For convenience we can divide physicians into two camps: those who follow the IDSA and those who follow ILADS. This is an over-simplification. Many physicians fall in between. I am seeing more infectious disease physicians cross over into the chronic Lyme side of things. Many other physicians are becoming more interested in treating Lyme as a chronic disease and treating it as such. The paradigm has broadened for many of us; chronic Lyme has evolved into chronic tick borne disease. Many patients do not improve or recover, at least not fully, unless other co-infections are treated as well. The treatment of co-infections exposes Lyme aware physicians to increased criticisms by IDSA leaning physicians because the presence of these entities is frequently more difficult to demonstrate than Lyme--Borrelia burdorferi.
Readers must be reminded that in the main, laboratory evidence suggesting the presence of Babesia tells the physician only one thing: the patient has been exposed to Babesia. Here I am referring to serological antibody tests. Other, more convincing tests, for the non-believers, include a blood smear which shows the organisms or a FISH test offered by IgeneX. These tests are not particularly sensitive missing most cases. Serologically, we can test for two strains of Babesia through commercial labs: B. microti and B. duncani. There are numerous other strains of Babesia for which no simple test exists. Clongen lab can perform a Babesia "species" PCR test which is very specific but not all that sensitive. It screens for the presence of Babesia DNA for about 15 species of Babesia.
In routine lab panels described elsewhere, anybodies directed against B. microti and B. duncani or WA1 are routinely obtained. It is always nice to have one's clinical suspicions mirrored in a laboratory test. But like most things Lyme: the diagnosis of Babesiosis is a clinical one.
Many clinical signs and symptoms have been ascribed to Babesiosis. In my practice the primary symptom is sweating. Patients have night sweats, sweats after a hot shower, day sweats or chills and flu like symptoms which recur cyclically. A secondary feature is muscle pains in preference to joint pain.
Another helpful test is the evaluation of a wet mount slide. Many patients show a crescent shaped organism which resembles Toxoplasmosis. I do not believe this organism is Toxo: many patients with the organism have negative serology (antibodies) directed against Toxo. I will explain why I mention this finding in connection with Babesiosis in a moment.
The standard treatment for Babesiosis has been Mepron, usually combined with Zithromax.
Mepron is a yellow liquid which is unpleasant tasting and very expensive. It contains a single ingredient: Atovaquone. Malarone, on the other hand, contains two anti-parasite ingredients: Atovaquone and Proguanil. Malarone is a less expensive, convenient tablet.
Malarone seems to address this crescent shaped parasite whereas Mepron does not. It is my suspicion that this other, yet unknown parasite, is responsible for much muscle pain, including that associated with fibromyalgia syndromes.
Even though the dose of Atovaquone in Malarone is only 1/3 of that present in Mepron, I have found it is effective for Babesia symptoms. My experience has informed me that it is the length of therapy, not the dose of Atovaquone which helps ameliorate Babesia related symptoms and presumably infection. Anti-Babesia or parasite therapy can be augmented by adding the herbal medicine, Artemsin, usually 200mg twice daily.
So yes, there are more positive serologies for B. duncani than B. microti here on the east coast which contrasts with the views of local health officials, still, the diagnosis of this syndrome is made strictly on clinical grounds. There exists a subset of patients with antibodies to Babesia who never exhibit symptoms of this infection. Most of these patients improve even though this specific co-infection has not been treated. Presumably, in these cases, the infection was mild and eliminated by a well functioning immune system. Even so, the presence of these antibodies can be used to substantiate the diagnosis of chronic Lyme in patients who are Lyme seronegative: where there is smoke there is usually fire.
A basic rule of thumb which has served me well for over 25 years of medical practice still holds: treat the patient, not the labs.
Another comment: Zithromax is not very is not very effective against Lyme disease; its cousin macrolide Biaxin is. Biaxin is frequently avoided when antibiotics are combined because of its it "sloppy" tendency to cause adverse drug to drug interactions: it doesn't play well with others.
Biaxin may reduce blood levels of Atovaquone by 40%. Still, in patients where the treatment of Lyme is imperative along with the treatment of Babesia, this combination has still been effective in many patients.
Another, quite effective drug can be mixed with Malarone for Lyme disease: Cleocin. But this drug carries its own unique risks, especially C. diff colitis, the nemesis of physicians treating chronic Lyme and related disorders. As always the need for probiotics can not be stressed enough. I prefer the combination of Sacchromyces with an Acidophilus mix.