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05/01/2012 08:29 AM

ACA-Skin Manifestations Of Lyme Disease

Posts: 1822
Senior Member

Blessings all-

I'm just stopping in to share this information with you all in the hopes that it might help one of you out there, or someone you love.

Without the tireless efforts that Betty puts forth in obtaining information for this site, I might not have found a picture of this and would never have been able to get the answer I needed. Betty, you have my sincere gratitude.

My father had a bullseye on his arm a few weeks ago, and I came here and searched for lyme rash pictures to show my parents when they got here for me to identify the bite mark.

I found a picture of the ACA instead, and have spent the past few weeks gathering all of the information that I could on it and have finally been given an answer to my almost two year dilemma.

I have had a weird skin manifestation on my hands since the beginning of my lyme treatment back in 2010, and never had a reason as to why. My doctor told me it was from washing my hands too much, then it was detox..he could never figure it out, and I wasn't satisfied with the answer.

I've spent the past few weeks trying to sort things out and have finally had my doctor's help in clinically diagnosing me with ACA...Acrodermatitis Chronica Atrophicans.

ACA is a manifestation of late stage chronic European Lyme from B. afzelii. It is usually only found in Europe, and rarely in people with European heritage in the US.

My family has German on my father's side of the family, and my mother's side is from England and Ireland.

Both of my parents have signs of ACA, which I will provide a link of a picture of their symptom for later, but not to the extent that I have it.

My father's mother also had the same symptoms on her hands, proving the lineage of this infection in my family.

I was worried that I was perhaps out of remission, or that I was never in remission at all. My doctor has reassured me that I am indeed in remission, I've been in remission for "many, many months", and this is something that I am left with as a result of having lyme disease.

I just wanted you all to know that I've spent the last few weeks very concerned about my status,..not that I care if I still have lyme, but that I didn't want to mislead anyone , especially myself, into thinking that I was in remission if I wasn't.

I work very hard to maintain truth and integrity in my life, and I did not want to speak something that wasn't my truth. If I had more work to be done, I would have done it with no hesitation, it's better to treat than to ignore.

This is my newfound truth/answer to my lyme journey... I have/had European lyme disease, and ACA will be something that I have left to remember it all by..there is nothing that will help my hands at this point, having been born with it has caused it to manifest into my skin and is something that cannot be cured.

Spraying it with colloidal silver is what helps alleviate most of what's left, so I will continue to use that and be grateful that this helps to the extent that it does.

This thread will be a compilation of all the information that I've found on the subject, and I pray that it will maybe help someone else who is going through the same or similar circumstances.

There's always the possibility that you might meet someone with this affliction, so please remember all of the possibilities that are out there in manifestations of lyme disease.

Remission is real, it's possible for all of us..we are just sometimes left with reminders..or battle scars if you will...of what we've been through and where we've been.

To finally have my answer has been such a gift, all of my pieces in my puzzle are finally solved. Love and blessings to you all.. please keep your faith and never give up on searching for your answers.

peace love and light-kim

What is ACA?

It is Acrodermatitis Chronica Atrophicans, a skin condition that frequently accompanies late stage Lyme borrelliosis (afzelii) but almost exclusively by those of European heritage.

Originally discovered and documented by Dr. Buchwald in 1883, it was not until 1902 when Dr's Herxheimer and Hartmann began to study the phenomena in earnest that clear evidence began to mount. (

The full name of the disease now carries the name of Dr. Herxheimer in most references.)

Now it is estimated that close to 10% of all Europeans with Lyme disease have ACA and in fact it is the most common late and chronic manifestation of European Lyme disease.

However, given the fact that most doctors in North America do not believe in chronic Lyme disease, it is not surprising that dermotologists would not be trained to recognize ACA, and even Lyme literate doctors are sadly lacking any significant training about ACA.

Acrodermatitis chronica atrophicans is a skin condition that takes a progressive course that leads to atrophy of the skin in a variety of ways but sharing certain common characteristics.

Not surprisingly, involvement of the peripheral nervous system is frequently observed as a part of ACA (numbness, tingling, pain...)

As we know, clinical manifestations of Lyme borreliosis are almost unlimited. They can affect the skin, nervous system, muscles, joints eyes, ears, any organ including the heart.

With ACA, the skin becomes papery thin and almost shiny and transparent so that the blood vessels, veins, arteries and tissue can be seen through the skin in various degrees which give the skin a pinkish/bluish color.

ACA is most commonly found on the hands and feet but can be found most anywhere on the body. Unfortunately, if you think you have it, there isn't a very good chance of diagnosis.

Doctors absolutely despise patients who come into their office armed with information from the internet. However, you may have a chance if you come armed with the following article from WebMD: This site also has some remarkable pictures at

For your own understanding of ACA, a picture is worth a thousand words.

There is a remarkable collection of pictures from (the lead picture for this post is from their site), make sure to click on your flag of nationality to read the text in the correct language:

Finally, there is a glaring and amazing point I would like to make - above and beyond the possible diagnosis that many may have been suffering with for years without a clue of its connection to chronic Lyme disease.

Perhaps you will have jumped ahead to the obvious question this post raises by the accepted and even honored research by Dr. Hartmann and Dr. Herxheimer over one hundred years ago.

Why and how can it be that the respected doctors of the day believed without a doubt in chronic Lyme disease and studied symptoms and treatment of such while our "advanced doctors have disregarded over a century of research and documentation to cling to their platform of "there is no such thing as chronic Lyme disease."

The next time you are challenged about chronic Lyme disease, you may want to bring up this ignored fact - that chronic Lyme disease is not debated in Europe. Do we even need to ask why?

Jenna Smith is a writer and amateur dressage rider who has published many articles on health and fitness. Struck down with Lyme disease in October 2006, Jenna has devoted her time to helping others with Lyme disease and other health concerns.

Jenna's goal is to help people discover cutting edge strategies for healing disease and obtaining optimum health.

Learn more about chronic Lyme disease, and claim your free ebooks on alternative treatment protocols at: and

Jenna also publishes a Lyme Blog, Lyme Video Blog and a Daily Inspiration Blog, all accessible from the websites, and has published a novel, "The Goddess of Sumer" available at Amazon.

Article Source:

Article Source:

enlarged text for easier reading, broke up longer paragraphs so we neuro lyme folks can be able to read all of this kim; bettyg, leader

Post edited by: Bettyg, at: 05/01/2012 11:24 PM


05/01/2012 08:30 AM
Posts: 1822
Senior Member

Blessings all-

The following link is pages long on the history of lyme disease. ACA was discovered back in 1883, which tells you that lyme has been around for too many years to not be given the epidemic status that it deserves. On pages 22 and 23, you will read of how the cold can attribute to a worsening of symptoms, like I get, and will also say that it is blood transferable, which gives credibility to us/me being born with it.

Sorry! Betty will have to fix this link, I don't know how to make it shorter!

peace love and light-kim

Post edited by: fabajenna, at: 05/01/2012 08:32 AM

edited by Lauren, hopefully fixed the formatting problem. Smile

Post edited by: WiscLamLymie, at: 05/01/2012 01:54 PM

05/01/2012 08:31 AM
Posts: 1822
Senior Member

Blessings all-

A link to pictures of ACA, as referred to In Jenna's Lyme Blog.. diagnose.htm

peace love and light-kim

05/01/2012 08:33 AM
Posts: 1822
Senior Member

Blessings all-

More pictures of ACA, the first link is what my parents have, as well as myself..the second link shows what mine look/looked like at their worst. LymeTBDRashes#5538492530746686530

peace love and light-kim

05/01/2012 08:36 AM
Posts: 1822
Senior Member

Blessings all-

Another article on ACA, straight from Europe..I'm posting one article, but there's several in the link provided..

Acrodermatitis chronica atrophicans

by Yvonne » Thu 27 Dec 2007 20:45

Acrodermatitis chronica atrophicans (ACA) is the third or late stage of European Lyme borreliosis (LCool. 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 ACA. Another genospecies of the Borrelia burgdorferi sensu lato complex, Borrelia garinii, has also been detected.

ACA is the only form of LB in which no spontaneous remission occurs. Its pathophysiology is not yet fully understood.

ACA 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 LB.

A restricted pattern of cytokine expression in ACA, 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.


In the US:

The occurrence of ACA is connected with the ecology of LB, which varies in different geographical regions of the world.

Despite a high incidence of LB in the United States (varying from 95 cases per 100,000 population in Connecticut to 1250 cases per 100,000 population in Nantucket County, Massachusetts [1996 data]), ACA is not seen in the United States, except in a few European immigrants.


The occurrence of ACA is connected with the ecology of LB, which varies in different geographical regions of the world.

Ixodes scapularis, Ixodes pacificus, and 4 other tick species distributed in North America transmit B burgdorferi sensu stricto, causing EM and LB arthritis.

Tick vectors of B afzelii, the main etiologic agent of ACA (and erythema migrans [EM]), are Ixodes ricinus, Ixodes hexagonus, and Ixodes persulcatus distributed in western and central Europe and in far eastern Europe and Asia.

Almost all of these hard tick species may also transmit B garinii, a causative agent of EM and neurologic symptoms of LB.

In Europe, LB with all its dermatologic manifestations occurs in almost all countries, predominantly in the central part of the continent.

The annual incidence per 100,000 population varies from 16 cases in France to 120 cases in northeastern Poland and Slovenia and to 130 cases in Austria (1995 data).

The frequency of ACA is about 1-10% of all European patients with LB, varying according to the region of the population sampled.

Among the group of patients with skin manifestations of LB observed in Vienna, the ratio of the number of EM cases to ACA cases and to Borrelia lymphocytoma (BL) cases was 30:3:1.

This ratio is 170:5:1 in the authors' as-yet-unpublished studies (provided in the group of patients with LB in northeastern Poland).

Because the clinical diagnosis of ACA is much more difficult than that of EM or BL, the condition is often underdiagnosed, and, in fact, the ratio of EM cases to ACA cases may be higher.

The total number of cases could increase with increasing frequency of untreated European LB. ACA is probably the most common late and chronic manifestation of the borreliosis in European patients with Lyme disease.

A Bulgarian survey found that borrelial lymphocytoma and ACA were rare (0.3%) (Christova, 2004

Mortality/Morbidity: The course of ACA is long-standing, lasting from a few to several years, and it leads to extensive flaccid atrophy of the skin and, in some patients, to the limitation of upper and lower limb joint mobility.

Chronic, difficult-to-treat ulcerations of atrophic skin may develop after minor trauma. Malignant degeneration has rarely been observed; one should not consider ACA to be a precancerous disorder.

The general status of patients with ACA remains good, though they may experience neurologic and/or rheumatologic signs and symptoms.

Race: ACA is not limited to any one nationality or race. It is much more frequent in whites than in other races, probably because of a far higher exposure to ticks transmitting B afzelii.

Sex: More than two thirds of patients with ACA are women. Among the authors' 19 patients, only 5 were men (Flisiak, 1999).

Age: The disease can occur in any age group, but it is most frequent in adults, usually in their 40s or 50s.

The youngest of the authors' patients was 26 years; the oldest was 73 years (Flisiak, 1999).

The mean age of the female group was 54.3 ± 12.8 years; the mean age of the male group was 46.2 ± 6.5 years.

ACA is rare in adolescents; however, it has been observed in children. A case in a 15-year-old girl was reported by Zalaudek et al in 2005.

History: Because of its late onset, patients with ACA 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. ACA 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 LB; 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.

ACA is most often unilateral, although bilateral ACA is also common.

Progressive allodynia, the exaggerated reaction to pain, is a characteristic symptom and, thus, may be a clue to the diagnosis of ACA.

Patients commonly complain of spontaneous acral pain and paresthesia or dysesthesia or cognitive dysfunction.

ACA 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.

ACA usually appears on the distal part of at least one extremity, predominantly on the extensor surfaces on the bony prominences.

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.

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.

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 ACA or develop simultaneously. The most common sites of these nodules are the elbows and the knees.

ACA does not heal spontaneously; gradual conversion into its atrophic phase may occur during many years of infection.

The skin becomes thin, atrophic, wrinkled, dry, and translucent.

The hair is lost; the number of sebaceous and sweat glands are decreased.

Even minor trauma may produce large, slow-to-heal ulcerations of the affected skin.

About 5-10% of patients with ACA develop sclerodermalike plaques. Anetodermalike skin lesions can be seen

concomitant with ACA.

ACA 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


The clinical recognition of ACA 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 ACA 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.

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 (see Image 1).

Skin changes are often associated with regional or generalized lymphadenopathy.

The later, atrophic phase of ACA 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.

Because of the loss of subcutaneous fat, the skin vessels become prominent.

Atrophy of the epidermis and lack of hairs, sebaceous glands, and often sweat glands make the skin poorly protected and vulnerable.

Large ulcerations can be observed, and malignant lesions may also occur.

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 ACA in both the inflammatory phase and the atrophic phase.

These changes are usually limited to the legs and the feet, but they occasionally occur on the trunk.

The lesions, similar to morphea and lichen sclerosus and atrophicus, may appear in regions where no ACA 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.

ACA 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 ACA was a 68-year-old woman first seen with prominent livedo racemosa on the leg where typical ACA inflammatory phase patches developed (Flisiak, 1999).

Others also observed the same phenomenon, so perhaps this may be more than a chance linkage.

Detailed clinical and neurophysiologic examinations in patients with ACA-associated polyneuropathy often show a sensory polyneuropathy.

Neuropathy symptoms, most often pain and/or paresthesia, are evident in one half of patients with ACA.

One of the authors' patients had paresis of the brachial plexus (Flisiak, 1999).

Marked abnormality of the vibratory threshold is a common finding.

Patients with localized or asymmetric neuropathy seem to have changes more often found in the extremities with, rather than without, visible ACA lesions.

Abnormalities in cerebrospinal fluid seldom have been found in patients with ACA.

ACA 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 LB facilitates ACA development.

Further Inpatient Care:

Patients with ACA without concurrent extracutaneous disease do not require hospitalization.

Consider a possible concurrent infection.

Co-infections include babesiosis, ehrlichiosis, and tick-borne encephalitis.

About 10% of patients with Lyme disease in southern New England are co-infected with babesiosis, and about the same percentage in parts of the midwestern United States have human granulocytic ehrlichiosis.

Babesiosis can cause a persistent infection and coexist with ACA, unlike ehrlichiosis, which is usually a short-lived infection

Further Outpatient Care:

Assure patients in the early phase of ACA that the resolution of symptoms may occur gradually during several weeks or months after treatment.

Inform patients treated in the atrophic phase that the disease progression can be stopped, but the symptoms may be only partially reversible.

Follow-up care should be performed initially every 3-6 months and later once a year.

Physical examination for signs and symptoms of cutaneous and extracutaneous manifestations of LB is important.

Quantitative serologic tests show a lack of changes in IgG antibody titer or show it declining only to a certain extent in most patients with ACA after antibiotic therapy.

Despite the persistence of IgG antibody response in late LB (serologic scar) similar to that observed in syphilis cases, the authors do serologic follow-up testing according to the recommendation for late syphilis.

A sudden increase in antibody titer can point to the activation of infection and precede a clinical recurrence of the disease

peace love and light-kim

broke up longer paragraphs, bettyg, leader

Post edited by: Bettyg, at: 05/01/2012 11:31 PM

05/01/2012 08:37 AM
Posts: 1822
Senior Member

Blessings all-

An article on ACA and peripheral neuropathy...this article will give you a visual diagram of the locations of where the neuropathy occurs.


peace love and light-kim

emphasized, bettyg, leader

Post edited by: Bettyg, at: 05/01/2012 11:32 PM

05/01/2012 08:38 AM
Posts: 1822
Senior Member

Blessings all-

I have more information and articles, but will leave this with you all for now. Keep the awareness going, and keep searching for your own answers. God bless.

peace love and light-kim

Post edited by: fabajenna, at: 05/01/2012 08:39 AM

05/01/2012 10:24 AM
Posts: 436

Does this require separate treatment from lyme, or will it resolve once the lyme is under control?

05/01/2012 01:56 PM
Posts: 1455
Group Leader

Great info here Kim! Thank you!!

And yes, huge thanks to Bettyg for all of her hard and diligent work on this board. Smile Many people fit so many of their puzzle pieces together with your hard work.

Lots of love to you all!


05/01/2012 02:44 PM
doglickPosts: 682

Strangely, my hands and feet look very much like the pictures. Go figure.

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