Bartonella

General or non-medical topics with information and discussion related to Lyme disease and other tick-borne diseases.
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Yvonne
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Bartonella

Post by Yvonne » Fri 6 Jun 2008 17:40

Bartonella species in blood of immunocompetent persons with animal and arthropod contact.

Abstract
Using PCR in conjunction with pre-enrichment culture, we detected Bartonella henselae and B. vinsonii subspecies berkhoffii in the blood of 14 immunocompetent persons who had frequent animal contact and arthropod exposure.

Attempts to isolate Bartonella sp. from immunocompetent persons with serologic, pathologic, or molecular evidence of infection are often unsuccessful; several investigators have indicated that Bartonella isolation methods need to be improved (1–4). By combining PCR and pre-enrichment culture, we detected B. henselae and B. vinsonii subspecies berkhoffii infection in the blood of immunocompetent persons who had arthropod and occupational animal exposure

The Study

From November 2004 through June 2005, blood and serum samples from 42 persons were tested, and 14 completed a questionnaire, approved by the North Carolina State University Institutional Review Board. Age, sex, animal contact, history of bites, environment, outdoor activity, arthropod contact, travel, and medical history were surveyed. Bacterial isolation, PCR amplification, and cloning were performed by using previously described methods (5–7). Each blood sample was tested by PCR after direct DNA extraction, pre-enrichment culture for at least 7 days, and subculture onto a blood agar plate (Figure). An uninoculated, pre-enrichment culture was processed simultaneously as a control. Methods used for DNA extraction and conventional and real-time PCR targeting of the Bartonella 16S-23S intergenic spacer (ITS) region and heme-binding protein (Pap31) gene have been described (7,8). Conventional PCR amplicons were cloned with the pGEM-T Easy Vector System (Promega, Madison, WI, USA); sequencing was performed by Davis Sequencing, Inc. (Davis, CA, USA). Sequences were aligned and compared with GenBank sequences with AlignX software (Vector NTI Suite 6.0 (InforMax, Inc., Bethesda, MD, USA) (7,8). B. vinsonii subsp. berkhoffii, B. henselae, and B. quintana antibodies were determined by using a modification of a previously described immunofluorescence antibody assay (IFA) procedure (9

Study participants included 12 women and 2 men, ranging in age from 30 to 53 years; all of them reported occupational animal contact for >10 years (Table). Most had daily contact with cats (13 persons) and dogs (12 persons). All participants reported animal bites or scratches (primarily from cats) and arthropod exposure, including fleas, ticks, biting flies, mosquitoes, lice, mites, or chiggers. All participants reported intermittent or chronic clinical symptoms, including fatigue, arthralgia, myalgia, headache, memory loss, ataxia, and paresthesia (Table). Illness was most frequently mild to moderate in severity, with a waxing and waning course, and all but 2 persons could perform occupational activities. Of the 14 participants, 9 had been evaluated by a cardiologist, 8 each by an infectious disease physician or a neurologist, and 5 each by an internist or a rheumatologist. Eleven participants had received antimicrobial drugs.

When reciprocal titers of >64 were used, 8 persons were seroreactive to Bartonella antigens (Appendix Table). B. henselae or B. vinsonii subsp. berkhoffii was detected or isolated from all 14 participants. At the time of initial testing, Bartonella DNA was amplified directly from 3 blood samples, from 7 pre-enrichment liquid cultures, and from 4 subculture isolates (Appendix Table). For 5 persons, results of PCR and culture of initial samples were negative. Overall, Bartonella DNA was amplified from 11 (28%) of 40 extracted blood samples, 13 (33%) of 40 pre-enrichment cultures, and 5 isolates. For 7 persons, B. henselae DNA was amplified at multiple time points. Bartonella DNA was never amplified from any PCR control or uninoculated culture control.

By using the ITS target region, 2 distinct B. henselae ITS and Pap31 strains were sequenced, B. henselae Houston I (HI) (GenBank NC-005956) and B. henselae San Antonio 2 (SA2) (GenBank AF369529). Within the noncoding ITS region, B. henselae SA2 strains have a 30-bp insertion (ATT GCT TCT AAA AAG ATT GCT TCT AAA AAG) located 518 bases downstream from the 16S gene. Only B. vinsonii subsp. berkhoffii types I and II were detected (8).

Conclusions
Persistent human infection with B. bacilliformis and B. quintana has been previously documented, whereas infection with B. henselae (cat-scratch disease [CSD]) is generally considered self-limiting (1,2,10). Recently, B. henselae DNA was amplified from the blood of a child 4 months after CSD diagnosis (11). Our study indicates that B. henselae and B. vinsonii subsp. berkhoffii can induce occult infection in immunocompetent persons and that detection can be enhanced by combining PCR with pre-enrichment culture. Considering only the results from initial blood samples, PCR detected Bartonella DNA in 3 samples, all of which were subsequently PCR positive by subculture or enrichment culture. In samples from 5 persons, pre-enrichment was necessary, and in 5 other persons, sequential sampling was necessary to detect Bartonella infection. Intermittent bacteremia, as occurs in B. henselae–infected cats (12), antimicrobial drug administration, low bacterial copy numbers, and low inoculum volume (1 mL) may have contributed to intermittent detection or inability to isolate Bartonella spp. from some participant samples. Although our approach is an improvement over historical isolation approaches, our results emphasize ongoing limitations associated with the detection of Bartonella infection. Obtaining stable Bartonella subcultures (n = 5 in this study) has proven problematic for other specialized laboratories that routinely culture for Bartonella spp. (3,4). To our knowledge, the B. vinsonii subsp. berkhoffii type II isolate described in our study is the only type II human isolate reported to date (8). Various combinations of B. henselae and B. vinsonii subsp. berkhoffii strain types were detected in the same blood sample or sequential blood samples. The coexistence of B. henselae genetic variants has been described among primary patient isolates, which suggests that multiple genotypes may emerge within the same person (13).

Overall, 57% of persons tested were seroreactive to 1 or all 3 Bartonella test antigens. Previous reports from the United States identified a B. henselae seroprevalence of 3% in healthy blood donors and a cumulative seroprevalence of 7.1% to both B. henselae and B. quintana antigens in veterinary professionals (1). In this and other studies, serologic test results did not correlate with PCR amplification or isolation results. Antigenic variability among B. henselae test strains can cause false-negative IFA results in persons with suspected CSD. Also B. henselae, B. quintana, or B. elizabethae antibodies were not detected in some persons with DNA evidence of active infection (1,3,4).

Animal contact, often to a wide spectrum of domestic and wild animal species, is an obvious consequence of the daily activities of the study population, which is biased by veterinary occupational exposure and by self-selection (volunteer bias). Cats are considered the primary reservoir host for B. henselae, whereas coyotes and foxes are considered reservoir hosts for B. vinsonii subsp. berkhoffii (1,2,8). Detection of B. vinsonii subsp. berkhoffii in 4 of 5 Californian participants could be related to the high prevalence of bacteremic coyotes in this region as well as to the potential transmission by a tick vector (1,2). All 14 participants reported frequent arthropod exposure. Although Bartonella spp.transmission by ticks has not been proven, several recent studies have identified Bartonella DNA in questing ticks, ticks attached to animals, and ticks attached to humans (1,2,14).

Despite reporting chronic or episodic illness, most participants continued to effectively maintain daily professional and personal activities. The symptoms described in the study patients are very similar to those described in a community and hospital-based surveillance study of CSD patients, in whom CSD-associated arthropathy was an uncommon chronic syndrome affecting mostly young and middle-age women (15). Our study was initiated to investigate the feasibility of combining PCR with pre-enrichment culture. Prospective studies, with appropriate controls, are needed to characterize the prevalence and clinical relevance of persistent Bartonella infection in immunocompetent persons.

http://www.cdc.gov/eid/content/13/6/938.htm
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Re: Bartonella

Post by Yvonne » Sat 16 Aug 2008 13:07

http://bloodjournal.hematologylibrary.o ... 106/4/1215

Infection of human CD34+ progenitor cells with Bartonella henselae results in intraerythrocytic presence of B henselae
Abstract

Although there is evidence that endothelial cells are important targets for human pathogenic Bartonella species, the primary niche of infection is unknown. Here we elucidated whether human CD34+ hematopoietic progenitor cells (HPCs) internalize B henselae and may serve as a potential niche of the pathogen. We showed that B henselae does not adhere to or invade human erythrocytes. In contrast, B henselae invades and persists in HPCs as shown by gentamicin protection assays, confocal laser scanning microscopy (CLSM), and electron microscopy (EM). Fluorescence-activated cell sorting (FACS) analysis of glycophorin A expression revealed that erythroid differentiation of HPCs was unaffected following infection with B henselae. The number of intracellular B henselae continuously increased over a 13-day period. When HPCs were infected with B henselae immediately after isolation, intracellular bacteria were subsequently detectable in differentiated erythroid cells on day 9 and day 13 after infection, as shown by CLSM, EM, and FACS analysis. Our data provide, for the first time, evidence that a bacterial pathogen is able to infect and persist in differentiating HPCs, and suggest that HPCs might serve as a potential primary niche in Bartonella infections.

Discussion

HPCs (erythroblasts, megacaryocytes, and myeloid progenitors) located in the bone marrow are the source of erythrocytes, platelets, and granulocytes. This highly important compartment of the body establishes the functional base for oxygen supply to the body, for clotting, and for eradication of pathogens. The role of HPCs has been widely investigated in hematology where these cells are used for bone marrow transplantation. However, the interaction of bone marrow–derived human stem cells with human pathogens has only rarely been analyzed.

Bartonella species cause several human diseases including trench fever, CSD, BA, BP, and other manifestations.5 However, in all of these infections, the primary niche of the pathogens remains unclear, although Bartonella species are capable of infecting a wide variety of different host cells. In particular, it has been shown that B henselae infects endothelial cells,20,22,26 epithelial cells,19 and monocytes or macrophages,29,30,32 and similar findings have been reported for B quintana.33,34

Intraerythrocytic presence of human pathogenic Bartonella species has been demonstrated several times in vitro by fluorescence mircroscopy using anti-Bartonella antibodies.12,35 It has already been assumed that a potential primary niche in Bartonella infections might be represented by HPCs.7 Consistent with this suggestion, there are currently 2 case reports describing immunofluorescence detection of Bartonella in erythroblasts from bone marrow aspirate.15,35 In addition, a rat animal model of trench fever using B tribocorum demonstrated that the pathogens appear intraerythrocytically in the bloodstream 4 to 5 days upon infection,4 and similar observations were made using a B grahamii mouse-infection model.36 Moreover, B henselae and B koehlerae have been detected in erythrocytes of naturally infected cats.37,38

The primary intracellular niche in which the pathogen is present and suggested to replicate within is, however, still unknown. A possible habitat might be represented by hematopoietic stem cells for several reasons, including: (1) Bartonella species remain undetectable in rat and mouse models for several days upon experimental infection,4,36 (2) these pathogens are detected intraerythrocytically during the course of infection, and (3) Bartonella can be detected in HPCs in human infections.15,35 These observations strengthen the hypothesis that hematopoietic stem cells are a possible niche for Bartonella, and it might be hypothesized that HPCs represent a sanctuary for chronic Bartonella infections responsible for recurrent intraerythrocytic bacteremia.35 These suggestions are consistent with our observations that coculture of human erythrocytes did not result in intraerythrocytic presence of B henselae (Figure 1).

The interaction of human pathogenic bacteria with HPCs has been described only rarely. It was shown that quiescent human HPCs are fully resistant to infections with Listeria monocytogenes, Salmonella enterica, and Yersinia enterocolitica, whereas these pathogens are taken up in a vacuolic compartment when HPCs are differentiated toward myeloid or monocytic cells.3 Moreover, it was shown that infection with these bacteria accelerated the maturation of HPCs along the myeloid lineage.39 Accordingly, human granulocytic ehrlichiosis (HGE), which is characterized mainly by cytopenia, also affects HPCs. CD34+ primary human bone marrow cells, stimulated to differentiate along myelomonocytic lineages, supported the replication of Anaplasma phagocytophilum (the agent of HGE), suggesting that HPCs represent potential target cells in this infection in vivo.

We showed microscopically and via gentamicin protection assays that B henselae does not infect erythrocytes within the first 48 hours of infection (Figure 1). In contrast, B henselae was able to infect HPCs to a similar extent as ECs, which represent one of the most likely primary targets for Bartonella infections (Figures 1 and 2). These data support the hypothesis that erythrocytes do not function as the primary target in B henselae infections. These observations might be explained by the fact that (1) B henselae binds to host cells via beta-1 integrins22 and (2) beta-1 integrins are expressed on HPCs but not on mature erythrocytes (Figure 3, Verfaillie et al,41 and Brittain et al

Moreover, we demonstrated by confocal and electron microscopy and flow cytometry that infection of HPCs with B henselae results in bacterial presence in differentiated erythroid cells. It would seem likely that a necessary prerequisite of B henselae is to be able to avoid host cell death upon infection. In fact, we did not detect a significant number of apoptotic progenitor cells upon B henselae infection as shown by TUNEL staining (Figure 7). This is consistent with previous observations that B henselae inhibits apoptosis of monocytes and ECs,27,29 most likely via the virB type IV secretion system.28 Additionally, we found that the amount of B henselae 16S rRNA was clearly elevated, indicating metabolic activity of B henselae and bacterial growth.20,43 Consistent data were obtained from gentamicin protection assays, which indicate replication of B henselae in erythroid differentiating HPCs over an incubation period of 13 days (Figure 6). Taken together, these data strongly suggest that B henselae persists and replicates within the host progenitor cells during differentiation of these cells toward erythrocytes

The extent of proliferation of B henselae–infected HPCs was, however, significantly lower compared with uninfected control cells. The mechanisms involved in such impaired cell proliferation of B henselae–infected HPCs cannot be explained by apoptotic cell death since apoptosis was not induced upon infection (Figure 7). It was described that adenosine triphosphate (ATP) induces proliferation of HPCs via P2 receptors.44 Proliferation of differentiating HPCs might be affected by the facultative intracellular B henselae, as bacterial presence is likely to result in increased metabolic demands of the host cells in order to cope with the bacterial infection. According to this suggestion, it has recently been shown that infection with B henselae results in ATP deprivation in several host cells (Kempf et al31 and Hanna Hartmann and V.A.J.K., unpublished data, November 2004). Therefore, it can be speculated that such ATP depletion may be responsible for the impaired proliferation of HPCs when infected with B henselae. Nevertheless, differentiation of HPCs into erythroid cells, quantified by FACS, was similar for uninfected and B hensleae–infected HPCs with strong GPA expression in both cases

Infection of several types of host cells with B henselae results in the secretion of IL-8 and VEGF.19,22,29-31 We observed that high amounts of IL-8 were secreted from HPCs when infected with B henselae, but surprisingly, in contrast to our earlier reports, the secretion of VEGF was reduced in HPCs (Figure 7). IL-8 has a strong mobilizing effect on HPCs, leading to the spreading of these cells in the bloodstream.45 In terms of Bartonella pathogenicity, it might be suggested that IL-8 secretion leads to propagation and systemic spread of the latent infection from the bone marrow. The mobilized HPCs could carry the pathogen to other sites of the body leading to subsequent infections in other organs such as the endothelium. Therefore, it might be speculated that infected HPCs may function as a vehicle to carry Bartonella species to the endothelial site where the vasculoproliferative disorders BA and PH are initiated. The fact that VEGF secretion is diminished in HPCs upon B henselae infection, in contrast to most other cells,31 remains unclear.

HPCs, which differentiate into erythroid cells, have never been analyzed for their capacity to interact with human pathogens. Moreover, it has never been described that bacterial pathogens persist in stem cells while these cells are undergoing differentiation, for example, toward erythrocytes. Our in vitro data provide evidence that infection of HPCs with human pathogenic bacteria (eg, B henselae) results in the presence of bacteria in differentiated cells (here: erythrocytes). These observations might suggest a newly described pathogenicity strategy of bacteria, in which the infection of human progenitor cells results in the spread of the bacteria via the differentiated cells
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Re: Bartonella

Post by Yvonne » Sat 16 Aug 2008 13:14

http://www.medscape.com/viewarticle/562276_2
Bartonella is an infection that may cause a rash, enlarged lymph node(s), and malaise and fatigue that resolve over several weeks.[1,2] Many animals and insects carry this infection. Bartonella has multiple vectors and infection sources including fleas, flea feces, cat licks or scratches, ticks, lice, and biting flies.[3-6] Young stray kittens are often able to infect humans due to flea feces on their paws, or through cat scratches, bites, or licks.[7-10]

Bartonella is found in cities, suburbs, and rural locations,[11-14] and is an emerging infection. In recent decades, Bartonella research publications are increasing, but psychiatric disorders were underreported in the soldiers of World War I and World War II. For example, approximately 1 million soldiers in WWI were affected with Bartonella quintana,[15] but medical journals did not report much about its psychiatric manifestations.

In the last 15 years, 9 Bartonella bacteria have been identified that are known to infect humans: B henselae, B elizabethae, B grahamii, B vinsonii subsp. arupensis, B vinsonii subsp. berkhoffii, B grahamii, B washoensis, and, more recently, B koehlerae and B rochalimae.[16-20] Currently, the largest national laboratories offer tests for only 2 species[21-23] (B quintana and B henselae).

Some Bartonella cases have "atypical" presentations with signs or symptoms lasting more than weeks, causing diverse medical problems. For example, Bartonella can cause vision abnormalities, prolonged fever, joint pain, lung inflammation, respiratory disease, and granulomas throughout the body. It can occasionally cause abdominal pain, liver and spleen tissue abnormalities, thrombocytopenic purpura, bone infection, papules or pustules, maculopapular rashes, arthritis, abscesses,[20, 24-30] heart tissue and heart valve problems,[31-37] and neurologic illnesses

Traditionally, cognitive neurology has been related to some psychiatric illnesses. A search of PubMed with "Bartonella" and the search words "depression," "mania," "bipolar," "major depression," "depression," "anxiety," "panic," "panic attack," "psychosis," and "schizophrenia" yielded the limited journal results below:

Depression


Dementia


Encephalopathy


Violent behavior


Confusion


Combative behavior


Substance abuse disorders[43-48]


Some articles link Bartonella to substance abuse. Bartonella is repeatedly linked with alcoholism in the presence of substandard living conditions. Intravenous drug users also have an elevated prevalence of antibodies to Bartonella organisms and may be at significant risk of becoming infected.[49-53] The 3 cases described below are consistent with past reports of Bartonella causing psychiatric symptoms, and add further clinical data to these past reports

Conclusion
We note that the number of Bartonella species that infect humans currently outpaces the number of Bartonella species that can be tested by top national labs. Some antibiotics seem to have an effect, but dosing and duration are not clearly established or indicated by a broad literature review. Further, clinical improvement and the cessation of symptoms do not always signify complete eradication. That is, it may be possible for a patient to relapse due to a significant medical stress to the body or a decrease in immune system capacity. Of greatest importance, we believe that Bartonella can enter the brain and cause not only well-documented neurologic disorders, but also some psychiatric disorders as well
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Re: Bartonella

Post by Yvonne » Tue 19 Aug 2008 12:10

http://jcm.asm.org/cgi/content/abstract/JCM.00832-08v1

Bartonella spp. bacteremia in patients with neurological and neuro-cognitive dysfunction
Abstract

We detected infection with a Bartonella species (B. henselae or B. vinsonii subsp. berkhoffii) in the blood of six immunocompetent patients who presented with a chronic neurological or neuro-cognitive syndrome including seizure, ataxia, memory loss, and/or tremor. 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 neuro-cognitive dysfunction
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Re: Bartonella

Post by Yvonne » Tue 19 Aug 2008 12:20

http://aac.asm.org/cgi/content/full/48/6/1921

Recommendations for Treatment of Human Infections Caused by Bartonella Species
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 µg/ml, as was rifampin. At this concentration, gentamicin was shown to enter erythrocytes slowly and to reach a peak level of 0.26 µg/ml after 24 h. However, when the ability of gentamicin to kill extraerythrocytic B. quintana at the concentration of 0.26 µg/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.


MICs correlate poorly with the in vivo efficacies of antibiotics in patients with Bartonella-related infections (74). The lack of a bactericidal effect of antibiotics against Bartonella spp. and the different niches that Bartonella occupies in the human host, e.g., sequestration in erythrocytes, may explain such discrepancies between in vitro and clinical data. For serious Bartonella infections, it is critical to use two antibiotics, each of which has good in vivo efficacy against Bartonella. This is particularly important if gentamicin is one of the drugs in the regimen, because the gentamicin protection assay with red blood cells infected in vivo, as well as the in vitro erythrocyte cell culture model, document that bartonellae residing within erythrocytes are protected from gentamicin (90, 93). Thus, with our current knowledge, addition of another antibiotic with good in vivo activity against Bartonella is crucial, because the two antibiotics may eradicate the bacteria in different niches in the host.

CONCLUSION

Bacteria of the genus Bartonella are responsible for emerging and reemerging diseases worldwide and can present as illnesses ranging from benign and self-limited diseases to severe and life-threatening diseases. Bartonella infections present a unique treatment challenge because they are persistent and often relapse and they involve an intraerythrocytic phase that apparently provides a protective niche for the bartonellae. The extreme diversity of disease manifestations is dependent on the infecting species of Bartonella and on the immune status of the patient. Because there are only two reports of randomized clinical trials for the treatment of Bartonella infections, an unequivocal treatment for all Bartonella infections does not exist, and thus, antibiotic treatment recommendations differ for each clinical situation. Treatment of Bartonella infections should be adapted to each clinical situation, to the infecting Bartonella species, and to whether the disease is in the acute or the chronic form. It is important that when the more severe Bartonella infections are recognized, diagnosed, and treated in a timely manner, the outcome is usually favorable
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Re: Bartonella

Post by cave76 » Tue 19 Aug 2008 15:08

Because there are only two reports of randomized clinical trials for the treatment of Bartonella infections, an unequivocal treatment for all Bartonella infections does not exist, and thus, antibiotic treatment recommendations differ for each clinical situation.

Treatment of Bartonella infections should be adapted to each clinical situation, to the infecting Bartonella species, and to whether the disease is in the acute or the chronic form.

It is important that when the more severe Bartonella infections are recognized, diagnosed, and treated in a timely manner, the outcome is usually favorable
I wanna know WHAT antibiotic is best for MY Bartonella. <g>

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Re: Bartonella

Post by Joe Ham » Wed 3 Sep 2008 19:12

The full PDF version of Yvonne's posting about neurological Bartonella (above) is attached -- just for those who like to go cross-eyed reading the fine print.
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Re: Bartonella

Post by Yvonne » Fri 28 Nov 2008 17:11

http://www.ajnr.org/cgi/reprint/26/6/1310.pdf

Optic Neuropathy Secondary to Cat Scratch Disease: Distinguishing MR Imaging Features from Other Types of Optic Neuropathies
BACKGROUND AND PURPOSE:

MR imaging characteristics of optic neuropathy caused by
cat scratch disease have not yet been described; this lack of information may result in incorrect
diagnosis and may contribute to initiation of inappropriate therapy. Our study was based on the
hypothesis that cat scratch disease–related optic neuropathy has distinct MR imaging features
compared with those of other types of optic neuropathies.

METHODS:
Eighty-two patients with various causes of optic neuropathy and available MR
imaging examinations were included in this study. Two readers blinded to the diagnosis
reviewed the MR images independently in regard to presence, location, and extent of optic nerve
enhancement. The MR imaging findings were correlated with the final diagnosis.

RESULTS:
Eleven percent (9/82) of the patients received a final diagnosis of cat scratch
disease. Optic nerve enhancement in patients with cat scratch disease (5/37) was localized to a
3- to 4-mm segment at the optic nerve– globe junction. All other patients with optic neuropathy
(31/37) with one exception showed enhancement away from the optic nerve– globe junction or a
long-segment enhancement when the optic nerve– globe junction was also involved. Four
patients with cat scratch disease did not show any optic nerve MR abnormalities.

CONCLUSION:
Unilateral, short-segment enhancement localized to the optic nerve– globe
junction is highly specific for cat scratch disease as the underlying cause of optic neuropathy
and may help in establishing the diagnosis of this condition.
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seanna
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Re: Bartonella

Post by seanna » Fri 28 Nov 2008 18:11


I'm unable to tolerate reading the very fine print though this is extremely interesting. My MRI showed "hematopoietic changes in my spine" when my symptoms first started though I've tested negative for Bartonella. The article states that "a possible habitat might be represented by hematopoietic stem cells"...hmmm.

Also interesting that fluroquines, doxycyclines, etc were not bactericidal, looks like rifampin the most effective?

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Yvonne
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Re: Bartonella

Post by Yvonne » Sun 7 Dec 2008 15:14

http://www.pubmedcentral.nih.gov/articl ... d=11777823

Natural History of Bartonella Infections (an Exception to Koch’s Postulate)
As for many vector-borne disease agents, it seems that the Bartonella species also have a natural cycle. The cycle contains a reservoir host in which the Bartonella species cause a chronic intraerythrocytic bacteremia and a vector that transmits the bacteria from the reservoir hosts to new susceptible hosts. These could be the natural reservoir hosts, new competent reservoir hosts, or incidental hosts. There is usually a specific association between the natural host, the vector, and the Bartonella species which determines the spectrum of hosts (natural or incidental) possible and the geographic distribution of the organisms.

Natural infection in the host. Natural Bartonella infections begin with the inoculation of the bacteria, and this is usually associated with the feeding of the arthropod vector. Differences in the clinical presentations of individuals with primary infections may be due to several factors. The size of the inoculum may vary, and this could explain the differences in the severities of the clinical signs that might occur. Variations in strain virulence may also, however, contribute to differences in the intensity of illness (72). Host responses, modulated by immune responses to Bartonella infections, can vary and can induce variations in the intensities of clinical signs during initial infections.

With all other known bacteria, prolonged bacteremia is associated with signs of septicemia in the host. Bartonella bacteremias in the natural hosts, however, can be asymptomatic. This is contrary to our present understanding of bacteremia and goes against the idea originated by Koch that bacteria do not occur in the blood of healthy animals or humans (12). Bartonella may be the single bacterial genus capable of producing asymptomatic bacteremia in mammals and, thus, may be an exception to Koch’s postulate. Using confocal microscopy, we have shown that B. henselae occurs within naturally infected asymptomatic cat erythrocytes (Fig. 2) (83) and that B. quintana occurs in human erythrocytes (unpublished data). As the Bartonella species are intraerythrocytic and, hence, might be less exposed to the immune system, their hosts may become adapted to the chronic bacteremia


CONCLUSION
The available data on the Bartonella species have expanded rapidly in recent years as this group of organisms has been found to be responsible for a growing spectrum of emerging and reemerging diseases. We now have new insights into the natural history of the Bartonella species and can see that these bacteria have adapted to their mammalian reservoir hosts in unique ways. They cause chronic intraerythrocytic infections, with up to half of the reservoir host populations being bacteremic at any one time. This bacteremia is the source of the vector infection. The Bartonella bacteremias, however, result in few (and, if present, very subtle) clinical signs in their specific reservoir hosts, and this contradicts Koch’s observation that the blood of healthy humans or animals is free of bacteria.
Listen to all,
plucking a feather from every passing goose,
but follow no one absolutely

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