Intrauterine Infections: General Characteristics and Routes of Transmission
Intrauterine infections comprise a broad group of disorders in which pathogens are transmitted from an infected mother to the developing fetus. Transmission can occur at various stages: prior to the onset of labor (antenatally) or during the passage of the infant through infected birth canals (intranatally).
According to statistical data, a significant proportion of infants ($\ge$ 10%) are exposed to intrauterine infection before or during delivery; however, clinical manifestation occurs far from universally — clinical signs, including pulmonary involvement, develop in only 1–10% of all infected newborns.
Several main routes of pathogen entry into the fetal organism are distinguished:
- Transcervical route (ascending infection) — plays the leading role in the development of pulmonary pathology.
- Transplacental route (hematogenous infection) — pathogen transmission via the maternal circulation.
- Rare transmission routes — these include descending infection (pathogen extension from the fallopian tubes in the presence of salpingitis) and iatrogenic infection during amniocentesis.
Ascending Infection: Etiology and Risk Factors
In ascending infection, the source of pathogens is the mucous membranes of the pregnant woman's vagina and cervix. The etiologic structure is dominated by bacterial agents. Considerably less frequently, the causes are specific microorganisms such as Chlamydia, Mycoplasma, Ureaplasma, as well as various viruses and pathogenic fungi.
A number of predisposing factors facilitate the infectious process and pathogen penetration to the fetus:
- Inflammatory diseases of the lower genital tract in pregnant women (vulvovaginitis, cervicitis).
- Premature rupture of membranes, compromising the sterile intrauterine environment.
- Prolonged anhydrous (ruptured membranes) period in labor, increasing fetal exposure time to the infected environment.
- Cervical incompetence (isthmic-cervical insufficiency), promoting gaping of the cervical os.
Pathogenesis of Pneumonia and Fetal Morphological Changes
The development of intrauterine pneumonia is inextricably linked to the condition of the amniotic fluid. When an ascending infection develops, amniotic fluid becomes contaminated with pathogenic microflora.
Fetal respiratory system injury occurs when respiratory movements are performed, resulting in infected amniotic fluid entering the respiratory tract directly. This aspiration leads to severe inflammation of the lung parenchyma — intrauterine pneumonia.
Morphological changes in intrauterine infection are not confined to the respiratory system alone. Other organs are also affected:
- Gastrointestinal tract: active fetal swallowing of contaminated fluid leads to inflammatory lesions of the mucosal lining of the digestive tract, including gastritis, enteritis, and colitis.
- Contact lesions: prolonged exposure of the fetus to infected amniotic fluid can cause injury to the skin and ocular mucous membranes.
The Role of Chorioamnionitis and the Inflammatory Cascade
An almost constant and critical sign of developing ascending infection is chorioamnionitis — marked inflammation of the fetal membranes. This process triggers a complex pathogenetic mechanism that not only leads to fetal infection but also provokes preterm labor.
Specific proteases released by bacteria and activated leukocytes degrade tissue structure, causing premature rupture of membranes. In response to infection, a powerful inflammatory cascade is initiated:
- Macrophages within the fetal membranes become activated and begin intensive synthesis of pro-inflammatory cytokines (IL-1, IL-2, IL-6, IL-8, tumor necrosis factor, and granulocyte-macrophage colony-stimulating factor).
- High cytokine concentrations stimulate the decidua and amnion to increase the synthesis of prostaglandins.
- Prostaglandins cause a sharp inhibition of progesterone synthesis, the principal hormone maintaining pregnancy.
- Decreased progesterone levels and prostaglandin action enhance uterine contractility and stimulate labor.
The clinical consequence of this pathological cascade is preterm delivery against the background of a severe infectious process. Estimates indicate that 20% to 40% of all preterm births are caused precisely by intrauterine infection of the fetal membranes.