Nematodes 2 Flashcards

1
Q

Ascarids: general features

A
  • LARGE (esp females)
    • males= 2 spicules & coilded tail
  • live in lumen (SI) gut content feeders
  • 3 large lips
    • esophagus may have ventriculus
    • +/- cervical alae
  • COMMON world wide
    • esp young animals
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2
Q

who produces this egg and how many?

A
  • Ascarids - thick shelled and highly resistant
  • a lot!! prolific egg layers (200,000 egg/day)
    • milky media
  • shed in feces & larva develops to infective stage inside egg & egg ingested
  • eggs are sticky
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3
Q

What is the general ascarid life cycle?

A
  • in environment (soil crucial for development) for 2-4 wks
  • direct LC w/ +/- transport host (earthworm)
  • egg laid in feces > larva develps to L3 in egg & egg ingested
    • free (L3) larvae penetrate SI/LI mucosa > enter portal venules to LIVER > LUNG> alveoli to bronchi- (HEPATOPULMONARY MIGRATION) > bronchi migration to trachea, pharynx and swallowed (TRACHEAL MIGRATION)
    • L4 reach SI about 2-3 wks post infection > adult in SI and lay eggs
  • PPP= 2 mo
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4
Q

What aspects of the ascarid life cycle are important to control?

A
  • young animals are clinically affected
  • older animals are reservoirs
    • strong exposure = induced immunity = lower burden
  • eggs are very resistant
  • zoonosis - humans are also definitve hosts
    • adults: ascaris suum - pig/human
    • larvae: toxocara canis and T. cati - ocular and visceral migrans
    • larvae: anisakids - eosinophilic gastritis (fish borne- consuming raw fish)
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5
Q

what is the ascarid that infects pigs? LC pattern?

A
  • Ascaris suum
  • Ascaris lumbricoides
    • site: SI
    • LC: direct +/- paratenic hosts
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6
Q

Pathogenesis of Adult Ascarids

A
  • less pathogenic
  • production & economic losses
    • luminal feeders, malnutrition, reduced weight gain, stunting (kids)
    • worms may secrete anti-pepsin and anti-trypsin enzymes
  • Clinical disease
    • diarrhea, colic, vomiting
    • intestinal ileus, blockage, rupture > peritonitis
    • bile duct occlusion (cholestasis)
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7
Q

Pathogenesis of what nematode & life stage?

A
  • larval ascarids
  • HPM - mechanial & inflammatory damage to organs
    • milk spots in pigs
  • “eosinophilic” pneumonia - calves, pigliets, pups, kittens, foals (asthma-like)
    • predispose to viral and bacterial pneumonia
  • A. suum in cattle lungs causes anaphylaxis
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8
Q

are ascarids host specific?

A

No, larval stages will undergo extensive migration

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9
Q

Ascarids of the horse?

A

Parascaris equorum

*SI and direct LC - very large worms

* peak egg counts in foals 15-18 wks old

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10
Q

Ascarids of dogs & cats

A

Toxocara canis - dog

Toxocara cati- cat

Toxascaris leonina - dog & cat

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11
Q

Toxascaris leonina (arrow worm)

  • Life cycle & host
A

cats and less frequently dogs

  • soft shelled eggs
  • larvae hatch and penetrate SI mucosa > L4 > adult
  • no migration
  • Paratenic hosts - rodents, arthropods, lizards
  • PPP= 7-10 wks
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12
Q

Toxocara canis

  • LIFE CYCLE
    • important migration/transmission patterns
A
  • egg thick shelled & sticky (adverse to environment)
    • 2 moults w/in egg - L3 infective stage in egg
  • egg ingested by a pup
    • hatch in SI > hepatopulmonary migration & moult L4 > tracheal migration > final moult in SI and lay eggs
    • PPP= 4-5 wks
    • as dogs mature tracheal migration less frequent
      • larvae pass though lung capillaries and distribute to other organs > encyst and developmentally arrest
      • female animals: somatic larvae activate and migrate in last weeks of pregnancy
        • transplacental migration - carried through umbilical vein to fetal liver> lungs
          • after birth: larvae undergo tracheal migration & develop to adults
            • pups pass eggs at 3 wks old
        • transmammary migration - infect while suckling and larva devlop to adult in SI
  • Paratenic host: mice, rats, lizards, arthropods
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13
Q

Who is most likely to have severe infection with Toxocara canis?

A

young, unweaned pups

*clinical signs can develop as young as 3 wks (coughing, failure to grow, pot belly)

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14
Q
A

A. Ascaris - pigs/humans

B. toxocara spp. - dogs, cats, cows

  • dark circular rough

C. toxascaris spp. - dogs/cats

  • smooth oval

D. parascaris equorum - horses

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15
Q

Toxocara cati

  • Life cycle
A
  • common parasite of cats
  • direct life cycle with traceal migration (paratenic hosts and transmammary migration possible)
    • trans colostral infection occurs
    • no transplacental
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16
Q

Nematode identification & preferred host?

A

A. Toxocara cati - cats

B. Toxocara canis - dogs

C. Toxascaris leonina- dogs/cats

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17
Q

who am I?

A

Toxocara canis & (bottom right - T. cati)

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18
Q

Public health significance of Toxocara spp.?

A

Visceral larval migrans

  • embryonated egg ingested by humans (18 mo - 4 yrs)
  • marked immune response to somatically migrating larvae (encapsulated in tissue for years)
  • clinincal signs
    • urticaria, fever, hepatomegally, eosinophilia, cough
    • usually self limiting
      • +/- eosinophilic encephalitis, myocarditis

Occular larval migrans

  • caused by single larva
  • 8yrs- adult
  • fibrotic lesions in retina > vision loss
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19
Q

Ascarids of ruminants

  • main route of infection?
  • Life cycle?
  • epidemiology?
A
  • Toxocara vitulorum
    • not common
    • excusively calves as transcolostral is the main route of infection
    • Direct LC- no tracheal migration
      • milk, muscles, lungs, liver > SI of calf (L3>L4>adult > eggs)
    • limited to north east coast of AU
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20
Q

Ascarids of birds & their identifying features

A
  • Ascaridia spp (small intestine)
    • esophagus club shaped
    • adult: 12 cm long
  • Heterakis spp (ceca)
    • esophagus with posterior bulb
    • adult: 1.5 cm long

** eggs identical & both males have precloacal suckers

-chickens, turkeys, geese, ducks

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21
Q

Life Cycle of Ascarida galli and Heterakis gallinarum

A
  • Ascarida galli (PPP- 6 wks) & Heterakis gallinarum (PPP= 3wks)
    • L3 develops in thick egg - 2 wks
    • fowl ingests egg > hatch in SI (Heterakis- larva migrate to cecum)
    • larva enter SI mucosa and moult 2x > reemerge to lumen and adults develop
    • quick immunity
    • transport hosts = earthworms
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22
Q

Pathogenesis of Ascarida galli

A
  • chicks 4-8wks old (older birds resistant)
    • larvae moult in SI wall
      • synchronous eruption > enteritis and hemorrhage
    • adult worms: intestinal occulsion
    • nutritional deficiency
      • increased susceptibility to disease
      • poor growth
        *
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23
Q

Pathogenesis of Heterakis gallinarum

A
  • little pathogenic significance (+/- cecal thickening) : LI
  • tranmission of Histomonas meleagridis through egg
    • protozoa not pathogenic to chickens but cause “black disease” in turkeys
    • necrotizing typhlitis and focal necrosis of liver
    • ** dont minx chickens and turkeys
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24
Q

How do you control this ascarid?

A
  • A: Ascardia galli
  • B: Heterakis spp
  • C: eggs are identical - compare to thin shelled strongylid eggs

Control extensive animals - challenging (rotate pastures esp young)

Control intensive animals

  • hygiene - prompt removal of feces
  • decontaminate with bleach
  • rodent/past control (cockroaches)
  • do not feed raw meat
  • treat nd quarantine new arrivals
  • deworm regularrly (esp young)
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25
Q

Treatment of ascarids - general

A

BZs (fenbendazol) & MLs (ivermectin) most common

  • water soluble drugs will kill ascarids in gut lumen
    • pyrantel
  • lipid soluble drugs will kill migrating larvae
    • Fendendozole
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26
Q

treatment of ascarids in an outdoor system

A
  • treat growers at 8 wks - to prevent high shedding in environment
  • treat sows and boars every 3 mo
  • treat sows 7-14 d prior to farrowing
  • test herd every 6 mo

in feed- levamisole, ivermectin, fenbendazole, morantel, piperazine

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27
Q

Treatment of ascarids in horses- who is most likely to have a heavy infection? How often do you treat? management?

A
  • foals and yearlings
  • deworm every 2 mo (rotate ML, BZ and pyrantel) for their first year of life
    • start at 2 mo/old
  • rotate pastures for mares and foals annually & fecal hygiene
  • FEC prior to deworming spring & autumn in adults
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28
Q

Treatment of Toxocara canis: pups vs adult dogs?

A

Pups

  • 2wks old q2wks until 10 wks old
  • deworm mother at same time

Adults

  • fecal examination 1-2x/yr
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29
Q

How do you treat ascarids during pregnancy?

A
  • does NOT kill arrested larvae - only kills when in circulation
    • want to prevent TP and TM to pups
  • Fenbendazole
    • 50mg/kg DAILY PO from D40 or pregnancy to +14d post whelping
    • off lable use
  • Selamectin
    • topically 40d and 55d of pregnancy
    • off lable use
  • Moxidectin
    • topical
    • labelled use
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30
Q

Treatment of Toxocara cati? Kittens vs adult cats?

A

Kittens

  • 3wk old > q2wks > until 8wks old > then monthly until 6mo

Adults

  • fecal exam and deworm according to risk (roaming/indoor)
  • apply selamectin, moxidectin and emodepside topically to mother at end of gestation
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31
Q

Life cycle of Anisakidae

A
  • indirect (stomach-SI)
    • need marine mammal to complete life cycle
    • acquired though L3 ingestion: raw or undercooked/smoked fish
  • zoonotic!
  • control: cook well or freeze >7d
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32
Q

Pathology of Anisakidiasis

A
  • invasive (1hr -2days)
    • penetrate gut mucosa
    • eosinophilic gastritis
    • acute vomiting and dxa
    • allergic respose to antigens
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33
Q

Where do you find the adult stage of oxyurids/pinworms?

A
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34
Q

Cecum, colon and rectum

***Direct life cycle and HIGHLY HOST SPECIFIC

A
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35
Q

Typical pinworms of Horses and Mice

A

Horses: Oxyuris equi

Mice: Syphacia obvelata

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36
Q

General life cycle of Oxyurids (example: Oxyuris equi)

A
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37
Q

How do you diagnose this nematode?

A

Oxyuris equi- oval shaped egg with mucus plug > use sticky tape method around anus

  • females can be 7.5cm long
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38
Q

Pathogenesis and clinical signs of Oxyurids (pinworms)? What oxyurid is most likely to cause clinical disease?

A

clinical signs

  • usually asymptomatic or mildly pathogenic
    • DD: ectoparasites
  • Syphacia obvelata (mice)
    • most commonly associated with disease
      • anal puritis + self multilation
      • dxa/ intussusceptions/ impactions
      • rectal prolapse
      • weight loss
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39
Q

How do you treat this nematode? control?

A

Syphacia obvelata- mice

  • challenging to control
    • bc eggs are so sticky
  • long course fenbendazole or piperazine in water, ivermectin
  • reduce overcrowding (esp in research lab)
  • HIGH STANDARD OF HYGIENE
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40
Q

Diagnosis? Where do you find this worm?

A. B.

A
  • Found in cecum or colon - both in mice
  • translucent hair like worm (male =1 mm & females 11 mm)

A: Syphacia obvelata

B: Aspiculuris tetraptera

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41
Q

3 features of Spiruids

A
  1. +/- 2 lateral lips
  2. esophagus with anterior muscle and posterior glandular sections
  3. unequal spicules
  4. eggs with L1 (oviparous) or L1 (viviparous)
  5. indirect LC - arthropod IH
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42
Q

Non-Filarid spiruids of horses & Life Cycyle

A

Habronema microstoma (IH: stomoxys) & Habronema muscae (IH: muscae)

  • near margo plicatus > no nodule formation
    • small ulcerations > hyperplasia and hyperplasia of mucus secreting cells

Draschia megastoma

  • IH: musca fly
    • chronic eosinophilic gransulomatous nodule (1-10cm) > ulcer
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43
Q

Apart from the stomach where else do you see “habronemiosis”?

A
  • Pulmonary
    • multiple abscesses filled with necrotic debris > contian parts of nematode larvae
    • eosinophilic inflammation
  • Cutaneous
    • around face, legs, mucosal areas
    • risk of secondary infection if not treated
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44
Q

Diagnosis of A & B…more pathogenic?

A

A: Draschia megastoma

  • big mouth -funnel shapped buccal capsule
  • causes majority of disease

B: Habronema spp.

  • cylindrical buccal capsule
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45
Q

After using a saline solution fecal floatation (SG > 1.20) on horse feces, we found a few of these eggs (may not see a lot bc adults are within a granulomatous nodule). What is this nematode and how will we treat?

A

Habronema spp.

  • oxfendazole, moxidectin
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46
Q

How do you treat cutaneous habronemiosis? Chronic infections? How do you control?

A
  • cutaneous lesions (L3) > treat topically
    • ivermectin
    • abamectin
    • moxidectin
  • chronic infections
    • corticosteroids
    • surgical debridement
    • MLs
    • cryotherapy

Control

  • fly control - dispose manure
  • face/eye masks
  • screens in stables
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47
Q

2 main stomach worms of dogs

A

Spirocerca lupi and Gnathostoma spinigerum

48
Q

3 main stomach worms of cats

A

Physaloptera praeputialis

Cylicospirura felineus

Cylicospirura ubequalis

49
Q

Life Cycle of Spirocerca lupi

A
  1. Ingest L3 with dung beetle > emerge in stomach and penetrate gastric arteries > aorta
  2. form nodules in aorta > L4> migrate from aorta to esophagus
  3. nodules in esophagus > adults emerge and lay eggs in esophagus
  4. eggs passed in feces (L1 inside egg) > ingested by dung beetle
50
Q

Dog in tropical/subtropical region presents with regurgitation, vomiting and weight loss. A few eggs were found in the feces (see picture). There are granulomas in the esophagus. What nematode is this and how do you treat?

A

Spirocerca lupi

  • hard to treat because adults in granulomas (also risk of aneurism from migration from aorta to esophagus > rupture and hemothorax)
  • Prophylactic : moxidectin (label use)
  • off label: doramectin, moxidectin and milbemycin for prolonged periods (up to 6 mo)
  • surgical removal of fibrosarcoma
  • air feeding - sitting upright
  • disallow scavenging/free roaming
51
Q

Gnathostoma Life Cycle:

A
52
Q

A dingo presents with gastritis, vomiting and anorexia, the fecal float had uni-plugged eggs. Will other dingos in the pack show the same clnical signs? What is the pathogenesis and how do you treat?

A

Gnathostoma

  • can be asymptomatic
  • adults embedded in submucosal gastric nodules with tract leading to gastric lumen
    • +/- secondary infection
    • adults appear dark red from ingesting blood - although anemia not common
    • adults also have cephalic bulb
  • treatment
    • ivermectin or moxydectin may be efficacious
53
Q

What is the main concern with Gnathostomes?

A

Human infection (zoonosis)

  • fish borne (under cooked)
  • DH= dogs, cats, pigs
  • L3 penetrate stomach and undergo larva migrans > highly puritic subcutaneous swellings
54
Q

Spiruid that is rarely pathogenic found in pigs and IH is an arthropod?

A
  • Gnathostoma hispidium
    • usually found in extensive farms
55
Q

Spiruid that is rarely pathogenic found in pigs and IH is a dung beetle?

A

A: Ascarops stongylina

B: Physocephalus sexalatus

56
Q

Clinical signs: blepharitis and mild to severe conjunctivitis, keratitis (opacitiy, ulceration, perforation)

A

Thelazia spp.

  • Don’t burrow
  • most commonly seen in cattle
57
Q

Spiruids of Cattle and their predilection?

A

A: Gonglyonema pulchrum - esophagus

B: Gonglyonema verrucosum - rumen

58
Q

Spiruids of Birds- predilection and IH

A
  1. Gonglyonema sp.
    • crop
    • IH: cockroach
  2. Acuaria spp. (picture)
    • proventriculus
    • IH: grasshoppers, beetles
  3. Tetrameres spp.
    • ventriculus
    • IH: grasshoppers, beetles
  4. Oxyspirura mansoni
    • conjunctival sac
    • IH: cockroach
59
Q

Name 5 features of Filarioidea

A
  • adults NOT in GI tract
    • liquid diet (blood/lymph)
    • majority vector borne - circulatory is a closed system
  • primarily viviparous > L1 = mff
  • indirect LC
    • IH= arthropod (mosquitoes, ticks, flies, flea)
  • female adults long
60
Q

General life cycle of filaria

A
  • L3 injected into host from Simulium bite
  • L3 in subcutaneous tissues > adults in nodule
  • L1 released in skin, lymphatics and blood
  • black fly takes blood meal and ingests L1
61
Q

Key features of filarioidea in humans

A
  • black flies as vector
  • onchocerca > river blindness
  • adults > nests in SC tissue
  • mmf
    • pruritic dermatitis (lizard skin)
    • die in eye = inflam> blindness
62
Q

What is culicoides (biting midge) a vector for in horses? What is the pathogenesis in the definitive host?

A
  • Onchocerca cervicals (adults in nuchal ligament)
    • edema & granulomatous nodules/fibrosis
    • “Queensland Itch”
  • Onchocerca reticulata (adults in flexor tendons)
    • mobility problems

Pathogenesis

  • dying mff in dermal tissue > puritic dermatitis
  • skin of ventral midline, neck, chest, forelegs
    • scales, crusts, ulcerations, alopecia
63
Q

How do you diagnose and treat Onchocerciasis?

A
  • skin snip or biopsy
    • mmf rarely in blood unless high burden
  • Ivermectin & moxidectin
    • highly efficacious against mff
  • permethrin pour on (reduce vector)
64
Q

3 Filarioidea of cattle with Culicoides vector and their predilection sites - what is the consequence?

A
  • Onchocerca gutterosa > nuchal lig
  • Onchocerca gibsoni > dermal brisket tissue
    • carcass condemnation
    • treat: ivermectin/moxidectin
  • Onchocerca lienalis > gastrosplenic ligament
65
Q

Heamatobia irritans (buffalo fly) is the vector for what filarioid of cattle? Predilection and path?

A
  • Stephanofilaria stilesi
    • adults live in dermis
      • lesions ventral thorax and abdo
        • ulcerative and exudative
        • chronic > hyperkeratiosis
          • secondary infection
    • treat with topical moxidectin
66
Q

What cattle filarioid has a mosquito as a vector and is common in Northern Australia?

A
  • Setaria spp.
    • large nematode
      • lies free in abdo cavity
      • mff in blood
67
Q

How do you diagnose filarioids in cattle?

A
  • skin snip
    • macerate in warm saline
    • stephanofilaria mff tiny (~50um)
    • onchocerca and setaria mff (>230um)
    • mff in blood = setaria
68
Q

3 control measure of Stephanofilaria

A

(common in northern and costal northern NSW)

  • non chemical control
    • walk through fly traps
      • buffalo flies cannot live off host for 1-2hr
    • dung beetles
  • synthetic pyrethroids or OPs
    • pour on, ear tags, dips
  • vector control
    • oral ivermectin
69
Q

Main Filarioids of dogs and cats

A
  • heartworm - dirofilaria immitis
  • subcutaneous nodule worms
    • dirofilaria repens
      • looks like D. immitis
    • Acanocheilonema spp
      • transmitted through fleas
  • lymphatic filaria
    • brugia spp
70
Q

Life Cycle of canine heartworm

A
  • mff in blood > ingested by mosquito
    • moult to L3 - 2-3 wks
  • L3 infective stage transferred to host
  • moult to L4 > migrate to chest muscles and abdo (9d to 2 mo)
  • moult to adult at 2-4 mo > migrate to pulmonary artery
  • in right ventricle after 3 mo

PPP= 6-7 mo

lifespan = 5-8 yrs

71
Q

Pathogenesis of right sided congestive heart failure from heartworm in dogs

A
  • presence of worm
  • proliferative endarteritis of pulm aa. > decreased compliance
    • PLUS thrombosis and thromboembolism
      • worms cause turbulence
      • red cells smash and platelets coagulate
  • pulmonary hypertension
    • heart pumps harder and cardiac mm thickens
  • ^ afterload for RV = RV hypertrophy and dilation
  • RSCHF and caval syndrome
    • loss of blood flow
    • blood pooling and edema in chest
    • organ failure
72
Q

What nematode causes pulmonary arterial disease

A

dirofilaria immitis

  • several worms or 1 knotted
  • thrombosis
  • inflammation
  • leakage
  • can be coughed out
  • +/- fluid in chest
73
Q

What are the 2 sequelae of caval syndrome caused by heart worm?

A
  • tricuspid valve insufficency
    • turbulence
      • mechanical hemolysis
        • jaundice
        • anemia
        • hemoglobinuria
        • glomerulonephropathy
  • obstuction of bloof flow
    • decreased cardiac output
      • congestion (ascites)
        • collapse of peripheral circ.syst
          • circulatory short/death
74
Q

What are the 4 classes/clinical stages of a heartworm infection

A

Class 1

  • early infection - asymptomatic
  • mild disease - cough

Class 2

  • moderate disease - pulmonary arterial disease
    • cough, exercise intolerance, abnormal lung sounds

Class 3

  • severe disease - heart murmur, coughing blood, ascites > heart dysfunction
  • guarded prognosis

Class 4

  • caval syndrome - heart failure
  • jaundice, hemoglobinurea, cardiac murmur
  • very poor prognosis
75
Q

what are 4 ways to diagnose heartworm in dogs

A
  1. history and clinical signs
    • endemic area
    • pups at least 6-7 mo old
  2. detection of mff in blood
    • unstained freshwater smear or buffy coat
    • concentration methods
      • knotts test
      • filtration
  3. ELISA to detect adults
    • Antigen only detected from adult FEMALES
  4. up to 30% may be occult
    • no mff in circulation
      • males, senile and immature dont produce mff
76
Q

Dirofilaria immitis vs Acanthocheilonema reconditium

A
  • use acid fast to stain
    • D. immitis
      • straight body and tail
      • clumpy and granular in stain
    • A. reconditium
      • curved body and hooked tail
      • diffuse stain
      • non-pathogenic
      • flea borne dermal filaria
77
Q

What does the anitgen heartworm test detect?

A
  • adult female worms
    • at least 3 females for consistent result
    • higher specificity
78
Q

What is the positive predicitive value

A

the number of results that are actually positive

79
Q

During days 0-70 of heartworm infection what stage are you killing and what do you use?

A

L3-L4

use monthly MLs (moxidectin, ivermectin, milbemycin)

80
Q

When can you kill heartworm adults and what compound are you using?

A

D 120-180 post infection

use an adulticidal - melarsomine

81
Q

What is the first step in treating a heart worm infection?

A
  • assess risk (class 1= low class 3/4= high)
  1. Strict rest - slow HR at least 4 wks post treatment
  2. corticosteroids
    • prednisolone: pre and 1 month post adulticide
    • reduce inflammation from dying worms
  3. doxycycline for 3-4 weeks
    • kill endosymbiota (worms bring in gram - bacteria)
82
Q

(step 2) how do you prevent new infections of heartworm and kill mff?

A

MLs (monthly or long term injectable) - on D0

  • kills circulating mff over 7-10d
    • dont want to kill too quickly > anaphylaxis
  • over longer term - 4-12 mo
    • kill juvenile and adults infertile
  • prevents new infections of L3
83
Q

How can you kill adult heart worms? when do you repeat the antigen test?

A
  • adulticide - melarsomine
    • deep IM lumbar injection
      • kills worms over 4 mo old
    • first injection
      • 2nd injection 1 mo later
      • 3rd injection 24 hrs later
  • repeat antigen test at 6 mo (after 3rd injection)
84
Q

What is the risk of surgical removal of heart worms when in class 4 (caval syndrome)

A
  • the heart is still in failure
85
Q

If melarsomine isnt available- how do you kill heartworm?

A
  • ML and doxy (1 mo on 2 mo off) over 9 -12mo
  • caution
    • clinical signs may worsen
    • resistance?
    • dont know when adults are dying
86
Q

name 4 chemo-prophylactic drugs for heartworm

A
  1. revolution
    1. selamectin
  2. proheart
    1. moxidectin
  3. advocate
    1. imidacloprid
  4. HeartGard
    1. ivermectin/pyrantel
87
Q

Life Cycle of Heartworm infection in cats

  • what are some main differences to dogs
A
  • less prevalent
  • most worms do not mature
  • prolonged PPP= 8 mo
  • no mff
  • shortened survival
  • aberrant migration (CNS)
  • smaller burden can cause disease
88
Q

clinical signs of heartworm in cats

A
  • Heartworm Associated Respiratoy Disease
    • acute
    • pulm arteriole hypertrophy
    • pulmonary edema
    • tachypnoea
    • cough
    • vomiting
    • weight loss
  • embolus of dead worms
    • collapse - death
89
Q

how does heartworm associated respiratory disease (HARD) develop in cats

A
  • juvenile worms in pulm a (3 mo)
    • eosinophilic vasculitis and pneumonitis (pulm edema)
      • compromise to pulm function (hypoxemia, cough)
  • worms mature to adults
    • asymptomatic or cough, dyspnea, vomit, neurologic
      • death, embolisation
        • acute resp distress, death
90
Q

When can you perform the antibody test for heartworm in cats? What other diagnositics?

A
  • as early as 8 wks post infection
    • need at least >1 female adult
  • radiographs
  • echocardiogram
    • parallel lines -echogenic cuticle of worm within main or right lobar pulm a.
  • lung lavage
    • rule out Aelurostrongylus
      • trial on moxidectin
91
Q

How do you treat heartworm in cats?

A
  • prednisolone
  • sx
  • ****adultacides contraindicated
92
Q

What are features of male and female enoplids?

A
  • male
    • single spicule or no spicule (trichinella)
  • female
    • oviparous (thick lemon shaped eggs- bipolar plugs)
    • viviparous L1= infective stage
93
Q

What kind of nematode?

A

enoplids

  • trichinella
    • food borne zoonosis
  • trichuris (whipworm)
    • humans, dogs, pigs
  • capillaria (hairworm)
    • poultry
94
Q

How do humans get Trichinellosis?

A
  • ingestion of undercooked meat
    • domestic pigs > T. spiralis (typically encysted)
    • hunted game meat
      • feral pig, cougar, bear, croc
95
Q

Is trichinella present in australia?

A

no - or unreported (only present in tasmania)

96
Q

What is the life cycle of trichinella?

A

domestic cycle

  • eat scraps
  • larvae travel to muscle and encycst

sylvatic cycle

  • predation/scavenge

DH1 = ingestion L1 > SI moult to adult > L1 enter circultaion > muscles (encyst) > DH2 ingest L1 encysted mm > SI to adult > circulation > L1 in mm

97
Q

What are the 2 groups of trichinella sp?

A

encapsulated

  • mammals only
  • L1 surrounded by collagen capsule and “nurse cell” within muscle tissue
  • no inflam response

non-encapsulated

  • mammals, birds, reptiles and marsupials
  • L1 free in muscle tissue
98
Q

What species of trichinella? encapsulated or not? What is the primary host and distribution?

A

Top

  • T. spiralis
    • domestic pigs
    • encapsulated
    • temperate and tropical regions (not AU)

Bottom

  • T. pseudospiralis
    • tassie devils
    • non encapsulated
    • tasmania
99
Q

What are the clinical signs of Trichinellosis?

A

Animals: NONE

Humans

  • per acute - intestinal phase (L1)
    • dxa, abdo pain, vomit, fever
  • acute (muscle invasion): 2-8 wks
    • eosinophilia- elevated CK
    • myalgia
    • vasculitits, cardiac/neuro complications > death
100
Q

How do you kill trichinella spp? Diagnose?

A

Treat: corticosteroids and albendazole to kill L1

Diagnose: serology, biopsy, PCR, histo with meat inspection

101
Q

Why does poverty lead to increased rates of trichinellosis?

A
  • cannot afford to feed pigs> roam and scavenge
  • backyard slaughter
  • lack of meat inspection
    • smoked rather than properly cooked meat
102
Q

When prevention and control practices can reduce cases of trichinellosis?

A
  • proper animal husbandry
    • prevent scavenging
    • certificate of trichinella-free produciton
  • meat preparation
    • cook over 77 C
  • meat inspection and certification
    • freezing
      • -20C for 2 weeks - T.spiralis
      • all exported farmed pork freeze certified
    • testing: artifical digestion methods and visualise larvae
      • look for encapsulated and unencapsulated forms
      • 5g of diaphragm from “high risk” meat
103
Q

What is significant about this egg?

A

Trichuris spp.

  • eggs take 3 weeks to embryonate
  • eggs highly resistant (4-5 yrs in environment)
104
Q

general life cycle of Trichuris spp? (whipworm)

A

ingest egg with L3 > larvae hatch in SI > bury schistosome in mucosa of cecum- feed on tissues and interstitial fluid > unembryonated eggs released in feces

PPP= 10-12 wks

105
Q

What host does each Trichuris species belong to?

  1. T. trichura
  2. T. vulpis
  3. T. suis
  4. T. campanula, T serrata
  5. T. discolor, T. globulosa
  6. T. ovis, T skrjabini
A
  1. T. trichura > human +++
  2. T. vulpis > dog +++
  3. T. suis > pig ++
  4. T. campanula, T serrata > cats +
  5. T. discolor, T. globulosa > cattle +
  6. T. ovis, T skrjabini > sheep +
106
Q

With a heavy load of Trichuris spp (especialy humans, dogs and pigs) what clinical signs do you expect?

A
  • congestion, submucosal edema, necrosis, fibrosis
  • watery and mucoid dxa, frank blood
  • tenesmus
  • rectal prolapse
107
Q

A dog presents with hyponatremia and hyperkalemia (similar to addisons disease)…what nematode causes this?

A

Trichuris vulpis

108
Q

How do you treat a whipworm infection?

A
  • oxantel & MLs & BZs
  • with pyranel pamoate salts

fecal oral control important > hygiene and lower stocking density

109
Q

What are 2 main hairworms that are pathogenic in poutry? What are their predilection sites?

A
  • Capillaria annulata : crop
  • Capillaria caudinflata : SI
110
Q

What is the behaviour of Capillaria eggs in the environment?

A

they embryonate in soil or in earthworms

  • eggs look like trichuris spp.
111
Q

Clinical signs of light vs heavy infection with Capillaria spp in chickens?

A

light

  • poor weight gain, production loss

heavy

  • catarrhal thickening, diptheritic inflammation of esophagus or crop
  • hemorrhagic enteritis
  • high mortality
112
Q

What are the main features of acanthoceohala? (thorny headed worms)

A
  • dioecious (male and female)
  • cylindrical and large
  • proboscis with hooks and spines (pathogenic effect)
  • no digestive tract
113
Q

General life cycle of acanthoceohalans?

A
  • eggs shed in feces (eggs live for a long time)
  • eggs ingested by intermediate host
    • Arthropod IH: dung beetle, cockroach etc
    • acanthor> cystacanth
  • cystacanth stage ingested by definitive host
    • proboscis jams into intestinal wall (SI)
114
Q

What is the acanthoceohalan of pigs and how do you treat?

A

Macracanthorhynchus hirudinaceus

  • absorb nutrients along the body
  • clinical signs : malnourishment, granuloma at site of attachment, enteritis +/- perforation
  • *** egg can look like a nematode egg- ciliated larva inside

Treat: ivermectin, levamisole, BZs

115
Q

What is the acanthoceohalan of cats and dogs?

A

Oncinola spp

  • common in SI of feral or stray cats/dogs
  • usually asymptomatic +/- enteritis
116
Q
A