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Parasitology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What parasite is responsible for Texas Cattle Fever aka Red Water Disease?

What serves as the major vector for this parasite?

How many hosts does this tick have?

What modes of transmission does this parasite undergo in the tick?

A

Babesia bigemina

Rhipicephalus annulatus

1

transovarian and transstadial

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2
Q

What happens to host animals that manage to survive infection of Babesia bigemina (Texas Cattle Fever)

A

They become carriers

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3
Q

What animal can serve as a natural reservoir for Babesia bigemina?

A

white-tailed deer

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4
Q

What acaracide drug are cattle coming from Mexico treated with before allowing entry into the US?

What other drugs can be used?

Why is this a problem?

A

Coumaphos, organophosphate acaracide applied in dipping vats or sprays

None

This is the only acaracide left that can kill ticks resistant to other drugs, but ticks are resistant to coumaphos as well. Cattle that are found to have ticks are dipped and sent back to Mexico, ticks that do not get killed by coumaphos are sent back (on the cattle) as well! resistance continues to grow!

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5
Q

What drugs are available to treat Babesia in cattle?

What is a drawback to these drugs?

A

diminazene aceturate and imidocarb dipropionate

Not used to treat affected cattle (illegal to do so) because no withdrawal periods have been established

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6
Q

What parasite is known as the “arterial worm”

A

Elaeophora schneideri

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7
Q

Which coccidia of cattle are we most concerned with?

Which one of these species is the most common cause of winter coccidiosis?

A

Eimeria bovis & Eimeria zuernii

Eimeria zuernii

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8
Q

Morphologically, how can you tell the difference between E. bovis & E. zuernii oocysts?

A

E. bovis is larger and oval/tapered, zuernii is smaller and round

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9
Q

True/False: Eimeria species of cattle are the only pathogenic species in ruminants

A

False, Eimeria species of sheep and goats are also pathogenic

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10
Q

What is a highly pathogenic species of Eimeria of llamas and alpacas?

What is a characteristic morphological trait of this species?

A

E. macusaniensis “E. mac”

very large in size, 92x67 um

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11
Q

Describe the life cycle of Eimeria in ruminants

A

Direct life cycle:

Ingestion of sporulated oocyst, each oocyst gives rise to 4 sporocysts, each containing 2 sporozoites, invasion of intestinal epithelial cells, schizogony occurs with merozoite formation, further schizogony occurs, final merozoite is released and invades an intestinal cell to form a male or female gamete, gametogony occcurs when male gamete invades a cell occupied by a female gamete, zygotes encyst and unsporulated oocysts are formed and shed

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12
Q

How fast can sporulation occur with ruminant coccidia once outside the host?

PPP of E. bovis & E. zuernii

A

2 days

2-3 weeks

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13
Q

What is causing the pathogenesis of coccidia inside the host?

What does the severity of disease depend on?

A

massive intestinal cell destruction due to rapid asexual reproduction of coccidia inside intestinal cells

number of oocysts ingested & immune status of host

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14
Q

What kinds of situations predispose cattle to severe coccidiosis?

A

Young cattle (that have not yet developed an immunity) that are confined in close quarters (feedlots) & large numbers of oocysts are being shed & subsequent accumulation of sporulated oocysts

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15
Q

What causes winter coccidiosis occur?

A

Cattle on range aggregate around water or feed during winter and shed oocysts around the communal areas

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16
Q

Is E. bovis or E. zuernii responsible for “nervous coccidiosis”?

A

E. zuernii

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17
Q

What are the 3 “main points” of coccidiosis in cattle?

A
  1. coccidia cause a greater economic loss than any other group of protozoa
  2. stress is usually involved in disease outbreaks
  3. highly specific immunity to individual Eimeria species does develop
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18
Q

What is a common sign of coccidiosis in goats?

A

CNS signs: hind limb ataxia, progression to recumbrence, coma, death

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19
Q

True/False: animals with coccidiosis can show clinical signs before shedding oocysts

A

True

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20
Q

What are some ways to control coccidiosis (management) and reasonings behind them?

A

Do not feed on ground: prevent animal from ingesting oocysts

Reduce stress: stressed animals predisposed to infection & disease

isolate affected animals even after clinical signs subside: oocyst production peaks after clearing of clinical signs

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21
Q

What are some common coccidiostats?

A

Sulfaquinoxaline & amprolium combination therapy

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22
Q

What is a common therapeutic method to prevent coccidiosis?

A

Continuous administration of meds in feed &/or drinking water in areas where coccidiosis is common

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23
Q

What drugs are approved for coccidia (E. mac) in camelids?

A

None, but ponazuril has shown to have the most efficacy against most life stages

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24
Q

Is coccidia in large animals considered zoonotic?

A

Nope

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25
Q

Why might you see Eimeria of large animals in the feces of a dog?

A

the dog is ingesting feces of large animals shedding oocysts, often these dogs have chronic coccidia infections that are not responsive to treatment

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26
Q

Regarding sporulation, how can you differentiate Eimeria and cystoisospora?

A

Eimeria have 4 sprocysts with 2 sporozoites each

Cystoisospora have 2 sporocysts with 4 sporozoites each

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27
Q

Which parasite is responsible for Cryptosporidiosis (genus and species)?

how big is this parasite?

pathogenicity?

A

Cryptosporidium parvum

5-6 um

HIGHLY pathogenic in young animals

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28
Q

Is C. parvum considered zoonotic?

A

YES

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29
Q

Describe the life cycle of cryptosporidium parvum

A

Ingestion of thick walled sporulated oocyst –> 4 sporozoites are released & invade microvilli of intestines –> induce host cells to form a cytoplasmic parasitophorous vacuole (PV) around the parasite on the SURFACE of the host cell –> schizogony, gametogony, fertilization, sporogony all occur inside the PV –> merozoites rupture out and enter new cells to form microgametes and undergo gametogony –> oocysts form inside the PV’s, sporulate, and can then give rise to thin-walled oocysts (20%) that release sporozoites to re-infect the host or give rise to thick-walled oocysts that are shed in feces that are immediately infective

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30
Q

Why does Cryptosporidium parvum not cause hemorrhagic diarrhea? (whereas coccidia can)

A

C. parvum technically does not invade the host cell and cause damage to the host cell while undergoing schizogony/gametogony, all reproductive processes occur inside the parasitophorous vacuoles located on the SURFACE of the host cell

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31
Q

What is the earliest time C. parvum’s prepatent period can be?

A

2 days

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32
Q

What kind of problems can C. parvum cause to its host?

A

malabsorption & maldigestion due to villous atrophy & decreased activity of membrane-bound digestive enzymes

immunocompromised animals can develop hepatobiliary or respiratory disease due to overwhelming multiplication of organisms (proliferation into airways)

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33
Q

Which kind of calves is C. parvum more common in: dairy/beef

What are some typical clinical signs?

A

Dairy calves as they are kept confined more

mild-severe diarrhea that persists for several days regardless of treatment, feces will be yellow/pale, watery, and contain mucus. Marked weight loss, emaciation, debilitation, and rarely death

often diarrhea is self-limiting

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34
Q

Diagnostic methods of C. parvum?

A

signalment/history (age, confinement), fecal float w/centrifugation, acid fast stain, ELISA, PCR

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35
Q

What treatment options are available for C. parvum? Which ones are FDA approved?

A

none besides good herd management and supportive care

no FDA approved therapies

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36
Q

What are some good management practices to avoid C. parvum outbreaks in your herd?

A

calves should be born in clean environment, fed w/adequate colostrum

calves need to be isolated for first 2 weeks of life

Diarrheic calves need to be isolated from healthy calves and kept isolated for several days after diarrhea ends

care must be taken to avoid mechanical transmission of C. parvum

calf-rearing houses must be vacated completely and thoroughly cleaned on a regular basis

pests control to prevent contamination of calf grain/milk feed storage areas

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37
Q

In terms of epidemiology, why is it so easy for other animals (including humans) to be infected with C. parvum?

A

Oocysts being shed are immediately infective, they sporulate inside the host

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38
Q

Regarding Giardia bovis, what is the difference between the cyst stage and trophozoite stage?

A

Cysts: reside in environment, infective stage,

Trophozoites: reside in small intestines, feeding stage,

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39
Q

PPP of Giardia bovis?

A

1-2 weeks

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40
Q

Describe the pathogenesis of Giardia bovis

A

Cysts are ingested, trophozoites are released and attach to epithelial cell surface, reduction in microvilli surface area leads to reduction in intestinal enzyme activity resulting in diarrhea

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41
Q

How will a calf typically present if it has giardia?

A

intermittent to continuous diarrhea for up to 6 weeks that is non-responsive to treatment, usually affecting calves 2-5 months of age

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42
Q

Treatment and control of giardia bovis?

Diagnostics?

Zoonotic?

A

Fenbendazole, prevent fecal contamination of feed/water

saline smears, fecal flotation with ZnSO4 w/centrifugation

Nope

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43
Q

What prominent ruminant cestode can measure up to 6 m long and 1.6 cm wide? Where does it reside in the host?

Does it have a direct or indirect life cycle? (If indirect, please list its I.H., and its associated life cycle stage)

How does the D.H. get infected?

A

Moneizia expansa, small intestine

indirect, oribatid mites, metacestode stage is a cysticercoid

ingestion of infected mite on grass while grazing

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44
Q

How can you diagnose Moneizia sp. in a ruminant?

Describe the morphology of a Moneizia sp. egg

A

presence of proglottids in feces, crushing proglottids and observing eggs, fecal float & observing egg w/pyriform apparatus, necropsy to find worms in small intestines

Large in size, +/- hexacanth embryo, 3-4 sided geometric egg,

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45
Q

What group of drugs used to treat cestodes in ruminants? (list 3 that belong in this group)

What other group of worms is this drug group efficacious for?

A

Benzimidazoles: Albendazole, fenbendazole, oxfendazole

Strongyles

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46
Q

What genus, species, and associated disease does the fringed tapeworm belong to?

What is its D.H. and where does this parasite reside in the D.H.?

What is its metacestode stage?

A

Thysanosoma actinoides, thysanosomiasis

Sheep, goats, antelope,(NOT CATTLE);small intestine (secodnarily bile ducts, gall bladder, pancreatic ducts)

Cysticercoid

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47
Q

Describe the morphology of thysanosoma actinoides

How can you diagnose it?

A

less than 1 foot long, creamy white in color, segments are short and conscpicuously fringed

Proglottids in feces

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48
Q

Treatment of Thysanosoma actinoides?

A

albendazole, fenbendazole

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49
Q

What parasite is responsible for Fascioliasis?

What species do we see this parasite usually affecting?

Where in the D.H do these reside?

A

Fasciola hepatica

Cattle, sheep, camelids

Bile duct

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50
Q

What is a unique morphological trait that can be used to distinguish (adult) fasciola hepatica from other flukes?

A

prominent “shoulder” just behind cephalic cone

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51
Q

What is the life cycle for Fasciola hepatica?

What is its PPP?

A

operculated eggs shed in feces, containing a miracidium –> miracidium hatches if egg deposited in water –> miracidium penetrates snail (I.H.) –> multiple cercariae exit snail from single miracidium –> cercariae are motile and find their way onto aquatic plant above water & develop into metacercariae–> plant w/metacercariae is ingested by D.H. –> immature flukes excyst in S.I. –> migrate to liver –> wander through parenchyma & feed on blood for ~6 weeks –> flukes enter bile ducts and matures to adult

2-3 months

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52
Q

Fasciola hepatica are more pathogenic in (cattle/sheep/goats), most pathology is caused by _______ of (immature/mature) flukes through ______

A

sheep/goats, migration, immature, hepatic parenchyma

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53
Q

Fasciola hepatica:clinical signs in sheep? cattle?

How can you diagnose fasciola hepatica?

A

SHEEP: acute disease (fever, anemia, sudden death w/o symptoms), chronic disease (bottle jaw, abdominal distension)

CATTLE: decreased gains, weak & unthrifty calves, decreased milk production & reproductive performance

Diagnosis: sedimentation

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54
Q

Which life stage of fasciola hepatica is more susceptible to anthelmintics? So when is the best time to start treatment?

What drugs are available for fasciola hepatica Tx?

What life stages are current drugs for fasciola hepatica approved for?

A

adults, when flukes are maturing or have matured

Clorsulon, albendazole

ONLY ADULTS

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55
Q

How can reasonable prevention/control of Fascioliasis be accomplished

Is this disease zoonotic?

A

removal of flukes in affected animals (stop them from shedding), reduction of snail population, prevention of livestock from grazing in snail-infested pasture

avoid wet pastures, DO NOT USE HAY FROM WET PASTURES

vaccinate against C. novyi

YES, ZOONOTIC

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56
Q

What parasite causes Fascioloidiasis?

What is its natural host?

What production animals is it seen in?

A

Fascioloides magna, “Giant Liver Fluke”, Deer Fluke

Deer

Cattle, sheep, goats

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57
Q

How can you morphologically differentiate fascioloides magna from fasciola hepatica?

A

fascioloides is much bigger (at least 2x size of mature fasciola), fascioloides does not have a prominent shoulder and cephalic cone (more uniform looking body)

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58
Q

What is different about the life cycle of Fascioloides magna when compared to Fasciola hepatica?

What is the difference between infection in cattle/sheep compared to deer?

What is the difference between infection in cattle compared to sheep?

A

Same until ingestion by definitive host, but Fascioloides sp. form cysts/capsules inside the liver with an opening on one end for egg release into bile ducts

Fascioloides does not release eggs in cattle/sheep, they are abnormal hosts

Fascioloides will become encysted in cattle, but will not encyst in sheep and continue to mirgate through the liver causing severe damage to parenchyma (but no release of eggs)

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59
Q

You own a herd of cattle/sheep, and they keep getting infected by Fascioloides magna, how is this occurring if Fascioloides does not release eggs in these abnormal hosts?

A

There is a nearby deer population that is serving as a reservoir for infection

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60
Q

Fascioloides magna causes more pathology in (cattle/sheep & goats), and cause predisposition to ______ infection.

A

sheep & goats, C. novyi

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61
Q

How would you diagnose Fascioloides magna infection in cattle, sheep, and goats (abnormal hosts)

A

since these abnormal hosts do not shed eggs, the only way to have a confirmatory diagnosis is by finding flukes inside the liver at necropsy and black pigmentation of liver

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62
Q

What treatments are effective for Fascioloides magna infection, are they FDA approved?

What is the most practical way to control (prevent) infection of these parasites?

A

Albendazole, clorsulon (not commercially available at concentration needed to kill flukes), none are FDA approved

Restrict deers’ access to grazing pasture

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63
Q

What parasites are responsible for Dictyocauliasis (aka Verminous Bronchitis, Verminous Pneumonia, Parasitic Bronchitis, Husk)

List the genus and species responsible in cattle and sheep

A

Cattle: Dictyocaulus viviparus - cattle lungworm

Sheep: Dictyocaulus filaria - sheep lungworm

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64
Q

Regarding Dictyocaulus vivparus infection in cattle, what is unique about its diagnostic stage? What is its diagnostic stage?

True/False: this is the only lung worm found in cattle

A

In cattle, this is the only parasite whose L1 is the diagnostic stage, the larval stage (L1) is the diagnostic stage

True

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65
Q

What is the diagnostic stage of Dictyocaulus filaria?

What are some characteristic morphological trait ofs the diagnostic stage?

A

L1 larvae

Tail is smooth and rounded. Anteriorly, it has a cephalic “button”

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66
Q

The life cycle for Dictyocaulus spp. is (direct/indirect)?

Describe the life cycle

Where do the adults reside?

Where do the eggs hatch?

A

Direct

L1 passed in feces –> develop to L3 –> L3 on grass ingested by host while grazing –> L3 penetrate intestines to lymphatics to mesenteric LN & develop to L4 –> migrate to vasculature –> arrive at lungs –> reach alveoli 5 days after ingestion –> adults lay eggs that are coughed up and swallowed

Adults in major airways, bronchi, trachea

Eggs hatch in small intestine

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67
Q

T/F: An animal infected w/Dictyocaulus spp. can die before presentation of clinical signs

A

True

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68
Q

What are the 4 phases of pathogenesis of Dictyocaulus spp.?

Which phases are associated with clinical signs/significant pathology?

What pathology is associated with these phases?

A

Penetration phase, prepatent phase, patent phase, post patent phase

Prepatent phase & patent phase

Prepatent: excessive inflammatory response to larvae in lung tissues/bronchioles resulting in frothy mucus that can block small bronchi/bronchioles

Patent: Adults damage epithelium, exudates blockbronchi & air passages, can lead to bronchitis, pneumonia, tracheitis, dyspnea, and death

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69
Q

What is the severity of Verminous Bronchitis, Verminous Pneumonia, Parasitic Bronchitis, Husk dependent on? (these are all the same disease FYI)

What happens to animals exposed periodically (not excessively) to the parasite that causes this disease?

What happens to an animal that develops immunity, is not exposed for a significant period of time, and is then re-exposed to large numbers of this parasite?

A

number of larvae ingested, rate of ingestion of larvae, number of larvae that reach the lungs

develop natural immunity, but immunity may wain in older animals

animal can develop severe infection

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70
Q

How can you diagnose Dictyocauliasis?

A

History of patient: repeated coughing, dyspnea, reduced gains, young animals on pasture

Baermann exam

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71
Q

What is one thing you have to worry about when treating animals w/Dictyocauliasis?

What drugs are available for treatment? Are the FDA approved?

A

Administration of anthelmintics can interfere with development of natural immunity

Albendazole, fenbendazole, ivermectin, moxidectin, levimasole

yes

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72
Q

How can Dictyocauliasis be controlled?

A

Vaccine is available (UK only)

have herds graze on dry pasture, cull chronically infected animals

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73
Q

What parasite is the lung worm of sheep, goats, and deer? Aka the hair lungworm

How can adult males be differentiated from females?

A

Muellerius capillaris

male: posterior end is a coiled spiral
female: S-shaped tail with spine

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74
Q

Muellerius capillaris: Is the life cycle direct/indirect? What is the diagnostic stage?

Describe the life cycle

A

Indirect, L1 larvae

eggs laid in lung tissue –> eggs hatch in lungs, L1 are coughed up and swallowed –> L1 shed in feces –> L1 ingested by snail/slug (I.H.)–> L1 develops into L3 –> infected snail ingested by host grazing on grass –> L3 penetrates intestines –> migrates through lymphatics, molts to L4 in mesenteric lymph nodes –> L4 migrates into circulation & molts to L5 (adult) in lung

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75
Q

What diagnostic technique can be used to diagnose Muelleriasis?

How can you differentiate larvae of Muelleria capillaris from Dictyocaulus spp. if you recover both on diagnostic testing?

A

Baermann exam

Muelleria sp. is shorter in length (300um), Dictyocaulus is 500um

Dictyocaulus has a rounded tail and a cephalic button

Muelleria has a S-shaped tail with spine (female) or spiraled tail (male)

76
Q

treatment options for Muelleria capillaris?

A

Levimasole, fenbendazole, albendazole, macrolides

77
Q

What parasite is known as the red lungworm?

What is its D.H.?

where does it reside in the D.H.?

How can you differentiate the larvae from other parasites whose larvae may be found in a Baermann exam?

A

Protostrongylus rufescens

sheep, goats, but is rare in U.S.

small bronchioles

can be a little smaller or similar size as Muelleria sp., tip of tail of larvae has a wavy outline, no dorsal spine

78
Q

What is the I.H. of protostrongylus rufescens?

How can you diagnose it?

What drugs are effective against it?

using just management techniques, how can you reduce infection rates of this worm?

A

snail/slug

Baermann exam

levimasole, albendazole, fenbendazole, macrolides

control pastures with snails/slugs

79
Q

What parasite causes nasal myiasis?

what is its definitive hosts?

A

Oestrus ovis

sheep, goats, humans (not a natural D.H.) so this is zoonotic

80
Q

What drugs can you use for Oestrus ovis?

A

Ivermectin 100% efficacy, moxidectin

81
Q

What is the natural definitive host for Elaephora schneideri?

Which animals is most pathology associated with?

Treatment options?

A

white tailed deer, mules, sheep, elk, goats

sheep, elk, goats

Ivermectin

82
Q

Describe the life cycle for Elaephora schneideri

A

Females deposit microfilaria into circulation –> microfilaria migrate to capillaries of face & forehead –> ingested by arthropod I.H. (flies) –> larvae develop into L3 in I.H. –> L3 deposited on skin of D.H. while I.H. feeds –> L3 move into wound left by I.H. on skin –> migrate to carotid, iliac, and mesenteric arteries to develop to adults

83
Q

What is the difference between microfilaria of Heartworms, Acanthocheilonema, and Elaephora?

A

Elaephora & Acanthocheilonema are shorter than Dirofilaria in length

Elaephora microfilaria are not found in peripheral circulation! Have tissue trophism for capillaries in face

84
Q

What parasite is known as the meningeal worm, brainworm, and deer worm?

What is the normal D.H.?

A

Parelaphostrongylus tenuis

White-tailed deer

85
Q

Describe the life cycle for Parelaphostrongylus tenuis

A

adults in venous sinuses of cranium lay eggs –> eggs pass into venous circulation –> develop to L1 –> larvae deposited in lung parenchyma –> L1’s are couhed up and swallowed to be shed in feces –> Snails ingest L1 (I.H.) –> L1 develops to L3 –> infected snail ingested while deer grazing on grass –> L3 penetrate abomasum –> migrates along spinal nerves to spinal cord –> adult worms migrate to meninges and venous sinuses to lay eggs

86
Q

What happens when L3 of Parelaphostrongylus tenuis is ingested by an aberrant host?

T/F: eggs are not shed in aberrant hosts

T:F clinical signs are seen in white-tailed deer

A

L3’s migrate to spinal cord and wander aimlessly, causing neural damage and inflammatory responses, damaging spinal cord, causing severe patholog

True

False

87
Q

What treatment option(s) are available for Parelaphostrongylus tenuis?

What life stage seems to be most susceptible?

What serious disease must be considered as a rule out?

A

Fenbendazole

migrating larvae

Rabies

88
Q

What parasite is responsible for Cysticercosis aka Visceral Cysticercosis?

What is the definitive host & where does the adult reside?

What is the metacestode stage, what I.H. (animals) does it reside in, and where?

A

Taenia hydatigena

Canines, small intestines

Cysticercus, SHEEP, goat, ox, moose, deer, pig, dog, cat, rodents, monkey, PEOPLE, peritoneal cavity

89
Q

Describe the life cycle of Taenia hydatigena

What is the PPP?

A

Ruminants ingest taenia type egg –> hexactnh embryo migrates through liver & encysts on peritoneum as cysticercus –> cysticercus in I.H. ingested by canids either from predation or viscera after slaughter (feeding scraps) –> adults mature in small intestine

PPP=2-3 mo.

90
Q

What treatments are available for taenia hydatigena ? which life stage is it for? which life stage do we not treat?

A

Praziquantel, adults, metacestode

91
Q

What parasites are responsible for Muscle Cysticercosis aka Beef Measles? (Clue: 2 of them)

A

Taenia saginata & Taenia ovis

92
Q

When comparing T. saginata to T. ovis, what are the differences/similarities in the D.H., I.H., metacestode stage & location, mode of infection, clinical signs?

A

T. saginata
D.H. = humans, I.H. = cattle/people, metacestode = cysticercus in cardiac and skeletal muscle, MoI = ingestion of cysticerci in muscle tissue of I.H., minimal to no clinical signs

T. ovis
D.H. = dogs, I.H. = sheep, metacestode = cysticercus in cardiac & skeletal muscles of sheep, MoI = ingestion of cysticerci in muscle tissue of I.H., minimal to no clinical signs

93
Q

Morphologically, how can you tell T. saginata from T. ovis?

A

T. saginata: large (4-8m long), cysticerci are small cysts 1.5 to 5 mm long in beef

T. ovis: cysticerci are ~6-8 mm long

94
Q

What parasites are responsible for Hydatidosis?

A

Echinococcus granulosus & Echinococcus multilocularis

95
Q

What is the I.H, metacestode stage, and D.H. for E. granulosus

A

sheep, swine, cattle, people, moose, etc.

hydatid cyst

canids

96
Q

What is the I.H, metacestode stage, and D.H. for E. multilocularis?

A

voles, lemmings, cattle, horses, swine, humans

alveolar hydatid

Dogs, foxes, cats

97
Q

Where are the hydatid cysts of E. granulosus found?

Where are the alveolar hydatids of E. multilocularis found?

Which one is more “malignant” and invasive?

A

E. granulosus: liver, lungs, pancreas

E. multilocularis: liver, lungs, pancreas

E. multilocularis

98
Q

Diagnostic stage of Echinococcus spp in the D.H., I.H.?

A

typical taeniid eggs in feces

metacestode stage in I.H. (E. granulosus = hydatid cyst, E. multilocularis = alveolar hydatid)

99
Q

What parasite is also known as Gid, Sturdy, Staggers?

D.H.?

I.H. (2)? Metacestode stage & location?

A

Taenia multiceps

canids

Sheep: coenurus, cranial cavity
Rodents: coenurus, brain, muscle tissue

100
Q

What is causing the clinical signs seen in animals infected with Taenia multiceps?

Is this parasite zoonotic?

A

Coenurus development in brain of infected animal, causing pressure on the brain.

Yes

101
Q

What parasite is responsible for Setariasis?

Where can it be found in the D.H.?

What is the I.H.?

What is special about its immature life stage?

PPP?

A

Setaria spp.

peritoneal cavity, pleural cavity, anterior chamber of the eye

Mosquito

Microfilaria (generally not found in circulation), similar in size to Dirofilaria (a little smaller)

8-10 mo.

102
Q

When would we see pathology of Setaria spp.?

A

when adults damage the eye or migrate into nervous tissues

103
Q

What protozoan parasite of cattle is transmitted venereally, reportable, and has a morphology identical to a parasite found in cats?

A

Tritrichomonas foetus

104
Q

Where does T. foetus reside in bulls? Cows?

A

Bulls: smegma of epithelial lining of penis, prepuce, distal urethra

Cows: vagina, uterus

105
Q

What is the main difference between Tritrichomonas foetus infections in bulls vs. cows?

A

Bulls, once infected, remain permanently infected

Cows can clear infection on own within 3 months after breeding (acquiring infection), but immunity is not long-lasting and they can become re-infected

106
Q

What are the important clinical signs of T. foetus in cows? What day of gestation does peak fetal loss occur?

Clinical signs in bulls?

A

Infertility is the most common sign, early abortion, poor connception rates

apparent infertility: early fetal resorption @ 1-16 weeks or early abortion @ 5-7 mo.

vulvovaginitis, cervicitis, pyometra

Peak fetal loss at day 50-70 of gestation

Usually no signs in bulls

107
Q

Tritrichomonas foetus infections usually result in late/early term abortions?

A

early

108
Q

True/False: if you, Dr. Random Vet, suspect Tritrichomonas foetus infection in a cow and send off a sample of semen to be tested at K-State, and the PCR test comes back negative, then that cow can be used for breeding.

A

False, samples can only be collected, handled, and shipped by a state CERTIFIED (special certification for Trich) veterinarian

109
Q

What happens to bulls (any Tx or other procedures) that have a confirmed diagnosis of Tritrichomonas foetus? Cows?

A

Bulls have no treatment, poor prognosis, will have a permanent, chronic infection, must be sent to slaughter or sold for slaughter

Cows have no Tx, good prognosis, will develop a short period of immunity, but can become reinfected

110
Q

What is the best way to control/prevent Tritrichomonas infection?

A

exclude infected animals from the herd, limit potential for neighbour’s herd to mate with your herd, purchase only virgin bulls, use artificial insemination, test any leased bulls, test female cows & heifers 60 days after breeding and cull open females, import semen only from sources that are confirmed to be trich negative

111
Q

What parasite is responsible for Eosinophilic myositis?

What is the I.H?

D.H.?

A

Sarcocystis cruzi

I.H. = cattle, bison

D.H. = canids, raccoons, jackals

112
Q

Sarcocystis cruzi undergoes _____ stages in the carnivore and ______ stages in the herbivore

A

sexual

asexual

113
Q

Describe the main points about the life cycle of Sarcocystis cruzi in carnivores vs. herbivores

A

Carnivores: sexual stages, infected via ingestion of meat containing sarcocysts, pass sporulated sporocysts in feces,

Herbivore: asexual stages, undergoes 2 schizogonic cycles in vascular endothelium with one additional schizogonic cycle in monocytes which releases merozoites that penetrate striated muscles/nerve cells/other tissues to form sarcocysts

114
Q

Regarding Sarcocystis cruzi, is more pathology associated in the I.H. (cattle/herbivore) or D.H. (canid/carnivore)

A

cattle/herbivore

edema, hemorrhage, serous atrophy of fat, placentitis, late term abortion, generalized lymphadenopathy

carnivores appear clinically normal

115
Q

Clinical signs of cattle infection of Sarcocystis cruzi?

A

Fever, muscle tremors, anorexia, lymphadenopathy, emaciation

sporogony process in endothelial cells in capillaries (obstruction) leads to loss of hair from tail, switch, neck, and back

late term abortion!

116
Q

What treatments are available for Sarcocystis cruzi infection?

Control methods?

Zoonotic?

A

no tx available

keep dogs out of areas where cattle graze, do not feed dogs raw beef

No

117
Q

What is the definitive host for Toxoplasma gondii? Paratenic hosts?

A

D.H. = cats

P.H. = ruminants and other warm blooded animals

118
Q

What kind of significant pathology does T. gondii cause in sheep and goats?

A

abortion, placentitis, multifocal encephalitis in fetus

abortion storm in 3rd trimester

lambs born dead or very weak

119
Q

What treatments for ruminants are available for T. gondii? FDA approved?

A

Monensin & lasalocid during late gestation, decoquinate fed daily

120
Q

What life stage of T. gondii do humans commonly get infected with? Sources?

A

Bradyzoites in undercooked pork or mutton, unpasteurized goat milk

121
Q

Which protozoan parasite of dogs historically has been misdiagnosed as T. gondii and is considered likely to be the #1 cause of abortion in dairy cattle?

A

Neospora caninum

122
Q

Where are tachyzoites of Neospora caninum found?

Bradyzoites?

A

macrophages, PMN’s, neural cells, spinal fluid, myocytes

brain and spinal cord

123
Q

D.H. of Neospora caninum?

I.H.?

mode of infection for each?

A

D.H. = dogs (canids), ingestion of infected tissues (bradyzoites

I.H. = cattle, ingestion of contaminated feed/water

124
Q

What are the 3 different ways cattle can get infected with Neospora caninum?

A

1) Horizontal: ingestion of contaminated feed/water
2) Transplacental: Pregnant cow can transplacentally infect developing fetus if exposed to sporulated oocysts
3) Transgenerational: Heifer calves that were infected in-utero can pass infections to offspring, which can happen in multiple pregnancies of same cow

125
Q

Clinical signs of Neospora caninum in dogs? Cattle?

T/F: Calves infected in-utero will have more significant pathology than cows infected from ingesting contaminated feed

A

Dogs: neurological signs

Cattle: mid-late term abortion, stillbirth of calves

F: calves are often subclinical & will not display any clinical signs

126
Q

What are the 4 outcomes associated with Neospora caninum infections of pregnant cows?

Which is the most common outcome? Which is the most common abnormal outcome?

A

4 is the most common, #2 is the most common abnormal outcome

1) early embryonic death (resorption, stillborn, present as infertile)
2) Abortions & stillbirth (usually at 5-7 months, mid-gestation abortion)
3) birth of feeble abnormal calf
4) birth of normal calf w/o clinical signs

127
Q

What are the best fetal tissues to send in for testing for Neospora caninum?

What Diagnostic tools are available?

A

Brain, heart, liver, placenta

IFAT, ELISA, PCR

128
Q

Why can you not definitively say that Neospora caninum caused a fetus to abort, even if the cow was seropositive?

A

Majority of live calves (congenital infections) born from seropositive cows are clinically normal, meaning that an infected cow will not always abort.

129
Q

What is the common name for the parasites belonging to the genus Gasterophilus (these are very annoying to horses)

What life stage is the parasitic stage?

How long does it take to complete the life cycle?

A

Bots

Larval

1 year

130
Q

Which bot fly parasite prefers to lay its eggs on the forelegs, belly, and flanks?

Which one prefers to lay eggs under the chin?

Describe what causes the eggs to hatch for each parasite?

A

Gasterophilus intestinalis, horse licking eggs

Gasterophilus nasalis, eggs hatch spontaneously in 4-5 days & 1st instars burrow into gums between molars

131
Q

What stage instar is the fly larvae when we are concerned with “bots”?

How can you tell the difference between 3rd instars of G. intestinalis and G. nasalis

A

3rd instar

Gasterophilus intestinalis: has 2 rows of spines on each segment, 1st row is larger than 2nd

Gasterophilus nasalis: has 1 row of spines on each segment

132
Q

Which instar larvae is responsible for gingivial myiasis? Describe the pathology associated briefly

Which instar larva is responsible for gastric myiasis? Describe the pathology associated briefly

A

Gingival: 1st & 2nd, ulceration of gums, secondary bacterial infections

Gastric: 3rd instars, mild inflammation, usually minimal pathology but severe infections can result in hemorrhage, ulcers, intestinal blockage @ pylorus

133
Q

What drug class is effective for bot flies when applied in fall or early winter?

A

macrocyclic lactones

134
Q

What parasites (2 genera) are responsible for Summer Sores, aka Habronemiasis?

Both genera of parasites are what type of worms? (we talked about these for the 1st exam)

A

Habronema muscae & Draschia megastoma

Spiruids (arthropod I.H., robust adult worms, larvated eggs)

135
Q

Where do adults of Habronema & Draschia reside in the definitive host?

How can you tell adults apart?

A

Stomach

Habronema: pharynx region has a distinct “H” shape

Draschia: occurs in nodules, head is constricted off body, no “H” structure of pharynx

136
Q

Describe the life cycle of Habronema & Draschia (only need to give 1 description, they are similar)

What is the intermediate host?

A

Larvated eggs shed in feces, larvae hatch and are ingested by fly maggots, larvae reach infective stage about same time fly maggot pupates, when adult fly emerges, the spiruid larvae migrates to proboscis, L3 transmitted to horses when flies feed on ocular secretions or other orifices and deposit infective spiruid larvae

House fly & Stable fly

137
Q

Why does cutaneous habronemiasis cause more significant pathology than the gastric form? Which form is referred to as “summer sores”?

A

Larvae deposited cutaneously are not at their natural destinations in the host, cause eosinophilic, granulomatous, pruritic lesions with serosanguinous drainage

Cutaneous form

138
Q

What drug is FDA approved for treatment of summer sores caused by Habronema & Draschia, but has variable efficacy?

A

Systemic macrolides: oral ivermectin

139
Q

What parasite of equine species is referred to as the “Threadworm”? What is the disease caused by this worm called?

A

Strongyloides westeri

Strongyloidiasis

140
Q

What happens eventually to animals infected by threadworms?

A

Will clear infection on own relatively soon

Foals usually clear infections on own by 6mo of age

141
Q

Describe the life cycle of Strongyloides westeri

A

L3 penetrate skin, undergo tracheal migration

Foals: S. westerii will ultimately end up in small intestines

Pregnant mares: larval stages in tissues can be activated by parturition to migrate to mammary tissue, transmammary transmission and larvae will undergo mucosal migration in the foal

142
Q

Strongyloides westeri: What is the range in time (days) that larvae can appear in mare’s milk postpartum?

PPP?

A

4-47 days postpartum

PPP = 8-14 days

143
Q

What drugs are available for treating Strongyloides westeri in horses?

Which one is effective for killing infective larvae in mammary tissue of the mare?

How can you prevent trasmammary transmission?

Which drug is not approved for horses under 6 months of age?

A

Ivermectin, fenbendazole, oxibendazole

Ivermectin

Routine ivermectin within 24 hours after foaling

Moxidectin

144
Q

Which parasite of horses produces an egg with similar morphology to the roundworms found in raccoons? (this is the largest parasite in horses)

A

Parascaris sp.

145
Q

Describe the life cycle of Parascaris sp.

PPP?

A

eggs shed in feces –> eggs larvate (infective stage) –> ingestion of infective larvated eggs –> eggs hatch, larvae undergo tracheal migration

3 months

146
Q

T/F: In parascaris infections, there is transplacental transmission but no transmammary transmission

How can foals become infected w/Parascaris sp. when suckling on a mare?

A

False, there is neither

Eggs are sticky, eggs in environment can become attached to various parts of body (including udders!) when mare lays down, which are then ingested when the foal suckles

147
Q

Clinical signs of Parascaris sp. infections?

A

respiratory signs apparent in 3rd-4th week of infection, pyrexia, nasal discharge, dry rales, pneumonia, these are due to larval migration through lungs

Colic due to bowel obstruction

Rarely, small intestinal impaction (FATAL)

148
Q

What is the main concern of clearing Parascaris sp. infections from horses?

Due to this concern, which drug class has been identified as the drug of choice?

If you decide to treat using pyrantel, what should be done first?

A

Slowly kill worms in heavy infections to avoid impactions of dead and dying worms

Benzimidazoles as these have not been shown to have a paralytic mode of action to cause acute intestinal impaction

FECRT

149
Q

Describe the basic plan for deworming programs (in consideration of Parascaris sp.) in foals (include drugs used and when)

A

Use Benzimidazoles (efficacy against ascarids): Fenbendazole, oxibendazole

Deworm at weeks 12, 24 (just before weaning). Deworm again at weeks 26 & 56 with treatments primarily aimed against strongyles

150
Q

Which parasite belonging to strongyloidea, has an oval buccal capsule with 2 ear shaped teeth at its base? The L3 form has 32 intestinal cells arranged in a double row.

A

Strongylus vulgaris

151
Q

In regards to large strongyles, what is the infective stage? What is the time of development of larvae dependent on?

A

Infective L3 on grass, temperaure and humidity

152
Q

What is unique about the larval development of Strongylus vulgaris?

Which larval stage penetrates arterioles and migrates to the cranial mesenteric artery?

Where do larvae migrate to molt to adults?

PPP?

A

Development takes place in arterial system

L4

Cecum & colon

6-7 months

153
Q

Where do larvae of Strongylus edantatus migrate to before heading to the cecum and colon to molt to adults (list 2 different locations, in sequential order)?

A

Liver, parietal peritoneum (form hemorrhagic nodules in peritoneum)

154
Q

What is different about the migratory pattern of Strongylus equinus compared to the other large strongyles?

A

L3’s go to cecum and colon first, then liver, then back to cecum and colon

155
Q

Of the large strongyles, which causes the most mortality and why?

A

Strongylus vulgaris b/c: larva penetrate arterial walls of small intestine and migrate through cranial mesenteric arteries, causing thromboembolic colic, can be fatal

156
Q

What diagnostic technique can be used for Strongylus vulgaris/edantatus/equinus?

How many intestinal cells are found in each species?

A

Baermann exam,

vulgaris: 32
edantatus: 18-20
equinus: 16

157
Q

What drugs are effective against large strongyles (which ones are effective against larvae & adults vs just adults)?

A

larvae & adults: macrocyclic lactones: ivermectin & moxidectin

Adults: benzimidazole & pyrantel

158
Q

Which parasite group makes up the “smal strongyles” of equine species?

A

Cyathostomins

159
Q

Describe the life cycle of Cyathostomins

PPP?

A

Eggs shed on pasture –> L1 hatch from egg and molt all the way to L3 –> L3 on grass are INFECTIVE –> L4 or undergo hypobiosis –> adults in large intestine & cecum

6 weeks - 3 months

160
Q

Which life stage of Cyathostomins causes the most pathology? L3, L4, Adult?

A

L4: these are much larger than the small L3 that originally encysted. Molting process causes release of antigens that elicit severe inflammatory response of cecum an colon, can result in colic

adults (at least in mild worm burdens) cause innocuous infections w/mild clinical signs, L3 insignificant

161
Q

When does larval cyathostomiasis occur?

A

synchronous emergence of L4 from intestinal mucosa and submucosa

162
Q

When do/can you treat a horse for Cyathostomiasis?

What drugs are efficacious for each life stage?

How can you help reduce infections in your horses?

A

Only if horse is showing clinical signs and if a quantitative egg count has been done and EPG >200

Adults: Benzimidazole, pyrantel, macrocyclic lactones,

encysted larvae: moxidectin

inhibited larvae: fenbendazole for 5 days

Remove poo from paddocks/pasture

163
Q

What genus & species do the 2 tapeworms of horses belong to? How can they be differentiated morphologically from other tapeworms and each other?

A

Anoplocephala perfoliata & Anoplocephala magna

Bodies are not made of proglottid segments

A. perfoliata has a scolex with suckers and lappets, shorter in length

A. magna has a scolex with suckers and no lappets, longer in length

164
Q

Describe the Life Cycle for Anoplocephala spp.

A

Oribatid mites serve as I.H., cysticercoid develops inside the mite –> horse ingests infected mite while grazing –> adult develops in small intestine or at ileocecal junction

165
Q

Which parasite of horses has a very large female adult worm with a pointed tail that passes an operculated, thin & narrow egg that is flattened on one side?

A

Oxyuris equi

166
Q

Describe the life cycle of Oxyuris equi

Zoonotic?

A

larvated eggs laid –> ingested w/food or water or when eggs are licked off inanimate objects –> hatched larvae migrate to cecum & ventral colon –> adult females migrate out of rectum and lay eggs perianally –> eggs become infective in 3-5 days

Not zoonotic

167
Q

Typical clinical signs of Oxyuris equi?

A

rubbing irritated areas near perineum, dull hair coat, broken hairs from rubbing on tail, loss of condition, restlessness,

168
Q

What happens to foals infected with pinworms usually?

What drugs are efficacious?

A

develop natural immunity by 18 months, unusualto see pinworm infections after that

ivermectin, moxidectin, benzimidazoles, pyrantel

169
Q

Which parasite is known as the equine lungworm?

Which animal does it cause more pathogenesis in, horses or donkeys? Why?

Why is it difficult to find eggs from these worms in feces?

A

Dictyocaulus arnfieldi

horses b/c they are not the natural definitive host, donkeys are natural D.H. and these worms will cause them little pathology

The eggs hatch very quickly once shed in feces

170
Q

How can you diagnose Dictyocaulus arnfieldi?

Describe the life cycle

A

Baermann exam, larvae in feces, tracheal wash, endoscopy exam (sometimes)

Eggs are coughed up and swallowed –> eggs passed in feces containing L1 –> L1-L3 in environment –> infective L3 on grass ingested –> larvae migrate to lungs via lymphatics & blood stream (larvae generally do not reach maturity in horses)

171
Q

What causes clinical signs in a horse infected with Dictyocaulus arnfieldi?

A

larvae & inflammatory reactions in small bronchi resulting in a chronic productive cough & nasal discharge and increased respiratory rate

172
Q

What parasite causes equine piroplasmosis and is considered to be a reportable foreign animal disease in the U.S. (actually 2 different organisms)

A

Babesia caballi & Theileria equi (Babesia equi)

173
Q

What is the definitive host for Babesia caballi & Theileria equi?

What kind of transmission do these parasites undergo in the D.H.?

A

Ticks!

Transovarian and transstadial

174
Q

Are acute infections or chronic infections of Equine Piroplasmosis more severe?

What happens to animals that manage to survive infection?

A

Acute form due to intravascular hemolysis & thrombocytopenia

Survivors become subclinical carriers that are reservoirs for transmission

175
Q

What happens to horses that test positive for Equine Piroplasmosis in the U.S.?

A

Quarantine and then:

1) enrolled in approved treatment program to eliminate infection and transmission risk
2) maintained under life-long quarantine
3) euthanized

176
Q

What treatment options are available for horses infected with Babesia caballi and/or Theileria equi?

Efficacy of Tx?

Why should treatment be done under supervision under regulatory personnel?

A

Imidocarb dipropionate

Often effective in resolving clinical signs but not always effective at eliminating parasites, thus horse can be a carrier/chronic infection

Adverse effects to Tx include colic, injection site reactions, diarrhea, liver & renal disease, and even death

177
Q

T/F: All imported horses to the U.S. must be negative to Equine Piroplasmosis unless it is accompanied by a state veterinarian and quarantined first.

A

False, all imported horses must be test negative before entry!

178
Q

What does EPM stand for?

What parasite is responsible for this disease?

A

Equine Protozoal Myeloencephalitis

Sarcocystis neurona

179
Q

What protozoal parasites that we have covered so far can cause encephalomyelitis in animals?

A

Sarcocystis neurona, Neospora caninum, Toxoplasma gondii

180
Q

What is the I.H. of Sarcocystis neurona? D.H.?

What is shed in the feces of infected definitive hosts?

What life stages are found in the I.H. and where?

A

I.H. = horses, D.H. = Opossum

sporocysts

Merozoites in CNS, sarcocysts (walled off bradyzoites) in muscle tissues

181
Q

Describe the life cycle of Sarcocystis neurona

A

Opossum (D.H.) ingests sarcocysts in infected muscle tissue –> bradyzoites form tachyzoites and invade intestinal epithelium –> gametogony occurs in small intestine of opossum –> oocysts produced & sporocysts released from intestinal epithelial cells –> Sporocysts shed in feces –> horse (I.H.) ingests sporocysts while grazing –> sporozoites excyst and invade vascular endothelial cell –> Schizogony occurs –> Tachyzoites are released and form bradyzoites –> either bradyzoites form in muscle tissue or tachyzoites/merozoites replicate inside neural cells and destroy them

182
Q

T/F: Horses infected with sarcocystis neurona can not transmit the disease to other horses

A

True

183
Q

What are typical signs of Equine Protozoal Myeloencephalitis?

A

Progressive asymmetric ataxia, rapid muscle atrophy at discrete location (gluteal area), vague hind leg lamenes, dysphagia, asymmetric gait abnormalities, death

184
Q

Why would a horse that is seropositive for EPM with consistent clinical signs, not necessarily have Sarcocystis neurona as the causative agent of the clinical signs?

What is another differential that always needs to be kept in mind?

A

Majority of seropositive horses do not show the typical clinical signs, thus, there could be a different reason this horse is displaying the CNS signs

RABIES

185
Q

What diagnostic tools are the most accurate for diagnosing current or recent exposure to Sarcocystis neurona?

A

Patient history & neurological exam with serological confirmatory diagnosis!

ELISA/IFA of serum and CSF: test for antibodies against whole S. neurona or merozoite surface antigens (snSAGs)

186
Q

What are our treatment options for treating horses with Equine Protozoal Myeloencephalitis caused by Sarcocystis neurona?

Why does this drug work?

Are acute or chronic cases more successfully treated?

A

Marquis Antiprotozoal Oral paste

It is able to cross the blood-brain-barrier

Acute

187
Q

What is a simple herd management strategy that can be used to help prevent your horses from being infected by Sarcocystis neurona?

Is Equine Protozoal Myeloencephalitis zoonotic?

A

Keep horse feed in a secure area where opossums can not reach (& defecate) in.

Not zoonotic

Parasitology (4 decks)

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