Exam 2 Flashcards

1
Q

Life Cycle of Nematodes

A
o	Eggs in dog/cat poo ->
o	Hatch in environement ->
o	L1 -> molt ->
o	L2 -> molt ->
o	L3 is infectious
o	Some nematodes lay live larvae
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2
Q

Diagnosis of Nematodes

A

o Fecal smear
o Fecal float
o Baermann
o Fecal Sedimentation

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3
Q

Basics of Ascarids & Species in Dogs, Cats & Raccoons

A
o	Common
o	Large w/ 3 lips
o	Adults live in small intestine
o	Some zoonotic
o	Eggs survive in envir for months

Dogs
• Toxocara canis
• Toxocaris leonina

Cats
• Toxacara cati
• Toxocaris leonina

Raccoons
• Baylisacaris procyonis

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4
Q

Toxocara canis Life Cycle

A

• Adult worms in intestine mate and produce eggs ->
• pooped into the environment ->
• Larva develops within the egg 4wks to the infectious L3 ->
• Dog ingests larvated egg ->
• Larvae hatches in intestine and enters blood stream ->
• Somatic migration
OR
• Tracheal migration

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5
Q

Somatic Vs Tracheal Migration & Ages

A

Somatic Migration
• Infective larvae accumulate in tissue
• In dogs older than 3-4 mo
• Becomes a parentenic host

Tracheal Migration
•	In dogs less than 3-4 mo
•	Larva enters alveolus ->
•	Coughed up & swallowed ->
•	Mature is intestine & produces eggs that are pooped out
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6
Q

Toxocara canis Transmission

A

Ingest a larvated egg from the environment

Eat an infected paratenic host

Transplacental transmission
o Arrested L3 in the tissues of the dam reactivated and migrate to the placenta during pregnancy > infects pups in utero
o Cause damage & inflammation to lungs

Transmammary transmission
o Arrested L3 in tissues of dam are reactivated and migrate to the mammary gland > ingested by pups in milk
o Go directly to small intestine

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7
Q

Toxocara canis Effects on Host

A

Small numbers
o mild mucoid enteritis,
o mild diarrhea,
o often asymptomatic

Large numbers
o obstruction or rupture of intestine,
o blockage of bile or pancreatic ducts

Adult worms
o Abdominal distension and discomfort,
o diarrhea or constipation,
o vomiting

Migration through lungs
o Respiratory signs

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8
Q

Toxocara cati Life Cycle & Transmission

A

Life Cycle
• Same as canis
• Very few do somatic migration

Transmission
• Ingest larvated egg from environment 

• Eat infected paratenic host (most)
• Transmammary transmission is possible but ONLY if the queen is infected during lactation

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9
Q

Toxascaris leonine Life Cycle & Transmission

A

Life Cycle
• Adult worms in intestine mate and produce eggs which are pooped into the environment ->
• Larva develops w/in egg to the infectious stage in 1wk
 ->
• Cat or dog ingests larvated egg ->
• Larvae hatches out in intestine and molts L4 > L5, adult Does not migrate in dogs and cats

Transmission
• No transmammary or transplacental

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10
Q

Baylisacaris procyonis

A
  • Same lifecycle as toxocara canis
  • Can undergo somatic migration in any mammal
  • Causes visceral & ocular larval migrans in humans
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11
Q

Visceral & Ocular Larval Migrans Due to Ascarids

A

Visceral Larval Migrans
• Children under 5yo
• Damage due to immune system against migrating larvae
• Asymptomatic or sever symptoms

Ocular Larval Migrans
• Eosinophilic granuloma surrounding larva in retina
• Can be mistaken for retinoblastoma

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12
Q

Treating Dogs/Puppies for Ascarids

A

Pyrantel pamoate
• Treat every 2 wks from 2wks old to 3mo

Piperazine
• Labeled for 6wk old pups

Fenbendazole

• Labeled for 6wk old pups
• Treat dams daily from day 42 of gestation to 14d post whelping

Macrocyclic lactones

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13
Q

Treating Cats/Kits for Ascarids

A
  • Don’t treat pregnant queens

* Lactating queens & kittens at 2, 4, 6, 8 wks w/ pyrantel pamoate

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14
Q

Basics of Hookworms & Species

A
  • Small, thin (~1 cm long) worms
  • Adults live in the small intestine
  • Blood suckers

Ancylostoma
o A. caninum - dogs in southern US

o A. brasiliense - dogs and cats in southern US
o A. tubaeforme - rare in US cat

Uncinaria stenocephala
o dogs in the N US

ID IN NOTES

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15
Q

Hookworm Life Cycle in Dogs Vs Cats

A

Dogs
o Adults mate and produce eggs ->
o eggs released into the environment ->
o L1 hatches out of the egg develops to L3 ->
o Dog eats L3 or paretenic host OR L3 penetrates skin ->
o Somatic or Tracheal migration route ->
o become encysted in tissues 
or intestinal mucosa ->
o Some molt to L4, then L5 and then to adult to produce eggs 

o No transplacental transmission

Cats
o Most L3 goes on tracheal route through lungs to intestine ->
o Molt to L4, then L5 and then to adult to produce eggs 

o No larval bank in cats

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16
Q

Hookworm Transmission

A

o Ingestion of L3 

o Penetration of skin by L3 

o Ingestion of paratenic hosts 

o Transmammary transmission occurs in dogs, and only occurs during acute infection in cats

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17
Q

Hookworm Damage to Host

A

o Inject anticoagulants into mucosa & suck blood
o Ulcers where worm feeds

Severe cases
• Caused by many Ancylostoma canium
• intestinal hemorrhage
• anemia

Asymptomatic Infection
• Caused by Unicinaria (inefficient bloodsucker)

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18
Q

Peracute Syndrome due to Hookworms

A

o transmammary transmission to neonatal pups
o Appear healthy in week 1
o deteriorate rapidly by week 2
o Anemia and bloody diarrhea

o Disease precedes egg production
o diagnosis is presumptive
o Treat immediately if suspected (prognosis is poor)

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19
Q

Acute Syndrome due to Hookworms

A

o sudden exposure to large number of environmental L3
o Anemia
& Diarrhea with blood

o Clinical disease precedes egg shedding by about a week
o Prognosis is good with prompt treatment

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20
Q

Chronic Compensated Syndrome due to Hookworms

A

o adult dogs with no clinical signs

o Eggs present in feces on routine fecal exams
o May have slightly low RBC or hemoglobin

o Treatment (cure) is challenging
o encysted larva in the larval bank are not affected by routine anthelmintic therapies

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21
Q

Chronic Decompensated Syndrome due to Hookworms

A

o adult and older dogs with comorbidities
o Profound anemia in emaciated animal
o Eggs detectable on fecal float
o Prognosis can be good if other factors are addressed
o Treatment requires protein administration + anthelmintics

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22
Q

Hookworm Diagnosis & Treatment of pups & adults

A

Diagnosis
o Clinical signs – anemia +/- bloody Ds
o Fecal float w/ visible strongyle eggs

Treatment
o Puppies – 2, 4, 6, 8 Pyrantel Pamoate
o Prevent transmammary transmission w/ Fenbendazole or high dose ivermectin
o Use Fecal Egg Count Reduction Test to differentiate between “larval leak” and anthelmintic resistance

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23
Q

Fecal Egg Count Reduction Test (FECRT)

A

o For Hookworm
o Perform fecal egg count using a quantitative fecal float before treatment and 2 weeks after treatment 

o Calculate the % difference 

o Number of eggs per gram should decrease by at least 95% two weeks after deworming 

o If the number of eggs per gram does not decrease by at least 75%, resistance is likely 


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24
Q

Hookworm Control/Prevention

A
o	Very hard to kill
o	Can freeze Ancylostoma eggs
o	Dispose of poo
o	Deworm regularly
o	Fecal floats
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25
Q

Cutaneous Larval Migrans Due to Hookworm

A

o In humans
o linear tortuous erythematous, intensely pruritic eruption caused by larva that have penetrated skin
o SE & Gulf Coats of US
o People in contact w/ soil

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26
Q

Basics of Heartworm & Geography

A
  • Dirofilaria immitis
  • Long, thin white worm
  • Adults live in the pulmonary artery
  • Dogs, Cats, Ferrets
  • Biologically vectored by mosquitoes
  • Filarid nematode produces live microfilariae not eggs

Geographic Distribution
o Mostly SE
o Reportable Dz in WA

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27
Q

Life Cycle of Dirofilaria

A

o Adults in pulmonary artery mate and produce microfilaria ->
o Microfilaria in blood are picked up by mosquito when it feeds on dog
->
o Microfilaria develop in mosquito to L3 ->
o Mosquito bites dog and deposits L3 on the skin, ->
o Moves into bite wound ->
o Molts to L4 in the skin in the first few days after the bite 
->
o L4s migrate through tissues for ~2 months 
->
o L5s enter circulation and are carried to pulmonary arteries 
->
o Finish maturation to adult and mate in pulmonary arteries (takes about 4 months to mature) 
->
o Microfilaria appear in blood 6 months after infection of the dog

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28
Q

Pathology in Dogs due to Dirofilaria

A

o Severity depends on # of worms, immune status, infection duration, host activity level
o Trauma & damage from worm Ags & excretions of arteries & heart

Caval Syndrome
• Worms fill right atrium and ventricle -> tricuspid valve insufficiency + pulmonary hypertension
• Acute severe lethargy + hemoglobinemia and hemoglobinuria
• Fatal if not treated surgically within 1-2 days

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29
Q

Clinical Signs of Dirofilaria in Dogs

A
o	Signs start when microfilaria in blood
o	Exercise intolerance and lethargy

o	Syncope- fainting from lack of blood flow to brain 
o	Soft cough
o	Acute respiratory distress

o	Sudden unexpected death
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30
Q

Dirofilaria Diagnosis in Dogs

A

Blood Ag test (SNAP)
• Detects uterine protein so female worm must be present
• Dogs develop immune complex -> false (-)

Microscopic exam
• Direct blood smear -> worms wiggle
• Knott’s test -> mix blood w/ formalin -> centrifuge -> methylene blue + pellet

Radiograph or echo of heart

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31
Q

Differentiating between Dirofilaria & Acanthocheilonema on Micro Exam

A
Dirofilaria
•	Pathogenic
•	High numbers
•	Wiggly w/o actually moving
•	Longer
Acanthocheilonema
•	Non-pathogenic
•	Very few
•	Wiggle moves them
•	Shorter
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32
Q

Wolbachia

A

o Symbiotic bacteria that Dirofilaria carries
o Killing bacteria can incapacitate worm
o Must kill bacteria to prevent bacterial infection around dead worms

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33
Q

Treatment of Dirofilaria in Dogs

A

o Complex
o Strict exercise restriction
o Surgical removal for caval syndrome

Macrocyclic Lactones - moxidectin
• Kills microfilaira & L3 & young L4

Doxycycline
• Kills Wolbachia & prevents secondary inflammation

Melarsomine
• Kills adults & late stage L5

If stable upon diagnosis
• Doxycycline & moxidectin for 2 mo –>
• After 2mo start melarsomine

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34
Q

Prevention of Dirofilaria in Dogs

A

Test all dogs >7MO yearly

Macrocyclic lactones
• ivermectin,
• selamectin,
• moxidectin

Mosquito repellent
• Pyrethrins
• Neonicotinoids

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35
Q

Dirofilaria immitis in Cats Vs Dogs

A
Dogs
•	30-250 worms 
•	Microfilariae usually present 
•	Large numbers required to cause pathology 
•	Usually easily diagnosed 
Cats
•	1-3 worms

•	Microfilariae usually absent 
•	Often fatal

•	Difficult to diagnose
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36
Q

Heartworm Associated Respiratory Dz in Cats Basics & Treatment

A

o Pathology in lungs due to migration of worms
o Cough, dyspnea, wheezing
o Very little cardiac issue

Treatment
• Only treat if cat is clinically affected
• Glucocorticoids ONLY
• Reduces immune response -> reduces clinical issue

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37
Q

Diagnosis of Heartworm Associated Respiratory Dz in Cats

A

Ag test
• Must have at least one female worm to test (+)

Ab test
• Can detect female & male worms
• Only indicates exposure not infection

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38
Q

Ollulanus; basics & transmission

A
  • Cat stomach worm
  • Tiny! < 1 mm long
  • Usually feral cats and catteries

Transmission:
• Direct by ingestion of larvae or adults in vomitus (NO fecal transmission)
• Internal autoinfection - Entire life cycle can occur in the stomach -> number of worms keeps increasing!

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39
Q

Ollulanus; clinical signs, diagnosis, treatment

A

clinical signs
• Heavy burdens- chronic gastritis and vomiting
• Can result in emaciation and death if left untreated

Diagnosis

• Demonstrate tiny worms in fresh (nonrefrigerated) vomitus by Baermann
• Endoscopy

Treatment

• 5 day course of fenbendazole
• Tetramisole

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40
Q

Physaloptera; basics & life cycle

A
  • Stomach worm of dogs and cats
  • Stout white worms up to 6 cm long
  • Most common in the midwest

Life Cycle
• Larvated egg shed in feces 
->
• L3 develops in beetles/crickets (Required intermediate host)
->
• Intermediate host can be eaten by birds or rodents (paratenic host) 
->
• Paratenic or intermediate host eaten by cat/dog 


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41
Q

Physaloptera; clinical signs, diagnosis, treatment

A

clinical signs

• Chronic gastritis

• Chronic vomiting (even if only 1-3 worms)

Diagnosis

•	Fecal floats often don’t work

•	Direct smear better for finding eggs 
•	Adults in vomitus
•	Endoscopy 

Treatment

• Pyrantel pamoate
• Fenbendazole

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42
Q

Strongyloides; basics & life cycle

A
  • Threadworm in small intestine
  • Very small- 2 mm long

Life Cycle
• Adults live in small intestine
• Larvae in feces
• Can have entire cycle in environment

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43
Q

Strongyloides; transmission & clinical signs

A
Transmission
•	L3 penetrates skin
•	L3 ingestion 
•	Internal autoinfection 
•	Propagation of infectious L3 by environmental stages leads to highly contaminated environments 

Clinical Signs
• Usually asymptomatic
• puppies and kittens are highly susceptible
• Dermatitis due to L3 penetration

• Bronchopneumonia due to lung migrations

• Adults in intestine = watery diarrhea, dehydration
• immunosuppression -> hyperinfection -> emaciation and death

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44
Q

Strongyloides; diagnosis, treatment, control

A

Diagnosis

• Fecal float to look for larva in feces

• Baermann of fresh fecal samples for larvae

Treatment

• Ivermectin
• Fenbendazole

Control
• Dry environment
• Potentially zoonotic- can be transmitted from dogs to humans

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45
Q

Trichuris Whipworm; basics & life cycle

A
  • Whip-shaped worm in large intestine of dog and cat
  • Thin hairlike anterior end embeds in the large intestinal mucosa

Life Cycle
• Ingestion of larvated egg from environment ->
• Eggs shed in feces ->
• larvate in environment
->
• Takes about 1 month in environment to become infectious ->
• Eggs are extremely environmentally resistant for years ->
• Eggs hatch when eaten ->
• larvae develop to adults in intestine

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46
Q

Trichuris Whipworm; clinical signs, treatment, control

A

clinical signs
• Usually asymptomatic

• Large numbers can cause bloody diarrhea, weight loss, dehydration
• Older dogs tend to have higher burdens

Treatment

• Fenbendazole

• Macrocyclic lactones- milbemycin, moxidectin
• Larva are not susceptible to anthelmintics
• Must treat every month for 3 months

Control
• Difficult
• Eggs survive in environment for a long time
• separate dogs from eggs
• Monthly heartworm preventive labeled for Trichuris

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47
Q

Trichuris Whipworm; Diagnosis

A

Fecal float

o Beautiful eggs in fecal floats- the fecal jewel
o Floats well but egg output is often low

Antigen ELISA
o used If no eggs on float

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48
Q

Oslerus osleri; basics, life cycle

A
  • Dog lungworm
  • Found in nodules at the bifurcation of the trachea

Life Cycle
•	Female worm deposits egg in trachea ->
•	hatches immediately
-> 
•	L1 coughed up and swallowed
-> 
•	infectious L1 larvae are shed in feces
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49
Q

Oslerus osleri; transmission, clinical signs

A

Transmission
• Direct transmission by ingestion of feces
• Nursing pups when dam licks them and L1 transferred via sputum

Clinical signs
• Hard dry cough brought on by cold or exercise
• Nodules can eventually obstruct air passages

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50
Q

Oslerus osleri; diagnosis, treatment

A

Diagnosis

• Bronchoscopy- nodules are pathognomonic
• Tracheal wash

• Fecal floatation: look for larvae in feces

Treatment
•	Difficult
•	goal is to reduce nodule size and clinical signs
•	cure is not often achieved 
•	Fenbendazole 
•	Ivermectin
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51
Q

Aelurostrongylus; basics, life cycle

A
  • Cat lungworm

  • Relatively common

  • Found in lung parenchyma

Life Cycle
• L1 shed in feces (not infectious) 
->
• L3 develops in snail/slug
(Required intermediate host) ->

• Intermediate host eaten by birds/rodents/reptiles (paratenic host) 
->
• Paratenic or intermediate host eaten by cat

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52
Q

Aelurostrongylus; clinical signs

A

Asymptomatic


Moderate:
o coughing and anorexia


Severe:
o coughing, panting, shortness of breath, death

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53
Q

Aelurostrongylus; diagnosis & treatment

A

Diagnosis:
• Fecal float to find larvae in feces 

• Baermann to look for L1 larvae in feces 


Treatment

• Fenbendazole 

• Ivermectin, selamectin- 2 treatments one month apart

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54
Q

Eucoleus; species & basics of each

A
E. aerophila
•	bronchial capillarid 
•	primarily in foxes (also dogs, cats)

•	Clinically inapparent to mild respiratory signs 
•	Cough, nasal discharge

E. boehmi-
• nasal capillarid
• Chronic rhinitis


55
Q

Eucoleus; diagnosis & treatment

A

Diagnosis
• fecal float for eggs

Treatment
• ivermectin and fenbendazole

56
Q

Dioctophyma; basics

A
  • Giant kidney worm of dogs
  • The largest nematode in veterinary medicine
  • Lives in the kidney (usually R)
  • Normal definitive host is the mink
57
Q

Dioctophyma; Life Cycle, Diagnosis, Treatment

A

Life Cycle
• Eggs shed in urine
->
• Intermediate host- aquatic oligochete worms ->
• Paratenic hosts: usually freshwater fish 
->
• Transmission to definitive host usually via undercooked freshwater fish or water containing infected oligochetes

Diagnosis:
• Eggs found in urine sedimentation 


Treatment:
• Surgical removal

58
Q

Personema plica; basics, transmission, clinical signs, treatment

A
  • Adults in bladder mucosa 

  • Eggs are in urine and look similar (but much smaller) than Dioctophyma!

Transmission:
• eggs released in urine
• Earthworms are intermediate host 


Clinical signs:
• usually asymptomatic 


Treatment:
• fenbendazole, ivermectin, levamisole

59
Q

Morphology of Cestodes

A

Scolex (head)
o Embeds & attaches to host tissue

Neck

Proglottid (segments)
• Further form head are more mature

Gravid segments
• Proglottids that are filled w/ eggs

60
Q

Two Cestodes Groups

A

Cyclophyllidae
• Common
• Hooks & suckers or one of either

Pseudophyllidea
• Rare
• No hook or suckers

61
Q

Cyclophyllidean General Life Cycle

A

o Adult tapeworms are in carnivore 
small intestine 
->
o Individual eggs or whole proglottids are shed in feces 
->
o Eggs/proglottids eaten by the intermediate host 
->
o Intermediate stages develop -> 

o Intermediate host eaten by definitive host 
->
o Adults develop in the definitive host’s small intestine

62
Q

Cyclophyllidean Clinical Signs & Treatment

A

Clinical Signs
o Intermediate stage of the tapeworm is the pathogenic stage
o Adult tapeworms tend to cause mild intestinal lesions

Treatment
o Praziquantel
o Fenbendazole

63
Q

Dipylidium caninum basics & life cycle

A

o Type of Cyclophyllidean
o Most common tapeworm of dogs and cats in many parts of the US
o Adult is 10-70 cm long
o 2 genital pores
o Proglottids found around anus or in poo

Life Cycle
• Infected dog or cat sheds proglottids ->
• Eggs in proglottid eaten by fleas
->
• Cysticercoid develops in the flea ->
• Dog (or cat or human) eats flea
->
• Cysticercoid in the flea develops into an adult tapeworm in intestine

64
Q

Dipylidium caninum; intermediate stage, clinical signs

A

Intermediate Stage
• cysticercoid
• small enough to fit in an arthropod
• baby tapeworm with an inverted scolex

Clinical Signs
•	Generally asymptomatic
•	scooting behavior 
•	Diarrhea, weight loss
•	Rarely cause intestinal blockage
65
Q

Dipylidium caninum; diagnosis, treatment, prevention, zoonosis

A

Diagnosis
• Eggs aren’t shed so will not be detected on fecal float
• Segments can be squashed and eggs packets visualized

Treatment

• Praziquantel

Prevention

• Control the FLEA

Zoonosis
• Humans infected w/ adult tapeworm if accidental ingestion of flea

66
Q

Taenia pisiformis; basics & life cycle

A
o	Type of Cyclophyllidean
o	Common tapeworm of dogs 
o	Found worldwide
o	Up to 2 m long 
o	Only 1 genital pore

Life Cycle
• Infected dog sheds proglottids and/or 
eggs 
->
• Proglottid/egg is eaten by a rabbit 
->
• Cysticercus develops in rabbit liver 
->
• Dog eats rabbit 
->
• Cysticercus from the rabbit develops into an adult tapeworm in dog intestine 


67
Q

Taenia pisiformis; intermediate stage, clinical signs, diagnosis, treatment

A

Intermediate Stage
• Cysticercus
• fluid-filled balloon with an inverted scolex

Clinical Signs
• Asymptomatic
• scooting behavior

Diagnosis

• Fecal float- eggs may be shed
• Segments crawling around the anus

Treatment
• Praziquantel
• Fenbendazole

68
Q

Taenia taeniaformis; basics, life cycles

A

o Type of Cyclophyllidean
o Common tapeworm of cats
o Found worldwide

o Up to 60 cm long

Life Cycle
• Infected cat sheds proglottids/eggs 
-.>
• Proglottid is eaten by mouse 
->
• Strobilocercus develops in the mouse liver 
->
• Cat eats mouse 
->
• Strobilocercus from mouse develops into adult tapeworm in cat intestine 


69
Q

Taenia taeniaformis; intermediate stage, clinical signs, diagnosis, treatment

A

Intermediate Stage
• strobilocercus
• Looks like a baby adult tapeworm

Clinical Signs
• Asymptomatic
• Increased grooming

Diagnosis

• Fecal float- eggs may be shed

• Segments crawling around the anus

Treatment

• Praziquantel
• Fenbendazole

70
Q

Echinococcus; basics

A
o	Type of Cyclophyllidean
o	Echinococcus granulosus 
o	Echinococcus multilocularis
o	Adult worms are very small and rarely seen 
o	1-3 mm

o	Important zoonotic potential
71
Q

Echinococcus; life cycle, intermediate stage

A

Life Cycle
• Infected dog sheds eggs 
->
• Eggs are eaten by intermediate host
->

• Hydatid cyst develops in the intermediate host 
->
• Dog eats intermediate host 
->
• Ingested hydatid cyst develops into many adult tapeworms

Intermediate Stage
• hydatid cyst

• Very large fluid-filled bladder with many scolices inside
• Some scolices are grouped together in membrane-bound sacks called brood capsules
• Public Health hazard!

72
Q

Echinococcus; clinical signs, diagnosis, treatment, prevention

A

Clinical Signs
• Adult tapeworm is asymptomatic in dogs

Diagnosis
• Fecal float to identify eggs
• Eggs are indistinguishable form Taenia

Treatment

• Praziquantel
• Fenbendazole

Prevention/Control
• Treat all dogs in endemic areas
• Practice good hygiene around dogs to prevent ingestion of eggs
• Do not feed dogs discarded viscera from slaughter/hunt

73
Q

Echinococcus granulosus Two Life Cycles

A

Dog definitive / Sheep intermediate

o Sheep-dense regions of Utah and California

Wolf definitive / Wild cervid intermediate
o circulates in WA and ID
o can spill over into dogs

74
Q

Echinococcus granulosus Hydatis Cysts

A
  • Non invasive
  • In sheep lung or liver
  • Can cause pressure atrophy
  • Ruptured cyst can cause allergic reaction
75
Q

Echinococcus multiloccularis; region, hosts, hydatid cysts

A
  • Circulates primarily in wild canids- mostly foxes
  • Alaska, Montana, midwest, Canada

Intermediate host:
• Rodents, other mammals including humans

Hydatid cyst
• multiloccular
• invasive

76
Q

Pseudophyllidean basics

A

o No hooks or suckers on scolex
o Eggs look like flukes
o 1 central genital pore
o requires two intermediate hosts

77
Q

Pseudophyllidean General Life Cycle

A
  • Adult tapeworms are in carnivore small intestine (definitive host) ->
  • Eggs are shed in feces and contaminate water bodies
->
  • Eggs hatch and ciliated larva eaten by the 1st intermediate host ->

  • Intermediate stage of tapeworms develop
->
  • First intermediate host eaten by the 2nd intermediate host ->
  • Second intermediate stage of the tapeworm develops ->
  • 2nd Intermediate host eaten by definitive host ->

  • Adults develop in the definitive host’s small intestine 

78
Q

Pseudophyllidean; clinical signs, diagnosis, treatment

A

Clinical signs
• Diarrhea, weight loss, and vomiting

Diagnosis
• Fecal Float to identify eggs
• Fecal sedimentation

Treatment
• Praziquantel- high off-label dose required

79
Q

Diphyllobothrium; basics & life cycle

A

• Type of pseudophyllidean

Life Cycle
• Infected dog/cat/human sheds eggs 
->
• Eggs get into water, hatch out and are eaten by a copepod (1st intermediate host) 
->
• Copepod is eaten by fish (2nd intermediate host) 
->
• Dog/cat/human/bear eats fish 
->
• Adult tapeworm develops in intestine of definitive host 


80
Q

Spirometra; basics & life cycle

A

• Type of pseudophyllidean

Life Cycle
• Infected dog/cat /raccoon sheds eggs 
->
• Eggs get into water, hatch out and are eaten by a copepod (1st intermediate host) 
->
• Copepod is eaten by snake or any non-fish vertebrate (2nd intermediate host) ->
• Dog/cat/raccoon eats snake 
->
• Adult tapeworm develops in intestine of the definitive host

81
Q

Proliferative Sparganosis

A
  • Caused by Spirometra
  • If a dog or cat consumes the copepod, they become an accidental 2nd intermediate host
  • The larva (sparanga) reproduce asexually and develop in all tissues 
(crazy amount of worms)
  • Very rare 

  • No effective treatment
82
Q

Basics of Flukes, diagnosis, treatment

A

o Flat leaf-like worms
o specific geographic ranges and organ preferences
o First host is always snail
o 

distribution tied to snail geography

Diagnosis
• Eggs mostly detected on fecal sedimentations
• Usually dark amber with an operculum
• Diagnosis is often made on geographic location and clinical signs!

Treatment
• Praziquantel
• Fenbendazole

83
Q

Nanophyetus salmoncola Basics

A
  • Adult fluke lives in the intestine of fish-eating carnivores (Dogs, bears, raccoons)
  • Adult fluke is tiny (~1 mm long)
  • Distributed throughout the Pacific Northwest
  • Transmit Neorickettsia helminthoeca (Salmon Poisoning Disease) in dogs
84
Q

Nanophyetus salmoncola Life Cycle

A
  • Adult fluke in small intestine 
->
  • 7 d after ingestion eggs shed in feces and contaminate water bodies 
->
  • Larva hatches and penetrates aquatic Oxytrema snail 
->
  • Larva exits snail and penetrate skin of salmonid fish 
->
  • Encysts in salmonid skin and viscera 
->
  • Definitive host ingests salmon 
->
  • Adult fluke develops in intestine 

85
Q

Nanophyetus salmoncola Clinical Signs, Diagnosis, Treatment

A

Clinical signs

• Fluke is asymptomatic
• Can transmit salmon poisoning

Diagnosis

• Fecal sedimentation
• Fecal float- sugar solution distorts and shrinks the egg
• Direct smear

Treatment
• Praziquantel
• Fenbendazole


86
Q

Nanophyetus salmoncola Dz Transmission & Clinical Signs of Dz

A
  • Bears & raccoons are sub-clinical & maintain cycle
  • Neorickettsia helmintheca replicate in macrophages
  • Markedly enlarged lymph nodes

  • Incubation period is 5-7 days
Clinical Signs
o	Fever

o	Diarrhea, vomiting

o	Dehydration

o	Anorexia/Weight Loss
o	Lymphadenomegaly
o	Splenomegaly
o	Lethargy/Depression 
o	Death w/o treatment after 6-10d
87
Q

Diagnosis & Treatment for Salmon Poisoning

A

Diagnosis
o Clinical history of eating salmon

o Nanophyetus eggs in fecal sedimentation, fecal float, or direct smear
o Rickettsia w/in macrophages in lymph node aspirates

Treatment
o Supportive therapy
o Parenteral oxytetracycline or doxycycline
o Praziquantel- only kills the fluke
o Dogs are usually/not always immune after recovery


88
Q

Paragonimus Basics & Life Cycle

A
  • Lung flukes of dogs, cats, many wild mammals, humans
  • Mississippi river region and the Great Lakes drainage system

Life Cycle
• Adults encyst in pairs in lung 
->
• Eggs coughed up and swallowed ->
• shed in feces 
->
• Larvae hatches out and penetrates snail host 
->
• Larvae burst out of snail 
->
• Larvae penetrate and encyst in crawfish intermediate host 
->
• Cat or dog eats crawfish 
->
• Migrates from intestine to lung and develops into adult 


89
Q

Paragonimus Clinical Signs, Diagnosis, Treatment

A
Clinical signs
•	respiratory signs depend on numbers of flukes and is often asymptomatic
•	Coughing
•	Dyspnea
•	Pneumothorax 
•	Bronchiectasis
•	Hemoptysis 

Diagnosis
• Fecal sedimentation to identify eggs

Treatment
• Fenbendazole
• Praziquantel

90
Q

Platynosomum Baiscs & Life Cycle

A
  • Adult live in bile ducts and gallbladder of cats
  • Found in SE US and Hawaii 

  • Requires 3 intermediate hosts 

  • Causes lizard poisoning disease 


Life Cycle
• Adults in bile ducts ->
• Eggs are shed in feces
->
• Larvae hatches out and penetrates snail (1st intermediate host)
->
• Larva exit snail and are eaten by pill bugs (2nd intermediate host) ->
• Pill bugs are eaten by lizard, frog, toad (3rd intermediate host)
->
• Cat eats these 3rd intermediate hosts ->
• Adults develop in bile ducts

91
Q

Platynosomum Clinical Signs

A

• Depends on numbers of flukes

Asymptomatic

Mild
o Fever, lethargy, anorexia, weight loss

Severe

o	Vomiting 
o	Jaundice
o	Diarrhea
o	Emaciation 
o	Chronic biliary/liver dz
92
Q

Platynosomum Pathogenesis of Liver/Biliary Dz

A
  • Flukes in bile ducts cause irritation and damage to the bile duct epithelium ->
  • Biliary epithelial hyperplasia ->
  • Reactive fibrosis ->
  • Severe bile duct damage ->
  • liver failure and/or Cholangiocarcinoma
93
Q

Platynosomum Diagnosis & Treatment

A

Diagnosis
• history of hunting behavior +
• Geographic location +
• Fecal sedimentation to identify fluke eggs
• May require corn oil & repeated fecal sedimentations

Treatment

• Praziquantel

94
Q

Alaria Basics & Life Cycle

A
  • Small intestinal flukes of dogs & cats
  • Mainly in Midwest US

Life Cycle
• Snail (1st intermediate host) ->
• Penetrates tadpole (2nd intermediate host) ->
• Tadpole ingested by a frog/mouse (paratenic host) -> 

• Undergoes lung migration in final host

95
Q

Alaria Clinical Signs, Diagnosis, Treatment

A

Clinical Signs
• Not much intestinal pathology
• May cause respiratory dz during pulmonary migration

Diagnose
• fecal sedimentation
• Basic fluke egg

Treatment
• Praziquantel

96
Q

Apicomplexa Basics

A

o protozoa
o Obligate intracellular parasites
o Stages that invade cells are called zoites
o Sexual and asexual replication

97
Q

Basic Life Cycle of Apicomplexa

A
  • Zoites enter host by Ingestion of oocysts or cysts or Injection via a vector (tick/mosquito) 
->
  • Zoite invades a cell & undergoes asexual replication ->
  • Zoites break out and invade new cells ->
  • more asexual replication ->
  • In the definitive host, eventually the parasite enters sexual replication and produces oocysts 
->
  • Oocysts go into environment
  • All of this = MANY zoites
98
Q

Toxoplasma gondii Life Cycle

A
  • Sexual replication occurs in the intestinal epithelial cells of cats ->
  • Oocysts are produced and shed in cat feces 
->
  • The oocyst sporulates in the environment 
->
  • The sporulated oocyst can be ingested by a variety of intermediate hosts 
->
  • Asexual replication occurs in intermediate hosts resulting in bradyzoite tissue cysts (also sexual rep in cats)
->
  • Ingestion of bradyzoite tissue cysts results in infection
99
Q

Toxoplasma gondii Transmission Basics & Transmission thu Ingestion of Oocyst

A
  • After 1st infection, Abs prevent re-infection
  • Abs mean exposure & presence of bradyzoite tissue cysts
  • Cats usually only shed cysts for 30 days one time in their life

Ingestion of an oocyst
o Oocysts are excreted by cats only ->
o Oocysts sporulate in environment (~ 1 day) ->
o VERY difficult to get out of environment
o When ingested, sporulated oocyst can infect any mammalian or avian host

100
Q

Toxoplasma gondii Transmission thu Ingestion of Bradyzoite cyst & trasplacental infection

A

Ingestion of bradyzoite tissue cyst
o Sporulated oocyst is ingested
usually in undercooked meat->
o Zoites break out of the oocysts and invade and proliferate in tissues throughout the body ->
o Tachyzoites stimulate a strong immune response -> clinical disease ->
o The immune response forces the parasites to slow down and encyst ->
o “bradyzoite” cyst

Transplacental infection
o Fetal death
o Humans: fetal death, still birth, birth defects
o Surviving fetuses may present later with vision loss or mental disability
o ONLY the tachyzoite is capable of passing through the placenta to the fetus

101
Q

Toxoplasma gondii Control & Treatment

A

Control
• Clean litter boxes daily
• Do no feed cats undercooked meat or let them hunt
• Exclude cats from garden beds
• Beware of undercooked meat & unwashed produce

Treatment in Cats
• Clindamycin

• Pyrimethamine
• Trimethoprim sulfa

102
Q

Toxoplasma gondii Clinical Signs in Cats & Dogs

A

Clinical Signs in Cats
• Usually asymptomatic
• If immunosuppressed…
o Depends on where the tachyzoites establish and
o replicate, and the degree of inflammatory response
o Commonly affect lymph nodes, liver, lung, CNS, and eye
o hemorrhage and necrosis
o May manifest as fever, weight loss, lethargy, neurologic signs, sight abnormalities, etc

Clinical Signs in Dogs
• Usually asymptomatic
• Clinical signs usually associated w/ distemper infection

103
Q

Toxoplasma gondii Diagnosis in Cats

A

• VERY difficult

Fecal flotation
o VERY UNRELIABLE

o Oocysts in feces look like other nonpathogenic protozoal oocysts
o Shed for a very short window of time

Tissue stages
o Needle in a haystack

Serologic diagnosis:
o Remember a positive titer is only evidence of past infection
o Must look for evidence of recent infection

Evidence of Active Infection
o Demonstrate IgM titer
o Demonstrate a four-fold or greater increase in IgG titer over time
o Clinical signs that aren’t attributable to other diseases
o Positive response to treatment

104
Q

Neospora canium Basics

A
  • Only dogs produce oocysts

  • Cattle are the primary intermediate host
  • Dogs become infected by eating the bradyzoite tissue cyst from cattle tissues
  • Dogs can be infected transplacentally
  • Not zoonotic
105
Q

Neospora canium Life Cycle

A
  • Dog produces oocysts ->
  • contaminate ruminant feed/water ->
  • cattle tissue cysts ->
  • dogs ingest bradyzoite from cow meat ->
  • Bradyzoites can reactivate in dogs and releases tachyzoites ->
  • transmit transplacentally
->
  • neonatal canine neosporosis
106
Q

Neonatal canine neosporosis

A
  • Usually manifests about 3-9 weeks of age

  • More than one puppy in a litter will develop hind limb paralysis with hyperextension
  • Muscle weakness and contracture develop
  • Dysphagia and eventually death
107
Q

Neospora canium Cinical Signs

A

• most infections are asymptomatic (Many dogs are seropositive)

Severe
• can occur in dogs of any age

• Due to tachyzoites disseminating throughout the tissues
• Immune responses result in granuloma formation and inflammation
• Prognosis is poor
• Aggressive treatment necessary to prevent death

108
Q

Neospora canium Diagnosis, Treatment, Prevention

A

Diagnosis
• Clinical signs and history + positive serology (IgM or increasing IgG titer)
• Oocysts are rarely seen in fecal floats

Treatment

• Clindamycin
• Trimethoprim plus pyrimethamine

Prevention
• Prevent dogs from eating raw tissues 

• Prevent contamination of cattle feed with dog feces 

• Do not breed bitches that have had neosporosis or have whelped puppies that have developed neosporosis

109
Q

Cystoisospora – Coccidiosis Basics & Diagnosis

A

o Intestinal coccidia
o Very host specific

o Multiple species in each host

Diagnosis
• Fecal float

110
Q

Cystoisospora – Coccidiosis Direct & Peratenic Life Cycle

A

Direct Life Cycle
• Dog or cat shed oocysts into the environment in feces ->
• Oocysts must sporulate to become infectious ->
• Dog/cat eats a sporulated oocyst ->
• Asexual replication occurs in intestinal epithelial cells ->
• huge increase in parasite numbers ->
• Sexual replication occurs in intestinal epithelial cells

Peratenic Host Life Cycle
• Sporulated oocysts are eaten by rodent
->
• Sporozoites come out of oocysts and encyst in the tissues of rodent ->
• Rodent eaten by cat/dog

111
Q

Cystoisospora – Coccidiosis Clinical Signs, Treatment, Control

A

Clinical signs
• Usually asymptomatic- especially in older dogs
• Young animals- diarrhea, weight loss, dehydration
• Severe in immunocompromised dogs

Treatment
• Sulfadimethoxine- approved and labeled for coccidiosis in dogs
• Trimethoprim sulfa, amprolium, ponazuril, toltrazuril, diclazuril

Control:
• Good sanitation!
• Oocysts survive well in environment and are resistant to disinfectants

112
Q

Tick Borne Apicomplexans Life Cycle

A
  • Asexual reproduction occurs in the dog or cat (intermediate host) ->
  • Gametes from asexual rep are picked up by the tick during a blood meal ->
  • Fusion of gametes = sexual reproduction (production of oocysts/sporozoites) occurs in the tick
113
Q

Hepatozoon americanum Basics & Life Cycle

A
  • Tick-borne apicomplexan
  • Emerging disease in dogs in the southern US
  • Transmitted by Amblyomma maculatum
  • 3 host tick


Life Cycle
• dog ingests an infected tick or a paratenic host that ate a tick ->
• Asexual reproduction occurs in dog muscle and forms “onion skin” cysts and pyogranulomas 
->
• Gamonts appear in leukocytes in peripheral blood 
->
• Ticks ingest gamonts when they feed ->
• sexual replication and production of oocysts occurs

114
Q

Hepatozoon americanum Pathogenesis & Clinical Signs

A

Pathogenesis
• Asexual replication in muscle tissue
• Inflammation & pain

Clinical Signs
• Muscle atrophy, soreness, stiffness and 
weakness 

• Neutrophilic leukocytosis 

• Fever, depression, weight loss, anemia 

• Mucopurulent ocular discharge 

• Periosteal bone proliferation, Diaphysis of long bones 


115
Q

Hepatozoon americanum Diagnosis, Treatment, Prevention

A

Diagnosis
• Muscle biopsy to find cysts

Treatment:

• “TCP”- Trimethoprim-sulfadiazine + clindamycin + pyrimethamine
• Follow with daily decoquinate for 2 years
• Supportive therapy
• Prognosis is poor

Prevention:
• acaracides,
• prevent exposure to ticks

116
Q

Babesia Sp. Basics

A
  • Tick-borne apicomplexan
  • Large Babesia species- B. canis

  • Small Babesia species- B. gibsoni
  • Transmitted by Rhipicephalus sanguineus
  • Treatment helps resolve clinical signs but it often DOES NOT eliminate infection
  • (+) dogs should never be used for blood transfusions
  • Immunosuppression or splenectomy will cause the infection to become symptomatic again
117
Q

Babesia sp. Life Cycle

A
  • Parasite replicates asexually in dog RBCs ->

  • Tick feeds on infected dog 
->
  • Sexual replication and development of oocysts 
occurs in tick 
->
  • Tick bites dog & transmits apicomplexan
  • Can also be transmitted during dog fights, blood transfusion, contaminated needles
118
Q

Large Babesia sp. Clinical Signs

A
o	Often asymptomatic 
o	Carriers are common 
o	Hemolytic anemia

o	Splenomegaly

o	Lethargy, fever, general weakness, depression, anorexia
119
Q

Large Babesia sp. Diagnosis, Treatment, Control

A

Diagnosis

o Piroplasms in blood smear

o PCR to detect carriers

o Serology- antibodies cross-react with other protozoans

Treatment

o Imidocarb diproprionate
o Clindamycin

Prevention
o Acaracides
o prevent blood contamination

120
Q

Small Babesia sp. Basics & Treatment

A
  • Most often seen in pit bulls -> dog fighting is likely a major route of transmission
  • Importance of tick transmission is questionable
  • Usually more pathogenic than large Babesia species

Treatment
o more difficult than for large Babesia
o Atovaquone + azithromycin is most effective

121
Q

Cytauxzoon sp. Basics

A
  • Tick-borne apicomplexan
  • Emerging disease in cats 

  • Transmitted by Amblyomma americanum 

  • Maintained in bobcats`
  • 3 host tick
  • Eastern US
122
Q

Cytauxzoon sp. Life Cycle

A
  • Cat is bitten by infected Amblyomma americanum ->
  • Asexual reproduction begins in endothelial associated macrophages which form huge schizonts ->
  • Clinical disease ->
  • Piroplasms invade erythrocytes ->
  • Ticks pick up parasites from infected cat and development of oocysts occurs in ticks (definitive host)
  • can also get this through blood transfusions, cat bites etc, but only the erythrocytic stage is transmitted and no schizonts develop = much less pathogenic
123
Q

Cytauxzoon sp. Clinical Signs, Diagnosis, Treatment

A

Clinical Signs
• usually get severe disease and >50% mortality
• High fever
• Anemia, jaundice

• Disseminated intravascular coagulation and shock
• Depression, lethargy, anorexia, dehydration

Diagnosis

• Piroplasms in blood smear
• Schizonts in macrophages in splenic, lymph node or bone marrow aspirate
• PCR (best)

Treatment
• Without treatment death occurs within 2-3 days after fever peaks
• Atovaquone + azithromycin

• Aggressive supportive care

124
Q

Giardia Basics & Life Cycle

A

o Type of Flagellate

Life Cycle
• Trophozoite in intestine rounds up into a cyst ->
• Cyst excreted into the environment ->
• Fecal-oral transmission of infective cyst

125
Q

Giardia Clinical Signs

A
  • Almost always asymptomatic

  • Commonly found in healthy animals
Young affected animals

•	Malabsorption syndrome
•	Chronic diarrhea 
•	Mal odorous feces and flatulence
•	Steatorrhea

•	Weight loss even with normal appetite 
•	No fever and no blood in feces


Older animals,
• diarrhea acute, intermittent, or chronic

126
Q

Giardia Diagnosis

A
  • Direct fecal smear of diarrheic feces to detect trophozoites & cysts (falling leaf twirling thing)
  • Fecal float
for Cysts
  • ELISA SNAP test for Ag in feces
  • Diagnosis can be difficult as shedding of cysts is intermittent
  • Retest several times over a period of a few days
127
Q

Giardia Treatment & Reasons for Treatment Failure

A
  • Fenbendazole for 3-5 days (most effective)
  • Metronidazole
(Treatment failures more common)
Treatment failures may result from: 
•	Reinfection - super common 

•	Inadequate drug levels 

•	Immunosuppression 

•	Drug resistance 

•	Giardia sequestering in the gallbladder or pancreatic ducts 

128
Q

Giardia Prevention & Zoonosis

A

Prevention
• Clean up dog poop IMMEDIATELY 

• Bathe animals on last day of treatment to remove cysts 


Zoonosis
• 8 taxonomic assemblages
• most animal assembalges can’t be passed to humans
• treating asymptomatic cases is controversial & depends on immune status of humans in household

129
Q

Tritrichomonas Basics, Clinical Signs, Transmission

A

o Type of flagellate
o Lives in large intestine of cats
o Only exists in trophozoite form
o Replicates by binary fission

Clinical Signs
• chronic large-bowel diarrhea

Transmission
• fecal-oral

130
Q

Tritrichomonas Diagnosis, Treatment, Control

A

Diagnosis
• PCR (best)
• Direct fecal smear (Looks like Giardia but has jerky movements)
• Feline InPouch TF Test kit (fecal culture)

Treatment
• Ronidazole

Control
• Clean litter box frequently
• Limit contact between infected and uninfected cats

131
Q

Leishmania Basics, Life Cycle, Transmission

A

o flagellate
o Foreign animal dz except n foxhounds in US

Life cycle
• Asexual reproduction in macrophages

Transmission
• endemic areas - vectored by sandflies
• US - transplacental and dog to dog via blood and secretions within the foxhound population

132
Q

Leishmania Clinical Signs & Diagnosis

A

Clinical Signs
• Commonly asymptomatic carriers
• Immunosuppression/pregnancy can cause clinical dz
• Fever, D, V, skin lesions, chronic wasting, loss of muscle, renal failure

Diagnosis
• Serology (infected asymptomatic animals can be seronegative for years) 

• PCR 

• Biopsy or aspirates to look for parasites in macrophages in spleen, liver, bone marrow, lymph nodes

133
Q

Leishmania Treatment & Zoonosis

A

Treatment 

• Pentavalent antimonials and maintenance therapy (for life) with allopurinol 

• Does not result in cure and relapses are common

Zoonotic potential: 

• Endemic areas can be transmitted from sandflies