6.10 – Strongylid Nematodes – Flashcards

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
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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
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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)
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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
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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
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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
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7
Q

Ancylostoma caninum; Morphological Features ‐ eggs

A
  • typical morulated egg (“hookworm egg”), oval and <70 μm in length
  • Features are: ‐ thin‐shelled ‐ morulated
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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
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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
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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
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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
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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
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13
Q

Hookworms ‐ Ancylostoma tubaeforme; pathogenicity

A
  • little known but presumed to be similar to canine hookworm
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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])
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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
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16
Q

Hookworms ‐ Uncinaria stenocephala; egg morphology

A
  • typical morulated egg (“hookworm egg”), oval, >70 μm in length
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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
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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
Q

Muellerius capillaris; Lesions/Clinical Signs

A
  • later infections show raised regions on the lung
  • some areas may calcify
  • goats may show more serious pneumonia but this may be multifactorial
26
Q

Muellerius capillaris; treatment

A
  • no registered compounds – may wish to try compounds such as levamisole or ivermectin registered against other nematodes in these hosts
27
Q

Filaroides and Oslerus spp.; general features; sites of infection, hosts

A
  • metastrongylid nematodes ‐ true lungworms
  • Oslerus osleri (= Filaroides osleri )
    ‐ tracheal or bronchial infections
  • Filaroides hirthi
    ‐ terminal bronchioles or alveoli
  • infects domestic or wild canids
28
Q

Filaroides and Oslerus spp.; morphology

A
  • 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
Q

Filaroides and Oslerus spp.; life cycle

A
  • 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
Q

Oslerus osleri PPP

A
  • Oslerus osleri ‐ 10 weeks
31
Q

Filaroides hirthi PPP

A
  • Filaroides hirthi ‐ 5 weeks
32
Q

Filaroides and Oslerus spp.; Pathogenesis/Lesions/Clinical Signs

A
  • 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
Q

Filaroides and Oslerus spp.; treatment

A
  • albendazole or levamisole have efficacy (off‐label)
  • F. osleri nodules may be removed surgically
34
Q

Filaroides and Oslerus spp.; diagnosis

A
  • 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
Q

Aelurostrongylus spp.; type of worm, hosts, site of infection

A
  • metastrongylid nematodes
  • true lungworm of cats
  • requires intermediate host
  • infects small bronchioles and alveoli
36
Q

Aelurostrongylus spp.; morphology

A
  • small (10mm) slender adults
  • larvae have a small bent tail with a dorsal spine
37
Q

Aelurostrongylus spp.; Life Cycle

A
  • 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
Q

Aelurostrongylus spp.; Pathogenesis/Lesions/Clinical Signs

A
  • 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
Q

Aelurostrongylus spp.; treatment

A
  • fenbendazole or levamisole have efficacy (off‐label usage)
40
Q

Crenosoma spp.; general features; type of worm, hosts, infection site

A
  • metastrongylid nematodes
  • true lungworm of dogs, wolves, foxes, racoons
  • requires molluscan intermediate host
  • infects small bronchioles and alveoli
41
Q

Crenosoma spp.; Morphology ‐ Adults

A
  • small (<16 mm) slender adults
  • anterior cuticle has prominent cuticular folds (crenations ‐ hence the name)
42
Q

Crenosoma spp.; Morphology ‐ Larvae

A
  • females deposit first stage larvae or thin‐ shelled eggs containing L1’s
  • larvae found in feces
  • detection by Baermann technique
43
Q

Crenosoma spp.; life cycle

A
  • 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
Q

Crenosoma spp.; Pathogenesis/Lesions/Clinical Signs

A
  • 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