Claim Missing Document
Check
Articles

Found 3 Documents
Search

UJI AKTIVITAS EKSTRAK ETANOL DAUN SAMBILOTO (Andrographis paniculata Nees) SEBAGAI ANTI BAKTERI Streptococcus pyogenes ATCC 19615 Prisillia Brigitta; Ni Nengah Dwi Fatmawati; Ni Nyoman Sri Budayanti
E-Jurnal Medika Udayana Vol 10 No 3 (2021): Vol 10 No 03(2021): E-Jurnal Medika Udayana
Publisher : Universitas Udayana

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24843/MU.2021.V10.i3.P15

Abstract

ABSTRAK Infeksi ialah masalah kesehatan global dan penyebab utama kematian, terutama di Indonesia. Salah satu penyebab infeksi yang sering ditemukan di Indonesia dan negara-negara berkembang lainnya adalah Streptococcus pyogenes. Untuk mengatasi penyakit infeksi dan menghindari resistensi obat-obatan kimiawi, dapat dilakukan dengan cara mengembangkan antibiotik baru dari sumber alam terutama tanaman. Daun sambiloto sering dijumpai di Indonesia dan dipakai oleh masyarakat sebagai tanaman obat untuk mengobati infeksi saluran kemih, pelega tenggorokan, dan lainnya. Pada daun sambiloto terdapat kandungan antibakteri seperti andrographolide, tanin, flavonoid, alkaloid, steroid, saponin, fenol, terpenoid, dan glikosida. Metode ekstraksi yang digunakan pada daun sambiloto adalah maserasi dengan pelarut etanol 96%, kemudian diencerkan dengan pelarut etanol 96% menjadi konsentrasi 20%, 60% dan 80%, kemudian uji aktivitas antibakteri menggunakan metode cakram difusi. Hasil dari penelitian ini menunjukkan bahwa secara signifikan ekstrak etanol daun sambiloto dapat menghambat pertumbuhan Streptococcus pyogenes ATCC 19615 (p=0.000). Hasil uji daya hambat berupa rerata diameter zona hambat yaitu 7 mm pada konsentrasi 20%, 8.8 mm pada konsentrasi 60%, dan 9.2 mm pada konsentrasi 80%. Dapat disimpulkan bahwa pada keseluruhan konsentrasi yang diujikan dapat menghambat pertumbuhan bakteri Streptococcus pyogenes ATCC 19615 dengan diameter zona hambat paling besar pada ekstrak daun sambiloto konsentrasi 80%. Kata kunci: Daun Sambiloto (Andrographis peniculata Nees), antibakteri, Streptococcus pyogenes
Fatal Disseminated Tuberculosis in Vaccinated Children with Failed BCG Scar Formation: A Clinical-Pathological Correlation and Immunological Review Delicia Rudy; Prisillia Brigitta; I Kadek Suarca
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 10 No. 2 (2025): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v10i2.1510

Abstract

Background: The Bacillus Calmette-Guérin (BCG) vaccine remains the cornerstone of preventative strategies against severe pediatric tuberculosis (TB), specifically disseminated forms such as miliary TB and tuberculous meningitis (TBM). While the formation of a cutaneous scar is historically viewed as a surrogate marker for successful vaccine uptake and delayed-type hypersensitivity (DTH), its absence is often clinically overlooked. This study investigates the correlation between the lack of BCG scarring, immunological anergy, and fatal disseminated disease outcomes. Case presentation: We report a clinical-pathological analysis of two pediatric patients admitted to a tertiary care center in Indonesia. Case 1, an 11-month-old male vaccinated at birth, presented with status epilepticus and was diagnosed with Probable TBM Stage III. Despite vaccination, he lacked a BCG scar and exhibited Tuberculin Skin Test (TST) anergy (0 mm). Case 2, a 2-year-8-month-old female vaccinated at birth, presented with Type 1 respiratory failure due to severe miliary TB. She demonstrated profound wasting and TST anergy (0 mm). Both patients succumbed to the disease (Day 9 and Day 14, respectively) despite aggressive management. Conclusion: The absence of a BCG scar in vaccinated children serves as a critical clinical indicator of "immunological silence." It correlates with a failure to mount the Th1-mediated granulomatous response necessary for containing lymphohematogenous spread. We recommend that scar failure be treated as a risk factor requiring enhanced surveillance and a lower threshold for preventative therapy.
Fatal Disseminated Tuberculosis in Vaccinated Children with Failed BCG Scar Formation: A Clinical-Pathological Correlation and Immunological Review Delicia Rudy; Prisillia Brigitta; I Kadek Suarca
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 10 No. 2 (2025): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v10i2.1510

Abstract

Background: The Bacillus Calmette-Guérin (BCG) vaccine remains the cornerstone of preventative strategies against severe pediatric tuberculosis (TB), specifically disseminated forms such as miliary TB and tuberculous meningitis (TBM). While the formation of a cutaneous scar is historically viewed as a surrogate marker for successful vaccine uptake and delayed-type hypersensitivity (DTH), its absence is often clinically overlooked. This study investigates the correlation between the lack of BCG scarring, immunological anergy, and fatal disseminated disease outcomes. Case presentation: We report a clinical-pathological analysis of two pediatric patients admitted to a tertiary care center in Indonesia. Case 1, an 11-month-old male vaccinated at birth, presented with status epilepticus and was diagnosed with Probable TBM Stage III. Despite vaccination, he lacked a BCG scar and exhibited Tuberculin Skin Test (TST) anergy (0 mm). Case 2, a 2-year-8-month-old female vaccinated at birth, presented with Type 1 respiratory failure due to severe miliary TB. She demonstrated profound wasting and TST anergy (0 mm). Both patients succumbed to the disease (Day 9 and Day 14, respectively) despite aggressive management. Conclusion: The absence of a BCG scar in vaccinated children serves as a critical clinical indicator of "immunological silence." It correlates with a failure to mount the Th1-mediated granulomatous response necessary for containing lymphohematogenous spread. We recommend that scar failure be treated as a risk factor requiring enhanced surveillance and a lower threshold for preventative therapy.