HLTA01 - Final Exam Notes.docx

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Health Studies
Caroline Barakat

HLTA01 – FINAL EXAM NOTES GENERAL Q’S  Plague – highly infectious ,usually fatal epidemic disease  Etiology (3) o Changes in environment = change in habits, food & conditions; parasites & disease become prevalent due to pop. Growth o Dense cities & close knit communities = easy transmission o “URUK” 5,500 years ago – development of ancient cities enabled:  Closer proximity to neighbours, smaller living spaces, waste secreted back into environment o 3 factors (revolutions) of population growth  Tool making  Cereal grains were harvested w/ ease b/c of tools, storage & processing of these grains  Used: baskets, mortar & pestles, techniques, storage pits  Agriculture  Population was less dense but people started domesticating animals & adopting sedentary lifestyle (food growth = exposure to parasites  Economic trade, ties, political structures & religious practices occur; selective advantages to those in control (group cohesion)  Irrigation practices = favorable environments for parasites b/c of abundant moisture – liquid medium of tranmission  Consequences: increase in human disease (easily transmitted), exposure of disease b/c of fertilization (favored disease), domestication (zoonotic)  Industrial  Technological advancements can speed disease control AND disease transmission; efficiency in transportation  Religion, “opiate of the masses” was a competitive advantage over societies = political stratification, governed the “settled” & commerce, baking & writing was invented = urbanization  (TWO checks needed to occur to set equilibrium of deaths/births (population growth) 1) External/environmental factors: limited food, space, resources, etc. 2) Self-regulating factors: fewer births, deliberate killing of offspring, OR increase in deaths b/c of accidents/ more virulent parasites o ** host resistance is counterbalance to virulence of parasite/degree of harm; how negatively a host will be affected is determined by host resistance and virulence HLTA01 FINAL EXAM NOTES –  Virulence – how mutation is filtered through natural selection: lethal vs. mild outbreak of d0sease, R must be > 1 o Factors that affect spread of disease  Seasonal patterns, climate  Size of population, overcrowding, density  Communal activities that bring susceptible  Close association w/ domestic animals ppl in contact w/ infectious MANDY TRAN 1  Character & quality of water supply, food, shelter  Counter measures used (quarantine,  Practice of using human excrement (night soil) as immunization, etc.) fertilizer = transmission of infective stages  Disease Ecology (7) o Main factors that influence the occurrence of a disease:  Host (to get sick), environment (exposure to contagion), agent (parasite) o Factors necessary for spread of disease  Must be infectious individuals  Must be susceptible individuals  Must have a means of transmission b/w the 2  NOTE: for an infection to persist in a population, each infected person must transmit the infection to at least 1 other o Reproductive ratio – “multiplier of disease” is the # of individuals each infected person infects at the beginning of the epidemic (R0)  Greater the population size = greater 0R )  Change in the high (0 ) = greater proportion of hosts infected (prevalence) & burden (incidence) of disease  R0> 1, transmission stages = expanding disease (epidemic) BUT in time, susceptibility is consumed & the epidemic may burn itself out/await new hosts through birth & immigration  R0< 1, parasite cannot establish itself  Size of population needed to maintain infection varies INVERSELY w/ transmission efficiency & DIRECTLY w/ death rate (virulence)  Therefore, virulent parasites (those that cause high # of deaths) need large population to be sustained o Modes of disease transmission  Direct – from person to person  Indirect – through a common route/vector  Portal of entry  Dermal – through skin  Ingestion – through mouth  Inhalation – during respiration  Aspiration – airway entry HLTA01 FINAL EXAM NOTES o Types of diseases –  Iceberg concept – broad spectrum of disease severity  Peak – see from a distance (common), know symptoms & how to avoid  Below surface – SUBCLINICAL, most severe b/c has infections but no symptoms = easy spread of outbreak MANDY TRAN 2 o Types of disease outbreaks  Endemic – usual occurrence of a disease given within a geographical area; normal  Epidemic – occurrence of a disease in excess of normal expectancy; exceeds normal tendencies  Pandemic – worldwide epidemic o Types of epidemic  TYPE 1 – population is large & shows regular series of outbreaks but never completely disappears – endemic, cases persist  # of susceptible ppl large enough to remain transmittable,0R > 1  TYPE 2 – peaks of infection are discontinuous but w/ regular pattern of occurrence cases; no endemicity, temporary absences of disease  # of susceptible ppl is not enough to keep chain of transmissio0, R < 1  TYPE 3 – occurs in populations of less than 10,000 w/ an increase in cases during irregular intervals & long periods of no disease  Chain of infection is interrupted b/c of remoteness0 R < 1 o Determinants of disease outbreaks [# of ppl immune/not at risk of disease VERSUS # of ppl susceptible/ at risk of disease]  Herd immunity – resistance of a group to a disease attack due to immunity (Ex: Measles, 94% population immune)  Incubation period – short = low disease outbreaks (contagious), longer = high disease outbreak (contagious during)  ** Attack rate – ratio of the # of ppl in whom a certain illness d÷vtotal # of ppl at risk  Terminology (7) o Parasites – organism that grows, feeds & is sheltered on or in a different organism & that does not contribute to the survival of its host (Ex: bacteria, protozoa – unicellular)  Unable to live on their own, must rely on host for nutrition & replication, can be in different forms:  Parasitism – the association of 2 different kinds of organisms (species) wherein 1 benefits (parasite) at the expense of others (the host) = harm o Virus – ultimate micro parasite, smaller than bacteria; neither cells or organisms & can only reproduce in host  Collection of genetic material engulfed in protein, only seen w/ electron microscope killed when RNA/DNA destroyed o Macro parasite – compose of many cells (multicellular) & cycles through transmission stages of eggs & larvae which pass into the external environment (Ex: plasmodium, ticks, flies)  Use the host for multiplication & cycles of transmission, can live on surfaces & the human body w/ complex or HLTA01 FINAL EXAM NOTES – simple life durations o 3 kinds of bacteria  Spherical (coccus), rod shaped (bacillus) & corkscrew (sprillium/spirochete) MANDY TRAN o Transmission – movement of a parasite from host to host 3  When it involves living organisms it’s called a vector & can be:  Mechanical (bite wound)  Developmental (parasites that grow & reproduce in snails) o Incubation period – interval of time required for development of disease (time b/w exposure & symptoms)  Parasite is replicating itself (or some activity within the host), the person can be affected/exposed to pathogen w/o showing any signs of symptoms o Latent period – seemingly inactive period b/w exposure to an infection & subsequent illness (time b/w exposure & being infectious)  Host doesn’t show any activity nor development of symptoms, the dormant stage: no signs o Parasite virulence – capacity of a parasite to cause disease  How strong/capable of inflicting harm & disease to host o Zoonotic infections – animals infections that can be transmitted to humans; originate from human sources DISEASE OF ANTIQUITY (2)  5000BC to 700AD, diseases during hunter gatherer society were o Those w/ high transmission rates, macro parasites and sexually transmitted diseases o Population was of low density, outbreak needed high transmission rates or parasites that sustain themselves externally, use vector or are sexually transmitted o Characterized by parasites w/ long lived transmission stages (Ex: Macro parasitic, laid eggs > larvae > infect human) o Person to person contact, due to environmental settings & population density  Pharaoh’s plague aka, snail fever/blood fluke disease/ endemic hematuria/schistosomiasis o 1900BC in the Nile valley of Egypt; agriculture & irrigation provided favorable conditions for spread of disease  Wars & migration carried the disease through trade routes of the world o Arithmetic disease – severity of its symptoms depends on exposure degree, continuous exposure = immunity (Africa) o Transmission stages  Start as eggs, (miracidia) then larvae (cercaria) then grow into adult worms that live in blood vessels  Enter human through contaminated water - Snail vector is mandatory*  “split body” b/c of ‘gynecorphic canal’ groove in males, paired worms move upstream to smaller vessels to deposit eggs – pass toward bladder = bleeding of hematuria (released) o Diagnosis: examining stools or biopsy of immunol methods, & urine to find eggs  1-2 months: early signs of infection w/ fever, chills, headache and cough HLTA01 FINAL EXAM NOTES –  6-12 months: accumulation of eggs = organ enlargement, abdomen is bloated, loss of appetite, anemia & dysentry o Prevention: education, treatment, control of snail vector, safe water supply, lining irrigation channels w/ cement  No preventive vaccine/drug  Treatment: praziquintel (biltricide, drug) MANDY TRAN 4  Dr. C Barlow volunteered and treated himself w/ IV of tartar emetic o Currently 1M deaths annually, not eliminated b/c developing countries have favorable conditions that promote its growth plus economic constraints  Plague of Athens o Dark ages (1200BC to 750BC, 450 years) o 430BC, infected Greek civilization who relied on wine & olive oil as a source of living o Route: Ethiopia > Egypt > Athens; Athenians defeated the war that lasted 27 years against Sparta o ** Disease is unknown; contributed to high death rates including “Pericles”, demoralized Athens’ citizenry  Roman Fever (*) o 27BC, roman empire established – series of colonies run by head & had had vast trade networks w/ agricultural changes o Increase in mosquito vectors = malaria, PLASMODIDUM FALCIPARUM (malignant form) to become prevalent  Thought to be a result from bad air; vapors from pontine marshes during summer = associate symptoms w/ smells from ground  Epidemics every 5-8 years: cyclical pattern o Rise of Christianity & religion to appease the multitude of gods so worshippers would receive benefit – became urban movement = universal salvation  Worshipped God’s truth, teachings to establish order, faith made life meaningful even at time of sudden death o Reduced life expectancy due to impact of various factors according to disease prevalence, lasted 2000 years  Antonine Plague (*) o AD166, named after the ruler Marcus Aurelius Antonius who died 7 days later after plague broke out o Route: Mesopotamia > Roman Empire > Europe – romans visited ancient ruins & contracted the disease o Symptoms were diverse and distinct, described by Galen & Hippocrates  Fever, thirst, diarrhea, inflammation of mouth/throat & rash that would appear  Telltale sign: pustules on skin after 9 days o Identity of plague not know but likely to be the first record of small pox; only disease humans have been able to eradicate  Caused more than 2000 deaths/day in Rome, contagion & transmission was high HLTA01 FINAL EXAM NOTES –  Cyprian Plague (*) o 250AD, route: Ethiopia > Egypt > roman colonies of North Africa & became pandemic that lasted 16 years o Symptoms: vomiting, diarrhea, gangrene of hands & feet, fever, sore throat – may be of first record of measles/smallpox (do not know origins/etiology of this plague) MANDY TRAN 5 o Christianity strengthened itself among Romans b/c it could deal w/ the horrors & hardships of plague = social & political development (Ex: St. Sabastien, protector of the plague who sufferers would seek salvation from)  (*) over the next 3 centuries, Rome collapsed under pressure b/c of Germanic tribes & recurrent outbreaks of disease: Roman fever, Antonine plague & Cyprian plague (4 HORSEMEN OF APOCALYPSE: disease, famine, war & death )  Justinian Plague o 541, Constantine, capital of E Roman Empire - 1 experience of pandemic of the Bubonic plague  Raged Europe > North Africa & the Middle East until 757AD (200 years)  1M ppl died in 5 year period, by 600AD mortality rate at 100M in Western Europe (50% of pop.) th o Highly contagious & high case fatality rate; recurred every 3-4 years for decades & effects lasted until the 17 century = the classical world – Greek & Roman civilizations shifted to Northerly lands o Symptoms: swellings (buboes), delirium & frantic restlessness & sometimes coma; ppl died within 5 days o Bubonic plague = 3 pandemics in course of 2000 years (Justinian, Black Death & 3 pandemic) PLAGUE – contributed to economic & social structure of England = change (aka Great Mortality, Great Persistence, Universal Plague)  Justinian Plague o Originated in Constantine & impacted Europe, Africa & Middle East  “Black Death” 1346 until 1352 in cities of Kipchak Khanate of the Golden Horde, NW of Caspien Sea o Origins in Caspian sea region & impacted/reduced population of Western Europe & Mediterranean: 20M deaths  Third Pandemic 1860’s in the Yunnan Region of China o Sporadic plague happening at 1 point to another, 1352 – 1722 o Spread through troop movements during war; railways & steamships = mobility of transmission  ** Plague originated from black rats spread to sea ports = major trade routes which invaded countries & spread to human populations  Impacts of plague o Quarantine “40 days in the sea” where they’d get better or die trying – stay in isolation to avoid transmission to others but rats were still able to move on land and infect humans at shores o Pest houses – where groups of sick people of infected were taken away & put in isolation together; no contact w/ others HLTA01 FINAL EXAM NOTES – o Quick burials – victims of plague were gotten rid of quickly by being buried together or burned to avoid transmission o Burning of clothes & bedding – avoid further contamination of disease o Studies of human anatomy – wanted to learn more as to what causes disease; emphasis on research MANDY TRAN 6 o Theory of contagion by Girolamo Fracastoro – certain diseases are contagious & transmission occurs from 1 person to th another (was dismissed before revived again in 19 century)  Infectious disease could be transmitted by SEMANARIA “germs” in 3 ways  Direct contact, through carriers (dirty linen), airborne transmission o Changes to farming – Ex: raise sheep instead of growing crops = more returns, less need for labour, readily available equates to the economic commodity of wool o Bigger ships = smaller crews, related to trade: less contact/ transmission for disease o New diversified economy – changed the way they live, income for less labour intensive devices/economies o Local universities – beginning to establish plus curriculum reform o Decline in papal authority – threat to churches w/ flagellants (counter culture) that claimed divine authorization to alleviate the plague b/c of spiritual revival  Cause o Plague microbe: YERSINIA PESTIS, 1898 plague linked to fleas on rats XENOPSYLLA CHEOPSIS (8+ species able to transmit disease)  Rod shaped, gram (-) bacterium; main factor of increase deaths was due to exposure more than susceptibility o Paul Louis Simone linked parasite to fleas (infected rodent > flea (carries infection from rat, bites human) > human)  Types o Bubonic plague, plus two other forms:  Appears 2 – 5 days after exposure  Symptoms: first sign is swelling of lymph nodes (Buboes), high fever after 3 days of deliriousness/hemorrhages of the skin, chills, general ill feeling, muscle pain, severe headache, seizures  Source: leftover microbes from previous pandemic that remained endemic for 7 centuries in susceptible black rats o (1) Septicemic (w/o development of buboes)  Infection occurs IN the blood, see signs ON skin  Symptoms: diarrhea, fever, low blood pressure, nausea, organ failure, vomiting along with abdominal pain & blood clotting problems – usually on limbs o (2) Pneumonic (bacteria moves through blood stream to the lungs – rapid, fatal form of the disease)  Infection IN lungs, death happens in hours  Symptoms: severe cough, frothy blood sputum, difficulty breathing, death occurs usually within 24 hours  Only form that is able to transmit person to person HLTA01 FINAL EXAM NOTES –  kills so fast that antibiotics are almost useless; can spread as easily as a sneeze o Normal cycle of transmission of Bubonic plague  Transmission of rodents & fleas, contact w/ humans = occurrence of plague  Cycle w/ domestic rodents & bubonic, could go straight to pneumonic – easy transmission b/w humans MANDY TRAN 7 o Plague today: NOT eradicated, remains endemic b/c of sylvatic & enzoonotic (death in 3-5 days, 50% mortality rate)  Antibiotics: streptomycin, gentamycin, sulfonamide, tetracycline st  1 vaccine invented by Waldemhar Haffkin using dead bacilli  VIDEO: 1345, biggest epidemic of plague – derived from marmots in Indonesia o Kindergarten teacher died of plague, everyone exposed but no secondary infections or other cases  Plague usually affects humans by accident, actually an animal disease; spread from squirrels to house hold pets o Still present today – San Francisco has teams of ppl trying to control plague  Deer mouse & ground squirrels are rodent reservoirs LEPROSY – “Hansen’s disease”  History o “disease of the soul” thought earlier to be a hereditary illness or caused by a curse or by punishment from God  Lepers were stigmatized (special clothing, notification of arrival, separate hospitals & often had to live in colonies called leprosarium/lazaretto/ leper colony/ lazar house) 1 leper house in England in 936AD  Lazarus was a patron saint of leper – the “order of lazarus” was the spiritual order of the knights infected  Mass of separation – practice by clergyman before people were separated under diagnosis  Mid 12 century, loss of civic status & removal from public office 13 century, 19,000 ‘leprosaria’ in use o 1550 BC Egyptian Papyrus document o 600 BC Indian writings, Charak Samhit o 320 BC records of ancient Greece, after the army of Alexander the Great returned from India o 250BC Asian textbook of medicine, Neichang wrote about disease o 62 BC in Rome w/ the return of Pompeii’s troops from Asia Minor o In 1179, 3 Lateran Council issued a decree urging the segregation of Lepers from society  Had to announce presence, wear distinctive clothing & had ritual burials o 1860 was the rediscovery of Leprosy due to foreign births – epidemic in Hawaii, used quarantine  1865 - 1974, Leper colony was established on Molokai  “Martyr of Molokai”- Father Damien joined as resident priest for 16 years: built homes, plumbing system, hospital reservoir & bandaged sores o 1917 leprosy bill was passed to established Carville Leprosarium in US  Drugs to control disease introduced in 1940’s but patients were still unable to marry, kids were put up for adopt–LTA01 FINAL EXAM NOTES o Up until 1960, public health laws restricted those w/ leprosy to use public transportation, airplanes or live free  1997, Clinton transferred it to a school/centre – patients will receive $30,000/year w/ lifelong medical care o **Pandemic reached epidemic levels in 12 century, peaked at 13-14 century & by 18 century Lazarettes had MANDY TRAN disappeared 8 o ** 3 countries: Brazil, Nepal & Timor leste HAVE NOT yet reached the target of 1 in 10,000 set in 1991 by the WHO  Canada & Leprosy st o D’Arcy Island, 1 case among Chinese railway workers in 1890s  Became prison for leprosy sufferers, “disease of the Chinese”  Left to deal on their own w/ 1 supply shift every 3 months for food, clothing, opium & coffins  Closed in 1957 when last person died o Sheldrake Island; Tracadie, NB, 1 case detected presumably b/c of sailors in 1815  1844, legislation passed to prevent the spread of the disease – isolated island, secluded for life  Lepers left unattended, living in a hut w/ weekly-monthly visits for rations otherwise no formal contact  Science contributions o 1873 1 objective &scientific appraisal, Dr. Hansen of Norway – “Hansen’s disease” discovered leprosy germ under a microscope; MYCOBATERIUM LEPRAE  M. LEPRAE is an acid fast bacillus w/ no known vectors OR reservoir hosts  NO way of detecting past infections or preventing apparent ones – what we know is derived from clinical cases  Cannot be grown in tissue culture, only humans, footpad of mice & 9 banded armadillos } 2 weeks to divide, slowly  Only 1-10 bacilli = infection within 5-6 months  Armadillos do not develop human type leprosy, disease usually more severe & fatal; incubation of 6months to 4years  Low body temperature may promote the disease (28-33C) o Excavations by V. Moller Christensen lead to description of the ‘facies leprosa’  Set of specific facial bone findings found in leprosy alone  Types (clinical manifestations) – immune systems determine how each spectrum is carried  Spectral disease: shows up in different forms & can get better or worse; can continue, revert or progress o Indeterminate (IL)  Earliest & mildest form w/ usually few lesions – scattered & nerve cells not usually targeted  Loss of sensation is rare, can continue, revert or progress in form of disease o Tuberculoid (TT)  1-2 years after exposure, less malignant  Development of large lesions, loss of sensation & affected nerves become thick = nerve damage, impairment o Borderline Tuberculoid (BT) HLTA01 FINAL EXAM NOTES –  Lesions are smaller but more numerous w/ more nerve damage o Borderline Lepromatous (BL)  Lesions are numerous but may now consist of papules, plaques & nodules  Punched out appearing lesions that look like inverted saucers are common MANDY TRAN 9 o Lepromatous (LL)  Most severe and never reverts back to less severe form  Early symptoms: nasal stuffiness, discharge, bleeding & swelling of legs and ankles  Only treatment will make better & even become more severe if untreated in due time  Nerve cells are impaired – bleeding, nasal discharge  Following problems may occur:  Skin thickens, eyebrows & lashes are lost, nose deformation/collapses, ear lobes thicken, photophobia (light sensitivity), blindness, enlarged liver & lymph nodes, hoarseness of voice, fingers & toes become deformed o Most patients develop Tuberculoid type which develops in 1-2 years after exposure vs. Lepromatous is longer  Due to Osteoporosis, death results most commonly from renal failure, pneumonia & tuberculosis  Patients DO have antibodies to M.LEPRAE antigens, just not productive  Leprosy is an endemic disease, those that are exposed don’t contract it Tuberculoid Lepromatous  Severe nerve damage  Cell mediated immunity w/ T-helper cells & Interleukin-  T Helper cells DO NOT respond to bacilli 2 secretion  Gamma interferon is not produced macrophages not activated  Bacteria multiplying in Schwann Cells that insulate  Bacteria multiply within macrophages & disease spreads nerves = numb w/ multiple organ involvement  b/c laminin, (outer surface of cells) is adhered to using  ^ Leads to facial deformity AND Osteoporosis & bacterial surface protein called H1P  invasion shortening of digits, damaged testes & no neutral  over time, immune system attacks Schwann cells & remission damage nerve: loss of sensation, degraded bones  Diagnosis o Based on clinical symptoms – lesions, loss of sensation  ** spread by bacilli shed from the skin, mostly from nasal secretions though route of entry is uncertain, possibly HLTA01 FINAL EXAM NOTES inhalation b/c bacteria cannot penetrate skin directly – o Skin smear observed for M. LEPRAE o Relies on microscopic examination & evaluation of the response of the patient to a pin prick or heat  Examination of ppl w/ tuberculoid lesions stained for acid fast – bacillus is diagnostic method – Hansen 1873 MANDY TRAN 10  Treatment o Chaulomoogra nut, oil extracts o Promin (1941), type of sulfone o Dapsone (1950) o WHO recommends multi drug therapy (MDT)  Combination of 3 drugs to deal w/ resistance to certain drugs of those victims of leprosy  Dapsone, Rifampicin & Clofazimine at a 6-24 month period for ppl w/ Lepromatous (LL) o BCG vaccination – a tuberculosis vaccination decreases susceptibility of contracting leprosy  Shows the closest antigenicity of all mycobacteria to M.LEPRAE o India has introduced own vaccine, Leprovac – 3 doses in 3 month intervals  MYCOBACTERIUM W (Mw) vaccine stimulates the immune tolerance & provoking an immune response that kills & clears disease from body  Resembles action w/ Tuberculosis vaccine, BCG & clearance of leprosy bacilli  Act by triggering the release of cytokines; enhance killing capacity of macrophages TUBERCULOSIS – “THE WHITE PLAGUE”  Transmission o Spread through the air by coughs/sneezes  Each droplet nuclei (airborne particles) can contain 1 & 3 bacilli  Each sneeze contains 100,000 nuclei droplets o Dry bacilli can remain viable for months, transmit though dust o In pulmonary TB, Granuloma forms in lung tissue upon inhalation  What happens when TB enters the body? o Tubercle bacilli can remain viable throughout the host’s lifetime  Can remain dormant OR cause active disease – when immunity /resistance of body fails o Distinguish b/w infection & active disease  Infection: disease is prevalent, multiplying, slight damage  Active: develop symptoms, etc.  10% chances of contracting active form in lifetime o Indefinite & variable incubation period HLTA01 FINAL EXAM NOTES –  Etiology o MYCOBATERIUM TUBERCULOSIS, an acid fast rod shaped bacillus  Evolved from M.BOVIS after domestication of cattle in 8000 – 400BC  After it is dyed, it does not decolorize on subsequent treatments to minerals MANDY TRAN 11  Paul Ehrlich retained colour w/ red fuschin & acid washed  Affects lungs & almost any other part of body – causes diseases in: meninges, intestines, lymph glands, skin, spine & genitals o 3 main types of the human bacillus  Type 1 – found in India; least virulent  Type A – Africa, China, Japan, Europe, N America  Type B – Exclusively Europe & N America o Forms – commonly affects infants & young children, fatal within few weeks/days  Pulmonary TB (most common form)  Bovine type may lead to Affects are constrained to lungs  Acute Miliary TB  grain like tubercles form in parts of the body  tends to be fatal in short weeks/days  Scrofula  Affect intestine & larynx  Lymph nodes in the neck are affected = swelling  Pott’s Disease  Fusion of the vertebrae & deformation of the spine – lead to hunchback  Lupis Vulgaris  Infection of the skin  Addison’s disease  The adrenal cortex is targeted, destroying adrenal function  Symptoms o Frequent & violent cough = purulent sputum sometimes w/ blood – only advanced stages do patients experience o Systematic symptoms: fatigue. Lethargy, aneorexia, weight loss, irregular menses, anxiety, chills, aches, sweats & fevers  Some ppl may even develop mold or asymptomatic cases where recovery happens before realization  Tubercle bacilli itself doesn’t damage body but cellular & tissue damage arise from allergic reaction – hypersensitivity (response contact) o HAVE A TB Infection  Feel sick, weak, lose appetite, weight loss, fever, night sweats HLTA01 FINAL EXAM NOTES – o Consistent coughing over 3 weeks = indication  Cough phlegm, mucous, etc.  Close to blood vessels, cough of blood  Chest pains when breathing MANDY TRAN 12 o Diagnosis – TB is a disease described by classic symptoms  Tuberculin test – not a cure but a diagnostic test  Smaller dose of PPD is injected into forearm, within 48-72 hours inflamed area appears if exposed to TB  ** (+) skin test does not mean an active infectious disease only exposure to  X rays – allows the tubercular lesions to be visible before apparent symptoms  Stethoscope –“acoustic picture”  Cannot identify cause of abnormal sounds  Positive sputum smear  Susceptibility/ Risk factors o Host dependent factors – age, gender, genetics  AGE – infancy, puberty & old age are periods of low resistance & high susceptibility  when younger = more likely primary infection become active – death, infants usually w/ military TB  NO IMMUNITY AFTER EXPOSURE: early exposure = high mortality rates in middle/old age  GENDER – female > male death during epidemic, but reverse during decline – after age 30  Due to the onset of menses = metabolic changes & need for more protein: when unavailable, resistance drops (Childbirth)  GENETICS – heredity does influence person’s risk (genetic pool is crucial to resistance) but mechanism of heredity hasn’t been determined  Jews are more resistant vs. population w/ no exposure = acute epidemics of disease o Environmental factors  Crowding - # people in a room = increase in a person’s changes of infection b/c of recycled air of those w/ disease in cramped quarters  Nutrition – protein is crucial to the resistance of tuberculosis  Working conditions – workers in “dusty trades” inhale particulate matter = inflammation of lungs, increase in risk of TB  Physical exertion, stress, smoking & socioeconomic status = combination of factors mean industrialization improves mortality & lowers both that & morbidity rates of TB o Persons most at risk for TB  Close contacts of a person w/ TB disease  From a country w/ high rates of TB  Those w/ weakened immune systems –LTA01 FINAL EXAM NOTES  People w/ HIV/AIDS  HIV & TB = lethal combination b/c HIV weakens the immune system, more likely to become sick by bacillus MANDY TRAN 13  TB is the leading cause of death among ppl who are HIV+ (opportunistic infections take over = death) THE GREAT POX SYPHILLIS  History o Began w/ eruption of MORBUS GALLICUS in late 15 century o 1494: King Charles VIII of France invades Italy o Outbreak of a new epidemic in Naples  The following year, mysterious affliction reported in England, France, Germany o Columbus return from the New World to Europe th o 19 century = worse o Pamphlet on syphilis, A fine treatise on the origin of the French evil appeared in different languages – printed during the course of a syphilis epidemic o Girolamo Fracastoro – Syphillis = seed of contagion, 1530 poem about shepherd boy named Syphilus  Not common term until 18 century o Philippe Ricord  Demonstrated that Gonorrhea & Syphilis were different diseases  Determined 3 stages o Rudolph Virchow  Established that syphilis was spread through the body by the blood  Explains how disease affects the rest of the body as well as psychological problems o Shaudinn & Hoffman  Discovered germ that cause syphilis, spirochete: Treponema Pallidum (spiral, threadlike & stains poorly)  “coiled hair” in chancres  Theories o 1) Introduced to Europe from the New World – Columbian theory  Written record – documented that men had similar lesions (transmission from new world)  Skeletal remains from the Americas  The pattern of spread of the disease – upon the return of Columbus o 2) Pre Columbian/Anti Columbian theory; NOT introduced  Unitarian vs. Non Unitarian theory th  Many populations of native Americans themselves were decimated by syphilis in the 16 century after the arrival HLTA01 FINAL EXAM NOTES – of the Europeans  Same organism that causes the disease: Yaws, Pintas, Endemic Syphillis, Veneral Syphillis but due to varying climates = different disease MANDY TRAN 14  OR series of mutations of Treponema bacteria that cause disease  Disease agent o TREPONEMA PALLIDUM, “pale corkscrew thread”  Difficult to diagnose & may affect the nervous system  mental instability  No spores, cannot be cultured but can be grown in rabbits & guinea pigs  Different subspecies look exactly the same; ALL susceptible from penicillin  Extremely fragile spirochete surviving only briefly outside the host – ONLY NATURAL HOST IS HUMAN  Transmission stages o Primary Stage  marked by the appearance of a single chancre  local tissue reaction at the site of spirochete inoculation  Untreated, may heal in 2-6 weeks on own o Secondary Stage, 6-8 weeks – early “latent stage”  skin rash and mucous membrane lesions  rough, red or reddish brown spots on the palms of the hands and bottoms of the feet  Occurs in first 2 years of infection, untreated will heal on itself after rash o Tertiary Stage/Latent  without treatment, the disease may damage the internal organs, including the blood vessels, bones, brain, eyes, heart, joints, liver and nerves  Present in all tissues, especially the blood  Affect heart and CNS = insanity  Difficult to diagnose o Infectious during the primary, secondary, early latent stage, NOT late tertiary stage  Methods of transmission o Sexually transmitted disease – direct w/ person to person contact, sores o Close contact w/ open lesion o In utero (mother to fetus) o Transfusion of infected blood HLTA01 FINAL EXAM NOTES –  Important events/stories (3) o John Hunter – founder of scientific surgery  Wanted to prove true/false that Gonorrhea & Syphilis were MANDY TRAN 15 often confused w/ each other as 1 in the same  Argued that they were the same but manifested in 2 different forms – wet & dry case  Undertook flawed self experimentation  He developed the signs of Syphilis & concluded the 2 infections were the same (Chancre, skin rash, etc.)  Eventually died of heart problem – tertiary syphilis  Injected himself w/ both disease but contracted only 1 o Tuskegee Syphilis study  Designed to document the natural history of disease – denied treatment to participants  Came to symbolize racism in medicine, ethical misconduct in medical research, paternalism by physicans & gov’t abuse of society’s most vulnerable  Oslo & Rosahn study } all 3 studies on the course of smallpox infection  Treatment – NO VACCINE ! o Mercury (John Hunter) o Penicillin (Sir Alexander Fleming) – drug of choice today  Magic bullet (Ehrlich)  Salvarsan, effective in reducing severity of disease but toxic used until 1943 o Treatment will kill the syphilis bacterium & prevent further damage but it will not repair damage already done o Diagnosis  Examine material from a chancre  Blood test: Wassermann Test  Serological reaction, tissues reacted (+) to syphilitic area  VIDEO o Come to depend on treatments = thinking that disease are simple, NOT  Epidemic of Syphilis & Gonorrhea; patients would rely on penicillin for treatment  Little was done to prevent & educate safe sex = AIDS o Naples welcomed soldiers into city and their beds  New disease, lets the body literally rot away  Deformations b/c of painless chancres and purple lesions/ulcer o AIDS is the modern day Syphilis of centuries ago o Used Syphilis as PROOF that the world was doomed HLTA01 FINAL EXAM NOTES –  People were being punished for being sexually active o First disease EVER to have a magic bullet; treatment targeted at a germ SMALLPOX MANDY TRAN 16  Historical context  Old world disease and an indiscriminate disease o Everyone may be susceptible, no relation to any specific grouping o Contagious if no immunity o Pox diseases derived through domestication of animals  10,000 BC - first agricultural settlements in NE Africa and spread to India by means of ancient Egyptian merchants  Earliest evidence on Egyptian mummies (1570–1085 BC) o Pharaoh Ramses V (died 1156 BC) – pockmarks  Described1122 BC in China and is mentioned in ancient texts of India o Evidence that it was prominent in Asian countries  100AD – Plague of Antonine o Combination of other diseases like Malaria  Europe - frequent epidemic during the Middle Ages  16 century became a serious disease in England and Europe o Was contained but w/ industrialization = spread  Effects of smallpox related to war outcomes o Plague of Antonine  Decline of Roman Empire b/c of returning soldiers from Italy o New world in the 16 century - fall of the empires of the Aztecs and the Incas  Local population infected b/c of exposure of disease o Contributed to the settlement of N America by the French & English (1617)  Native population hit with epidemic of small pox disease  Smallpox in Canada o In1796, Dr. John Clinch forwarded a letter to Dr. Edward Jenner in Gloucestershire requesting information about using cowpox pustule matter  As a way of life long protection w/ vaccination  1799 - vaccinating people in Newfoundland o Became common practice th  Development in the 20 Century o DID NOT INCUR LIFE LONG IMMUNITY BY VACCINE  Only from past exposure = “childhood disease” HLTA01 FINAL EXAM NOTES –  Late 19th century, it was realized that subsequent revaccination was necessary  Mortality rates declined as vaccination became common o In 1950s, smallpox was eradicated in many areas in Europe and N America MANDY TRAN 17  Public health centers involve  Change in infrastructure, hygiene, etc.  Picked up practice of vaccination = eradication  Social/contextual events of vaccination = riots, squads & public policy vs. public health o In 1958 – report of smallpox in 63 countries  WHO organization formed after WW2 o Program of eradication began in 1967  Different features of disease = how to ensure eradication  No longer existed in 1977  Impact on populations o Global campaign succeeded - smallpox eradicated in 1977 o On May 8, 1980, the World Health Assembly announced that the world was free of smallpox  Recommended the seize of vaccination o August 1978 - Janet Parker (1938 – 1978) o University of Birmingham Medical School  Last person to contract disease through indirect contact due to inhalation  Not natural case  Developed variola major grown in research lab o Her mother contracted the disease but survived o Radical changes in how dangerous pathogens are studied  Researcher committed suicide o Debate over stocks of vaccine  Keep, destroy or transfer them?  Decided to store in the case of event of their uses to be used in one point or another o Biological warfare  First instance w/ smallpox o French-Indian War (1754–1767) - deliberate use of smallpox  Was used to tame hostile people against British troops HLTA01 FINAL EXAM NOTES –  Amerhyst used smallpox to diminish American Indian population  Purposely infected blankets, set off epidemic amongst Indians = gaining control of the fort  Directed outcome of the war o Slave trade MANDY TRAN 18  Became practiced to supplement the dwindling labour force  Disease was prominent in old world Africa = spread to Americas when slaves were brought over  Related etiology o Virus : Genus - Orthopoxvirus, fami
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