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Infection

Infection

When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
The chain begins with pathogens: bacteria, viruses, fungi, prions, or parasites such as protozoa helminths. These can be present on the skin as transient or resident flora, or they can be acquired from the environment. Identifying and treating the type of infection and...

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Pneumonia II: Pathophysiology

The pathophysiology of pneumonia involves the following steps:

Urinary Tract Infection II: Pathophysiology

Urinary Tract Infection II: Pathophysiology

The pathophysiology of urinary tract infections (UTIs) encompasses several progressive stages, beginning with bacterial colonization and culminating in potential systemic complications if untreated. UTIs are primarily initiated by bacteria, such as Escherichia coli, which often originate from the gastrointestinal tract and migrate to the urinary system through the periurethral area. This migration can occur via several routes, including improper hygiene practices, sexual activity, or...

Acute Inflammation II: Local and Systemic Effects

Acute Inflammation II: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...

Bacterial Meningitis II: Pathophysiology

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...

Acute Pancreatitis II: Pathophysiology

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...

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Updated: May 12, 2026

Cecal Ligation Puncture Procedure

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Published on: May 7, 2011

The pathogenesis of sepsis.

¹Rush Medical College, Chicago, Illinois.

Annals of Internal Medicine

|September 15, 1991

Summary

Sepsis involves numerous mediators, not a single cause. Understanding target cell activation and mediator interactions is key to managing this lethal condition.

Area of Science:

* Pathophysiology of sepsis and its sequelae (sepsis syndrome, septic shock).
* Infectious disease and critical care medicine.

Background:

* Sepsis and its sequelae are increasingly common and potentially lethal diagnoses.
* Numerous mediators contribute to sepsis pathogenesis, including cytokines, lipids, and cellular components.

Purpose of the Study:

* To review the complex cascade of mediators involved in sepsis pathogenesis.
* To discuss the challenges in identifying a central mediator and extrapolating animal study findings.

Main Methods:

* Literature review of described mediators and mechanisms in sepsis.
* Analysis of proposed pathogenic pathways and regulatory feedback loops.

Main Results:

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* No single central mediator for sepsis has been identified; tumor necrosis factor alpha (TNF alpha) is insufficient.

* Sepsis pathogenesis likely involves complex interactions of target cell activation, mediator presence, and feedback mechanisms.

* Endothelial damage results from persistent inflammatory insults, leading to loss of regulatory control.

Conclusions:

* Sepsis is a multifactorial condition influenced by target cell state and mediator interplay.
* Effective management requires understanding the complex inflammatory response and potential for endothelial damage.
* Further research is needed to elucidate the precise mechanisms and develop targeted therapies.