6.10 – Strongylid Nematodes – Flashcards
(44 cards)
1
Q
Strongylids;
General Features
A
- contains the trichostrongyles, strongyles, hookworms and lungworms
- most have a single host (exception lungworms)
- wide range of hosts that vary depending on group of strongylid
2
Q
Introduction to Strongylids; General Morphology ‐ Adults
A
- mainly smaller nematodes (2 ‐ 5 cm)
- trichostrongyles and lungworms slender
- hookworms and strongyles more stout bodied
3
Q
Introduction to Strongylids; General Morphology ‐ Eggs
A
- thin‐shelled, morulated eggs (most 60 ‐ 150 μm)
- called various things depending on host (GIN, hookworm egg or strongyle egg)
4
Q
Introduction to Strongylids; General Life Cycle
A
- direct in most cases (exception lungworms)
- eggs or larvae in feces
- primarily oral transmission (some penetrate skin)
- some have extra‐intestinal migrations as larvae
5
Q
Hookworms ‐ Ancylostoma caninum; General Features; geographic range, site of infection, feeding method
A
- commonly found in south & temperate regions
- common hookworm of canine small intestine
- less common in this region
- vicious blood‐sucking worm
6
Q
Ancylostoma caninum
Morphological Features ‐ Adults
A
- stout worm with bend at buccal cavity
- may be dark red if filled with blood
- buccal cavity has 3 large pairs of teeth
7
Q
Ancylostoma caninum; Morphological Features ‐ eggs
A
- typical morulated egg (“hookworm egg”), oval and <70 μm in length
- Features are: ‐ thin‐shelled ‐ morulated
8
Q
Ancylostoma caninum
Life Cycle
A
- direct life cycle
- morulated eggs passed, L1’s develop to L3’s
- L3’s penetrate skin of dogs (or man) and undergo tracheal migration in young dogs
- somatic migration occurs in older dogs
- # ingestion of L3’s can give rise to patent infections through a mucosal migration
- pups infected by transmammary infection
- mature dogs may have patent infections resulting from reactivation of hypobiotic larvae
- paratenic hosts may play a minor role
- environment will affect L3’s
- PPP ‐ 21⁄2 weeks for transmammary ‐ 3 ‐ 4 weeks for other routes
9
Q
Hookworms ‐ Ancylostoma caninum; Pathogenesis/Lesions/Clinical Signs
A
- blood‐feeding worms lead to:
‐ anemia and protein losses (hypoproteinemia)
‐ enteritis - per acute infections result from 50 ‐ 100 worms and may die before patency
- less acute infections can result in anemia, melena and emaciation
- may get edema from hypoproteinemia
10
Q
Hookworms ‐ Ancylostoma caninum; treatment
A
- same anthelmintics used against ascarids are effective against hookworms with the exception of piperazine (not active against hookworms)
- selamectin (Revolution®) has label activity against feline hookworms but not canine hookworms
11
Q
Hookworms ‐ Ancylostoma tubaeforme; general features; host, adult morphology, egg morphology
A
- common hookworm of cats
- adults are similar to A. caninum but smaller
- typical morulated egg (“hookworm egg”), oval and <70 μm in length
12
Q
Hookworms ‐ Ancylostoma tubaeforme; life cycle
A
- direct life cycle
- morulated eggs passed, L1’s develop to L3’s
- L3’s penetrate skin of cats (or man) and undergo tracheal migration in young cats
- somatic migration presumed to occur in older cats
- paratenic hosts may (or may not) be involved
13
Q
Hookworms ‐ Ancylostoma tubaeforme; pathogenicity
A
- little known but presumed to be similar to canine hookworm
14
Q
Hookworms ‐ Ancylostoma tubaeforme; treatment
A
- same as roundworms in cats with fewer compounds available than for dogs
- pyrantel pamoate‐based treatments (Pyr‐a‐Pam®, Pyr‐a‐Pam II®, Pyran®, Drontal® [mixed with praziquantel])
15
Q
Hookworms ‐ Uncinaria stenocephala; range, hosts, morhpology
A
- the northern hookworm
- infects both dogs and cats
- morphologically similar to Ancylostoma but has a pair of cutting plates in the buccal cavity instead of three large pairs of teeth
16
Q
Hookworms ‐ Uncinaria stenocephala; egg morphology
A
- typical morulated egg (“hookworm egg”), oval, >70 μm in length
17
Q
Hookworms ‐ Uncinaria stenocephala; life cycle
A
- direct life cycle
- morulated eggs passed, L1’s develop to L3’s
- L3’s are hardy and freeze‐tolerant
- L3’s are ingested, unlike the other hookworms
- skin penetration by L3’s not common
- no extra‐intestinal migration
- PPP‐21⁄2weeks
18
Q
Hookworms ‐ Uncinaria stenocephala; Pathogenesis/Lesions/Clinical Signs
A
- much less pathogenic than Ancylostoma spp.
- blood‐feeding worms lead to:
‐ anemia and protein losses (hypoproteinemia)
‐ mild enteritis
19
Q
Hookworms ‐ Uncinaria stenocephala; treatment
A
- same anthelmintics used against ascarids are effective against hookworms with the exception of piperazine (not active against hookworms)
20
Q
Control of Roundworms and Hookworms in Puppies; objectives and solutions
A
Objectives:
* reduce/eliminate egg‐shedding by puppies
(public health benefits plus reduced future problems)
Solutions:
* if a problem is suspected/known ‐ aggressive therapy starting at two weeks and then every 2 weeks out to 12 weeks (what stages/species are likely to be controlled this way?)
* normally‐treatment at 4‐6 weeks of age (minimum age for label usage of many anthelmintics) followed by treatment in response to continued positive fecals
21
Q
Lungworms; what are the true lungowrms? what is their general reproductive strategy/ first life stage?
A
- metastrongyloid nematodes‐true lungworms
- most shed larvae instead of eggs
- Examples:
Metastrongylus* Protostrongylus Muellerius* Filaroides* Oslerus* Aelurostrongylus*
22
Q
Muellerius spp.; general features; hosts, life cycle
A
- metastrongylid nematodes ‐ true lungworms
- DH – sheep, goats
- IH – snails and slugs
- Indirect life cycle that involves ingestion of IH followed by migration to predilection site of the alveoli and terminal bronchioles
23
Q
Muellerius spp.; diagnostic stage
A
- L1’s shed in feces are diagnostic stage
24
Q
Muellerius capillaris; pathogenesis
A
- alveolar rupture
- focal interstitial pneumonia
- some granuloma formation
25
Muellerius capillaris; Lesions/Clinical Signs
* later infections show raised regions on the lung
* some areas may calcify
* goats may show more serious pneumonia but this may be multifactorial
26
Muellerius capillaris; treatment
* no registered compounds – may wish to try compounds such as levamisole or ivermectin registered against other nematodes in these hosts
27
Filaroides and Oslerus spp.; general features; sites of infection, hosts
* metastrongylid nematodes ‐ true lungworms
* Oslerus osleri (= Filaroides osleri )
‐ tracheal or bronchial infections
* Filaroides hirthi
‐ terminal bronchioles or alveoli
* infects domestic or wild canids
28
Filaroides and Oslerus spp.; morphology
* adults small and slender
* thin‐walled, fully larvated eggs are laid by female (and these quickly hatch in bronchi or trachea)
* small larvae ~300 μm long passed in feces
29
Filaroides and Oslerus spp.; life cycle
* direct life cycle
* L1’s shed in environment are infective
* tracheal migration gives adults in trachea/bronchi (O. osleri) or in brochioles/alveoli (F. hirthi)
30
Oslerus osleri PPP
* Oslerus osleri ‐ 10 weeks
31
Filaroides hirthi PPP
* Filaroides hirthi ‐ 5 weeks
32
Filaroides and Oslerus spp.; Pathogenesis/Lesions/Clinical Signs
* F. hirthi ‐ usually asymptomatic
* O. osleri ‐ nodules and released eggs/larvae give rise to tracheitis/bronchitis with wheezing cough
* heavy infections may give dyspnea
* larvae diagnosed in sputum or with Baermann
* nodules can be visualized by bronchoscopy
33
Filaroides and Oslerus spp.; treatment
* albendazole or levamisole have efficacy (off‐label)
* F. osleri nodules may be removed surgically
34
Filaroides and Oslerus spp.; diagnosis
* use a Baermann technique
* larvae crawl from fecal mass
* more definitive diagnosis can be made on morphology of larvae
* requires fresh, unfixed fecal specimens (≥20g if possible)
35
Aelurostrongylus spp.; type of worm, hosts, site of infection
* metastrongylid nematodes
* true lungworm of cats
* requires intermediate host
* infects small bronchioles and alveoli
36
Aelurostrongylus spp.; morphology
* small (10mm) slender adults
* larvae have a small bent tail with a dorsal spine
37
Aelurostrongylus spp.; Life Cycle
* larvae passed in feces infect snail/slugIH
* frogs/rodents/lizards/birds act as PH’s (probably most common source of infections)
* larvae migrate from stomach to lungs
* adults in terminal respiratory tract/lung parenchyma
* PPP‐5 to 6 weeks
38
Aelurostrongylus spp.; Pathogenesis/Lesions/Clinical Signs
* adults and released eggs/larvae give rise to focal pneumonia with granulomas
* heavy infections may give chronic cough & dyspnea
* larvae diagnosed in sputum or with Baermann
39
Aelurostrongylus spp.; treatment
* fenbendazole or levamisole have efficacy (off‐label usage)
40
Crenosoma spp.; general features; type of worm, hosts, infection site
* metastrongylid nematodes
* true lungworm of dogs, wolves, foxes, racoons
* requires molluscan intermediate host
* infects small bronchioles and alveoli
41
Crenosoma spp.; Morphology ‐ Adults
* small (<16 mm) slender adults
* anterior cuticle has prominent cuticular folds (crenations ‐ hence the name)
42
Crenosoma spp.; Morphology ‐ Larvae
* females deposit first stage larvae or thin‐ shelled eggs containing L1’s
* larvae found in feces
* detection by Baermann technique
43
Crenosoma spp.; life cycle
* larvae passed in feces infect snail/slug IH
* DH gets infected by eating snail or slug containing an infective L3 larva
* larvae migrate from stomach to lungs
* adults in bronchi and brochioles
* PPP ‐ 19 days (experimentally)
44
Crenosoma spp.; Pathogenesis/Lesions/Clinical Signs
* adults and released eggs/larvae give rise focal lesions
* heavy infections may give rhinotracheitis, bronchitis with or without nasal discharge
* larvae diagnosed in sputum or with Baermann
