Home Sickness
I had been working for 5 days before my first night on call. I was worried about how I’d handle an emergency, even though I was the backup vet on call. I think every new vet worries about these things. I secretly wonder if some of the more experienced vets worry about these things.
I had been feeling pretty good about surviving my first week as a vet, so as a celarbration I had bought a somewhat less-than-thrilling hamburger from the shop down the road. I regretted the burger when I was eating it (not at all worth $7). I regretted it even more as it left me puking my guts out every half hour, whilst suffering acutely violent diarrhoea from 8pm to 4am.
I was as sick as a parvo puppy and I was almost in an emergency clinic, not fit to be veting for one.I have odd thoughts when I’m being violently sick. I try to guess which species of bacteria it is that poisoned me based on the time of onset and duration of illness. I’m betting campylobacter. Its a lot more interesting when it’s not you with the symptoms, but you have to think of something at times like that.
Being so violently ill wasn’t quite what I had pictured when I thought I might get homesick.
I’m on call again tonight. I’m hoping that the phone doesn’t ring after mudnight. It’s a Friday, so I am making the generalisation that the people awake at that time aren’t going to be sober enough to notice something mildly wrong with their pets. If they do, it’ll be something just under $300 to get me out of bed in the tiny hours of the morning.
I’m a little bit worried about it, but at least I’m not puking my guts out tonight.
6 comments
Dr. Ferox, I’m sure you’ll do great in the event that an emergency situtation does come up, and yup, even the experienced emergency vets sometimes worry. I once had one of Moki’s vets tell me that experience doesn’t always mean you know the answer, it just means that some times your better at covering up the fact that you do not know…
On a different note, I had a question to ask you. After spending the past two years trying to figure out whats been going on with Moki, I think I have finally found the answer. It only took enrolling in a virology class to connect the dots…Anyway after reviewing Moki’s medical records for the millionth time, I noticed some thing that everyone seemed to have missed and that is that Moki was vaccinated with an FVRCP vaccination approximately two weeks before he got sick. Of course this now makes a vaccine induced version of Panleukopenia seem highly probable…
I know that with MLV vaccines, vaccince induced viruses can occur although be it rarely. I also know that vaccine induced viruses can cause nucleotide subsitutions to occur, but am not sure if these subsitutions occur within the vaccinated host, or during the manufacture of the vaccine itself. So I was wondering if maybe you could clarify for me at which point the subsitutions occur and how buddling viruses together into one vaccine might be affected by these subsitutions if they do occur during the manufacturing of the vaccine. I tired asking my instuctor, but he isn’t all that familiar with the bundling of viruses into one vaccine, he tends to be more familiar with human vaccines versus veterinary vaccines, so I was hoping maybe you might know the answer…
Hope that makes sense…
P.S.
Glad to hear your feeling better. Food poisioning is no fun. No fun at all!
The ‘vaccine induced viruses’ you refer to are a small but recognised risk of using modified live (aka attenuated) vaccines. During production of these vaccines, a given type of virus is grown through many cycles in a laboratory situation on a tissue culture. During the many replication cycles, mutations build up, initially randomly and then over time favouring the new mutants that survive and replicate best in the artificial environment (small-scale evolution). These adaptations that favour the new environment make the virus less suited for life in a living host, and eventually a strain is found that causes minimal or no disease at all in a host. This strain is then used to create the vaccine. The virus is still capable of replication and this replication drives a stronger immune response (which is why they’re used), as the body can detect more signals of infection. The slight risk is that during these reproductive cycles, the previous mutations can re-mutate which result in the virus in the vaccine producing a new strain which is capable of causing disease. It is most likely that this “reversion to virulence” as it is known will produce similar clinical signs as the original virus, although that isn’t guaranteed. This production process is performed separately for each virus that will go into the vaccine, and only mixed together once the strains are stable and right for packaging.
Specific answer 1: reversion to virulence occurs in the host not at manufacture, otherwise many animals exposed to the same batch would be affected. There are many monitoring and quality control systems in place to detect problems and minimise the risk of that happening.
Specific answer 2: recombination of multiple types of attenuated viruses used in a combination vaccination is not going to happen as the structure of the different viruses genomes are very different (Feline herpes- dsDNA, Feline calici- (+)ssRNA, Feline panleukopenia- ssDNA).
Having had a look at your blog, I wouldn’t think that a mutated panleukopenia infection from the virus would fit with Moki’s presentation particularly well, mainly with the relapsing nature of it. Panleukopenia is typically a very acute disease with recovery leading to complete clearing of the virus and a good immune response. And his improvement on the anti-influenza (very different type of virus) medication doesn’t fit very well either. Although the vomiting, bloody stools and diarrhoea etc do fit well! Herpesvirus infections can become chronic with relapses such as you’re seeing and is the FVR in that vaccine. Ultimately though as long as your thoughts on why things are happening guide effective treatment and help keep him happier and healthier, the rest is academic. Sounds like a very caring one when he’s unwell and a great life for Moki when he’s healthy
Hi Dr. Ugg,
Thank you so much for taking the time to write such a detailed and informative response. I found it most useful. I had suspected that the mutation took place in the host, for the reasons you stated, but wanted to confirm the notion with someone who knew a little bit more about it. (I myself am still a student and have much left to learn.)
With that said, here is the reasoning behind the panleukopenia theory:
1. Feral kittens are at high risk for immunosuppression. Moki entered the shelter as a feral kitten, which opens up the possibility that Moki was immunosuppressed at the time of vaccination.
2. At the height of moki’s illness a parvo snap test was administered. The parvo snap test came back negative. While it is possible that Moki was indeed free of parvo, there is another possibility which should be taken into consideration and that is, parvo snap tests can render false negative results if the virus particles are so thoroughly coated with antibodies that they cannot react with the chemicals of the test. At the time that the test was administered, Moki’s WBC was 0.7. Something was obviously depleting his WBC’s, so it stands to reason that if Moki did in fact have parvo, with his depeleted WBC, the virus particles would have been thoroughly coated with antibodies.
3. Given Moki’s age at the time of infection he may still have had some protection from passive immunity. This passive immunity in theory could possibly explain his initial short lived immune response as seen in step 2 above.
4. My understanding of the panleukopenia virus is that while the virus needs a host’s cell to replicate, it does not needs a host’s cell to survive in the system. With that said if Moki was immunosuppressed and the virus depeleted whatever passive immunity he had left, then the virus in theory could remain in Moki’s system until such a point in time that his immune system regained the ability to rid itself of it.
5. If we take into consideration all of the above possibilities, then the next question becomes why does Moki only appear to get better when on Tamiflu? I think the answer to this question can be found in a research article published in the Journal of Virology, titled “Host-Selected Amino Acid Changes at the Sialic Acid Binding Pocket of the Parvovirus Capsid Modulate Cell Binding Affinity and Determine Virulence.” According to the research conducted, “sialic acid is a common attachment factor for parvoviruses infecting different species…The treatment of susceptible cells with neuraminidase, which removes SA moieties from cell surfaces, abolishes MVM infection, suggesting that the primary receptors for MVM contains terminal SA residues.”
6. So with that said, if the above research is correct, if Moki’s own immune system couldn’t fight off the virus, then it would stand to reason that the virus could survive in his system for a period of time. The goal of the virus of course is to replicate, which would explain why initially Moki kept getting sick. Of course I didn’t see signs of the virus until it’s replication was well underway. When Moki did/does show symptoms, he was/is immediately put back on the Tamiflu which keeps the virus from replicating further.
7. As Moki has gotten older, he seems to be suffering from fewer and fewer outbreaks. I think this might be a result of an increased number of memory cells having been formed from prior outbreaks.
8. It seems to me that his immune response is still much slower than that of a normal cat, but has definitely improved with age. My guess is that we will continue to see improvement as he ages.
9. Now two interesting things to note are Moki’s cerebellar condition and Moki’s thoracic inlet condition. If Moki does in fact have a vaccine induced version of panleukopenia, it would stand to reason that at the age of vaccination (approx., 3 months, keeping in mind that this is an estimate because he was feral,) the virus would have attacked the cerebellum, since the cell line would have still be undergoing rapid division. As for the thoracic inlet, I am guessing that thoracic inlet problem is somehow related to panleukopenia’s known pattern of attacking the rapidly dividing thymus cell line.
Now of course all of the above is hypothetical, but it does seem to make some sense. ..Parvoviruses are known for mutating and if Moki has a vaccine induced version of Panleukopenia, it’s possible that the mutated version of the virus may not follow to a T all of the same symptoms of the original version of the virus.
As for the Herpes virus, it was a virus that we initially tested for, but all of Moki’s symptoms didn’t quite fit the viruses pattern. The herpes virus theory still left us seeking answers as to the cause of Moki’s neurological condition as well as his thoracic inlet issues…
After reading all of the above, maybe you can offer some additional insight or input. Again I am still just a student and there is much I could be missing, over looking etc. I’m just trying to hash out any and every possible explanation and leave no rock unturned in the process…
Thanks in advance for you input, interest, and response!
Thats a pretty comprehensive reply… The cerebellar hypoplasia (hadn’t got that far back in your posts earlier) is a classic outcome of a panleukopenia infection. I’m interested in what the orthopaedic problem / thoracic inlet issue is, but without radiographs its tough and if its beaten all of UC Davis, its out of my league! I haven’t learnt enough about the Tamiflu / parvovirus / neuraminidase link yet to make a truly informed comment. I’ve come across contradictory evidence about whether sialic acid affects parvoviral binding or not (”The Natural Host Range Shift and Subsequent Evolution of Canine Parvovirus Resulted from Virus-Specific Binding to the Canine Transferrin Receptor” stood out), but quite possibly that mechanism accounts for his improvement on the Tamiflu.
While antibody binding of viruses can block their detection in ELISA tests, I would have thought that with such a severe leukopenia, viruses would have been in excess. But thats just guessing now. So yes, negative Snap test doesn’t always = no virus.
One thing I struggle with is the idea of the virus persisting so well in the little guy’s body so long despite him recovering several times. Yes, the virus only needs cells to reproduce not exist, but normally (not necessarily applicable to Moki) clinical recovery is followed by complete elimination as circulating antibodies mop up any stray floaters. One possibility off the top of my head is the Tamiflu is interfering with the viral binding and release cycle and promoting its persistence within him, but your virology course probably sets you up better to assess whether thats a possibility or not than me.
Good to hear he has come so far through so much and is still such a wonderful pet. Good luck with him in the future and I hope he recovers permanently soon!
You know, you two seem to be handling this discussion well on your own. You should flick through moki’s brain scans Ugg, they’re quite interesting.
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