Babesia, re-visited

Those in the chronic Lyme community have a narrative for explaining the chronicity of Lyme disease or at least the persistence of Borrelia despite the onslaught of immune responses and antimicrobiobials, including such things as: genetic switching - up and down regulating of key surface proteins at key times, protection of the bacteria within a niche, polymorphic switching from spirochetes to cysts and then back again, biofims, and other proven effective stratagies for survival. Despite this evidence, we are still convincing the few.

With chronic Babesiosi we lack such a narrative. Patients are frequently treated for months or longer without clinical resolution. Patients have repeatedly shown me positive FISH(RNA)results for Babesia after extensive therapy, still sick with the disease. As one of my patients recently described in a YouTube video, two ID specialists at Johns Hopkins dismissed this evidence claiming that IgeneX is not a trustworthy lab and suggested the patient seek psychiatric care.

Although there is a great deal of overlap between the symptoms of Lyme and Babesia, certain symptoms are quite specific for babesiosis, inlcuding: recurrent flu like symptoms with low grade fevers, air hunger and night sweats.

Frequently the diagnosis of babesiosis is made on clinical grounds. There are over 100 known species of Babesia but only a few are though to cause human disease. In the US we look for B. microti and B. duncani. Another, yet unnamed species, MO1 has been shown to cause human disease in the US. Others are likely.

Babesia in humans is an infection of red blood cells. The protozoa invade and reproduces within red blood cells. When the cells rupture Babesia forms quickly attach to other red blood cells. Babesia has two hosts: mouse and tick, both of which are required for the parasite's normal life cycle. The tick is considered the definitive host because this is where sexual reproduction of the organism occurs. Humans are considered an unintended, bystander host, unlucky enough to have been bitten by the wrong tick. In humans Babesia is seen as any of three forms: sporozoites which microscopically have a spherical form, trophozoites which have a ring appearance and merozoites which may have the "Maltese cross" (tetrad) appearance.

Unfortunately, Babesia sp infect only a small percent of circulating red blood cells and direct evidence of its presence via microscopy is rarely evident.

Standard, and largely unchallenged dictum states that the microbe lives only within red blood cells, it does not hide in tissues, all of the forms are killed by the same antimicrobials/antiparasitics. The narrative to support the parasite's longevity seems lacking. Well, lets look at some recent medical literature: Clinical Infectious Diseases, 2008, Florescu, highlighted as important by the IDSA.

Two cases of Spenic Infarct are discussed. Both patients were critically ill, one succumbed. At autopsy Babesia-infected red blood cells were noted with the spleen, liver and lymph nodes. One then wonders, is the parasite seeking safe harbor within the microvasculature of these organs?

Of interest, the authors observed that the first patient who survived was co-infected with anaplasmosis "which may have contributed to the prolonged course of the illness." The implication is obvious to chronic TBD believers. The authors report that Babesia has been associated with retinal damage, ostensibly as a consequence of "microobstruction" of tiny blood vessels (by the parasites).

The authors report that multifocal coagulative necrosis has been shown to occur with B. duncani at least in Syrian hamsters. This means that Babesial infection within narrow blood vessels likely caused blood clotting associated with multi-organ damage.

In May 2011, The CDC reports a study of Babesia sp. EU1 (of reindeer) which found hemosiderin laden macrophages in multiple tissues, meaning that infected red blood cells were ingested by macrophages. Babesia DNA was found in: bone marrow, brain, heart, kidney, liver, lung, lymph nodes, small intestinal wall and spleen. Perhaps Babesia can sequester itself with organs.

In summary: Babesia can likely cause blood clotting with localized tissue damage. It may persist only within tiny blood vessels or it may be able to exist within tissues. There are many species of Babesia. They may exhibit different biological behavior. Little is known here.

The evolving science may help us uncover a better narrative by which we may describe patho-anatomic-physiological mechanisms supporting the notion of chronic Babesiosis.

In the meantime, our clinical experience and our supporting laboratory data cannot and should not be ignored.