Home Forums General Discussion "Severe Anemia After Treatment of Babesiosis"

Viewing 11 posts - 1 through 11 (of 11 total)
  • Author
    Posts
  • #458169
    Suzanne
    Participant

    From The People’s Pharmacy:

    Severe Anemia After Treatment of Babesiosis

    “Severe Anemia After Treatment of Babesiosis
    Even after receiving appropriate and complete antibiotic treatment, some patients recovering from babesiosis develop severe anemia.”

    Mom of teen daughter with Poly JIA since age 2. Current med: azithromycin 250 mg MWF.

    #458171
    Maz
    Keymaster

    Unfortunately, the “appropriate” treatment may not be appropriate enough. Very often, long term combo antibiotics as needed for at least 4 months and sometimes in rounds, because this red blood cell parasite lives inside red blood cells and red blood cells have a lifespan of about 4 months.

    Regarding treating the chronic anemia after “appropriate” treatment for babesiosis, it’s worth looking at the Krause, etal, Studies of babesiosis patients who were asplenic or on immune suppressants were found to develop lymphoma.

    http://Www.pubmed.com/18181735

    It’s all a bit worrying, considering that the blood supply is not screened for babesiosis (last I read) and the very sick patients getting infected transfused blood end up in really poor shape. This happened to my gym trainer’s Mom, here in CT, who was hospitalized for severe anemia, given a blood transfusion and sent home. Days later, she broke out with a severe fever and it took several days, after she had to be packed in ice, to figure out what had happened.

    Agh…we don’t need a rotten Lyme season up here in the NE. I saw the Lyme article that you posted on the other thread, on the CNN website, today and was cringing. Thanks for posting it, Suzanne. It’s important info for all of us.

    #458172
    Suzanne
    Participant

    I had the same thought about what they might consider “appropriate” treatment. I also was surprised at how they treated the anemia – “Two-thirds of the patients in the report required immune-suppressing drugs to reverse their severe anemia.”

    Mom of teen daughter with Poly JIA since age 2. Current med: azithromycin 250 mg MWF.

    #458173
    Maz
    Keymaster

    Yes, surprising and very concerning. I wondered at the asplenic patients in the Krause study. Babesiosis can lead to autoimmune hemolytic anemia (infection in spleen), so did those patients lose their spleens to chronic previously undiagnosed babesiosis? Why in heavens name would they put someone who is already severely immune compromised on a biologic (Rituximab) drug? Just makes no sense. There is something very odd about the timelines of some of these studies.

    #458174
    Suzanne
    Participant

    I think the study was about people infected after they were on Rituxan or had their spleens removed. The study is saying they had the worst outcomes. I will read it again.

    Mom of teen daughter with Poly JIA since age 2. Current med: azithromycin 250 mg MWF.

    #458175
    Suzanne
    Participant

    “All case patients were immunosuppressed at the time of acute babesiosis, compared with <10% of the control subjects. Most case patients experienced B cell lymphoma and were asplenic or had received rituximab before babesial illness.”

    They were being treated with Rituxan for lymphoma when they got babesiosis.

    Mom of teen daughter with Poly JIA since age 2. Current med: azithromycin 250 mg MWF.

    #458176
    Maz
    Keymaster

    “All case patients were immunosuppressed at the time of acute babesiosis, compared with <10% of the control subjects. Most case patients experienced B cell lymphoma and were asplenic or had received rituximab before babesial illness.”

    They were being treated with Rituxan for lymphoma when they got babesiosis.

    Yes, this is what I’m questioning. If they were asplenic, why? Did they have previously undiagnosed babesiosis? If put on immune-suppressant medication (for lymphoma?), could latent babesiosis have been reactivated? How did they know the patients had been infected afterwards? Had they been tested for the infection prior to being put on Rituxamab? Babesiosis is a similar protozoan piroplasm as malaria, which can reactivate with signs/symptoms of acute infection, throughout life when a person is run-down. There are just a lot of assumptions and unknowns with this. I think to be convinced, I’d have to know if the patients had been tested for babesiosis prior to treatment with the biologic. What seems a bit too coincidental is that these patients all developed lymphoma, all had babesiosis and were all immune-compromised.

    There was a lady here with SD who later developed lymphoma and discovered she had co-existent babesiosis. She had achieved remission on AP for the SD, but the lymphoma was a later manifestation. Just have to wonder if there is some connection to lymphoma with babesiosis and that minocycline alone wasn’t enough to treat the babesiosis. Oh…lots and lots of unanswered questions.

    #458204
    Suzanne
    Participant

    Lymphoma patients may have their spleens removed as treatment.

    Mom of teen daughter with Poly JIA since age 2. Current med: azithromycin 250 mg MWF.

    #458206
    Maz
    Keymaster

    Interesting, Suzanne, thanks. Also interesting is that babesiosis can cause splenomegaly, sometimes requiring splenectomy. So my question is, which came first, the chicken or egg?

    https://www.ncbi.nlm.nih.gov/pubmed/21375849

    http://www.nejm.org/doi/full/10.1056/NEJMoa1612165#close

    http://www.annclinlabsci.org/content/38/4/390.full

    Forgive my digging around here….I’m a connect-the-dots kind of person. I think it’s so important for researchers to find root causes of diseases, like lymphoma, which can affect rheumatic patients. If a person has an undiagnosed tickborne infection, like babesiosis, and is then given an anti-rheumatic biologic drug, where the risk for lymphoma is increased by the drug, this is important to know. Also interesting is the proclivity of Lyme to infiltrate the lymphatic system and babesiosis is a common coinfection of Lyme disease. Helicobacter pylori, also a spirochete, has been implicated in malt lymphoma, so why not Lyme and other forms of lymphoma, as discussed in this study?

    http://www.bloodjournal.org/content/111/12/5524?sso-checked=true

    #458216
    Suzanne
    Participant

    What seems a bit too coincidental is that these patients all developed lymphoma, all had babesiosis and were all immune-compromised.

    [/quote]

    from the study: “We compared the immunologic status, clinical course, and treatment of 14 case patients who experienced morbidity or death after persistence of Babesia microti infection, despite repeated courses of antibabesial treatment, with those of 46 control subjects whose infection resolved after a single course of standard therapy.”

    It isn’t a coincidence if they were studying people who died (14) to compare to controls (46) who got better. Those who died, not surprisingly to me, had immune suppression in common.

    Researchers are connecting the dots. Here is an explanation (found within an abstract) of gain of function and loss of function mutations:
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4672729/
    Genetic alterations including missense/nonsense point mutations, insertions and deletions can bestow gain of function (GOF) or loss of function (LOF) activity on proteins expressed in hematopoietic cells. Such mutations can affect various functions of the immune system, including leukocyte survival and differentiation, antibody production, and/or cytokine signaling, compromising our ability to combat specific infections. Although the majority of PIDs are attributed to LOF alleles inherited in an autosomal recessive fashion, autosomal dominant GOF alleles have been implicated in several PIDs over the past decade (3). Although these GOF mutations are all hypermorphic, disease manifestations are often paradoxically linked to a greater susceptibility to infection or malignancy. This review highlights salient discoveries related to two recently described PIDs linked to definitive GOF mutations in key signal transduction molecules. Herein we examine underlying molecular mechanisms and shared pathological features that provide new insights on these distinct diseases and their clinical management. In doing so, we emphasize a common theme: immune signaling pathways are finely tuned, such that loss or gain of signal transduction capability can ultimately manifest as immunodeficiency. Although other GOF mutations are linked to multiple autoimmune and inflammatory disorders often classified as PIDs (3), these will not be discussed here.

    Mom of teen daughter with Poly JIA since age 2. Current med: azithromycin 250 mg MWF.

    #458222
    Linda L
    Participant

    “Two-thirds of the patients in the report required immune-suppressing drugs to reverse their severe anemia.”

    I don’t understand how they wanted to treat anemia with the immune-suppressing drugs. I was on MTX and Prednisone so many years and my anemia was severe all the time.

    RA tried everything: Methotraxate, Arava, Humira. Pneumonia three times. Anemia. Very low iron. Hypothyroidism
    AP from April 2014 till August 2015. No luck.
    Current medications: Natural thyroid, Mobic, supplements,
    vitamins and minerals.
    MTHFR heterozygous

Viewing 11 posts - 1 through 11 (of 11 total)

You must be logged in to reply to this topic.