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An infection caused by bacteria.

An infection involves invasion and multiplication of an infectious agent in a host. Bacteria are one possible cause; an agent capable of causing disease is a pathogen. The National Cancer Institute defines infection through invasion and growth in the body. ^[ref].

In a SIR model, acquiring infection moves a member of the susceptible compartment into the infectious compartment. That immediate transition is a model assumption: the SEIR model instead includes an exposed stage before infectiousness. Specify these states when translating a biological process into compartmental models.

Sensory and behavioural processes reducing exposure to pathogens, such as avoidance of contamination. This broader defence usage should be distinguished from cellular and molecular immunity.

Reduction of pathogen burden through prevention or control of infection. It differs from disease tolerance, which reduces damage at a given burden.

Reduction of health or fitness damage for a given pathogen burden. Low symptoms alone cannot distinguish tolerance from successful disease resistance.

Removal or avoidance of contaminated material or infected individuals, potentially reducing exposure of an individual or group to pathogens. disease reduction must be measured rather than inferred from cleaning alone.

Experimental manipulation intended to stimulate an immune response. A nonreplicating inflammatory stimulus separates some host responses from effects of a live pathogen, but need not reproduce natural infection.

A workable scheme has to deal with both transport and final disposal. At the house, collect excreta in suitably flushed closets; use sound, impermeable drains with sufficient fall and provision for inspection and cleaning. Traps interrupt communication between house air and sewer air, while appropriate sewer ventilation prevents the system from discharging its atmosphere into dwellings. Keep the drinking supply physically protected from drains and leakage. A sewer that carries filth away from a courtyard but releases it beside a downstream drinking intake has merely moved the danger.

Convey sewage promptly to a controlled outfall or disposal site, with pumping where the terrain requires it. One contemporary proposal was application to land by sewage irrigation, using land and drainage arranged to receive the flow rather than allowing stagnant pools. A period report on sewage irrigation at the Cumberland Asylum appeared in January 1866, establishing that this was an available contemporary option, not a later technology projected into the examination.^[ref]

The word “best” needs conditions. Water-carriage sewerage requires a dependable supply, engineering maintenance and an acceptable destination for the effluent. Where these cannot be provided, watertight removable receptacles with organized frequent collection can be preferable to an unreliable water system. Dry-earth sanitation was another period alternative, useful where systematic collection and suitable dry material could be assured. Neither an overflowing cesspool nor occasional removal after a nuisance has developed is a satisfactory urban service. Contemporary proposals competed over these very questions; there was no demonstrated single apparatus suitable for every town.^[ref]

Other waste organic matter requires a parallel service: covered receptacles, frequent collection of kitchen refuse and animal waste, cleaning of markets and slaughtering places, and controlled treatment or disposal away from dwellings and drinking supplies. Bulky refuse should not be pushed into house drains and allowed to obstruct them. The practical objective is continuous removal from contact with people, rather than accumulation followed by attempts to suppress the smell.

The present public health qualification is crucial: sanitation includes safe containment, emptying or conveyance, treatment and final disposal or controlled reuse. Neither chemical deodorization nor the apparently clear appearance of an effluent establishes removal of pathogens. Land application of untreated sewage must therefore not be presented as automatically safe for workers, crops or downstream users. Modern evaluation follows the whole service chain and its exposure routes.^[ref]

The proposed asymmetry is not generally defensible: animal behaviour and immunity form a reciprocal system, and “more” has no common meaning without an outcome, scale and intervention. Avoiding infection, controlling pathogen growth, tolerating tissue damage and changing social contact are different outcomes. Their causal effect sizes cannot be ranked by counting examples in either direction.

The definition of immunity matters first. In its narrower physiological sense, it concerns cellular and molecular defences. A behavioural immune system describes actions that reduce exposure before those defences are challenged, while social immunity includes protection generated by interactions among group members. If avoidance is defined as part of immunity, a statement that animal behaviour influences immunity becomes partly true by definition. A useful analysis instead specifies whether an action changes exposure, immune activity, pathogen burden or the damage associated with that burden. disease resistance reduces burden; disease tolerance reduces damage at a given burden. Lower illness alone does not distinguish these routes.

One strong route from animal behaviour to defence is the management of exposure. Choice of food, mates and social partners determines contact with infectious material. grooming can remove external parasites, and hygienic behaviour can remove contaminated material from a nest. Conversely, aggregation and some forms of close social contact can increase opportunities for transmission. These effects depend on the pathogen's transmission route: removing one kind of contact need not reduce infection spread by an environmental reservoir. An observed association between sociability and infection can also arise because infection changes sociability, making temporal or experimental evidence essential.

honeybee colonies selected for hygienic behaviour provide a causal evolutionary and experimental example. Selection based on brood-removal assays was combined with exposure to American foulbrood disease, allowing disease outcomes in selected and comparison colonies to be assessed. Removal of infected brood can reduce a colony's infectious reservoir and protect other individuals. ^[ref] The result concerns colony protection, not a demonstration that each worker's cellular immunity is stronger. Selection can change correlated traits as well as brood removal, so a mechanistic follow-up should match colony size, brood age, exposure and background, and manipulate the opportunity for removal. Colonies are independent experimental units; scoring many cells within one colony does not create many independently selected colonies.

Choice of an offspring’s food plant can also change the chemical environment encountered by parasites. Infected monarch butterflies preferentially laid eggs on plants that reduced parasite growth and disease in their offspring. This supported transgenerational medication: neither a simple cure of the mother nor merely a demonstration that a toxic plant can inhibit a parasite. ^[ref] The inference needs both the infection-dependent change in oviposition and the offspring benefit. Tests should include infected and uninfected mothers offered the same plant alternatives, standardized parasite exposure of offspring, and measurements of larval growth and survival as well as parasite burden. Nutritional quality and general plant preference are competing explanations. A cost of the medicinal plant in parasite-free conditions would additionally help explain why every individual does not always choose it.

animal behaviour can influence physiological immunity as well as exposure. Activity, feeding and sleep affect resource acquisition and allocation, while social interactions can alter endocrine and neural signals. These are plausible routes, but a study must measure the relevant immune process and not infer it from survival alone. An immune assay can increase because the animal is more infected, rather than because it has greater protective capacity. randomization, controlled nutrition and repeated observations can help separate these interpretations. Any claim of a trade-off should identify the limiting resource and the competing biological fitness demands; a change in one circulating marker is insufficient.

The reverse direction is equally substantive. Immune challenges can change activity, appetite, social investigation and priorities, producing sickness behaviour. Such changes may conserve resources, reduce exposure to further hazards or alter transmission, but some can instead reflect damaging inflammation or a pathogen's manipulation. Reduced activity after infection is therefore not automatically adaptive host defence. Comparing host biological fitness with and without the response, and separating immune activation from direct pathogen action, is necessary for an evolutionary interpretation.

lipopolysaccharide provides one experimental way to induce an inflammatory response without a replicating pathogen. Work on lactating house mice showed that the resulting effects depended on the activity and environmental context: pup retrieval could be maintained, and cold conditions elicited nest building despite the challenge. ^[ref] This supports a reorganization of competing motivations rather than simple global paralysis. It does not show that all illness-related inactivity is strategic. Controls should match handling and injection, assess motor capacity and temperature, and distinguish loss of appetite from inability to acquire food. Dose and timing also matter: an artificial inflammatory challenge need not reproduce a natural infection's trajectory. Blocking a candidate immune mediator, followed by a rescue intervention, would provide stronger evidence for a specific immune-to-neural pathway than a challenge alone.

Immune influences are not confined to overt sickness. In house mice, work on interferon-gamma linked immune deficiency and altered social preference to changes in neural connectivity and inhibitory physiology. Immune restoration and targeted signalling interventions strengthened a mechanistic interpretation beyond a correlation between illness and social withdrawal. ^[ref] The experiments support a role for immune signalling in the tested neural and behavioural context; they do not establish a universal explanation of sociability or justify extrapolating a house mouse social-preference assay directly to human psychiatric conditions. Sensory ability, general activity, anxiety-related responses, housing and genetic background remain important controls when interpreting such assays.

The two directions can form the same feedback loop. An immune response changes social contact; changed contact alters subsequent exposure and infection; the new infection state changes the immune response again. The medication example similarly links infection-dependent action to offspring defence. Neither direction is an independent input fixed while the other acts. A useful factorial design would manipulate a specific action or opportunity for action and a specific immune challenge, then measure both behavioural and physiological outcomes over time. Baseline health, age, sex and reproductive state should be controlled, and the manipulation of action should avoid introducing injury or stress that independently changes immunity.

A claim that one direction is larger would require comparable interventions and a shared endpoint, such as lifetime reproductive success or pathogen transmission, with uncertainty over an explicitly chosen time horizon. Different answers may follow for individual survival, colony persistence and epidemic spread. The evidence supports bidirectional, context-dependent regulation: actions govern exposure and defence, while immune signals govern behavioural priorities and sometimes normal neural function. A universal ranking conceals precisely the causal distinctions needed to understand this system.

An inflammatory disease of the lung. Nineteenth-century series concern historical clinical diagnoses; they should not be assigned a particular modern causative pathogen without evidence.

Primary publication record or author/institutional full text.

By Marla Spivak. Coauthor: Gary S. Reuter. Apidologie 32, pp. 555–565; selected hygienic colonies, brood assays and pathogen challenge.

Collective protection against pathogens arising through interactions among individuals, including hygienic behaviour. A colony-level reduction in infection need not be increased cellular immunity in every worker.