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- Border Collie 4 years AIHA (secondary, maybe)
Hi all,
my name is Alberto and I’m from Italy.
I’m the lucky owner of a Border Collie (beauty line) and he’s 4 years old.
On the half of April 2017 we saw him really depressed and tired and in a while, he started collapsing (he had a temperature of 40.3 more or less).
We took him in Clinic where the temperature was confirmed and he’s spleen was found bigger than normal. The day after (they told us) it was diagnosed piroplasmosis got from a tick. He wasn’t anemic but was a bit thrombocytopenic (he was at about 50.000 platelets).
He was treated with imidocarb and than with doxycycline antibiotic for a month. After a couple of days, his platelets were at 16.000 so they gave him cortisone (1st-day ad 1mg/kg/die and from the second at 2mg/kg/die).
In about a week platelets were ok, but his bilirubin climbs up from 2 to 5.9 and so his liver enzymes (alanine aminotransferase reached 5500).
On the 1th of May with blood panel correct (he was a 5mils blood cell and he had about 7mils blood cells on a couple of weeks before infection) we started reducing cortisone (less than 1/4) and from that moment blood cells started reducing from about 100k to 200k units a week so we reintroduced cortisone ad 42mg/day (2mg/kg/day).
We had no response for the next 20 days and on the 22nd of May (3 days after my daughter was born) they climb up to 5.3mills from 4.2 in 4 days.
Again from that moment up now we never had another increase in blood cells count. On the 1st of July we added to cortisone (2mg/kg/day) also ciclosporin 100mg (2 capsules/day) and also after that we got another strong reduction on the 10th of July, of blood panel 300k units in a week with haemoglobin at 9.7 and MCV (cell volume) of 78.6.
On the 27 of June, we also made an examination of the bone marrow and the response was (I hope the translation will be understandable): “Hemopoietic sample with adequate cellularity, with excellent preservation of cellular morphology. The myeloid relationship: erythroid appears to be increased. Depending on the erythroid series, moderately
represented, occasional episodes of erythrophagocytosis are observed. The granule-monocyte chain appears hyperplastic mainly in the maturation sector. The megacaryocyte chain also hyperplastic shows signs of obesity compatible with osteoclastic-like appearance. The
ancillary cells show a moderate infiltrate of plasmacellules and small lymphocytes. You do not observe neoplastic cellular infiltrates or etiologic agents. Conclusions: The overall picture appears compatible with a chronic flogistic process, nonspecific. With regard to the evidence of spherocytosis to the evaluation of the streak it is likely that anemia base and peripheral macrocytosis there is a chronic hemolytic picture. It seems appropriate
Do a search for anti-erythrocyte antibodies to test/exclude a possible immunomediated mechanism.”
Since then we have done no other controls and we are about to move to Padova for a full check up in one of the best clinics in Italy.
Meanwhile, we got a couple of stomach flu and a “light” pnemonia, but the dog seems to feel quite good – a little slowed but good.
By the end they think it might be an “Immunohistochemical hemolytic anemia” (hope is correct), they also thought it was secondary anemy due to piroplasmosis but they don’t understand if it’s the dog who doesn’t respond to ciclosporin, of if there’s another cause they can’t understand.
Thanks for you time and for reading. Any advice idea or suggestion is welcome. We only know we are not ready – as all of you I think – to let him pass aways.
Hope this might help.
Alberto
I just want to add that my boy is called Skye and in his bone marrow exam they revealed also:
anisocytosis; macrocytes; spherocytes and stomatocytes.
Thanks again.
We have a young baby, a girl Emma, and it’s hard to stand the idea that they might never make a run together…
Alberto,
Thank you for the complete history, this is very helpful.
This is actually babesiosis and is known in dogs while piroplasmosis is referenced in horses, not dogs. Similar diseases but babesiosis is what you are looking at now. Some breeds can actually be carriers of this disease, such as Pit Bulls, and pass it on during fighting with other dogs. It is certainly very well known in the US, with Greyhounds another breed severely impacted.
Babesiosis is a tick disease and the spleen is the organ that is most active in fighting it off. In fact, when the spleen must be removed due to illness in humans or dogs, doctors or vets will recommend that they avoid traveling to other countries where they can contract babesiosis, as the spleen has the greatest ability to control the disease. Without a spleen, it is difficult to survive this condition. Once the disease is brought under control by the body, it often remains dormant and can return in the future. Your vet used one of the most important drugs to fight it and I am so happy that they thought to use this.
So the spleen will be enlarged when there is infection by babesiosis. The spleen is a very active contributor to our immune system functions. It produces some of our white blood cells, it cleans the blood of old blood cells and it looks for and destroys RBC that contain parasites.
One of the routine functions of the spleen is to evaluate the health of RBCs. So when the body is at rest, the spleen will sequester a lot of blood. It has circuitous and convoluted pathways that require the RBC to squeeze through. Old cells fall apart and are scavenged for “parts.” RBC that contain parasites such as tick diseases will be destroyed by the immune system during this process. One sign that this is occurring is to see spherocytes in the blood. These are RBC that have had a part of them pinched off, or bitten off, by the spleen. They are smaller round, not concave, cells.
In IMHA, immune mediated hemolytic anemia and AIHA autoimmune hemolytic anemia, there is destruction of RBC in circulation. This can be assisted by the spleen. The spleen can become overactive and begin to destroy way too many RBC as well. In earlier times vets sometimes removed the spleen to stop this destruction. That surgery has mostly gone out of favor as it wasn’t shown to be completely effective in stopping the immune damage.
If you are offered to remove the spleen, I would get a second opinion. The spleen is particularly important in keeping the babesiosis under control.
A friend keeps a website about tick diseases and it would be important for you to read what she has collected.
https://sites.google.com/site/tickbornediseaseindogs/babesiosis
Now for the bone marrow. I actually have an important paper for you to read about the effects of babesiosis on dog’s bone marrow on our website. Go to this page:
https://www.secondchanceaihadogs.com/parasite-resources/
And scroll to the bottom and click on this paper:
Evaluation of blood and bone marrow in selected canine vector-borne diseases
It will open the paper in a small window, click on the arrow in the right hand corner to make it full screen. You can save and print the paper as you wish once you have done this. It is a difficult read and I don’t expect you to understand most of it, but I did want you to have something in your hand that mirrors the findings of your bone marrow biopsy.
If I could explain this the in a way you might understand, it would be to show you a picture of what the cells look like inside of the bone marrow. Each type of cell goes through a series of stages that transform it from the same basic template cell (precursor) to the mature stage. This should allow you to hover over these words and see a graphic of these cells: HSC Hematopoietic Stem Cells This is a simplified presentation of what is really a far more complex series of events. The bone marrow biopsy is looking at all these cells and evaluating the health of them and how many there are. Some are showing damage at certain steps along the way and that indicates maturation arrest. The immune system is responsible for this damage inside the bone marrow and is immune mediated bone marrow failure.
So what is the best treatment? I want you to read and print a protocol developed by Dr. Dodds of Hemopet.org. IMMUNE MEDIATED HEMATOLOGIC DISEASE and BONE MARROW FAILURE. Go to this page:
https://www.secondchanceaihadogs.com/hemopetresources/
click on the picture of the title of the protocol and it will open in the window, click on the upper right arrow to make it full screen.
This protocol is designed to hit the bone marrow with very high dose immunosuppressives. I used this protocol to save Chance’s life when he was diagnosed with a similar (but slightly different) bone marrow failure. Dr. Dodds helped me for a year while we treated him and his health was restored. The recovery happened specifically when I put him on this protocol and we introduced the high dose cyclosporine (Atopica) treatment. It took about 4 weeks at the PULSE DOSING treatment, which she outlines carefully in this protocol, make sure you vet sees this!
I also strongly suggest you contact Dr. Dodds for an owner consultation. She can further advise you on exactly how you should be dosing him with these meds and what the prognosis is that you can suppress the babesiosis sufficiently. The link to that site is on the same page, second from the top. Owner Consultation. It is $150 and she will evaluate your paperwork and advise you. She will even consult with your vet. Please let us know if you need help to do this.
Dr. Dodds saved many of the dogs that we have helped on this site. This is what she does all day long and has done for over 35 years, canine blood diseases and canine blood bank resources. She is compassionate and will be concerned about Skye.
Do you have more questions for me?
my best, patrice
First of all, thanks for your rapid answer and for the information. We are going to see our vet today and I’ll talk to her about this forum and you Vet reference.
It’s somehow less difficult to know that other people had to deal with the same horrific illness.
I just wanted to precise some elements that maybe in my first reconstruction seemed to be confusing.
Atm Skye feels “quite” well.
He walks, sometimes he plays with wood, he eats, he barks when he hears the door ring…
You wouldn’t say he’s sick if you don’t know.
What’s is really strange of his IMHA (if I understood well this is the correct name of his illness) are the following things:
– babesiosis seems to be completely defeated since the 2nd day at the clinic (there was no trace in blood and PCR made on the 29th of June was negative;
– his spleen is normal;
– his bilirubin value grown up after more or less a week from illness beginning passing from 3 to 6 in 3 days, but now is in range;
– his liver enzymes started growing up more or less with bilirubin a week after everything started, but now they are quite normal (only gamma GT are still high but slowly lowering);
– he got that form of “light” pnemonia that seems to mean that ciclosporin is working…
One of our most strange question is: ” where this destroyed blood go? No sign anywhere… is it possible is completely reabsorbed?
It seems we cannot arrest this slow continuos anemia (he never had a strong reduction of blood cells count)…
It’s hard, really (and I come from a family of Doctors) to understand what’s happening…
Ah… he had also a little liver damage.
This was the exam of liver function made on the 20th of July.
Lipase DGGR (IU/L): 36 (6-120)
Total Steel (μg/dL): 325 (100-220)
UIBC (μg/dL): 138 (140-250)
TIBC (μg/dL): 462 (300-410)
Saturation (%): 70.2 (28-60)
Ferritin (ng/mL): 176 (10-123)
Bile acids pre meal (μmol/L): 18.60 (0-9)
Bile acids post meal (μmol/L): 43.51 (0-30)
Nothing really serious but we decided to leave the azathioprine as last medicine to try.
Last time he made blood exams he also presents a low numbers of reticulocyte but thay told us it was because the haematocrit was only at 29.4 where only under the limit of 30 the bone marrow start to release them.
Here are the results (18th July):
RBC /μL 3.740.000 (5.100.000 – 8.500.000)
Hb g/dl 9,7 (11,5 – 18)
Hct % 29,4 (35 – 55)
MCV μL 78,6 (62 – 76)
MCH pg 25,9 (20 – 25)
MCHC g/dl 33,0 (30 – 36)
RDW % 11,4 (11 – 16)
Reticulocyte = 63.580/ul
CRP = 1,1%
RI = 0,6
WBC/μL 17.600 (6.000 – 18.000)
C. corr. WBC/μL 0
Neutrofil “banda” /μL 0 (0 – 300)
Segmented neutrophils /μL 17.248 (3600 – 14000)
Lymphocyte /μL 352 (1000 – 6000)
Monocyte /μL 0 (0 – 1600)
Eosinophil /μL 0 (0 – 1500)
PLT K/μL 417 (120 – 500)
MPV fl 5,5 (5,5 – 8,5)
Pct % 0,22 (0,1 – 0,4)
PDW % 12,6 (10 – 27)
Estimate PLT: adequate.
Thanks again
One last thing, sorry.
Skye has various allergies to plants and food (an exam told us, he had only some stomach problems in the past) that’s why we prepare his food by ourselves.
Than his 1st blood count recuduction happened in the same time we gave his the “interceptor” (med againstheartworm) and the collar “seresto” (http://www.seresto.it) used against tick and flea.
Thanks.
Update.
Things are getting more strange.
Today we made check and luckily the pneumonia is almost ok.
In the blood test, on the other hand, even with cyclosporine amount in blood = 500 (limit at 300), we got:
RBC /μL 3.900.000 (5.100.000 – 8.500.000)
Hb g/dl 10,2 (11,5 – 18)
Hct % 28,7 (35 – 55)
MCV μL 73,6 (62 – 76)
MCH pg 26,2 (20 – 25)
MCHC g/dl 35,5 (30 – 36)
RDW % 11,7 (11 – 16)
Reticulocyte = 89.700/ul
CRP = 1,5%
RI = 0,8
Total Proteins 8,0 g/dl
WBC/μL 18.400 (6.000 – 18.000)
C. corr. WBC/μL 0
Neutrofil “banda” /μL 0 (0 – 300)
Segmented neutrophils /μL 15.824 (3600 – 14000)
Lymphocyte /μL 1.104 (1000 – 6000) <—- even with cyclosporine and cortisone at top
Monocyte /μL 1.472 (0 – 1600)
Eosinophil /μL 0 (0 – 1500)
Basophil /μL 0 (0 – 400)
PLT K/μL 84 (120 – 500) <——-
MPV fl 6,5 (5,5 – 8,5)
Pct % 0,05 (0,1 – 0,4)
PDW % 12,5 (10 – 27)
Estimate PLT: adequate.
So what?
Should be allarming if count of piastins decreased from 417k to 84k, in just one week, with blood stabilizing…
Is this ever happened to you?
Thanks for you time. This illness it’s so hard to manage, everytime you think you got something good (like 4 month of good numebers in piastins or 1st sign of stabilization and than something worsening…) you get something terrible…
Alberto