posted
I'm writing for a friend who has a question about her babesia treatment.
She's been treated for Lyme for years. Recently, her FSH test was positive and her doctor pt her on a regimen of mepront, bactrim and ketek for babesia.
After 12 days of this, her symptoms (low grade fevers, fatigue, weakness, muscle and joint pain) seem to be getting worse. Her normal condition is so severe, that when she tells me she's getting worse, that's pretty bad.
She would like to know if this is a typical reaction or a sign that the regimen is not working. I thought that maybe she was herxing from her Lyme on this regimen, but she is clear that this is not what she feels like when she herxes from Lyme treatment.
Anybody have any thoughts about this? Thanks, Ellen
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Posts: 819 | From New York, NY | Registered: Oct 2001
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You didn't mention a rash so I would say her symptoms are a babesia herx. Several people including hubby have had possible allergic reactions to Mepron which usually show up on Day 10 of treatment.
See the thread below regarding artemesinin and babesia herxes.
Bea Seibert
Posts: 7306 | From Martinsville,VA,USA | Registered: Oct 2004
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Tincup
Honored Contributor (10K+ posts)
Member # 5829
posted
Yo Bozo...
I am not experienced with using Ketek/bactrim with Mepron. I used Zith and Mepron. Herxing was on the 4th day (for at least a week to 10 days).... and again on the 30 day.. like clockwork for me.
Now.. this could be a herx she is having.. the symptoms sound like they fit with Babs stuff... and with them getting worse after starting meds, it would make it seem they were "acting" like a herx...
However... thought here...
Since she is normally quite bad.. could it be she didn't notice the herx like symptoms building up any sooner than the 12th day? Or did she wait to say "Uncle" because she is tuff spirited and was holding her own till now?
Gotta think this out... hmmmmmmmmm...
Ya know.. sure as I am sitting here...
I wouldn't hesitate to give the doc a ring a ding... oh ding a ling.
I don't want to assume it is a herx like reaction because to ME it isn't a "clear cut" thing or something I see regularly when folks herx.. so best take care and call the doc.
Chances are it could be a herx... but I don't want to climb out on that limb. And you know I would if I could.. cause I don't like to call the doctor!!!
One last thought...
HA! Forgot it that quick...
Oh... well... bells on butterflies.. forgot again!
OK.. I don't tend to lean to the side of the regimen not working for her. But.. I do want to add...
If she is getting Lyme worse... which I think from your writing she doesn't think so??? Well...
Has she been treated for Bartonella? I just saw a DVD thingy (lecture) where Dr. B noted that folks who relapse quickly when off Lyme meds.. ya might need to check for Bartonella in that case. Also.. temps/fever.. if higher in the AM.. think Bart.
No matter what it is.. if she gets any worse.. do call the doc. Otay?
She may need to back off meds and let the "gunk" clear out a bit.. then go back on. I know Dr. J (NC) is now doing three weeks on.. one off.. for that purpose. Finding month round very hard on some folks.
Hope that helps some. But most of all.. I hope she feels better soon.
posted
Babesia herxes are different from Lyme herxes. I would agree with backing off the meds a bit and see if she feels better. Then she will know if it's a herx or not.
Those meds can cause pretty rough herxing. But yes, have her run it by her dr just to make sure of what to do.
-------------------- --Lymetutu-- Opinions, not medical advice! Posts: 96227 | From Texas | Registered: Feb 2001
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david1097
Frequent Contributor (1K+ posts)
Member # 3662
posted
I think you have already answered your question.... Ketek.... Did she ever have it before? Ketek can result in a pretty bad symtom flare of the lyme symptoms. Also the change in antibiotics (if it as been changed) can accentuate the regular flareup cycle so you should compare the timing with the ones before the start of treatment.
I am leaning to a antibiotic lyme effect since I have restarted mepron/ketek 3 times, 2 of those for severe relapse. None resulted in the herxhiemer effect. I just got better. Some claim a herxhiemer effect but I have been unable to find any published information indicating that this happens, even for quinine based treatment or malaria treatment. Thus my tendency to attribute the observation to a change in antibiotic.
If someone has information on herxhiemers and babesia please sound in as I would really like to figure this one out.
Posts: 1184 | From north america | Registered: Feb 2003
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Michelle M
Frequent Contributor (1K+ posts)
Member # 7200
posted
Well, I haven't got any research cause no one seems to think it's important enough to spend any money on, a'course.
However, I was pretty bad before starting Mepron/Zith/Art. As in daily headaches, brain fog, limping through workday.
Discovered babesia WA1 and added the babesia meds about six weeks ago. In short order, my headaches went from a 7 to about a 15 (on a scale of 1 to 10). It became so bad I thought I would have a stroke and die. I sort of mumbled for days and walked around holding my head, considering a visit to be ER to be knocked out with a shot.
It let up, and things improved greatly.
It hurt even worse than lyme herxes have hurt, if possible.
I'm definitely convinced.
I am negative for bartonella.
Of course I agree she should check with her doctor; however, I'd give it more time as things may soon get MUCH better.
I hope so!
Michelle
Posts: 3193 | From Northern California | Registered: Apr 2005
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groovy2
Frequent Contributor (1K+ posts)
Member # 6304
posted
I agree with Michell
Babs herx was WAY worse than Lyme Herx for me--
Feels diffrent too-
I had a bad migrane for 19 solid days 24X7--Was worth it tho--
Babs was By Far my worst bug-- Hang in there--Jay--
Posts: 2999 | From Austin tx USA | Registered: Oct 2004
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trueblue
Frequent Contributor (1K+ posts)
Member # 7348
posted
Ellen, I have long untreated Babesia and started taking just Artemesinin a week ago. Not even up to the part where I add in the anti-malarial and the Ketek.
I suppose it's not called a herx with Babs but I'm having a similar experience as your friend with only 200 mgs of Artem.... a day. Also lot's of shaky, waves of whoozy feeling, weird breathing problems and nausea.
Apparently, hitting on Babs is very, very different than anything I've dealt with with lyme.
I began to feel really bad on the 4th/5th day like TC said and am waiting until it lets up.
It sounds to me and feels like something is working but would also call the doc and make sure it's not too much at once, considering.
I hope she feels better soon.
-------------------- more light, more love more truth and more innovation Posts: 3783 | From somewhere other than here | Registered: May 2005
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JimBoB
Unregistered
posted
I STILL can't figure out why some people are STILL hell bent on a killer drug like Ketek. But that being said, IF I were her I would call her doc the first thing Monday morning, and maybe get off it till then, right now, or maybe she won't even be able to call him on Monday.
TrueBlue, check YOUR thread; I have posted on it about West Nile tonight. Very similar symptoms, and I am having them right now too, AND I know I have been bitten by one or more mosquitos this past week or so.
I'm pretty sure that she was on ketek a while before the babesia diagnosis and it was helping her Lyme. But I'll double check.
I'm gonna call her to discuss some of these responses as soon as there's a commercial in Grays' Anatomy. There are some programs she's trained me not to interrupt.
I'm really surprised at all the suggestions to check with the doctor. I think maybe I wasn't reacting as if this was serious enough, so I really appreciate the feedback Ellen
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Posts: 819 | From New York, NY | Registered: Oct 2001
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I'm pretty sure that she was on ketek a while before the babesia diagnosis and it was helping her Lyme. But I'll double check.
I'm gonna call her to discuss some of these responses as soon as there's a commercial in Grays' Anatomy. There are some programs she's trained me not to interrupt.
I'm really surprised at all the suggestions to check with the doctor. I think maybe I wasn't reacting as if this was serious enough, so I really appreciate the feedback Ellen
--------------------
Posts: 819 | From New York, NY | Registered: Oct 2001
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I'm pretty sure that she was on ketek a while before the babesia diagnosis and it was helping her Lyme. But I'll double check.
I'm gonna call her to discuss some of these responses as soon as there's a commercial in Grays' Anatomy. There are some programs she's trained me not to interrupt.
I'm really surprised at all the suggestions to check with the doctor. I think maybe I wasn't reacting as if this was serious enough, so I really appreciate the feedback Ellen
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Posts: 819 | From New York, NY | Registered: Oct 2001
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charlie
Frequent Contributor (1K+ posts)
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posted
Bactrim is a pretty good cheapo substitute for mepron IMO
Posts: 2804 | From Texas | Registered: Oct 2000
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posted
Hi folks, I forgot to get back to you after speaking with my friend.
I called her that night with all your responses. She was so grateful. It's really hard for her because she can't use her hands to type and hasn't been able to afford decent equipment to be able to talk her email.
So this has really helped her keep her feeling in touch with other Lyme patients.
When I called her, she was already feeling better, so for now she's assuming it was a herx. But these illnesses being what they are, I have an uncomfortable feeling that I'll have to be back in touch about other complications.
THanks so much for your help. Ellen
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Tincup
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trueblue
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posted
I glad to hear your friend is feeling better, Ellen. Long may it continue!
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Michelle M
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posted
Ellen, glad your friend weathered what I HOPE was the worst of it. Fingers crossed that things continue to look up. Glad she's got you for a friend!!
Michelle
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treepatrol
Honored Contributor (10K+ posts)
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Hemmer RM, Ferrick DA, Conrad PA. Role of T cells and cytokines in fatal and resolving experimental babesiosis: protection in TNFRp55-/- mice infected with the human Babesia WA1 parasite. J Parasitol 2000 Aug;86(4):736-42
The full discussion section from this reference is cited below, because the authors give a thorough explanations for the role of TNF-a and other cytokines (including a lot of references) - and this is possibly a common pathogenetic 'pathway' for several (all?) intracellular parasitic infections ?
DISCUSSION:
TNF-a is a pleiotropic cytokine that appears to be an integral component of the immunologic defense network. TNF-a seems to be required for resistance to several intracellular facultative bacteria and parasites, including Listeria monocytogenes and Leishmania major (Havell, 1989; Green et al., 191990; Kaufmann, 1993). In contrast, other evidence demonstrates the detrimental effects of TNF-a on the host. TNF-a is involved in triggering the lethal effects of cachexia, septic shock syndrome, inflammation, and other systemic manifestations of disease (Tracey and Cerami, 1994). The fact that this cytokine is crucial in organizing the events involved in both immunity and disease demonstrates the complexity of TNF-a function. Previous studies from this laboratory demonstrated that WA1 babesial infection results in pulmonary edema, infiltration and adhesion of mononuclear cells to the pulmonary veins, and endothelial cell activation, as demonstrated by hypertrophy and upregulation of intracellular adhesion molecule-1 (Hemmer et al., 1999). There is much evidence that these inflammatory responses can be mediated by TNF-a (Mulligan et al., 1993; Urquhart, 1994; Luca et al., 1997). The effector functions of TNF-a include increased vascular permeability, upregulation of adhesion molecule expression on endothelial cells, and stimulation of other changes in vascular endothelium that contribute to tissue injury. Thus, the pathology observed in WA1-infected mice correlates with known biological effects of TNF-a and suggests a role for its activity in the WA1-associated disease.
In the present study we examined the difference in TNF-a production by CD4+, CD8+, and gd+ splenic T-cell subpopulations in fatal and resolving Babesia infections. Upregulation of TNF-a production by gd+ T cells in fatal WA1 infections, but not in resolving infections, suggested that TNF-a production was detrimental to the host. Additional support for the role of TNF-a in the pathogenesis of WA1 came from infections of TNFRp55-/- mice. These mice are resistant to either lipopolysaccharide or bacterial superantigen-induced septic shock, a syndrome mediated by TNF-a (Pfeffer et al., 1993). Furthermore, in the characterization of TNFRp55-/- mice, it was shown that inoculation of TNF-a triggered mononuclear cell infiltration of lung, liver, and kidney in C57BL/6 mice, but not in TNFRp55-/- mice (Neumann et al., 1996). This provides evidence that the TNFRp55 receptor is necessary for TNF-a mediated leukocyte adhesion to activated endothelium. In our study, the TNFRp55-/- mice survived a lethal WA1 infection, thus demonstrating that abolishing TNFRp55 function eliminated an important pathogenic mechanism of the WA1 parasite. This result suggests that during a WA1 infection, signaling through TNFRp55 promotes the recruitment of leukocytes to the lungs, and the outcome is activation of the vascular endothelium, pulmonary edema, respiratory distress, and death. Taken together, these results implicate TNF-a as an essential component of the WA1-associated pathology.
In addition to TNF-a, other cytokines were involved in Babesia infections. IFN-g, another proinflammatory cytokine, was shown to have significanfly higher peak expression by CD8+ T cells in WA1-infected mice compared to mice infected with B. microti. IFN-g is the principal macrophage-activating cytokine and central in the regulation of TNF-a (Rudin et al., 1997). There is evidence that IFN-g synergizes with TNF-a to enhance an inflammatory response (Tracey and Cerami, 1994). Upregulation of both of these cytokines during the WA1 infection could account for the severity of the WA1-associated disease.
In resolving B. microti infections, increased production of both IL-10 and IL-4 by gd+ T cells occurred as the parasite load was decreasing. Thus. in B. microti infections, increased expression of IL-10 and IL-4 was important for resolution of the parasitemia.
One striking observation was that gd+ T cells were the major cytokine-producing cells in both WA1 and B. microti infections. gd+ T cells act as a first line of defense against a pathogen and response of gd+ T cells to antigen happens faster than that ab+ [?, hard to read on my copy] T cells (Boismenu and Havran, 1997). These responses indicate that the cytokine profile of gd+ T cells may regulate the functional activities of both innate and acquired immune responses. Production of IFN-g by gd+ T cells has been shown to prime macrophages for TNF-a expression (Nishimura et al., 1995). Other studies of intracellular organisms imply that control of pathogen dissemination and host tissue damage requires the regulatory influence of gd+ T cells (Rosat et al., 1993; Fu et al.. 1994). These studies cast gd+ T cells as an important regulatory cell for both innate and acquired immune responses. Despite the fact that gd+ T cells were the predominant cytokine-producing cells detected in our experiments, gd-/- mice behaved similar to controls when they were infected with either WA1 or B. microti. This result is not entirely surprising in light of the fact that gd+ T cells make up a small percentage of all T cells, approximately 2-5% in the mouse spleen. Certainly other cell types are major producers of cytokines. Macrophages and natural killer cells that produce TNF-a and IFN-g, respectively, could contribute to the WA1-associated pathology. The flow cytometry results showed limited involvement of cytokine production by CD4+ and CD8+ T cells. This was probably not due to technical difficulties, because IFN-g production was observed in CD8+ T cells, and IL-2 expression was detected in CD4+ T cells (data not shown). It is possible that the cytokine expression was below the level of detection for this assay, or that cytokines other than the ones we tested are involved in Babesia infections. It is important to note that in this study, the T cells were not restimulated in vitro, and this may explain the paucity of cytokine expression by CD4+ T cells. Because it was well established that CD4+ and CD8+ T cells have many important functions in defense against intracellular pathogens, we used CD4-/- and CD8-/- mice to study the effects of an absence of these T-cell subpopulations on the outcome of WA1 and B. microti infections. There was a significant delay in parasite clearance in both WA1- and B. microti-infected CD4-/- mice. A similar persistence in parasitemia was observed in mice depleted of CD4+ T cells by monoclonal antibody treatment (Shimada et al., 1996). These results demonstrate a role for CD4+ T cells in the elimination of parasites from the blood. Following WA1 inoculation, CD8-/- mice had a moderately increased survival rate. One possibility is that because CD8+ T cells are a major source of lFN-g, the absenec of CD8+ T cells reduces the overall availabilty of IFN-g (Boehm et al., 1997). Consequently, the synergistic effects of IFN-g and TNF-a are inhibited, leading to a reduced inflammatory response and increased survival. The protection in B. microti-infected CD4-/- and CD8-/- mice suggests that either CD4+ or CD8+ T cells, without the other subset present, but in the presence of B cells, gd+ T cells, and innate immune cells can be sufficient for immunity. Our results emphasize the plasticity and redundancy of CD4+ and CD8+ T-cell functions in response to intracellular pathogens.
These studies were undertaken to gain a more complete understanding of the role of T cells and cytokines in the pathogenesis of WA1 infections and the resolution of B. microti infections. We have shown that cytokine responses of splenic T cells were different during fatal and resolving infections and that cytokines contribute to both host pathology and host immunity. TNF-a activity through TNFRp55 was essential to the WA1-associated disease. Additional studies of T cells, B cells, endothelial cells, and innate immune responses are needed to elucidate the different mechanisms involved in fatal and resolving Babesia infections. Future experiments will be directed at studying the role of cytokine-stimulated endothelial cells and macrophages in WA1 pathology.
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