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Parasitology
exam 5
| Question | Answer |
|---|---|
| Nematode parasites of the respiratory system generally feed on what | host cellular tissue. |
| What do most Nematode parasites of the respiratory system require for development | to develop into infective stage in obligate intermediate host |
| Metastrongyloide common name | Dog lung worm |
| Types of Metastrongyloide (dog lung worm) | 1.filaroides hirthi 2.filaroides osleri |
| filaroides hirthi are parasitic in what tissue | lung parenchyma. need to do surgical biopsy |
| filaroides hirthi pp | 35 days. 5 wks |
| filaroides osleri are parasitic in what tissue | nodules in the trachea and bronchi. |
| with filaroides osleri infection when can nodules be detected | at 2 months |
| filaroides osleri pp | 6-7 mo |
| Filaroides life cycle | direct. tracheal migration by hepatic circulation |
| puppies are infected with filaroides via | 1. coprophage 2.regurgitated stomach contents |
| filaroides infective stage to final host | 1st larval stage |
| filaroides diagnosis fecal exam | 1. baermann 2.zinc sulfate flotation |
| filaroides diagnostic characteristic | kinked tail |
| Baermann is preferential for what | recovery of live larvae in fecal samples and cultures. active migration of larvae out of fecal sample suspended in water. larvae concentrate in stem. wet mouth of larvae from bottom |
| filaroides clinical sig. | asymptomatic. hard, dry cough. stim by cold air or exercise. possible obstruction of trachea with nodular formation in hyperinfections |
| filaroides pathology | focal areas of inflammation and necrosis in parenchyma of lung lobe |
| filaroides treatment | IVM preferred. prevention |
| Angiostrongylus vasorum common name | french heartworm |
| Angiostrongylus vasorum found in what tissue | right heart/ pulmonary artery |
| Angiostrongylus vasorum clinical sig | pulmonary thombosis, clotting disorders, hemorrhage from deposited eggs and larvae |
| Angiostrongylus vasorum treatment | Milbemycin. standard monthly heartworm prophylactic dose. |
| Angiostrongylus costaricensis clinical sig | abdominal pain, fever, vomiting from worms living in mesenteric arteries |
| Angiostrongylus costaricensis is found where | central and south America and Caribbean. |
| Angiostrongylus costaricensis spread in Florida | associated with deaths in primate colonies. raccoons and opossums trapped near zoo also affected. |
| Angiostrongylus costaricensis spread in Africa | Cuban mercenaries in Angola in 1980s |
| Angiostrongylus cantonensis clinical sig | neurologic disease from larvae in meninges and inflammatory response. zoonotic |
| Angiostrongylus costaricensis in South Asia | naturally occurring in rats. spread with distribution of giant African Snail. |
| Angiostrongylus costaricensis in North America spread | Wharf rats from Asia. |
| Aleurostrongylus abstrusus common name | cat lung worm |
| Aleurostrongylus abstrusus lifecycle | indirect. 1st stage larvae passed in feces ingested by snail/slug |
| Aleurostrongylus abstrusus paratenic hosts | mice/birds |
| Aleurostrongylus abstrusus pp | 5-6 wks |
| Aleurostrongylus abstrusus found where | terminal bronchioles and alveolar ducts. eggs are laid in lung parenchyma |
| Aleurostrongylus abstrusus pathology | "nests" of worms appear as small nodules with associated inflammatory response and focal necrosis |
| Aleurostrongylus abstrusus clinical sig | most common lungworm in companion animal. coughing and dysorexia with moderate infection. polypnea in severe cases. |
| Aleurostrongylus abstrusus deaths are associated with what | anethesia. shelter run spay neuter program |
| Aleurostrongylus abstrusus diagnosis | fecal exam. Baermann, zinc sulfate |
| Aleurostrongylus abstrusus treatment | FBZ. prevention |
| Troglostrongylus in Europe and Mediterranean | Agent of feline respiratory disease |
| Troglostrongylus live where | frontal sinuses, bronchi, trachea |
| Capillaria aerophilia are parasitic where | bronchi |
| capillaria bohemi are parasitic where | nasal sinuses |
| capillaria lifecycle | direct. facultative indirect with earthworms |
| capillaria clinical signs in dogs/cats | slight cough, sneezing. bronchopneumonia, rattling wheezy respiration, coughing, ADR |
| capillaria treatment | macrocyclic lactone drug |
| Muellerius capillaris species infect | goats and sheep |
| Muellerius capillaris are parasitic where | embedded in respiratory tissue (parenchyma) |
| Muellerius capillaris lifecycle | obligate indirect. short migration. 1st stage ingested by snails/slugs |
| Muellerius capillaris clinical sig | in immunocompromised animals, coughing and rapid breathing, weight loss |
| Muellerius capillaris treatment | macrocyclic lactone drugs |
| Dictyocaulus arnfeldi species infect | horse and donkey |
| Dictyocaulus viviparus species infect | cattle |
| Dictyocaulus filaria species infect | sheep and goat |
| Dictyocaulus lifecycle | direct. migrate to lungs via mesenteric lymphnodes and thoracic duct. |
| Dictyocaulus pp | 4wks |
| Dictyocaulus clinical sig | heavy infection occlude airway and obstruct airflow. increased respiration, harsh breathing, occasional crepitation. decreased eating/weight grain from increased stress to beath |
| Dictyocaulus host resistance comes from | age, vigor, genetics, established infection, acquired immunity |
| Dictyocaulus epidemiology and optimal env conditions | moderate temp, damp pasture |
| Dictyocaulus treatment | macrocyclic lactones |
| Dirofilaria immitis common name | canine heartworm |
| Dirofilaria immitis lives where | pulmonary artery and vasculature of dog/cats/mammals |
| Dirofilaria immitis vermiform embryonic stages is called | microfilaria. functional equivalent of egg. diagnostic for infection status |
| Dirofilaria immitis dog infected via | mosquitoes harboring infective stage larvae. |
| Dirofilaria immitis larvae migration | SQ tissue. colonize the pulmonary artery. become reproducing adult worms. |
| Dirofilaria immitis when do microglariae begin circulating | 6mo PI. |
| Dirofilaria immitis lifecycle | female mosquitoes feeding on microfilaremic dogs complete lifecycle, transmission to new host where the microgilariae then develop into infective heartworm |
| mosquito factors that affect heartworm transmission | 1.vector efficiency 2.mosquito feeding activity 3.microfilarial activity in host 4.source and average # blood meals taken 5.night/day time temp variation |
| heart worm pathogenesis | obstructive fibrosis, pulmonary endothelial damage, narrowing of vasculature bed w/ impaired blood flow. Reduced cardiac output |
| heart worm radiograph | pulmonary hypertension induced compensatory hypertrophy w/ enlargement of the right side of the heart. enlarged, thickened and tortuous pulmonary artery. pulmonary infiltrates in caudal long lobes. |
| heart worm and kidney disease | caused from obstruction of glomeruli. Microfilaria get stuck and block flow. |
| what bacteria is most commonly associated with heartworm | Wolbachia pipientis. primary factor of disease process! |
| what species is the vector for wolbachia pipentis | arthropods |
| how is wolbachia pipentis transmitted | in utero from adult female worms to their microfilariae |
| Caval syndrome with heart worm | large number of worms in right atrium into vena cava. obstructs blood flow and interferes with action of tricuspid valve. blood hemolyzed. |
| what are the clinical signs of caval syndrome | jaundice, hemoglobinemia, hemoglobinuria. fatal if not attended to properly |
| How does caval syndrome cause death | 1. disseminated intravascular coagulation 2.massive action and consumption of proteins involved in coagulation 3.uncontrolled hemorrhaging |
| heart worm preventative med | DEC and Oxibendazole. DEC is extremly microfilarcidal |
| how does heart worm preventative med work | targets L3 a at molt to L4 stage |
| proheart 6 | Moxidectin |
| heartgaurd | ivermectin and pyrantel pamoate |
| sentinel | milbemycin oxime, lefenuron |
| advantage muli | moxidectin, imidacloprid |
| trifexis | milbemycin oxime, spinosad |
| revolution | seleamectin |
| ivermectin sensitivity is in animals w/ what mutant allele | MDR1. collie breeds (white footed breeds). neurological effects |
| tests with poor Sensitivity are susceptible to what | many false neg |
| poor specificity leads to excessive what | false pos |
| predictive value | probability that the test correctly discriminates b/w subjects w/ and w/o infection |
| three phases of heart worm treatment | 1.pre adulticide clinical eval and treatment 2.adulticide treatment 3.post adulticide eval and treatment to eliminate microfilaria if necessary |
| pre adulticide clinical eval and treatment | lungs relatively clear, clinical eval. removal of HW larvae and wolbachia. symptomatic or asymptomatic (Mild to severe). |
| adulticide treatment | melarsomine dyhydrochloride to kill adult worms >100 days post infection in pulmonary artery. 2 or 3 injection protocols available. |
| post adulticide eval and treatment to eliminate microfilaria if necessary | antigen testing to verify treatment effectiveness. microfilaria testing and treatment |
| primary goal of adulticidal treatment | removal of adult worms in pulmonary artery/rt ventricle. |
| "slow kill" adulticial treatments | original- ivermectin 24 months. ongoing HW inflammation new- ivermectin 6 months, doxycycline for 30 days. killed microfilaria by 12 wk moxy-doxy- doxycycline for 30 days. killed microfilaria by 21 days |
| concerns with adulticial treatment | 1.post adulticidal risk of thromboembolisim 2.reduction of inflammatory response and complication |
| post adulticidal risk of thromboembolisim | dead, dying, deteriorating worms in vascular circulation. natural part of disease clearing process. reduce exercise. use corticosteroids. |
| what is the only FDA approved adulticidal treatment | Melarsomine |
| are microfilaria produced in cats with HW | No. wolbachia still factor |
| HW in cats | usually only 1 worm. ectopic sites, sudden death. worms may migrate to brain, |
| Heart worm associated respiratory disease (HARD) | inflammation in pulmonary vasculatre. occlusion of airways. asthma-like. esoinophilia, basophilia |
| clinical signs of HARD | dyspnea, coughing, vomiting, tachypnea, anorexia, lethargy |
| 3 phases of HARD | 1. w/ clinical signs 2. w/o clinical signs due to immunomodulatory activity by parasite 3. w/ clinical signs as parasite control of host response diminishes |
| management of feline HW | No approved adulticidal regimen. manage symptomatically.monthly HW prophylaxis (ivermectin/ doxycycline) |
| HW in ferrets is caused by what disease | Dirofilaria immitis. transmission like dogs and cats |
| How is HW in ferrets similar to dogs and cats | dog: recovery of adult worms cat: low and tansient microfilaremia. |
| where is Capillaria plica found | urinary tract |
| Capillaria plica is found in what sp | dogs, foxes, wolves, coyotes, cats |
| where is Capillaria feliscati found | urinary bladder |
| Capillaria feliscati is found in what sp | cats |
| Capillaria sp. in urinary tract life cycle | direct. obligate indirect w/ earthworm as IH. |
| Capillaria sp. in urinary tract PP | 60 days |
| Capillaria sp. in urinary tract clinical signs | re;atively harmless. occasional cystitis, difficulty w/ urination |
| Capillaria sp. in urinary tract treatment | ivermectin. control w/ env hygine |
| Dioctophyma renale common name | giant red kidney worm |
| Dioctophyma renale found where | renal tissues of mammalian DH. pelvis of kidney. |
| Dioctophyma renale infect dog | opportunistically. reservoir hosts: wild canidae, bear, mink, raccoon, otter |
| Dioctophyma renale life cycle | obligate indirect. free living aquatics annelids (IH). crayfish, frog, fish (PH) |
| Dioctophyma renale route in body | 1. infective larvae penetrate bowl 2. develop in peritoneum 3. penetrate kidney 4. dev to adults and repro. |
| Dioctophyma renale pp | 138 days |
| Dioctophyma renale clinical signs | without symptoms. parasitize rt kideny. renal function impaired in 1 kidney. |
| Dioctophyma renale disease is caused by what | destruction of parenchyma. eventually only capsule remains |
| Dioctophyma renale what happens when they extend down ureter | blockage/tissue destruction results in uraemia. kidney failure/death |
| Dioctophyma renale free in the peritoneum causes | inflammation, adhesoins, peritonitis |
| Dracunculus sp common name | Guinea worm. fiery serpent |
| Dracunculus sp found where | subcutaneous tissue of North American Carnivores mammals. Limb. |
| Dracunculus sp infect pet dogs/cats | opportunistically. Reservoir hosts are wild canidae, raccoon, otter, muskrats. |
| Draculculus insignis lifecycle | free living aquatic copepods (IH). frogs (PH). accidental ingestion of IH. Predatory ingestion of PH. ` |
| Draculculus insignis path in body | ingested larvae migrate through intestinal wall, reach subcutaneous tissues (3wks), sexual maturity and repro (6-7 wks) |
| Draculculus insignis host reaction | blister/ulcer at end of migration tunnel. female protrudes uterus when stim by contact w/ water |
| Draculculus mediensis sp infect | humans residing in Africa. No effective treatment |
| Thelazia sp common name | eye worm |
| Thelazia sp found where | conjunctival and lacrimal sacs |
| Thelazia sp . sp infect | dogs, cats, horses, cattle, sheep, people |
| Thelazia sp lifecycle | obligate indirect. Flies (IH)- feed on lachrymal secretions. Transmission back to DH when return to feed |
| Thelazia sp clinical sig | minimal. irriation and conjunctivities. increased tearing attracts flies |
| Thelazia sp treatment | macrocyclic lactones. ivermectin, moxidectin |
| Paraelaphostrongylus tenuis common name | meningeal worm |
| Paraelaphostrongylus tenuis sp infect | white tail deer. non pathogenic |
| Paraelaphostrongylus tenuis life cycle | obligae indirect |
| Paraelaphostrongylus tenuis in moose and elk | significant morbidity and mortality |
| Paraelaphostrongylus tenuis clinical sig | lateral recumbency, dysorexia, ADR, ataxia, head tilt, circling, paraparesis w/ advanced disease |
| Paraelaphostrongylus tenuis seasonal epi | infective larvae acquired in summer. clinical signs appear during fall/ early winter. consistent w/ deep activity |
| Paraelaphostrongylus tenuis in goats | transient often get better |
| Paraelaphostrongylus tenuis in camelids | detection late in clinical course. |
| Paraelaphostrongylus tenuis treatment | FBZ. IVM (migrating larval stages) |
| Paraelaphostrongylus tenuis prognosis | 10-20% unable to stand. 75-80% able to stand w/o assistance |
| Paraelaphostrongylus tenuis prevention | limit contact with white tail deer. gravel/limestone barriers to snail/slug migration around fence lines, improve drainage |
| Paraelaphostrongylus tenuis prophylactic IVM treatment | migrating larvae. may facilitate IVM resistance to Haemonchus |
Created by:
ejohnson17
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