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Pathophysiology · Chapter 7. Infectious Process

Portals of Entry for Infection

Port d'entrée de l'infection — the specific site of pathogen penetration into the macroorganism. The localization of this area often determines which specific nosological form of the disease will develop in the patient.

Main roleDetermine the form of the disease (for example, Streptococcus causes tonsillitis or erysipelas depending on the portal of entry).
Inside macrophagesCertain pathogens (mycobacteria, brucellae) are capable of multiplying inside phagocytes.
Barrier functionEvolutionary mechanisms of mucous membranes inhibit the penetration and multiplication of pathogens.
Routes of disseminationMicrobes spread via the blood, lymph, intercellular spaces, and serous cavities.
4 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Types of portals of entry

Pathogenic microorganisms use various anatomical structures for invasion. The following main localizations serving as portals of entry are distinguished:

  • Skin integument: pathogens of malaria, epidemic typhus, and cutaneous leishmaniasis penetrate through it.
  • Mucous membranes of the respiratory tract: a typical route for respiratory pathogens such as influenza and measles viruses, as well as bacteria causing scarlet fever.
  • Mucous membranes of the gastrointestinal tract (GIT): the site of introduction of intestinal infection pathogens, for example, typhoid fever and dysentery.
  • Mucous membranes of the urogenital organs: specific portals for sexually transmitted infections (syphilis, gonorrhea).
  • Walls of blood and lymphatic vessels: provide entry of the pathogen directly into the blood or lymph, bypassing external integuments. This occurs during bites of blood-sucking arthropods and animals, medical injections, or surgical interventions.

Clinical significance of localization

The site of initial microbial introduction is of paramount clinical significance, as it often determines the nosological form of the developing disease. The same pathogen can cause completely different pathologies depending on the tissues through which it entered the macroorganism.

A classical example of the dependence of the disease form on the portal of entry is streptococcal infection:

  • If Streptococcus invades the tonsillar tissue, the patient develops tonsillitis.
  • When the pathogen penetrates through the skin, erysipelatous inflammation (erysipelas) or pustular skin lesions (pyoderma) occur.
  • If the mucous membrane in the uterine region becomes the portal of entry, the infectious process leads to the development of endometritis.
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Methods of dissemination in the body

After successfully overcoming the primary barriers, bacteria begin to spread (disseminate) through the tissues of the macroorganism. Four main routes of such spread are distinguished:

  1. Through intercellular spaces. The advancement of microbes in tissues is possible due to the presence of defects in the epithelial cover or the production of specific enzymes by pathogens (e.g., bacterial hyaluronidase), which break down the intercellular substance.
  2. Lymphogenic route. Pathogens penetrate into lymphatic capillaries and are carried away by the lymph flow.
  3. Hematogenous route. Spread occurs via blood vessels with the blood flow.
  4. Through fluids of serous cavities and the spinal canal. Pathogens migrate together with cerebrospinal fluid or exudate within enclosed spaces of the body.

Barrier systems of the macroorganism

In the course of evolution, humans have developed powerful defense systems. Their main task is to prevent the penetration of pathogens, halt their reproduction, and prevent the realization of pathogenic effects. A special role in this process belongs to factors that inhibit the invasion of pathogenic and opportunistic bacteria (barrier function).

Each section of the GIT has its own unique set of protective factors:

GIT sectionMain defense factors
OropharynxLysozyme enzyme, proteolytic enzymes of saliva, secretory immunoglobulins (Ig), as well as competition from the endogenous microflora.
StomachAggressive acidic environment, proteolytic enzymes, and active peristalsis.
Small intestineBile acids, protective mucus (mucin), secretory Ig, proteolytic enzymes, constant desquamation of epithelial cells, lymphoid formations, peristalsis, and intestinal microflora.
Large intestineAbundant intestinal microflora, mucin, secretory Ig, epithelial desquamation, and peristalsis.

Phagocytosis and intracellular survival

The most important mechanism of macroorganism defense is phagocytosis. Its protective role consists in the sequential detection, engulfment, and destruction of microorganisms by specialized cells.

However, there is a serious problem: pathogens of certain infectious diseases have developed resistance to the effector mechanisms of phagocytes. Instead of perishing, they are capable of actively multiplying inside macrophages.

Microorganisms that multiply in macrophages include:

  • Viruses: poxviruses and herpesviruses.
  • Rickettsiae: the causative agent of epidemic typhus (Rickettsia prowazekii).
  • Bacteria: tubercle bacillus (Mycobacterium tuberculosis), Mycobacterium leprae (Mycobacterium leprae), brucellae (Brucella), and the causative agent of legionellosis (Legionella pneumophila).
  • Protozoa: toxoplasmas, leishmanias, and trypanosomes.
How to memorize

How to remember the routes of microbial dissemination: CLIM — Clood (hematogenous), Lymph (lymphogenic), Interstitium (intercellular space), Medullary canal (and serous cavities).

Class and exam questions

Does the same pathogen always cause the same disease?

No, this depends on the portal of entry. For example, Streptococcus on the tonsils causes tonsillitis, whereas penetration through the skin causes erysipelas or pyoderma.

Due to what do bacteria manage to penetrate through the intercellular space?

This is facilitated by defects in the epithelial cover, as well as the production of special enzymes by microbes, such as bacterial hyaluronidase.

Why does phagocytosis not always protect against infection?

A number of pathogens (e.g., Mycobacterium tuberculosis, herpes viruses, toxoplasmas) are resistant to the effector mechanisms of phagocytes and can multiply directly inside them.

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What else to study on this topic

  • Mechanisms of action of bacterial hyaluronidase during dissemination
  • Defense factors of various GIT sections (oropharynx, stomach, intestines)
  • Features of intramacrophage multiplication of bacteria and viruses
  • Role of secretory immunoglobulins (Ig) in the barrier function of mucous membranes
  • Differences between hematogenous and lymphogenic routes of infection spread

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