Morgellons Disease: A Chemical and Light Microscopic Study
Research Article Open Access
Morgellons Disease: A Chemical and Light Microscopic Study
Marianne J. Middelveen1, Elizabeth H. Rasmussen2, Douglas G. Kahn3 and Raphael B. Stricker1*
1International Lyme and Associated Diseases Society, Bethesda, MD
2College of Health Sciences, University of Wyoming, Laramie, WY
3Department of Pathology, Olive View - UCLA Medical Center, Sylmar, California
Raphael B. Stricker, MD
450 Sutter Street, Suite 1504
San Francisco, CA 94108, USA
Fax: (415) 399-1057
Received date: January 27, 2012; Accepted date: March 12, 2012; Published date: March 16, 2012
Citation: Middelveen MJ, Rasmussen EH, Kahn DG, Stricker RB (2012) Morgellons Disease: A Chemical and Light Microscopic Study. J Clin Exp Dermatol Res 3:140. doi: 10.4172/2155-9554.1000140
Copyright: © 2012 Middelveen MJ, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Morgellons disease is an emerging multisystem illness characterized by unexplained dermopathy and unusual skin- associated filament production. Despite evidence demonstrating that an infectious process is involved and that lesions are not self-inflicted, many medical practitioners continue to claim that this illness is delusional. We present relevant clinical observations combined with chemical and light microscopic studies of material collected from three patients with Morgellons disease. Our study demonstrates that Morgellons disease is not delusional and that skin lesions with unusual fibers are not self-inflicted or psychogenic. We provide chemical, light microscopic and immunohistological evidence that filaments associated with this condition originate from human epithelial cells, supporting the hypothesis that the fibers are composed of keratin and are products of keratinocytes.
Morgellons disease; Digital dermatitis; Lyme disease; Borrelia burgdorferi; Spirochetes; Keratin
Morgellons disease (MD) is an emerging dermatological disorder and multisystem illness. The disease is characterized by unexplained dermopathy associated with formation of unusual filaments found both subcutaneously and emerging from spontaneously appearing, slow-healing skin lesions . Filaments associated with MD appear beneath unbroken skin [1,2], thus demonstrating that they are not self-implanted. Filaments have been observed protruding from and attached to a matrix of epithelial cells . This finding demonstrates that the filaments are of human cellular origin and are not textile fibers. These filaments have not been matched with known textile fibers, and dye-extracting solvents have failed to release coloration; the fibers are also very strong and heat resistant [4,5]. MD filaments are physically and chemically consistent with keratin, a biofiber produced in the epithelium by keratinocytes. A recent report from the Centers for Disease Control and Prevention (CDC) confirmed that these filaments have a protein composition that is consistent with keratin .
Lyme disease-like symptoms in MD such as neurological disorders and joint pain are evidence of systemic involvement [1,2,7] . Objective clinical evidence of disease has been demonstrated by its association with peripheral neuropathy, delayed capillary refill, decreased body temperature, tachycardia, elevated pro-inflammatory markers, cytokine release, selective immune deficiency and elevated insulin levels, suggesting that an infectious process is involved [8,9]. Patients may demonstrate abnormal laboratory findings indicative of low-grade anemia, endocrine dysfunction, immune dysfunction and inflammation [8,10]. Patients with MD are predominantly seroreactive to Borrelia burgdorferi (Bb) antigens, suggesting a likelihood of Lyme borreliosis or related spirochetal infection [1,10]. Patients also demonstrate a higher than expected percentage of positive laboratory findings for other tick-borne diseases, suggesting the possible involvement of coinfecting pathogens .
The observation of unusual filaments forming in lesions is not unique to humans afflicted with MD. Similarities between MD and bovine digital dermatitis (BDD) have been described . BDD is an emerging disease afflicting cattle and is characteristically associated with unusual filament formation in skin above the hooves . Latestage proliferative lesions demonstrate elongation of keratinocytes, hyperkeratosis, and proliferation of long keratin filaments [12-14]. Consistent detection of spirochetes associated with lesions is evidence of spirochetal etiologic involvement [15-20]. Experimental induction of lesions with tissue homogenates  and pure cultured treponemes  supports a role for spirochetes as primary etiologic agents.
Like BDD, MD is associated with apparent spirochetal infection and unusual filament production . A comparison between BDD and MD suggests that the unusual fibers seen in MD patients may result from hyperkeratosis and filament production as described in BDD. It appears that MD fibers are likewise composed of keratin produced by keratinocytes, a phenomenon that has been demonstrated in BDD . The following three case studies provide further evidence supporting this hypothesis.
Materials and Methods
Human and bovine samples
Three patients meeting the clinical criteria for Morgellons disease collected calluses, scabs, filaments, and other dermatological debris and submitted the material for microscopic examination. The collected samples were examined by bright-field microscopy at 100x magnification. Specimens were illuminated either superior or posterior to the specimen. Some specimens were also illuminated with ultraviolet (UV) light.
Biopsies from cattle with BDD were kindly provided by Dr. Dorte Dopfer, Faculty of Veterinary Medicine, University of Wisconsin, Madison, WI. Biopsy material from proliferative late stage BDD was examined for comparison to MD samples with 8x magnification under a dissecting microscope. This material was also tested for fluorescence under UV light.
For the chemical experiments, samples of normal hair, filaments from Cases 1 and 2 and BDD fibers were studied for reactivity to three caustic agents: sodium hypochlorite 12%, sodium hydroxide 10%, and potassium hydroxide 10%. Each sample was suspended in 150 μl of the chemical solution for up to two hours, and serial light microscopy was performed at 0, 1, 10, 30, 60 and 120 minutes. Dissolution of fibers was assessed by fraying, loss of shape and/or disintegration at each timepoint.
For the immunohistological experiments, filament samples from Cases 1 and 2 were stained for keratin using monoclonal antibodies. Briefly, formalin-fixed paraffin-embedded filaments were incubated with monoclonal antibodies AE1/AE3 (Dako North America Inc, Carpinteria, CA) and AE5/AE6 (Cell Marque Corporation, Rocklin, CA) directed against cytokeratins 1/3 and 5/6, respectively, using the Envision® + Dual-Link System-HRP (Dako) according to the manufacturer’s instructions. The samples were stained using a horseradish peroxidase label, and the brown staining of keratin was visualized under light microscopy.
The patient is a 72-year-old grandmother and former fashion model who developed painful lesions on her hands while working in her garden in San Antonio, Texas, in 1994. The lesions were punctate with ragged edges and healed slowly, leaving visible scarring. Fibers were observed in the lesions and under intact skin on her hands using a 60x handheld microscope. Topical steroids had no effect. The patient also noted the onset of fatigue, joint pain and muscle aches, and systemic steroid treatment exacerbated these symptoms without any improvement in the skin lesions. Medical evaluation was negative for autoimmune or infectious diseases, and neuropsychiatric evaluation was entirely normal. Biopsy of a lesion demonstrated hyperkeratosis and parakeratosis with no visible organisms or evidence of vasculitis. However “textile fibers” were noted in the dermal layer of the biopsy specimen.
In 2001, after numerous visits to dermatologists and other medical specialists and treatment with topical emollients and antiinflammatory medications, the patient had persistent skin lesions on her hands, fatigue and musculoskeletal pain. Despite the use of gloves to avoid scratching, her lesions persisted and she was unable to work in her garden or hold her grandchildren due to pain in her hands and joints. She recalled numerous tickbites but never saw an erythema migrans (EM) rash, and she was found to have positive testing for B. burgdorferi, Babesia microti and Bartonella henselae. She was treated with antimicrobial medications and her fatigue and musculoskeletal pain improved significantly. However her skin lesions persisted. She received anti-parasitic medication, and the lesions improved to the point that she could once again do gardening. The lesions persist but are “manageable” (Figure 1A).
Figure 1A: Lesions on hands of Case 1 following extensive antimicrobial treatment. Note erythematous base with ragged edges.
The patient is a 49-year-old registered nurse who had numerous tickbites while hiking, camping and horseback riding in Missouri, Texas and Northern California over more than a decade. She never saw an EM rash. In 1997 while living in San Francisco she developed painful lesions on her face, trunk and extremities. The lesions were punctate with ragged edges. Some lesions healed slowly, leaving visible scarring, while others did not heal at all, and fibers that were resistant to extraction were observed within several lesions. Fibers were also observed under intact skin using a 60x handheld microscope. Topical steroids had no effect. Biopsy of a lesion on her leg revealed hyperkeratosis and parakeratosis without evidence of infection or vasculitis. However, “textile fibers” were noted in the dermal layer of the biopsy specimen. She also developed fatigue and musculoskeletal pain, and systemic steroid treatment exacerbated these symptoms without any improvement in the skin lesions. Medical evaluation was negative for autoimmune or infectious diseases, and neuropsychiatric evaluation was completely normal.
Because of persistent fatigue, musculoskeletal pain and her history of tick exposure, the patient was evaluated for Lyme disease in 2004 and had positive testing for B. burgdorferi and Ehrlichia chafeensis. Antibiotic therapy led to improvement in the fatigue and musculoskeletal pain, but the skin lesions persisted. She received antiparasitic medication and her skin lesions improved somewhat, but new lesions appeared and healing lesions caused painful scarring. She has received intermittent courses of antibiotics over the past six years, and her skin lesions continue to wax and wane (Figure 1B).
Figure 1B: Lesions on back of Case 2. Note punctate appearance of open lesions and scarred appearance after healing. Lesions occur in locations that could not be easily reached by the patient.
The patient is a 47-year-old business manager who was in excellent health until he developed a “bullseye” rash, fever, chills, severe headache, musculoskeletal pain and malaise after hiking in the woods near Atlanta, Georgia, in 1995. He had pulled ticks off his dog, which also became ill at the same time. He was diagnosed with fibromyalgia and treated with pain medications, but by 2000 he had become progressively disabled by muscle pain and fatigue. In 2002 he developed crawling sensations on his head, face, groin and other body areas where there was hair. The sensations were accompanied by painful skin lesions. He was diagnosed with folliculitis and put on a topical antibiotic, which made his skin symptoms worse. He began to notice painful fibers coming out of the skin on his face, head and other hirsute areas, and he could not sleep because the fibers were so painful. He extracted fibers from his facial lesions, but new ones appeared. He was diagnosed with trichotillomania and delusional parasitosis.
He went to several dermatologists and was treated with topical lindane and oral cephalexin without benefit. Treatment with oral ketoconazole and fluconazole provided marginal improvement in the crawling sensations and skin lesions. A scalp biopsy demonstrated increased numbers of catagen and telogen follicles with fragmented hair fibers and inner root sheath consistent with trichotillomania. There were no visible organisms or evidence of vasculitis. Medical evaluation was negative for autoimmune or infectious diseases, and neuropsychiatric evaluation revealed reactive depression. He was treated with antidepressants without benefit. Finally in 2005 a physician noted fibers under his skin using a 60x hand-held microscope. Testing for Lyme disease was indeterminate in 2006, and treatment with doxycycline was given for one month without benefit. The patient continues to suffer from crawling sensations, skin lesions, musculoskeletal pain, disabling fatigue and depression. He is reluctant to see any more physicians about his skin condition (Figure 1C).
Figure 1C: Head of Case 3 photographed at disease onset in 2002 (top) and during disease flare in 2011 (bottom). Note punctate lesions with ragged edges in bottom picture. Patient shaved his head in effort to decrease pain from scalp lesions.
MD Microscopic observations
Case 1: Microscopic examination revealed a wide range of filaments in various stages of formation ranging from early stages that demonstrated either single or clusters of hyaline, tentacle-like projections with tapered ends (tentacle diameter approximately 5 μm) to macroscopic masses or mats of tangled fibers (approximately 1 mm diameter) (Figures 2A-2H). Floral-like formations of early-stage filaments were observed in some samples that were collected on different dates and years (Figure 2A). These structures had tapered ends with bases originating at a central point and were found in groups anchored to a dried dermal matrix. The reverse side of some of these specimens revealed a layer of pavement epithelial cells (Figure 2B). Epithelial matrices anchoring longer hyaline fibers were observed, suggesting that as the tentacle-like projections increase in length individual fibers may become tangled, or clumped (Figure 2C). Various structures composed of clumps, strings, and nest-like balls of hyaline filaments were observed and some of these were glued together by clotted or dried exudate (Figure 2D). This suggests that tangled filaments may eventually separate from the supporting epithelial matrix and form balls and other tangled structures.
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