The previous page on bartonella, linked here, was written a number of years ago and like every other page, has new information that could be added that many may find helpful. At the 2018 ILADS conference in Chicago there was a very interesting breakout session on Bartonella infection diagnosis, treatment, and complications which had many interesting pieces of of information, some new, some old, all important.

The afternoon was chaired by Robert Mozayeni, MD, Marna Ericson, PhD, Tania Dempsey, MD and Ed Breitschwerdt, DVM.

Original research was presented in which the linear tracks that practitioners very often see in bartonella had biofilim and collagen damage implicated in their genesis. These same mechanisms were shown to be present in some case studies in which osteoarthritis seemed to be at least associated with bartonella infection.

Bartonella is an infection that can become systemic, live in the blood chronically, and go on to affect a variety of different tissues but especially the microvascular areas of the nerves, brain, skin, collagen and cartilage. Careful examination with the physician may find signs of bartonella especially with the neurological exam, as this may be the most sensitive way to find small vessel disease. In fact, central nervous system signs such as poor cognition / executive function, a "disconnect" from reality, slow processing can be some of the earlier signs because the circulation to the white matter areas of the brain can be compromised early. Other symptoms can include cysts, a migrating peripheral neuropathy such as pins and needles or burning pains, POTS or dizziness when patients stand up, muscle twitching, tremors, muscle pain, joint pain and fatigue.

There is a significant overlap between bartonella infection symptoms as well as lyme symptoms. Of note, lyme is transmitted by the deer tick vector, whereas bartonella is thought to be transmitted through this vector as well, but is present in and transmitted also by fleas, cats, lice, dust mites, bed bugs amongst other vectors.

While bartonella can often be coinfection in lyme patients, bartonella can present its own primary infection problem and be the "main trigger" for a patient's widespread symptoms. The speaker's opinion was that bartonella infection may even cause a false positive IgM lyme western blot, and this is something to be considered when the IgM is positive without seroconversion to IgG. Data was presented at an earlier conference in which patients with PCR, culture or IFA positivity to bartonella were more likely to the be the ones who had an IgM western blot for lyme positive, with IgG western blot for lyme negative. Molecular testing, by PCR and also culture, were considered good testing options for bartonella. Antibodies to bartonella may stay elevated for long periods after the patient is well (whereas in the veterinary examples antibodies often fell as recovery came on).

Bartonella can also deplete IgG1 and IgG3 due to the immunosuppressive effects of some of its compounds. CD57 also appears to be lowered in such infections. There may be mild liver enzyme elevations, a mild white blood cell decrease, an elevated c4a inflammation marker as well.

Similar to discussions in chronic lyme cases, considerations of the host vs the bug are very important. In many patients, infections such as lyme and bartonella are tolerated, sometimes without symptoms, and without problems, while for others the patients can become very ill. While this may be due to differences in the strains of the infections, it is clear that the host response is very important in ascertaining if a patient becomes chronically sick from such infections or not. In some aggressive infections, such as "flesh eating disease" - the infection is so aggressive that the host response may play little role in the damage caused to the tissue. In other infections, such as chronic lyme or bartonella, the host response is responsible for the majority of the symptoms involved, and the goal becomes ascertaining if the infection is a persisting issue exagerrating the host response or if has acted mainly as a trigger, such as in some cases of mast cell activation syndrome. Ebola was given as an example where the host response is responsible for the majority of the problem, and of course in this example the primary goal is eradication of the trigger. This may or may not be the case in chronic lyme or bartonella patients, depending on the case and response to treatment.

In many cases of lyme disease treatment failure, we have to consider bartonella as a possibility due to the similar findings in symptoms.

Treatment of bartonella in some cases is similar to lyme, with subsets of patients responding over many months of treatment. Partly the long duration of treatment is explained similarly to lyme, in which both infections have a very long division time of 22-24 hours. Further, the biofilm formation makes it difficult for antibiotic penetration, and even within the biofilm there is infection that is in different stages. As nutrients become more and more sparse deeper in the biofilm, the bartonella deeper in these lesions is much more dormant.

It is not simply a matter of prescribing doxycycline or rifampin, as the skill set behind it in managing the nuances of treatment are important, especially appreciating the downstream effects such as hormone support that are necessary both because of the illness as well as because of certain medications.

The speaker's experience has often been that a duration of 6 months is necessary once at the full dose of antibiotics. Often, clarithromycin, rifampin/rifabutin is used as well as medications for hormone support as needed. The speaker has not found as good results with the usual doxycycline / rifampin or rifampin / sulfa drug combinations. Hydrocortisone as the main adrenal support has been most important.

Importantly, an inflammation of the eye called uveitis should be considered when using rifabutin. There has been literature published describing uveitis with the clarithromycin / rifabutin combination, as well as with bartonella infection itself.

A case was presented which was very similar to many of mine own patients. The case was presented as an example to show the synergistic effects of bartonella infection in a child who also had developed mast cell activation disorder and had mold exposure.

In this example bartonella testing was positive but lyme testing negative, and a panel called the Cunningham panel was done to evaluate for inflammation directed against the nervous system, which was positive.

In this example, and in many of my patients, there was an infectious trigger likely, which led to an antibody response by the immune system. The antibodies in this case then cross reacted and started attacking the nerves. The immune system and especially the mast cells became over-reactive, and testing such as histamine levels, chromogranin-A, and tryptase is sometimes abnormal in such cases.

The mast cell activation seemed to be secondary to the infectious trigger, though the tendency for this to be present to a lesser extent can be present before the actual trigger. The mast cells release a variety of inflammatory mediators, only one of which is histamine. This important condition is described elsewhere on this site.

Often times in such cases, gentle and supportive treatment is done first, often trying to stabilize the mast cells with medications such as ketotifen, cromolyn, quercetin, or the DAO enzyme. Antihistamines can be very useful. There can be signicant changes in the symptoms with this alone, and then infection can be treated. If there is a further plateau, looking at treating other toxicity including the mycotoxin is important and in many cases helps to dramatically improve if not resolve the symptoms.

In summary, bartonella infection is a commonly missed and inadequately treated infection that can cause symptoms that are very similar to lyme disease. Either infection can act as a trigger for mast cell activation syndrome, and through multiple mechanisms can cause many neurologic and psychiatric symptoms as well. We often have to think about mast cell activation when treating the underlying infections does not completely resolve the condition.