For Clinicians | Strep Throat vs. Sore Throat

Do You Need Antibiotics?

By Dr. Jamie Wilkey, PharmD — Director of Clinical Strategy, Jase
Medically reviewed and edited by Kristen Carpenter, PA-C

Most sore throats don’t need an antibiotic. Most of us already know that.

What’s harder to keep straight is the one patient who does, and what happens if that visit gets waved through like all the others. A kid with a sore throat, no cough, tender glands, running a fever, looks almost exactly like the kid down the hall with a garden-variety virus. The difference matters for antibiotic stewardship and, more importantly, for their health. Untreated Group A strep can progress to rheumatic fever: permanent heart valve damage that can show up weeks after the sore throat is long forgotten. Rheumatic fever is rare enough in the US that a lot of us learned about it as a historical disease that isn’t around anymore. But, it isn’t gone. It’s just rare enough, and quiet enough, that it’s easy to lose track of why the testing and treatment ritual around strep exists.

Today we’re talking about the tool that resolves that tension: the Centor score (McIsaac-modified for kids), what it tells you, and why the treatment on the other side of a positive test hasn’t changed in decades.

Do you need antibiotics for a sore throat?

Most of the time, no. The majority of sore throats, especially in adults, are viral. As you know antibiotics don’t affect a virus, and prescribing one anyway doesn’t get the patient better faster. It just adds an unnecessary drug, and an unnecessary risk, to their day. And contributes to antimicrobial resistance.

But roughly 5-15% of adult sore throats, and 20-30% of pediatric cases, are Group A strep. Symptom judgment alone doesn’t reliably separate the two: exudate can show up with mono, fever can show up with either, and “it just looks bad” isn’t a diagnostic criterion. The actual clinical problem isn’t “treat everyone” versus “treat no one.” It’s how to tell, reliably, which patient in front of you is which.

The four-question tool: the Centor score

The Centor score, McIsaac-modified with an age adjustment, turns that judgment call into a short checklist:

• Tonsillar exudate
• Tender anterior cervical lymphadenopathy
• Absence of cough
• History of fever
• Age adjustment: add a point for ages 3-14, subtract a point for ages 45 and up

Add it up. The score runs from -1 to 5, and each end points to a different action. A score of 0 or below means under 10% odds of an actual GAS infection: treat it as viral, skip testing. A score of 4 or 5 means over 50% odds: test to confirm if you want, but treating before the result comes back is reasonable. Everything in between, 1 through 3, is the test-before-you-decide zone, where a rapid strep swab settles it.

Take a 52-year-old with a cough, no exudate, no tender nodes, and no fever: zero criteria met, minus one for age 45 and up, for a total score of -1, the bottom of the range. Skip testing. Now take an 8-year-old with exudate, tender anterior cervical nodes, no cough, and a fever: four criteria met, plus one for age 3-14, for a total score of 5, the top of the range. Test and likely treat.

Using this little checklist in practice cuts unnecessary initial antibiotic prescribing by close to half, without missing the strep infections that matter. It settles the question directly: which patient in front of you actually needs the prescription.

When to test, and when the rapid test needs backup

A score in the test-before-you-decide zone (1 through 3) means swab and run a rapid antigen detection test (RADT). 

• Positive RADT: treat. No backup culture needed, in adults or kids. The test’s specificity is high enough to act on directly.
• Negative RADT in children and adolescents: back it up with a throat culture before ruling out strep. RADT sensitivity isn’t perfect, and this is the population carrying most of the rheumatic fever risk.
• Negative RADT in adults: no backup culture needed. The downstream risk is low enough that a negative result can stand on its own.

In practice, a lot of this happens before you’re even in the room. Plenty of practices swab everyone with a sore throat during rooming now, since newer RADT platforms turn around a result in about 15 minutes, often faster than the visit itself. That’s fine: RADT specificity is high enough that a positive result still means treat, even in a patient who scored a 0 and never should have been swabbed by the letter of the algorithm. The score’s real job in that kind of workflow isn’t gatekeeping who gets tested. It’s telling you how much to trust a negative, and in whom.

Why penicillin, still, after all these years

Once you’ve got a positive result, the treatment hasn’t changed: penicillin V or amoxicillin for a full 10 days. Group A strep has never developed resistance to penicillin. Which is impressive since clinicians have been prescribing it for decades for this. There’s no clinical reason to reach for a macrolide or a cephalosporin here unless the patient has a true penicillin allergy.

The full 10 day course really does matter too. The rheumatic fever prevention data behind this whole guideline was built on the 10-day course, not a shorter one, and stopping early is still the most common way an adequately-treated strep infection turns into a recurrence.

The bottom line

Most sore throats are viral, and most clinicians already know not to reach for the prescription pad on symptoms alone. The Centor score turns that instinct into a number: four questions that tell you which patient is worth testing, and which one just needs reassurance and time. When the test comes back positive, the treatment hasn’t changed in decades: penicillin or amoxicillin for the full 10 days.

We built Jase on that same idea: don’t guess who needs antibiotics, use a real framework to decide. Appropriate medical preparation takes the same logic behind the Centor score, defined criteria instead of a feeling, and applies it earlier: deciding ahead of time which predictable, self-limiting conditions are safe to prepare for before symptoms even start. In no way a replacement for a clinician’s judgment call. Just that same judgment, applied sooner.

Sources

1. Centor RM, Witherspoon JM, Dalton HP, Brody CE, Link K. The Diagnosis of Strep Throat in Adults in the Emergency Room. Medical Decision Making. 1981;1(3):239-246.
2. McIsaac WJ, White D, Tannenbaum D, Low DE. A clinical score to reduce unnecessary antibiotic use in patients with sore throat. CMAJ. 1998;158(1):75-83.
3. Shulman ST, Bisno AL, Clegg HW, et al. Clinical Practice Guideline for the Diagnosis and Management of Group A Streptococcal Pharyngitis: 2012 Update by the Infectious Diseases Society of America. Clinical Infectious Diseases. 2012;55(10):e86-e102.
4. CDC. Clinical Guidance for Group A Streptococcal Pharyngitis.
5. Hamilton JL, McCrea L. Streptococcal Pharyngitis: Rapid Evidence Review. American Family Physician. 2024;109(4):343-349.
6. Gerber MA, Baltimore RS, Eaton CB, et al. Prevention of Rheumatic Fever and Diagnosis and Treatment of Acute Streptococcal Pharyngitis: A Scientific Statement From the American Heart Association. Circulation. 2009;119(11):1541-1551.

For Clinicians | Head Lice Myths

Permethrin Resistance, and What Actually Works Now

By Dr. Jamie Wilkey, PharmD — Director of Clinical Strategy, Jase
Medically reviewed and edited by Kristen Carpenter, PA-C

A few years ago when I was working as a pharmacist a patient handed me a small plastic baggie. I thought it was empty as I was holding it and she asked, “Is this lice?” I turned it over, looking for whatever she wanted me to see. She asked again: “Is this lice??” She’d pulled it from her daughter’s head and needed someone behind a counter to tell her what she was looking at.

I’ve had patients hand me a lot of things over a pharmacy counter. I’d never had someone hand me a baggie of lice and ask me to identify it. Every time lice comes up, I think of that baggie and patient. Patients are asking about this and as we are headed back to school this month it is the perfect time for a lice refresher course for all of us.

Is head lice a sign of a dirty house?

Nope. Lice don’t care how clean the house is, how often the kid showers, or how expensive the shampoo is. If anything, lice attach more easily to clean hair than dirty hair, so the kid who washes every night isn’t safer than the one who skips a day (or three).

They also don’t come from the family dog or cat. Human head lice are species-specific: they feed on human blood and can’t survive on fur. The lice that show up on pets are a different species entirely, and they stay on pets.

The couch, the car seats, the stuffed animals are also fine. Lice survive 24 to 48 hours off a human scalp, so that outdated bagging-everything-in-the-house instinct is solving a problem that doesn’t really exist. Head-to-head contact is how lice spread, almost always. Not shared hats, not the family dog, not the couch cushions.

The house is fine. The nit still in her hair might get her sent home anyway.

What the AAP says about nits and school

Quick refresher, since this is where most of the confusion starts: a nit is the egg, not the bug. It’s glued to a hair shaft close to the scalp and takes roughly a week to hatch. A live louse is the actual insect, crawling and feeding on the scalp. Finding a nit doesn’t mean there’s an active infestation, especially once hair growth has carried it away from the scalp. Most of the panic, and most of the school policy, is built on the wrong half of that distinction.

Plenty of schools still send a kid home for a single nit, or won’t let them back until every last one is combed out. That policy has been out of step with the actual guidance for going on two decades now, and the AAP tightened its language further in 2022.

The AAP’s clinical report states that children shouldn’t be restricted from school attendance over head lice, given how low classroom contagion actually is.¹ It goes further than earlier guidance, too: screening for nits alone isn’t an accurate way to predict which kids are or will become infested, and school nit-checks haven’t been shown to reduce how much lice actually circulates in a school over time.

The distance rule is specific: nits found more than roughly a quarter inch from the scalp are usually already hatched or dead. Diagnosis is supposed to rest on finding a live louse, not counting nits.

Empower a parent who’s arguing with a front office over a nit check with that information, and they have something to bring back to the school.

Why doesn’t permethrin work like it used to?

A parent buys the same box of Nix everyone’s grandmother used, follows the instructions exactly, and the lice are still crawling around seemingly unfazed. In most of the country that’s not user error anymore. Resistance is here!

A 2016 study sampled lice from 138 sites across 48 states and tested them for the genetic marker tied to pyrethroid resistance. The average resistance-allele frequency came back at 98.3 percent, and 42 of the 48 states sampled had populations at 100 percent.² Permethrin resistance isn’t a pocket problem. In most US communities, it’s the baseline.

That marker measures the gene, not the treatment outcome in any one kid’s head, so it’s not a guarantee that a specific box of Nix will fail. But at that frequency, reaching for permethrin as a first-line fix is closer to hoping than treating.

So what actually works?

When first-line permethrin or over-the-counter pyrethrins fail, the next rungs aren’t exotic. They’re underused mostly because parents, and a fair number of clinicians, still think of Nix as the only option.

• Benzyl alcohol 5% lotion (Rx): works by asphyxiating lice rather than poisoning them, so permethrin resistance doesn’t carry over. Two applications, a week apart.
• Malathion 0.5% lotion (Rx): an organophosphate, still effective against most resistant populations. Flammable formulation, so no hair dryers or open flame during application.
• Spinosad 0.9% topical suspension (Rx): kills both lice and eggs, often effective in a single application.
• Ivermectin 0.5% lotion (Rx): a single 10-minute application cleared lice in 74 percent of patients at day 15 in trial, against 18 percent for the vehicle control.³
• Oral ivermectin (Rx): 400 mcg/kg on days 1 and 8 beat malathion lotion for treatment-resistant lice in trial.⁴ No ovicidal action, so the second dose is what catches nymphs that hatch in between. Off-label for lice specifically, and generally avoided under 15 kg over a theoretical CNS risk.

The practical marker for when to move up the ladder instead of reaching for another box of the same product: check 8 to 12 hours after treatment5. A few lice still moving slowly is normal, the medicine just needs time to finish the job. It’s a different story if you don’t find any dead lice at all, or the live ones look just as active as before treatment. That’s the point to switch classes, not double the dose.

A pharmacist can walk a parent through this ladder at the counter faster than most primary care visits allow.

The bottom line

The myths about lice haven’t caught up to the evidence, and neither has the drugstore treatment that used to work. The no-nit exclusion was never real AAP policy. A second failed box of permethrin isn’t bad luck anymore, it’s the baseline. Next time a parent hands you a baggie and asks if it’s lice, you’ve got a straight answer for the house, the school, and the drugstore shelf.

Sources

1. Nolt D, Moore S, Yan AC, Melnick L; American Academy of Pediatrics. Head Lice. Pediatrics. 2022;150(4):e2022059282.
2. Gellatly KJ, et al. Expansion of the Knockdown Resistance Frequency Map for Human Head Lice in the United States Using Quantitative Sequencing. Journal of Medical Entomology. 2016;53(3):653-659.
3. Pariser DM, Meinking TL, Bell M, Ryan WG. Topical 0.5% Ivermectin Lotion for Treatment of Head Lice. New England Journal of Medicine. 2012;367(18):1687-1693.
4. Chosidow O, et al. Oral Ivermectin versus Malathion Lotion for Difficult-to-Treat Head Lice. New England Journal of Medicine. 2010;362(10):896-905.
5. Centers for Disease Control and Prevention. Treatment of Head Lice. cdc.gov/lice/treatment.

For Clinicians | Doxycycline Uses

Lyme Prophylaxis, Malaria Prevention, Acne, and the Doxy-PEP Debate

By Dr. Jamie Wilkey, PharmD — Director of Clinical Strategy, Jase
Medically reviewed and edited by Kristen Carpenter, PA-C

We’re continuing our series on the antibiotics we see most often come up in medical preparation conversations, one drug at a time. This week it is ….drum roll please…..doxycycline’s turn.

Doxycycline is basically the Swiss Army knife of antibiotics, except instead of a bottle opener and tiny scissors, you get malaria prevention and clearer skin. Want stellar proof? It works on Lyme disease protocol, a malaria prevention plan, an acne prescription, and now a post-exposure STI regimen. Doxycycline really does treat five unrelated problems. It isn’t that the drug just has killer marketing (although, it totally does that). It’s pharmacology: one mechanism, several targets, and, as it turns out, a guideline landscape that doesn’t fully agree on how to use it.

Take the tick bite question. The Infectious Diseases Society of America, the American Academy of Neurology, and the American College of Rheumatology all endorse a single 200 mg dose within 72 hours of a high-risk bite¹. The International Lyme and Associated Diseases Society doesn’t². Same drug and window, yet different answer depending on which guideline you’re using.

What is doxycycline used for?

More than you’d expect from one antibiotic. Doxycycline treats Lyme disease, prevents malaria, clears chlamydia, controls acne and rosacea, and, as of a 2024 CDC update³, prevents certain bacterial STIs after exposure in specific patients. 

That’s not doxycycline being a jack-of-all-trades in the vague sense. It comes down to mechanism. Doxycycline blocks protein synthesis in bacteria, the same core action tetracyclines have always had. It also disrupts a structure inside the malaria parasite called the apicoplast, a leftover organelle the parasite can’t survive without.

Quick reference: doxycycline by indication

Treatment: Lyme disease (a 10-day course performs as well as longer regimens⁴), rickettsial infections, chlamydia, and acne or rosacea.

Prevention: a single 200 mg dose within 72 hours of a high-risk tick bite, or daily dosing started before travel to a malaria-endemic area⁵.

Adjunct: reduces gum-pocket depth after periodontal treatment⁶.

Anthrax exposure: 100 mg twice daily for 60 days⁷., the CDC’s long-standing post-exposure regimen following high-risk Bacillus anthracis exposure. This one’s been on the Strategic National Stockpile for over two decades, not a new addition.

Emerging and debated: a single post-exposure dose to reduce the risk of certain bacterial STIs. That one’s newest, and it’s not settled, so it gets its own section next.

Five categories, one drug. Four of which are on well-worn clinical ground.

Where this fits into appropriate medical preparation

Three of these five uses are built for a standby kit: the single tick-bite dose, prescribed before symptoms show up; the pre-travel malaria regimen, started before a patient ever sets foot somewhere with risk; and doxycycline kept on hand ahead of a possible anthrax exposure. These work only because they’re prescribed ahead of need, not after.

That’s what we mean by appropriate medical preparation: a bounded, clinician-controlled step for conditions where the evidence is strong and the timing is predictable well in advance.

Acne, chlamydia treatment, and Doxy-PEP don’t fit that same frame. Each is answering a different clinical question, on a different timeline. None of this is a replacement for primary care. It’s the same clinical standard we’d apply at the time of symptoms, just applied earlier, for the narrow slice of doxycycline’s uses where earlier actually helps.

The bottom line

Doxycycline’s breadth isn’t hype or overuse. It has a great mechanism that allows one antibiotic to serve in several clinical roles since it blocks protein synthesis in bacteria and disrupts a different structure entirely in the malaria parasite. Most of that list is settled, well-worn clinical ground. Doxy-PEP isn’t. CDC’s 2024 guidance applies it to a defined population, adults with a bacterial STI diagnosis in the past 12 months, not sexually active adults broadly³. That population has already been redrawn once: WHO issued its own endorsement in 2026, broadly aligning with CDC, while Europe’s ECDC held back, citing resistance concerns over a population-level rollout⁸ ⁹. 

The uses that actually belong in a standby kit, prescribed ahead of need, are the tick-bite dose, pre-travel malaria regimen, and anthrax exposure backup. That’s the appropriate medical preparation slice of this list, and it’s the piece Jase is built around.

Sources

1. IDSA/AAN/ACR 2020 Lyme guideline, single 200 mg dose within 72 hours of a high-risk tick bite. Infectious Diseases Society of America. idsociety.org/practice-guideline/lyme-disease
2. ILADS treatment guidelines (the dissenting position). ilads.org/patient-care/ilads-treatment-guidelines
3. CDC Clinical Guidelines on Doxycycline Postexposure Prophylaxis, MMWR 2024. Confirms 200 mg within 72 hours, population is MSM and transgender women with a bacterial STI in the past 12 months. cdc.gov/mmwr/volumes/73/rr/rr7302a1.htm
4. Shorter versus longer antimicrobial therapy for early Lyme disease, systematic review and meta-analysis, confirming no significant difference between ≤10-day and longer courses. sciencedirect.com/science/article/abs/pii/S0732889324000440
5. CDC Yellow Book, Malaria chapter, chemoprophylaxis dosing and timing. cdc.gov/yellow-book/hcp/travel-associated-infections-diseases/malaria.html
6. Subantimicrobial-dose doxycycline (Periostat), FDA-approved 1998 as adjunct to scaling and root planing, reduces pocket depth. ncbi.nlm.nih.gov/pmc/articles/PMC6473443
7. CDC Anthrax Doxycycline Emergency Use Instructions, 100 mg twice daily for 60 days post-exposure. stacks.cdc.gov/view/cdc/56837/cdc_56837_DS1.pdf
8. WHO news release, first recommendation on doxycycline PEP, May 28, 2026. who.int/news/item/28-05-2026-who-issues-first-recommendation-on-doxycycline-post-exposure-prophylaxis
9. ECDC guidance on doxycycline for STI prevention, January 2026, recommends against population-level rollout. ecdc.europa.eu/en/news-events/ecdc-issues-guidance-doxycycline-sti-prevention

For Clinicians | Food Poisoning, Stomach Flu, or H. Pylori

Do You Actually Need Antibiotics?

By Dr. Jamie Wilkey, PharmD — Director of Clinical Strategy, Jase
Medically reviewed by Kristen Carpenter, PA-C — Clinical Advisory Board Member

Three patients, same complaint. One had a rough day after a backyard barbecue and is already turning the corner. One picked up whatever’s going around at daycare and brought it home to the whole family. One has lived with vague stomach discomfort for years. Ask any of the three if they have “a stomach infection” and they’d probably all say yes.

Only one of them actually does, in the literal sense. And not commonly tested for.

Food poisoning and the stomach flu get lumped in with real stomach infections constantly. Food poisoning and norovirus are usually done doing their damage by the time a patient’s in front of you, so there’s nothing left for an antibiotic to fix. There’s one specific presentation where reaching for antibiotics anyway doesn’t just fail to help, it can actively hurt the patient. And H. pylori sits underneath all of it: a real bacterial infection that can live in the stomach for years without a single symptom, then show up as heartburn nobody connects to the actual cause, and it’s the one of these three that almost always needs a real antibiotic course once someone thinks to look for it.

Getting this right changes what happens at the pharmacy counter and in urgent care. Here’s where the actual lines are for these top 3 ‘stomach bug’ presentations.

Do You Need Antibiotics for Food Poisoning or the Stomach Flu?

Almost never.
The reason is different for each.

Norovirus, the actual “stomach flu,” is viral. There’s no antibiotic target. Fluids and time are the entire treatment, and most people are through the worst of it in one to three days.

Food poisoning is where people expect a prescription and usually don’t need one. Most cases, Salmonella, Campylobacter, the toxin-producing bugs from undercooked meat or food left out too long, are self-limited in a healthy adult. IDSA’s own 2017 guidelines back this up directly: for uncomplicated Salmonella and Campylobacter in immunocompetent patients, the recommendation is supportive care, not antimicrobial therapy.¹ Antibiotics don’t reliably shorten the illness in these cases, and for Salmonella specifically, treating an otherwise uncomplicated infection can prolong how long someone keeps shedding the bacteria afterward.

There is only one big exception and that’s important for you to know. 

Bloody Diarrhea and Fever: Why Reaching for Antibiotics Can Backfire

This is the one every instinct in the room gets wrong, patient and clinician alike. Bloody diarrhea with fever looks like exactly the presentation that needs an antibiotic fast. It’s also the presentation where giving one, before you know what you’re treating, can make things worse.

The organism to worry about is Shiga toxin-producing E. coli, STEC, the kind behind most O157:H7 outbreaks. Killing the bacteria with an antibiotic can cause it to release more Shiga toxin as it dies, and that toxin is what drives hemolytic uremic syndrome, the kidney injury that’s the real danger here, especially in kids. CDC is direct about this: clinicians treating a patient whose presentation suggests STEC should know that giving an antimicrobial may raise the risk of HUS rather than lower it.² IDSA’s own guidelines back this with a strong recommendation: empiric antibiotics for bloody diarrhea, given before results are back, are not recommended in immunocompetent children or adults.³ For STEC confirmed to produce Shiga toxin 2, or when the toxin type isn’t yet known, IDSA goes further and says antimicrobial therapy should be avoided outright.⁴

The same logic applies to anti-diarrheal medications like loperamide. Slowing the gut down means the toxin sits in contact with the colon longer, and that’s also linked to higher HUS risk. The instinct to reach for Imodium while waiting on results is worth stopping while you’re at it.

This isn’t a blanket rule against ever treating bacterial diarrhea, and the mechanism explains why switching drugs isn’t a clever workaround: fluoroquinolones and trimethoprim-sulfamethoxazole are both potent triggers of the same bacterial stress response that ramps up Shiga toxin production. The largest look at real-world outcomes hasn’t found any antibiotic class that’s actually safer than the others. The safe default while you’re waiting on a stool culture and Shiga toxin testing stays the same: don’t treat empirically, and don’t reach for anti-motility agents, until you know what you’re dealing with.

1. Pylori: The Infection That Can Sit for Years Before Anyone Tests for It

This is the one that doesn’t announce itself. H. pylori can live in the stomach lining for years without a single symptom, then surface as heartburn, bloating, or vague upper-abdominal discomfort that gets blamed on stress, coffee, diet, or just getting older. By the time someone brings it up, they’ve often been living with it for a decade.

It won’t show up on a routine stool culture. Culture works by growing an organism, and H. pylori isn’t detected that way.⁵ Finding it takes a test built for it specifically: a urea breath test, which picks up the byproduct of the bacteria’s own urease enzyme, or a stool antigen test, which looks for H. pylori antigen directly. Either has to be ordered by name; neither is part of a standard workup.

The stakes here go past symptom relief. WHO’s cancer research arm classified H. pylori as a human carcinogen back in 1994, and the evidence has only held up since: it’s a major driver of non-cardia gastric adenocarcinoma, and nearly every patient with gastric MALT lymphoma tests positive for it.⁶ That’s the actual argument for testing someone whose “just stress” stomach discomfort has gone on for years, not just comfort, an infection tied to cancer risk that’s fully treatable once it’s found.

And when it’s confirmed, treatment isn’t a guess. Fourteen days now beats the older 7 to 10 day courses, eradication rates run meaningfully higher.⁷ Which drugs matter too: clarithromycin-based triple therapy only holds up where local resistance is low and the patient hasn’t had a macrolide recently, and bismuth-based quadruple therapy is the safer default when resistance status is unknown.⁸ This is a real regimen decision, not a reflexive prescription.

Quick Reference: Which One, Which Answer

Norovirus (viral “stomach flu”): No test needed in typical cases. No antibiotics, there’s no target. Fluids and time, usually resolved in 1 to 3 days.

Uncomplicated food poisoning (Salmonella, Campylobacter, toxin-mediated): Stool culture only if severe, prolonged, or high-risk. Antibiotics not recommended for uncomplicated cases in immunocompetent patients. Supportive care is the treatment.

Bloody diarrhea with fever (possible STEC): Stool culture plus Shiga toxin testing, ordered specifically, before treating. Avoid empiric antibiotics and avoid anti-motility agents like loperamide until results are back. Avoid antimicrobials outright if Shiga toxin 2 is confirmed or the toxin type is unknown.

1. pylori: Urea breath test or stool antigen test, ordered by name, not caught by routine stool culture. When confirmed, a real 14-day antibiotic course, bismuth quadruple therapy if resistance status is unknown, clarithromycin triple therapy only where local resistance is low.

What to Tell Your Patient

Most stomach bugs, the kind that hit hard and fast after a bad meal or a bug going around, don’t need antibiotics at all. Fluids, rest, and a few days usually settle it.

One exception: if diarrhea turns bloody and comes with fever, that’s a reason to call rather than push for an antibiotic. In some cases, antibiotics can make it worse instead of better, and that’s not an intuitive thing for a patient to already know.

The other stomach conversation to bring up: years of stomach discomfort chalked up to stress, coffee, or getting older is worth a specific test, not a shrug or an Rx for omeprazole. If it turns out to be H. pylori, it’s treatable.

The Bottom Line

Three complaints, one label, three different right answers. Most stomach bugs, viral or bacterial, resolve on their own and never need an antibiotic. The one case where reaching for one anyway can genuinely hurt a patient is bloody diarrhea with fever: test for Shiga toxin before treating, and skip the anti-motility agents too until you know what you’re dealing with. And the condition patients have been living with for years without a name, chronic dyspepsia blamed on stress or diet, deserves a specific test rather than another round of empiric PPI. If it’s H. pylori, a real 14-day course clears it.

Getting the label right is the whole job here. Getting it wrong either denies someone a cure they’ve needed for a decade, or pushes a treatment that makes a dangerous case worse.

Sources

1. IDSA, 2017 Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea: for uncomplicated Salmonella and Campylobacter infection in immunocompetent patients, the recommendation is supportive care rather than antimicrobial therapy, and treating uncomplicated Salmonella can prolong the carriage state: https://pmc.ncbi.nlm.nih.gov/articles/PMC5848254/
2. CDC, Information for Clinicians: E. coli Infection: administering antimicrobial agents to a patient whose presentation suggests STEC may increase the risk of hemolytic uremic syndrome; anti-motility agents in STEC infection may increase the risk of toxic megacolon, HUS, and neurologic complications: https://www.cdc.gov/ecoli/hcp/guidance/index.html
3. IDSA, 2017 Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea, Recommendation 30: empiric antimicrobial therapy for bloody diarrhea while awaiting diagnostic results is not recommended in immunocompetent children and adults (strong recommendation, low-quality evidence): https://pmc.ncbi.nlm.nih.gov/articles/PMC5848254/
4. IDSA, 2017 Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea, Recommendation 35: antimicrobial therapy for infections attributed to STEC O157 and other STEC producing Shiga toxin 2, or when the toxin type is unknown, should be avoided (strong recommendation, moderate-quality evidence): https://pmc.ncbi.nlm.nih.gov/articles/PMC5848254/
5. Merck Manual, Helicobacter pylori Infection: bacterial culture has limited use for H. pylori because of the organism’s fastidious nature; urea breath testing and stool antigen testing are preferred for initial diagnosis: https://www.merckmanuals.com/professional/gastrointestinal-disorders/gastritis-and-peptic-ulcer-disease/helicobacter-pylori-infection
6. National Cancer Institute, H. Pylori and Cancer fact sheet: the World Health Organization’s International Agency for Research on Cancer classified H. pylori as a human carcinogen in 1994; it increases the risk of non-cardia gastric adenocarcinoma, and nearly all patients with gastric MALT lymphoma show signs of infection: https://www.cancer.gov/about-cancer/causes-prevention/risk/infectious-agents/h-pylori-fact-sheet
7. Cochrane, Ideal length of treatment for Helicobacter pylori eradication (Review CD008337): across 45 studies, extending PPI-based triple therapy from 7 to 14 days raised the eradication rate from 72.9% to 81.9% (NNT 11): https://www.cochrane.org/CD008337/UPPERGI_ideal-length-of-treatment-for-helicobacter-pylori-h.-pylori-eradication
8. American Academy of Family Physicians, H. pylori Infection: ACG Updates Treatment Recommendations: clarithromycin should be avoided where local resistance exceeds 15%; bismuth quadruple therapy should be strongly considered first-line where clarithromycin resistance is high or with any prior macrolide exposure; no regimen achieves a 100% cure rate: https://www.aafp.org/pubs/afp/issues/2018/0115/p135.html

For Clinicians | Cyclospora 101

Transmission, Diagnosis, and Treatment Behind the Current Case Surge

By Dr. Jamie Wilkey, PharmD — Director of Clinical Strategy, Jase
Medically reviewed by Kristen Carpenter, PA-C — Clinical Advisory Board Member

Your patients have probably already asked about this one. A parasite outbreak, spreading state by state, case counts climbing every week they check the news. Now almost every case of diarrhea is getting extra scrutiny and worry.

Here’s what most of the coverage isn’t quite getting right. CDC has been direct about it: there is no evidence of a single Cyclospora outbreak linking all the cases making headlines.¹ What’s actually happening is several separate clusters, each under its own traceback investigation, landing in the same news cycle because they’re all surfacing in the same few weeks of summer. A single traceable outbreak comes with a recall and an end date you can hand a worried patient. Several under-investigation clusters come with neither, plus a parasite that’s easy to miss on the test most of us recommend first.

So this isn’t another case-count update article. It’s the backstory: what Cyclospora cayetanensis actually is, why it shows up every summer, why the two things patients think are protecting them aren’t, why a clean stool workup doesn’t clear it, how to treat it, and what to tell the patient who’s allergic to the first-line drug. That’s how we want to help this week, whether you’re seeing the patient in the office or filling the prescription at the pharmacy counter.

What Cyclospora Actually Is, and Why It’s a Summer Problem

Cyclospora cayetanensis is a single-celled parasite, not a bacterium and not a virus, and that distinction is exactly why the stool tests built for bacterial pathogens keep missing it. It gets into the body the way most foodborne illnesses do: contaminated food or water, usually fresh produce that picked up the parasite in the field before it ever reached a grocery shelf.

That’s also why this tends to show up in the warmer months instead of everywhere at once. Documented outbreaks have clustered in spring and summer, tracking harvest windows for produce implicated before: cilantro, basil, raspberries, snow peas, bagged salad mixes.² The parasite needs warm, wet growing conditions to survive on a leaf or in irrigation water, which is most of why the season tracks the produce. CDC itself is upfront that the seasonal pattern isn’t fully understood and can vary year to year.

Symptoms start an average of a week after exposure, with a range from two days to two weeks or longer,³ which is plenty of time for most patients to have forgotten which salad or smoothie they’d even blame by the time they’re in front of you.

The traceback complaints you’ve probably heard about aren’t a competence problem. Contamination happens upstream, on the farm or in the wash water, long before the product reaches a shelf. By the time a cluster gets reported, the implicated produce is usually gone, and the oocyst itself is hard to detect on food even when investigators know exactly where to look. That’s most of why this season, like most Cyclospora seasons, is landing without a single, obvious recall notice to point patients to.

Now remember,  this isn’t Giardia. Even though the two get confused constantly and both cause watery diarrhea traced back to contaminated food or water. Giardia shows up on a routine stool antigen test or standard multiplex panel without any special request. Cyclospora doesn’t.

Does Washing Produce Protect Against Cyclospora?

No, and this is the myth worth correcting every single time it comes up. Washing produce under the tap, even scrubbing it, does not reliably remove Cyclospora oocysts.⁴ Standard chlorine-based sanitizers, the same ones that work fine against most bacteria on fresh produce, don’t reliably inactivate this oocyst either. The only thing that reliably kills it is heat: cooking, boiling, baking.

That’s worth really communicating to a worried patient, because the instinct is to blame their own kitchen habits. They didn’t wash carelessly. The oocyst gets onto produce in the field or in irrigation water, well before anyone in their house ever touched it, and no amount of rinsing at home was going to undo that. This is a supply chain and traceback problem, not a hygiene-compliance problem, and patients need to hear that distinction instead of walking away thinking they did something wrong.

What About Person-to-person Spread?

The second myth is about who else in the house is at risk. Direct person-to-person spread is unlikely, and the reason is mechanical: the oocysts shed in a bowel movement aren’t infectious yet. They need roughly one to two weeks outside the body to sporulate before they can infect anyone else.⁵ A parent with cyclosporiasis is not a transmission risk to their kids the way a parent with norovirus is. The exposure that mattered already happened, probably at a meal everyone ate together, which is why cases often cluster by household without any household member infecting another.

The Symptom Pattern That Gets Mistaken for Recovery

Watery diarrhea is the leading symptom, often profuse and explosive enough that patients bring it up before you even ask. Most also report cramping, nausea, low-grade fever, and a fatigue that feels disproportionate to the diarrhea itself. Anorexia and real weight loss show up often enough to ask about directly. Blood or mucus in the stool is less common, and when it shows up, it’s worth considering whether something else, on top of the Cyclospora, is also going on.

The detail that matters most clinically is the shape of the illness, not just the symptom list. Left untreated, cyclosporiasis can run for weeks to months,⁶ and it rarely runs in a straight line. Some patients get a single, self-limited stretch that resolves on its own. Many more get a waxing-and-waning course: a few days of feeling noticeably better, then a relapse that brings the diarrhea and fatigue right back. That pattern is exactly what makes this so easy to write off. A patient who feels better on day ten looks recovered. A patient who’s still cramping on day twenty-five gets told it’s probably just taking longer than usual, or that it’s turned into post-infectious IBS. Neither read is wrong often enough to catch, because the actual explanation, an active infection nobody tested for, isn’t on either differential.

Watch this more closely in infants, older adults, and immunocompromised patients, where the same illness runs harder: more dehydration, more real malnutrition risk, and a rare but real mortality risk in the most vulnerable of that group.⁶

Does a Stool Culture or Routine O&P Detect Cyclospora?

Short answer: not reliably. Don’t assume a standard panel catches it.

A routine ova and parasite exam uses wet-mount and trichrome stains that Cyclospora oocysts don’t take up well.⁷ The organism can be there and still go unseen, or show up faint enough to write off as debris. Finding it reliably takes a stain built for this organism specifically, a modified acid-fast stain or a safranin stain, and neither is standard on a routine O&P order. It has to be requested by name.

Multiplex PCR panels solve part of the problem, but only if Cyclospora is actually on the panel. Coverage varies by manufacturer, and plenty of the GI panels in wide clinical use don’t include it as a target at all.⁷ Before trusting a negative PCR, confirm Cyclospora was actually one of the organisms that panel was built to detect.

Then there’s shedding. Patients don’t shed oocysts in every bowel movement, so a single specimen, even with the right stain or the right panel, can come back falsely negative.⁸ Microscopy-based testing typically needs specimens collected on separate days to be reliable; a targeted PCR is more forgiving and can often catch it from one well-timed sample. A patient with three weeks of symptoms and one negative stool study hasn’t been ruled out. They’ve had one attempt at the wrong test, or one attempt at the right test on an unlucky day.

Quick Reference: Ordering for Cyclospora

• Test to order: modified acid-fast stain or safranin stain on microscopy, or a GI multiplex PCR panel confirmed to include Cyclospora as a named target.
• Why routine testing misses it: standard O&P wet-mount and trichrome stains don’t reliably visualize the organism, and not every PCR panel tests for it.
• If microscopy is negative: don’t stop at one sample. CDC recommends three or more specimens spaced 2 to 3 days apart before ruling it out.
• If PCR is negative: confirm Cyclospora was actually on that panel. If it was, one well-timed sample is usually sufficient.

Cyclosporiasis Treatment: TMP-SMX Dosing, and What to Do for the Sulfa-Allergic Patient

Trimethoprim-sulfamethoxazole is first-line, and for most adults it works well. The standard course is one double-strength tablet (TMP 160mg/SMX 800mg) by mouth, twice a day, for seven to ten days.⁹ Most patients start feeling meaningfully better within the first few days. Patients with HIV may need a longer course to fully clear it.

The sulfa-allergic patient is the real open problem in this article, and it deserves a straight answer instead of a reassuring one. CDC’s own language here is blunter than most clinicians expect: no highly effective alternative to TMP-SMX has been identified.¹⁰ Ciprofloxacin gets reached for first, but the evidence behind it is thin. One small study in HIV-positive patients in Haiti showed modest activity, and against that sits a lot of anecdotal clinical experience suggesting it just doesn’t work well in immunocompetent patients. Nitazoxanide gets prescribed too, and it’s also less effective than TMP-SMX where it’s actually been studied.

So what do you actually do? For a patient who’s truly sulfa-allergic, CDC lists three real paths, not two backup drugs to cycle through: observation with symptomatic treatment while the infection runs its course, a trial of one of the less-proven antibiotics with the patient told upfront that it may not work, or referral for TMP-SMX desensitization. Desensitization doesn’t come up enough in conversations about this parasite, and it’s worth having in your back pocket for the patient who needs a real cure and can’t take the drug that reliably delivers one.

What to Tell Your Patient

First, washing all produce helps in general, just not with this one specific parasite. It’s not their fault, and it’s not a reason to scrub harder next time.

Second, they’re not about to infect the rest of the household. The exposure already happened, probably at a shared meal, and there’s nothing contagious about sitting next to them at dinner tonight.

If a stomach bug has dragged on more than a week or two, especially with cramping, fatigue, or weight loss that won’t quit, that’s not “give it more time” anymore. That’s “ask whether anyone’s tested specifically for a parasite.”

The Bottom Line

Cyclospora cayetanensis is having a real season, and the headlines are outrunning what’s actually confirmed about it. That part will sort itself out as the traceback investigations close.

What won’t sort itself out on its own is the diagnostic habit. A routine O&P or an untargeted GI panel can come back clean and still miss this. If a patient has weeks of watery diarrhea, cramping, and fatigue that won’t resolve, name the test: modified acid-fast stain, or a PCR panel confirmed to include Cyclospora. Treat with TMP-SMX first. And if the patient’s allergic to it, know going in that the backup options are weak, so observation, a documented trial of a less-proven drug, or desensitization done through an allergist, and only for patients without a life-threatening allergy, are the real conversation…. not a quick swap to ciprofloxacin and moving on.

That’s the difference between a case that resolves in a week and one that drags on for a month before anyone catches it.

Sources

1. CDC statement that there is no evidence of a single Cyclospora outbreak linking current cases, several clusters remain under separate traceback investigation, as reported by CBS News Texas, July 2026: https://www.cbsnews.com/texas/news/cyclosporiasis-texas-diarrhea-2026-cdc/
2. CDC, Clinical Overview of Cyclosporiasis: seasonality varies by setting and is not fully understood: https://www.cdc.gov/cyclosporiasis/hcp/clinical-overview/index.html. CDC, U.S. Foodborne Outbreaks of Cyclosporiasis, 2000–2017: past outbreaks have been linked to fresh produce including cilantro, basil, raspberries, snow peas, and bagged salad mixes: https://stacks.cdc.gov/view/cdc/118740 
3. CDC, Clinical Overview of Cyclosporiasis: incubation period averages one week, ranging from 2 days to 2 weeks or more: https://www.cdc.gov/cyclosporiasis/hcp/clinical-overview/index.html
4. FDA, Cyclosporiasis and Fresh Produce: standard washing and chlorine-based sanitizing do not reliably remove or kill Cyclospora oocysts; only cooking reliably inactivates them: https://www.fda.gov/food/foodborne-pathogens/cyclosporiasis-and-fresh-produce
5. CDC, About Cyclosporiasis: oocysts require roughly 1 to 2 weeks outside the body to become infectious, so direct person-to-person transmission is unlikely: https://www.cdc.gov/cyclosporiasis/about/index.html
6. Mathison and Pritt, “Cyclosporiasis—Updates on Clinical Presentation, Pathology, Clinical Diagnosis, and Treatment,” Microorganisms (2021): untreated illness may last weeks to months with a relapsing-remitting course, and runs more severe in infants, older adults, and immunocompromised patients: https://pmc.ncbi.nlm.nih.gov/articles/PMC8471761/ 
7. CDC, DPDx Cyclosporiasis: routine wet-mount, trichrome, and Giemsa stains are not adequate for reliable detection; modified acid-fast or safranin stains are required, and not all commercial multiplex PCR panels include Cyclospora as a target: https://www.cdc.gov/dpdx/cyclosporiasis/index.html
8. CDC, DPDx Cyclosporiasis: oocysts are shed intermittently and in low numbers, so a single negative specimen does not rule out infection; three or more specimens at 2- to 3-day intervals may be required: https://www.cdc.gov/dpdx/cyclosporiasis/index.html
9. CDC, Clinical Care of Cyclosporiasis: TMP-SMX dosing of one double-strength tablet twice daily for 7 to 10 days in adults, with longer courses considered for patients with HIV: https://www.cdc.gov/cyclosporiasis/hcp/clinical-care/index.html
10. CDC, Clinical Care of Cyclosporiasis: no highly effective alternative to TMP-SMX has been identified; options for sulfa-allergic patients include observation with symptomatic care, an alternative antibiotic supported by limited data, or TMP-SMX desensitization for selected, allergist-evaluated patients without a life-threatening allergy: https://www.cdc.gov/cyclosporiasis/hcp/clinical-care/index.html. The ciprofloxacin data point traces to a 2000 randomized trial in 42 HIV-infected patients in Port-au-Prince, Haiti: TMP-SMX outperformed ciprofloxacin, 95% versus 70% negative stool tests by day 7 (Annals of Internal Medicine, 2000): https://pubmed.ncbi.nlm.nih.gov/10836915/. Nitazoxanide as a sulfa-allergy alternative, with the caveat that treatment failure may occur, is per Mathison and Pritt (Source 6).