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Bacterial Infection

Subtypes

Description

Diseases caused by bacterial pathogens that can invade tissues, produce toxins, and trigger inflammatory responses.

Effect of Fasting

During fasting, dietary amino acids and glucose stop entering the bloodstream within hours, forcing the body into a conservation mode. Cells activate autophagy to recycle internal proteins, while blood amino acid and glucose levels drop sharply after 24-48 hours. This creates a nutrient-poor environment that starves both sugar- and amino-acid-utilizing bacteria. Some bacteria can secrete proteases to digest host tissue, but fasting reduces blood flow, mucus turnover, and nutrient leakage—making tissue harder to invade. At the cellular level, mTOR shuts down, autophagy increases, and barrier integrity strengthens, forming a metabolic defense state where cells “close up” and become less permissive to infection. The result is a low-nutrient, high-defense physiological state that suppresses bacterial growth and enhances immune clearance.

Treatment Options

Fasting
Antibiotics

Susceptibilities

Systemic Inflammation

Sources

[1] Ketogenesis promotes tolerance to Pseudomonas aeruginosa pulmonary infection
[ 1 ] Kira L Tomlinson et al. (2023) DOI PMCID PMID
[2] Modeling Neisseria meningitidis metabolism: from genome to metabolic fluxes
[ 2 ] Gino J E Baart et al. (2007) DOI PMCID PMID
[3] Role of the pyruvate metabolic network on carbohydrate metabolism and virulence in Streptococcus pneumoniae
[ 3 ] Haley Echlin et al. (2020) DOI PMCID PMID
[4] Carbon source regulates polysaccharide capsule biosynthesis in Streptococcus pneumoniae
[ 4 ] Lukas J Troxler et al. (2019) DOI PMCID PMID
[5] Metabolic adaption to extracellular pyruvate triggers biofilm formation in Clostridioides difficile
[ 5 ] Yannick D N Tremblay et al. (2021) DOI PMCID PMID
[6] Dietary trehalose enhances virulence of epidemic Clostridium difficile
[ 6 ] J Collins et al. (2018) DOI PMCID PMID
[7] Clostridioides difficile Toxins: Host Cell Interactions and Their Role in Disease Pathogenesis
[ 7 ] Md Zahidul Alam et al. (2024) DOI PMCID PMID
[8] Carbon metabolism of intracellular bacteria
[ 8 ] Ernesto J Muñoz-Elías et al. (2006) DOI PMID
[9] Rapid Growth and Metabolism of Uropathogenic Escherichia coli in Relation to Urine Composition
[ 9 ] Larry Reitzer et al. (2019) DOI PMCID PMID
[10] Dinner Date: Neisseria gonorrhoeae central carbon metabolism and pathogenesis
[ 10 ] Aimee D Potter et al. (2024) DOI PMCID PMID
[11] Helicobacter pylori Physiology Predicted from Genomic Comparison of Two Strains
[ 11 ] Peter Doig et al. (1999) DOI PMCID PMID
[12] Pathway analysis using (13) C-glycerol and other carbon tracers reveals a bipartite metabolism of Legionella pneumophila
[ 12 ] Ina Häuslein et al. (2016) DOI PMID
[13] Glucose and Glycolysis Are Required for the Successful Infection of Macrophages and Mice by Salmonella enterica Serovar Typhimurium
[ 13 ] Steven D Bowden et al. (2009) DOI PMCID PMID
[14] CcpA Regulates Staphylococcus aureus Biofilm Formation through Direct Repression of Staphylokinase Expression
[ 14 ] Mingxia Zheng et al. (2022) DOI PMCID PMID
[15] The Catabolite Control Protein E (CcpE) Affects Virulence Determinant Production and Pathogenesis of Staphylococcus aureus*
[ 15 ] Torsten Hartmann et al. (2014) DOI PMCID PMID
[16] Metabolic Versatility of Mycobacterium tuberculosis during Infection and Dormancy
[ 16 ] Dorothy Pei Shan Chang et al. (2021) DOI PMCID PMID
[17] Proteus mirabilis and Urinary Tract Infections
[ 17 ] Jessica N Schaffer et al. (2015) DOI PMCID PMID