Pinta

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.^[2] Pinta is characterized by chronic skin lesions that occur primarily in young adults.^{[3, 4, 5, 6]}

The name pinta originates from the Spanish word for "painted." The disease is known by different names in different regions. For example, it is known as mal de pinto in Cuba and Mexico, enfermedad azul (blue sickness) in Chile and Peru, and carate in Colombia and Venezuela.^[7]

• References

Pathophysiology

The precise mechanism of transmission is unknown, although recurrent skin-to-skin contact is most plausible. Pinta is not known to be a blood-borne disease or to be transmitted vertically. Young adults with pinta skin lesions are considered to be the disease's main reservoir.^{[7, 8]}

Like other treponematoses, pinta is classified into stages. The infection is thought to be limited to the epidermal and dermal layers despite systemic dissemination, although potential bone involvement has been reported.^[9]

After an incubation period that ranges from 1 week to 2 months, the initial lesion appears on the skin. The primary lesion is a papule or erythematous and squamous plaque usually found on exposed surfaces of the legs, dorsum of the foot, forearm, or hands. The lesion enlarges slowly and becomes pigmented and hyperkeratotic and may last months or years. It is often accompanied by regional lymphadenopathy.

The secondary stage is characterized by disseminated lesions, referred to as pintids. The lesions appear after several months and may coexist with the primary lesion. Pintids are similar to the primary lesion and can vary in size and location and usually become pigmented with time. The primary and secondary lesions are rich in bacteria and are considered highly infectious.^{[7, 4, 5, 6, 8]}

Late or tertiary pinta usually develops 2-5 years after the initial infection. Late 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.^{[1, 3, 6, 7, 2]}

• References

Epidemiology

Frequency

United States

Pinta does not occur in the United States.

International

It is unclear whether pinta still occurs in scattered foci in rural areas of Central and South America.^[10]

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. Today, it is unclear whether pinta still exists. If so, it might be restricted to very circumscribed parts of Latin America; known recent foci have involved the Tikuna tribes living in the Amazon Trapeze and inhabitants of a Panamanian village. The most recently reported case of pinta involved a Cuban female who was visiting Austria in 1999.^{[11, 12, 2, 7]}

Mortality/Morbidity

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

No neurologic or cardiac manifestations occur. No congenital form is known to exist.

Sex

Both sexes are affected with equal frequency.

Age

Pinta affects children and adults of all ages.^[13]

The peak age of incidence is 15-30 years.

• References

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.

• References

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.

• References

Physical

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

View Image

Erythematosquamous plaque of early pinta. Perine PL, Hopkins DR, Niemel PLA, et al. Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pi....

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

View Image

Violaceous psoriatic plaque of early pinta. Perine PL, Hopkins DR, Niemel PLA, et al. Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and ....

The regional lymph nodes may enlarge.

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

View Image

Late pigmented pinta (blue variety). Perine PL, Hopkins DR, Niemel PLA, et al. Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pinta. ....

Approximately 3-9 months after infection, more lesions may appear distal to the initial lesion and expand. Late lesions become treponeme-free and achromic or treponeme-containing and hyperpigmented.

• References

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.

• References

Laboratory Studies

Pinta is most often a clinical diagnosis.

Serological tests are considered the standard laboratory method for the diagnosis of endemic treponematoses, including 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.^[10]

New rapid point-of-care treponemal tests have become available in resource-poor settings. Whole-genome fingerprinting techniques and polymerase chain reaction (PCR) are also available but currently limited for research purposes.^[10]

• References

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.^{[9, 4]}

• References

Medical Care

The World Health Organization (WHO) recommends treatment of pinta with a single-dose intramuscular injection of long-acting benzathine penicillin (1.2 MU for adults; 0.6 MU for children). Penicillin render lesions noninfectious within 24 hours.^[2]

Lesions become noninfectious within 24 hours of treatment.

Skin lesions heal slowly.

After treatment, nontreponemal titers should decline and can (but do not always) revert to negative.

The WHO has started a campaign to eradicate yaws (caused by T pallidum pertenue) by 2020 based on the mass treatment of endemic communities with an oral dose of azithromycin. T carateum is most likely sensitive to azithromycin, and this intervention could therefore have a concomitant effect on pinta in regions of Latin America where both yaws and pinta might still coexist.^[2]

• References

Surgical Care

Surgery has no role in pinta treatment.

• References

Complications

Early pinta lesions usually improve with penicillin treatment, although the late changes of pinta are irreversible, often causing stigmatization in communities.^[2]

• References

Prevention

Treatment of close contacts and household members is recommended to prevent the development of infection.^[1]

• References

Long-Term Monitoring

Long-term monitoring of pinta is unnecessary. Treatment resolves early lesions and, in persons with late infections, arrests progression. A fall in two or more dilutions in the nontreponemal tests may be seen after treatment with penicillin, but serology results might not revert to negative.^[1]

• References

Medication Summary

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

• References

Penicillin G benzathine (Bicillin LA)

• Dosing, Interactions, etc.

Clinical Context:  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.

• References

Azithromycin (Zithromax, Zmax)

• Dosing, Interactions, etc.

Clinical Context:  Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest. Dosing is usually 30 mg/kg single dose (max dose of 2 g).

• References

Tetracycline (Achromycin, Sumycin)

• Dosing, Interactions, etc.

Clinical Context:  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).

• References

Class Summary

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

• References