QuestionSBA
QuestionChoice
This is not required
32037
e
HIV testing
QuestionChoice
Dapsone inhibits folic acid synthesis and should be given with folate supplementation. It does not affect B12 levels
32036
d
Vitamin B12 levels
QuestionChoice
Dapsone does not cause arrhythmias or cardiovascular events
32035
c
Electrocardiogram (ECG)
QuestionChoice
Dapsone undergoes hepatic metabolism and does not require dosage adjustment in renal impairment
32034
b
Renal function testing
QuestionChoice
Dapsone carries the risk of severe haemolytic anaemia in patients with severe G6PD deficiency
32033
a
Glucose-6-phosphate dehydrogenase (G6PD) levels
QuestionComment
weird question. I think very niche too - not high yield memorising Rx of haemolytic anaemia in pt with G6PD
12160
User
subscriber
Versicolor Sclerosis
QuestionComment
Does routine HIV testing post-diagnosis of TB not extend to other Mycobacterium infections?
62063
QuestionComment
i tried looking this up and there doesn't seem to be much evidence in favour of TB association with leprosy. however, if you have both, the leprosy might flare more (i guess reasonably so because of the diminished immune response). but there's no guidance to test everyone (i got it wrong as well tho)
62094
User
subscriber
Vaccine Complement
User
subscriber
Amnesia Syndrome
Concept
Chapter
# Summary
 
 
Leprosy is a disease endemic in many developing countries. The disease can manifest in various ways depending on host immunology and bacterial virulence. The two main forms are multibacillary (lepromatous) and paucibacillary (tuberculoid) leprosy. Differential diagnoses to consider include inherited diseases, endocrine disorders, and other conditions such as AL amyloidosis. Diagnosis is primarily based on clinical assessment and the presence of acid-fast bacilli in biopsies or smears. Management involves the use of medications such as dapsone, rifampicin, and clofazimine, with close monitoring for potential side effects and immunological complications. 
 
 
# Definition
 
 
Leprosy is a mycobacterial disease caused by *Mycobacterium leprae* which typically presents with dermatological and neurological manifestations.
 
# Epidemiology
 
Leprosy is endemic in a number of developing countries across the world. Most new cases occur in Southeast Asia.
 
It is associated with severe morbidity, reduced psychosocial functioning and stigmatisation. While difficult to transmit, it is thought to be spread by the respiratory route via nasal discharge.
 
# Aetiology
 
 - Leprosy is spread through droplets from the respiratory tract. Prolonged close contact (over months) is required to transmit the disease.
 - Leprosy manifests in a number of different ways owing to a range of factors, the most important being host immunology and bacterial virulence/initial infectious load
 - *M. leprae* grows best at 27–33° so it prefers to grow at **cooler** areas of the body (eg. skin, nerves close to the skin, mucous membranes)
 - There are five types, but broadly it can be classified as lepromatous and tuberculoid leprosy
 - In disseminated lepromatous/multibacillary leprosy, bacteria become widely disseminated due to poor Th1 cell-mediated responses. This causes symmetrical peripheral nerve damage through demyelination of peripheral nerves, as well as classical skin changes.
 - In tuberculoid/paucibacillary leprosy, there is a robust Th1 cell-mediated response, leading to better control by the immune system and milder clinical manifestations.
 
# Symptoms & Signs
 
The clinical features of leprosy exist on a spectrum. At one end is **disseminated lepromatous/multibacillary leprosy**:
 
 - Coppery or hypopigmented anaesthetic patches; ≥5
 - Classic facial changes include nose destruction and ear swellings – leonine faces
 - Nerve thickening may be felt on palpation, with the most commonly affected nerves being the ulnar, median, radial cutaneous, greater auricular, common peroneal and posterior tibial nerves to control of the infection
 
Clinical features of **tuberculoid/paucibacillary leprosy** include a milder form of nerve damage and dermatological manifestations (<5 lesions)
 
Nerve damage in all forms can lead to contractures, ulceration and deformity in the long term
 
# Differential diagnosis
 
 
The differential diagnosis for other causes of thickened peripheral nerves include:
 
 - **Inherited diseases** – Charcot–Marie–Tooth disease, Refsum's disease and neurofibromatosis. These can also cause peripheral neuropathies and cutaneous manifestations alongside a family history.
 - **Acromegaly** - coarsening features & nerve compression (especially carpal tunnel syndrome). Symptoms are more generalised and complications such as diabetes mellitus can develop.
 - **AL amyloidosis** - may be associated with symptoms of multiple myeloma (hypercalcaemia, renal dysfunction, anaemia, bone pain).
 - **Peripheral neuropathy** secondary to diabetes mellitus, alcohol use or, more acutely, Guillain-Barré syndrome. This is usually preceded by poorly controlled diabetes or alcoholism, or by a recent infection (precipitating GBS)
 
 
# Diagnosis
 
Leprosy is diagnosed with one or more of the following clinical features and laboratory tests:
 
 - Loss of sensation in a hypopigmented or reddened skin patch
 - Thickened peripheral nerve and sensory loss/weakness in the area supplied by the nerve
 - Slit-skin smear demonstrating acid-fast bacilli with a special stain
 
 
# Treatment
 
Early diagnosis and treatment can reduce illness severity and long-term sequelae.
 
 - Treatment of multibacillary leprosy involves the use of dapsone, rifampicin and clofazimine (an immunosuppressive agent) for at least 12–24 months
 - Patients commenced on medications need to be monitored closely throughout the course of their treatment for immunological complications known as type I and II (erythema nodosum lepromum) reactions, which require hospital inpatient treatment. Treatment should continue with the addition of prednisolone, aspirin or thalidomide under specialist guidance.
 - Side effects of dapsone include methaemoglobinaemia, agranulocytosis, Stevens–Johnson Syndrome and the DRESS syndrome; it can also trigger a haemolytic crisis in G6PD deficiency
 - Clofozamine can cause abnormal skin pigmentation
 - Rifampicin can cause orange secretions and is a cytochrome P450 inducer, hence has several drug interactions
 - Treatment of paucibacillary leprosy involves rifampicin and dapsone for 6 months
 
 
# References 
 
 [BNF: Leprosy treatment summary](https://bnf.nice.org.uk/treatment-summaries/leprosy/#:~:text=Paucibacillary%20leprosy%20should%20be%20treated,is%20sufficient%20to%20treat%20tuberculosis.)
 
 [Click here for the WHO page on leprosy](https://www.who.int/news-room/fact-sheets/detail/leprosy)
 
 
 [Leprosy: review of the epidemiological, clinical, and etiopathogenic aspects - Part 1 - PMC (nih.gov)](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4008049/)
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Leonine facies.
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Hypesthetic patches seen in someone with leprosy.
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Leprosy
Topic
58
Infectious Diseases
6407
Dapsone carries the risk of severe haemolytic anaemia in patients with severe G6PD deficiency
A 55 year old man presents to his GP with a 6 month history of multiple hypopigmented patches over his torso. He also has multiple burn marks on his hands from accidentally touching hot pans whilst cooking. Nerve conduction studies reveal reduced conduction velocity in the ulnar and median nerves. He is diagnosed with leprosy and started on dapsone.

Which one of the following tests should be performed before starting treatment?
a