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Natural Disasters Part One: Pathophysiology Part Two: Environmental Physiology Part One - Pathophysiology Definition : The functional changes associated with or resulting from disease or injury; the study of such changes (distinguished from s structural defect)

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Natural Disasters

Part One: Pathophysiology

Part Two: Environmental Physiology


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Part One - Pathophysiology

  • Definition: The functional changes associated with or resulting from disease or injury; the study of such changes (distinguished from s structural defect)

  • Web site on medical physiology & pathophysiology textbook: http://www.mfi.ku.dk/ppaulev/content.htm


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Infectious Disease in the Aftermath of a Natural Disaster

  • Widespread outbreaks of infectious disease such as cholera or typhoid after hurricanes are not common in areas where such diseases do not naturally occur i.e. pre-existing level of disease in a community affected by disaster is a significant parameter, however there was a discovery of an endemic focus of Vibriocholerae in the US

  • A disease may be brought into a disaster area from elsewhere even by relief workers e.g. 1976 Guatemalan Earthquake occurred in the winter influenza season in North America thus relief workers from NA could have brought influenza with them(however, most outbreaks that occur are almost always from diseases that were already in the disaster-affected area before the disaster struck)


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Infectious Disease in the Aftermath of a Natural Disaster

  • Communicable disease outbreaks of diarrhea & respiratory illness can occur when water & sewage systems are not working & personal hygiene is difficult to maintain as a result of a disaster – food storage & water purification become major issues as is adequate shelter and warmth


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Infectious Disease in the Aftermath of a Natural Disaster

  • Decaying bodies create very little risk for major disease outbreaks

  • Short bouts of diarrhea/upset stomach & colds/respiratory diseases sometimes occur among those living in large groups in shelters (close contact with minimal sanitation & available clean water)

  • Drowning (after hurricane/flooding) may be more of a risk than contacting infectious disease

  • Clean water (boiled minimum of 1 minute), food stored properly and personal hygiene (including handwashing & clean wound management) very NB


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Can a Natural Disaster Lead to an Epidemic?

  • Web page for discussion (& photos)

    http://ndms.chepinc.org/data/files/3/84.pps

    (“disease after disaster” on web browser: Infectious Disease Issues in Natural Disasters)

  • Phases of a Disaster:

  • Impact phase (0-4 days) extrication & some soft tissue infections

  • Post impact Phase (4 days-4 weeks): airborne, food-borne, waterborne diseases

  • Recovery Phase (>4 weeks): those with long incubation periods & of chronic disease


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Can a Natural Disaster Lead to an Epidemic con’t?

  • Environmental Factors:

  • Climate (cold = airborne; warm = water-borne)

  • Season (e.g. US = winter = influenza; summer = enterovirus

  • Rainfall e.g. El Nino years increase malaria

  • Geography e.g. isolation from resources


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Types of Disasters & types of Problems

  • Earthquake – crush & penetrating injuries

  • Hurricane & flooding – water contamination, vector borne diseases

  • Tornado – crush injuries

  • Volcano – water contamination & airway disease


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Examples of Epidemics after Disasters – a Short History

  • San Francisco – 1907 – Fire – Plaque (quarantine failure)

  • Duluth, Mn. – 1918 – Forest Fire – Influenza – (crowding, epidemic)

  • Haiti – 1963 – Hurricane – malaria (vector control stopped)

  • Italy – 1976 – Earthquake – Salmonella Carriers (water sanitation stopped)

  • Dominican Republic – 1976 - Hurricane – typhoid, GI, hepatitis, measles (crowding, flooding, chronic disease)


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Examples of Epidemics after Disasters – a Short History

  • Popaya, Colombia – 1983 – Earthquake – viral hepatitis (water sanitation)

  • Equador – 1983 – Flooding – Malaria (vector increase)

  • US – 1992 – Hurricane Andrew

  • SE Asia – 2004 – Tsunami –

  • US – 2005 – Hurricane Katrina & Rita

  • Pakistan – 2005 - Earthquake


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Infectious Disease in the Aftermath of a Natural DisasterSpecial Considerations/Example – Mold

  • After flooding/hurricanes, massive mold contamination of buildings submerged in water likely a certainty especially for buildings/structures soaked for >48 hours (e.g. after Katrina, ~60-80% of residential structures in New Orleans sustained severe flood damage)

  • Exposure routes can vary but primarily are aerosol and ingestion (also through open skin wounds is a possibility) – people can be infected by either spores or mycelial fragments


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Infectious Disease in the Aftermath of a Natural DisasterSpecial Considerations – Mold

  • Symptoms/Disease effects can range from immunologic/allergic response to hyper-sensitivity pneumonitis to long-term ingestion of toxins (which could lead to cancer – not likely a serious consequence after a flood)

  • Pathophysiology of mold then due to either an immunological, infectious or toxic interaction with host

  • It is common for several of these mechanisms to contribute to pathogenesis of a fungal-induced disease


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Infectious Disease in the aftermath of a Natural DisasterSpecial Considerations – Mold

  • Immunological response – IgE-mediated (allergic) responses (IgE is an immunoglobulin (antibody) protein in nature secreted by plasma cells (some Igs secreted by lymphocytes) whose production is elicited by exposure to an allergic substance (allergen – in this case, mold spores or mycellium) – mostly bound to mast cells & basophils that have a IgE specific receptor (it has a high CHO content) – IgE attaches to foreign substance & assists in destroying them – IgE is 1 of 5 major classes of Immunoglobulins present primarily in skin & mucous membranes – mediates type 1 hypersensitivity (can be involved in allergy, asthma, eczema, allergic conjunctivitis, allergic rhinitis and anaphylaxis)


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Infectious Disease in the aftermath of a Natural DisasterSpecial Considerations – Mold con’t

  • Atopy (genetic predisposition to form IgE responses to aeroallergens) is a risk factor

  • Normal immune response to an antigen is to produce antibodies which mark the foreign substance for removal by phagocytosis

  • Pathophysiology of an allergic response is primarily due to repeated exposure to antigen in which IgE molecules attached to mast cell recognize & bind again to the allergen but this time causing degranulation of the cell (triggered by cross-linking of adjacent IgE molecules) = this stimulates release of histamine & other chemicals


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Infectious Disease in the aftermath of a Natural DisasterSpecial Considerations – Mold con’t

  • histamine cause dilation & increased permeability of small blood vessels leading to typical allergy symptoms (sneezing, runny nose, tearing eyes & smooth muscle contractions that can lead to breathing difficulties (antihistamines are used to treat these symptoms) & a decrease in blood pressure

  • Histamine is a physiologically active amine which can also be released after tissue injury as well as during neutralization of foreign material

  • its release in skin, causes edema (swelling), can cause acute urticaria (rapidly appearing hives accompanied by sever itching)


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Infectious Disease in the aftermath of a Natural DisasterSpecial Considerations – Mold con’t

  • Anaphylaxis – an acute allergic response which may lead to a whole-body, life-threatening reaction that can occur within seconds of exposure to an allergen – develops when widespread mast cell degranulation triggers abrupt dilation of peripheral blood vessels, causing a precipitous drop in blood pressure - death may occur within minutes (more often seen with exposure insect venom, peanuts or allergy to Penicillin than to molds seen after flooding)


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Infectious Disease in the aftermath of a Natural DisasterSpecial Considerations – Mold con’t

  • Infectious response (either humoral &/or cell-mediated immune responses) – (exposure to mold after sever flooding/hurricane can result in 2 types of inhalation fevers: a. humidifier fever & b. organic dust toxic syndrome – both can be characterized by fever, flu-like symptoms, general weakness, headache body chills, coughing) these are not thought to be associated with immune response but rather a nonspecific inflammatory response & usually removal from antigen is sufficient for recovery - not to be confused with hypersensitivity pneumonitis which is based on an immune response – accurate history is of paramount importance) – next pages on immune response


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Humoral & Cell-mediated Immunity (associated with response to infective agents)

  • Humoral immune response – involves the activation & clonal selection of B cells (B lymphocytes), resulting in the production of secreted antibodies that circulate in blood and lymph

  • Cell-mediated immune response involves the activation & colonal selection of cytotoxic T cells (T lymphocytes) which directly destroy certain target cells

    Central to the acquired immune response is the helper T cell which responds to peptide antigens displayed on antigen-presenting cells & ion turn stimulates the activation of nearby B cells & cytotoxic T cells


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Cytotoxix T cells: a response to infected cells (& cancer cells)

  • Effectors of cell-mediated immunity

  • Eliminate body cells infected by viruses or other intracellular pathogens (& cancer cells & transplanted cells)

  • When binds to specific antigen complexes on an infected body cell, these cells are activated & differentiated into an active killer

  • Cytokines secreted from nearby helper T cells promote this activation

  • Activated cytotoxic T cells secrete proteins that act on bound infected cell leading to its destruction


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B Cells: A Response to Extracellular Pathogens

  • Antigens that elicit a humoral immune response are typically proteins & polysaccharides present on surface of bacteria or incompatible transplanted tissue

  • Activation of B cells is aided by cytokines secreted from helper T cells activated by the same antigen

  • B cell proliferates & differentiates into a clone of antibody-secreting plasma cells & clone of memory B cells – depending on type of antibody produced, various mechanisms of disposal of antigens are initiated (e.g. viral neutralization, agglutination of antigen-bearing particles & precipitation of soluble antigens enhances removal by phagocytosis {often by neutrophils) where as activation of complement system & pore formation lead to cell lysis)


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Infectious Disease in the aftermath of a Natural DisasterSpecial Considerations – Mold con’t

  • Toxic response – many common molds can produce metabolites with a wide range of toxic activities such as antibiotic (e.g. penicillium), immune-suppressive (e.g cyclosporine), carcinogenic (e.g. aflatoxins), emetic and hallucinogenic (e.g. ergot alkaloids) – ingestion is a common route (but inhalation & dermal contact also possibilities) – mycotoxin production depends on species & strain of mold plus environmental conditions (e.g. temperature, water activity, light) & growth substrate – huge variability in pathophysiology of mycotoxins ranging from disruption of membrane permeability & functioning of ion channels (e.g. leakage of K & influx of Na) to changes


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Infectious Disease in the aftermath of a Natural DisasterSpecial Considerations – Mold con’t

  • Toxic reaction con’t: to changes in pH to DNA breaks, chromosomal abnormalities & inhibition of protein synthesis (can be a biological weapon) – several theories on how a mycotoxin can inhibit protein synthesis: one is related to toxin’s affinity for a part of the ribosomal subunit, therefore inhibiting protein synthesis at the initial step while another theory suggests that it is due to inactivation of peptidyl transferase which inhibits the terminal step of protein synthesis


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Opportunistic organisms

  • Many organisms do not cause disease and live basically symbiotically with humans

  • However, provided the “right” environmental conditions, some organisms not originally pathogenic (disease-causing) become pathogenic capitalizing on the “opportunity” e.g. Pseudomonas after a sever burn to the skin

  • Natural disasters may provide ideal environments for opportunistic organisms to cause disease


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Infectious Disease in the aftermath of a Natural DisasterSpecial Considerations – Mold con’t

  • Greatest risk posed to those with impaired host defense systems (immunodeficity diseases, organ transplant recipients, stem cell recipients, cancer-themotherapy patients, individuals taking corticosteroids, etc.) in which exposure to mold could lead to death


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Infectious Disease in the aftermath of a Natural DisasterSpecial Considerations/Example: Cholera

  • Causitive agent – Vibrio cholerae (gram negative bacterium

  • Major symptom – severe watery diarrhea with 50% mortality if untreated

  • Bacterial model for toxin mediated disease


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Infectious Disease in the aftermath of a Natural DisasterSpecial Considerations: Cholera con’t

  • Pathophysiology:

  • Organisms enter small bowel & colonize – pilus required – hemagglutanins – accessory colonizing factor – porin like proteins

  • Produces toxin – A with 5 B subunits – A cleaves to A1, activates adenylate cyclase (enzyme involved with converting ATP to cAMP) – leads to increase Cl secretion & decreased Na absorption resulting in a net flow of H2O, K & HCO3 into the bowel


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Infectious Disease in the aftermath of a Natural DisasterSpecial Considerations: Cholera con’t

  • May be asymptomatic; most cases show no symptoms before diarrhea - some people develop rapid diarrhea (with some emesis) most sever day 1-2 (usually stops by day 6 or individual may lose 10% body weight in 2 days (children & elderly at risk) with accompanying “thickening” of blood, shoke & death occurring in 2-48 hours (18 average) – infected people are carriers until they develop diarrhea, then they “have” cholera

    (e.g. Of non-cholera dysentery: Giardia, E. coli, Salmonella, Shigella, Campylobacter, Yersinia, Viral hepatitis)


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Importance of Other Related Sciences/Studies & their Definitions

  • Etiology

  • Epidemiology

  • Pathology

  • Pathogenesis

  • Endemic vs. Pandemic vs. Epidemic

  • Virology vs. Bacteriology vs. Parasitology

  • Clinical Symptoms, Predisposing Factors, Infectivity, Carrier-state


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Part Two - Environmental Physiology - Introduction Definitions

  • Provides a basic understanding of physiological responses to natural and man-made environmental conditions

  • Sub-topics often studied in environmental physiology include comparative aspects of temperature regulation, the effects of altitude and hudrostatic pressure, life existing without light and the dive reflex across the species


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Introduction con’t Definitions

  • It is important to study animals in the context of their own habitat and their real needs – this adds traditional natural history to the study of comparative physiology

  • Primary aim of ecological or environmental physiology is to understand how animals function in and respond to their natural environments, at all stages of their life cycles


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Environmental Changes Definitions

  • Overall, environments may be very stable on all timescales relevant to living organisms, e.g. deep seas or,

  • They may vary on an evolutionary and geological timescale of tens or hundreds or thousands of years as land masses move, sea levels rise and fall, material erode and deposit elsewhere, an rivers change their courses

  • There may also be changes with a regular annual, lunar, or daily cyclicity

  • There are changes on a much shorter timescale of hours or minutes or seconds, as the weather changes


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Environmental Changes con’t Definitions

  • Magnitude of change is a relative phenomena – short-term changes are especially important in relation to very local microenvironments & therefore to very small animals (e.g. the difference between the environment above a leaf & the environment below it may be profound, and both may change within seconds in relation to varying solar radiation {insulation}, air movements & rainfall)

  • Changeable environments put a high selective premium on versatility or tolerance in animals, rather than on precise adaptations to particular conditions (this may be particularly true where man has intervened in the natural ecosystem to put new stresses on animals, whether from habitat destruction, climate modification or the introduction of many kinds o toxic chemicals)


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Environmental Changes con’t Definitions

  • It is significant to note, that many animals, for most of their lifetime do not need extreme physiological adaptation & reply instead on behavioral strategies to avoid the worst of their difficulties – however, in the wake of a natural disaster (as well as in the cumulative damage done through pollution), their environments are drastically changed, some temporarily, some permanently


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What does an organism need from its environment? Definitions

  • Source of palatable water

  • Source of oxygen (note: some organisms are anaerobic)

  • Source of energy (& other nutrients)

  • Climate within tolerable limits

  • Shelter (including appropriate breeding “grounds”) - depends on species

  • & for survival of the species, access to potential mates & protection/defense from predators


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Natural Disasters Change Environments often Drastically & Suddenly

  • No time for “evolutionary” adaptations; adjustments must be made quickly

  • Relationships between animals & their environments maybe forever changed

  • Items provided by the environment may be reduced or totally lost (habitat, nesting grounds, breeding grounds, feeding grounds, prey reduction &/or predator loss (either can upset the natural “balance”), other food source loss or reduction, contaminated water or water source loss, permanent changes to landscape (e.g. large crevices, river direction) may separate populations, environmental cues which drive behavior may be gone, etc.

  • = survival “strategies” no longer effective


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Natural Disasters as an Extreme Type of Abiotic Stress Suddenly

  • Abiotic stress – a wide range of threats to animal health not associated with other living organisms which would include nutrient deficiencies, nutrient & non-nutrient toxicities, drought, temperature and salinity stresses (extreme weather and pollution of all types would be examples of abiotic stresses)

  • Within limits, animals have adaptive abilities to cope with moderate changes in their environments, especially if these changes are temporary (e.g. seasonal temperature fluctuations) & not extreme (e.g. some animals may hibernate, enter torpor or migrate) but they have limited ability to adjust to sudden & drastic/permanent changes – only those individual able to acclimatize to these extreme changes carry on


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Bottleneck Effect Suddenly

  • Genetic drift resulting from a reduction in a population, typically by a natural disaster, such that the surviving population is not longer genetically representative of the original population

  • By chance, among the survivors certain individuals may be over-represented while others may be under-represented; some may be lost entirely


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Bottleneck Effect Suddenly

  • Genetic drift may continue to have substantial impact for many generations


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A web site for more info Suddenly

  • http://www.pbs.org/wgbh/evolution/darwin/origin/index.html


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