scott@vtx-cpd.com
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Replying to Rosemary S. 01/11/2021 - 11:25
Hello.
Thank you for your brilliant question.
Bone marrow suppression, especially anaemia, is the most common clinical syndrome associated with FeLV infection, resulting from infection of both hematopoietic stem cells and bone marrow stromal cells. Most commonly anaemia will be non-regenerative. Progressive infection with active viral replication is usually required for bone marrow suppression. Regressive infection is only rarely associated with myelosuppression. Thus, in a FeLV antigen-negative cat with bone marrow suppression, testing bone marrow for FeLV by PCR is only sometimes helpful. The most common form of FeLV-induced anaemia is pure red cell aplasia, a severe nonregenerative anaemia with marked depletion and maturation arrest of erythroid precursors in the bone marrow (with the characteristic finding of a lack of reticulocytes but a high mean corpuscular volume [MCV]). Regenerative anaemia in FeLV-infected cats, indicated by increased reticulocytes and, in some cases, nucleated red blood cells (RBCs), is less common than nonregenerative anaemia and is often associated with coinfection with Mycoplasma haemofelis or other haemotropic Mycoplasma spp..
Some cats with immune-mediated haemolytic anaemia are progressively FeLV-infected, and in some, haemolysis precedes the emergence of myeloproliferative disease or lymphoma. This would be a specific reason to test in these cases.
Even if myeloproliferative disease was not to develop in these cases, the would be possible management benefits of knowing the FeLV/FIV status:
1. Progressively FeLV-infected cats should be kept indoors to avoid spread to other cats and exposure of the cat to other infectious agents carried by other animals.
2. βRoutine vaccination programsβ should be maintained in cats with progressive FeLV infection. They might not be able to mount an adequate immune response to vaccines and protection might not be comparable to that in a healthy cat. Therefore, testing for the immune response (e.g., antibody measurement after feline panleukopenia virus vaccine) and protecting against exposure should be considered.
Hope that helps a little.
Scott π
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This reply was modified 3 years, 4 months ago by
scott@vtx-cpd.com.
Replying to Ilse v. 31/10/2021 - 06:09
Hello.
This is a brilliant question that I am not sure I am going to be able to give a definitive answer to. The consensus statement states:
“We suggest that thromboprophylaxis be initiated at the time of diagnosis and continued until the patient is in remission and no longer receiving prednisone or prednisolone”.
I must admit that I often do not continue this long. The maximum risk period for mortality associated with IMHA appears to be the first 2 weeks after initiation of treatment. This period represents the phase when pathophysiologic risk factors for thrombosis are maximal, likelihood of transfusion is highest, and any prothrombotic effect of immunosuppressive medications is greatest, if related to dosage. The risk of haemorrhage from recommended antithrombotic dosages is likely to be small. As the disease process responds to immunosuppression, the likelihood of thrombosis may diminish, but the continued use of immunosuppressive medications may generate ongoing thrombotic risk. Some dogs may require lifelong low doses of glucocorticoids to maintain remission. We suggest that thromboprophylaxis be discontinued if such dogs have been in remission for 6 months and no other risk factors exist.
I would usually use a combination of rivaroxaban and clopidogrel. I would normally discontinue the rivaroxaban after the first couple of weeks and discontinue the clopidogrel once the weaning of the steroid dose starts.
Hope that helps.
Scott π
Replying to Rosemary S. 01/11/2021 - 11:30
Hey.
Really good question. I hope you are safe and well. The reasoning behind prophylactic use of omeprazole will be different between the Palladia and the NSAIDs. I presume the reasoning behind the use of omeprazole prophylactically with the Palladia will be to prevent gastrointestinal side effects. Although the NSAIDs will also cause gastrointestinal side effects, the mechanism of this is different with both drugs.
I must admit… I had to phone a friend with the actual answer to this question! I spoke to two oncology specialist colleagues, neither of them use omeprazole prophylactically with Palladia. If there is gastrointestinal upset with this drug, it is unlikely that the modification of gastric pH will help the situation. An antiemetic possibly, but often the drug has to be withdrawn.
Hope that helps a bit.
Scott π
Replying to Alison Docherty 01/11/2021 - 12:34
Hey Alison.
I hop you are well and enjoying the course.
I would also love to hear what everyone’s thoughts are. I tend to use the MILA systems for this. I really do love their products. They can be on the wee bit more expensive side, but I think works really well:
Hope that helps.
Scott π
Replying to Becky Cooper 01/11/2021 - 15:17
Hello.
I hope you are well. It was indeed! We had to do a bit of editing… not sure everyone needed to hear my social catch up with Mairi at the beginning!
Will be uploaded in the next couple of days.
Hope you are enjoying the course.
Scott π
Replying to Emma Holt 26/10/2021 - 20:05
Thanks Emma.
I would totally agree. I still always assess vulvar conformation in recurrent UTI cases.
I would indeed consider surgery where there were recurrent problems and everything else had been ruled out.
Hope you are enjoying the course.
Scott π
Replying to Synnove S. 27/10/2021 - 08:23
Synnove.
Thank you so much for your question and your kind words.
Regarding bladder wall culture, this really has to be a tissue biopsy. Taking a roll prep from the bladder wall surface would probably still only represent what was going on in the bladder. The culture really has to be from the tissue to get an understanding of what is going on in the actual bladder wall. This can be done with surgical or cystoscopic biopsies.
The main issue with treating the inflammation and not infection is that there are many other factors at play regarding host immunity that will also be dealing with the infection. Whether bladder colonization causes clinical disease ultimately depends on bacterial gene expression. Bacteria contain genomic islands encoding fitness factors that promote commensalism and/or virulence factors and dictate the severity of the UTI.
The NSAIDs are just dealing with the inflammation. The hope would be that multiple other body factors will be dealing with the infection. There is no doubt that these situations when there are clinical signs, will require antibiotics.
I hope that helps.
Let me know if you have any other questions.
Scott π
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This reply was modified 3 years, 4 months ago by
scott@vtx-cpd.com.
Replying to Jeanette Tungesvik 27/10/2021 - 13:24
Hello Jeanette.
This is a brilliant question. Basically, I would not treat in this case if there are no associated clinical signs.
Subclinical bacteriuria is not uncommon, even in individuals with no known predisposing factors. Rates of 2.1β12% have been reported in healthy dogs, with higher rates (15β74%) in groups such as dogs with diabetes mellitus,
morbidly obese dogs, puppies with parvoviral enteritis, dogs with acute disk herniation, chronically paralyzed dogs and dogs treated with cyclosporine or glucocorticoids. Study of subclinical. No evidence of an association between
subclinical bacteriuria and risk of development of cystitis or other infectious complications has been reported in dogs or cats, although study has been limited. A study of 101 healthy female dogs identified bacteriuria in nine (8.9%) and found no association with subsequent cystitis development over a 3 month follow-up
period. Bacteriuria was not associated with fever or survival in a study of paralyzed dogs. In humans, there is abundant support that antimicrobial treatment is not needed for asymptomatic bacteriuria. Treatment guidelines such as Infectious Diseases Society of America Guidelines for the Diagnosis and Treatment of Asymptomatic Bacteriuria in Adults and European Association of Urology guidelines on urological infections do not recommend treating asymptomatic bacteriuria in almost all patient groups. While treatment might eliminate the current bacteriuria event,
recolonization often follows. A systematic review in humans concluded that while bacteriuria may be
eliminated in the short-term, the effect is not sustained and recolonization is common, leading to no impact on overall morbidity or mortality.I would definitely not treat and monitor for now. I don’t think that there would be much value in culturing this sample.
Do you think the dog is underweight due to nutrition?
Hope that helps a bit.
Scott π
Replying to elaine elder 12/10/2021 - 17:52
Hey Elaine!
They do indeed! Various studies have shown that Ξ±2-agonists reduce the perioperative levels of stress-related hormones and thus attenuate the stress response of surgery in dogs. Alpha2-agonists, typically xylazine, have been reported to induce an increase in serum glucose by suppressing insulin release, stimulating glucagon release, or both, in Ξ² and Ξ± cells of the pancreas, respectively. However, medetomidine given at doses of 10 and 20 ΞΌg/kg BW, IV, decreased insulin values significantly but was not found to alter plasma glucose concentrations in normal beagles. Differences in plasma glucose concentrations are likely associated with the greater specificity of medetomidine, compared with that of xylazine, at the Ξ±2-adrenoreceptors. The hyperglycemia associated with xylazine has been attributed to the actions at both the Ξ±2- and Ξ±1-adrenoreceptors.
The following study did demonstrate this effect in cats:
Effects of dexmedetomidine on glucose homeostasis in healthy cats
Abstract
Objectives
Alpha(Ξ±)2-agonist administration has been documented to increase blood glucose concentrations in many species. The aim of this study was to further describe the effect of dexmedetomidine on glucose and its regulatory hormones in healthy cats.Methods
A randomized crossover study using eight healthy cats with a 14 day washout period was used to assess the effect of dexmedetomidine (10 ΞΌg/kg IV) and saline on glucose, cortisol, insulin, glucagon and non-esterified fatty acid (NEFA) concentrations at 0, 20, 60, 120 and 180 mins post-administration. Glucose:insulin ratios were calculated for each time point.Results
Within the dexmedetomidine group, significant differences (P <0.05) were detected: increased median (range) blood glucose concentrations at 60 mins (11.55 mmol/l [5.9β16.6 mmol/l]) and 120 mins (12.0 mmol/l [6.1β13.8 mmol/l]) compared with baseline (6.05 mmol/l [4.8β13.3 mmol/l]); decreased glucagon concentrations at 120 mins (3.8 pmol/l [2.7β8.8 pmol/l]) and 180 mins (4.7 pmol/l [2.1β8.2 pmol/l]) compared with baseline (11.85 pmol/l [8.3β17.2 pmol/l]); decreased NEFA concentrations at 60 mins (0.281 mmol/l [0.041β1.357 mmol/l]) and 120 mins (0.415 mmol/l [0.035β1.356 mmol/l]) compared with baseline (0.937 mmol/l [0.677β1.482 mmol/l]); and significantly larger (P <0.05) glucose:insulin ratios at 60 mins compared with baseline. Insulin and cortisol concentrations were not significantly changed after dexmedetomidine administration.Conclusions and relevance
Feline practitioners should be aware of the endocrine effects associated with the use of Ξ±2-agonists, particularly when interpreting blood glucose concentrations. The transient effects of dexmedetomidine on glucose homeostasis are unlikely to significantly affect clinical practice.Hope that helps.
Scott π
Replying to Anisha A. 14/10/2021 - 15:21
Hello Anisha.
I hope you are well and enjoying the course.
I put your question to Felipe in the live Q&A last night. It was the first question I asked him in fact!
The recording will be available by the end of the week.
If you have any other questions let me know.
Scott π
Replying to Rebecca C. 18/10/2021 - 19:16
Hello again.
Hope you are safe and well. I have popped some thoughts down regarding your other questions too:
The amount of blood vs. EDTA can definitely have am effect on the sample. What tubes do you use. It might be having a chat with the lab/manufacturer about the variability. Collection of a small blood volume with placement into a standard EDTA tube will cause shrinkage of red blood cells, because EDTA is hypertonic. This will cause a false decrease in the mean cell volume (MCV) and false increase in mean cell hemoglobin concentration (MCHC) of red blood cells. Crenation of red blood cells (echinocyte formation) will also be evident on the blood smear. This is a common artifact that we see in hematologic samples. Too much blood compared to EDTA will increase the risk of clot formation.
There is not an exact gauge guideline. Venipuncture should be minimally traumatic to minimize platelet activation and should be done using a minimum of a 23G needle, 21-22G is also fine for small animals. I would not go lower than 23G.
Regarding smears; any smears (blood or FNA) are best kept out the fridge once air dried. It is best to get them to the lab (as with everything) as soon as possible.
Hope that helps. Let me know if you have any questions.
Scott π
Replying to Shona M. 25/10/2021 - 19:04
Hey.
Our half term was last week in Scotland… so kids were not so much of an issue up here! π
Will get the recording up ASAP.
Scott π
Replying to Lesley M. 25/10/2021 - 19:46
Hey!
No pressure to speak. I am just conscious that I sometimes speak too muck and want to make sure people have time to ask questions too.
Hope you enjoyed the session.
Scott π
Replying to Emma A. 25/10/2021 - 23:51
Hello.
Thank you so much for your lovely feedback.
I will pass these questions on to Jon and get back to you ASAP.
Scott π
Replying to Anisha A. 14/10/2021 - 15:21
Hello Anisha.
I hope you are safe and well.
I will make sure to ask Felipe this question tonight at the Q&A.
Hope you are enjoying the course.
Scott π
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This reply was modified 3 years, 4 months ago by
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