IB 114

Dynamics: SIR model

R- recovered, resistant or dead disease will increase if ΔI positive, (host density above threshold) as disease spreads, individuals enter resistant class or die when resistant class becomes sufficiently large, density of susceptibles get too low and disease dies out

Visher et al paper

influenza: high levels of productivity, high burden on health care infrastructure. no vomiting A: generally talked about H_N_ B: only in humans, more stable than A, less antigenic drift. children/milder disease C:rarely reported, mild symptoms, not associated with epidemic disease avian: alpha-2-3-linked in respiratory/GI tract human: alpha-2-6-linked sialic acid in upper respiratory Mutation rate matters: 1. high mutation rates may help with host shift 2. high mutation rates constatnly generate novel variants 3. Fast evolution makes control difficult mutational robustness Quasispecies model- fitness of variant depends on mutational neighborhood leads to brittle and robust genotypes Methods: 1. Made random mutants across genome 2. Directly compete mutants against wt strian to measure fitness H/N higher fitness if mutated? influenza similar to those of same genome size novel treatment options: lethal mutagenesis

Endoparasites

intimate association

Virus

intracellular obligate parasites -use cell components to replicate -DNA or RNA + proteins -transferred extracellulary (plasmids, transposons) FMD disease, first viruses. highly variable in size, structure and complexity

Leeuwenhoek

invented microscope-

Macroparasites

large bodied-nematodes/tapeworms/fleas longer generation times adults release infective stages that can persist outside of host persistent infection no lasting immunity impact is a function of number of parasites per host

Megavirus and Mimivirus

largest viruses. 1million bp DNA and 1000 genes.

ectoparasites

less intimate association

Phage Lambda

linear dsDNA in virion, circulizes on cell entry, large genome infects e. coli DNA virus: recombination following multiple infection use host's recombinational machinery 1. Lytic 2. Integrated into host genome; lysogenic

Parasites

macroparasites

Toxoplasma gondii

manipulates host behavior, more risk taking mice sniffs cat pee and likes it

Mixed infection

may cause genetically different strands in same virion

Infectious Disease history

much of our emotional and moral attitude to disease is legacy of past history principles of disease biology apply to plants, animals, humans. Studying plant/animal disease helps to understand human.

Antigenic drift

mutations cause small changes in H or N antigens on surface of virus

Negative virus

need to replicate complementary strand which is then transcribed and translated need to be converted to positive sense RNA by RNA polymerase before translation don't seem to produce dsRNA and may evade host immunity

Upward incorporation

new definitive host, typically higher up a food web and which preys on original definitive host is added Original host becomes intermediate host, in which reproduction is suppressed Advantages: - avoid mortality due to predator -greater body size at maturity, higher fecundity (more space to grow)

Downward Incorporation

new intermediate host is added at a lower trophic level Advantages: - reduces mortality -facilitates transmission to original definitive host

SARS

newly emergent Asia, spread worldwide. 774 died. Transmission through direct person-to-person contact

Disease cause

non-infectious: caused by internal and external conditions infectious agents: replicating entities that multiply in or on hosts, and are transferred from host to host; when these agents cause harm to the host, we call them pathogens or parasites; when they enter a host we say the host is "infected", manifestations of the harm that they cause is termed a disease infectious disease: infectious disease is product of interaction between host and pathogen or parasite

Rabies

none in Switzerland

leptokurtic

normal curves that are tall and thin, with only a few scores in the middle of the distribution having a high frequency advance is faster than with normal

Disadvantage vertical transmission

not efficient way for pathogen to increase reproductive rate, at best only same level of disease on avg, indivudal leaves only one mature offspring in constant population. Transmitting to one offspring doesn't spread disease not sustained unless 100% transmission Always trade-offs, increase transmission in one pathway reduces transmissinon by other. Intracellular transmission Reproductive organs are where pathogen is located Persist to reproduction No adaptation for dispersal needed To persist as vertical pathogen must: 1. Have additional horizontal transmission mode OR 2. increase reproductive success of host- By definition makes it a mutualist

Parsimonious

not overwhelmed by unknowns. We want to have it be as simple and straightforward as possible

Intellectual fossilization

not pushing forward. erroneous paradigm.

βxIxs

number of newly diseased individuals per time interval

S

#healthy/susceptible

Basic Reproductive Number

#secondary infections produced by single infected host in susceptible population You need susceptibles for chain of infection to establish

Transposons

(jumping genes) short strands of DNA capable of moving from one location to another within a cell's genetic material

Tobacco Mosaic Virus (TMV)

+ssRNA Virus that affects many species of plants e.g. tomatoes Symptoms: a mosaic pattern on the leaves - parts of the leaves become discoloured The discolouration prevents the plant from photosynthesising as well, thus the virus affects growth

Samy et al

- Socioeconomic model criticized by disease biologists human densities as ZIka informer higher people densities will increase spraying public health much higher risk for bees

Bacterial classification

1. Morphology 2. Staining 3. Serology 4. Biochemical properties

Bacteria variation generation

1. Mutation -replication error (have DNA repair) -transposons 2. Recombination -transformation -transduction -conjugation 3. Plasmids 4. Infection by phages that integrate into genome

Virus generate new variant mechanism

1. Mutation/Errors during replication 2. recombination

Different host adoption phylogenetic frameworks

1. Vertebrate first 2. Mollusc first 3. Blend

Bacteria

1. freeliving or extracellular or intracellular 2. no nucleus or membrane bound organelles 3. Genome consists of singular circular dsDNA/ smaller plasmids 4. Small, visible in light microscope

HIV new variants

1. mutation: reverse transcriptase has no error repair. rate per base pair: 3x 10-5. 9100 bp. Produces 10^9 virions per day. 2. Recombination: virion diploid; two RNA molecules, code for identical genes

Viral Classification

1. ssDNA, dsDNA, ssRNA, dsRNA 2.Replication via DNA or RNA 3. positive or negative translation 4.Replication site- nucleus or cytoplasm 5. Capsid morphologies A MESS!

Vertebrate host

1.further dispersal 2.predation survival 3. Find a mate- vertebrates larger so more different types that can potentially be there (no use in mating with same genes)

Viroids

3-400 bases, no protein coding, infect platns, circular naked ssRNA (no protein coat)

Ringworm

40 types of fungi can cause, Diseases: athlete's foot (tinea pedis) / jock itch (tinea cruris ) reproduce asexually in "conidia", sexual stages unknown

Microviridae

5000 bases, circular encapsulated ssDNA, 10 genes, 6 partially overlapping genes

positive frequency dependent selection

Phenotypes are favored only when common. Example is warning coloration or DVD vs blu-ray. Equivalent but DVD died since it was less common as blu ray was more common and was able to afford licensing more movies and selling them making more money.

negative frequency dependent selection

Phenotypes favored only when rare. Example is left-handed fighting ability, converse shoes. As host type becomes popular, then there's common so lots of things trying to infect common host as it increases their own proability of reproducing. Selection pressure to infect common host. Host will then survive better if rare which drives down the frequency in population of common host type.

Malaria

Plasmodium species, protoza phylum Apicomplexa disease of reptiles, birds, mammals Humans: P. falciparum, Pvivax P. malariae Life cycle: human and mosquito ANopholes mosquito Vector: female Anopholes mosquito definitive host: where sexual reproduction occurs, not just a vehicle High historic importance locations became permanently or seasonally uninhabitable. huge impact on armies, high cause of hospitalization ~50deaths/hour

Gram positive

Positive stain blue for peptidoglycan cell wall constituents

Antigenic shift

Acquisition of entirely new antigens when influenza viruses reassort looks totally different

niche models

Species Distribution Modelling (SDM) applied in ecology biogeography correlative

Plague

Yersinia Pestis

Mutational robustness

ability of organism to maintain phenotype when genotype changes

Exogenous prion

abnormal protein is ingested

Prions

abnormal proteins that cause neural degeneration but are transmissible transmissile, abnormal folding of specific normal "prion proteins" that are found most abundantly in brain Normal folding: helices Abnormal: sheets abnormal folding of prion proteins leads to brain damage and characteristic signs and symptoms of disease Ex: Creutzfeldt- jakob infectious protens Endogenous origin: mutation in gene coding causes it to fold into "sheet" fconformation

Chestnut blight

accelerated speed, leptokurtic

Coitocaecum parvum

accelerates devlopment and rapidly reach precocious maturity in crustacean intermediate in absence of chemical cues from fish definitive host Worms were longer when exposed to control water than fish-conditioned water

Transduction

accidental transfer of bacterial DNA by bacteriophage

Aerial transmission

aerosoles, airborne spores

Robert Koch

anthrax caused by bacterium bacilis anthracis. Experimental criteria to establish causal relationship between microorganisms and disease 1. Microorganism has to be present in diseased and not healthy individuals 2. Has to be isolated and grown in pure culture 3. When re-inoculated into host must cause same disease 4. Same organism must then be re-isolated from experimentally diseased host

t

arbitrary time interval

carrier

asymptomatic but still infectious

latent

asymptomatic for disease

Abundance

average # parasites across all hosts (prevalence*intensity)

Intensity

average # parasites within infected host mean # worms/host usually macroparasites only

R0

average number of new cases that each primary infection produces over infectious period in completely susceptible population must be >1 for invasion

Rust fungi

caused by numerous Uredinales species alternate hosts Wheat rust- Puccinia graminis Alternates barberry and wheat- Uredinia produces urediniospores. Asexual summer cycle on wheat (rust color) Basidiospores in spring go to barberry Barberry eradication program

Dikaryon stage

cell genetically diploid but nuclei remian separate

Lytic vs non-lytic

cell lysis of virion production and release

incidence

change in number of cases or prevalence per unit time

Causes of disease

concept of contagion remained undefined and vague for centuries.

core

contains nucleic acid,

Macroparasite population biology

count number of worms or parasites in body , number matters tapeworm

Microparasite population biology

count whether infected or not- binary, particulates don't really matter flu/rabies/measles

Threshold density

critical community size

Pathogenicity

degree of damage to host tissue by pathogens

virulence

describes negative effects of parasites on host fitness (disease-induced mortality, or severity of infection)

Horizontal transmission routes

direct contact transmission aerial transmission waterborne transmission soil borne vector transmission trophic transmission

Potato blight

direct observation of germs-organisms= disease Miles Berkeley- potato blight caused by fungus

Positive strand virus

directly codes for mRNA viral RNA similar to mRNA, immediate translation in and of itself infectious even without full viral particle

At equilibrium...

disease is endemic not epidemic. not all population is diseased

zoonotic

disease primarily transmitted from animals to humans

β

disease transmission coefficient per individual contact rate cx 𝛿 hard to measure directly

Seasonality

disease transmission is not constant during year childhood disease- more transmission in term time

α

disease-induced host mortality rate

Baculoviridae

dsDNA virus insect form crystal-like structures in cells of insects (inclusion bodies or polyhedra) polyhedrosis viruses polyhedra: DNA-protein complexes that can survive outside the cell biocontrol

V. cholerae ecology

endemic in estuaries/oceans. parasites of crustaceans Hindgut of crabs, influences osmo-regulation

Wolbachia

endosymbiotic bacterium. changes males to females, more females increases transmission kills males: good if progeny compete- more resources for females- good if progeny eat each other bad for host population as it may lead to too few males to fertilize females

Trematodes

flatworms/flukes internal parasites of molluscs and vertebrates most trematodes have complex life cycle with at least 2 hosts primary host where flukes sexually reproduce is a vertebrate intermediate host, asexual reproduction, usually snail

Cercaria

free swimming larval stage of trematodes (flukes) they leave host and then enter again, may want to have upstream density

Nematodes

free-living and parasitic on plants and animals complex morphology; separate sexes, females lay eggs Larvae have deterministic development, fixed number of larval stages separated by "molts" 3rd stage larvae are dispersal or infectious stage Medical symbol Ex: Loa loa, Root knot disease, Guinea worm. Dracunculus

Vertical transmission

generations from parent to offspring female to offspring most common Types: -Cytoplasmic -transplacental -perinatal (during birth) -postnatal (lactation)

Transmission factors

greater number of livestock, greater transmission/risk of infection certain species transmit more and are more susceptible

Fungi

grows as hyphae to produce mycelium or yeast-like forms. Reproduce asexually by spore production fertilization (syngamy) occurs by hypahal fusion, fusion of single cells, or fusion of spore with hypha meiosis may occur directly after fusion or after extended dikaryon stage greatest cause of species extinction or extirpation events

INfected

harboring disease agent

Neuraminidase

helps release virions from the host cell after replication and assembly

b

host birth rate, per capita

d

host natural mortality rate

morbidity

host weakness or lethargy caused by disease

SIR assumptions

hosts uninfected at birth infection doesn't affect host fecundity recovered hosts remain resistant for life population large enough that stochastic processes can b ignored

Bacterial pathogens

humans: cholera, syphilis, plague Plants: citrus greening disease, fire blight

Avian influenza

in birds, occurs worldwide. Highly pathogenic form caused by H5 and H7 viruses. Antigenic shift: genetic reassortment with human influenza virus to enable person-person transmission. First cases of avian influenza in humans in HK 1997a

Clonal amplification

in their first intermediate host leads to average 4-fold expansion of numbers of individuals at next life stage. Trophic transmission to definitive host results in no numerical change. (getting eaten)

Downsides of complex life cycle

increased chances of not finding host and dying Evidence that life cycle truncation has evolved independently many times

Complex life cycle parasites

indirect life cycle parasites parasites that sequentially infect different hosts over lifecycle curse NOT multi-host NOT same as vector-transmitted parasites/pathogens

virions

individual particles have core and capsid may or may not be coated with membrane from host cell may or may not be accompanied by cell lysis

Susceptible

individual who will acquire infections if exposed to pathogen

Leucochloridium paradoxum

infected snails will position themselves in more exposed/illuminated places and situated higher in vegetation hopes to get eaten by birds

I

infected/infectious

nosocomial

infections occuring primarily in hospitals

Paragordius tricuspidatus

infects wasps, makes them fall in water and worms come out

Lytic viral particles

infects, multiplies and bursts bacterial cell (lysis) producing more virus

Zika

Aedes aegypti, A. Albopictus birth defects sexual transmission Flaviviridae Americas/Brazil prevention: life immunity, hard to limit transmission when don't know infectious mosquito removal- habitat removal/spraying (hard to get information for spraying)

Messina et al.

Alt. model -brazilian data -accounts for change in virus since discovery -may not represent a "typical" year florida/lower USA yes bees at risk.

parasitoids

An organism that lays eggs inside other organisms. always harmful

Carlson et al.

Conservative model: -used african data -assumed zika hasn't changed -limited by small data mostly in tip of Florida

Complex life cycle parasite diseases:

Dracunculiasis (guinea worm disease) caused by Dracunculus medinensis Schistosomias caused by digenetic blood trematodes "swimmer's itch" caused by Trichobilharzia regenti

Transplacental

HIV at low percentage, german measels (rubella)

Perinatal

HIV at substantial, gonorrhea, seed borne viruses and fungi in plants

postnatal

HIV through breast feeding seeds under parental trees get soil borne pathogens from parents

Humoral theory

Hippocrates- natural causes Humoral theory: Elemental ideas (Aristotle) disease caused by disequilibria and imbalances key people weren't medical scientists imbalances caused by stars/weather/behavior/decoposition. disease contagious but mechanism of spread was by "smells and miasmas" STILL influences us. words still reflect theory- cold, ulcers.

Cucumber mosaic virus, CMV

Host: cucumber and wide range of wild/cultivated plants particulate virus- needs 3 virions

Holding types

IP- infected premise CP- contiguous premise DC- dangerous contact

fomites

objects on which diseases are transmitted (objects are vector)

Protozoa

one-celled organisms that are more complex than bacteria Ex: Giardia Trypanosomes: sleeping sickness, chagas, coffee phloem necrosis, dourine horse STD

Waterborne transmission

oral-fecal

OID

ordinary infectious disease aerial, soil, waterborne, non sexual contact diseases number of contacts increase with crowding Density-dependent or "mass action" transmission Ex: hookworm abundance or microsporidians in Daphnia

Endemic

parasite consistently present, no large or sudden fluctuations in prevalence

Male to offspring transmission

pathogens may adhere to sperm, enter sperm, or carried in seminal fluid. Problem in human infertility and cattle insemination Chlamydia adheres to sperm pathogens adhere to pollen grains

FMD Keeling et al

peak in late March, long tail after May. rapidity in culling would have been ideal. 1. We need robust set of models to deal with range of human/livestock diseases 2. Models should be in place before disease invades 3. Need suite of powerful statistical techniques to rapidly ascertain parameter values 4. Excellent lines of communication between vets, scientific advisors, policy makers 5. Rapidity key to success: in terms of detection, decisions and control farm as unit environmental niche modeling stochasity heterogeneities large farms, more infectious prompt culling

𝛿

per contact probability of infection Probability of gettind disease given contact was made

c

per individual contact rate number of contacts per individual per unit time

Naled

pesticide for mosquito highly effective applied in small amounts rapidly degenerates kills bees on exposure

Reservoir hosts

place for storage alternate or passive host or carrier that harbors infectious organism without harm to itself and can serve as source of infection for other individuals or species mainly refers to among-species transmission so depends on reference host species

Ring vaccination or culling

pre-emptive: prevent new infections within prescribed area -local vacc -killing/culling individuals locally Ex. citrus canker, FMD in england Rabies switzerlandn

Isolation

prevent dispersal of infectious individuals -infected needs to be identified rapidly prevent dispersal of whole population -if diseased individuals are not easily recognized

Quarantine

prevent immigration of infected individuals by keeping them through the incubation period

Transformation

process in which one strain of bacteria is changed by a gene or genes from another strain of bacteria direct uptake of exogenous DNA

Strand switching

produces recombinant RNA molecule from reverse transcriptase

DISEASE is not the causal agent

product AIDS: disease HIV: pathogen

infectious disease

product of interaction between host and pathogen/parasite.

Prevalence

proportion of hosts infected or expressing disease (#infected/ total N)

βxI

rate at which each susceptible individual becomes infected

γ

recovery rate probability a diseased individual recovers in a unit of time

Herd immunity

reduced probability of infection due to the presence of a high proportion of individuals in the population with immunity.

Immunity

resistance to infection incurred through exposure to previous infection

Influenza Virus

segmented -ss RNA virus, enveloped host: most vertebrates bind through hemagglutinin synth viral proteins secreted through neuraminidase Exit: membrane rupture multiple infection recombination- highly pathogenic avian can recombine with human making a highly pathogenic human strain

Disease

semi-permanent bodily condition that reduces an individual's well-being biological organism: any semi-permanent bodily condition that has a negative effect on an individual's fitness product of interaction between host and parasite

Segmented

several RNA molecules in one virion

Particulate

several virions needed for infection

Particulate virus

several virions needed for successful infection

Direct contact transmission

sexual vs non sexual

STD

sexually transmitted disease contacts relatively independent of density, tranmission depends on fraction of individuals diseased "frequency-dependent transmission"

HIV

sexually transmitted, attacks T-helper cells of immune system CD4 or CCR5, destruction of immune system, death by opportunistic infections (AIDS) Control issues: 1. Delayed disease onset, undetectable without testing 2. High genetic variability 3. Integrated into host genome and can remain cryptic 4. Sexually transmitted

Bassi

silkword disease caused by fungal infection. germs- organisms-disease

Dynamics conclusion

simple models can capture a range of disease dynamics: endemic, outbreak, sequential epidemics SIR model with demography (births, deaths) and forcing is enough to explain the different dynamics of childhood diseases

Microparasites

small- protozoa, viruses, bacteria, fungi rapid multiplication in host short generation time usually leads to crisis in host...

Critical community size

smallest population of susceptible hosts below which disease goes extinct, and above which disease persists mealses and whooping cough persist in large cities but "Fade out" in smaller towns

Nt

some parasites have critical population size for establishment

Benedict Prevost

spores could produce fungus

Basidiomycetes

spores produced externally on basidium

Ascomycetes

spores produced internally in ascus

Norovirus

ssRNA, non enveloped gastroenteritis Cyclical dynamics: common driven by seasonality, transmission increases with weather conditions pulses of susceptibles Hypothesis: Winter vomiting: moisture/temperature/humidity, how long viruses can stay in airor can persist longer in water sources

Koskella et al paper

study Potamopyrgus antipodarum (frewhater new zealand snail, high clonal diversity) Microphallus sp. (sterilizing trematode with complex life cycle NO direct horizontal transmission-good for lab. Asexual reproduction in snails and sexual in the ducks that eat snail (here it's mice) Coevolution drive changes in host population composition Recycled: common clone frequency decrease compared to control parasites are targeting common clone. Cross-inoculated with parasties from field population and those from experimental populations. Prevalence stays same because each running as fast as it can to escape it. Prevalence doesn't change but no forward progress, genetically changes rapidly. Red Queen hypothesis

Epidemic

sudden increase in prevalence or intensity (sharp rise in new cases): parasites characterized by periodic outbreaks

Linnaeus

suggested diseases caused by living organisms- Systema Naturae "Chaos"

N

total population size S+I

Conjugation

transfer of bacterial DNA via conjugative plasmid

iatrogenic

transmission because of medical attendants ( humans are vectors)

Disease fails to spread if:

transmission low few susceptible hosts high virulence rapid host recovery

Horizontal transmission

transmitting within one generation between unrelated individuals.

Influenza Pandemic 1918-1919

unusually severe and deadly strain. 50-100m deaths worldwide. more killed than WWI.

Retrovirus

uses own reverse transcriptase enzyme to produce DNA from RNA genome new DNA incorporated into host cell genome by integrase enzyme Host cell treats viral DNA as part of own genome, translating and transcribing viral genes along with cell's own genes

Pathogen

usually thought of as smaller than parasites pathogen

Smallpox

variola virus new world bioterrorism (Aztecs, Delaware) eliminated worldwide through vaccination since 1979 but cultures exist in laboratories

Cytoplasmic vertical transmission

vector borne diseases in the vector (west nile, lyme )

VTD

vector transmitted diseases Relation to density complex: 1. Contacts increase 2. Contacts stay constant- vector search compensates for changes in host density 3. Vectors numbers per host declines and so do contacts "dilution effect" Pollinator transmitted disease: anther smut

Vector transmission

vectors may be passive or biological

Excision

virus "jumps out" and lyses cell

Lysogenic

virus in this stage is called prophage replicates with bacterial host integrated in host genome

spatial modelling

capture local spread of disease

Stochastic

capture random nature of transmission

Life cycle truncation

-rare or missing host hypothesis -environmental instability hypothesis (inconsistency of hosts over time) -developmental time hypothesis (can't wait) -cannibalism hypothesis (adults eat babies of same species) -latitudinal gradient hypothesis (expanded range)

Transmission conclusions

-vertical or horizontal -vertical not efficient, may lead to modifications of sex ratio - horizontal transmission may be expected to be different between ordinary, sexual and vector transmitted -frequency dependence and density dependence transmission

Viral replication

1. Adsorption 2. Entry 3. Uncoating 4. Transcription/mRNA production 5.Synthesis of virus components 6. Virion assembly 7. Release (liberation stage

Endogenous origin of lethal disease Inheritance???

1) late onset of disease (post-reproduction) 2) Recessive allel encoding misfolding Selection is less efficient, esp if there's a selective advantage of allele in early life 3) Heterozygote advantage, Homozygous is deleterious but heterozygous is helpful

Fungal disease

Ascomycetes: Trichopyhton (ring worm) , Entomophaga (summit disease of insects) Basidiomycetes: Puccinia (wheat rust) Cryptococcus (meningitis/pneumonia in humans), Microbotryum (anther smut

Recombination

DNA viruses can undergo recombination using cell's enzymes and generates variation if multiple infections within same host RNA viruses can't use cell's enzymes to recombine sporadic cases of recombination reported in some -ssRNA

Mutation/Errors during replication

DNA viruses: DNA polymerase has error repair. lower mutation rate. 1 x 10-9 RNA viruses: replicate either by RNA replicase or by generating DNA by reverse transcriptase. No error repair. Mutation rate: 1x 10-4 bp

Fracostoro

De Contagione first accurate description of contagion/infection.

Controlling epidemic spread

Isolation quarantine Ring vaccination Culling

Cholera

LARGE complex genome wide range of plasmids and integraded phages Virulent: CTXf intense diarrhea, loss of body fluids, loss of electrolytes 6 vibrio species associated with cholera-like symptoms V. cholerae is very variable ca.180 serotypes -transmitted mainly through water -incubation period 1-3 days -bacteria adhere to intestinal wall -secretes toxin stimulating hyperproduction of water and salt -diarrhea: water loss of 10-15 liters during infection antibiotic resistant plasmid- up to 7 on single plamid. Not easily treatable with antibiotics

Germ theory accepted

Pasteur- microorganisms responsible for fermentation MIcro-organisms not spontaneously generated but from reproduction of pre-existing micro organisms Microbes responsible for specific diseases

John Snow

Mapped the occurrence of cholera in London, water source

Enveloped vs. non-enveloped viruses

Membrane from host cell coating - enveloped viruses need more intimate contact in order to infect a host cell, but they are able to change their outside appearance more easily without causing problems for the virus itself allowing it to evade the immune surveillance - non-enveloped viruses are sturdies and can survive longer outside the host, so they can invade easier, but they are limited in their ability to change outside appearance and thus are more recognizable by immune system

Anther-Smut disease

Microbotryum spores carried from flower to flower by pollinators Host: white campion Smutted flowers- XY and have stamens. Diseased females develop stamen from normally XX but get stamens for more infection

Hemagglutinin

One of the enzymes found on the surface of the Influenza virus. It is responsible for binding the virus to the cell that is being infected.

capsid

Outer protein coat of a virus

Gram negative

Red stain, many pathogenic stains in phylum Proteobacteria, no peptidogylcan cell wall constituents

Syphilis

Small genome, plasmid like no known conjugation/sex in spirochaetes rare bacteriophage multi-gene family. Sensitive to penicillin sexually transmitted, can't be cultured in vitro lesions- local allergic hypersensitivity rxns tertiary stage effects largely result of body rxns to pathogen dementia

Simple microparasite model

SIR. useful for translating individual-level events to population-level processes Epidemilogists: measure and model disease changes over time and space

Human evidence of contagion

Semmelweis- childhood fever can be prevented by physicians washing hands Snow- cholera waterborn Lister- antiseptics

Same agent can cause different diseases

Varicella-Zoster Virus= Human Herpes Virus 3; Prions

Etiology

cause of disease

Damped oscillations

births/deaths leads to endemic state

Why do complex life cycle parasites exist?

break out of growth/reproduction trade off

Measles

can e explained by simple mechanisms 1. SIR individuals 2. Seasonal transmission

Crown gall

cancerous like disease of plants, infects wide range. Agrobacterium tumefasciens Inserts piece of Tumor inducing plasmid region into plant cell Cell produces opalines (amino-acid like) that only bacterium can metabolize.

Trophic transmission

cannibalism or feeding on intermediate hosts

correlative vs mechanistic

where do we find species? where else is similar to where we find it? how does its physiology work? where would we expect it?

Soil borne transmission

with or without long lived resting stages