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
What is propagated progressive source epidemic?
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
When is an epidemic not an epidemic?
The successive epidemic waves await replenishment of susceptibles → host-parasite relationship may eventually dampen down to a stable equilibrium (endemic) state
27
What is endemic equilibrium?
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
What does persistence depend on?
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
What happens when you increase infectious period but maintain R0?
→ likely low host mortality → eliminates cycles - improves persistence → increases prevalence
30
How does Ebola virus have continual incidence?
1976 - Sudan 1976 - Zaire 1995 - Multiple small outbreaks 2013-2016 - West Africa 2014 - Congo → many seemingly isolated outbreaks - suggests reservoir host
31
What are the features of Ebola virus?
→ 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
What are the characteristics of gastrointestinal helminth worms for endemic persistence?
→ 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
What is the aim of intervention?
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
How can transmission be prevented?
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
How can intervention be done after transmission?
Infectious curtailment → tracing, isolation, or culling → e.g. SARS, hospital MSRA (humans) → FMD, BSE, avian influenza (animals)
36
What is the logic behind interventions?
Re = S x c x p x D = S x R0 → reduce number susceptibles → reduce time infectious → reduces contact
37
How many people should be vaccinated?
Pc = the minimum proportion of individuals you need to vaccinate for herd immunity to be effective S = 1 - Pc Pc = 1 - 1 / R0
38
What is herd immunity?
Large proportion of population immune - spread of disease unlikely → remaining unvaccinated people gain protection by reducing the infectious fraction - prevents virus reaching susceptibles
39
Is herd immunity reached without intervention?
No → active immunisation is required
40
What is the first ever eradicated disease?
Smallpox 1980 → only human one → last case in 1975 → first vaccine created by Edward Jenner
41
How can you estimate R0 from average age of infection and life expectancy (demography)?
R0 = 1 + L / A → A = average age of infection → L = life expectancy A / L = proportion of lifetime before infection
42
Why is measles virus controlled not eradicated unlike small pox?
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
How was ring culling used in avian influenza?
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
What are some vector-borne infections?
Mosquitoes → Plasmodium spp - malaria, arboviruses - dengue, yellow fever Black flies → Onchocerca volvulus - onchocerciasis Tsetse flies → Trypanosome spp - african sleeping sickness
45
What does anthroponotic mean?
Transmission: human → arthropod → human
46
What is vectorial capacity (C)?
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
What are some vector controls?
Human bait traps → e.g. insecticide treated nets Non-human bait traps Urban breeding site source reduction Rural drainage of breeding sites
48
Why does climate change have a big effect on vector-borne diseases?
Climate change brings extreme weather events → environmental parasites stages sensitive to climate, seasonally, breeding sites → white host environment relatively robust