Marine Mammal Toxicology Flashcards

1
Q

What are the four categories of hydrocarbons? Which is the most toxic?

What are some effects of benzene exposure?

The toxicity of petroleum on wildlife depends on several factors - what are they?

A
  • General Oil Toxicity
    • The distillation process of crude oil can either decrease or increase proportion of components that are acutely or chronically toxic within the resultant product.
    • Crude and refined petroleum products contain thousands of different organic and inorganic compounds.
      • Oils – 98% hydrocarbons, also sulfur, nitrogen, oxygen, trace metals, porphyrins.
    • Hydrocarbons are categorized into 4 categories:
      • Alkanes.
      • Naphthenes
      • Alkenes
      • Aromatics
        • Considered the most toxic
        • Rings of six carbons connected by alternate C-C bonds
        • Benzene strongly associated with carcinogenicity, organopathies, death at high exposure levels in vertebrates.
          • Readily available to biological systems due to high water solubility.
          • Often only really found immediately following a spill since they are so volatile.
        • Many compounds containing two or more aromatic rings i.e. polynuclear aromatic hydrocarbons, have caused carcinogenicity, repro failure, immunotoxicity in lab animals.
          • Significant exposure to these larger compounds may take place through ingestion of exposed prey items, grooming, preening.
    • Toxicity of petroleum to wildlife is dependent upon:
      • Ode of exposure
      • Duration of exposure
      • Characteristics of the product (i.e. crude vs refined vs fresh vs weathered)
      • Species sensitivity
      • Age and health of individual
      • Numerous other variables
    • May impact foraging behaviors, migration patterns, ecological distributions in addition to impacting individuals.
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2
Q

How do oil spills affect otters?

What are some of the clinical signs of affected otters?

Why are they so susceptible?

What are the long-term effects of exposure?

A
  • Sea Otters
    • One of the most at-risk spp during spill events.
      • Dense fur coat rather than blubber or fat layer, unable to repel water when oiled -> hypothermia.
      • Otters must also constantly groom to maintain trapped air layer within the pelage, can result in significant internal exposure.
      • High metabolic rate, increases to compensate for loss of insulation and increased activity levels in trying to groom.
      • Dietary intake can result in internal exposure to PAHs and petroleum compounds contained in prey.
      • Physiological and behavioral problems.
        • CNS depression, resp distress, interstitial pulmonary emphysema and aspiration pneumonia, anemia, adrenal gland dysfunction, hepatic necrosis and GI erosions, hepatic/renal lipidosis.
        • Some of those may be compounded by shock and chronic stress associated with capture and rehab.
    • Long-term effects: Decreased survival rates.
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3
Q

What are some of the more common effects of oil exposure in pinnipeds?

How does oil affect pups differently than adults?

A
  • Pinnipeds
    • High prevalence of conjunctivitis and burns in Galapagos sea lions oiled in 2001, no long-term impacts on the population detected.
    • Documented clinical and histopathologic effects of oil in pinnipeds:
      • Ambulatory restrictions, dermal irritation, thermoregulatory imbalance, conjunctivitis, corneal edema, gastrointestinal irritation, liver and renal tubular necrosis.
      • Seal pups may drown due to inability to swim.
      • Oiling does not appear to disrupt mother-pup interactions.
      • Harbor seals observed exhibiting abnormally tame or lethargic behaviors that may be explained by brain lesions caused by toxic systemic effects of inhaled hydrocarbons in some individuals.
      • Oil may be ingested through prey spp, grooming, nursing.
      • Low-molecular-wt petroleum hydrocarbons rapidly absorbed and distributed to various target organs such as liver and blubber.
      • Toxicity depends on chemical composition of ingested oil and leads to organ damage and/or acute death.
      • Internal exposure is the route of greatest concern other than young pups/fur seals more reliant on fur for thermal insulation.
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4
Q

Do cetaceans actively avoid oil spills? How?

How did the Exxon Valdez spill affect killer whale populations?

What were some of the effects of the Deep Water Horizon spill on the bottlenose dolphins there?

A
  • Cetaceans
    • Cetaceans far less susceptible to oiling than marine birds.
    • May be able to see sheen of oil on water surface, but aversive behaviors only seen after animals came into contact with it.
    • Less likely or able to avoid oil at night (supports visual cues).
    • Thin sheens resulted in erratic responses and suggested that the sheen was not detectable acoustically or visually, did not produce a strong tactile response.
    • Ability to detect sheen related to the thickness of the slick and composition of oil.
      • One study – Could detect 6mm crude, residual, and refined motor oils and 17 mm thick slicks of diesel fuel, but could not detect 6 mm thick slicks of leaded gasoline or transparent mineral oil.
    • After Exxon Valdez, significant changes in killer whale stocks in/around PW Sound noted.
      • Feed primarily on harbor seals and Dall’s porpoises, ingest/inhale significant amounts of petroleum from oiled prey and succumb from toxicosis.
    • One study found like live BND captured in LA, USA where heavy and prolonged oil occurred during Deep Water Horizon spill showed evidence of hypoadrenocorticism (thin adrenal cortices) and were 5x more likely to have moderate to severe lung dz.
      • Increased risk of bacterial pneumonias.
      • Only 20% of pregnant dolphins in the area produced viable calves. Fetal distress, higher incidence of Brucella spp infections ID via lung PCR.
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5
Q

How do oil spills affect sirenians?

A
  • Sirenians
    • Aquatic herbivores, prefer low-salinity protected waters with abundant vegetation.
    • Effects of oil on sirenians is undocumented, no experimental studies.
    • Most likely to contact near-shore oil spills (not deepwater).
    • At risk for oil inhalation as nares are raised just above water surface during respiration.
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6
Q

How are polar bears affected by oil?

A
  • Polar Bears
    • Little is currently known, presumed similar to other heavily furred mammals.
    • Thermoregulatory issues, health effects due to ingestion from food items or grooming.
    • Impacts to denning females and cubs from oiling and disturbance from cleanup activities.
    • Ingestion of oil lead to anorexia, dehydration, anemia, and renal failure in one report.
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7
Q

What are the agencies that organize the response to an oil spill in the US?

Who is in charge of the wildlife response?

A
  • General Response to Oil Spills
    • US – All activities related to disaster response are coordinated through a defined Incident Command System (ICS).
      • Delineated by the National Incident Management System (NIMS).
        • Under Federal Emergency Management Agency (FEMA).
        • NIMS – Provides systematic, proactive approach to guide departments and agencies at all levels of government, nongovernmental operations, private sector to work together to manage incidents to reduce loss of life, property, and harm to the environment.
        • Unified Command (UC) – Governing body ultimately responsible for all decision-making processes.
          • Marine spills – Made up of a federal onscene coordinator FOSC (i.e. Coast Guard captain), a state on-scene coordinator SOSC, and a qualified individual from the responsible party.
          • +/- local government representatives.
  • Wildlife Response Activities During Oil Spills
    • Wildlife response activities exist within the Operations Section (Wildlife Branch) of the ICS or Environmental Unit of the Planning Section.
      • ICS activates Wildlife Branch -> Reconnaissance for affected and at-risk animals, deterring animals away from the region, search and collection of live and dead animals in the area, treatment, rehab, release of live oiled animals, documentation and necropsy of recovered dead animals. NOAA National Marine Fisheries Service has structures for different scales of response.
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8
Q

What is the most effective method to prevent marine mammal injuries from oil?

What is this called?

What methods are used?

A
  • Hazing
    • Most effective means to protect marine mammals from injuries assoc with oil exposure is preventing them from contacting oil in the first place.
    • Removing or keeping animals away from oil.
    • Deterrence actions only effective if there are safe locations to situate displaced animals, when species will not quickly return, and when the geographic area involved is small enough it can be effectively controlled.
    • Must be done under appropriate authority and oversight since it is designated as harassment or take under the US Marine Mammal Protection Act.
    • Methods – Close-range i.e. Oikomi pipes, explosive seal control devices, acoustic deterrents, prerecorded predatory or conspecific calls, vehicular traffic, or long-range i.e. acoustic harassment that causes pain, chemotattractants, air guns, midfrequency sonar.
    • No reports of success or failures of such activities has been publishes or analyzed.
    • Hazing plan must be developed that addresses benefits of keeping mammals away and risks to people and wildlife assoc with hazing, also costs and benefits assoc with taking no action.
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9
Q

When are live captures of marine mammals authorized?

Why is it important dead animals are collected during a spill event?

A
  • Search and Collection
    • Aka wildlife recovery.
    • All stranded marine mammals in the spill area that appear injured, debilitated, or otherwise nor normal should be collected if possible.
      • US – Has to be under appropriate wildlife management permits, data and samples must be collected following legally binding procedures.
      • Risk is higher for birds overall, but depends on marine mammal species and region.
        • Also depends on concentration i.e. high haul-out/pupping areas.
        • Marine mammal experts should be involved.
    • Live captures.
      • Captures should only be contemplated if they can be performed safely for people and animals.
      • Potential benefits of capture must outweigh potential negative consequences. I.e. small amt of oil on pinniped fur does not warrant capture.
      • In general, no rescue should be initiated on free-swimming or beached pinnipeds unless the animal in question is in obvious distress.
      • Rescuers should not enter rookeries, where disturbance might cause female/pup separation or cause other disruptions.
      • No active rescue on free-swimming cetaceans should be initiated where oiling is the primary problem, unless that cetacean is moribund, can be approached without avoidance behavior, and the capture vessel has the appropriate capabilities to take the cetacean on board safely.
      • Unless specifically authorized, no nondebilitated/nonstranded live animals will be collected.
    • Collecting dead animals.
      • Reduces contamination in environment, potential for secondary contamination of scavengers, prevents secondary oiling of the carcass at a later date, confirms source of oil, provides data for impacts.
      • Transport dead oiled mammals to a facility for evaluation.
        • Depending on dize and condition of carcass, resource availability and location.
      • Only a fracture of what has died will be seen.
        • Natural Resource Damage Assessment (NRDA) requires an impact assessment be done in a systematic and quantitative manner to estimate the impacts.
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10
Q

How are oiled marine mammals transported to care facilities?

How are life animals categorized in terms of oiling? What data needs to be collected on them?

On necropsy, what tissues need to be collected? Are there

A
  • Transport
    • Depending on size of spill may want to have dedicated transport personnel.
    • Smaller pinnipeds should be in a quiet, sheltered, well ventilated area in separate transport boxes, kennels, or cages.
    • Kennels containing fur seals or sea otters should be fitted with a raised bottom grate to avoid additional fur fouling.
    • Cetaceans and sirenians should be placed in a stretcher and placed on foam or soft substrate that is wetted continuously or covered with light, wet towels to prevent sunburn and desiccation. Can also transport at night.
    • Vehicles must have adequate ventilation.
    • Field stabilization techniques for live marine mammals prior to transport if will be > 1-2 hours before reaching the rehab facility.
      • Thermoregulation, fluids, remove excess oil from eyes and nares, emergency meds.
    • Monitor animals periodically during transports > 1 hour.
    • Chemical sedation during transport not recommended, can exacerbate difficulties with thermoregulation.
    • Hyperthermic animals can be sprayed gently with water, icea cubes can be added to top of cage and allowed to drip as it melts, or placed under a grate in the kennel.
    • Do not allow water to accumulate in the bottom of transport cages -> drowning.
  • Processing
    • Documentation and sampling activities.
    • Complete necropsy of collected animals.
    • Determine if death was due to exposure, and if animal was exposed.
    • Effort should be made to avoid implying that animals not appearing oiled on initial evaluation are truly oiled.
    • Categories: Visibly oiled (external, internal), not visibly oiled, or pending. Impacts from nonvisible oiling must come from further evaluation of samples i.e. histo or PAH analysis of biological samples.
    • Live animals – Minimize animal handling time. Collect demographic data i.e. species, age class, sex, photograph each animal, Collect external oil sample, begin intake form.
    • Necropsy approach specific to oiling – Sampling strategies for PAH analyses, where external skin swabs or scraping should be collected.
      • Tissues to collect in decreasing order of preference:
        • Bile, urine, whole blood, stomach and intestinal contents, blubber/fat, liver, kidney, lung, intestine, brain, muscle.
        • Fluids should be collected with sterile syringes or pipettes, transferred to Teflon vials (blood) or amber class vials (bile, urine).
        • Tissues should be cleaned with alcohol between samples, stored in solvent-rinsed Teflon-lined glass jars.
        • Collect duplicate samples when possible.
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11
Q

Describe the intake and prewash care of oiled marine mammals.

How are these animals triaged?

What data needs to be collected?

What samples need to be collected?

What care should be provided before these animals are washed?

A
  • Intake
    • Initial PE, medical evaluation of live, oiled animals.
    • Triage based on species legal status, age class, historical success of that spp/age class in rehab, medical status, and characteristics of spill response.
    • Key data to collect – Oiling evaluation, basic demographics, attitude/alertness, body condition, morphometrics, rectal temp, respiratory status, hydration status.
      • All oiled animals are assumed to be at least 5% dehydrated.
    • Systems to include – Neurologic, head/mouth, eyes/ears, heart/lungs, gastrointestinal, musculoskeletal, integument.
    • Collect blood for hematology (EDTA) and chemistry (serum separator). Blood should be taken on intake, prior to washing, and prior to release.
    • Other biomedical samples i..e. urine, fecal, microbiological swab, blubber bx, milk can be collected.
  • Prewash Care
    • Make sure physiologically stable prior to washing.
    • Address thermoregulatory problems, rehydration, feeding, and emergency case so animal is not in negative metabolic balance prior to washing.
    • If ingestion of highly volatile oil is suspected, activeated charcoal can be administered.
    • Young and malnourished animals can become easily hypoglycemic.
    • Criteria to be met to ensure animals are stable enough to withstand cleaning – good alertness/attitude, blood values WNL, PE.
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12
Q

What agents are used to clean oiled marine mammals?

If oil is tarry or weathered, what pretreatments can be helpful before the detergent?

Describe the oil removal process for sea otters, pinnipeds, cetacean & manatees.

A
  • Cleaning
    • Goal – Remove all external contamination to allow the affected animal to regain normal function.
    • Detergent to remove oil, rinse to remove the soap.
    • Drystep step needed for heavily furred mammals to allow a trapped layer of air to return to the undercoat.
    • Large, aggressive, or densely furred animals likely require anesthesia for cleaning.
    • Large volumes of temp controlled water needed for washing and rinsing.
    • Liquid dishwashing detergents shown to be safest and most effective for removing oil from wildlife. i.e. Dawn.
    • Pretreatment products i.e. methyl soyate, methyl oleate, vegetable oil may be helpful if the oil is tarry or weathered.
    • Sea otters – Multiple application sof dilute 5% Dawn.
      • Hand dry and then dry with pet dryers.
    • Others – Consider freshness of the product, extent of oiling, overall health of individual, available support for the procedure, and whether additional diagnostics/procedures are necessary that can be coupled with the wash effort to minimize restraint events.
      • Clipping away tar patches can be done in pinnipeds if small areas.
      • Pinnipeds other than fur seals – Dishwashing detergent 1:1 ratio.
        • Can air dry in outdoor pen or with supplemental heat.
      • Cetaceans and manatees.
        • Cleaning skin, blowhole, eyes.Wupe with disposable towels, skin washed with Dawn 1:1.
        • Beach cleaning of oil can be considered on a case by case basis.
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13
Q

Following the removal of oil from oiled marine mammals, how are animals prepared for return to the wild?

What steps for fur seals and sea otters need to be taken?

How are animals monitored when released?

A
  • Postwash Care, Release, and Postrelease Monitoring
    • Goal of postwash care – Allow time and support to regain normal physiological and behavioral function in anticipation of release.
    • Sea otters and fur seals – Must be gradually reintroduced to aquatic environments, do not emerge from the wash completely waterproof.
      • Portable cages or pens with limited access to water.
      • Warmed, softened, fresh water within these pens can significantly reduce recovery time.
      • Once waterproofing is close to normal, can move into large outdoor pools.
    • Return to aquatic environments, appropriate nutrition.
    • Criteria must be met and then a written release plan and timeline is developed.
    • Tracking methods should be used when possible for animals that will be released.
    • Flipper/dorsal fin tags and or/freeze branding can be performed for passive monitoring and ID of animals that have been completely rehabilitated.
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14
Q

What are toxic elements that accumulate in marine mammals?

Marine mammals have evolved levels of antioxidants - what are they?

A

Elements

o Greatest concern: mercury, cadmium, lead, organotins

Antioxidants

o Block damaging compounds before they attack (increase oxidative stress, produce oxidants)

o Ex: vit E, glutathione peroxidase (GPx)

o Diving mammals have higher activities of GPx compared to terrestrial mammals

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15
Q

Describe the relationship between selenium and the toxicity of mercury in marine mammals.

Mercury is highest in which marine mammals, and lowest in which?

Are there geologic points of higher exposure?

What organ has high tissue levels.

How does selenium prevent mercury toxicity?

How does mercury prevent selenium toxicity?

A

Mercury and Selenium: Toxicant and Nutrient Interaction

  • Mercury (Hg): nonessential toxic element, biomagnifies in food webs esp in neurotoxic form
  • High in piscivorous marine mammals
  • Geologic exposure, point sources (ie near Amazon river dolphin habitat and San Francisco Bay region)
  • Very high in liver tissue
  • Lower in baleen whales and sirenians that feed lower in food web
  • Selenium (Se): serves protective role against Hg toxicity
  • High levels of both frequent in marine mammals
  • Se dependent detox processes (glutathione peroxidase, selenoproteins)
  • High Se selenosis; Hg deficiency
  • Proposed mechanisms:
  • Transfer of Hg away from kidney and other sensitive organs to muscle and other tissues
  • Competition for binding sites
  • Formation of Hg-Se complex
  • Conversion of toxic forms of Hg to less toxic forms (i.e. methylated to divalent)
  • Prevention of oxidative damage
  • Detox via formation of Hg-Selenide complexes which sequester Hg and allow for elimination via cellular sloughing
  • Se key component of GPx family of enzymes
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16
Q

What protein binds mercury in marine mammals?

What form of mercury is toxic?

How does mercury accumulation affect the liver histologically?

A study explored the effects of high (25 mg/kg) and low (0.25 mg/kg) doses of mercury in harbor seals. What did that study find?

What cohort of animals are most vulnerable to adverse effects?

What are some ways of measuring mercury?

A
  • Metallothionein (MT) and Mercury
  • MT-bound Hg low proportion of total Hg in tissues but can be important intermediate Hg processing step
  • Metal binding proteins involved w/ uptake, transfer, excretion
  • Mercury and Immunotoxicity
  • Methylated form = neurotoxic; immune system as target
  • Mercury and Histology
  • Hepatic Hg concentration w/ tissue pathology – few studies
  • Lipofuscin like pigment granules and liver lesions in T. truncatus w/ high liver [Hg]
  • But animals were also older – accumulation over time
  • Liver distribution is zonal in belugas but homogenous in harbor porpoises
  • In vitro dosing with methyl mercuric chloride
  • Verified demethylation and selenium interaction
  • 25mg/kg daily in harp seals within 20-26 days renal failure, uremia, toxic hepatitis, death; no obvious lesions with 0.25mg/kg.
  • Nonspecific low level of structural damage to sensory cells of organ of corti (missing or damaged stereocilia, reticular scars, collapsed sensory cells)
  • Alteration of gonadal and adrenal steroid synthesis with 0.25mg/kg
  • Critical cohort exposure
  • Fetal and neonatal exposure likely most vulnerable to adverse health effects – limited detoxification and elimination processes available
  • Keratinized tissues (whiskers and lanugo) – noninvasive matrices to evaluate exposure
  • Harbor seal pups – highest in hair compared to liver, kidney, muscle
  • Increased between mid and late gestation and at early lactation
17
Q

What are organohalogens?

How do they accumulate in the environment and in the food chain?

How do concentrations change within exposed marine mammals with time and reproduction?

A
  • Organohalogens (OH)
  • o Halogens = fluorine, chlorine, bromine, or iodine bound to carbon
  • o Some occur naturally, some don’t
  • o Organochlorines most studied in marine mammals
  • Highly lipophilic
  • o Terrestrial runoff, atmospheric transport on particulate matter, biomagnification in food webs, ingested and concentrated in fatty tissues (i.e. blubber, CNS)
  • o Cyclic changes in blubber (seasonal, reproductive) – variation in amount of lipid stored and [OH]
  • Transplacental, lactational – proven in ringed seal blubber samples, CSLs
  • CSLs: DDTs higher compared to PCBs and higher among late term compared to premature fetuses
  • High lactational transfer rates proven in common dolphins and gray seals; increases over course of nursing
  • Endocrine disruption likely exacerbated in young animals in important developmental periods
18
Q

What are polychlorinated biphenyls?

What were they used for?

What marine mammal groups had the highest levels? Which had lower levels?

A

Polychlorinated biphenyls (PCBs)

  • 209 OC Congeners produced by the industrial chlorination of biphenyls
  • Widespread application in industry (electrical transformers, capacitors, hydraulics, heat transfer systems, plastics, inks
  • Most nations banned its used in70s and 80s due to environmental contamination
  • Highest concentrations in males of piscivorous and or marine mammal consuming species from inshore locations and in diseased individuals w/ poor BCS
  • Low concentrations in nonpiscivorous spp and females
19
Q

List a few organochlorine pesticides.

What is their mechanism of action on their target organisms?

What effect do they have on the reproduction and endocrine systems of marine mammals?

What possible association exists on their effects on the immune system and epizootics?

A
  • Organochlorine pesticides and metabolites
  • i.e. DDT + many others
  • Some act as neurotoxins on target organisms
  • Some hydrophobic, some hydrophilic
  • Effects of organochlorines on reproduction and endocrine systems
  • Alteration of menstrual cycles, embryo absorption, abortion, stillbirths, impaired growth ans survival of young
  • Harbor seals fed more OC contaminated fish had lower reproductive success likely due to failure at implantation (endocrine mediation disruption)
  • Ringed seals in Baltic Sea w/ uterine stenosis and occlusions had elevated DDT in blubber and PCBs compared to pregnant females
  • Baltic gray seals – uterine leiomyomas associated w/ PCV and DDT concentrations
  • Some studies failed to find associations w/ uterine pathology and OCs
  • Higher PCBs in CSLs aborting fetuses and producing stillbirths; but had confounding factors like lepto
  • Elevated PCBs affected repro in belugas of st Lawrence river (repro pathology in stranded carcasses)
  • Adrenocortical dysfunction
  • Skull asymmetry and bone lesions potentially related to hyperadrenocortical effects corresponding to increased pollution in seals of Baltic sea
  • Lower thyroid hormones in bottlenose dolphins with increasing blubber PCBs
  • Effects of organochlorines on immunocompetence and epizootics
  • Many studies could not find an association except one onstriped dolphins from Med Sea that died during morbillivirus epidemic (high PCBs in blubber compared to other marine ammamls)
  • Several vitro studies have been performed but difficult interpretation and variable exposures compared to real wild animal situations in vivo
  • Other organohalogens
  • Fluorinated hydrocarbons, PBBs, octachlorostyrene and PBDEs
  • Flame retardants, low concentrations
20
Q

How do organochlorine and polychlorinated biphenyls afffect marine mammal populations over time.

Are there geographic areas of greater exposure?

A
  • Population Impacts
  • Young in utero and nursing – unknown long term impacts
  • Bottlenose dolphins in Sarasota Bay – higher concentrations of PCBs among first born calves compared to 3rd or 5th born calves
  • 50% mortality rate for 1st born compared to 30% for subsequent calves
  • Possible that 1st born gets brunt of offloaded contaminants
  • May help survival rate of subsequent calves
  • Increases in prevalence and concentrations over time
  • Higher concentrations if near developed coastal areas
21
Q

How do PCBs adn other OC affect thyroid function in polar bears?

What enzyme is upregulated or downregulated depending on toxin exposure?

Are males or females more suceptible?

A

Polar Bear Case Study

  • Negative relationship between PCB concentrations and T4 in plasma and muscle
  • PCBs, OH PCBs, and PBDEs positively correlated with type 1 and 2 deiodinase activities; OC pesticides and byproducts were negatively associated w/ D1and 2 activities
  • Blood PCB concentration higher in females and young compared to males and significantly related to reduced BCS
  • Biomarkers of Se status and T3 concentrations positively related to Hg in al mature polar bears. TT4 negatively related w/ blood PCBs in solitary females
  • Females more susceptible to changes in blood based biomarkers to selenium and thyroid status than males
22
Q

What are the effect of microplastics and plasticizers on the marine environment?

A

Chemical Plasticizers and Microplastics

  • Beads, fragments or filaments <5mm in diameter
  • Filter feeders, ingestions due to similarity in appearance to prey, up the food web
  • Even inverts are ingesting it
  • Microbial communities can colonize plastics
  • Plasticizers that are chemicals added to plastics to enhance or alter structural properties usually will leach into the environment. Metabolized by the body.
  • Many potential physiologic, endocrine, reproductive consequences
23
Q

How does feeding style affect how affected a marine mammal is by environmental contaminant?

How do marine mammals maintain toxin levels in the marine environment?

A

Ecophysiologic Considerations

  • Diet and feeding strategy can affect how much miomagnification has occurred
  • Higher trophic level, higher variability
  • Variability in metabolism by species
  • i.e. polar bears metabolize OC pesticides more effectively than other spp

Marine Mammals as “Hazmat”

  • Chemicals shed or excreted – exposure route for other organisms
  • Biotransport of contaminants during movement over great distances
  • “Whale fall” – contaminant rich decaying tissue consumed by other animals – recycling bioaccumulated toxins

One Health and Population Implications

  • sentinels of environmental and human health
  • immunity impacts can help the spread of infectious diseases
24
Q

What are harmful algal blooms? What causes them?

How are they diagnosed?

How are they treated?

What is the general prognosis?

How are they controlled?

A
  • Algae: large amount discolor water, release biogenic toxins which are transferred into food web via water or biota
    • Cyanobacteria (blue-green algae) – oxyphototrophs; grow better in warmer water/weather. Longer seasons due to global warming
    • Biotoxins – neurotoxin or hepatotoxin; lipophilic (brevetoxin) or hydrophilic (saxitoxin, domoic acid, microcystin, nodularin)
      • Functional groups: neurotoxins, cytotoxins, dermatotoxins, irritant toxins
      • Freshwater cyanobacteria: Microcystis, Anabaena, Panktothrix; microcystin most common toxin produced
      • Alkaloid toxins: anatoxin, saxitoxin, cylindrospermopsin, lyngbayatoxin a
  • Biotoxins should be suspected for neurological signs when head trauma absent
    • Clinical signs: seizures, disorientation, ataxia, improper positioning @ water surface, facial/body twitching
      • If inhaled then increased respiratory rate or dyspnea (manatees w/ brevetoxin)
    • Accumulate in bivalves – human and animal risk of consumption
  • Diagnosis: environmental confirmation of bloom, presence of toxin in prey, presence of cells/toxins/toxic dietary items in GIT, toxin in tissue
    • Hydrophilic toxins – shorter half-life in blood/urine
    • Lipophilic – 1-2 day half life
    • Minimum samples from deceased animals – urine, feces, GI contents, liver, kidneys
    • Can examine a wet mount from water or GI contents
    • IHC for detecting toxins in formalin fixed tissues
  • Treatment – supportive care, stop seizures
  • Prognosis – varies with biotoxin & taxa. CA sea lions + sea otters with acute DA or manatees with brevetoxicosis = fair to good px if seizures controlled
  • Control of cyanobacterial blooms
    • Environmental treatment expensive and impractical
    • Common algicides – CuSO4, diquat, simazine aluminum sulfate (alum), lime
      • Alum & lime – remove phosphorus from water; cause coagulation of the algae 🡪 flocculation so decrease toxin release into farms/lakes but hippos will wade and disrupt the sludge
      • Cu reported to be effective in natural waters
      • Decomposing barley or hay may reduce growth
      • Bacillus cereus in floating plastic carriers – controlled Microcystis blooms (99% decrease in 4 days)
25
Q

What is the mechanism of action for brevetoxin?

Is it lipophilic or hydrophilic?

What organism produces it?

How is it transmitted?

How is it diagnosed?

How do you treat exposed animals?

A
  • Brevetoxin (lipophilic, neurotoxic; PbTx) – bind to voltage-gated Na channels so that inactivation is prevented (cannot perform another action potential)
    • Karenia brevis – top 2 marine mammal mortalities
      • Florida red tide dinoflagellate (east coast/Gulf of Mexico)
      • Manatee & bottlenose dolphin mass mortalities – respiratory or neuro signs
    • Consume orally or inhalation
    • Humans affected: neuro and GI
    • Few stranded cetaceans with brevetoxicosis survive
    • Diagnosis: Heterophilic & eosinophilic leukocytosis, hemoconcentration, electrolyte abnormalities, immune changes
      • Nx manatee: congestion of nasopharynx, airways, meninges; hemorrhage liver-kidney-lung
    • Treatment – keep animals from drowning
26
Q

What is the mechnism of domoic acid?

Is it hydrophilic or lipophilic?

How does it affect people?

How does it affect

What species are affected?

How is it diagnosed?

What treatments are recommended for acute intoxication?

A
  • Domoic acid (hydrophilic) – activate glutamate receptors in the brain – NEURO SIGNS
    • Pseudo-nitzchia (diatom) – top 2 marine mammal mortalities
      • West coast
      • CA sea lions + various dolphins
    • Amnesic shellfish poisoning
      • Humans: Neuro and GI
    • Affects pinnipeds, cetaceans, sea otters
    • May cause spontaneous abortion in pinnipeds as well as various neuro signs; may be vertically transmitted (in utero, milk)
    • Few cetaceans that strand due to DA intoxication live more than 24 hours, if at all
    • Diagnosis: urine most useful, may also be in amniotic fluid; eosinophilia on CBC
      • Cortisol levels decreased in sea lions with chronic and acute exposure
      • MRI – hippocampal atrophy from chronic exposure
      • Antibodies in chronic sea lions
    • Sea lion treatment: phenobarbital, lorazepam (if in status); pregnant sea lions – give dexamethasone for abortion
27
Q

What is the mechanism of action for saxitoxin?

Is it hydrophilic or lipophilic?

What organism produces it?

What species is commonly affected?

What clinical signs occur in people and marine mammals?

A
  • Saxitoxin (hydrophilic) – bind to voltage gated Na channel and block Na influx into cells therefore no action potential
    • Alexandrium (dinoflagellate) – humpback whales
    • Paralytic shellfish toxin
      • Humans affected: neuro (numbness; can progress to respiratory suppression)
      • Mammals – muscle paralysis and respiratory arrest
28
Q

What is the mechanism of action for microcystin toxins?

How are sea otters exposed to this toxin?

What organism produces this toxin? How does temperature play a role?

Describe the effect of this toxin on fish.

Describe the effect of this toxin on flamingos.

Describe the effect of this toxin on African wildlife.

A
  • Microcystins – hepatotoxin (@ acute toxic doses – loss of hepatocyte structure, massive liver hemorrhage, death from hypovolemic shock or hepatic insufficiency, hepatogenic photosensitization; ruminal stasis if applicable; death in 1-2 weeks).
    • Freshwater
      • Sea otters were exposed to these freshwater toxins via downstream affected shellfish; develop neurologic signs
    • Humans: GI, piloerection, pallor
    • Microcystis aeruginosa – growth temperature dependent (limited @ < 15 C, optimal growth 25-32 C, maximal toxin production @ 20C) – aka cold weather = decreased growth
      • Light intensity plays a role in buoyancy of the algae, eutrophication (higher water nitrogen : phosphorous ratio) 🡪 more algae at surface of water where animals drink
      • Fertilizer & waste run-off + availability of Fe2+ (ferrous) & Zn2+: also increases algae at surface
    • Mass mortalities of fish: contributing factors include low water level, high H2O temp, high pH, high NH4+, low DO, presence of other toxin producing organisms
      • Exposure when toxins pass over gills – gill epithelium undergoes cell degeneration and necrosis, Cl channels disrupted
      • Interfere with development and organ function
      • Adult fish – kidneys and liver affected
      • Species in oligotrophic (minimal plant life) habitats more sensitive than eutrophic habitats
    • Lesser flamingos (Africa) – death from microcystin & anatoxin a producing Arthrospira fusiformis
      • Neuro signs, cyanosis, respiratory failure, death
    • Cattle, sheep, goats, wildlife – will consume concentrated areas of the algae bloom instead of less concentrated
    • Kruger National Park
      • 2005 - Dry summer, warm autumn & early winter + low river levels 🡪 large algae bloom occurred in dammed water bodies
        • 52 animals died: white rhinos, lions, cheetahs, zebra, wildebeest, hippo, giraffe, warthog, kudu
      • 2007 – 22 animals
      • Elephants, buffalo, hippos – underrepresented – perhaps because wade into deeper water
29
Q

What are the effects of these less commonly encountered harmful algal bloom toxins:

Nodularin

Cylindrospermin

Lyngbyatoxin

Aplysiatoxin

Cyanotoxin

Okadeic acid

A
  • Nodularin – hepatotoxic
  • Cylindrospermopsin – irreversible inhibitor of protein biosynthesis, affects liver
  • Lyngbyatoxin a – tumor promoter
  • Aplysiatoxins – dermatotoxic, inflammation of skin, potent tumor promoters
  • Diagnosis of cyanotoxin exposure in sea otters – diffuse icterus, swollen/hemorrhagic liver
  • Okadaic acid – protein phosphatase inhibitor & tumor promoters
    • Diarrheic shellfish poisoning