Infectious disease Flashcards
What is infectious disease?
Product of an interaction between 2 species. The host is a resource for the pathogen.
Which diseases are especially bad for children in Sub Saharan Africa?
Malaria and measles
Example of clinical latency?
HIV. Clinical latency before it gets worse and opportunistic factors take over due to lack of CD8+ cells. HIV can mutate and escape the CD8+ T cell responses. Uses certain receptors in order to attack CD8+ cells, but can move between certain cells when they run out of resources. Escapes antibody response, as HIV has a massive capacity to change the epitopes on their lipid envelope. Arms race metaphor.
Example of antigenic variation?
Malaria. P. Falciparum can undergo antigenic variation. Large part of life-cycle is spent in red blood cells. Alter the membrane to express PfEMP1, allowing it to stick to receptors on endothelium, stopping the RBCs from being moved into the spleen and destroyed. Pathogen carries 60 different copies of the protein, which it sequentially expresses. Eventually runs out of new mutations.
How does TB evade the immune system?
Finds and hides in macrophages. Makes it invisible to immune system until reactivation.
What is the colonising strategy?
Pathogen enters a population and lies dormant. Allows it to colonise patches.
Basic infection equation?
dy/dt = rate of infection x susceptible population
Infection equation incl B?
B is a combination of parameters relating risk of infection to prevalence of infection. (lander=By).
For directly transmitted pathogens: B=beta x N (beta - probability of transmission, N is population size)
For sexually transmitted pathogens: B = beta x c (c - average number of partners)
For vector borne pathogens: B = m x a^2 x b x c x H (m- no of vectors per host, a - biting rate, b - proportion of bites leading to infection, c - proportion of bites on infectious hots leading to infections, h - lifespan of vector).
Infection equation including death of hosts?
dy/dt = By (1 - y) - uy
u-death rate of host
Will level out at 1 - u/B
Describe the Herpes Simples Virus?
Enter peripheral sensory nerves and migrates along axons to sensory nerve ganglia in the CNS. Allows the virus to escape immune response and become latent.
Also other Herpes viruses, including chicken pox (95% of people) and Epsom barr.
What is the Basic reproduction number?
Represents the average number of secondary cases generated by a primary case in a totally susceptible population. Fundamental measure of the transmission potential of a pathogen in a given setting (max spread).
What is the carrying capacity?
K = 1 - (1/R0)
R0 = B/u
What is the instrinsic growth rate of infection?
r = B - u
What is the SIR model?
Short infection then immune.
Example of SIR model?
Natural immunity to measles is known to last at least 65 yrs.
Evidence to show that immunity doesn’t have to be “boosted” - natural immunity to measles lasts at least 65 years. In 1781 measles disappeared from Faroe islands and was not re-introduced until 1846. Individuals older than 65 years were still protected.
SIR model equation?
dy/dt = By (1-z) - oy
y - infectious population
z - previously infected
Seasonal fade outs.
Difference in infection patterns before and after vaccinations?
Before vaccinations: regular biennial epidemics with small annual epidemics in between
After vaccines: much lower incidence and more irregular epidemics.
Get smaller oscillations due to births, but a smaller susceptible population.
SIR type and SI type examples?
SIR:
Measles, mumps, rubella.
Lifelong immunity and a short infectious period
SI:
HIV, Herpes viruses, Syphilis
Lifelong carriage.
How can diseases be eradicated?
Reduce the average number of secondary cases generated by an index case to less than 1. To achieve this, the proportion immunised must exceed the fraction immune at equilibrium in the absence of vaccination.
Why is influenza so hard to vaccinate against?
The Receptor-Binding Site of the Measles Virus Hemagglutinin Protein Itself Constitutes a Conserved Neutralizing Epitope, so doesn’t change.
The influenza hemagglutinin protein has evolved to mutate the top of the HA to change shape and hold glycans.
Malaria also varies its antigens, using its genes. Strains co-circulate.
