Professional Documents
Culture Documents
CliniCal Findings
Leprosy is primarily a disease of developing countries, especially in the tropical areas. India has
two thirds of the global leprosy burden. In the United States, new indigenous cases are reported
mainly in Louisiana and Texas. The prevalence of leprosy has been decreasing in the past
decade because of the effectiveness of multidrug therapy. Mycobacterium leprae is an
intracellular organism most commonly transmitted from human to human. The course and
presentation of an individual infected with M. leprae depends on the host response to the
bacillus. The incubation period of leprosy is variable, on average 5 years. The organism is of low
infectivity and transmission requires prolonged and/or close contact. The portal of entry is
thought to be skin, upper respiratory tract, particularly the nasal mucosa. The spectrum of clinical
presentation and histopathologic findings of leprosy are currently classified according to the
RidleyJopling classification. At one end of the spectrum is tuberculoid leprosy, which is a
paucibacillary form with few lesions. On the other end is lepromatous leprosy, in which there are
numerous lesions with myriad bacilli. In between are the clinical forms classified as borderline-
tuberculoid, borderline, and borderline-lepromatous leprosy. This clinical-histologic
classification has been shown to correlate closely with the level of cell-mediated
immunity to the pathogen. Indeterminate leprosy is a form better recognized in the endemic
regions, seen before the appearance of well-developed lesions of leprosy. It usually manifests as
single or multiple ill-defined hypopigmented or slightly erythematous macules, usually on the
limbs. Slight impairment of sensation may be present. Most indeterminate leprosy lesions heal
spontaneously, but approximately 25% of cases progress. Tuberculoid leprosy is a relatively
stable form seen in patients with strong immunologic host resistance and a markedly positive
lepromin test. Very well demarcated annular patches or plaques with raised erythematous
borders and central clearing are distributed asymmetrically on the trunk or extremities. Sensory
impairment is an essential feature and enlarging regional nerves often lead to palsy. The lesion is
characteristically anesthetic and anhidrotic. Borderline-tuberculoid leprosy is usually associated
with more numerous, smaller lesions than classic tuberculoid leprosy. Hair impairment and
hypoesthesia are more prevalent.
Borderline leprosy represents the middle of the spectrum; but it is unstable, with patients quickly
upgrading or downgrading to a more stable stage. Cutaneous lesions are larger, usually ill-
defined, erythematous or copper-colored, annular patches or plaques (Fig. 3-42). Borderline-
lepromatous leprosy has more numerous and poorly defined lesions than borderline leprosy.
These lesions are shinier and less anesthetic than the tuberculoid type. Nodular lesions may be
present. Lepromatous leprosy occurs in patients with minimal or absent host response (Fig. 3-
43). The cutaneous lesions are usually symmetric, poorly demarcated, erythematous and
hypopigmented macules, patches, and nodules, frequently involving the earlobes and nasal
mucosa. Multiple facial nodules, which spare the eyebrows, give a classical leonine appearance.
When local nerves are involved, lepromatous leprosy causes hypoesthesia of the affected areas.
Multiple autoantibodies are frequently detected in lepromatous leprosy, and there is
an increased incidence of vitiligo.
figure 3-42 leprosy. Ill-defined erythematous patches and plaques are present in the face
(borderline leprosy).
fiGure 3-45 lepromatous leprosy. a, Dense diffuse sheets of histiocytes are present. B, the
infiltrate includes many foamy histiocytes. c, Acid-fast bacilli are numerous.
anCillary studies
Fite stain helps to identify microorganisms. Polymerase chain reaction tests are more sensitive.
diFFerential diagnosis
Sarcoidosis may be difficult to differentiate from tuberculoid leprosy if the Fite stain is negative.
Finding the elongate tuberculoid leprosy lesions that follow neurovascular bundles and the
remnants of nerves (via silver stain) within granulomas are helpful clues. Cutaneous
tuberculosis and tuberculoid leprosy are histologically similar. Culture and clinical findings are
important in differentiating these two diseases. Any tendency to involve the nerves points toward
a diagnosis of leprosy. Similar to lepromatous leprosy, sheets of foamy histiocytes occur in
xanthoma. However, Fite stain is negative in the latter. The round intracytoplasmic inclusions
within the histiocytes of rhinoscleroma and histoplasmosis distinguish these from lepromatous
leprosy. Granular cell tumor may mimic lepromatous leprosy because the neoplastic cells have a
perineural distribution and granular cytoplasm. However, a granular cell tumor is usually
overlaid by pseudoepitheliomatous hyperplasia and the cytoplasm appears more eosinophilic
than the macrophages in leprosy.