Relationship between Fever Level and Leukocyte Levels in Children with Typhoid Fever

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Huỳnh Thanh Thu


Salmonella typhi spreads typhoid fever, a multisystem illness. The bacteria that cause typhoid fever may promote the generation of endotoxins that alter haematological assays, particularly those involving leukocytes. Exogenous pyrogens, such as bacteria or an immune reaction, produce fever. Pyogen may be an interleukin-1-like protein. This chemical may stimulate the hypothalamus to create more prostaglandin E2, causing fever. We also found lymphocytosis, monocytosis, eosinophilia, and thrombocytopenia. Endotoxin and endogenous mediators may reduce bone marrow, causing leucopenia. Recent research shows that the average leukocyte count is normal or slightly elevated, despite the idea that 25% of the population has leucopenia. This research examines whether fever and leukocyte counts are linked in hospitalized typhoid patients. This cross-sectional study was undertaken in the hospital's pediatrics and medical records departments. The sample included typhoid-hospitalized children. Forty persons were randomly recruited for this study. Chi-Square was used for univariate and multivariate analysis. (p = 0.816; OR = 1.181; 95% CI = 0.292-4.778). In typhoid-hospitalized youngsters, fever and leukocyte counts are unrelated.


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Thu, H. T. (2022). Relationship between Fever Level and Leukocyte Levels in Children with Typhoid Fever. Journal of Asian Multicultural Research for Medical and Health Science Study, 3(4), 16-21.


Bunce, M., Rosendo, S., & Brown, K. (2010). Perceptions of climate change, multiple stressors and livelihoods on marginal African coasts. Environment, Development and Sustainability, 12(3), 407-440.

Cramer, M. N., Gagnon, D., Laitano, O., & Crandall, C. G. (2022). Human temperature regulation under heat stress in health, disease, and injury. Physiological reviews, 102(4), 1907-1989.

Crowl, R. M., Stoller, T. J., Conroy, R. R., & Stoner, C. R. (1991). Induction of phospholipase A2 gene expression in human hepatoma cells by mediators of the acute phase response. Journal of Biological Chemistry, 266(4), 2647-2651.

Kjellstrom, T., Holmer, I., & Lemke, B. (2009). Workplace heat stress, health and productivity–an increasing challenge for low and middle-income countries during climate change. Global health action, 2(1), 2047.

Moshage, H. (1997). Cytokines and the hepatic acute phase response. The Journal of Pathology: A Journal of the Pathological Society of Great Britain and Ireland, 181(3), 257-266.

Teadt, S., Burns, J. C., Montgomery, T. M., & Darbes, L. (2020). African American adolescents and young adults, new media, and sexual health: scoping review. JMIR mHealth and uHealth, 8(10), e19459.

Watson, D. W. (1960). Host-parasite factors in group A streptococcal infections: pyrogenic and other effects of immunologic distinct exotoxins related to scarlet fever toxins. The Journal of Experimental Medicine, 111(2), 255-284.

Xia, N., Horke, S., Habermeier, A., Closs, E. I., Reifenberg, G., Gericke, A., ... & Li, H. (2016). Uncoupling of endothelial nitric oxide synthase in perivascular adipose tissue of diet-induced obese mice. Arteriosclerosis, thrombosis, and vascular biology, 36(1), 78-85.