Topic: Will those with ACA presentation please step forward?
Melanie Reber
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(please see my questions at the end of this post)
Acrodermatitis Chronica Atrophicans
Background Acrodermatitis chronica atrophicans (ACA) is the third or late stage of European Lyme borreliosis (LB). This unusual, progressive, fibrosing skin process is due to the effect of continuing active infection with Borrelia afzelii. Buchwald first delineated it in 1883; Herxheimer and Hartmann described it in 1902 as a tissue paper-like cutaneous atrophy. It is evident on the extremities, particularly on the extensor surfaces, beginning with an inflammatory stage with bluish red discoloration and cutaneous swelling and concluding several months or years later with an atrophic phase. Sclerotic skin plaques may also develop. Physicians should use serologic and histologic examination to confirm this diagnosis.
Pathophysiology B afzelii is the predominant, but may not be the exclusive, etiologic agent of acrodermatitis chronica atrophicans. Another genospecies of the Borrelia burgdorferi sensu lato complex, Borrelia garinii, has also been detected.
Acrodermatitis chronica atrophicans is the only form of Lyme borreliosis in which no spontaneous remission occurs. Its pathophysiology is not yet fully understood. Acrodermatitis chronica atrophicans appears to be associated with long-term persistence of Borrelia organisms in the skin; several nonspecific reactions together with a specific immune response may contribute to its manifestations.
The persistence of the spirochetes despite a marked cutaneous T-cell infiltration and high serum antibody titers may be connected with resistance of the pathogen to the complement system; the ability to escape to immunologically protected sites (eg, endothelial cells, fibroblasts); and the ability to change antigens, which may lead to an inappropriate immune response. Lack of protective antibodies, with a narrow antibody spectrum and a weak cellular response with down-regulation of major histocompatibility system class II molecules on Langerhans cells, has been observed in patients with Lyme borreliosis.
A restricted pattern of cytokine expression in acrodermatitis chronica atrophicans, including the lack of interferon-gamma, may contribute to its chronicity. Cross-reactive antibody responses could take part in autoimmune damage, but whether autoimmune reactions play any role in the pathogenesis of the disease is unclear. The pathogenic mechanism of atrophic skin changes has also not been clarified. Perhaps periarticular regions are favorite sites because of reduced acral skin temperatures or reduced oxygen pressure.
History Because of its late onset, patients with acrodermatitis chronica atrophicans rarely remember a tick bite. Instead, they recall having been in the woods or grassy areas a few months or years previously, especially in a geographically endemic region. A history of EM is recalled by about 20% of patients. Acrodermatitis chronica atrophicans can develop directly from EM or after 6-36 months, often involving the same region of the body. Sometimes, the disease may be preceded by a latent phase (lasting up to several years) or by other manifestations of Lyme borreliosis; the latter can also develop simultaneously.
* The patient notices localized cutaneous swelling on the distal extremity or on only one of the digits and sometimes discovers that one foot is larger than the other when buying shoes. Acrodermatitis chronica atrophicans is most often unilateral, although bilateral acrodermatitis chronica atrophicans is also common.
* Progressive allodynia, the exaggerated reaction to pain, is a characteristic symptom and, thus, may be a clue to the diagnosis of acrodermatitis chronica atrophicans.
* Patients commonly complain of spontaneous acral pain and paresthesia or dysesthesia or cognitive dysfunction.
* Acrodermatitis chronica atrophicans starts with an inflammatory phase, characterized by few to several soft, erythematous, slowly enlarging cutaneous swellings or flat infiltrations of various sizes or with diffuse bluish red discoloration and edema of the skin.
o Acrodermatitis chronica atrophicans usually appears on the distal part of at least one extremity, predominantly on the extensor surfaces on the bony prominences.
o Common sites are the foot, the lower leg or the hand, the forearm, and the olecranon area; however, they uncommonly appear proximally on the upper arm and the shoulder or the thigh and the buttock.
o Sometimes, the erythema is slight and swelling may dominate, or the signs are very subtle and may be overlooked by the patient or the physician.
o Lymphadenopathy may be noticed.
* Only one part of an extremity may be affected for many months or years. With time, the skin lesions may extend on one extremity or appear on additional ones and also involve other parts of the body.
* Fibrotic nodules (often multiple, localized linearly in the vicinity of joints) are typical. They can precede acrodermatitis chronica atrophicans or develop simultaneously. The most common sites of these nodules are the elbows and the knees.
* Acrodermatitis chronica atrophicans does not heal spontaneously; gradual conversion into its atrophic phase may occur during many years of infection.
o The skin becomes thin, atrophic, wrinkled, dry, and translucent.
o The hair is lost; the number of sebaceous and sweat glands are decreased.
o Even minor trauma may produce large, slow-to-heal ulcerations of the affected skin.
* About 5-10% of patients with acrodermatitis chronica atrophicans develop sclerodermalike plaques. Anetodermalike skin lesions can be seen concomitant with acrodermatitis chronica atrophicans.
* Acrodermatitis chronica atrophicans is accompanied often by peripheral neuropathy, musculoskeletal pains, and joint damage underneath the cutaneous plaques. Involvement of the small joints of the hands and the feet by the fibrotic reaction is often seen.
Physical The clinical recognition of acrodermatitis chronica atrophicans may be difficult, even in typical cases. A detailed history, including epidemiologic data, is helpful. Physicians should confirm the clinical diagnosis by histopathologic examination and serologic test results.
* The early, inflammatory phase of acrodermatitis chronica atrophicans is marked by soft, painless, poorly demarcated, bluish reddish plaques tending to coalescence or by diffuse erythema and edema localized on the distal extremities that spread proximally.
o In the authors' experience, not only the distal extremities but also the proximal parts, the trunk, and the face may be involved in the early stage. Others have also observed skin-colored facial edema as an initial manifestation of acrodermatitis chronica atrophicans.
o Skin changes are often associated with regional or generalized lymphadenopathy.
* The later, atrophic phase of acrodermatitis chronica atrophicans is more characteristic clinically. The affected skin has a dark red or brownish red discoloration; focal hyperpigmentation; telangiectasias; and a thin, wrinkled, cigarette paper-like, translucent appearance.
o Because of the loss of subcutaneous fat, the skin vessels become prominent.
o Atrophy of the epidermis and lack of hairs, sebaceous glands, and often sweat glands make the skin poorly protected and vulnerable.
o Large ulcerations can be observed, and malignant lesions may also occur.
o The atrophic poikilodermic changes are often bilateral and most noticeable over the knees, the elbows, and the dorsal surfaces of the hands and the feet. They may also involve the trunk (particularly the chest) and the face.
* Sclerodermalike changes may appear in patients with acrodermatitis chronica atrophicans in both the inflammatory phase and the atrophic phase.
o These changes are usually limited to the legs and the feet, but they occasionally occur on the trunk.
o The lesions, similar to morphea and lichen sclerosus and atrophicus, may appear in regions where no acrodermatitis chronica atrophicans is present.
* Single or multiple fibrotic nodules or bands may be seen on the extensor surfaces of the elbows and the knees or adjacent to other joints. They are generally firm; bluish-red, yellowish, or skin-colored; and 0.5 to 2-3 cm in diameter.
* Acrodermatitis chronica atrophicans has been described in association with localized amyloidosis, eczema, psoriasis, lupus erythematosus, leprosy, and Hodgkin disease. These associations may be coincidental. One of the authors' patients with histologically and serologically confirmed acrodermatitis chronica atrophicans was a 68-year-old woman first seen with prominent livedo racemosa on the leg where typical acrodermatitis chronica atrophicans inflammatory phase patches developed. Others also observed the same phenomenon, so perhaps this may be more than a chance linkage.
* Detailed clinical and neurophysiologic examinations in patients with acrodermatitis chronica atrophicans-associated polyneuropathy often show a sensory polyneuropathy.
o Neuropathy symptoms, most often pain and/or paresthesia, are evident in one half of patients with acrodermatitis chronica atrophicans.
o One of the authors' patients had paresis of the brachial plexus.
o Marked abnormality of the vibratory threshold is a common finding.
o Patients with localized or asymmetric neuropathy seem to have changes more often found in the extremities with, rather than without, visible acrodermatitis chronica atrophicans lesions.
o Abnormalities in cerebrospinal fluid seldom have been found in patients with acrodermatitis chronica atrophicans.
* Acrodermatitis chronica atrophicans can produce deformities of the fingers and the toes if it is not treated promptly. Persistent reducible deformities of the fingers may be consistent with Jaccoud arthropathy.
Causes Lack of adequate or appropriate treatment of early Lyme borreliosis facilitates acrodermatitis chronica atrophicans development.
I have a few questions for those with ACA presentation:
Have you been diagnosed clinically or through serology? Has your LLMD offered treatment options, and if so, what are they? Have you been able to halt the progression with treatment? Do you know for certain where you were infected? Have you ever traveled to Europe or to other places outside of the states? Do you have photographic evidence of your condition? How long were you ill before this presented? What other diseases besides Lyme have you been diagnosed with? What are your main symptoms? Do you know of others with ACA?
Thank you so very much in advance for any information you can provide, Melanie
SForsgren
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I think it is rare to see this in the US b/c it is from the European strains and an advanced sign. I did see it once on a teenager that had it but doesn't seem to be common here
-------------------- Be well, Scott Posts: 4617 | From San Jose, CA | Registered: Jul 2005
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Melanie Reber
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Thank you Scott, How are you BTW?
I know that the current thought by many is that it is uncommon in the states, however, new research is proving that it is transferred by Borellia ssp. that is yet to be coded. I will try to locate that finding and post it.
I have since heard from many who are presenting with the exact images that I now have...and they have never traveled out of the country.
Acrodermatitis chronica atrophicans is a dermatological condition that takes a chronically progressive course and finally leads to a widespread atrophy of the skin. Involvement of the peripheral nervous system is frequently observed, predominantly a sensory polyneuropathy. Acrodermatitis chronica atrophicans follows a peculiar geographical distribution forming clusters of high prevalence in certain regions.
Acrodermatitis chronica atrophicans is a clinical manifestation of borreliosis, an infectious disease transmitted by ticks. Clinical manifestations of borreliosis are multiple. They most often affect the skin, nervous system, joints and heart. Cutaneous pseudolymphomas, erythema chronicum migrans of Afzelius, acrodermatitis chronica atrophicans of Pick-Herxheimer, meningo-radiculitis and various arthropathies are the most commonly encountered diseases.
Melanie Reber
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Cutaneous manifestations of Lyme borreliosis Elisabeth Aberer1 and Herta Klade1 Infection Volume 19, Number 4 / July, 1991
Summary
The dermatological symptoms of Lyme borreliosis present with a typical clinical pattern and characteristic time of appearance. In contrast to other manifestations of Lyme borreliosis they are easily recognizable in most of the cases. In the first stage, erythema migrans arises at the tick bite site. With this symptom the diagnosis of Lyme borreliosis can be established. During all manifestations of Lyme borreliosis the history of erythema migrans is an important parameter to verify the diagnosis. In the early stage of disease a lymphocytic proliferation can appear at the tick bite site, at the ear lobe, or at the mamilla.
Borrelia lymphocytoma can be diagnosed when antibodies againstBorrelia burgdorferi are positive. Years after infection, acrodermatitis chronica atrophicans arises at distal body sites causing livid swelling and gradually skin atrophy. Skin lesions can be accompanied by neuropathies, mostly of the lower legs, which in contrast to the skin lesions, do not respond well to antibiotic therapy. There is evidence that some cases of Shulman syndrome, morphea and lichen sclerosus et atrophicus might be related to a borrelia infection as indicated by cultivation ofB. burgdorferi from skin biopsies of morphea and response to antibiotic treatment in some cases.
The classical dermatological symptoms of Lyme borreliosis, erythema migrans, borrelia lymphocytoma and acrodermatitis chronica atrophicans respond to oral antibiotic treatment. In acrodermatitis chronica atrophicans parenteral antibiotic therapy is sometimes necessary.
Melanie Reber
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Lyme disease: the evolution of erythema chronicum migrans into acrodermatitis chronica atrophicans. Patmas MA. Community Medical Center, Toms River, New Jersey. Cutis. 1993 Sep;52(3):169-70.
Erythema chronicum migrans and acrodermatitis chronica atrophicans are both recognized to be lesions associated with Lyme disease, although they are thought to be distinct entities. In this paper, the clear evolution of erythema chronicum migrans into acrodermatitis chronica atrophicans is demonstrated.
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Melanie Reber
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Is Serological Follow-Up Useful for Patients with Cutaneous Lyme Borreliosis? [JOURNAL ARTICLE] Mullegger RR, Glatz M Curr Probl Dermatol 2009.:178-182.
Serologic follow-up examinations are frequently performed in patients with erythema migrans, borrelial lymphocytoma, and acrodermatitis chronica atrophicans (the 3 dermatoborrelioses) to evaluate treatment efficacy. There is, however, substantial proof in the literature that antibody titer development after therapy is unpredictable and variable, and moreover it is largely uncorrelated with the clinical course and mode of antibiotic treatment.
For example, persistent positive IgG and/ or IgM antibody titers do not indicate treatment failure. Thus, repeated serologic testing is of very limited value for assessing therapy efficacy, and therefore not recommended in the follow-up of dermatoborrelioses patients. Since cultivation of the etiologic agent, Borrelia burgdorferi sensu lato, and polymerase chain reaction are also inadequate for this purpose, the assessment of patients with cutaneous manifestations of Lyme borreliosis in the follow-up rests primarily on the clinical picture.
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Melanie Reber
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The expanding spectrum of cutaneous borreliosis. [Journal Article] Eisendle K, Zelger B G Ital Dermatol Venereol 2009 Apr; 144(2):157-71.
The known spectrum of skin manifestations in cutaneous Lyme disease is continuously expanding and can not be regarded as completed. Besides the classical manifestations of cutaneous borreliosis like erythema (chronicum) migrans, borrelial lymphocytoma and acrodermatitis chronica atrophicans evidence is growing that at least in part also other skin manifestations, especially morphea, lichen sclerosus and cases of cutaneous B-cell lymphoma are causally related to infections with Borrelia.
Also granuloma annulare and interstitial granulomatous dermatitis might be partly caused by Borrelia burgdorferi or similar strains. There are also single reports of other skin manifestations to be associated with borrelial infections like cutaneous sarcoidosis, necrobiosis lipoidica and necrobiotic xanthogranuloma. In addition, as the modern chameleon of dermatology, cutaneous borreliosis, especially borrelial lymphocytoma, mimics other skin conditions, as has been shown for erythema anulare centrifugum or lymphocytic infiltration (Jessner Kanof) of the skin.
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Melanie Reber
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Dermatological aspects of Lyme borreliosis. [JOURNAL ARTICLE] Lipsker D Med Mal Infect 2007 Mar 26.
Lyme borreliosis is a tick-borne zoonosis due to bacterial infection by Borrelia (B.) burgdorferi sensu lato The disease presents differently in Europe or North America and may be called European borreliosis when acquired in Europe. Lyme borreliosis evolves in 3 stages. The main manifestations include cutaneous, neurological, and joint involvement.
Erythema migrans (EM) is the most specific and most frequent finding in patients with Lyme borreliosis. It is the hallmark of early-localized borreliosis. EM is a slowly expanding red macula that occurs in about 60-80% of patients contracting Lyme borreliosis. Central clearing of the red patch can occur. It appears at the site of the tick bite, 7 to 20 days after the bite.
Borrelial lymphocytoma (BL) occur rarely in patients with the early-disseminated stage of the disease. BL is a red or brown nodule or plaque located on the nipple, the earlobe, the scrotum, or the face. It should not be confused with cutaneous B-cell lymphoma.
Acrodermatitis chronica atrophicans (ACA) is the cutaneous manifestation of late borreliosis. It starts as a violaceous patch, usually located on the extensor surface of a limb. Periarticular nodules and cords can also be present. Without treatment, it will evolve over weeks or months to the typical atrophic stage with extensive dermo-epidermal atrophy and visibility of superficial veins. Only these 3 manifestations are clearly related to an infection with B. burgdorferi. The relationship between infection with B. burgdorferi and other dermatoses, especially morphea, lichen sclerosus, and interstitial granulomatous dermatitis is still debated.
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Melanie Reber
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Course of Borrelia burgdorferi DNA Shedding in Urine after Treatment. [Journal Article] Aberer E, Bergmann AR, Derler AM, Schmidt B Acta Derm Venereol 2007; 87(1):39-42.
Diagnosis of Lyme borreliosis by urine polymerase chain reaction (PCR) has been recognized as having better diagnostic sensitivity in patients with erythema migrans than serological methods. We made serial tests with 192 urine specimens from 70 patients with erythema migrans and 60 urine specimens from 21 patients with acrodermatitis chronica atrophicans to evaluate the course of positive urine PCR after antibiotic treatment.
Before treatment, urine samples from patients with erythema migrans showed a positive PCR in 27/34 samples (79%), and those from patients with acrodermatitis chronica atrophicans in 7/11 (63%). The specificity of bands was proven by hybridization with GEN-ETI-KTM-DEIA kit in 40/41 samples. Borrelia DNA in urine decreased gradually within the observation period of one year in both patients with erythema migrans and acrodermatitis chronica atrophicans, and persisted without clinical symptoms in 4/45 patients with erythema migrans (8%) after 12 months. Urine PCR can serve as a diagnostic method in early Lyme borreliosis and also in seropositive patients with unclear clinical symptoms.
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Melanie Reber
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Focus floating microscopy: "gold standard" for cutaneous borreliosis? [Journal Article] Eisendle K, Grabner T, Zelger B Am J Clin Pathol 2007 Feb; 127(2):213-22.
Borrelia burgdorferi is difficult to detect in routine biopsy material from patients with skin lesions of borreliosis. In this study, a new immunohistochemical method, focus floating microscopy (FFM), was developed to detect B burgdorferi in tissue sections and was compared with polymerase chain reaction (PCR).
By using standard histologic equipment, tissue sections stained with a polyclonal B burgdorferi antibody were simultaneously scanned through 2 planes: horizontally in serpentines and vertically by focusing through the thickness of the section. Borrelia were detected in 47 of 71 ticks, 34 of 66 tick bites, 30 of 32 erythema chronicum migrans cases, 41 of 43 borrelial lymphocytomas, and 50 of 51 acrodermatitis chronica atrophicans cases.
FFM proved to be more sensitive than PCR (96.0% vs 45.2%) and nearly equally specific (99.4% vs 100%). All 169 control cases, except 1 false-positive case of secondary syphilis, were negative with FFM. FFM is an easy, quick, and inexpensive method to reliably detect Borrelia in cutaneous tissue sections.
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Marnie
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I wonder if the skin could be treated with light like they do for psoriasis?
Although psoriasis can be linked to H.Pylori.
Or...if you chose abx, go here to see what was Rx'd, how much and for how long:
glm1111
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I have/had this Melanie.
As I get rid of the infections...parasites/worms/bb etc that I believe are inhabiting the small intestine my hands are coming back to normal.
It seems like the infections in the small intestine were spilling over and desseminated into the hands/head/organs etc. I hope this makes sense,
Gael
-------------------- PARASITES/WORMS ARE NOW RECOGNIZED AS THE NUMBER 1 CO-INFECTION IN LYME DISEASE BY ILADS* Posts: 6418 | From philadelphia pa | Registered: Jul 2008
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Marnie
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P.S. Are we using the wrong class of abx. to combat OspB?
Melanie Reber
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An American Case of Acrodermatite Chronica Atrophicans Ang�lique Gagn�-Henley; Dominique Hanna; Bruno Maynard, Centre hospitalier universitaire de Sherbrooke CHUS, Sherbrooke, QC
Introduction: Lyme disease is due to infection with a spirochete, Borrelia, and is transmitted by Ixodes ticks. Borrelia species in North America (Borrelia burgdorferi sensu stricto) are different from the European species (B. afzelii, B. garinii), which explains a different presentation of the disease. Acrodermatitis chronica atrophicans is well described following infection by the European species of borrelia (almost always B. afzelii) but is extremely rare in North America. It appears months to years after the infection, as a slowly progressive bluish-red patch that becomes atrophic.
Methods: We describe the case of a 36-year-old woman with a several year history of lesions on her knees and ankles. The lesions were asymptomatic, but more prominent since her pregnancy. She spent her summers, as a child, on the coasts of New England.
Results: Complete blood work was normal. The skin biopsy was compatible with acrodermatitis chronica atrophicans. Finally, serology by ELISA and Western blot were positive for Borrelia burgdorferi and confirmed Lyme disease.
Treatment: The treatment is beneficial for all stages of disease and if treated early, it is completely curable. Our patient received a sixty day treatment of Amocixicyllin 500 mg per os QID. Surprisingly, with this treatment, the lesions healed, leaving a discrete atrophic patch.
Conclusion: Acrodermatitis chronica atrophicans caused by American species of Borrelia, although very rare, has been described in a few case reports. We present a patient with chronic lesions, skin biopsy and serology compatible with Acrodermatitis chronica atrophicans.
BEAUTIFUL Miss Marnie!!! Thank you!!!Posts: 7052 | From Colorado | Registered: Mar 2003
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Melanie Reber
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"P.S. Are we using the wrong class of abx. to combat OspB?"
From what I understand, Penicillin is the preferred treatment method for ACA...either old simple oral or IM Bicillin.
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sammy
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Interesting, thank you for sharing with your research with us Melanie:)
To answer your questions, yes I have been diagnosed with ACA.
Have you been diagnosed clinically or through serology? Pos. western blot
Has your LLMD offered treatment options, and if so, what are they? Not specifically for ACA, treating Lyme in general. You mentioned Bicillin, tried that for about 6mo. Switched to various orals. Have been on IV Rocephin for about 8wks now.
Have you been able to halt the progression with treatment? Hopefully yes, I have not noticed any new or worsening areas recently.
Do you know for certain where you were infected? Yes, about 5yrs ago, went hiking in near my home in OH, developed EM and symptoms shortly after.
Have you ever traveled to Europe or to other places outside of the states? Yes. London, city only, about a week in the winter. Asia, South and Latin America for longer periods of time.
Do you have photographic evidence of your condition? No but I guess I could try to take pictures if needed.
How long were you ill before this presented? 3-4years. Diagnosed with Lyme about a year ago. Dermatologist diagnosed ACA a couple months after Lyme dx.
What other diseases besides Lyme have you been diagnosed with? Babesia, Cpn, Mycoplasma P, secondary Addisons. Also have Lichen sclerosis.
What are your main symptoms? Too many. Fatigue, cognitive difficulties, neuropathy (peripheral and Vagal/GI), vision problems, these are probably the worse right now.
Do you know of others with ACA? Nope.
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Melanie Reber
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"Have you been diagnosed clinically or through serology? Pos. western blot"
Thank you Sammy. Was your WB for Bb or one of the other strains?
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sammy
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Yes, it was Bb.
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TO LIFE
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Dear Melanie,
I hope you don't have it.
My Lyme MD has always seened the Euro strain in me, which we have talked about ACA some. Let me explain my SX.
1.Inflammation with elevated sed. rate. Cardio MD wanted Vasculitis ruled out. My skin had a purple look to it. I had so much inflammation in the Brachial Plexus, I had to have my subclavicle artery released.
2. I get a blood blister rash come and go about every 3 weeks, just when I think their gone new ones appear. Their getting better, but still get some.
3. My skin on my arms and hands are thin. I used to do hairdressing so I thought it was from that.Arms are getting alot better.
4. I have a prior DX of RSD, which is very rough burning nerve pain with allodynia. I will look for a couple articles relating RSD to Lyme if anyone is interested.
5.Some left Vertricle heart damage. which I believe I am healing from.
6. I was bedridden for nearly 2 years.
7. Weak and fatigued.
8. Swollen lymph nodes.
9. Broken capullaries are in my skin.
10. Hair loss on my legs and arms, but not my head.
I have had to have very aggresive therapy. My Lyme MD has never given up on me and is very postive for my recovery. I have been on antibiotic treatment for 2 years. 7 months of various IV's.
I am doing 50% to 70% better. I believe I will have my life back, and be an asset to society again.
Jill E.
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Yes, my mother has it - she is American, not European. My LLMD confirmed it when doing a visual exam on my mother and saw ACA in several places, and I had already suspected it with my mom.
My mother has really bad lipomas, some are covered with ACA, but she also has ACA on non-lipoma areas of her body.
Jill
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Melanie Reber
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Thanks to each of you Jill, Life Sammy and Gael,
Do any of you have photos you would like to share with me? I am trying to compile visual evidence. I would keep the patient information strictly anonymous. Thank you for considering helping others in this manner. M
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Melanie Reber
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Lyme borreliosis (LB) is a multisystemic infectious disease involving the skin, joints, nervous system, heart, and eyes. Today at least three subtypes pathogenic for humans have been identified: Borrelia burgdorferi sensu stricto, Borrelia garini, Borrelia afzelii. Different genospecies strains of Borrelia have been associated with different clinical manifestations. LB is classically described as having three clinical stages or, similarly to syphilis, an early phase and a late one. The early infection corresponds to the first stage, the late infection includes the second and the third stages. LB skin manifestations could be divided into five classes. Erythema migrans, lymphadenosis benigna cutis, and acrodermatitis chronica atrophicans are proven skin manifestations of LB.
Lichen sclerosus et athrophicus, morphea, scleroderma, scleredema Buschke, atrophodermia of Pierini and Pasini, Parry-Romberg progressive facial hemiatrophy, and Shulman fasciitis are controversial LB manifestations. Granuloma annulare, atypical persistent pityriasis rosea, and pityriasis lichenoides are skin lesions occasionally related to LB. Urticaria, erythema nodosum, and papular acrodermatitis (Giannotti Crosti disease) are reactive LB skin manifestations. Nodular panniculitis (Pfeifer-Weber-Christian) (I think this is what I have growing inside of me!!!), B-cell cutaneous lymphoma, and juvenile chronic myeloid leukemia are exceptional skin manifestations of LB.
In the last years, there have been numerous and important advances of many aspects of Lyme borreliosis (LB). However, it appears that many questions concerning this disease remain unanswered. It is not clear, how spirochetes behave when they enter into the human body. They can produce pathognomonic lesions, skin manifestations mimicking other diseases, or clinical pictures that can be induced also by other etiologic agents.
We became aware of the complexity of this disease since genetic studies can identify different species of Borrelia burgdorferi (Bb) sensu lato responsible for human infections: Bb sensu stricto, B. garinii and B. afzelii. In Japan a new species was recently described, B. japonica, which does not appear to be a human pathogen. In future, additional species of Borrelia will probably be identified. The recurrent fever also is caused by several species of Borrelia, and the vectors are different ticks (B. recurrentis transmitted by Pediculus sp. in epidemic relapsing fever, B. caucasica, B.crocidurae, B. duttonii, B.hermisii, B. hispanica, B. mazzottii, B. parkeri, B. persica, B. turicatae, B. venezuelensis transmitted by Ornithodoros sp. in endemic relapsing fever). Diagnosis of LB is certain, when the infection is transmitted by a hard tick of genus Ixodes, and erythema chronicum migrans (ECM) appears.
Different Bb species and strains can have different organ tropisms and can induce different clinical manifestations. B. afzelii has been found in patients with acrodermatitis chronica atrophicans (ACA), while Bb sensu stricto in patients with arthritis and B. garinii in patients with neuroborreliosis. A possible Bb follicular hair tropism can explain the ECM with hair loss.
Atypical LB skin manifestations could be ordered in the following classes:
1. Controversial LB skin manifestations 2. Skin manifestations occasionally related to LB 3. Reactive LB skin manifestations 4. Exceptional skin manifestations during LB.
Skin lesions that appear immediately after tick-bite should also be mentioned: they can be mild and transient reactions, or, sometimes, edematous papular dermatitis of some centimeters of diameter, exceptionally with tissue necrosis.
Bb infection requires certain preconditions:
* Infected tick * Attachment of the tick to the skin * Appearance of enlarging erythema after an incubation period of at least 4-5 days
During the visit the tick can be observed on the skin, or sometimes the patient shows a detached tick in a little box. In such cases the tick bite is certain, while in all other cases the tick bite may be only supposed.
1. Controversial manifestations of LB
Essentially the following atrophic and sclerosing (sclerodermatous) disorders can be included:
Lichen sclerosus et atrophicus (LSA) has been related to Borrelia infection by Asbrink who noticed the frequent association between LSA and ACA. Aberer demonstrated the presence of Borrelia in LSA. It is characterized by sclerotic atrophic patches, sometimes confluent, and often located on genitals. In 3 children affected by LSA living in endemic areas, borrelial DNA was found in the involved skin, by PCR (2). No specific DNA was found in 4 cases affected by LSA living in non endemic area. The same authors confirmed the relation of morphea to Borrelia infection, while others maintain that there is no such correlation. Probably morphea can be caused sometimes by Borrelia afzelii (1).
The possible relationship between LB and LSA or morphea is suggested by the following evidence:
* Clinical and histological similarities between morphea, LSA and ACA. * The presence of antibodies against Borrelia burgdorferi in some patients with LSA and/or morphea. * Identification of borrelial organisms in histological sections. * The coexistence of ACA, LSA and/or morphea in the same patient. * A response to antimicrobial therapy in many cases of LSA and morphea.
2. Skin manifestations occasionally related to LB
Granuloma annulare (GA) has been described in association with LB. In some cases the author was able to find positive serological tests or spirochetal bodies in the affected skin by silver stain. In his experience the GA is very seldom related to LB. In 3 patients he detected Borrelia in the affected skin by PCR, but in these cases clinical evolution has been unusual and the treatment by nimesulide hasn't been effective.
Atypical persistent pityriasis rosea, lasting longer than 4-5 months, could be suspected of being related to LB.
The author is studying some children who developed a papular dermatitis with perifolliculitis, mimicking pityriasis lichenoides (2). In one case he was able to isolate Borrelia sp. in BSK from the involved skin. Further studies are necessary to confirm the relationship with Lyme disease (3).
3. Reactive skin manifestations of LB
Such manifestations can be observed also in other infectious diseases:
* urticaria, * erythema nodosum and * papular acrodermatitis
Two varieties of urticaria can be distinguished:
* diffuse * localized
The first form appears usually in early LB, whereas the localized form is more frequent in late LB. The localized form often involves the skin adjacent to the affected joints.
Erythema nodosum has also been observed during active LB. Recently, the author has reported two children who have developed papular acrodermatitis (Gianotti-Crosti disease) after borrelial infection.
4. Exceptional skin manifestations described during LB
Hassler (4) has reported an association between LB and involvement of subcutaneous tissue (Pfeifer-Weber Christian disease) and he has been able to demonstrate the presence of Borrelia in the affected skin even after several antibiotic treatments. There is also the problem of a possible correlation between LB and cutaneous B-cell (or T-cell) lymphomas. Evolution of borrelial lymphadenosis benigna cutis (LABC) towards malignancy has been supposed, but this hypothesis needs further investigations.
.......
I know there are a lot of big and confusing medical terms in this article, so if you just highlight what you, or anyone else, doesn't understand and open a new window to look it up, you will be able to make your way through this more clearly...at least that is what I had to do! Posts: 7052 | From Colorado | Registered: Mar 2003
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Melanie Reber
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From the 2006 IDSA Guidelines...(I know, I know...but at least it is acknowledged) read treatment guidelines with this in mind.
Background and Diagnosis of Acrodermatitis Chronica Atrophicans
Acrodermatitis chronica atrophicans is a late skin manifestation of Lyme disease that develops insidiously several years after initial infection (range, 0.5-8 years) [109, 242]. Approximately 20% of patients have a history of a preceding erythema migrans lesion, usually of the same extremity [242]. Acrodermatitis chronica atrophicans is diagnosed most frequently in women greater than 40 years of age. Although any of the species of Lyme Borrelia may cause the lesion, by far the most common etiologic agent is B. afzelii. Therefore, this manifestation is much more common in Europe than in the United States [243-246].
Acrodermatitis chronica atrophicans occurs most often on the extensor surfaces of the hands and feet, and early lesions are characterized by a slight bluish-red discoloration and doughy swelling. Initially unilateral, the lesion may later become bilateral. The lesion enlarges slowly over months to years, in association with resolution of the edema and development of skin atrophy (figure 4) (sometimes referred to as ``cigarette paper skin''). Nodules may develop over bony prominences, such as the elbow or patella [197, 242, 247]. In some patients, sclerosing lesions develop. Because of atrophy of the skin, the veins become prominent, which may lead to a misdiagnosis of venous insufficiency [109, 197, 242]. Approximately two-thirds of patients have an associated peripheral neuropathy, typically involving the affected extremity, manifested primarily as local sensory loss [248, 249].
The diagnosis of acrodermatitis chronica atrophicans is based on appropriate epidemiology, clinical characteristics, histological findings, and IgG seropositivity. Histopathology shows a pronounced lymphoplasmacellular infiltration of the skin and sometimes also of the subcutis, with or without atrophy [195].
Evidence to support treatment recommendations.
Acrodermatitis chronica atrophicans does not appear to resolve spontaneously. There are no prospective, randomized studies on treatment. Oral or parenteral antimicrobial therapy (table 2) given for 3 weeks (range, 2-4 weeks) has resulted in improvement in pain and swelling, diminution in fibrous nodules, and gradual fading of the lesion within 2-6 months [250-252].
Atrophic areas often persist, and little objective improvement can be demonstrated in the neuropathy in uncontrolled studies, regardless of whether antibiotics are administered parenterally. However, progression of neurologic involvement is halted, and the neuropathic symptoms of pain and paresthesia are improved [251, 252]. In the United States, treatment of Lyme disease-associated peripheral neuropathy with intravenous ceftriaxone usually results in improvement. The reasons for the differences in the experience with this manifestation of the disease in the United States and Europe are not clear.
Recommendations
1. Available data indicate that acrodermatitis chronica atrophicans may be treated with a 21-day course of the same antibiotics (doxycycline [B-II], amoxicillin [B-II], or cefuroxime axetil [B-III]) used to treat patients with erythema migrans (tables 2 and 3). A controlled study is warranted to compare oral with parenteral antibiotic therapy for the treatment of acrodermatitis chronica atrophicans.
Jill E.
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Hi Melanie,
I don't think I can ask my mom to take photos - she is really resistant to going through Lyme/co treatment at this late stage of her life. She has seen me, and then my dad, suffer so much with this illness that I can't bring it up at the moment. But if things change, I'll let you know.
Jill
-------------------- If laughter is the best medicine, why hasn't stand-up comedy cured me? Posts: 1773 | From San Diego | Registered: Apr 2006
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Melanie Reber
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As I get rid of the infections... parasites/worms/bb etc that I believe are inhabiting the small intestine my hands are coming back to normal.
It seems like the infections in the small intestine were spilling over and desseminated into the hands/head/organs etc.
Hello Gael, I actually ran across something the other day that DID speak to fillial (sp) worms. Gosh my memory is so bad right now...but I will try to find it again and post. Thank you!
I completely understand Jill, not to worry.
THANK YOU Sammy!!!
Roz, I'm so happy you have a new comp. I would be more than happy to help you with any photo questions, just ask, OK? I am not real sure exactly WHAT I have right now...still trying to lean as much as I can and put the mystery together. But, I AM making progress! Posts: 7052 | From Colorado | Registered: Mar 2003
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Melanie Reber
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CLINICAL AND LABORATORY INVESTIGATIONS
Morphoea: a manifestation of infection with Borrelia species? K. Eisendle, T. Grabner and B. Zelger Department of Dermatology and Venereology, Innsbruck Medical University, Anichstra�e 35, 6020 Innsbruck, Austria
Background Morphoea or localized scleroderma is a cutaneous inflammatory disease with still unknown aetiology. Borrelia burgdorferi as causative agent has been discussed controversially.
Objectives To assess the evidence for infection with B. burgdorferi in patients with morphoea by focus-floating microscopy (FFM).
Methods Using standard histological equipment, tissue sections stained with a polyclonal B. burgdorferi antibody were simultaneously scanned through in two planes: horizontally as in routine cytology, and vertically by focusing through the thickness of the section, i.e. FFM. Part of the material was also investigated with a Borrelia-specific polymerase chain reaction (PCR).
Results One hundred and twenty-two cases of morphoea and 68 controls (58 negative and 10 positive by PCR) were investigated for the presence of Borrelia within tissue specimens. Using FFM Borrelia was detected in 84 cases (68�9%) of morphoea and in all positive controls, but was absent in all negative controls.
Borrelia was significantly more frequent in early inflammatory-rich (75%) than late inflammatory-poor (53%) cases (P = 0�018). What seemed to be vital microorganisms were mostly found close to the active border, while degenerated forms were more common in fibrosclerotic parts. The presence of B lymphocytes determined by CD20 staining proved to be a good positive predictor of the microorganism (correlation 0�85, P < 0�001). Borrelia-specific DNA was detected in only one of 30 cases of morphoea analysed by PCR.
Conclusions FFM is a reliable and highly sensitive method to detect Borrelia in tissue sections. The frequent detection of this microorganism in morphoea points to a specific involvement of B. burgdorferi or other similar strains in the development of or as a trigger of this disease.
Health
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Hi,
I would say I have ACA, and it started to progress even while IN lyme treatment, and now I am treating Babesia and it is getting better I would say, my facve almost looks normal,
I was starting to get it on my face, and that is very upsetting. I am on Mepron and Azithromycin for about 10 months now, and had to stop this treatment because it was too strong, but now have been back on it for some time now.
I feel because my Babesia in the past had not been treated long enough, I have the strain Babesia Duncani, and this strain my LLMD says takes 10 or more months of treatment,
as well I had untreated lyme for about 15 years, and untreated Babesia for about 18 years.
I will post on here occasionaly to put in my comments, I hope that I dont have the ACA permanent.
If Babesia is not treated, for me anyways, the Lyme got worse, because immune system worse.
I have also had the hands ITCH like heck from this Mepron and Azithromyin where the ACA is, the ACA that is on me is not as bad as the pictures, and I hope that treating,
the Babesia and then the Lyme again, and possibly Bartonella? I will no longer have any ACA signs.
If you have ACA treat Babesia if you have not.
I also got sick in Europe and I live in Canada.
So maybe got it over there.
Hope this helps.
Will post another time, if I get worse or better.
I even have the ACA starting to show on eye lids, and had the eye lids itch like heck from herxing, now I look pretty good almost normal.
My face is getting better, through treating babesia.
Trish
Posts: 1250 | From Canada | Registered: Aug 2004
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hshbmom
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Hi Melanie,
My hands look very dry and leathery regardless of the time of year. My kids say I have "Grandma hands." I'm not THAT old. Ha ha.
Some day I'll take some photos and send them to you.
I never remember to ask my good doctor about them.
My family member has the swelling all over that you described recently. Diuretics don't help. It looks like they take massive doses of steroids. I think it's vasculitis. The fluid & protein leaks out of the blood vessels, then more fluid follows to dilute the protein.
Your skin coloring looks like mine, how is your circulation?
I am doing much better. I believe 100% you can go into remmision with ACA as well. I am 65% percent better and have been in treatment for 2 years.
How are you doing as far as detoxing goes?
My treatment right now is red clover therapy, it has several herbs in it and is supposed to cleanse the blood. My thinking is, if the blood is clean no disease can live.
I am also taking just a couple humaworm tablets a day.
I just bought this real cheap tent sauna for 129.-maybe it will help as well.
I am still trying to trace down the people that took photo's of my arm before treatment.
Melanie Reber
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Livedo racemosa: an unusual late manifestation of borreliosis? Baumann M, Tebbe B, Arnold M, Krengel S, Goerdt S, Orfanos CE. Hautarzt. 2000 Aug;51(8):593-6.
Klinik und Poliklinik f�r Dermatologie, Universit�tsklinikum Benjamin Franklin, Freie Universit�t Berlin.
Classic variants of cutaneous borreliosis are erythema chronicum migrans (ECM), lymphadenosis benigna cutis (LBC) and acrodermatitis chronica atrophicans (ACA). Other dermatoses have been reported in the literature as possibly linked to borreliosis.
A 59-year old female patient was seen in the late phases of cutaneous borreliosis with histologically confirmed ACA. In addition, prominent livedo racemosa was seen on the legs, also showing tissue changes similar to those of ACA.
Borrelia burgdorferi infection was serologically confirmed by the presence of anti-IgM and anti-IgG antibodies. The clinical spectrum of late cutaneous borreliosis should be enlarged to include livedo racemosa.Posts: 7052 | From Colorado | Registered: Mar 2003
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Melanie Reber
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Acrodermatitis chronica atrophicans in a 15-year-old girl misdiagnosed as venous insufficiency for 6 years. Zalaudek I, Leinweber B, Kerl H, M�llegger RR. Department of Dermatology, Medical University of Graz, Graz, Austria. J Am Acad Dermatol. 2005 Jun;52(6):1091-4.
Acrodermatitis chronica atrophicans, the characteristic cutaneous manifestation of late Lyme borreliosis, typically occurs in elderly women. To our knowledge, only 4 cases of acrodermatitis chronica atrophicans in children have been described. Prompt diagnosis and treatment are important to prevent progression of disease and extracutaneous complications.
We describe a 15-year-old girl with acrodermatitis chronica atrophicans of the left leg that had been misdiagnosed as chronic venous insufficiency for 6 years. Because of the long-standing disease course, skin changes expanded and progressed to marked atrophy. The correct diagnosis was finally based on clinical, histopathologic, and serologic findings. The girl was treated with oral doxycycline for 6 weeks, but her skin changes did not fully normalize.
This case illustrates the possibility of acrodermatitis chronica atrophicans appearing in childhood and the difficulties in differentiating vascular disorders from acrodermatitis chronica atrophicans on the basis of the clinical appearance alone.
Posts: 7052 | From Colorado | Registered: Mar 2003
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Melanie Reber
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Well, it is official... the reason I am a wrinkled smurf is because I have ACA! I LOVE my LLMD!
So, we are going to anti-smurf me soon. Up for more possible ACA people?
Melanie Reber
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Yes... it is sort of odd that after 6 years (how many 30 day treatments would that make? Ummm 73 rounds of curative treatment) of MASSIVE ABX...
I still am presenting with an acute Borrelia infection.
Hmmmm, someone has to be misinformed here somewhere. I wonder who that could be?
Shoes would be lovely, but only if they go with my new pink toenails. Posts: 7052 | From Colorado | Registered: Mar 2003
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Pinelady
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Great Work. Are the bottoms the same and is the
toe flaring signs of neuro involvement?
I would love to
see um whats his names face at the IDSA review
when and if they get to see that hot pink!
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Melanie Reber
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Good morning Lady of the pines,
Are you asking if the bottoms of my feet are smurfing too? If so, actually no, they remain either yellow or white or red, I am almost patriotic, huh?
However, the inside of my palms under the thumbs... and both of my forearms are turning blue too now.
Mostly things change pretty rapidly, so I am very happy that I have kept up with the photos to chronicle this weirdness, as I don't think anyone would believe me otherwise.
Having said that... while in my LLMD apt yesterday morning; I showed the docs my purple (red AND blue) freezing feet and my blue palms and forearms. While at the same time, my yellow and blue hands were burning hot. So, at least they were witness to this weirdness.
Yes, I do think the toe flaring is something weird as well. This is new for me. But I am also experiencing severe cramping... so who knows what the actual cause is. Could be multiple reasons.
Although, one sign of ACA IS an outward flaring of the extremity digits... ~sigh~
Hope YOU are doing well? M
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Melanie Reber
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IDSA 'Recommendations' from above guidelines:
1. Available data indicate that acrodermatitis chronica atrophicans may be treated with a 21-day course of the same antibiotics (doxycycline [B-II], amoxicillin [B-II], or cefuroxime axetil (Ceftin) [B-III]) used to treat patients with erythema migrans (tables 2 and 3). A controlled study is warranted to compare oral with parenteral (IM or IV) antibiotic therapy for the treatment of acrodermatitis chronica atrophicans.
*21 day course... OK, my mistake... so that means I have actually done 104 curative courses.
*doxycycline... Ah, I guess that first 2 weeks of Doxy didn't do it after all? Nor did the other few months of Doxy, well into treatment?
*amoxicillin... And the 3 months of Amoxy up to 6 grams, that followed the Doxy, wasn't enough either?
*cefuroxime axetil (Ceftin)... OK, so now I see where I went wrong... I have never taken Ceftin!
*compare oral with parenteral (IM or IV) antibiotic therapy... Hmmm, the 15 months of IV and subsequent 4 months of IM as compared to the continuous 6+ years of oral therapy really HAS been worth studying. ...
What is it that guy with the mustache says? GIVE ME A BREAK!
(Can you tell I am a bit peeved? )
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Pinelady
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OK thanks for asking. I haven't hit the ER so I guess I'm good. Bump up to Eric555 about 5inches up. He's got Ceftin. Hang on to that humor and you will get through this.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Tincup
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I thought the upward toes are how it is suppose to be when you CA dudes are surfing on those boards?
Truthfinder
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Melanie, I probably have some kind of ACA presentation, but I'm stumbling over all the medical terminology that describes what ACA is or resembles. I've looked at the photos; some look similar but the resolution on my screen isn't the best.
Like TO LIFE, two different punch biopsies on my back came back as Lichen Simplex Chronicus. That was several years ago. The LSC starting kicking in about the same time as other Lyme symptoms began to emerge (didn't know it at the time, of course).
But I have two different, new things going on the last 2-3 years, too, though one manifestation is similar to the LS in how it changes and damages my skin.
First, I get all these strange color changes in my skin when I shower. Redish blotches on my arms and other areas. My hands or fingers can change color. It eventually fades and returns to normal. When I look down at my feet, I've noticed this dusky color where my leg meets my foot - that wasn't there until about a year ago. I've noted no changes in skin texture or appearance with this. But I have noticed that my ankles are much thicker than they ever were, and I have pooling `edema' below my ankle bone.
But there's something else, too, similar to the LS. The Lichen Simplex stuff starts off with a tiny itch - like one single pore in my skin is irritated. So, I scratch it. If I continue to scratch it, it becomes a rash with several pores irritated. Then the texture of the skin changes, it gets a reddish color, kind of hard and inflexible, often with little scales, and I have a full-blown patch of Lichen Simplex.
I was told at Mayo Clinic to treat them with a prescription steroid cream, which does work. But the skin is often `wrinkled, dry, and translucent' when it's all over.
These latest `patches' look similar - slightly darker than normal skin or reddish, and can either be scaly or not. But there is never any itch associated with them - they just appear. I've had one on my L knee, and one on my right thigh and now the knuckles of both hands are affected. They last for several months. I don't know if steroid cream would work as I haven't tried it. But nothing else works that I've tried.
Eventually, the `rash' fades and leaves the skin `wrinkled, dry, and translucent'. Or in the case of my knuckles, it's almost like scar tissue or like when you get a sunburn - like kind of hard and not as flexible. It's almost like dead skin - it isn't anything like the skin I had before. Maybe that would be termed `sclerotic'. And none of these areas has ever returned to normal.
BTW, I've never been to Europe.
So, I'm not sure what I have, really. I do know that we have B. bissettii and B. parkeri here in Northern Colorado and in this county (found that in an old NIH document), which could be implicated.
B. bissettii is a common Borreliosis culprit in parts of Europe (like Slovenia). Here in Northern Colorado, reservoirs for B. bissettii appear to include chipmunks and ground-squirrels.
As it turns out, I had both a wild chipmunk and a wild ground-squirrel as pets between the ages of about 9 and 15. I don't know if ACA is common in B. bissettii infections in Europe, though, so I'm not sure if there is a connection. I handled both animals a lot and don't recall any fleas or ticks on them, nor was I ever bitten that I remember.
I suspect I'm in the ACA group, but just not sure.
-------------------- Tracy .... Prayers for the Lyme Community - every day at 6 p.m. Pacific Time and 9 p.m. Eastern Time � just take a few moments to say a prayer wherever you are�. Posts: 2966 | From Colorado | Registered: Dec 2005
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Melanie Reber
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Good morning Tracy,
Thank you so much for stepping forward! Yes, the medical terminology is/was very difficult for me as well. I have/had to keep looking up every other word in every abstract or article I read... so that slows things way down.
By now, though, I am beginning to get a tad more familiar with most terms.
I get all these strange color changes in my skin when I shower. Redish blotches on my arms and other areas.
Yes! I could NOT have described this better myself. It is as if the skin looks burned from the warm shower water! But, it is patchy in unexpected places, but mostly for me, on my hands, feet and certain areas of my legs.
I don't know WHAT this is, but feel it has to be connected somehow. My theory is... we have very poor circulation that goes along with ACA, most times, my extremities are freezing cold- thus the bluish hues. So, when exposed to warm water, the circulation increases to those cold areas, turning them red.
It is almost the same phenomena as frostbite. The frozen skin changes color to a bluish hue, and when re-exposed to warmth, if it is not too late, it turns bright red.
But I have noticed that my ankles are much thicker than they ever were, and I have pooling `edema' below my ankle bone.
My exact experience. And the photos I posted verify this. I need to take recent pictures, as the edema has subsided, but still there remains a blob right behind the ankle bone.
I was told at Mayo Clinic to treat them with a prescription steroid cream, which does work. But the skin is often `wrinkled, dry, and translucent' when it's all over.
So sorry... but I shudder to even hear that name. I'm sure you are aware by now as to why? As you know, the `wrinkled, dry, and translucent' skin IS the atrophy process associated with ACA.
Goodness, knowing you are in CO and have never been to Europe really intrigues me. I lived there (Durango and then Denver) for 23 years and was bitten by numerous ticks the whole time. CO is known to have some very interesting ticks that carry very interesting diseases. One just needs to dig a bit deeper to find the proof, and I am so thankful that you have done just that!
No, I never saw ONE flea while in CO either. But, when I moved here to CA, my cat became immediately infested. I didn't even know what one was supposed to do for fleas! But we figured it out. Unfortunately, by that time, the damage had been done... the cat became very ill and I relapsed terribly.
When I can make the time and find the energy to research your theory of B. bissettii... I will be certain to post it.
Meanwhile... I am not a physician, obviously, but what you are describing, at least to me, most certainly puts you in the ACA/ Scleroderma category. I'm so terribly sorry, but also so pleased that you have shared such valuable information. I do hope you will seek the help you need to take care of this before it progresses further.
We are currently collecting stories like yours and photos for educational use. If you would be willing to send some photos my way, it would be more than appreciated!
Melanie Reber
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up... for others?
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Melanie Reber
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Solitary borrelial lymphocytoma in adult patients. [Journal Article] Maraspin V, Cimperman J, Lotric-Furlan S, Ruzić-Sabljić E, Jurca T, Picken RN, Strle F Wien Klin Wochenschr 2002 Jul 31; 114(13-14):515-23.
During the period from 1986 to 2000, 85 adult patients with solitary borrelial lymphocytoma were diagnosed at the Department of Infectious Diseases, University Medical Centre Ljubljana, Slovenia. There were 36 (42.4%) females and 49 (57.6%) males with a median age of 49 (15-74) years.
Borrelial lymphocytoma was located on the breast (nipple--areola mammae region) in 68 (80%) patients, on the ear lobe in eight (9.4%), and in other locations in nine (10.6%). A concomitant erythema migrans enabling clinical diagnosis of Lyme borreliosis was registered or reported in 67 (78.8%) patients. Fifteen (17.6%) patients had no accompanying symptoms, 34 (40%) reported local and constitutional symptoms, 23 (27.1%) recounted only local symptoms, and 13 (15.3%) patients had solely constitutional symptoms.
Clinical findings indicating early disseminated borrelial infection were observed at the first visit in 12 (14.1%) patients: six (7.1%) had multiple erythema migrans, one had meningitis, one meningoradiculitis and arthritis, one radiculoneuritis and arthritis, one peripheral facial palsy and concomitant meningitis, and two arthritis. In addition, one of the patients with borrelial lymphocytoma on the breast had acrodermatitis chronica atrophicans.
A seropositive response to borrelial antigens was found in 30 (35.3%) patients at the initial examination. In 11/46 (23.9%) patients, infection with Borrelia burgdorferi sensu lato was confirmed by isolation of the agent from lymphocytoma tissue. Eight out of nine (88.9%) typed borrelial strains were found to be B. afzelii, and one (11.1%) B. bissettii.
Patients were treated with doxycycline, azithromycin, amoxycillin, cefuroxime-axetil, phenoxymethylpenicillin, or ceftriaxone. Median time to complete disappearance of lymphocytoma was 28 days (range 7-270 days) after the institution of antibiotic treatment; disappearance took longer in patients with prolonged duration of the skin lesion prior to treatment.
Treatment failure was registered in 11 (12.9%) patients who were later re-treated. The outcome of borrelial infection assessed at the end of a follow-up period of one year was favourable.
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Melanie Reber
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Borreliosis--increasing clinical problem [Journal Article] Dybowska D Wiad Lek 2006; 59(1-2):23-6.
Lyme disease (LD) is due to infection with Borrelia burgdorferi (B. burgdorferi). We analysed some aspects of epidemiology and clinical manifestation of borreliosis. We tried to estimate the efficiency of diagnostic methods and treatment.
We analyzed medical documentation of 300 patients with LD treated in our department between 1993-2001. The diagnosis was made according to Lyme Disease Foundation's criteria. Patients suffering from LD were divided into 3 groups according to stages of the disease.
The most frequent manifestation of LD was erythema migrans (EM). The number of LD cases had increased during the observation time. The exposition to tick-bites was greater during summer and early autumn. The great number of patients with EM was observed at the same time.
Cases of Lyme arthritis (LA), disseminated EM, Lyme carditis (LC) and neuroborreliosis represented the group number 2.
LA, uveitis and acrodermatitis chronica atrophicans (ACA) were diagnosed in the third group of patients.
Serological markers of B. burgdorferi infection were found in about 50% of cases of EM and in each patient in group 2 and 3. Complete recovery after antibiotic therapy was observed in every case in early LD and partial one in the late stage.
Posts: 7052 | From Colorado | Registered: Mar 2003
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Truthfinder
Frequent Contributor (1K+ posts)
Member # 8512
posted
Melanie,
Interesting that you found a case where B. Bissettii may be implicated in ACA.....
I think B. bissettii is a `new name' for what were once classified as European DN127 type strains..... it gets confusing. I do have a small collection of excerpts and links regarding Colorado strains if you want me to send those to you. It's been awhile since I did any research on it.
Not much attention is given to B. bissettii here in the USA, I think mostly because of articles that say stuff like this (vintage 2004 - Allen Steere was involved in this one, no surprise):
quote:Similarly, in Colorado, wood rats and I. spinipalpis ticks may be infected with Borrelia bissettii, one of the nonpathogenic species, in a cycle that is not known to cause human infection (13). http://www.jci.org/articles/view/21681/version/1
Well, that's just not true in Europe, so the above statement is extremely misleading.
As for photos, I've had a digital camera for 3 years and still haven't taken the time to figure out how to download the software and get photos transferred onto my computer, lol. This computer has been such a snarled up mess since I got it that it sort of takes the fun out of using it.
Anyway, I've been checking my body the past few days for picture-worthy `examples' of possible manifestations..... very disappointing! I haven't had a single after-shower reddish splotch show up, except a couple of very small, vaguely-pink spots that won't show up on camera. I'm sure they will be back, but for now they are quiet.
I should get someone else to take pics of the odd skin on my knuckles. And perhaps the thick ankles and pooling edema below my ankle bones. Those are the only things that MIGHT show up decently on film.
Oh, and I forgot to mention that I, too, have the `droopy eyelid' thing, only it's different on each eye. It isn't really the eye `lids' themselves, so much; it's that skin below my eyebrow (like in your photo). AND, I developed a puffiness below my eyes - mostly one side - in that `dark circle' area, too. That happened about a year and a half ago. The puffiness comes and goes, but never completely leaves.
Also forgot to mention that before I posted last time, I had some kind of skin eruption on my scalp - like 2 pimples or bug bites - right near the hairline on the back of my neck. I'd never had that before, but saw something similar in your photos.
I think you are probably right about the circulation issues. My feet are often very cold, but they will still sweat, which just makes things worse. So, I have clammy, cold feet in both winter and summer.
Last winter, I finally broke down and bought several pairs of Smartwool socks (washer-friendly), and it DID make a difference. For some reason, my feet either don't perspire as much, or the moisture gets wicked away. I even bought 3 summer-weight pairs recently but don't know how they will work out yet. I usually itch terribly from wool but I haven't had a problem with the Smartwool. (I did wash them a couple of times before wearing.)
I also have periods when my feet are hot and burning. Though I don't have the color changes you mentioned, it always reminded me of frostbite - first freezing cold, then when they get warm, they go to the extreme.
This appears to be related to what I eat and how much I eat more than anything. And if I don't eat enough, or try to stick with mostly vegetables, I can't get warm. Even in bed with lots of blankets and comforters. I'm just not generating enough heat (circulation again?). It's just so crazy.
Re fleas: I feel so lucky that I just haven't had a problem. Fleas around here can carry the Plague, among other things. Cats are particularly susceptible since they hunt birds and rodents.
And with the crazy deer sleeping in my back yard several days a week, squirrels in my trees (that someone imported from somewhere 10 years ago), Mourning Doves that appear to be nesting in my darn chimney (!) right here in town, you'd think I'd have lice, fleas, and ticks to deal with in my cats and dog. But I haven't yet. The only time I ever had fleas here was when I boarded my dog for few days and he came home with fleas. What a mess.
I realized that I never answered the questions you posted .... well, I won't be much help there but here are the answers:
"Have you been diagnosed clinically or through serology?" Neither, really. Had an ultimate high-positive Bowen test in 2005 and low CD57 test last year.
"Has your LLMD offered treatment options, and if so, what are they?" I don't have an LLMD, or a Lyme doc of any kind.
"Have you been able to halt the progression with treatment?" Haven't been on any specific medical protocol.
"Do you know for certain where you were infected?" Nope. Probably had this since I was a kid and I grew up here. Spent countless hours out in the brush with livestock, horses, pets, and critters of every kind, had attached ticks regularly in summer. There were some early symptoms but nothing overt until mid-1980s.
"Have you ever traveled to Europe or to other places outside of the states?" Nope. Spent time in both Alaska and Hawaii, traveled through Canada and some into Mexico, but never have been overseas.
"Do you have photographic evidence of your condition?" Not yet, but if I get some, I'll send it to you.
"How long were you ill before this presented?" Hmmm. If we consider the `Lichen Simplex' issue, then I've had this going on since about 1992.
"What other diseases besides Lyme have you been diagnosed with?" Actual diseases? Not many. If we include conditions and syndromes, then the list is pretty long. I'd have to think about it, but if you want all that, I can gather the info.
"What are your main symptoms?" Musculo-skeletal problems (bulging disks, degeneration), fatigue and sleep issues, cognitive issues, and digestive/elimination problems. Those are my top 4 at this moment.
"Do you know of others with ACA?" No.
Gee, sorry this is so long!
-------------------- Tracy .... Prayers for the Lyme Community - every day at 6 p.m. Pacific Time and 9 p.m. Eastern Time � just take a few moments to say a prayer wherever you are�. Posts: 2966 | From Colorado | Registered: Dec 2005
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Melanie Reber
Frequent Contributor (5K+ posts)
Member # 3707
posted
Good morning Tracy,
yes I would be very interested in seeing what you have re: the strains in CO. As you may or may not know; I am trying to keep track of each state's known ticks and diseases that they carry on the Lyme Memorial site, and would really like to add to the CO page with more info that you can provide.
Yes, things do get confusing in the naming of these buggers, as they change so quickly as more are discovered. It takes a lot of research to try and keep things straight.
For example, if you read the abstract below, you will see that new strains of Borrelia have been found just recently in the Carolinas. B Bissettii was also implicated as 'a diverse group' found in the wildlife there.
I can completely relate to trying to learn new tech things when ill. I had a printer for over 2 years before I finally was well enough to figure out how to hook the darn thing up. (still have not tackled the fax capabilities)
As far as transferring photos from your camera... you may want to try what I have done with the borrowed camera I am using.
Get a cable that hooks into your camera on one end and into your comp USB port on the other. Then, you can turn on the camera while in the replay pictures mode, and open up a new window of 'My Computer'. Now you will see the camera listed, simply double click on the camera icon, and your PC should walk you through an instant download wizard w/out any additional software.
Hope that was clear enough? It is certainly worth a try, and if it works for you, you will not have to do anything else to download any images from now on.
I find it really interesting that you have found circulation and body temp issues are related to what you eat. I too go through periods, almost daily, when I sort of crash mid-afternoon. I just have to lay down or fall down. So I make my way to the sofa and cover up with down. Even pull it over my head.
It matters not what temperature is is inside.. I begin to shiver uncontrollably until I fall asleep. usually to awaken in a sweat.
I think most of that has to do with my endocrine system being pretty messed up. But my doc keeps harping on my eating habits, which are basically nil. She tells me that if I would just eat consistently throughout the day, this crazy pattern would begin to regulate itself.
I'm still smiling about the flea comments. I lived at 7,200 elevation there, and NEVER saw a flea.
You don't have a Lyme doc? At all? Who is treating you then? Sorry to pry, I am just concerned.
And please do not apologize for the length... you are providing wonderful information, and I really do appreciate it! M
Melanie Reber
Frequent Contributor (5K+ posts)
Member # 3707
posted
Borrelia carolinensis sp.nov. - a new (14th) member of Borrelia burgdorferi sensu lato complex from the southeastern United States. [JOURNAL ARTICLE] Rudenko N, Golovchenko M, Grubhoffer L, Oliver JH J Clin Microbiol 2008 Nov 19.
Approximately 118 Borrelia isolates were cultured from a variety of rodents, birds and ticks collected in the southern USA. In addition to a highly diverse group of Borrelia bissettii strains, and a homogenous group of Borrelia burgdorferi sensu stricto strains, a group of 16 isolates with unusual characteristics was found.
Isolates were cultured from ear biopsies of the rodents Peromyscus gossypinus and Neotoma floridana trapped at 5 localities in South Carolina. Multilocus sequence analysis of rrf-rrl intergenic spacer, 16S rRNA, flagellin, ospA and p66 genes were used to clarify the taxonomic status of the new group of B. burgdorferi sensu lato isolates. Thirteen species of B. burgdorferi sensu lato complex were used as controls. Unique RFLP patterns of rrf-rrl intergenic spacer region and flagellin gene were recognized. Unique signature nucleotides were also found in the 16S rRNA gene. Phylogenetic analysis shows that the 16 new isolates cluster together but separately from the other species in the B. burgdorferi sensu lato complex.
Our data strongly support the recognition of the 16 isolates as a new B. burgdorferi sensu lato species. We propose to name this genospecies Borrelia carolinensis with respect to the place of its currently known geographic location.Posts: 7052 | From Colorado | Registered: Mar 2003
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