Epidemiology (23-28) Flashcards

1
Q

What is epidemiology of infectious diseases?

A

The study of infectious disease in populations:
→ transmission
→ contact patterns
→ rate of spread and recovery
→ immunity
→ control of disease
→ population structure
→ genetic disposition

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2
Q

What causes infectious disease?

A

Microparasites - small, difficult to count, multiply in their host
→ viruses, bacteria, fungi, protozoa

Macroparasites - large, can be counted, multiply external of the host
→ endoparasites (worms), ectoparasites (ticks, flees, lice)

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3
Q

What are some transmission routes of disease?

A

One-to-one contact → direct, indirect, droplet

Non-contact → airborne, vehicle, vector borne

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4
Q

What is DALYs?

A

Disability Adjusted Life Year
→ the number of healthy years of life lost due to pemature death and disability

DALY = YLD (years lived with disability) + YLL (years of life lost)
→ most affected by lower respiratory infections, diarrhoea diseases, HIV/AIDS

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5
Q

What is the plague?

A

Ancient bacterial disease caused by Yersinia pestis
→ vector borne disease - fleas, rodents are hosts/carriers

bubonic plague → lymphatic system
septicaemia plague → blood
pneumonic → lungs

→ caused ‘Black death’: 14th venturing, 50mil deaths in Europe

high mortality without treatment, high survival with treatment

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6
Q

Whats the difference between the different types of plague symptoms?

A

Bubonic → painful lymph nodes, fever, headache, chills, weakness, mortality: 30%
Pneumonic → fever, headache, weakness, pneumonia - shortness of breath, chest pain. cough, blood/watery mucus, mortality: 80%
Septicaemic → fever, chills, abdominal pain, shock, bleeding into the skin and other organs, skin/tissue may turn black, mortality: 100%

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7
Q

What caused the incidence of plague in Madagascar 2017?

A

Pneumonic → human-human transmission possible, changes to dynamic of disease enabled outbreak

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8
Q

What are some examples of arthropod vector-borne protozoan micro parasites?

A

Trypanosoma cruzi → human Chagas disease in central and S. America
Trypanosoma brucei spp → African sleeping sickness in Africa
Plasmoodium spp → malaria on many continents

(vector: living organism that can transmit infectious disease between humans or from animals to humans)

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9
Q

What is Chagas Disease?

A

Caused by Trypanosoma cruzi
→ endemic in 21 countries
→ 6-7 million persons infected
→ 10,000-14,000 deaths per year
→ 100mil at risk

transmission → 80% vector-borne, 20% transfusion of infected blood, congenital: mother to foetus

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10
Q

Whats the difference between acute and chronic Chagas disease?

A

Acute → pseudocysts form (replication sites) - rapture release inflammatory mediators, localised cell damage and inflammation, cute myocarditis

Chronic → type III hypersensitivity - kidney disease, chronic myocarditis - fibrosis and necrotic damage

70-80% of people infected remain asymptomatic

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11
Q

What are some characteristics of macro parasites?

A

Chronic recurring infections
High morbidity, low mortality (most vectors evolve not to kill host)
Endemic in nature
Continual reinfection
Age-related exposure, burden, pathology

soil transmitted helminths: round worms, hook worms, tape worms

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12
Q

What is an epidemic?

A

An increase in incidence of disease in excess of that expected in a given population
→ incidence: number of new cases per unit time

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13
Q

What is the compartmental model for the sequence of host stages?

A

susceptible → infected → recovered

S → I - effected contact rate
I → R - recovery rate

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14
Q

What is R0?

A

Basic core reproduction number
→average number of secondary cases arising from one infected individual introduced into a population of wholly susceptible individuals

endemic occurs when R0 > 1

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15
Q

How can you estimate R0 for a pathogen?

A

R0 = p x c x D

p → probability that a contact results in transmission
c → the frequency of host contacts between infectious and susceptible individuals
p x c → effective contact rate
D → average amount of time the host is infectious

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16
Q

What is effective R (Re)?

A

Restrained growth rate
→ R0 for a ‘virgin’ population where all individuals susceptible
→ Re is the true reproductive rate = R0 x fraction od susceptible individuals

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17
Q

Why do endemics end?

A

The pool of susceptible is depleted
→ Re declines to < 1
→ Re cannot return above 1 until new susceptibles are generated

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18
Q

How do endemics continue?

A

Susceptibles
→ born, migration
No lasting immunity
Pathogen mutates and can re-infect/continually infected individuals
Immunity wanes

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19
Q

What is epidemic fade-out?

A

The elimination of infectious agent due to chance
→ in small populations
→ generation (birth) of threshold susceptibles is slow, numbered of infecteds is low

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20
Q

What is waning immunity?

A

Loss of immunity post recovery from infection
recovered → susceptible

21
Q

What can patterns in epidemic data tell us?

A

→ infecteds through time: prevalence and incidence
→ origin of the outbreak
→ mode of spread through the population
potential incubation period through time of exposure
→ clues to identify the infectious agent (R0 value comparisons)

22
Q

What is the difference between incubation and latent period?

A

incubation period → the period between infection and clinical onset of the disease
latent period → the time from infection to infectiousness

23
Q

What is a point epidemic?

A

Single common exposure and incubation period
→ does not spread by host-to-host transmission
e.g. food-borne disease outbreaks

24
Q

What is continuous source epidemic?

A

Prolonged exposure to source over time
→ cases do not all occur within the span of a single incubation period
→ curve decay may be sharp or gradual
e.g. water-borne cholera (inc period 1-3 days)

25
Q

What is propagated progressive source epidemic?

A

Spread between hosts
→ larger curves until susceptibles are depleted or intervention
→ this pattern most likely in a small population
→ in a larger population it would all ‘merge’ together

26
Q

When is an epidemic not an epidemic?

A

The successive epidemic waves await replenishment of susceptibles
→ host-parasite relationship may eventually dampen down to a stable equilibrium (endemic) state

27
Q

What is endemic equilibrium?

A

Stability in the incidence of infection
→ persistence of the parasite in the host population
→ each infection produces 1 secondary (new) infection on average Re = 1
Re > 1 means epidemic

28
Q

What does persistence depend on?

A

Critical community size → the minimum host population size required (particularly micro-parasites)
Rate of contact for transmission
Duration of infectious period
Survival of host

29
Q

What happens when you increase infectious period but maintain R0?

A

→ likely low host mortality
→ eliminates cycles - improves persistence
→ increases prevalence

30
Q

How does Ebola virus have continual incidence?

A

1976 - Sudan
1976 - Zaire
1995 - Multiple small outbreaks
2013-2016 - West Africa
2014 - Congo
→ many seemingly isolated outbreaks - suggests reservoir host

31
Q

What are the features of Ebola virus?

A

→ zoonotic pathogen
→ transmitted animal to human
→ fruit bats primary reservoir host - not diseased
→ constant human cases in isolated communities
→ human to human transmission drives large outbreak

32
Q

What are the characteristics of gastrointestinal helminth worms for endemic persistence?

A

→ host density (CCS) not limit factor to transmission
→ external ‘reservoir’ of transmission stages
→ long generation time and period of infectiousness
→ immunity is transient (short)
→ continual re-infection
→ mode of transmission - often contaminative, not requiring host-host

33
Q

What is the aim of intervention?

A

Control → maintains parasite population to an acceptable level
Elimination → zero incidence in a defined geographical area
Eradication → zero incidence worldwide
Extinction → infectious agent no longer exists in nature or lab

34
Q

How can transmission be prevented?

A

Mass (random) or targets vaccination → e.g. small pox
Vaccination of risk group → e.g. child MMR
Spatial vaccination → e.g. ring vaccination
Reduction in contact → hand washing, condoms, sanitation

35
Q

How can intervention be done after transmission?

A

Infectious curtailment → tracing, isolation, or culling
→ e.g. SARS, hospital MSRA (humans)
→ FMD, BSE, avian influenza (animals)

36
Q

What is the logic behind interventions?

A

Re = S x c x p x D = S x R0

→ reduce number susceptibles
→ reduce time infectious
→ reduces contact

37
Q

How many people should be vaccinated?

A

Pc = the minimum proportion of individuals you need to vaccinate for herd immunity to be effective

S = 1 - Pc
Pc = 1 - 1 / R0

38
Q

What is herd immunity?

A

Large proportion of population immune - spread of disease unlikely
→ remaining unvaccinated people gain protection by reducing the infectious fraction - prevents virus reaching susceptibles

39
Q

Is herd immunity reached without intervention?

A

No
→ active immunisation is required

40
Q

What is the first ever eradicated disease?

A

Smallpox 1980
→ only human one
→ last case in 1975
→ first vaccine created by Edward Jenner

41
Q

How can you estimate R0 from average age of infection and life expectancy (demography)?

A

R0 = 1 + L / A

→ A = average age of infection
→ L = life expectancy

A / L = proportion of lifetime before infection

42
Q

Why is measles virus controlled not eradicated unlike small pox?

A

Measles and small pox share properties
→ no animal reservoir, safe cheap effective vaccine, high morbidity/mortality

Measles differs as:
→ transmitted more readily, R0 higher (requires higher Pc), highly infectious though not as virulent

43
Q

How was ring culling used in avian influenza?

A

2003 Dutch avian influenza A virus epidemic
→ R0 = 5.8
→ 30mil birds slaughtered from 1145 farms
→ ring culling 1km zones around farms
→ movement restrictions in affected regions

44
Q

What are some vector-borne infections?

A

Mosquitoes
→ Plasmodium spp - malaria, arboviruses - dengue, yellow fever
Black flies
→ Onchocerca volvulus - onchocerciasis
Tsetse flies
→ Trypanosome spp - african sleeping sickness

45
Q

What does anthroponotic mean?

A

Transmission: human → arthropod → human

46
Q

What is vectorial capacity (C)?

A

The average number of potentially infective bites that will be delivered by al the vectors feeding upon a single host in 1 day, units: per day

R0 = C x d

47
Q

What are some vector controls?

A

Human bait traps → e.g. insecticide treated nets
Non-human bait traps
Urban breeding site source reduction
Rural drainage of breeding sites

48
Q

Why does climate change have a big effect on vector-borne diseases?

A

Climate change brings extreme weather events
→ environmental parasites stages sensitive to climate, seasonally, breeding sites
→ white host environment relatively robust