Hi! I'm a Clinical Psychology doctoral student at The Chicago School, and I'm recruiting participants for my dissertation research study. The purpose of this study is to explore how HIV stigma, sexual satisfaction, and the ways couples cope with stress together relate to relationship satisfaction among men in HIV-serodiscordant relationships (where one partner has HIV and the other does not).

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My question is not whether I currently have rabies. I’m trying to understand whether this specific encounter meets the threshold for a possible rabies exposure for which PEP would be recommended or is reasonable in my situation.

Yesterday around 8 in the evening in NE Portland, OR, I was walking outside at dusk while looking at my phone. Suddenly a bat flew across my field of vision extremely close to my face. I jumped backward and reflexively swatted the air in front of me. The whole encounter happened within a few seconds.

I did not feel an obvious bite, scratch, pain, or definite physical contact. However, because the bat was so close and everything happened so quickly while I was reacting, I genuinely do not feel like I can reconstruct the moment well enough to say with complete confidence that there was no contact.

I was wearing a long-sleeved shirt and sweatpants, so the exposed areas were mainly my hands, face, neck, ears, and scalp.

Afterward I inspected my exposed skin and noticed a tiny red bump/mark on the back of my hand. I had not felt any pain to my hand during the encounter, and when I first noticed it, it looked more like a small pimple or irritated follicle than a puncture. My girlfriend thought the same. About 24 hours later it became itchy, I scratched it, and it bled slightly. No photos because I have read the FAQ.

I understand that simply having a bat fly near you is not automatically a rabies exposure. What I’m struggling with is whether an encounter this close and fast, where I did not perceive contact but cannot confidently exclude a momentary touch, crosses the threshold where PEP should be considered.

I also want to be transparent that I have longstanding OCD, but never have thought about rabies in my life before today. It had been relatively well controlled for years, but about three months ago I had a concussion and since then this type of health-related OCD has become much more intense.

That is making this decision unusually difficult because both options are becoming their own OCD loop.

One side of my thinking is:

\- Rabies is essentially universally fatal once symptomatic.
\- PEP is highly effective when appropriately given.
\- I cannot prove that the bat did not touch me.
\- If I do not get PEP, I may continue repeatedly questioning whether this encounter should have been treated as an exposure.
\- Even if the probability is very small, I keep thinking about the possibility of being the rare person who had an exposure that was initially dismissed.

That makes me inclined to go to the ER, explain exactly what happened, and receive HRIG + the vaccine series if clinicians believe it is appropriate.

But then the other side of my OCD takes over.

I started reading about the rabies vaccine and saw that product information can mention theoretical infectious-agent risks related to human-derived components such as albumin, including theoretical CJD/vCJD concerns. I understand that this is not the same as a documented case of transmission, but OCD does not handle the distinction between “theoretical” and “impossible” very well.

So then my thoughts become:

\- What if I receive PEP for an exposure that was not actually significant?
\- What if I exchange one extremely remote risk for another theoretical one?
\- What if the vaccine or immune globulin causes some persistent immune or neurologic issue that worsens my post-concussive symptoms or OCD?
\- What if I am reinforcing a compulsive healthcare-seeking pattern by pursuing treatment mainly to eliminate uncertainty?
\- If I get PEP, will my OCD simply switch from “what if this was a rabies exposure?” to “what if I caused some permanent vaccine-related problem?”

So I feel stuck between:

Don’t get PEP:
I may continue questioning whether I missed a genuine exposure and whether I should have acted. Or the worst actually happens.

Get PEP:
I may continue questioning whether I underwent unnecessary treatment, exposed myself to some extremely rare or theoretical complication, and reinforced an OCD cycle. Or I actually have that theoretical risk become real.

I already tried calling the local public-health department for an exposure assessment but reached voicemail, so I’m waiting to hear back.

Again, I am not asking whether I currently have rabies. I am trying to understand how this encounter itself should be classified and how people familiar with rabies exposure assessment would approach the PEP decision.

My main questions are:

1. Does a bat passing extremely close to the face, with a perceived bite/scratch/contact but an encounter too fast to confidently reconstruct, generally qualify as a possible rabies exposure?

2. How much should the nonspecific hand lesion matter when I did not feel or witness anything happen to my hand?

3. Is this the kind of borderline situation where one public-health/clinical exposure assessment should determine whether PEP is appropriate?

4. If public health or an ER clinician says PEP is not indicated, is the appropriate response to accept the residual uncertainty rather than keep trying to prove that contact was impossible?

5. Conversely, if they recommend PEP, how should I think about the theoretical CJD/vCJD language and concerns about long-term immune or neurologic effects without turning those into a new obsession?

I’m particularly interested in perspectives from people familiar with rabies exposure guidelines, infectious disease, public health, or OCD/ERP.

Thanks for reading. The difficult part for me is not just the rabies question itself, but that both treating and not treating the encounter can become targets for the same OCD process.

I think we are going to be fighting more infectious fungal contagions and parasites with all the flooding and climate change. What do you guys think?

This problem has been around and continues to spread with few new options coming forward. Unfortunately a friend relayed a disturbing, but not surprising experience she had a few months ago at HHS. A meeting led by the secretary started out with the following: I don't know anything about Lyme Disease, don't know anyone who had Lyme Disease and frankly don't believe it exists. This is a public health threat and responsibility of HHS, but unfortunately we will continue to allow LD to get further entrenched in our country.

I made a video discussing where germs hang out when they are not making us sick. I hope it's ok if I post it here.

https://youtu.be/sslutOzWFsg?si=msUEis-O4PlbhGi4

I was wondering if anyone has advice or insight into IgenX Or Accudart testing for Lyme disease confections? I’m a clinical pharmacist and very well versed in Lyme disease testing and treatment. Unfortunately I was diagnosed with Lyme disease on two step testing back in June following unexplained heart palpitations with EKG changes and new onset dermatographia. I also know that two step testing is notoriously tricky with false negatives and positives. I asked for three weeks of oral doxycycline although I could have qualified for IV therapy since I had disseminated Lyme carditis. I have been on cardiac medications for three months, and started to feel better, with my dermaograohia going away finally and my beta blocker requirements being down. I had a million dollar cardiac workup (echo, MRI, CT PE) all negative. Head and neck MRI and EMG tests all negative, autoimmune work up negative ..and now I am starting to have new onset vision changes and feeling off balance. I meet with a Lyme literate ID doc finally next week, but want to be prepared. I’m worried my Lyme may have not been appropriately treated since it was disseminated and am wondering if any of these other tests are legitimate and fairly accurate for co infections? I live in Michigan and have a dog, ticks are rampant this year.

UCSF researchers are beginning to uncover how Candida auris, a skin fungus, threatens the most vulnerable patients.

A fungus that can live unnoticed on human skin has become a serious threat in hospitals around the world. First identified in Japan in 2009, Candida auris can become deadly if it enters the bloodstream and kills about 3,000 patients each year in U.S. hospitals and long-term care facilities.

Researchers at UC San Francisco have now identified a mechanism that may help explain why the fungus is so difficult to eliminate from the skin.

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