Dog/Cat Heartworms and Lungworms Flashcards
Superfamily Filarioidea (classic heartworm)
Dirofilaria immitis
Filarioidea are tissue dwelling. They’re never in the intestines; they’re either in the organs or the subcutaneous tissue
Have insect vectors as intermediate hosts
Primitive forms release eggs, whereas more highly evolved forms release live L1 or microfilaria (MF)
nb: MF can show periodicity in blood (in d. immitis, not STRONGLY periodic)- increase in number of MF around 10pm-2am– evolutionary adaption- get into blood when IMH/vector is biting!
Dirofilaria immitis
Host: dog, cat, ferret, sea lion, man (in man presents as cyst, never causes a patent infection)
IMH: mosquito
Site: CV system–> right ventricle, posterior VC, pulmonary artery
Distribution: USA, warm temperate zones (Europe), tropics
Life cycle of dirofilaria immitis
Adults in the heart–> release MF into blood (300 microns (teeny tiny)
MF infested by mosquito when it takes a blood meal–> develops L1-L3 in 10-14 days under optimal conditions (temp dependent)
L3 is infective form for the host–> transmitted by feeding mosquito via infected head/mouth parts
L3->L4->Adult in subcutaenous tissue. nb: this skin development is really important because this is where we can use prophylaxis
Juvenile adult migrates to heart
NB: adults are 20-30 cm long and white
Pathogenesis of D. immitis
Pathogenesis of D. immitis- depends on worm burden. Low numbers can result in no apparent ill-effects.
With high numbers, get loads of problems
HW is very pathogenic because of were it lives. D/t its shape and size (long and slender) it’s adapted for life in blood vessels.
More pathogenesis of D. immitis
Associated with adults in the heart–> chronic congested right-sided heart failure
Can cause pulmonary embolism: important when thinking about the treatment of infected animals–adults block the vessels
Vena cava syndrom: blocked by mass of worms and collapses
Endocarditis in valves, pulmonary endarteritis (local inflammatory response)
Glomerulonephritis–> deposition of immune complexes in kidney (occurs in heavily infected dogs)
Clinical signs of D. immitis
CV dysfunction
Listless/gradual loss of condition
Exercise intolerance
Chronic soft cough
Diagnosis of D. immitis
Detection of microfilaria in blood (wet film, strain dry blood film)
Detection of circulating antigens–> females pump of ES product– antibody can detect antigen from serum)
Clinical signs and history
Microfilaria in blood film- highly motile, much bigger than bacteria/rickettsia
PPP=6 months
Antigen tests can detect a single female, but not male (d/t ES product produced by female)
Start testing by 6-7 months of age.
Antigen test more sensitive than MF detection- some dogs have occult infections (adults but no MF), possibly due to IR clearing MF but not adults
Epidemiology of D. immitis
Major pathogen in US, has spread rapidly over the last two decades. Present in southern europe. Mosquitos are present in UK that can transmit but only dogs with HW in UK were imported.
Factors affecting epidemiology of d.immitis
Dog: density of dogs (esp. lots of untreated strays), MF present for long period, poor immunity, poor owner complicance
Mosquito: distribution of susceptible vectors (not all mosquitos can transmit), capacity for rapid population increase, short developmental period from MF-L3
Control of D. immitis
much easier to control than treat
do we control parasite or vector? depends on tropical or temperate zone.
D. immitis requires 24 hour daily temperature of >18 degrees c for 1 month for parasite to develop in the mosqutio (that’s why there’s no transmission cycle in the UK)
Prophylaxis is the basis of control- use year round in the tropics. In temperate zone, use one month before mosquito season, during the seaosn and 2 months after the season
D. immitis prophylaxis
Macrocyclic lactones (e.g. ivermectin etc) monthly- kills L3 and L4 up to 6 weeks post-infection
DEC (diethylcarbamazine) daily- very cheap
NB: prophylactic drugs do NOT kill adult worms
May have a sterilizing effect on female worms
Must check MF status of dogs. IVM and particularly DEC are also microfilaricidal at prophylactic doses. If MF +ve dog is treated, can induce anaphylactic shock if high MF counts because MF are lysed and there’s a huge release of contents.
In endemic areas, puppies should be treated prophylactically by 8 weeks of age.
Other prevention measure of D. immitis infection
keep animals indoors at peak mosquito biting times
insectidie collars or spot-on
attempt to reduce mosquito population
D. immitis treatment of infected animals
Surgical removal of adult worms, usually in specialized HW clinics
Treatment with melarsomine (immiticide, but no license in UK)- give drug VERY carefully to avoid embolism (nb this is arsenical compound)
Treat to kill MF
Experimental D. immitis treatment
many species of filarial worm harbor a bacterial endosymbiont called wolbachia. killing wolbachia negatively affects adult worms.
Combo therapy of IVM and doxy appears to kill adult D. immitis. All filarial worms in humans have wolbachia. if you give infected humans doxy, these adult worms die.
D. immtis infection in cats
Not well adapted to cats, but VERY pathogenic if cat becomes infected/susceptible
Adult worms live for a shorter period of time compared to dogs (2-3 years)
MF are transient
Usually carry around <6 adults
lungs are most affected
potentially fatal, complex diagnosis
no approved treatment
3 prophylactic drugs approved inthe US
D. immitis infection in dogs
Dogs are very susceptible
Adult worms live 5-7 years
Many worms present (30+ adults)
Persistent microfilaremia
Heart and lungs most affected
Pathogenicity depends on worm burden
Simple diagnosis
Adult tx= melarsomine
7 prophylactic drugs available
Treatment of D. immtis in cats
Pathology in cats relates to the inflammatory response to worms/worm death and NOT from the biomass of adults (as in dogs, i.e. obstruction of blood flow due to large numbers of worms).
If no clinical signs, can allow spontaenous recovery with monitoring.
NB: melarsomine is VERY toxic in cats.
Superfamily metastrongyloidea
Angiostrongylus vasorum- small HW of dogs
Aelurostrongylus abstrusus- small HW of cats
Oslerus osleri
Metastrongyles
Indirect life cycles
clinically mild/asymptomatic
IMH-molluscs (slugs, snails)- exception: pig metastrongyle has earthworm as IMH
Oslerus osleri: direct life cycle and increased pathogenicity
Angiostrongylus vasorum (French Heartworm)
Host: dog and fox
IMH: molluscs
Site: right ventricle, pulomonary artery
Small brown worms of roughly 2.5 cm
Angiostrongylus vasorum life cycle
Adults in heart–> female releases eggs–> eggs hatch in pulmonary capillaries
L1 break into the alveoli and migrate up the lungs–> coughed and swallowed and L1 end up in feces
L1 to L3 in IMH (possibly penetrate soft parts of slug/snail
L3 released from IMH (not sure how it happens)
L4–> adult–> adults migrate to right side of heart
PPP~7 weeks
Pathogenesis of Angiostrongylus vasorum
Chronic infection
Pathology is associate with adults in large vessels and eggs in pulmonary capillaries.
Chronic congestive cardiac failure, fibrosis in arteries (feels like a pipe stem), mottled lungs d/t penetrating L1
Subcut bleeding
Fluffy, ill-defined opacities (alveolar pattern) in caudal lung field due to L1 worms.
Clinical signs of angiostrongylus vasorum
Early on, asymptomatic
Later: increased resp. rate, exercise intolerance +cough
If heavy worm burden, can show symptoms (fainting) in resting dog.
Subcutaenous hematoma- parasite ES products interfere with blood clotting–> can be confused with warfarin poisoning.
Can be associated with brain and spinal cord hemorrhage
Diagnosis of Angiostrongylus vasorum
Diagnosis Baermann on fecal smaple; L1 is characteristic with a small spine of tail; PCR, antigen test
Epidemiology of angiostrongylus vasorum
found in UK and europe; hot-spots in SW UK; distribution is increasing in UK. May be associated with warm, damp winter and increase in slugs.
Aelostrongylus abstrusus
Cat equivalent of angiostrongylus vasorum
Host: cat
IMH: mollusc
Site: lung parenchyma and small bronchioles
Cat becomes infected by eating molluscs containing L3
Pathogenesis of Aelurostrongylus abstrusus
Not very pathogenic
Small lung granulomas, rarely see larger lesions.
Can get muscular hypertrophy/hyperplasia
Granulomas often resolve
If you section through lung tissue, you can see a worm
Clinical signs, diagnosis and epidemiology of Aelurostrongylus abstrusus
chronic moist cough, following handling sneezing and coughing, mild dyspnea
Diagnosis of L1
Epidemiology: widespread, ubiquitous IMH, wide range of paratenic host, UK prevalence >5%
Oslerus osleri
Host: dog and wild canilids
NO IMH- direct life cycle
Site: nodules at tracheal bifurcation
Worms are thin, 1-1.5cm long
Dogs become infected by ingestion of L1.
Oslerus osleri clincial signs
Usually asymptomatic +/- dry cough
Exercise intolerance if a heavy egg burden
most obvious in working dogs and 6-12 month old dogs
Oslerus osleri diagnosis
History of chronic dry cough/ exercise intolerance
L1 in sputum (or feces)
Bronchoscopy- nodules and L1
L1 has a distinctive “S” shaped curly tail (coiled toil)
Oslerus osleri epidemiology
Nursing bitch often the focus of infection- @ tracheal bifurcation. L1 in sputum, lick pups, pups get immediate infection.
L1 is immediately infection
6% prevalence in the UK
