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Home » Dermatology » Dermatology Clinics


RASH ON FACE, TRUNK, AND EXTREMITIES

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SLIDESHOW

1 / 1


SLIDE



 * CASE STUDY:

 * EXPLANATION:

A 60-year-old Black woman presents with a 30-day history of a nonitchy rash. The
rash is located on her face, trunk, and extremities. She reports that she has
tried topical steroids on the rash, which did not help. The patient has no other
medical conditions and takes no medications. She notes that she had unprotected
sex with a new partner about 4 months prior to presentation. On physical
examination, the patient has many scattered erythematous scaly papules on her
face, abdomen, back, and upper and lower extremities including the palms and
soles.

Syphilis is an infection from exposure to the bacterium Treponema pallidum that
spreads through sexual transmission or vertically from mother to baby. The only
known natural host of T pallidum is humans, affecting 16% to 30% of individuals
who have...

Submit your diagnosis to see full explanation.

Syphilis is an infection from exposure to the bacterium Treponema pallidum that
spreads through sexual transmission or vertically from mother to baby. The only
known natural host of T pallidum is humans, affecting 16% to 30% of individuals
who have had sexual contact with a syphilis-infected person within the last 30
days.1 The bacterium can inoculate intact mucous membranes or microabrasions
leading to anogenital ulcer and then spread to the regional lymph nodes and are
carried in the blood to other parts of the body.2

Throughout the centuries, sexually transmitted diseases (STDs) were seen as a
single disease. However, Ricord helped differentiate syphilis from gonorrhea in
an 1831 study. The discovery of the etiologic agent of syphilis around 1905 by
Schaudinn and Hoffman further helped identify syphilis as its own separate
disease. The use of dark-field microscopy and serologic tests for the diagnosis
of syphilis were introduced in the early 1990s.3

Due to its wide-ranging manifestations, syphilis has been broken down into 3
distinct stages. Primary syphilis presents as a single chancre at the site of
inoculation. Chancre appearance begins about 3 weeks after exposure with an
incubation period of 10 to 90 days. As the disease progresses, T pallidum
spreads to other tissues and manifests as secondary syphilis around 3 months
after initial infection. Most commonly, secondary syphilis presents as a
disseminated mucocutaneous rash and maculopapular lesions in 50% to 70% of
patients. In about 10% of patients, secondary lesions are accompanied by
condylomata lata, highly infectious lesions favoring warm and moist areas of the
body.1,2 After healing of clinical lesions, patients enter the latency stage,
which is characterized by positive serologic tests in the absence of symptoms.
Approximately 70% of untreated individuals will remain in latency for the rest
of their lives.4 Clinical manifestations of tertiary syphilis may appear 20 to
40 years after initial infection and include gummas (localized bone
destruction), cardiovascular syphilis (aortic insufficiency or aneurysm), and
neurosyphilis.1,2

Syphilis affected 129,813 individuals in 2019, which represents a 74% increase
from 2015. Of the 30,644 cases in 2017, 88% occurred in men with 58% of overall
cases occurring in men who have sex with men. Syphilis rates have increased
among women every year since 2003 and in every age group. Primary and secondary
syphilis disproportionately affects Black men and women and Hispanic men.5 From
2012 to 2016, the rates of congenital syphilis increased by 86.9%, from 8.4
cases in 2012 to 15.7 cases per 100,000 live births in 2016.6

To initiate infection, T pallidum uses proteins such as TP0155 and TP0483 to
bind matrix fibronectin and adhere to epithelial cells. The protein TP0751 also
strategically uses its zinc-dependent protease domain to degrade laminin and
fibrinogen. T pallidum moves through tight junctions between endothelial cells
to enter the perivascular space. T pallidum also induces the production of
matrix metalloproteinase-1 (MMP-1), which promotes the breakdown of collagen and
facilitates systemic spread in secondary syphilis by allowing T pallidum to move
to and from the bloodstream and penetrate tissues. Endothelial cells, dendritic
cells, and macrophages recognize the lipid moiety by toll-like receptors on the
cell surface and promote an immune response.1,7

The clinical presentation of primary syphilis includes an anogenital chancre
that is typically indurated and painless and is accompanied by enlarged regional
lymph nodes. However, atypical presentations can also occur as soft, multiple,
or painful lesions, and lesions may occur in other sites such as the lip or
fingers. The primary chancre may not be recognized by the patient.2,4 In terms
of exposure site, heterosexual men experience syphilis most commonly on the
penis, homosexual men are more likely to experience syphilis on the rectum and
anal canal, and women develop syphilis typically on the labia or cervix.1

In secondary syphilis, a generalized rash, generalized lymphadenopathy, and
condylomata lata are common clinical findings. Systemic symptoms include sore
throat, muscle aches, malaise, low-grade fever, and weight loss. The rash of
secondary syphilis consists of scaly, nonpruritic, macules or papules that vary
from pink to violaceous to red-brown in color.The exanthem is distributed on the
trunk and extremities with the palms and soles involved in 40% to 80% of
cases.2,4,5 Less common presentations of secondary syphilis include patchy
alopecia, split papules at the oral commissure, granulomatous nodules and
plaques, uveitis, retinitis, and hepatosplenomegaly.2,4

The most sensitive and specific test for diagnosis of primary syphilis is
dark-field microscopy of fluid from the chancre. Antibodies to cardiolipin can
be measured with the rapid plasma regain (RPR) or Venereal Disease Research
Laboratory (VDRL) assay, and these antibodies are present in about 80% of
patients with clinical symptoms of primary syphilis. Antibodies to T palladium
are detected via microhemagglutination T pallidum (MHA-TP) and fluorescent
treponemal-antibody absorption (FTA-ABS) assays. These assays are positive in
approximately 90% of patients with symptoms of primary syphilis and remain
positive for life; therefore, dark-field microscopy is required to differentiate
between primary syphilis and an earlier infection. Secondary syphilis is
diagnosed via dark-field microscopic examination of serous exudates from lesions
of skin and mucous membranes (except those of the oral cavity) and via antibody
serologic tests.4

The histopathologic features of secondary syphilis demonstrate extensive
variability. The epidermis may be normal, psoriasiform, ulcerated, or necrotic.
The dermis contains infiltrates of plasma cells, histiocytes, and lymphocytes;
these infiltrates may be perivascular, nodular, lichenoid, or diffuse. Dilated
blood vessels and vascular proliferation may also be present.4,8 In a review of
106 cases of secondary syphilis, the most common histologic features were
endothelial swelling, interstitial inflammatory pattern, irregular acanthosis,
and elongated slender rete ridges.9

The diverse histologic and clinical presentations of secondary syphilis have led
to the nickname the great masquerader because symptoms can mimic those of other
conditions. As a result, there are many conditions to consider in the
differential diagnosis of syphilis such as alopecia areata, bullous pemphigoid,
cutaneous lymphoid hyperplasia, granuloma annulare, histiocytoma, mycosis
fungoides, pemphigus vulgaris, pityriasis lichenoides et varioliformis acuta
(PLEVA), eczematous dermatoses, sarcoidosis, vasculitis, leprosy, lichen planus,
and lupus erythematosus.8 Differential diagnosis of a truncal rash should
include acute HIV infection, viral exanthems, pityriasis rosea, drug eruption,
and psoriasis. In addition, clinicians should eliminate erythema multiforme;
hand, foot, and mouth disease; and Rocky Mountain spotted fever for a
palmoplantar rash. 5

Treatment guidelines from the World Health Organization (WHO), Europe, United
States, and United Kingdom recommend penicillin as the drug of choice for
syphilis.1,2 For early syphilis (which includes primary, secondary, and early
latent syphilis acquired <1 year previously), penicillin should be administered
as intramuscular benzathine penicillin 2.4 million units as a single dose.2,4 An
alternative treatment for individuals allergic to penicillin includes oral
doxycycline, tetracycline, ceftriaxone, or azithromycin.2 However, a rise in the
prevalence of macrolide-resistant T pallidum has occurred as a result of
increased usage of azithromycin.1,7 Patients with early syphilis who are
pregnant require 2 doses of weekly intramuscular benzathine penicillin 2.4
million units. While patients with concurrent HIV infections are at higher risk
for neurologic involvement and treatment failure, there is no evidence for
alteration of treatment regimens to prevent these outcomes.2,4 All patients
diagnosed with syphilis should also be tested for HIV infection. Patients with
ocular symptoms should be assessed for uveitis and neuroretinitis.4

The patient in this case had a positive RPR; a punch biopsy of her rash further
confirmed a diagnosis of secondary syphilis. She was treated with 1 dose of
intramuscular benzathine penicillin 2.4 million units.

Sarah K. Friske, BBA, is a medical student at Baylor College of Medicine in
Houston, Texas; Tara L. Braun, MD, is a resident physician at Baylor College of
Medicine.

REFERENCES

1. Lafond RE, Lukehart SA. Biological basis for syphilis. Clin Microbiol Rev.
2006;19(1):29-49. doi:10.1128/CMR.19.1.29-49.2006

2. Goh BT. Syphilis in adults. Sex Transm Infect. 2005;81(6):448-452.
doi:10.1136/sti.2005.015875

3. Tampa M, Sarbu I, Matei C, Benea V, Georgescu SR. Brief history of syphilis.J
Med Life. 2014;7(1):4-10.

4. Stary G, Stary A. Sexually transmitted infections. In: Dermatology. Bolognia
J, ed. Elsevier Limited; 2018:1447-1469.

5. Forrestel AK, Kovarik CL, Katz KA. Sexually acquired syphilis: laboratory
diagnosis, management, and prevention. J Am Acad Dermatol. 2020;82(1):17-28.
doi:10.1016/j.jaad.2019.02.074

6. Rowe CR, Newberry SM, Jnah AJ. Congenital syphilis: a discussion of
epidemiology, diagnosis, management, and nurses’ role in early identification
and treatment. Adv Neonatal Care. 2018;18(6):438-445.
doi:10.1097/ANC.0000000000000534

7. Ho EL, Lukehart SA. Syphilis: using modern approaches to understand an old
disease. J Clin Invest. 2011;121(12):4584-4592. doi:10.1172/JCI57173

8. Carlson JA, Dabiri G, Cribier B, Sell S. The immunopathobiology of syphilis:
the manifestations and course of syphilis are determined by the level of
delayed-type hypersensitivity. Am J Dermatopathol. 2011;33(5):433-460.
doi:10.1097/DAD.0b013e3181e8b587

9. Flamm A, Parikh K, Xie Q, Kwon EJ, Elston DM. Histologic features of
secondary syphilis: a multicenter retrospective review. J Am Acad Dermatol.
2015;73(6):1025-1030. doi:10.1016/j.jaad.2015.08.062

QUESTION

What is your diagnosis?
 * Bullous pemphigoid
 * Pemphigus vulgaris
 * Secondary syphilis
 * Pityriasis lichenoides et varioliformis acuta (PLEVA)

1/1
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Please mark all the Question(s) to submit your Quiz.


TOPICS:

Case Studies Dermatology Dermatology Clinic Sexually Transmitted Infections


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