Presentation on theme: "Infectious Disease Epidemiology EPIET Introductory Course, 2006 Lazareto, Menorca Prepared by: Mike Catchpole, Johan Giesecke, John Edmunds, Bernadette."— Presentation transcript:
Infectious Disease Epidemiology EPIET Introductory Course, 2006 Lazareto, Menorca Prepared by: Mike Catchpole, Johan Giesecke, John Edmunds, Bernadette Gergonne
Epidemiology: Why Bother? Human disease does not occur at random Epidemiology leads to the identification of causal and preventive factors in human disease
Burden of disease in adult men and women, Established Market Economies: 1990 Source: World Bank *Pertussis, polio, measles and tetanus
Epidemiology: basic concepts The study of the distribution and determinants of disease frequency in (human) populations Frequency Distribution Determinants
What is special about infectious disease epidemiology?
Specific concepts Attack rate, immunity, vector, transmission, carrier, subclinical disease, serial interval, index case, source, exposure, reservoir, incubation period, colonization, generations, susceptible, non-specific immunity, clone, resistance, repeat episodes … But why do we need these concepts?
Infectious disease: the unique factor Infectious diseases can be spread from human to human (or animal to human)
Chain of Transmission Portal of exit Portal of entry Agent Susceptible Host Mode of transmission Reservoir Person to person transmission
Chain of transmission Reservoir Human Person with symptomatic illness Carriers: Asymptomatic Incubating Convalescent Chronic Animal: zoonosis Environmental: soil, plant, water
Chain of transmission Direct Direct contact Secretions, Blood, Faeces/urine Droplet spread Indirect Food/water Aerosol Animal vectors Fomites Medical devices and treatments Mode of Transmission
Respiratory tract Mouth (faecal-oral transmission) Skin Mucous membranes Blood Portal of entry Chain of transmission
Level of disease occurence Sporadic level: occasional cases occurring at irregular intervals Endemic level: persistent occurrence with a low to moderate level Hyperendemic level: persistently high level of occurrence Epidemic or outbreak: occurrence clearly in excess of the expected level for a given time period Pandemic: epidemic spread over several countries or continents, affecting a large number of people
What causes incidence to increase? Portal of exit Portal of entry Agent Susceptible Host Mode of transmission Reservoir
Why does an epidemic occur ? Agent and host in adequate number Recent increase in amount of the agent Recent increase in infectivity / virulence of the agent Recent introduction of the agent Enhanced mode of transmission Increase of host exposure Change in the susceptibility of the host response to the agent Introduction through new portals of entry
Agent Host Environment Age Sex Genotype Behaviour Nutritional status Health status Infectivity Pathogenicity Virulence Immunogenicity Antigenic stability Survival Weather Housing Geography Occupational setting Air quality Food Factors influencing disease transmission
Infectious Disease Epidemiology: five major differences 1.A case can also be an exposure 2.Sub-clinical infections influence epidemiology 3.Contact patterns play major role 4.Immunity 5.There is sometimes a need for urgency
1. Case = exposure Unique to infectious disease epidemiology. Usually, the sets of exposures and outcomes are completely apart e.g. smoking and cancer.
The average number of cases an infectious individual will generate Dependent on 4 factors: 1) The number of contacts made (c) 2) The probability of infection given contact (p) 3) The duration of infectiousness (D) 4) The proportion of contacts who are susceptible (S)
The basic reproduction number, R 0 Useful summary statistic Definition: the average number of secondary cases a typical infectious individual will cause in a completely susceptible population Measure of the intrinsic potential for an infectious agent to spread
The basic reproduction number, R 0 If everyone is susceptible then the average number of secondary infections generated by a single infectious individual is given by: R 0 = p x c x D Can be estimated if we know p, c, & D, or from proportion susceptible, outbreaks in susceptible populations, the average age at infection (and many other ways)
R 0, threshold for invasion If R 0 < 1 then infection cannot invade a population implications: infection control mechanisms unnecessary (therefore not cost-effective) If R 0 > 1 then (on average) the pathogen will invade that population implications: control measure necessary to prevent (delay) an epidemic
After invasion: the effective reproduction number, R(t) As pathogen invades, the number of susceptibles declines through recovery (or death) Eventually, insufficient susceptibles to maintain chains of transmission On average each infectious person infects < 1 other, epidemic dies out Initial invasion, R(t) = R 0 Peak of epidemic R(t) = 1
Changes to R(t), over an epidemic R=R 0 R>1 R=1 R<1
Determinants of STI incidence R 0 = p c D p Risk of transmission c Rate of sexual partner change D Duration of infectivity
STI Control Strategies R 0 = p c D p condoms, acyclovir, zidovudine c health education, negotiating skills D case ascertainment (screening, partner notification), treatment, compliance, health seeking behaviour, accessibility of services
Cases of Gonorrhoea and Genital Herpes seen in STI clinics in England,
Determinants of STD incidence c T = 1 p D c T Critical threshold for maintenance p Risk of transmission D Duration of infectivity
Sexual partners in last 12 months * * UK National Study of Sexual Attitudes and Lifestyles
Sexual partners in last 12 months c Herpes c GC
2. Subclinical infections R 0 = p x c x D A case can be a case without being recognised as a case. – What do we mean by ´asymptomatic´? – How do recognise these? – What level of infectious risk do they pose?
Asymptomatic Infections Genital Chlamydia trachomatis infection % infected women asymptomatic Poliomyelitis - 90% asymptomatic or non-specific fever HIV - majority asymptomatic or non-specific symptoms pre-AIDS SARS-CoV - ??
Rates of genital chlamydial infection in the general population, UK 2000 Adj OR 0.58 ( ) Adj OR 0.43 ( ) Adj OR 1.37 ( ) Adj OR 0.90 ( ) Source: Natsal 2000
Undiagnosed HIV Infection Among Men Who Have Sex With Men, STI Clinic Attendees, London 2003
3. Contact patterns R 0 = p x c x D Do all cases contribute equally to the spread of disease? How can we identify and control 'super spreaders'?
SARS, Inner Mongolia
Small world How big probability that there is a sexual chain between two random people? 'Six degrees of separation' Do people choose sexual partner at random? If not, how does this affect epidemiology?
Reported new sexual partners from outside the UK in the past 5 years, by gender and age-group Source: Natsal 2000
4. Immunity R 0 = p x c x D –Can we measure it? –How can we change it (positively or negatively)? –Can we predict the consequences of changing immunity?
Vaccination coverage required for elimination Pc = 1-1/Ro rubellameasles
Consequences of Changing Immunity Not always what you might intuitively expect
Proportion of pregnant women susceptible to rubella Athens, % 10% 20% 30% 40% Year % susceptible Infant vaccination introduced 1975 data from Panagiotopoulos et al, BMJ, 1999
Age distribution of outpatient rubella cases, Athens 0% 10% 20% 30% 40% Age group Proportion of cases 1986 (n=113) 1993 (n=326) from Panagiotopoulos et al, BMJ, 1999
Rubella and CRS in Greece, JanFebMarAprMayJunJulAugSepOctNovDec Month Rubella Notifications CRS cases Rubella notifications
5. A need for urgency R 0 = p x c x D What EPIET is very much about…
Five major differences 1.A case can also be an exposure 2.Sub-clinical infections influence epidemiology 3.Contact patterns play major role 4.Immunity 5.There is sometimes a need for urgency
If you enjoyed this… Further reading: McNeill, WH. Plagues and Peoples Diamond J. Guns, Germs, and Steel: The fates of human societies.