Exam 2 Flashcards
(133 cards)
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
2
Q
Diagnosis of Nematodes
A
o Fecal smear
o Fecal float
o Baermann
o Fecal Sedimentation
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
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
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
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
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
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
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
10
Q
Baylisacaris procyonis
A
- Same lifecycle as toxocara canis
- Can undergo somatic migration in any mammal
- Causes visceral & ocular larval migrans in humans
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
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
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
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
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
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
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)
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)
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
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
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
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
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
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
25
Cutaneous Larval Migrans Due to Hookworm
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
26
Basics of Heartworm & Geography
* 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
27
Life Cycle of Dirofilaria
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
28
Pathology in Dogs due to Dirofilaria
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
29
Clinical Signs of Dirofilaria in Dogs
```
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
```
30
Dirofilaria Diagnosis in Dogs
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
31
Differentiating between Dirofilaria & Acanthocheilonema on Micro Exam
```
Dirofilaria
• Pathogenic
• High numbers
• Wiggly w/o actually moving
• Longer
```
```
Acanthocheilonema
• Non-pathogenic
• Very few
• Wiggle moves them
• Shorter
```
32
Wolbachia
o Symbiotic bacteria that Dirofilaria carries
o Killing bacteria can incapacitate worm
o Must kill bacteria to prevent bacterial infection around dead worms
33
Treatment of Dirofilaria in Dogs
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
34
Prevention of Dirofilaria in Dogs
Test all dogs >7MO yearly
Macrocyclic lactones
• ivermectin,
• selamectin,
• moxidectin
Mosquito repellent
• Pyrethrins
• Neonicotinoids
35
Dirofilaria immitis in Cats Vs Dogs
```
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
```
36
Heartworm Associated Respiratory Dz in Cats Basics & Treatment
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
37
Diagnosis of Heartworm Associated Respiratory Dz in Cats
Ag test
• Must have at least one female worm to test (+)
Ab test
• Can detect female & male worms
• Only indicates exposure not infection
38
Ollulanus; basics & transmission
* 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!
39
Ollulanus; clinical signs, diagnosis, treatment
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
40
Physaloptera; basics & life cycle
* 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
41
Physaloptera; clinical signs, diagnosis, treatment
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
42
Strongyloides; basics & life cycle
* 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
43
Strongyloides; transmission & clinical signs
```
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
44
Strongyloides; diagnosis, treatment, control
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
45
Trichuris Whipworm; basics & life cycle
* 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
46
Trichuris Whipworm; clinical signs, treatment, control
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
47
Trichuris Whipworm; Diagnosis
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
48
Oslerus osleri; basics, life cycle
* 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
```
49
Oslerus osleri; transmission, clinical signs
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
50
Oslerus osleri; diagnosis, treatment
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
```
51
Aelurostrongylus; basics, life cycle
* 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
52
Aelurostrongylus; clinical signs
Asymptomatic
Moderate:
o coughing and anorexia
Severe:
o coughing, panting, shortness of breath, death
53
Aelurostrongylus; diagnosis & treatment
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
54
Eucoleus; species & basics of each
```
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
Eucoleus; diagnosis & treatment
Diagnosis
• fecal float for eggs
Treatment
• ivermectin and fenbendazole
56
Dioctophyma; basics
* Giant kidney worm of dogs
* The largest nematode in veterinary medicine
* Lives in the kidney (usually R)
* Normal definitive host is the mink
57
Dioctophyma; Life Cycle, Diagnosis, Treatment
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
Personema plica; basics, transmission, clinical signs, treatment
* 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
Morphology of Cestodes
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
Two Cestodes Groups
Cyclophyllidae
• Common
• Hooks & suckers or one of either
Pseudophyllidea
• Rare
• No hook or suckers
61
Cyclophyllidean General Life Cycle
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
Cyclophyllidean Clinical Signs & Treatment
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
Dipylidium caninum basics & life cycle
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
Dipylidium caninum; intermediate stage, clinical signs
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
Dipylidium caninum; diagnosis, treatment, prevention, zoonosis
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
Taenia pisiformis; basics & life cycle
```
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
Taenia pisiformis; intermediate stage, clinical signs, diagnosis, treatment
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
Taenia taeniaformis; basics, life cycles
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
Taenia taeniaformis; intermediate stage, clinical signs, diagnosis, treatment
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
Echinococcus; basics
```
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
Echinococcus; life cycle, intermediate stage
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
Echinococcus; clinical signs, diagnosis, treatment, prevention
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
Echinococcus granulosus Two Life Cycles
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
Echinococcus granulosus Hydatis Cysts
* Non invasive
* In sheep lung or liver
* Can cause pressure atrophy
* Ruptured cyst can cause allergic reaction
75
Echinococcus multiloccularis; region, hosts, hydatid cysts
* Circulates primarily in wild canids- mostly foxes
* Alaska, Montana, midwest, Canada
Intermediate host:
• Rodents, other mammals including humans
Hydatid cyst
• multiloccular
• invasive
76
Pseudophyllidean basics
o No hooks or suckers on scolex
o Eggs look like flukes
o 1 central genital pore
o requires two intermediate hosts
77
Pseudophyllidean General Life Cycle
* 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
Pseudophyllidean; clinical signs, diagnosis, treatment
Clinical signs
• Diarrhea, weight loss, and vomiting
Diagnosis
• Fecal Float to identify eggs
• Fecal sedimentation
Treatment
• Praziquantel- high off-label dose required
79
Diphyllobothrium; basics & life cycle
• 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
Spirometra; basics & life cycle
• 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
Proliferative Sparganosis
* 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
Basics of Flukes, diagnosis, treatment
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
Nanophyetus salmoncola Basics
* 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
Nanophyetus salmoncola Life Cycle
* 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
Nanophyetus salmoncola Clinical Signs, Diagnosis, Treatment
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
Nanophyetus salmoncola Dz Transmission & Clinical Signs of Dz
* 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
Diagnosis & Treatment for Salmon Poisoning
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
Paragonimus Basics & Life Cycle
* 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
Paragonimus Clinical Signs, Diagnosis, Treatment
```
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
Platynosomum Baiscs & Life Cycle
* 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
Platynosomum Clinical Signs
• 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
Platynosomum Pathogenesis of Liver/Biliary Dz
* 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
Platynosomum Diagnosis & Treatment
Diagnosis
• history of hunting behavior +
• Geographic location +
• Fecal sedimentation to identify fluke eggs
• May require corn oil & repeated fecal sedimentations
Treatment
• Praziquantel
94
Alaria Basics & Life Cycle
* 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
Alaria Clinical Signs, Diagnosis, Treatment
Clinical Signs
• Not much intestinal pathology
• May cause respiratory dz during pulmonary migration
Diagnose
• fecal sedimentation
• Basic fluke egg
Treatment
• Praziquantel
96
Apicomplexa Basics
o protozoa
o Obligate intracellular parasites
o Stages that invade cells are called zoites
o Sexual and asexual replication
97
Basic Life Cycle of Apicomplexa
* 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
Toxoplasma gondii Life Cycle
* 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
Toxoplasma gondii Transmission Basics & Transmission thu Ingestion of Oocyst
* 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
Toxoplasma gondii Transmission thu Ingestion of Bradyzoite cyst & trasplacental infection
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
Toxoplasma gondii Control & Treatment
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
Toxoplasma gondii Clinical Signs in Cats & Dogs
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
Toxoplasma gondii Diagnosis in Cats
• 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
Neospora canium Basics
* 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
Neospora canium Life Cycle
* 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
Neonatal canine neosporosis
* 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
Neospora canium Cinical Signs
• 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
Neospora canium Diagnosis, Treatment, Prevention
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
Cystoisospora – Coccidiosis Basics & Diagnosis
o Intestinal coccidia
o Very host specific
o Multiple species in each host
Diagnosis
• Fecal float
110
Cystoisospora – Coccidiosis Direct & Peratenic Life Cycle
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
Cystoisospora – Coccidiosis Clinical Signs, Treatment, Control
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
Tick Borne Apicomplexans Life Cycle
* 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
Hepatozoon americanum Basics & Life Cycle
* 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
Hepatozoon americanum Pathogenesis & Clinical Signs
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
Hepatozoon americanum Diagnosis, Treatment, Prevention
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
Babesia Sp. Basics
* 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
Babesia sp. Life Cycle
* 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
Large Babesia sp. Clinical Signs
```
o Often asymptomatic
o Carriers are common
o Hemolytic anemia
o Splenomegaly
o Lethargy, fever, general weakness, depression, anorexia
```
119
Large Babesia sp. Diagnosis, Treatment, Control
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
Small Babesia sp. Basics & Treatment
* 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
Cytauxzoon sp. Basics
* Tick-borne apicomplexan
* Emerging disease in cats
* Transmitted by Amblyomma americanum
* Maintained in bobcats`
* 3 host tick
* Eastern US
122
Cytauxzoon sp. Life Cycle
* 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
Cytauxzoon sp. Clinical Signs, Diagnosis, Treatment
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
Giardia Basics & Life Cycle
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
Giardia Clinical Signs
* 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
Giardia Diagnosis
* 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
Giardia Treatment & Reasons for Treatment Failure
* 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
Giardia Prevention & Zoonosis
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
Tritrichomonas Basics, Clinical Signs, Transmission
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
Tritrichomonas Diagnosis, Treatment, Control
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
Leishmania Basics, Life Cycle, Transmission
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
Leishmania Clinical Signs & Diagnosis
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
Leishmania Treatment & Zoonosis
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
