HW Flashcards
Def caval syndrome
- Acute manifestation of HW disease
o Large # of HW in R heart → 30-200 worms
o Intertwined, trapped in TV apparatus
Prevalence caval syndrome
uncommon
o Sex predilection: 75-90% males
Pathophys caval syndrome
- Mass of worm in RV → RA
o Worms trapped in TV apparatus → acute/severe TR
Can be exacerbated by PH from HW
Can develop R sided CHF
o ↓CO in pulmonary circulation → L sided volume underload → ↓ systemic CO → poor perfusion - IV hemolysis → hemoglobinemia/uria
o From shear stress on RBCs forced to flow around the worms at high velocity
RBC more fragile in dogs with caval syndrome → alteration of RBC membrane
Etiology caval syndrome
HW get from PA → R heart
* Normally held in place into PA against gravity because of forward flow
o Found in RV at necropsy since blood stops at time of death
* Start in PA → descend into RV → ascend into RA = MIGRATION
o From 5-17months after infection
o Any event resulting into transient or sustained ↓PA forward flow
High HW burden → PH → poor CO → ↓ blood flow
Arrhythmias can occur w severe dz → ↓ PA blood flow
o Once in RV → can use TV to pull themselves into RA
Leading worms can be forced into VC
C/s caval syndrome
- Cardiogenic shock and circulatory collapse
o Anorexia, depression, weakness
o Respiratory signs: dyspnea, tachypnea, coughing - Dark brown to black urine
PE caval syndrome
- Heart murmur: R sided systolic apical murmur (87% of cases), loud/split S2, gallop
- R-CHF: ascites, hepatomegaly, jugular vein distension
Dx BW/UA caval syndrome
o Hemoglobinemia/uria → pathognomonic
o Other signs are secondary to hypoperfusion, hepatic congestion and inflammation
Moderate regenerative anemia: reticulocytes, ↑ RBC volume, nucleated RBC
* Target , schistocytes, spur , spherocytes
Inflammatory leukogram: neutrophilia with L shift
Eosinophilia
↑liver enzymes
Hyperbilirubinemia
Azotemia
Proteinuria, bilirubinuria, hemoglobinuria
o Disseminated intravascular coagulation: thrombocytopenia,↑ clotting time, hypofibrinogenemia
Intravascular hemolysis
Metabolic acidosis
↓hepatic fct → impaired removing of circulating procoagulant
o Can lead to hepatic or renal failure → products of hemolysis
o Microfilaremia (85% of dogs)
CTX caval syndrome
R heart enlargement, tortuous PA, interstitial parenchymal changes
ECG caval syndrome
R axis deviation
o Deep S wave in lead I,II,III, aVF (56%)
o Arrhythmias: sinus tachycardia (33%), APC (28%), VPC (6%)
Echo caval syndrome
o Presence of worms in the R heart: high # of worms in RA moving into RV in diastole
o RA/RVE
o Paradoxical septal motion from ↑RVP
o Indications of PH
PA dilation
Reduced L sided parameters
TR, PI
Cardiac KT caval syndrome
↑ pressures in RA, RV, PA
Px caval syndrome
- Guarded to poor: 30-40% mortality with appropriate tx
- Death in 24-72h w/o tx
Complications after tx
o Organ failure
o DIC
Tx caval syndrome
- Surgical removal of worms via jugular vein
- Supportive care: corticosteroids, heparin, ATBs
o IV fluids to improve CO
Initial should be aggressive if shock and - Normal venous pressures <5mmHg → 10-20ml/kg
- Increased venous pressures >10mmHg → 1-2ml/kg
o Prevent or reverse DIC
o Prevent Hb nephropathy
o Reverse lactic acidosis
What causes complications in caval syndrome
- Maceration of worms → massive AG release
o Can lead to severe pulmonary vasoconstriction
o DIC
o Administration of parenteral corticosteroids + heparin necessary
After procedure (caval syndrome) care
o Adulticide should be given → kill remaining worms
o Disappearance of TR, ↑CO and ↓RAP may take several days
Vector of dirofilaria immitis
- Vector: 60 species of mosquitoes, important ones <12
o Risk of HW infection correlated to lifestyle: outside dogs 4-5x more likely than indoor
o Cats less likely to be bitten by mosquitoes
1 species (Culex) more likely than other
Life cycle of dirofilaria immitis
- Adult HW: L5 → reside in PAs
- Completion of life cycle 184-210 days
o Microfilaremia occurs as early as 6mo
Typically 7-9 months
Seasonal/diurnal periodicity: ↑# in evening and summer
Microfilariea live up to 30 months
Steps of infection/life stages dirofilaria immitis
- After mating → mature adult females (L5) produce microfilariae (L1) → released into circulation
- L1 ingested by female mosquitoe
- L1 then undergo 2 molts: L1 →L2 and L2 → L3 over 8-17 days
o Temperature dependent: requires 2w of T > 27C
Development does not occur <14C
o Wolbachia pipipentis: symbiotic bacteria necessary for maturation - L3 is infective → transmitted to host (dog) by feeding
- After infection:
o Molt occurs in subQ, adipose and skeletal muscle tissue (1-12 days): L3 → L4
o Final molt L4 → L5 (immature adult) is after 2-3months (50-68 days) - L5 (1-2cm length) migrate into vascular system → heart/lungs
o Final maturation to mature adult: males 15-18cm, females 25-30cm
o Mating: microfilariae detected after 6mo
Life span worms
5-7years
Pathophys: what causes c/s and disease severity
- HW reside primarily in caudal pulmonary vascular tree
o Can migrate in PAs, R heart, great veins
o Obstructions of pulmonary vessels by worms is little clinical significance unless high worm burden in small patient
Worms mainly in caudal PAs until #>25 worms (in 25kg dog)
o Disease severity and onset depend on # of worms (1 to 250)
>100 worms at high risk for caval syndrome - Damage of PAs and lungs
Severity of lesions to lungs are related to
# of worms
Duration of infection
* Reversible in 4-6wks if brief infection
Host and parasite interaction
Worms are triggered by
toxic substances, immunologic response, physical trauma
Histo lesions lung vessels
Villous myointimal proliferation
Inflammation
Pulmonary hypertension
Disruption of vascular integrity
Fibrosis
Arterial obstruction/vasoconstriction from live worms
Thromboemboli of dead worms
When do pulmonary vascular lesions develop and order
3 days to 3 months post infection
o Endothelial damage/sloughing/swelling
↑ vascular permeability → protein/water leakage into perivascular interstitium
o Villous proliferation
Rapidly dividing SM + collagen
o Widened intercellular junctions
o Activation/attraction of leucocyte/platelets
Trophic factors released: platelet derived growth factor
Stimulate migration/multiplication of SM in tunica media
* 3wks: migration of SM from media → intima
o More severe rx with dead worms
Thrombosis, granulomatous and rugous villous inflammation
Gross exam
o Enlarged, tortuous PAs
Thick walls
Rough endothelial surfaces
o Vessels of caudal lung lobes more severely affected
o Partially reversible changes
Effect of exercise
exacerbate signs of TE HW disease
o Unclear role in pulmonary vascular dz or PH development
o PAs: thrombosed, thickened, dilated, tortuous, noncompliant, funtionnally incompetent
Cannot be recruited if ↑ demand → exercise intolerance
Etiology of pulmonary vasoconstriction
o Vasoactive substances released by worms
o Endothelin-1 from vascular endothelial
o Vasoconstrictive substances: serotonin, adenosine diphosphate, thromboxane A2
o Hypoxia: ventilation-perfusion mismatch from PTE
o Eosinophilic pneumonitis
Immune mediated destruction of microfilariae in pulmonary microcirculation → amicrofilaremiae
Antibody coated microfilaremia → entrapped in pulmonary circulation
Inflammatory reaction
o Pulmonary consolidation
Pathophys of PTE
spontaneous or post adulticide from dead worms
o Precipitate/worsen c/s
o Producing/aggravating PH, R-CHF, pulmonary infarction
o Worsen vascular damage
Exuberant villous proliferation
Granulomatous inflammation
o Enhance coagulation → thrombus formation
Wolbachia
- Wolbachia pipientis: symbiotic relationship
o Identified in glomerulus and lungs of infected HW dogs
o Contribute to inflammatory response by producing proteins
Comorbidities from HW
- Pulmonary eosinophilic granulomatosis
o Associated with HW disease
o Similar pathogenesis to eosinophilic pneumonitis
Microfilariae trapped in lungs → surrounded by neutrophils/eosinophils → granulomas and bronchial lymphadenopathy - Glomerulonephritis: from AG/AB complexes
o Proteinuria
o Uncommonly associated w renal failure
Occult infection prevalence
20% of cases
Causes of amicrofilarial infections
o Prepatent period
o Single sex infection
o Infertile adult worms from drug therapy
o IM destruction of microfilariae
Dx occult infection
- Can be detected by serologic testing
Prepatent period
Winter and spring months if infected during previous late summer/fall
Appear after 6 months post inoculation
Female worms → detectable AG (7-8 months post inoculation)
Single sex infection
More frequent in regions w low HW incidence
Fewer larvae inoculated in host
Infertile adult worms from drug tx
Long term (>6mo) administration of prophylactic macrolide agents
Monthly macrolide in immature infection → induce occult infection if worms not killed
Can usually be detected by AG testing
IM destruction of microfilariae
Hypersensitivity to microfilarial AG
AB (IgG) excess → predispose to occult infection
* AB-dependent leucite adhesion to microfilariae in pulmonary capillaries → micrfilarial entrapment
* Microfilaria-leucocyte complexes → phagocytosis → granulomatous inflammation
Clinical syndromes associated w/ IM destruction of worms
- Allergic pneumonitis
- Pulmonary eosinophilic granulomatosis
C/s depend on
of worms, duration of infection, host response
C/s
o Dyspnea
Pulmonary vascular/parenchymal changes
↑PVR → ventilation/perfusion mismatch
o Coughing
o Exercise intolerance
↓ ability to recruit arteries when high blood flow rate is needed for exercise
o Syncope
o Hemoptysis
PE
split S2, R apical gallop, crackles
Classification of syndrome
- Class 1: asymptomatic/mild symptoms
o Px: excellent - Class 2: moderate dz
- Class 3: severe dz
o Px: poor
Dx: what improves testing accuracy of microfilariae
- Testing accuracy is improved if >1 test is used
o Most sensitive: modified Knott test and milipore filtration
Concentrate microfilariae
o More sensitive than ELISE in infection <6-7mo
Tests for dx Microfilarial testing
o Microscopic identification on direct blood smear
o Above buffy coat in microhematrocrit tube
o Modified Knott test
o Milipore filtration
Microscopic identification on direct blood smear
Permit examination of larval motion
Distinction of Dirofilaria Immitis and Dipetalonema reconditum
* D. reconditum does not require adulticide tx
* ↓ [microfilariae]
Microfilarial testing: False negative results
o Amicrofilaremic infections can occur
Prepatent infection (young dog)
Single sex infection
IM destruction of microfilariae
Drug-induced amicrofilaremiae: macrocyclic lactones
* Can clear microfilariae in 6-8 mo
* Embryostasis may be permanent
o Small # of microfilariae
o Small amount of blood
When should microfilarial detection should be performed
- Should be performed in AG + dogs to determine microfilarial status
o If large #: pre-treatment or schedule observation time
o # of circulating microfilariae ≠ predict worm burden
Immunodiagnostic antigen test
- Detect AG from adult female worms
o Semi quantitative ELIS assay → rapid strong reaction = high burden
o Sensitivity 70%, specificity 97%
Immunodiagnostic antigen test: false negatives
o 1st 5 to 8 months of any infection
Late summer infection tested around May-April
o All-male infection
o Low female worm burden infection (<3 female worm)
Immunodiagnostic antigen test: false positives
uncommon
o Problem if low prevalence
o Weakly + result should always be repeated.
What is the only effective test in dogs receiving monthly preventatives.
Immunodiagnostic antigen test
Best test to evaluate severity of infection
CTX
and evaluate pulmonary parenchymal changes
Prevalence of abn CTX
- Abnormalities present in 85% of cases, develop early in dz course
CTX changes
o RVE 85%
o Prominent MPA 70%
o Enlarged lobar PAs
o ↑ size/density of PAs 50%
o Tortuous PAs and pruning 50%
* ↑ interstitial density
sensitive indicator of HW associated CHF
- Marked enlargement of cranial lobar PA
What causes ↑ interstitial density
from ↑ vascular permeability → perivascular fluid leakage + inflammatory cells accumulation
o Most severe parenchymal lung changes after adulticide tx
Dead worms washed into distal PAs
o More severe lesions in caudal lung lobes
CBC changes
o Mild/moderate regenerative anemia (10% mild, 60% severe)
o Neutrophilia (20-80%)
o Eosinophilia (85%), basophilia (60%): common, not specific
Commonly higher count in Dipetalonema
o Thrombocytopenia: chronic HW, caval syndrome, DIC
Most common 1-2weeks after adulticide
Chem changes
↑ liver enzyme(10%), hyperbilirubinemia,
o Hypoproteinemia (severe infection) → from protein-losing glomerulonephropathy
UA changes
albuminuria (10-30%)
ECG
not very useful, normal in 90% of cases
Echo: clinical utility
- Evaluation of R sided function
- Estimate # and location of HW
- Determine severity of PH
Prophylaxis
Diethylcarbamazine
Macrocyclic lactone (macrolide) antibiotics
Diethylcarbamazine: risks, target and dosing
- Safe only in amicrofilaremic dogs, effective
o Need yearly HW test prior to give
o IM reaction in 30% of microfilaremic cases
C/s w/I 1h: depression, ptyalism, V+, D+, cardiogenic shock (weak pulses, pale MM, ↓CRT), bradycardia - Kill L3 and early L4 tissue migrating larvae
- Daily
Macrocyclic lactone: target, dosing
- Interrupt larval development (L3 and L4) during 1st 2 mo of infection
- Monthly
o Retroactive efficacy: grace period if dose forgotten
o Dual roses as microfilaricide
Which dogs will have less severe rx to tx w/ macrocyclic lactones
- Microfilaremic dog
Types of macrocyclic lactones
Ivermectin (Heartguard)
Milbemycin oxime (Interceptor)
Selamectin (Revolution)
Moxidectin (Advantage multi)
Ivermectin
- Derived from avermectin B1, obtained from Streptomyces spp
o Effective against wide range of endo/ectoparasites
o Safe in puppies >6w - Adverse rx in only 10% of dogs
o Related to high microfilarial counts
o Starts w/I several hours
o Lethargy, V+, D+ → self limiting - 2mo lapses
o Extended if continuous 12mo administration post exposure: lapses 3-4mo - Microfilaricidal at preventative doses → gradual ↓ in microfilarial #
o Kills microfilariae in 90% of dogs in 21 days, most killed/I hours
Milbemycin oxime
- Nonmacrolide member of a family of milbemycin macrocyclic lactone ATB derived from species of Streptomyces
- Broad spectrum parasiticide at preventative dose
o Effective against hook/round/whipworms - Safe in puppies <8w
- Microfilaremic dogs: ↑ potential of adverse rx
o Potent microfilaricide at preventative doses
Moxidectin
- Narrow spectrum HW preventative
- Gradual microfilaricidal effect
o No adverse effects - Safe in Collies, careful in puppies <6mo and cats
Which dogs will benefit from adulticide tx
- All HW infected dogs = acceptable candidates
o Class 1 and 2: high success rate
o Class 3: ↑ risk of severe, life-threatening pulmonary complication post adulticide
o If serious concommittant problems → not good candidates
Hepatic insufficiency = CONTRA INDICATED
Renal failure
Nephrotic syndrome
Monitoring after adulticide tx
stop If anorexia, perisistent vomiting, icterus
o Rise in liver enzymes is often seen in dogs tolerating tx
Adulticide agents
Melarsomine dihydrochloride
Thiacetarsamide
Melarsomine dihydrochloride: target, protocol
- Organic arsenical
- Highly effective against all age/sex HW
o Good efficacy against immature/young HW
o Effective against migrating larvae - Protocol
o Dosage 2.5mg/kg, deep IM injection into epaxial lumbar musculature
Lameness and sciatic nerve damage can occur if injected in hind leg
o 2 injections at 24h interval
Eliminate adult worms in 75% of infected dogs
Seroconversion occurs by 8mo after tx
o 2 injections can be repeated 4mo later
Eradicate any remaining worms - Modified protocol: for high worm burden
o 1st injection → kill 50% of worms
↓ severity of thromboembolic complications
o Followed by 2 injections at 24h interval 1 month later
Kills remaining worms
Melarsomine dihydrochloride: toxicity
- Toxic reactions: tx with Dimercaprol (British anti-Lewisite (BAL))
o Parenterally administered heavy metal chelating agent
o Used to treat arsenic, gold, copper and mercury poisoning.
Thiacetarsamide: determinant of efficacity, protocol
- Determinant of efficacy: duration of worm exposure to minimum effective concentration
o ½ life = 45min, 80% of drug eliminated in 48h
Worm kill is ↓ in dogs with rapid clearance
o Highest tissue concentration in kidneys and liver - Protocol: 4 IV injection over 48h
o Interval btw injection <12h
o ↑ dose → ↑ # worms killed but ↑ risk of adverse rx
o IV into peripheral vein as distally as possible
o Avoid multiple injection at same site
o Extravasation: pain, swelling
Thiacetarsamide: disadvantages
o Narrow therapeutic index
o Lack efficacy against young female worm
o IV administration
Thiacetarsamide: toxicity
- Acute hepatic toxicity can occur → abort protocol
o Most often after 1st injection
o 20% of dogs
Ancillar drug therapy w/ adulticide
- Heparin
o Treat symptomatic PTE after adulticide tx
PTE: most frequent 5-21 days post adulticide
BW: inflammatory leukogram, thrombocytopenia, prolonged activating clotting time
o Dose adjusted to prolong aPTT 1.5-2x normal
o Continued for 5-21days, gradually weaned off - Aspirin: not recommended in asymptomatic dogs
- Corticosteroids
o Can help eosinophilic pneumonitis, pulmonary infiltrates, eosinophilic granulomas
o Prednisone 1mg/kg SID
o Monitor improvement with CTX
Tx modification w/ severe HW dz
- Heartworm extraction
- Modified melarsomine protocol
- Aspirin and cage rest
o ↓ platelet fct with aspirin
o Restrict exercise 3wks prior to thiacertasamide tx - Long term low dose heparin: controversial
o Prophylaxtic use to reduce risk of PTE
Assessment of treatment efficacy
- Seroconversion usually by 3 months
o Can occur as late as 5 months - False negative can occur if <1-2 adult worms <8mo/old
If persistent positive result, decision to treat again based on several factors
o No treatment
Weak positive result
↓ strength in AG test result compared to pre tx
Mild/no c/s
No evidence of pulmonary pathology on CTX
Marked improvement of CTX changes
Nonworking dog
Serious concomitant problems
o Treat
Strong, persistent antigenemia
Initially severe clinical/CTX abnormalities
Persistent c/s
Working dog
No apparent contra indication for retreatment
HW related clinical syndromes
Eosinophilic pneumonitis
Pulmonary granulomas
- Eosinophilic pulmonary granulomatosis
- Lymphomatoid granulomatosis
Post adulticide pulmonary thromboembolism
Eosinophilic pneumonitis: cause, prevalence
- Hypersensitivity type pneumonitis
o 10-15% of dogs with IM mediated occult HW infection
AB dependent leucocyte adhesion to microfilariae
Entrapment in pulmonary capillaries
o Hypersensitivity develops → abnormally high # of eosinophils in inflammatory response
Pulmonary infiltrates with eosinophilia
Eosinophilic pneumonitis: c/s
progressive over few weeks → 6mo
o Coughing, dyspnea
o Mild cyanosis, anorexia, weight loss if severe
Eosinophilic pneumonitis: CTX
diffuse, bilateral, lineal interstitial and alveolar pulmonary infiltrates
Eosinophilic pneumonitis: BW
eosinophilia, basophilia, hyperglobuminemia
Eosinophilic pneumonitis: dx
- Transtracheal lavage: sterile, eosinophilic exsudate
Eosinophilic pneumonitis: tx
corticosteroids
o Rapid, complete resolution of c/s and CTX changes in 3-5 days
o Steroids can be stopped when resolved
Eosinophilic pulmonary granulomatosis: distinguish from
metastatic pulmonary neoplasia, systemic mycoses, lymphmatoid granulomatosis
Eosinophilic pulmonary granulomatosis: lesions
o Thickened interalveolar septa: fibrous connective tissue, lymphocytes, plasma
o Eosinophilic granular material and macrophage in alveoli
Proliferation of pneumocytes type II
o Granulomas: dense accumulation of large epithelioid , macrophages, eosinophils obliterating normal architecture
Eosinophilic pulmonary granulomatosis: c/s
o Chronic coughing and dyspnea
o HW treated or untreated dogs
Eosinophilic pulmonary granulomatosis: CTX
o Multiple pulmonary masses: 1-20cm
o Mixed interstitial-alveolar, bronchial lung patterns
o Hilar lymphadenopathy
o Pleural effusion
o Mediastinal, intra-tracheal masses
Eosinophilic pulmonary granulomatosis: BW
eosinophilia, neutrophilia (2/3 of dogs)
Eosinophilic pulmonary granulomatosis: tx
o Most repond to immunosuppressive and cytotoxic drug
o Prednisone can produce partial, occasionally complete remission
Eosinophilic pulmonary granulomatosis: px
o Progression or relapse occurs in most cases after 1-3mo
o Additional chemo usually ineffective
Lymphomatoid granulomatosis: prevalence
- Rare
- Pleomorphic lymphoid neoplasm
Lymphomatoid granulomatosis: gross lesions
solitary/multiple firm, nodular pulmonary masses
Lymphomatoid granulomatosis: histo
pleomorphic mononuclear cell infiltration
o Angiocentric pattern → vascular obliteration
Lymphomatoid granulomatosis: tx
prednisone and cyclophosphamide
Post adulticide pulmonary thromboembolism: CTX
marked enlargement of lobar PA + parenchymal pulmonary infiltrates
Post adulticide pulmonary thromboembolism: tx
rapid response
o Strict cage rest for 3wk
Features/species differences: feline HW
- < % infective larvae will mature into adults in cats (1-25%) vs dogs (40-90%)
- Worm burden is ↓ compared to dogs: 1-9 worms
o Adult worm can reach significant size: female 21cm, male 12cm
o Slower development
o Shorter life span (<2y, vs 5y in dogs) - Infective larvae (L3)
o Natural resistance in cats, but still susceptible hosts
↓ period of patency
↓ # of HW
Lack of micrfilaremia
o Infective larvae poorly oriented
Adult worm more likely to develop at ectopic sites (brain, eye, subQ) - Death of migrating larvae
- SubQ nodules
- Granulomas
o Average time to develop circulating microfilariae = 8 months - Microfilariae = uncommon (<20% of cases)
o Inconsistent among cats and transient
o Low # produced → less risk of adverse reactions with treatment of preventatives
o Negative test does not r/o HW
Pathophys feline HW
- Similar to dogs
- Pulmonary vascular lesions common, more severe in caudal PAs
o Muscular hypertrophy and hyperplasia, severe in smaller PAs
o Villous endarteritis
o Adventitial cellular infiltrates - Pulmonary fibrosis
Epidemiology feline HW
o No age predilection
o Not associated to FIV/FeLV
C/s feline HW
- May die acutely, exhibit c/s or be asymptomatic
o Sudden death: from circulatory collapse and respiratory failure from acute PTE/lung injury
o C/s usually late fall, early winter months (4-7mo after exposure)
AG testing usually negative since worms are immature - C/s: most commonly associated w immature worms arriving in lungs OR death of mature worms
o Cardiopulmonary: coughing, dyspnea, syncope - Collapse, shock
- Hemoptysis
- Dyspnea/coughing
Pneumonitis
o GI: V+ → from release of inflammatory mediators → CRTZ stimuation
o Nervous system: uncommon
Blindness, seizures, ataxia, coma, circling
o Non specific: weight loss, lethargy
C/s are caused by
acute lung injury
* Type II alveolar cells hypertrophy
* Lungs become hemorrhagic and necrotic
Embolization is major contributing factor of initiating c/s
PE feline HW
usually normal
o Systolic murmur over TV and gallop can be present
o Harsh lung sounds is most frequent abnormality
Feline HW: caval syndrome
rare, w high worm burdens
o Hemoglobinuria is not consistent finding
o C/s seem to be associated w poor venous return and TR
Dx feline HW: best screening test
- Thoracic radiographs = best screening test
o Non specific pulmonary parenchymal changes
Interstitial infiltrates, perivascular densities, lung atelectasis
Can change rapidly
o Enlarged PAs with ill defined margins
Most important in caudal lung lobes
Blunting and tortuosity can be seen but less common vs dogs
Feline HW: non selective angio
dilated PAs, pruning and filling defects (worms)
Dx feline HW: serology
o Antibody → detect felin AB against adult AG
Immunofluorescent antibody test → detect AB against microfilarial cuticular AG
* Diagnostic 1/3 of time
Enzyme-linked immunofluorescent assay (ELISA) → detect AB against adult HW AG
* Positive titers detected 2-3mo after exposure
o Positive result means: cat was infected by L3, molt → L4 and lived at least 2-3mo
o Could be + w/o adult worm present if macrolide tx was instituted
* Titers will ↓ gradually post infection, undetectable after 4-6mo
o Antigen → detect adult female reproductive tract AG
ELISA or colloid gold
* Will become + 8mo post infection
False negative feline HW serology
Immunofluorescent antibody test
o Immature, sterile, unisex infection
o Absence of host response
ELISA Ag
immature infection, low worm burden (1-7 worms), male infection only
Knott’s test feline HW
o Microfilaremia: short duration and low # → usually not present at testing (>80% of cats are afilaremic)
o ↑ accuracy with large quantity of blood
Feline HW: echo/ ECG
chronic infections can have HW in PA, R heart
most often normal, can show R heart enlargement
Feline HW: CBC/chem
o Mild, non regenerative anemia
o Eosinophilia → depend on stage of infective larvae
Transient
o Basophilia: rare but suggestive of HW
Feline HW: tracheal wash/BAL
eosinophils
o 4-7mo post infection
Feline HW: DDX
HW will cause unique PA changes
* Aerulostrongylus abstrutus (lung worm)
* Paragonimus kellicotti infection
* Bronchitis/asthma
* Cardiomyopathy
Feline HW: tx
- Shorter longevity of adult HW in cats
o Natural death: can be associated with severe respiratory c/s - Conservative treatment
o Corticosteroid
May help reduce coughing, vomiting
Radiographic lesions usually progress
Do not prevent acute respiratory distress and death - Adulticide treatment
o Asymptomatic: risk and severity of post adulticide complications > risk of spontaneous HW death and embolization
o Thiacetarsamide sodium
Generally tolerated w/o immediate complication (hepatic/renal toxicity)
Strong + AG test cat: more likely to develop complications - Post adulticide rx are peracute
- Pulmonary edema: unpredictable complication during 2 days of tx
- Close monitoring 1st 2wks after tx
o Assessment of efficacy
Immature worm resistant to thiacetarsamide
AG test should be negative 12wks after
Feline HW: preventative
- Milbemycin oxime: 50mcg/kg once month
- Ivermectin: 25mcg/kg once month
