pinta (tropical syphilis)
TRANSCRIPT
Pinta (disease)
Allysha Tan 40A
What is Pinta?
Pinta is an endemic treponematosis caused by infection with
a spirochete, Treponema carateum.
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.
Pinta is characterized by chronic skin lesions that occur
primarily in young adults.
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
Pinta occurs in scattered foci in rural areas of Central and South America. 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.
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.
The peak age of incidence is 15-30 years.
Clinical Picture
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 Clinical Picture
The initial lesion is a papule
that slowly enlarges to
become a pruritic plaque
Erythematosquamous plaque of
early pinta.
The dorsum of the foot and
legs are the most common
sites of lesions
Violaceous psoriatic plaque of
early pinta.
The regional lymph nodes
may enlarge.
Lesions become pigmented
with age and may change
colors from copper to grey
to slate blue.
Late pigmented pinta (blue variety).
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.
Differential Diagnoses
Leprosy
Syphilis
Yaws
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 pallidumhemagglutination [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.
Treatment
Medical Care
After penicillin therapy, lesions become
noninfectious in 24 hours.
Surgical Care
Surgery has no role in pinta treatment.
Medication
The goals of pharmacotherapy are to eradicate the infection, to
reduce morbidity, and to prevent complications.
Antibiotics
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.
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 (Erythrocin, E-Mycin, EES)
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.
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