10. Infectious Diseases

An infectious, or communicable, disease is caused by a pathogen and can be transmitted from an infected host to an uninfected host. A pathogen is the disease-causing infectious agent; the disease is the resulting illness or poor health, not the agent itself.

• Cholera → Vibrio cholerae → bacterium
• Malaria → Plasmodium species → protist
• Tuberculosis (TB) → Mycobacterium tuberculosis and M. bovis → bacteria
• HIV/AIDS → human immunodeficiency virus (HIV) → virus

These named diseases are all infectious because a pathogen is involved and the infection can spread between hosts. The organism type identifies the agent; it does not by itself state how that disease is transmitted or controlled.

Do not call a mosquito the pathogen in malaria: it is a vector, while Plasmodium is the protist pathogen. Do not treat HIV/AIDS as a bacterium, or confuse a pathogen with the disease it causes. Transmission routes belong to 4624; prevention, diagnosis and treatment belong to 4625. No image generated or bound.

Transmission occurs when a pathogen leaves an infected source, remains viable in a route or medium, and reaches a new host. The route is disease-specific: water/food, an insect vector, droplets or direct exchange of body fluids.

• Cholera — contaminated water or food: infected people egest Vibrio cholerae in faeces; water becomes contaminated, and another person can acquire the bacterium through contaminated water, washing in it or food exposed to it.
• Malaria — vector and blood route: a female Anopheles mosquito takes up Plasmodium with a blood meal from an infected person, then passes the protist into the blood of the next person it feeds on. Blood transfusion, reused unsterile needles and passage across the placenta are also listed routes.
• Tuberculosis — droplets or animal-product route: an infected person with active TB releases droplets containing Mycobacterium tuberculosis when coughing or sneezing; another person inhales them. M. bovis can pass from cattle to humans through contaminated meat or unpasteurised milk.
• HIV/AIDS — direct body-fluid exchange: HIV reaches a new person through exchange of infected body fluids, including sexual intercourse, blood exposure or shared needles, and mother-to-child transfer across the placenta, during birth or through breast milk.

A mosquito is a vector, not the malaria pathogen; a cough-related route for TB is droplet infection, not a generic label for every contact; HIV requires direct body-fluid exchange rather than casual contact. These are transmission chains only: prevention, diagnosis and treatment belong to later cards. No image generated or bound.

Transmission is successful only when a pathogen leaves an infected source, remains able to infect within a suitable route or medium, and reaches a susceptible new host. The route must connect the source to the host; contact alone is not enough.

• Source and exit: the pathogen must be present in an infected person, animal or body fluid and reach an exit route such as faeces, droplets or blood.
• Viable route or medium: the pathogen must survive long enough in the relevant medium or carrier. Cholera depends on contaminated water or food; malaria uses a female Anopheles mosquito as a vector; TB commonly uses inhaled droplets; HIV requires direct exchange of infected body fluids.
• New host exposure: the route must deliver the pathogen to a person who can become infected. The same labels are not interchangeable: a mosquito is a carrier of Plasmodium, a droplet is an inhaled medium for TB, and casual contact does not provide the body-fluid exchange required for HIV.

Transmission therefore depends on the combination of pathogen, route, environmental or contact conditions and host exposure. Conditions such as contaminated water, crowded air spaces or access to infected blood can increase opportunities for the matching route, but they do not change the pathogen into a different type.

A disease is not transmitted simply because its pathogen is present: the pathogen must reach a new host by a compatible route. This card explains the conditions that make transmission possible; the four disease-specific route chains are established in the neighbouring card, while prevention, diagnosis and treatment are separate learning tasks.

Infectious-disease prevention and control work best when the measure targets the pathogen, route or host susceptibility involved. Feasibility also depends on biological conditions, social organisation and available resources, so one measure is not equally effective everywhere.

• Cholera: sewage treatment and clean, chlorinated piped water reduce contamination of the water/food route; vaccination can help in areas where cholera is common. Oral rehydration supports affected people, while monitoring and antibiotics in severe cases are control measures rather than route prevention.
• Malaria: insecticides, reducing breeding sites where feasible, biological control of larvae, insecticide-treated bed nets and reducing exposed skin target the Anopheles vector or human–vector contact. Preventive drugs, rapid diagnosis, effective treatment and vaccines are additional tools, but resistance, side effects, cost and mosquito breeding in small water bodies limit universal control.
• Tuberculosis: BCG vaccination reduces susceptibility; contact tracing and testing identify exposed cases. Testing cattle, pasteurising milk and properly cooking meat address M. bovis, while overcrowded housing increases the social opportunity for droplet spread.
• HIV/AIDS: screened blood, sterile needles, condoms/femidoms/dental dams and education reduce opportunities for infected body-fluid exchange. Testing, contact tracing, antiretroviral drugs and treatment of HIV-positive mothers and babies support control; long asymptomatic stages and unequal access to testing, drugs and safer alternatives affect feasibility.

The same intervention category can act at different points: vaccination changes host susceptibility, sanitation or barriers reduce exposure, vector control removes a transmission opportunity, and diagnosis or treatment reduces the number or duration of infectious cases. Layered measures are useful because biological resistance, infrastructure, behaviour and funding can weaken any single control.

Control is not a list of universally interchangeable actions: match the measure to the disease route and local constraints. This card synthesises prevention, diagnosis and treatment choices; the neighbouring cards establish the pathogen and transmission routes, so this card does not redefine those routes or add unlisted drug mechanisms or policy details.

Penicillin stops new peptidoglycan molecules from forming the cross-links that strengthen a growing bacterial cell wall.

• A growing bacterium makes small holes in its wall so the wall can stretch; enzymes called autolysins continue to create these holes.
• Normally, new peptidoglycan is added and cross-linked to reinforce the wall. Penicillin prevents the cross-linking step.
• The holes therefore accumulate while reinforcement is reduced, so the wall becomes progressively weaker.
• Bacteria take up water by osmosis. A weakened wall cannot withstand the pressure from inside indefinitely, so a growing susceptible bacterium can burst.

The effect depends on growth: once bacterial growth is complete, autolysins no longer create new holes and no further cross-links form, so this penicillin mechanism is most effective while the bacterium is growing.

Penicillin weakens a bacterial wall by interrupting its reinforcement; it does not dissolve every bacterium immediately. This card stops at the cell-wall mechanism: the distinction between bacterial and viral targets and the development of antibiotic resistance belong to the neighbouring cards.

Antibiotics work against bacterial structures or processes, but a virus is not a bacterial cell. A virus therefore does not provide the bacterial targets that an antibiotic such as penicillin is designed to affect.

• Bacterial target exists: an antibiotic can interfere with a bacterial cell-wall process, membrane protein, enzyme, DNA process or protein-synthesis process. Penicillin, for example, acts on strengthening a growing bacterial cell wall.
• Viral target is absent: viruses have no bacterial-style cell wall and do not carry out growth and reproduction as independent bacterial cells. During replication they use the host cell’s transcription and translation machinery.
• Treatment consequence: blocking a bacterial target cannot stop the virus from using host-cell machinery, so an antibiotic does not treat the viral infection.

This is a target-matching rule, not a diagnosis from symptoms alone. Cholera and TB are bacterial diseases for which antibiotics may be relevant, whereas HIV is viral and is not treated by antibiotics.

“Antibiotics do not affect viruses” means that antibacterial targets are absent from viruses; it does not mean that no medicine can ever act against a virus. Resistance and other reasons for treatment failure are separate topics, not part of this target distinction.

Antibiotic resistance is a population change: a chance mutation can produce a resistance allele, and antibiotic treatment selects bacteria that survive, allowing resistance to become more common.

• Variation first: random mutation creates genetic variation; the antibiotic does not direct a bacterium to mutate.
• Selection: treatment kills susceptible bacteria, while a bacterium with a resistance allele survives with less competition.
• Frequency increases: the resistant survivor reproduces, so its allele is passed to more offspring and becomes more frequent in the population. Short generation times, clonal offspring and horizontal gene transfer can speed spread.
• Clinical consequence: commonly used antibiotics can become less effective; multidrug-resistant strains can make infections difficult to treat and require complicated, expensive treatments that may not be available to everyone.

• Reduce selection: prescribe antibiotics only when needed, do not use them for viral infections, avoid unnecessary wide-spectrum use, complete the prescribed course and tighten control of antibiotic use in agriculture.
• Limit spread: maintain good hygiene, especially handwashing or sanitiser use in clinical settings, and isolate infected patients when resistant strains could spread.
• Maintain options: develop new antibiotics and alternatives, recognising that this is expensive and time-consuming.

Antibiotics select pre-existing resistant variants; they do not train every bacterium or create a targeted mutation. Resistance is a change in allele frequency in a bacterial population, not immunity of the patient. The penicillin wall mechanism and the virus target boundary are covered by the neighbouring cards.