ScienceDaily (Nov. 24, 2008) -- Bacteria that can cause serious heart disease in humans are being spread by rat fleas, sparking concern that the infections could become a bigger problem in humans. Research published in the December issue of the Journal of Medical Microbiology suggests that brown rats, the biggest and most common rats in Europe, may now be carrying the bacteria.
Since the early 1990s, more than 20 species of Bartonella bacteria have been discovered. They are considered to be emerging zoonotic pathogens, because they can cause serious illness in humans worldwide from heart disease to infection of the spleen and nervous system.
"A new species called Bartonella rochalimae was recently discovered in a patient with an enlarged spleen who had travelled to South America," said Professor Chao-Chin Chang from the National Chung Hsing University in Taiwan. "This event raised concern that it could be a newly emerged zoonotic pathogen. Therefore, we decided to investigate further to understand if rodents living close to human environment could carry this bacteria."
Scientists have found that rodents carry several pathogenic species of Bartonella, such as B. elizabethae, which can cause endocarditis and B. grahamii, which was found to cause neuroretinitis in humans. Although scientists are unsure about the main route of transmission, these infections are most likely to be spread by fleas. Ctenophthalmus nobilis, a flea that lives on bank voles, was shown to transmit different species of Bartonella bacteria. These pathogens have also been found in fleas that live on gerbils, cotton rats and brown rats.
"We analysed bacteria found in Rattus norvegicus in Taiwan. The brown rat is also the most common rat in Europe," said Professor Chang. "By analysing the DNA of the bacteria, we discovered a strain that is most closely related to B. rochalimae, which has been isolated recently from a human infection in the United States".
The researchers took samples from 58 rodents, including 53 brown rats, 2 mice (Mus musculus) and 3 black rats (Rattus rattus). 6 of the rodents were found to be carrying Bartonella bacteria; 5 of these were brown rats. Four of the rodents were carrying B. elizabethae, which can cause heart disease in humans, and one of the black rats was found to be harbouring B. tribocorum. However, the scientists noticed one strain that had not been identified in rodents previously. The strain was finally shown to be close to B. rochalimae.
"Because of the small sample size used in this study, we cannot say for sure that the common brown rat is spreading B. rochalimae," said Professor Chang. "However, several different Bartonella bacteria are surely transmitted by rodents. These results raise concerns about the existence of other reservoirs and vectors for this emerging infection. This certainly warrants further investigation."
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posted
Discovery Of New Bartonella Species That Infects Humans 07 Jan 2009
Researchers at North Carolina State University and the Centers for Disease Control and Prevention have produced the first link between a species of bacteria most commonly found in sheep and human illness.
Dr. Edward Breitschwerdt, professor of internal medicine at NC State's College of Veterinary Medicine, and NC State colleague Dr. Ricardo Maggi isolated the bacterium Bartonella melophagi from samples of human blood.
B. melophagi is such a newly discovered member of the genus Bartonella it is considered a "Candidatus" species, meaning that its name has yet to be formally accepted. In nature, sheep are the most likely hosts for B. melophagi and transmission among sheep is thought to occur via a wingless fly known as a ked. The route(s) of transmission to humans is unknown.
Their results are published in the January edition of Emerging Infectious Diseases.
The blood samples Breitschwerdt and Maggi tested came from previously healthy women who were suffering from symptoms including muscle fatigue and weakness. One of the patients had been diagnosed with pericarditis, an inflammation of the membrane surrounding the heart. B. melophagi was present in blood samples from both women; Bartonella henselae, a strain of the bacterium which has been associated with human neurological illnesses and fatigue, was isolated from one of the samples.
The research marks the first time that this particular strain of Bartonella has been cultured from human blood and associated with human illness.
"Over the past decade, there has been a rapid expansion in the number of Bartonella species that are documented human pathogens," Breitschwerdt says. "From this preliminary data, it looks as though we may be able to add another species to that list."
"A small number of Bartonella in the bloodstream can cause infection, and this fact, coupled with the large variety of transmission routes by which people can become infected, make the diagnosis, treatment and prevention of the illnesses caused by this bacteria a real challenge," Maggi adds. "I think it's critical that we discover more about how this bacteria infects people, and how Bartonella infection relates to the subsequent development of progressive illnesses in humans."
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1: Am J Clin Pathol. 2009 Feb;131(2):250-6. Related Articles, Links Click here to read Evaluation of immunohistochemistry in identifying Bartonella henselae in cat-scratch disease.
Department of Pathology, Baystate Medical Center, Tufts University School of Medicine, Springfield, MA, USA.
Cat-scratch disease (CSD) is largely due to infection with Bartonella henselae. Microbiologic detection is difficult, and molecular testing is not readily available. A monoclonal antibody (mAB) to B henselae has become commercially available. We evaluated the usefulness of immunohistochemical analysis (IHC) for diagnosing CSD on surgical specimens and compared these results with polymerase chain reaction (PCR) detection and serologic testing for B henselae. We studied 24 formalin-fixed, paraffin-embedded (FFPE) cases of lymphadenitis with histologic and/or clinical suspicion of CSD. Control cases included 14 cases of lymphadenopathy other than CSD. FFPE tissue sections were evaluated with an mAB to B henselae, Steiner silver stain (SSS), and PCR that targeted B henselae and Bartonella quintana. Positive cases were as follows: SSS, 11 (46%); PCR, 9 (38%); and IHC, 6 (25%). Only 2 cases (8%) were positive for all 3 studies. All control cases were negative for IHC and PCR. The diagnostic sensitivity of these 3 tests is low for CSD. SSS seems to be the most sensitive test but is the least specific. PCR is more sensitive than IHC and may, therefore, serve as a helpful second-line test on all IHC- cases.
Publication Types:
* Evaluation Studies
PMID: 19141385 [PubMed - indexed for MEDLINE]
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posted
Someone had sent me a pm with some questions about the skin manifestations of Bart. Out of the fourty or so that Dr. James Schaller illustrates and describes in his book, my son and I seem to have had 37 of them.
To answer this person's question more specifically in reference to the purple river stretch marks and vessels....
The purple river strecth marks my son has, are the kind of stretch marks that occur where normally they do not. His are located along his lower back and hips, and occured without any signifigant growth to his body. The purple river strecth marks for those with Bartonella, tend to go against the structural lines of normal skin, although some do not. The more purple they are, they more active they are perceived and are commonly referred to as striations, but they really do look like stretch marks to me.
In both the child and adult, you will find stretch marks where there really shouldn't be any, such as the mid arm on the outer part, the antecubital, along the back, the backs of the knees, and the peripheral arm pit margins.
Yes, with Bart you will also commonly encounter new vessels appearing under the skin. Vessels, resembling chains of broken tiny capillaries, spider veins, or varicose veins. Bartonella secretes VEGF in which stimulates vessel growth. You can find these anywhere, and usually they seem to progress where you start out with one or two areas, easily explained with aging, and then you continue to get them.
You may see these in common areas where the ones we acquire through aging appear, but you will also find them in the unusual as well. Such as the inside of the mid arm, along the stomach, and the lateral margins of your feet, esp. around the ankles and clustered in the arches. These can appear as little capillaries or veins. Someone mentioned green vasculature, and I am not sure where the source for the information was, but I don't recall that being discussed by Dr. James Schaller, but there were fourty or so he covered.
Hope this helps with your son.
Lauirel
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posted
Great information... I have dark purple stretch marks behind my knees and on my inner thigh that go up indstead of across like the ones from gaining weight in pregnancy... SO I can see my pregnancy stretch marks which are silvery and then ones going up and down which are purple... I also have them on my inner arms going from my armpit almost down to my elbow... they were VERY purple last year and have been getting dimmer to a light pink and some silvery.
I also have the purple ones at the top of my thigh running down. I can see the silvery ones from pregnancy and then these purple ones which have gotten lighter but are still dark and wider than the pregnancy ones.
At my next doc appt, she is doing that VEGF test. Before I got pregnant, hence before I was EVER sick... I had a small kitten off the street... I gave it a home and it gave me hundreds of flee bites all over. This is when all the madness started... SEVERE anxiety that kept me in the hosue.. I even had to drop out of college. I then became pregnant and the rest is history, I have been sick ever sicne with BAD neuro symptoms that have left me bedridden since my daughter was born 2 years ago.
Here is the million dollar question.....
WHAT is the best treatment for Bartonella??
I have been on
Doxy (1 month) Tetracycline (2 months) Zith (6 months) Septra Bicillin (could only do a month and a half) Omnicef (short course) Mepron Mino while doing the MP for 6 months Rifampin (short course)
Now I am off all ABX and doing herbs, and other things...
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posted
Lauirel, you did a fabulous job explaining those Bart skin rashes. Thank you!
Just thought I'd add that another skin manifestation that is seen with Bartonella is a skin condition called Livedo Reticularis. Click on the photo on this link to see a close-up.
In the medical literature, one will frequently see this skin condition attributed to Lupus or other conditions. Rarely, have I seen it attributed to Bartonella in the literature I've managed to read. This is unfortunate because Bartonella can be a chief cause of Livedo Ret. in many patients (according to what's been shared with me by LLMD's).
I've got Livedo Ret. as one of my many Bart symptoms. My lacy-web-type rash has larger patterns. The lace pattern has a larger empty center and it is not as dense and concentrated as in the photo above. Also, most of the time the lacy-web-looking rash is red or pink and usually doesn't turn the angry purple that is seen above.
The rash appears on the entire trunk of my body (the front), the entire length of my arms and legs.
Sometimes astute doctors who see this in patients will also look for symptoms of vasculitis, which can Bartonella can also cause (See, the PubMed article posted above on Bartonella causing vasculitis/polyneuropathy). The vasculitis can sometimes accompany the Livedo Reticularis.
Yet another skin manifestation that can appear from Bartonella is Raynaud's Disease (or Phenomenon). Lyme doctors have also shared with me that they also see Raynaud's with other tick borne infections. By the way, Raynaud's can also be caused by non-tick borne infection sources as well. I've read that it can be a side effect from certain medications.
Shandy, I saw a list somewhere containing information on the combination antibiotic approach that is used for treating Bart when it's present with Lyme and other Co-infections.
I'm not confident I'll be able to find it again (I didn't save it). But I'll try!
Fuzzy
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Alv
Unregistered
posted
Perfect description-this is exactly what I needed .I knew it was bart and My son had done the VEFG and was high since last year ..but I was curious in what you see in your son .
All I wanted to know how would you perscribe it in every little detail and ACTUALLY that is WHAT me and my son had all along and that is where all neurosymtoms started.
posted
Very interesting link FuzzySlippers! I have some questions and a couple of observations concerning my experience with Livedo Reticularisor LR.
First a description of myself. If you all are familar with Dr. J.S. then you will also be familar with the skin manifestation of Bartonella called the stacked clams. This was the very first noticable sign for me. I would like to describe my skin for those unfamilar.
I noticed one day a strange type of skin discoloration on my legs. At this point it was in sporadic areas just on my thighs. White spots surronded by light pink borders, or just lighter spots surrounded by normal skin. When i would get cold, these areas would become even more noticable. Because of the hypopigmentation I saw, I wondered if I had acquired a fungal infection. I made an appointment with a dermatologist, a prominent, reknowned tri-state duck. He diagnosed me with a skin fungal infection.
Over time, my stacked clams spread to encompass my entire thighs, stopping at my knees. They then progressed to Livedo Reticularis. I couldn't find the term for it for the life of me, and Thank you FuzzySlippers for doing that for me. What timing. I also acquired it across my entire back and the outside of my upper arms.
My question is prior to you developing the Livedo Reticularis, did you noticed what I described, in your skin as well? The stacked clams?
I was also wondering whether on your link you posted whether you had clicked on the other links related to the disease? One was the antiphospolipid syndrome? This is something I experienced because of my Lyme and how it affected by immune system.
As far as treatments we did, they seemed to help me more than my son.
A a whole slew of herbals to synergize with. I can't find the list, but when I do, I will post.
We also used oils with Bay Laurel as Bay is supposed to help with bartonella. I picked that up here from a poster I can't remember her name either. i claim lyme alzheimers.....lol I keep wanting to say Jeannie or something like that.
Warning, got a hell of a candida fight from it even with pre and probiotics.
And yes, we did these all at the same time. Don't ask me about our liver enzymes. But it did really help me. my purple rivers went away, but my sons did not. We still struggle.
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posted
Lauriel - I can sympathize because I have the same symptoms. I am on IV EDTA and IV Zithromax at the moment. I herxed rather badly and only been on it for one week. I understand that Dr's are wanting to test for elevated VEGF, but like my Dr said...if the pathogen is killed...the VEGF goes away and isnt relevant. Of all the misunderstandings, I dont understand why these striations and stretch marks dont go away. My doctor may try IV Gentamicin. I will let you know if anything works and please let me know. If any others are having luck, espicially with the stretch marks and striations, please let me know. Thanks.
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When I posted my last post on this subject, I really was at a point where I was going to throw my hands up in the air. We have been battling Bart for well over a year. Ironically, since that last post, something has happened.
My son, in which did not seem to be helped with the antibiotics as much as I, has recently had a change. He was going shirtless yesterday and is quite unusual considering his embarrassment over these purple rivers. Being stealth, I sneaked glances trying to get a good visual and became a raving lunitic.
It seems his purple rivers are dissappearing, not just fading. We have been rotating the things recommeded for over a year. We had that period of antibiotics, and then continued the rotational stuff for Lyme, Babesia, and Bartonella. We also did a rotation of antivirals just recently due to everyone coming down with the flu and also to correlate with my Candida fight. Our rotations overlap and often include many targets at once. We also continually treat for fungal and candida issues by natural means. And we have been supplementing our detoxification pathways and are also pretty fanatic on detoxification period. Out of all this, there were only three new rotations I added. One was Mangosteen, one was Pau de Arco, and the other a topical ozonated olive oil directly to the purple rivers.
I have no idea if what we recently added has had an effect or whether it was the continual rotation of the naturals we used and over time has lead to this improvement. From what I know of Bart, I wouldn't think it was anything recent, but maybe it was the tipping factor.
Timing is kinda funny as I was just about to go back to the drawing board. I have never stopped treating all three at anytime, we have just changed our rotationals after a period of time and combinations. We use the same things over and over again, I just switch them up every couple of months.
My son's protocol isn't any different than my own. Because he is in school, it was hard to get the mid day thing so it made it difficult for me to gauge his progress or lack there of. So by putting myself on the same protocol, it made it easier for me to pick the rotationals and combinations and correlate his reactions to my own.
I know the detail is lacking but I didn't write it down, I just went on our symptoms and reactions. Now I wish I had. I have a headache from hell right now, but I do have a basic protocol that I used as my base and worked and added from there. I gleaned it from another Lymie in which cured himself, his wife, and his two dogs. I will try to write it down later and post if anyone is interested.
I am not claiming cure, but we have had an improvement of late. Please keep good thoughts going for my son. He has been through the teenage ringer with Lyme and company added to it and then losing our home on top of everything. I sure hope this means we are getting somewhere. Time will tell.
Many regards to all....Lauirel
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CD57
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posted
Lauriel, it would be great it you could post your detailed treatment. I think you may be onto something and rotating these meds and herbs may work . Someone on another forum was talking about pulsed quinolone (a month?) followed by high dose HH capsule (like 15 per day), and then switching back and forth between those.
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Journal of Clinical Microbiology, September 2008, p. 2856-2861, Vol. 46, No. 9
American Society for Microbiology. All Rights Reserved.
Bartonella sp. Bacteremia in Patients with Neurological and Neurocognitive Dysfunction
E. B. Breitschwerdt,1* R. G. Maggi,1 W. L. Nicholson,2 N. A. Cherry,1 and C. W. Woods3
Intracellular Pathogens Research Laboratory, Center for Comparative Medicine and Translational Research, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina,1 Rickettsial Zoonoses Branch, Centers for Disease Control and Prevention, Atlanta, Georgia,2 Duke University Medical Center, Durham, North Carolina3
Received 1 May 2008/ Returned for modification 16 June 2008/ Accepted 10 July 2008
We detected infection with a Bartonella species (B. henselae or B. vinsonii subsp. berkhoffii) in blood samples from six immunocompetent patients who presented with a chronic neurological or neurocognitive syndrome including seizures, ataxia, memory loss, and/or tremors. Each of these patients had substantial animal contact or recent arthropod exposure as a potential risk factor for Bartonella infection. Additional studies should be performed to clarify the potential role of Bartonella spp. as a cause of chronic neurological and neurocognitive dysfunction.
posted
Ok, well, I'm not too thrilled with the cautious manner this author used in opining, but here is what the IDSA said about the study in the previous link immediately above.
At least the article below seems to advise docs to remember the possibility of Bartonella.
Bartonella Bacteremia and Neurological Symptoms Khalil Ghanem, MD
A case series published in the September issue of the Journal of Clinical Microbiology suggests an association between chronic neurological symptoms and Bartonella species bacteremia in patients with documented animal or arthropod exposures.
The authors report six cases of immunocompetent patients who presented with a myriad of subacute to chronic neurological symptoms (including seizures, paralysis, headaches, fatigue, memory loss, and visual disturbances) and who were found to have bacteremia with Bartonella henslea and/or Bartonella vinsonii subspecies berkhoffii. All six patients reported clear exposures to cats (mostly scratches or bites), arthropods, farms, or farm animals. The duration of neurological symptoms lasted from one month to five years. In most of these cases, treatment of the infection led to subjective improvement of the neurological symptoms.
In addition to serological testing, the investigators used broth enrichment methods coupled with molecular diagnostics to document infection. These methods are not routinely available in clinical laboratories.
The association noted in this paper is interesting but far from definitive. Given that infectious diseases clinicians are often asked to evaluate patients with neurological symptoms of unclear etiology, the possibility of Bartonella infection can be entertained when evaluating patients with clear animal or arthropod exposures. (Breitschwerdt et al., J Clin Microb. 2008:46; 2856-2861.)
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posted
This might have some useful info to use as a launching pad for further research.
I don't agree with some of what's been written here -- the self-limiting nature of Bartonella, that chronicity occurs only in HIV infected patients, nor the poor sanitation/hygiene remarks relating to trench fever. Bartonella Quintana (Trench Fever) has been seen plenty as a co-infection with Lyme Disease, regardless of hygiene and HIV status.
I'm sure many of you will not agree with the remarks in this article about the rarity of some of the strains as well as the stated rarity of some of the symptoms/complications seen with those strains.
Nevertheless, I'm posting this in case it might help people who are interested in researching.
Bartonella are Gram-negative bacteria and are facultative intracellular parasites.
* They are found in various vertebrates, rodents and their flea vectors, and are associated with an increasing range of diseases. Transmission is generally considered to be by arthropod vectors. * Three species of the genus Bartonella are known to be important causes of human disease, although other species are increasingly being recognised as important.1 The range of infection varies from mild lymphadenopathy seen in cat scratch disease, to life-threatening systemic disease in immunocompromised patients.2 Infections caused by Bartonella species include: o Cat-scratch disease: B. henselae - Bacillary angiomatosis is a disseminated form of B. henselae infection, found most commonly in HIV-positive patients o Oroya fever/verruga peruana: B. bacilliformis o Trench fever: B. quintana; louse-borne, variable fever with persisting severe shin and other bone pain * Endocarditis is sometimes associated with Bartonella infection (including B. henselae, B. quintana, B. elizabethae). Homelessness and alcoholism are risk factors for B. henselae endocarditis. * Bartonella encephalopathies are rare in patients with normal immunity but may occur in HIV-positive patients, especially with B. henselae and B. quintana infection. Features include meningoencephalitis, encephalopathy and neuropsychiatric disorders. * B. henselae osteomyelitis and hepatitis have been reported.
* Epidemiology: o It is caused by B. quintana (formerly Rochalimaea or Rickettsia quintana.) o Urban trench fever is now seen in alcoholics and the homeless. o Poor sanitation and lack of personal hygiene strongly correlate with transmission by the body louse Pediculus humanus. * Presentation: o Fever develops after an incubation period of a few days to a month. Usually, several episodes of fever develop and each episode lasts about 5 days. o Other symptoms include joint and muscle aches, headache, dizziness, and pain behind the eyes. Some patients have diffuse symptoms without fever. o May cause culture-negative endocarditis. o On examination there are injected conjunctivae, nystagmus, hepatosplenomegaly, lymphadenopathy, a maculopapular rash and tender muscles and joints. * Differential Diagnosis: o Other causes of fever, headache, focal neurology and lymphadenopathy, e.g. CMV, HIV seroconversion. Other causes of culture-negative endocarditis include Legionellosis, Q Fever and slow-growing streptococci. * Investigations: o Serology testing is the most cost-effective method to confirm the diagnosis. o Culture for Bartonella may be useful in patients who have other manifestations of either B henselae or B quintana infection (e.g. fever of unknown origin, neuroretinitis, encephalitis, culture-negative endocarditis). Fresh media is required to increase the chance of isolating the organism. * Management: o Doxycycline is given for at least two weeks and a longer course when the liver or other organs are involved. Chloramphenicol may be used in severe cases.3 * Complications: o Persistent bacteraemia with B. henselae may develop in people with AIDS. * Prognosis: o Usually self-limiting. Trench fever reinfection may recur within 3-6 months, because antibodies do not give full protection. o Bartonella endocarditis: the recommended treatment is doxycycline for 6 weeks, with gentamicin for 2 weeks.3 Surgical resection of heart valves is usually required. Mortality rate of bartonella endocarditis is 30%.
Bacillary Angiomatosis and Peliosis Hepatitis
* Both B. quintana and B. henselae are associated with these conditions. * Bacillary angiomatosis was initially described in people infected with HIV infection. * Symptoms depend on the anatomical site involved and may include fever, tender lymphadenopathy, and skin lesions. Cystic hepatitis (peliosis) often occurs in bacillary angiomatosis. * Homeless persons and alcoholics typically develop B. quintana endocarditis. * Presentation: o Lesions are often dark purple and resemble Kaposi's sarcoma. o There may be enlargement of the liver, lymph nodes, or spleen if infected. * Investigations: o Patients should have HIV antibodies and CD4 lymphocyte counts checked. o Usually causes anaemia and elevated serum alkaline phosphatase. * Management: o Effective antibiotics include erythromycin, doxycycline, azithromycin, clarithromycin, or a fluoroquinolone. o Doxycycline combined with rifampin is effective for patients with severe disease.3 * Prognosis: o Untreated patients have a high mortality. o Immunocompromised patients with bacillary angiomatosis or peliosis hepatitis respond well to antibiotics. o Relapses are common.
Oroya Fever and Verruga Peruana
Synonym: Carrion disease
* Epidemiology: o B. bacilliformis is common in the Peruvian Andes and transmission is limited to elevations of 1000-3000 meters because of the habitat of the sand fly vector. * Presentation: o Bacteraemia of Oroya fever begins 3-12 weeks after a sand fly bite. o May be mild where endemic (Andean Peru, Ecuador, Colombia, Chile, Bolivia, and Guatemala) but may be severe in newly infected patients, with profound haemolytic anemia, which is often fatal if untreated. o Severe illness causes fever, headache, dyspnoea, mental state changes, and seizures. o Weeks or months later, untreated survivors develop verruga peruana lesions (angiomatous skin lesions), which begin as small nodules and then grow. They then form vascular lesions, which ulcerate, bleed, and then heal by fibrosis over several months. * Differential Diagnosis: o Other serious causes of fever in a patient who has returned from a developing country include dengue fever, malaria, tuberculosis and babesiosis. * Investigations: o Haemolytic anaemia, thrombocytopenia and abnormal liver function tests. o Serology testing is the most cost-effective method to confirm the diagnosis. * Management: o Both chloramphenicol or doxycycline are effective and need to be given for at least one week. Chloramphenicol is usually reserved for severe cases.3 * Prognosis: o Untreated patients have a 95% mortality rate. o Persistent bacteraemia may occur in survivors.
Other Associations
* B. elizabethae is a rare cause of endocarditis. * B. washoensis is associated with cardiac disease (ground squirrel host). * B. vinsonii (subspecies arupensis) causes fever and neurological symptoms. * B. grahamii associated with neuroretinitis, as is B. henselae.
Document references
1. Edwards B; Bartonellosis; eMedicine, March 2006 2. Anderson BE, Neuman MA; Bartonella spp. as emerging human pathogens.; Clin Microbiol Rev. 1997 Apr;10(2):203-19. [abstract] 3. Rolain JM et al; Recommendations for treatment of human infections caused by Bartonella species. Antimicrob Agents Chemother. 2004 Jun;48(6):1921-33.
Acknowledgements EMIS is grateful to Dr Colin Tidy for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. �EMIS 2009. DocID: 1354 Document Version: 22 DocRef: bgp346 Last Updated: 30 Oct 2007 Review Date: 29 Oct 2009
Bartonella, transmitted from cats, can cause 22 human diseases and cat scratch disease is only the "tip of the iceberg."
[click on link for listing of some of those 22 human diseases and also more info in general]
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This report describes a case of granulomatous inflammation, involving the bone marrow and skin, due to Bartonella infection in an immunocompetent patient. The clinical presentation included prolonged fever, pancytopenia, rash and hepatitis. Bartonella infection should thus be added to the growing list of entities that produce marrow granulomas and fever.
[click on link for remainder of article]
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posted
I'd forgotten about this until I saw tosho's recent post on another thread. This is from Doc B's Guidelines. This section lists co-infection symptoms.
I'm including it here as a basis of comparison for Lyme, Bart and other Co-Infections.
Thanks, Tosho!
CLASSIC LYME (Bb infection)-
� Gradual onset of initial (viral-like) symptoms- this often makes it difficult to pinpoint when the infection began.
� Multisystem- almost always, in disseminated stages, involves more than one part or system (i.e. joint pain plus cognitive dysfunction).
� Migratory- first a knee will hurt, then over time this may lessen and the elbow or shoulder acts up, and later the joints calm down but headaches worsen.
� Stiff joints and loud joint crepitus, especially the neck (``Lyme shrug'').
� Headaches are often nuchal and associated with stiff, painful and crepitant neck.
� Afternoon fevers, often unnoticed- most Lyme patients have subnormal temperatures in the AM but rise to 99+ by early to mid-afternoon. No obvious sweats.
� Tiredness and limited stamina- often is a strong need to rest or even nap in the afternoon, especially when the flushed face and elevated temperature appears.
� 4-week cycles- Bb activity, and thus symptoms, wax and wane in a cycle that repeats roughly every four weeks. This cycle, if clear, can guide your treatments.
� Slow response to treatment, with an initial symptom flare in most (``Herxheimer-like reaction'') then improvement over weeks, punctuated by the monthly symptom flares. Likewise, if treatment is ended too soon, an initial period of well-being will gradually, over a few weeks, be replaced by a return of symptoms.
� EM rash in 25% to 50%
BARTONELLA & ''BARTONELLA-LIKE ORGANISMS''-
� Gradual onset of initial illness.
� CNS symptoms are out of proportion to the musculoskeletal ones- if a patient has no or minimal joint complaints but is severely encephalopathic (see below), then think of Bartonella/BLO.
� Obvious signs of CNS irritability can include muscle twitches, tremors, insomnia, seizures, agitation, anxiety, severe mood swings, outbursts and antisocial behavior.
� GI involvement may present as gastritis or abdominal pain (mesenteric adenitis).
� Sore soles, especially in the morning.
� Tender sub-cutaneous nodules along the extremities, especially outer thigh, shins, and occasionally along the triceps.
� Occasional lymphadenopathy.
� Morning fevers, usually around 99. Occasionally light sweats are noted.
� Elevated vascular endothelial growth factor (VEGF) occurs in a minority, but the degree of elevation correlates with activity of the infection and may be used to monitor treatment.
� Rapid response to treatment changes- often symptoms improve within days after antibiotics are begun, but relapses occur also within days if medication is withdrawn early.
� May have papular or linear red rashes (like stretch marks that do not always follow skin planes), especially in those with GI involvement.
BABESIA SPECIES-
� Rapid onset of initial illness, often with sudden onset of high fever, severe headaches, sweats and fatigue, thus it is easy to know when infection began.
� Obvious sweats, usually at night, but can be day sweats as well.
� Air hunger, need to sigh and take a deep breath; dry cough without apparent reason.
� Headaches can be severe - dull, global (involves the whole head, described like the head is in a vise).
� Fatigue is prominent, does not clear with rest, and is made worse with exercise.
� Mental dullness and slowing of reactions and responses.
� Dizziness- more like a tippy feeling, and not vertigo or purely orthostasis.
� Symptoms cycle rapidly, with flares every four to six days.
� Hypercoaguable states are often associated with Babesia infections.
� Rarely, splenomegaly
� Very severe Lyme Disease can be a clue to Babesia infection, as it will make Lyme symptoms worse and Lyme treatments less effective.
EHRLICHIA/ANAPLASMA-
� Rapid onset of initial illness with fever, headache, prostration.
� Headaches are sharp, knife-like, and often behind the eyes.
� Muscle pain, not joint pain, and can be mild or severe.
� Low WBC count, elevated liver enzymes, and (rarely) inclusions seen in the WBCs.
� Rarely see diffuse vasculitic rash, including palms and soles (less than 10%).
� Rapid response to treatment.
DNA VIRUSES (HHV-6, EBV, CMV)
� Persistent fatigue, made worse with exercise.
� Sore throat, lymphadenopathy, and other viral-like complaints.
� May see elevated liver enzymes and low WBC counts.
� Autonomic dysfunction.
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I would love to read more about the herbs you used to combat Bart--and Lyme and Babs if used-- and the method in which you used them, i.e., continued with antibiotics--which ones?
Did you rotate the herbs? Antibiotics? Rotation schedule?
Thanks!
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Thanks to Lymetoo for posting this article. I'm adding it to this thread.
Medical research benefits local veterinarian suffering from MS
by Margaret Palermo - Staff writer
What if you were struggling with a neuromuscular disease that left you pretty much unable to walk or work and kept getting worse, even with treatment?
And then, through an incredible series of coincidences, a diagnosis of a degenerative neuromuscular disease meets up with a bacterium that shows up on a blood test and suddenly your life is handed back to you?
A year ago, local veterinarian John Barnes was facing the possibility of spending the rest of his life in a wheelchair as his body degenerated. He was unable to walk with more than a shuffling pace and found it difficult to work.
It started one day in December of 2004, he said. I was the only one in the house and I woke up about 2 or 3 in the morning with fever and vomiting and thought I had food poisoning, he said. A thermometer pegged his fever at 103, though he said he thought it might have gone higher.
I took a shower and I felt like an octopus on the land, he said describing the weakness accompanying his sudden-onset illness. I felt like I had no bones.
And from that point on, things only got worse. I was a jogger and had been for years, he said. I was jogging and noticed when I went around the third lap of the track, my left leg started to trip a little bit. The next week or two, it was the second lap. I knew I had a problem in one of my neck discs. I thought it was related to that.
He talked to friends who were doctors and they told him he probably had some kind of virus and he should get over it in a couple of months.
But the problem didn't go away. It just kept getting worse. My neurology friends said we better do some testing on you and find out, he said. An MRI and spinal taps were done. It was a fairly clear-cut picture that I had MS.
Treatments for multiple sclerosis were started. We started the typical MS protocol which is interferon shots, said Barnes. With the interferon, he was having relapses about every six months, something typical with MS. Interferon, he explained, is a maintenance drug for MS, but not a cure.
Then in July 2005, he was talking to a friend who is a world-class veterinary internist at Texas A&M University at College Station about an oncology case they shared. Barnes said his friend was unaware of his medical condition.
She asked how I was doing. I said you know how it is with MS. You have your good days and your bad days, he said. I started talking to her about it and I made the comment to her that I'm not balking at the diagnosis of MS, but I'm exposed to so many weird things, I would like to know that's all I have.
He said his friend agreed with him and said his timing was perfect because she had a friend who was doing a study. She gave Barnes an e-mail address for Dr. E.B. Breitschwerdt, co-director of the Vector-Borne Disease Laboratory at the North Carolina State University College of Veterinary Medicine in Raleigh, N.C.
Breitschwerdt has been working with something called polymerase chain reaction, or PCR, testing which can be used to detect and diagnose bacteria by looking for genes or portions of genes in a patient's sample.
The advantage of PCR testing is that it can be used to amplify any gene that had been identified, speeding up the identification process.
Breitschwerdt also called Barnes' timing perfect and agreed to use him in his study. He drew Bartonella out of my blood, said Barnes, explaining that other types of tests can show that you've been exposed to Bartonella, but not that you currently have the bacteria still active in your body.
Typically, Bartonella is self-limiting, he said. When he drew it out of me the first time, he was working with a Duke University infectious disease guy. Dr. (C.W.) Woods was not excited about me being positive, but said he would test me again in a couple of months. He tested again and it was there again.
Barnes said they wanted to test the second sample to find out what species of Bartonella it was since there are at least a dozen different species of the bacteria. Then they lost my sample and a bunch of other samples. I was with my neurologist and they were doing some IV-IG therapy and I was undergoing that.
Barnes said the next round of testing his blood for Bartonella had to wait until he finished the IV-IG treatments. Another couple of months go by and they take another sample again and, sure enough, I'm positive again, he said.
This was about April 2007 that Dr. Breitschwerdt saw that my sample was positive, said Barnes. He said the sample turned out to be Bartonella henselae-San Antonio strain. I said great, what do we do? He said we still don't know.
Barnes also has a cardiologist, Dr. Jamil Bitar. I was talking to him about it and he said I should talk to his brother Camil Bitar, who is an infectious disease expert in Louisiana, said Barnes. Dr. Woods is not sure, but he's thinking about an antibiotic protocol.
Barnes talked about the protocol with Dr. Camil Bitar, explaining that it included taking two antibiotics, one of which could have a bad effect on the liver. We started by the month to see how my liver was doing, he said. I asked him how long should I be on it and Dr. Bitar said until you're well.
That was the first time anyone had ever told me this might make me well and he said absolutely, said Barnes. I was excited about that part of it, that this could reverse some of my clinical signs. Dr. Bitar agreed that I should stay on the drug as long as I could handle it. I just finished in August 2008.
Barnes said he saw changes in himself from the first month, however. The first month, I could see a change in, believe it or not, the color of my toes, he said. He said his toes had been gray, but regained their normal color.
My fatigue slowly got better, he said. In September of this year, after he had already finished the antibiotic regimen, he discovered he could bring his right leg up past his knee without having to lift it with his hand. By October he could move his legs as if he were jogging. He shared news of his progress with Dr. John Shudde. Dr. Shudde said 'Simple pleasures are, indeed, the best!' said Barnes.
What Dr. Camil Bitar says, and I agree, is that Bartonella was the trigger for my MS, he said. They don't know what triggers MS. He and I would both agree that I should not go so far as to say I don't have MS. Since they don't know what causes MS is, it's hard to say what's going on.
I think what we have is Bartonella-induced MS. I thank God every day that I'm getting better. I told myself if I don't get any better, if I can't jog again, at least I'm doing better in other things.
The potential for helping others with strange illnesses that could be related to Bartonella is obvious. What's so exciting to me about this is that we don't know how many people are being undiagnosed or misdiagnosed, said Barnes. At this point, he said, there is no way to know how many problems could be the result of Bartonella.
With diagnostic tests getting better, it is now possible to treat the actual disease rather than just treating symptoms. Dr. Breitschwerdt told me about the dean of a veterinary school who came down with neurologic signs and his 12-year-old daughter had fatigue. They were tested and they found Bartonella in his spinal fluid and in the girls' blood and in their dog's mouth. They are being treated and doing well, said Barnes.
Of the six research subjects, including Barnes, that Breitschwerdt used in his study, two were veterinarians who reported frequent bites from cats, dogs, pocket pets and other animals, one reported a severe scratch from a cat, one had frequent arthropod exposure and had been bitten by a pig and pecked frequently by various fowl, another owned a horse farm and had frequent arthropod exposure and cat scratches and the sixth was a teenager who developed sever debilitating migraine headaches after a tick was removed from his ankle.
The most exciting thing about Ed's work is the hope which will be instilled in so many, said Barnes.
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New Study Identifies Louse-borne Diseases That Ravaged Napoleon's Army
ScienceDaily (Dec. 15, 2005) -- Using dental pulp extracted from the teeth of soldiers who died during Napoleon's disastrous retreat through Russia in 1812, a new study finds DNA evidence that epidemic typhus and trench fever ran rampant among the French Grand Army. The study, published in the Jan. 1 issue of The Journal of Infectious Diseases, now available online, identifies the specific species of louse-borne pathogens that were a major cause of death among the remains of the retreating army.
Napoleon marched into Russia in the summer of 1812 with a half-million soldiers. Only a few thousand staggered out again, victims of war, weather, and disease. Twenty-five thousand arrived in Vilnius that winter, but only 3,000 lived to continue the retreat. The dead were buried in mass graves.
Construction work in 2001 unearthed one such grave, containing between 2,000 and 3,000 corpses. Didier Raoult, MD, PhD, from the Universit� de la M�diterran�e in Marseille, France, and colleagues identified body segments of five lice in a forensic excavation of two kilograms of earth containing fragments of bone and remnants of clothing. Three of the lice carried DNA from Bartonella quintana, which causes the disease commonly known as trench fever, which afflicted many soldiers in World War I.
The team analyzed dental pulp from 72 teeth, taken from the remains of 35 soldiers. Dental pulp from seven soldiers contained DNA from B. quintana, and pulp from three soldiers contained DNA from Rickettsia prowazakii, which causes epidemic typhus. Testing for other organisms gave negative results, and other appropriate controls were negative.
In all, 29 percent of the soldiers tested had evidence of either R. prowazkii or B. quintana infection, suggesting that louse-born diseases such as typhus and trench fever may have been a major factor contributing to Napoleon's retreat from Russia. The authors conclude that searching for DNA of infectious agents in dental pulp may become an important tool for investigating the history of communicable diseases.
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21st Century Plague? Rat Fleas Spread Heart-damaging Bacteria
Brown rats may now be carrying bacteria that can cause serious heart disease in humans. Rat fleas can spread the disease.
ScienceDaily (Nov. 24, 2008) -- Bacteria that can cause serious heart disease in humans are being spread by rat fleas, sparking concern that the infections could become a bigger problem in humans. Research published in the December issue of the Journal of Medical Microbiology suggests that brown rats, the biggest and most common rats in Europe, may now be carrying the bacteria.
Since the early 1990s, more than 20 species of Bartonella bacteria have been discovered. They are considered to be emerging zoonotic pathogens, because they can cause serious illness in humans worldwide from heart disease to infection of the spleen and nervous system.
"A new species called Bartonella rochalimae was recently discovered in a patient with an enlarged spleen who had travelled to South America," said Professor Chao-Chin Chang from the National Chung Hsing University in Taiwan. "This event raised concern that it could be a newly emerged zoonotic pathogen. Therefore, we decided to investigate further to understand if rodents living close to human environment could carry this bacteria."
Scientists have found that rodents carry several pathogenic species of Bartonella, such as B. elizabethae, which can cause endocarditis and B. grahamii, which was found to cause neuroretinitis in humans. Although scientists are unsure about the main route of transmission, these infections are most likely to be spread by fleas. Ctenophthalmus nobilis, a flea that lives on bank voles, was shown to transmit different species of Bartonella bacteria. These pathogens have also been found in fleas that live on gerbils, cotton rats and brown rats.
"We analysed bacteria found in Rattus norvegicus in Taiwan. The brown rat is also the most common rat in Europe," said Professor Chang. "By analysing the DNA of the bacteria, we discovered a strain that is most closely related to B. rochalimae, which has been isolated recently from a human infection in the United States".
The researchers took samples from 58 rodents, including 53 brown rats, 2 mice (Mus musculus) and 3 black rats (Rattus rattus). 6 of the rodents were found to be carrying Bartonella bacteria; 5 of these were brown rats. Four of the rodents were carrying B. elizabethae, which can cause heart disease in humans, and one of the black rats was found to be harbouring B. tribocorum. However, the scientists noticed one strain that had not been identified in rodents previously. The strain was finally shown to be close to B. rochalimae.
"Because of the small sample size used in this study, we cannot say for sure that the common brown rat is spreading B. rochalimae," said Professor Chang. "However, several different Bartonella bacteria are surely transmitted by rodents. These results raise concerns about the existence of other reservoirs and vectors for this emerging infection. This certainly warrants further investigation."
Journal reference:
1. Jen-Wei Lin et al. Isolation of Bartonella species from rodents in Taiwan including a strain closely related to 'Bartonella rochalimae' from Rattus norvegicus. Journal of Medical Microbiology, 2008; 57 (12): 1496 DOI: 10.1099/jmm.0.2008/004671-0
Adapted from materials provided by Society for General Microbiology, via AlphaGalileo.
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CD57
Frequent Contributor (1K+ posts)
Member # 11749
posted
Is there any way to sticky this list at the top?
Fuzzy, who gave you the symptom list?
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You talking about the Babesia/Bartonella Symptom Questionnaire at the top of this thread? If so, I was given this list by one of my LLMD's during an office visit. Months later, I later saw this same list published in Dr. K. Singleton's book, "The Lyme Disease Solution." Doc S was not the doctor who gave me this list by the way.
I posted a separate thread about a year ago which contains just the questionnaire. It's called the "Bartonella/Babesia Symptom Questionnaires." That particular post used to have a sticky on it but it was unstickied with a bunch of other threads after a few members complained of their being too many stickies at the top of the Medical Forum.
This article is called, "The Role of Bartonella spp. in Veterinary and Human Medicine With Special Emphasis on Pathogenicity Mechanisms," by V.A. J. Kempf, and F. Kramer. It was published in December, 2008 in EJCAP.
It contains some photos photos of Bartonella rashes and has a great chart listing different strains of bartonella, the reservoir and vectors for each strain, and the human diseases that the strains cause.
Fuzzy
Posts: 503 | From Maryland | Registered: Oct 2007
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Macrolides are produced by Streptomyces erythreus. Their chemical structures contain large lactone rings linked through glycoside bonds with amino sugars.
Macrolides are inhibitors of protein synthesis. They are effective against Gram-positive bacteria and most Gram-negative bacteria, Neissera, Legionella, and Haemophilus, but not Enterobacteriaceae. The most important macrolides are:
*
Erythromycin *
Oleandomycin
question-
effective against "most" gram negative bacteria?
What KIND of gram negative bacteria is bartonella specifically? (Neissera, Legionella, Haemophilus, OR Enterobacteriaceae??
I have a BAD case of bart, and am trying to beat the bart load down w/ some biaxin before rifampin, but am wondering how effective biaxin is for bart?
I don't care what doctors said what, I am curious to know what kind of gram negative bacteria bartonella specifically is, in order to effectively choose antibiotics.
anyone?
THANKS
-D
-------------------- "Experience is not what happens to you; it is what you do with what happens to you."
I don't know about Biaxin and I haven't tried Rifampin yet. I've had some success using Bactrim, but have found this antibiotic difficult because I have the MTHFR C677T genetic variant, which makes handling drugs which affect folate absorption a challenge.
I am seeing alot of results with Factive. It's still early days with this therapy, so I can't speak to whether it will deal with my Bart infection completely.
I'm not a microbiologist and don't have a scientific background, but my understanding is that Bartonella is a proteobacterium. It's also a gram negative bacterium (bacillus). I think this classification stands for all spp. (species) in the class of Bartonella genus or family. This includes Bartonella Henselae, Bartonella Quintana, etc.
Fuzzy
Posts: 503 | From Maryland | Registered: Oct 2007
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posted
I forgot to include this for you, D. This info was linked awhile ago in this thread, but I'll paste it here again. I hope it helps.
The article is titled, "Recommendations for Treatment of Human Infections Caused by Bartonella Species," by J. M. Rolain,1 P. Brouqui,1,2 J. E. Koehler,3 C. Maguina,4 M. J. Dolan,5 and D. Raoult1,2*
Members of the genus Bartonella are facultative intracellular bacteria belonging to the alpha 2 subgroup of the class Proteobacteria and are phylogenetically closely related to Brucella species (15, 73). Until 1993, only three diseases were known to be caused by Bartonella species: Carrion's disease (Bartonella bacilliformis), trench fever (Bartonella quintana), and cat scratch disease (CSD; Bartonella henselae). The genus now comprises B. bacilliformis, species of the former genera Rochalimea and Grahamella (14, 18), and additional, recently described species (Table 1). In mammals, each Bartonella species is highly adapted to its reservoir host; the bacteria can persist in the bloodstream of the host as the result of intraerythrocytic parasitism (49). Intraerythrocytic localization of B. henselae has been demonstrated in cat erythrocytes (88), and B. bacilliformis bacilli have been observed within erythrocytes during the acute phase of Carrion's disease (Oroya fever) (88). Bartonellae also have a tropism for endothelial cells, and intracellular B. henselae can be identified in endothelial cells infected in vitro (28), although intraendothelial cell bacilli have not been identified in vivo.
Bartonella species cause long-recognized diseases, such as Carrion's disease, trench fever, and CSD, and more recently recognized diseases, such as bacillary angiomatosis (BA), peliosis hepatis (PH), chronic bacteremia, endocarditis, chronic lymphadenopathy, and neurological disorders (Table 2) (73). A remarkable feature of the genus Bartonella is the ability of a single species to cause either acute or chronic infection and either vascular proliferative or suppurative manifestations.
The pathological response to infection with Bartonella spp. varies substantially with the status of the host immune system. Indeed, infection with the same Bartonella species (e.g., B. henselae) can result in a focal suppurative reaction (CSD in immunocompetent patients), a multifocal angioproliferative response (BA in immunocompromised patients), endovascular multiplication of the bacteria (endocarditis), or an exaggerated inflammatory response without evidence of bacteria in patient tissues (meningoencephalitis) (86).
Some of the diseases due to Bartonella species can resolve spontaneously without treatment, but in other cases, the disease is fatal without antibiotic treatment and/or surgery. The clinical situations are so different that a single treatment for all Bartonella-related diseases has not been identified, and the approach to treatment must be adapted to each species and clinical situation (49). Moreover, the database of clinical studies with a standard case definition, culture confirmation, rigidly defined disease outcomes, and patients with similar host defenses is very limited. Thus, case reports with a very limited number of subjects often serve to dictate therapy. The objective of this minireview is to summarize the antibiotic treatment recommendations for the different infections caused by Bartonella species. We have compiled the in vitro antibiotic susceptibility data and our knowledge of the in vivo efficacies of antibiotics for each clinical manifestation, and finally, we have summarized and ranked our treatment recommendations according to the Infectious Diseases Society of America (IDSA) practice guidelines (see Table 5) (51).
ANTIBIOTIC SUSCEPTIBILITIES OF BARTONELLA SPECIES
Culture of Bartonella spp. Because Bartonella spp. are facultative intracellular organisms, isolation can be performed in either cell cultures or axenic media with blood-enriched agar plates (63) (Fig. 1 and 2). However, Bartonella bacteria are very fastidious, and primary isolation is difficult, with detection of colonies only after 1 to 4 weeks of incubation on blood agar plates (63). The growth of subcultured isolates on blood agar plates is more rapid, usually yielding colonies after 3 to 5 days. Cell coculture systems have been reported to be more sensitive and allow more rapid growth of bartonellae than blood agar plates (63). Since 1992, several studies have reported on the isolation of B. henselae from the blood and lymph nodes of patients with CSD, with confirmation by serology, PCR, or culture (9, 71). However, isolation of B. henselae from the lymph nodes of CSD patients is very rare compared to the more frequent detection of B. henselae DNA in these patients by PCR assays (63, 109). At present, there is no optimal procedure for the isolation of Bartonella species; rather, several techniques and agars (e.g., cocultivation with eukaryotic cells, in addition to plating onto rabbit blood and chocolate agars) should be combined in order to isolate strains.
In vitro susceptibilities of Bartonella species to antibiotics. The results of susceptibility testing with Bartonella spp. are summarized in Table 3. Evaluation of susceptibilities to antibiotics has been performed either in the presence of eukaryotic cells or without cells, i.e., in axenic media. Use of these different methods of culture for the determination of the bacteriostatic activities of antibiotics yielded similar results. Determination of antibiotic susceptibility in axenic media has been carried out either with solid media enriched with 5 to 10% sheep or horse blood or with liquid media (74, 97). It should be noted that the conditions required to grow Bartonella during susceptibility testing do not meet the standardized criteria established by NCCLS. Bacteria of the genus Bartonella are susceptible to many antibiotics when they are grown axenically, including penicillin and cephalosporin compounds, aminoglycosides, chloramphenicol, tetracyclines, macrolide compounds, rifampin, fluoroquinolones, and co-trimoxazole (74, 79). However, the in vitro and the in vivo antibiotic susceptibilities of Bartonella do not correlate well for a number of antibiotics; for instance, penicillin has no in vivo efficacy, despite the very low MICs observed in vitro.
In vitro antibiotic susceptibilities of Bartonella species cocultivated with eukaryotic cells have also been examined. As with agar-based susceptibilities, these studies demonstrated that Bartonella spp. are susceptible to many antibiotics in vitro (46). However, all of these antibiotics (48) had only bacteriostatic activity (47, 48). It was recently demonstrated in vitro that aminoglycosides alone are bactericidal against Bartonella species grown either in liquid medium (91) or in endothelial cells (78). With a recently established erythrocyte coculture model, it was found that most of the antibiotics tested (i.e., doxycycline, fluoroquinolone compounds, and beta-lactams) were not bactericidal against Bartonella (90). Gentamicin was bactericidal at 4 �g/ml, as was rifampin. At this concentration, gentamicin was shown to enter erythrocytes slowly and to reach a peak level of 0.26 �g/ml after 24 h. However, when the ability of gentamicin to kill extraerythrocytic B. quintana at the concentration of 0.26 �g/ml achieved in the erythrocyte was tested, it was found that gentamicin was not bactericidal, even after 96 h of incubation (90). We hypothesize that erythrocytes may be a reservoir for B. quintana and that the bactericidal activity of gentamicin that was observed occurs mainly when the bacteria emerge from the erythrocytes and are found extracellularly.
[click on link for remainder of article]
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posted
^ for anyone interested.
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Tracy9
Frequent Contributor (1K+ posts)
Member # 7521
posted
Thanks for bumping this up, it's a GREAT thread, and now that I am finally experiencing the hell of Bart treatment, I appreciate all of Fuzzy's and everyone else's efforts.
I know several of us right now are going through the torturous Rifampin treatment.
I have a question; I have experienced all the horrors of Bart mainly since starting to treat it. Does the Rifampin bring it out of hiding? Is it toxins dying off?
I feel I should know the answer, but what exactly IS it that makes us feel so much worse when we suddenly start treating? I never had all the symptoms of Bart until I swallowed the darned Rifampin...then it was a textbook list of symptoms hitting me!
13 years Lyme & Co.; Small Fiber Neuropathy; Myasthenia Gravis, Adrenal Insufficiency. On chemo for 2 1/2 years as experimental treatment for MG. Posts: 4480 | From Northeastern Connecticut | Registered: Jun 2005
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In my personal experience, I have found the literature pertaining to Bartonella infections to be frustratingly sparse in terms of what we can expect as patients during treatment. We can read about herxheimer reactions and/or drug reactions with plenty of other infections, such as MRSA, Mycoplasmas, Syphillis, and even Borrelia; however, the information about what to expect as far as herxheimer reactions during Bartonella treatment is hard to come by.
I guess our best resources will be our own LLMD's who have seen the progression of this disease, it's growth cycles, responses to treatment, first hand in their patients. And then, our next best resources will be talking with patients who've been through it.
Fuzzy
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BARTONELLA Over 20,000 cases of disease caused by the Bartonella family of bacteria occur each year in the United States. The most commonly known Bartonella infectious disease is ``cat scratch fever.'' Although most cases are due to flea bites from infested, infected animals; cat or dog bites or scratches may also directly cause the illness in humans.
Studies in recent years have found Bartonella and Bartonella-like microorganisms, which live inside cells, in some species of ticks. Scientists suspect that ticks may be transmitting Bartonella to humans in some cases. Further studies are needed.
Reported symptoms from suspected tick-borne Bartonella henselae may include unusual streaked rashes often recurring on the body, visual problems, fatigue with agitation, poor sleep, joint and muscle pain and stiffness, low grade fevers, sweats, headaches, recurring sore throat, lymph node enlargement, lower abdominal pain, ringing in the ears, anxiety, panic disorder, irritability, rage, seizure disorder, tremors, and other neurological problems.
Diagnosis is made clinically; antibody titers and PCR analysis may be helpful but are not always sensitive. Prescribed treatment is often quinolone and tetracycline.
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posted
Excellent article by Dr. Edward B. Breitschwerdt, et. al., "A Groundhog, a Novel Bartonella Sequence, and My Father's Death," from CDC's publication, Emerging Infectious Diseases, Volume 15, Number 12-December 2009.
A Groundhog, a Novel Bartonella Sequence, and My Father's Death
Edward B. Breitschwerdt, Ricardo G. Maggi, Maria Belen Cadenas, and Pedro Paulo Vissotto de Paiva Diniz Author affiliation: North Carolina State University College of Veterinary Medicine, Raleigh, North Carolina, USA
During the summer of 2007, migratory joint pain developed in my (E.B.B.) 86-year-old father, previously an ironworker, farmer, and World War II veteran. Because of occasional tick attachments, a Borrelia burgdorferi ELISA was performed; antibodies were not detected, and no treatment was instituted. In the fall, subtle memory loss developed, and he fell twice a few weeks apart. Dad jokingly blamed the falls and the memory loss on "old timer's disease." Subsequently, episodes of subtle confusion and more frequent memory loss generated family concern as to what the future might hold. On December 15, he broke his left femur during a fall while climbing 2 stairs to enter our home. Despite having successfully climbed those stairs thousands of times in the past, he would never climb those or any other stairs again.
Retrospectively obvious, a pattern of insidious illness characterized by joint pain, memory loss, and incoordination, not recognizable by my father or other family members, had begun before that summer. Medically stable historical problems included coronary artery disease, atherosclerosis, carotid artery occlusion, hypertension, and atrial fibrillation. During the previous year, a normocytic, normochromic, nonregenerative anemia persisted. Despite normal serum iron, total iron binding capacity, ferritin, and vitamin B12 values, anemia was attributed to intestinal blood loss. When examined in May 2007, before anesthesia for endoscopy, mood and affect were appropriate, recent and remote memory were intact, insight and judgment were good. A hiatal hernia, mild antral gastritis, and duodenitis were visualized.
Initial Hospitalization
When my father was hospitalized December 15, 2007, with a broken femur, a resting pill roll tremor and cogwheel rigidity were suggestive of Parkinson disease. Preoperative neurologic consultation identified severe confusion, inattention, and an inability to answer questions. Short-term memory and problem-solving abilities were decreased. There was mild ptosis of the right eye, normal cranial nerves, mild asterixis, and hand weakness. Laboratory abnormalities included anemia, hypercreatinemia, an elevated aspartate aminotransferase level, and hyperglobulinemia. Due to the severity of the femoral fracture, the femoral head was excised and replaced with a bipolar femoral prosthesis.
Postoperatively, poor mentation was considered a sequela of general anesthesia and peri-operative analgesics. For more than a week, dementia persisted. He did not recognize family members and had near constant hallucinogenic activities, including agitation, tying knots, sawing motions, and constantly pulling covers, bed clothes, and fluid lines. Severe hematuria developed after he pulled an inflated Foley catheter from his urethra. Concurrent gastrointestinal bleeding of undetermined cause necessitated multiple blood transfusions. Other complications included difficulty swallowing and paralytic ileus. Repeat abdominal radiographs, in conjunction with stool softeners and laxatives, failed to alleviate gastrointestinal complications. Eventually, he refused food and became severely bloated. Endoscopy performed on December 26 identified severe necrotizing esophagitis, multiple plaques, and a stricture attributed to Candida albicans and herpes zoster. C. albicans esophagitis is known to accompany HIV infection, leukemia, or an unidentified source of immune suppression (1,2). Shingles, caused by herpes zoster, occurred during the previous Thanksgiving and can be associated with immunosuppression, stress, or an aging immune system (3,4). Mentation and gastrointestinal abnormalities improved after starting treatment with fluconazole, acyclovir, and symptomatic medications for erosive esophagitis. However, confusion, lack of orientation, hyponatremia, hypokalemia, and hyperglycemia remained problematic until discharge to a physical therapy center on December 31.
Second Hospitalization
During the next week, strength and mental capacities improved rapidly and discharge to the home environment was scheduled for January 9. On that morning and while driving to Maryland to build entry ramps, I was informed by cell phone that my father fell out of a chair and became nonverbal and that a stroke was suspected. For me, the roller coaster illness ultimately leading to his death would take an unbelievable turn of events. Upon his transfer to the neurology service, encephalopathy, asterixis, Parkinsonian-type tremor, hypoactive reflexes, pinpoint and minimally reactive pupils, and cogwheel rigidity were found. Verbal communication was absent, but he would grimace with pain whenever extremities were manipulated. An urgent computed tomography scan did not identify intracranial abnormalities.
When I was a boy, my father used the expression "something is fishy in Denmark" to imply that something was astray. Based upon historical events, I suspected something was being missed. Laboratory findings included anemia (hemocrit 34%), a normal leukogram (leukocytes 9,100 cells/μL, 2% band neutrophils), mild hypokalemia, hypoalbuminemia, hyperglycemia, increased serum alkaline phosphatase level, erythrocyte sedimentation rate of 79, and hypergammaglobulinemia. Thoracic radiographs identified mild bilateral pleural effusion. Because an undefined infectious source of immunosuppression seemed plausible, and fever (maximum temperature 38.6�C) occurred 24 hours after neurologic decompensation an infectious etiology was pursued. Nasal methicillin-resistant Staphylococcus aureus, blood, urine, and cerebrospinal fluid (CSF) cultures were negative. CSF results, including those for special stains, were unremarkable. Serologic results for Treponema pallidum, Borrelia burgdorferi, Rickettsia rickettsii, Bartonella henselae, Bartonella quintana, and HIV were negative. Results of CSF herpes simplex PCR and a test for T. pallidum antibodies were negative.
On January 11, results of magnetic resonance imaging and magnetic resonance angiography were interpreted as a left posterior stroke with no active bleeding. Initial treatment included intravenous acyclovir, fluconazole, vancomycin, ceftriaxone, ampicillin, and dexamethasone.
Translational Research and the Practice of Medicine
Because I direct the Intracellular Pathogens Research Laboratory (IPRL) at the North Carolina State University College of Veterinary Medicine, aseptically obtained blood and CSF samples were kindly provided for testing. Results of PCR (5,6) specific for Anaplasma, Ehrlichia, and Rickettsia species were negative. Bartonella 16S-23S intergenic spacer primers (7) repeatedly generated amplicons of different sizes from blood and CSF, respectively. Compared with GenBank sequences, the blood amplicon was most similar (434/465bp) to Candidatus Bartonella volans (strain FSq-1, EU294521) isolated from a southern flying squirrel (Glaucomys volans) and Candidatus Bartonella durdenii (391/422bp) amplified from Orchopeas howardi (GenBank accession no. DQ 336386), a flea found on eastern US gray squirrels (Scinrus carolinensis), and a Bartonella sp. (446/492bp, EF125214) identified in ground squirrels (Spermophilus danricus) in the People's Republic of China. The novel rodent Bartonella sequence obtained from my father's blood had an 18-bp insert at positions 2047 or 334 in EU294521 and DQ336386, respectively. Previously, our laboratory had never worked with rodent Bartonella species and had never amplified a 300-bp internal transcribed spacer region amplicon from >3,000 animal or human blood samples. After several unsuccessful cloning attempts, the CSF amplicon was most similar (393/394 bp) to B. henselae (NC-005956). Blood and CSF, cultured by using Bartonella α Proteobacteria growth medium (BAPGM) (8), did not result in the growth of a Bartonella species.
Clinicians and Scientists Working Together
After Bartonella PCR results became available, treatment with piperacillin and tazobactam were continued for 3 weeks until discharge. Levetiracetam was added to the patient's treatment because a generalized seizure occurred shortly after antimicrobial drugs were given. On January 18, severe dependent edema of the right elbow resulted in fluid leakage through intact skin. For 3 weeks, Dad remained semicomatose, disoriented, agitated, and encephalopathic. Hallucinations continued, accompanied by frequent involuntary motor movements. Diabetes mellitus and a large decubital ulcer on the right heel developed. During the fourth week, mentation improved, and he could rise and stand for brief periods. On January 28, he was discharged to a rehabilitation facility, with instructions to receive doxycycline and rifampin 2�/d for 13 days. Blood samples, obtained aseptically before discharge, were again submitted to the IPRL. After BAPGM pre-enrichment and subculture, B. vinsonii subsp. berkhoffii genotype II was isolated, and sequential serologic testing identified a rising titer to B. vinsonii subsp. berkhoffii but did not detect B. henselae antibodies (Table). After a brief, emotionally traumatic stay at the rehabilitation facility, Dad returned home to be cared for by 4 sons, his wife of 60 years, and other family members. Each week a different son slept by his bed, which was relocated to the family living room.
Home Again at Last
During the next 3 weeks, there was substantial and progressive improvement in physical capabilities and a return of normal mental capabilities, including exceptional short- and long-term memory. Appetite normalized, and despite severe atrophy, muscle strength increased so he could stand, walk with assistance, and, although a daily struggle, access the bathroom. A February 10 blood sample obtained while he was receiving oral antimicrobial drugs was Bartonella PCR negative, and no bacteria were isolated in BAPGM. During this precious 3 weeks, our father joked, laughed, and vividly recalled wartime friends and other experiences. On March 1, 2008, he opened Christmas presents with our family. I should have been there.
Third and Final Hospitalization
On March 4, ≈2 weeks after the course of oral antibiotics was completed, agitation and disorientation returned, and mental status deteriorated. Within 24 hours, Dad was hospitalized, where fine motor tremors of the right hand and wrist, asymmetric edema involving the right leg, and edema of the penis and scrotum were noted. He was afebrile and nonverbal and could not follow simple commands. Hematocrit was 30.2%, platelet count 557,000 cells/μL, and leukocyte count 7,800 cells/μL with a normal differential count. Serum biochemical abnormalities included hyperglycemia (glucose 218 mg/dL), hyperglobulinemia (3.6 g/dL), and increased alkaline phosphatase activity (169 IU/L). Urinalysis abnormalities included proteinuria with occasional hyaline casts.
Lorazepam was administered to control the agitation and restlessness. The warfarin dose was increased and heparinization initiated for a potential cerebrovascular accident. Due to the prior documentation of Bartonella infection, intravenous doxycycline, rifampin, and gentamicin were administered, and total parenteral nutrition was instituted. Again, shortly after initiation of antimicrobial drugs, a seizure occurred. Bartonella spp. were not amplified or isolated from a 1-mL blood sample obtained 4 days after initiation of treatment with antimicrobial drugs. During the next 3 weeks, while intravenous antimicrobial drugs were administered, our father again remained encephalopathic, with frequent hallucinations, severe agitation, and near-constant mental confusion. On March 14, intravenous methylprednisolone for potential immune-mediated vasculitis elicited no improvement in mental status. Similar to the previous treatment course, improvement in mental status, coherent communication, and renewed ability to recognize family members occurred during the fourth hospitalization week.
A Battle Lost
On April 4, Dad was discharged to our home and oral antimicrobial drugs (doxycycline and rifampin) were dispensed. Despite all efforts by medical professionals, members of our family, and our tough 86-year-old father, protracted illness and prolonged hospitalizations had resulted in mental and physical debilitation, severe muscle wasting, and profound weakness. More important, he had lost his desire to live. After discharge, there was minimal neurologic improvement. Before the availability of April 4 IPRL test results, he began to refuse all medications. The identical rodent Bartonella DNA sequence was again amplified from his blood, but no bacteria were isolated.
Four weeks later my father died, on Friday, May 2, at 5 pm, around quitting time for an old iron worker. My mother and youngest brother were at his side. After his death, blood culture results from another sample obtained by the hospice nurse on April 28, 2008, became available. B. vinsonii subsp. berkhoffii genotype II was amplified and sequenced from the enrichment BAPGM blood culture. As direct extraction of DNA from blood was negative, growth of viable bacteria in liquid culture was implicated (8,9).
Groundhogs, Fleas, and the Genus Bartonella
Following our father's death, I recalled a small, 0.5-cm, raised, firm lesion within his right eyebrow that developed during the summer of 2007 and would spontaneously hurt or burn, causing him to rub or squeeze the lesion. The mass disappeared after he began taking antimicrobial drugs in 2008. Retrospectively, I suspected a rodent flea bite above the eye had transmitted a novel Bartonella species, which we sequenced from his blood after each hospitalization. All known Bartonella spp. have preferential animal reservoir hosts, and each uses arthropods or animal bites and scratches as the primary modes of transmission (10-12). Dad would occasionally capture mice, rats, skunks, and groundhogs in the barns. Groundhogs were transported in the car trunk to a distant location for release, potentially leaving behind fleas. Therefore, 3 Candidatus Bartonella spp. isolates were provided by Dr. William Nicholson, a colleague at the Centers for Disease Control and Prevention in Atlanta. After sequencing, the 16S-23S intergenic spacer region of a ground squirrel (Candidatus Bartonella durdenii), a flying squirrel (Candidatus Bartonella volans), and a groundhog (Candidatus Bartonella monaxi) isolate, the most similar GenBank sequence was Candidatus Bartonella volans. There was no perfect match with these 3 isolates. However, sequences from Dad's blood clustered with a squirrel Bartonella subgroup. This observation supports the presence of a novel Bartonella species on the eastern shore of Maryland, an as yet undefined animal reservoir, and an unknown arthropod vector.
Regardless of the mode(s) of transmission, repeated molecular documentation of a novel rodent Bartonella sp. and B. vinsonii subsp. berkhoffii supports the unexpected failure of 2 intensive courses of intravenous and oral antimicrobial drugs to eliminate these fastidious, intravascular bacteria. During the first two hospitalization periods, there was similar and progressive improvement in neurologic signs and mental capabilities that began during the fourth week of antimicrobial drug administration. Pre-enrichment BAPGM growth of B. vinsonii subsp. berkhoffii from blood obtained 4 days before death supports persistence of viable organisms. Recently, antimicrobial drug resistance genes have been characterized in B. bacilliformis, B. henselae, and B. quintana by in vitro serial passage (13-15). Retrospectively, the relapse in encephalopathic signs might have been avoided if antimicrobial drugs were continued for a longer interval after discharge from hospital 2, and blood cultures were optimally obtained and sequentially tested to confirm therapeutic elimination.
Elimination of Bartonella spp. by antimicrobial drugs in immunocompetent patients may be more difficult to achieve than is currently appreciated (16). Although co-infection with B. henselae and B. vinsonii subsp. berkhoffii has been previously reported, DNA of 3 Bartonella spp. was detected in our father. Based on repeatable PCR testing, a small quantity of B. henselae DNA was in the January CSF sample. Because PCR amplicon contamination was never detected in any negative control, laboratory error is considered unlikely. Although the BAPGM enrichment approach has improved molecular detection and isolation of some Bartonella spp. from human patient samples (9,16-18), a rodent Bartonella sp. isolate was not obtained. Unfortunately, 8 weeks can be required from inoculation of BAPGM until a subculture agar plate isolate is characterized by DNA sequencing. Therefore, IPRL test results were often not available to Dad's physicians in a timely manner.
Age, Bartonella spp., and Immune Suppression?
Suspicion of an undetermined source of immune suppression and recent tick exposures were primary factors motivating testing in the IPRL. Previously, B. vinsonii subsp. berkhoffii was shown to induce immunosuppression in experimentally infected dogs (19,20). In retrospect, occult infection with Bartonella spp. may have contributed to shingles at Thanksgiving and necrotizing C. albicans esophagitis after hospitalization for the fractured femur. Recently, B. quintana lipopolysaccharide was found to have antiinflammatory properties (21). Immune suppressive factors may facilitate persistent intravascular Bartonella infection without inducing obvious infection indicators, such as fever, tachycardia, leukocytosis, and CSF pleocytosis. Fever was documented once and mild neutrophilia for 3 of 48 blood counts. Thrombocytosis, previously associated with B. henselae (22), was documented 14 times.
Ecologic Complexity of Bartonella spp.
Because of my father's long-standing atherosclerosis and because BAPGM will grow a spectrum of seemingly difficult to isolate bacteria (8,23), pre-enrichment blood cultures and Bartonella internal transcribed spacer region PCR had been performed in September 2005 and August 2006 (Table). Bartonella spp. were not amplified or isolated, which suggests infection occurred after the summer of 2006. Transmission of B. henselae, B. vinsonii subsp. berkhoffii, and B. alsatica can occur as a result of a scratch from a cat, a dog, or a wild rabbit, respectively (17,24-26). Cats are the primary reservoir for B. henselae, whereas dogs and coyotes are the only reported reservoir hosts for B. vinsonii subsp. berkhoffii genotype II in North America (27). Recently, B. vinsonii subsp. berkhoffii genotype II was isolated by BAPGM blood culture from a cat with recurrent osteomyelitis (E.B. Breitschwerdt, unpub. data), which suggests that a bacteremic cat might facilitate transmission of this subspecies. My parents had an old (≈21 years of age) exclusively outdoor barn cat that would occasionally scratch. The cat could not be tested because it died in 2007. B. henselae and B. clarridgeae have been transmitted experimentally by transfusion to cats (24). Because B. vinsonii subsp. berkhoffii seroconversion occurred during hospitalization, transfusion-associated transmission is also possible. The exact timing and mode of transmission of B. henselae, B. vinsonii subsp. berkhoffii, and the rodent Bartonella sp. to our father cannot be established. However, his illness serves to illustrate the medical and ecologic complexity of this genus.
Occult Infection and Chronic Illness
Reconstructing the history of a chronic illness is always difficult and remains an unexacting science due to known, unknown, and undetermined factors that influence disease expression over time. Experimental studies that used rodent models have emphasized the ability of Bartonella spp. to invade erythrocytes and vascular endothelial cells (28). In vitro studies indicate that B. henselae can infect macrophages, microgial cells, dendritic cells, and CD34+ progenitor cells (29). B. henselae and B. vinsonii subsp. berkhoffii have been amplified from dog lymph node aspiration samples (30). Thus in a given patient, Bartonella organisms likely infect a substantial number of cellular targets. B. henselae infection induces chronic arthritis in a subset of cat scratch disease (CSD) patients, and atypical CSD manifestations are more likely to develop in elderly patients (31,32). In the context of arthritis, B. henselae and B. vinsonii subsp. berkhoffii were repeatedly isolated from joint fluid from a dog in which repeated antimicrobial drug therapy was not successful (33). Although a spectrum of acute and generally self-limiting neurologic manifestations have been historically described in CSD patients, B. henselae and B. vinsonii subsp. berkhoffii were only recently isolated from patients with chronic neurologic and neurocognitive abnormalities (16).
We propose that the initial arthritic signs, short-term memory loss, and incoordination were premonitory signs of Bartonella spp. infection, and that persistent infection contributed to localized edema, nonregenerative anemia, thrombocytosis, hyperglobulinemia, and a protracted debilitating illness accompanied by hallucinations, agitation, seizures, and death. Agitation, disorientation, and combative behavior have been reported in association with CSD and physicians have implicated Bartonella spp. as contributors to agitation and treatment-resistant depression (34,35). Memory loss and a spectrum of neurocognitive complaints have also been reported in immunocompetent persons infected with B. vinsonii subsp. berkhoffii and B. henselae (9,16,17).
[click on link for remainder of article]
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Link to Dr. Breitschwerdt's lab website. Currently they are in the protocol validation stage for human testing. Once the validation testing is complete, they will begin human testing for Bartonella.
Galaxy Diagnostics provides an advanced testing methodology for the enhanced detection of hard-to-detect, vector-borne bacteria called Bartonella. Popularly known as Cat Scratch Disease (CSD), Trench Fever, Carrion's Disease, and Orroyo's Fever, Bartonella infection has been identified as an important source of emerging infectious disease in animal and humans. Recent medical evidence has linked Bartonella infection to serious chronic disease processes in immuno-competent patients, as well as to acute infections in immuno-suppressed patients.
Our Bartonella test combines state-of-the-art DNA detection with a patented enrichment culture developed by research scientists at the North Carolina State University College of Veterinary Medicine in response to the serious false negative rates of conventional testing. Our results are highly accurate and significantly more effective than any other available method for detecting active Bartonella spp. infection.
Galaxy's Bartonella Enrichment Culture+PCR platform offers a new standard of patient care in the diagnosis of Bartonella infection. We also offer optimized serology and conventional PCR testing to test for evidence of past/current infection.
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Bacteria transmitted by fleas-and potentially ticks-can be passed to human babies by the mother, causing chronic infections and raising the possibility of bacterially induced birth defects, a scientist has discovered.
Dr. Ed Breitschwerdt, professor of internal medicine in the Department of Clinical Sciences, is among the world's leading experts on Bartonella, a bacteria that is maintained in nature by fleas, ticks and other biting insects, but which can be transmitted by infected cats and dogs as well.
The most commonly known Bartonella-related illness is cat scratch disease, caused by B. henselae, a strain of Bartonella that can be carried in a cat's blood for months to years.
Cat scratch disease was thought to be a self-limiting, or ``one-time'' infection; however, Breitschwerdt's previous work discovered cases of children and adults with chronic, blood-borne Bartonella infections-from strains of the bacteria that are most often transmitted to cats (B. henselae) and dogs (B. vinsonii subsp. berkhoffii) by fleas and other insects.
In his most recent case study, Breitschwerdt's research group tested blood and tissue samples taken over a period of years from a mother, father and son who had suffered chronic illnesses for over a decade. Autopsy samples from their daughter-the son's twin who died shortly after birth-contained DNA evidence of B. henselae and B. vinsonii subsp. berkhoffi infection, which was also found in the other members of the family.
Both parents had suffered recurring neurological symptoms including headaches and memory loss, as well as shortness of breath, muscle weakness and fatigue before the children were born. In addition, their 10-year-old son was chronically ill from birth and their daughter died due to a heart defect at nine days of age.
Results of the parents' medical histories and the microbiological tests indicated that the parents had been exposed to Bartonella prior to the birth of the twins, and finding the same bacteria in both children, one shortly after birth and the other 10 years later, indicates that they may have become infected while in utero.
``This is yet more evidence that Bartonella bacteria cause chronic intravascular infections in people with otherwise normal immune systems, infections that can span a decade or more,'' Breitschwerdt says. ``Also this new evidence supports the potential of trans-placental infection and raises the possibility that maternal infection with these bacteria might also cause birth defects.''
Breitschwerdt's research appears online in the April 14, 2010 Journal of Clinical Microbiology .
Posts: 503 | From Maryland | Registered: Oct 2007
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I'm a little hesitant to post this one ... don't want to unncessarily frighten some folks who've had this. But, I think some of the information in the article is very helpful regarding treatment.
Of particular importance is their conclusion. "Effective antibiotic therapy for Bartonella endocarditis should include an aminoglycoside.
Investigative article on the "Outcome and Treatment of Bacterial Endocarditis."
richedie
Frequent Contributor (1K+ posts)
Member # 14689
posted
The thing that really scares me when I see this is that my pain never moves or changes! WHY? My left arm always hurts like heck....and always in the same spots. Not the right arm....just the left.
-------------------- Mepron/Zith/Ceftin Doxy/Biaxin/Flagyl pulse. Artemisinin with Doxy/Biaxin. Period of Levaquin and Ceftin. Then Levaquin, Bactrim and Biaxin. Bactrim/Augmentin/Rifampin. Mepron/Biaxin/Artemisinin/Cat's Claw Rifampin/Bactrim/Alinia Plaquenil/Biaxin Posts: 1949 | From Pennsylvania | Registered: Feb 2008
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Biotechnology scientist Donna Needham works with blood samples. Dr. Edward Breitschwerdt and Ricardo Maggi of NCSU founded Galaxy Diagnostics to cultivate the Bartonella bacteria.
BY SARAH AVERY - Staff Writer
A bacterial infection typically spread by fleas, lice and biting flies could be more prevalent than many think, and may have been transmitted from a mother to her children at birth, scientists from N.C. State University say.
Dr. Edward Breitschwerdt, an infectious disease veterinarian and one of the world's leading researchers of bacteria called Bartonella, has for the first time documented evidence that the pathogen may have been passed between family members.
Although more studies are needed to back up his findings, Breitschwerdt and colleagues describe the case of a mother and father who began battling chronic aches, fatigues and other symptoms soon after they were married. When their twins were born in 1998, the daughter died after nine days from a heart defect, and the son developed chronic health problems.
Using tissue from the daughter's autopsy and blood from the surviving family members, Breitschwerdt's team discovered that the entire family was infected with the same species of Bartonella bacteria, despite having no shared exposures to flea or lice infestations. Bartonella is known to causes such illnesses as trench fever and cat scratch disease, and it is increasingly suspected of triggering a variety of aches and inflammations that doctors have been unable to diagnose.
"I think we have stumbled across something that is of monumental medical importance," said Breitschwerdt, whose findings were published recently in the Journal of Clinical Microbiology.
Proving the mother-child transmission could be difficult, however. Little funding is available for such research because the bacteria are still not considered a major source of human disease.
Dr. Michael Kosoy, who heads the Bartonella laboratory for the Centers for Disease Control and Prevention in Fort Collins, Colo., said scientists are only beginning to build evidence that Bartonella infections may be more common than previously thought.
"Bartonella are circulated around the world in many animals, but there are different Bartonella species, and the question is how can they be transmitted to humans?" Kosoy said, noting that most known cases have been transmitted from biting insects. He said the NCSU findings about the potential family transmission are compelling but inconclusive.
Dozens of strains
At least 26 strains of Bartonella have been named worldwide, and the list is growing. The most notorious Bartonella infection is cat scratch disease, a fever illness passed to humans from flea-infected cats. Fleas are the primary hosts, and they spread the bacteria in their feces.
Other Bartonella strains spread more serious diseases. Kosoy is studying how often heart inflammation is caused by a Bartonella that thrives among rat fleas in Thailand. He has already established that about 25 percent of unexplained fever illnesses among a group of patients there was caused by Bartonella .
"This is not limited to cat scratch," Kosoy said. "That's just the tip of the iceberg."
Breitschwerdt said he thinks the bacteria may be the hidden cause behind a host of chronic symptoms - muscle aches, neurological problems, fatigue, arthritis - that defy diagnosis.
About two years ago, Breitschwerdt began testing blood samples from a doctor in Maryland, who was curious whether Bartonella infections might be causing problems for some of his patients.
"There are lab tests showing inflammation," but no discernible cause, said Dr. Robert Mozayeni, a Yale-educated rheumatologist who practices in Rockville, Md.
Mozayeni contacted Breitschwerdt and his NCSU colleague, Ricardo Maggi, who together developed a more sensitive test for Bartonella. Routine blood tests fail to detect Bartonella because they search for antibodies that the body is slow to produce.
Instead, Breitschwerdt and Maggi figured out how to cultivate the bacteria in the laboratory from blood samples of infected people. They founded a company called Galaxy Diagnostics to handle the laboratory volume.
Of Mozayeni's mystery patients tested at the lab, nearly 20 percent had Bartonella infections.
"I suspect this is going to be one of the causes of rheumatoid arthritis and a few other things, but it's too speculative right now to say," Mozayeni said.
Human testing
More studies are needed, and Mozayeni has joined Breitschwerdt and Maggi in the diagnostic company to oversee human testing.
"Certainly, the prevalence of Bartonella infection in people with chronic illness is higher than I would have ever guessed, but we still don't know what that means," Breitschwerdt said.
Among the biggest unknowns is how to treat people who have been infected. The effectiveness of antibiotics depends on which strain of Bartonella is at work, and with so many strains, treatments can be hit or miss.
Breitschwerdt said the family in his most recent study declined to comment about their experience. He said they were having difficulty finding a doctor.
"It is very difficult to find a physician who wants to see someone with a chronic illness that is poorly defined," he said, adding that many such patients often think they have Lyme disease, a tick-borne bacterial infection with similar symptoms - and stigma. "With an unexplained illness, it becomes problematic."
mojo
Frequent Contributor (1K+ posts)
Member # 9309
posted
Tracy - Rifampin can be a difficult drug to take but I think it's very effective for Bart. I couldn't take it because it sent my Liver Enzymes sky high.
Make sure to get your Liver Enzymes checked regularly.
My sister took it for 8 months or so and she was very ill the entire time (but liver was OK). She was not herself - very cranky and always felt sick. It really did a lot for her, though.
It also treats Lyme so that could be another reason people herx hard.
I wish I could go back on this one!
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Tracy9
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Member # 7521
posted
I've been very lucky; my liver enzymes have been fine. Is it the Bart coming out that makes us so sick, toxins dying off, or what? The Rifampin seems to be doing a good job, whatever it is.
Also I am on JUST Rifampin. Several people have said you have to be on something else with it but my LLD says no, Rifampin alone is fine.
13 years Lyme & Co.; Small Fiber Neuropathy; Myasthenia Gravis, Adrenal Insufficiency. On chemo for 2 1/2 years as experimental treatment for MG. Posts: 4480 | From Northeastern Connecticut | Registered: Jun 2005
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Tracy9
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Member # 7521
Published Fri, May 21, 2010 05:10 AM Modified Fri, May 21, 2010 07:54 AM
The pain of Bartonella
A bacterial infection typically spread by fleas, lice and biting flies could be more prevalent than many think, and may have been transmitted from a mother to her children at birth, scientists from N.C. State University say.
Dr. Edward Breitschwerdt, an infectious disease veterinarian and one of the world's leading researchers of bacteria called Bartonella, has for the first time documented evidence that the pathogen may have been passed between family members.
Although more studies are needed to back up his findings, Breitschwerdt and colleagues describe the case of a mother and father who began battling chronic aches, fatigues and other symptoms soon after they were married. When their twins were born in 1998, the daughter died after nine days from a heart defect, and the son developed chronic health problems.
Using tissue from the daughter's autopsy and blood from the surviving family members, Breitschwerdt's team discovered that the entire family was infected with the same species of Bartonella bacteria, despite having no shared exposures to flea or lice infestations. Bartonella is known to causes such illnesses as trench fever and cat scratch disease, and it is increasingly suspected of triggering a variety of aches and inflammations that doctors have been unable to diagnose.
"I think we have stumbled across something that is of monumental medical importance," said Breitschwerdt, whose findings were published recently in the Journal of Clinical Microbiology.
Proving the mother-child transmission could be difficult, however. Little funding is available for such research because the bacteria are still not considered a major source of human disease.
Dr. Michael Kosoy, who heads the Bartonella laboratory for the Centers for Disease Control and Prevention in Fort Collins, Colo., said scientists are only beginning to build evidence that Bartonella infections may be more common than previously thought.
"Bartonella are circulated around the world in many animals, but there are different Bartonella species, and the question is how can they be transmitted to humans?" Kosoy said, noting that most known cases have been transmitted from biting insects. He said the NCSU findings about the potential family transmission are compelling but inconclusive.
Dozens of strains
At least 26 strains of Bartonella have been named worldwide, and the list is growing. The most notorious Bartonella infection is cat scratch disease, a fever illness passed to humans from flea-infected cats. Fleas are the primary hosts, and they spread the bacteria in their feces.
Other Bartonella strains spread more serious diseases. Kosoy is studying how often heart inflammation is caused by a Bartonella that thrives among rat fleas in Thailand. He has already established that about 25 percent of unexplained fever illnesses among a group of patients there was caused by Bartonella .
"This is not limited to cat scratch," Kosoy said. "That's just the tip of the iceberg."
Breitschwerdt said he thinks the bacteria may be the hidden cause behind a host of chronic symptoms - muscle aches, neurological problems, fatigue, arthritis - that defy diagnosis.
About two years ago, Breitschwerdt began testing blood samples from a doctor in Maryland, who was curious whether Bartonella infections might be causing problems for some of his patients.
"There are lab tests showing inflammation," but no discernible cause, said Dr. Robert Mozayeni, a Yale-educated rheumatologist who practices in Rockville, Md.
Mozayeni contacted Breitschwerdt and his NCSU colleague, Ricardo Maggi, who together developed a more sensitive test for Bartonella. Routine blood tests fail to detect Bartonella because they search for antibodies that the body is slow to produce.
Instead, Breitschwerdt and Maggi figured out how to cultivate the bacteria in the laboratory from blood samples of infected people. They founded a company called Galaxy Diagnostics to handle the laboratory volume.
Of Mozayeni's mystery patients tested at the lab, nearly 20 percent had Bartonella infections.
"I suspect this is going to be one of the causes of rheumatoid arthritis and a few other things, but it's too speculative right now to say," Mozayeni said.
Human testing
More studies are needed, and Mozayeni has joined Breitschwerdt and Maggi in the diagnostic company to oversee human testing.
"Certainly, the prevalence of Bartonella infection in people with chronic illness is higher than I would have ever guessed, but we still don't know what that means," Breitschwerdt said.
Among the biggest unknowns is how to treat people who have been infected. The effectiveness of antibiotics depends on which strain of Bartonella is at work, and with so many strains, treatments can be hit or miss.
Breitschwerdt said the family in his most recent study declined to comment about their experience. He said they were having difficulty finding a doctor.
"It is very difficult to find a physician who wants to see someone with a chronic illness that is poorly defined," he said, adding that many such patients often think they have Lyme disease, a tick-borne bacterial infection with similar symptoms - and stigma. "With an unexplained illness, it becomes problematic."
13 years Lyme & Co.; Small Fiber Neuropathy; Myasthenia Gravis, Adrenal Insufficiency. On chemo for 2 1/2 years as experimental treatment for MG. Posts: 4480 | From Northeastern Connecticut | Registered: Jun 2005
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Bartonella vinsonii subsp. berkhoffii and Bartonella henselae bacteremia in a father and daughter with neurological disease
Edward B Breitschwerdt1 , Ricardo G Maggi1 , Paul M Lantos2 , Christopher W Woods2 , Barbara C Hegarty1 and Julie M Bradley1
1 Intracellular Pathogens Research Laboratory, Center for Comparative Medicine and Translational Research, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough St., Raleigh, NC, USA 2 Duke University Medical Center, 2301 Erwin Rd, Durham, NC, USA author email corresponding author email
Received: 4 February 2010 Accepted: 8 April 2010 Published: 8 April 2010 � 2010 Breitschwerdt et al; licensee BioMed Central Ltd.
Abstract
Background Bartonella vinsonii subsp. berkhoffii is an important, emerging, intravascular bacterial pathogen that has been recently isolated from immunocompetent patients with endocarditis, arthritis, neurological disease and vasoproliferative neoplasia. Vector transmission is suspected among dogs and wild canines, which are the primary reservoir hosts. This investigation was initiated to determine if pets and family members were infected with one or more Bartonella species.
Methods PCR and enrichment blood culture in Bartonella alpha Proteobacteria growth medium (BAPGM) was used to determine infection status. Antibody titers to B. vinsonii subsp. berkhoffii genotypes I-III and B. henselae were determined using a previously described indirect fluorescent antibody test. Two patients were tested sequentially for over a year to assess the response to antibiotic treatment.
Results Intravascular infection with B. vinsonii subsp. berkhoffii genotype II and Bartonella henselae (Houston 1 strain) were confirmed in a veterinarian and his daughter by enrichment blood culture, followed by PCR and DNA sequencing. Symptoms included progressive weight loss, muscle weakness, lack of coordination (the father) and headaches, muscle pain and insomnia (the daughter). B. vinsonii subsp. berkhoffii genotype II was also sequenced from a cerebrospinal fluid BAPGM enrichment culture and from a periodontal swab sample. After repeated courses of antibiotics, post-treatment blood cultures were negative, there was a decremental decrease in antibody titers to non-detectable levels and symptoms resolved in both patients.
Conclusions B. vinsonii subsp. berkhoffii and B. henselae are zoonotic pathogens that can be isolated from the blood of immunocompetent family members with arthralgias, fatigue and neurological symptoms. Therapeutic elimination of Bartonella spp. infections can be challenging, and follow-up testing is recommended. An increasing number of arthropod vectors, including biting flies, fleas, keds, lice, sandflies and ticks have been confirmed or are suspected as the primary mode of transmission of Bartonella species among animal populations and may also pose a risk to human beings.
Background
When a genus of bacteria is discovered or, in the case of Bartonella, rediscovered; numerous clinical, microbiological and pathological concepts related to disease causation and microbial pathogenesis are sequentially redefined. Subsequently, the medical relevance of the genus undergoes continued maturation; as knowledge of the organism, the host immune response, diagnostic test sensitivity and specificity, treatment efficacy and epidemiology expand. Since the early 1990s, this paradigm of discovery and ongoing biological and medical redefinition has clearly been applicable to the genus Bartonella. Prior to 1990, only two pathogenic Bartonella species, B. bacilliformis and B. quintana, were known to exist. Since 1990, greater than 22 Bartonella species have been described, of which at least half have been implicated or confirmed as human pathogens [1,2].
Bartonella vinsonii subsp. berkhoffii was initially isolated from a dog with endocarditis in 1993 [3]. Subsequently, four genotypes of B. vinsonii subsp. berkhoffii were described, based upon analysis of blood samples from coyotes, dogs and foxes [4]. To date, genotype II has been the most frequently isolated genotype sequenced from dog and human blood samples [5-8]. Previously, B. vinsonii subsp. berkhoffii genotype II was documented in a healthy dog on 8 of 10 culture attempts spanning a 16-month period, thereby supporting the potential for persistent intravascular infection in pet dogs [9]. Although tick transmission of B. vinsonii subsp. berkhoffii has been suggested, the mode(s) of transmission among canines has not been determined [10]. In contrast to the canine reservoir for B. vinsonii subsp. berkhoffii, domestic and wild felids represent the primary reservoir in nature for Bartonella henselae, an organism transmitted among cats by fleas (Ctenocephalides felis); a factor that contributes to a worldwide distribution for this Bartonella sp. [1,2]. Similar to dogs, outwardly healthy cats can remain bacteremic with B. henselae for months to years [11,12]. However, despite what seems to be exceptional evolutionary adaptation of B. vinsonii subsp. berkhoffii in canines and B. henselae in felines, both of these two bacterial species can be pathogenic in both cats and dogs.
In this study, intravascular infection with B. vinsonii subsp. berkhoffii genotype II and B. henselae were foundin a veterinarian and his daughter. The father presented with progressive weight loss, muscle weakness and lack of coordination; his daughter had developed headaches, muscle pain and insomnia. Both individuals were being evaluated by a neurologist at the time of initial testing for evidence of Bartonella infection. Multiple courses of antibiotics were administered before the patients' clinical status improved and before microbiological, molecular and serological evidence of infection diminished or was negative.
Patients, pets and methods
In October, 2007, the primary author was contacted by the father of a family residing in North Carolina, who requested Bartonella testing as a component of an IRB approved study (North Carolina State University Institutional Review Board, IRB#s 4925-03 and 164-08-05). For all family members and pets (Institutional Animal Care and Use Protocol 07-014-0) tested in this study, a previously described approach that combines PCR detection of Bartonella spp. DNA and enrichment culture of blood and serum samples in Bartonella alpha Proteobacteria growth medium (BAPGM) was used [8]. The three part BAPGM diagnostic platform incorporates PCR amplification of Bartonella spp. following direct DNA extraction from patient blood and serum samples, PCR amplification following enrichment culture in BAPGM for 7 to 14 days, and PCR from isolates obtained following BAPGM subculture inoculation onto trypticase soy agar with 10% rabbit blood. Agar plates are incubated for 4 weeks and checked weekly for evidence of bacterial growth. To assess for potential laboratory contamination, an un-inoculated BAPGM culture flask was processed simultaneously and in an identical manner with each batch of patient blood and serum samples tested. Specifically, while establishing cultures using a batch of samples in the biosafety hood, the top was removed from the BAPGM un-inoculated control flask until all patient samples had been processed. Methods used for testing sample cultures, including DNA extraction, PCR amplification targeting the Bartonella 16S-23S intergenic spacer region (ITS), and sequencing procedures were performed using previously described methods [5-8]. Following the standard operating procedures in the Intracellular Pathogens Research Laboratory, sample preparation including BAPGM cultures and agar plate sub-inoculation, DNA extraction, PCR preparation and PCR amplification and analysis were performed in separate laboratory rooms to avoid culture as well as DNA contamination. In addition, negative and positive Bartonella DNA test control samples, consisting of bacteria-free blood DNA and DNA spiked with B. henselae genomic DNA at 0.5 genome copies per microliter, respectively, were used for each batch of DNA tested. For all results reported in this study, PCR products consistent in size with a Bartonella spp. (400-600 bp amplicon size) were sequenced to confirm the species and ITS strain. Sequences were aligned and compared with GenBank sequences using AlignX software (Vector NTI Suite 6.0, InforMax, Inc.).
Serology was performed using modifications of a previously described indirect fluorescent antibody test [13]. Bartonella vinsonii subsp. berkhoffii and B. henselae antibodies were determined following traditional immunofluorescence antibody assay (IFA) practices with fluorescein conjugated goat anti-human IgG. Bartonella vinsonii subsp. berkhoffii genotypes I, II and III and B. henselae (Houston I strain) were passed from agar grown cultures of each organism into DH82 (a continuous canine histiocytic cell line) cultures to obtain antigens that would seemingly be expressed by an intracellular bacteria localized to erythrocytes or endothelial cells within the vasculature. Heavily infected cell cultures were spotted onto 30-well Teflon coated slides (Cel-Line/Thermo Scientific), air dried, acetone fixed and stored frozen. Serum samples were diluted in phosphate buffered saline (PBS) solution containing normal goat serum, Tween-20 and powdered nonfat dry milk to block non-specific antigen binding sites. Patient sera were screened at dilutions of 1:16 to 1:64. All sera that remained reactive at a titer of 1:64 were further tested with twofold dilutions out to a final dilution of 1:8192.
Results
Father The father was a 50-year-old veterinarian whose symptoms began in 2006 with arthralgias and fatigue, which became progressively severe over ensuing 18 months. He described pain and stiffness of the joints, muscles, and neck that were most severe in the morning but improved throughout the day. He did not have fevers, but he suffered from profound fatigue. He had also experienced an 80-pound weight loss, though this was partially intentional. Beginning in September 2007, and of greatest concern to the patient, was progressive difficulty maintaining his balance while standing or ambulating. His history was notable for extensive occupational and domestic animal exposure. International travel was minimal. He was initially evaluated by a neurologist, and because of his exposure to zoonotic pathogens he was referred for infectious disease evaluation. He had not received any empiric courses of antibiotics.
On physical examination, the patient had a blood pressure of 141/88 mm Hg, a pulse of 98 beats/min, and a temperature of 37�C. He was in no acute distress and had a normal sensorium. Notable abnormal findings included a positive Romberg sign and difficulty with heel-toe walking. Cranial nerves, muscle strength, sensation, and deep tendon reflexes were normal and symmetrical, and his funduscopic examination was normal. There was no lymphadenopathy, no organomegaly, and no rash. Lumbar puncture revealed normal cerebrospinal fluid indices and opening pressure. Magnetic resonance imaging of the brain was notable for an increase in signal intensity throughout the pons and upper medulla lateralizing to the left of the midline (Figure 1).
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Int J Med Sci 2009; 6:131-132 �Ivyspring International Publisher
Ocular Bartonellosis
Massimo Accorinti
Institute of Ophthalmology, University ``La Sapienza'' of Rome (Italy) How to cite this article: Accorinti M. Ocular Bartonellosis. Int J Med Sci 2009; 6:131-132. Available from http://www.medsci.org/v06p0131.htm
Bartonella henselae is a gram negative aerobic bacillus and is the etiologic agent of cat-scratch disease. The infection is present around the world and may affect patients of all ages, including immunocompetent individuals. Humans are usually infected through a cat's scratch or bite, but a bite by cat fleas may also be the origin of infection. More common in children and young adults, it usually presents with a wide range of systemic and ocular symptoms. Other Bartonella species have been described as causing ocular lesions, as shown in Table 1.
Systemic signs and symptoms usually precede ocular involvement and are constituted by the appearance, 3 to 10 days after inoculation of bartonella by scratch or bite, of an erythematous papule on the skin on the site of inoculation. Seven to 14 days after the exposure a follicular conjunctivitis may appear. Fourteen to 21 days after the inoculation regional lymphoadenopathy may occur which is usually associated with myalgias, fatigue and low-grade fever. The association of conjunctivits and regional lymphoadenopathy is well known as Parinaud's oculoglandular syndrome (POGS).
Ocular signs
The most frequent ocular manifestation is neuroretinitis which is usually unilateral. If neuroretinitis is bilateral, it is quite asymmetric. Rarely, posterior pole involvement may be characterized by the presence of a focal inflammatory mass, either of the retina or of the optic disk. Central or paracentral scotoma or physiologic blind spot enlargement are the main alterations of the visual field, while fluorescein angiography usually presents a diffuse leakage from the optic nerve head along with the retinal vessels. Sometimes vascular occlusion with intraretinal haemorrhages and cotton-wool spots are present at the posterior pole. Anterior uveitis, intermediate uveitis and orbital abscess may also be observed in bartonellosis. In HIV-seropositive patients, some cases of bacillary angiomatosis and subretinal neovascular granuloma have been reported.
Diagnosis and Differential diagnosis
Enzyme immunoassay and Western Blot, along with PCR analysis, are usually used for diagnosis, although past history of contact with cats should lead to suspect the proper diagnosis. Serologic tests show a specificity and sensitivity of 90% in immunocompetent patients and only 70% in immunodeficient subjects.
Parinaud's syndrome is a clinical entity that may be due to numerous infections, including tularaemia, sporotrichosis, tuberculosis, syphilis, mononucleosis, coccidioidomycosis, while neuroretinitis with macular star may be observed in vascular disorders, toxoplasmosis, syphilis, tuberculosis, Lyme disease, and viral infection.
Table 1
[The Table didn't copy well -- please see link for the table which includes information on Bartonella pathogens and the eye]
Cat scratch disease is usually a self-limited disease in immunocompetent patients. Bartonella henselae is sensitive to many antibiotics in vitro, but only aminoglycosides have bactericidal activity. In immunocompetent patients doxycicline 200 mg/day is usually administered because of its property to cross the blood-brain and blood-ocular barrier. Caution should be made if administered to children, because it may cause dental changes. Ciprofloxacin (1,5 gr/day), gentamicin (3-5 mg/kg/day), erythromycin (2 gr/day), trimethoprim-sulphamethoxazole (Bactrim � 2 tablets/day) are good alternatives and, like doxycicline, are usually given for 14 to 28 days. Azythromicin may also be given to patients affected by cat scratch disease at 500 mg/day for 3 to 5 days. Immunodeficient patients need a more prolonged course of treatment, usually up to 4 months.
Ocular lesions are treated with antibiotics and with topical steroids for conjunctival lesion, topical steroids and mydriatics for anterior segment involvement and with peribulbar (sub-tenon) steroid injection and/or systemic steroids for retinal and optic nerve involvement. In this last case it is important to start steroid therapy after at least 48 hours from starting specific antibiotic treatment, especially if given locally in a depot preparation.
Bartonella henselae is a gram negative aerobic bacillus and is the etiologic agent of cat-scratch disease. The infection is present around the world and may affect patients of all ages, including immunocompetent individuals. Humans are usually infected through a cat's scratch or bite, but a bite by cat fleas may also be the origin of infection. More common in children and young adults, it usually presents with a wide range of systemic and ocular symptoms. Other Bartonella species have been described as causing ocular lesions, as shown in Table 1.
Systemic signs and symptoms usually precede ocular involvement and are constituted by the appearance, 3 to 10 days after inoculation of bartonella by scratch or bite, of an erythematous papule on the skin on the site of inoculation. Seven to 14 days after the exposure a follicular conjunctivitis may appear. Fourteen to 21 days after the inoculation regional lymphoadenopathy may occur which is usually associated with myalgias, fatigue and low-grade fever. The association of conjunctivits and regional lymphoadenopathy is well known as Parinaud's oculoglandular syndrome (POGS).
Ocular signs
The most frequent ocular manifestation is neuroretinitis which is usually unilateral. If neuroretinitis is bilateral, it is quite asymmetric. Rarely, posterior pole involvement may be characterized by the presence of a focal inflammatory mass, either of the retina or of the optic disk. Central or paracentral scotoma or physiologic blind spot enlargement are the main alterations of the visual field, while fluorescein angiography usually presents a diffuse leakage from the optic nerve head along with the retinal vessels. Sometimes vascular occlusion with intraretinal haemorrhages and cotton-wool spots are present at the posterior pole. Anterior uveitis, intermediate uveitis and orbital abscess may also be observed in bartonellosis. In HIV-seropositive patients, some cases of bacillary angiomatosis and subretinal neovascular granuloma have been reported.
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I also acquired it across my entire back and the outside of my upper arms.![[Frown]](frown.gif)
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