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Tuesday, February 19, 2019

Babesia confusion

Babesia is a protozoan, a higher life form than bacteria. Both are single cell organisms.  The primary difference is protozoa have an organized nucleus containing DNA. It is a member of the phylum Apicomplexa.  This is a relatively small group of organisms. Its closest relative is Malaria; only Babesia and Malaria (Plasmodium spp.) are intraerythrocytic, meaning live inside red blood cells. Because of this, many therapies against malaria are also effective against Babesia.  Mainstream medicine offers two therapies only: quinine/clindamycin and Zithromax/Mepron (atovaquone). These approaches frequently fail and additional approaches are required. 
Historically, Babesia was first described in the 1950s as a cattle disease.  The first human cases, B. microti were described around Nantucket Island in the 1960s.  Many physicians have stubbornly, erroneously clung to the belief that human babesiosis on the east coast, is virtually always caused by B. microti.  Although B. duncani was first described on the West Coast, it currently accounts for the majority of speciated cases diagnosed on the East Coast as well.  More often than not the diagnosis is made without speciation. (the species of Babesia causing the illness is not identified).  There are more than 100 species of Babesia known.  Other species, MO1, CA1 are recognized human pathogens in the US.  B. divergens, a bovine species, is known to have jumped species, cow to human.
Most Lyme doctors make the diagnosis empirically, based on symptoms.  Underused diagnostic tools include Giemsa stains and FISH tests.  Many Babesia symptoms are nonspecific.  In my practice I especially pay attention to a triad:  night sweats +/- feeling feverish, air hunger and change in emotional state – especially random bouts of tearfulness. 
For many patients the two “standard” therapies, as stated above, proves ineffective or only partially effective.  Other therapies may be effective and medically necessary.  Therapies must be science based and rational. The term evidence based refers to mainstream treatment vetted through a peer reviewed process and frequently, not always FDA approved.  Second tier drugs and therapies are used when “evidence based” treatments have failed.  Science based approaches require biological plausibility, e.g. med works well against malaria and/or their use is supported by body of empirical evidence, e.g. traditional herb has been used for a century to treat malaria.  Doctors prescribing these therapies need to be knowledgeable about the disease.  
One approach/theory must be debunked.  This is the idea that 4 months of treatment is all that is required.  The basis for this thinking is that red blood cells only live 120 days. Therefore, after 4 months every infected red blood cell will have been replaced. It may sound plausible, but the reasoning is not sound. Every red blood cell (RBC) has a different birthday and at a different point in its lifecycle.  Cells are destroyed and made every day.  Infected senescent cells may transfer merozoites (infecting stage of parasite) to new born cells on any given day.  There is no specific duration that will always be effective. A short course of therapy, e.g. 3 weeks of quinine/clindamycin could at times achieve compete remission. 
Antimalaria drugs make work well but not all antiprotozoal drugs kill Babesia. This seems to be a common misconception.  Some drugs used to treat toxoplasmosis (like Mepron) may be effective against Babesia.  Drugs active against, Giardia, Amoeba, Leishmaniasis and other protozoans will likely not be effective.  Flagyl is a broad-spectrum drug with activity against Giardia and Amoeba. It is also an effective anti-Lyme drug. It has no activity against Babesia. 
Anti-worm drugs, such as ivermectin, is active against microfilaria, and has no antibabesia properties.  If the drug provides relief of symptoms it is doing something else.
Unless you are a scientist -- reading about complex cellular biology, biochemistry, etc. is likely only to confuse. A patient copied and pasted something from the internet which claims that Babesia infection suppresses the production of nitric oxide.  The truth is that Babesia infection activates macrophages and stimulates the production of nitric oxide (NO).  Nitric oxide is an extremely complex signaling molecule and an entire science journal is dedicated to this one compound. Reading about cytokines and metabolic pathways, killer T cells, Th1, Th2 etc. and trying to apply it to your illness is an example of how a little knowledge can be dangerous.
The Mepron/ Zithromax combinations is the most widely used initial approach.  The higher dose, Zithromax 500-600 mg and Mepron 2 tsp twice daily is more likely to be effective.  Medication doses are within FDA recommended levels.  This is generally the best place to start. 
Quinine/clindamycin is too toxic for most to tolerate but is very effective. 
Malarone has been used in lieu of Mepron but the dose of the active ingredient, atovaquone is quite low. 
The traditional herb artemisinin has a long track record and is a very helpful adjunct to treatment.  Combining active artemisinin with the whole plant (artemisia) may enhance adsorption and bioavailability.
The FDA approved Coartem contains artemether, a more active derivative of artemisinin and is very effective. 
Liposomal artemisinin available through a compounding pharmacy is a potent alternative. 
Artesunate is another artemisinin derivate, available in other countries; it may also be highly active.  An oral version of the agent is also available through TCM (Traditional Chinese Medicine) sources. 
There are many traditional herbs, this is a partial list.   Cryptolepis can be very effective at times, sold as a single agent through a compounding pharmacy.  
Herbal combination therapy, described by Buhner: cryptolepis, sida acuta and alchornea may be an effective option. 
Daraprim (with leucovorin) folic acid antagonist, a drug typically used to treat toxoplasmosis and has some anti-Babesia properties.  It may be helpful adjunctively. 
Larium, related to quinine (with doxycycline) is very effective but its use has been limited because the side effect depression. 
Antibiotics, generally not effective as single agents.  IV clindamycin can be effective in stubborn cases. 
Bactrim touted to have anti-babesia properties is typically ineffective. 
Other, novel approaches have been used in patients with very resistant disease.  For example, the anticoagulant heparin coats merozoites and inhibits RBC penetration. (works in mice, some human data).

Babesia can be associated with numerous symptoms: fever, feeling flulike, malaise, fatigue, chills, sweats, headache, air hunger, cough, joint pain, muscle pain, cough, abdominal pain, nausea, depression, changes in emotional state and many others.

Clinically, Babesia is usually seen as a coinfection with Lyme and other tickborne pathogens and symptoms may be more confused.  Babesia is the second most common tickborne infection after Lyme. Long term remission is attainable in the vast majority of patients, time frame unpredictable.

Wednesday, February 13, 2019

Lyme ADD

Attention deficit disorder, ADD/ADHD brains operate in much the same way.  For purposes of this piece I will only discuss ADD. ADD is common, perhaps much more than appreciated. It may affect 20% of the general population. Symptoms vary tremendously in degree  and severity from one person to the next. 

ADD is closely associated with “executive function” disorder. Brain housekeeping functions controlled by the frontal lobe are askew.  Patients have problems with focus, attention and staying on task.  Minds wander. Patients are impatient and interrupt. They don’t follow conversations; their minds are elsewhere. Their memories are full of holes. They lose their keys, wallets and misplace important papers. They forget where they parked their car at the mall. Routine tasks don’t get done, like washing dishes or filing tax forms. If something interests the ADD brain the person may hyper-focus: play a video game for hours on end, stay up all night reading a book despite predictable exhaustion the next day.  It is not all bad. People with ADD can be extremely creative, interpret the world in unique ways.  For example, only an ADD Einstein could imagine what it is like to travel next to a beam of light and discover relativity.  The same Einstein never learned to drive a car, he lacked the required focus. (Einstein’s brain was unique in other ways as well). ADD people are risk takers, which may be good or bad. They have other unique personality traits/quirks. 
These are the symptoms I hear every day from Lyme patients. They have ADD. Adult ADD. Or do they?
Adult ADD is a misnomer.  ADD is a genetic brain glitch. You are born with it. Symptoms should be present in elementary school or before.  Preexisting ADD may be discovered at any age.  Once it was believed that ADD, a pediatric disorder resolved over time. Perhaps the hyperactivity component resolves in many cases; the important frontal lobe executive dysfunction does not. 
The important question for a Lyme patients is: were you like that before?  If the answer is: no, I was precise, organized and orderly. Then the diagnosis is not ADD.  It is Lyme masquerading as ADD, or “Lyme ADD.”  Findings on functional brain scans, like SPECT may be similar to those seen with ADD.  Patients with preexisting ADD are afflicted the most. They experience ADD on steroids. 
Of course, Lyme, Lyme brain, Lyme encephalopathy, neuroborreliosis (synonyms) are treated with antibiotics etc.  But “Lyme ADD” patients can also be effectively treated, if only temporarily with classic ADD drugs and experience much improvement. 
Stimulants tend to be the most effective agents and may be multipurpose since most patients are suffering with severe fatigue as well.  Drugs like Nuvigil work only for wakefulness, not for ADD.  The principal drugs are Ritalin and Adderall and there are multiple variants. 
Proper dosing, side effect are other clinical details are outside the scope of this discussion. 

Appropriate treatment may drastically improve quality of life for many suffering with "Lyme brain."

Thursday, February 7, 2019

Lyme and Hashimoto's.

It has been reported by “Lyme doctors” that Lyme infection is associated with endocrinopathies (disorders of the endocrine system). The most frequent is thyroid disease, generally autoimmune hypothyroidism AKA Hashimoto’s disease.  When looking at Lyme associated endocrine disorders, we need to take them one at a time.  A patient I saw today gained 70 pounds and was first diagnosed with hypothyroidism prior to Lyme. Thyroid supplementation helped him loose the weight. Thyroid disease, particularly autoimmune Hashimoto’s disease is very common. Lyme is very common. But do Lyme patients have hypothyroidism more frequently than would be expected on the basis of chance? Is there is a causal relationship? Hypothyroidism is almost entirely autoimmune. Anti-TPO and other anti-thyroid autoantibodies are invariably present. First off, we know that Hashimoto’s is a familiar disorder, e.g. mom and 2 daughters all suffer with it.  It has been well established that there is genetic predisposition, i.e. HLA DR3, DR5 mutations. 
Autoimmune disease likely is caused by several different mechanisms, one is called molecular mimicry. It has been reported that Bb shares certain amino acid sequences with thyroid proteins.  Antibodies directed against Lyme, in genetically predisposed individuals, may precipitate the productions of self-directed antibodies.  In other words, Lyme antibodies accidentally trigger anti-thyroid antibodies in some cases. 
It appears there may be a causal relationship.  I don’t think there is anything published confirming this suspicion. 
Most endocrine disorders are not autoimmune, including: hypothalamic, pituitary, adrenal disorders, sex hormones and (? POTS -- angiotensin 1 receptor).  If relationships exist, other factors are in play. 
All of my Lyme patients, who invariably complain of fatigue, have their thyroid functions checked.  Most doctors just screen with TSH.  T3 and T4 may be helpful but anti-thyroid antibodies are essential.  If these antibodies are present the patient will need thyroid supplementation sooner or later. If they have exhaustion – sooner, irrespective of the other numbers (except with hyperthyroidism or Grave’s disease).