A thirty seven year old female presented for an evaluation at the end of 2010. She had previously been in good health until 18 months before the visit. She had been diagnosed with chronic fatigue syndrome and fibromyalgia by several other doctors. She had been informed that blood tests, including a Lyme test, had all been normal. She had recently moved back to Maryland from North Carolina. She had previous lived in Maryland 2007 to the beginning of 2009.
Her symptoms had included: fatigue, swollen glands, joint pain and swelling, headaches, nausea, vertigo, blurred vision, dizziness, loss of balance, facial twitches, tremor, memory loss, decreased appetite, muscle cramps, abdominal pain, flulike symptoms, night sweats, shortness of breath, numbness and tingling, disorientation, confusion, poor cognitive processing, random lactation, hot flashes and chills.
She is not an outdoor person although she has had many cats. She does recall walking barefoot through tall grasses on several occasions. There is no history of tick bite. There is no history of an EM (bulls eye) rash.
After 6 months of treatment, including 5 months of Rocephin she is feeling reasonably well. She is still weak but has good endurance. The fatigue is all but gone. Cognitive problems have largely resolved. Muscles pains are gone. Overall, she is about 80% better.
Response to antibiotics is extremely variable amongst patients. Currently the combination of Tindamax and Levaquin have been very effective. The addition of Cortef seems to have been very helpful.
I would like to suggest that I(we) frequently do not know what we are really treating. We do not have a microsopic view of tissues, the immunological responses, microbiological responses or cellular functions.
For example. From many quarters it would be assumed that I am treating Lyme, Bartonella and adrenal fatigue. Perhaps this is mostly wrong.
Regarding Lyme, we have no data regarding microbial resistance. A patient yesterday asked me if Lyme is a "super bug." Actually a good question. We know Lyme has a complex genome and we know Lyme should have the ability to develop drug resistance. Super bugs like MRSA and VRE have evolved the ability to resist multiple antibiotics. Efflux pumps within the bacteria pump out antibiotics of differing classes rendering these antibiotics to be ineffective.
Perhaps Levaquin works, and/or Tindamax, because the offending germs have not developed resistance to these antibiotics.
And Cortef. Treating adrenal fatigue? Maybe not. Patients with treatment refractory Lyme may have very high levels of cytokines such as IL6 and TNF alpha. These are potent mediators of inflammation. It is well know that one of the ways Lyme makes people so ill is because it causes excessive inflammatory reactions. Steroids are the best way to tamp down these excessive immunological responses.
I really started writing this blog because of the patients measurable immune responses to the germ. Currently, the standard WB shows no reactivity but the C6 peptide, 1.55, is positive for the first time. The WB sent to Stony Brook showed only 41 IgM and IgG bands. One year ago, a Labcorp WB was positive for IgG bands (4/10) 66,58,41 and 28 and IgM band 23. Six months prior to that, Labcorp found IgG bands (3/10) 66,58 and 41 and a positive IgM (2/3) 39 and 41. Previous C6 peptides had been 0.4 and 0.7.
It shows that either the tests are completely unreliable or that immune responses are extemely variable over time. Maybe some of both.
Friday, July 27, 2012
Sunday, July 8, 2012
Toxoplasmosis and Lyme
The Archives of General Psychiatry has published two studies from Denmark demonstrating the relationship between toxoplasmosis and suicide. Especially violent suicide. Toxoplasma parasities hide within neurons and glial (supporting brain cells) in cystic forms.
Toxoplasma are persistent brain parasites. The immune system is unable to eradicate them. No effective antimicrobial therapy is available. As with Lyme infection, the organisms manipulate the immune system and are associated with alterations in cytokine levels including interleukin 6. Toxoplasma infection and Lyme also impacts metabolic pathways which lead to the production of kynurenic acid and quinolinic acid from tryptophan.
Elevated quinolinic acid levels has been associated with neuroborreliosis in at least one frequently cited study. These neuro-active substances are associated with glutamic acid excito-toxicity.
Toxoplasma infection has been long associated with depression, schizophrenia, autism, congenital disorders and many other brain disorders.
Toxoplasma infection is common, infecting up to 1/3 of the world's population.
As the microbiome projects has shown. Microorganisms inhabit communities within special niches. Many bacteria commonly found in places as prosaic as the skin remain unknowns. It is clear our bodies are loaded with unknown "mystery bugs."
Perhaps the brain also frequently hosts communities of microbes: Toxoplasmosis, Lyme, other spirochetes. Of course, only those in the Lyme community think of Lyme, Babesia, Bartonella and other co-infections as frequent denizens of the human brain.
An unknown, perhaps endogenous, protozoan has been observed within human cells and the nervous system (unpublished) with genetic/morphological features borrowed from both Malaria and Toxoplasma. (We may all be born infected with this unknown parasite). This is all I can say regarding this topic at the present time).
One investigator has suggested such organisms could even be symbiotic? mutalistic at times. This is certainly the case with many other microbial communities, natural flora. At times usually beneficial organisms, under the right opportunistic conditions can become troublesome.
Most Toxoplasma infected individuals have no symptoms or apparent ill effects. The same is likely true for most individuals harboring brain infection with many of the other microbes listed here.
Why or when infected individuals is unpredictable. Experience has shown that other infection, trauma or stress can provoke illness with Lyme. It does seem clear that mixes of co-infection increase the severity of Lyme syndromes including neuroborreliosis. One could postulate that at times Toxoplasmosis acts a co-infection.
Many patients with extensive, systemic Lyme seem to have immune dysfunction. Many have subtle decreases in varying IgG subclasses. This may turn out to be a key factor.
From a treatment perspective, anti-Babesia drugs are used for chronic forms of the disease. It should be noted that many anti-psychotic medications also have anti-parasitic properties.
The authors note that two other studies have shown the association of toxplasmosis with suicide, one in Maryland, my home state. Great.
Toxoplasma are persistent brain parasites. The immune system is unable to eradicate them. No effective antimicrobial therapy is available. As with Lyme infection, the organisms manipulate the immune system and are associated with alterations in cytokine levels including interleukin 6. Toxoplasma infection and Lyme also impacts metabolic pathways which lead to the production of kynurenic acid and quinolinic acid from tryptophan.
Elevated quinolinic acid levels has been associated with neuroborreliosis in at least one frequently cited study. These neuro-active substances are associated with glutamic acid excito-toxicity.
Toxoplasma infection has been long associated with depression, schizophrenia, autism, congenital disorders and many other brain disorders.
Toxoplasma infection is common, infecting up to 1/3 of the world's population.
As the microbiome projects has shown. Microorganisms inhabit communities within special niches. Many bacteria commonly found in places as prosaic as the skin remain unknowns. It is clear our bodies are loaded with unknown "mystery bugs."
Perhaps the brain also frequently hosts communities of microbes: Toxoplasmosis, Lyme, other spirochetes. Of course, only those in the Lyme community think of Lyme, Babesia, Bartonella and other co-infections as frequent denizens of the human brain.
An unknown, perhaps endogenous, protozoan has been observed within human cells and the nervous system (unpublished) with genetic/morphological features borrowed from both Malaria and Toxoplasma. (We may all be born infected with this unknown parasite). This is all I can say regarding this topic at the present time).
One investigator has suggested such organisms could even be symbiotic? mutalistic at times. This is certainly the case with many other microbial communities, natural flora. At times usually beneficial organisms, under the right opportunistic conditions can become troublesome.
Most Toxoplasma infected individuals have no symptoms or apparent ill effects. The same is likely true for most individuals harboring brain infection with many of the other microbes listed here.
Why or when infected individuals is unpredictable. Experience has shown that other infection, trauma or stress can provoke illness with Lyme. It does seem clear that mixes of co-infection increase the severity of Lyme syndromes including neuroborreliosis. One could postulate that at times Toxoplasmosis acts a co-infection.
Many patients with extensive, systemic Lyme seem to have immune dysfunction. Many have subtle decreases in varying IgG subclasses. This may turn out to be a key factor.
From a treatment perspective, anti-Babesia drugs are used for chronic forms of the disease. It should be noted that many anti-psychotic medications also have anti-parasitic properties.
The authors note that two other studies have shown the association of toxplasmosis with suicide, one in Maryland, my home state. Great.
Saturday, July 7, 2012
Fatigue in a complicated patient
After a long struggle, the patient is doing fairly well. The cognitive improvements have been superb. But the fatigue and lack of endurance have recently been unbearable. The fatigue has improved and worsened in fits and starts. Recently, she has pushed herself just a little too much; rebound fatigue with no endurance became unbearable. No reserves.
Long term intravenous antibiotics, 7 months and counting, have worked great. For three months, IV Flagyl as mono-therapy has been effective.
Despite normal lab studies, I clinically diagnosed adrenal fatigue. I treated her with Cortef and Florinef with a very positive result. Fatigue and energy much improved.
She has a history of very clear cardiac Lyme and has a permanent pacemaker. Her cardiologist has been carefully adjusting the pacemaker, recently increasing the top heart rate. The increased heart rate allowed with exercise seems to have helped as well.
POTS cannot be easily diagnosed. Her heart rate, recent exam, decreased with standing rather than vice-versa expected with POTS.
Surprising, at our last visit she reported relief in other symptoms. Her face was oily for the first time in more than a year (under autonomic/sympathetic control). A sensation of incomplete bladder emptying resolved (under autonomic/parasympathetic control) control. The sensation of hot/cold temperature dysregulation improved. These are POTS symptoms, not generally considered adrenal fatigue symptoms.
I prescribed Florinef, a mineralcorticoid analogue of aldosterone made by the adrenals for the treatment of Adrenal fatigue. This hormone is widely prescribed for POTS because it increases salt and water retention helping with postural dizziness. A strictly symptomatic therapy. In this case it was prescribed for adrenal fatigue, not POTS.
Adrenal fatigue patients describe salt cravings. Perhaps this is due to adrenal/aldosterone dysfunction.
My treatment of adrenal dysfunction seemed to improve dysautonomia. An unexpected outcome.
She also started taking Ritalin again which has been very helpful for fatigue. Many clinicians prescribe Provigil/Nuvigil for fatigue. Ritalin usually works the same but is much more affordable.
Stimulants like Ritalin/Adderall, augment the effects of dopamine and norepinephrine. Adrenal insufficiency is associated with decreased norepinephrine excretion - stress hormones.
Taking Ritalin hopefully does not make adrenal fatigue worse. Like cortisol, it may take pressure off a mis-firing adrenal system. Anyway, it helps.
Improvements of symptoms and function hopefully help the overall healing process.
Too much stimulant may have a negative effect causing dependence - decreased endogenous neuro-transmitter function.
It is all complicated and outside the box, but working for this heretofore desperate and hopeless patient.
Long term intravenous antibiotics, 7 months and counting, have worked great. For three months, IV Flagyl as mono-therapy has been effective.
Despite normal lab studies, I clinically diagnosed adrenal fatigue. I treated her with Cortef and Florinef with a very positive result. Fatigue and energy much improved.
She has a history of very clear cardiac Lyme and has a permanent pacemaker. Her cardiologist has been carefully adjusting the pacemaker, recently increasing the top heart rate. The increased heart rate allowed with exercise seems to have helped as well.
POTS cannot be easily diagnosed. Her heart rate, recent exam, decreased with standing rather than vice-versa expected with POTS.
Surprising, at our last visit she reported relief in other symptoms. Her face was oily for the first time in more than a year (under autonomic/sympathetic control). A sensation of incomplete bladder emptying resolved (under autonomic/parasympathetic control) control. The sensation of hot/cold temperature dysregulation improved. These are POTS symptoms, not generally considered adrenal fatigue symptoms.
I prescribed Florinef, a mineralcorticoid analogue of aldosterone made by the adrenals for the treatment of Adrenal fatigue. This hormone is widely prescribed for POTS because it increases salt and water retention helping with postural dizziness. A strictly symptomatic therapy. In this case it was prescribed for adrenal fatigue, not POTS.
Adrenal fatigue patients describe salt cravings. Perhaps this is due to adrenal/aldosterone dysfunction.
My treatment of adrenal dysfunction seemed to improve dysautonomia. An unexpected outcome.
She also started taking Ritalin again which has been very helpful for fatigue. Many clinicians prescribe Provigil/Nuvigil for fatigue. Ritalin usually works the same but is much more affordable.
Stimulants like Ritalin/Adderall, augment the effects of dopamine and norepinephrine. Adrenal insufficiency is associated with decreased norepinephrine excretion - stress hormones.
Taking Ritalin hopefully does not make adrenal fatigue worse. Like cortisol, it may take pressure off a mis-firing adrenal system. Anyway, it helps.
Improvements of symptoms and function hopefully help the overall healing process.
Too much stimulant may have a negative effect causing dependence - decreased endogenous neuro-transmitter function.
It is all complicated and outside the box, but working for this heretofore desperate and hopeless patient.
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