|
|||||||||||||||||||||||
|
High Risk Groups for Tuberculosis Following the collapse of the state in 1991, all health institutions, including the National TB Control Program, were destroyed. As a result, all open TB cases were released to the general population, transmitting the disease. Extreme poverty, malnutrition, lack of clean water, basic sanitation increased morbidity and mortality from TB. Pathogenesis The primary complex (Ghon) of TB consists of portal of entry and the regional lymph nodes that drain the area of the primary focus. The infection may occur anywhere in the body, although the primary site is the lungs in >95% of cases. It may occur dissemination leading to Miliary T.B. Clinical Forms of Tuberculosis I) Endo Thoracic Diseases I) The Endo Thoracic Diseases. II) Extra Thoracic Diseases. Skeletal TB Abdominal and Gastrointestinal TB Renal TB Superficial lymph nodes TB (Scrofula). Prenatal TB The Case of Mohamed Amin Abdik arim Hagi This is a study of Mohamed Amin Abdikarim Hagi, a seven-year old Somali boy, who visited Arafat Specialist Medical Center on 17 November 2002 . He was brought in as an outpatient to the Department of Pediatrics. The young patient had a high-grade fever, intermittent and continuous, for three months prior to the visit. In addition, he had a chronic productive and irritant cough that was progressively worsening by the day. Also, the child was experiencing chest pain, dyspnea, palpitations, poor appetite, anorexia, nausea, recurrent vomiting, progressive weight loss, malaise and prostration. Furthermore, the child was not responding to antipyretic and antibiotic treatment. Past History Past history, birth history, nutritional history and developmental history were all normal. However, he was not given any immunization since birth. Family and social history indicate that both parents were young, not educated and nomadic. There is a history of consanguinity, though no history of known hereditary diseases was reported. The child had 5 siblings (3 males and 2 females), who were all alive and healthy. He was the 3 rd offspring and according to the family background there were no infectious diseases or known history of TB in the family, including cohabitant grandmother. Physical Examination General condition: Patient was sick with a toxic appearance. He looked pale and had severe respiratory distress. Vital signs: temperature 39.5c; RR=42 beats per minute; pulse=136 beats per minute; BP= was not recorded because the appropriate cuff was out of order. Neck, eyes, ears, and throat were all unremarkable. WT= 18 kg (<10 th percentile); HT= 150 cm (25-50 th percentile); HC= 50 cm (< 50 th percentile). Chest : Inspection showed a severe respiratory distress with sub costal, intercostals, and supra-sternal recessions. On palpation, there was dullness on both sides of the hemi-thorax, though more on the left. On auscultation, there was reduced air entry on both sides of the lung bases and harsh egobronchophany on the left upper lung. Cardiovascular System: S1+S2 normal; heart is rhythmic and regular, however he had tachycardia and murmur grade II/VI all over the pericardial areas, possibly due to anemia. Abdomen: Was soft with a mild tenderness, mainly on the left hypochondriac region. Spleen was palpable in 3-4 cm BCM, while the liver was just palpable, and no abdominal mass was felt. Genitalia, male with normal configurations and both testicles were in the scrotum. Central Nervous System: No neck rigidity, muscle power, tone, motor, and sensitivity were grossly unremarkable. Case Management: During the Course of the Treatment The 1 st chest X-ray showed huge opacity on the left lung with consolidation-collapse. We started to treat the patient with Kenya-label anti-T.B. drugs with Isoniazid 10 mg /kg /day, Rifampicin 10 mg /kg /day, Ethambutol 15 mg /kg/day, Multivitamin one tablets BID and Paracetamol 500 mg PRN as an outpatient, and Iron tablets BID. The 1st ESR = 140mm/hr; RBC=3.35; WBC=18000; HGB=6.5; HCT=22.1; PLT=814; Urea=18; Creatinin=0.9 mg; SGOT=73; SGPT=21; Blood Sugar = 74 mg. Stool analysis results showed Ascaris Lumbricoid, and was treated with Albendazole 200 mg single dose. The patient continued to have the above signs & symptoms with no improvement after two days of follow-up as an outpatient. Blood film for Malaria done showed P.F. +ve and anti-malaria treatment with Cotecxin syrup was administered, and child showed some progress but remained sick. So, we considered supra-infection and initiated an antibiotic treatment with 3 rd generation Cephalosporin (Cefatax) of 100 mg/kg/day (IV) TDS & Gentamycin 5 mg/kg/day (IV) BID along with anti-T.B. treatment for tree days. Still the child remained sick. A repeated blood film test for Malaria was “-ve”. The second chest X-ray was worse on the 7th day with complete consolidation of the left lung and a huge opacity of the right upper and middle lobes. On the 7 th day, we discontinued the Kenya-labeled anti-T.B. products. Instead, we switched to Chinese Anti-T.B. drugs, while keeping Cephalosporin & Gentamycin for two-weeks course, soon after switching on to the Chinese anti-T.B. product, then the majority of the signs and symptoms subsided. The child became comfortable, gaining weight gradually, and the 3 rd chest X-ray showed dramatic improvement. We continued the Chinese Anti-T.B. drugs for 9 months and thereafter discontinued. The second ESR=75 mm/hr, then a repeated ESR=35mm/hr, and the fourth chest X-ray showed completed resolution. Epidemiological Data of Childhood TB in Somalia • After two years of intensive work in the Pediatric Department of Arafat Specialist Medical Center, we received 33,874 children. Some of these children came for a routine medical check-up, while the majority were seeking treatment for different diseases, such as chest infection (upper and lower respiratory tract infections), diarrhea, intestinal parasitosis, anemia, malnutrion (Marasmas, kwashiorkor), malaria falciprum, viral hepatitis, meningitis, various skin infections, etc. Of these 33,874 patients, only 26 were affected by TB This means that less than 1% of our study had TB = 0.07675%. The P value (P< 0.0001) is statistically highly significant, and the distribution of the affected cases went as follows : 2 cases were TB Meningitis; 3 had peritoneal TB; 4 had TB lymphadenitis; and remaining 17 cases suffered from pulmonary TB. Tuberculosis Diseases (TB) TB remains one of the most serious infectious diseases in the world. It afflicts 1-2 billion people worldwide, causing 1.3 million deaths per year, most of which are children in developing countries. Etiology The major agents of human TB are mycobacterium tuberculosis and Mycobacterium Bovis, which are both rare in developed countries, because milk pasteurization, veterinary health control, and proper screening of slaughtered animals are mandatory. However, TB infection is significantly associated with untreated bovine milk and meat, which are regularly consumed in underdeveloped countries. The Bacilli are non-motile, non-spore forming, pleomorphic, and weak gram positive (+ve). The hallmark of Mycobacterium is Acid Fastness; the dye is not readily removed by rinsing with Ethanol plus Hydrochloric Acid. The Bacilli appears red when stained with Fuchsine (Zeihl – Neelsen Or Kynyoun Stain). Conclusion Since there are no permanent medical educational programs in Somalia for the last 14 years, and no governmental body to control the national health system, a large number of unscrupulous profit-seeking health professionals continue to practice medicine. Also, some NGOs and businesspersons import expired products—i.e., drugs, beverages and food products--without formal authority and quality control. Thus, Somalis are not only dying of bullets, diseases and starvation, but also of medical malpractice and consumption of dangerous products. Good Governance could be the only Solution. Bibliography • Starke JR, Correa AG. Management of Mycobacterial Infection and disease in children. Pediatr Infect Dis J 1995; 14: 553. • Schaaf HS, Beyers N, Gie RP, et al. Respiratory tuberculosis in childhood: the diagnostic value of clinical features and special investigations. Pediatr Infect Dis J 1995; 14: 189. • American Academy of Pediatrics Committee on Infectious Diseases. Chemotherapy of tuberculosis in Infants and children. Pediatrics 1992; 89: 161. • Miller FJW. Tuberculosis in children. New York : Churchill Livingstone, 1981. • Lincoln EM, Sewell EM. Tuberculosis in children. New York : McGraw-Hill,1963.
|
||||||||||||||||||||||
| ©JUBBALAND.ORG ®All rights reserved. Contact us at: info@jubbaland.org Site designed by Ramaas Software | |||||||||||||||||||||||