NeuRA and UNSW Professor Cynthia Shannon Weickert and NeuRA PhD student Helen Cai. Photo: NeuRA


In one of the biggest breakthroughs in schizophrenia research in recent times, Cynthia Shannon Weickert, a professor from Neuroscience Research Australia (NeuRA) and UNSW Sydney, has identified immune cells in greater amounts in the brains of some people with schizophrenia. 

The study, published in Molecular Psychiatry, has the potential to transform global schizophrenia research and open new avenues for developing targeted immune cell therapies​.

One in every 100 Australians lives with schizophrenia. No single cause of schizophrenia has been identified, and this has prevented the development of a cure.

The current treatments for schizophrenia are designed to suppress symptoms rather than target underlying causes of the disorder. These drugs only partially relieve symptoms and can produce unwanted side effects.

Most scientists have had a long held belief that immune cells were independent from the brain pathology in psychotic illnesses, Shannon Weickert said.

“In our study, we challenged this assumption that immune cells were independent of the brain in psychiatric illness and made an exciting discovery. We identified immune cells as a new player in the brain pathology of schizophrenia,” Shannon Weickert added.

Current schizophrenia research has focused on the status of three brain cells: the neurons; the glial cells that support the neurons; and the endothelial cells that coat the blood vessels.

Employing new molecular techniques allowed Shannon Weickert and her team to identify the presence of a fourth cell, the macrophage, a type of immune cell in the brain tissue of people with schizophrenia who show high levels of inflammation.

“Immune cells have previously been ignored as they had long been viewed simply as travelers just thought to be passing by, undertaking surveillance work. They have never been a suspect until now,” Shannon Weickert said. “To find immune cells along the blood brain barrier in increased amounts in people with schizophrenia is an exciting discovery. It suggests immune cells themselves may be producing these inflammatory signals in the brains of people living with schizophrenia. We have observed in people with schizophrenia, the glial cells, one of the local residents, become inflamed and produce distress signals which change the status of the endothelial cells. We think this may cause the endothelial cells to extend sticky tentacles, so when the immune cells travel by some are captured. These cells may transmigrate across the blood brain barrier entering the brain in greater amounts in some people with schizophrenia compared to people without the disorder.”

This discovery shows that specific immune cells are in the brains of some people with schizophrenia in close enough proximity to the neurons to do damage.

Peter Schofield, CEO of NeuRA, said this innovative new research has the ability to possibly alter the diagnosis and treatment schizophrenia.

“This breakthrough demonstrates the value of the NSW Government’s support for Professor Shannon Weickert as NSW Chair of Schizophrenia Research, which has delivered new insights that the community seeks,” Schofield said.

Shannon Weickert is encouraging a cross-collaborative approach between neuroscientists and immunologists globally, to work together to develop treatments targeting this abnormal immune pathology of schizophrenia.

“This opens whole new avenues for therapy, because it suggests that the pathology of schizophrenia could be within the immune cells and the immune cells could be contributing to the symptoms of schizophrenia,” Shannon Weickert concluded.


**Comment**  LLMD, Dr. Horowtiz, goes on record stating that antibiotics are effective in Schizophrenia. With irony he points out that the authors attribute the reason minocycline helped these patients is due to its ability to affect glutamate pathways in the CNS, blocking nitric oxide-induced neurotoxicity, and inflammation in the brain. He reminds them that minocycline is a tetracycline antibiotic that very well may be treating an infection. He also emphatically states that he has had several schizophrenic patients test positive for Bb, the agent of Lyme Disease. After taking doxycycline they improved significantly and with the help of their psychiatrist, were able to reduce and in some cases eliminate all of their antipsychotic medication. It is important to note that patients remained stable on antibiotics but their symptoms returned if they stopped treatment.  BTW:  Mino was one of the most effective meds for my neuro issues and severe occipital headaches.  It crosses the blood brain barrier.  In this presentation, Dr. Markes questions if psychiatric disorders are inflammatory diseases. She lists: Autism, Alzheimer’s, Schizophrenia, Bipolar, PTSD, Depression, Stress, Sleep Deprivation, Self-harm, and Suicide Attempts. She also describes a study in England observing children for over a decade in which children with a high IL-8 at age 8 have an 81% change of developing depression by age 18 and a 2-fold chance of becoming psychotic.  

She states that TBI’s (Tick Borne Illness) causes an impaired Hypopituitary Axis (HPA) which on a chronic basis decreases cortisol and increases inflammation.

Neurotoxins in the brain contribute to mental illness by causing problems with Homosysteine metabolism, which supresses remethylation, but that apoptosis (cell death) can be reversed by supplementing with SamE.

She says Post Treatment Lyme Syndrome (PTLS) is like a “dog whistle,” and usually demonstrates a bias on behalf of the authors who believe that 3 weeks of antibiotics cures LD. She then goes on to tell of a study that revealed that nearly 50% of those labeled as PTLS (with persistent symptoms) had anti-brain antibodies compared to 16.5% of Post Treatment Healthy Controls (no symptoms).

Depersonalization, Violence, self-harm, and schizophrenia can be a part of the picture with TBI’s. At 41:20 she tells the story of a little girl who would throw horrific temper tantrums in which she would destroy her room and then feel absolutely horrible after the fact. She also had a psychotic episode. Her MSIDS testing came back flagrantly positive.



Tick infestations of wildlife and companion animals in Ontario, Canada, with detection of human pathogens in Ixodes scapularis ticks.

Smith KA, et al. Ticks Tick Borne Dis. 2018.


The growing risk of transmission of tick-borne zoonotic pathogens to humans in Ontario, Canada, warrants investigations into regional tick distribution, tick burdens of local peridomestic animals, and prevalence of tick-borne pathogens. The objectives of this study were to investigate the geographic distribution and magnitude of tick infestations in opportunistically sampled mammalian wildlife and companion animals (i.e., dogs) in southern Ontario and to test these ticks for evidence of zoonotic tick-borne pathogens. Ticks collected from wildlife carcasses, live-trapped wildlife and companion animals (2015-2016), as well as wildlife diagnostic cases (2011-2013), were identified to species and life stage.

Ixodes scapularis ticks were tested by real-time PCR for Anaplasma phagocytophilum, Babesia microti, Borrelia miyamotoi and Borrelia burgdorferi sensu stricto (s.s.). Amblyomma americanum ticks were tested for Ehrlichia chaffeensis. A total of 1687 ticks of six species were collected from 334 animals, including 224 raccoons (n = 1381 ticks) and 50 dogs (n = 67 ticks).

The most common tick species collected from parasitized raccoons were Ixodes texanus (n = 666 ticks) and Dermacentor variabilis (n = 600 ticks), which were removed from 58.5% (median: 2 ticks; range: 1-36) and 49.1% (median: 2 ticks; range: 1-64) of raccoons, respectively. Of I. scapularis tested, 9.3% (4/43) were positive for Bo. burgdorferi s.s. and 2.3% (1/43) for A. phagocytophilum. These results reveal that numerous tick species parasitize common, peridomestic wildlife and that at least two zoonotic, tick-borne pathogens circulate in southern Ontario. Host-tick vector-pathogen dynamics should continue to be monitored in the face of global climate change, landscape alterations and expanding human populations.



This researcher obviously hasn’t read his own countryman’s work:   Another problem with the climate change models is they overlook the fact that deer ticks were established in northwestern Ontario, southern Manitoba and were already in central Canada prior to 1970. What they predict to happen in the future has already happened in Canada. Their oversight caused a skewed rate of tick expansion and a miscalculation of northward projected movement.

“For blacklegged ticks, climate change is an apocryphal issue.” -John Scott

adj. Of questionable authorship or authenticity
adj. Erroneous; fictitious

Lemons and Lyme by Stanley Plotkin

Carl Tuttle
Hudson, NH

SEP 20, 2018 —
A copy of the letter below was forwarded to the Tick Borne Disease Working Group as the information currently published is an extension of the thirty year racketeering scheme. The mishandling of Lyme disease can be traced back to vaccine development when the infection was classified as “easily diagnosed and treated” Publications prior to Dearborn (1994) painted an entirely different picture. One of those publications from 1977 is highlighted below.


The picture attached to this update was found at the following Wikipedia Plotkin page:

Letter to Stanley Plotkin regarding the Lyme vaccine:
———- Original Message ———-
From: Carl Tuttle <>
Date: September 19, 2018 at 9:48 AM
Subject: Lemons and Lyme by Stanley A. Plotkin
Journal of the Pediatric Infectious Diseases Society
13 September 2018 P L O T K I N C O L U M N
Lemons and Lyme

Stanley A. Plotkin
Emeritus Professor of Pediatrics, University of Pennsylvania, Doylestown


“It is odd that there is a lobby against the development and deployment of a vaccine against the disease by people who think they are suffering from Lyme infection in a chronic form, the existence of which remains doubtful. They believe that the first vaccine against Lyme disease caused chronic arthritis.”

Sept 19, 2018
Perelman School of Medicine
University of Pennsylvania
3400 Civic Center Boulevard Building 421
Philadelphia, PA 19104

Dr. Plotkin,

“It is odd” that the two principal investigators of the previous Lyme vaccines, Allen Steere for SmithKlineBeecham’s LymeRix and Gary Wormser for Connaught’s vaccine (which never made it to market) have been named in a racketeering lawsuit. (See attached court document)
It is believed that Lyme disease was pigeonholed into its current status by the two principal investigators of the previous Lyme disease vaccines as these investigators conceptualized a disease that would enable vaccine development.
A preventive vaccine for Lyme disease would not satisfy the FDA if a chronic persistent infection and seronegative disease exist. The lead author of the one-size-fits-all IDSA Lyme treatment guideline (which matches the conceptualized disease) was the principal investigator of Connaught’s Lyme vaccine, Dr. Gary Wormser. This is a flagrant conflict of interest. Have we been dealing with an antibiotic resistant/tolerant superbug purposely concealed to promote vaccine development?

Forty one years ago Allen Steere knew that antibiotics used to treat Lyme disease were not working:
Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three connecticut communities. (1977)
Steere AC, Malawista SE, Snydman DR, Shope RE, Andiman WA, Ross MR, Steele FM.


“The best treatment for this illness is not clear. Some physicians have reported that penicillin or tetracycline results in disappearance of the skin lesion (41,42), but others find antibiotics ineffective. Four of the patients with expanding skin lesions received penicillin but still developed arthritis.”

A search will find hundreds of papers reporting persistent Borrelia infection.

I would like to point out the following 1995 case study from Stony Brook Lyme clinic. I understand the patient received thirteen spinal taps, multiple courses of IV and oral meds, and relapsed after each one, proven by CSF antigens and/or PCR. The only way this patient (said to be a physician) remained in remission was to keep her on open ended clarithromycin- was on it for 22 months by the time of publication.

Seronegative Chronic Relapsing Neuroborreliosis.
Lawrence C.a · Lipton R.B.b · Lowy F.D.c · Coyle P.K.d
aDepartment of Medicine, bDepartment of Neurology, and cDivision of Infectious Diseases, Albert Einstein College of Medicine, and dDepartment of Neurology, State University of New York at Stony Brook, New York, NY., USA
Eur Neurol 1995; 35:113–117 (DOI:10.1159/000117104)

We report an unusual patient with evidence of Borrelia burgdorferi infection who experienced repeated neurologic relapses despite aggressive antibiotic therapy. Each course of therapy was associated with a Jarisch-Herxheimer-like reaction. Although the patient never had detectable free antibodies to B. burgdorferi in serum or spinal fluid, the CSF was positive on multiple occasions for complexed anti-B. burgdorferi antibodies, B. burgdorferi nucleic acids and free antigen.

The following pilot study recently identified chronic Lyme disease in twelve patients from Canada. All of these patients were culture positive for infection (genital secretions, skin and blood) even after multiple years on antibiotics so there was no relief from current antimicrobials. Some of these patients had taken as many as eleven different types of antibiotics.

Persistent Borrelia Infection in Patients with Ongoing Symptoms of Lyme Disease

Dr. Plotkin, your commentary published in the Journal of the Pediatric Infectious Diseases Society is little more than perpetuation of a thirty year racketeering scheme to suppress evidence of persistent infection for the purpose of vaccine development. An astute fifth grader with access to PubMed could uncover this blatantly obvious charade.

Carl Tuttle
Lyme Endemic Hudson, NH
Attachment: Lyme Disease RICO Lawsuit Court Document
Cc: Theoklis Zaoutis, MD, MSCE EDITOR-IN-CHIEF
Attorney Daniel Dutko of Hanszen Laporte
The Honorable Chris Smith and Collin Peterson


Edward B. Breitschwerdt, DVM, DACVIM
Chief Scientific Officer, Galaxy Diagnostics, Inc.
Professor, Internal Medicine, NCSU, Raleigh, NC
Adjunct Professor of Medicine, Duke University Medical Center
Bartonella species are fastidious gram-negative bacteria that are highly adapted to a mammalian reservoir host and within which the bacteria usually cause a long-lasting intraerythrocytic bacteremia.  1-3  These facts are of particular importance to veterinarians and physicians, as an increasing number of animal reservoir hosts have been identified for various Bartonella species. Among numerous other examples, Bartonella henselae has co-evolved with cats, Bartonella vinsonii subsp. berkhoffii has co-evolved with dogs and wild canines, and Bartonella bovid has co-evolved with cattle.  1-2  Importantly, the list of reservoir-adapted Bartonella species, including a large number of rodent species that might serve as “pocket pets,” continues to grow exponentially, as new Bartonella spp. are discovered. Prior to 1990, there were only two named Bartonella species, whereas there are now at least 24 named and numerous unnamed or candidatus species, based upon deposited Gen Bank sequences or preliminary reports, respectively, seventeen Bartonella spp. including B.alsatica, B. bacilliformis, B. clarridgeiae, B. doshiae, B. elizabethae, B. grahamii, B. henselae (Houston 1 and San Antonio 2 strains), B. koehlerae, B. melophagi, B. quintana, B. rochalimaea, B. tamiae, B. vinsonii subsp. berkhoffii (Genotypes I, II and III), and B. washoensis have been associated with an expanding spectrum of human diseases.
Epidemiological evidence and experimental flea transmission studies support an important role for fleas in the transmission of B. henselae, B. clarridgeae and most likely B. koehlerae among cats. 1  Three other Bartonella species, B. bovid, B. quintana and B. vinsonii subsp. berkhoffii have been isolated from cat blood, but the modes of transmission and the reservoir potential of these species in felids has not been definitively established. Recently, we isolated Bartonella vinsonii subsp. berkhoffii from a cat with recurrent osteomyelitis spanning an eighteen month time period. 2  Thus, cats can maintain a chronic bacteremia with at least six Bartonella spp., of which five are known zoonotic pathogens.  1-3 In addition to fleas, an increasing number of arthropod vectors, including biting flies, keds, lice, sandflys and ticks have been implicated in the transmission of Bartonella species. Although there is clinical and epidemiological evidence to support tick transmission of B. vinsonii subspecies berkhoffii to dogs and coyotes, the mode of transmission of this Bartonella subsp. to cats and dogs has not been determined. Recent evidence supports tick transmission of B. henselae by Ixodes scapularis and Ixodes ricinus. Considering the diversity of Bartonella species and subspecies, the large number of reservoir hosts and the spectrum of arthropod vectors, the clinical and diagnostic challenges posed by Bartonella transmission in nature may be much more complex than is currently appreciated in human and veterinary medicine.
In the natural reservoir host, such as a cat or rodent, chronic bacteremia with a Bartonella species can frequently be detected by blood cultre or PCR in outwardly healthy individuals.  1-3  In contrast, the diagnostic detection of a Bartonella spp. in a non-reservoir adapted host, such as a dog, horse or human patient, can be extremely difficult. Most, although not all diseases caused by Bartonella spp. occur in accidental hosts and these organisms are being increasingly implicated as a cause of zoonotic infections.  4-8  It is important to recognize that strains of a Bartonella sp. vary in their virulence. Therefore, highly pathogenic strains of B. henselae, for which the cat is the primary reservoir, can induce granulomatous myocarditis in cats, presumably following flea transmission.  Until recently, mechanisms that facilitate persistent Bartonella bacteremia in mammals were not well understood. Recent reports have identified an intra-endothelial, as well as intra-erythrocytic localization for these bacteria, which represents a unique strategy for bacterial persistence. Non-hemolytic intracellular colonization of erythrocytes in conjunction with the ability to invade and replicate within endothelial cells would preserve the organisms for efficient vector transmission, protect Bartonella from the host immune response, and potentially contribute to decreased antimicrobial efficacy. Although the clinical implications are not understood, other in vitro studies indicate that Bartonella spp. can infect dendritic cells, microglial cells, monocytes and CD34+ bone marrow progenitor cells.
For over a century regional lymphadenopathy has been associated with animal contact, particularly cat scratches. Over the years, numerous microorganisms were implicated as the cause of CSD. In 1992, Regnery and colleagues at the Centers for Disease Control, identified seroreactivity to B. henselae antigens in 88% of 41 human patients with suspected CSD compared to 3% of controls.  Subsequently, additional support for B. henselae as the predominant cause of CSD was provided when Bartonella DNA was amplified from lymph node samples of 21 of 25 (84%) patients with suspected
CSD, using a polymerase chain reaction assay. A similar study from Sweden identified B. henselae DNA, but failed to identify A. felis DNA, in a large number of patients with suspected CSD. Prior to the
recognition of B. henselae as the cause of CSD, Afipia felis, named for the Armed Forces Institute of Pathology, was considered the sole cause of CSD. Subsequently, we blood cultured B. henselae or B. clarridgeae
from 17 of 19 cats owned by 14 patients with CSD, which indicated that bacteremia is a frequent occurrence in cats that transmit B. henselae
to a human being. 1-2
Historically, atypical manifestations of CSD have included tonsillitis, encephalitis, cerebral arteritis, transverse myelitis, granulomatous hepatitis and/or splenitis, osteolysis, pneumonia, pleural effusion, and thrombocytopenic purpura. With the advent of specific diagnostic techniques, (culture, serology, and PCR), there has been a dramatic increase in reports describing human patients with “atypical” manifestations of CSD. Osteomyelitis, granulomatous hepatitis and granulomatous splenitis have been increasingly recognized in children infected with B. henselae, who frequently lack the classical lymphadenopathy of CSD. Previously, Bartonella infection would not have been considered a likely differential diagnosis by the physician in patients lacking a history of lymphadenopathy or animal contact. As evidenced by reports in the past four years, the spectrum of human disease associated with the genus Bartonella continues to expand, requiring periodic reassessment as new information becomes available. On a comparative medical (“One Health”) basis, our research group has documented many of the same CSD atypical manifestations in cats or dogs, including encephalitis, transverse myelitis, granulomatous hepatitis, osteolysis, pleural effusion, and thrombocytopenic purpura. In this context, a highly prevalent, naturally-occurring human disease (CSD) can be used as a “model” to determine the potential behavior of these bacteria in companion animal patients.
Because cat scratch disease generally denotes a self-limiting illness characterized by fever and lymphadenopathy and because the recognized spectrum of human disease manifestations associated with Bartonella infections (which may not include fever or lymphadenopathy) has expanded considerably in recent years, it is becoming obvious that the designation CSD lacks clinical, microbiologic and zoonotic utility. Although cats are a major reservoir for B. henselae, B. clarridgeiae, and B. koehlerae, some patients deny the possibility of a cat scratch or bite wound, or indicate no contact with cats. Transmission from environmental sources, various arthropod vectors, perinatally or by other animal hosts is probable and the more inclusive term bartonellosis may facilitate enhanced future understanding of diseases caused by members of the genus Bartonella. As physicians have been taught that CSD is self-limiting, there is an ongoing lack of appreciation that B. henselae can cause chronic, asymptomatic or intermittently symptomatic illness, accompanied by persistent bacteremia in people. In this context, the documentation of chronic, relapsing bacteremia in cats, dogs and other animal species provides a “model” for better understanding human bartonellosis.
Endocarditis can be induced by a spectrum of Bartonella species in dogs and human patients and is the best example of documented disease causation for this genus. Historically, Bartonella species have been a cause of culture-negative endocarditis in people and dogs because the diagnostic methods used by microbiology laboratories were not adequate to isolate these bacteria. Now, by using
specialized techniques, a spectrum of Bartonella species have been identified in research and diagnostic laboratories in different parts of the world—in heart valves or in blood cultures from dogs
and people with endocarditis. 3  It is important for physicians and veterinarians to recognize that some of these Bartonella species are found in the blood of cats, dogs, rats, ground squirrels, and rabbits.
Because conventional microbiological techniques lack sensitivity, bartonellosis is usually diagnosed by PCR amplification of organism specific DNA sequences and/or through serological testing. Recently, the development of a more sensitive isolation approach, using BAPGM (Bartonella alpha Proteobacteria growth medium) followed by PCR has greatly facilitated the molecular detection or isolation of Bartonella species from the blood of sick or healthy animals, including cats, dogs, horses and human beings. Most importantly, the use of this enrichment growth medium prior to PCR testing has allowed our research group to confirm that immunocompetent human patients, in particular veterinarians and veterinary technicians, can have chronic intravascular infections with Bartonella spp. 4-5 Information relative to this EnrichmentPCRTM testing platform for animal and human patients is available at
It is increasingly clear that no single diagnostic strategy will confirm infection with a Bartonella sp. in the immunocompetent patient population.  As described in studies from our NCSU laboratory, B. henselae, B. koehlerae and B. vinsonii subsp berkhoffii seroreactivity was found in only 58.6% of the patients in which Bartonella spp. infection was confirmed by EnrichmentPCR TM and sequencing. Therefore, Bartonella serology lacks sensitivity and can only be used to implicate prior exposure to a Bartonella sp. Even when serum from cat scratch disease patients, which is caused by B. henselae, is used in various diagnostic laboratories for IFA testing, test sensitivities have ranged from 14 to 100%.
Previously, we described B. quintana bacteremia in a woman who was tested following the development of an infected cat bite lesion involving the hand. 6  Two months later, the feral cat that had
induced the bite wound was captured and was also shown to be B. quintana bacteremic. In a cumulative study involving 392 patients with occupational animal contact or extensive arthropod exposure 31.9% were bacteremic with one or more Bartonella spp., when blood, serum and BAPGM enrichment culture PCR results were combined. Although this high prevalence of bacteremia is biased by testing at risk, sick individuals, it clearly demonstrates that intravascular infection with Bartonella sp. is much more common in immunocompetent patients, than was previously suspected. By IFA testing, only 75 out of 128 (58.6%) PCR positive patients were seroreactive to a panel consisting of five Bartonella sp. test antigens.
In a recent study, Bartonella vinsonii subsp. berkhoffii, Bartonella henselae or DNA of both organisms were amplified and sequenced from blood, BAPGM enrichment blood cultures or autopsy tissues from four family members. 7  Historical and microbiological results derived from this family support human perinatal transmission of Bartonella species. To date, there have been a limited number of studies that address the potential impact of intravascular infection with a Bartonella sp. on reproductive performance, however, studies involving experimentally-infected cats, rodents and naturally-infected cows with various Bartonella sp. have identified decreased reproductive performance involving both males and females. The parents of these children had attempted to conceive children for several years prior to resorting to in vitro fertilization.
We have also described a veterinarian, who experienced a needle stick while obtaining a fine needle aspiration sample from a cutaneous histiocytic neoplasm. 8  Subsequently symptoms, including headaches, fatigue and intermittent paresthesias (numbness) developed. This patient seroconverted to B. vinsonii subsp. berkhoffii genotypes I and III and B. vinsonii subsp. berkhoffii genotype I DNA was amplified and sequenced from sequentially obtained blood samples, whereas genotype III DNA was amplified from the cytological specimen. All symptoms resolved following antibiotic treatment.
It is increasingly evident that dogs can serve as a source for human infection with B. vinsonii subsp. berkhoffii. Bartonella vinsonii subsp. berkhoffii genotype II was amplified and sequenced from
a liver biopsy from a patient with epithelioid hemangioendothelioma (soft tissue tumor considered a vascular cancer), after which the organism was isolated by BAPGM blood culture. 9  The unique capability of Bartonella to invade and induce long lasting intraerythrocytic and intraendothelial infections, in conjunction with the ability of at least three Bartonella spp. (Bh, Bq, and B. bacilliformi) to induce VEGF-mediated vasoproliferative disease in immunocompromised or immunocompetent individuals suggests that these novel emerging bacterial pathogens might contribute to the development of vascular tumors.
Bartonella koehlerae bacteremia was documented in eight immunocompetent patients by PCR amplification and DNA sequencing, either prior to or after BAPGM enrichment blood culture.10  Presenting symptoms most often included fatigue, insomnia, joint pain, headache, memory loss, and muscle pain. Four patients were also infected with Bartonella vinsonii subsp. berkhoffii genotype II. Bartonella koehlerae antibodies were not detected (titers<1:16) in 30 healthy human control sera, whereas five of eight patient samples had B. koehlerae antibody titers of 1:64 or greater. Studies are needed to determine if B. koehlerae is a cause or cofactor in the development of arthritis, peripheral neuropathies or tachyarrhythmias in human patients. Co-infection with B. henselae and two hemotropic Mycoplasma variants resembling Mycoplasma obis were also found in the blood of a veterinarian with a historical diagnosis of multiple sclerosis. 11
Due to extensive contact with a spectrum of animal species, veterinary professionals appear to have an occupational risk of infection because of frequent exposure to Bartonella spp., therefore these individuals should exercise increased precautions to avoid arthropod bites, arthropod feces (i.e. fleas and lice), animal bites or scratches and direct contact with bodily fluids from sick animals. As Bartonella spp. have been isolated from cat, dog or human blood, cerebrospinal fluid, joint fluid,aqueous fluid, seroma fluid and from pleural, pericardial and abdominal effusions, a substantial number of diagnostic biological samples collected on a daily basis in veterinary practices could contain viable bacteria.
The increasing number of defined Bartonella spp., in conjunction with the high level of bacteremia found in reservoir adapted hosts, which represent the veterinary patient population, ensures that all veterinary professionals will experience frequent and repeated exposure to animals harboring these bacteria. Therefore, personal protective equipment, frequent hand washing and avoiding cuts and needle sticks have become more important as our knowledge of this genus has improved and various modes of transmission have been defined.
Physicians should be educated as to the large number of Bartonella spp. in nature, the extensive spectrum of animal reservoir hosts, the diversity of confirmed and potential arthropod vectors, current limitations associated with diagnosis and treatment efficacy, and the ecological and evolving medical complexity of these highly evolved intravascular, endotheliotropic bacteria.
1  Chomel BB, et al. Vet Res 2009;40:29.
2  Breitschwerdt EB, et al. J Vet Emerg Crit Care 2010; 20:8.
3  Chomel BB, et al. Ann N Y Acad Sci 2009;1166:120.
4  Breitschwerdt EB, et al. J Clin Microbiol 2008;46:2856.
5  Breitschwerdt EB, et al. Parasit Vectors 2010;3:29.
6  Breitschwerdt EB, et al. J Clin Microbiol 2007;45:270.
7  Breitschwerdt EB, et al. J Clin Microbiol 2010;48:2289.
8  Oliveira AM et al. J Vet Intern Med 2010;24:1229.
9  Breitschwerdt EB, et al. J Clin Microbio 2009;47:1957.
10 Breitschwerdt EB, et al. Parasit Vectors 2010;3:76.
11 Sykes JE, et al. J Clin Microbiol 2010;48:3782.

Avril Lavigne – Head Above Water (Lyric Video)

Video Created by: Jonah Best
Produced by: Magic Seed Productions

I’ve gotta keep the calm before the storm
I don’t want less
I don’t want more
Must bar the windows and the doors
To keep me safe to keep me warm

Yeah my life is what I’m fighting for
Can’t part the sea
Can’t reach the shore
And my voice becomes the driving force
I won’t let this pull me overboard

God keep my head above water
Don’t let me drown
It gets harder
I’ll meet you there at the altar
As I fall down to my knees
Don’t let me drown
Don’t let me drown

So pull me up from down below
‘Cause I’m underneath the undertow
Come dry me off and hold me close
I need you now I need you most

God keep my head above water
Don’t let me drown
It gets harder
I’ll meet you there at the altar
As I fall down to my knees
Don’t let me drown
Don’t let me drown
Don’t let me drown
Keep my head above water above water

And I can’t see in the stormy weather
I can’t seem to keep it all together
And I can’t swim the ocean like this forever
And I can’t breathe

God keep my head above water
I lose my breath at the bottom
Come rescue me
I’ll be waiting
I’m too young to fall asleep

God keep my head above water
Don’t let me drown
It gets harder
I’ll meet you there at the altar
As I fall down to my knees
Don’t let me drown
Don’t let me drown
Don’t let me drown
Keep my head above water above water

To find resources on Lyme Disease PREVENTION, educate yourself on doctors and TREATMENT, learn more about the most current scientific RESEARCH…and JOIN OUR FIGHT AGAINST LYME,


Glandular Tularemia

  • Laura Marks, M.D., Ph.D.,
  • and Andrej Spec, M.D.

A 68-year-old man from Missouri presented to the primary care clinic with a history of 1 week of fever followed by 2 months of progressive, painful swelling on the right side of his neck. Approximately 2 days before the onset of the patient’s symptoms, his outdoor cat died from a subacute illness; a veterinarian had diagnosed feline leukemia without laboratory testing, and the cat had been treated with prednisone, which the patient administered. The patient’s physical examination revealed three erythematous, tender lymph nodes. The remainder of the physical examination was normal. Serologic testing with IgM antibody was positive for Francisella tularensis (titer, 1:1280). A diagnosis of glandular tularemia was made. Glandular tularemia is the second most common manifestation of tularemia after the ulceroglandular form. Because culture requires biosafety level 3 conditions, diagnosis is often confirmed serologically. Domestic cats can become infected through the consumption of infected prey and can transmit the bacteria to humans. The patient was treated with doxycycline for 4 weeks; the lesions improved within 5 days and resolved within 3 weeks.

Laura Marks, M.D., Ph.D.
Barnes–Jewish Hospital, St. Louis, MO

Andrej Spec, M.D.
Washington University in St. Louis, St. Louis, MO




I remember hearing Timothy Lepore, MD, FACS, surgeon at Nantucket Cottage Hospital, at a Lyme conference.  He explained that Tularemia is also a disease of those who work with the land such as landscapers and farmers, as well as those who get bit by a tick. There are cases reported in every state but Hawaii, and many other wild and domestic animals can be infected. The highest rates of infection are in Arkansas.  Please see this link for more details but know that this is a bioweaponized pathogen:  The WHO estimates that an aerosol dispersal of 50 kg of F. tularensis over an area with 5 million people would result in 25,000 incapacitating casualties including 19,000 deaths.

For hunters:  “The frequency of about seven percent shows that hunting dogs can also become infected regularly. As vectors of the disease, even without symptoms, the animals must also be considered unexpected carriers,” Posautz adds.

Approx. 4 Min.



We shouldn’t be eating hardly anything presented here.  The apple, natural honey, butter, mayo, and cottage cheese are about it.

For homemade mayo.  Makes 2 1/2 C.  Put all into blender:

2 eggs

1 tsp salt

2 T honey

2 T apple cider vinegar

1 T Dijon mustard

Blend for 1 min.  With motor running slowly drizzle 1 C of safflower oil, then 1/8 C lemon juice, then 1 more C of safflower oil.  Continue blending until emulsified.  This won’t keep forever so store in frig and use within 2 weeks.

Interesting note on butter….so a patient went to his doc having allergy-type symptoms and said the only thing was that he was using a different brand of butter.  The doc called the manufacturing facility and learned they put a a thin layer of crushed shellfish on the butter to help keep it’s shape when it’s warmed.  The man was allergic to shell fish.

Until the food industry is required to honestly label ALL ingredients (even things like minute amounts of shellfish used for shape) patients will struggle with figure out why they react to so many things.