

References: Comparison of Clostridioides difficile Stool Toxin Concentrations in Adults With Symptomatic Infection and Asymptomatic Carriage Using an Ultrasensitive Quantitative Immunoassay

 Lemierre syndrome (LS) originates as a complication of bacterial throat infections – it is characterized by a thrombophlebitis of the internal jugular vein and evidence of disseminated infection (often septic pulmonary emboli). LS is most commonly caused by Fusobacterium necrophorum, an anaerobic, gram-negative bacilli that is part of the normal flora in the pharynx, GI tract, and female genital tract. It’s not clear as to whether F. necrophorum acts predominantly as a primary or secondary pathogen; in addition to direct infection, it’s postulated that mucosal damage of the pharynx caused by other bacterial or viral infections (e.g. streptococcal infection or acute EBV) leads to conducive conditions for a fusobacterial superinfection. Following epithelial invasion at the pharynx, F. necrophorum are believed to track along vascular planes, eventually invading the carotid sheath. Subsequent inflammation is thought to trigger a local hypercoagulable process, promoting thrombosis of the cervical veins and the release of septic emboli into systemic circulation. The most frequently affected organ is the lungs (85%), but joints, liver, kidney, brain, bones, heart and meninges can all be involved.

References: Lemierre Syndrome