anth final

infectious disease

communicable disease

chronic disease

non communicable disease

casual agent

microorganisms that use hosts resources to reproduce, resulting in an immune response or physiological disruption

host

organism that is the target of an infecting action of a specific infectious agent
-Most microorganisms don't cause disease (ex: gut bacteria) →those that do are called pathogens (germs)

6 major groups of pathogens that affect humans

viruses, bacteria, protozoa, fungi, helminths, prions
-variation in exposure and susceptibility (ask questions about pop density, occupation, individual experiences, immune compromised, socioeconomic status, resources)

Death and major infectious diseases

many dying in infancy, not making it to old age
-differences due to public health
-global morality: 25% of deaths

Who is most affected by infectious disease

-younger people →don't have same level of immune development, don't have antibodies to remember for defense against disease , weaning when no longer antibodies from breastfeeding
-old people-immune system ages

high income deaths

heart disease and old age

low income deaths

Highest death in respiratory infection (majority communicable disease)
Less access to care

US deaths

Highest death from heart disease
Those that die from pneumonia/flu are most exposed
-people die of different things at different ages in different places

epidemic curve

Epidemic-increase in incidence of infection in a population at a specific time
“Flattening the curve”

why do we still have infectious disease

-globalization (new interactions)
Conflicts between pathogens and host

pathogens reproduce more quickly than hosts thus evolve faster

Some may be more or less deadly than others depending on on host/environment
Ex: antibiotic resistance

novel environments-new diseases

Ex: zoonotic diseases (zoonosis/zoonoses)-infectious diseases caused by pathogens that spread between animals (usually vertebrates) and humans

changes in virulence

Virulence:severity of disease brought on by pathogen

Robert Kock (1843-1910)-Germ theory of disease

Anthrax exposure always causes specific set of symptoms
-Pathogen must always be found in person with disease
-Must be isolated and grown in pure culture
-Culture should cause disease when introduced into a healthy individual
-Can be isolated from second individual and grown into culture

viruses

DNA or RNA surrounded by protein
Obligate parasites-cant exist without host
Mimic host cell proteins in order to bind with receptors on host cells
Host is a carrier of the virus

bacteria

-Single celled prokaryotic organisms (no nucleus)
-Reproduce by duplicating their DNA and dividing
-Over 400 identified genera;40 known to cause disease in humans
-10x the number of bacterial cells as humans
-Healthy gut bacteria: 5400 species; 3.3 lbs
-Variability
-->Survivability outside host, capsules, flagella, pili, spores, aerobic and anaerobic, virus-like

protozoa

-Single celled eukaryotic organisms (has nucleus)
-Able to evade host's defenses
-Infections are difficult to treat and symptoms may be chronic because their cellular structures are similar to host mammal
Variability
-->Growth and reproduction stages in different organs, intermediate species insect vectors, intracellular, extracellular
Vector-any agent which carries/transmits an infectious pathogen into another living organism

fungi

Eukaryotic organisms (have cell nucleus)
70,000 species, though only a few are harmful to humans
Low virulence, unless host is immunocompromised
Variability
Yeasts, spores

helminths

Multicellular organisms
3 diseases in humans
-->Roundworms, tapeworms, flukes
50% world's population is infected today
historically -most humans infected
Difficult to treat-->Tough outer coatings
Transmission
-->Intermediate hosts and water, soil, food

prions

Infectious proteins
Unclear how to replicate : no RNA or DNA
Transmission spongiform encephalopathies
Human
-->Creutzfeldt-Jakob disease
-->KURU
Non human
-->Bovine spongiform encephalopathy
-->Scrapie
Transmission
-->Exposure to brain tissue and spinal cord from infected individuals
Untreatable and fatal

direct transmission

Epithelial cells-exploitation of most permeable parts of hosts body
Skin, respiratory tract, respiratory and digestive tract
EX: breast tissue

droplet transmission

Microbes are spread in mucus droplets that travel short distances (>1 meter)
Coughing sneezing
EX: TB spread

vector borne transmission

Intermediate species or material that can take a pathogen from one hose to another
Insects animals(zoonosis) food water, fecal oral, utensils, needles

Paul Ewald

-evolution of virulence

Factors favoring selection for higher virulence

Intermediary disease vectors
Transmission does not require host to be mobile

Factors favoring selection for low virulence

Casual human-to-human transmission
Transmission required host to be mobile
-Domesticating disease requires disrupting modes of transmission, which will create conditions for the pathogen to evolve to mildness

first line of defense

Skin
Mucous membrane
-->Cilia
-->Coughing and sneezing
-->Secretions of the skin and mucous membranes
------->Low ph of stomach acid

symptoms

Vomiting and diarrhea;coughing sneezing
Fever
Iron sequestering
To treat or not to treat
Individual comfort vs evolutionary adaptation vs public health

(video)resistance is a

man made problem, accelerated evolutionary process,most dangerous bacteria will not be treatable
-more or less harm depending on transmission
Close contact-mild
insects/food/water-severe

example of severe resistance

cholera in SA, extreme diarrhea from waste in water-became more toxic
Still getting infections but so mild-need to change to domestic bacteria

immune system overview

1)recognize pathogen 2)destroy pathogen 3)Communication between cells of immune system to coordinate 1 and 2

identify “self” vs “non-self”

Problems with “self/non-self dichotomy”
-->Many cells in the body are non-self and not pathogenic
-->Many cells in the body are self and are pathogenic

Criterion of continuity

immune system recognizes strong discontinuities in molecular pattern, whether exogenous or endogenous origin

innate

Older, more multicellular organisms
Responds quickly (minutes, hours)
Broad recognition of pathogens
-->Recognizes generalized molecular patterns of pathogens
Destroys pathogens
Principal cells; phagocytes (ex: macrophage)
Phagocytes recognize molecular patterns that are common across pathogens and which cannot be modified by pathogens to avoid detection (ex: sugars in cell walls)
No memory

adaptive

Vertebrates only
Responds slowly (days)
High specificity of recognition of pathogens
Principal cells;lymphocytes(white blood cells; T cells, B cells)
Lymphocytes recognize specific epitopes in pathogens
Systems can remember 100 million epitopes
-Evolution of adaptive is advantage because vertebrates have longer lives so more encounters with disease so memory allows better protection
Which cells require an immunological response and which do not

Epitopes

sections of pathogen proteins that are identifiable as non self

Antigen

large molecule or cell with epitopes on its surface

lymphocytes

b cells
Bone marrow
Monitor extracellular spaces (blood and other fluids)
part of immune system are reproducing to get rid of pathogen-stays with you for a few days
replicate in response to pathogen
Memory cells-remain after infection is resolved
More rapid response if pathogen returns→immunity

t cells

Thymus
Monitor intracellular infection
Specificity-each lymphocyte recognizes a single epitope
Proliferation-swelling of lymph nodes as lymphocytes respond to pathogen

antigen

receptor proteins on b cells surface

antibodies

immunoglobulins - IgA, IgD, IgE, IgG, IgM

b cell recognizes antigen-->

Proliferation of antibody-Y shaped
Antibody binds to antigen and “labels” pathogen for destruction by other cells of the innate system
-Innate and adaptive systems help the body protect itself from harmful pathogens(antigens)
-Allergic immune response when the immune system responds to non threatening antigens (allergens)

Why are atopic disease rates increasing over time and higher among industrialized populations?

Hygiene and helminth/ “old friends” hypothesis

Hygiene and helminth/ “old friends” hypothesis

Improvements to hygiene result in fewer childhood diseases, altering development of immune system
Exposure to pathogens that trigger TH1 responses→prevents Th2 responses from overreacting
No exposure to Th1 stimuli→Th2 responses are left unchecked and atopic reactions can be triggered by harmless antigens

evidence for Hygiene and helminth hypothesis

Japanese children exposed to tb found that compared to children negative to tb→ higher Th1 levels and lower lgE and lower rates of allergies
Children with older siblings have lower incidence of allergies/asthma than only and eldest children
More older siblings have lower rates than children with fewer older siblings
Day care have lower rates than children at home
Living in farms lower rates of atopy than children in urban areas (wealthy countries only)

Th1

intracellular

Th2

extracellular pathogen

Lack of exposure presents diff environment

Th1 become overactive because no balance

Pathogen recognition and destruction: innate immune system

1st immune response after pathogen has penetrated body’s barrier defense
Macrophages have cell surface receptors that have broad recognition for molecular patterns of pathogens
Macrophages engulf pathogens and destroy them through phagocytosis

B cells floating in body or other fluids

directly recognize extracellular pathogens via antibodies on the b cell surface
Each b cell makes one kind of antibody that matches only one antigen
Unique binding to only one antigen

Proliferation of antibodies (recognize and make more to get rid of it)

Antibodies can disable pathogen or labeling of pathogen for destruction by phagocytes (innate system)
Production of memory b cells to respond quickly with antibody if same pathogen encountered again

T Cells recognize intracellular pathogens via antigen presenting cells that contain major histocompatibility complex (MHC) molecules

MHC molecules move pieces of pathogenic proteins out of the surface of the cell where t cells often recognize them
T cells with matching receptors bind to MHC + pathogenic protein and depending on the pathogen

Cytotoxic t cells

destroy the pathogen containing cell or helper t cells (Th1 or Th2) are produced which secrete cytokines to activate
Th1→Macrophages (active cell of innate)
Th2→B cells

allergies

immune response to foreign substances in the environment that are harmless to most people (allergens)

evolutionary reason for allergies-increasing incidence

Variation in suffering due to hygiene hypothesis
Relationship between improvement in hygiene and decreased childhood diseases alters immune system
Infancy (bias to more Th2 cellular response-more active)

allergens

Dander, mold, pollen, insect bites/stings, drugs, foods (peanuts, shellfish, milk, eggs)
Reactions:mild (coughing sneezing congestion wheezing vomiting diarrhea)
Severe: (anaphylaxis)

asthma

a chronic disease of the branches of the windpipe (bronchial tubes) characterized by recurrent attacks of breathlessness and wheezing
During attack, lining of tubes swell, causing airways to narrow and reducing flow of air into and out of the lungs

asthma triggers

indoor allergens (house dust, mites in bedding, pollution and pet dander)
Outdoor allergens (pollen and molds)
Tobacco smoke, chemical irritants in workplace, air pollution

asthma stats

-estimates 235 people suffer from asthma
-most common NCD among children
-most deaths in low/lower middle income countries
-Under diagnosed and under treated

Equality

give same tools and expect same outcome

Equity

people underserved MORE resources
→universal healthcare

Tuberculosis spread

-Highly contagious infectious disease that typically targets lungs and respiratory system
Mainly spread through droplet transmission (cough sneeze)
Sit and wait→can survive on surfaces for months on surfaces

active TB

systematic/contagious
Only 5-10% of those with pathogen will develop active TB

latent TB

asymptomatic/not contagious
Most people will stay in dormant phase

TB stats

About ¼ of world's population is infected
10 million new cases→1.5 million people died
One of top 10 ten causes deaths around the world
Expected to cost world 15-20 trillion dollars

Targets most vulnerable members of society

lower socioeconomic status, co immunocompromising conditions

-how does the body protect itself from harmful pathogens(antigens)

-innate and adaptive systems

-what happens when the immune system responds to non threatening antigens (allergens)

-allergic immune response

-why are atopic disease rates increasing over time and higher among industrial populations

-hygiene and helminth /old friends hypothesis

innate system

Older, most multicellular organisms
Responds quickly (minutes, hours)
Principal cells (phagocytes ex macrophage)
Specificity of pathogen recognition-broad recognition of pathogens
Memory-no

adaptive system

Vertebrates only
Responds slowly (days)
Principal cells (lymphocytes ex white blood cells, T cells, B cells)
Specificity of pathogen recognition-highly specific; recognizes epitopes
B cells (antibodies)
T cells (T cell receptor + MHC)
Proliferation-swelling of lymph nodes respond and replicate
Memory-yes

macrophages

have cell surface receptors that have broad recognition for molecular patterns of pathogens→engulf pathogens and destroy them through phagocytosis

b cells

Made in bone marrow (monitor extracellular spaces ex blood and other fluids)
Recognize extracellular pathogens via antibodies on the b cell surface
-each b cell has a unique antigen binding site
Proliferation-antibodies can disable pathogen or “label ” pathogen for destruction by phagocytes (innate)
Production of memory B cells to respond quickly with antibody if same pathogen is encountered again

t cells

Made in thymus-monitor intracellular function
Recognize intracellular pathogens via antigen presenting cells that contain Major histocompatibility complex (MHC) molecules
MHC molecules move pieces of pathogenic proteins out to surface of the cell where T cells can recognize them
T cells with matching receptors bind to MHC + pathogenic protein and depending on pathogen:
Cytotoxis t cells destroy pathogen containing cell or
Helper t cells (TH1 or TH2) are produced which secrete cytokines to activate
-macrophages (TH1)
-B cells (TH2)

vaccination

administration of antigenic material to stimulate and individuals immune system to develop adaptive immunity to a pathogen
-Through natural selection, made less virulent

Passive immunity

uses pre-formed antibodies from other individuals
-through mother in utero or breastfeeding

active immunity

provokes immune system to generate memory cells which provide long term protection against pathogens
-Live attenuated (Ex MMt) or inactive vaccines (Ex flu)
-Vaccines made from parts of pathogens (Ex Hep B)
-mRNA (Ex covid 19)

b cell response to vaccines

B cell detects antigen on antibody cell surface of the vaccine material (ex attenuated measles virus)
B cells multiply creating clones
B cells become plasma cells that produce antibodies or memory b cells
Plasma b cells secrete large amounts of antibodies and tag the vaccine material for destruction by other cells of the immune system
Primary response takes place over several days
Exposure to pathogen vaccinated against, memory b cells quickly recognize the antigen
Memory b cells rapidly multiply
Memory b cells develop into plasma and produce a large amount of antibodies
Antibodies tag the pathogen for destruction by other cells of the immune system

measles stats

Prior to vaccines, 2.3 million deaths annually →2019 over 7 million globally infected causing 100,000 deaths
Young children and malnourished most at risk

measles transmission

one of the most contagious diseases, spread through direct contact, droplet transmission and can live on live surfaces for up to 2 hours

measles symptoms

high fever, runny nose, cough watery eyes, white spots on inside cheeks (Koplik spots) and rash

measles Morbidity and Mortality

complications include blindness, encephalitis, severe diarrhea ear infections and pneumonia

herd immunity

Indirect protection from large infectious diseases that occur when a large percentage of population becomes immune to an infection, therefore providing a measure of protection for individuals who are not immune
Protects those who cannot receive vaccinations (infants, immunocompromised, allergic)

human stress is unique

threat to survival (rarer) and social situations (common)
Timing-immediate, anticipated and recalled threats/importance of perception
Frequency-chronic

animal stressors

threat to survival or reproduction
Predators, competition, temp extremes, food shortages
Timing-immediate

Did hunter gatherer ancestors live with as much stress as we do now?

Mismatch between and ancestral and contemporary environments
Kin based social groups vs social stratification

defining poverty

should poverty be estimated with a cut off line that reflects a level below which people are in some sense ‘absolutely impoverished’ or level that reflects minimum standards of living common to that country in particular

absolute poverty

based on subsistence, minimum standard needed to live
Rowntree-identified ‘poverty line’ on the basis of minimum needs

relative poverty

based on a comparison of poor people with others in society
Townsend- ’poverty is a dynamic, not a static concept… our general theory then should be that individuals and families whose resources over time fall seriously short of the resources commanded by the average person or family in the community in which they live…are in poverty’
Orshansky- ‘poverty, like beauty, lies in the eyes of the beholder’

SES(socioeconomic status)

a composite measure that includes income, occupation, education and housing conditions

“SES gradient”

every step downward in SES correlates in poorer health
Risk of some diseases vary 10 fold from highest vs lowest SES category
5-10 year mortality difference between highest and lowest SES category in some countries

Health → SES

Maybe chronic illness→missed educational and employment opportunities→lowered SES

SES → Health(most evidence)

Ex: postmortem studies on adrenal glands
Blood pressure studies in “low stress” groups

wealthier countries have higher life expectancy

able to meet basic needs
Inequality triggers stress related diseases in wealthy countries still

Stress responses are more likely to be activated when individuals

Feel as if they have minimal control over stressor
Have no predictive information about duration and intensity of stressor
Have few outlets for the frustration caused by a stressor
Interpret stressor as evidence of circumstances worsening
Lack social support for duress caused by stressor

Whitehall studies

Studies of health in British civil service workers
Stratified by rank-hierarchical
Universal health care
Significant differences in risks of many diseases and mortality
Findings replicated in other countries with socialized medicine
Findings still hold when corrected for health-seeking behaviors (access to healthcare and poor behavioral drivers like low exercise,smoking alcohol use)
risk factors (smoking, exercise, etc) accounted for >½ of the effect

Lower SES increases risk factors and decreases protective factors

campaigns have good intention but create blame and solutions rely on individual behavior changes