Cutaneous Tuberculosis Disease

CHAPTER -1 CUTANEOUS TUBERCULOSIS INTRODUCTION: In this innovative world while progress in medicine has helped up to deal with many diseases Tuberculosis and Cutaneous Tuberculosis is still a challenge for doctors. A resurgence of Cutaneous Tuberculosis in areas of high HIV incidence, drug resistant present in patients with pulmonary tuberculosis and in immunosupressed patients are the main challenges for clinicians. (6) Cutaneous TB is caused by Mycobacterium tuberculosis, Mycobacterium bovis, Bacillus Calmette-Guerin (BCG) vaccinations & and the Tuberculids whose pathogenesis is poorly understood. Cutaneous TB is very variable in its clinical presentation, significance & prognosis. Factors which effect on variability are:

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  • The pathogenesity of the organism involved.
  • The Previous treatment given.
  • The Immune status of the patients which can be related to the presence of Acquired Immunodeficiency Syndrome (AIDS) or Immunosuppressive therapy.
  • The Port of infection.
  • Any Local factors like, the recent Trauma, the lymphatic drainage, the vascularity of area and the proximity to lymph nodes).

PREVALANCE: Thirty years ago it was assumed world wide that tuberculosis would be eradicated in the developed countries, as its incidence increased only on by average 6 % in the United States and 10% in Europe between the years 1953 and 1985. However, in 1983 tuberculosis was declared a global emergency by the world Health Organization because of a sharp increase in incidence. (9) Among infectious diseases, Tuberculosis is an important cause of death. Tuberculosis was responsible for 6% of deaths worldwide. Global prevalence of TB currently is greater than 32%. More than 50% of new patient occurrences were in 5 Asian countries, i.e. India (largest worldwide patient load), China, Indonesia, Bangladesh, and Pakistan(ref ?) The current global burden of Tuberculosis is mind boggling. In 1997, the incidence of new Tuberculosis patients approached 8 million in addition to more than 16 million patients already diagnosed. Around 2 million people died of Tuberculosis in 1997 with a global fatality rate of 23%, fatality rates exceed 50% in some African countries in which there is a high HIV incidence. Approximately 8% of tuberculosis patients are HIV infected. (2) Prevalence of tuberculosis infection in 1985, 1995 and 2005 (10) Prevalence of tuberculosis has increased between 1985 and 2005.According to the World Health Organization case reports statistics, in 1985 there were around 3 million patients of tuberculosis of all types with the highest no of cases in Asia and Africa. In Asia the highest numbers of cases were in India, Pakistan, China, Philippines, Bangladesh, Afghanistan and Vietnam. In Africa the highest number of case were in Ethiopia, Nigeria, South Africa, Congo, Morocco and Tanzania. (10) During the last two decades the number of cases increased all over the world. In 1995 the total number of cases increased to 4.6 million and in 2005 to 7.5 million worldwide. In Asia in 2005 the highest numbers of cases were in India, China & Pakistan. In Africa in 2005 the highest numbers of cases were in South Africa, Ethiopia & Congo. (10) There is an increasing rate of tuberculosis in the developing countries is approximately 500/100,000/y. Great alarm has been the progressive increase in numbers of strains of tuberculosis that are resistant to antibiotics. Since 1984, that incidence of extra pulmonary tuberculosis has increased at even faster rate than that of pulmonary tuberculosis and is considered to be a diagnostic criterion in the case definition for AIDS. Because immunocompromised individual are at increased risk of extra pulmonary tuberculosis, so dermatologist are renewing their historic role in the diagnosis of cutaneous lesions of tuberculosis. (11) EPIDEMIOLOGY: Epidemiological analysis is used to detect the changing trends in the incidence and prevalence of mycobacterial disease in the community. The main objectives of these methods are to determine the natural behavior of disease and factors which affect his behavior and to calculate future trend if possible to help in the design of any control measures and to assess the usefulness of these measure.(8) Even though 1 of 3 individuals on this planet is infected with tubercle bacillus, the incidence of Cutaneous TB appears low. In areas such as India or China where TB prevalence is high, cutaneous manifestations of TB (overt infection or Tuberculids) are found in less than 0.1% of persons seen in dermatology clinics. The frequency of patients with Cutaneous Tuberculosis seen between 1980 and 1993 in a hospital dermatology clinic in Madrid was 16 per 10,304 which was 0.14%. In a ten year retrospective survey of patients seen in governmental dermatology clinics in Hong Kong between 1983 and 1992, the detected incidence of Cutaneous Tuberculosis among patients was 179 per 267,089 which was 0.07%. Among patients with Cutaneous Tuberculosis only15% had classic Cutaneous Tuberculosis and 85% had tuberculids. In that classical cutaneous tuberculosis approximately 5% had lupus vulgaris, 5% had Tuberculosis Verrucosa cutis and 5% had scrofuloderma. (2) In a tertiary-care hospital in northern India, 0.1% of dermatology patients seen between 1975 and 1995 had Cutaneous Tuberculosis. Lupus vulgaris was the most common manifestation around 55%, followed by scrofuloderma 27%, TB Verrucosa cutis 6%, tuberculous gumma 5%, and tuberculids occurred in 7%. (2) FREQUENCY: USA: In the United States, tuberculosis cases decreased from 84,304 cases in 1953, when national reporting was first began, to 22,201 in 1985.  This represented fairly steady decline of about 5.8% per year. However, the turn down in tuberculosis cases stopped in between 1985 and 1992. In 1992 the annual number of cases increased by 20% to 26,673 cases. (12) The increases were concentrated geographically in several states, with over 90% of the 14,871 cases in California, Florida, New Jersey, New York, and Texas and demographically tuberculosis occurred in racial and ethnic minorities, in people aged 25 to 44, males and in those born abroad. Especially troubling, and indicative of increasing transmission of new infections, was a 36% increase in tuberculosis among children 4 years old or younger. Tuberculosis appears to be on the decline again in the United States as numbers with only 14,871 cases in 2003. (12) Reported tuberculosis cases in United States, 1982-2002 (12) The percentage of Tuberculosis patients who were born abroad individuals was 42%. People born in Mexico, the Philippines, and Vietnam account for one half of born abroad Tuberculosis patients in the United States. The Tuberculosis rate among born abroad people was 4 to 6 times higher than for US-born peoples. Minimum estimates of the proportion of TB patients with coincident HIV infection were approximately 10-15%. Among people aged 25-44 years, this proportion increased to 20-30%. (12) The fundamental origin of this new Tuberculosis epidemic in troubled states reflects a minimum of four major factors including (1) the involvement of Tuberculosis with the HIV epidemic, (2) the increased migration from countries where Tuberculosis is common, (3) the spread of Tuberculosis in congested settings (health-care facilities, prisons, homeless shelters), and (4) the worsening of the basic health-care infrastructure. (2) Molecular typing of Mycobacterium tuberculosis isolates in the United States in a restriction fragment-length polymorphism study suggests more than one third of new patient incidence results from people-to-people transmission, and the remainder result from reactivation of latent infection. Approximately 1 of 13 Mycobacterium tuberculosis isolates currently shows a form of drug resistance. (2) The modern introduction of biological agents that block tumor necrosis factor-alpha in the treatment of rheumatoid arthritis, psoriasis, and several other autoimmune disorders has additional raised about the necessity of the identification of patients with latent Tuberculosis. At present, several hundred cases of Tuberculosis have been reported in patients who receive these tumor necrosis factor-alpha antagonists. (2) HISTORY: Tuberculosis has an ancestry which can be traced to the earliest history of mankind. It was recognized as a contagious disease by the time of Hippocrates and Aristotle in 350 BC. Signs of skeletal Tuberculosis were identified in Europe since Neolithic times and in ancient Egypt around 3700 BC in mummified bodies. Evidence of TB appears in Biblical scripture, in Chinese literature dating back to around 4000 BC, and in religious books in India around 2000 BC. (5) During1600’s and 1800’s tuberculosis was known ass the “Great White Plague” in Europe.  Other names for Tuberculosis were Phthisis which was from Greek term phthinein, meaning to waste away, scrofula which were used for swellings of the lymph nodes of the neck and consumption which were used as progressive wasting away of the body.(2) In 1826 Laennec first reported cutaneous tuberculosis which he called PROSECTOR WART. Following Laennec, Rokitansky and Virchow described the histological features in detail comparing them to those of visceral tuberculosis. (6) The Incidence of TB increased with population density and urban development so that by the Industrial Revolution in Europe in 1750, it was responsible for more than 25% of adult deaths. Indeed, in the early 20th century, TB was the leading cause of death in the United States. In 1882, a German biologist ROBERT KOCH presented his discovery of the organism that caused TB. NEIL FINSEN won the Nobel Prize in Medicine in 1903 for introducing UV light into the treatment of skin TB. (2) With the help of better living conditions and the introduction of the antibiotic streptomycin on 20th November 1944, the number of reported TB patients in the United States steadily declined around 126,000 TB patients in 1944, 84,000 in 1953, 22,000 in 1984, and 14,000 in 2004.(2) MODE OF TRANSMISSION: Tuberculosis is an airborne contagious disease that occurs after inhalation of infectious droplets expelled from patients with laryngeal or pulmonary Tuberculosis during coughing, sneezing, or speaking. Each cough can generate more than 3000 infectious droplets. Droplets are so small around 1 to 5 micro meter, that they remain airborne for hours. (2) The likelihood that disease transmission will occur depends upon the infectiousness of the tuberculous patient, the environment in which exposure takes place, and the duration of exposure. Roughly 20% of people in the infected household contact develop infection. Micro epidemics have occurred in closed environments such as transcontinental flights and submarines. Tuberculin sensitivity develops 2 to 10 weeks after infection and usually is lifetime. ????(2) Because Tuberculosis induces a powerful immune response, individuals with positive tuberculin reactions are at a considerably lower risk of acquiring new tuberculous infection. In HIV-infected individuals, active Tuberculosis is more likely to occur from reactivation of existing disease than from superinfection with a new mycobacterial strain. (2) Without treatment, an estimated 10% lifetimes possibility exists of developing active disease after tuberculous infection, 5% occurs within the first 2 years and 5% thereafter. An Increased risk of acquiring active disease occurs during HIV infection, Intravenous drug abuse, diabetes mellitus, silicosis, immunosuppressive therapy, cancer of the head and neck, hematological malignancies, end-stage renal disease, intestinal bypass surgery or gastrectomy, chronic malabsorption syndromes and low body weight. Infants younger than two years are associated with increased risk. (2) 1) DIRECT INHALATION: The most common mode of entry via portal in to the lungs usually resulting from the Inhalation of airborne droplets containing a few bacilli, expectorated by individuals with “open” pulmonary disease.(8) 2) INDIRECT INHALATION: A) Ingestion: Less often bacilli may be swallowed and lodge in to the tonsil or in the wall of the intestine. These infections are chiefly related to the consumption of contaminated milk products. (8) 3) INOCULATION: Cutaneous tuberculosis manifestations depend upon the method of cutaneous inoculations, which may be exogenous that is from an out side source, may occur by autoinoculation, or may be by endogenous .Direct exogenous inoculation in an individual not previously infected with tuberculosis causes primary tuberculosis infection, will led to the tuberculous ‘chancre’ or to tuberculosis Verrucosa cutis depending upon the immune status of the patient. Another example of exogenous transmission is lupus vulgaris at the site of BCG vaccination. (9) Endogenous transmission can occur by continuous extension of tuberculous process underlying the skin as in scrofuloderma, by the way of lymphatic as in lupus vulgaris and by hematogenous spread as in acute miliary tuberculosis or lupus vulgaris. (9) Infrequent mode of transmission is direct implantation in to the skin through cuts and abrasions. These troubles usually in persons, working with infected material or cultures of tubercle bacilli. These skin lesions were called as “Prosector warts” (8) CLASSIFFICATION OF CUTANEOUS TUBERCUCLOSIS: Cutaneous tuberculosis clinical manifestations comprise a considerable number of skin changes, usually sub classified in to more or less distinct disease forms. Classification depends on morphology & more recently mode of transmission or the immunological state of host, but none of them satisfies completely.

1)INOCCULATION TUBERCUCLOSIS (Exogenous Source) Tuberculosis chancre
Warty tuberculosis(Verruca cutis)
Lupus vulgaris(some)
2) SECONDARY TUBERCULOSIS (Endogenous source)
A) Contiguous spread Scrofuloderma
B) Auto-inoculation Orifical tuberculosis
3)HAEMATOGENOUS TUBERCULOSIS Acute miliary tuberculosis
Lupus vulgaris(some)
Tuberculous gumma
A) Micropapular Lichen scrofulosorum
B) Papular Papular/Papulonecrrotic TB
C) Nodular Erythema induratum(Bazin)
Nodular Tuberculids

(CLASSIFICATION OF TUBERCULOSIS, MODIFIED FROM beyt et al) (4) CHAPTER-2 CLASSIFICATION OF MYCOBACTERIA: Tuberculosis is an infectious disease which is caused by the Mycobacterium species. Mycobacteria are acid fast, non-sporulating, non-motile & weakly gram positive organisms. TEM micrograph of Mycobacterium tuberculosis Table 3:

Kingdom Bacteria
Phylum Actinobacteria
Order Actinomycetales
Suborder Corynebacterineae
Family Mycobacteriaceae
Genus Mycobacterium

Scientific classification by Lehmann & Neumann. (3) In 1950’s Runyon classified the atypical mycobacteria according to their ability to form pigment, their rate of growth & colony characteristics. This classification also includes obligate human pathogens and facultative human pathogens. (1) Today more then 60 species of mycobacteria are identified. Around 41 of these were included in the approved lists of bacterial names in 1980. (9) 30 species of mycobacterium are known that can cause disease in humans. The most common causative organism includes:

  • Mycobacterium tuberculosis
  • Mycobacterium Leprae.
  • Atypical mycobacteria.

The species which produce disease in tuberculosis primary complex include:

  • Mycobacterium tuberculosis.
  • Mycobacterium Bovis.
  • Mycobacterium Africanum.

Sometimes Bacillus Calmette Guerin (BCG) may also cause disease. (1) MEDICAL CLASSIFICATION: For the purpose of diagnosis & treatment mycobacteria can be classified in several major groups. Mycobacterium tuberculosis complex, which can cause tuberculosis by the pathogens Mycobacterium tuberculosis, M Bovis, M Africanum & M microti. Mycobacterium Leprae, which causes Hansen’s disease. Nontuberculous mycobacteria are the mycobacteria which can cause pulmonary disease, lymphadenitis, and skin disease & disseminated disease.

1)Obligate human pathogens M. tuberculosis-bovis group including bacillus Calmette-Guerin(BCG) & M Africanum (not included in runyon classification
2)Facultative Human pathogens
M. kansasii I
M. marinum I
M. simiae I
M. scrofulaceum II
M. szulgai II
M. gordanae II
M. avium-intracellualr complex III
M. haemophilum III
M. Ulcerans III
M. xenopi III
3) Nonpathogens
M. flavescen II
M. terrae complex III
M. trivale III
M. gastri III
1))Facultative Human pathogens
M. fortuitum I V
M. chelonae I V
M. abscessus I V
2) Nonpathogens
M. smegmatis I V
M. phlei I V
M. vaccae I V

STAINING CHARACTERISTICS OF MYCOBACTERIA: Mycobacteria are aerobic, facultative, intracellular non-spore forming and non-motile curved rods measuring 0.2- 0.5 by 2-4 um. Mycolic acid rich long chain glycol lipids and phospholipoglycans, a mycocides present in the cell wall of mycobacteria protect them. (2) Mycobacteria do not gram stain readily but their most valuable staining characteristic is Acid Fastness. This ability retains carbol fuchin dye after washing with acid or alcohol occurs because of the high content of cell wall mycolic acids, fatty acids & other lipids. Other staining methods used include Dietrele, auramine-Rhodamine and phenolic acridine orange stains. Nocardia rhodococcus, legionella dadei, isospora & cryptosporidium also share acid fastness. (1) The Ziehl-Neelson acid-fast stain, while highly specific for mycobacteria, is relatively insensitive, and recognition requires at least 10,000 bacilli per mL; most clinical laboratories currently use a more sensitive auramine-rhodamine fluorescent stain (auramine O). Routine culture uses a nonselective egg medium called Lowenstein-Jensen or Middlebrook 7H10 and often requires more than 3-4 weeks to grow because of the 22-hour doubling time of mycobacterium tuberculosis. Radiometric broth culture, BACTEC radiometric system of clinical specimens significantly reduces time 10 to 14 d for mycobacterial recovery. DNA probes specific for mycobacterial ribosomal RNA categorize species of clinically significant isolates after recovery. In tissue, polymerase chain reaction (PCR) amplification techniques can be used to detect Mycobactereria tuberculosis-specific DNA sequences and thus, small numbers of mycobacteria in clinical specimens. (2) The cell wall of mycobacteria consist of: (3)

  • Outer lipids
  • Mycolic acid
  • Polysaccharides(arabinoglactan)
  • Peptideglycan
  • Plasma membrane.
  • Lipoarrabinomannan(LAM)
  • Phosphatidylinositol mannoside.
  • Cell wall skeleton.

PATHOGENESIS: The most common site for Tuberculosis disease is lungs and 85% of TB patients present with pulmonary symptoms. The most common sites of extrapulmonary disease are mediastinal, retroperitoneal, and cervical lymph nodes, vertebral bodes, adrenals, meninges, and the GI tract. Pathology of these lesions is similar to those in the lung. Extrapulmonary TB can occur as part of a primary or late generalized infection or as a reactivation site that may, coexist with pulmonary reactivation. (2) Mycobacterium tuberculosis is an obligate pathogen. It is a slender aerobic rod, characterized by high lipid content. This lipid is responsible for resistance to phagocytosis. Identification of organism is easy in tuberculous chancre, scrofuloderma, orificial lesions and the miliary variant. This may be difficult to find or absent in lupus vulgaris, gummata and warty tuberculosis. The organism is highly resistant to drying to drying and therefore can retain infectivity by inoculation or contamination of minor wounds. (19) The reaction of the bacterium depends on:

  • the size of inoculum.
  • the virulence of organism.
  • The immune state of patient.

After mycobacteria have invaded the host, either they may multiply and caused progressive infection or their multiplication is checked or completely arrested. The balance between bacterial multiplication and damage is depend not only properties of the invading organism but also by the ability of the host to control such infection. (9) Once the bacteria have invaded, the interaction of T-lymphocyte and mycobacteria antigens, displayed on the surface of antigen presenting cells, induces the liberation of lymphokines, interlukins and intereferons. These substances encourage the activation and expression of MHC molecule II antigens and IL-2R on T-Lymphocytes. Macrophages gather and a granuloma is formed. During the initial sensitization T cells generated and these will remain for decades in affected organ and the circulation. (6) In HIV infection, cell mediated immunity is impaired and therefore there may be reactivation of disease. (6) With the onset of host-immune response, lesions that develop around mycobacterial foci can be either proliferative or exudative. Both types of lesions develop in the same host, since infective dose and local immunity differ from site to site. (2) Proliferative lesions develop where the bacillary load is small and host cellular-immune responses dominate. These tubercles are condensed with activated macrophages admixed and are bounded by proliferating lymphocytes, plasma cells, and an outer rim of fibrosis. Intracellular killing of mycobacteria is effective, and the bacillary load remains low. (2) Exudative lesions predominate when large numbers of bacilli are present and host defenses are weak. These loose aggregates of immature macrophages, neutrophils, fibrin, and caseation necrosis are sites of mycobacterial growth. Without treatment, these lesions progress and infection spreads. (2) Even though mycobacteria are spread by blood all over the body during initial infection, primary extrapulmonary disease is rare except in severely immunocompromised hosts. Resistant hosts control mycobacterial growth at distant foci before expansion of active disease. Infants, older persons, or otherwise immunosuppressed hosts are incapable to control mycobacterial growth and develop disseminated Tuberculosis. Patients who become immunocompromised months to years after primary infection also can develop late generalized disease. (2) HISTOLOGY: The tubercle is the feature of the tuberculosis and infections with some of the atypical mycobacteria. In early stages of the skin lesion there is non specific inflammation but tubercle formation occur with in a month. (20) A tubercle granuloma consists of foci of epitheloid cells, containing variable, but usually sparse number of langerhan’s giant cells, with surrounding by a rim of mononuclear cells. The centre of this tuberculoid granuloma may shown a caseation necrosis which may calcify. (20) Even though tuberculoid granuloma is highly characteristic for several forms tuberculosis, but it is not pathognomic. Syphilis, leprosy, deep fungal infection and some other disease can also produce similar type of lesions. However differentiation of tuberculosis from these conditions sometimes may not be easy. (20) MICROSCOPIC ASPECTS: The involvement of an organ by tuberculosis is related with an inflammatory reaction at the affected site. There are three consecutive stages of inflammation, which are acute, subacute and chronic. These stages have different histological aspects. (21) 1) THE ACUTE PHASE: Infection first leads to a rapid, nonspecific inflammatory reaction apparent by exudative lesions, which are not predominantly specific to tuberculosis. The focus of inflammation is the site of serous-fibrous exudates with abundant macrophages in the centre. (21) 2) THE SUBACUTE PHASE: Lysis of the bacilli liberates the phospholipids from their capsule, provoking a specific tissue reaction and the formation of follicles “Koester follicles”. Two kinds of follicular lesions may be observed. (21) A) The epitheloid giant cell follicle: These are rounded focus containing numerous epitheloid cells, which are monocyte with egg-shaped centre, abundant cytoplasm and indistinct cytoplasmic edges. Several Langhans giant cells, generally situated din the centre of the follicle. These are large cells with abundant cytoplasm, indistinct edges and multiple centres arranged in the shape of a crown or horseshoe. Langhans cells are formed by the fusion of epitheloid cells. Epitheloid cells and langhans cells created by the monocyte, under the action of lymphokines. There is also a peripheral crown of lymphocytes. (21) This follicle does not contain necrosis and is not specific for tuberculosis. It is common to tuberculous leprosy, sarcoidosis and connective tissue diseases. (21) B) The necrotizing granuloma: The epitheloid giant cell follicle presents with central Caseating necrosis. This lesion is very specific for tuberculosis. Caseating necrosis is a fine-grained, homogeneous eosinophilic necrosis. (21) 3) THE CHRONIC PHASE: The tuberculous follicle gradually develops in to a fibrous follicle. Collagenous fibres invade the tuberculous focus, which is enclosed in a fibrous shell with fibroblast and lymphocytes; forming a fibro-Caseating follicle that is then transformed into a fully fibrous follicle this follicle can become entirely calcified. (21) The key examination for confirming the diagnosis of tuberculosis is bacteriology. Histology does play an important role in confirming diagnosis of extra pulmonary tuberculosis. Combination of both histological techniques and bacteriology increase the yield of histology. (21) MICROBIOLOGY: Tubercle bacilli are aerobic, with lipid-rich walls and a slow rate of growth. They take 20 hours on average to double in number. The lungs, dark and oxygen rich, at a temperature of 37°C, provide an ideal environment for the bacilli to replicate .Tubercle bacilli are rapidly destroyed in the ambient environment by ultraviolet rays. It is difficult to stain the bacilli with stains commonly used for other bacteriological examinations. They require special stains that can penetrate the wax-rich wall of the bacillus. For bacteriological examination, the quality of the samples sent to the laboratory is of fundamental importance. For pulmonary tuberculosis: The specimen that should be collected for examination is sputum obtained from the patient after coughing; more rarely the sample is obtained by gastric aspiration or bronchoscopy. As sputum can be contaminated by other bacteria, it must be collected in clean sputum non-sterile containers that can be firmly sealed. For extrapulmonary tuberculosis: Fluid from serous effusion, cerebrospinal fluid or biopsied fragments can be sent to the laboratory for culture. All sampling must be performed in strictly sterile conditions so that culture can be performed directly without prior decontamination. Samples must never be placed in formol, which kills the bacilli. bacteriological techniques Microscopy A smear of a selected part of a submitted specimen is made on a slide, then examined by microscope after staining • Staining methods There are several staining methods used for the tubercle bacillus; it is important for the method or methods used to be standardized for each country. The stains that are the most effective are Ziehl-Neelsen (ZN) staining and auramine staining. Ziehl-Neelsen staining The smear is covered with carbol fuchsin, and then heated. The smear is then destained successively using sulfuric acid and alcohol. All of the smears must be almost totally destained, and then restained with methylene blue. The bacilli are stained red by the fuchsin and are resistant to the acid and alcohol, hence the name acid-fast bacilli (AFB). Destaining by the successive application of acid and alcohol can also be done using only 25% sulfuric acid; however, it should be applied several times until the smear is completely destained. This is the method recommended by the IUATLD, as it is less delicate and does not require alcohol (which is not always available in some countries). On microscopic examination of the stained smear, the tubercle bacilli look like fine, red, slightly curved rods that are more or less granular, isolated, in pairs or in groups, and stand out clearly against the blue background. Fluorescent auramine staining The fuchsin is replaced by auramine; the bacilli fix the fluorescent stain and retain it after the acid and alcohol staining. • Reading by microscopy After Ziehl-Neelsen staining The stained smear is examined using a binocular microscope with an immersion lens (magnification ¥100). The number of AFB per 100 fields ,about one length and one width of a slide are counted. This technique is simple, rapid and fairly in expensive. After auramine staining The stained smear is examined by fluorescence microscopy with a dry lens of low magnification (*25 or 40). This microscope has an ultraviolet lamp to enable the fluorescent bacilli to be seen: they are clearly visible in the form of greenish-yellow fluorescent rods. The sensitivity and specificity of examination by fluorescence microscopy are comparable to those of microscopy after ZN staining. The main advantage is the easy and rapidity of reading: on the same slide surface, the results of 10 minutes’ reading by optic microscope are obtained in 2 minutes on fluorescence microscopy. As this technique requires more costly equipment (the microscope itself, and the lamps, which need to be replaced frequently ,on average after 200 hours of use, it is cost-effective only if more than 30 slides are examined each day. A constant electricity supply and trained technicians are also indispensable CHAPTER -3 TYPES OF CUTANEOUS TUBERCULOSIS: INTRODUCTION: Scrofuloderma and lupus vulgaris are the two most common forms of tuberculosis. However, the pattern of cutaneous tuberculosis is changing, as the tuberculid, lichen scrofulosorum, is becoming more common over recent years and has occurs almost as frequently as scrofuloderma and lupus vulgaris. 1) SCROFULODERMA: Syn- Tuberculosis colliquativa, scrofulous gumma. DEFINITION: Scrofuloderma is a subacute form of subcutaneous tuberculosis which causes cold abscess formation and secondary breakdown of overlying skin. PATHOGENESIS: Scrofuloderma results from the contiguous involvement of the skin overlying another tubrculous process for example, tuberculous lymphadenitis, tuberculosis of bone and joints, or tuberculous epididymitis. (9) INCIDENCE: Scrofuloderma may affect all groups but historically, a high prevalence of scrofuloderma was seen in children infected with Mycobacterium bovis from contaminated nonpasteurized milk (which type cow ??). CLINICAL FEATURES: Lesions present as firm, painless, subcutaneous nodules that progressively enlarge and suppurate and then form ulcers and sinus tracts to the overlying skin. Typical ulcers have undermined edges and a floor of granulation tissue. Typical tubercles with acid-fast bacilli are found in the lower dermis and the walls of the ulcer or abscess. Tubercle bacilli usually can be isolated from the purulent discharge. Tuberculin sensitivity is usually marked. Natural healing can occur but often takes years and may be accompanied by the formation of hypertrophic scars. Lupus vulgaris may develop in the locality of healing scrofuloderma. (2) Cervical lymph nodes are infected most commonly on the same side of the neck as the primary tuberculous complex. In the neck submandibular, preauricular, tonsillar, postauricular, occipital and supraclavicular lymph nodes are usually implicated. Occasionally discharging sinuses may occur over areas devoid of lymph nodes. Over weeks to months the involved lymph nodes enlarge, turn livid red, suppurate and then perforate with resultant ulceration and fistula formation. (11) Progression of disease with scarring produces irregular adherent masses, densely fibrous in places and fluctuant or discharging in others. Fungating tumors may arise from the excessive granulation tissue and after healing characteristic puckered scaring at the site of the infection. (4) COURSE: Spontaneous healing does occur (what % ? ) but it takes years before it is a completed. The typical cribriform or criss-crossed scarring and localized recurrence are common. 2) LUPUS VULGARIS: Syn: Tuberculosis cutis Luposa DEFINITION: In most reporting publication, Lupus Vulgaris is the most common form of Cutaneous TB and has the most unpredictable presentation. Lupus vulgaris is a chronic and progressive form of Cutaneous TB that occurs in tuberculin-sensitive patients. Hypersensitivity to tuberculin is high although immunity is low to moderate. (11) The mode of infection is not entirely clear in the individual case but it is considered that Lesions appear in normal skin either as a result of direct extension of underlying tuberculous foci, in lymphatic or hematogenous spread, after primary inoculation, after BCG vaccination, or in the scars of old scrofuloderma. INCIDENCE: Traditionally, lupus vulgaris was most common in northern Europe and less common in Asian countries ( figures???), with affected females outnumbering males by 2-3:1. All age group affected equally. (2) CLINICAL FEATURES: Lesions are small, sharply marginated; red-brown papules of gelatinous consistency called apple-jelly nodules. This apple-jelly nodule slowly evolves by peripheral extension in to large plaques with central atrophy. Lesions are frequently solitary, and more than 90% involve the head and neck. Re-emergence of new active tuberculosis nodules within earlier atrophic or scarred lesions is characteristic. If the Cartilage of the nose and ears is involved, it is gradually destroyed. This destruction of tissue is known as lupus vorax. Bone usually is spared. Buccal, nasal, and conjunctival mucosa may be involved primarily or by extension. (2) Lupus Vulgaris is more common in western countries on the face, especially on cheeks, nose, ears, and on the extensor surface of the extremities, also on the breast & buttocks. In many developing countries including India the lower extremities mainly the buttocks are the primary site of involvement. Mucous membrane involvement is very rare in Lupus Vulgaris. (11) VARIANTS OF LUPUS VULGARIS: There are many clinical types depending upon the local tissue response to infection. 1- PLAQUE FORM OR LUPUS VULGARIS EXFOLIATIVE: This form of lupus vulgaris is characterized by the plaques. Scaling frequently occurs on the lower legs where it may resemble psoriasis. As the lesion enlarges they become softer. Over a period of time a polycystic or serpiginous configuration can develop with central clearing and atrophy in the lesion. Irregular scarring is frequent and the active edge may be thickened and hyperkeratotic. (2) 2) ULCERATING AND MUTILATING LUPUS VULGARIS: Scarring and ulceration be the main clinical features. Crusts form over areas of necrosis. Deep tissues and cartilage are invaded and ultimate scarring of the disease produces contractures and distortion. (2) 3) LUPUS VULGARIS VEGETANS OR LUPUS PAPILLOMATOSUS: This form of lupus vulgaris is characterized by necrosis, ulceration, and proliferative and papillomatous granulation tissue. It involves mucous membranes sometimes, and invades and destroys the cartilage when involving nasal and auricular cartilage. (2) 4) NODULAR FORM OF LUPUS VULGARIS: In this form of lupus vulgaris large soft tumors appears usually on ear lobes. These are characterized by an absence of ulceration and scarring. (2) 5) LUPUS POSTEXANTHEMATICUS: It is disseminated, papular and nodular form that commonly arises after a transient impairment of immunity predominantly after measles.(9) ( complete lesion picture) 6) LUPUS VULGARIS OF MUCOUS MEMBRANE: Mucous membrane tuberculous lesions are extremely rare. These lesions are small soft, gray or pink papules, ulcers or granulating masses that bleed easily. They arise in mucous membrane by direct extension of skin lupus to buccal, nasal or conjunctival mucosa. This form can produce severe destruction & can produce stenosis of the larynx and scarring deformities. (9) DIAGNOSIS OF LUPUS VULGARIS: Lupus vulgaris is difficult to diagnose when it occur in unusual sites like popliteal fossa. Special stains and mycobacterial cultures may be having frequently negative in these sites. However, it is possible to reach the correct diagnosis of Lupus vulgaris by using clinical and histopathological findings. In such cases, to confirm the diagnosis at times, a therapeutic trial with antitubercular agents may be required. (17) COURSE: Lupus vulgaris is a very destructive disease and without treatment can progress slowly over years or even decades. It can cause severe scarring and disfigurements like Ectropion, and others distortion of the mouth and severe damage to the nose may occur. (11) CUTANEOS TUBERCULOSIS IN CHILDREN: Cutaneous tuberculosis in children is a most important health problem in India. It accounts for about 1.5% of all the cases of extra pulmonary tuberculosis Overall the clinical patterns are comparable with adults. However, children can have widespread and severe involvement because many unusual and infrequent patterns are known to occur in children. Underlying systemic involvement(what invovlment??) is more common in children with lupus vulgaris, compared to adults with lupus vulgaris. (13) Cutaneous tuberculosis is extensive in Pakistan but has not been adequately documented. One study was conducted to establish the clinical patterns, incidence and prevalence of the disease in Larkana, Sindh province, Pakistan. This study showed the number of patients was reasonably has large, thus suggesting a high incidence of cutaneous tuberculosis in Larkana. Lupus vulgaris, a form of cutaneous tuberculosis, was extensive in this area and prevalent in adults, while scrofuloderma was prevalent in children. Additionally, the obtainable rate of the disease was higher in children aged under ten years of age and lower in adults. This showed that children are more prone to this disease than adults in Larkana.(complete ratio of patients????) (14) Ocular scrofuloderma with orbital tuberculosis is a rarely described presentation of childhood tuberculosis. Bilateral eye involvement had never been reported. One case report from India,in which a three year old boy who presented with bilateral infraorbital swellings of tubercular etiology. Computed tomography (CT) scan of the upper face revealed enhanced soft tissue lesions in both the lower lids of the eyes, with extraconal extension into the orbits and with erosion of the right zygomatic bone. The cause was confirmed by using the Ziehl Neelsen staining of the aspirate from the lesions, which was positive for acid-fast bacilli and growth of Mycobacterium tuberculosis in the aspirate culture. The patient showed marked improvement of his lesions on anti-tubercular treatment. (15) Localized tuberculid has been reported occasionally in the data. The majority of these case reports are of papulonecrotic tuberculid localized to the penis, an entity selected as “penis tuberculid.” In females, such a localized genital tuberculid has not been reported frequently. There is one case report from India, in which an 11-year-old girl with lichen scrofulosorum confined to the vulva, associated with cervical and inguinal tubercular lymphandenitis is reported. (16) UNUSUAL MANIFESTATION OF TUBERCUCLOSIS: Long standing lupus vulgaris can be complicated by Squamous cell carcinoma. Latency period may be 10- 20 years. I am presenting a case report from Romania in which 59 years old farmer lady had lupus vulgaris on right ear lobule, since childhood. which started after her empiric perforation for earrings. The development was progressive, strange, involving the pinna and the right cheek in the meantime. At the time of first examination, a diffuse mass of red-yellowish infiltration was found at the level of the right ear and the right cheek. In the following two years, an ulcer-vegetating tumor developed at the level of the right ear lobule, along with retromandibular adenopathy, of about 1 cm, histopathological examination confirmed the diagnosis of squamous cell carcinoma developed from a lupus vulgaris. (18)

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Cutaneous Tuberculosis Disease. (2017, Jun 26). Retrieved January 25, 2022 , from

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