ANTH 323 Final Study Guide PDF

AUGUST 30TH STRESS “Health is a state of complete physical, mental and social well-being and not merely the absence of infirmity” – WHO General stress response: ➔ Activation of sympathetic nervous system (environmental, physiological, psychological) ➔ Release of stress hormon...

AUGUST 30TH STRESS “Health is a state of complete physical, mental and social well-being and not merely the absence of infirmity” – WHO General stress response: ➔ Activation of sympathetic nervous system (environmental, physiological, psychological) ➔ Release of stress hormones: cortisol, adrenaline, deviation from homeostasis ‘resting state’ Bioarcheologists study long-term, chronic stress understood as illness. Stress as a proxy for health: Skeletal evidence of biological disruption from stress responses is one way to pinpoint health PALEOEPIDEMIOLOGICAL STRESS MODEL SEPTEMBER 11TH BIOARCHAEOLOGY AND PALEOPATHOLOGY Analysis of human skeletal remains also known as osteoarcheology Methods: - Macroscopic observation: visual analysis of skeletons to develop biological profile - Microscopic: histology, bone tissue, parasitology - Biological/geological/chemical analysis: ancient DNA sequencing, stable isotope analysis Skeletal analysis: 1) Describe physical remains: MNI (minimum number of individuals1) and biological profile (age, sex, stature) 2) Integrate cultural context ➔ Age: Juveniles 1 Because of bone fragments, inventory. Might have more skeleton than one  - Epiphyseal fusion2 - Dental development3 Adults - Pubic symphysis4 - Auricular surface of ilium5 - Cranial suture closure6 - Sternal rib ends7 - Degenerative changes (osteoarthritis) 8 - Dental wear9 ➔ Sex: Relies on sexual dimorphism: expression of phenotypic differences between males and females of the same species (most apparent after puberty so it’s hard to do this for juveniles) Degree of dimorphism can vary by population: differences are averages, not absolute – sex may be undetermined (should not compare if no similar environment or genetic background) Estimation methods: Post cranial: - Pelvis10 Cranial: - Cranium11 - Mandible12 2 Growth plates not yet fused together/cartilage. There are different ages for all bone fusions so it is easier to identify a juvenile because some bones have not yet fused. 3 In-coming teeth – babies won’t have showing teeth yet. 4 Two sides of pelvic bone, connected by cartilage. How much micro-trauma and how worn down or changed can indicate age of adult. 5 Where sacrum meets pelvis in cartilage 6 Soft spot on baby’s head – suture lines are healed over. The more closed or obstructed, the older the skeleton is 7 Sternum and rib connection, rib ends change shape 8 No scale for this. Like pubic symphysis, but people mostly develop this over time or there is a pre- existing condition/trauma but no concrete range 9 Teeth wear down at the crown 10 Childbirth: evolutionary constraint on pelvis so it’s more cup-chapes, hole is bigger, angle at the bottom is more open 11 Males: heavier glabella, square jaw, not as accurate as pelvis because cranium can also be tied to environment 12 Square jaw  ➔ Stature: Factors impacting growth: - Genetics - Nutrition - Stress - Health Key methods: - Anatomical method13 - Mathematical method 14 Paleopathology Study of ancient disease and illness – individual data focused Conditions that disrupt typical biological function: traumatic injuries and infectious diseases ➔ Differential Diagnosis: Find evidence of disease and diagnose most likely disease. Differentiating abnormal bone morphology from natural variation Porosity and remodeling is normal at certain ages but not at later ages 15 Bone has limited response to trauma: form new bone or resorb existing bone to replce a missing one) Abnormal growth/formation, chronic not acute conditions, abnormal absence Methods - non-macroscopic: - Radiology - Ancient DNA - Paleo proteomics - Parasitology 13 Measure every bone that has to do with height. Most accurate method because it’s specific to the individual 14 Population-based calculations: compare one population’s reference data to one person. Most practical method because often we’re dealing with broken bone and not full ones 15 Just like epiphyses fusion Non-specific stress indicators: - Periosteal reaction (bone growth) 16 - Osteomyelitis (bone loss) 17 - Cribra obitalia and porotic hyperostosis (porosity) 18 Fractures Partial or complete discontinuity of a bone, described by rate and distribution mechanism (surface area or velocity) Dislocation: separation of two ends of the bone where they meet at joint Body modification: deliberate altering of the human anatomy or human physical appearance Types of mechanical stress: - Compression = pushing on the bone which causes negative elongation - Tension: pulling on the bone which causes positive elongation - Shear stress: forces that act on opposite sides of a body with the same magnitude but opposite direction Rate of force: - Blunt force (broad area/slow load) - Sharp force (force goes through the bone, narrow point of force (size of entry), more cut than broad cracks - High velocity (projectile) Timing: - Antemortem = before death, evidence of healing - Perimortem = around time of death, little to no evidence of healing - Postmortem = after death, evidence of change from burial environment Osteological Paradox: - Hidden heterogeneity in frailty: skeletal samples are made of individuals with unknown variation in individual fragility to stressors. Can be biological (stronger immune system) or cultural (exposure, nutrition) 16 Thin, protective layer like saran-wrap 17 Holes in bone 18 Roof of eye socket. Don’t always know why this is caused  - Selective mortality: we only see the people who died, biased representations of living populations - Demographic non-stationarity: cemetery assemblages can be derived from migratory populations or changes in fertility/mortality and this can affect the interpretation of age-at-death distributions, infant mortality rates. September 13th PALEO GENOMICS Characteristics of DNA: - Recumbent nuclear DNA - Mitochondrial DNA: passed from biological mother - Y DNA: passed only to males from father Role of DNA: gives instructions for bodily function, cellular repair and growth Ancient DNA characteristics: - Studied by paleo geneticists - Has existed outside of body for a while and is degraded. Retrieving ADNA: - Bone, teeth, mummified tissue - Belongings (chewing gum, pipe stems) - Environment (human feces, soil samples) Issues working with ADNA: - Contamination: DNA is mixed with other DNA from environment - Difficulty: sampling the DNA we are interested in Good conditions: - Permafrost: preserves cells - No fluctuating pH temperature and humidity - Stable wet environments (aerobic water environment) Bad conditions: - Highly acidic soils, high heat humidity, and water movement - Soft tissue, except in anaerobic conditions or mummified remains Characteristics of a lab: - Positive pressure - Cleanroom environment: HEPA air filtration - Unidirectional workflow - PPE - Decontamination: UV light to bleach and sterilization of equipment - Use of extraction negatives Steps to extraction: - Decontamination - Pulverization - Digestion - Extraction - Amplification - DNA sequencing Applications of analysis: Use of MtDNA: - Hypervariable/control region - Different individual to individual - More copies available than nDNA (before invention of PCR) - Limiting view of ancestry: it only shows mother line Use of YDNA: - Very little DNA, only looks at paternal ancestry Use of nDNA: - More complete genetic profile: both parents’ information - Allowed for realization that there are biases when studying one sex of the population at a time (just one lineage, not the other) - Looking at environmental adaptions to answer questions about evolution Metagenomics: Definition metagenomics: - Sequencing all genomic material in a sample  - Sequencing DNA from different species and organisms all together - Non-targeted sequencing: universal primers amplify all DNA September 18th PARASITOLOGY A parasite is an animal that gets nutrients by living on or in an organism of another species Complementary information given by parasite remains can help remedy the osteological paradox: parasites don’t always leave skeletal lesions, but the remains of the parasites can give us an idea of the symptoms. They can also help us identify what a non-specific lesion pattern is caused by. Three types: ectoparasites, helminths, protozoans Ectoparasites: - Live outside of host (mosquitos, ticks, fleas, lice, leeches) - Can be pathogen vectors – capable of transmitting pathogens to host - Can actually be seen, caught somewhere, but they leave pathogen traces around Helminths: - Parasite worm, typically live in gastro-intestinal tract (flatworm/flukes, tapeworm, roundworm)19 - Feed off nutrients from host, and use host to reproduce - Feces fertilizer, not properly washed meat, eggs, death Protozoans: - One-celled microscopic organisms - Live in intestines or blood or tissues - Spread through contaminated food or water, person-to-person contact or through the bite of a vector (malaria) ➔ Types of Protozoans: - Amoeba: form temporary false feet (pseudopods) to move. Entamoeba histolytic causes dysentery. 19 Trematode, cestode, nematodes  - Ciliates: use short, hair-like structures (flagella) to move and sense surroundings. Giardia intestinalis causes giardiasis; Trypanosoma brucei causes sleeping sickness. - Sporozoan: plasmodium causes malaria Paleoparasitology: Studies human and animal parasites and their host pathogen co-evolution through time Study parasitic organisms through the recovery of their preserved remains in archaeological, paleontological, palaeoecological, and medical contexts Ways of life: - Paleopathologies - Hygiene - Dietary/food habits - Waste management Identification: Macro-remains: observe the preserved parasite directly - parts of adult worm or larvae - typically, will degrade, preservation is rare because they are soft-bodied - Preservation requires extreme dry or cold, or humid environments, or conditions favoring mineralization - Natural, environmental mummification: cold, dry; hot, dry, salt saturated or water clogged anaerobic environments - Intentional/cultural mummification: cultural treatment that prevents decay - Also belongings (clothing, combs) and living space (natural sheds) of ectoparasites Dissemination and reproductive forms: how it moves between hosts, eggs - Eggs - Individual level: assess burial soil for parasite remains (control for environmental contamination) - Population level: assess water areas like latrines Biomolecules: aDNA of parasite recovered (and antigens, toxins) - Antigens: toxins that indices immune response in host - Possible to detect paleoantigens of parasitic protozoa - Specific: allows for direct identification of parasites - Ancient DNA: species that do not produce many eggs; different strains of same species to study evolution in relation to human population; confirm differential diagnosis of potential pathogen and disease Interdisciplinary: - Understand ecology of past environment - Geographic distribution of pathogen and/or vector - Human culture and behaviour (past and present), parasite exposure - Clinical knowledge of impact of parasite on host health September 20th AGRICULTURAL REVOLUTION Also referred to as Neolithic Revolution. Hunting/gathering/foraging subsistence to intensive farming during the Holocene - Increased food production - Storage of food surplus: reduced risks of bad harvest - Property ownership: where people are growing - Social hierarchy - Task specialization: specific crafts - Increased fertility and population size = big marker Shifts from diverse foraging diet to limited diet of complex carbs form crops - Nutritional deficiencies - Worsening dental health Sedentary population: - Close proximity to domestic animals (vectors of disease) - Poor sanitation = not being great with waste is risky - Increased interpersonal violence Foraging had a more diverse amount of food versus agriculture which will grow one thing specifically. Why agriculture? We don’t really know. Interacting variables: - Climate change in the Pleistocene and Holocene (cold and wet to warmer and dryer) - Evolution of animals/plants adapted to new landscapes - Local factors such as water availability and knowledge of local fauna and flora by human populations Dietary isotopes: - Previous research relied on remains of food which is impacted by preservation bias - Stable isotopes are evidence of the chemical composition of an individual’s diet - Allows us to see how much of different types of food individuals are eating - Terrestrial versus marine (C13); C3 vs C4 plants; trophic level of food consumed (N15). - Lets us look at specific individuals, quantify how diet was changing, adaptability of plants over time to be grown together Malnutrition: Shift to reliance on carbs resulted in a change in nutritional quality of diet - Maize: deficient in amino acids lysine, isoleucine, and tryptophan; causes low iron absorption; low bioavailability of vitamin B3 (niacin) - Millet and wheat: iron deficient - Rice: protein deficient; inhibits vitamin A Anemia: porotic hyperostosis (symptom of anemia) Deficiency of red blood cells, can have many causes - Causes expansion of blood-forming tissues to increase. Causes bone on surface of skull to become porous: porotic hyperostosis 20 - Elevated frequency of porotic hyperostosis in agricultural settings (reduced availability of dietary iron and intestinal parasites are more likely - Stress indicator, osteological markers: non-specific (symptom not disease) Growth disruption: - Reduced growth rates of children - Reduced adult height (but stature can rebound) - Can be caused by nutrition or stressors (increased infectious diseases/pathogens) Enamel defects: - Non-specific indicator stratigraphically - Linear enamel hypoplasia (defect from disruption of cells forming enamel) - Evidence of growth disruption during childhood, when enamel forms 20 Hard shell becomes squishy inside like a chocolate bar or whippet  - Non-specific = caused by a variety of diseases, nutritional disruption, or combo of stressors - Comparison of farmers and foragers shows increase in frequency of enamel defects, probably due to nutritional defects Dental microwear: - Analysis of microscopically visible wear on the chewing surfaces of teeth: pits and scratches evidence of consistency of food consumed (oatmeal/porridge = less damage; nuts/seeds = more damage) inclusion of particles introduced by food preparation (metal grind stones, mortar and pestle = food processing) - Aging adults: population level analysis, teeth ground down to a certain level Dental caries: Cavities or lesions resulting from tooth decay - Cariogenic bacteria adhere to tooth enamel - Metabolize sugars from carbs -> produce acid -> demineralize enamel - Infected tooth can affect surrounding tissue and bone, lead to tooth loss - Increased carb consumption (domesticated plants) = increased tooth decay and worse oral health - Rice is an exception, unsure if cariogenic Infectious disease: Populations increase in size and decrease in mortality = conditions of spreading and maintenance of infectious disease Adoption of agriculture in a sedentary environment = more diseases and can’t easily move away Syphilis, tuberculosis, leprosy September 25th ANIMAL DOMESTICATION Co-evolution process that arises from mutation. One species (domesticator) constructs an environment where they can manage the survival and reproduction of other species (domesticate. Allows domesticator to receive resources and/or services: - Protection - Labour - Pest management - Transport Humans control animal behaviour, nutrition, reproduction, range of movements, life span, etc. In turn, humans provide healthcare, protection against predators, starvation, uncontrolled population growth, negative climactic influences, etc. Animal populations tend to live longer domesticated because of our intervention. Expand to geographical regions and environments that are not accessible for wild forms Domestication process: unintentional long-term interactions 1) Tamed likely young animals 2) Assembling and managing of groups of tamed or controlled animals 3) Inter-breeding tames animals allowed selection of desirable traits 4) Expanded use of animals and integration into society Evidence: ➔ Animal demography at site (distribution, age sex, compared to wild = does it match hunting pattern or co-living pattern?) ➔ Morphological changes: physical structure (wild cattle versus domestic) = domestic animals are smaller and easier to control ➔ Genetic changes: invisible changes in temperament, coat colour, amount of wool produced = selective breeding pressures) ➔ Paleopathology: when animals were used differently than in the wild (lesions in bones)21 ➔ Evidence of care and social relationships: - Different biological stressors: LEH in response to stress because of closer proximity - Diet is more restricted = evidence of human interaction - Healthcare = veterinary help (fractures, broken teeth) and intentional comingled burials Osteoarthritis in domestication will show younger than wild because we ask to stress earlier than they 21 would in the wild = we change the type of activity + muscle marker Simultaneous domestication: Dogs and wolves in Europe ---- 33,000 – 18,000 Sheep and goats ---- 11,000 – 10, 500 Pig, cows, and ox ---- 8,000 Camels and guinea pigs ---- 3000 Horses and donkeys ---- 5,500 Zoonotic disease: zoonosis An infectious disease that has jumped from a non-human animal to humans: may spread back to animals or may evolve to become human-only infectious strains Zoonotic pathogens may be: bacterial, viral, parasitic Endemic: only in humans Enzootic: only in animals Can spread to humans through direct contact or through food, water, or environment - Animal and blood saliva - Respiratory droplets - Contaminated water - Animal waste - Animal products (meat, eggs) Animals serve as a vector and reservoir of many pathogens and parasites. Animals that have been domesticated for the longest period share more diseases with humans than other species with shorter domestication histories. Identifying zoonotic disease: Genomic evidence of pathogen co-evolution: pathogen can jump from animals → humans; mutations help identify strains across hosts Paleopathology: differential diagnosis of disease in animals and humans = shared disease in same place. Requires development of domestication to have the animal group Paleoparasitology: animals are vectors that spread parasites. Studying parasites can help us evidence zoonotic disease direct and indirect. Eggs can be found near human/animal body. Study environment: don’t know if disease did animals first then humans which is the geneal trajectory but sometimes there is back spill thus genetic evidence and strains makes it easier to see where disease originated from. September 27th GLOBALIZATION “Complex connectivity” – dense network of interactions and interdependencies interconnecting through long distance flow of goods, ideas, and individuals Identified by correlation between increased flow of products and people and evidence for the array of cultural changes associated with globalization. Health impacts: As populations grew, they developed cultural and technical innovations that allowed them to move more easily: domestication of animals and building roads/ships. When people moved, pathogens moved with them. Parasites on Silk Road: 2000-year-old personal hygiene sticks with cloth recovered from latrine Eggs of Chinese liver fluke, roundworm, whipworm, Talnia tapeworm. Closest region endemic for Chinese liver fluke is over 1000km away Ancient travelers migrated along Silk Road with parasites. Health impacts: Cultural change can impact quality of life and introduce a bunch of new stressors Increased human mobility that can introduce new pathogens in new populations: human conflict and death European colonization: South/North America, European contact and colonization caused severe decline in Indigenous populations: estimates between 75-95% of population Little Ice Age = indigenous deaths not agriculture so carbon back in environment? Local disease landscape: Paleopathological evidence that Indigenous populations already experienced disease local to their environments: - Treponematosis (syphilis, nonvenereal) - Tuberculosis - Poliomyelitis (polio) - Rabies Endemic diseases rarely occur in epidemic proportions (‘endemic’ = already circulating) Adapted to in environment so this didn’t kill them Novel pathogens: European pathogens were introduced at different places and times: - Influenza - Measles - Mumps - Smallpox Resulted in waves of epidemics, rather than single event because it came at different times and spots. Pathogen co-evolution: Most lethal pathogens were zoonotic: measles, mumps, tuberculosis = bovine reservoirs European populations had adapted immunity since animal domestication but in Americas, transition to farming evolved regionally; some populations alternating between hunter/gatherer and farming through time. Red Queen Hypothesis: Pathogens need their hosts to stay alive long enough for them to reproduce and spread to other hosts. Humans are trying to adapt to the pathogen to survive. Pathogen tries to be just virulent enough for the host to live long enough. Limited number of pre-contact epidemics: - Hemorrhage fever epidemic “cocoliztli” caused by salmonella enterica at the time of contact in Mexico - Parasite Trypanosoma cruzi (chagas disease)  - Tuberculosis infection from seals – limited human to animal pathogen reservoir Immunological naivety: No adaptive/acquired immunity to pathogens – only have innate generalized immune response Innate immunity: attacking foreign bodies “Virgin Soil Epidemics” – Alfred Cosby: everyone in a population gets simultaneous infection because of no circulating host/herd immunity. Acquired Immunity Active Passive Natural exposure Mom to baby Artificial vaccine Serum medicine Acquired immunity: Infectious disease is the strongest selective process affecting the evolution of the human genome Mycobacterium leprae (leprosy) was most prelevant in Europe around the 12th-14th centuries and declined in the 16th while simultaneously increasing in other regions. This may be explained by selective changes in host immunity to better combat M. leprae infection. Ancient DNA analysis of M. leprae have revealed low mutation rate without reduction in virulence compared to modern strains. Study both pathogen and how pathogen forced genome evolution. Leprosy pathogen didn’t change – host immunity changed. October 2nd INDUSTRIALIZATION Profound changes: - Mechanization of industry and farming - Rapid urbanization - Increased pollution - Population growth from fertility rates and migration - Technical, environmental social change The initial wave of poor health during 18th-19th centuries shifted to increased life expectancy and decreased levels of infectious disease in later 19th century linked to public health measures. More life than death: migration, increased population levels Rapid population growth: close quarters, more disease, poor health trends, but increase in life expectancy because of health measures taken Multiple industrial revolutions – for us: British (coal and textiles) First: 1700-1800s then introduction of gas, 1950s nuclear and technologies, renewable energies Happened multiple places around the same times: - South Africa and Australia = mining - France, Japan, US = coal November 11th DIET AND NUTRITION Nutrients and their functions: Provide energy, regulating chemical processes. Types of nutrients: Macronutrients: metabolically transformed into cellular energy. Quantified in calories, energy comes from breaking of chemical bonds - Carbs: source of energy for body. Essential for the function of the heart, kidneys, and nervous system. Structural aspects of the formation of cells. Soluble in water. Simple carbs: sucrose and glucose (basic unit of sugar); complex carbs: need to break down into simple sugars. Fiber: passes through digestive system undigested (can’t give us energy in the same way as complex carbs) - Lipids: composed of carbon, hydrogen, and oxygen. Form structural component of cell structure. Insoluble in water, provide storage of energy, help with protection of vital organs and isolates tissues to preserve body heat. Types: phospholipids, sterols, triglycerides. - Proteins: chains of amino acids. Gives access to enzymes, messenger proteins, antibodies, structure of bones, muscles, and cells, transport and storage. Not a great source of energy. Micronutrients: need in lesser amounts but still critical (needed for biological functions)  - Vitamins: need to get from plants and animals (cannot be synthesized); insoluble in water, regulate body processes like immune system, nervous system, bone mineralization, synthesis of red blood cells. - Minerals: inorganic crystal substances. Trace minerals: few mg (zinc, iron, iodine). Macro minerals: hundreds of mg (calcium, potassium). Functions: regulate body processes, necessary for cellular function and comprise body tissue. - Non-nutrients contained in food: harmful = toxins absorbed with food. Beneficial/neutral = preservatives, fiber, probiotics, antioxidants, dyes. Paleodietary analysis: How do we study diet in the past? - Stable isotopes: proportion of macronutrients (carbs and protein especially), not good for understanding micronutrients - Coprolites: macro remains of food, seeds, carbonized plant seeds, bone. - DNA: dietary biomolecules on dental calculus. Can help reveal what kind of nutrients were available - Paleopathology: skeletal lesions can be signs of deficiencies in micro or macronutrients. Metabolic bone disease: Condition which disrupts bone modelling and remodelling. Impacted by: - Age - Sex - Ancestry - Environment Effects of metabolic bone disease: - Normally, osteoclasts = removes the old bone; osteoblasts = builds new bone tissues. Dietary deficiencies impact these processed October 23rd MALNUTRITION October 25th MICROBIOME Characteristics: - Ecological community: commensal, symbiotic, and pathogenic organisms that share our body space. - Refers to the microbial life in the distal colon and oral region (surface of tongue, buccal mucosa, surface of teeth) - Important in digestion of fiber - The immense genetic diversity makes it an accessory genome/super organism - Halobiont: symbiosis between bacteria and human organisms Major functions: Digestion - In animals: use bacteria to digest fiber (cellulases) = symbiotic relationship (koala and eucalyptus) - In humans: hunter/gatherers and rural agriculturalists have more diverse microbiome than urban industrialists. Pathologies of the colon and obesity correlate with less microbial diversity - Feedback between host and bacteria: mice swapped microbiome = swapped phenotype Vitamin production and drug metabolism - Vitamin K primary source - Vitamin Bs (folate, biotin, etc.) - Metabolism of drugs: some are only absorbable if metabolized by bacteria like oral contraceptives Gut cellular health o First 3 years of life establishes good immunity (formation of gut microbiome) o Digestion of dietary fibre by gut bacteria creates fatty acid by-products like butyrate, which is a primary nutrient for colonic cells (if there is a butyrate deficiency, there is inflammation of the colon and colonic cell atrophy) o Inflammation and immune regulation issues play a role in periodontal disease, systemic inflammation leads to the growth of unhealthy communities of bacteria.  Defense against pathogens o Outcompeting pathogenic bacteria o Creating an environment that only favours themselves and blocks off pathogens (ex: lactobacillus in vaginal microbiome create a highly acidic environment that reduces pathogen std infection) Issues with unhealthy microbiome o Transient bacteremia: bacteria from oral microbiome linked to gingivitis periodontal disease led to cardiovascular infections-> produce plaque 2-Bioarcheological studies of the microbiome 2.1Ancient DNA studies: Focus on dentin and bones: difficulty of accessing the microbiome o Dry cold conditions: gut bacteria desiccate and produce coprolites which produces a long-term record of the gut microbiome o Dental plaque of the dental biome calcifies and persists after death in a mineralized state o Gut + oral = most diverse and important and diverse microbiomes in human body Recent advances o Coprolites: found in fossilised human faeces (frozen dry or desiccate dry caves) Source tracker using Bayesian probability to assign what proportion of the bacteria found in a sample comes from which source: ▪ rural human gut ▪ primate gut ▪ urban human gut ▪ oral microbiome Issues with the study of coprolites: ▪ Coprolite don’t preserve well enough at the bio molecular level to find them in faeces ▪ Hard to analyse fossilised gut contents because bacteria digest each other after the death of the host and proportions drastically change (fossilised faeces can often be just like compost) Solution to issues with coprolite analysis: ▪ looking for fossilisation contexts where all water is removed extremely quickly (ex: remains preserved in slat) à salt mines latrines analysis of bacterial populations in the modern gut vs the ancient gut: o similar in both ancient and modern gut microbiome: pseudomonas, clostridium, actinobacterium, coprococcus, blautia, roseburra, prevotella faecalibacterium o Microbial populations in ancient guts that diverge from the average modern microbiota of an adult: Bifidobacterium ▪ common in infant guts, metabolises milk, uncommon in populations that don’t consume milk. ▪ found in Austrian ancient sample but not in Iranian ancient sample (gives diet indication) Treponema: ▪ Present in both ancient samples (Australian and Iranian) ▪ otherwise usually found in termite gut, pigs gut, great apes, human hunter gatherers, early rural agriculturalists ▪ not at all in urban human populations ▪ à Bioarcheological question: why is this component of the ancestral gut microbiome lost in urban populations? 2. Analysis of the oral microbiome: calculus samples from medieval Germany o Advantages of studying calculus o only part of the human body that fossilised while we’re still alive (no post-mortem modification like with coprolites) o laminated (like an onion, layers formed during life, calcification over 2 weeks and new plaque deposit) o Soil doesn’t enter the calcium layers of calculus (no post-mortem modification) o If calculus is decalcified and gram strained, the cells stay intact allows to see diverse morphology of bacteria in calculus matrix. o Good DNA preservation  in bone, cell count is very low and there is a lot of soil contamination (in dentine samples, only 0,1 to 8% of human DNA is found vs 100% when the individual was alive), whereas dental plaque is very cell dense, so it has a very low burden of soil contamination (60% to 80% is oral bacteria) Carious teeth also have very little DNA even within highly diseased (infected) bone tissue à calculus is unique in its dense cell proportion and uncontaminated DNA quantity. o Ubiquity of calculus across all human populations (and also a lot of animals): allows for good differential study and comparative analysis of different populations. o Abundant resource (lots of plaque can be pulled from a single tooth) Disadvantages of studying calculus: o Starts forming in early 20s so it allows the analysis of dental records after the end of dental formation (stops at adulthood) o layered record of diet temporally ordered but we don’t know what amount of time separates each layer. Microbiome from carries vs from plaque o Decomposition in tooth: active decay, bacteria produce acid that dissolves the minerals of the tooth and exposed more collagen to eat. o in calculus there is no dental pulp to build up the bacterial population that can decalcify. There are no changes in mineralogy (very different decomposition profile) o Difference in bacterial communities depending on calculus or dentine/ carious dentine. Bacteria from human and oral dental studies correlate with calculus ADNA while soil + burial environmental DNA correlates more with dentine. Proteins in calculus: large number of bacterial proteins but also a lot of human proteins (more than human DNA proportion)-> secretory protein Other components (other than bacteria) in calculus: 0,7 eukaryotic DNA, mostly DNA and some plant DNA, some archaea, some bacteriophage 2.3-Study of ancient disease: lots of opportunistic pathogens present in calculus can give insight into illnesses that occurred o opportunistic pathogens don’t necessarily cause infections they can be carried by the host asymptomatically.  o major periodontal pathogens found can confirm macroscopic signs of bad dental health (reactive inflammation, alveolar resorption, periodontal osteoporosis etc.) Combination of findings o we can have both the virulence factor expressed in aDNA and the protein secretive corresponding to that virulence factor also fossilised in the calculus. Reconstruction bacterial genomes: o allows to compare to modern strains of the bacteria and see what virulence factors it has acquired through evolution (ex: ancient bacteria missing tetracycline transposed element) Host and food relations analysed through calculus: o Human secretory proteins in calculus are linked to the innate immune system specific to neutrophils (early reaction to bacteria, produce bactericidal proteins) o Proteins observed are directly linked to the immune response against the bacterial protein / ADNA observed + the pale pathology findings (osteological signs of illness) o Food: Presence of connective tissue and photolytes from plants (barley), starch granules (pea, beans) o Milk proteins (beta lactic globulin) produced by ruminants found in Viking calculus helps analyse the spread of dairying across Europe through a sequence-based approach. distinguishing species milk originates from, not only analysis of non-specific lactic acid. October 30th PLAGUES I: EPIDEMIOLOGY 1-Plague outbreaks in the past 1.1 Historical records of plague Body-lined streets mass graves in churchyards overfilled. Putrid smell (need to cover faces with cloth soaked in herbs)  Not a lot of people experiencing plague were literate, and lots of death causes little eyewitness testimonials. 1.2 Plague variant symptoms Excruciatingly Plainfield swollen lymph nodes, buboes at groin and armpits (15% survival) Fevers, rashes and blisters (death soon after developing these symptoms) Tubercular nature (death after lengthy period of illness) 1.3 Social impact Infected people shunned. A lot of priests refusing to give service. Some turned to religion and prayer, self-flagellation (atone for potential sins of the body that could’ve caused the plague) Rise of hedonism (if we’re going to die, we might as well feel pleasure) Entire communities wiped out. 1.4 Important outbreaks: plagues: same bacillus, but epidemiology and etiology differ (evolutionary shifts) o 6th century Justinian plague (end of Roman Empire) Potentially originated from China and then moved to the Roman Empire through trade routes to Egypt and Constantinople plague’s devastation hindered the efforts to reunite the eastern and western roman empires (not enough active farmland to be taxed to pay for military expenses and not enough able-bodied young men to have a strong military) Plague accelerated the fall of the Roman Empire (shaped Europe we know today) o 14th century medieval Europe (kept reappearing periodically midler forms until the 17th century) Most devastating Shift in the nature of plague over the episodic outbreaks ▪ 14th century England: mostly targeted healthy individuals, as opposed to immunocompromised people  ▪ o 19th century: plague in Asia Outbreaks in China and India (80% of infected died) Alexandre Yersin and Shibasaburo Kitasato isolate plague in laboratory Yersin Identified rats as a vector of the disease (fleas jump from rat to human and bite humans) à Zoonosis 1.5 Nature and epidemiology of plague in the 20th century Spread of plague o Fleas that are infected aren’t necessarily infectious. Ventriculus Proventriculus regulates the food that fleas are ingesting before it gets to the stomach When fleas feed on infected rodents: blockage of the bacteria and blood forms so nourishment can’t get to the stomach. Fleas start biting more aggressively and frequently to get nourishment, until the blockage is regurgitated (into the bloodstream of the host the flea is biting Need for rat hosts: bacteria percentage in blood of human is not enough to trigger the Ventriculus Proventriculus, but it is in rats. So there needs to be a rat host, that dies of plague, forcing the rat flea to find another food source (humans) Types of plague: o Bubonic plague: very similar to other zoonotic disease -> Ebola Difficult human to human transmission (only if you burst the buboes to try to administer treatment) Much research on bubonic plague is based on current Ebola (comparison of modern vs Middle Ages phenomenon) ▪ Ebola is a virus, not a bacterium, but originates from a similar zoonotic jump (jumped to humans from fruit bats) Comparison to HIV/AIDS: also a virus, but zoonotic disease (jumped from monkeys to humans, from consumption of infected meat) ▪ 10-20% of people descended from medieval populations of Western Europe are immune to HIV ▪ Gene mutation CCR5-delta 32 prevents HIV virus from entering the cells  ▪ Odd: HIV originated in modern Africa, while gene mutation is present in populations from the Middle Ages -> virus causing hemorragic fever was potentially the cause of this mutation (so possible that the plague in the Middle Ages was not caused by Yersinia Pestis), maybe a smallpox virus (also zoonotic, like bubonic plague, also transmitted via contact with rodents) o Pneumonic plague: respiratory system, not lymphatic system Starts with bubonic form, which then reaches the lungs from the lymphatic system. Transmissible from person to person: caregiver of someone with plague comes into contact with blood, sputum, saliva and becomes infected. Early forms of hazmat suits: fresh smelling herbs in mask Death from internal hemorrhaging 1-2 days after infection= death o Septicaemic plague: bacteremia Least common form of plague Can start off as bubonic. Causes disseminated intravascular coagulation (DIC)-> formation of small blood clots. Blood clots cause localized ischemic necrosis (death of tissue due to lack of circulation) Blood loses the ability to clot if bacteremia is advanced: internal bleeding, produces red bumps/lumps on skin. Final sign: vomiting blood You can die within 24 hours of showing symptoms. 2-Repercussions of the Black Death 2.1 Effects in populations directly affected by the black death loss of skilled labor economic, social, and political world needed to reinvent themselves social structures dismantled: lower class takes advantage of new upward mobility plays a role in the renaissance of the 16 century (might have been delayed a couple of centuries otherwise)  church: did not resolve the crisis, so any dissatisfaction with the authority of the church that existed pre-plague was amplified. o Decline in devout believers. o Martin Luther reform might have taken longer to materialize without the plague. 2. Effects on the plague today Fear of the plague: reappearing in waves over 3 centuries keeps people on edge, not knowing when the Black Death is going to return. Rise of other diseases causing plagues after the last plague epidemics in medieval Europe: smallpoxàsyphilisàcholeraàinfluenza Black Death functions as a touchstone of comparison for people to process the significance of later pandemics + figure out how to function and response. o Ex: practice of quarantine was prevalent during the Black Death o Comfort: humanity did survive the Black Death o Offers perspective: things are bad with x pandemic, but they could be worse (like the plague) o Gave language to talk about the HIV/AIDS epidemic. o Plague in medieval Europe could be a useful guide for those working on the effects of a modern epidemic in progress (this was the case for AIDS crisis) o Social associating between vampires and mass epidemics (was the case for AIDS) à supernatural creatures transformed through the sharing of blood. Antibiotic crisis: bacteria develop resistance (what if Y. Pestis becomes resistant to treatment) o we’ve seen these bacteria mutate before: became less virulent after initial outbreak in 14th century (needs to have life hosts to survive) o World is much more interconnected: already spread quickly just through sea travel and trade routes. What about now? o Countries with lack of medical personnel/ equipment and with political instability: primary target from new pandemics, we need local systems designed for response to infectious disease. o Lateral gene transfer: Y. Pestis takes genetic material from E. coli and Salmonella à gaining resistance factors. 3rd pandemic has never been declared over (recent outbreak in India, 1994) o Natural disasters like earthquakes: displaced large quantities of rats and there was a zoonotic jump (wasn’t caught because people don’t pay attention to plague anymore)  o Took the form of pneumonic plague: easy to transmit between people (flu symptoms in the beginning, only noticeable when coughing up blood) o Started in poor neighborhoods: close quarters, not a lot of medical resources. o 78% of confirmed cases were in the poor neighborhoods. o Shortage of antibiotics, medical professionals abandoned their posts, etc. o Presence of media: sensationalist headlines à like in the Middle Ages, cause people to move around a lot (go to the countryside, pilgrimage, etc.) instead of just staying put. November 1st PLAGUES II: PALEOPATHOLOGY OF THE BLACK DEATH 1- Overview of the 3 plague pandemics pandemics throughout Europe: there were outbreaks in between but not to the magnitude of these events o Outbreaks continue still today, not travelling around huge populations and distances over short periods of time o What allowed the plague to travel: Trade routes allowed vectors (rats) carrying the flees to travel around the world People moving around-> fleas (on human body) Globalisation affects connections between populations It took a while to figure out that Yersenia pestis caused all 3 plague pandemics because: o Co-infections with other bacterial infections o Confusion because of different symptomatic expressions o Osteological remains show large scale death evidence but not specific a pathogen (highly virulent disease, doesn’t leave skeletal markers besides the mass graves burials) o Not everyone was buried in mass graves o Historical records: can have biases or incorrect information  Advantages of using aDNA to study plague o Before aDNA studies, it was hard to tell what pathogen caused a disease because a lot leave no highly diagnostic lesions o aDNA allows to extract bacterial DNA from Osteological remains in plague pits and confirm the pathogen that caused the disease 2-Transmission of plague Reservoir: rodents Fleas: vector (spread the bacteria to people) Different expressions of the same infection affect the way plague is transmitted. o Bubonic plague 50% mortality big blood welts most identifiable plague, easy to see who is sick and isolate them animal to human transmission only (from flea bites) When the rodents were eliminated, bubonic plague became less common because less flea bites o Pneumonic plague 90% mortality infects lungs. respiratory droplets spread the bacteria and allow human to human transmission. easily confused with other illnesses that aren’t plague (flu symptoms), harder to effectively quarantine people o Septicaemic plague 100% mortality sepsis, bacteria in the bloodstream more advanced stage of the disease infection is everywhere o You can go from bubonic to pneumonic, bubonic to sceptic, from pneumonic to sceptic: there can be combinations, but it’s important to keep in mind the original type because it impacts type of transmission Factors that impact Contact:  o Urban vs rural environment has an impact on risk of transmission or the type of plague. o Occupation: high deaths amongst priests because live in small, cloistered communities and tend to the sick, doctors in contact with infected people o Attempts to stop the disease. quarantine, protection from infection (masks) piercing of buboes 3-Evidence bio archaeologists use to understand the Black Death What can bio archaeological investigations do to understand the Black Death o How do people interact o risk factors involved in contracting the bacteria o Epistemological study of affected populations was plague a universal killer? Did everyone have an equal chance of being infected and/or dying from the plague? looking at factors like age, sex, socioeconomic status, etc. o What was health like and what were the risk factors in the period of the Black Death Consensus is that health was getting worse before the Black Death ▪ nutrition deficiencies ▪ non specific stressors that indicate poor health etc ▪ creates good conditions for the plague Mostly universal killer ▪ some episodes affected some demographics more: older people having lived during an outbreak had acquired immunity while the younger generation didn’t ▪ Overall no differentiation in sex or age factors ▪ Occupational and socioeconomic factors did have an impact Link with Osteological paradox: o hidden heterogeneity: not everyone has the same risk of dying of something comorbidities, genetic predisposition, socioeconomic factors, rural or urban environments, occupation help understand how plague moves through populations  Analyzed with paleo demography à cemetery and population scale (no paleopathological analysis on the individual scale) We can see who was dying in the period prior to the plague, during the plague and after the plague (demographic of the cemetery changes) 4-Impact of the plague on the population (not looking at osteological indicators, but analysis of health before and aafter the black death) General trend towards more healthy populations (less people with immune challenges and nutrition deficiency) Social changes: reduced population = more food and resources to go around, people’s labour valued more Genetic impact (understood through aDNA studies) o infectious disease can exert a selective pressure on a population Effect a pathogen can have on the immune function of future generations Some genes related to immune function (HLA gene) -> different combinations of alleles affect gene expression-> allele change is adaptive to immune response (signature of selection in the genes related to immune function) -> people who survived the plague had an advantageous allele combination that was passed down o Understanding how human genetics were impacted by the plague o Host-pathogen coevolution analysis (see how the bacteria evolves through time from one pandemic episode to another) o Strain analysis from different plague cemeteries over different regions -> track phylogeny —> strain that evolved in China was a descendant of mediaeval European strain -> plague moved east to west and west to east 5-The plague today Still exists in the save reservoirs and vectors. Plague not endemic in Europe anymore (not sure why) November 15th SMALLPOX 1-Characteristics of the smallpox virus: Variole virus -> genus of orthoxvirus o Two varients of the virus Variole major (most cases of smallpox, most mortality (30%)) Variole minor (1% mortality, more recent strain of the virus-> 19th century) o 4 types of disease 85% of infections -> typical form Modified form: less severe, seen in people who are inoculated (previous exposure causes immune response that protects you from re infection) Flat type /malignant: ▪ difference in appearance of lesions: lesions merge together, no scabbing, flatter softer version of the fans over the whole body ▪ More common in children, very fatal Hemorrhagic: ▪ Internal bleeding instead of skin lesions -> death from organ failure and hemorrhaging ▪ More common in pregnant women ▪ Very fatal These different expressions do not depend on the strain of variole, it depends on the host immune system and the factors that impact it (genetic predisposition, comorbidities, age, pregnancy, etc.) Disease progression: o Incubation period: 10-14 days After exposure to the virus, not enough viral load to be sick yet, not contagious yet Virus building up to the stage that can make you sick o Initial symptoms: 2-4 days  High fever, fatigue (related to the organs that are most attacked, like kidneys), back pain, abdominal pain and vomiting à non specific viral symptoms No rash yet Not contagious yet (by the time people are contagious they are already very sick and secluded) o Early rash: 4 days Starts around face, mouth (mucus membranes) and hands, then spreads to rest of body Blister/soft bumps filled with clear liquid Contagious (as soon as rash shows up, early rash is when most contagious) o Pustular rash: 10 days Hard pustules, spread throughout body Characteristic of smallpox o Scabbing: 6 days Pustules scabs, when all the scab falls off = no longer contagious (can take 3-4 weeks to stop being contagious after the rash starts) o Blindness, scars create long term health impact on people Transmission o Human to human contact only, no animal reservoir not like TB where animals can spread some strains adapted to humans) zoonotic jump thousands of years ago, no known animals now that can be infected with smallpox o Spread through inhalation airborne droplets from saliva close contact with sick people, face to face prolonged exposure o Fluid inside of the sores (need for precaution when caring for people with smallpox) o Shed scabs spread the virus, the virus can be in the environment 1 year outside of the body and still be infectious -> smallpox blankets)  o No asymptomatic spread o Crowded environments in urban areas created more transmission. 2-Origin of Smallpox Historical records and archeological evidence of smallpox Egypt, Asia and Asia Minor, then Europe and then the Americas Zoonotic jump in Egypt or near east: o large populations, trade routes and population movements o gerbille or camel origin o Origin not confirmed (zoonotic jump event not clear) First major pandemic: Roman Empire, Antonin plague àsmallpox becomes endemic in the old world (seasonal and regional outbreaks up until the 19th century) First increased in Europe in the 11th century from people coming back from the crusades, silk roads, etc. à becomes endemic Globalisation o introduction through South America up to North America (early European settlements and trade routes) o spread rapidly across the planes, big outbreak in north America BC o evidence of intentional spread of the disease: biological warfare (smallpox infected items given to indigenous people) o European slave trade into the Americas also increased the number of infections and spread them (poor immune status of enslaved people, easier to become infected and spread the disease) 3-Bioarchaeology of smallpox: Archeological evidence that can be used o Limited Osteological changes for people who have the disease. o Most prevalent form of evidence is oral history and historical records (ex: crusades) o Mummified tissues: paleopathology of soft tissues of early mummies that had lesions that looked like smallpox lesions o Ancient DNA of mummified tissue or evidence of an immune response (no conclusive evidence yet for older samples ) o Child mummy (17th century à later version of the disease) à similar smallpox scars, variola virus found successfully o A DNA not used a lot because expensive and destructive, more a way of confirming Paleopathological analysis of lesions o Mass graves, paleodemography analysis sites that show evidence of being abandoned or less populated than before)-> drop in population = sign of epidemics o Changes in burial practices: American planes: quick burials isolated from the rest of the population historical records = sign of smallpox o Mothers buried with infants: maternal/newborn mortality link is clue of smallpox because close contact between mother/infant= spread o Not a lot of evidence on skeletal remains Osteomyelitis variolosa o Fused joints/dislocation bc of bone infection smallpox = targets joints more than other bones o Very small percentage of people who get smallpox have this (similar to TB in that way) o Usually symmetrical inflammation, but one side can have more deformity. o Usually in epiphysis of the bones: more dramatic in children because bone is still growing (no epiphyseal fusion yet) o You have to live long enough for the bones to heal: typical infection probably, not more fatal versions Vaccine development o First disease to have vaccination o Earliest form of vaccine: variolation (intentional exposure to the disease à fluid from blister, crushing up scabs and inhaling the powder à controlling the amount of the virus you get exposed to (but a bit of a gamble, because virus is still alive and virulent) à more localised version of the virus if done correctly. o Jenner:  link between smallpox and cowpox came from John Fewster (doctor) who was variolating people and saw people who got cowpox were protected from the variolation. Jenner ran with it (1796) Jenner took cowpox (another ortho virus, causes similar disease but doesn’t make you as sick) doing variolation with cowpox= less risky but giving exposure to the same genus Vaccine campaign eradicated the virus Zombie viruses: o Viruses recovered from remains and that have been reanimated concern with the fact that currently eradicated diseases could come back because they still exist in Osteological remains o Permafrost Alaska excavation: influenza that caused the 1918 pandemic of the flu o Siberia example of smallpox: genetic material recovered o Ability to recover the virus doesn’t necessarily mean it’s infectious o Anthrax: example of infection from permafrost frozen remains o Climate change: potential for re introduction à we are not protected with natural immunity bc no vaccine currently November 20th TUBERCULOSIS How was tuberculosis conceptualized and what impact did this have on society? Social differences, lower classes consider sickness as such, but upper classes considered Virgin Mary-esque. Different treatments: wouldn’t always disclose that higher class women had the disease. How did medicinal practice around people arise? TB started with sanitarium treatments – care facilities for chronic infectious diseases. People didn’t really know what to do but eventually increasing understanding of direct sunlight, clean air, and water was useful for combatting bacteria. Laying out in the sun came out of treating widespread infection in society with sanitariums. Ranging standards of sanitation but in literature, people also self-treat by going outside and on holidays. Mycobacterial infections: Leprosy (Hansen’s Disease): Mycobacterium leprae / lepromatosis (two main species which cause leprosy. Different animal hosts that they likely evolved from before making zoonotic jump. In North America, armadillos are reservoir for leprosy, don’t cuddle armadillos, current understanding: infected by people post-colonization. Post-reservoir now but did not exist as reservoir before) Tuberculosis: Mycobacterium tuberculosis (complex) = broad group, set of strains Primary, people to people, is above. Multiple host specific animal versions of pathogen: cattle, camelids, seals, deer, other primates. Can jump into humans as secondary host. Most likely route of transmission for both are inhaling droplets from another infected individual. Leprosy needs longer, closer contact. TB is easier to contract but can also be infected through meat or animal products = infected milk form cow, infected meat from deer. What Are Possible Risk Factors of TB Exposure and Disease? Agglomeration, poor ventilation, lack of sunlight, malnutrition, vitamin D deficiency Unpasteurized milk, working with animals/product = more TB after agricultural revolution, TB Mary First instances of TB: pre-dynastic Egypt, Pre-neolithic More significant mortality: TB in modern time with agglomeration, 19th-20th century, then declines with treatment of disease, but now on the rise again Symptoms: - Chest pain - Appetite loss - Chills - Weight loss - Fatigue - Night sweats - Fever - Blood coughing  - Prolonged cough Respiratory transmission => pulimary TB Ingesting => gastro-intestinal TB LATENT/DORMANT TB: the body encapsulates the bacteria in a cocoon, stopping the spread. Not symptomatic or contagious, bacteria is stuck in body. Sometimes people experience a reactivation of TB = SECONDARY - Suppression of immune system: can’t continue to encapsulate, bacteria replicates, moves through body, symptoms come back, contagious again, TB spread and becomes extrapulmonary: lymphatic system, cardiac muscles. Skeletal TB: We can’t see TB unless it causes skeletal changes. Majority of people w TB, we have no evidence they died to TB. But for this small group that develop skeletal TB, it gives us evidence. Heterogenic disparity: hard to diagnose age of death - Underrepresents infection in archaeological record - Spinal TB is highly diagnostic: TB spondylitis or Potts Disease What happens: targets specific bones in the body, no even distribution. Localized areas of changes and lesions = cancelus/spongey bone? Bone in disk of vertebrae, tons of oxygenation and blood supply and this is what TB goes for. Bones near respiratory bones, metathesis and apotheoses of long bone? Three sections: diathesis, shaft, metathesis, growth plate, apotheoses, bones separate then merge into metathesis when grown. Oxygenated areas of bone, pathogen targets those areas, TB related arthritis can be caused. Lytic/Destructive lesions: bone destruction from pathogen, Potts. As the lytic lesions invade the bone, vertebras, it starts to collapse in on itself. It causes kyphosis, the curvature caused by collapse of vertebrae. Spinal infection is characteristic of TB but in other areas, we may be underdiagnosing individuals with skeletal TB because without clear indications of disease, hard to diagnose. We can identify skeletal TB, it’s hard, we may be misdiagnosing, underrepresenting the amount of TB circulating in populations, underscores our understanding. What is a deviant burial? What does it tell us about the individual who was buried? When the burial deviates from the normal burial ground. Usually because they have some sort of social identity in life that make people treat them differently in death. A common factor is disease or disability. There have been vampire burials = TB infected people so prevent them from coming back lol. Lots of visual similarities between the two. Must be treated a specific way when they died: - Poland: 14 burials, decapitated, face down, weighed with stones = unhealthy people most likely, maybe TB. Pathologies say no correlation between lesions and anti- vampire burial but Vampire Panic in New England mad people crazy. - Buried separately, pulmonary infection = it is potential that some deviant burials are TB burials. Still don’t know for sure why they were treated that way. Deviant burials tell us very little about person buried but much more about people that did the burial. There was also malnutrition, so death wasn’t determined by age necessarily. November 29th ARCHAEOLOGY OF MEDICINE How people have dealt with pathogens and disease, health challenges in the past, what is possible to see in bioarcheological environment. Agency of people in terms of pathogens, human experience of pathogens rather than focusing on the pathogen itself as we have been doing Medicine – Neanderthal herbalists Working with remains in northern Spain, 47000-50000 years ago, looking at dental calculus. Pre-genomic analysis. Mass spectronomy: identified compounds from two different non-nutritional plants. Chamomile (calming) and yarrow (stringent). Being in dental calculus implies ingestion, neanderthals could eat yarrow even if it tasted bitter but they had genetic predisposition towards bitterness Follow-up analysis years later, meta-genomics: identified additional species with probable medical properties. One guy had severe tooth infection, ate aspen which produces penicillin, painkilling properties, antibiotic properties to heal tooth infection. Plants in medicine: discussion among archaeologists, suggested that the reason we don’t always find animal remains was because animal bones were used in medicine like Chinese medicine. In Germany, they found mammal remains, rounded out end of long bone – evidence of grinding bone for powder for medicine maybe. We have evidence of plants, maybe animals, hard to find evidence, easily erased. Dental care – Upper Paleolithic dentistry 14000 BC Mans has carious lesion, dental cavity, dark pit in tooth, Scanning electron microscopy found striation alongside of lesion, replicated, and decided it was evidence of someone trying to cut away at diseased tissue or trying to remove shit stuck in cavity = someone dealing with their cavity. The Greeks, romans, Egyptians = removing carious lesions by drilling them out, removing infected teeth. Trephination and Surgery Reading = more depth, bioarcheology of care Drilling hole to reduce swelling, pressure relief Even if someone heals, the hole will never close because the skull does not knit back over. So, people had something placed over the hole to protect. Obvious form of early surgery: cut marks, marks in bone, healing evidence Amputation: mans from Borneo, early case of amputation, not taphinotic damage in burial, but example of surgical amputation then survived for 6-7 years ish. If they can’t move around very easily, who helped them move around and survive? Prosthetics Relacing visual aspect not so much functionality Warfare function, societal acceptance, confidence