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R0 Value & Herd Immunity

Principal Scientist & Act. Head of Epidemiology Division, Indian Veterinary Research Institute at Indian Veterinary Research Institute
Sep. 14, 2017
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R0 Value & Herd Immunity

  1. R0 VALUE & HERD IMMUNITY (HERD EFFECT/ COMMUNITY IMMUNITY/ POPULATION IMMUNITY/ SOCIAL IMMUNITY) DR. BHOJ R SINGH, PRINCIPAL SCIENTIST (VM) HEAD DIVISION OF EPIDEMIOLOGY INDIAN VETERINARY RESEARCH INSTITUTE, IZATNAGAR-243122, BAREILLY, UP, INDIA. TELEFAX +91-581-2302188 THE PROPORTION OF IMMUNE INDIVIDUALS IN A POPULATION ABOVE WHICH A DISEASE MAY NO LONGER PERSIST IS THE HERD IMMUNITY THRESHOLD.
  2. R0 VALUES The average number of secondary cases arising from an average primary case in an entirely susceptible population. The basic reproduction number (basic reproductive rate, basic reproductive ratio R0) of a contagious disease is the number of cases than a case of the disease generates (on an average) over the course of its infectious period in a susceptible population.
  3. FACTORS DETERMINING THE R0  R0 will vary from agent to agent depending on the infectiousness of the agent.  R0 may also vary from population to population depending on population density.  Course of infectiousness of the disease. Incubation period, latent periods and period of infectiousness).  Mode of transmission and contagiousness.
  4. FACTORS AFFECTING R0 It can be explained by the epidemiological triad  Host Factor: Mixed Population, different age group of animals, difference in nutritional status, inbred population, parasitic load and mobility of host.  Environment Factor: Seasonal Variation e.g., FMD (autumn and spring) and Malaria (hot and humid climate).  Agent Factor: The agent may not spread at the same rate in all the countries. Genetic changes in the host factors like Genetic drift and genetic shift. Evolution of new antigenic variant strains.
  5. COURSE OF SOME INFECTIOUS DISEASES IN DAYS Infectious disease Incubation period Latent period Infectious period Measles 8-13 6-9 6-7 Mumps 12-26 12-18 4-8 Pertussis 6-10 21-23 7-10 Rubella 14-21 7-14 11-12 Diphtheria 2-5 14-21 2-5 Chickenpox 13-17 8-12 10-11 Hepatitis B 30-80 13-17 19-22 Poliomyelitis 7-12 1-3 14-20 Influenza 1-3 1-3 1-3 Smallpox 10-15 8-11 2-3 Scarlet fever 2-3 1-2 14-21
  6. Infectious disease Host R0 Measles Humans (UK) 12-18 Pertussis (whooping cough) Humans (UK) 12-18 Chickenpox (varicella) Humans (UK) 10-12 (16-18 in India) Rubella Humans (UK) 5-7 Smallpox Humans 3.5-7 Feline immunodeficiency virus (FIV) Domestic Cats 1.1-1.5 Rabies Dogs (Kenya) 2.44 Phocine distemper Seals 2-3 Tuberculosis Cattle 2.6 Influenza (Pandemic) Humans 2-4 Foot-and-mouth disease Livestock farms (UK) 3.5-4.5 Mumps Humans 4-12 Poliomyelitis (polio) Humans 5 HIV/AIDS Hetro 2-5 HIV Male homosexuals UK 4 HIV Female prostitutes in Kenya 11 Malaria Humans ≈ 100 SARS Human 2-5 IBR Cattle (UK) 7 TB Cattle 2.6 R0 of Some Diseases
  7. R0 IS AFFECTED BY MODE OF TRANSMISSION Disease Transmission R0 Measles Airborne 12–18 Pertussis Airborne droplet 12–17 Diphtheria Saliva 6–7 Smallpox Social contact 5–7 Polio Fecal-oral route 5–7 Rubella Airborne droplet 5–7 Mumps Airborne droplet 4–7 HIV/AIDS Sexual contact 2–5 SARS Airborne droplet 2–5 Influenza (1918 pandemic strain) Airborne droplet 2–3
  8. CALCULATION OF R0  R0= β/ γ  γ= 1/ average infectious period  β= Transmission rate (Number contacts by infective case in defined time, contact rate)  If susceptible fraction of a population is >1/R0 then only disease can progress. We can get is by vaccination, preventive therapy or control measures.  When initial fraction of susceptible population is less than γ/β or 1/R0 then infection can not progress and dies out, it is called the threshold fraction.  R0 is also defined as inverse of relative removal rate (the already got infected during the period).  1- 1/R0 is also defined as fraction of the population to be vaccinated for getting herd immunity.
  9. HOW TO REDUCE R0 VALUE? R0 can be reduced through intervention at any point in the transmission cycle by the following methods:  Reducing or eliminating the shedding of the agent by the infected host. e.g., by antibiotics and segregation and quarantine.  Reducing the duration of environmental survival of the agent. e.g., sunlight, fumigation, aeration etc.  Reducing or eliminating vehicle contamination and fomite transmission.  Controlling the Vector Population for biological transmission.  Reducing the exposure of susceptible host. e.g., density reduction, provision of protective gears as masks, goggles, aprons, gloves, gumboots etc.  Increasing the resistance of susceptible host by vaccination, passive immunization etc.
  10. IMPORTANCE OF RO  For an infectious disease with average infectious period 1/γ and transmission rate β, Ro = β/γ:  For a closed population, an infectious disease can only invade if there is a threshold fraction of susceptible individuals greater than 1/Ro .  If R0 is 2.5 then 1/R0 is 0.4, i.e., for control of the disease less than 0.4 fraction of the population be susceptible or more than 60% be non-susceptible or immune.  Vaccination policy: if proportion of susceptible individuals is reduced to below 1/Ro the disease can be eradicated.
  11. LIMITATIONS  When calculated from mathematical models, particularly using ordinary differential equations, R0 is, in fact, simply a threshold, not the average number of secondary infections.  There are many methods used to derive such a threshold from a mathematical model, but many of them often give an hypothetical value sometimes far away from the the true value of R0. This is particularly problematic if there are intermediate vectors between hosts, such as malaria.  Methods include the survival function, rearranging the largest value from the Jacobian matrix, the next-generation method, calculations from the intrinsic growth rate, existence of the endemic equilibrium, the number of susceptibles at the endemic equilibrium, the average age of infection and the final size equation.  Few of these methods agree with one another, even when starting with the same system of differential equations. Even fewer actually calculate the average number of secondary infections. Since R0 is rarely observed in the field and is usually calculated via a mathematical model, this severely limits its usefulness
  12. HERD IMMUNITY  The term herd immunity was first used in 1923.  It was an integral part During the Small Pox eradication in the 1960s and 1970s.  The practice of Ring Vaccination, of which herd immunity is integral to, began as a way to immunize every person in a "ring" around an infected individual to prevent outbreaks from spreading.  Vaccination controversies and opposing of vaccination are mainly due to failed herd immunity, either it was not be established or disappeared in certain communities, allowing preventable diseases to persist in or return to these communities.  Topley, W. W. C.; Wilson, G. S. (May 1923). "The Spread of Bacterial Infection. The Problem of Herd- Immunity". The Journal of Hygiene (London). 21 (3): 243– 249. PMC 2167341 . PMID 20474777. doi:10.1017/s0022172400031478.  Strassburg, M. A. (1982). "The global eradication of smallpox". American journal of infection control. 10 (2): 53– 9. PMID 7044193. doi:10.1016/0196-6553(82)90003-7.
  13. DEFINITION OF HERD IMMUNITY As per John TJ, Samuel R. European Journal of Epidemiology 2000;16, Herd Immunity can be defined as follows: 1. The resistance of a group for attack by a disease because of the immunity of a large proportion of the members and the consequent lessening of the likelihood of an affected individual coming into contact with a susceptible individual. 2. The prevalence of immunity in a population above which it becomes difficult for the organism to circulate and reach new susceptible is called herd immunity. 3. It is well known that not everyone in a population needs to be immunised to eliminate disease.
  14. HERD IMMUNITY  The indirect protection from infection of susceptible livestock in a herd, and the protection of the herd as a whole, which is brought about by the presence of immune individuals.  The number of individuals in a population (herd) who are (relatively) immune to infection with an infectious agent may depend on the proportion who have previously been infected with the agent and the proportion who have been vaccinated with an efficacious vaccine.
  15.  A measure of the level of population-immunity or herd- immunity is the proportion who are thus immune from further infection.  For many infections, the level of herd immunity may have an effect on the transmission of the infection within the population and, in particular, may affect the risk of an uninfected becoming infected.  For such infections, increasing the level of herd immunity will decrease the risk of an uninfected person becoming infected.  If the herd effect reduces the risk of infection among the uninfected sufficiently then the infection may no longer be sustainable within the population and the infection may be eliminated.  This concept is important in disease elimination or eradication programmes. It means, for example, that elimination can be achieved without necessarily vaccinating the entire population.
  16. TYPES OF HERD IMMUNITY Innate (Inherent) Herd Immunity: It is genetically determined physiological changes with respect to antibody production or other defence mechanism in a herd. It does not depend on the previous exposure of herd with infection or it may arise in a herd through prolonged exposure to an infection or natural selection.
  17.  Some population of domestic fowl have innate resistance to pullorum disease due to an inherited difference in lymphocyte numbers immediately after hatching.(Robert & Card,1926)  Inheritance of resistance to influenza virus in mice is probably due to a single dominant autosomal allele. (Lindermann, 1964)  Cameroon et al have shown that resistance to brucellosis in swine may be genetically determined.
  18. Acquired Herd Immunity: It is a type of herd immunity where a sufficient number of its members have actually been exposed naturally or artificially to infectious agents during their lifespan.  This kind of exposure may be made very early in life.  Polio in paralytic form are rare in countries with poor hygiene and sanitation where exposure to the virus occurs in early part of life but in countries where the hygiene is better and exposure is delayed till school age then paralytic manifestations are higher.
  19. ADVANTAGES OF HERD IMMUNITY  Potential for infection elimination.  Reduced risk of infection for those refusing vaccination (“free riders”).  Vaccination against sexually transmitted diseases (STIs) targeted at one sex result in significant declines in sexual disease in both sexes.  Reduced risk of infection for those for whom vaccination is contraindicated (e.g., immune-suppressed) or who cannot be vaccinated e.g., cancer patients, too young animals and pregnant animals.  Prioritization of vaccination towards target groups or High Risk groups in the community may lead to protection of the whole community e.g. prioritization of vaccinating children against pneumococcus and rotavirus, school-age children for seasonal flu immunization reduces of the disease burden in the whole community.
  20. Limitations  Herd immunity generally applies only to diseases that are contagious. It does not apply to diseases such as tetanus, botulism food borne infections and intoxications.  Raise the average age of infection among those who are infected.  Particular problem for those infections where the severity of infection increases with age (e.g. polio, rubella, varicella, measles, hepatitis A).  It is not a permanent attribute, depending on the duration of the immunity conferred after vaccination the structure of herd for susceptible versus immune rapidly changes.  Herd immunity might be associated with emergence of variants of pathogens more dangerous than the existent due to Evolution Pressure on the pathogen or Selection Pressure on the antigen variant.  Herd immunity may lead to antigenic variation among pathogens at much faster rate than it would have been in the absence of herd immunity. Leading to Serotype Replacement.  Herd immunity not work for many of the infectious diseases like Tetanus, Botulism, and similar toxico-infections.
  21. BACTERIAL DISEASES OF LIVESTOCK Sl. No Name of the Disease Host Range Type of Vaccine Used Duration of Immunity 1 Haemorrhagic Septicemia Cattle, Sheep & Goat, Pig Inactivated alum adjuvant vaccine 6 months 2 Black Quarter Cattle, Sheep & Goat Inactivated alum adjuvant vaccine 6 months 3 Anthrax Cattle, Sheep & Goat Sterne-avirulent spore vaccine 1 year 4 Brucellosis Cattle, Sheep & Goat Live freeze dried vaccine Life Long 5 Enterotoxemia Sheep Inactivated alum adjuvant vaccine 6 months 6 Leptospirosis Canine Killed Mixed Vaccine 1 year
  22. DISEASE ELIMINATION & HERD IMMUNITY  If the herd effect reduces the risk of infection among the uninfected sufficiently then the infection may no longer be sustainable within the population and the infection may be eliminated.  The “effective reproduction number” (R) has to be reduced below 1.  If a proportion (P) of the population are immune then R = (1- P) R0 So, to get R down to about 1, P must be more than 1-1/ R0. Thus if R0 = 5 then vaccine coverage will have to be in excess of 80%.
  23. QUIZ  What are the factors affecting reproduction ratio (R0 ) of a disease?  Give R0 values for important animal diseases.  How is associated with herd immunity?  Give herd immunity values required for prevention of FMD, HS, BQ, Enterotoxemia, Goat Pox, Sheep Pox, PPR, Brucellosis, Classical swine fever.  What are different types of herd immunity in animals?  An useful link https://www.historyofvaccines.org/content/herd- immunity-0
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