Sechenov School
Home › Pathology › Intrauterine Infections

Intrauterine Infections

Infectiones intrauterinae

For medical students2 min readUpdated 2026-10-10

Intrauterine infections encompass a group of diseases in which the pathogen is transmitted from the mother to the fetus during pregnancy. In pathology, they are considered one of the leading causes of symmetrical intrauterine growth restriction (IUGR) and severe hypoxic damage associated with the aspiration of infected amniotic fluid.

Main pathogensCytomegalovirus (CMV), Toxoplasma, herpes simplex virus, and rubella virus
Threat to the fetusMortality rates in infants with IUGR are 3–5 times higher than average
AspirationIn chorioamnionitis, microbes and maternal leukocytes are found in the fetal lungs
Timing of damageInfectious IUGR develops early—during the 1st and 2nd trimesters

Role of Infections in Intrauterine Growth Restriction (IUGR)

Intrauterine growth restriction is diagnosed when the birth weight falls below the 10th percentile for gestational age. Intrauterine infections (cytomegalovirus infection, toxoplasmosis, herpes, rubella) are fetal causes of IUGR and result in its most severe form.

Fetal infection leads to the development of the hypoplastic (symmetrical) variant of IUGR:

Endocrine Alterations in Growth Pathology

Normal fetal growth is regulated by specific hormones whose balance can be disrupted by infectious and placental pathologies:

  1. Insulin and Insulin-like Growth Factors (IGFs): Play a key role. Insulin is synthesized by the fetus itself (it does not cross the placenta), ensuring fat and glycogen storage and protein synthesis. IGFs stimulate the cell cycle. In intrauterine malnutrition, fetal blood levels of C-peptide are frequently decreased.
  2. Growth Hormone (Somatotropin): Does not affect physical growth in utero because fetal receptors are not yet developed.
  3. Thyroid Hormones: Do not determine body weight, but are absolutely essential for proper cellular differentiation and maturation.

Intrauterine Hypoxia and Aspiration Syndrome

Against the background of an infectious process (e.g., placental inflammation), placental insufficiency often develops, leading to intrauterine hypoxia. Oxygen deprivation triggers a cascade of pathological reactions:

Lung morphology during aspiration: Lanugo hairs (lanugo), epithelial scales, and clumps of meconium are found within the lumens of bronchi and alveoli. If hypoxia occurs alongside a maternal infection (endometritis, vaginitis, chorioamnionitis), the amniotic fluid becomes infected. Microscopic examination of the fetal lungs reveals massive numbers of microorganisms and maternal leukocytes. By comparison, during the aspiration of non-infected fluid, the fetal response differs—macrophages appear after 12–16 hours, while neutrophils join only on the second day.

Impact on Lung Development (Respiratory Distress Syndrome)

Chronic intrauterine hypoxia, IUGR, and infections exhaust the compensatory mechanisms of the fetus, increasing the risk of respiratory distress syndrome (RDS), also known as hyaline membrane disease.

Its core mechanism is a deficiency of surfactant, which is normally synthesized by type II pneumocytes. Until 32–34 weeks, synthesis proceeds via the imperfect ethanolamine methylation pathway, which is extremely sensitive to hypoxia and acidosis. With surfactant deficiency, alveoli collapse (atelectasis), the endothelium is damaged, and fibrinous exudate accumulates in the alveoli. It forms homogeneous eosinophilic sheets—hyaline membranes—which completely block gas exchange, locking in the vicious cycle of hypoxemia.

Mnemonic

To remember the profile of symmetrical (infectious) IUGR: "Symmetry means Systemic." The entire body is affected systematically from early stages, which is why all parameters are uniformly reduced.

Frequently asked questions

What surfactant synthesis pathways exist in the fetus and at what gestational ages do they function?

The fetus has two main surfactant synthesis pathways that function at different gestational ages.

  • Ethanolamine methylation pathway — the primary pathway until 32–34 weeks of intrauterine development. It is imperfect and easily depleted during hypoxia, acidosis, or hypothermia.
  • Choline pathway — becomes active later in pregnancy.

Synthesis begins at 20–24 weeks, when surfactant is detectable in trace amounts. From 24 weeks onward, the activity of producing cells rapidly increases, reaching peak synthetic activity by 35 weeks.

What morphological changes in the placenta are characteristic of intrauterine infections?

Intrauterine infections are characterized by inflammatory processes in various placental structures depending on the route of transmission.

  • Villitis — inflammation of the villi (focal or diffuse, exudative or productive), which is the primary indicator of hematogenous infection. Chronic processes lead to stromal sclerosis of the villi and obliteration of fetal vessels.
  • Chorioamnionitis — focal or diffuse leukocyte infiltration of the extraplacental membranes in ascending infections.
  • Funisitis — inflammation of the umbilical cord vessels (initially veins, then arteries), complicated by thrombosis.

In specific infections (such as listeriosis), necrosis foci and granulomas form within the villous stroma.

What specific congenital anomalies does the rubella virus cause in the fetus?

The rubella virus causes multiple congenital malformations in the fetus. The classic triad includes:

  • Cataracts.
  • Sensorineural hearing loss.
  • Congenital heart defects.

Congenital rubella is also characterized by ocular lesions, including chorioretinitis, and central nervous system involvement. CNS manifestations include meningoencephalitis and impaired myelination processes. CNS damage combined with deafness and blindness leads to intellectual disability.

Which infections cause IUGR in the fetus?

The main pathogens leading to growth restriction include cytomegalovirus (CMV), rubella virus, herpes simplex virus, and Toxoplasma.

What is the difference in the lungs between the aspiration of infected vs. non-infected amniotic fluid?

When infected fluid is aspirated (associated with chorioamnionitis), microbes and maternal leukocytes are immediately detected in the lungs. In sterile aspiration, a local macrophage response develops first (after 12–16 hours), and neutrophils appear later.

How do infections contribute to the development of hyaline membranes?

Infections are frequently accompanied by fetal hypoxia and acidosis. These conditions exhaust the immature enzyme systems of type II pneumocytes, suppressing surfactant synthesis, which directly leads to atelectasis and hyaline membrane formation.

Which hormone is critically important for fetal growth but does not cross the placenta?

Insulin. The fetus must secrete it independently. Its deficiency or impaired receptor sensitivity leads to severe intrauterine growth restriction.

Go deeper

More topics in Pathology

Hemolytic AnemiasPrecancerous States and HeredityPathogenesisGestosis: Pathogenesis, Pathology and ComplicationsInfectious Dermatoses and Bullous Skin DisordersBone TumorsChildhood Infections: Polio, Varicella, and Pertussis PathologyPediatric Neoplasms and HemangiomaPulpitis: Pathology, Classification and Clinical FormsInternational Classification of DiseasesBirth Injury: Types, Pathophysiology and Clinical PresentationCarbohydrate DystrophiesPathology →