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11. Acquired heart dz > HW > Flashcards

HW Flashcards

1
Q

Def caval syndrome

A
  • Acute manifestation of HW disease
    o Large # of HW in R heart → 30-200 worms
    o Intertwined, trapped in TV apparatus
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2
Q

Prevalence caval syndrome

A

uncommon
o Sex predilection: 75-90% males

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3
Q

Pathophys caval syndrome

A
  • 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
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4
Q

Etiology caval syndrome

A

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

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5
Q

C/s caval syndrome

A
  • Cardiogenic shock and circulatory collapse
    o Anorexia, depression, weakness
    o Respiratory signs: dyspnea, tachypnea, coughing
  • Dark brown to black urine
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6
Q

PE caval syndrome

A
  • Heart murmur: R sided systolic apical murmur (87% of cases), loud/split S2, gallop
  • R-CHF: ascites, hepatomegaly, jugular vein distension
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7
Q

Dx BW/UA caval syndrome

A

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)

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8
Q

CTX caval syndrome

A

R heart enlargement, tortuous PA, interstitial parenchymal changes

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9
Q

ECG caval syndrome

A

R axis deviation
o Deep S wave in lead I,II,III, aVF (56%)
o Arrhythmias: sinus tachycardia (33%), APC (28%), VPC (6%)

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10
Q

Echo caval syndrome

A

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

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11
Q

Cardiac KT caval syndrome

A

↑ pressures in RA, RV, PA

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12
Q

Px caval syndrome

A
  • Guarded to poor: 30-40% mortality with appropriate tx
  • Death in 24-72h w/o tx
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13
Q

Complications after tx

A

o Organ failure
o DIC

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14
Q

Tx caval syndrome

A
  • 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
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15
Q

What causes complications in caval syndrome

A
  • Maceration of worms → massive AG release
    o Can lead to severe pulmonary vasoconstriction
    o DIC
    o Administration of parenteral corticosteroids + heparin necessary
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16
Q

After procedure (caval syndrome) care

A

o Adulticide should be given → kill remaining worms
o Disappearance of TR, ↑CO and ↓RAP may take several days

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17
Q

Vector of dirofilaria immitis

A
  • 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
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18
Q

Life cycle of dirofilaria immitis

A
  • 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
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19
Q

Steps of infection/life stages dirofilaria immitis

A
  • 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 > 27C
     Development does not occur <14C
    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
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20
Q

Life span worms

A

5-7years

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21
Q

Pathophys: what causes c/s and disease severity

A
  • 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
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22
Q

Severity of lesions to lungs are related to

A

 # of worms
 Duration of infection
* Reversible in 4-6wks if brief infection
 Host and parasite interaction

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23
Q

Worms are triggered by

A

toxic substances, immunologic response, physical trauma

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24
Q

Histo lesions lung vessels

A

 Villous myointimal proliferation
 Inflammation
 Pulmonary hypertension
 Disruption of vascular integrity
 Fibrosis
 Arterial obstruction/vasoconstriction from live worms
 Thromboemboli of dead worms

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25
Q

When do pulmonary vascular lesions develop and order

A

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

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26
Q

Gross exam

A

o Enlarged, tortuous PAs
 Thick walls
 Rough endothelial surfaces
o Vessels of caudal lung lobes more severely affected
o Partially reversible changes

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27
Q

Effect of exercise

A

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

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28
Q

Etiology of pulmonary vasoconstriction

A

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

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29
Q

Pathophys of PTE

A

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

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30
Q

Wolbachia

A
  • Wolbachia pipientis: symbiotic relationship
    o Identified in glomerulus and lungs of infected HW dogs
    o Contribute to inflammatory response by producing proteins
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31
Q

Comorbidities from HW

A
  • 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
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32
Q

Occult infection prevalence

A

20% of cases

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33
Q

Causes of amicrofilarial infections

A

o Prepatent period
o Single sex infection
o Infertile adult worms from drug therapy
o IM destruction of microfilariae

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34
Q

Dx occult infection

A
  • Can be detected by serologic testing
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35
Q

Prepatent period

A

 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)

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36
Q

Single sex infection

A

 More frequent in regions w low HW incidence
 Fewer larvae inoculated in host

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37
Q

Infertile adult worms from drug tx

A

 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

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38
Q

IM destruction of microfilariae

A

 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

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39
Q

Clinical syndromes associated w/ IM destruction of worms

A
  • Allergic pneumonitis
  • Pulmonary eosinophilic granulomatosis
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40
Q

C/s depend on

A

of worms, duration of infection, host response

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41
Q

C/s

A

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

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42
Q

PE

A

split S2, R apical gallop, crackles

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43
Q

Classification of syndrome

A
  • Class 1: asymptomatic/mild symptoms
    o Px: excellent
  • Class 2: moderate dz
  • Class 3: severe dz
    o Px: poor
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44
Q

Dx: what improves testing accuracy of microfilariae

A
  • 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
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45
Q

Tests for dx Microfilarial testing

A

o Microscopic identification on direct blood smear
o Above buffy coat in microhematrocrit tube
o Modified Knott test
o Milipore filtration

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46
Q

Microscopic identification on direct blood smear

A

 Permit examination of larval motion
 Distinction of Dirofilaria Immitis and Dipetalonema reconditum
* D. reconditum does not require adulticide tx
* ↓ [microfilariae]

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47
Q

Microfilarial testing: False negative results

A

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

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48
Q

When should microfilarial detection should be performed

A
  • 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
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49
Q

Immunodiagnostic antigen test

A
  • Detect AG from adult female worms
    o Semi quantitative ELIS assay → rapid strong reaction = high burden
    o Sensitivity 70%, specificity 97%
50
Q

Immunodiagnostic antigen test: false negatives

A

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)

51
Q

Immunodiagnostic antigen test: false positives

A

uncommon
o Problem if low prevalence
o Weakly + result should always be repeated.

52
Q

What is the only effective test in dogs receiving monthly preventatives.

A

Immunodiagnostic antigen test

53
Q

Best test to evaluate severity of infection

A

CTX
and evaluate pulmonary parenchymal changes

54
Q

Prevalence of abn CTX

A
  • Abnormalities present in 85% of cases, develop early in dz course
55
Q

CTX changes

A

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

56
Q

sensitive indicator of HW associated CHF

A
  • Marked enlargement of cranial lobar PA
57
Q

What causes ↑ interstitial density

A

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

58
Q

CBC changes

A

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

59
Q

Chem changes

A

↑ liver enzyme(10%), hyperbilirubinemia,
o Hypoproteinemia (severe infection) → from protein-losing glomerulonephropathy

60
Q

UA changes

A

albuminuria (10-30%)

61
Q

ECG

A

not very useful, normal in 90% of cases

62
Q

Echo: clinical utility

A
  • Evaluation of R sided function
  • Estimate # and location of HW
  • Determine severity of PH
63
Q

Prophylaxis

A

Diethylcarbamazine
Macrocyclic lactone (macrolide) antibiotics

64
Q

Diethylcarbamazine: risks, target and dosing

A
  • 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
65
Q

Macrocyclic lactone: target, dosing

A
  • 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
66
Q

Which dogs will have less severe rx to tx w/ macrocyclic lactones

A
  • Microfilaremic dog
67
Q

Types of macrocyclic lactones

A

Ivermectin (Heartguard)
Milbemycin oxime (Interceptor)
Selamectin (Revolution)
Moxidectin (Advantage multi)

68
Q

Ivermectin

A
  • 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
69
Q

Milbemycin oxime

A
  • 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
70
Q

Moxidectin

A
  • Narrow spectrum HW preventative
  • Gradual microfilaricidal effect
    o No adverse effects
  • Safe in Collies, careful in puppies <6mo and cats
71
Q

Which dogs will benefit from adulticide tx

A
  • 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
72
Q

Monitoring after adulticide tx

A

stop If anorexia, perisistent vomiting, icterus
o Rise in liver enzymes is often seen in dogs tolerating tx

73
Q

Adulticide agents

A

Melarsomine dihydrochloride
Thiacetarsamide

74
Q

Melarsomine dihydrochloride: target, protocol

A
  • 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
75
Q

Melarsomine dihydrochloride: toxicity

A
  • 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.
76
Q

Thiacetarsamide: determinant of efficacity, protocol

A
  • 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
77
Q

Thiacetarsamide: disadvantages

A

o Narrow therapeutic index
o Lack efficacy against young female worm
o IV administration

78
Q

Thiacetarsamide: toxicity

A
  • Acute hepatic toxicity can occur → abort protocol
    o Most often after 1st injection
    o 20% of dogs
79
Q

Ancillar drug therapy w/ adulticide

A
  • 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
80
Q

Tx modification w/ severe HW dz

A
  • 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
81
Q

Assessment of treatment efficacy

A
  • Seroconversion usually by 3 months
    o Can occur as late as 5 months
  • False negative can occur if <1-2 adult worms <8mo/old
82
Q

If persistent positive result, decision to treat again based on several factors

A

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

83
Q

HW related clinical syndromes

A

Eosinophilic pneumonitis

Pulmonary granulomas
- Eosinophilic pulmonary granulomatosis
- Lymphomatoid granulomatosis

Post adulticide pulmonary thromboembolism

84
Q

Eosinophilic pneumonitis: cause, prevalence

A
  • 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
85
Q

Eosinophilic pneumonitis: c/s

A

progressive over few weeks → 6mo
o Coughing, dyspnea
o Mild cyanosis, anorexia, weight loss if severe

86
Q

Eosinophilic pneumonitis: CTX

A

diffuse, bilateral, lineal interstitial and alveolar pulmonary infiltrates

87
Q

Eosinophilic pneumonitis: BW

A

eosinophilia, basophilia, hyperglobuminemia

88
Q

Eosinophilic pneumonitis: dx

A
  • Transtracheal lavage: sterile, eosinophilic exsudate
89
Q

Eosinophilic pneumonitis: tx

A

corticosteroids
o Rapid, complete resolution of c/s and CTX changes in 3-5 days
o Steroids can be stopped when resolved

90
Q

Eosinophilic pulmonary granulomatosis: distinguish from

A

metastatic pulmonary neoplasia, systemic mycoses, lymphmatoid granulomatosis

91
Q

Eosinophilic pulmonary granulomatosis: lesions

A

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

92
Q

Eosinophilic pulmonary granulomatosis: c/s

A

o Chronic coughing and dyspnea
o HW treated or untreated dogs

93
Q

Eosinophilic pulmonary granulomatosis: CTX

A

o Multiple pulmonary masses: 1-20cm
o Mixed interstitial-alveolar, bronchial lung patterns
o Hilar lymphadenopathy
o Pleural effusion
o Mediastinal, intra-tracheal masses

94
Q

Eosinophilic pulmonary granulomatosis: BW

A

eosinophilia, neutrophilia (2/3 of dogs)

95
Q

Eosinophilic pulmonary granulomatosis: tx

A

o Most repond to immunosuppressive and cytotoxic drug
o Prednisone can produce partial, occasionally complete remission

96
Q

Eosinophilic pulmonary granulomatosis: px

A

o Progression or relapse occurs in most cases after 1-3mo
o Additional chemo usually ineffective

97
Q

Lymphomatoid granulomatosis: prevalence

A
  • Rare
  • Pleomorphic lymphoid neoplasm
98
Q

Lymphomatoid granulomatosis: gross lesions

A

solitary/multiple firm, nodular pulmonary masses

99
Q

Lymphomatoid granulomatosis: histo

A

pleomorphic mononuclear cell infiltration
o Angiocentric pattern → vascular obliteration

100
Q

Lymphomatoid granulomatosis: tx

A

prednisone and cyclophosphamide

101
Q

Post adulticide pulmonary thromboembolism: CTX

A

marked enlargement of lobar PA + parenchymal pulmonary infiltrates

102
Q

Post adulticide pulmonary thromboembolism: tx

A

rapid response
o Strict cage rest for 3wk

103
Q

Features/species differences: feline HW

A
  • < % 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
104
Q

Pathophys feline HW

A
  • 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
105
Q

Epidemiology feline HW

A

o No age predilection
o Not associated to FIV/FeLV

106
Q

C/s feline HW

A
  • 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

107
Q

C/s are caused by

A

acute lung injury
* Type II alveolar cells hypertrophy
* Lungs become hemorrhagic and necrotic
 Embolization is major contributing factor of initiating c/s

108
Q

PE feline HW

A

usually normal
o Systolic murmur over TV and gallop can be present
o Harsh lung sounds is most frequent abnormality

109
Q

Feline HW: caval syndrome

A

rare, w high worm burdens
o Hemoglobinuria is not consistent finding
o C/s seem to be associated w poor venous return and TR

110
Q

Dx feline HW: best screening test

A
  • 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
111
Q

Feline HW: non selective angio

A

dilated PAs, pruning and filling defects (worms)

112
Q

Dx feline HW: serology

A

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

113
Q

False negative feline HW serology

A

 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

114
Q

Knott’s test feline HW

A

o Microfilaremia: short duration and low # → usually not present at testing (>80% of cats are afilaremic)
o ↑ accuracy with large quantity of blood

115
Q

Feline HW: echo/ ECG

A

chronic infections can have HW in PA, R heart

most often normal, can show R heart enlargement

116
Q

Feline HW: CBC/chem

A

o Mild, non regenerative anemia
o Eosinophilia → depend on stage of infective larvae
 Transient
o Basophilia: rare but suggestive of HW

117
Q

Feline HW: tracheal wash/BAL

A

eosinophils
o 4-7mo post infection

118
Q

Feline HW: DDX

A

HW will cause unique PA changes
* Aerulostrongylus abstrutus (lung worm)
* Paragonimus kellicotti infection
* Bronchitis/asthma
* Cardiomyopathy

119
Q

Feline HW: tx

A
  • 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
120
Q

Feline HW: preventative

A
  • Milbemycin oxime: 50mcg/kg once month
  • Ivermectin: 25mcg/kg once month

11. Acquired heart dz (18 decks)

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