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AOD Exam 2 Stronglyes

Terms in this set (166)

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Strongylida
Trichostrongylidae
Strongyle family typically found in large animal
HOT Complex
Haemonchus spp.
Ostertagia spp.
Trichostrongulus spp.
Trichostrongylidae examples
Ancylostomatoidea
Strongyle family typically found in dogs and cats
Ancylostomatoidea
Hookworms fall under which strongyle super family?
Hoomworks (canine and feline)
Common name for Ancylostoma spp
Strongyloidea
Strongyle family typically found in horses
Eggs look the same
Direct life cycle
Transmit disease through L3 in the environment
Undergo hypobiosis
Commonatlities of stronglyes
Direct life cycle
Life cycle of strongyles
Though L3 in the environment
How are strongyles transmitted?
The eggs of strongyles all look the same
How do you identify the difference in strongyle spp eggs.
Hookworms
A 1-year-old, MN, Greyhound dog presents for a 2-week history of diarrhea with a normal appetite. On physical exam, he is BAR, TPR is WNL, abdominal discomfort on palpation, and dried fecal material is noted around perineum. Sarge is down approximately 2% of his body weight from his previous visit 6 month ago for routine vaccination.

Other important information
On year-round heartworm prevention (HWP)
Every Saturday, Sarge goes to the dog park to hang out with his girlfriend Lulu the Shih Tzu
No other animals in the house

We performed a direct fecal smear and CBC and found that he has no ova or motile forms in fecal smear and that he has mild regenerative anemia, hypochromcic and microcytic RBC (pale and small RBCs) --> iron deficiency anemia.

What is your diagnosis?
small intestine
Canine hookworms live where in the dog?
Bloodsuckers
Canine hookworms are generalized as
Short PPP: ~2-3 weeks are all routes of infection
PPP of canine hookworms
thin shelled
morulated
ovoid
55-90 um to 55 um
zoonotic
Describe the egg of canine hookworms
Yes! zoonotic
Are canine hookworms zoonotic?
Ancylostome caninum (most common in USA and worldwide, voracious bloodsucker)
Ancylostome braziliense (associated with cutaneous larval migrans in people, SE USA)
Uncinaria stenocephala (Norther USA)
Three types of canine hookworms to worry about in the USA and where
Ancylostoma caninum
Most common hookworm in the USA (very active in southern states)
You cannot tell the difference. You just write them off as canine hookworm eggs.
How do you tell the difference between canine hookworm eggs?
Cutaneous larval migrans in people from canine hookworms
mice, rats, beetles, roaches
paratenic host of canine hookworms
Toxocara canis
Hookworm life cycle is similar to the life of what?
per os
paratenic (rodents, beetles, roaches)
transmammary (most important route for puppies)
transplacental (about 2% of puppies are infected by this route)
percutaneous (important in human transmission)
Canine hookwars are transmitted through..
In the environment
Hookworm eggs hatch and develop into infective L3 where?
1. migrate to trachea --> SI --> adults (similar migration path as ascaris suum in pigs or toxocara canis in dogs)
2. L3 migrate to somatic tissue --> hypobiotic in muscle --> can re-emerge to develop to adults in SI
3. L3 enter intestinal mucosa and become hypobiotic --> can re-emerge to develope to adults in SI
What routes might an L3 hookworm take after being ingested?
Infective L3 penetrate the skin and migrate via lymphatics and circulation, taking either the tracheal route back to mature in the intestine or the somatic route and become hypobiotic in muscle
Describe skin penetration of hookworms
Oral route
percutaneous
paratenic host
Thought to be the most common route of infection of hookworms in adults
1. migrate to mammary tissue in lactating bitch - transmammary transmission to puppies (MOST EFFECTIVE route for hypobiotic larvae)
2. trick infection or larval lead form muscle, tracheal route, adults in SI --> especially after deworming
3. some thought to be mobilized in pregnant bitch and migrate to fetus - very minor
What is the fate hypobiotic hookworm (ANCYLOSTOMA CANINUM) larvae if they become activated?
The larvae develop DIRECTLY inthe intestine (no tracheal migration)
What happens after an adult dog ingests a Ancylostoma caninum paratenic host?
Bleeding, malabsorption, pain
Blood loss --> microcytic hypochromic anemia from an Iron deficiency anemia
Clinical signs of Ancylostoma caninum
They are plug feeders with teeth, so they chew and lacerate tissue, causing bleeding and malabsorption, and they ingest up to 0.1ml per worm per day.
How does Ancylostoma caninum cause blood loss?
Ancylostoma caninum (canine hookworms)
What is pictured?
Fecal flotation (primary method, prolific egg layers, floats easy with most solutions)
Hookworm ELISA (identified protein on ADULT worms)
Occult blood fecal test (not sensitive or specific for hookworms) (not recommended)
Common diagnostics of Ancylostoma caninum
Sanitation around home
Routine fecal exams
Preventative measure for Ancylostoma caninum
Hookworm fecal ELISA
Persistent infections of Ancylostoma caninum is diagnosed by
1. most dewormers only kill adult worms and do not target hypobiotic worms
2. lavae hypobiotic in the muscle tend to become reactivated in small numbers and migrate to the gut --> larval leakage
3. there is now proven resistance in Ancylostoma caninum
Why might a Ancylostoma caninum infection be persistent?
Trichostrongylidae (HOT complex)
Ruminant stronglyes are often
Haemonchus spp., Ostertagia spp., and Trichostrongylus spp.

Type of trichostrongylidae (ruminant stronglyes)
HOT complex
a mixed nematode species infection
(a disease complex...Thus, HOT complex)
Gastroenteritis in ruminants are generally caused by...
"strongyle-type eggs"
since it is difficult to ID specific parasite species by their egg on fecal flotation, we designate them as....
Direct life cycle (trichostrongyles)
Trichostrongyles have what type of lifecycle
Ingestion of larvae (L3) in the environment
How are ruminants infected with Trichostrongyles?
abomasum or SI
Where does Trichostrongyles live in a ruminant animal?
Adults mate and eggs pass in the feces. Eggs hatch and develop directly on the ground (L1 to L3). Infective larvae move away from the fecal mechanically and on their own. The L3 are ingested while grazing, exsheath while on their way to the abomasum/SI. They enter the abomasum/SI and mature to adults.
Describe the Trichostrongyles life cycle
brown stomach worm
Common name for ostertagia ostertagi
ostertagia ostertagi
What is the most important nematode in cattle worldwide?
overgrazed
overstocked
ostertagia ostertagi is more common is herds that are ______ or _______
younger animals
ostertagia ostertagi tends to infect ruminants of what age most?
Adults mate and eggs pase in the feces. Eggs hatch and develop on the ground (L1 to L3). Infective larvae move away form the fecal mechanically and on their own. The L3 are ingested while grazing, exsheath while on their way to the abomasum. The larvae enters the gastric glands. It develps into the L4 in 4-5 days and continues to grow, increasing in size 10x and become L5 in 12-14 days. As young adults, they leave the gastric gland, causing destruction of the gastric gland. In the lumen, they mate and lay eggs in about 3 weeks (PPP)
Describe the life cycle of ostertagia ostertagi
4-6 weeks
PPP of ostertagia ostertagi
ostertagia ostertagi larvae in gastric glands of abomasum
Yes, is can go in a hypobiotic state.
Can ostertagia ostertagi go into a hypobiotic state?
Exposure to:
late fall conditions (in the north)
late spring conditions (in the south)
Unfavorable weather

They remain there until late winter or early spring and then resume development (north)
Why might ostertagia ostertagi larve go into a hypobiotic state?
gastric gland
Where does hypobiosis of ostertagia ostertagi occur in the ruminant?
Pregnancy
Stress
Relaxation of immunity
Spring?
What events trigger the development of hypobiotic ostertagia ostertagi larvae to adults?
3 phases
How many major phases of diease are there in ostertagia ostertagi?
Larvae invade the gastric gland. During growth and molting to L4, they damage zymogen, parietal, and mucus secreting cells, which are replaced with undifferentiated cells
Describe phase 1 of ostertagia ostertagi
Day 1 - 17
Phase 1 of ostertagia ostertagi occurs during what days?
Day 17 - 35
Phase 2 of ostertagia ostertagi occurs during what days?
Young adults (L5) emerge and destroy parietal cells, causing HCl production to stop. Bacteria proliferate. No pepsinogen to pepsin. Cell junctions lost so pepsinogen goes into plasma and plasma proteins are lost to guy, causeing hypoalbuminemia.
Describe phase 2 of ostertagia ostertagi
Day 35 - 70 days
Phast 3 of ostertagia ostertagi occurs over what days?
Gradual loss of worms (They have completed their life span) and gradual return to function
Describe phase 3 of ostertagia ostertagi
A group of proteins that can also be described as an inactive enzyme, in the stomach these proteins are mainly activated by HCl
What is zymogen?
Zymogen form of pepsin
What is pepsinogen?
An enzyme that breaks down proteins into pepties (main digestive enzymes in the stomach)
What is pepsin?
Mainly albumine which is responsible for oncotic forces in the peripheral blood
What are plasma proteins?
Diarrhea
weight loss
inappetance
bottle jaw, AKA submandibular edemia (hypoalbuminemia)
hyperplastic gastric glands resulting in a "moroccan leather" appearance on gross examination
Clinical signs of ostertagia ostertagi
Hyperplastic gastric gland (AKA moroccan leather) as a result of ostertagia ostertagi
Bottle jaw as a result of hypoalbuminemia, can be a result of many diseases.
Type 1 Ostertagiosis (summer ostertagiosis)
Type 2 Ostertagiosis (winter ostertagiosis)
What are the two major types of ostertagiosis?
Dependent on season. In temperate climates with cold winters, both types occur
What are the types of ostertagiosis dependent on?
calves during their first grazing season as a result of massive larval ingestion 3-4 weeks earlier
Type 1 Ostertagiosus (summer) is usually seen in....
In north america in Mid-july and onward
Where and when do you usually see Type 1 Ostertagiosus?
Bright green diarrhea
What does the poop in Type 1 ostertagiosus look like?
Unable to process nutrients, so the grass just comes out
Why is the poop green in Type 1 ostertagiosus?
High morbidity
Is the morbidity of Type 1 ostertagiosus high or low?
yearlings in the late winter or early spring following their first grazing season
Type 2 Ostertagiosus (winter) is usually seen in....
maturation of larvae ingested the previous autumn. The hypobiotic worms over the winter emerge in the late winter/early spring to begin development.
Type 2 Ostertagiosus results from....
Profuse watery diarrhea (bright green)
Dull
Severe dehydration
High morbidity
Clinical signs of Type 1 Ostertagiosus
Profuse watery diarrhea, usually intermittent
Dull
anorexia
thirst (dehydration)
hypoalbuminemia --> bottle jaw
Clinical signs of Type 2 ostertagiosus
Type 2 (winter) because they emerge at different times and at different rates, so it gives us a false since of how infected or how much the nematode load is in the abomasum
Which type of ostertagiosus would ostertagia be more difficult to detect on fecal egg counts?
Clinical signs
season and grazing history
fecal egg counts
plasma pepsinogen (not very sensitive or specific)
Necropsy (ID of small red worms or larvae in glands on histology)
How might you diagnose Type 1 ostertagiosis?
Clinical signs
Season and grazing history
+/- fecal egg counts (often negative)
Plasma pepsinogen (not very sensitive or specific)
Necropsy, +/- ID of small red worms or larvae in glands on histology
How might you diagnose Type 2 ostertagiosis?
Strongyle-type eggs
found in ruminant
Responds well to anthelminthics. Following treatment, move to pasture not grazed by cattle that same year
Treatment and prevention method of Type 1 ostertagiosis
More difficult to treat than Type 1. Must address the hypobiotic larvae. Use short and long acting anthelminthic. (long acting kills hypobiotic). Move animals off pasture, and graze pasture with sheep or goats until following June.
Treatment and prevention method of Type 2 ostertagiosis
1. Edema is present and it is not common in ostertagia
2. Ostertagia is usually seen in younger animals, and henry is older
Henry is a 1.5 year old llama. On presentation had a HCT of 6%. One month prior he had a history of diarrhea and we was dewormed with ivermectin. This past weekend, owners noticed that Henry's mucous membranes were pale and he was hyporexic.

Results of physical exam:
Attitude: QAR (Quiet, alert, responsive)
Temperature: 100.4 F (Slightly febrile)
Pulse: 140 bpm
Respiration: 60 breaths/ minute
Cardiovascular and Pulmonary: WNL
BCS: 2/5
PCV/ TP: 6%, 4.2 g/dL (Normal=26-45%, 6-8 g/dL)
Mild submandibular edema noted

What is different about this presentaiton versus Ostertagia?
Same low protein and enemia(?)
Henry is a 1.5 year old llama. On presentation had a HCT of 6%. One month prior he had a history of diarrhea and we was dewormed with ivermectin. This past weekend, owners noticed that Henry's mucous membranes were pale and he was hyporexic.

Results of physical exam:
Attitude: QAR (Quiet, alert, responsive)
Temperature: 100.4 F (Slightly febrile)
Pulse: 140 bpm
Respiration: 60 breaths/ minute
Cardiovascular and Pulmonary: WNL
BCS: 2/5
PCV/ TP: 6%, 4.2 g/dL (Normal=26-45%, 6-8 g/dL)
Mild submandibular edema noted

How can we make some of these signs fit with the life cycle we know from Ostertagia?
Direct life cycle (Haemonchua contortus)
Haemonchua contortus life cycle type
Effs hatch and larvae develop to the infective L3 (ensheathed and resistant to the environment). L3 is ingested. Exsheath in rume to abomasum. Penetrate between gastric epithelial cells. Emerge as L4 and moult to adult.
Describe the life cycle of Haemonchua contortus
When unfavorable conditions occur (autumn, winter, or dry), the L4 will undergo hypobiosis and encyst in the gut wall until conditions become favorable
When might hypobiosis occur in Haemonchua contortus?
acute hemorrhagic anemia from bloodsucking habits of adults and L4s
Presentation of acute Haemonchua contortus
reinfection is negligible but occurs when pasture becomes nutrient depleted and hypobiotic larvae mobilize
Presentation of chronic Haemonchua contortus
Anemia (occurs 2 weeks after infection --> dramatic decrease in PCV and protein)
Iron deficiency anemia
Hypoproteinemia from blood loss --> edema (bottle jaw)
Dehydration
Clinical signs of acute Haemonchua contortus
mild anemia (usually regenerative)
progressive weight loss
inappetance
weakness
Clinical signs of chronic Haemonchua contortus
No, diarrhea is not a common feature
Is diarrhea a common feature of Haemonchua sp. infections?
Season, history, and clinical signs
fecal egg counts
FAMACHA (use mucous membranes to determine if animals affected by Haemonchus contortus should be dewormed)
Necropsy
Diagnosis of Haemonchua sp. is based on
Haemonchua has develpoed resistance to all groups of anthelminthics.
Can Haemonchua sp. be treated with anthelminthics?
Pasture rotations
Prevention of Haemonchua contortus
Multiple blood transfusions
Animals severely affected with Haemonchua sp. may be treated with...
Sheep, goats, camelids (sheep and camelids are most severely infected)
Definitive hosts of Haemonchua contortus
18-21 days, but have hypobiotic states
PPP of Haemonchua contortus
Live in abomasum or C3
Where does Haemonchua contortus reside within an animal?
Very common
Is Haemonchua contortus a common disease?
common small intestinal ruminant nematode
Nematodirus Spp.
thin necked intestinal worm
Nematodirus Spp. is also known as...
15-26 days
PPP of Nematodirus Spp.
Direct life cycle (Nematodirus Spp.)
Type of life cycle of Nematodirus Spp.
adults live in the SI
where do adult Nematodirus Spp. live in the animal?
Females lay very few eggs, so finding ONE egg on a float is significant and should prompt treatment
Do female Nematodirus Spp. lay a lot of eggs or few eggs?
It is direct life other strongyles. Except, the larval stage develop within the egg and do not hatch until L3. Therefore, the eggs/L3 can survive on pasture for extended periods of time. They can survive freezing. They are susceptible to desiccation (tend not to see these infection in arid climates)
How is the life cycle of Nematodirus Spp. similar and different from other stronglyes
After ingestion, the L3 exsheaths in the abomasum. Migrates between the villi in the SI. Emerge as adults 15-26 days (PPP). May undergo hypobiosis in intestingal mucosa
Describe the life cycle of Nematodirus Spp.
Larval stages can cause massive damage to intestinal wall resultingin unthriftiness, poor weight gain, and diarrhea
Large numbers of adult worms may retard growth in younger animals
Clinical signs of Nematodirus Spp.
Fecal float or quantitative fecal flotation
The eggs are the largest of the strongyle type eggs (2-3x the size of a typical strongyle type egg)
Not heavy eggs shedders, thus finding any in a fecal likely means heavy worm burden
Diagnosis of Nematodirus Spp.
Nematodirus Spp. egg
Nematodirus Spp. egg amongst many typical strongyle type eggs
Size (large and small strongyles)
Equine strongyles are characterized into two groups based on...
Strongylus vulgaris -> cecum
Strongylus edentatus -> colon
Strongylus equinis -> cecum
What are the three large equine strongyles?
Cyanthostomes -> colon and cecum
What is the small equine strongyle?
No, the eggs have identical morpholgy
We can cell which species an equine stonglye is on fecal float alone?
Horses and donkeys
Definitive host of equine strongyles
Cecum and colon
Where does equine strongyles. live in the animal?
6 months
Equine strongyles PPP
L3 (not egg)
Horses are infected with equine strongyles by ingesting which stage of the species?
worm burden and infected with larvae or adults. Larvae cause greater pathology
Clinical signs of equine strongyles are dependent on
Yes, large problem
Is anthelminthic resistance of small equine strongyles a problem?
Morphologically the same
Are the eggs of large and small equine strongyles morphologically the same or different?
ingestiong of L3 by horse. L3 perforates the SI and migrates along cecal and colonic arteries. Enters the root of the cranial mesenteric artery. Spends 3-4 months in the cranial mesenteric artery and then migrate and returns to the conol/cecum via the lumen of the arteries. Encyst in the submucosa of the colon and cecum until they rupture out to become adults. Will begin producing eggs in approximately 6-8 weeks form this point. Eggs passed in the feces to external environment.
Describe the life cycle of Strongylus vulgaris
6-7 months
PPP of Strongylus vulgaris
Little pathology with low worm burdens. Aggressive plug feeders --> do not eat blood but can result in severe blood loss and ulceration. 30mL of blood can be lost per day with 75-100 adults in a foal
Pathogenesis/clinical signs of Strongylus vulgaris adults
Most significant pathology associated with migration via arteries and disruption of Virchow triangle. Arteritis, endothelial wall thickening and potentially thrombi formation. Colic from migration --> painful. Thromboembolic colic --> necrosis of intestines
Pathogenesis/clinical signs of Strongylus vulgaris larvae
Strongylus sp. (on right) attatched to cecum/colon lumen (on left)
S. vulgaris (left)
S. edentatus (middle)
S. equinus (right)
Name the strongyles
Severe artertitis due to massive larval migration
The artery on the left is normal, so what is wrong with the artery on the left?
Horses are infected by ingesting larvae (L3) while grazing. There they pass through the stomach to the SI then onto the cecum and colon. Larvae enters the crytps and encysts in the submucosa of cecum and colon. The larvae will emerge form the submucosa and develop to adutls in the lumen of the ventral and dorsal colon. Adults produce eggs that are excreted in feces and develop to larvae in the environment.
Describe the life cycle of Cyanthostomes
6-14 weeks, but larvae can arrest for longer periods of time depending on many factors
PPP of Cyanthostomes
Yes, it can
Can Cyanthostomes undergo hypobiosis?
2.5 years
Cyanthostomes can lie in enysted for up to how long?
larval cyanthostomiasis
Synchronous emergence of Cyanthostomes in early spring can result in...
Neutrophilia, hypoalbuminemia, hyperglobulinemia, acute diarrhea, larvae in feces (eggs may not be present in the feces)
Clinical signs of larval cyanthostomiasis
...
Why might larval cyanthostomiasis eggs not be present in the feces?
usually less severe than larval stages --> weight loss
still plug feeders but have shallow mouthparts so feed mainly by grazing on mucosal surface
however cumulative effects of heavy worm burden can lead to diarrhea
Pathogenesis/clinical skills of adult Cyanthostomes
genergally, more severe in animals < 2 years with heavy infection
Hemorrhagic, caterrhal and fibrinous enteritis
colonic ulceration
Pathogenesis/clinical skills of larvae Cyanthostomes
adult cyanthostome
history
clinical signs
culture to infective L3 for identification
How might we diagnose large and small equine strongyles?
strongyle type egg (equine strongyles)
Good management and a strategic deworming program using fecal egg counts (FEC) (parasitic resistance is a huge problem, especially in small strongyles)
Strict sanitation
Good pasture management
Compost manure
Good nutrition
Prevention and control methods of equine strongyles
Equine pinworms
Common name for Oxyuris equi
all equids
Oxyuris equi infects...
larvated egg
The infective stage of Oxyuris equi is...
terminal large intestine
where does Oxyuris equi reside in the animal?
<18 months old
Oxyuris equi is more common in horses ages...
perianal itching
broken tail head hairs
clinical signs of Oxyuris equi
5 months
PPP of Oxyuris equi
Adult's mate, female migrates out of the anus and lays eggs in the perianal region. The eggs are kept there with sticky substance, which is very irritating. Eggs fall or are rubbed off and drop to ground or in feed. Egg develops to the infective larval L3 stage in 3-5 days. Larvated (L3) egg is ingested. Egg hatches and the larvae migrate into the mucosal crypts of ventral colon and caecum. Develop and return to the lumen
Describe the life cycle of Oxyuris equi
Adults do little damage
Pathogenesis of adult Oxyuris equi
Larvea in the mucosa may cause problems when numbers are high
Pathogenesis of larvae Oxyuris equi
Eggs in perianal region
intense pruritus
cause rubbing of tail head
restless and loss of condition
hair loss, rat tailed appearance
damage to premise
Clinical signs of Oxyuris equi
Clinical signs and history
Find eggs in perianal region (use non-opaque stick tape and place on glass slide)
Observe adults in freshly voided feces
Diagnoses of Oxyuris equi
Fecal flotation may not yield eggs
Can you use a fecal float to diagnose Oxyuris equi?
Oxyuris equi eggs
Damage to tail hair due to irritation caused by Oxyuris equi infection
Remove egg masses with soap and warm water
Sanitation in stalls and paddocks
Treat infected animals (most anthelminic approved for horses are efficacious)
Prevention and control of Oxyuris equi
Histomanas melagridis (protazoan, not nematode)
What is heterakis gallinarum the intermediate host for?
transmammary
What is the most common route of transmission ot T cati to kittens?
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