Final Exam Flashcards
P. tenuis zoonotic?
No
General types of parasties
cestodes- tapeworms
trematodes- flukes
nematodes- round worms
ectoparasite- fleas: ticks, mites, lice, bot flies, biting flies, midges, mosquitoes
protozoans (single- celled parasites)
- hemaprotozoans (blood parasites)
- enteric protozoans (intestinal parasites)
-tissue inhabiting protozoans (eg toxoplasmosis)
Protozoans
single celled parasites
hematoprozoans
enteric protozoans
protozoans are…
microscopic
some ectoparasites
ectoparasites
generally not life threatening especially in wildlife
can be a complicating factor when other diseases are present (ie anemia)
can be debilitating in young animals
do commonly serve as vectors for other diseases
exception to harmless ectoparasites: hair loss syndrome
disease of mule deer and BTD
exotic louse of Damalinia/ Cervicola or Bovicola sp.
Normal hosts: European and Asian cervids
hypersensitivity (allergy)- itch hair loss
may be fatal (esp to fawns in late winter) because they depend on their hair to keep them warm
Exception to harmless ectoparasites: winter tick
D. albipictus
also causes hair loss in moose (elk)
AKA Ghost Mouse
may be fatal
- exsanguination (blood loss) or hypothermia (freezing)
Exception: mange
mites. Many species cause individual animal problems
Psoroptes spp. mites cause population level issues in BHS
hair loss and extreme crusting of ears
not currently an in issue for TX Desert BHS
Deer Nose Bots
ectoparasite
Cephemnemyia fly larvae
not an accurate term, hang out in the pharyngeal pouch and when the deer dies they come out of the nose
enters deer nose, lays eggs there, deer inhales the eggs and they hatch in the pharyngeal pouch.
not considered too bothersome but the deer don’t like them
worldwide distribution
large host distribution- more common in deer
generally not pathogenic
the cause of concern for hunters re carcass quality
NOT zoonotic (also like papilloma virus- very common)
in general, ectoparasites are a big concern in wultildlife when:
when they transmit other infectious agents
Nematodes- Round Worms
P. tenuis- meningeal woem, brain worm
Elaeophora schneideri- carotide artey worm of mule deer
setaria cervi- peritoneal worms
Histomonaaaaas/ hetrakis- blackhead in turkeys
Elaeophora schneideri- carotid artery worm of mule deer
elaeophora means deer
Schenider- person who found it
a filarid worm ( like Setaria and heartworms)
adults found in carotid or maxillary artery but can occur in any large artery
spread by biting flies (horseflies- Tabindae)- carrying the microfilaria
symptoms depend on the location of the worm
16 documented species that serve as intermediate hosts
first described in sheep as “poll evil” or “sorehead”
E. schneideri
almost never a problem in mule deer (the natural host)
occasional problem in WTD
pathogenic to elk, moose, red deer, sika deer, BHS, auodad, Ibex, domestic sheep and goats
causes unilateral blindness (not common for it to be in both eyes), antler deformation, dry necrosis of ear or nose of elk, sever neurological disease
can be fatal
not ZOONOTIC
life cycle of carotid artery worm
adults in the arteries give birth to microfilaria (not eggs)
microfilaria migrate to the capillaries of the skin
biting fly ingest microfilaria with blood meal
microfilaria L1, L2, L3 in fly
L3 migrate to mouthparts of fly to be definitive host to venous blood and migrate through circulatory system to arteries and mature
Sorehead of sheep and goats
if sheep and goats are affected with Elaephora they may get the same signs as wildlife, more often they die suddenly (3-5 weeks after infection) after a short bout of neurologic signs (incordination, circling and convulsion).
death more common in young animals
those that survive often develop sorehead due to microfiliarial dermatitis 6- 10 months later
Diagnosis of E. schenideri
dead animal- disect the carotid an internal maxillary aretry and look for worms
live animals- skin biopsy
must be endemic area of mule deer ( ocasionally WTD infected)
Treatment for E. schenideri
Piperazine salts are effective
complete recovery in 2-3 weeks, damage to ear, antlers may remain
only effective before neurologic disease develops
not practical for free ranging wildlife
Parelaphostronglyus tenuis
meningeal worm
moose sickness
“extrapulmonary lungworms”
P. tenuis
Phylum Nematoda ( round worms or nematodes) have complete digestive tract (mouth though anus)
6 stages: eggs, larva (1-4), adults (both sexes)
L3 is what infects the definitive host
may have direct (no intermediate host) or indirect (intermediate host) life cycle)
Order Strongylida
most stronglyes are parasites if GIT not P tenuis!
p. Tenuis is common almost everywhere with…
WTD, usually no Disease
Debilitating on other species such as elk, moose llamas, sheep, goats, exotic ungulates
P. tenuis breakdown of name
para= near
elapho= deer
strongylus= round worm
tenuis- tenuous
P. tenuis life cycle
adults in blood vessels of brain meninges
release eggs-> heart> lungs> develop into L1
L1 coughed up, swallowed, out GIT
L1 penetrate snails > L2 >L3 (ineffective stage)
deer accidentally eats snails
L3 penetrate abomasum> nerves> spinal cord
L4> L5-> cranium (adult)
P. Tenuis
in abnormal hosts (not WTD)
no road map
cause pathology
often fatal
problems with Diagnosis of P, tenuis
there are other species of Parelaphostrongylus that are found in deer
P. andersoni is the muscle worm of WTD
P. odocoilei is found in the muscle of mule deer, BTD and woodland caribou
all have dorsal spined larvae and very difficult to separate microscopically
problems with treatment for P. tenuis
- since drugs do not cross the BBB, Ivermectin and other drugs are ineffective against adults
- Ivermectin can control the larvae for a period of time
treatment can interfere with diagnosis prior to movement of animals - movement implications
Meningeal worm concerns
As WTD expand range will P. tenuis as well?
could have major complications for moose, elk. mule deer and exotics
will drier conditions prevent westward expansion? (fewer snails and slugs)
environment plays a role! Some exotics don’t do well in wetter areas.
Histomonas/ heterakis
crater like lesions- pathopneumonic
Blackhead of Gallincacious Birds
parasite within a parasite within a worm
histomnas meleagridis- the damaging parasite ( a protozan)
heterakis gallinae- a mostly harmless cecal nematode parasite
earthworm: an optional paratenic host
Terminology review
direct lifecycle= no intermediate host needed, parasite transmitted from one definitive host to another, no intermediate host is needed
indirect life cycle- parasite requires 2 or ore different species to complete its cycle
definitive host: hosts the sexually mature stage of the parasite
intermediate host: hosts one or more of the sexually immature stage(s) of the parasite
paratenic (transport) host- not required for completion of life cycle and in which no development occurs, Usually a prey species of the definitive host
vector transmits parasite, usually an arthropod
Review
P. tenuis has an indirect life cycle
E schneideri has a indirect life cycle as well because they have intermediate hosts
definitive host for P. tenuis is WTD- accidental host
E. schenederi defnitive host is mule deer
intermediate host for P. tenuis is snail
flies are the intermediate host for E. schedderi
Bird cecum
human appendix is a rudimentary cecum
most birds have a well developed ceca at the junction of the small and large intestine (some species have two, some have one)
Lifecycle
Histomonas multiply by binary fission. H. meleagridis uses the cecal nematode, H. gallinae to protect it in the environment. Histomonads invade the nematode egg. those eggs are then often eaten by earthworms and when the bird eats the nematode egg develops in the cecum and release the histomonads
Species susceptibility to H. mileagridis
Gallinaceous birds: chukar, pheasant, quail, grouse, wild turkey, jungle fowl, guinea fowl, peafowl
Turkeys (domestic and wild) are VERY susceptible!
Domestic chickens are VERY resistant
Signs of Blackhead
7- 12 days after infection: incubation period
typically in turkeys
listlessness, reduced appetite, drooped wings, unkempt feather, sulfur yellow feces, rarely cyanosis of head (combs, waddles, etc)
Lesions
inflammation and ulceration of ceca
yellow thick- green exudate or cheesy pus in ceca
liver necrosis- maybe focal crater like entire liver, may be green or tan
Diagnosis
history and signs- presumptive
lesions- pathognomonic
direct microscopic examination of liver or cecal scraping- look for histomonads or PCR- definitive
Treatment of H. meleagridi
specific anitprotozoal medicine not approved for food producing animals
anthelminths Controlling the nematode, eliminates the protozoan
nothing realistic for wild birds
Controlling of H. meleagridis
can cause catastrophic losses of wild turkeys (over 75% mortality reported)
keep domestic chickens out of wild turkey habitat
partially effective vaccine available for domestic turnkeys
Introduction of nilgai to TX
did not introduce any new diseases
occurred at the time when WTD populations were at historic lows
Nilgai expanded their range and did well
–few predators
–high fecundity 2-3 calves/ year; live 12- 14 years)
valued game animals
do well in S. TX environment- drought tolerant, heat loving
CONT
Texas Cattle Tick Fever (Babesiosis)
caused by protozoa: Babes bovis and B. bigemia
carried by ticks: R. annulatus and R. microplus
cause hemolysis, anemia and death (90% in naiive cattle)
3 life tick, 1 host tick
transovarial transmission- affected tick passes through the ovaries, lay 4000 eggs on gound
CONT
Distribution
used to be all along the South, now only on the Texas Mexico border
Texas Cattle Fever History
1893: Texas Livestock Sanitary Commission (became TX Animal Health Commission)
1906: role of ticks recognized and eradication effort began
1940s: pushed back to Texas/ mexico border and permanent buffer zone created
eradication effort included Vacating pastures for 9 months to starve the ticks out
Texas Cattle Fever resurgence via Nilgai and WTD
range of fever ticks and disease has expanded well beyond the permanent quarantine zone
cattle are inspected and treated before leaving the zone
impossible to treat live Nilgai before they migrate out
some treatments possible for WTD
Control of Texas Catle Fever Tick
Cattle treatments (dipping, spraying, injectable
acarracide (Doramectin), quarantine, movement
restrictions
• Restrictions on hides of Nilgai and WTD
• Treatments of WTD: ivermectin corn and
permethrin rubbing posts
• Still looking for good Nilgai treatment
Cestodes- Tapeworms
Echinoccous granulous: hydatid cysts, worldwide distribution, predator, prey hosts
definitive host- wolves, coyotes, foxes jackals, hyenas, bear, domestic dogs (cats for E. multilocularis)
intermediate hosts- moose deer, pigs, cattle, sheep ( iintermediate hosts get the hydatid cysts)
ZOONOTIC
Echinococcus is zoonotic!
when humans become the intermediate hosts, in rare cases where humans become defiinitive host- no symptoms
biggest risk: farmers. ranchers whose ranch dogs who scavenge livestock/ wildlife carcasses
carnivore biologists at risk
location of hydatid cyst determines symptoms
Echinococcus importance
not population limiting
zoonotic
humans= dead end host (accidental host)
metacestode (cyst) remains in proliferative stage; invades and
Echinococcus diagnosis
carnivores, look for eggs in feces
humans (difficult at surgery)
Echinoccous treatment/ control
domestic dogs are given drugs
reduction of stray dogs (developing countries)
hygiene! wash hands after handling carniovres
Trematodes-flukes
Fascioloides magna- giant liver fluke
not zoonotic (relatives are)
geographic distribution- primarily in America but introduced to Europe
host distribution- primarily cervids and bovids
implications for translocation
Fascioloides magna life cycle
adults reside in the liver and shed eggs via bile system to sm intestine and our in feceds
eggs hatch in water and miracidia invade snails )snails = intermediate host)
within the snail miracid=cica develop into cervariae
when snail is
pic should say accidental
Fascioloides magna
definitive hosts: cervids: WTD, MD, elk
2 types of accidental hosts: aberrant hosts( can complete migration, may kill host) sheep
dead end hosts: trematodes reach live but cant produce eggs that reach the small intestine. hosts dont die include bovids, suids, llams, and moose
Fungal diseases of wildlife
rarely pathogenic, estimates are that there be 1.5 millionn species of fungi
only 120 known human pathogens
even fewer wildlife pathogens involved
Pharmacology
the branch of medicine concerned with the uses, effects, and modes of actions of drugs
pharmokinetics
how drugs move through the body
Goals of pharmacology
curative- curing
paliative- making it feel betwe
restorative- restoring normal function
pharmacokinetics and pharmocodynamics
ADME- absorption, Distribution, Metabolism and Elimination
things that effect the 4 key features of a odys reaction to a drug are effecrting the PK and PKD of a drug
liophilicty- can cross the BBB, viscosity, ph, route of administration
Temp, pph, BP, fat content,
schedule 1 drug
illegal, no medicinal use
What is a drug?
a substance that causes a physiologica effect when introduced into an organism
a drug/ toxin is a chemical but a chemical id not always a drug/ toxin
drug and toxin can be used interchangeably, but toxin has a negative connotation and is biologically created
How drugs work
agonist- full (when causes an effect on the receptor, it causes the full effect), partial( still has effect but does ot bind to all receptors and does not act in the full potential), inverse
antagonist (blocks effect of receptor)- competitive( drug takes up the binding site), allosteric- indirect binding, irreversible (cannot separate- permanent change), functional
How drugs work
agonist- full (when causes an effect on the receptor, it causes the full effect), partial( still has effect but does ot bind to all receptors and does not act in the full potential), inverse
antagonist (blocks effect of receptor)- competitive( drug takes up the binding site), allosteric- indirect binding, irreversible (cannot separate- permanent change), functional- binds causes the protein to change so its no longer able to react with the natural chemical in the body
what makes a good drug?
only ideal, not an actual thing yet universal dosing among species potency and efficacy low ED(effective dose) 50 and (high lethal dose)50 multiple routes of administration rapid effect reversible specificity (little or no side effects)
How are drugs classified in the US
they are scheduled-
schedule 1: no medical use and high potential for abuse (most dangerous)
schedule 2: high potential for abuse with use potentially leading to sever psychological or physical dependence( dangerous)
schedule 3:
schedule 4:
schedule 5:
lipids do not have the physiologic effect
Posion vs Toxin vs Venom
both poisons and venoms are toxins
a toxin is a biologically produced that id absorbed through epithelial membranes such as the skin or the gut wall
a venom is a biological produces toxin that is injected into an organism
drug abuse toxicity
a drug can become a toxic thing
anything can become toxic if they have too much
three types of changes: functional changes, structural changes, biochemical changes
measure of toxicity of a drug
toxic part of a drug is a side-effect
How drugs are administered
transdermal ingestion IM IV subcutaneous inhalation sublingual intraventricular rectal many more!
how the drugs are administered effects how the drugs go throughout the body
tools for delivering drugs to wild animals
hand syringe ( rare for chemical immobilaztion, more common for antibiotic type drugs and vaccines
pole syringe
dart guns and darts (pneu dart vs dan inject)
baits
use of drgs in wildlife and exotic animals
grey area!
must drugs in wild and exotic animals is done extra- label and the use of drugs is left up to the digression of the veterinarian in charge of the health of the animal
only a few cases where exotic animals are listed as acceptable for immobilizing drugs and they are very specific
Types of drugs used in wildlife and exotic animals
essentially the same as the ones in vet med
analgesics
anesthetics
vaccinations, antibiotics, antiviral parasites
hormones- FSH and LH
no matter what drug is used, kniw that there are potential side effects
reasons for drug exposure in wildlife and exotic animals
exotic pet, zoo, wildlife vet work chemical immobilization'prevention of disease transmission vaccinations- her health prevent or treat stress research accidental exposure
anti parasitic drug use in S. Texas ungulates
program implented in South Texas to reduces fever ticks in exotic nilgai antelope and WTD permithin infused scratching posts ivermectin infused coen moderately effective in killing ticks Nilgai
cape buffalo capture for transportation
BAM and hyaluronidase (tip of sperm cell)
atipamezole delivered via hand injection IM as reversal
chemical immobilization with a drug combination delivered by dart gun for transportation to another ranch
amphibian accidental exposure to hormones
supplemental hormones intended for human use were introduced into the environment via water contamination causing hermaphroditic frogs
synthetic estrogen contaminated water near urban areas affecting frogs (transdermal)
MT Antibiotic research in TX ungulates
upper resp and infection among deer in breeding pens and Draxxin us the preferred antibiotic
Hemaprotozoan (protozoan parasites of blood)
Babesia bigemina- TX Cattle fever
Theileria cervi- WTD
Plasmodium- malaria
Trypanozoma- Chagas’ Disease
Anaplasma spp
A rickettsial organism- not a Hemaprotozoan
Texas Redwater Fever. Texas Tick Fever, Bovine Babesiosis
Babesia bovis and B. bigemina- a tick borne parasite of red blood cells
the cause of Texas Tick Fever, or Texas Redwater Fever
along the rio grande in Texas- occasionally moves North
Carries by Rhipichephalus (Boophilus) ticks
Now found on WTD and Nilgai antelope
Basics on B. anthracis
- ancient distribution with worldwide distribution
- gram positive, spore forming bacterium
- all mammals are viable hosts
- able to persist for decades in natures harshest environments
- classified as a tier 1 biological select agent
Anthrax Life Cycle
- B. anthracis spore exposure to host
- spores germinate into vegetative bacteria within host and multiply
- vegetative bacteria release anthrax toxins into the blood
- host dies of toxic shock or cardiac arrest and sheds the vegetative bacteria
- bacteria sporulate on exposure to O2
- fly transmission pathways
Symptoms of infection in animals
- 3 to 7 days after exposure
- death is within 2 days of noticeable signs
- usually no symptoms but an acute infection will cause difficulty breathing, fever, seizure, dark blood oozing
- trembling, staggering and collapse
Is Anthrax zoonotic?
Yes it is!
Humans and animals can be infected in 3 ways: inhalation, cutaneous ad gastrointestinal
Cutaneous anthax
- spores enter the body through a cut or scrape
- most frequently but least deadly
- symptoms appear within a week of exposure
Diagnosis and Treatment for anthrax
test for antibodies and/ or toxins in the blood
- bacterial culture on bodily fluids
x- ray or CT for inhalation anthrax
- treat with a combination of antibiotics and antitoxins for 60 days
Chytridiomycosis (Chytrid) spread due to
trade in African frogs for lab use
trade in frog fr food and pets
other amphibians for fish bait
now considered to be worldwide
Chytrid
specific fungus: Bd
considered t be the most spectacular loss of biodiversity.
caused the decline or extinction of 200 frog species
how it kills frogs: infects the skin (reddening), underside
Humans kind of get chytrid too
athletes foot
amphibians
breath through their skin and excrete water through their skin
amphibians can absorb toxins through their skin alot more readily than mammals
Solution to Bd?
fungal treatments
research on this disease is needed
essentially impossible to treat free ranging amphibians
managing wetlands to prevent/ control Bd (water levels and movement)
slowing the spread to other areas (disinfection practices)
What are other wildlife diseases with major pop level impacts to wildlife?
whitenose syndrome is the second most important population level disease (also a fungal disease)
CWD is 4
Bighorn pneumonia is number 3
What are some wildlife diseases with major potential to impact domestic animals?
Rabies, Canine Distemper
BT
Brucellosis
TB
What are some important diseases that are not zoonotic?
Chytrid Whitenose CWD Bighorn sheep pneumonina BT/ EHD Canine Distemper
