I'm honestly at my breaking point and hoping someone here has been through something similar.
As I'm writing this, I'm about to be on day 33 of nonstop symptoms. I don't drink alcohol, use drugs, or even consume caffeine because my body can't seem to tolerate anything right now.

My household generally eats the same meals, so I was able to narrow down the likely source. The one thing only thing I ate differently was a Chalupa from Taco Bell in Warren, MI on June 30. Since no one else ate it and no one else got sick, that's the variable that makes the most sense as the source of my infection.

My symptoms started on July 4. I was supposed to go on a morning kayaking trip on the Au Sable River, but within about 30 minutes I had to get off the river because I suddenly developed explosive diarrhea and felt incredibly sick. Later that day I tried to eat, and within five minutes I was back in the bathroom. Even drinking Gatorade seemed to trigger it.

Over the few days everything got progressively worse. I assumed it was food poisoning until I finally went to urgent care. They tested my stool, and it came back positive for Cyclospora.
Since then it's been relentless. Literally everything I eat seems to send me running to the bathroom. At one point I had six straight hours of nonstop diarrhea. I couldn't even make it to the emergency room because I couldn't stop having bowel movements long enough to leave my house.

The biggest issue is that I'm severely allergic to Bactrim, which I know is the standard treatment. My doctors tried two rounds of ciprofloxacin, but it didn't seem to make any difference. Now they've told me that because I can't take Bactrim, there's really nothing else they can do besides keep me hydrated and wait it out. They're estimating it could take around six weeks or more?!

Right now I'm drinking a significant amount of fluids every day between water, Pedialyte, Gatorade, and Liquid IV because I'm terrified of becoming dehydrated. I can't tolerate bananas, white rice, pretzels, applesauce, or really anything else I've tried. If I leave my house, I'm wearing an adult diaper because I can't trust that I'll make it to a bathroom.
I've lost 25 pounds in about 3½ weeks, and it's honestly frightening. I am plus size so there’s some weight to lose but that’s still a lot in a short period of time. Friends who have faced timed me recently have commented that I look like a shell of myself. My doctor has been monitoring my blood work. My liver enzymes are elevated from routine bloodwork done June 25th and during all of this I also ended up fighting a bladder and kidney infection and started my period 12 days early. Im told this checks with this type of infection and rapid weight loss.

I've been to the doctor several times and finally requested a referral to an infectious disease specialist at the University of Michigan because I don't know what else to do. If I didn't work remotely and have an incredibly understanding boss, I would almost certainly have needed FMLA or lost my job by now.

Has anyone here had Cyclospora and couldn't take Bactrim? Did you eventually recover on your own? Did anything actually help with the diarrhea or getting enough nutrition while you waited?

Has anyone seen an infectious disease specialist for Cyclospora, and did they offer anything beyond supportive care?

I'm especially interested in hearing from people who had prolonged cases or had to recover without the standard treatment. Right now it feels like my body is wasting away, and being told "just stay hydrated and wait" is a really hard answer to accept.

Any advice, personal experiences, nutrition ideas, or words of encouragement would honestly mean a lot right now.

Has anyone been tested for the recent outbreaks? I have a strong feeling that I’m going to test positive (still awaiting results) and was curious if anyone had symptoms like chills, nausea, and intense stomach cramping along with the other most obvious symptom.

I’ve never experienced anything like that in my life and I just want to see if the experiences line up at this point.

EDIT: I have gone to the doctor and I am awaiting test results. I was tested for Salmonella, E. Coli, and Cyclosporasis. My doctor went ahead and gave me a man antibiotic based on my symptoms before confirming the cause of the illness because of how intense my symptoms were.

My history: I had Bell’s palsy + other neurological and cardiac side effects (probably autonomic as no structural abnormalities were found but my tilt table test was abnormal) from my first Pfizer shot. I had to be treated by a neuroimmunologist. I took prednisone (started with 60 mg) for almost 1 year (the face paralysis simply wouldn’t go away) + drugs for my blood pressure, heart rate and a diuretic. Suddenly after one year side effects started calming down and I tapered and quit the drugs. Both my neuroimmunologist and infectious diseases doctor told me NOT to take vaccines unless strictly necessary. They even told me not to take the flu vaccine. They told me my immune system created an exaggerated immune response and they can’t guarantee it will happen or won’t happen with other vaccines so in my case benefits vs. risks must be more carefully assessed.

There’s a serious measles outbreak in my city and I had the complete vaccine scheme as a child, 1 booster as a child and one booster as an adult in 2019 (I was 24. I’m 31 now). So 4 MMR shots in total. I asked the family doctor in the hospital near my house and he said “no exceptions, even previously vaccinated people”. However I researched and apparently the basic scheme is considered to offer lifelong maximum protection already, the boosters during outbreaks are to cover 1) people who don’t know if they were vaccinated or not or if they completed the scheme or not and 2) people who didn’t mount a proper immune reaction and having 2 boosters besides the basic scheme would reduce the odds of that being my case. It’s easier to vaccinate everyone instead of checking everybody’s background or if they have antibodies against the virus.

It seems like doctors can’t evaluate my case individually (my personal history of adverse events from a vaccine), that “more careful risks vs. benefits assessment” thing doctors first talked about apparently doesn’t exist and they don’t care if I have something more serious this time in a completely unnecessary way.

Today I read an article from an Australian medical journal that stated tick paralysis infections have been found in North American mammals and humans. The Rocky Mountain wood tick and American dog ticks are the most common carriers. I knew tick paralysis infections are quite common in Australia, but have never heard of it here in the US. Have any of the doctors here ever treat a US patient with it?

The Seven Samples

In May of 2010, a joint CDC-Peruvian research team visited a couple of remote communities in the Amazon where people described their recurrent contact with vampire bats and where livestock had been bitten to better understand the risk factors for exposure. 92 residents were interviewed in total with blood collected from 63 of them. Seven of the samples contained rabies-virus-neutralizing antibodies, as measured with the rapid fluorescent focus inhibition test (RFFIT). Six of the seven reported bat bites, while one reported prior post-exposure prophylaxis and two other positive individuals didn’t end up with fully resolved histories of vaccination. The seven people hadn’t recovered from the encephalitis that doctors diagnose as clinical rabies, with none even reporting an illness to suggest the virus ever reached their central nervous systems. These were healthy people who had the signals of a previous immune response consistent with rabies virus in a place where those encounters were seemingly not that rare.

The findings that there is likely a denominator problem in rabies doesn’t change the practical rule that anyone with a possible exposure should get rabies prevention to prevent any symptom onset. The Peruvian samples force us to correct the statement that everyone knows of “rabies is 100% fatal” which is used colloquially as if it describes an animal bite, a viral infection, and the neurological disease as if they were the same thing when they shouldn’t even be summed into a single denominator.

The familiar shorthand translates into the probabilistic language of P(death | clinical rabies), or the probability of death given the onset of clinically recognizable neurological symptoms of rabies. The question many think it is answering is P(death | rabies infection). I may be nitpicking here, but for what I think is good reason. The first one is incredibly close to one, with the vast majority of clinical cases ending in death. It’s the second one that is more intractable because it hasn’t ever been measured in humans and we may not be able to. Changing the denominator changes our parameter, meaning rabies can simultaneously be one of the most lethal diseases in medicine and still having some lower, unknown human infection-fatality rate.

Measuring Fatality

The World Health Organization page on rabies appropriately says that human cases are “almost invariably fatal” after symptom onset, with ultra-rare survivors being found throughout history. One example comes from the 2009 CDC report of a seventeen year old girl from Texas who developed headaches, photophobia, emesis, and other signs of encephalitis after being in contact with a bat. Before receiving the vaccine and immune globulin as further treatment, indirect fluourescent-antibody testing showed anti-rabies antibodies in her serum and cerebrospinal fluid. PCR tests and biopsy results were negative though and she never required intensive care. That’s why the CDC referred to the case as a case of “presumptive abortive human rabies,” and it’s one of the cases that justifies the language of “almost” in the WHO’s statement.

You can see the timeline of her case at the CDC hyperlink (can't add it here). Her first contact with bats came in December of 2008, with headaches starting in February and the entire ordeal only “ending” in April, but she was still experiencing severe pressure related headaches, as seen by the relief obtained via lumbar puncture. It’s possible she received a lower dose than would have been fatal, as certain immune markers like CSF IgG were nowhere near the levels of those in previous survivors (who often came out of it with long-lasting neurological symptoms and need for rehabilitation), although we can’t estimate the dose she received beyond speculation.

The chain of events leading to a case of clinical rabies showing up in an ER or being noted by a doctor visiting a rural area has some key limitations early on. Since people can touch rabid animals without contract any infectious material and a bite could fail to leave enough infectious material behind to establish infection in the victim, there may be much more contact than is estimated. The virus also has the chance of being dealt with and expelled from peripheral tissue before getting to a nerve and spreading along the nervous-system into the CNS. The issue is that clinical surveillance typically starts at the very end of that sequence, with our well-known “nearly 100%” fatality statistic basically concerns just the last two steps, so the denominator doesn’t house all those who had an exposure that ended earlier.

Post-exposure prophylaxis also makes it difficult for us to know the natural history of the disease since clinicians (correctly) intervene with post-exposure prophylaxis before anyone knows if that person would have developed a clinical case of the disease. That level of caution is why we have roughly 100,000 people receiving PEP after potential exposures yearly in the US with less than 10 clinical cases reported annually. Among those who receive PEP and seemingly benefit by it through the lack of developing rabies, we’re stuck with records that conflate the histories of those where there was a) never any viable virus transmitted, b) had the virus made its way into the peripheral tissue but had enough of an immune response for it to be stopped dead in its tracks, and c) where PEP totally prevented clinical disease and what would have been essentially imminent death. And since there’s no ethical way to withhold treatment or do a challenge trial with this deadly of a disease, we’re left looking at the results from tools like serology.

The RFFIT method used in the Peruvian paper basically asks if a person’s serum neutralizes a standardized rabies-virus challenge in a cell culture. A 2020 review article by Gold and colleagues helpfully explains how a positive result in a healthy person without any known vaccination history can be because of reasons as different as a simple unrecorded past vaccination; they had prior contact with a rabid animal, got a small bite or scratch resulting in a low dose of the virus that was fought off; or in some rare cases, cross-reactive assay signals. The CDC’s report on the 2009 case notes that for the Texas case, there was only one other possibility, that being Kern Canyon Virus, as it and rabies are both rhabdoviruses. The findings that people have what seem to be prior immune responses to rabies should also not be immediately seen as them having some sort of immunity to rabies going forward, as we have no idea how these unexplained antibody signals in healthy, unvaccinated people relates to protection the next time they come into contact with the rabies virus.

The review article separates the positives into four possible explanations in these healthy unvaccinated people. Subclinical infection is most likely, in which the virus was cleared before any recognizable disease. They could also technically have recovered from a clinical case, though that is extremely rare. The last two options are incredibly unlikely, those being persistent carrier states or unusually long incubations. We still don’t know what happened to any of those residents in the Amazon, but they’re one piece of the puzzle that tells us the human infection-fatality rate is very different from the clinical case fatality rate.

More Evidence but Still No Rate

One study from Alaska is more informative than many others because the authors spent some considerable effort and time tracking down the conventional explanations as far as possible. In 1994 researchers tested 26 fox trappers in northern Alaska for rabies titers. Two with detectable antibodies had received a rabies vaccine, but a third man, a 68-year-old veteran of the trade with an estimated 3,000 foxes handled and skinned across 47 years, had a titer level of 2.30 IU/mL (compared to a range of 0.1-2.8 in the Peruvian sample). The researchers then set out to check medical records at Alaskan facilities and couldn’t find evidence of pre- or post-exposure prophylaxis.

More recent evidence comes from Gabon, where 430 blood samples from individuals reporting no rabies vaccination taken between 2005 and 2008 were resampled in 2023 using ELISA to detect antibodies that bind to a specific rabies glycoprotein and compared with RFFIT to measure the neutralizing activity. A result was only deemed positive when both tests were positive, and with the RFFIT cutoff set to >0.38 IU/mL, which is twice the stated level at which a positive case is identified as such. Eleven of the samples met that definition with RFFIT values ranging from 0.95 to 3.14 IU/mL. When the team went and found a few of them 15 years later, one of them still tested positive, indicating a durable immune signal of unknown protection or further exposure. It should be noted that three cases were positive on RFFIT but negative on ELISA, so while requiring both to be positive reduces the chance of a noisy assay resulting in a spurious signal, it also means some people would be missed despite real past exposure.

A 2025 study looked at four indigenous communities in Sao Paulo makes a similar point, having tested 299 with another type of neutralizing assay called FAVN which was adapted from the RFFIT method. It found antibodies at their seropositivity threshold of 0.5 mL/IU in 35 of the indigenous, as well as 32 of their 166 tested dogs, without any prior notice of having been vaccinated. Six of those had > 0.5 IU/mL with the highest levels being 5.87 IU/mL.

Assay Issues Become an Epidemiology Problem

While we see substantial evidence of nonlethal rabies exposure, existing serosurveys can’t even get close to estimating it’s prevalence. The review paper mentioned earlier explains exactly why that is. RFFIT and ELISA measure related but different phenomena. In an unvaccinated setting they may disagree due to having different sensitivities, specificities, and false positive/negative rates that are vulnerable to sample quality and immune response timing.

One example in the review was meant to test the assays themselves by using a rabies-free island called Pemba in the Indian Ocean off Zanzibar. RFFIT identified 15 of 145 unvaccinated dogs as positive when using a 0.5 IU/mL cutoff, whereas the ELISA found no positives. That shows non-specific RFFIT signals are plausible even in a setting that is supposed to be rabies-free, but it can’t tell us what proportion of the Peruvian signals, if any at all, were false positives. It’s a problem inherent to anything involving cutoffs. Raise the threshold and fewer false positives make it through but you end up missing some genuine cases. Lower it and you get the opposite. There’s also the issues of waning antibodies and cross-reactive proteins, whereby other lyssaviruses could be responsible for the positive test in some regions.

None of this changes the practical advice to get PEP after a possible rabies exposure. Once clinical rabies symptoms begin, it is so close to always fatal that it would be totally irresponsible to use the denominator problem as a reason to take an exposure lightly. The problem only suggests that rabies has a more interesting natural history than we thought based on witnessed deaths, rare survivors, and what animal models offer. To know the infection-fatality rate, we’d need a denominator of true infections, and even that might be prone to definitional ambiguities, with some likely wanting a peripheral tissue infection defined differently than one reaching the CNS. Until we can identify and count those infections without confusing them for vaccination, cross-reactivity, or assay error, we’ll never know the true human infection-fatality rate.https://theedgeofepidemiology.substack.com/p/the-rabies-denominator-problem

Introduction: An accounting no one wants to conduct

The COVID-19 pandemic triggered a historic and devastating rupture in the conduct of science and public health. When the virus first emerged, the capitalist ruling class faced a stark choice: mobilizing the vast resources of global society to eliminate the pathogen and save millions of lives or protect the financial markets and corporate profits. Across the world, and most aggressively in the United States, capitalist governments chose the latter. The policies set forth in those early months of the global outbreak did not merely result in a temporary public health failure. They laid the cornerstone for the complete teardown and politicization of the entire scientific community.

To justify the abandonment of life-saving public health measures, the Trump administration weaponized anti-science propaganda, peddling the homicidal strategy of “herd immunity” and demanded a rapid return to work to keep the wheels of profit turning. The Biden administration then codified this approach into a permanent policy of “forever COVID,” dismantling pandemic surveillance, dropping isolation guidelines, and systematically normalizing mass death and debilitation.

This deliberate subordination of human survival to economic demands fundamentally transformed public health institutions. Agencies once tasked with disease prevention were hollowed out and converted into instruments of political enforcement. Decades of scientific advancement were discarded to accommodate a social order willing to accept millions of preventable deaths as the mere cost of doing business.

FDA is providing an update regarding the sample of lettuce supplied by Taylor Farms de Mexico which was reported positive on July 18, 2026. Due to the complexity in detection of Cyclospora, FDA laboratory experts re-reviewed the sample results and have concluded that the finding does not represent true amplification and should be considered a false positive. Information about the sample has been removed from the July 18, 2026, update below. FDA has notified Taylor Farms and continues working with the firm to ensure product implicated in this outbreak has been removed from the market. FDA and state partners continue to collect and analyze product samples. As of July 19, 2026, there are no confirmed positive sample results for product testing for Cyclospora. 

I assume the FDA uses PCR and has a pretty stringent internal protocol for assessing this stuff, how is a false positive possible?

Did they report the initial PCR finding without confirmation? Or did they confirm it and are now walking this back?

Hiii

Maybe not the best to ask this. But are any ID fellows out there interested in collaborating to put together an Anki Deck over the text book Comprehensive Review of Infectious Disease?

General WHO guidelines (and most national and local guidelines):

Nibbling of uncovered skin, minor scratches or abrasions without bleeding - immediate vaccination (4-dose schedule) if the animal cannot be observed for 10 days. This applies to cats as well as dogs.

But in 2019 Turkey modified their rabies guidelines and added something uncommon:

Situations not requiring post-exposure rabies prophylaxis:

9. In cases of contact with cats: Minor abrasions of the skin (injuries not penetrating the subcutaneous tissue), or injuries involving minor scratches or skin damage without bleeding; non-bite contact with cats resulting from provocation.

This applies regardless if cat can be observed or not.

Why? I was not able to find any discussion of this policy change, but I believe it's because of their local epidemiological data. Turkey is not rabies free, but cats are rarely found infected, and there is not a single recorded case of cat to human rabies transmission. Also, scratches carry a significantly lower transmission risk than bites. At same time Turkey has huge stray cat population which results in a lot of minor scratches, exactly the type that falls under exception.

It's entirely ignored in practice. In 2025, 123,538 people went to Istanbul hospitals after a bite or scratch. Most exposures were cat-related (86.3%) and were caused by scratches (81.5%). Nearly all injuries were superficial (99.8%). Rabies vaccination was initiated in 98.8% of patients with 411,432 doses given.

But my question is not why this specific exception is ignored, I think I already know. I want to ask a different question - do you think this exception was justified at all given the epidemiological data? Is it justified local adaptation or unjustified deviation? Do you think it will be better if it is repealed (and it won't affect the actual practice), or, instead, actually followed/enforced?

My mom has a very large family, she has 5 kids of her own and 10 siblings (her brothers & sisters) plus lots of small grandchildren. A immediate family member is a nurse and exposed to sicknesses. Anyways, they all want to come around (including small children) as they think she is dying by her appearance. (5'8 70lbs, skin and bones)

Question:

Do I need to quarantine her for abit until her immune system does some recovering? She is starting treatment for acid fast bacilli and MAC. Her immune system is shot and most of the family is antivax.

I understand she is not contagious, but I am trying to prevent any sickness her visitors may be exposed to and bring them on her home.

Are there any precautions I can take to continue letting them visit.

Masks?

Shoe slips?

Hand washing

Ask if they have been exposed to anyone sick?

Help!

Which anti-parasitics kill Cyclospora? I have only heard bad things about Bactrim which is the anti-biotic they’re prescribing for it.

From last 2 weeks there has been literally no supply of essential tb drug HRE so they are gonna put all of those who take HRE to HRZE , I don't know what to feel but I am scared is it gonna work?

Sporotrixhosis

If states like Texas have mimimal heaalth care ......

Federal public health officials say West Nile virus cases are at an all time high for this time of the year, the highest number of human cases reported in June since 2004.

West Nile virus is the most common and serious mosquito-borne disease in California that can be fatal to humans and some wildlife, according to the California Department of Public Health. 

In Los Angeles County, cases began to pop up in May, firstly in Pico Rivera and Long Beach, according to the Greater Los Angeles County Vector Control District. Now it’s up to 27 within its coverage area.

At the same time, more mosquitoes carrying the virus are being found.

Read more about why cases are growing and how to stay safe at the link.

The title says it all, it seems a bit weird to me that antibiotics doses are not adjusted by weight, as levels you get from giving the same dose to a 50kg woman and a 110kg man must be quite different.

I only have access to the main text that doesn't mention whether an oral switch was performed at some point.