Lecture 7 Pop Dyn Dz & Sm Mammals

Lecture 7 Pop Dyn Dz & Sm Mammals - WILDLIFE...

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Unformatted text preview: WILDLIFE MANAGEMENT AND DISEASE PRINCIPLES & Small Mammal Diseases Glenn H. Olsen, DVM, PhD Patuxent Wildlife Research Center Laurel, Maryland, 20708 Declining Wildlife Populations Wildlife relatively abundant from colonial times to late 1800's. Bobwhite quail populations noted as declining in 1880 White-tailed deer populations locally declining 1870-1900 California quail declining in 1890 Organized Study of Ecology and Wildlife Management Begins Herbert L. Stoddard publishes "The Bobwhite Quail" 1931 Aldo Leopold publishes "Game Management," 1933, first professor of wildlife studies, considered father of wildlife management/wildlife biology Paul L. Errington publishes papers on wildlife management, harvest theory, 1936 Further Declines in Wildlife Numbers, 1940-1970 Lehman (1937) describes loss of wildlife as native areas converted to intensive agriculture US Government starts Savannah River Project, 100,000 ha, wildlife studies begin DDT banned in US, hawk, eagle and osprey numbers start to increase again Errington's Theories of Harvest Annual "doomed" surplus hypothesis Hunting harvest or take has little effect on population Is harvest mortality additive or compensatory? Emergence of Research, 1970s, 1980s Bioenergetics Research, Professor Robert J. Robel Species and habitat modeling "Art" versus "Technology" of wildlife management Scientific analogy, bobwhite vs. chicken Management Implications of Disease - Introduction Disease suppression in medicine by: a. Direct chemical attack on disease producing organism b. Immunization c. Nutrition to eliminate or reduce disease d. Environmental conditions Situation with Wildlife Population disease control, not individual treatment Indirect control over nutrition Indirect control over movement, reproduction, survival Limited control of environment Limited resources Significant indigenous disease levels indicate an imbalance in the wildlife/environment relationship Slight decline in reproduction or nutrition to multiple severe disease outbreaks Three levels of disease in relation to environment virtual absence, covert disease, overt disease Biotic Potential and Environment Populations have a biotic potential limited by environmental resistance Environmental resistance determined by carrying capacity, disease, reproduction, etc. Environmental Resistance/ Carrying Capacity Carrying capacity function of food supply, water, cover, etc. Cover required for protection from predators, from environmental extremes, reproduction Food supply directly related to nutrition, reproduction, development, and body weight Wildlife/Environment Relationship Phase I, virtual absence of disease Under populated Wildlife (herd) in balance with environment Reproductive rate, nutritional level, weight normal Phase II, covert disease present Acute overpopulation Population can exceed carrying capacity Eventual damage to environment Reprod rate, nutrition, body weight normal Phase III, overt disease Chronic overpopulation Population declines Carrying capacity declines Parasite counts elevated Phase III, continued Reproductive rate, nutritional level, body weights all decreasing Unusual losses of adults or fawns Depleted fat reserves Gross lesions/ pathology Nutrition and Disease Malnutrition reduces resistance to infection Infectious diseases can have a direct metabolic effect Nutrition as Related to Reproduction and Development On a low nutritional diet, yearling does produce 0.6 fawns/doe On a high nutritional diet, yearling does produce 1.6 fawns/doe On a low nutritional diet, yearling bucks develop only spike antlers On a high nutritional diet, yearling bucks grow 6-8 point antlers Food Supply and Over Population Carrying capacity can be related to quantity and quality of available food throughout the year As an example, deer can eat 40-60% of current growth of woody plants and the plants survive When deer eat >80% plants eventually die Deer can exceed carrying capacity Herbivores feed selectively, choosing plants with highest nutritional value first First plants removed from environment can be the most needed Lost plant species replaced by less nutritionally desirable species Nutritional deficiencies become pronounced Synergistic Effects of Nutrition on Infectious Disease Reduced host capacity to form antibodies Decreased WBC activity Alterations in tissue integrity Decreased inflammatory response Changes in intestinal flora Decreases in wound healing Variations in endocrine functions Extreme Temperatures Loss of Body Heat and Starvation Example: 200 g bobwhite, 60% water, 80 g dry mass, 20% fat (16 g), 13.6 g fat available for metabolism 39.3 kJ/g energy from fat X 13.6 g =534.5kJ At 0o C daily energy requirement is: Y=205.1-3.52T = 205.1kJ/day Stored fat energy would last 2.6 days Extreme Temperatures Loss of Body Heat and Starvation Example: 200 g bobwhite, 60% water, 80 g dry mass, 20% fat (16 g), 13.6 g fat available for metabolism 39.3 kJ/g energy from fat X 13.6 g =534.5kJ At 0o C daily energy requirement is: Y=205.1-3.52T = 205.1kJ/day Stored fat energy would last 2.6 days Extreme Temperatures Gain of Body Heat/Hyperthermia Air temperature alone is a poor indicator of potential hyperthermia Operative temperature, composite of air temperature, wind, sunlight effects At 35-40o C maximum heat dissipation falls below rate of heat gain for quail Therefore operative temperature leading to hyperthermia is below body temp. (41.5o C) Body temperature may rise and stabilize at some non-lethal temperature Animal experiences non-lethal hyperthermia and recovers as temperature drops Death from hyperthermia possible if core body temperature rises above 46.5o C Death from hyperthermia may be rare, but may limit habitat usage Energy of Foods Metabolized energy (ME) of foods varies ME for fat is 39.3 kJ/g, for carbohydrates and proteins 16.7 kJ/g Animals have limited time periods to obtain food, and have a maximum quantity For quail that can consume 17 g daily, ME>(1/17)(205.1-3.52T)>12.06-0.21T If ME=12.06-0.21T, then At 0o C, T=0, so ME=12.06kJ/g will balance energy loss Importance in wildlife biology is that food quality based on ME is directly related to time, temperature and food intake rate Carrying Capacity Number of animals that can live on an area for a year Often based on food available Other factors affecting carrying capacity can include water resources, cover, nesting habitat, etc. Energy Based Carrying Capacity C = PDEQ C = Carrying capacity P = dry mass of food produced or available in kg/ha-yr E = Mean metabolizable energy in kJ/kg D = Mean energy requirement of animal in animal-day/kJ C = PDEQ PDE = (kg/ha-yr)(kJ/kg)(animal-days/kJ) =animal-days/ha-yr, which is one way of identifying carrying capacity Q = standard animal-yr/animal-day, taking into account that an animal may inhabit the area <365 days Calculating Carrying Capacity P = 16.9 kg/ha for average rangeland E = 12,558 kJ/kg D = 1/(205.1-3.52[15])=0.0066 quail-day/kJ at an average yearly temperature of 15o C Q = 1/365 = .003 C = (16.9)(12,558)(0.0066)(0.003) = 4.2 animal-yr/ha-yr (Guthery, 2002) Problems with Calculated Carrying Capacity Energy-based carrying capacity model is simplified Not all food produced may be available due to competition with other species, loss of food to other causes (degradation of food, sprouting of seeds, etc.) Twelve fundamental Categories of Morbidity and Mortality Abnormalities Stress Trauma Suffocation Neoplasms Toxicoses Nutritional Disease Viral and Richettsial Diseases Bacterial Diseases Mycotic Diseases Parasitic Diseases Anomalies Rare in wildlife Often confined to an occasional animal Only of major concern in endangered populations Stress Varying degrees of morbidity or mortality Depends on type of stress or stressors Stress can also reflect other conditions such as chronic malnutrition or extreme parasitism Trauma Frequent cause of wildlife mortality Automobile collisions Power line collisions for birds Tower collisions migratory birds Wind generators birds Building collisions Trauma - Reduction For automobile collisions, improved fencing, underpasses for wildlife Power line collisions primarily daytime, markers on lines in areas of high collision potential Tower collisions primarily at night, modify aviation warning lights Trauma - Reduction Wind generators site generators in areas not used frequently by birds Building collisions seek architectural solutions, avoid open glass areas that animals can see through, turn out lights at night, etc. Suffocation Degree of mortality related to cause of suffocation Drowning of some occasional animals seen Neoplasms A variety of neoplasms are documented in wildlife Cause only occasional mortality Indicator of environmental health adenocarcinomas in Mississippi sandhill cranes Toxicoses Wildlife exposure to man-made chemicals is increasing May cause substantial morbidity and mortality, especially over a local area Potential to be devastating when a species congregates in one area whooping cranes on the Intercoastal Waterway, Swainson's hawk in Argentina (monocrotophos) Nutritional Diseases Malnutrition due to deficient energy and protein intake Potential to be a major source of morbidity and mortality for a population Often associated with infectious diseases Most severe in very young and old animals. Often associated with overpopulation, extreme environmental conditions Methods to Reduce Starvation Losses Reduce population to level more compatible with existing food supply Increase carrying capacity of habitat cutting, planting, burning, fertilizing Provide supplemental feeding during emergency situations can compound the next crisis, grains fed deer can cause metabolic disturbances, rumen overload Viral Diseases Capable of inflicting widespread and rapid mortality Introduced viral diseases pose major threat to wildlife West Nile Virus, foot and mouth disease Bacterial Diseases Capable of inflicting considerable morbidity and mortality especially in dense populations Special care given to clinical signs, lesions and cultures to make diagnosis Some diseases disseminated by contamination of the environment by carcasses Mycotic Diseases Primary fungal diseases are not normally considered a major cause of wildlife mortality Chytrid fungus of amphibians Secondary invader following other diseases Some fungi produce mycotoxins that kill wildlife sandhill cranes feeding on peanuts Parasitic Diseases Morbidity or mortality of an insidious nature, over long duration Associated with overpopulation and subsequent malnutrition Large scale arthropod control programs such as screwworm fly benefit deer, burning reduces tick populations Senility Not an important factor in wildlife morbidity and mortality Occurs in markedly under harvested deer herds Wildlife Disease Control Disease control activities influenced by type of disease, environmental factors, species involved, political factors, etc. Initial response can include carcass pickup and disposal, diagnosing and monitoring cause of mortality, organizing people involved, public relations Wildlife Disease ControlManagement Disease management activities include: Population manipulation Habitat manipulation Decontamination of the infected environment Surveillance Analysis Population Manipulation Deny wildlife use of an area by: Motorized hazing with aircraft, boat, snowmobile, motorbike, etc. Propane exploder Audio system, loud speakers Cracker shells Pumps to drain wetland areas Population Manipulation Concentrate and maintain wildlife on a desirable area by: Supplemental feeding of grain, corn, etc. Move water into an area, flood and area to provide habitat Close area to hunting to provide temporary refuge area Habitat Manipulation Vegetation removal Drainage, allowing air and sunlight to destroy microbes Controlled burning Planting crops for wildlife to lure animals away from potentially harmful situations such as treated agricultural fields Wildlife Surveillance, Sampling and Monitoring Wildlife capture Wildlife marking visible marking, permanent marking: legbands radio transmitters After disease control operations are over, continue monitoring area 10-30 days Analysis Learn from past mistakes, evaluate what was done correctly, what could be improved What impact did the disease have on the wildlife population? Improve detection methods for wildlife disease Small Mammal Diseases RABIES Squirrrel / rodent Canine Feline Rabies General: 55,000 people die each year worldwide Few die in U.S. from rabies ~40,000 exposed 93 /100 from wild animals Raccoons > bats > skunks > foxes Worldwide U. S. Rabies Etiology: Rhabdovirus Signs: 2 forms Furious & Dumb Furious Vicious attacks on animals/ humans Self mutilation Dumb aimless wandering, unusually tame, hind limb weakness or paralysis, lethargy, Hosts: All warmblooded mammals; most common in bats & carnivores Rabies Diagnosis: No method for live animal diagnosis; quarantine Wild animals euthanize & submit arcass/head to Health Dept. Transmission: Bite from infected animal fresh wound exposure to saliva of rabid animal organ transplant Lesions: No specific gross lesions Good body condition Rabies Prevention: People: preexposure prophylaxis (PEP) vacc. Wildlife: experimental vaccination ORV = oral rabies vaccination programs Zoonotic: Extremely dangerous only 12 known humans survived after symptoms appeared Raccoon Oral Rabies Vaccination Activity United States (2005 and beyond) 1) Static, incomplete ORV barrier 2) Incomplete, moving ORV barrier 3) Incomplete ORV with focal large land mass treatment RACCOON ORV Squirrel / Rodent Diseases Squirrel Pox / Fibroma Squirrel Pox / Fibroma Etiology Signs Hosts Diagnosis Trans. P o x virus R a is e d o r fla tte n e d n o d ule s ; us ua lly re g re s s S q uirre ls , wo o d c h uc ks G ro s s le s io ns ; c o n firm b y VI Mo s q u ito /tic k ve c to rs Significance Fo u nd in m o s t S E US p o p ula tio n s DDX Wa rb le s Squirrel Warbles / Cuterebra Etiology Names Signs Hosts Diagnosis Trans. La rva e o f Cuterebra flies Wa rb le s , b o ts R a is e d s we llin g s with c e n tra l b re a th ing p o re S q u irre ls , ra b b its , o th e r ro d e nts G ro s s le s io ns ; re c o ve ry o f la rva e Flie s Significance Fo un d in m o s t S E US p o p u la tio ns DDX Fib ro m a / p o x Endemic Diseases Squirrel Dermatophytosis -Fungi Etiology Names Signs Hosts Diagnosis Trans. Trichophyton, Mucor, Phaeoannellomyces Ba ld S q uirre l Dis e a s e , R ing wo rm Alo p e c ia , c irc u la r s kin le s io ns , h a ir "s tu b s " S q uirre ls , ra b b its , o th e r ro d e n ts G ro s s le s io ns ; I. D. fung us Dire c t c o n ta c t Significance Fo u nd in m o s t S E US p o p ula tio n s Zoonotic Lo w ris k to p e o p le Squirrel Mange Etiology Names Signs Hosts Diagnosis Trans. Notoedres mites Ma n g e S c ra tc h in g , a lo p e c ia , th ic ke n e d /c rus te d ` s kin S q uirre ls , ra b b its , o th e r ro d e n ts S kin s c ra p e ; I. D. m ite s Dire c t c o n ta c t Significance Fo u nd in m o s t US p o p u la tio ns Zoonotic O c c a s io n a l tra n s m is s io n to p e o p le Tularemia Relatively common, often fatal septicemia of rodents, rabbits and certain gallinaceous birds Etiology: bacterial, Francisella tularencis Transmission: all known epidemiologic routes Clinical signs: roughened hair coat, depression, huddling, anorexia, ataxia, death Gross Pathology: numerous pinpoint white foci of necrosis in the liver and spleen Tularemia Diagnosis: isolation of organism, serological testing Treatment and control: Tetracycline and streptomycin Zoonotic: transmissible to humans, do not handle carcasses without proper precautions Prevention: Vaccine available for humans, none for animals Wildlife management implications: causes sporadic severe localized mortality in rodents (especially muskrats) and rabbits Tyzzer's Disease Etiology: Clostridium piliformis Names: Errington's disease, Tyzzer's Hosts: Rodents especially muskrats Signs: None reported; rapid death Transmission: Ingestion of bacterial spores Lesions: Hemorrhage, edema, ulceration, necrosis in intestines & ceca Liver small white foci of necrosis Thoracic and abdominal cavities Bloodtinged fluids Not known to be zoonotic Ascarid Roundworm Etiology: Baylisascaris procyonis raccoon; B. columnaris skunk B. procyonis and B. columnaris rabbits Others? Signs: None in host species; severe in other nontarget animals and humans Migrating larvae produce neurologic signs Diagnosis: Fecal exam Control: None Prevention: Do not translocate infected animals to "clean" areas Plague Plague is a bacterial disease of rodents that can be spread to humans and other animals by infected fleas Etiology: Yersinia pestis; SW U.S. Hosts: Rodents prairie dogs, squirrels, rabbits; also cats Signs: 3 forms in people: Bubonic plague (infection of the lymph glands) Septicemia plague (infection of the blood) Pneumonic plague (infection of the lungs) Transmission: Flearodent cycle flea bites direct contact with tissues/ body fluids of a plagueinfected animal inhaling infectious airborne droplets laboratory exposure to plague bacteria Treatment & Prevention: Treatable with antibiotics if detected early Control rodent fleas; controversial depopulation of rodents Education of the public where plague occurs Preventive medicines and vaccines as appropriate Canine Distemper Acute or subacute febrile disease Etiology: Morbillivirus Hosts: Many species of the order Carnivora: Canidae, gray wolf, dog, jackal, dingo coyote, maned wolf, foxes, raccoon dog Hyaenidae: hyaena Mustelidae: fisher, weasel, mink, ermine, blackfooted ferret, European ferret, sable, badger, skunk, otter Procyonidae: raccoon, lesser panda, coati, kinkajou Aquatic mammals: seals, dolphins, porpoises, whales, manatee, polar bears Canine Distemper Signs: generalized infection Heperkeratosis = "hard pad" foot lesions Central nervous system disturbance Erythema of skin, chin, muzzle, foot pads, Elevated body temperature Diarrhea Listlessness Anorexia Nasal / ocular discharge Canine Distemper Transmission: aerosol or direct contact Pathogenesis: dogs, virus present in nasal tissues, lungs, spleen and blood in 2 days, viral antigen in lymphatic tissue in 5 days Ferrets, virus present in cervical lymph nodes in 2 days, antigen present in 9 days Gross pathology: enlarged spleen, lungs congested and consolidated, hyperemia and hemorrhage of mucosa of gastrointestinal tract and urinary system Canine Distemper Diagnosis: signs, fluorescent antibody test Prognosis: poor, mortality in mink 2090%, raccoons 50% Prevention and: vaccination for captive animals, passive transfer, disinfection with phenol 0.75% or roccal 0.2% Treatment: Supportive (fluids, etc.); trx of individual animals not recommended: potential to spread disease, high mortality rate, no known cure Importance: As wildlife mortality factor varies, not completely understood Feline Panleucopenia Distemper Synonyms: feline infectious enteritis, feline distemper, feline agranulocytosis Hosts: Felidae family, Mustelidae, Procyonidae Etiology: Parvovirus; single strand DNA virus Transmission: inhalation or ingestion from infected feces, urine or saliva Virus can be shed for months after recovery Virus resistant to heat and drying Feline Panleucopenia Signs: sudden onset of depression anorexia, elevated temperature Vomiting, diarrhea, abdominal tenderness Abortions, cortical hypoplasia resulting in uncoordinated young at birth (tumbing kitten) Gross pathology: dehydration, empty intestines, hemorrhagic enteritis, mesenteric lymph nodes swollen, bone marrow hypoplastic Feline Panleucopenia Prognosis: mortality during acute phase can be 6090%, mild form can cause high morbidity but low mortality Prevention: vaccination for captive wildlife Supportive treatment: electrolyte solutions, whole blood transfusions, antibiotics for secondary bacteria, antidiarrheal medications Disinfection: dilute sodium hypochlorate Importance: As mortality factor in wildlife not well known Where to Go for Information Southeastern Cooperative Wildlife Disease Study (SCWDS) Univ. of GA; Athens, GA www.scwds.org Association of Fish & Wildlife Agencies (AFWA); Washington, DC USGS National Wildlife Health Center (NWHC); Madison, WI www.nwhc.usgs.gov Contact Information Glenn H. Olsen, DVM, PhD Patuxent Wildlife Research Center Laurel, Maryland, 20708 Glenn_olsen@usgs.gov ...
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This note was uploaded on 01/09/2012 for the course ANSC 252 taught by Professor Cindydriscoll during the Spring '11 term at Maryland.

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