Fact-checked by Grok 2 weeks ago

Infectivity

Infectivity is the proportion of individuals exposed to a causative infectious agent who subsequently become infected, representing the agent's capacity to establish infection in a susceptible host upon contact.^[1] This concept is central to infectious disease epidemiology, where it quantifies the likelihood of transmission independent of whether the infection leads to clinical disease.^[2] Distinct from pathogenicity—the proportion of infected individuals who develop symptoms—and virulence—the proportion of persons with clinical disease who become severely ill or die—infectivity focuses solely on the initial establishment of infection.^[1] For instance, pathogens like Shigella dysenteriae exhibit high infectivity with an infectious dose 50 (ID50) as low as 10 organisms, meaning half of exposed individuals become infected with minimal exposure, whereas Vibrio cholerae requires 10^6 to 10^11 organisms.^[3] Measurement typically involves the secondary attack rate, the percentage of susceptible contacts of an infected case who acquire the infection, particularly for directly transmitted diseases.^[2] Factors influencing infectivity include characteristics of the infectious agent, such as its minimal infective dose and mode of transmission (e.g., airborne, vector-borne, or direct contact); host factors like age, immune status, and genetic susceptibility; and environmental elements including sanitation, climate, and population density.^[2]^[3] These determinants collectively shape transmission dynamics and contribute to the basic reproduction number (R0), an estimate of secondary infections generated by one case in a fully susceptible population, where R0 > 1 signals potential for epidemic spread.^[2] Understanding infectivity is crucial for public health strategies, including vaccination programs, quarantine measures, and vector control, as it informs predictions of disease outbreaks and the effectiveness of interventions in reducing global infectious disease burden.^[3] For example, high-infectivity pathogens like SARS-CoV-2 have driven rapid pandemics, underscoring the need for targeted epidemiological surveillance.^[4]

Definition and Basic Concepts

Definition of Infectivity

In infectious disease epidemiology, infectivity is the proportion of susceptible individuals exposed to a causative infectious agent who subsequently become infected, representing the agent's capacity to establish infection in a susceptible host upon contact.^[1] Biologically, this capacity refers to the ability of a pathogen, such as a bacterium, virus, fungus, or parasite, to enter a susceptible host, evade initial immune defenses, survive within host tissues, and multiply sufficiently to establish a productive infection. This fundamental property enables the pathogen to initiate the infectious process, which may or may not lead to overt disease. The biological mechanism underlying infectivity typically proceeds through sequential steps: adhesion to host cell surfaces via specific ligands or receptors, invasion into host cells or tissues, intracellular or extracellular replication, and initial colonization of the infection site, often occurring asymptomatically in the early stages.^[5] The concept of infectivity emerged in late 19th-century microbiology, with the term first documented in 1871 to describe the quality of being able to produce or transmit infection.^[6] It gained formalization in early 20th-century research on bacterial pathogens, particularly through studies of tuberculosis during the 1920s, where scientists like Albert Calmette and Camille Guérin investigated the attenuated virulence of Mycobacterium bovis strains in developing the BCG vaccine.^[7] An illustrative example is the poliovirus, which exhibits potent infectivity via the fecal-oral route; ingested virions resist gastric acidity, adhere to receptors on gastrointestinal epithelial cells, replicate locally in the oropharynx and intestine, and establish initial colonization before potentially disseminating systemically.^[8] Infectivity is distinct from virulence, which quantifies the severity of harm or disease caused in the infected host.^[3] Infectivity refers to the capacity of a pathogen to establish an infection in a susceptible host upon exposure, whereas pathogenicity describes the proportion of infections that progress to clinical disease in the infected host. For instance, a pathogen may have high infectivity, successfully colonizing many exposed individuals, but low pathogenicity if most infections remain subclinical without causing noticeable symptoms. Pathogenicity is often quantified by metrics such as the fraction of infected individuals who develop symptomatic illness, distinguishing it from infectivity's focus on initial host invasion. Virulence, in contrast, measures the degree or severity of harm caused by a pathogen once infection is established, encompassing factors like tissue damage, organ impairment, or lethality in diseased hosts. While infectivity and virulence can correlate—for example, some pathogens with high infectivity also exhibit elevated virulence— they are not synonymous; a pathogen like rhinovirus demonstrates high infectivity in causing upper respiratory infections but low virulence, typically resulting in mild, self-limiting common colds rather than severe outcomes. This distinction highlights that infectivity pertains to the pathogen's ability to enter and replicate within the host, independent of the subsequent intensity of disease. Transmissibility differs from infectivity by emphasizing a pathogen's overall potential to spread from one host to others in a population, incorporating elements like shedding duration, environmental stability, and contact patterns, beyond just the efficiency of host invasion upon direct exposure. Infectivity focuses narrowly on the pathogen's success in infecting an exposed individual, while transmissibility integrates broader epidemiological dynamics of propagation. For example, measles exhibits high transmissibility largely due to its airborne mode of spread, allowing efficient dissemination in crowded settings, whereas HIV shows high infectivity in specific high-risk exposures such as blood transfusions but negligible transmissibility through casual contact like hugging or sharing utensils.

Measurement and Quantification

Direct Measures of Infectivity

Direct measures of infectivity quantify the pathogen's capacity to establish infection in exposed hosts through empirical assessments in laboratory or field settings. The attack rate serves as a fundamental field-based metric, defined as the proportion of a defined population that becomes infected following exposure during an outbreak. It is calculated as the number of new infections divided by the total number at risk, often expressed as a percentage: (number infected / total exposed) × 100. In practice, attack rates are frequently based on reported clinical cases, but for precise measurement of infectivity, confirmation of infection via methods like PCR or serology is preferred, especially to account for subclinical cases. For instance, during seasonal influenza outbreaks in unvaccinated populations, attack rates typically range from 10% to 20%, highlighting the virus's potential to infect a substantial portion of susceptible individuals in community settings.^[9] Infectious dose metrics provide laboratory-derived estimates of the minimal pathogen quantity required to initiate infection, focusing on dose-response relationships in controlled models. The ID₅₀, or median infectious dose, represents the amount of pathogen that infects 50% of exposed hosts, while the ID₉₀ indicates the dose infecting 90%, both determined through titration experiments in cell cultures, animal models, or human challenge studies.^[10] These metrics underscore pathogen virulence; for example, norovirus exhibits an exceptionally low ID₅₀ of approximately 18 viral particles in human volunteers, enabling infection from minimal exposures.^[11]^[12] The secondary attack rate refines attack rate assessments by measuring the probability of infection among susceptible contacts of an index case, particularly in close-contact scenarios like households.^[1] It is computed as the number of new infections among contacts divided by the total number of susceptible contacts, typically during the index case's infectious period, offering insights into direct transmission efficiency in defined exposure contexts. To accurately capture infectivity, infections are ideally confirmed through testing rather than relying solely on symptomatic cases. Laboratory assays enable precise quantification of viable infectious units by directly assessing pathogen replication potential. For viruses, plaque assays involve infecting cell monolayers with serial dilutions of the pathogen, overlaying with agar to restrict spread, and counting resulting plaques—each representing a single infectious focus—to yield plaque-forming units (PFU) per milliliter.^[13] In bacteria, colony-forming units (CFU) are determined by plating dilutions on nutrient media and enumerating visible colonies, each derived from a viable, infectious bacterial cell capable of proliferation.^[14] These methods distinguish infectious particles from total counts, emphasizing functional infectivity in experimental evaluations. Unlike broader transmissibility concepts, direct measures like attack rates center on the initial infection establishment in exposed individuals.^[15]

Reproduction Numbers and Metrics

The basic reproduction number, denoted as R_0, represents the average number of secondary infections produced by a single infected individual in a completely susceptible population under ideal transmission conditions.^[16] This metric integrates key elements of infectivity, including the pathogen's transmission rate (influenced by its inherent infectiousness), the contact rate between individuals, and the duration of the infectious period.^[17] In simple compartmental models of disease dynamics, R_0 is calculated as R_0 = \beta \times D, where \beta is the transmission rate (combining contact frequency and probability of infection per contact, modulated by infectivity) and D is the average duration of infectiousness.^[17] For instance, early estimates for SARS-CoV-2 in 2020 placed R_0 at approximately 2–3, reflecting its moderate to high airborne and contact-based infectivity in crowded settings.^[18] Similarly, Ebola's R_0 has been estimated at 1.5–2.5 during outbreaks, underscoring its moderate infectivity primarily through direct contact with bodily fluids.^[19] The effective reproduction number, denoted as R_t or R_e, extends R_0 by accounting for real-world changes over time, such as population immunity, behavioral interventions, and vaccination coverage, providing a dynamic measure of ongoing transmission potential. This metric incorporates partial immunity or susceptibility within a population, estimating the average secondary infections per case adjusted for the proportion of immune individuals, and is particularly useful in partially vaccinated or previously exposed groups, where it typically falls below R_0 but above or below 1 depending on herd immunity thresholds.^[20]^[21] Unlike the static R_0, R_t varies temporally and indicates epidemic growth when above 1, stability at 1, or decline below 1.^[20] For example, during COVID-19 lockdowns in China in early 2020, R_t dropped below 1 within about 30 days, demonstrating how mobility restrictions could suppress transmission driven by infectivity.

Factors Influencing Infectivity

Pathogen-related factors encompass the inherent biological properties of infectious agents that dictate their capacity to establish and propagate infection within a host. Central to this are structural features, particularly surface proteins that facilitate attachment and entry into host cells. For instance, in enveloped viruses such as coronaviruses, the spike (S) protein protrudes from the viral envelope and mediates binding to host receptors like angiotensin-converting enzyme 2 (ACE2), enabling membrane fusion and viral entry, which is essential for infectivity.^[22] Similarly, in Gram-positive bacteria, surface-anchored proteins such as adhesins promote adherence to host tissues and evasion of immune clearance, directly enhancing the pathogen's ability to initiate infection.^[23] Replication efficiency further modulates infectivity through the rate of pathogen proliferation and genetic variability introduced by mutations. High replication rates allow pathogens to rapidly amplify viral load or bacterial numbers within the host, overwhelming initial defenses and increasing transmission potential. RNA viruses, including influenza, exhibit elevated mutation rates—often 10^{-5} to 10^{-4} substitutions per site per replication cycle—enabling antigenic drift that evades pre-existing immunity and sustains infectivity across seasons.^[24] This mutational plasticity contrasts with more stable DNA pathogens but underscores how replication dynamics shape adaptive evolution.^[25] The minimum infectious dose (MID), defined as the smallest number of pathogen particles required to initiate infection in 50% of susceptible hosts, varies markedly due to intrinsic stability traits. Respiratory viruses like influenza and adenovirus demonstrate exceptionally low MIDs, often below 1 tissue culture infectious dose (TCID50), owing to their structural robustness and efficient receptor engagement.^[26] Prions exemplify extreme stability, resisting proteolytic degradation and environmental stressors, which permits infection at doses as low as a few protein aggregates, far below thresholds for less resilient agents.^[27] Evolutionary pressures on pathogens often reveal trade-offs between infectivity and virulence, where heightened transmission potential may coincide with increased host damage. In plant pathosystems, such as those involving fungal pathogens like Zymoseptoria tritici, high infectivity—measured by lesion formation and spore production—positively correlates with virulence, as aggressive replication within host tissues boosts both damage and dispersal, though this balance evolves to optimize fitness.^[28] These dynamics highlight how pathogen genomes adapt intrinsic traits to maximize propagation while navigating host interactions. A illustrative case is Mycobacterium tuberculosis, whose infectivity is bolstered by its aerosol stability and intracellular persistence. The bacterium's waxy cell wall confers resistance to desiccation, allowing prolonged viability in airborne droplets for hours, facilitating respiratory transmission.^[29] Once inhaled, M. tuberculosis survives within alveolar macrophages by arresting phagosome-lysosome fusion and modulating host cell apoptosis, thereby establishing latent infection and enhancing overall transmissibility.^[30] Host-related factors significantly modulate a pathogen's ability to establish and sustain infection by altering the host's defensive capabilities at the point of entry, during replication, and in dissemination. These factors encompass the host's immune competence, genetic profile, age-related changes, and nutritional condition, each interacting with pathogen mechanisms to either facilitate or hinder infectivity. Innate and adaptive immune responses, for instance, can block pathogen attachment or limit viral replication windows, while genetic polymorphisms may render certain hosts inherently resistant. Understanding these dynamics is essential for tailoring interventions like vaccination or nutritional support to vulnerable populations. The immune status of the host, encompassing both innate and adaptive components, profoundly influences pathogen infectivity. Innate barriers, including the physical integrity of skin and mucosal linings, act as the primary shield against microbial invasion by preventing pathogen adhesion and penetration.^[31] Compromised mucosal integrity, such as through inflammation or injury, heightens susceptibility by exposing underlying tissues to pathogens. Adaptive immunity further refines this defense; in HIV-1 infection, the onset of CD8+ T-cell responses during acute infection reduces viral load by up to 35% daily, thereby shortening the high-infectivity transmission window before chronic persistence sets in.^[32] Prior immune priming, as seen in vaccine trials like RV144, can elicit early antibody responses that modestly curb initial viral dissemination, though full sterilizing immunity remains elusive.^[33] Genetic susceptibility introduces variability in host-pathogen interactions, with specific polymorphisms altering receptor availability or immune signaling to impede infection. The CCR5-Δ32 mutation exemplifies this, as homozygous carriers lack functional CCR5 coreceptors on CD4+ T cells, blocking HIV-1 entry and conferring near-complete resistance to R5-tropic strains prevalent in early infection.^[34] Similarly, the sickle cell trait (heterozygous HbAS) provides partial protection against Plasmodium falciparum malaria by promoting abnormal erythrocyte sickling under low-oxygen conditions, which disrupts parasite replication and reduces infection intensity by inhibiting merozoite invasion.^[35] These genetic adaptations highlight how host alleles can evolutionarily counter pathogen tropism without eliminating susceptibility entirely. Age and physiological state further exacerbate or mitigate infectivity by altering immune vigor and tissue homeostasis. In elderly hosts, age-associated immunosenescence diminishes T-cell proliferation and cytokine production, elevating the risk of latent pathogen reactivation; for varicella-zoster virus, this leads to herpes zoster incidence rising from 3-5 cases per 1,000 person-years in young adults to over 10 in those over 80.^[36] Immunocompromised individuals, including the elderly with comorbidities or those on immunosuppressive therapy, face amplified infectivity due to impaired viral clearance, resulting in disseminated disease rather than localized reactivation. Nutritional deficiencies compound these vulnerabilities by weakening mucosal immunity; malnutrition impairs secretory IgA production and epithelial barrier function, increasing Vibrio cholerae adherence and toxin-mediated damage in the gut, as evidenced by higher case-fatality rates in undernourished children during outbreaks.^[37] Vitamin A deficiency, in particular, reduces mucosal antibody responses to cholera toxin, prolonging bacterial colonization and fluid loss.^[38]

Environmental Factors

Environmental factors play a crucial role in modulating the infectivity of pathogens by influencing their survival, transmission efficiency, and exposure opportunities outside the host-pathogen interface. Physical conditions such as temperature and relative humidity significantly affect the stability of airborne pathogens. For instance, influenza virus exhibits higher infectivity in cold, dry air because low relative humidity (around 20-35%) enhances the stability of infectious aerosols, allowing prolonged suspension and transmission, as demonstrated in experimental models using guinea pigs.^[39] In contrast, higher humidity levels accelerate viral inactivation, reducing aerosol persistence and overall transmission potential.^[40] Transmission routes mediated by environmental vectors or media further alter the dose and likelihood of pathogen exposure. In tropical climates, warmer temperatures (typically 25-30°C) accelerate the development of Plasmodium parasites within Anopheles mosquitoes, shortening the extrinsic incubation period and thereby enhancing infectivity by increasing the proportion of infectious vectors.^[41] This temperature-dependent vector competence exemplifies how environmental conditions in endemic regions amplify malaria transmission compared to cooler areas where parasite maturation is inhibited below 16°C.^[42] Human behaviors intertwined with environmental settings, such as crowding and hygiene practices, profoundly influence contact-based infectivity. Poor sanitation in densely populated areas facilitates norovirus spread through fecal-oral routes via contaminated water or food, with outbreaks commonly reported in settings like evacuation shelters where inadequate facilities lead to rapid person-to-person transmission.^[43] Crowded indoor environments exacerbate this by increasing close-contact opportunities, as seen in mass gatherings where poor hygiene amplifies enteric pathogen dissemination.^[44] Climate change is altering vector competence for arboviruses, with post-2020 studies highlighting how rising temperatures expand transmission risks. For dengue, warmer conditions improve Aedes aegypti mosquito survival and virus replication, leading to higher vector infection rates and prolonged transmission seasons in regions like India, where projected warming could increase dengue incidence by 49–76% by mid-century.^[45] Similarly, urban heat islands combined with global warming enhance arboviral infectivity by optimizing extrinsic incubation at elevated temperatures around 29°C.^[46] A prominent example is the SARS-CoV-2 virus during the 2020-2022 COVID-19 pandemics, where infectivity was markedly amplified in indoor spaces with poor ventilation, as stagnant air allowed accumulation of infectious aerosols, contributing to superspreading events in enclosed, crowded settings.^[47] This environmental factor underscored the role of airflow in modulating respiratory pathogen transmission dynamics.^[48]

Infectivity Across Pathogen Types

Viral Infectivity

Viral infectivity is fundamentally tied to the mechanisms by which viruses enter host cells, often relying on receptor-mediated endocytosis or direct membrane fusion facilitated by viral glycoproteins. In receptor-mediated endocytosis, viruses bind to specific host cell receptors, triggering invagination of the plasma membrane to form endocytic vesicles that internalize the virion. For instance, human immunodeficiency virus (HIV) primarily enters CD4+ T cells through binding to the CD4 receptor and chemokine coreceptors like CCR5 or CXCR4, followed by endocytosis and subsequent fusion within endosomes driven by the viral envelope glycoprotein gp41.^[49] Fusion proteins, such as those in enveloped viruses, undergo conformational changes to merge viral and host membranes, enabling genome delivery; this process is pH-dependent in many cases, occurring in acidic endosomal compartments.^[50] A hallmark of viral infectivity is the capacity for latency and persistence, allowing viruses to evade immune detection and establish chronic infections. Herpesviruses, such as herpes simplex virus type 1 (HSV-1), maintain their circularized genomes as extrachromosomal episomes in the host cell nucleus in a non-replicative state, particularly in sensory neurons where they remain dormant for the host's lifetime.^[51] Reactivation from latency can be triggered by stressors like UV light or immunosuppression, leading to viral replication and shedding; during latency, viral gene expression is minimal, limited to non-coding RNAs that promote neuronal survival and immune evasion.^[52] This persistent reservoir sustains long-term infectivity, enabling recurrent outbreaks without continuous transmission.^[53] High mutation rates in viral RNA polymerases drive genetic variability, enhancing infectivity through antigenic drift and shift that allow evasion of host immunity. In influenza A viruses, error-prone replication results in point mutations (drift) accumulating in hemagglutinin and neuraminidase genes, gradually altering antigenicity and necessitating annual vaccine updates, leading to annual seasonal epidemics due to these changes.^[54] Antigenic shift occurs via reassortment of gene segments in co-infected hosts, potentially creating novel subtypes with pandemic potential, as seen in the 2009 H1N1 emergence.^[55] This evolutionary dynamism maintains infectivity in diverse host populations. Zoonotic transmission underscores viral adaptability, with viruses jumping from animal reservoirs to humans via mutations enhancing human receptor binding. SARS-CoV-2, originating from bats, features a furin cleavage site in its spike protein that primes the protein for efficient entry into human ACE2-expressing cells, facilitating airborne spread and high infectivity.^[56] Similarly, Ebola virus demonstrates potent infectivity through direct contact with bodily fluids, where its filovirus glycoprotein binds to host receptors like NPC1 in endosomes, promoting endothelial cell invasion and vascular leakage that amplifies dissemination.^[57] These adaptations highlight how structural innovations sustain cross-species infectivity.

Bacterial Infectivity

Bacterial infectivity refers to the capacity of prokaryotic pathogens to colonize host tissues, evade defenses, and propagate within a host, often through autonomous replication and secretion of virulence factors rather than reliance on host cellular machinery. Unlike viruses, bacteria employ diverse strategies encompassing both extracellular lifestyles, where they remain outside host cells and deploy toxins to disrupt tissues, and intracellular modes, where they invade and persist within cells to avoid immune detection. These mechanisms enable bacteria to establish acute or chronic infections, with infectivity modulated by structural adhesins for initial attachment and secreted effectors for deeper invasion.^[58]^[59] Adhesins such as pili and fimbriae facilitate bacterial attachment to host epithelial surfaces, a critical initial step in infectivity. For instance, type 1 fimbriae of uropathogenic Escherichia coli bind mannose-containing receptors on uroepithelial cells, promoting colonization of the urinary tract and resistance to mechanical clearance by urine flow. Complementing these, exotoxins secreted by extracellular bacteria induce cytotoxicity and tissue damage, aiding invasion by disrupting host barriers and promoting bacterial dissemination. Exotoxins provoke local inflammation and breakdown of extracellular matrix, as seen in various Gram-positive and Gram-negative pathogens, thereby enhancing spread from the site of entry.^[60]^[61] Biofilm formation represents a key strategy for persistent bacterial infectivity, particularly in chronic infections where communities of bacteria encased in a protective matrix resist antibiotics and host immunity. In cystic fibrosis patients, Pseudomonas aeruginosa forms biofilms in the lungs, shielding cells from phagocytosis and antimicrobial agents while maintaining a niche for ongoing replication and transmission. Similarly, intracellular pathogens like Salmonella enterica employ type III secretion systems to inject effectors into host cells, remodeling phagosomes to create replicative vacuoles that evade lysosomal degradation and support bacterial survival. These adaptations allow intracellular persistence, contributing to systemic spread.^[62]^[63] Evolution of antibiotic resistance further amplifies bacterial infectivity by enabling survival in treated environments, such as hospitals, where resistant strains outcompete susceptible ones. In methicillin-resistant Staphylococcus aureus (MRSA), mutations in regulatory genes like agrC reduce toxin production to minimize host inflammation, facilitating asymptomatic carriage and nosocomial transmission. A notable example is Vibrio cholerae, whose cholera toxin (CT) hyperactivates intestinal adenylate cyclase, causing massive secretory diarrhea that expels up to 10^9 bacteria per gram of stool, thereby amplifying fecal-oral transmission in contaminated water sources. Bacteria also briefly evade host immunity through capsule production or molecular mimicry, sustaining infectivity across infection stages.^[64]^[65]^[66]

Infectivity in Parasites and Fungi

Infectivity in parasites and fungi, as eukaryotic pathogens, is characterized by intricate life cycles that often involve multiple host species and developmental stages adapted for transmission and persistence. Unlike simpler prokaryotic pathogens, these organisms employ morphological transformations and environmental resilience to establish infection, exploiting host vulnerabilities such as immunosuppression or vector interactions. For instance, protozoan parasites like Plasmodium species require alternation between insect vectors and vertebrate hosts, where specific stages ensure efficient dissemination and invasion.^[67] Fungal pathogens, meanwhile, leverage dormant forms like spores or cysts to withstand harsh conditions before reactivating in susceptible hosts, highlighting their evolutionary adaptations for survival and propagation.^[68] A hallmark of parasitic infectivity is the multi-host life cycle, exemplified by Plasmodium falciparum, the causative agent of severe malaria. In the mosquito vector (Anopheles species), sexual reproduction produces infectious sporozoites, which are inoculated into the human bloodstream during a blood meal; these sporozoites rapidly invade hepatocytes in the liver, where they differentiate into merozoites that burst forth to infect erythrocytes, perpetuating the cycle.^[69] This stage-specific infectivity relies on the parasite's ability to evade innate immunity during transit and replication, with sporozoites exhibiting high motility to reach the liver within minutes of inoculation.^[70] Similarly, in fungal infections, spore resilience enables survival in adverse environments; Cryptococcus neoformans, an opportunistic yeast, produces a polysaccharide capsule that shields yeast cells from phagocytosis by macrophages, particularly in immunocompromised individuals such as those with AIDS, allowing unchecked dissemination from the lungs to the central nervous system.^[71] The capsule not only inhibits engulfment but also modulates host immune responses, enhancing the fungus's invasiveness in hosts with depleted CD4+ T cells.^[72] Vector-mediated transmission further amplifies infectivity in parasites like Trypanosoma brucei, responsible for African sleeping sickness. During a blood meal, infected tsetse flies (Glossina species) inject metacyclic trypomastigotes into the mammalian host's skin, where these flagellated forms evade local defenses and enter the lymphatic system to initiate systemic infection.^[73] This process depends on the parasite's developmental progression within the fly's midgut and salivary glands, ensuring a high proportion of viable infective stages.^[74] Parasites such as Toxoplasma gondii demonstrate targeted exploitation of host immunosuppression through oral routes; ingestion of tissue cysts from contaminated food or water leads to cyst rupture in the small intestine, releasing bradyzoites that convert to rapidly dividing tachyzoites, which disseminate and reform latent cysts in muscles and the brain, persisting lifelong in immunocompetent hosts but reactivating in those with weakened immunity.^[75] These cysts provide a reservoir for reinfection and transmission, underscoring the parasite's strategy for chronicity.^[76] Dimorphic fungi like Histoplasma capsulatum illustrate pulmonary infectivity tied to environmental exposure. Inhalation of microconidia from soil enriched with bird or bat guano allows the fungus to convert to its pathogenic yeast form at body temperature, primarily within alveolar macrophages in the lungs, where it multiplies intracellularly while suppressing phagolysosomal fusion to avoid destruction.^[68] This macrophage tropism facilitates initial colonization and potential hematogenous spread to disseminated sites, particularly in endemic areas where soil disturbance aerosolizes spores.^[77] Overall, the infectivity of parasites and fungi hinges on these adaptive mechanisms, enabling them to navigate host barriers and environmental challenges with remarkable efficiency.

Applications in Epidemiology and Public Health

Role in Disease Dynamics

Infectivity plays a central role in the Susceptible-Infected-Recovered (SIR) model, a foundational framework in epidemiology that simulates disease spread within a population by modeling transitions between compartments. In this model, originally developed by Kermack and McKendrick, the rate at which susceptible individuals (S) become infected (I) is directly proportional to the product of the susceptible population size and the number of infectious individuals, with infectivity determining the contact rate parameter that governs this transition. The model's differential equations capture how high infectivity accelerates the depletion of susceptibles, leading to epidemic peaks and eventual decline as herd-level immunity builds. R0, the basic reproduction number, serves as a key input parameter reflecting average infectivity in a fully susceptible population. The herd immunity threshold, derived from SIR dynamics, is calculated as 1 - (1/R0), representing the proportion of the population that must be immune to prevent sustained transmission. High infectivity elevates this threshold, necessitating greater vaccination coverage to achieve control; for instance, measles with an R0 of 12–18 requires 94–95% immunity to halt outbreaks. This threshold underscores how pathogens with elevated infectivity, like measles, demand near-universal protection to avoid resurgence in partially immune populations. Infectivity influences whether a disease establishes as endemic or triggers epidemic waves, as seen in the 1918 influenza pandemic where the virus's high transmissibility drove multiple successive waves of infection across global populations. The pandemic's dynamics, characterized by rapid escalation followed by temporary declines, exemplified how potent infectivity can overwhelm susceptible pools before natural immunity curbs spread, resulting in an estimated 50 million deaths. In contrast, lower infectivity may sustain endemic circulation without explosive outbreaks. Superspreading events highlight the heterogeneous impact of infectivity, where rare individuals or gatherings disproportionately amplify transmission beyond average rates. During the COVID-19 pandemic, a 2020 choir practice in Skagit County, Washington, illustrated this: one symptomatic attendee infected 52 of 60 participants (87% attack rate), driven by aerosol-generating activities in a confined space. Such events, representing a small fraction of transmissions but contributing disproportionately to overall spread, complicate disease dynamics by creating localized surges that seed broader epidemics. Persistent infectivity via environmental routes poses ongoing challenges to eradication efforts, as in poliomyelitis where fecal-oral transmission sustains circulation in areas with poor sanitation. Despite global vaccination campaigns reducing wild poliovirus cases by over 99% since 1988, low-sanitation environments in regions like parts of Africa and Asia enable silent circulation and vaccine-derived outbreaks, hindering the final push toward elimination.

Strategies to Mitigate Infectivity

Strategies to mitigate infectivity encompass a range of evidence-based public health interventions designed to interrupt pathogen transmission by targeting key stages such as host entry, replication, exposure dose, and environmental persistence. These approaches, including vaccination, pharmacological treatments, behavioral measures, and sanitation practices, have been shown to reduce the effective reproductive number (R_e) of infectious diseases by limiting the pathogen's ability to infect susceptible hosts.^[78] Vaccination represents a primary strategy to mitigate infectivity by inducing host immunity that blocks pathogen attachment and entry into cells. For instance, the human papillomavirus (HPV) vaccine generates neutralizing antibodies that bind to the virus's L1 capsid protein, preventing its interaction with heparan sulfate proteoglycans on host cells and thereby inhibiting initial infection. Clinical trials have demonstrated that this mechanism confers near-complete protection against vaccine-targeted HPV types, reducing cervical precancer incidence by over 90% in vaccinated populations.^[79]^[80] Antiviral and antibacterial agents mitigate infectivity by inhibiting pathogen replication within the host, thereby shortening the duration of the infectious period and reducing viral or bacterial shedding. Oseltamivir, a neuraminidase inhibitor, exemplifies this for influenza by accelerating viral clearance; randomized controlled trials indicate it shortens the symptomatic illness duration by approximately 1 day in adults and reduces the time to viral negativity by 0.5 to 1 day compared to placebo. This reduction in shedding limits onward transmission, with observational data showing decreased household secondary attack rates by up to 55% when administered early.^[81] Behavioral interventions, such as masking and physical distancing, lower infectivity by decreasing the exposure dose required for transmission, effectively raising the threshold for successful infection. During the COVID-19 pandemic, mask-wearing reduced the risk of SARS-CoV-2 infection by 70% among close contacts in a U.S. Navy outbreak investigation, as masks capture respiratory droplets containing viable virus particles. Cluster-randomized trials further support that community-level mask promotion, combined with distancing, can avert up to 30% of symptomatic infections by diluting aerosol transmission.^[82]^[83] Disinfection and sanitation practices target environmental reservoirs to diminish pathogen viability and infectivity outside the host. Chlorination of drinking water, for example, inactivates waterborne bacteria like Vibrio cholerae and Escherichia coli by damaging their cell membranes and genetic material, achieving over 99.99% reduction in culturable pathogens at standard residual doses of 0.2-0.5 mg/L. Field studies in low-resource settings have shown that point-of-collection chlorination reduces diarrheal disease incidence by 20-40% in children under five, directly linking to lowered bacterial infectivity in contaminated sources.30315-8/fulltext)^[84] Ring vaccination strategies exemplify targeted mitigation for highly infectious outbreaks, focusing on contacts of cases to rapidly contain transmission chains. In the 2014-2016 West African Ebola outbreak, the rVSV-ZEBOV vaccine was deployed in a ring vaccination trial, vaccinating over 7,000 contacts and demonstrating 100% efficacy against Ebola virus disease when administered within 10 days of exposure. This approach interrupted high-infectivity clusters, contributing to outbreak control by reducing the effective R_e below 1 in affected communities.32621-6/fulltext)^[85]

References

[1]
Epidemiology Glossary | Reproductive Health - CDC
May 15, 2024 · INFECTIVITY. The proportion of persons exposed to a causative agent who become infected by an infectious disease. INFERENCE, STATISTICAL. In ...
[2]
Infectious diseases epidemiology - PMC - NIH
Infectivity is the ability of an infectious agent to cause a new infection in a susceptible host, and in directly transmitted diseases it is measured by the ...
[3]
Principles of Infectious Diseases: Transmission, Diagnosis ...
Infectivity is the likelihood 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 ...
[4]
Epidemiology and Transmission Dynamics of Infectious Diseases ...
Infectious disease epidemiology, a branch of epidemiology that studies why infectious diseases emerge and how they spread, can provide helpful information on ...
[5]
Virus Infectivity - an overview | ScienceDirect Topics
Infectivity is the intrinsic ability of a retrovirus particle to establish infection of a target cell.
[6]
https://www.merriam-webster.com/dictionary/infectivity
[7]
INFECTIVITY Definition & Meaning - Merriam-Webster
Nov 4, 2025 · The meaning of INFECTIVITY is the ability to produce or transmit infection : the quality or state of being infective; specifically : the ...
[8]
History of BCG Vaccine - PMC - NIH
In 1900 Albert Calmette and Camille Guérin began their research for an antituberculosis vaccine at the Pasteur Institute in Lille. They cultivated tubercle ...
[9]
Chapter 18: Poliomyelitis | Pink Book - CDC
May 1, 2024 · The virus enters through the mouth and multiplies in the oropharynx and gastrointestinal tract. The virus is usually present in nasopharyngeal ...
[10]
Principles of Epidemiology | Lesson 3 - Section 1 - CDC Archive
Thus, an attack rate is the proportion of the population that develops illness during an outbreak.
[11]
Principles of Epidemiology | Lesson 3 - Section 5 - CDC Archive
Here are the formulas: Attack Rate (Risk) Attack rate for exposed = a ⁄ a+b. Attack rate for unexposed = c ⁄ c+d.
[12]
Risk factors for in-hospital mortality and secondary bacterial ... - PMC
Mar 31, 2023 · During epidemics, attack rates of influenza in unvaccinated populations were estimated to be 10–20% globally [1]. Most people recover from mild ...
[13]
ID50 (Median Infectious Dose) - an overview | ScienceDirect Topics
The median infective dose (ID 50) is defined as the minimal dose of a biological agent that will infect 50% of a population exposed to that agent under ...Missing: ID90 | Show results with:ID90
[14]
Updated Norovirus Outbreak Management and Disease Prevention ...
Mar 4, 2011 · Norovirus is extremely contagious, with an estimated infectious dose as low as 18 viral particles (41), suggesting that approximately 5 ...Missing: ID50 | Show results with:ID50
[15]
Norwalk virus: How infectious is it? - Teunis - Wiley Online Library
Jun 12, 2008 · We estimate the average probability of infection for a single Norwalk virus particle to be close to 0.5, exceeding that reported for any other virus studied to ...Missing: ID50 | Show results with:ID50
[16]
Principles of Epidemiology | Lesson 3 - Section 2 - CDC Archive
Overall attack rate is the total number of new cases divided by the total population. A food-specific attack rate is the number of persons who ate a specified ...
[17]
Two Detailed Plaque Assay Protocols for the Quantification of ...
May 31, 2020 · Infectious virus titers are measured in plaque-forming units (PFU). As such, plaque assays remain the gold standard in quantifying ...INTRODUCTION · Basic Protocol: SARS-CoV-2... · Alternate Protocol: SARS-CoV...
[18]
Colony-Forming Unit - an overview | ScienceDirect Topics
The colony forming unit (CFU) is a measure of viable colonogenic cell numbers in CFU/mL. These are an indication of the number of cells that remain viable ...
[19]
Complexity of the Basic Reproduction Number (R0) - CDC
Nov 27, 2018 · R0 is an estimate of contagiousness that is a function of human behavior and biological characteristics of pathogens. R0 is not a measure of the ...Abstract · Variations In R · R And Vaccination Campaigns
[20]
[PDF] Have You “Herd”? Modeling Influenza's Spread - CDC Stacks
The basic reproduction number (R0) is used to determine the ability of the virus to spread. R0 = (k) × (d) × (p). R0 = average number of persons each ...
[21]
Estimating the basic reproductive ratio for the Ebola outbreak in ...
Feb 24, 2015 · The basic reproductive ratio R 0 for Liberia resulted to be 1.757 and 1.9 for corrected and uncorrected case data, respectively.
[22]
Behind the Model: CDC's Tools to Assess Epidemic Trends | CFA
Oct 4, 2024 · The basic reproductive number, R0 (pronounced R-naught), is defined as the expected number of new infections caused by each infected person ...
[23]
Epidemic theory (effective & basic reproduction numbers, epidemic ...
The effective reproductive number (R) is the average number of secondary cases per infectious case in a population made up of both susceptible and non- ...
[24]
Structural and functional properties of SARS-CoV-2 spike protein
Aug 3, 2020 · The S protein on the surface of the virus is a key factor involved in infection. It is a trimeric class I TM glycoprotein responsible for viral ...
[25]
Surface Proteins on Gram-Positive Bacteria - ASM Journals
Surface proteins are critical for the survival of gram-positive bacteria both in the environment and to establish an infection.
[26]
Viral Mutation Rates - PMC - NIH
The resulting rates range from 10−8 to10−6 s/n/c for DNA viruses and from 10−6 to 10−4 s/n/c for RNA viruses.
[27]
A speed–fidelity trade-off determines the mutation rate and virulence ...
Jun 28, 2018 · Our data indicate that viral mutation rates have evolved to be higher as a result of selection for viruses with faster replication kinetics.
[28]
Minimum Infective Dose of the Major Human Respiratory and Enteric ...
Doses of <1 TCID50 of influenza virus, rhinovirus, and adenovirus were reported to infect 50% of the tested population. Similarly, low doses of the enteric ...
[29]
Transmission of prions - PNAS
A striking feature of prions is their extraordinary resistance to conventional sterilization procedures, and their capacity to bind to surfaces of metal and ...
[30]
The evolution of virulence and pathogenicity in plant pathogen ...
Here we define virulence as the degree of damage caused to a host by parasite infection, assumed to be negatively correlated with host fitness, and ...
[31]
Comparison of ambient air survival of Mycobacterium tuberculosis ...
This study compared the ambient air survival of two clinical strains of Mycobacterium tuberculosis that had caused significantly different numbers of cases ...
[32]
Molecular basis of mycobacterial survival in macrophages - PMC
Here, we describe mechanisms by which intracellular pathogens, with an emphasis on mycobacteria, manipulate macrophage functions to circumvent killing and live ...
[33]
Innate immune system - Autoimmunity - NCBI Bookshelf - NIH
The innate immune system includes physical and anatomical barriers as well as effector cells, antimicrobial peptides, soluble mediators, and cell receptors.
[34]
The immune response during acute HIV-1 infection - PubMed Central
Understanding the early events and immune responses is crucial to devising vaccine strategies that can improve the weak protection offered by current HIV ...
[35]
https://www.pnas.org/doi/10.1073/pnas.1804388115
[36]
The CCR5-Delta32 Genetic Polymorphism and HIV-1 Infection ... - NIH
Our meta-analysis suggests that the CCR5-delta32 homozygous genotype (delta32/delta32) confer possible protection against HIV-1, especially the exposed ...
[37]
Resistance to Plasmodium falciparum in sickle cell trait erythrocytes ...
Jun 26, 2018 · Sickle cell trait (AS) confers partial protection against lethal Plasmodium falciparum malaria. Multiple mechanisms for this have been proposed, ...
[38]
Herpes zoster in the older adult - PMC
Risk factors for reactivation of VZV include older age and immunocompromised status from such conditions as HIV-1 infection, lymphoma, leukemia, bone marrow ...
[39]
Impaired mucosal antibody response to cholera toxin in vitamin A ...
Effects of undernutrition on infection with Vibrio cholerae O1 and on response to oral cholera vaccine. Pediatr Infect Dis J. 1989 Feb;8(2):105–109. [PubMed] ...Missing: malnutrition infectivity
[40]
Malnutrition Decreases Antibody Secreting Cell Numbers Induced ...
Feb 13, 2020 · Our results indicate that deficient diet impairs B cell mucosal, and systemic immune responses following HRV vaccination, and challenge.
[41]
Roles of Humidity and Temperature in Shaping Influenza Seasonality
Experimental studies in guinea pigs demonstrated that influenza virus transmission is strongly modulated by temperature and humidity.
[42]
Inactivation of influenza A viruses in the environment and modes of ...
Several investigators found that aerosolized influenza virus survives well at low RH and is inactivated quickly at medium and high RH.<|separator|>
[43]
Adapting to the shifting landscape: Implications of climate change for ...
Jul 19, 2024 · Warmer temperatures can accelerate the development of the Plasmodium parasite within the mosquito, increasing transmission potential.
[44]
Climate Drivers of Malaria Transmission Seasonality and Their ...
Malaria parasite development is not possible at temperatures below 16°C and temperatures above 40°C have adverse effects on mosquito population turnover ( ...
[45]
Outbreak of Norovirus Illness Among Wildfire Evacuation Shelter ...
May 22, 2020 · Norovirus is highly infectious, spreads quickly in congregate settings (4) through contaminated food and beverages and person-to-person contact ...Missing: crowding | Show results with:crowding
[46]
Mass Gatherings | Yellow Book - CDC
Apr 23, 2025 · Travelers to mass gatherings face unique risks because these events are associated with both communicable diseases (from crowding, poor hygiene ...
[47]
Dengue dynamics, predictions, and future increase under changing ...
Jan 21, 2025 · The global burden of dengue disease is escalating under the influence of climate change, with India contributing a third of the total.Missing: competence post-<|separator|>
[48]
Interactions between climate change, urban infrastructure and ...
Dec 11, 2023 · Air and water temperature affect numerous biological processes in mosquitoes that regulate population dynamics and vector competence (e.g., ...Missing: post- | Show results with:post-
[49]
Coronavirus disease (COVID-19): How is it transmitted?
Dec 23, 2021 · Indoor locations, especially settings where there is poor ventilation, are riskier than outdoor locations. Activities where more particles are ...Missing: 2020-2022 | Show results with:2020-2022
[50]
Superspreading Event of SARS-CoV-2 Infection at a Bar, Ho Chi ...
Crowds in enclosed indoor settings with poor ventilation may be considered at high risk for transmission ... infectivity ... (COVID-19) in the United States, 2020– ...
[51]
HIV: Cell Binding and Entry - PMC - NIH
The HIV envelope protein binds to the host cell receptor CD4 and then to a cellular coreceptor. This triggers fusion of the viral and host cell membranes, ...
[52]
Virus Entry: Looking Back and Moving Forward - PMC
Epstein–Barr virus is a good example; a receptor on B cells mediates entry by direct fusion, while another one in epithelial cells leads to micropinocytosis ...
[53]
A cultured affair: HSV latency and reactivation in neurons - PMC
Herpesviruses rely on latency for long-term persistence ... ICP0 is required for efficient reactivation of herpes simplex virus type 1 from neuronal latency.
[54]
Molecular basis of HSV latency and reactivation - NCBI - NIH
The genome, however, persists in neurons in a latent state from which it reactivates periodically to resume replication and produce infectious virus.
[55]
Herpesvirus latency - PMC - PubMed Central
May 4, 2020 · Herpesviruses infect virtually all humans and establish lifelong latency and reactivate to infect other humans. Latency requires multiple ...
[56]
Evolution of Influenza A Virus by Mutation and Re-Assortment - NIH
Aug 7, 2017 · Every mutation, which helps the virus to evade the host immune ... Evasion of influenza A viruses from innate and adaptive immune responses.
[57]
The evolution of seasonal influenza viruses - Nature
Oct 30, 2017 · New antigenic variants of A/H3N2 viruses appear every 3–5 years, whereas new antigenic variants of A/H1N1 and influenza B viruses appear less ...
[58]
Genomic determinants of Furin cleavage in diverse European SARS ...
May 30, 2022 · Our results provide evidence that furin cleavage sites can be natural acquired in the bat reservoir and thus support a natural origin of SARS-CoV-2.
[59]
Ebolavirus glycoprotein structure and mechanism of entry - PMC
The EBOV glycoprotein (GP) is the only virally expressed protein on the virion surface and is critical for attachment to host cells and catalysis of membrane ...Zebov GpΔmucΔtm Prefusion... · Zebov Gp Glycosylation &... · Cathepsin Cleavage Enhances...
[60]
Bacterial Adhesion and Entry into Host Cells - ScienceDirect.com
Successful establishment of infection by bacterial pathogens requires adhesion to host cells, colonization of tissues, and in certain cases, cellular invasion.<|separator|>
[61]
The Role of the Type III Secretion System in the Intracellular Lifestyle ...
In this article, we review the mechanisms by which T3SS effectors contribute to these different lifestyles.
[62]
Type 1 Fimbriae, a Colonization Factor of Uropathogenic ... - NIH
Feb 20, 2009 · In E. coli, type 1 fimbriae play a crucial role during urinary tract infections by mediating adhesion to mannose-containing receptors on the ...
[63]
Bacterial endotoxins and exotoxins in intensive care medicine - NIH
Exotoxins can cause local inflammation and tissue breakdown, helping bacterial spread. •. Diagnosis of toxic shock syndrome can be difficult. Treatment should ...Missing: aiding | Show results with:aiding
[64]
Pseudomonas aeruginosa biofilm formation in the cystic fibrosis ...
The CF lung is chronically inflamed and infected by Pseudomonas aeruginosa, which is a major cause of morbidity and mortality in this genetic disease.
[65]
Salmonella SPI-2 Type III Secretion System Effectors
Aug 9, 2017 · In this Review, we summarize the biochemical activities, host cell interaction partners, and physiological functions of SPI-2 T3SS effectors.
[66]
MRSA virulence and spread - PMC - NIH
... MRSA clone in hospital settings involves reduced aggressive toxicity. Nevertheless, the agrC mutation in contemporary CC30 clones (such as EMRSA-16 ...
[67]
Modulation of Host-Microbe Metabolism by Cholera Toxin
Apr 6, 2023 · Vibrio cholerae requires cholera toxin (CT) to cause diarrheal disease, which is thought to promote the fecal-oral transmission of the pathogen.
[68]
Evasion of the Host Immune System by Bacterial and Viral Pathogens
In this review, we highlight and compare some of the many molecular mechanisms that bacterial and viral pathogens use to evade host immune defenses.
[69]
Plasmodium—a brief introduction to the parasites causing human ...
Jan 7, 2021 · The Plasmodium life cycle begins when parasites known as sporozoites produced in the insect vector enter the blood of the vertebrate host ...
[70]
Histoplasma capsulatum, lung infection and immunity - PMC
Upon inhalation of spores, H. capsulatum transforms into the pathogenic yeast phase. This form replicates within macrophages that carry the yeast from lungs to ...
[71]
DPDx - Malaria - CDC
Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle.
[72]
Malaria parasite pre-erythrocytic stage infection: Gliding and Hiding
... Plasmodium sporozoite reaches the liver and subsequently develops into blood stage-infectious merozoites. However, current experimental data provide ...
[73]
Role of Phagocytosis in the Virulence of Cryptococcus neoformans
The C. neoformans capsule is the most well-studied fungal antiphagocytic factor. The capsule inhibits the phagocytosis of the fungus by macrophages (5, 44, 63), ...
[74]
Interactions of Cryptococcus neoformans with Host Phagocytes - PMC
Oct 27, 2020 · The capsule also physically inhibits phagocytosis by increasing cell size. Upon entry of C. neoformans into the host environment, capsule ...
[75]
DPDx - Trypanosomiasis, African - CDC
Life Cycle. lifecycle · View Larger. During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into ...
[76]
understanding Trypanosoma brucei morphology in the tsetse - PMC
These trypomastigotes are thought to subsequently form the infective metacyclic trypomastigote (MT) population in the SG. When a SG infected tsetse feeds on its ...
[77]
Replication and Distribution of Toxoplasma gondii in the Small ...
Natural infection by Toxoplasma gondii occurs via oral ingestion of tissue cysts that rupture in the small intestine, releasing zoites that infect locally.
[78]
Bradyzoite Pseudokinase 1 Is Crucial for Efficient Oral Infectivity of ...
The tissue cyst formed by the bradyzoite stage of Toxoplasma gondii is essential for persistent infection of the host and oral transmission.
[79]
Histoplasmosis - StatPearls - NCBI Bookshelf - NIH
It is a soil-based fungus, and when it is disturbed, the conidia become airborne and can be inhaled. Often the infections are asymptomatic, but a granulomatous ...
[80]
Infection prevention and control - World Health Organization (WHO)
Infection prevention and control (IPC) is a practical, evidence-based approach preventing patients and health workers from being harmed by avoidable infections.
[81]
HPV pathogenesis, various types of vaccines, safety concern ... - NIH
May 24, 2023 · In response to an HPV vaccine, the body produces antibodies that attach to the virus and stop it from infecting cells in subsequent contacts ...
[82]
Understanding and learning from the success of prophylactic human ...
Sep 10, 2012 · This report documents the mechanisms by which VLP antibodies can prevent cervicovaginal HPV infection. Article CAS PubMed PubMed Central ...
[83]
Reducing Influenza Virus Transmission: The Potential Value of ...
Of note, oseltamivir treatment in IPs did not significantly decrease viral shedding in this study. A trial conducted during the 2008–2009 season, comparing ...Reducing Influenza Virus... · Nonclinical Studies · Clinical Studies
[84]
Effectiveness of Mask Wearing to Control Community Spread ... - NIH
During a COVID-19 outbreak on the USS Theodore Roosevelt, persons who wore masks experienced a 70% lower risk of testing positive for SARS-CoV-2 infection.
[85]
Impact of community masking on COVID-19: A cluster-randomized ...
Dec 2, 2021 · We conducted a cluster-randomized trial to measure the effect of community-level mask distribution and promotion on symptomatic severe acute ...
[86]
The Disinfection of Drinking Water - NCBI - NIH
The goal of disinfection is to eliminate pathogens. Chlorination is the most common method, but sterilization is not attempted. Other methods like ozone, ...
[87]
Effectiveness of Ring Vaccination as Control Strategy for Ebola Virus ...
Our results suggest that ring vaccination could substantially reduce the potential size and duration of outbreaks if other control measures are also in place ( ...