Archive for the ‘Bartonella’ Category

Case of Cerebral Vasculitis Due to Neurobartonellosis

A case of cerebral vasculitis due to neurobartonellosis

Meryim Poursheykhi, Farhan Mithani, Tanu Garg, Christian Cajavilca, Siraya Jaijakul, Steve Fung, Richard Klucznik, Rajan Gadhia

We report a case of a 60-year-old right-handed woman with hypertension, hyperlipidemia, and hypothyroidism who presented with a three-week history of:

  • recurrent thunderclap headaches 
  • photophobia (aversion to light)
  • phonophobi (aversion to sound)
  • nausea
  • vomiting

She reported one brief episode of:

  • slurred speech
  • expressive aphasia (inability to understand and formulate language)
  • right facial droop
  • right hemiparesis suggestive of a TIA

Family history was remarkable for primary angiitis of the CNS (PACNS) in the mother. Neurologic examination was unremarkable. CT of the head was negative; CT angiography (CTA) of the head and neck suggested fibromuscular dysplasia in bilateral cervical internal carotid arteries and distal right vertebral artery. MRI of the brain showed no correlating abnormalities. A digital subtraction angiography (DSA) revealed multivessel intracranial medium and large vessel narrowing and fusiform dilatations, suggestive of reversible cerebral vasoconstriction syndrome (RCVS) vs vasculitis. Subsequent MR intracranial vessel wall imaging (IVWI) showed multifocal concentric vessel wall thickening and enhancement consistent with vasculitis (figure). Transcranial Doppler showed no evidence of elevated intracranial velocities. CSF studies were unremarkable with an opening pressure of 10 cm H2O, 2 white blood cells (normal 0–5/mm3), 2 red blood cells (normal 0–1/mm3), 58 mg/dL glucose (normal 40–70, serum glucose 87), 41 mg/dL protein (normal 15–45), normal Q-albumin ratio, normal IgG synthetic rate, and IgG index. Serum inflammatory and infectious studies had been negative thus far. Empiric high-dose IV steroids lead to complete symptom resolution.

Final infectious workup revealed strongly positive serum Bartonella IgM titer of 1:256 and negative IgG, consistent with her reported cat exposure.

She was started on an outpatient two-week course of doxycycline, rifampin, and oral steroids. Four weeks later, repeat vessel wall MRI and Bartonella serologies (IgM titer 1:80) showed improvement.

FigureVessel imaging

(A) Angiogram of the left internal carotid artery showing multifocal narrowing and fusiform dilatations (arrows) pretreatment. (B) Intracranial vessel wall MRI showing multifocal concentric vessel wall thickening and enhancement (arrows) pretreatment. (C) Intracranial vessel wall MRI showing reduction in vessel wall enhancement (arrows) posttreatment. (D) Magnetic resonance angiography (MRA) head showing multifocal stenoses (arrows) pretreatment. (E) MRA head showing improvement of stenoses (arrows) posttreatment.


We present an individual with symptoms initially concerning for RCVS vs vasculitis who was subsequently found to have secondary CNS vasculitis due to cat-scratch disease (CSD). To our knowledge, this is the first adult case of Bartonella henselae-associated CNS vasculitis, particularly without encephalopathy as the presenting symptom.

CSD typically presents with self-limited regional lymphadenopathy and fever.1 Neurologic complications are rare, occurring in 2% of cases with encephalopathy as the most common manifestation.2 Neuroretinitis, seizures, coma, myelopathies, and cranial and peripheral nerve involvement have also been reported. CNS vasculitis associated with CSD, however, has only been reported in 2 pediatric cases which presented with strokes.3,4

Diagnostically, identifying primary and secondary CNS vasculitis can be challenging both clinically and radiographically. No specific studies in serum or CSF are available for the diagnosis of CNS vasculitis. As in neurobartonellosis, CSF may be unremarkable or reveal nonspecific mild lymphocytic pleocytosis. Cerebral vasculopathies can present with similar luminal patterns, and therefore, imaging modalities such as DSA, magnetic resonance angiography (MRA), and CTA provide nonspecific results leading to difficulties identifying and differentiating between common etiologies of intracranial disease including vasospasm, atherosclerosis, and inflammation. Although DSA remains the gold standard for vessel imaging, it is an invasive study that provides information limited to the vessel lumen. Conversely, IVWI allows direct visualization of the vessel wall by subtracting the signal of blood in the vessel lumen and has shown to improve diagnostic specificity.5 In CNS vasculitis, IVWI shows multifocal concentric vessel wall enhancement and thickening as seen in our patient. In RCVS, vessel wall thickening may be present but with minimal or no enhancement.5

At this time, there is no clear evidence-based treatment regimen or duration for neurologic manifestations of CSD including CNS vasculitis.1 We recommend concomitant treatment of the infection with antibiotics and secondary vasculitis with high-dose steroids. Our patient received a 2-week combination of doxycycline 100 mg and rifampin 300 mg twice daily per current expert opinion.6 In addition, we initiated 5 days of high-dose IV steroids, followed by a 1-week oral steroid taper. To avoid recurrent invasive testing, we repeated IVWI 4 weeks later for treatment monitoring and found significant reduction in vessel wall enhancement (figure).

Our case reiterates the importance of ruling out rare causes of CNS vasculitis including assessing animal exposure before diagnosing PACNS. Detection of the etiology of vasculitis is essential to guide treatment and for prognostication. Noninvasive imaging such as an IVWI provides valuable diagnostic information and can be useful in assessing the treatment response over time by minimizing the need for repeat invasive DSA.

Study funding

No targeted funding reported.


M. Poursheykhi, F. Mithani, T. Garg, C. Cajavilca, S. Jaijakul, S. Fung, R. Klucznik, and R. Gadhia report no disclosures. Go to for full disclosures.


The authors thank Dr. Gadhia for his mentorship.



Since Bartonella is a vascular disease, it follows that it will cause vasculitis pretty much anywhere in the body.

It also creates tumors, many neurological manifestations including PANS and other mental health issues.

The concern with their treatment is it wasn’t long enough and she could relapse, which is common.  Bartonella, in my opinion, is as bad if not worse than Lyme disease and together it’s a one, two punch – you are out.

Marna Ericson’s work has demonstrated it to survive right along side a PICC line with antibiotics being pumped directly into the body:  The subject is her son who has chronic bartonellosis.




Kills Bartonella: A Brief Guide

Kills Bartonella: A Brief Guide – Dr. Marty Ross

updated 6/24/20

“New experiments show effective Bartonella treatments must do more than kill growing germ forms – they should also kill hibernating persister forms of Bartonella and include agents to remove biofilms.”   Marty Ross MD

Recent research published in 2019 and early 2020 is changing the approach I take to treat Bartonella. Previous research showed Bartonella has rapidly growing germ forms – thus the antibiotics I recommended in the past treated growing forms only. New research shows that Bartonella also has non-growing forms called persisters. Think of a persister as a hibernating form of the germ that ignores most antibiotics and immune system attacks. In addition, this new research shows that Bartonella can form protective sugar-slime coverings called biofilms. These biofilms can block the immune system and antibiotics from reaching Bartonella. This new research is based on petri dish laboratory experiments.

In this updated article I review the best treatment approaches to eradicate Bartonella based on my clinical experience and this new science. (See link for article)



In my experience Bartonella is as bad or worse than Lyme.  It is what both my husband and I struggle with when we relapse.  Unlike Dr. Ross, our doctor HAS had good results with A-Bart from Byron White for Bartonella maintanance.  For US it has been Berberine that has kept us at bay.  We take 500 mg 3X/day with good success.  Berberine is a wonderful herb and does 1,000 different things.  For more:

Bartonella Treatment:

Disseminated Cat Scratch Disease in Pediatric Patients in Hawaii

. 2020 May 1; 79(5 Suppl 1): 64–70.
PMCID: PMC7260883
PMID: 32490388

Disseminated Cat Scratch Disease in Pediatric Patients in Hawaii


Cat scratch disease is known to be a generally benign, self-resolving illness associated with non-specific symptoms, including lymphadenopathy, fever, fatigue, anorexia, and headaches. However, it can also cause disseminated disease with a wide range of manifestations, including liver and spleen microabscesses, osteomyelitis, encephalitis, and uveitis.

Eighteen pediatric cases of disseminated cat scratch disease at a single center in Hawaii are described. This case series emphasizes the importance of disease recognition and use of appropriate diagnostic tools and disease management. The disease burden of pediatric patients with disseminated cat scratch disease in the state of Hawaii has a high incidence and should be considered in pediatric patients with prolonged febrile illnesses.



This is important because few doctors will consider Bartonella in pediatric patients.  Like the article states, most doctors consider Bartonella to be a benign, self-resolving disease when nothing could be further from the truth.  In fact, I’d go as far to say it can be as bad as Lyme if not worse.  It’s very tenacious.

For more:  University of Hawaii study shows Hawaii keiki are more than three times more likely to get severe forms of cat scratch disease than mainland kids.

This is an interesting finding.  I wouldn’t blame only cats. Bartonella can be transmitted from many, many things:

Mode of Transmission: Arthropod vectors including fleas and flea feces, biting flies such as sand flies and horn flies, the human body louse, mosquitoes, and ticks; through bites and scratches of reservoir hosts; and potentially from needles and syringes in the drug addicted. Needle stick transmission to veterinarians has been reported. There is documentation that cats have received it through blood transfusion. 3.2% of blood donors in Brazil were found to carry Bartonella in their blood. Bartonella DNA has been found in dust mites. Those with arthropod exposure have an increased risk, as well as those working and living with pets that have arthropod exposure. 28% of veterinarians tested positively for Bartonella compared with 0% of controls. About half of all cats may be infected with Bartonella – as high as 80% in feral cats and near 40% of domestic cats. In various studies dogs have close to a 50% rate as well. Evidence now suggests it may be transmitted congenitally from mother to child – potentially leading to birth defects.

**On a personal note**

If my husband and I have symptoms – they are typically Bartonella symptoms. After years of treatment, we both use Berberine, which has served as a wonderful maintenance treatment for both of us:


Formidable Evidence For Sexual Transmission of Lyme Disease – First Study to Document ACA Rashes in Canadian Patients

healthcare-08-00157-v2 Full study Here

Presentation of Acrodermatitis Chronica Atrophicans Rashes on Lyme Disease Patients in Canada

John D. Scott

International Lyme and Associated Diseases Society, 2 Wisconsin Circle, Suite 700, Chevy Chase, MD 20815-7007, USA;; Tel.: +1-519-843-3646 Received: 13 May 2020; Accepted: 29 May 2020; Published: 4 June 2020


Lyme disease (Lyme borreliosis) is a complex multisystem illness with varying clinical manifestations. This tick-borne zoonosis is caused by the spirochetal bacterium, Borrelia burgdorferi sensu lato (Bbsl) and, worldwide, presents with at least 20 different types of rashes. Certain cutaneous rashes are inherently interconnected to various stages of Lyme disease. In this study, five Canadian Lyme disease patients from a multi-age range presented various phases of the acrodermatitis chronica atrophicans (ACA) rash. In each case of ACA, the underlying etiological pathogen was the Lyme disease spirochete. Although ACA rashes are normally found on the lower extremities, this study illustrates that ACA rashes are not directly correlated with a tick bite, geographic area, age, Bbsl genospecies, exercise, or any given surface area of the body.

  • Case 4 provides confirmation for an ACA rash and gestational Lyme disease (club feet at birth).  Both parents tested positive for Bbsl.
  • One patient (Case 5) puts forth a Bbsl and Bartonella sp. co-infection with a complex ACA rash.
This study documents ACA rashes on Lyme disease patients for the first time in Canada.


The study states that about 63% of patients infected with Lyme develop chronic Lyme disease.  Authorities keep telling us it’s only 10-20%. It also states Lyme colonizes in many immune-privileged sides including bone, brain, eye, ligaments & tendons, heart, kidney, bladder, liver, muscle, synovial cells, central nervous system, claim and neuronal cells, and fibroblasts/scar tissue.  It states Lyme can be an insidious neurologic pathogenesis with demyelination, and even fatal.

The study points out that Bb is pleomorphic with diverse forms (spirochetes, round bodies, blebs, granules, and biofilms). The study also touches upon the hopelessness many patients can experience which can lead to despair and suicide. Lyme may be potentially transmitted via intimate relations as well as gestationally.

For more:  

Rashes-larger-blog-4Various studies showing how many get the EM rash.

Intracranial Infection in Homeless Patient – Bartonella Diagnosis By Molecular Approach

. 2020 May 19;20(1):357.

doi: 10.1186/s12879-020-05088-2.

Unusual Subdural Empyema in a Homeless Patient Diagnosed by Molecular Approach: A Case Report

Affiliations expand


Background: We report a case of subdural empyema in a homeless patient caused by Bartonella quintana. B. quintana is a facultative intracellular bacteria for which bacterial growth is fastidious. The molecular biology approach has been a real help in establishing the diagnosis.

Case report: A 59-years old homeless patient, with a history of chronic alcohol abuse, was brought to the emergency department with a massive subdural empyema. Extensive microbiological evaluation didn’t reveal any pathogen in the pus collected before antibiotic treatment. B. quintana was detected in the pus from the empyema using a 16S rRNA-based PCR. Histology of intraoperative samples was consistent with the diagnosis and a serological assay was positive. The patient responded well to a treatment that included craniectomy with drainage of the loculated pus, total removal of the infected capsule and a combination of antibiotics.

Conclusion: This unique case of B. quintana-related empyema illustrates the risk of secondary infection of subdural hematoma with B. quintana since such infections have recently reemerged, predominantly among the homeless populations. Patients with subdural empyema in at-risk populations should be systematically evaluated for B. quintana with an appropriate diagnostic approach involving molecular biology.


For more: