Teodora Deaconu

Mrs. Teodora Deaconu


Research Focus & Metrics

Academic Career Length

2Years (2025-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
4 February 2025 in Microorganisms
Verified
Journal Article
Open access
PDF file
SBSerban Nicolae Benea
Serban Nicolae Benea
VMVALENTINA RUXANDRA MOROTI-CONSTANTINESCU
VALENTINA RUXANDRA MOROTI-CONSTANTINESCU
TDTeodora Deaconu
Teodora Deaconu
CCCorina Ciont
Corina Ciont
MBMihaela Anca Benea
Mihaela Anca Benea
ISIlinca Savulescu-Fiedler
Ilinca Savulescu-Fiedler
Streptococcus suis is a common germ in pig populations, with high carrier rates. Recent studies identify it as an emerging zoonotic pathogen, particularly in Southeast Asia, where raw pork is traditionally consumed. Data on Streptococcus suis infection in Europe, especially Eastern European countries like Romania, are limited. Our study reviewed data from an infectious diseases tertiary hospital in Bucharest between 2001 and 2024, including eight patients diagnosed with a Streptococcus suis invasive infection. The median age was 53.3 years, with a male-to-female ratio 3:1. Three patients had risk factors such as contact with pigs or handling fresh pork. Seven patients were initially diagnosed with meningitis and one with endocarditis. During hospitalization, an additional endocarditis case was identified among the meningitis patients. Laboratory samples indicated bacterial infection, with Streptococcus suis isolated from CSF in six cases and blood cultures in two cases. All strains tested were susceptible to beta-lactam antibiotics, but resistant to lincosamides and macrolides. There were no deaths, but half of our patients experienced severe meningitis-related sequelae, mainly hearing loss. Clinicians should be aware of Streptococcus suis as an etiologic agent of meningitis in non-endemic areas like Romania, especially in patients with risk factors (contact with pigs, pork).

4 February 2026 in Life
Verified
Journal Article
Open access
PDF file
Roxana-Nicoleta SilisteRoxana-Nicoleta Siliste
Roxana-Nicoleta Siliste
SBSerban Nicolae Benea
Serban Nicolae Benea
CHCorina Homentcovschi
Corina Homentcovschi
TDTeodora Deaconu
Teodora Deaconu
Constantin CaruntuConstantin Caruntu
Constantin Caruntu
ISIlinca Savulescu-Fiedler
Ilinca Savulescu-Fiedler
Myocardial and vascular injury secondary to SARS-CoV-2 infection and vaccination has emerged as a clinically relevant phenomenon, with distinct but overlapping mechanisms. Myocardial injury in COVID-19 results from a complex interplay between direct viral effects and immune-mediated inflammation, supported by histopathological studies revealing macrophage-rich infiltrates, microthrombosis, and supporting fibrosis in isolated areas. In contrast, vaccine-associated myocarditis—reported predominantly following mRNA vaccines—has a self-limiting clinical course, with mechanisms likely involving molecular mimicry, aberrant immune activation, or hypersensitivity reactions, although these pathways require further validation. Although mRNA vaccines have been associated with a small increase in myocarditis, particularly in young men, the risk is significantly lower than that associated with COVID-19 infection, and the cardiovascular benefits of vaccination far outweigh these rare adverse events in most populations. After the end of the pandemic, the number of patients with severe forms of COVID-19 has decreased significantly, but we consider that cardiac involvement remains an important issue for the acute and long-term prognosis of patients with SARS-CoV-2 infection. Our paper synthesizes the latest epidemiological and mechanistic evidence on the link between COVID-19, vaccination, and myocardial and/or vascular injuries, highlighting the clinical implications and providing practical recommendations for management, as well as future perspectives on risk assessment, targeted immunotherapy, advanced diagnostic tools, and long-term monitoring.

24 December 2025 in Preprints.org
Verified
Preprint
Open access
PDF file
Roxana-Nicoleta SilisteRoxana-Nicoleta Siliste
Roxana-Nicoleta Siliste
SBSerban Nicolae Benea
Serban Nicolae Benea
CHCorina Homentcovschi
Corina Homentcovschi
TDTeodora Deaconu
Teodora Deaconu
Constantin CaruntuConstantin Caruntu
Constantin Caruntu
ISIlinca Savulescu-Fiedler
Ilinca Savulescu-Fiedler
Cardiovascular involvement in SARS-CoV-2 infection and following vaccination has emerged as a clinically relevant phenomenon with distinct yet overlapping mechanisms. Myocardial injury in COVID-19 results from a complex interplay between direct viral ef-fects, immune-mediated inflammation, endothelial dysfunction, oxidative stress, and, in rare occasions, cytokine storm. The virus primarily binds to ACE2 receptors, which are highly expressed in endothelial cells and pericytes, leading to microvascular damage and a systemic prothrombotic state. Additional viral entry pathways, including CD147, Neu-ropilin-1, and CD26, further contribute to vascular and myocardial injury, which is a ra-ther immune-driven process rather than a direct cytopathic one. Histopathological studies that reveal macrophage-rich infiltrates, microthrombosis, and patchy fibrosis support the immune-driven process theory. In contrast, vaccine-associated myocarditis – predomi-nantly reported following mRNA vaccines – presents a self-limiting clinical course, with mechanisms probably involving molecular mimicry, aberrant immune activation, or hy-persensitivity reactions. Despite an increased incidence in young males after the second dose, the overall risk remains low compared to infection-related myocarditis. Under-standing the pathophysiological interplay between infection- and vaccine-related cardiac involvement is essential for accurate risk assessment, improved diagnostic strategies, and targeted therapeutic approaches. Future research should focus on elucidating immune pathways, refining biomarkers, and developing personalized management strategies in order to mitigate cardiovascular sequelae of both COVID-19 and vaccination.

1 June 2025 in GERMS
Verified
Journal Article
Open access
ISIlinca Savulescu-Fiedler
Ilinca Savulescu-Fiedler
TDTeodora Deaconu
Teodora Deaconu
RSRoxana Siliste
Roxana Siliste
CHCorina Homentcovschi
Corina Homentcovschi
AGAdriana Gurghean
Adriana Gurghean
SBSerban Benea
Serban Benea
Inflammation may induce dysautonomia, which is revealed by the decrease in heart rate variability (HRV) parameters. Our pilot study compares changes in HRV and the association between HRV and inflammatory markers in three RNA viral infections: acute (SARS-CoV-2, measles) and chronic (HIV). We evaluated 25 patients with viral infections and 8 control patients without viral disease, with similar mean age and comorbidities. Patients with measles and COVID-19 were hospitalized for mild to moderate respiratory symptoms, while those with HIV were assessed during follow-up visits. HRV parameters were assessed in time and spectral domains, under standardized conditions. Significant differences were identified between patients with measles and COVID-19 regarding SDNN (p=0.016), rMSSD (p=0.002), and between patients with COVID-19 and HIV, both for SDNN (p=0.029) and rMSSD (p=0.017). SDNN and rMSSD had the highest value in the COVID-19 group and the lowest value (lower than in the control group) in patients with HIV and measles. All frequency-domain parameters reached their highest values in patients with COVID-19, whereas they were consistently lower in those with HIV and measles. A significant correlation of LF/HF ratio with serum fibrinogen was observed only in patients with measles and HIV infection (r=0.793, p=0.011, respectively r=0.955, p<0.001). Our study showed a significant decrease in HRV parameters in patients with measles and HIV, with a more stable autonomic response in mild-moderate COVID-19 forms. A correlation between inflammation and markers of sympathetic dominance was found in patients with measles and HIV but not in COVID-19. Further studies may assess the relation between inflammation in viral infections and subtle changes in HRV parameters.