Norwegian Scabies Infestation

Abstract: An 84-year-old elderly woman with 3 months history of pruritic skin eruption

History: The patient is an 84-year-old nursing home resident who presents for evaluation  of pruritic skin eruption for the past three months. She first noted pruritic lesions on her hands when she was in a hospital for a back surgery. Since then her skin was progressively worsening and the eruption spread to her face, arms, abdomen and legs. She notes she was getting thick scales in the involved areas. She has chronic back pain and has gone through several operations past 3 months. Her other medical history includes congestive heart failure, hypertension, and COPD. Due to pain and her recent skin eruption, she has been taking prednisone, hydromorphone, doxepin, and Ativan. She feels sedated and confused at times. The patient is with her daughter who had significant contact and similar symptoms.

Clinical photos:

O/E: The skin exam shows a somewhat sleepy, but oriented, elderly woman in a wheelchair with yellow to green thick scaly plaques on the hands, forearms, elbows,  face,  ears, abdomen and legs. Dermoscopic evaluation shows multiple triangle jet signs with burrows. Scraping prep with mineral oil showed multiple scabies mites. Photo shows a portion of a 10X field on which 11 mites were seen.

Diagnosis: Norwegian scabies

Questions: We'd appreciate your recommendations on this patient's care. 

Discussion: Crusted Norwegian scabies is an uncommon hyperkeratotic variant of scabies infestation. Norwegian scabies are known to be as opportunistic pathogens. Our patient has been under significant stress physically and emotionally due to recent back surgeries and her skin eruption has progressed under the eyes of a medical staff.  Her medications contributed to the development of Norwegian scabies by suppressing her immune response (prednisone) and blunting her itch perception (Dilaudid, doxepin and Ativan).  In a way, this was a perfect storm.   Due to severity of involvement, the patient will be treated with oral ivermectin 200 micrograms per kilogram weekly for 3 weeks and permethrin 5% cream weekly for 4 - 5 weeks. Her daughter and all close family members will be also treated with topical medication. The nursing home will be informed.  It is estimated that the mite load of patients with Norwegian scabies can be as high as 15 million which accounts for the  highly contagious nature of this variant.  All of the staff and residents of her nursing home should receive scabies treatment.

References:
1. Towersey L, Cunha MX, Feldman CA, et al. Dermoscopy of Norwegian scabies in a patient with acquired immunodeficiency syndrome. An Bras Dermatol. 2010;85(2):221-223

2. Problems in diagnosing scabies, a global disease in human and animal populations.

Walton SF, Currie BJ.  Clin Microbiol Rev. 2007 Apr;20(2):268-79.  Excellent review, available open access fulltext.

3. Reflectance confocal microscopy for quantification of Sarcoptes scabiei in Norwegian scabies. Cinotti E, Perrot JL, et. al J Eur Acad Dermatol Venereol. 2013 Feb;27(2):e176-8.  PubMed listing.

Complicated Speckled Lentiginous Nevus

Presented by Yoon Cohen, D.O.
Alta Dermatology
Mesa, Arizona

Abstract: An 8-year-old girl with large congenital nevus on the chin, the anterior neck and the right aspect of shoulder and the chest

History: The patient is an 8-year-old girl who was born with congenital nevi on the mid anterior neck and possibly another similar lesion over the right side of the mandible. Over the years, she has developed many 1-3 mm in diagmeter tan papules in and around the chin and submental region. She was seen recently for follow up. Her nevus is slowly maturing but still benign in appearance and there are no outlier lesions in the large defect. Some of the tumor is bilateral.

Clinical photo:

O/E: The skin examination shows a healthy, pleasant child with numerous scattered 1 to 3 mm brown macules and papules in a background of light tan pigmentation on the chin, the anterior neck and the right aspect of the upper chest. There is a well marginated 25 mm in diameter brown patch on the lower mid anterior neck. There is a 3.5 x 4.0 cm hypopigmented patch on the right shoulder

Diagnosis: Complicated Speckled Lentiginous Nevus (SLN)

Questions: Please share your experiences in managing patients with SLN similar conditions.  Do you feel there is a concern that this lesion may undergo malignant transformation.  What do you think of the hypopigmented area?

Discussion: A speckled lentiginous nevus (SLN, Nevus Spilus) can be a congenital or acquired pigmented lesion. More recently arguments are in favor of speckled lentiginous nevi as subtype of congenital nevi including the following observations: frequent presence at birth or noted soon therafter; patterns of distribution reflecting embryonic development; hamartomatous behavior with various types of nevi; and histologic features of congenital melanocytic nevi within the lesions. There are two types of speckled lentiginous nevus -- Nevus spilus maculosus and nevus spilus papulosus. The macular type is characterized by dark speckles that are completely flat and rather evenly distributed on a light brown background, resembling a polka-dot pattern. In contrast, nevus spilus papulosus is defined by dark papules that are of different sizes and rather unevenly distributed, reminiscent of a star map. Perhaps, the most pressing concern is its potential malignant transformation. The propensity to develop Spitz nevi appears to be the same in both types of speckled lentiginous nevus whereas the development of malignant melanoma has been reported far more commonly in nevus spilus maculosus. Torchia and her colleague argue that malignant transformation of melanocytes might occur in SNL not because the hyperpigmented background features any specific procarcinogenic abnormality but because there are more melanocytes with SNL, yielding a slightly higher likelihood of developing any type of melanomcytic lesion. It is our best interest that we monitor our patients with SNL pediodically to detect any early signs of malignant transformation.

References:
1. Happle R. Speckled lentiginous naevus: which of the two disorders do you mean? Clin Exp Dermatol. 2008;34:133-135
2. Paraskevas LR, Halpern AC, Marghoob AA. Utility of the Wood's light: five cases from a pigmented lesion clinic. Br J Dermatol. 2005 May; 152(5): 1039-44
3. Menon K. Dusza SW, Marghoob AA, et al. Classification and prevalence of pigmented lesions in patients with total body photographs at high risk of developing melanoma. J Cutan Med Surg. 2006 Mar-Apr; 10(2):85-91
4. Schaffer J. Orlow S, Lazova R, et al. Speckled Lentiginous Nevus Within the Spectrum of Congenital Melanocytic Nevi. Arch Dermatol. 2001; 137:172-78
5. Torchia D. Schachner L. Is speckled lentiginous nevus really prone to dysplasia/neoplasia? Pediatr Dermatol. 2012 Jul-Aug; 29(4):546-7

Comments:
1. Dr. Ashfaq Marghoob: 
These patients (SLN of maculosa type) are at slightly higher risk for developing MM. Continued surveillance for focal change is what I do for these patients.

2. Dr. Rudolph Happle:
Thank you very much for letting me see this interesting case! Apparently, this is a classical example of papular SLN (papular nevus spilus).  Why is your diagnosis "Complicated SLN"? I would call this a complicated case if a melanoma would develop, but the risk is rather low because It's not a macular nevus spilus.

3. Dr. Harper Price: 

Thank you for sharing this interesting case.  It does look very classic for a SLN.

The risk of malignant transformation is very low and likely starts at puberty so I would follow her yearly and if there was a lot of change, even more frequently and use photography to help.  These SLN can have many other nevi within in as stated, including Spitz and blue nevi.

Hers looks quite good and not worrisome.  The area of hypopigmentation, if new, may represent vitiligo or if present early on, a hypochromic nevis (“twin spotting”).

These SNL certainly carry a much lower risk than a typical congenital melanocytic nevus of this size for melanoma development. 
Lifelong follow-up is my recommendation

Hemorrhagic Blister

Abstract: A 58-year-old man with 2-day history of deep purple to black papule

History: A 58-year-old man presents for evaluation of a skin lesion on the right lower abdomen that has been present approximately 2 days. The patient does not remember having any trauma on that area. It seems the lesion appeared quite abruptly and the color has been darkened over past 2 days. No history of non-melanoma skin cancers or melanoma.

O/E: The skin exam shows a healthy and pleasant man with skin type III. There is a sharply demarcated 6 mm deep dark purple oval shaped papule on the right lower abdomen. It is somewhat compressible.

Clinical & Dermatoscopic Photos:

Polarized Dermatoscopic Photo

Non-Polarized Dermatoscopic Photo

Diagnosis: Hemorrhagic blister

Discussion: The lesion was lanced with an 11 blade. Blood product was drained and confirmed the diagnosis of hemorrhagic blister. Initially, the lesion did not obviously look as  a hemorrhagic blister. The dermatoscopic image did not show a typically appearing hemangioma. Our biggest concern was to make sure this is not a melanoma. Conventionally, melanoma would not appear in a 2-day period. A careful history led us to consider a hemorrahagic blister with a simple lancing. 

Reference:
1. Bullous malignant melanoma: an unusual differential diagnosis of a hemorrhagic friction blister.

Vogt T, Brunnberg S, Hohenleutner U, et al. Dermatol Surg. 2003 29(1): 102-4

Source

BACKGROUND:

A 66-year-old woman presented to our outpatient clinic with a 3 x 2.5-cm tense, hemorrhagic-appearing bulla on her forefoot. Histopathology and immunohistochemistry confirmed a transtumoral-transepidermal blister formation within an advanced acrolentiginous malignantmelanoma (MM).

OBJECTIVE:

To study bullous malignant melanoma.

METHODS:

Blistering in MMs represents a rare but clinically important pitfall in clinical differential diagnosis. The blisters are typically due to the disruption of the cohesion between neoplastic cells and keratinocytes, but physical friction may also contribute.

RESULTS:

Hemorrhagic blistering is, in many cases, a relatively insignificant finding in which frictional forces are imposed.

CONCLUSION:

The case reported here underscores that in rare cases MMs, particularly if acrally located, can be complicated by hemorrhagic blistering. Because of the life-threatening consequences, one should be aware of this rare differential diagnosis.

Rosacea-Like Demodeciasis

Abstract:  47 yo woman with ab 8 month history of a facial eruption
 

The patient is a 47 yo woman with a rosacea-like eruption for eight months.  Dr. Yoon Cohen suggested demodicosis and performed a scraping.  It was loaded with demodex mites.  We are considering this an example of rosacea-like demodexinfestation and treated the patient with ivermectin 250 microgram/kg x 2 a week apart and permethrin 5% cream 2 - 3 times a week. 

Photos:

 After one week:

Diagnosis:  Rosacea-like Demodeciasis (most probably)

Discussion: It seems that this acneiform eruption is due to Demodex, but we need more time to be certain. Since Samuel Ayers, Jr. described this entity in 1930 it has been in the literature but there are still doubters in the dermatologic community.

Reference:

1. Dermatol Online J. 2007 Oct 13;13(4):9.

Granulomatous rosacea-like demodicidosis. Free Full Text

Lee JY, Hsu CK.

Abstract

Demodicidosis may present as pityriasis folliculitis, papulopustular lesions, rosacea-like eruptions, and granulomatous rosacea-like eruptions. We report a case of demodex granuloma presenting with recurrent granulomatous rosacea-like papules on the face in a middle-aged woman. The diagnosis of demodicidosis was made by finding extrafollicular mites in the perifollicular inflammatory infiltrate. The papules resolved after 3 weeks of systemic and topical metronidazole, and low-dose oral prednisolone therapy. In summary, demodex granuloma may be mistaken for granulomatous rosacea-like papules. Correct diagnosis can be facilitated by finding extrafollicular demodex mites in skin biopsy specimens.

2.  Cutis. 2007 Aug;80(2):149-51.

Recalcitrant papulopustular rosacea in an immunocompetent patient responding to combination therapy with oral ivermectin and topical permethrin.  Full Text PDF

Allen KJ, Davis CL, Billings SD, Mousdicas N.

Abstract

A 68-year-old healthy man presented with papulopustular rosacea (PPR) recalcitrant to multiple therapies, including permethrin cream 5%. Histologic examination detected the presence of chronic folliculitis and numerous Demodex organisms. A diagnosis of rosacealike demodicidosis was rendered, and the patient was treated with oral ivermectin and permethrin cream 5%, resulting in resolution of the folliculitis. Demodex infestation should be considered in any patient with rosacealike dermatitis resistant to conventional rosacea therapies. If infestation is demonstrated in these patients, oral ivermectin in combination with topical permethrin is a safe and effective therapeutic option.

Follicular Mucinosis?

Abstract: 80 yo man with intensely pruritic papules face and neck for 2 months

HPI:  This 80 yo man has a 2 month history of 2 – 3 mm erythematous papules, mostly on face and neck. These are few in number.  A trial cobetasol ointment was without relief.  His medications are: amlodipine, HCTZ, metroprolol, Vytorin (ezetimibe and eimvastatin), Pantoprazole.  He is in good general health.

ClinicalPhotos: These show how subtle the lesions are.

Because of symptoms a Biopsy was done.

Histopath shows: focal erosion and ulceration and ectatic blood vessels.  There is a moderate to dense superficial and deep perivascular perifollicular lymphohistiocytic infiltrate with numerous eosinophils, marked mucin deposition and conspicuous disruption of the follicular epitheliumThe pathologic diagnosis includes, “infectious etiology,” eosinophilic folliculitis, and follicular mucinosis.

Diagnosis:  Acneiform Follicular Mucinosis might be the best fit.

Reference:

Chronic Ulcers

Presented by Yoon Cohen, D.O.
Alta Dermatology Residency
Mesa Arizona

Abstract: 66-year-old woman with 3 year history of leg ulcers

HPI: The patient is a 66-year-old retired elementary school teacher who was seen for evaluation of chronic leg ulcers. The most recent injury was sustained on her right lower leg when she bumped into her grandson’s toy.  This  eventually caused a new leg ulcer. Subsequently, she was hospitalized, and seen and evaluated by the Plastics Wound Clinic at a major hospital center. The patient presented for continuity care after discharge from the hospital.  Her chronic leg ulcers started in 2011 when she had a cat scratch on the right foot which resulted in cellulitis and ulcer on the right leg. After that episode, she noticed the development of ulcers whenever she gets even minor injury to her legs. She has a long history of rheumatoid arthritis that she has been on multiple treatments including prednisone, methotrexate and Remicade. Her current medications include prednisone 5mg daily, methotrexate 20mg weekly with folic acid, Celebrex 200mg bid, and oxycontin 50mg daily.

O/E: The skin exam shows a pleasant, somewhat depressed woman with several various seized leg ulcers with healthy granulation tissues at base on the lower legs.
A) R lateral calf: fibrinous base, 3.3 cm x 1.3 cm
B) L dorsal foot: Fibrinous base, 1.8 cm x 1.0 cm
C) L lateral calf: Fibrinous base, 2.5 cm x 1.6 cm
D) L medial calf: Clean granulation tissue at base, 5.0 cm x 4.8 cm x 0.5 cm
Pedal pulses 1+ and 2+ pitting edema bilaterally

Clinical Photos:

Hospital Courses:
1. Diagnosis: Her chronic ulcers were considered to be multifactorial. Likely contributors include trauma, infection, rheumatoid arthritis, venous insufficiency, ulceration from methotrexate toxicity.
2. Procedures: Debridement and Kenalog injection(10mg/cc) to the left medial calf
3. Diagnostic Studies: Wound culture (pending)
4. Dressings: Acticoat 7 for lesions A and D, and then continue hydrofera blue to lesions A and D. Santyl, adaptic, gauze, kerlex for lesions B and C.
5. Compression: Soft cotton between the skin and the SurePress; will try penumoboots for home and leg elevation.

Discussion: The possible etiologies can be trauma, rheumatoid arthritis, venous insufficiency, infection, or prolonged use of methotrexate or Remicade. There are 9 reports of ulcerations from methotrexate and 1 report of ulcerations  of foot from Remicade (infliximab) according to Litt’s DERM Drug Eruptions & Reactions Manual. There are two major questions. What is (are) causing these ulcerations which occur with even minor injuries? Could it be methotrexate toxicity? Could this be a variant form of pyoderma gangrenosum related to RA? She does not heal well even in other locations of her body. It seems to be more than just venous insufficiency. Lastly, how can we help heal these ulcers? 

Questions: 
What are your thoughts regarding the etiology of this woman's leg ulcers? 
How would you manage her to facilitate healing?
Do you think her medications play a role?  or her rheumatoid arthritis?

References:
1. Ben-Amitai D, Hodak E, David M. Cutaneous ulceration: an unusual sign of methotrexate toxicity - first report in a patient without psoriasis. Ann Pharmacother. 1998; 32 (6): 651-3
Abstract
Objective: To describe a case of skin ulcer related to methotrexate toxicity
Case Summary: A 67-year-old white man with seronegative arthralgia developed recurrent skin ulcer concurrent with 3-year treatment with methotrexate 5 mg daily. The skin ulcer resolved on discontinuation of methotrexate
Discussion: To the best of our knowledge, this is the first reported case of skin ulcer believed to be induced by methotrexate in a patient without psoriasis
Conclusions: Skin ulceration should be added to the list of possible toxic adverse effects of methotrexate, not only in psoriatic patients but also in those without psoriasis.

2. Stolman LP, Rosenthal D, Yaworsky R, et al. Pyoderma Gangrenosum and rheumatoid arthritis. Arch Dermatol. 1975; 111(8): 1020-3. 
Abstract
Two patients had pyoderma gangrenosum and rheumatoid arthritis. Biopsy specimens of the cutaneous ulcers in the paitents showed a necrotizing vasculitis. Complement (C3) and immunoglobulines were not detected in the skin lesions. There was no important impairment of cell-mediated immunity observed.

3. Seitz CS, Berens N, Brocker EB, et al. Leg ulceration in rheumatoid arthritis -- an underreported multicausal complication with considerable morbidity: analysis of thrity-six patients and review of the literature. Dermatology. 2010; 220 (3): 268-73
CONCLUSIONS: The majority of leg ulcers in patients with RA are due to underlying venous/arterial malfunction while vasculitic or traumatic ulcers are less common. Additionally, we identified a relevant subgroup of patients with 'inactivity ulcers' due to impaired mobility and consecutive lymphedema. Morphology and localization of ulcerations as well as duplex sonography provide the most important clues for accurate diagnosis, ensuring adequate treatment.

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A potentially lethal disease

presented by Dr Henry Foong
Ipoh, Malaysia

Abstract:  19 yo man with skin lesions and gastro-intestinal infarcts

History: A 19 yr old student presented with multiple discrete mildly pruritic papules on the trunk and thighs of 9 months duration.  It started as papules on the trunk that become enlarged resulting a central depression.  2 months ago, he had severe abdominal pain,  underwent emergency laparotomy and was told he had a "perforated appendix".  The surgeon noted several shallow ulcers on the large and small intestines.  He was worried about typhoid but serology was negative.  

Exam:  Multiple discrete papules/plaques 3-6 mm diameter with a central porcelain white atrophied depression and a raised border on the trunk and thighs.  There was a rim of telangiectasia on the periphery in some of the lesions. No purpura was noted.

Clinical Photos:

Pathology: A skin biopsy was performed.  Biopsy showed an atrophied epidermis with evidence of arteritis in the deeper dermis.  (see below)

Lab: His blood counts and biochemistry was unremarkable.

Diagnosis:  Degos disease (Malignant atrophic papulosis) appears most likely.  Could this some form of cutaneous lymphoma?

Questions:  Have any of our readers seen and treated similar patients? There are only around 200 cases of Degos Disease reported in the literature.  Treatment is difficult and often ineffective.  Aspirin and dipyridamole has been tried to reduce the complications of vessel thrombosis.  Some cases has been associated with connective tissue disease but by and large those with gastrointestinal complications have poor prognosis. IV immunoglobulins and eculizumab has been tried with some success.

Cost Considerations:  
In the U.S.: 
Eculizumab is ~$7000 per dose at low end

A four dose course of IVIG for a 70 kg person at 2 g/kg would cost $25 000-$26 000. Or ~ $21,000 for a 60 kg person. 

While these drugs may be 40% cheaper in Malaysia can your patient's family afford a trial or does the government pick up the cost?

References:
1. Cynthia M. Magro, MD, Jonathan C. Poe, PhD,et. al.  A C5b-9/Interferon-α–Mediated Endotheliopathy Syndrome.  Am J Clin Pathol 2011;135:599-610

2. Scheinfeld N. Commentary on 'Degos disease: a C5b-9/interferon-α-mediated endotheliopathy syndrome' by Magro et al: a reconsideration of Degos disease as hematologic or endothelial genetic disease.  Dermatol Online J. 2011 Aug 15;17(8):6. Excellent discussion and available Free Full Text 

3. Zhu KJ, et al. The use of intravenous immunoglobulin in cutaneous and recurrent perforating intestinal Degos disease (malignant atrophic papulosis) Br J Dermatol. 2007 Jul;157(1):206-7.

Histopath demonstrates an atrophied epidermis with evidence of arteritis in the deeper dermis.

Innoculation Eschar

Abstract: 6 yo  boy with one month history of an eschar on the neck

History:  This six year old boy has had an indurated nodule on the left posterior nuchal area for around a month.  He is a high functioning patient on the autism spectrum.  No history of antecedent trauma or envenomation is available.  He is well otherwise with no complaints of constitutional symptoms or headache.

O/E:  1 cm escharotic lesion left posterior neck.  Surrounding area is indurated.  No other cutaneous findings.

Clinical Photo:

photo courtesy of Yoon Cohen, D.O.

Labs:  A wound culture was obtained.

The eschar was sharply dissected.  We attempted to anesthetize the area for an incisional biopsy but patient was not compliant.

Discussion:  The patient lives in an endemic area for Lyme disease.  There are many ticks in the environment.  The wound may represent a reaction to a tick bite.  The differential diagnosis in patients with similar eschars includes rickettsial infections, cutaneous anthrax, tularaemia, necrotic arachnidism (brown recluse spider bite), scrub typhus (Orientia tsutsugamushi), rat bite fever (Spirillum minus), staphylococcal or streptococcal ecthyma, and Lyme disease.

Diagnosis:  Considering where this patient lives, the most likely diagnosis is tick bite reaction.

References:
1.  Tick-borne lymphadenopathy (TIBOLA) acquired in Southwestern Germany Free Full Text

Siegbert Rieg1 et. al  siegbert.rieg@uniklinik-freiburg.de

BMC Infectious Diseases 2011, 11:167 doi:10.1186/1471-2334-11-167

2.  African tick-bite fever: a new entity in the differential diagnosis of multiple eschars in travelers. Description of five cases imported from South Africa to Switzerland.

Althaus F, Greub G, Raoult D, Genton B.  Int J Infect Dis. 2010 Sep;14 Suppl 3:e274-6. doi: 10.1016/j.ijid.2009.11.021. Epub 2010 Mar 15.

Abstract:  African tick-bite fever (ATBF) is a newly described spotted fever rickettsiosis that frequently presents with multiple eschars in travelers returning from sub-Saharan Africa and, to a lesser extent, from the West Indies. It is caused by the bite of an infected Amblyomma tick, whose hunting habits explain the typical presence of multiple inoculation skin lesions and the occurrence of clustered cases. The etiological agent of ATBF is Rickettsia africae, an emerging tick-borne pathogenic bacterium. We describe herein a cluster of five cases of ATBF occurring in Swiss travelers returning from South Africa. The co-incidental infections in these five patients and the presence of multiple inoculation eschars, two features pathognomonic of this rickettsial disease, suggested the diagnosis of ATBF. Indeed, the presence of at least one inoculation eschar is observed in 53-100% of cases and multiple eschars in 21-54%. Two patients presented regional lymphadenitis and one a mild local lymphangitis. Though a cutaneous rash is described in 15-46% of cases, no rash was observed in our series. ATBF was confirmed by serology. Thus, ATBF has recently emerged as one of the most important causes of flu-like illness in travelers returning from Southern Africa. The presence of one or multiple eschars of inoculation is an important clinical clue to the diagnosis. It can be confirmed by serology or by PCR of a biopsy of the eschar. Culture can also be done in reference laboratories. Dermatologists and primary care physicians should know this clinical entity, since an inexpensive and efficient treatment is available.

3.  Histologic features and immunodetection of African tick-bite fever eschar. Free Full Text

Lepidi H, Fournier PE, Raoult D.    Emerg Infect Dis. 2006 Sep;12(9):1332-7.

African tick-bite fever (ATBF) is a rickettsiosis caused by Rickettsia africae. We describe histologic features and immunodetection of R. africae in cutaneous inoculation eschars from 8 patients with ATBF, which was diagnosed by culture or association of positive PCR detection and positive serologic results. We used quantitative image analysis to compare the pattern of inflammation of these eschars with those from Mediterranean spotted fever. We evaluated the diagnostic value of immunohistochemical techniques by using a monoclonal antibody to R. africae. ATBF eschars were histologically characterized by inflammation of vessels composed mainly of significantly more polymorphonuclear leukocytes than are found in cases of Mediterranean spotted fever (p < 0.05). Small amounts R. africae antigens were demonstrated by immunohistochemical examination in 6 of 8 patients with ATBF. Neutrophils in ATBF are a notable component of the host reaction, perhaps because ATBF is a milder disease than the other rickettsioses. Immunohistochemical detection of rickettsial antigens may be useful in diagnosing ATBF.

4. The Expanding Spectrum of Eschar-Associated Rickettsioses in the United States Free Full Text

W. Chad Cragun, MD; Brenda L. Bartlett, MD; Michael W. Ellis, MD; Aaron Z. Hoover, MD; Stephen K. Tyring, MD, PhD, MBA; Natalia Mendoza, MD; Todd J. Vento, MD, MPH; William L. Nicholson, PhD, MS; Marina E. Eremeeva, MD, PhD; Juan P. Olano, MD; Ronald P. Rapini, MD; Christopher D. Paddock, MD, MPHTM

Arch Dermatol. 2010;146(6):641-648. doi:10.1001/archdermatol.2010.48.

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