Epidemiological triad.pptx, rothmann pie model

ssuserd05ae8 0 views 34 slides Oct 07, 2025
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Epidemiological triad model, rothmann pie model


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Health and Disease Epidemiological triad model Natural history of diseases Risk Factors

The epidemiological triad model helps to understand the dynamics of disease transmission by focusing on the relationship between the agent, host, and environment. Each component of the triad plays a crucial role; for instance, changing one element can significantly alter disease outcomes, such as controlling an agent's spread through vaccination or improving environmental conditions. This model emphasizes the importance of a multi-faceted approach to public health by integrating biological, behavioral, and environmental strategies to combat diseases. The epidemiological triad is particularly useful in outbreak investigations, helping to identify sources of infection and potential interventions. Developed in the 19th century, this model has evolved to include complex interactions such as social determinants of health and emerging infectious diseases. The epidemiological triad model

Host Agent Environment Time Traditional Epidemiological Triad Model Agent- Cause or what of the triangle (infectious microorganism) Host- Host and Host Factors (Who of the disease) Environment- external factors that influence or allow disease transmission (i.e., the “where” of the triangle) Time-include the time characteristics, incubation/latency period, the length of the disease process, trends and cycles of the disease (i.e., vector), seasonality of the disease, and the personal characteristics of the people in the population (i.e., herd immunity) that affect the disease trajectory

The epidemiologic triad model, as modified by Miller . The modern epidemiology tries to demystify the „what,‟ „who,‟ „where,‟ „when,‟ „why,‟ and „how‟ questions of communicable and non-communicable diseases (NCDs). Agent- Infectious Organisms, natural disasters, road traffic accidents, genetics, psychological, and idiopathic conditions Host- The distribution of disease refers to the person, place, and time it occurs (otherwise known as „who‟, „where‟, and „when‟? The determinants of health-related problems or disease are factors that lead to the outbreak of a disease or health problem (otherwise known as „why‟? Obstructions of diseases are factors that can hinder the progress of a disease or health-related condition (otherwise known as the „how‟). The deterrents of a disease condition also connote the „control measures or interventions‟ in public health.

Schematic representation of the variations in the equilibrium of the ecological triad. The dynamics of the ecological triad will favor or determine the transition of the subject in the health-disease continuum, as expressed by Milton Terris and Hernan San Martín, based on the complex balance of the susceptibility-resistance binomial of man that allows him to defend himself constantly from the environmental conditions and potentially pathogenic agents, making it possible to obtain a positive balance

Infectious disease Epidemiological Triad model An infectious disease can be defined as an illness due to a pathogen or its toxic product, which arises through transmission from an infected person, an infected animal, or a contaminated dead object to a susceptible host. Infectious agents may be parasites (helminths or protozoa), fungi, bacteria, viruses, or prions. Environmental factors determine if a host will become exposed to one of these agents, and subsequent interactions between the agent and host will determine the exposure outcome. Agent and host interactions occur in a cascade of stages that include infection, disease, and recovery or death

Potential outcomes of host exposure to an infectious agent. (a) Following an exposure, the agent and host interact in a cascade of stages that can result in infection, disease, recovery, or death. (b) Progression from one stage to the next is dependent upon both agent properties of infectivity , pathogenicity, and virulence, and host susceptibility to infection and disease, which is in large part due to both protective and adverse effects of the host immune response

Recovery from infection can be either complete (elimination of the agent) or incomplete. Incomplete recovery can result in both chronic infections and latent infections. Chronic infections are characterized by the continued detectable presence of an infectious agent. In contrast, latent infections are distinguished by an agent that can remain quiescent in host cells and can later undergo reactivation. For example, the varicella zoster virus, the agent causing chicken pox, may reactivate many years after a primary infection to cause shingles. From a public health standpoint, latent infections are significant in that they represent silent reservoirs of infectious agents for future transmission.

Determinants of Infectious Disease Agent Factors Infectivity is the possibility that an agent will infect a host, given that the host is exposed to the agent. Pathogenicity refers to the ability of an agent to cause disease, given infection. Virulence is the possibility of causing severe disease among those infected. Virulence reflects structural and/or biochemical properties of an infectious agent. Agent characteristics can be measured in various ways. Infectivity is quantified in terms of the infectious dose 50 (ID50), the amount of agent required to infect 50% of a specified host population. Virulence is measured in terms of lethal dose 50 (LD 50), the amount of dose required for the death of 50% of the population. Infectivity and pathogenicity can be measured by the attack rate, the number of exposed individuals who develop disease. Virulence is often measured by the case fatality rate or proportion of diseased individuals who die from the disease.

Host Factors The outcome of exposure to an infectious agent depends, in part, upon multiple host factors that determine individual susceptibility to infection and disease. Susceptibility refers to the ability of an exposed individual (or group of individuals)to resist infection or limit disease as a result of their biological makeup. Factors influencing susceptibility include both innate, genetic factors and acquired factors such as the specific immunity that develops following exposure or vaccination. The malaria resistance afforded carriers of the sickle cell trait exemplifies how genetics can influence susceptibility to infectious disease ( Aidoo et al., 2002 ). Susceptibility is also affected by extremes of age, stress, pregnancy, nutritional status, and underlying diseases . Mechanical and chemical surface barriers such as the skin, the flushing action of tears, and the trapping action of mucus are the first host obstacles to infection.

The innate and adaptive immune responses are critical components of the host response to infectious agents Comparison of innate and adaptive immunity Innate Immune Response Adaptive Immune Response Immediate response within seconds. Gradual response; initially generated over 3–4 days (primary response) Targets groups of pathogens, Targets-specific pathogens No memory Memory Immune Response

Immune memory is the basis for the use of vaccines that are given in an attempt to stimulate an individual’s adaptive immune system to generate pathogen-specific immune memory. An immune host is someone protected against a specific pathogen(because of previous infection or vaccination), such that subsequent infection will not occur, or if it does, the severity of the disease will be diminished. The duration and efficacy of immunity following immunization by natural infection or vaccination vary depending upon the infecting agent, quality of the vaccine, type of vaccine (i.e., live or inactivated virus, subunit, etc.), and ability of the host to generate an immune response Vaccination

Environmental factors Environmental determinants of vulnerability to infectious diseases include physical, social, behavioral, cultural, political, and economic factors. Climate/weather- EI Niño- persistent, above-normal rainfall /Flooding- Increased vegetation promoting increase in rodent reservoir or Expansion of vertically infected mosquitoes and secondary vectors- Hantavirus pulmonary syndrome, Rift Valley fever. Water resource development and management, Forest fragmentation- Expansion of irrigated rice farming creating vector breeding sites, Loss of biodiversity, expanding natural reservoirs- Japanese encephalitis, Lyme Animal husbandry- Small-scale poultry farming facilitating animal-to-human virus transfer-H5N1 avian influenza Commercia l-Import of infected animals-Monkeypox Politics - Government response -Denial of viral etiology epidemic -HIV/AIDS Economics- Low income- lack of protection against vector- Dengue Social/ behavioral -Forest encroachment, bushmeat hunting, Live-animal markets- Exposure to infected bush animals, Close contact facilitating animal virus jumping species to humans- Ebola, SARS

The classical epidemiologic triad consists of the pathogen, environment, and host. Disrupting the connections will stop transmission of the pathogen. This simplistic representation is excellent for communicable diseases, but not adequate to explain the complexities of vector-borne diseases. To adapt the triad to vector-borne diseases, the insect vector is generally placed in the middle, where it influences the other three points

Social Chain of Infection by SARS-CoV-2 COVID-19- SARS-CoV-2- Flattening the curve. Disease Triangle

Natural history of disease: “ natural history of disease signifies the way in which a disease evolves from the earliest stage of its pre-pathogenesis phase to its termination as recovery, disability, or death in the absence of treatment or prevention ”

Natural history of disease timeline

Phases of disease History

The natural history of diseases is conventionally divided into two phases- Pre-pathogenesis phase Pathogenesis phase The pre-pathogenic phase refers to the period before the onset of a disease in humans, occurring prior to the appearance of signs and symptoms. During this phase, disease-producing agents are present in the environment but have not yet entered the human host. Three essential factors—agent, host, and environment—are necessary for the development of a disease, collectively known as the epidemiological triad. Diseases cannot occur in the absence of any one of these factors. When these three factors are present, and an individual is susceptible and physically weakened, the causative agent can enter the body, leading to the development of the disease.

The pathogenesis phase begins when the disease agent enters the host and starts causing changes at the cellular and tissue levels. This phase includes several sub-stages : Incubation: The incubation period is the time interval between the entry of the disease agent into the host and the appearance of the first symptoms or signs. During this period, the agent multiplies, spreads, or produces toxins, but the host remains asymptomatic. The length of the incubation period varies greatly depending on the disease: Short incubation periods:  Common cold (1-3 days), influenza (1-4 days) Medium incubation periods:  Measles (7-14 days), mumps (12-25 days) Long incubation periods:  Tuberculosis (4-12 weeks), hepatitis B (45-180 days), HIV (months to years)

T he P rodromal period: C haracterized by the appearance of non-specific symptoms. These might include general malaise, fatigue, low-grade fever, or mild discomfort. During this stage, the disease is beginning to manifest, but specific symptoms that would allow diagnosis have not yet appeared. The prodromal period typically lasts from a few hours to a few days. From a public health perspective, this period is particularly concerning because individuals are often contagious during this time but may not realize they are ill. This can lead to the unintentional spread of communicable diseases.

The Clinical D isease period M arked by the appearance of specific signs and symptoms that are characteristic of the particular disease. During this period, the disease becomes fully apparent and can usually be diagnosed. The manifestations during this period result from: Tissue damage:  Direct damage caused by the disease agent Immune response:  The body’s reaction to the agent Physiological dysfunction:  Altered functioning of affected organs or systems The duration and severity of this period vary widely depending on the disease, the individual’s health status, and whether any interventions are implemented.

O utcome stage, C an take several forms: Complete recovery:  The disease resolves with no residual effects Recovery with disability:  The individual recovers but is left with some degree of impairment Chronic condition:  The disease continues in a prolonged form Death:  The most severe outcome when the disease process overcomes the host’s defenses

A cohort study can well establish the natural history of disease As these studies are costly and laborious, understanding the natural history of disease is largely based on other epidemiological studies, such as cross-sectional and retrospective studies.

Iceberg Concept of Diseases Visible Clinical Cases Hidden cases Asymptomatic individuals Mildly symptomatic individuals Unrecognized cases

A risk factor is any attribute, characteristic, or exposure of an individual that increases the likelihood of developing a disease or injury (WHO 2017b ). Risk factors are statements of association between exposure to a particular agent and the occurrence of disease. Risk factors—spanning behaviors, lifestyles, socio-demographics, and environmental exposures—are identified and measured in epidemiology, with emphasis on chronic diseases. Common examples include cardiovascular diseases, cancers, chronic respiratory diseases, diabetes, and arthritis.   Risk factors play an important role in shaping public health interventions and policies. Risk Factors

Types of Risk Factors Behavioral (steerable): Smoking, poor diet, inactivity. Environmental: Housing, Sanitation, workplace, pollution, toxic exposure. Agentic: These are behaviors that are related to personal agency and are also largely modifiable. Risky behaviors like unprotected sex. Non-agentic (socio-demographic): Age, sex, genetics, occupation, ethnicity. Risk factors may also be modifiable (lifestyle) or non-modifiable (age, genetics). They often act synergistically rather than independently.

Importance of Identification & Measurement Early identification allows timely prevention . Accurate measurement enables assessment of disease risk , prediction of future trends, and evaluation of public health strategies . The opportunity to modify the risk of disease by modifying risk factors has important epidemiologic implications. Risk factors, as determinants of diseases, therefore, assume importance when it is acknowledged that preventive programs that prioritize them are essential. Guides resource allocation and equitable health service planning. The belief that diseases and their determinants may be preventable increases interest in risk factors.

Methods of Identifying Risk Factors Observational studies (Epidemiological studies): There are several types of epidemiological research studies, including cohort, case-control, and cross-sectional studies. Observational studies can identify that there are differences in the incidence of a health outcome with exposure or non-exposure to a lifestyle factor; they cannot conclude or argue causality. Epidemiological studies are likely to help in delineating population trends with respect to risks for health in different parts of the world, identifying trends, and allowing planning of interventions .

Clinical trials (RCTs): Gold standard for causal links and intervention evaluation; The gold standard method to identify and evaluate risk factors is the randomized controlled trial, also known as a clinical trial. Clinical trials are conducted in a controlled setting with known conditions, clearly defined inclusion and exclusion criteria, and a well-defined comparator. Clinical trials have two arms (with 'no treatment' as an exception) and can be conducted on, for example, participants, healthy volunteers, or communities. In general, clinical trials consist of a set of phases, followed by phases I–IV. They provide a systematic approach to determine the safety, effectiveness, and potential risks of new treatments, ultimately improving healthcare outcomes for individuals and communities worldwide. Clinical trials and observational cohorts are inextricably related to each other in that the results of the former play a critical role in describing the associations between risk factors and diseases The results from cohort studies may be the impetus for specific interventions to be evaluated in clinical trials.

Quantitative Measurement Relative Risk (RR): Compares disease incidence between exposed and unexposed groups, also known as the risk ratio, successive ratio, or incidence ratio. This remarkable measure grants us valuable insights into the magnitude of the risk associated with developing a particular disorder or symptom of interest, such as lung cancer, stroke, or even mortality. Odds Ratio (OR): Odds ratio is a measure of how strongly an event is associated with exposure. It helps to show how likely an exposure will lead to an outcome. It’s a ratio of two odds: the odds of the outcome occurring in the exposed group and the odds of the outcome occurring in the unexposed group .

Attributable Risk (AR): Proportion of disease incidence explained by a risk factor. assesses the proportion of disease incidence that can be attributed to a specific or a group of risk factors. By understanding this proportion, interventions can be effectively targeted to reduce the risk associated with these factors. Understanding and estimating the attributable risk of a disease can have important practical implications in terms of resource allocation. Population Attributable Risk (PAR): Percentage of cases in the population due to a risk factor—key for policy decisions.

Challenges and Limitations : Confounding variables: The determination of whether or not risk factors or causal associations are present can be complicated by extraneous factors, such as confounding variables. Such variables can systematically distort the results of an otherwise valid study. Failure to control for confounding variables may result in a conclusion that diseased and non-diseased individuals are equally likely to be exposed, when the reality might be quite different. As new evidence emerges, previously identified risk factors may be reassessed, new associations may be discovered, and existing knowledge may be revised. It is important for researchers and policymakers to remain vigilant and up-to-date in their understanding of risk factors to inform effective preventive measures and interventions Bias in study design: Selection, information, and publication bias reduce validity. Complexity of interactions: Multiple risk factors interact dynamically. Measurement issues: Accurately quantifying exposures is difficult.

Conclusion Risk factors are central to predicting disease and guiding prevention .Both observational and interventional studies are needed. Quantitative measures strengthen risk evaluation but must account for confounders and bias Policymakers and researchers must stay updated to ensure effective, evidence-based interventions. Risk factors rarely act alone, need precise measurement, and require robust methodologies (epidemiological studies + clinical trials) to inform public health strategies for reducing chronic disease burden.
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