Pinta 

Updated: May 19, 2017
Author: Natalie C Klein, MD, PhD; Chief Editor: Mark R Wallace, MD, FACP, FIDSA 

Overview

Background

Pinta is an endemic treponematosis caused by Treponema carateum.[1] It is an ancient disease that was first described in the 16th century in Aztec and Carib Amerindians. In 1938, treponemes indistinguishable from those that cause yaws and syphilis were demonstrated in lesions of a Cuban patient.[2] Pinta is characterized by chronic skin lesions that occur primarily in young adults.[3, 4, 5, 6, 7]

Pathophysiology

Like other treponematoses, pinta is classified into an early and late stage. The early stage comprises the initial lesion and the secondary lesions, while the late stage comprises the latent phase and tertiary stage.

After an incubation period of approximately 2-3 weeks, the initial lesion appears on the skin. The primary lesion is a papule or erythematosquamous plaque usually found on exposed surfaces of the legs, dorsum of the foot, forearm, or hands. The lesion slowly enlarges and becomes pigmented and hyperkeratotic. It is often accompanied by regional lymphadenopathy.

Disseminated lesions, referred to as pintids, are similar to the primary lesion and may appear 3-9 months after infection. These secondary lesions vary in size and location and become pigmented with age.

Late or tertiary pinta is characterized by disfiguring pigmentary changes, hypochromia, achromic lesions, and hyperpigmented and atrophic lesions. The pigmentary changes often produce a mottled appearance of the skin. Lesions may appear red, white, blue, violet, and brown.

Epidemiology

Frequency

United States

Pinta does not occur in the United States.

International

Pinta occurs in scattered foci in rural areas of Central and South America.[8] In the 1950s, about 1 million cases of pinta were reported in Central and South America. In the 1980s, 20% seropositivity was found in remote rural areas of Panama. The current prevalence of pinta is unknown, but only a few hundred cases have been reported per year.[9, 10]

Mortality/Morbidity

Pinta is the most benign of the endemic treponematoses. The skin is the only organ involved.

No neurologic, bone, or cardiac manifestations occur. No congenital form exists.

Sex

Both sexes are affected with equal frequency.

Age

Pinta affects children and adults of all ages.[11]

The peak age of incidence is 15-30 years.

 

Presentation

History

The exact mode of transmission is unknown, but pinta is probably transmitted by direct skin or mucous membrane contact.

The initial lesion is usually found on an exposed part of the body.

Pinta causes no constitutional symptoms.

Physical

The initial lesion is a papule that slowly enlarges to become a pruritic plaque (as seen in the image below).

Erythematosquamous plaque of early pinta. Perine P Erythematosquamous plaque of early pinta. Perine PL, Hopkins DR, Niemel PLA, et al. Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pinta. Geneva, Switzerland: World Health Organization; 1984.

The dorsum of the foot and legs are the most common sites of lesions (as seen in the image below).

Violaceous psoriatic plaque of early pinta. Perine Violaceous psoriatic plaque of early pinta. Perine PL, Hopkins DR, Niemel PLA, et al. Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pinta. Geneva, Switzerland: World Health Organization; 1984.

The regional lymph nodes may enlarge.

Lesions become pigmented with age and may change colors from copper to grey to slate blue (as seen in the image below).

Late pigmented pinta (blue variety). Perine PL, Ho Late pigmented pinta (blue variety). Perine PL, Hopkins DR, Niemel PLA, et al. Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pinta. Geneva, Switzerland: World Health Organization; 1984.

Late lesions become achromic or hyperpigmented.

Causes

T carateum is the causative agent and is considered to be a separate species from Treponema pallidum.

T carateum can be grown only in primates, and less is known about this treponeme than any of the others.

 

DDx

Differential Diagnoses

 

Workup

Laboratory Studies

Pinta is most often a clinical diagnosis.

The nontreponemal and treponemal serologic tests used in diagnosing venereal syphilis are used for serodiagnosis of pinta.

Treponemes can be demonstrated by darkfield examination of exudates from early lesions.

Nontreponemal test results (ie, rapid plasma reagent [RPR], Venereal Disease Research Laboratory [VDRL] test) are positive in all stages of pinta except very early lesions. Confirmatory treponemal test results (ie, T pallidum hemagglutination [TPHA], microhemagglutination T pallidum [MHA-TP], fluorescent treponemal antibody absorption [FTA-Abs]) are also positive but are not practical in remote areas.

Histologic Findings

Findings of pinta and yaws are similar, but pinta does not cause ulcer formation. In early lesions, mild acanthosis is present with migration of lymphoid cells into the epidermis. In the late stage, irregular acanthosis or epidermal atrophy occurs. Treponemes can be demonstrated in the epidermis in primary and secondary lesions using silver stain. They are absent in late achromic lesions.[12]

 

Treatment

Medical Care

After penicillin therapy, lesions become noninfectious in 24 hours.

Surgical Care

Surgery has no role in pinta treatment.

 

Medication

Medication Summary

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications.

Antibiotics

Class Summary

Benzathine penicillin is the DOC but should not be administered to patients who are allergic to penicillin. Alternative therapies include tetracycline or erythromycin.

Penicillin G benzathine (Bicillin LA)

Interferes with cell wall synthesis during active multiplication, resulting in bactericidal activity against susceptible microorganisms. Should not be administered to patients who are allergic to penicillin.

Tetracycline (Achromycin, Sumycin)

Alternative to benzathine penicillin for patients who are allergic to penicillin. Treats gram-positive and gram-negative organisms, as well as mycoplasmal, chlamydial, and rickettsial infections. Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s).

Erythromycin ethylsuccinate (E.E.S., EryPed)

Indicated for the treatment of infections in children who are allergic to penicillin or women who are pregnant. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest. In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, one half of the total daily dose may be taken q12h. For more severe infections, double the dose.

 

Follow-up

Further Inpatient Care

Lesions become noninfectious within 24 hours of treatment.

Skin lesions heal slowly.

After treatment, nontreponemal titers should decline and eventually revert to negative.

Prognosis

The prognosis is good. The skin is the only organ affected. Primary and secondary lesions usually heal within 6-12 months. Pigmentary changes persist in late lesions.