Nematodes: Horse and ruminant gastrointestinal strongyles Flashcards
Basic morphological description of nematodes
Cross-section is round
Unsegmented, tapering at end
Cuticle – tough and flexible (NOT called a tegument in these ones)
Pseudocoelom – body cavity with inner fluid, hydrostatic skeleton
Longitudinal internal organs
Digestive system of nematodes
Fully developed digestive system (so not like flatworms).
Mouth is called a stoma.
- some have two/three lips
- some have tentacles at the lips
Buccal capsule, some have teeth/ blades.
Some can be surrounded by a “leaf crown”.
Cloaca in males
Anus in female
Reproductive system of nematodes
Dioecious, meaning have males and females separately. Repro syst. designed to produce extremely large numbers of eggs.
Females are smaller
- Repro syst. either monodelphic, Didelphic branch system or multidelphic branch. So one, two or three branches of uterus.
- Ovary – oviduct – uterus, common vagina and vulva
Male are larger
Single tube repro tract.
Testes
- Class Secernentea have one
- Class Adenophorea - two
Vas deferens - ejaculatory duct, cloaca
Accessory male organs in nematodes
Copulatory spicules (sorta like worm penis)
gubernaculum guides the spicule for copulation
Copulatory bursa - cuticula modification in order Strongylida. Called bursate if they have them and non-bursate if they don’t.
Used for grasping female for copulation.
Cuticular modifications in nematodes,
Identification between the species:
Diff. species may have diff ones of the below:
Copulatory bursa in males
- Bursal rays and lobes
Cuticle alae, „side wings“
- Cervical and caudal alae
Cephalic and cervical vesicle
Cervical and caudal papillae
Leaf crown
Papillae
Nematode basic life cycle
In the environment:
egg, embryo, vermiform, microfilaria etc.
I molt
second larval stage
II molt
third larval stage
III molt
Then in host:
fourth larval stage
IV molt
adulthood (5th stage of development)
define hypobiosis
or facultative arrested development stage of some larva
development is delayed temporarily
Triggering factors:
- Seasonal arrestment - cold autumn/winter or dry summer.
- Caused by the immunity
- Caused by overcrowding
Epidemiological importance:
- Important in parasite distribution - increases nematode survival
- Maturation of the arrested larvae increases environment contamination
Nematode Migratory phase in the final host
In many species the larva travels/ migrates in the final host before they reach their preferred site.
Most common: hepatic-tracheal migration
E.g. image diagram depicts migration between organs in pig host.
Explain: Periparturient rise (PPR) in fecal egg count
Called “Spring rise” = increase in egg amounts around parturition
Reason: relaxation of immunity in dams
+ hypobiotic larva resuming development
So sources of these extra eggs:
- Maturation of arrested larvae
- Increased acquired infections
- Increased fecundity of existing adult nematodes
Thus, Metaphylactic treatment important before parturition.
How do strongyle larvae overwinter? (2)
2 ways:
- as preparasitic stage-L3 on grass or
- as arrested larvae within host tissues
depends on local climate and worm species.
What class does nematode order strongylida belong to?
Secernentea
What 4 bursate superfamilies belong to Order Strongylida?
Strongyloidea
Trichostrongyloidea
Metastrongyloidea
Ancylostomatoidea
Which superfamily of order strongylida has an indirect life cycle?
he 4 superfamilies:
Strongyloidea
Trichostrongyloidea
Ancylostomatoidea
Metastrongyloidea has an indirect life cycle meaning a molluscan or annelid
intermediate host is required for development of I stage larva to III stage larva.
Name the 2 classes of nematoda to have vet med clinical significance.
Secernentea & Adenophorea
Name the 5 orders of class Secernentea to have vet med clinical significance.
Oxyurida
Strongylida
Ascaridida
Spirurida
Rhabditida
Strongylus edentatus, bursa copulatrix
Equine enterostrongylidosis is a
parasitosis with a chronic course caused
by roundworms of the Strongylida order
parasitizing the large intestine, which is
characterized by loss of appetite,
indigestion, reduced work capacity and
emaciation.
Their migrating larvae cause
thromboembolic colic, pancreatitis,
nodular colitis and sometimes death.
Equine enterostrongylidosis hosts
Final host: horses
No intermediate hosts!
Usually Young horses - less than a year or less than 6 years.
Transmission of strongylidosis into horses?
Transmission: ingestion of L3 larvae that are waiting in grass
Organ preference of strongylidosis
Habitat: caecum or colon
When is incidence of strongylidosis infection highest?
Overwintering larvae, encysted larvae lead to: Infection highest in Spring and then Autumn
Strongyle size
There are both small and large strongyles and infections can be with a mix of both so they may be discussed as a strongyles group instead of specific spp.
Most prevalent and pathogenic larval form of parasites in horses
Equine SMALL strongyles
Equine SMALL strongyles Larvae live in
caecum, inside nodules.
Larval cyathostominosis is
the result of a mass emergence of encysted arrested cyathostome larvae (small stongyle larva) in the wall of the large intestine, cecum, or both.
- acute typhlocolitis, profuse watery diarrhea, ventral oedema
- high mortality
cyathostomes = small strongyles (which are the most prevalent parasite of horses)
typhlo- = refers to the cecum
PS: fecal flotation and EPG is not diagnostic at larval cyathostominosis stage
Clinically healthy horses can harbor burdens of small strongyles.
Describe small strongyles morpology:
Small strongyles are Small (5-25 mm)
Cylindrical short buccal capsule
No teeth, no lips
Males have a bursa copulatrix
Small species differentiation:
- Buccal capsule
- Internal/external leaf crowns
The basic life cycle of all strongyles is
similar - but here are differences in the larvae migration!
Life cycle:
Direct - females ovoparous (lay eggs)
L1-L3 develops outside
Horse eats infective L3
Within the horse:
Within 1-2 weeks L3 encysts in a fibrous capsule and then molts into L4 in 5-6 weeks.
OR
Early L3 may enter hypobiosis (2-3 months).
L4 emerges into gut lumen, molts into L5.
In the environment development is 2 weeks
Prepatent period 2-3 months
What life phases of small stongyles live in the open environment?
eggs get deposited outside and develop into L1, L2 and L3 outside. L3 is then eaten by a horse.
Clinical signs of larval cyathostominosis/ small stongyles infestation.
Massive tissue destruction, lesions from the encysted larvae.
- Weight loss and subcutaneous oedema due to hypoalbumenemia, anemia
- Profuse, sudden onset of diarrhea
- Death common & colics
Adults in the intestine:
- Unspecific signs, spoor/shaggy coat, colic,
inappetence, reduced performance
Clinically most important and destructive equine parasites
Equine LARGE strongyles, especially S. vulgaris (due to the migratory phase) is highly pathogenic.
S. vulgaris
S. edentatus
S. equinus
are all equine large strongyles with extensive larvae migration. In which organs do each species migrate?
S. vulgaris - anterior mesenteric and nearby arteries
S. edentatus - liver and subperitoneal connective tissues
S. equinus - liver, pancreatic ducts and renal region
All have Long prepatent period (due to migratory phase)
Describe the morphology of equine LARGE strongyles.
Large strongyles are 1 – 5 cm.
Have Large buccal capsule
Teeth may be present
Two leaf crowns
Males have bursa
Large species differentiation:
size/presence/shape of teeth
Length of the following large strongyles?
And prepatent period?
Strongylus vulgaris
Strongylus edentatus
Strongylus equinus
Length
Strongylus vulgaris 1,5-2,5 cm, 6-7 months
Strongylus edentatus 2,5-4,5 cm, 10-11 months
Strongylus equinus 2,5-5,0 cm, 8-9 months
spp.?
Strongylus vulgaris
spp.?
Strongylus edentatus
spp.?
Strongylus equinus
Steps Strongylus vulgaris takes in the host
Larva penetrates submucosa
After 1 week migrates in the arteries
upstream - to cranial mesenteric artery
Develops there in clots for several months
Blood carries back to intestinal wall arteries
Encapsulated in nodules (1cm)
Adults in caecum and colon
Prepatent period 6-7 months
steps Strongylus edentatus takes in the host
Larva penetrates intestinal wall
Through portal vein travels to liver
Moults in nodules in parenchyma
- 2 week post infection
- 2 months travels in liver tissue
Forms nodules in the tissue and moults.
Then travels under the peritoneum and moults; migrates there several months
Adults hang out in large intestinal wall
Prepatent period 10-12 months
Steps Strongylus equinus takes in the host
Larva penetrates submucosa
Formation of nodules in caecum/colon mucosa
Larva travels to liver parenchyma (in contact with cecum) - migrates there for months
Then travels in/around the pancreas or peritoneal cavity
Adult penetrates cecum/colon wall and travels to intestines
Prepatent period 8-9 months
Describe the image pathogenesis.
Adult strongyles feeding on plugs of intestinal mucosa and consume blood:
they cause Haemorrhages, ulcers, scars
pyrexia, loss of appetite, anemia,
emaciation
Severe infection with S. vulgaris larva can cause:
Thromboses, arteritis, embolism,
intestinal infarct (rare!)
Thromboembolic colic
Fever, enteritis, peritonitis
Death due to infarcted intestine possible
Diagnostic methods for strongylus infection.
Anamnesis: grazing history, clinical signs not valuable.
Response to treatment: Faecal egg count reduction test (FECRT).
Detecting the eggs: Fecal flotation method
Identification of species:
- Fecal culture method – for larvae identification (L3).
- Baermann method - larvae in the feces (small strongyle L4).
PS: FEC (fecal egg count) not valuable in case of larval cyathostominosis.
- Diagnosis is through anamnesis, clinical signs.
- Emerged L4 can be found in feces using the Baermann method.
Molecular methods (pre-adult stage DNA) and serology (larval antigen).
Intestinal mucosa biopsy or post mortem (necropsy).
Arteriography in small horses (S. vulgaris).
S. vulgaris: rectal examination – palpation of cranial mesenteric artery.
What is FECRT?
Fecal egg count reduction test
A response to treatment test.
for estimating the reduction in fecal egg counts and its corresponding confidence interval. The results of this test can be used to determine the anthelmintic resistance status of the animals.
What is the Baermann technique in parasitology?
technique is based on the active migration or movement of larvae. Faeces are suspended in water. The larvae move into the water. They sink to the bottom and can be collected for identification.
Eggs of Order Strongylida (except superfamily Metastrongyloidea) are
similar.
Most species eggs are not distinguishable from each other.
Larvae are used to distinguish species.
Describe strongylida eggs.
Shape: ellipsoidal
Size: 70-100 µm
Shell: smooth and thin
Content: embryo (blastomeres)
Color: brownish
Describe the Larval culture method.
What is it?
How is it performed?
enables differentiation of strongyle larvae to genus/species level.
Preparation of the sample:
*Mix the feces with sawdust
*Transfer the culture medium to the screw
jar until it is half full. Loosen the cover.
*Incubate culture at 26° C for 5-8 days
(80% humidity).
*Fill the glass with water, place the petri
dish on top of the glass, turn the glass
over, fill up with water, leave to stand for
6-12 hours → Larvae migrate.
*Perform microscopic genus/species
diagnosis of the L3
Treatment options for Strongylidosis.
Diagnose before treatment! Treat if FEC (fecal egg count) is over 200 EPG (eggs per gram of feces). Minimum possible treatment.
Broad-spectrum anthelmintics against adults:
- Benzimidazoles (resistance problem)
- Pyrantel (resistance problem)
- Macrocyclic lactones (ivermectin)
Treatment options for larval cyathostomosis.
Against larval cyathostomosis once a year after the grazing season - foals and young horses:
- Fenbendazole
- Moxidectin single doses
Supportive therapy for reducing diarrhea (Rehydration and corticosteroids).
What is the disease called when a horse is infested with encysted larvae of the Strongylida order?
larval cyathostomosis
cya-tho-sto-mosis
Prevention and control options for Strongylidae.
Monitoring 1-3 times per year (monitor S. vulgaris separately) - FEC and FECRT once a year.
Strategic deworming: spring and autumn (egg shedding peaks).
Class of drugs should be rotated annually/biannually.
New horse: deworm + quarantine for 72 hours.
Paddock rotation system - nursing mares and foals go first!
Avoid pasture overgrazing/overstocking.
Enterostrongylidosis of ruminants is a
parasitoses caused by roundworms of
the order Strongylida parasitizing
the
abomasum, small intestine and
large intestine of domestic and wild
ruminants, characterized by
indigestion, weakness, anemia and
emaciation.
GIS =
Ruminant gastrointestinal strongyles (GIS)
cause the disease enterostrongylidosis
in Superfamily Trichostrongyloidea, all members are parasites of the alimentary tract except for
except genus Dictyocaulus (they are lungworms)
Describe enterostrongylids broadly.
Small, hair-like worms
Males with well developed bursa and two spicules.
Teeth usually absent
Life cycle is direct and usually non-migratory, but hypobiotic stage is common.
Infective stage is free L3
Location: abomasum and the small intestine
Important in ruminants (widespread morbidity) & common in grazing ruminants.
Clinical disease: digestive disorders, anorexia, apathy, weakness
Where in the body do Dictyocaulus like to live?
respiratory system
Which Strongyloides spp. like to inhabit the abomasum? (4)
Ostertagia spp.
Haemonchus spp.
Teladorsagia spp.
Trichostrongylus axei
Which Strongyloides spp. like to inhabit the small intestine? (5)
Cooperia spp.
Nematodirus spp.
Bunostomum spp.
Oesophagostomum spp.
Chabertia spp.
Life cycle of GIS
GIS = gastrointestinal strongyles
Exogenous = free-living stage:
Eggs to L1-L3 in feces, takes around 2 weeks.
L3 travel to herbage and become infective.
Endogenous stage = parasitic stage:
Host eats the herbage with larva
Larva into the abomasal/ intestinal glands, then molts.
Adult emerges from gland 2-3 weeks later.
L3 can become arrested: hypobiosis up to 6 months.
Which species of GI strongyle actually has a percutaneous infection and migratory phase? (rather than alimentary transmission)
Bunostomum spp.
Seasonal dynamics of gastrointestinal strongyles (GIS)
Overwintering larvae usually die in June.
Early spring the infection rate low.
Worm generation:
3 weeks in host
1 week outside
Beginning 2-3 month on pasture there is intensive contamination of pastures.
Animals become infected July/August, also first clinical signs occur then.
Ostertagiosis is caused by?
give latin name and english name
Parasite:
Ostertagia ostertagi
Brown stomach worm
A similar disease to Ostertagiosis but affecting sheep is caused by what parasite?
So Ostertagiosis is caused by Ostertagia ostertagi.
The similar disease in sheep is caused by Teladorsagia circumcincta.
Where does Ostertagia ostertagi/ Brown stomach worm like to reside in a host?
Prepatent period?
surface of the abomasal mucosa, in nodules
PPP: 3 weeks
Morphology of Ostertagia ostertagi/ Brown stomach worm?
Slender, reddish-brown color worm, up to 1cm.
Ostertagiosis pathogenesis
Heavy infection: when adult worm burdens are 40,000 epg or more - parasites are emerging from gastric gland.
Reduction in the acidity of the abomasal fluid (3 weeks post infection)
- pH increases from 2.0 to 7.0 - loss of bacteriostatic effect - pepsinogen not activated to pepsin
– protein digestion decreases - increase of pepsinogen leakage to circulation -
hyperpepsinogemia - Elevated plasma concentration – loss of plasma proteins into lumen
– hypoalbuminaemia, oedema
Enhanced permeability of the abomasal epithelium.
Physical changes/pathologies due to Ostertagiosis.
Formation of nodules, cell degeneration, strong inflammation of mucosa, enlarged regional lymph glands.
Ostertagiosis pathogenesis:
Type I (summer ostertagiosis)
Calves in their first grazing season, mid-July onwards.
High morbidity
Profuse watery diarrhea – bright green color.
Ostertagiosis pathogenesis:
Type II (winter ostertagiosis)
Yearlings
Late winter or spring – larvae being arrested after first grazing season.
Profuse intermittent watery diarrhea with anorexia and thirst
Submandibular oedema
Morbidity low, mortality high when left untreated with anthelmintics effective against adults and arrested larvae.
Haemonchus spp. known as what in english?
Barber’s pole worm
Describe Barber’s pole worm morphology:
- white ovaries winding spirally around the blood-filled intestine (barber’s pole)
- buccal cavity small with small lancet-like tooth
- large: 2-3cm
Location of predilection for barber’s pole worm?
Abomasum
this is Haemonchus spp.
Prepatent period of barber’s pole worm/ Haemonchus spp.?
2-3 weeks in sheep and 4 weeks in cattle
Haemonchus spp. (barber’s pole worm) causes similar pathology to that of ostertagiosis with one main difference:
Feces: mostly normal to firm consistency
dark to blackish colored additional blood loss!
In which species do the following live:
H. contortus:
H. placei:
H. similis:
H. contortus: mainly in sheep and goats
H. placei: mainly in cattle
H. similis: mainly in cattle
Describe Cooperia spp.
Location:
Morphology:
PPP:
Location: small intestine
Morphology: small, less than 1 cm, pinkish-white when fresh
Often mixed with Ostertagia ostertagi
Prepatent period: 2-3 week
Describe Oesophagostomum spp.
English name:
Location:
Morphology:
PPP:
- Nodular worms
Location: colon, skin penetration can be possible
Morphology: whitish, 1-2 cm long, stout
Prepatent period: 5-7 weeks
Forms nodules in the large intestine or abomasum. L4 may remain arrested in nodules for up to 1 year.
Describe Nematodirus spp
English name:
Location:
Morphology:
PPP:
Thread-necked worms
Location: small intestine
Morphology: white, slender and long: 1-2,5cm, anterior end is thinner, body twisted and coiled
Life cycle: L1-L3 inside the egg!
Describe Bunostomum spp.
English name:
Location:
Morphology:
Life cycle comment:
English name: hookworms
Location: small intestine , anterior jejunum/duodenum
Morphology: 1-3 cm, white, anterior end bent large buccal capsule with cutting plates
Life cycle comment: the larvae can have migratory phase!
Pathogenesis with 100-500 worms:
* Progressive anaemia, hypoalbuminaemia
* Loss of weight
Pathogenesis with 2000 worms: death
Haematophagus parasite
Describe Trichostrongylus spp
Location:
Morphology:
PPP:
Location: small intestine
Morphology: slightly reddish/brown, slender, hair-like, less than 7mm. No obvious buccal cavity.
Distinct excretory notch in oesophageal region.
PPP: 2-3 weeks
Describe Chabertia ovina
English name:
Location:
Morphology:
PPP:
English name: Large mouthed bowel worm
Location: colon (largest nematodes in colon of ruminants)
Morphology: up to 2cm, white.
anterior end is large and bent ventrally
very large buccal capsule - bell shaped, no teeth
PPP: 6-7 weeks
Clinical signs of GIS.
Ruminant gastrointestinal strongyles
inappetence, weight loss and diarrhoea
Diagnosis of GIS in general.
Ruminant gastrointestinal strongyles
Detecting the eggs:
Fecal flotation method
Followed by fecal culture method for species identification
Antibody detection – milk ELISA (bulk-tank milk or individual)
Routine post mortem examination
- valuable parasitological data about the herd status.
FAMACHA for Haemonchus spp.
Diagnosis of GIS - ostertagiosis specifically
- Increased plasma pepsinogen levels
- Season – In Europe type I occurs from July to September; type II occurs from March to May
- Grazing history
- type I: the calves have grazed in one area for several months
- type II: the calves have been moved between different areas
- fecal egg count (FEC)
- type I: >1000 epg
- type II: usually low and of limited value (arrested larvae!)
Treatment of GIS
Widespread anthelminthic resistance in GIS of small ruminants, especially with benzimidazoles and macrocyclic
lactones.
NEW treatment concepts: selective, targeted treatment:
Refugia - preserve a proportion of the parasite population in “refugia”, unexposed to treatment.
Currently, 3 classes of anthelmintics commonly used in ruminants:
* benzimidazoles (including albendazole, fenbendazole)
- macrocyclic lactones/avermectins (including ivermectin, moxidectin)
- cholinergic agonists (including levamisole/morantel)
Control and therapy of GIS
Effective pasture/farm management
* pasture change/ rotation – horses-cattle-sheep-crops – 1 year for one
* rotate adults and youngsters/ keep separate – young animals go graze first!
* Diagnose – fecal analysis – always before treatment.
Do not treat the whole flock
- treat certain groups (young, pregnant)
- treat unwell animals (scouring (diarrhetic), anaemic, thin, etc)
- Do not treat animals with mild clinical signs
- let them develop immunity
