1. Cara diagnosis?

2. Diagnosis penyakit tersebut?

Pasien mengalami LEPROSY

Klasifikasi kusta menurut Madrid 1953:

Klasifikasi berdasarkan manifestasi klinis, pemeriksaan bakteriologis, dan pemeriksaan
histopatologi, sesuai rekomendasi dari International Leprosy Association di Madrid tahun
1953. Yaitu:
Intermediate
Tuberculoid
Lepromatous
Borderine
Ridle dan Jopling:
Pada klasifikasi ini penyakit kusta adalah suatu spektrum klinis mulai dari daya kekebalan
tubuhnya rendah pada suatu sisi sampai mereka yang memiliki kekebalan yang tinggi
terhadap M.leprae di sisi yang lainnya. Kekebalan seluler (cell mediated imunity = CMI)
seseorang yang akan menentukan apakah dia akan menderita kusta apabila individu tersebut
mendapat infeksi M.leprae dan tipe kusta yang akan dideritanya pada spektrum penyakit
kusta.
1. Tuberkuloid Tuberkuloid (TT)
2. Borderline Tuberkuloid (BT)
3. Borderline Borderline/= Mid Boderline (BB)
4. Borderline Lepromatose (BL)
5. Lepromatose Lepromatose (LL)
WHO
Pada tahun 1982, WHO mengembangkan klasifikasi untuk memudahkan pengobatan di
lapangan. Dalam klasifikasi ini seluruh penderita kusta hanya dibagi menjadi 2 tipe yaitu tipe
Pausibasiler (PB) dan tipe Multibasiler (MB). Sampai saat ini Departemen Kesehatan
Indonesia menerapkan klasifikasi menurut WHO sebagai pedoman pengobatan penderita
kusta. Dasar dari klasifikasi ini berdasarkan manifestasi klinis dan hasil pemeriksaan
bakteriologi.

PB: kusta tipe I, TT dan sbg besar BT dgn BTA negatif menurut klassifikasi Ridley-Jopling
dan type I dan T menurut klassifikasi Madrid
MB: Kusta type LL, BL, BB dgn sebagian BT menurut klassifikasi Ridley-jopling dan type
B dan L menurut klassifikasi Madrid dan semua type kusta dgn BTA positif

Pada skenario kasus, dikatakan bahwa ada benjolan-benjolan/nodul, sehingga dapat dicurigai
pasien mengalami leprosy tipe MB. Namun untuk memastikan perlu dihitung jumlah
bercaknya ataupun smear melalui pemeriksaan bakteriologi.

3. Patogenesis penyakit?

4. Cara Penularan?
Cara penularan belum diketahui secara pasti, namun ada 3 kemungkinan pintu keluar dari
tubuh, yaitu kulit, traktus GI, traktus respiratorius.

Transmission by contact
The term 'contact' in leprosy is generally not clearly defined. All that we know at
present is that individuals who are in close association or proximity with leprosy
patients have a greater chance of acquiring the disease. It is with reference to this
observation that the early workers appear to have used the term 'contact' as method of
transmission. However, it is the definition of contact by later workers with
qualifications such as 'skin to skin', 'intimate', 'repeated', etc. that has made it appear
as if the disease could be acquired only under such conditions, and that the

transmission involved some kind of 'inunction' or rubbing in of the organisms from

the skin of affected persons into the skin of healthy subjects. Certainly, there is no
proof that transmission takes place only through such inunction. In general, closeness
of contact is related to the dose of infection which in turn is related to the occurrence
of disease. Of the various situations that promote close contact, contact within the
household is the only one that is easily identified. In that area the relative risk for
contacts was about four times that of non-contacts. The actual incidence among
contacts and the relative risk for them appear to vary considerably in different studies.
Attack rates for contacts of lepromatous leprosy have varied from 6.2 per 1000 per
year in Cebu (Doull et al, 1942) to 55.8 per 1000 per year in a part of South India
(Noordeen & Neelan, 1978).
Transmission through contacts
The possibility of transmission of leprosy through the respiratory route is gaining
increasing attention in recent years. It is interesting to note that as early as 1898 this
possibility has also been discussed at some length by Schiffer (Schiffer, 1898). The
possibility of transmission through the respiratory route is based on (a) the inability of
the organisms to be found on the surface of the skin, (b) the demonstration of a large
number of organisms in the nasal discharge, (c) the high proportion of morphologically
intact bacilli in the nasal secretions, and (d) the evidence that M.leprae could survive
outside the human host for several hours or days.
Transmission through insects
With the available evidence on intracutaneous inoculation as a successful method of
transmission of M.leprae in the mouse footpad model and a similar situation possibly
existing in human beings, the question arises whether insects could play any role in
natural infection. Although a large number of experiments had been conducted in the
past demonstrating AFB in biting insects, the question whether insects actually
transmitted infection had remained unanswered.

5. Bagaimana perawatan penyakit tersebut?

6. Perawatan luka pasien?

Efficacy of metronidazole was assessed in 20 leprosy cases with trophic ulcers with poor
response to oral and topical antibiotic. Oral metronidazole 400 mg three times daily for one
week and topical metronidazole gel 1% for three weeks were found to be very effective.

Pada sebuah case report di University Hospital of the Faculty of Medicine of Ribeirao
Preto, Sao Paulo University (Brazil), terdapat 3 orang pasien penderita leprosy yang
dilakukan perawatan. Ketiga pasien memiliki ulser pada bagian soft palate, dan 2
pasien di antaranya memiliki ulser di hard palate.
Perawatan:
Pasien dirawat dengan MDT, 600mg rifampisin daily, 300mg clofamizine sekali
sebulan atau 50mg perhari, dan 100mg dapsone perhari, dengan total 24 doses.
Seluruh pasien kemudian sembuh dari lesi oral maupun mukosa dari leprosy ini.

7. Manifestasi oral?
MORPHOLOGY
The oral lesions in leprosy are slow to progress and are usually asymptomatic. The
spectrum of lesions may vary from relatively non-specific ones like enanthem of
palate or uvula, which, on histopathology, may show no changes or non-specific
infiltrate to more specific lesions like papules, nodules and ulcers, which may show
bacillary positivity.[14] Table 1 enumerates the various non-specific and specific
lesions seen in the oral cavity in leprosy. However, no lesion can be referred to as
pathognomonic for leprosy. The number of oral lesions increases with age. Scheepers
et al. report the prevalence of oral lesions to be higher among males compared with
females.[15] Females tend to present at a younger age, probably because of the
greater cosmetic concern. The same authors observe the presence of family history of
leprosy to be a significant factor in determining the severity of the oral lesions.

Lepros involvement of the lips may present as macrocheilia, presence of flat-topped nodules
and microstomia.[16] The swollen and rigid appearance of the lips may be marked and hence

cosmetically quite troublesome. In a study by Handa et al., leprous macrochelia was seen in
10.7% of the 28 patients presenting with chronic macrocheilia.[17] The tongue may be
involved in 1725% of the cases.[18,19] Commonly observed lesions include multiple
superficial ulcers, mild glossitis, loss of papillae, chronic atrophic candidiasis and fissured
tongue.[20] Nodular lesions may be present over the anterior part of the tongue, giving a
pavement-stone appearance and ultimately lead to scarring. The muscles of the tongue are
usually spared unlike the extensive involvement seen in other subcutaneous muscles. The
buccal mucosa may appear paler than normal. In advanced cases, there may be diffuse
infiltration, swellings, papulonodules and ulceration.

Hard palate, as already mentioned, is the most common site of involvement and shows the
most varied type of lesions. The disease may present as erythematous or reddish papules that
gradually increase in size and number and coalesce to form a generalized nodular submucosal infiltrate [Figures [Figures114]. As the disease progresses, the mucosa loses its
shininess and gives a matt-like appearance.[21] Ultimately, there may be palatal ulceration
and perforation leading to communication between the oral and nasal cavity. At this time,
patients may develop functional abnormalities like difficulty in swallowing, eating and
drinking. Bucci et al. reported erythema nodosum leprosum to be an important but rare cause
of destruction of the hard and soft palate.[22] Noduloulcerative lesions over the palate may at
times mimic squamous cell carcinoma.[23] Further in the course of disease, the mucosa of the
soft palate, uvula and fauces of tonsils become infiltrated with the appearance of miliary
papules or nodules. These may break down forming superficial ulcers, especially during
leprosy reactions. The uvula may initially appear swollen and later completely effaced or may
become adherent to the soft palate. Scarring in the region of fauces may lead to a triangular
deformity instead of the normal faucial arch.

Involvement of gums may be in the form of gingivitis, periodontitis and

periodontoclasia. Gums appear swollen with shiny and purplish mucosa and bleed easily
with decreased sensitivity to pain. Dental involvement has been less extensively studied.
Miranda et al. described three different types of leprotic involvement of teeth: specific
pulpitis, dental anomalies and periapical granulomas. Marti et al. further concluded that
leprosy patients tend to have poor dental and periodontal health, unrelated to the
presence of facial destruction or the type of leprosy.[24] In addition, it has been
postulated that oral chronic infections may be associated with the recurrence of leprosy

reaction episodes. Motta et al. compared 38 patients with leprosy 19 with and 19
without oral infections and found the latter group to show clinical improvement in
leprosy reactions after dental treatment.[25]
Histopathological examination of the mucosal lesions may show variable features.
Scheepers et al. described epithelial atrophy to be a feature seen only in patients with
lepromatous leprosy.[15] Grenz zone, which is a consistent feature in skin lesions, is
rarely seen in oral lesions. Intense infiltration of macrophages, lymphocytes and plasma
cells is prominently seen in oral lesions of lepromatous leprosy, with abundance of acid
fast bacilli. Hyperkeratosis is observed in some cases and is believed to be analogous to
desquamation of skin, as seen in reversal or downgrading reactions. Abreu et al. studied
19 patients with multibacillary leprosy between 2000 and 2002, and concluded that
clinical alterations in the oral mucosa do not imply disease involvement and should be
confirmed by histopathological examination.[26] Conversely, the normal oral mucosa
can show specific histopathological changes.

DP:
1. Tony B, Stephen B, Neil C, Chridtopher G. Rooks Textbook of Dermatology. 8th ed.
Oxford: Wiley-Blackwell. 2010: 32.1-32.19.
2. Paul AK, Susan CT. Dermatology for Skin of Color. Washington: Mc-Graw-Hill.
2009: 441-6.
3. Ana CFM, Marilena CK, Claudia HLS, etc. Leprosy-specific oral lesions: A report of
three cases. Med Oral Patol Oral Cir Bucal. 2008;13(8): 479-82.
4. Ruchi G, Hemanta KK, Minakshi B. Revalidation of various clinical criteria for the
classification of leprosy A clinic-pathological study. Lepr Rev (2012) 83: 354362.
5. Vathsala N, Raghavendra K, Smit S, Anjali S. Leprosy Specific Orofacial Aspect. J of
Indian Academy of Oral Medicine and Radiology. 2011; 23(3):216-20.
6. Shambulingappa P, Soheyl S, Anupreet K, Amit A, Ravinder S. Oral cavity and
leprosy. Indian Dermatol Online J. 2012; 3(2): 101104.
7. Richard WT Pushpendra S, Rahul S, etc. Probable Zoonotic Leprosy in the Southern
United States. N Engl J Med. 2011; 364:1626-1633
8. Mishra S, Singh PC,Mishra M. Metronidazole in management of trophic ulcers in
leprosy. Indian J of Dermatology, Venereology and Leprology. 1995; 61(1): 19-20.