The frequency of complication of Diabetes mellitus in patients with pulmonary tuberculosis is high. Lupus vulgaris is a progressive form of cutaneous tuberculosis that occur in a patient with moderate or high degree of immunity. Cutaneous tuberculosis is an infrequent first sign of disseminated tuberculosis. Cutaneous tuberculosis in immunocompetent diabetic patient should be considered as a D/D of cutaneous abscess or ulcers due to fungal infection and tuberculoid. PCR is an efficient and sensitive method for the diagnosis of cutaneous tuberculosis.
Introduction
Problems associated with diabetic foot are world
wide. However there may be regional variation among risk factors and clinical presentation, differences concerning age, diabetes duration, peripheral vascular disease and precipitaing factors contributing to injury are also considered. Clinical presentation of cutaneous tuberculosis is varying. There is an increasing trend of cutaneous tuberculosis over the years. Scrofuloderma was the most common clinical presentation followed by Lupus vulgaris, tuberculosis verucca cutis and tuberculids.1
Cutaneous tuberculosis is an infrequent first sign of disseminated tuberculosis. The authors describe a case with cutaneous tuberculous ulceration on the dorsum of left foot.
Case Report
Mr. B Age 68 years retired, wireman by profession complaining of painful erythematous, ulceration with oedema and oozing of watery fluid admixed with necrotic cheesy material on dorsum of left foot since 3 months was seen in surgery OPD of Shree Mumbadevi Hom Hospital.
Ulcers measuring 3 x 2 x 3 cms; indurated margin with black discolouration, floor of the ulcer shows necrotic yellowish cheesy material (Fig. 1).
P/H Diabetes Mellitus, Insect bite. No H/O Pulmonary Tuberculosis.
F/H No Diabetes Mellitus
O/E
No Lymphadenopathy, BP 120/80 mm Hg in supine position, RR 18/min, Pule 88/min. RS, CVS NAD
Laboratory work up revealed WBC 10,900 Hb, 16.6 gm% N 70%, L 30%, FBS 79 mg%, PPBS 107.7 mg%. Swab from wound for aerobic culture revealed Staphylococcus aureus, Coagulase and Catalase Test positive having maximum inhibition for Gatifloxacin. Glycosylated Hb 8.0% (Ion exchange resin) Normal Range : 4-7% Non diabetic 8-9% Good Control, 9-10% Poor control.
HIV status : normal, HBsAg : negative, ECG : normal
Patient was followed up in surgical OPD for one month with Inj. Magnamycin, Amikacin with no marked improvement. Patient was referred to Ortho OPD for 2nd opinion. Surgical exploration with debridement was done under GA, tissue was send for paraffin section.
The histopathological findings suggested granulomatous changes with central necrosis and Langhan giant cells (Fig. 2).
Mycobacterium tuberculosis was identified from tissue by imprint smear, staining with modified ZNCF method.
A tuberculin skin test showed 11 mm erythema. A preclusive anti-tuberculosis chemotherapy AKT4 was started with remarkable rapid remmision of cutaneous lesion.
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| Fig. 1 : Ulcer showing indurated margins, with black discoloration. Floor shows necrotic yellowish red cheesy material. |
Fig. 2 : (H.P. 400 X) H and E stained section shows granulomatous changes with central necrosis and Langhan's giant cells. |
Discussion
Our case was a diabetic clinically controlled but still the healing was poor since the basic pathology was due to atypical Mycobacterium tuberculosis probably scrofuloderma and due to diabetes the local defence was modified even though immunocompetent, because of which the cutaneous mycobacterial infection entered through the insect bite. The pathogenesis of innoculation of cutaneous tuberculosis requires a break in the skin through minor abrasion allowing the entry of organism.8
We speculated that in older patients and in diabetics oxygen pressure alters in the lower limbs2 which may favour the growth of organism like Staphylococcus and tubercle bacilli even the artherosclerotic changes of vessels may enhance the pathogenesis.
Cutaneous tuberculosis in immunocompetent diabetic patient should be considered as a D/D of cutaneous abscesses or ulcers due to fungal infection and tuberculid3,4 which are hypersensitivity reaction to mycobacterium tubercle (MTB).5
Cutaneous tuberculosis is more frequent in diabetes than in non-diabetic.6 Tuberculosis aggravates diabetes and increases the frequency of complication compared with diabetics without tuberculosis.7
Atypical mycobacterium are important human pathogens. Although they often cause systemic disease, mycobacterium infection may present solely as cutaneous lesion. It is not easy to detect non-tuberculosis mycobacterium by traditional, histochemical Ziehl Neelsen stain or by culture on specific media.9 The author stresses the importance of PCR (polymerase chain reaction) to identify non-tubercle mycobacterium in skin lesion. Since tuberculosis and diabetes frequently coexist in the population at risk for tuberculosis. Clinician should suspect tuberculosis in the diabetics with or without abnormality on chest roentgenogram. Aggressive diagnostic measures and specific chemotherapy should be given and monitored to treat cutaneous tuberculosis.10
Acknowledgement
We thank Dr. NO Goel, the superintendent of the hospital for giving permission to publish the data. We also express our thanks to Dr. Rakesh Gupta house surgeon for preparing case record.
References
- Yasmeen N, Kanjee A. Cutaneous tuberculosis : a three year prospective study. J Pak Med Ass 2005; 55 (1) : 10-2.
- Perez-Guzman, Toress-Cruz A, et al. Progressive age - related changes in pulmonary tuberculosis images and the effect of diabetes. Am J Respir Crit Care Med 2000; 162 (5) : 1738-40.
- Sos G, Arvieux Cazalets C, et al. Factors of immuno suppression in patients with tuberculosis. Presse Med 2005; 34 (6) : 420-4.
- Rotoli M, Capizzi R, et al. Cutaneous tuberculosis : a case of difficult classification. Recent Prog Med 1995; 86 (1) : 21-4.
- Jordaan HF, Schneider JW, Abdulla FA. Nodular tuberculid - a report of four patients. Pediatr Dermatol 2000; 17 (3) : 183-8.
- Almagro M, Del Pozo J, et al. Metastatic tuberculosis abscesses in an immunocompetent patient. Clini Exp Dermatol 2005; 30 (3) : 247-9.
- Mboussa J, Monabeka H, et al. Course of pulmonary tuberculosis in diabetes. Rev Pneumol Clin 2003; 59 (1) : 39-44.
- Wang HW, Tay YK, Sim CS. Papular eruption on a tattoo, A case of primary innoculation tuberculosis. Australas J Dermatol 2005; 46 (2) : 84-7.
- Collina G, Morandi L, Lanzoni A. Atypical cutaneous mycobacteriosis diagnosed by polymerase chain reaction. Br J Dermatol 2002; 147 (4) : 781-4.
- Morris JT, Sea Worth BJ, Mc Allister CK. Pulmonary tuberculosis in diabetes. Chest 1992; 102 (2) : 539-41.
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THINKING BEYOND DEWORMING
These worms infect more than a third of the world’s population, of whom 300 million have severe and permanent ill health as a result. The highest rates of infection are usually in children aged 5-15 years, but those most at risk of severe morbidity are pre-school children (age 2-5 years), school-age children, adolescent girls, and women of childbearing age.
Anaemia, vitamin A deficiency, stunted growth, poor intellectual development, impaired cognitive function, and damage to the liver, intestine, and urinary tract are all sequelae of chronic worm infection.
Yet worm control is possible with cheap and effective drugs. A substantial reduction in the burden of disease associated with schistosomiasis and soil-transmitted helminths can be achieved by regular (once or twice a year) treatment of all high-risk populations. A single tablet of albendazole or mebendazole is effective against the common soil-transmitted worms, and praziquantel for schistosomiasis can be given as a single dose according to height. All these drugs are cheap.
Deworming in childhood leads to improvements in intellectual development that are related to income in adulthood Hungry children become more malnourished when infected with worms.
Worm infections increase children’s vulnerability to other infectious diseases. For example, there is some evidence that the frequency of malaria attacks is increased in those with worm infections, and that the disruption of immune responses with worm infections hastens the progression from HIV to AIDS.
Lancet, 2004; 364 : 1993.
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