Nematodes: lungworms Flashcards
Lungworms affect what animal species?
All sorts!
Diff spp. of lungworm affect diff animal species.
Name the 3 main families to belong to SuperFamily Metastrongyloidea.
Metastrongylidae
Protostrongylidae
Angiostrongylidae
Bovine lungworm infection in caused by what species of nematode?
Dictyocaulus viviparus
Common names for bovine lungworm disease (5)
dictyocaulosis
Parasitic bronchiolitis
Parasitic pneumonia
Verminous pneumonia
“Husk” or ”Hoose”
Geographical distribution of Dictyocaulus viviparus.
And seasonality?
bovine lungworm
worldwide
In climates with heavy rainfall
Endemic areas in northern hemisphere
Symptoms seen from July to September
Signs of Dictyocaulus viviparus is usually seen in what age and breed demographic?
bovine lungworm
Calves in their first grazing season.
Dairy and dairy-cross breed or autumn-born beef calves in early summer.
Parasitic bronchitis from bovine lungworm in Adults is only seen in 2 cases:
- Herd/age phenomenon - failed to acquire natural immunity+heavy infection
- Individual phenomenon - penned in heavily contaminated calf paddock
Describe Immunity toward bovine lungworm:
Patent infection lasts 2-3 months due to immunity (otherwise is longer).
Re-infection important to maintain immunity
Older cattle with lungworm typically have no clinical signs
Bovine lungworm survival strategies in endemic areas:
- Fungus Pilobolus (image) helps in larva distribution
- Mechanical transmission: boots, feet, birds
- Paratenic hosts (act as a reseroir)
- Overwintered L3 from autumn to late spring
- Carrier animals with inhibited worms in bronchi (yearlings)
Morphology of bovine lungworms.
Threadlike adults With small buccal capsule
Adult 4-8cm - Well developed bursa - Two short spicules
L1 has granular appearance, 300–360 μm
To distinguish from sheep lungworm D. filaria:
Has an anterior knob
Life cycle of bovine lungworm/ Dictyocaulus viviparus.
Direct
L3 infective and ingested
In the host:
Larva travels to lungs & alveoli through lymph, blood by 1 week after infection.
Adults in bronchi, trachea
Eggs produced in lungs
Ovoviviparous - the larvae hatch very fast
L1 travels to trachea, coughed up, swallowed to intestines, end up in feces.
Outside:
Develops in 4 - 12 days
Larva distributed with fungus spores (Pilobolus)
Prepatent period: 3-4 weeks, 21 days
Patency: several years
Pathogenesis and clinical signs of bovine lungworm/ Dictyocaulus viviparus.
Four stages, describe the 1st.
- Penetration phase (day 1-7 pi)
- Larvae migration - no signs
(2. Prepatent phase (day 8-25 pi) follows
- Larvae develop in the lungs
Signs: cough, increased respiratory rate)
Pathogenesis and clinical signs of bovine lungworm/ Dictyocaulus viviparus.
Four stages, describe the 2nd.
- Prepatent phase (day 8-25 pi)
- Larvae develop in the lungs
* haemorrhages
* necrosis
* alveolitis
* bronchiolitis
* bronchitis
Signs: cough, increased respiratory rate
(3. Patent phase (day 25-60) follows)
Pathogenesis and clinical signs of bovine lungworm/ Dictyocaulus viviparus.
Four stages, describe the 3rd.
- Patent phase (day 25-60)
Two lesions:
a) parasitic bronchitis - larvae in bronchial lumen
b) dark-red collapsed areas - aspiration of eggs and L1 into alveoli
- Pulmonary compression, emphysema,
granulomatous pneumonia, lobular atelectasis - caudal lobes
Signs:
increased respiratory rate, dyspnea
cough, crepitation, harsh sounds - air hunger
nasal discharge
emaciation - not feeding - growth depression
apathy (saw-horse position)
fever
deaths common (with sec. bacterial infection)
Pathogenesis and clinical signs of bovine lungworm/ Dictyocaulus viviparus.
Four stages, describe the 4th.
- Post patent phase (day 60+)
a) Recovery phase in untreated animals
b) In 25% of heavily infected animals a flare-up of clinical signs occurrs
Caused by:
1. Lung epithelialization, gas exchange impaired + interstitial emphysema, oedema
Aspiration of dead/dying larva into alveoli
- Sec. bacterial infection + imperfectly healed lungs
Mild – cough intermittently, when exercised
Moderate – bouts of coughing at rest, tachypnoea
Severe – severe tachypnoea, „air-hunger“, salivation, anorexia, sounds on auscultation, dyspnea. Reduced milk yield in older cattle
Name 3 small ruminant lungworms, english + latin.
Dictyocaulus filaria/ large lungworm
Protostrongylus rufescens/ red lungworm
Muellerius capillaris/ nodular lungworm
(Most common)
Most common small ruminant lungworm?
Muellerius capillaris/ nodular lungworm
Small ruminant lungworms:
Hosts and epidemiology
(final and intermediate hosts
Final hosts: sheep, goat, deer, wild small ruminants
Intermediate hosts: snails, slugs
Prevalence increases with age
D. filaria prevalence lower in adults though.
Ewes may carry hypobiotic larvae in their lungs during winter.
Usually mild with no clinical signs
Coughing and weight loss in heavy infections
Small ruminant lungworms:
Latin name and Morphology of small ru large lungworm.
Dictyocaulus filaria/ small ru large lungworm
D. filaria (4-10cm) - white
- L1 dark Food granules (intestine visible)
- Blunt tail in female L1
- Male spicules dark, stout
Small ruminant lungworms:
Latin name and Morphology of small ru red lungworm.
Protostrongylus rufescens/ red lungworm
P. rufescens (4-6cm) - reddish
- Conoid tail in female L1
- Small bursa in male
- Long comb-like spicules
Small ruminant lungworms:
Latin name and Morphology of small ru nodular lungworm.
Muellerius capillaris/ nodular lungworm
(Most common out of the small ru lungworms)
M. capillaris (12-25cm) - grey-reddish
- L1 S-shaped wavy tail in female
- Male tail spirally coiled
- Male bursa folded inwards, small
- Embedded deeply into lung tissue
identify
Protostrongylus rufescens/ small ru red lungworm
P. rufescens (4-6cm) - reddish
- Conoid tail in female L1
- Small bursa in male
- Long comb-like spicules
identify
Muellerius capillaris/ nodular lungworm
(Most common out of the small ru lungworms)
M. capillaris (12-25cm) - grey-reddish
- L1 S-shaped wavy tail in female
- Male tail spirally coiled
- Male bursa folded inwards, small
- Embedded deeply into lung tissue
Life cycle of D. filaria.
Dictyocaulus filaria/ small ru large lungworm life cycle similar to bovine lungworm life cycle.
Prepatent period 26-30 days (4+ weeks)
In the final host:
L3 travels to lungs - lymphatic-vascular migration route
Moults in lymph nodes and lungs
Female ovoviviparous – lays eggs in lungs and they hatch fast
L1 travels to intestines and passed in feces
In the intermediate host:
L1 penetrates the mollusc feet and develops to L3
Prepatent period: 5-9 weeks
Patency: several years
Life cycle of Fam. Protostrongylidae.
Indirect, infection from intermediate host with L3.
In the final host:
L3 travels to lungs - lymphatic-vascular migration route
Moults in lymph nodes and lungs
Female ovoviviparous – lays eggs in lungs and hatches fast
L1 travels to intestines and passed in faeces
In the intermediate host:
L1 penetrates the mollusc feet and develops to L3
Prepatent period: 5-9 weeks
Patency: several years
Name 3 spp. Pig lungworms.
Genus Metastrongylus
Species:
M. apri (elongatus)
M. pudendotectus
M. salmi
Final & Intermediate hosts of pig lungworms.
Final hosts: Pig, wild boar
Intermediate host: Earthworms
Geographical distribution & Localization: of pig lungworms.
Geographical distribution: worldwide
- High prevalence in wild boar & outdoor raised.
Localization: lumen of small bronchi and bronchioles (lung), posterior lobes
Pig lungworms Morphology.
Adults up to 6 cm White worms
Female posterior end hook-shaped
Females have prevulvar swelling
EGGS are passed in feces, NOT LARVAE.
Eggs larvated 55-61x45-50 μm
Rough shell
Pig lungworm species:
M. apri (elongatus)
M. pudendotectus
M. salmi
Life cycle of pig lungworms.
Indirect - Infection from intermediate host with L3.
In the host:
L3 travels to mesenteric lymph nodes
Further travels to heart and lungs
Larva settles in the bronchi and lays eggs
Eggs in the feces
In the intermediate host:
Ingests L1 or egg
L1 develops into L3
Development lasts 1 month
Lives for 7 years
Prepatent period: 4 weeks
Describe Horse lungworms and give spp. in latin.
Dictyocaulus arnfieldi
Final hosts: horses and donkey
Prevalent in donkeys, which serve as reservoir hosts. Worldwide distribution.
Localization:
Small and large bronchi
→ Dictyocaulosis in horses usually
only when kept together with
donkeys or on pasture which has been
grazed by donkeys.
White worms (3-9 cm)
Eggs: 74-96 x 46-58 µm,
thin-shelled, with larva
Describe the Horse lungworm life cycle.
Dictyocaulus arnfieldi
Final hosts: horses and donkey
Dictyocaulosis in horses usually
only when kept together with
donkeys or on pasture which has been
grazed by donkeys.
Clinical signs of lungworm infection in Sheep
Generally asymptomatic
Mildly – sporadic coughing, unthriftiness
Severely – predisposed by secondary bacterial infection
- Emaciation, oedema, loose wool, high morbidity
Clinical signs of lungworm infection in Goats
Severely infected – coughing and dyspnea, pneumonia
Clinical signs of lungworm infection in Pigs
Older pigs - mostly light and asymptomatic
Young animals – Coughing, dyspnea, nasal discharge
+ Secondary bacterial infection – inappetence
Purulent Staphylococcus infection
- many viruses spread with pig lungworm eggs and larvae.
Clinical signs of lungworm infection in Horses
Cough, tachypnoea, unthriftiness in older horses.
To which Superfamily does Dictyocaulus belong?
Trichostrongyloidea
To which Superfamily do Muellerius and Protostrongyllus belong?
Metastrongyloidea
Cat lungworm in latin (3 spp.).
Family Metastrongylidae
Species:
Aelurostrongylus abstrusus
Troglostrongylus brevior
Capillaria (Eucoleus) aerophila
Life cycle of Aelurostrongylus abstrusus.
cat lungworm
Life cycle indirect
Cat lungworm infection.
Localisation of A. abstrusus:
Localisation of T. brevior:
Localisation of A. abstrusus:
Pulmonary tissue - from subpleural nodules
Localisation of T. brevior:
Upper airways: trachea, bronchi and bronchioles
Cat lungworm infection.
Intermediate host:
Paratenic hosts:
Intermediate host: Invertebrate gastropod (Snails and slugs)
Paratenic hosts: birds, rodents
Cat lungworm Epidemiology
Prevalence higher in:
Wild cats and free-roaming cats
kittens (T. brevior) - often fatal.
Cat lungworm Morphology.
Describe the Cat lungworm Life cycle.
Indirect - infection from intermediate host or paratenic host.
In the final host:
L3 penetrates intestinal mucosa
Via lymphatics reaches lungs - develops and matures.
Adult worms live in the alveolar ducts, bronchioles.
Eggs laid and hatched in the pulmonary ducts, alveoli.
L1 migrates to pharynx - swallowed and passed into feces.
In the intermediate host/ in paratenic host:
L1 penetrates snails, slugs - develop to L3
Possibly paratenic hosts in the life cycle
Prepatent period: 35-48 days
Patency: several years
Cat lungworm Pathogenesis: explain pathologies associated with infestation.
Kittens more susceptible.
Host inflammatory response -> Larvae and eggs are surrounded by granulomas and inflammatory cells.
Reduction of the available surface area for gas exchange.
Vascular pathologies:
Hypertrophy and hyperplasia of smooth muscles of pulmonary arteries - OBSTRUCTION of BRONCHI.
NB: Risk in sedation or anesthesia - hypoxia, hypotension, cardiovascular arrest.
Cat lungworm Clinical signs
Subclinical to variety of respiratory signs:
Dyspnoea, open-mouth abdominal breathing
Coughing, wheezing, sneezing,
Mucopurulent nasal discharge
Shaggy coat, emaciation
Enlarged mandibular lymph nodes
Possible severe cases with concurrent infections in kittens:
Pneumothorax, pyothorax
Vomiting, diarrhoea, pyrexia
Hyperinfection syndrome in immunosuppressed kittens.
Name 4 lungworms to affect Dogs.
Eucoleus boehmi & Eucoleus aerophilus
(also known as Capillaria aerophila)/ canine nasal capillarids
Angiostrongylus vasorum/french heartworm/dog heartworm
Crenosoma vulpis/ fox lungworm
fox lungworm in latin
Crenosoma vulpis
Final host: fox
Reservoir host: dog
Emerging in dogs
Dog lungworm Morphology.
L1: oral end bluntly conical
posterior end tapering smoothly
200 - 300 μm long
Adult:
18 to 26 cuticular folds with small backwardly directed spines on their margin encircle the body and give the adult worms their crenated appearance.
Size: 4-16mm
identify
Crenosoma vulpis/ fox lungworm
L1: oral end bluntly conical posterior end tapering smoothly
identify
Crenosoma vulpis/ fox lungworm
Adult:
18 to 26 cuticular folds with small backwardly directed spines on their margin encircle the body and give the adult worms their crenated appearance.
Dog lungworm infection:
Pathology and clinical signs
Eosinophilic bronchopneumopathy
Chronic bronchitis, bronchiolitis
Especially in small breeds
Signs:
Chronic productive cough
Bronchial sounds
Wheezes
Weight loss, lethargy
Anaemia
C. aerophila - chronic tracheobronchitis
Capillaria boehmi life cycle.
(also known as Capillaria aerophila)/ canine nasal capillarids)
Hosts: dogs
1. Dog ingests the paratenic host or egg
- In the duodenum, the larva hatches and
migrates to lungs through liver and heart. - From the lungs the larva migrates to
nasal passages – develops to adult and
lays eggs. - Eggs travel from mouth to intestines
and out with feces.
What is he French heartworm in latin?
Dog lungworm - Angiostrongylus vasorum
Capillaria aerophila common name?
Hosts?
tracheal worm
Hosts: dogs and cats
Capillaria aerophila life cycle and alt. name?
tracheal worm
- Ingestion of infective eggs from the environment or via paratenic host (earthworm).
- Larvae hatch in duodenum and migrate via the bloodstream to the lungs (through the liver and heart).
- In the lungs they settle in the bronchi - molts, matures.
- Following maturation of the worms reproduction starts- eggs are laid, coughed up, swallowed and excreted.
- Prepatent period is about 6 weeks.
In the environment, infective larva develops in the egg in 5 – 6 weeks.
Out of the following - which affect dogs?
Angiostrongylus
Filaroides
Out of the following - which affect sheep and goats?
Muellerius
Protostrongylus
Out of the following - which affect pigs?
Metastrongylus
Out of the following - which affect ruminants and equidae?
Dictyocaulus
Diagnosis of lungworm infection.
Anamnesis and clinical signs
Early detection during prepatent infection:
Detection of eggs or larvae in lungs by:
- examination of sputum
- bronchial mucous (BAL)
- bronchoscopy
- tracheal secretions
Later detection during patent infection:
Detection of larvae or eggs in feces:
Larvae in the faeces (Fam. Protostrongylidae, Dictyocaulidae)
- Baermann method – detection of L1 (NB: shedding intermittent)
Eggs in the faeces (Fam. Metastrongylidae - in pigs)
- Flotation method (saturated magnesium sulphate) (but Often present in normal pig)
Samples should be taken from several animals.
Mini-FLOTAC is a more sensitive test.
Detecting larvae from post mortem (necropsy) is also possible via histology.
Dictyocaulus viviparus L1
Metastrongylus apri egg
Up to which week, diagnosis rests entirely on the history and clinical signs and why?
Until the fourth week, no larvae are shed in the feces and diagnosis rests entirely on the history and clinical signs.
Early detection during prepatent infection stage:
Detection of eggs or larvae in lungs:
- examination of sputum
- bronchial mucous (BAL)
- bronchoscopy
- tracheal secretions
Larvae in the faeces can be detected by what method?
(Fam. Protostrongylidae, Dictyocaulidae)
- Baermann method – detection of L1 (NB: shedding intermittent)
Eggs in the faeces can be detected by which method?
(Fam. Metastrongylidae - in pigs)
- Flotation method (saturated magnesium sulphate)
Treatment of lungworm infection.
Anthelmintics are highly effective.
Always treat the whole herd!
- Broad-spectrum - also effective against GIN
- Macrocyclic lactones
- Benzimidazoles - effect against hypobiotic stages! (do this in autumn!)
Antimicrobials for secondary bacterial infections.
Anti-inflammatory drugs as needed
Hydration fluids
Name some anthelminthics effective against lungworm.
ivermectin
doramectin
fenbendazole
albendazole
milbemycin
moxidectin
etc.
Describe Large animal lungworm Immunity
Immunity depends on the infection dose of the primary infection.
Intensive treatment of calves before first grazing season will prevent immunity.
The acquired immunity will be lost after 12 months in the absence of reinfection.
Development of complete immunity through natural infection.
Vaccination with attenuated larvae possible.
Prevention and control of lungworm infection in large animals.
Large animals:
Separation of young and old animals
Young animals to clean pastures
Avoid wet pastures
Give feed/water from clean container
Improve herd management
Rotational grazing
Anthelmintic metaphylactically?
- In early spring to second year cattle
- Local grazing epidemiology
Vaccination in cows: BOVILIS® HUSKVAC
- to calves over 8 weeks
Prevention and control of lungworm infection in small animals.
Control difficult for intermediate hosts.
Keeping cats indoors - avoid predation.
Do not let your dog eat slugs/snails.
Strongyloides belong to what Order and Superfamily?
Order Rhabditida
Superfamily Rhabditoidea
Common name for strongyloides spp.?
What disease do they cause?
Location in the host?
threadworms
Strongyloidoses
Location: crypts of small intestine
Transmission of strongyloides spp.? (5)
Transmission:
- ingestion of L3 larva - alimentary
- penetration of skin by L3 – percutaneous
- via infected colostrum – lactogenic
- via transplacental – intrauterine
- autoinfection
Morphology of strongyloides spp.?
Adult female 9 mm
Only females are parasitic!
Uterus is intertwined with intestine
- looking like a twisted thread
Filariform (L3)
- Parasitic generation
- Straight-sided oesophagus
- Tail blunt
Rhabditiform (L1)
- Free-living generation
- Cilindrical oesophagus with double bulb
Morphology of strongyloides spp. eggs?
Eggs
Size: Small eggs (45-60 μm,)
Shape: Oval with flattend poles,
Shell: thin-shelled,
contents: U-shapped embryo or larva
strongyloides spp. egg
Size: Small eggs (45-60 μm,)
Shape: Oval with flattend poles,
Shell: thin-shelled,
contents: U-shapped embryo or larva
What are the two morphological shapes for strongyloides spp. larvae and what larval stage is each?
Filariform (L3)
- Parasitic generation
- Straight-sided oesophagus
- Tail blunt
Rhabditiform (L1)
- Free-living generation
- Cilindrical oesophagus with double bulb
Life cycle of strongyloides spp.
Direct, but complex.
Homogony – parasitic cycle:
L3 turns into infectious form
Migrates from circulatory system to lungs
Migrates from trachea to intestines
Parthenogenesis – asexual reproduction
Eggs or larva in faeces after one week
Heterogony – free-living cycle:
Sexual reproduction only outside
Can follow parasitic cycle
Important: arrested larvae in adults for years. In subcutaneous fat.
Activate before birth - transmitted via milk or in uterus. First source of infection to young animals.
What two types of life cycles can strongyloides spp. have?
Homogony – parasitic cycle:
Homogonic development – direct new parasitic generation from L3 - females.
Parthenogenesis – asexual reproduction.
Heterogony – free-living cycle:
Heterogonic development – indirect, free-living generations that produce parasitic generations. Sexual reproduction only outside.
Describe autoinfection in strongyloides spp. infections.
Autoinfection:
non-infective rhabditiform larvae (L1) becomes infective filariform larvae (L3) before leaving the body.
a) external autoinfection
- penetration of the perianal region
b) internal autoinfection
- penetration of the intestines
L3 starts new migration in the organism
(Also nematode Capillaria philippinensis can cause this kind of autoinfection)
In this way, the host can be infected for several years!
Clinical signs of strongyloidoses.
Light infections asymptomatic.
Heavy infection in young animals
- (10-14 days)
Skin lesions – larval migration:
Dermatitis, erythema - abdomen, thighs
Lung lesions – larval migration:
Cough (bronchopneumonia)
Intestinal lesions - adults
- Anorexia, weight loss
- Bloody diarrhoea
- Anaemia
- Stunting
- High mortality
Describe strongyloides in ruminants.
S. papillosus in cattle is almost
universally prevalent, but rarely causes
detectable illness.
Signs are usually in lambs and calves.
Penetration of Stongyloides larvae into
the skin may cause erythema, oedema
and allergic reactions.
Clinical signs of strongyloidoses in dogs.
Which spp. is in dogs?
S. stercoralis in dogs
Mostly in summer and in dog kennels
Symptoms similar to other species.
Diarrhea, emaciation and no appetite
Diagnosis of strongyloidoses.
Anamnesis and clinical signs.
Detection of eggs/larvae in faeces:
- Fresh samples – later larvae moves out from egg!
- Fecal flotation method - many samplings
- Baermann method – if there are already larvae in faeces!
- Culture method – If the sample is really fresh – eggs still hatching.
Detection of adults/ larva during post mortem (necropsy):
- Direct microscopic examination
- Histology
- Mucosa scrapings – adults
Detection of adults/larvae in duodenal aspirates:
- BAL (bronchoalveolar lavage)
- Duodenal biopsy
Treatment of strongyloidoses.
Against intestinal infection
- Macrocyclic lactones (ivermectin, moxidectin)
- Benzimidazoles (fenbendazole) in increased dosages
- Levamisole
Before and after parturition.
Suppression of larval excretion via milk
- Ivermectin
Prevention and control of strongyloides.
Pigs:
Strict hygiene
- Especially in farrowing houses
All-in all-out system
Use of anthelmintics prior to farrowing.
Good nutrition helps.
Foals:
Anthelmintic treatment in 1-2 week of age
Humans: use of footwear
Describe strongyloides eggs.
Eggs 59
Size: Small eggs (45-60 μm,)
Shape: Oval with flattened poles,
Shell: thin-shelled,
contents: U-shapped embryo or larva
