All Posts Tagged With: "myalgia"

Human isolates of Bartonella tamiae induce pathology in experimentally inoculated immunocompetent mice

Full article: http://www.biomedcentral.com/1471-2334/10/229

Excerpt:

Results

Following inoculation with B. tamiae, mice developed ulcerative skin lesions and subcutaneous masses on the lateral thorax, as well as axillary and inguinal lymphadenopathy. B. tamiae DNA was found in subcutaneous masses, lymph node, and liver of inoculated mice. Histopathological changes were observed in tissues of inoculated mice, and severity of lesions correlated with the isolate inoculated, with the most severe pathology induced by B. tamiae Th239. Mice inoculated with Th239 and Th339 demonstrated myocarditis, lymphadenitis with associated vascular necrosis, and granulomatous hepatitis and nephritis with associated hepatocellular and renal necrosis. Mice inoculated with Th307 developed a deep dermatitis and granulomas within the kidneys.

Conclusions

The three isolates of B. tamiae evaluated in this study induce disease in immunocompetent Swiss Webster mice up to 6 weeks after inoculation. The human patients from whom these isolates were obtained had clinical presentations consistent with the multi-organ pathology observed in mice in this study. This mouse model for B. tamiae induced disease not only strengthens the causal link between this pathogen and clinical illness in humans, but provides a model to further study the pathological processes induced by these bacteria.

Clinical manifestations and neuroimaging in neuroborreliosis

Full article: https://www.thieme-connect.com/ejournals/abstract/neuropediatrics/doi/10.1055/s-2006-974121

Excerpt:

Neuroborreliosis often presents with cranial nerve palsy, aseptic meningitis or meningoencephalitis. Cerebral arteriopathy has rarely been reported as single cases. Here we present a retrospective analysis from 1997 to 2005 in the Berlin area. In this period neuroborreliosis was confirmed in 47 children through the finding of specific antibodies against Borrelia burgdorferi in CSF.

22 (47%) suffered from facial palsy as a presenting symptome, in one of them the palsy was bilateral. Four children (9%) had palsies of other cranial nerves, and four patients (9%) presented with paresis of an arm, hemiparesis, or spastic paraparesis. 16 children (34%) reported headache on admission, 15 (32%) presented with myalgia and/or arthralgia. Two patients (4%) had paraesthesia, another two (4%) were atactic. Ten (21%) had unspecific symptoms such as fever, fatigue, loss of appetite, or nausea. Other symptoms included general slowdown, sensoric or motoric aphasia, agitation, confusion, incomplete Horner’s syndrome, and mucosa haemorrhage, each in one patient.

In 19 patients (40%) cerebral imaging was performed. 13 (68%) were found to be normal, or rather revealed typical lesions in a patient with an underlying neurofribromatosis type 1. In one child with hemiparesis, and in one with multiple cranial nerve palsies, arterial subtraction angiography (DAS) confirmed multifocal vasculitis and dissection of the left Aa. vertebralis and basilaris, respectively. In one girl with hemiplegia, MRI revealed an infarction of the according internal capsule. Although angiography was not done this finding is suspicious of focal arteriopathy. The girl also had a homozygous mutation of factor V Leiden.

Bartonella

Full article: http://www.lymeneteurope.org/forum/viewtopic.php?f=7&t=1336#p9502

Excerpt:

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.

Lyme Encephalopathy

Encephalopathy is like fine art: Most people know it when they see it, but there is very little agreement on how to define it. At the 14th International Lyme Disease Conference, Brian A. Fallon, MD,[1] of Columbia University and the New York State Psychiatric Institute, New York, NY, tried to do just that. More importantly, he described the different ways one can define encephalopathy, the strengths and limitations of each approach, and significantly, what other aspects of life can give the impression of encephalopathy where none exists. First, one must evaluate patients with persistent Lyme encephalopathy by asking the following questions:

Is the diagnosis correct?
Are there comorbid psychiatric disorders that could be treated better? Does the patient have a psychogenic medical illness? What was the patient’s response to prior antibiotics?
Was previous treatment adequate? How long was the course, and what was the route of administration? Was there a subsequent relapse Continued

Lyme Encepalopathy

Encephalopathy is like fine art: Most people know it when they see it, but there is very little agreement on how to define it. At the 14th International Lyme Disease Conference, Brian A. Fallon, MD,[1] of Columbia University and the New York State Psychiatric Institute, New York, NY, tried to do just that. More importantly, he described the different ways one can define encephalopathy, the strengths and limitations of each approach, and significantly, what other aspects of life can give the impression of encephalopathy where none exists.
First, one must evaluate patients with persistent Lyme encephalopathy by asking the following questions:

Is the diagnosis correct?
Are there comorbid psychiatric disorders that could be treated better? Does the patient have a psychogenic medical illness? What was the patient’s response to prior antibiotics?
Was previous treatment adequate? How long was the course, and what was the route of administration? Was there a subsequent relapse Continued