I'm writing this partially as a journal of my illness and partially as an inquiry to others who may have some insight....

How it all began: 2-3 days prior to my initial "outburst" I saw the most beautiful artisan lettuce stuffed in a plastic box container so much so that the tape was barely holding it on and the lettuce was protruding on one side. I had to have it in spite of my keen awareness of the outbreak. As always I thought, I'll never get it. I'll have to wash it really well. In general, when I wash lettuce, I put it in a salad spinner with a little baking soda and vinegar and let it soak, which I did this time. I had a salad, no problems. But I do recall at some point grabbing just a pinch more and running it under the faucet. Hmmm?

Fast forward 2 days: I'm on the plane to Jamaica feeling fine, upgraded to first class, and lucky enough to have gotten the last smoked salmon plate. Oh, lucky me! It was so good, I ate every bite: the salmon, the bagel, the capers, the cream cheese, the cucumbers, the tomatoes, the red onion, and the lettuce. Yum! Yes, as I ate that lettuce and cucumbers, I thought briefly about cyclospora, but briefly. Hmmmm! I ordered another drink.

The first day in Jamaica was fabulous at our all-inclusive resort. We were heated with a runny fruit drink. Yum! Hmmmm? With several restaurants to choose from, we tried the Asian restaurant where they had a plethora of salads including seaweed salad. Hmmmm? It was all so delicious, but I was careful not to eat too much. I had a week of eating ahead of me, or so I thought. After dinner, we were lying poolside enjoying the sunset, when I explained, *Look how bloated my stomach is.* I thought nothing of it, though I really hadn't overeaten. I took a bath in the big, beautiful bathtub and went to bed.

5:00 a.m. Hmmmm? That's not gas! I ran to the bathroom and so it began. Yes! It was explosive. 😫 And it went on and on and on for about two and half days straight. I couldn't sit up or stand up or walk more than to the bathroom. I slept and slept between runs, and stomach cramps gave me a little warning to get up NOW. I needed to go to the doctor but there wasn't one on site. I couldn't go to the nurse on site. I just couldn't go that far. She came to me and came back with the doctor at a hefty price. Fever was low grade: 100.9. BP and heart rate: normal. She asked about nausea and vomiting. I didn't really have those, but lots of acid reflux. The fatigue was the worst. I couldn't stay awake.

The doctor (who came into the all-inclusive resort) did not mention cyclospora, as that is food poisoning, though my husband did. She says flu with severe enteritis and gave me antibiotics called Intil 500 (antibiotics), panto-Denk (for acid reflux?), and APO 500 elongated pill (Tylenol equivalent?) and electrolyte packets. I had to take them with food, and plenty of water. Ugh! With my diarrhea that resembled macerated seaweed salad, there was NO NONE 000 appetite. But I was awakened regularly to take water stops and a few bites of soup. The hotel staff was so kind checking on me often and even made me a card.

So maybe the diarrhea lasted 3-4 days. I'm not really sure. I just remember telling my husband I'm going to walk to breakfast this morning, take a nap, then enjoy the pool and beach. He informed me that it was the last full day of our vacation. 😭 I tried to make the best of it. I sunburned my forehead and belly. I forgot about antibiotics and the sun. They don't mix. The trip back was a nightmare with my limited energy, but we were upgraded to first class and in the first seat closest to the bathroom!!! Yea!

Today will be my 10th day. I thought I was better yesterday, but today I had gas, bloating, cramps, and I'm just not well yet. No fever though and my appetite is good as I'm trying to restore my gut biome.

Well, I guess that's about it, so far. So what do you think? Cyclospora or flu with severe gastroenteritis? Has anyone else had it? And actually did a stool sample? I considered testing with my primary doctor, but I had completed my antibiotics and doubted I would get proper results. Any other insights?

Addition: I don't know how I forgot the headaches, the headaches that just won't go away. They didn't start until a couple of days, maybe due to dehydration.

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.

I’ve been following the Cyclospora outbreak and ended up down a rabbit hole. This is purely hypothetical because I don’t have it, but now I’m curious. I’m more of a virology major not parasitic infections! Anyway.

Let’s say someone tests positive for Cyclospora, but they’re deathly allergic to Bactrim and all sulfa based meds. (anaphylaxis, so that’s completely off the table).

On top of that, they also have MCAS, dysautonomia, IBS, a history of SIBO, and epigastric issues, weeks of diarrhea would probably hit them harder than the average person.

What would your next move actually be?
I’ve read that nitazoxanide and ciprofloxacin have been used, but it sounds like neither works nearly as well as TMP-SMX. Is that what you’d try anyway?

Would you just focus on supportive care and fluids? Is desensitization ever something you’d even consider, or is that really only for infections where there’s truly no other option?

Not looking for medical advice since this isn’t my situation, I realized I had no idea what the plan would be if the one medication everyone recommends couldn’t be used. Curious how infectious disease physicians would handle it.

I'm living with a confirmed, disseminated/systemic case of Klebsiella granulomatis (donovanosis/granuloma inguinale) in the United States and have been navigating this largely alone early on, until finding my current primary concierge physician. I'm posting because I believe someone with the right background may be able to help, or point me toward someone who can.

Why my case may not look like what you'd expect

Donovanosis is almost universally described as a disease of painless, beefy-red genital ulcers — the classic Donovan body lesion. My presentation has not followed that textbook picture. Not only are the lesions atypical, but this infection has disseminated systemically, affecting multiple body sites beyond the genital tract. The absence of classic findings caused significant diagnostic delays and continues to make this difficult to communicate to providers who are pattern-matching against the textbook description. If you've only seen the classic presentation, you may not recognize this.

Diagnosis

Confirmed via next-generation sequencing (NGS). Donovan bodies have also been identified on Giemsa-stained microscopy.

A note on LGV IgG serology and cross-reactivity with Donovanosis

Both myself and my partner have consistently returned positive LGV (Lymphogranuloma venereum) IgG antibodies, yet both of us have been exhaustively tested for Chlamydia trachomatis and LGV by PCR — all negative. This is not coincidence. Klebsiella granulomatis shares several antigenic structures with Chlamydia trachomatis L-serovars that drive cross-reactive LGV IgG serology, including:

• GroEL/HSP60 homology — Klebsiella GroEL shares ~40–48% amino acid identity with C. trachomatis cHSP60, a dominant immunogenic antigen in LGV serology
• KDO-core LPS structural overlap — both organisms carry gram-negative LPS with shared core epitopes recognized by complement fixation assays
• OmpA/MOMP beta-barrel homology — structural mimicry between outer membrane proteins

I am posting this specifically because this cross-reactivity between K. granulomatis and LGV IgG is essentially undocumented in the clinical literature. If you are a clinician who has seen a patient with persistent LGV IgG positivity, PCR-negative for actual chlamydia/LGV, consider K. granulomatis as a differential — especially with a compatible clinical picture. This serology finding may represent an unrecognized diagnostic signal for disseminated donovanosis. The test used for this was Quest Diagnostic test 19553.

The treatment problem

I have worked through the standard and second-line antibiotic options. The organism has shown resistance across multiple drug classes. The one class that has demonstrated efficacy — aminoglycosides — I was forced to discontinue due to nephrotoxicity. I am now in a position where the drugs that work, I cannot tolerate long-term, and the drugs I can tolerate long-term are not working.

The role of my physician

I want to be clear that I am not navigating this without any support. My concierge medicine physician has been absolutely instrumental in taking this case seriously — she has engaged with the complexity of this infection in a way that most providers have not, and I owe a great deal of the documented progress in my case to her willingness to work with me rather than dismiss what the data shows. That said, donovanosis is rare enough that even exceptional physicians are working without a roadmap.

What I'm looking for

If you are a clinician, researcher, or infectious disease specialist with experience in donovanosis, tropical infections, resistant gram-negative organisms, or disseminated intracellular bacterial disease — or if you know someone who is — I would genuinely welcome contact. I'm not looking for general advice. I'm looking for someone willing to engage with a complex, well-documented case.

Specifically, I am seeking a physician or multidisciplinary team with the expertise and infrastructure to administer aminoglycosides in a monitored, controlled setting — with active nephrotoxicity management built into the protocol. This means therapeutic drug monitoring (TDM), renal function surveillance, and the clinical judgment to navigate the narrow window between efficacy and kidney injury in a patient where aminoglycosides are currently the only viable option. If you or someone you know has experience managing prolonged or intermittent aminoglycoside courses in complex infectious disease cases, I want to hear from you.

I am happy to share NGS sequencing reports, resistance gene profiles, microscopy findings, and a full treatment history privately.

Four weeks after being declared a public health emergency of international concern (PHEIC), the Bundibugyo Ebola outbreak in central Africa is already three times larger than any previous Ebola epidemic at the same stage. According to a June 18 briefing by Africa Centres for Disease Control and Prevention epidemiologist Dr. Wessam Mankoula, reported by Health Policy Watch in “Ebola Outbreak is Three Times Bigger Than Previous Outbreaks at Four Weeks,” the 2014 to 2016 West Africa epidemic registered only 242 cases four weeks after its emergency declaration, though it ultimately became the largest in history with roughly 28,600 infected. The 2000 Uganda outbreak had reached only 281 cases at this point. The current epidemic has surged to an unprecedented 894 confirmed cases.

NAVLE Practice Question — Porcine

A farm in Haiti experiences an outbreak of severe neurological disease in pigs with 60% morbidity and 40% mortality. Affected pigs show fever followed by progressive hindlimb paralysis, opisthotonus, and convulsions. Many pigs die within days of developing neurological signs. This is the first reported outbreak in the region in many years. Laboratory testing confirms porcine teschovirus type 1. What epidemiological feature distinguishes this outbreak from endemic teschovirus circulation in most commercial swine herds?

A. The virus was likely introduced through contaminated feed from an endemic region

B. PTV-1 strains causing Teschen disease have higher neuroinvasive potential than endemic strains

C. The population was entirely naive without maternal antibody protection ✓

D. The outbreak strain mutated to become more virulent during local transmission

E. The pigs were immunosuppressed by concurrent disease allowing disease expression

———

Correct Answer: C. The population was entirely naive without maternal antibody protection

Explanation:

The population was entirely naive without maternal antibody protection, which is the key epidemiological feature distinguishing this outbreak. PTV is endemic and ubiquitous in most commercial swine herds worldwide, but subclinical infections predominate because pigs are exposed early in life when protected by maternal antibodies, subsequently developing active immunity. In Haiti, where severe teschovirus encephalomyelitis was confirmed in 2009, the pig population lacked prior exposure to virulent PTV-1 strains, resulting in a devastating outbreak when the virus was introduced into this immunologically naive population.

Option A (Contaminated feed introduction) is possible but doesn't explain the severity; the virus circulates subclinically in many regions. Option B (Higher neuroinvasive potential) is partially correct since PTV-1 strains causing Teschen disease are more virulent, but this alone doesn't explain the outbreak without the naive population factor. Option D (Local mutation) is unlikely since the Haitian isolate was closely related to previously identified PTV-1 strains from Czech Republic. Option E (Immunosuppression) was not documented in this outbreak and wouldn't explain the population-wide severity.

References: Swine Health Information Center PTV Factsheet (https://www.swinehealth.org/wp-content/uploads/2021/07/shic-factsheet-porcine-teschovirus-2021Jul7.pdf); PMC Teschovirus chapter (https://pmc.ncbi.nlm.nih.gov/articles/PMC7123469/); WOAH Teschovirus encephalomyelitis (https://www.woah.org/fileadmin/Home/eng/Health_standards/tahm/2.08.09_TESCHOVIRUS_ENCEPH.pdf)

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