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Cutaneous Tuberculosis Presenting as Necrotizing Fasciitis in an Elderly Patient
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CASE REPORT
CUTANEOUS TUBERCULOSIS PRESENTING AS NECROTIZING FASCIITIS IN AN ELDERLY PATIENT Wen-Chin Cho1, Yung-Chia Pai1,2, Yung Hsiung1, Wai-Mau Choi1* 1
Department of Emergency Medicine, Hsinchu Mackay Memorial Hospital, Hsinchu, and 2 Mackay Medicine, Nursing and Management College, Taipei, Taiwan.
SUMMARY We report a case of cutaneous tuberculosis presenting as cellulitis and necrotizing fasciitis of the bilateral lower legs. The patient was a 79-year-old male who denied any history of chronic medical diseases such as hypertension, diabetes or old cerebrovascular accident. He had developed itchy skin papules since August 2008. His clinical cellulitis failed to respond to antibiotic therapy. Subsequent investigations involving both acid-fast bacilli cultures and smears of neck lymph nodes were positive, and established the alternative diagnoses of cutaneous tuberculosis, hyper-IgE syndrome and eosinophilia. The skin eruption cleared after treatment with isoniazid, rifampicin and pyrazinamide. This case represents a most unusual presentation of tuberculosis in the skin. The atypical features may reflect the patient’s general medical state. [International Journal of Gerontology 2008; 2(2): 79–82] Key Words: cellulitis, cutaneous tuberculosis, eosinophilia, hyper-IgE syndrome, necrotizing fasciitis
Introduction
Case Report
Cellulitis, an inflammatory disease that involves the skin and subcutaneous tissues, frequently leads to office visits and hospital admissions. Most cases of cellulitis can be attributed to an infectious cause. However, physicians may be challenged by cases that do not respond to the initial antimicrobial regimen. Cutaneous involvement is a rare manifestation of tuberculosis (TB). The correct diagnosis is often significantly delayed, because cutaneous TB is not routinely considered in the differential diagnoses or investigations fail to reveal the presence of Mycobacterium tuberculosis. Here, we report an elderly man with cutaneous TB presenting as necrotizing fasciitis.
A 79-year-old male, denying any other systemic diseases such as hypertension and diabetes, was sent to the emergency department because of progressive itchy skin papules that had affected both his lower limbs for several months. He had previously visited Chang Gung Memorial Hospital but no diagnosis was made, and the lower limbs subsequently became swollen and shiny. Two weeks prior to his admission, there was discharge from ruptured vesicles over both lower legs, and he could not walk without cane support. On arrival at our hospital, he was ill-looking. Physical examination revealed multiple excoriations with scarring vesicles over the lower limbs, swelling of both legs with erythematous change, hypopigmented macules over the abdomen, and enlarged lymph nodes over the inguinal area and neck (Figure 1). The remaining findings of the examination were unremarkable. He had a body temperature of 37.9°C, pulse rate of 103 beats/minute, respiration rate of 22 breaths/minute, and blood pressure of 104/55 mmHg. Laboratory examinations showed
*Correspondence to: Dr Wai-Mau Choi, Department of Emergency Medicine, Hsinchu Mackay Memorial Hospital, 690, Section 2, Guangfu Road, Hsinchu, Taiwan. E-mail: [email protected] Accepted: March 10, 2008
International Journal of Gerontology | June 2008 | Vol 2 | No 2 © 2008 Elsevier.
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lymph node biopsy revealed perivascular lymphohistiocytic infiltrates, fat necrosis, and numerous granulomas with central caseating necrosis. Ziehl-Neelsen staining was positive for acid-fast microorganisms. A culture for TB bacilli was positive. A diagnosis of cutaneous TB was made, and the patient was started on isoniazid 300 mg, rifampin 450 mg, ethambutol 800 mg and pyrazinamide 1,500 mg. His fever subsided gradually and the skin lesions also improved. Owing to the improvements in his spirit and general condition, he was discharged with oral medication and followed up in the outpatient department. Figure 1. Multiple excoriations with scarring vesicles over the lower limbs and swelling of both legs with erythematous change are noted.
Figure 2. Extensive infiltration or edema within the subcutaneous fat and fasciae of both lower extremities are noted.
a white blood cell count of 24,600 cells/µL with 33% neutrophils and 57% eosinophils, hemoglobin 9.9 g/dL, hematocrit 29.6%, platelet count of 77,000/µL, C-reactive protein 5.28 mg/dL, sodium 133 mEq/L, potassium 3.9 mEq/L, plasma glucose 102 mg/dL, IgE 48,147 IU/mL (normal range, < 87 IU/mL), and eosinophil count of 9,700/µL. Chest radiography revealed a fibrocalcified infiltrate at the left upper lung field. Computed tomography of the lower legs showed extensive infiltration or edema within the subcutaneous fat and fasciae of both lower extremities, compatible with necrotizing fasciitis (Figure 2). After admission, empirical antimicrobial therapy with Tapimycin (piperacillin 2.0 g/tazobactam 0.25 g) two vials every 8 hours plus Amikin 500 mg every day was started. A skin biopsy from the thigh and a neck 80
Discussion Cellulitis is an inflammation of the connective tissue underlying the skin and can be caused by bacterial infections. It can be due to either normal skin flora or exogenous bacteria, and often occurs at sites where the skin has been broken, such as cracks, cuts, blisters, burns, insect bites, surgical wounds or sites of intravenous catheter insertion. Skin on the face or lower legs is most commonly affected by this type of infection, although cellulitis can occur in any part of the body. Cellulitis may be superficial (affecting only the surface of the skin) but can also affect the tissues underlying the skin and spread to the lymph nodes and bloodstream1. Cellulitis of the lower leg is a common problem with considerable morbidity. Although the risk factors are well identified, the relationships between the consequences of cellulitis and further episodes are less well understood. Edema is a risk factor for multiple episodes of cellulitis/erysipelas of the lower leg2. Necrotizing fasciitis is an infection that affects the skin and the tissues under the skin (subcutaneous tissues). It is similar to cellulitis but is always very serious. Various bacteria can cause necrotizing fasciitis, but it is most commonly due to Streptococcus bacteria. Necrotizing fasciitis is one of the fastest-spreading infections identified to date. It is sometimes referred to as the “flesh-eating” disease. However, the bacteria that cause this infection do not actually eat flesh. Instead, the bacteria release toxins that destroy the nearby tissues, such as skin and muscle tissue. Similar to the case for cellulitis, the infection for necrotizing fasciitis typically starts from a wound in the skin, and this is often a very minor wound such as a scratch, which allows bacteria into the skin. Typically, the affected International Journal of Gerontology | June 2008 | Vol 2 | No 2
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Skin TB Presenting as Necrotizing Fasciitis
skin initially becomes very painful but is often without any obvious redness or inflammation during the early stages. The disease then progresses rapidly (over hours), and the affected tissues typically become swollen and red and may blister. Fairly quickly, the affected skin becomes violet or purple, blisters, and dies (necroses) along with the subcutaneous tissues. The toxins and infection can affect the rest of the body, causing organ failure. Severe cases progress within hours, and the death rate from this infection is high (30% or more), even with treatment3. Aeromonas infection, Vibrio infection, cancer, hypotension and band form neutrophil count greater than 10% are independent positive predictors of mortality in patients with necrotizing fasciitis4. TB continues to be a health problem in some countries. The development of resistance to antituberculous drugs and the increases in diseases and conditions associated with immunodeficiency, such as AIDS and chemotherapy, have caused TB to increase recently. As a result, the incidence of cutaneous TB has also been increasing5. Cutaneous involvement is a rare manifestation of TB. The correct diagnosis is often significantly delayed, because cutaneous TB is not routinely considered in the differential diagnoses or investigations fail to reveal the presence of M. tuberculosis. The clinical features of cutaneous TB are diverse and result from exogenous and endogenous spread of M. tuberculosis and immune-mediated mechanisms. Recognition of cutaneous TB is important, because the diagnosis is frequently overlooked, resulting in delayed treatment6. Diagnosis of cutaneous TB is challenging and requires correlation of the clinical findings with diagnostic testing. In addition to traditional acid-fast bacilli smears and cultures, there has been increased utilization of polymerase chain reaction owing to its rapidity, sensitivity and specificity. Because most cases of cutaneous TB are manifestations of systemic involvement and the bacillary load in cutaneous TB is usually lower than that in pulmonary TB, the treatment regimens are similar to those of TB in general. In immunocompromised patients, such as HIV-infected patients with disseminated miliary TB, rapid diagnosis and prompt initiation of treatment are paramount. Unfortunately, despite even the most aggressive efforts, the prognosis for these individuals is poor when multidrug-resistant mycobacteria are present. An increased awareness of the re-emergence of cutaneous TB will allow for the proper diagnosis and management of this increasingly common skin disorder7. International Journal of Gerontology | June 2008 | Vol 2 | No 2
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Hyper-IgE syndrome is a rare immunodeficiency characterized by recurrent staphylococcal infection of the skin, lung infections, atopic dermatitis and high serum levels of IgE. These patients are also at increased risk of osteoporosis and spontaneous bone fractures8. There are two main forms of hyper-IgE syndrome: one inherited as an autosomal dominant trait, and the other inherited as an autosomal recessive trait. Both involve defects of the immune system and elevated levels of IgE (hyper-IgE) in the blood. For years, researchers considered these forms to be different expressions of the same disorder, but they are currently considered to be similar, yet distinct, disorders9. Eosinophilic cellulitis (Wells syndrome) is characterized by acute pruritic dermatitis10. Patients typically present with one or a few erythematous plaques, which may resemble infectious cellulitis. The lesions evolve over 2 to 3 days and resolve completely without scarring in 2 to 8 weeks. The disease usually recurs. Peripheral eosinophilia, which is manifested during the acute phase, and dermal eosinophilic infiltration help to differentiate this entity from infectious cellulitis. Wells syndrome may be idiopathic or associated with conditions such as myeloproliferative, immunologic and infectious disorders, and medications11,12. Most cases respond favorably to oral corticosteroid treatment13.
References 1.
2.
3. 4.
5.
6.
7.
Kroshinsky D, Grossman ME, Fox LP. Approach to the patient with presumed cellulitis. Semin Cutan Med Surg 2007; 26: 168–78. Cox NH. Oedema as a risk factor for multiple episodes of cellulitis/erysipelas of the lower leg: a series with community follow-up. Br J Dermatol 2006; 155: 947–50. Roldan CJ. Necrotizing fasciitis. J Emerg Med 2008; 34: 457–8. Hsiao CT, Weng HH, Yuan YD, Chen CT, Chen IC. Predictors of mortality in patients with necrotizing fasciitis. Am J Emerg Med 2008; 26: 170–5. Kivanç-Altunay I, Baysal Z, Ekmekçi TR, Köslü A. Incidence of cutaneous tuberculosis in patients with organ tuberculosis. Int J Dermatol 2003; 42: 197–200. Lai-Cheong JE, Perez A, Tang V, Martinez A, Hill V, Menagé Hdu P. Cutaneous manifestations of tuberculosis. Clin Exp Dermatol 2007; 32: 461–6. Barbagallo J, Tager P, Ingleton R, Hirsch RJ, Weinberg JM. Cutaneous tuberculosis: diagnosis and treatment. Am J Clin Dermatol 2002; 3: 319–28.
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Dewitt CA, Bishop AB, Buescher LS, Stone SP. Hyperimmunoglobulin E syndrome: two cases and a review of the literature. J Am Acad Dermatol 2006; 54: 855–65. 9. Tomic J, Odri I, Pasic S, Jovanovic M. Destructive staphylococcal pleuropneumonia in a two-year-old boy with hyperimmunoglobulin-E syndrome. Med Pregl 2005; 58: 78–84. 10. Moossavi M, Mehregan DR. Wells’ syndrome: a clinical and histopathologic review of seven cases. Int J Dermatol 2003; 42: 62–7.
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11. Bogenrieder T, Griese DP, Schiffner R, Büttner R, Riegger GA, Hohenleutner U, et al. Wells’ syndrome associated with idiopathic hypereosinophilic syndrome. Br J Dermatol 1997; 137: 978–82. 12. Seçkin D, Demirhan B. Drugs and Wells’ syndrome: a possible causal relationship? Int J Dermatol 2001; 40: 138–40. 13. Weiss G, Shemer A, Confino Y, Kaplan B, Trau H. Wells’ syndrome: report of a case and review of the literature. Int J Dermatol 2001; 40: 148–52.
International Journal of Gerontology | June 2008 | Vol 2 | No 2
CASE REPORT
CUTANEOUS TUBERCULOSIS PRESENTING AS NECROTIZING FASCIITIS IN AN ELDERLY PATIENT Wen-Chin Cho1, Yung-Chia Pai1,2, Yung Hsiung1, Wai-Mau Choi1* 1
Department of Emergency Medicine, Hsinchu Mackay Memorial Hospital, Hsinchu, and 2 Mackay Medicine, Nursing and Management College, Taipei, Taiwan.
SUMMARY We report a case of cutaneous tuberculosis presenting as cellulitis and necrotizing fasciitis of the bilateral lower legs. The patient was a 79-year-old male who denied any history of chronic medical diseases such as hypertension, diabetes or old cerebrovascular accident. He had developed itchy skin papules since August 2008. His clinical cellulitis failed to respond to antibiotic therapy. Subsequent investigations involving both acid-fast bacilli cultures and smears of neck lymph nodes were positive, and established the alternative diagnoses of cutaneous tuberculosis, hyper-IgE syndrome and eosinophilia. The skin eruption cleared after treatment with isoniazid, rifampicin and pyrazinamide. This case represents a most unusual presentation of tuberculosis in the skin. The atypical features may reflect the patient’s general medical state. [International Journal of Gerontology 2008; 2(2): 79–82] Key Words: cellulitis, cutaneous tuberculosis, eosinophilia, hyper-IgE syndrome, necrotizing fasciitis
Introduction
Case Report
Cellulitis, an inflammatory disease that involves the skin and subcutaneous tissues, frequently leads to office visits and hospital admissions. Most cases of cellulitis can be attributed to an infectious cause. However, physicians may be challenged by cases that do not respond to the initial antimicrobial regimen. Cutaneous involvement is a rare manifestation of tuberculosis (TB). The correct diagnosis is often significantly delayed, because cutaneous TB is not routinely considered in the differential diagnoses or investigations fail to reveal the presence of Mycobacterium tuberculosis. Here, we report an elderly man with cutaneous TB presenting as necrotizing fasciitis.
A 79-year-old male, denying any other systemic diseases such as hypertension and diabetes, was sent to the emergency department because of progressive itchy skin papules that had affected both his lower limbs for several months. He had previously visited Chang Gung Memorial Hospital but no diagnosis was made, and the lower limbs subsequently became swollen and shiny. Two weeks prior to his admission, there was discharge from ruptured vesicles over both lower legs, and he could not walk without cane support. On arrival at our hospital, he was ill-looking. Physical examination revealed multiple excoriations with scarring vesicles over the lower limbs, swelling of both legs with erythematous change, hypopigmented macules over the abdomen, and enlarged lymph nodes over the inguinal area and neck (Figure 1). The remaining findings of the examination were unremarkable. He had a body temperature of 37.9°C, pulse rate of 103 beats/minute, respiration rate of 22 breaths/minute, and blood pressure of 104/55 mmHg. Laboratory examinations showed
*Correspondence to: Dr Wai-Mau Choi, Department of Emergency Medicine, Hsinchu Mackay Memorial Hospital, 690, Section 2, Guangfu Road, Hsinchu, Taiwan. E-mail: [email protected] Accepted: March 10, 2008
International Journal of Gerontology | June 2008 | Vol 2 | No 2 © 2008 Elsevier.
79
■
■
W.C. Cho et al
lymph node biopsy revealed perivascular lymphohistiocytic infiltrates, fat necrosis, and numerous granulomas with central caseating necrosis. Ziehl-Neelsen staining was positive for acid-fast microorganisms. A culture for TB bacilli was positive. A diagnosis of cutaneous TB was made, and the patient was started on isoniazid 300 mg, rifampin 450 mg, ethambutol 800 mg and pyrazinamide 1,500 mg. His fever subsided gradually and the skin lesions also improved. Owing to the improvements in his spirit and general condition, he was discharged with oral medication and followed up in the outpatient department. Figure 1. Multiple excoriations with scarring vesicles over the lower limbs and swelling of both legs with erythematous change are noted.
Figure 2. Extensive infiltration or edema within the subcutaneous fat and fasciae of both lower extremities are noted.
a white blood cell count of 24,600 cells/µL with 33% neutrophils and 57% eosinophils, hemoglobin 9.9 g/dL, hematocrit 29.6%, platelet count of 77,000/µL, C-reactive protein 5.28 mg/dL, sodium 133 mEq/L, potassium 3.9 mEq/L, plasma glucose 102 mg/dL, IgE 48,147 IU/mL (normal range, < 87 IU/mL), and eosinophil count of 9,700/µL. Chest radiography revealed a fibrocalcified infiltrate at the left upper lung field. Computed tomography of the lower legs showed extensive infiltration or edema within the subcutaneous fat and fasciae of both lower extremities, compatible with necrotizing fasciitis (Figure 2). After admission, empirical antimicrobial therapy with Tapimycin (piperacillin 2.0 g/tazobactam 0.25 g) two vials every 8 hours plus Amikin 500 mg every day was started. A skin biopsy from the thigh and a neck 80
Discussion Cellulitis is an inflammation of the connective tissue underlying the skin and can be caused by bacterial infections. It can be due to either normal skin flora or exogenous bacteria, and often occurs at sites where the skin has been broken, such as cracks, cuts, blisters, burns, insect bites, surgical wounds or sites of intravenous catheter insertion. Skin on the face or lower legs is most commonly affected by this type of infection, although cellulitis can occur in any part of the body. Cellulitis may be superficial (affecting only the surface of the skin) but can also affect the tissues underlying the skin and spread to the lymph nodes and bloodstream1. Cellulitis of the lower leg is a common problem with considerable morbidity. Although the risk factors are well identified, the relationships between the consequences of cellulitis and further episodes are less well understood. Edema is a risk factor for multiple episodes of cellulitis/erysipelas of the lower leg2. Necrotizing fasciitis is an infection that affects the skin and the tissues under the skin (subcutaneous tissues). It is similar to cellulitis but is always very serious. Various bacteria can cause necrotizing fasciitis, but it is most commonly due to Streptococcus bacteria. Necrotizing fasciitis is one of the fastest-spreading infections identified to date. It is sometimes referred to as the “flesh-eating” disease. However, the bacteria that cause this infection do not actually eat flesh. Instead, the bacteria release toxins that destroy the nearby tissues, such as skin and muscle tissue. Similar to the case for cellulitis, the infection for necrotizing fasciitis typically starts from a wound in the skin, and this is often a very minor wound such as a scratch, which allows bacteria into the skin. Typically, the affected International Journal of Gerontology | June 2008 | Vol 2 | No 2
■
Skin TB Presenting as Necrotizing Fasciitis
skin initially becomes very painful but is often without any obvious redness or inflammation during the early stages. The disease then progresses rapidly (over hours), and the affected tissues typically become swollen and red and may blister. Fairly quickly, the affected skin becomes violet or purple, blisters, and dies (necroses) along with the subcutaneous tissues. The toxins and infection can affect the rest of the body, causing organ failure. Severe cases progress within hours, and the death rate from this infection is high (30% or more), even with treatment3. Aeromonas infection, Vibrio infection, cancer, hypotension and band form neutrophil count greater than 10% are independent positive predictors of mortality in patients with necrotizing fasciitis4. TB continues to be a health problem in some countries. The development of resistance to antituberculous drugs and the increases in diseases and conditions associated with immunodeficiency, such as AIDS and chemotherapy, have caused TB to increase recently. As a result, the incidence of cutaneous TB has also been increasing5. Cutaneous involvement is a rare manifestation of TB. The correct diagnosis is often significantly delayed, because cutaneous TB is not routinely considered in the differential diagnoses or investigations fail to reveal the presence of M. tuberculosis. The clinical features of cutaneous TB are diverse and result from exogenous and endogenous spread of M. tuberculosis and immune-mediated mechanisms. Recognition of cutaneous TB is important, because the diagnosis is frequently overlooked, resulting in delayed treatment6. Diagnosis of cutaneous TB is challenging and requires correlation of the clinical findings with diagnostic testing. In addition to traditional acid-fast bacilli smears and cultures, there has been increased utilization of polymerase chain reaction owing to its rapidity, sensitivity and specificity. Because most cases of cutaneous TB are manifestations of systemic involvement and the bacillary load in cutaneous TB is usually lower than that in pulmonary TB, the treatment regimens are similar to those of TB in general. In immunocompromised patients, such as HIV-infected patients with disseminated miliary TB, rapid diagnosis and prompt initiation of treatment are paramount. Unfortunately, despite even the most aggressive efforts, the prognosis for these individuals is poor when multidrug-resistant mycobacteria are present. An increased awareness of the re-emergence of cutaneous TB will allow for the proper diagnosis and management of this increasingly common skin disorder7. International Journal of Gerontology | June 2008 | Vol 2 | No 2
■
Hyper-IgE syndrome is a rare immunodeficiency characterized by recurrent staphylococcal infection of the skin, lung infections, atopic dermatitis and high serum levels of IgE. These patients are also at increased risk of osteoporosis and spontaneous bone fractures8. There are two main forms of hyper-IgE syndrome: one inherited as an autosomal dominant trait, and the other inherited as an autosomal recessive trait. Both involve defects of the immune system and elevated levels of IgE (hyper-IgE) in the blood. For years, researchers considered these forms to be different expressions of the same disorder, but they are currently considered to be similar, yet distinct, disorders9. Eosinophilic cellulitis (Wells syndrome) is characterized by acute pruritic dermatitis10. Patients typically present with one or a few erythematous plaques, which may resemble infectious cellulitis. The lesions evolve over 2 to 3 days and resolve completely without scarring in 2 to 8 weeks. The disease usually recurs. Peripheral eosinophilia, which is manifested during the acute phase, and dermal eosinophilic infiltration help to differentiate this entity from infectious cellulitis. Wells syndrome may be idiopathic or associated with conditions such as myeloproliferative, immunologic and infectious disorders, and medications11,12. Most cases respond favorably to oral corticosteroid treatment13.
References 1.
2.
3. 4.
5.
6.
7.
Kroshinsky D, Grossman ME, Fox LP. Approach to the patient with presumed cellulitis. Semin Cutan Med Surg 2007; 26: 168–78. Cox NH. Oedema as a risk factor for multiple episodes of cellulitis/erysipelas of the lower leg: a series with community follow-up. Br J Dermatol 2006; 155: 947–50. Roldan CJ. Necrotizing fasciitis. J Emerg Med 2008; 34: 457–8. Hsiao CT, Weng HH, Yuan YD, Chen CT, Chen IC. Predictors of mortality in patients with necrotizing fasciitis. Am J Emerg Med 2008; 26: 170–5. Kivanç-Altunay I, Baysal Z, Ekmekçi TR, Köslü A. Incidence of cutaneous tuberculosis in patients with organ tuberculosis. Int J Dermatol 2003; 42: 197–200. Lai-Cheong JE, Perez A, Tang V, Martinez A, Hill V, Menagé Hdu P. Cutaneous manifestations of tuberculosis. Clin Exp Dermatol 2007; 32: 461–6. Barbagallo J, Tager P, Ingleton R, Hirsch RJ, Weinberg JM. Cutaneous tuberculosis: diagnosis and treatment. Am J Clin Dermatol 2002; 3: 319–28.
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Dewitt CA, Bishop AB, Buescher LS, Stone SP. Hyperimmunoglobulin E syndrome: two cases and a review of the literature. J Am Acad Dermatol 2006; 54: 855–65. 9. Tomic J, Odri I, Pasic S, Jovanovic M. Destructive staphylococcal pleuropneumonia in a two-year-old boy with hyperimmunoglobulin-E syndrome. Med Pregl 2005; 58: 78–84. 10. Moossavi M, Mehregan DR. Wells’ syndrome: a clinical and histopathologic review of seven cases. Int J Dermatol 2003; 42: 62–7.
82
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11. Bogenrieder T, Griese DP, Schiffner R, Büttner R, Riegger GA, Hohenleutner U, et al. Wells’ syndrome associated with idiopathic hypereosinophilic syndrome. Br J Dermatol 1997; 137: 978–82. 12. Seçkin D, Demirhan B. Drugs and Wells’ syndrome: a possible causal relationship? Int J Dermatol 2001; 40: 138–40. 13. Weiss G, Shemer A, Confino Y, Kaplan B, Trau H. Wells’ syndrome: report of a case and review of the literature. Int J Dermatol 2001; 40: 148–52.
International Journal of Gerontology | June 2008 | Vol 2 | No 2