Skin Disorders and Lyme
Skin Disorders that may be associated with Lyme disease include:
Acrodermatitis Chronica Atrophicans (ACA) see below for more
Pityriasis Rosea (click on link for abstracts)
Acrodermatitis Chronica Atrophicans (ACA) see below for more
Pityriasis Rosea (click on link for abstracts)
From Dr Ray Charles Jones site: (Follow link for Pictures)
Chronic Lyme Disease- Rashes & Manifestations
"Acrodermatitis chronica atrophicans (ACA) represents the persistent late stage of borreliosis in which Borrelia species may survive for decades. Occasionally, B-cell lymphoma may develop and additional neoplastic complications such as basal cell carcinoma or squamous cell carcinoma (SCC) have been reported along with ACA. Patients with ACA manifestations can also experience acral pain, paresthesia, dysesthesia, cognitive dysfunction, peripheral neuropathy, lymphadenopathy, musculoskeletal pains, destruction of small joints, atrophy of the epidermis, morphea, lichen sclerosus atrophicus, facial edema, paresis of the brachial plexus and fibrotic nodules or bands (most often elbows and knees). Edema with or without a bluish discoloration of the skin may occur. Chronically ill Lyme patients have been misdiagnosed with scleroderma, livedo, venous insufficiency, Reynaud’s syndrome, edema or an ongoing aging process.
Acrodermatitis Chronica Atrophicans Bozena Chodynicka, MD; Chief Editor: Dirk M Elston MD. Medscape http://emedicine.medscape.com/article/1051695-overview#aw2aab6b2b2
Pathophysiology and Etiology:
B afzelii is the predominant etiologic agent of ACA but may not be the sole cause. Borrelia garinii, another genospecies of the Borrelia burgdorferi sensu lato (“in the broad sense”) complex, has also been detected in this setting.
ACA is the only form of Lyme borreliosis 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 the following factors:
* Resistance of the pathogen to the complement system
* The pathogen’s ability to escape to immunologically protected sites (eg, endothelial cells, fibroblasts)
* The pathogen’s 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 characterized by downregulation of major histocompatibility system (MHC) class II molecules on Langerhans cells, has been observed in patients with Lyme borreliosis.
A restricted pattern of cytokine expression in ACA, including 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 also has not been clarified. Perhaps periarticular regions are favored sites because of reduced acral skin temperatures or reduced oxygen pressure.
Lack of adequate or appropriate treatment of early Lyme borreliosis facilitates the development of ACA.
For further information from this Medscape article click on this link
Pathophysiology and Etiology:
B afzelii is the predominant etiologic agent of ACA but may not be the sole cause. Borrelia garinii, another genospecies of the Borrelia burgdorferi sensu lato (“in the broad sense”) complex, has also been detected in this setting.
ACA is the only form of Lyme borreliosis 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 the following factors:
* Resistance of the pathogen to the complement system
* The pathogen’s ability to escape to immunologically protected sites (eg, endothelial cells, fibroblasts)
* The pathogen’s 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 characterized by downregulation of major histocompatibility system (MHC) class II molecules on Langerhans cells, has been observed in patients with Lyme borreliosis.
A restricted pattern of cytokine expression in ACA, including 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 also has not been clarified. Perhaps periarticular regions are favored sites because of reduced acral skin temperatures or reduced oxygen pressure.
Lack of adequate or appropriate treatment of early Lyme borreliosis facilitates the development of ACA.
For further information from this Medscape article click on this link
Extra References / Readings - Thanks to Medline
Bhate C, Schwartz RA. Lyme disease: Part I. Advances and perspectives. J Am Acad Dermatol. Apr 2011;64(4):619-36; quiz 637-8. [Medline].
Bhate C, Schwartz RA. Lyme disease: Part II. Management and prevention. J Am Acad Dermatol. Apr 2011;64(4):639-53; quiz 654, 653. [Medline].
Buchwald A. Ein Fall von diffuser idiopathischer Haut-Atrophie. Vrtljschr Derm. 1883;10:553-6.
Herxheimer K, Hartmann K. Ueber Acrodermatitis chronica atrophicans. Arch f Dermatol u Syph (Wien). 1902;61:57-76.
Smetanick MT, Zellis SL, Ermolovich T. Acrodermatitis chronica atrophicans: a case report and review of the literature. Cutis. May 2010;85(5):247-52.
[Medline].
Aberer E. Country report - Austria. Report of WHO Workshop on Lyme Borreliosis Diagnosis and Surveillance, Warsaw. Warsaw, Poland: World Health Organization; 1995.
Christova I, Komitova R. Clinical and epidemiological features of Lyme borreliosis in Bulgaria. Wien Klin Wochenschr. Jan 31 2004;116(1-2):42-6. [Medline].
Flisiak I, Schwartz RA, Chodynicka B. Clinical features and specific immunological response to Borrelia afzelii in patients with acrodermatitis
chronica atrophicans. J Med. 1999;30(3-4):267-78. [Medline].
Zalaudek I, Leinweber B, Kerl H, Mullegger RR. Acrodermatitis chronica atrophicans in a 15-year-old girl misdiagnosed as venous insufficiency for 6
years. J Am Acad Dermatol. 2005;52:1091-4. [Medline].
Andres C, Ziai M, Bruckbauer H, Ring J, Hofmann H. Acrodermatitis chronica atrophicans in two children. Int J Dermatol. Feb 2010;49(2):180-3. [Medline].
Leverkus M, Finner AM, Pokrywka A, Franke I, Gollnick H. Metastatic squamous cell carcinoma of the ankle in long-standing untreated acrodermatitis chronica atrophicans. Dermatology. 2008;217(3):215-8. [Medline].
Danz B, Kreft B, Radant K, Marsch WCh, Fiedler E. Skin-coloured facial oedema as an initial manifestation of acrodermatitis chronica atrophicans. J Eur
Acad Dermatol Venereol. Jun 2008;22(6):751-3. [Medline].
Mullegger RR, Glatz M. Skin manifestations of lyme borreliosis: diagnosis and management. Am J Clin Dermatol. 2008;9(6):355-68. [Medline].
Maraspin V, Ogrinc K, Ružic-Sabljic E, Lotric-Furlan S, Strle F. Isolation of Borrelia burgdorferi sensu lato from blood of adult patients with borrelial lymphocytoma, Lyme neuroborreliosis, Lyme arthritis and acrodermatitis chronica atrophicans. Infection. Feb 2011;39(1):35-40. [Medline].
Bhate C, Schwartz RA. Lyme disease: Part I. Advances and perspectives. J Am Acad Dermatol. Apr 2011;64(4):619-36; quiz 637-8. [Medline].
Bhate C, Schwartz RA. Lyme disease: Part II. Management and prevention. J Am Acad Dermatol. Apr 2011;64(4):639-53; quiz 654, 653. [Medline].
Buchwald A. Ein Fall von diffuser idiopathischer Haut-Atrophie. Vrtljschr Derm. 1883;10:553-6.
Herxheimer K, Hartmann K. Ueber Acrodermatitis chronica atrophicans. Arch f Dermatol u Syph (Wien). 1902;61:57-76.
Smetanick MT, Zellis SL, Ermolovich T. Acrodermatitis chronica atrophicans: a case report and review of the literature. Cutis. May 2010;85(5):247-52.
[Medline].
Aberer E. Country report - Austria. Report of WHO Workshop on Lyme Borreliosis Diagnosis and Surveillance, Warsaw. Warsaw, Poland: World Health Organization; 1995.
Christova I, Komitova R. Clinical and epidemiological features of Lyme borreliosis in Bulgaria. Wien Klin Wochenschr. Jan 31 2004;116(1-2):42-6. [Medline].
Flisiak I, Schwartz RA, Chodynicka B. Clinical features and specific immunological response to Borrelia afzelii in patients with acrodermatitis
chronica atrophicans. J Med. 1999;30(3-4):267-78. [Medline].
Zalaudek I, Leinweber B, Kerl H, Mullegger RR. Acrodermatitis chronica atrophicans in a 15-year-old girl misdiagnosed as venous insufficiency for 6
years. J Am Acad Dermatol. 2005;52:1091-4. [Medline].
Andres C, Ziai M, Bruckbauer H, Ring J, Hofmann H. Acrodermatitis chronica atrophicans in two children. Int J Dermatol. Feb 2010;49(2):180-3. [Medline].
Leverkus M, Finner AM, Pokrywka A, Franke I, Gollnick H. Metastatic squamous cell carcinoma of the ankle in long-standing untreated acrodermatitis chronica atrophicans. Dermatology. 2008;217(3):215-8. [Medline].
Danz B, Kreft B, Radant K, Marsch WCh, Fiedler E. Skin-coloured facial oedema as an initial manifestation of acrodermatitis chronica atrophicans. J Eur
Acad Dermatol Venereol. Jun 2008;22(6):751-3. [Medline].
Mullegger RR, Glatz M. Skin manifestations of lyme borreliosis: diagnosis and management. Am J Clin Dermatol. 2008;9(6):355-68. [Medline].
Maraspin V, Ogrinc K, Ružic-Sabljic E, Lotric-Furlan S, Strle F. Isolation of Borrelia burgdorferi sensu lato from blood of adult patients with borrelial lymphocytoma, Lyme neuroborreliosis, Lyme arthritis and acrodermatitis chronica atrophicans. Infection. Feb 2011;39(1):35-40. [Medline].
