An infection is the successful invasion and multiplication of pathogenic microorganisms within a host’s tissues. This complex biological mechanism, known as pathogenesis, requires the pathogen to overcome multiple layers of host defense. For a disease to manifest, a microorganism must complete a specific, sequential series of steps. Understanding this sequence reveals the strategies microbes use to survive and propagate inside a living system, starting with finding a way inside.
Source and Portal of Entry
The initiation of infection begins with the pathogen’s origin, known as the reservoir or source. These sources are diverse, including environmental locations like contaminated soil or water, animal populations, or human carriers who may or may not show symptoms. The microbe must successfully transfer from this source to a new host to continue its life cycle.
Once transferred, the microorganism must gain access to the host’s internal environment through a specific opening called the portal of entry. Pathogens are often highly selective, adapted to utilize a particular entry point that offers ideal conditions for survival and replication.
The respiratory tract is a common pathway, allowing entry of microbes contained within inhaled airborne droplets. The gastrointestinal tract is another frequent route, especially for pathogens introduced through contaminated food or water that can survive stomach acid. Other significant entry points include the urogenital tract and the parenteral route, which involves direct deposition beneath the skin or mucous membranes through mechanisms like insect bites, cuts, or needle sticks. The skin is a robust physical barrier, meaning any breach can serve as an opportunistic gateway for invading organisms.
Adherence and Colonization
Gaining entry is followed by the challenge of resisting mechanical clearance mechanisms designed to wash the pathogen away. The body employs defenses like the continuous flow of mucus, the flushing action of urine, and the rhythmic contractions of the gut (peristalsis) to physically remove foreign particles. To counteract these forces, microorganisms must establish a strong and stable foothold within the host.
This establishment relies on adherence, where specialized structures on the pathogen surface bind tightly to specific receptor molecules on host cells. Many bacteria utilize surface proteins called adhesins, often located on hair-like appendages such as fimbriae or pili, allowing them to stick to target tissues. The specificity of this interaction determines which tissue types the microbe can successfully infect.
Once adherence is achieved, the microbe begins to multiply rapidly, leading to colonization. This involves the exponential growth of the pathogen population at the site of entry, forming a microbial community. The number of organisms required to successfully establish colonization and cause disease is defined by the infectious dose, which varies dramatically among pathogens.
Some bacteria enhance colonization by forming complex, protective structures called biofilms, consisting of a matrix of extracellular polymeric substances. This dense, self-produced scaffolding shields the microbes from mechanical forces, immune responses, and antimicrobial treatments. The successful formation of a stable colony marks the transition from contamination to a developing infection.
Immune System Evasion
With a colony established, the pathogen must confront the host’s sophisticated immune system. This requires the pathogen to employ specific strategies to avoid detection and destruction by both the innate and adaptive branches of immunity. Pathogens have evolved three primary tactics to ensure their survival.
Hiding from Surveillance
One strategy involves hiding from immune surveillance, often by seeking refuge inside host cells. Certain bacteria and viruses exhibit intracellular replication, where they are taken up by cells like macrophages but prevent normal destructive processes, allowing them to multiply unseen. Other microbes utilize latency, entering a dormant state where their genetic material remains within host cells without actively replicating, thus becoming invisible to the immune system.
Camouflage
A second major tactic is camouflage, which involves altering or masking the surface structures the immune system uses for identification. Pathogens achieve this through antigenic variation, periodically changing the proteins and sugars displayed on their outer surface. Many bacteria also surround themselves with thick polysaccharide capsules that mimic host molecules or prevent phagocytic immune cells from engulfing them.
Active Sabotage
The third strategy involves active sabotage, where the microbe directly interferes with or disables the host’s immune machinery. Some pathogens secrete enzymes or protein toxins that specifically target and destroy immune cells, such as T-lymphocytes or neutrophils. Other secreted factors can disrupt the communication networks of the immune system, interfering with the signaling pathways necessary for cells to coordinate a robust defense. The success of these evasion techniques determines whether the infection remains localized or spreads throughout the body.
Tissue Damage and Symptom Onset
The final stage occurs when the multiplying pathogen begins to cause measurable harm, leading to the observable signs of disease. Pathogens damage the host through two distinct mechanisms: the production of powerful toxins and the direct destruction of host cells. This damage translates the biological event of infection into the physical experience of illness.
Toxins are highly potent molecules that can travel far from the colonization site and interfere with specific cellular functions. Exotoxins are proteins secreted by live bacteria that disrupt nerve impulses or damage cell membranes, potentially leading to severe systemic disease. Endotoxins are components of the outer membrane of certain bacteria, released only when the cell dies, often triggering an excessive inflammatory response like fever and shock.
Beyond toxins, many pathogens cause direct cytopathic effects by physically disrupting the structure and function of the cells they invade. Viruses, for instance, often hijack the host cell’s machinery to produce new viral particles, causing the cell to burst and release progeny to infect neighboring cells. The collective damage from toxins and cellular injury triggers the host’s inflammatory response, manifesting in common symptoms such as localized pain, swelling, and fever.