1. Leprosy is caused by Mycobacterium leprae and affects the skin and peripheral nerves. It is classified based on clinical, histopathological, immunological and bacteriological parameters.
2. The Ridley-Jopling classification from 1966 is widely used, categorizing leprosy into tuberculoid, borderline, and lepromatous types.
3. WHO classifications from 1982 onward divided leprosy into paucibacillary and multibacillary types based on bacterial load for purposes of treatment.
Leprosy is caused by Mycobacterium leprae, an obligate intracellular organism. It manifests as a spectrum of diseases from lepromatous leprosy (LL) to tuberculoid leprosy (TT), with severity inversely related to cell-mediated immunity status. Diagnosis is by clinical signs and microscopy examination of skin/nerve lesions. Treatment involves multidrug regimens over 6-12 months. Prevention focuses on active case finding, effective treatment, and reducing transmission through awareness and early detection of cases.
Leprosy is a chronic infectious disease caused by Mycobacterium leprae that affects the skin and peripheral nerves. It is transmitted through respiratory droplets, skin contact, or feeding. There are different classifications of leprosy depending on clinical presentation and bacterial load. Treatment involves multidrug therapy with dapsone, rifampicin, and clofazimine over 6-12 months depending on type of leprosy. Prevention focuses on isolation of infectious individuals to reduce transmission.
- Mycobacterium leprae is the causative bacteria of leprosy (Hansen's disease), which was first recognized in ancient times and described by Hippocrates. The bacteria was discovered in 1873 and causes a chronic granulomatous disease primarily affecting the skin, nerves, and respiratory tract.
- Leprosy has a long incubation period of 5-7 years on average and can be classified based on clinical presentation and bacterial load as tuberculoid, borderline, or lepromatous. Effective treatment involves multidrug therapy with rifampicin, dapsone, and clofazimine for 6-12 months depending on classification.
- Without treatment, le
M. tuberculosis and M. leprae are acid-fast bacilli that cause tuberculosis and leprosy, respectively. M. tuberculosis was discovered in 1882 and is transmitted through droplets. It has a cell wall containing mycolic acids and is a slow growing obligate aerobe. Laboratory diagnosis involves acid-fast staining of samples from sputum or tissues, as well as culturing on media like LJ. Treatment uses multi-drug therapy including isoniazid and rifampin. M. leprae causes a chronic granulomatous disease affecting skin and nerves. It is not cultivable but can be propagated in animals. Classification systems include tuberculoid, lepromatous, and
This document provides an overview of leprosy (Hansen's disease):
- It is caused by Mycobacterium leprae and mainly involves the peripheral nerves and skin. It can also involve other organs like the mouth, eyes, bones, and testes.
- Leprosy exists in several forms along a spectrum from tuberculoid leprosy to lepromatous leprosy. It is transmitted through droplets from the nose and mouth during close and frequent contact with untreated cases.
- Diagnosis involves clinical symptoms, skin smears, skin biopsies, and nerve biopsies to look for acid-fast bacilli and determine bacterial load and immune response patterns. There is
This document contains an MCQ discussion on leprosy. It begins with 13 multiple choice questions about leprosy, including topics like who discovered the causative bacteria, the generation time of Mycobacterium leprae, clinical presentations of leprosy, types of leprosy, treatment, and more. The document then provides explanations and key facts about leprosy, including that it is caused by Mycobacterium leprae, clinical features, types according to skin smear and clinical classification, signs and symptoms, pathogenesis, diagnosis including skin smear microscopy, and treatment with multidrug therapy.
This document discusses leprosy (Hansen's disease), including:
- Gerhard Armauer Hansen discovered Mycobacterium leprae in 1873.
- Clinical features include skin lesions and loss of sensation in fingers and toes.
- Lepromatous leprosy is the most infectious form, characterized by numerous acid-fast bacilli in skin scrapings.
- Diagnosis involves skin smears and biopsies to identify acid-fast bacilli within macrophages.
- Multi-drug therapy (MDT) uses dapsone, rifampicin, and clofazimine to treat paucibacillary and multibacillary forms of the
Leprosy is caused by Mycobacterium leprae, an obligate intracellular organism. It manifests as a spectrum of diseases from lepromatous leprosy (LL) to tuberculoid leprosy (TT), with severity inversely related to cell-mediated immunity status. Diagnosis is by clinical signs and microscopy examination of skin/nerve lesions. Treatment involves multidrug regimens over 6-12 months. Prevention focuses on active case finding, effective treatment, and reducing transmission through awareness and early detection of cases.
Leprosy is a chronic infectious disease caused by Mycobacterium leprae that affects the skin and peripheral nerves. It is transmitted through respiratory droplets, skin contact, or feeding. There are different classifications of leprosy depending on clinical presentation and bacterial load. Treatment involves multidrug therapy with dapsone, rifampicin, and clofazimine over 6-12 months depending on type of leprosy. Prevention focuses on isolation of infectious individuals to reduce transmission.
- Mycobacterium leprae is the causative bacteria of leprosy (Hansen's disease), which was first recognized in ancient times and described by Hippocrates. The bacteria was discovered in 1873 and causes a chronic granulomatous disease primarily affecting the skin, nerves, and respiratory tract.
- Leprosy has a long incubation period of 5-7 years on average and can be classified based on clinical presentation and bacterial load as tuberculoid, borderline, or lepromatous. Effective treatment involves multidrug therapy with rifampicin, dapsone, and clofazimine for 6-12 months depending on classification.
- Without treatment, le
M. tuberculosis and M. leprae are acid-fast bacilli that cause tuberculosis and leprosy, respectively. M. tuberculosis was discovered in 1882 and is transmitted through droplets. It has a cell wall containing mycolic acids and is a slow growing obligate aerobe. Laboratory diagnosis involves acid-fast staining of samples from sputum or tissues, as well as culturing on media like LJ. Treatment uses multi-drug therapy including isoniazid and rifampin. M. leprae causes a chronic granulomatous disease affecting skin and nerves. It is not cultivable but can be propagated in animals. Classification systems include tuberculoid, lepromatous, and
This document provides an overview of leprosy (Hansen's disease):
- It is caused by Mycobacterium leprae and mainly involves the peripheral nerves and skin. It can also involve other organs like the mouth, eyes, bones, and testes.
- Leprosy exists in several forms along a spectrum from tuberculoid leprosy to lepromatous leprosy. It is transmitted through droplets from the nose and mouth during close and frequent contact with untreated cases.
- Diagnosis involves clinical symptoms, skin smears, skin biopsies, and nerve biopsies to look for acid-fast bacilli and determine bacterial load and immune response patterns. There is
This document contains an MCQ discussion on leprosy. It begins with 13 multiple choice questions about leprosy, including topics like who discovered the causative bacteria, the generation time of Mycobacterium leprae, clinical presentations of leprosy, types of leprosy, treatment, and more. The document then provides explanations and key facts about leprosy, including that it is caused by Mycobacterium leprae, clinical features, types according to skin smear and clinical classification, signs and symptoms, pathogenesis, diagnosis including skin smear microscopy, and treatment with multidrug therapy.
This document discusses leprosy (Hansen's disease), including:
- Gerhard Armauer Hansen discovered Mycobacterium leprae in 1873.
- Clinical features include skin lesions and loss of sensation in fingers and toes.
- Lepromatous leprosy is the most infectious form, characterized by numerous acid-fast bacilli in skin scrapings.
- Diagnosis involves skin smears and biopsies to identify acid-fast bacilli within macrophages.
- Multi-drug therapy (MDT) uses dapsone, rifampicin, and clofazimine to treat paucibacillary and multibacillary forms of the
Leprosy is a chronic infection caused by Mycobacterium leprae that primarily affects the skin and peripheral nerves. It was first identified and isolated in 1873 by Gerhard Hansen in Norway. While leprosy has affected humans for thousands of years, it remains endemic in some developing countries today. Treatment involves multidrug therapy with rifampicin, dapsone, and clofazimine over the course of months to years depending on the type of leprosy.
This document discusses leprosy, its causes, symptoms, transmission, diagnosis and treatment. It notes that leprosy is a chronic infectious disease caused by Mycobacterium leprae that mainly affects nerves and skin. Symptoms start subtly with numbness and loss of sensation, and can progress to ulcers and disfigurement if untreated. It is transmitted through droplets from the nose of untreated patients. Diagnosis involves clinical examination, skin smears and biopsies. Treatment is multidrug therapy administered over 6 months to 1 year. Control relies on early detection, treatment and social support to prevent stigma and disability.
This document discusses leprosy, a chronic disease caused by Mycobacterium leprae. Key points include:
- Leprosy affects the skin and nerves and can cause deformities if left untreated. It is transmitted through droplets.
- M. leprae is an acid-fast bacillus that is intracellular and can be seen in bundles or "globi" inside cells.
- Leprosy manifestations depend on host cell-mediated immunity and range from tuberculoid leprosy with good immunity to lepromatous leprosy with poor immunity.
- Diagnosis involves examination of skin and nasal smears for acid-fast bacilli as well as le
Leprosy is caused by Mycobacterium leprae and primarily affects the skin and nerves. It exists on a spectrum from tuberculoid to lepromatous leprosy. Transmission occurs through droplets or nasal secretions, though most new cases have no known contact. Treatment involves multidrug therapy over 2 years for multibacillary or 6 months for paucibacillary cases. Reactions like reversal and erythema nodosum leprosum are immune-mediated flare-ups that may occur during or after treatment. Prevention focuses on early diagnosis and evaluation of contacts to reduce disability and transmission.
Leprosy, also known as Hansen's disease, is caused by the bacteria Mycobacterium leprae. It primarily affects the nerves, skin, and mucous membranes of the body. Leprosy is curable with multidrug therapy. While leprosy is moderately contagious, about 95% of people have natural immunity. Left untreated, leprosy can cause permanent damage to the skin, nerves, limbs, and eyes. Clinical signs include pale skin lesions with loss of sensation. Diagnosis involves skin smears and biopsy to detect bacteria. Treatment depends on the classification of leprosy into paucibacillary or multibacillary forms.
Leprosy is a chronic infectious disease caused by Mycobacterium leprae bacteria. It mainly affects nerves and skin. The disease presents on a spectrum depending on the host's immune response. Patients with strong immunity typically have localized tuberculoid leprosy lesions, while those with weak immunity are more likely to develop disseminated lepromatous leprosy with high bacterial loads. Leprosy is classified using systems that consider clinical features and bacterial loads. Treatment involves multidrug therapy to cure the disease and prevent disability and transmission.
"A Study of Clinical Profile of Leprosy in Post Leprosy Elimination Era"iosrjce
IOSR Journal of Dental and Medical Sciences is one of the speciality Journal in Dental Science and Medical Science published by International Organization of Scientific Research (IOSR). The Journal publishes papers of the highest scientific merit and widest possible scope work in all areas related to medical and dental science. The Journal welcome review articles, leading medical and clinical research articles, technical notes, case reports and others.
Key facts
Leprosy is a chronic infectious disease caused by a type of bacteria, Mycobacterium leprae.
The disease predominantly affects the skin and peripheral nerves. Left untreated, the disease may cause progressive and permanent disabilities.
The bacteria are transmitted via droplets from the nose and mouth during close and frequent contact with untreated cases.
Leprosy is curable with multidrug therapy (MDT).
Leprosy is reported from all the six WHO Regions; the majority of annual new case detections are from South-East Asia.
Overview
Leprosy is an age-old disease and is described in the literature of ancient civilizations. It is a chronic infectious disease which is caused by a type of bacteria called Mycobacterium leprae. The disease affects the skin, the peripheral nerves, mucosa of the upper respiratory tract, and the eyes. Leprosy is curable and treatment in the early stages can prevent disability. Apart from the physical deformity, persons affected by leprosy also face stigmatization and discrimination.
Scope of the problem
Leprosy is a neglected tropical disease (NTD) which still occurs in more than 120 countries, with more than 200 000 new cases reported every year. Elimination of leprosy as a public health problem globally (defined as prevalence of less than 1 per 10 000 population) was achieved in 2000 (as per World Health Assembly resolution 44.9) and in most countries by 2010. The reduction in the number of new cases has been gradual, both globally and in the WHO regions. As per data of 2019, Brazil, India and Indonesia reported more than 10 000 new cases, while 13 other countries (Bangladesh, Democratic Republic of the Congo, Ethiopia, Madagascar, Mozambique, Myanmar, Nepal, Nigeria, Philippines, Somalia, South Sudan, Sri Lanka and the United Republic of Tanzania) each reported 1000–10 000 new cases. Forty-five countries reported 0 cases and 99 reported fewer than 1000 new cases.
Transmission
The disease is transmitted through droplets from the nose and mouth. Prolonged, close contact over months with someone with untreated leprosy is needed to catch the disease. The disease is not spread through casual contact with a person who has leprosy like shaking hands or hugging, sharing meals or sitting next to each other. Moreover, the patient stops transmitting the disease when they begin treatment.
Diagnosis
The diagnosis of leprosy is done clinically. Laboratory-based services may be required in cases that are difficult to diagnose.
The disease manifests commonly through skin lesion and peripheral nerve involvement. Leprosy is diagnosed by finding at least one of the following cardinal signs: (1) definite loss of sensation in a pale (hypopigmented) or reddish skin patch; (2) thickened or enlarged peripheral nerve, with loss of sensation and/or weakness of the muscles supplied by that nerve; (3) microscopic detection of bacilli in a slit-skin smear.
Based on the above, the cases are classified into two types for treatment
Leprosy is a chronic infectious disease caused by Mycobacterium leprae that mainly affects the skin and peripheral nerves. It develops slowly and can have an incubation period of 2-20 years. Clinical features vary depending on immune response, from single hypopigmented lesions with distinct sensory impairment in tuberculoid leprosy to numerous symmetrical lesions with less severe sensory disturbance in lepromatous leprosy. Classification systems are based on histology and bacillary load. Treatment involves multidrug therapy to prevent disability and transmission.
Objective :
Describe the morphology and structure of mycobacterial tuberculosis ?
What are the tests required for mycobacterial infection :
Mantoux skin test
Sputum examination using Ziehl-Neelsen staining
Sputum culture using lowenstein-jensen media
Discuss the clinical features and transmission of mycobacterial tuberculosis.
What are the pathological changes in mycobacterium tuberculosis?
How to control mycobacterial infection in the environment and vaccine available?
done by : asem shadid , college of medicine .
This document provides information about leprosy (Hansen's disease), including:
- It is caused by Mycobacterium leprae and primarily affects the skin, nerves, and mucosa.
- There are several classification systems including paucibacillary, multibacillary, lepromatous, tuberculoid, and borderline. Classification depends on immune response and bacterial load.
- It remains a major public health problem with millions of cases worldwide, especially in India, Brazil, and African countries. Treatment involves multidrug therapy to prevent disability.
This document provides an overview of immunofluorescence (IF) techniques used in dermatology. IF can be used to directly detect antigens in tissue or indirectly detect circulating antibodies in serum. It involves using fluorescently-labeled antibodies that bind to target antigens, which are then viewed under a fluorescence microscope. Direct IF is used to detect in vivo antigen deposition in skin biopsies, while indirect IF detects circulating antibodies in serum. Modifications include antigen mapping to determine structural protein localization in epidermolysis bullosa, and salt split skin techniques to differentiate subepidermal bullous disorders. IF plays a key role in diagnosing immunobullous diseases and providing insight into the pathogenic mechanisms of various skin conditions.
This document provides information about leprosy (Hansen's disease) including:
- It is caused by slow-growing bacteria that can affect nerves, skin, eyes and nose.
- Signs include pale or reddish skin patches with loss of sensation and thickened nerves.
- It is diagnosed through skin smears and biopsies looking for acid-fast bacilli.
- Treatment involves multidrug regimens to cure it and prevent complications like paralysis.
- Nursing care focuses on nutrition, hydration, eye and nasal care to preserve function.
With
nursing
intervention,
patient is able to
perform ADLs with
minimal
assistance.
lesions all
over the
body
-loss of
sensation
on the skin
lesions
Dependent: With
nursing
intervention,
patient is able to
perform ADLs with
maximum
assistance.
Assessment:
Impaired
skin
integrity
related to
presence
of skin
lesions
Planning:
-Provide
clean
dressing
daily
-Monitor
for signs of
infection
-Teach
proper skin
care
Intervention:
-Cleansed
skin lesions
with normal
saline
1. Immunosuppressants and immunomodulators used in pregnancy include corticosteroids, azathioprine, cyclosporine, hydroxychloroquine, intravenous immunoglobulin, mycophenolate mofetil, rituximab, and tofacitinib.
2. The risk of these drugs depends on the gestational period, with higher risks in the first trimester and third trimester. Drugs are categorized by the FDA based on risk, from A (no risk) to X (contraindicated).
3. The document provides details on specific drugs, including their mechanisms of action, placental passage, FDA risk categories, and potential adverse effects
1. Lupus erythematosus is an autoimmune disease where the immune system attacks healthy tissue. It is characterized by a red rash and can cause skin, joint, kidney, and other organ involvement.
2. The document discusses the classification, epidemiology, pathogenesis, clinical features, investigations, management, and prognosis of both cutaneous and systemic lupus erythematosus.
3. Treatment involves general measures, local and systemic medications like antimalarials, corticosteroids, and immunosuppressants to control disease activity and damage. Monitoring is important to assess disease status and damage over time.
Leprosy is a chronic infection caused by Mycobacterium leprae that primarily affects the skin and peripheral nerves. It was first identified and isolated in 1873 by Gerhard Hansen in Norway. While leprosy has affected humans for thousands of years, it remains endemic in some developing countries today. Treatment involves multidrug therapy with rifampicin, dapsone, and clofazimine over the course of months to years depending on the type of leprosy.
This document discusses leprosy, its causes, symptoms, transmission, diagnosis and treatment. It notes that leprosy is a chronic infectious disease caused by Mycobacterium leprae that mainly affects nerves and skin. Symptoms start subtly with numbness and loss of sensation, and can progress to ulcers and disfigurement if untreated. It is transmitted through droplets from the nose of untreated patients. Diagnosis involves clinical examination, skin smears and biopsies. Treatment is multidrug therapy administered over 6 months to 1 year. Control relies on early detection, treatment and social support to prevent stigma and disability.
This document discusses leprosy, a chronic disease caused by Mycobacterium leprae. Key points include:
- Leprosy affects the skin and nerves and can cause deformities if left untreated. It is transmitted through droplets.
- M. leprae is an acid-fast bacillus that is intracellular and can be seen in bundles or "globi" inside cells.
- Leprosy manifestations depend on host cell-mediated immunity and range from tuberculoid leprosy with good immunity to lepromatous leprosy with poor immunity.
- Diagnosis involves examination of skin and nasal smears for acid-fast bacilli as well as le
Leprosy is caused by Mycobacterium leprae and primarily affects the skin and nerves. It exists on a spectrum from tuberculoid to lepromatous leprosy. Transmission occurs through droplets or nasal secretions, though most new cases have no known contact. Treatment involves multidrug therapy over 2 years for multibacillary or 6 months for paucibacillary cases. Reactions like reversal and erythema nodosum leprosum are immune-mediated flare-ups that may occur during or after treatment. Prevention focuses on early diagnosis and evaluation of contacts to reduce disability and transmission.
Leprosy, also known as Hansen's disease, is caused by the bacteria Mycobacterium leprae. It primarily affects the nerves, skin, and mucous membranes of the body. Leprosy is curable with multidrug therapy. While leprosy is moderately contagious, about 95% of people have natural immunity. Left untreated, leprosy can cause permanent damage to the skin, nerves, limbs, and eyes. Clinical signs include pale skin lesions with loss of sensation. Diagnosis involves skin smears and biopsy to detect bacteria. Treatment depends on the classification of leprosy into paucibacillary or multibacillary forms.
Leprosy is a chronic infectious disease caused by Mycobacterium leprae bacteria. It mainly affects nerves and skin. The disease presents on a spectrum depending on the host's immune response. Patients with strong immunity typically have localized tuberculoid leprosy lesions, while those with weak immunity are more likely to develop disseminated lepromatous leprosy with high bacterial loads. Leprosy is classified using systems that consider clinical features and bacterial loads. Treatment involves multidrug therapy to cure the disease and prevent disability and transmission.
"A Study of Clinical Profile of Leprosy in Post Leprosy Elimination Era"iosrjce
IOSR Journal of Dental and Medical Sciences is one of the speciality Journal in Dental Science and Medical Science published by International Organization of Scientific Research (IOSR). The Journal publishes papers of the highest scientific merit and widest possible scope work in all areas related to medical and dental science. The Journal welcome review articles, leading medical and clinical research articles, technical notes, case reports and others.
Key facts
Leprosy is a chronic infectious disease caused by a type of bacteria, Mycobacterium leprae.
The disease predominantly affects the skin and peripheral nerves. Left untreated, the disease may cause progressive and permanent disabilities.
The bacteria are transmitted via droplets from the nose and mouth during close and frequent contact with untreated cases.
Leprosy is curable with multidrug therapy (MDT).
Leprosy is reported from all the six WHO Regions; the majority of annual new case detections are from South-East Asia.
Overview
Leprosy is an age-old disease and is described in the literature of ancient civilizations. It is a chronic infectious disease which is caused by a type of bacteria called Mycobacterium leprae. The disease affects the skin, the peripheral nerves, mucosa of the upper respiratory tract, and the eyes. Leprosy is curable and treatment in the early stages can prevent disability. Apart from the physical deformity, persons affected by leprosy also face stigmatization and discrimination.
Scope of the problem
Leprosy is a neglected tropical disease (NTD) which still occurs in more than 120 countries, with more than 200 000 new cases reported every year. Elimination of leprosy as a public health problem globally (defined as prevalence of less than 1 per 10 000 population) was achieved in 2000 (as per World Health Assembly resolution 44.9) and in most countries by 2010. The reduction in the number of new cases has been gradual, both globally and in the WHO regions. As per data of 2019, Brazil, India and Indonesia reported more than 10 000 new cases, while 13 other countries (Bangladesh, Democratic Republic of the Congo, Ethiopia, Madagascar, Mozambique, Myanmar, Nepal, Nigeria, Philippines, Somalia, South Sudan, Sri Lanka and the United Republic of Tanzania) each reported 1000–10 000 new cases. Forty-five countries reported 0 cases and 99 reported fewer than 1000 new cases.
Transmission
The disease is transmitted through droplets from the nose and mouth. Prolonged, close contact over months with someone with untreated leprosy is needed to catch the disease. The disease is not spread through casual contact with a person who has leprosy like shaking hands or hugging, sharing meals or sitting next to each other. Moreover, the patient stops transmitting the disease when they begin treatment.
Diagnosis
The diagnosis of leprosy is done clinically. Laboratory-based services may be required in cases that are difficult to diagnose.
The disease manifests commonly through skin lesion and peripheral nerve involvement. Leprosy is diagnosed by finding at least one of the following cardinal signs: (1) definite loss of sensation in a pale (hypopigmented) or reddish skin patch; (2) thickened or enlarged peripheral nerve, with loss of sensation and/or weakness of the muscles supplied by that nerve; (3) microscopic detection of bacilli in a slit-skin smear.
Based on the above, the cases are classified into two types for treatment
Leprosy is a chronic infectious disease caused by Mycobacterium leprae that mainly affects the skin and peripheral nerves. It develops slowly and can have an incubation period of 2-20 years. Clinical features vary depending on immune response, from single hypopigmented lesions with distinct sensory impairment in tuberculoid leprosy to numerous symmetrical lesions with less severe sensory disturbance in lepromatous leprosy. Classification systems are based on histology and bacillary load. Treatment involves multidrug therapy to prevent disability and transmission.
Objective :
Describe the morphology and structure of mycobacterial tuberculosis ?
What are the tests required for mycobacterial infection :
Mantoux skin test
Sputum examination using Ziehl-Neelsen staining
Sputum culture using lowenstein-jensen media
Discuss the clinical features and transmission of mycobacterial tuberculosis.
What are the pathological changes in mycobacterium tuberculosis?
How to control mycobacterial infection in the environment and vaccine available?
done by : asem shadid , college of medicine .
This document provides information about leprosy (Hansen's disease), including:
- It is caused by Mycobacterium leprae and primarily affects the skin, nerves, and mucosa.
- There are several classification systems including paucibacillary, multibacillary, lepromatous, tuberculoid, and borderline. Classification depends on immune response and bacterial load.
- It remains a major public health problem with millions of cases worldwide, especially in India, Brazil, and African countries. Treatment involves multidrug therapy to prevent disability.
This document provides an overview of immunofluorescence (IF) techniques used in dermatology. IF can be used to directly detect antigens in tissue or indirectly detect circulating antibodies in serum. It involves using fluorescently-labeled antibodies that bind to target antigens, which are then viewed under a fluorescence microscope. Direct IF is used to detect in vivo antigen deposition in skin biopsies, while indirect IF detects circulating antibodies in serum. Modifications include antigen mapping to determine structural protein localization in epidermolysis bullosa, and salt split skin techniques to differentiate subepidermal bullous disorders. IF plays a key role in diagnosing immunobullous diseases and providing insight into the pathogenic mechanisms of various skin conditions.
This document provides information about leprosy (Hansen's disease) including:
- It is caused by slow-growing bacteria that can affect nerves, skin, eyes and nose.
- Signs include pale or reddish skin patches with loss of sensation and thickened nerves.
- It is diagnosed through skin smears and biopsies looking for acid-fast bacilli.
- Treatment involves multidrug regimens to cure it and prevent complications like paralysis.
- Nursing care focuses on nutrition, hydration, eye and nasal care to preserve function.
With
nursing
intervention,
patient is able to
perform ADLs with
minimal
assistance.
lesions all
over the
body
-loss of
sensation
on the skin
lesions
Dependent: With
nursing
intervention,
patient is able to
perform ADLs with
maximum
assistance.
Assessment:
Impaired
skin
integrity
related to
presence
of skin
lesions
Planning:
-Provide
clean
dressing
daily
-Monitor
for signs of
infection
-Teach
proper skin
care
Intervention:
-Cleansed
skin lesions
with normal
saline
1. Immunosuppressants and immunomodulators used in pregnancy include corticosteroids, azathioprine, cyclosporine, hydroxychloroquine, intravenous immunoglobulin, mycophenolate mofetil, rituximab, and tofacitinib.
2. The risk of these drugs depends on the gestational period, with higher risks in the first trimester and third trimester. Drugs are categorized by the FDA based on risk, from A (no risk) to X (contraindicated).
3. The document provides details on specific drugs, including their mechanisms of action, placental passage, FDA risk categories, and potential adverse effects
1. Lupus erythematosus is an autoimmune disease where the immune system attacks healthy tissue. It is characterized by a red rash and can cause skin, joint, kidney, and other organ involvement.
2. The document discusses the classification, epidemiology, pathogenesis, clinical features, investigations, management, and prognosis of both cutaneous and systemic lupus erythematosus.
3. Treatment involves general measures, local and systemic medications like antimalarials, corticosteroids, and immunosuppressants to control disease activity and damage. Monitoring is important to assess disease status and damage over time.
Secukinumab, an IL-17A inhibitor, demonstrated high efficacy and a favorable safety profile in treating severe chronic plaque psoriasis in pediatric patients in a 52-week randomized controlled trial. At week 12, 80.0% and 77.5% of patients receiving secukinumab low and high doses, respectively, achieved PASI 75 scores compared to 14.6% of placebo patients. 70.0% and 60.0% of patients receiving low and high doses achieved IGA mod 2011 0 or 1 scores compared to 4.9% of placebo patients. Efficacy was maintained through week 52 and secukinumab showed a favorable safety profile.
The document discusses the causes, symptoms, diagnosis and treatment of ingrown toenails. It begins by defining ingrown toenails as a common condition where the nail edge grows into the skin, causing pain. Risk factors include poorly fitting shoes and improperly trimmed nails. Symptoms progress from pain to infection if left untreated. Diagnosis is usually clinical. Treatment ranges from conservative approaches like soaking the toe and splinting the nail, to surgical techniques like partial nail removal or chemical ablation of the nail matrix. The goal of treatment is to relieve symptoms and prevent recurrence.
This document provides information on deep cutaneous mycosis, specifically focusing on subcutaneous mycoses. It discusses several types of subcutaneous mycoses including sporotrichosis, mycetoma, and chromoblastomycosis. For each condition, it describes the causative organisms, epidemiology, clinical presentation, diagnosis, and treatment. Sporotrichosis is caused by Sporothrix schenckii and can manifest as lymphatic or fixed cutaneous lesions. Mycetoma is characterized by grain formation and can be caused by fungi or actinomycetes. Chromoblastomycosis features slow growing exophytic lesions caused by pigmented fungi that form sclerotic bodies in tissue.
Graft-versus-host disease (GvHD) is a complication of allogeneic hematopoietic stem cell transplantation where donor T cells attack the recipient's organs, most commonly affecting the skin, liver, and gastrointestinal tract. It is classified as either acute or chronic GvHD depending on time of onset post-transplant. Acute GvHD presents within 100 days as a rash, diarrhea, and liver dysfunction while chronic GvHD appears after 100 days with skin sclerosis, lichenoid eruptions, and other organ involvement. Treatment involves immunosuppression with corticosteroids, calcineurin inhibitors, or other agents depending on GvHD severity and organ systems affected
This document provides an overview of nail anatomy through a presentation. It discusses the basic structure of the nail including the nail matrix, nail bed, nail plate, cuticle, and lunula. It describes the blood supply and nerve innervation of the nail. It also reviews nail growth and factors that can affect the rate of growth such as age, gender, season, and certain medical conditions. The presentation provides details on nail development during embryology and changes that occur in childhood and old age.
about various genodermatoses and classified according to clinical presentation.
mentioned are introduction clinical features histology management of each disease.
Mercurius is named after the roman god mercurius, the god of trade and science. The planet mercurius is named after the same god. Mercurius is sometimes called hydrargyrum, means ‘watery silver’. Its shine and colour are very similar to silver, but mercury is a fluid at room temperatures. The name quick silver is a translation of hydrargyrum, where the word quick describes its tendency to scatter away in all directions.
The droplets have a tendency to conglomerate to one big mass, but on being shaken they fall apart into countless little droplets again. It is used to ignite explosives, like mercury fulminate, the explosive character is one of its general themes.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
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Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
2. INTRODUCTION
• Caused by Mycobacterium leprae.
• It is highly contagious, but its morbidity is low
• Affects mainly the skin and peripheral nerves.
• Diagnosis is established based on skin and neurologic examination of
the patient.
• Early diagnosis is very important.
• The timely and proper implementation of treatment will prevent
sequelae and physical disabilities.
3. NEED FOR CLASSIFICATION
• To know variation in the disease presentation, its course, prognosis and complication.
• The correct classification helps to decide the treatment options.
• The frequency and the type of leprosy reaction also become clear.
• The infectivity of a case and its epidemiological importance can also be determined.
• A uniform classification helps in communication with the other workers, sharing the
ideas on a common platform and the comparison of data becomes more clear and
realistic.
4. • Leprosy may be classified based upon
• Bacteriological,
• Immunological,
• Clinical or Histopathological
• Parameters individually or by using a correlated combination of these.
• Bacteriological Criteria: BI is a measure of the density of the organisms
• Immunological Criteria :CMI against M. leprae, is measured indirectly by
lepromin testing and the patients classified as lepromin positive (good
immunity) to lepromin negative (poor immunity) on a standard scale.
5. • Histopathological Criteria :
• It is most definitive criteria for defining the different entities.
• The interpretations are not influenced by external factors, are less prone to
the subjective errors .
• However, it is not practicable to apply them universally over a large leprosy
population.
• Clinical Criteria :
Based on the clinical features is the easiest to apply .
Clinical features can be identified with some training by even a health worker in
the field.
7. 2. The Strassbourg classification (1923) :
based on location of bacilli in various tissue of the body.
1. Skin leprosy 2. Nerve lepros 3. Mixed
3. The Manila classification (1931):
• International system of classification for the first time use
• This formed basis of future classifications
4. The Cairo classification (1938)
5. The Pan American classification (1946)
6. The Havana classification (1948)
7. WHO expert committee (1952)
8. 8. The Madrid classification (1953)
9. The Indian classification (1955)
10. Ridley-Jopling classification (1966)
11. The New IAL classification (1981)
12. Job & Chacko classification
13. WHO classification (1982)
14. WHO classification (1988)
15. WHO classification based on the number of
lesions (1998)
16. Classification under NLEP, India (2009)
9. CLASSIFICATION
PREMANILA NODULAR
ANAESTHETIC
MANILA 1931 CUTANEOUS
NEURAL
MIXED
CAIRO 1938
Cutaneous' replaced by the term 'lepromatous' and
neural' was retained
Disadvantages. Use of the term 'neural', because nerves
are affected in both types.
Neuromacular simple
Neuromacular tuberculoid
Neuroanesthetic
PANAMERICAN 1946
Based on histological grounds.
term neural was replaced by the tuberculoid.
Disadvantages. Use of the term Uncharacteristic leprosy
Tuberculoid leprosy
Lepromatous leprosy
Uncharacteristic leprosy
HAVANA 1948
Uncharacteristic' was replaced by 'indeterminate'
Tuberculoid leprosy
Lepromatous leprosy
Indeterminate leprosy
10. RECOMMENDATION OF THE W.H.O EXPERT COMMITTEE 1952
Recommended adding a borderline group to the
three types accepted at Havana.
Therefore, leprosy was divided into four main
classes:
1. Lepromatous leprosy
2. Tuberculoid leprosy
3. Borderline leprosy
4. Indeterminate leprosy
11. The Madrid classification (1953)
Two types : Definite and typical clinical entities
1. Lepromatous type (L)
• Macular
• Diffuse
• Infiltrated
• Nodular
• Neuritic, pure (?)
2. Tuberculoid type (T)
• Macular (Tm)
• Minor tuberculoid (micropapuloid) (Tt)
• Major tuberculoid (plaques, annular lesion
etc.) (TT)
• Neuritic, Pure (Tn)
Two Groups’ were less distinct, nontypical
entities
3. Indeterminate group (I)
• Macular (Im)
• Neuritic type (In)
4. Borderline (Dimorphous) group(B)
• Infiltrated
• (Others?)
The major problem with this classification was that the pure neuritic type was included in I, L and T
groups.
12. The Indian classification (1955)
Almost similar to the Madrid classification, but maculoanesthetic and pure
neuritic were kept as separate categories.
The classification was kept simple for field workers.
1. Lepromatous (L)
2. Tuberculoid (T)
3. Maculoanesthetic (MA)
4. Polyneuritic (P)
5. Borderline (B)
6. Indeterminate (I)
13. Ridley-Jopling classification (1966)
• The main advantage It is based on
bacteriological, immunological,
histopathological and clinical features
of leprosy.
• For these reasons, this classification
has been widely accepted.
• The main drawback is that there is no
specific place for the indeterminate
and pure neuritic leprosy in the
spectrum.
1. Tuberculoid leprosy (TT)
2. Borderline tuberculoid leprosy (BT)
3. Mid-borderline leprosy (BB)
4. Borderline lepromatous leprosy (BL)
5. Lepromatous leprosy (LL)
14. • The New IAL classification (1981)
MA Leprosy was merged with T
1. Lepromatous (L)
2. Tuberculoid (T)
3. Polyneuritic (P)
4. Borderline (B)
5. Indeterminate (1)
WHO classification (1982)
Base on Bacterial index
1. Paucibacillary leprosy (BI<2+)
2. Multibacillary leprosy (BI≥2+)
15. WHO classification (1988)
.
• Categorized into PB or MB
leprosy depending upon Slit-skin
smears
• All the patients with
demonstrable acid fast bacilli in
SSS without any reference to
bacterial index were to be
categorized as multibacillary
1. Paucibacillary leprosy: It included
only smear negative cases belonging to
• Indeterminate (I), tuberculoid (TI),
• and borderline tuberculoid (BT) cases as
classified under Ridley-Jopling classification
and
• Indeterminate (I), and tuberculoid (T) cases
under Madrid classification
2. Multibacillary leprosy: included all
• Mid-borderline, borderline lepromatous ,
and lepromatous under Ridley-Jopling
classification
• Borderline (B) and lepromatous (L) cases
under the Madrid classification
• Any other smear positive case
16. WHO classification based on the number of lesions (1998)
• Based upon the total number of leprosy lesions in the
patient and categorized into PB and MB types .
• If skin smear facilities are available or any patient, the
smear positive cases should be placed in
multibacillary type irrespective of the number of
lesions.
• With the use of this classification, some MB cases may
wrongly be classified into PB types resulting in under
treatment.
• Paucibacillary single lesion
leprosy (SLPB);
• Paucibacillary leprosy (2-5
skin lesions);
• Multibacillary leprosy- six or
more skin lesions and , also,
all smear positive cases.
• WHO 2017
17. Classification under National Leprosy Eradication
Programme, India (2009)
• Number of nerves involved also consideration along with the skin
lesion count.
• If skin smear is positive, irrespective of number of skin and nerve
lesions, the disease is classified as MB leprosy;
• But if skin smear is negative it is classified on the basis of the number
of skin and nerve lesions.
18. 1. Paucibacillary (PB)
• Skin lesions - 1-5 lesions
• Peripheral nerve involvement - No nerve or only one nerve with or
without 1-5 lesions
• Skin smears - Negative at all sites
2. Multibacillary (MB)
• Skin lesions – 6 and above
• Peripheral nerve involvement - More than one nerve irrespective
of the number of skin lesions
• Skin smears - Positive at any site
19. ETIOPATHOGENESIS
M. leprae, was identified by Norwegian physician Gerhard Armauer
Hansen in 1873. Therefore, it is also called Hansen’s bacillus.
• class Schizomycetes
• order Actinomycetales
• family Mycobacteriaceae
• genus Mycobacterium
It is a straight or slightly curved rod, with rounded ends, measuring 1.5-8
microns in length by 0.2-0.5 micron in diameter.
In smears, stains red with carbol fuchsin using the Ziehl-Neelsen (ZN)
stain, acid-alcohol resistant because of mycolic acid.
20. • Arranged in parallel chains, just like cigarettes in a pack, forming the
globi.
• M. leprae infects mainly macrophages and Schwann cells.
• It has never been grown in artificial media.
• Reproduction (about 12-14 days) in the foot pads of mice.
• 27 ºC and 30 ºC.
• Cooler areas preferred skin, peripheral nerves, testicles, and upper
airways, and lower visceral involvement.
• Immune privilege sites- scalp, axilla, groin, transverse band of skin
over lumbosacral area, midline back.
22. IMMUNOPATHOLOGY
• Ability of the host to develop different degrees of cellular immune
response to M. leprae, led to the spectral concept of the disease.
• The first barrier to infection with M. leprae is innate immunity,
represented by the integrity of epithelia, secretions, and surface
immunoglobulin A(IgA).
• In addition, natural killer (NK) cells, cytotoxic T lymphocytes, and
activated macrophages.
23. Genes involved in the immuno-pathogenesis of
leprosy
1. MHC genes
2. Cytokine genes
3. Low molecular weight Proteases 2 and 7
4. Transporters associated with peptide loading 1 and 2
5. Protein tyrosine phosphatase non-receptor type 22
6. Single-nucleotide polymorphism involving lymphotoxin-a, VIT D
receptor (VDR), TNF-a, IL-10, IFN-Y, HLA genes, and TLR1
24. • leprosy patients may have different MHC patterns with HLA variability.
• The spectrum of disease at one end
• little or no bacillary proliferation,
• positive lepromin reaction and
• epithelioid granulomas.
• Other end
• .Bacillary proliferation,
• lepromatous or foam cell granulomas and
• negative lepromin reaction.
• The dual response of macrophages and monocytes to leprosy bacilli may be
responsible for the clinico-pathological bipolarity of leprosy
25. Key steps in the immunopatho-genesis of leprosy
1. The portal of entry for M. leprae is via the nose and then it spreads
to the skin and nerves via the circulation.
2.Invasion and multiplication in dermal lymphatics and vascular
cells play a major role in the hematogenous spread.
3. M. leprae invades peripheral nerves via blood vessels of the
perineurium.
26. 4. The clinical phenotype depends on the immunological response mounted
by the host.
5. In tuberculoid leprosy the monocytes destroy the organism completely,
whereas in lepromatous leprosy, microvacuolated monocytes (phagocytes)
with bacillary debris may persist.
6. The specific response in Th1 or Th2 is dependent on the cytokines/chemokines
that are released after the mycobacterial lipoproteins are recognized by the Toll-
like receptors on innate immune cells following uptake of M leprae by the
dendritic cells.
conti.
27. 7. TLR1 and TLR2 activation leads to Th1-type cytokines, and Th2-type
cytokines are associated with inhibition of this activation.
monocytes and DCs in TT lesions have a stronger expression of TLR1
and TLR2 as compared with LL lesions.
8. The CD4/CD8 T-cell ratio is 2:1 in tuberculoid leprosy lesions, leading to a
Th1-like profile with secretion of pro-inflammatory cytokines IL-2, IFN-y,
TNF and IL-12 that induce strong CMI and phagocytic activity.
9. In lepromatous leprosy there is weak CMI, but strong humoral response, CD4/CD8
ratio is 1: 2, and Th2-like profile characterized by anti-inflammatory cytokines IL-4
and IL-10.
conti.
28. 10. A polyclonal B-cell response and autoantibodies production with
no effect on M. leprae results in formation of immune complexes.
11. The borderline forms are immunologically unstable, shifts
between the two polar forms occur; causing reactions that are a
feature of the borderline states.
conti.
29.
30. Tuberculoid lesions Lepromatous lesions
• Predominance of T helper (CD4+)
• CD4:CD8 ratio of 2:1, the same ratio found in blood
• CD4+ cells in tuberculoid lesions express the
phenotype memory-T cells (CD45R0+)
• Predominance of the population of T CD8+
lymphocytes with CD4:CD8 ration of 1:2
• most CD8+ cells belong to the CD28- phenotype,
suggesting that they are T-suppressor cells
• cytokines involved
• interferon-gamma (IFN-γ), interleukin-2 (IL-2), and
TNF-α.
• Suppressor cytokines of macrophage activity
• interleukin-4 (IL-4), interleukin-5 (IL-5), and IL-10
• Th1 pattern
• enhancers of cell-mediated immunity and reduced
proliferation of M. leprae.
• Th2 pattern
• Contribute to the stimulation of B lymphocytes,
with increased humoral immune response and
production of antibodies
• IL-7 and IL-12 - growth and differentiation factors
of T cells
• IL-13 seems to play a role in the
immunosuppression of lepromatous lesions.
• In type 1 reaction, sudden influx of CMI and T CD4+
cells and production of IL-1, TNF-α, IL-2, and IFN-γ
in the lesions, Th1 response pattern.
• In ENL, immune complexes reaction, characterized
by increased IL-6, IL-8, and IL-10 in the lesions,
suggesting Th2 response
31. Divergent macrophage pathways for antimicrobial
activity versus phagocytosis
• Toll like receptor (TLR) induced IL-15 triggers
↓
• Upregulation of the Vit D receptor (VDR) and CYP27b1.
↓
• CYP27b1 converts inactive 25D3 to active 1, 25 D3 which can then
↓
• Bind the to VDR and initiate transcription of cathelicidin and in conjunction with IL-1,
↓
• Results in Defensin beta 4 production.
↓
• Cathelicidin initiates autophagy and autophagolysosomal fusion resulting in the killing of mycobacteria.
32.
33. Phagocytic pathway
• IL-10 induces
↓
• A scavenger receptor program
↓
• Resulting in enhanced phagocytosis of mycobacteria and oxidized
lipid
↓
• Resulting in foam cell formation and microbial persistence.
• IL-10 and IL-4 can suppress TLR expression.
34. SCHWANN CELL (SC)
• Initial Target: Laminin a2 -> PGL 1 of M. leprae binds to it
• Laminin a2 seen in Schwann cell, Striated muscle, Placenta
• H1p/LBP21-> potentiates interaction of M. leprae with SC
• SC processes antigen & presents it through MHC - II
• CD4+ T Cells then get activated & releases ILs-> leads to
• Macrophage activation -> kills bacteria
• Concurrent nerve demyelination occurs due to inflammatory events
35.
36. MECHANISM OF ENTRY INTO NERVE
• SC membrane has laminin 2 and a laminin 2 receptor (a-dystroglycan)
• Laminin 2 has a G domain on the a2 chain
• PGL-1 of M. leprae binds to this domain.
• This PGL-Laminin-2 complex interacts with a-dystroglycan, leading to
uptake of M. leprae.
• Laminin binding protein 21 (LBP21) of M. leprae also binds to a-DG on
SC membrane, leading to its entry.
37. Important innate immune cells
Macrophages:
• Role in immune response to M. leprae
• Phagocytic and antimicrobial function
• M1 M ↑ in TT spectrum: Antimicrobial
• M2 M ↑ in LL spectrum: Phagocytic
• Cytokine release modulates the adaptive Th response
38. Dendritic cells (DC)
•Professional antigen presenting cells; release
proinflammatory cytokines
• Marked deficit in LL
• Activation and maturation of DCs inhibited by M.
leprae
• PGL-I impairs DC maturation and activation
39. Keratinocytes
• ↑ ICAM expression in TT
• Upregulation of human beta-defensins 2 and 3 on
stimulation with M. leprae
• Major producer of CXCL-10 in TT
• Present M. leprae to CD4+ T cells
40. PGL-1
• It is a major glycolipid antigen of M. leprae.
• Is unique to M. leprae.
• It is part of lipid capsule.
• Accounts for 2% of mass of bacilli
• Has an antigenically distinct trisaccharide linked to phenol, which is
linked to 29C phthiocerol, which are attached 2 mycoserosic acids.
41. PGL-1 (contd.)
• Specific IgM antibodies develop to it, more at lepromatous spectrum.
• Antigen specificity resides in terminal sugars, which has been
exploited for serodiagnosis.
• Helps in entry and colonization within phagocytes.
• Once inside phagocytes, it can scavenge ROS and helps the bacteria
survive intracellularly.
42. REACTIONAL STATES
• Leprosy reactions result from changes in the immune balance
between the host and M. leprae.
• Such reactions are acute episodes that primarily affect the skin and
nerves, being the main cause of morbidity and neurological disability.
• They may occur during the natural course of the disease, throughout
treatment or after it.
• They are classified into two types: type 1 reaction and type 2
reaction.
43. TYPE 1 REACTION
• Delayed-type hypersensitivity reactions.
• It M/C occurs in the immunologically unstable borderline forms of leprosy (BT,
BB & BL)
• Expression of MHC II on the surface of the infected cells leading to antigen
presentation resulting in cell damage mediated by CD4 lymphocytes through
cytokines such as TNF alfa.
• Th1 response ensues and pro-inflammatory cytokines, such as IFN-Y, IL-12, IL-
8, monocyte chemoattractant protein (MCP)1
• And inducible nitric oxide synthase (iNOS), are expressed in the lesions.
44. Conti. T1R
• Rise in serum TNF-a levels is observed 4-8 weeks prior to T1R, highlighting the key role
of TNF-a in leprosy immunopathogenesis.
• A microsatellite polymorphism in the tlr2 gene have been found to predispose to an
increased frequency of T1R;
• Increase in Tregs during T1R. It perform the role of controlling the exacerbated CMI seen
in T1R with beneficial consequences for the host
• On the other hand, Tregs to be depleted in T2R. The unregulated inflammation may
cause extensive clinical manifestations associated with widespread tissue damage.
45.
46. cont T1R
• Th17, an increase in T2R is consistently and in T1R variably
• The cytokine much higher levels in T1R skin lesions than T2R lesions,
• T1R is a hyperimmune response characterized by a selective increase
of CD4+ IFN- gama producing cells resulting in the clearing of bacilli
and concomitant tissue damage,
47. TYPE 2 REACTION
• T2R is immune complex mediated affects patients with BB, BL, and LL forms .
• It is initiated by the release of mycobacterial antigens, resulting in immune
complex formation and activation of complement pathway and mononuclear
cells releasing cytokines mediating tissue damage.
• Monocytes also play a significant role in leprosy reactions and associated
tissue damage.
48. conti.T2R
• It is possible that T-cell activation leading to cytokine-mediated killing
of bacilli may release pathogen-related antigens which then bind to
existing antibodies to create immune complexes.
• There are reports of increased absolute neutrophil count, in ENL.
• IFN-y is the hallmark cytokine for T2R.
The cell wall attached to the plasma membrane is composed of peptidoglycans bound to branched chain polysaccharides, consisting of arabinogalactans, which support mycolic acids, and lipoarabinomannan(LAM),
. Lipoarabinomannan (a major lipoglycan of the cell wall envelope)—resistance to oxidative metabolites;
2. Mycolic-acid glycolipids, wax D, and trehalose dimycolate (cord factor)—granuloma formation and adjuvant activity;
3. Sulfatides—inhibition of phagolysosome fusion.
The capsule, the outermost structure, has lipids, especially phthiocerol dimycocerosate and phenolic glycolipid (PGL-1), which has a trisaccharide bound to lipids by a molecule of phenol.