Delicia Rudy
General Practitioner, Air Force Hospital, Surabaya, Indonesia

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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 (2026): 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 (2026): 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.