Bryan Child
MEDI 7003
Tropical Medicine Paper
Topic: Hansen’s Disease
Although it may be a common topic for this assignment, I have chosen to discuss the topic of Hansen’s disease, or leprosy. I wanted to discuss something that I have actually seen here in
Epidemiology: The prevalence of leprosy varies greatly from country to country, with the vast majority of cases presenting in developing countries. Very few cases are newly detected in the
Microbiology/Transmission: Leprosy is actually caused by Mycobacterium leprae, an acid-fast bacillus. It is an obligate intracellular parasite that multiplies very slowly (generation time of 12.5 days). It grows best at temperatures from 27-33 degrees Celsius. As such, it most commonly affects cooler areas of the body such as the skin, nerve segments near the skin, and the mucous membranes of the upper respiratory tract. The definitive rout of transmission of leprosy has not actually been proven. However, it is believed to be spread via the respiratory route, similar to TB, since the nasal discharge of untreated patients often contains large numbers of bacilli. From the respiratory tract, hematogenous dissemination can occur, spreading to the skin and nerve. It is also possible that the organism occasionally enters through breaks in the skin, as there have been some reports of contact with infected armadillos. The bacilli can survive for several days in the environment. The incubation period is 2-5 years for TT cases and 8-12 years for LL cases (classifications discussed later). Most people develop an effective immune response and clear the bacteria. Only a small minority, about 5%, fail to do so and develop clinical leprosy.
Risk factors: People in close contact with infected people have a greater, but still small, chance of becoming infected. The type of leprosy that a person is in close contact with also appears to be a risk factor, with contacts of the multibacillary patient having a higher risk than contacts of paucibacillary or single lesion patients. Older persons also appear to be at an increased risk of leprosy. Although it is difficult to separate the contribution of genetic factors from that of close contact, it does appear that there is some genetic component to leprosy susceptibility. This is likely related to the type of cell-mediated immune response that is elicited.
Classification: There are two principal classification systems for leprosy, the WHO and the Ridley-Jopling systems. The WHO classification system is simpler and is based upon the number of skin lesions and the number of bacilli detected on skin smear. Paucibacillary (PB) leprosy is defined as five or fewer skin lesions without detectable bacilli on skin smears. Patients with only one skin lesion are classified separately as single lesion PB. Multibacillary (MB) leprosy is defined as six or more lesions and may be skin smear positive. On the skin smear, the number of acid-fast bacilli found can range from a bacterial index (BI) of 0 to a BI of 6+. A BI of 2 or more at any skin site is an indication to treat as MB leprosy. The Ridely-Jopling system classifies leprosy on the basis of skin, motor, and sensory changes as well as biopsy findings. The classifications are: indeterminate (I), tuberculoid (TT), borderline tuberculoid (BT), mid-borderline (BB), borderline lepromatous (BL), and lepromatous (LL). Under most circumstances, the simpler WHO classification is easier to use and I, TT, and BT disease are generally equivalent to PB, while BB, BL, and LL disease are generally equivalent to MB.
Clinical Features: Indeterminate disease usually presents with a solitary hypopigmented 2-5 cm lesion. The center may show sensory loss, though the patient and the doctor are often uncertain about this loss. TT cases have skin lesions with well-defined borders and sensory loss. The patch is dry from loss of sweating and hairless. There may be one or more peripheral nerves affected, occasionally presenting as a mononeuropathy. BT disease presents with irregular plaques with raised edges and sensory loss. Satellite lesions are present at the edges. There is also asymmetrical peripheral nerve involvement. BB leprosy has many lesions with punched out edges and satellites are common. There is widespread nerve enlargement and sensory and motor loss. BL has many lesions with diffuse borders and variable anesthesia. Finally, LL presents with numerous nodular skin lesions in a symmetrical distribution. The lesions are not dry or anesthetic. There are also often thickened shiny earlobes, loss of eyebrows, and skin thickening. BL and LL have similar nerve involvement to BB. The most commonly affected nerves are: ulnar and median (claw hand), common peroneal (foot drop), posterior tibial (claw toes and plantar insensitivity), facial, radial cutaneous, and great auricular. It is important to note that the ulceration and digit loss seen in leprosy is due to secondary damage in neuropathic hands and feet and is not an intrinsic disease feature.
Diagnosis: Diagnosis of leprosy is based upon the following: a typical skin lesion (with loss of sensation in TT/BT patients), thickened peripheral nerves, and a skin smear from a lesion edge or ear lobe positive for mycobacteria. As such, the skin lesions need to be tested for sensation. The peripheral nerves should be palpated to assess for enlargement and/or tenderness. Nerve function should also be assessed by testing the small muscles’ power and sensation in the hands and feet. Eye function should also be checked, including visual acuity, corneal sensation, and eyelid closure.
Treatment: Management of leprosy consists of chemotherapy to treat the infection, education of the patient, and prevention of disability. The WHO recommended multi-drug therapy regimens are very effective. Relapse rates are 0.1% per year. Clinical improvement is rapid and adverse reactions are rare. For paucibacillary (2-5 lesions) leprosy, rifampicin 600 mg is administered monthly and dapsone 100 mg is administered daily for a total of six months. For multibacillary (more than 5 lesions) leprosy, rifampicin and dapsone are still taken as in paucibacillary leprosy, but the patient also is administered clofazimine 300 mg monthly and clofazimine 50 mg daily. Treatment is continued for a full year. The patient should be educated that within 72 hours of beginning treatment, they are non-infectious and can lead a normal social life. There are no limitations on touching, sex, or sharing utensils. They should also be taught that leprosy is not a curse from God or a punishment and that gross deformities are not the inevitable endpoint of the disease. Care and awareness of their limbs are as important as chemotherapy. Finally, care should be taken to prevent disability. Sensation and muscle power should be monitored in the patient’s hands, feet, and eyes as part of routine follow-up so that new nerve damage is detected early. Any new damage can be treated with prednisolone.
Resources
- Robert Jacobson, James Krahenbuhl, and Leo Yoder. Overview of Leprosy, from Up To Date. Updated September 4, 2008.
- Michael Eddleston, Robert Davidson, Andrew Brent, and Robert Wilkinson.
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