The part of the cyclosporiasis outbreak no one is talking about | Opinion

Every summer now, it seems, we get the same headline: a cluster of cyclosporiasis cases traced to fresh produce, a recall, a brief wave of concern and then silence until next year. The news coverage almost always frames this as a food safety story – contaminated basil, bad lettuce, a supplier that slipped through the cracks.

I want to offer a different diagnosis, because I've watched this exact pattern before, in a very different disease, and I recognize it immediately.

Cyclospora cayetanensis has not changed. It hasn't mutated into something more virulent. It hasn't developed some new mechanism of transmission. Its biology is exactly what it was a decade ago: an oocyst shed in stool that requires days to weeks in the environment – typically through contaminated water used for irrigation or washing – before it becomes infectious to the next person who eats that produce.

This is a slow, environmentally dependent parasite with no capacity to outrun a functioning surveillance system. It has no ability to evolve its way past inspection.

It only needs one thing to spread further than it used to: for us to stop looking as carefully as we once did.

Cyclosporiasis isn't just a food safety failure

That's the part of this story nobody is telling.

Import inspection capacity, produce sampling at the border, the state public health labs running whole-genome sequencing to match an isolate from a sick patient to a specific lot number, the epidemiologists converting scattered case reports into a recognized cluster – this is the immune system protecting our food supply.

And like any immune system, when you starve it of resources, you don't get a healthier host. You get a slower, blinder response to a threat that was always there.

I recognize this pattern because I spent over a decade in HIV medicine, and Cyclospora is not a stranger to that world; it's classified as an AIDS-defining opportunistic infection. In a healthy adult with an intact immune system, cyclosporiasis is typically a self-limited, if miserable, illness.

In a patient with advanced, untreated HIV and a severely depleted CD4 cell count, that same unchanged parasite can cause weeks of debilitating diarrhea and wasting, and can become life-threatening without treatment.

The organism didn't change between those two patients. The infrastructure around them did, whether they were linked to care, virally suppressed and being monitored by a clinician who knew to test for it. I watched outcomes diverge for years based entirely on that infrastructure, never on the pathogen.

This outbreak is telling us the exact same thing, just outside the clinic instead of inside it.

Consider how contamination actually happens. Cyclospora spreads through fecal contamination of water in the field or during processing, which means the epidemiologic chain runs directly through the bodies of the workers doing the harvesting.

A field worker without bathroom access, without paid sick leave, without a doctor of their own isn't a bystander to an outbreak. Where that worker's health and safety end is exactly where the produce's contamination risk begins. We have built two separate monitoring systems – one for food safety, one for farmworker health – to track what is functionally a single point of failure.

Cyclosporiasis isn't getting smarter. Our infrastructure is weaker.

Even diagnosis reflects this divide.

Detecting Cyclospora requires a specific test – stool microscopy with acid-fast staining or targeted polymerase chain reaction – that a clinician has to actively think to order. A patient with a primary care relationship gets that workup completed.

A patient cycling through urgent care, or with no consistent access to care at all, gets sent home with a diagnosis of "viral gastroenteritis" and never enters the case count.

The number of confirmed cases we report every summer isn't a measure of how much cyclosporiasis exists. It's a measure of who had a doctor willing to keep asking questions – the same access gap I watched drive undiagnosed HIV for years.

And solving any of it – actually tracing an outbreak back to its source – is fundamentally a labor question. It requires interviewers calling patients to reconstruct meals from up to two weeks earlier, epidemiologists cross-referencing those interviews to find the common ingredient, and inspectors walking the distribution chain backward to confirm it. Every one of those is a funded position, and funded public health positions are often the first line item cut when budgets tighten.

When that workforce disappears, the outbreak doesn't resolve. It goes unsolved. The contaminated supplier keeps shipping. We simply lose our ability to prove where it came from.

Cyclosporiasis this summer is not a story about a parasite getting smarter. It's a sentinel event – the same warning sign that undiagnosed HIV gave us a generation ago – telling us that the public health infrastructure meant to catch threats like this before they reach a dinner plate is quietly failing.

The organism is constant. Whether we notice in time never was.

Tyler B. Evans, MD, MPH, DTM&H, is founder and CEO of Wellness Equity Alliance and the author of "Pandemics, Poverty, and Politics." He served as the first chief medical officer for New York City's COVID-19 response and has worked in global health across dozens of countries for nearly three decades.

This article originally appeared on USA TODAY: The part of the cyclosporiasis outbreak no one is talking about | Opinion

Reporting by Dr. Tyler B. Evans, Opinion contributor / USA TODAY

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This story was originally published July 16, 2026 at 1:49 PM.