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Parasitology > Ruminant protozoa, cestodes, blood > Flashcards

Ruminant protozoa, cestodes, blood Flashcards

1
Q

Eimeria bovis

A

most common protozoal parasite in cows, causes damage to small and large intestine; oval cysts

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2
Q

Eimeria zuernii

A

Pathogenic in cows, most common cause of winter coccidiosis, sporulation in spilled hay; round cysts

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3
Q

Eimeria macusaniensis

A

in llamas and alpacas, 92 by 67 oocysts

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4
Q

Eimeria has coccidian lifestyle

A

multiplication in SI (schizogony) with sexual repro in the large intestine (gametogony), develops in environment to sporulated oocyst (within 2 days)

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5
Q

What is the PPP for eimeria?

A

2-3 weeks

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6
Q

How is the host damaged in Eimeria?

A

Due to cellular infiltrates-parasite destroys intestinal lining, disease associated with secondary pneumonia, severity depends on immunity of the host and number of oocysts ingested (young animals or animals on winter pasture)

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7
Q

What is nervous coccidiosis?

A

Occurs from E. zuernii, seen in animals older than 6 months and may be related to toxin or electrolyte imbalance. There are 3 points. 1) Cause greater economic loss than other protozoa 2) stress involved in disease outbreaks 3) highly specific immunity to Eimeria develops

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8
Q

What are the necropsy lesions associated with coccidiosis?

A

Cattle-damage to mucosa of small intestine, cecum, colon (white nodules). Goats-lesions only in small intestine (hemorrhage and ulcers, yellowish plaques)

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9
Q

What are the clinical signs of enteric coccidiosis?

A

Calves-unthrifty and have fecal stained perineal areas.; severe cattle may have thin bloody diarrhea and may be feverish and anorexic **tenesmus common
Acute-some calves may die from diarrhea or other secondary infections, bloody scours

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10
Q

What are the clinical signs of nervous coccidiosis?

A

Sudden onset in a few animals: muscle tremors, hyperesthesia, nystagmus. Often seen during or after severe winter and sudden stimuli trigger cows

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11
Q

Small ruminant coccidiosis

A

Many shed oocysts with no signs, stress may go to diarrhea, CNS problems are common

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12
Q

Diagnosis of coccidiosis

A

Lab findings must correlate to clinical signs. do fecal float, disease outbreaks may occur every year on same farm.

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13
Q

Treatment and control of coccidiosis

A

Change management practices, reduce stress, increase water supplies, because oocysts are resistant do not feed on ground; may need individual animal support with fluids and electrolytes. Keep affected animals isolated after clinical signs resolve because they are shedding high oocysts. Manage and medicate the whole herd. Can use sulfas or amprolium. No approved drug for E. mac but use ponazuril.

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14
Q

Epidemiology of coccidiosis

A

treat before you ship the cows. Summer dz by dry weather and crowding, winter by manure contaminated grass. Not zoonotic and can be prevented by medication in feed.

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15
Q

Can dogs get Eimeria?

A

YES. Look for micropyle (cap on end) and differentiate between Cysto. Dogs eat poop. Also has 4 sporocysts whereas in cysto there are 2.

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16
Q

Cryptosporidiosis

A

Cryptosporidium parvum is 5-6 micrometers in the small intestine and are pathogenic to the young. Andersoni is in the abomasum and is non-pathogenic.

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17
Q

Crypto life cycle

A

Ingest thick walled sporulated oocysts, invade microvilli of intestinal tract, development/schizogony/gametogony/sporogony in parasitophorous vacuoles (enclosed by host cytoplasm, a feeder organelle develops, this allows the parasite to develop protected from phagolysosomes). organisms on top of brush border. oocysts sporulate rapidly in PVs, thin walled release sporozoites in lumen that invade host cell for autogenous infection and thick walled are passed into the environment and are immediately infective.

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18
Q

What are the types of merozoites in crypto?

A

Type 1-rupture out and can recycle indefinitely in immunocompromised or develop into type 2. Type 2-rupture out, enter new cells, form macrogametes.

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19
Q

What is the crypto PPP?

A

as little as 2 days

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20
Q

Crypto pathology

A

Do not cause as much cell damage as Eimeria but result in malabsorption and maldigestion due to villous atrophy and decreased enzyme activity. Calves susceptible until functional rumen develops. Can lead to hepatobiliary or respiratory dz.

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21
Q

Clinical signs of crypto

A

C. parvum seen more in dairy cows because of environmental differences, young calves up to three weeks old have mild to severe diarrhea that persists regardless of treatment. Feces are yellow, watery, and have mucus.

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22
Q

Diagnosis of crypto

A

Clinical signs and history. Do fecal float, acid fast, or PCR.

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23
Q

Treatment of crypto

A

Good management control-no licensed therapeutics for food animals-DON’T give anything to them. Immune response usually clears them. Dairy cows should be in clean environment, kept separate for 2 weeks, and isolated from healthy if have diarrhea.Avoid mechanical transmission and change gloves. Calf houses should be cleaned out, and give fluid and electrolyte therapy to sick.

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24
Q

Epidemiology of crypto

A

C. parvum and C. hominis infect humans. Immediately infective when passed, vets and students at risk. Water plays a role

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25
Q

Bovine giardiasis

A

Giardia intestinalis assemblage E. Cysts (infective stage) in environment, trophozoites in small intestine. Calves ingest cysts, trophozoites feed, cysts passed in feces. PPP 1-2 weeks. Trophozoites attach to intestinal epithelial cells which decrease microvilli surface area and reduce intestinal enzyme activity leading to diarrhea. Other enteropathogens involved (crypto)

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26
Q

Giardia clinical signs

A

may be none or some persistent diarrhea in calves 2-5 months of age.

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27
Q

Giardia diagnosis and treatment

A

zinc sulfate fecal float, use fenben and good control. prevent fecal contamination of feed and water. Not zoonotic.

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28
Q

Monieziasis

A

Adults live in the small intestine of ruminants, are cestodes, eggs or proglottids in feces, oribatid mites are IH, no to few clinical signs.

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29
Q

Clinical signs of Moniezia

A

sheep: slight intestinal disturbances, some growth retardation, usually no clinical signs. Cattle: more serious, may kill young but not usually clinical signs

30
Q

Diagnosis and treatment of moniezia

A

Presence of proglottids or eggs in the feces, fecal float to observe egg with pyriform apparatus. Use fenben.

31
Q

Thysanosoma actinoides

A

Rare, in sheep, in small intestine, segments are conspicuously fringed, may obstruct bile ducts, use fenben to treat

32
Q

Fasciola hepatica

A

Common liver fluke, occur in bile ducts, operculated eggs passed in feces, miracidium develops if in water, penetrate snail, cercariae exit and are ingested, go to the small intestine, penetrate and enter the peritoneal cavity to go to the liver. They wander in the liver parenchyma and feed on blood for 6 WEEKS.

33
Q

What is F. hepatica’s PPP?

A

2-3 months

34
Q

What is the most pathogenic in liver flukes?

A

The young liver fluke! A second bacterial disease, Black disease, from C. noyvi can develop. More pathogenic in sheep and goats.

35
Q

Clinical signs of liver flukes?

A

Sheep: fever, anemia in acute disease. in more chronic infections you may see bottle jaw (like in Haemonchus) and fasciolosis can be fatal. Cattle: decreased weight gain and conception rates, livers condemned at slaughter so decreased profits.

36
Q

Diagnosis and treatment of liver flukes?

A

Sedimentation exam, timing is critical for success and transmission is weather dependent, treat when the flukes are in the animal! Adults flukes more susceptible, use albendazole. NO PRODUCT kills migrating flukes. Control: remove flukes in animals, avoid wet pastures, vaccinate against C. novyi. Zoonotic if eat watercress.

37
Q

Fascioloides magna

A

Giant liver fluke. No shoulders, twice the size of F. hepatica. Found in hepatic parenchyma in cysts, not usually in bile ducts. Same life cycle as other until enter host. Deer: capsules around flukes open to ducts to help eggs escape. Cattle: abnormal, dead end host, become encapsulated and eggs don’t escape. Sheep/goats: abnormal hosts, no capsules form, flukes cause damage to liver and other organs, no eggs deposited

38
Q

Clinical signs of F. magna?

A

Cattle: none; sheep/goats: emaciation, weakness, death

39
Q

Diagnosis and treatment of F. magna?

A

No eggs in feces, have to look at necropsy for flukes or black pigmentation in liver. Use albendazole in sheep but none approved. Control deer on property!

40
Q

Dictyocauliasis

A

viviparus: cattle, filaria: sheep; lungworm, only one in cattle! L1 is diagnostic stage found in the feces. Direct life cycle: seasonal, L3 sensitive to drying and cold. DH ingest L3 on grass->penetrate intestine->lymphatics->mesenteric l.n->vascular system->lungs->alveoli within 5 days. Adults in airways, bronchi, trachea. Eggs are coughed up, swallowed, hatch in intestine.

41
Q

Pathogenesis of dictyocauliasis

A

Penetration phase: Larvae ingested and migrate to lungs. Prepatent phase: 7-25 days after infection, larvae enter lung tissue and bronchioles and cause clinical signs like eosinophilic exudates and frothy mucus. Patent phase: Adults lay eggs in bronchioles, Adult worms damage bronchi and lead to bronchitis, alveoli collapse, edema. Post patent phase: surviving animals recover and few flukes remain.

42
Q

Clinical signs, diagnosis, treatment of dictyocauliasis

A

Numbers determine severity of disease. Immunity develops rapidly but may wane in older animals. species, age, level of exposure determine severity. Acute Verminous Pneumonia: 7-25 d post infection, several animals affected at one time on pasture, usually young animals. Subacute Verminous Pneumonia: sudden onset, scouring, lower mortality, labored breathing and susceptible to other dzs. Do history and Baermann. Timing critical for success. Use alben and fenben.

43
Q

Prevention of dictyocauliasis

A

THERE’s a vaccine! only in the UK. keep pasture dry and eliminate chronically affected animals.

44
Q

Muellerius capillaris

A

Hair lungworm in sheep and goats. Occurs in lung parenchyma. L1 is diagnostic stage. Transmission depends on larvae survival and snail IH. L1 in feces ingested by snail, develops to L3, snail ingested and L3 penetrates intestine to lymphatics, molt in mesenteric l.n., get to lungs through circulation. Form small fibrous nodules under pleura, can be calcified.

45
Q

Clinical signs, diagnosis, treatment by M. capillaris

A

Minimal but related to resp disease. Find larvae in Baermann. use fenben, keep snails off pastures.

46
Q

Protostrongylus rufescens

A

red lungworm in sheep and goats, in small bronchioles, L1 in feces. Same life cycle as M. capillaris.

47
Q

Clinical signs, treatment, diagnosis in P. rufescens

A

irritation and inflammation in bronchioles, dz depends on number of worms. vague and nonspecific signs. find larvae in feces.use fenben, keep snails off.

48
Q

Nasal myiasis

A

Oestrus ovis-sheep, goats, humans. Looks like honeybee. Maggots in nasal sinuses are yellow. Females viviparus, shoot fluid with larvae at sinuses. Go to frontal sinuses and molt twice, larvae fall and pupate. Adults live less than a month

49
Q

Pathogenesis, signs, treatment of nasal myiasis

A

1st instar causes mucoid nasal discharge. other instars cause bloody discharge. Sheep are restless and keep nose to ground, recover larvae from sinuses at necropsy. Ivermectin. causes eye and nasal infections in humans.

50
Q

Babesiosis

A

Babesia bigemina and Babesia bovis, Red Water Disease, found as pyriforms in the RBC, transmitted by Rhipicephalus annulatus that feeds on cattle and transmits sporozoites (one host tick). Ticks ingest RBC with piroplasms, undergo gametogony in tick, transovarian and transstadial transmission. Infected RBC removed by intravascular hemolysis. Death from pulmonary edema. Subclinical infection is protective.

51
Q

Clinical signs, diagnosis, treatment of babesiosis

A

Anorexia, anemia, increased HR/RR, before collecting samples contact state vet. Demonstrate parasites in RBC, do PCR. All cattle out of Mexico or quarantine zone are hand inspected and treated with coumaphos. If not killed, cattle go back. Affected cattle are not treated because withdrawal times unknown.

52
Q

National Cattle Fever Tick Eradication Program

A

Mandated dipping of cattle which killed tick life stages. Have quarantine zone. White tailed deer may carry and mexican cattle cross border.

53
Q

Elaeophora schneideri

A

Aterial worm, adults in carotid/iliac/mesenteric arteries. Microfilariae in capillaries move through circulation until they reach capillaries of face and forehead where they are ingested by horse flies (IH). Develop to L3, deposited on skin when feeding, move into wound, microfilariae not in peripheral circulation. Can cause thrombosis, inflammation, fibrosis of arteries.

54
Q

Clinical signs, diagnosis, treatment of elaeophora

A

Filarial dermatitis, lesion on poll, may be on face/nostrils/hind feet. May cause brain damage. Find by characteristic lesions and microfilariae in blood-warm saline will cause migration. Ivermectin is treatment. Deer are natural hosts and no signs in them.

55
Q

Parelaphostrongylus tenuis

A

White tailed deer are normal hosts, llama and moose are most sensitive. Adults in venous sinuses of cranium, eggs in venous circulation. larvae carried through the blood stream to the lungs and penetrate parenchyma. L1 passed in feces and snails eat them. L3 penetrates abomasum and travels to the spinal cord. Lay eggs on meninges. Aberrant hosts have brain damage from migration.

56
Q

Diagnosis and treatment of parelaphostrongylus tenuis

A

Signs after 45 days of ingesting snail. do CSF tap to see increased eosinophils and rule out rabies, thiamine deficiency. Use fenben against migrating larvae. Drain and fence wet areas

57
Q

Taenia hydatigena

A

In small intestine of canines, cysticercus in peritoneal cavity of sheep (IH), Taenia type egg in dog feces, ruminant eats egg and it encysts on peritoneum as cysticercus. Pathology from migration from intestine through liver to peritoneum. Dullness, loss of appetite, pyrexia. Dog is DH. Use prazi.

58
Q

Taenia saginata

A

adults in human SI, cysticercus in cardiac and skeletal muscle of cattle and people. Taenia type eggs in feces of DH. No treatment or signs in IH. Diagnose by necropsy

59
Q

Taenia ovis

A

adults in dog SI, cysticercus in cardiac and skeletal muscle of sheep. Taenia type eggs in feces of DH. No treatment or signs in IH. Diagnose by necropsy.

60
Q

Echinococcus granulosus

A

canids DH, hydatid cyst is metacestode; liver, lungs, pancreas, find taenia type eggs in feces, not treated, treat dogs with prazi.

61
Q

Echinococcus multilocularis

A

dogs and cats DH, alveolar hydatid is metacestode; exogenous budding, like neoplasm, find taenia type eggs in feces.

62
Q

Taenia multiceps

A

DH is canids, small scolex, large coenurus in sheep that takes long time to mature. Larvae migrate to brain when eggs ingested from DH. Find coenurus in sheep or eggs in feces. Zoonotic.

63
Q

Setaria

A

peritoneal and sometimes pleural cavity or anterior chamber of eye. Sheathed microfilariae, mosquitoes deposit L3 near wound. Non pathogenic in peritoneal cavity, invade spinal canal of sheep/goats/cattle. No treatment.

64
Q

Tritrichomonas foetus

A

Same as in cats!, vagina and uterus in cows, venereal disease that has no symptoms in bulls but early abortion in cows, reportable disease. Causes vaginitis and metritis. epithelial crypts in bulls deepen for organism, immunity not long lasting for cows. Virgins most susceptible. Trophozoites cause inflammation of uterus and invade fetal tissues, can see pyometra after abortion. Fetal loss 50-70 days after gestation. Infertility most common sign. Vaginal exudate with pus and trichomonads

65
Q

Diagnosis of T. foetus

A

History, after intro of new animal into herd followed by decreasing fertility. Find DNA. Vets must be certified to collect samples. Bulls must be tested before change of ownership and transfer. ONLY PCR, ship overnight, inpouch. May collect, incubate, frozen, shipped. Cows usually have to have calf by side or be 120 days pregnant.

66
Q

Treatment for T. foetus

A

none for bulls, must be identified and sent to slaughter if positive. Bulls less than 4 years less carriers, can become chronic. Can use killed, whole cell vaccine for cows to reduce shedding, don’t need if good biosecurity. Cull open females.

67
Q

Sarcocystis cruzi

A

Beef cattle! eosinophilic myositis (meat condemned at slaughter), canids are DH. Dogs eat meat with sarcocysts, pass sporulated sporocysts in feces. Two schizogonic cycles in vascular endothelium and one in monocytes in cows, merozoites enter striated muscle and create sarcocysts. Can see edema, hemorrhage of fat, placentitis and late term abortion. Bradyzoites in tongue, heart.

68
Q

Clinical signs of S. cruzi

A

Fever, muscle tremors, loss of hair from tail switch and back of neck, no treatment.

69
Q

Toxoplasma gondii

A

Sheep and goats, bradyzoites in tissue like other species, cats are DH. Others are PH. Abortion storm 3rd trimester!, placentitis. In sheep, if ingest sporulated oocysts early in gestation will lead to resorption. In goats, will see abortion or weak, won’t abort again.

70
Q

Signs and treatment for T. gondii

A

No treatment but can feed monensin. People infected by eating undercooked pork or unpasteurized goat milk.

71
Q

Neosporosis

A

Neospora caninum, main cause of abortion in dairy cows, fatal in dogs. Tachyzoites in PMNs, tissue cysts in brain or spinal cord. Dogs are DH, eat infected tissue, pass oocysts in feces, IH infected by ingesting sporulated oocysts in feed or water by horizontal transmission. Sporozoites enter intestinal cells and become tachyzoites which enter circulation. Can also be transmitted transplacentally. Congenital cows with it are raised and pass it to offspring via transgenerational. Vertical form most common. Dogs have to eat infected tissue cysts, not oocysts.

72
Q

Signs and treatment of N. caninum

A

neurological signs, encephalitis and myocarditis in fetus. No signs in adult. If pregnant cow is infected: 1) early embryonic death 2) most common, abortion and still birth 3) birth of feeble and abnormal calf 4) normal calf with no signs; most calves have no signs. Submit all or part of aborted fetus to diagnose (brain!). Serology based on tachyzoite antigens, a positive titer does not mean N. caninum was responsible for abortion. No treatment. Embryo transfer to control vertical transmission. Test and cull. Keep away from feces. UNLIKE T. GONDII IT IS NOT ZOONOTIC.

Parasitology (21 decks)

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