The fall of the biopsychosocial model

While both CBT and GET are not often discussed directly in biopsychosocial terms, its alluded to frequently.
GET is of course the bio- part;
CBT (under a presumption of a psychosomatic illness) is the -psycho- part,
and denying patients support and benefits that will enable their illness is the -social part.

Source: http://forums.phoenixrising.me/entry.php?1347-The-Rise-and-Fall-of-the-Biopsychosocial-Model

One Link Established- Chronic Fatigue Syndrome (CFS), Lupus, Fibromyalgia, Autoimmune disease and Chronic Lyme Disease

http://www.envita.com/lyme-disease/finally-one-link-established-chronic-fatigue-syndrome-cfs-lupus-fibromyalgia-autoimmune-disease-chronic-lyme-disease

An Easy Explanation to Idiopathic (unknown Cause of Disease) – But is it the Right One? 

Idiopathic disease is defined as one that develops without any apparent or known causes.  That is the term used for fibromyalgia, autoimmune diseases, including Lupus and Chronic Fatigue Syndrome. While many of these diseases have recognizable signs and symptoms, the lack of causality haunts medical schools, doctors, practices, and hospitals. The only one benefitting from the lifelong symptom treating associated with Chronic Fatigue Syndrome, Lupus, Autoimmune disease, or Fibromyalgia are the pharmaceutical companies who sell billions in medication to treat them. A long list of pain medications, sleep-aids, anti-depressants and anti-inflammatories is not sufficient because the diagnosis is incorrect. So let’s look at what the possible causes are to these diseases.

Here is the conventional Scientific Overview of What Causes (Chronic Fatigue Syndrome) CFS and Fibromyalgia

Below, is a quick list of causes and we will give a clinical review and explanation as to what takes place.

• Brain abnormalities
• Genetic factors (HPA) axis
• A hyper-reactive immune system
• Viral or other infectious agents like (Chronic Lyme disease Complex)
• Psychiatric or emotional conditions

Are Genetics to Blame? Fibromyalgia and Chronic Fatigue Syndrome

Chronic Fatigue Syndrome and Fibromyalgia have been linked with genes involved in the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. These genes regulate response to trauma, injury, and other stressful events. 10 years of Envita’s clinical experience shows that while such traumas could play a role in the etiology (the trigger to exhibiting symptoms) of the disease, they are not likely the causes of these conditions.

What is the HPA (Hypothalamic-pituitary- adrenal axis)?  Does Lyme Disease Play a Role?

HPA makes up a multi-set of direct influences and feedback interactions among the hypothalamus, the pituitary gland (a pea-shaped structure located below the hypothalamus), and the adrenal, also called “suprarenal,” glands which are small, conical organs on top of the kidneys.
The interactions among these organs constitute the HPA axis, a major part of the neuroendocrine system that controls reactions to stress and regulates many body processes including digestion, the immune system, mood, emotions, sexuality, as well as energy storage and expenditure. Infectious disease, such as chronic Lyme Disease Complex, impacts the HPA-axis via neurotoxins that compete for the same receptor sites used by the HPA-axis. In fact, such infections can bring about identical symptoms of some idiopathic diseases listed above and many of the symptoms associated therewith. This should bring our attention to the Lyme Disease Complex, which is composed of a number of infections and neurotoxins that bring about even more symptoms than those listed earlier in this article.

Does HPA Affect Fibromyalgia and Chronic Fatigue Syndrome?

Abnormal levels of certain chemicals regulated in the HPA axis area of the brain system, have been proposed as a cause of Chronic Fatigue Syndrome and also have some influence in Fibromyalgia. This system controls important functions, including sleep, stress response, and depression. Of particular interest to researchers, are the chemicals and other factors listed below that are controlled by the HPA axis.
The HPA axis is involved in the neurobiology of mood disorders and functional illnesses, including anxiety disorder, bipolar disorder, insomnia, post-traumatic stress disorder, borderline personality disorder, ADHD, major depressive disorder, burnout, chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome, and alcoholism. Antidepressants, which are routinely prescribed for many of these illnesses, serve to regulate HPA axis function. All of these conditions and their symptoms are commonly seen in Chronic Lyme disease patients that contain a host of infections and neurotoxins that block serotonin receptors in the brain.

How Can Chronic Lyme Disease Complex or Infectious Disease Affect HPA?

Patients may have contracted an infection at any point in their life-time; however, the symptoms of Chronic Lyme disease Complex or its co-infections may remain unseen or dormant until the individual is weakened by a trauma or trigger. This could be anything from child birth or a car accident to the death of a loved one, a divorce, or even a vaccine as seen among children with weakened immune systems.
In the etiology of chronic infectious disease, the traumatic event is a trigger but not the cause of autoimmune disease, Chronic Fatigue Syndrome, or Fibromyalgia. Nevertheless, treating these triggers is critically important to the new patient’s care. What we find is that infection and not genetic defects are at the root of HPA axis disruption in the brain itself.

The Major Impact of Epigenetic Changes

A number of studies have found that alterations in genes are caused by infections involving immune function, intercellular communication and energy transfer.
Researchers have identified many different genes in patients with Chronic Fatigue Syndrome that relate to blood disease, immune system function, and infection. However, despite these identifications, there is no clear pattern to them and it is quite possible that it is the infections alone that are altering these genes and are responsible for impacting mental and emotional health as well. It is very possible that the infections can alter these genes that impact mental and emotional health as well.

Important Neurotransmitters Changed by Neurotoxins Competing for Receptor Sites

Some patients with Chronic Fatigue Syndrome have abnormally high levels of serotonin – a neurotransmitter (chemical messenger in the brain), and also show deficiencies in dopamine – an important neurotransmitter associated with feelings of reward. In some cases there is also a demonstrable imbalance between norepinephrine and dopamine.
A number of studies on Chronic Fatigue Syndrome have shown patients with lower cortisol levels, a stress hormone produced by the adrenal glands. It has been suggested that such cortisol deficiencies are responsible for Chronic Fatigue Syndrome patients having impaired or weakened responses to psychological or physical stresses like worry, infection, or exercise. However, administering replacement cortisol improves symptoms only in some patients. Why? Infection and their toxins (neurotoxins) must be cleared before hormone replacement can begin to be effective in these patients. It is also common for these patients to have thyroid, testosterone and cortisol issues.

Idiopathic Diseases are at the Root of Many Psychological Disorders: Sleep disorders Explained

Evidence suggests that certain CFS, Fibromyalgia, and Autoimmune patients have disturbed circadian rhythms (disorder of the sleep-wake cycle), which is regulated by the so-called circadian clock, a nerve cluster in the HPA axis. These are commonly seen in Lyme Disease Complex along with a number of other neurological symptoms.
A mentally or physically stressful event, such as a viral infection, may disrupt natural circadian rhythms. An inability to reset these rhythms results in a perpetual cycle of sleep disturbances. Medications that improve sleep can be very helpful for certain patients with Chronic Fatigue Syndrome, Fibromyalgia, and Autoimmune diseases. But, until the infections are cleared and hormones are rebalanced, long-term improvement is unlikely.
Psychological, personality, and social factors are strongly associated with Chronic Fatigue Syndrome, Fibromyalgia, and Autoimmune disease like Lupus. There is a distinct complex relationship between physical and emotional factors.

What Specific Infections are Responsible

Because most of the features of Chronic Fatigue Syndrome resemble those of a lingering viral illness, many researchers have focused on the possibility that a virus or some other infectious agent, in some cases, causes the syndrome.
At Envita, we have clinically determined that these patients usually have a group of viral, bacterial, parasitic, and fungal infections that make up what we call Lyme Disease Complex. Some patients may or may not have actual Lyme disease but may have another type of tick-borne illness along with a host of co-infections that have brought about immunological, hormonal, and neuroendocrine changes.
Still, not all Chronic Fatigue Syndrome patients show signs of infection. And although experts have long been divided on whether infections play any role in this disorder at all, it does seem clear that subtypes of both viral and non-viral Chronic Fatigue Syndrome exist. That being said, researchers have seemingly overlooked the complexity of mute-infections, multi-toxins, and heavy metal components that complicate these conditions making them extremely difficult to diagnose on a case to case basis. When a complex of infections exists, they can affect the activation and replication of each other via biofilm communities. To be certain, most patients are never tested thoroughly and correctly for all the infections that make up, chronic Lyme Disease Complex.

Infections, Looking More Like the Cause

The theory for Chronic Fatigue Syndrome having a viral cause is not based on hard evidence, rather, on an ever-growing series of observations that suggest this association:
Chronic Fatigue Syndrome as well as Fibromyalgia and Autoimmune disease patients are often found with elevated levels of antibodies to many organisms that cause fatigue and other Chronic Fatigue Syndrome symptoms. Such organisms include those that cause Lyme disease, Candida (“yeast infection”), herpes virus type 6 (HHV-6), human T cell lymph tropic virus (HTLV), Epstein-Barr, measles, coxsackie B, cytomegalovirus, or parvovirus.
Many of these infectious agents are very common; however, none have emerged as a definitive cause of CFS. Well-designed studies of patients who met strict criteria for CFS without any known cause have not found an increased incidence of any specific infection(s).
In up to 80% of cases, CFS starts suddenly with a flu-like condition. In the U.S., there have been reports of cluster outbreaks of CFS occurring within the same household, workplace, and community (but most have not been confirmed by the Centers for Disease Control and Prevention). However, most cases of CFS occur sporadically in individuals, and do not appear to be contagious. These all have the pattern of infections and more importantly, complexes of infections taking over the patient’s immune system, which is clearly seen in the depressed CD57 markers found in almost all of this population.

Infection Complexes Leading to Immune System Abnormalities and Immuno-Compromised States

CFS is sometimes referred to as “Chronic Fatigue Immune Dysfunction Syndrome.” In many cases, studies have detected many immune system irregularities. Some components appear to be over-reactive, while others appear to be under-reactive, but no consistent picture has emerged to explain CFS as a disease of the immune system in conventional medical practices. Chronic Lyme Disease patients almost always have depressed CD57 marker called the striker panel and this is almost never run on chronic fatigue patients when they go to their doctor. Almost 100% of the time we find decreased key immune function in all CFS patients because we are running the correct diagnostics.

Environmental Toxins Impact Chronic Fatigue Syndrome and Fibromyalgia

Some studies have reported that a majority of CFS patients have allergies to foods, pollen, metals (such as nickel or mercury), or other substances. One theory is that allergens, like viral infections, may trigger a cascade of immune abnormalities leading to CFS. However, most allergic people do not have CFS. In our clinical setting, patients often have pesticide, heavy metal and chemical toxicity along with chronic infections which explains the abnormal and inconstant responses to allergies. Environmental toxins complicate these conditions and require targeted treatments to overcome them.

Autoimmunity Overlaps with other Conditions

The risk profile for CFS is similar to the risk profiles for a number of autoimmune diseases. Studies are inconsistent with regards to the presence of auto-antibodies (antibodies that attack the body’s own tissues) in CFS, so the disease is unlikely to be due to auto-immunity – making it more likely connected to infectious disease. In Lyme disease patients, we typically see that the patient was diagnosed at one time or another with several autoimmune diseases but almost certainly the previous physicians were confused.

Where Can You Find Help?

Envita Medical Centers has been leading the way in comprehensive, personalized patient care.  Contact us for more information. We will answer any health questions you may have.

http://www.envita.com/lyme-disease/finally-one-link-established-chronic-fatigue-syndrome-cfs-lupus-fibromyalgia-autoimmune-disease-chronic-lyme-disease

The Invitation by Oriah

It doesn’t interest me
what you do for a living.
I want to know
what you ache for
and if you dare to dream
of meeting your heart’s longing.

It doesn’t interest me
how old you are.
I want to know
if you will risk
looking like a fool
for love
for your dream
for the adventure of being alive.


It doesn’t interest me
what planets are
squaring your moon...
I want to know
if you have touched
the centre of your own sorrow
if you have been opened
by life’s betrayals
or have become shrivelled and closed
from fear of further pain.


I want to know
if you can sit with pain
mine or your own
without moving to hide it
or fade it
or fix it.


I want to know
if you can be with joy
mine or your own
if you can dance with wildness
and let the ecstasy fill you
to the tips of your fingers and toes
without cautioning us
to be careful
to be realistic
to remember the limitations
of being human.


It doesn’t interest me
if the story you are telling me
is true.
I want to know if you can
disappoint another
to be true to yourself.

If you can bear
the accusation of betrayal
and not betray your own soul.
If you can be faithless
and therefore trustworthy.


I want to know if you can see Beauty
even when it is not pretty
every day.
And if you can source your own life
from its presence.


I want to know
if you can live with failure
yours and mine
and still stand at the edge of the lake
and shout to the silver of the full moon,
“Yes.”


It doesn’t interest me
to know where you live
or how much money you have.
I want to know if you can get up
after the night of grief and despair
weary and bruised to the bone
and do what needs to be done
to feed the children.


It doesn’t interest me
who you know
or how you came to be here.
I want to know if you will stand
in the centre of the fire
with me
and not shrink back.


It doesn’t interest me
where or what or with whom
you have studied.
I want to know
what sustains you
from the inside
when all else falls away.


I want to know
if you can be alone
with yourself
and if you truly like
the company you keep
in the empty moments.


By Oriah © Mountain Dreaming,
from the book The Invitation
published by HarperONE, San Francisco,
1999 All rights reserved

http://www.oriahmountaindreamer.com/

Chronic diseases can stem from infectious agents

Evidence now confirms that noncommunicable chronic diseases can stem from infectious agents. Furthermore, at least 13 of 39 recently described infectious agents induce chronic syndromes.

Identifying the relationships can affect health across populations, creating opportunities to reduce the impact of chronic disease by preventing or treating infection. As the concept is progressively accepted, advances in laboratory technology and epidemiology facilitate the detection of noncultivable, novel, and even recognized microbial origins. 

A spectrum of diverse pathogens and chronic syndromes emerges, with a range of pathways from exposure to chronic illness or disability. Complex systems of changing human behavioral traits superimposed on human, microbial, and environmental factors often determine risk for exposure and chronic outcome. Yet the strength of causal evidence varies widely, and detecting a microbe does not prove causality.

Nevertheless, infectious agents likely determine more cancers, immune-mediated syndromes, neurodevelopmental disorders, and other chronic conditions than currently appreciated.

full paper
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291059/

Potential Pathogens cause of Fibromyalgia

Fibromyalgia (FM) is a commonly misunderstood, sometimes misdiagnosed rheumatic disease. The main symptoms are achiness, pain (more in the muscles than in the joints), stiffness, fatigue, accompanied by headaches, depression, sleep disorders, Raynaud's and irritable bowel syndrome. The sites of pain are located in specific areas called tender or trigger points.

The painful tender points are located where the ligament attaches the muscle to the bone. There are 18 tender point locations. Sensitivity at 11 points defines a diagnosis of fibromyalgia. FM is not life threatening nor does it cause physical deformities. Many lab tests are within normal range. In fact, most patients look extremely well and fit, making it difficult to account for the degree of clinical suffering they are experiencing, yet 10-30% of fibromyalgia patients are disabled to some degree because of their disease symptoms.
It is 9 times more common among women than men, usually between the ages of 40 and 60, is more common in Caucasians than other races, and is the second or third most common disorder treated by rheumatologists.

Potential Pathogens
As is the case of most forms of "arthritis," no known cause has been established, but a number of possibilities are mentioned in the medical literature. Like many forms of arthritis, the cause of FM is probably not limited to one single factor.

1.      55% of patients identify a "flu-like" or viral type illness,

2.      33% physical trauma/injury and

3.      14% emotional stress as a precursor to the onset of symptoms. 

The connection of FM to infections is well documented in the literature, especially in relation to Lyme disease, mycoplasma, Chlamydia pneumoniae., Hepatitis C, Parvovirus B19, HIV, and Epstein-Barr.

Source: www.cpnhelp.org

Association of Active HHV-6, -7 and Parvovirus B19 in ME/CFS

http://downloads.hindawi.com/journals/av/2012/205085.pdf

Adv Virol. 2012;2012:205085. Epub 2012 Aug 13.

Association of Active Human Herpesvirus-6, -7 and Parvovirus B19
> Infection with Clinical Outcomes in Patients with Myalgic
> Encephalomyelitis/Chronic Fatigue Syndrome.
>
> Chapenko S, Krumina A, Logina I, Rasa S, Chistjakovs M, Sultanova A,
> Viksna L, Murovska M.
> August Kirchenstein Institute of Microbiology and Virology, Riga
> Stradins University, Ratsupites Street 5, LV-1067 Riga, Latvia.
>
> Abstract
>
> Frequency of active human herpesvirus-6, -7 (HHV-6, HHV-7) and
> parvovirus B19 (B19) infection/coinfection and its association with
> clinical course of ME/CFS was evaluated.
>
> 108 ME/CFS patients and 90 practically healthy persons were enrolled
> in the study.
>
> Viral genomic sequences were detected by PCR, virus-specific
> antibodies and cytokine levels-by ELISA, HHV-6 variants-by restriction
> analysis. Active viral infection including concurrent infection was
> found in 64.8% (70/108) of patients and in 13.3% (12/90) of
> practically healthy persons.
>
> Increase in peripheral blood leukocyte DNA HHV-6 load as well as in
> proinflammatory cytokines' levels was detected in patients during
> active viral infection.
>
> Definite relationship was observed between active betaherpesvirus
> infection and subfebrility, lymphadenopathy and malaise after
> exertion, and between active B19 infection and multijoint pain.
> Neuropsychological disturbances were detected in all patients. The
> manifestation of symptoms was of more frequent occurrence in patients
> with concurrent infection.
>
> The high rate of active HHV-6, HHV-7 and B19 infection/coinfection
> with the simultaneous increase in plasma proinflammatory cytokines'
> level as well as the association between active viral infection and
> distinctive types of clinical symptoms shows necessity of simultaneous
> study of these viral infections for identification of possible subsets
> of ME/CFS.
>


>
> Full paper: http://downloads.hindawi.com/journals/av/2012/205085.pdf

My question to dr Schwarzbach

http://www.ilads.org/lyme_programs/boston/speakers/bio_schwarzbach.php

Sunday, Nov. 4, 2012
8:10-8:40am

Chlamydia Pneumoniae and Borrelia Burgdorferi as Intracellular and Cystic Bacteria: A Study About Symptoms, Laboratory Problems and Therapeutical Consequences

Dr. Armin Schwarzbach, MD, PhD is a specialist in laboratory medicine from the Borreliose Centrum Augsburg/ Germany. He began by studying biochemistry at Hoechst AG, Frankfurt/Germany where he worked as a medical assistant in internal medicine and infectiology. By 1993 he had started specializing in laboratory medicine. Dr. Schwarzbach is the Chair of the laboratory test, international and international membership committees of ILADS. His friends call him the German Lyme Fighter.
Company: Infectolab
Address: Morellstr. 33, Augsburg, Germany D-86399
Phone: 0049(0)8214550740
Website: www.infectolab.de

My question:

Could Lyme symptoms be mimicked by chlamydia pneumonia + chronic EBV + chronic CMV (and others) + low B12 + adrenal insufficiency + hypothyroid + low ATP + ANA antibodies + low VIP + monocytosis + partial immunoglobulines deficiency + MCS + mycoplasma + calcifications in joints + artritis like lesions?

 

Dr Schwarzbach:

Absolutely! I got the impression, that not Lyme is worldwide problem no 1, but Chlamydia and Mycoplasma pneumoniae and the symptoms are nearly the same according literature. Also EBV and all other problems you mention can overlap this situation and the symptoms.

For more information about the intracellular bacterial infection Chlamydia Pneumonia, please visit www.cpnhelp.org
Symptoms, diagnosis, related illnesses, protocols, forum, patient stories, ...

Chlamydia pneumonia is more than an energy parasite

http://www.cpnhelp.org/pdfs/Host:CellEnergyDepl.pdf

The pathogenesis of Systemic Chlamydial Infections: Theoretical Considerations of Host Cell Energy Depletion and its metabolic consequences

Chlamydiae are prokaryocytes that
develop in eukaryotic cells and utilize
part of the host cell metabolism.

...
Moreover,
electron microscopic studies have shown
that replicating chlamydiae are always
found in close proximity to mitochondria.
Therefore, it has been suggested
that chlamydiae behave in the reverse
manner of mitochondria in that mitochondria
import ADP from the host cell
cytoplasm and export ATP, while
chlamydiae import ATP and export ADT.
...
Depletion of host cell energy by the
intracellular infection with Chlamydia
species might cause additional energyrelated
complications. As fewer electrons
are available to move through the
electron transport chain of the host cell
mitochondrial matrix membrane, the
citric acid cycle produces more succinyl-
CoA which. in turn, promotes increased
synthesis of d-ALA. The net result is an
increased amount of heme precursors
and heme porphyrins. The presence of
porphyrins in the mitochondrial matrix
may damage the cell as these molecules
are unstable and form free radicals.
...
The clinical result of the intracellular
and extracellular accumulation of porphyrins,
if extensive, could be an tissue/
organ specific secondary porphyria
which might produce the classical manifestations
of porphyria including neuropsychiatric
symptoms and signs. As
the chlamydial-infected host cells lyse,
as can happen in the normal life cycle
of Chlamydia, the intracellular porphyrins
are released and result in porphyria

Source:
http://www.cpnhelp.org/pdfs/Host:CellEnergyDepl.pdf
http://en.wikipedia.org/wiki/Porphyria

Latent CMV impairs NK-cells after acute exercise

rain Behav Immun. 2012 Jan;26(1):177-86. Epub 2011 Sep 10.

NK-cells have an impaired response to acute exercise and a lower expression of the inhibitory receptors KLRG1 and CD158a in humans with latent cytomegalovirus infection.

Bigley AB, Lowder TW, Spielmann G, Rector JL, Pircher H, Woods JA, Simpson RJ.

Source

Laboratory of Integrated Physiology, Department of Health and Human Performance, University of Houston, 3855 Holman Street, Houston, TX 77204, USA.

Abstract

NK-cells and γδ T-cells are cytotoxic effectors of the immune system that are preferentially mobilized into the blood compartment in response to acute stress and exercise.
...
EBVpos had higher proportions of CD8+ NK-cells, but cellular responses to exercise were not influenced by EBV. The frequency and exercise-responsiveness of γδ T-cells was not affected by CMV or EBV serostatus (p>0.05). In conclusion, latent CMV infection is associated with lowered numbers of NK-cells expressing inhibitory receptors and a blunted mobilization of NK-cells in response to acute exercise. This may indicate a compromised immune response to "fight-or-flight" situations in those infected with CMV.
Copyright © 2011 Elsevier Inc. All rights reserved.

http://www.ncbi.nlm.nih.gov/

pubmed/21933704

Sanitary cover up of bartonella?

What if bacterial infections were the cause of an epidemic of chronic illnesses but your government looked the other way?

Let's say bartonella was prevalent in 90% of beef cattle. Would you still feel comfortable eating it?
What if your cat could transmit bartonella by its flees or a scratch, would you still pet it?
What if your child could get if via head lice in school, would you believe it?
What if your endocarditis, muscle or joint paint was not due to getting old, but to a bacteria that is hard to find by a bloodtest, would you doubt about a negative result?
What if you knew antibiotics had a hard time against bartonella, would you find the courage to continue?

Read more:
http://veterinarymedicine.dvm360.com/vetmed/article/articleDetail.jsp?id=660519&pageID=1&sk=&date=
Bartonellosis: An emerging and potentially hidden epidemic?

PCR detection of Bartonella bovis and Bartonella henselae in the blood of beef cattle.

Cherry NA, Maggi RG, Cannedy AL, Breitschwerdt EB.

Source

Intracellular Pathogens Research Laboratory, Center for Comparative Medicine and Translational Research, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606, United States.

Abstract

Although an organism primarily associated with non-clinical bacteremia in domestic cattle and wild ruminants, Bartonellabovis was recently defined as a cause of bovine endocarditis. The purpose of this study was to develop a B. bovis species-specific PCR assay that could be used to confirm the molecular prevalence of Bartonella spp. infection. Blood samples from 142 cattle were tested by conventional PCR targeting the Bartonella 16S-23S intergenic spacer (ITS) region. Overall,Bartonella DNA was detected in 82.4% (117/142) of the cattle using either Bartonella genus primers or B. bovis species-specific primers. Based upon size, 115 of the 117 Bartonella genus ITS PCR amplicons were consistent with B. bovis infection, which was confirmed by PCR using B. bovis species-specific primers and by sequencing three randomly selected, appropriately sized Bartonella genus PCR amplicons. By DNA sequencing, Bartonella henselae was confirmed as the two remaining amplicons, showing sequence similarity to B. henselae URBHLIE 9 (AF312496) and B. henselae Houston 1 (NC_005956), respectively. Following pre-enrichment blood culture of 12 samples in Bartonella alpha Proteobacteria growth medium (BAPGM) B. henselae infection was found in another three cows. Four of the five cowsinfected with B. henselae were co-infected with B. bovis. To our knowledge this study describes the first detection of B. henselae in any large ruminant species in the world and supports the need for further investigation of prevalence and pathogenic potential of B. henselae and B. bovis in cattle.

https://sites.google.com/site/marylandlyme/pets/cows