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How pathogens cause disease and damage tissues

Infection and responseCommunicable diseases

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What is binary fission?

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A form of asexual reproduction in bacteria in which the cell copies its DNA and divides into two identical cells.

Key concepts

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Pathogens and the infectious life cycle

A pathogen is any microorganism that transmits a communicable disease from one organism to another and then reproduces or replicates inside that host. The basic cycle consists of entry into a host, multiplication, damage to the host, and transmission to new hosts. Many pathogens survive briefly outside a host but cannot reproduce without infecting living cells. Pathogen traits such as ease of airborne transmission or survival outside a host determine how rapidly an infection spreads through a population. High infectivity and fast reproduction increase the chance of transmission before immune clearance.

Bacterial reproduction: binary fission and limiting factors

Bacteria reproduce asexually by binary fission, where one bacterial cell divides to form two genetically similar daughter cells. Under ideal conditions bacterial populations can double repeatedly and can increase in number very rapidly; some bacterial colonies can double their population in around 20 minutes. Rapid asexual reproduction produces large numbers of cells that can overwhelm host defences. Limiting factors control bacterial growth in the body. Temperature, nutrient availability, oxygen concentration (for aerobic bacteria), pH and immune responses reduce reproduction rate or cause death of bacteria. Antibiotics reduce bacterial numbers by targeting bacterial structures or processes, but bacterial populations can evolve resistance when reproduction produces rare resistant variants that survive treatment.

Viral replication inside host cells and cell damage

Viruses are not metabolically active outside cells and replicate only by entering living host cells and using the host cell’s machinery to produce new virus particles. A virus attaches to a specific host-cell receptor, injects or releases its genetic material into the cell, and hijacks the cell’s enzymes and ribosomes to make viral proteins and genomes. New virus particles assemble and leave the cell. This process is called replication. Viral replication often damages or destroys the infected cell. Cell damage arises from depletion of cellular resources, disruption of normal cell processes, and cell lysis when large numbers of new viruses exit the cell. Cell death and tissue damage explain many symptoms of viral disease. The need for host cells to replicate viruses explains why antiviral treatments target steps of the viral life cycle rather than bacterial features.

Bacterial toxins and tissue damage

Some bacteria cause harm by producing chemical poisons called toxins. Toxins act locally or systemically to disrupt normal cell function, destroy cells, or interfere with physiological pathways. Bacterial toxins can break down cell membranes, inhibit protein synthesis, or trigger excessive immune responses that cause collateral tissue damage. The immune system produces specific antitoxins (antibodies) that bind and neutralise toxins, reducing their harmful effects. Antitoxin production forms part of the specific immune response that helps to clear toxin-mediated damage while phagocytes and other mechanisms remove the bacteria themselves.

Key notes

Important points to keep in mind

Pathogens infect, multiply, damage tissues, and spread to new hosts.

Bacteria reproduce by binary fission; short doubling times enable rapid population growth.

Viruses replicate only inside host cells and use the cell’s machinery, causing cell damage.

Bacterial toxins are chemicals that damage cells or disrupt body systems; antitoxins neutralise them.

Limiting factors for microbial growth include temperature, nutrients, oxygen and host immune responses.

Antibiotics target bacteria and not viruses; misuse of antibiotics selects for resistant strains.

Transmission route influences outbreak speed: airborne and contaminated water spread infections quickly.

Replication inside cells explains why antiviral strategies target viral entry, replication or release steps.

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