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11. Acquired heart dz > Infectious myocarditis > Flashcards

Infectious myocarditis Flashcards

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1
Q

Def and features of myocarditis

A
  • Inflammation of the myocardium
    o Focal/diffuse involvement
     Leucocytic infiltration
     Nonischemic myocyte degeneration/necrosis
    o Consequences depend on location, extent and duration
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2
Q

Dx myocarditis

A

endomyocardial biopsy is gold standard
o Elevated TnI suggest myocardial injury

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3
Q

most common etiology of myocarditis dogs

A

T cruzi
Parvovirus

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4
Q

Viral myocarditis

A

Parvovirus
West Nile virus
Distemper
K9 herpesvirus

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5
Q

Parvovirus: affected individuals

A
  • Neonatal parvovirus infection
    o Severe and fatal peracute myocarditis
     C/s from birth to 8wks
  • Cardiac form often w/o enteric involvement
     High mortality in litters btw 3-10wk/o
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6
Q

C/s parvovirus myocarditis

A

Vocalization, retching, dyspnea, sudden death

tachycardia, arrhythmia, gallop, apical systolic murmurs
 Cardiomegaly, pulmonary infiltrates

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7
Q

Survivors of parvovirus myocarditis

A

can develop fibrous scar tissue and develop arrhythmia/contractile dysfct

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8
Q

Pathophys parvo

A

cardiomyocytes mitotically active until 15 days after birth
o Viral tropism for active cells
 Major mechanism of cells death is apoptosis
 Cell cycle arrest: DNA damage
 Necrosis
o Infect the heart via leucocytes or in blood/lymph

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9
Q

Phases of pavoviral infection

A

o Acute phase: day 0-3 → viremic phase
 Systemic viremia → virus binding to myocyte coR → virus invasion into cardiomyocytes
 Virus replication → myocytolysis

o Subacute phase: day 4-14 → inflammatory phase
 Clearance of virus by natural killer cell, cytokins, perforins, neutralizing antibodies
 Mononuclear cell (cytotoxic T and B lymphocytes) enter myocardium → extensive cell damage
* Ongoing immune response perpetuates cell damage and death

o Final/chronic phase: >day 15 → healing phase
 Myofiber dropout and replacement fibrosis
 Viral persistence may lead to chronic inflammation → repetitive cycles of myocardial injury/repair → apoptosis, coronary microvascular spasms, autoimmune effects

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10
Q

Other than neonatal parvo myocarditis, what is another clinical presentation

A

o 2nd form of dz: juvenile dogs <1y/o
 Clinical presentation similar to DCM

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11
Q

Necropsy findings parvo myocarditis

A

o Pale myocardium with pale streaks
o Dilated/enlarged hearts
o +/- pericardial effusion

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12
Q

Histo findings parvo myocarditis

A

mild to severe multifocal lymphoplasmocytic myocarditis with degeneration and necrosis, fibrosis and intranuclear bodies
o Multifocal to locally extensive cardiomyocyte degeneration and necrosis
 Variable fiber size and staining affinity
 Fragmentation
 Loss of cross striation
o Mononuclear cells infiltration
 Lymphoplasmocytic
o Dense basophilic intranuclear inclusion
 Peripheralized the chromatin
o Interstitial fibrosis

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13
Q

Immunohistochemical analysis findings parvo myocarditis

A

canine parvovirus antigen found in nuclei +/- cytoplasm or myocytes

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14
Q

West nile virus myocarditis: features

A
  • Uncommon in dogs
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15
Q

West nile virus myocarditis: c/s

A

o Lethargy, inappetence, neurologic signs, fever, arrhythmias

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16
Q

West nile virus myocarditis: histo

A

o Sever lymphocytic neutrophilic myocarditis and vasculitis
o Focally extensive hemorrhage and myonecrosis

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17
Q

West nile virus myocarditis: dx

A

o Immunohistochemistry
o Reverse transcriptase polymerase chain rx testing
o Virus isolation
o Serology

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18
Q

Protozoal myocarditis agents

A

Chagas: trypanosoma cruzi
Neosporosis
Leishmaniosis

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19
Q

Chagas: prevalence

A

reported in young dogs in Southern US, Central/South America
o Zoonosis

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20
Q

Chagas hosts

A

raccoons, armadillos, opossums, dogs, cats, Guinea pigs

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21
Q

Chagas etiology

A

Trypanosoma cruzi: hemoflagellate protozoan parasite

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22
Q

Chagas life cycle/infection

A

o Transmitted by blood sucking insect of Triatoma subfamily
 Trypomastigote enters insect after feeding on infected host → transforms to epimastigote → multiply by binary fission → transforms back to trypomastigote in hindgut → excreted in feces deposit into fresh wound during feeding
 Infection in blood → remain free in circulation or trypomastigote infect macrophages → evade immune system and spread
 Hematogenous spread → infect cardiomyocytes → amastigotes → multiply by binary fission → convert back to trypomastigotes → rupture and release from cell back into circulation

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23
Q

Chagas: acute infection = c/s

A

weight loss, D+, lethargy, anorexia, lymphadenopathy, spleno/hepatomegaly, myocarditis, sudden death
 Parasitemia: as early as 3 days after infection, peak after 17 days, subpatent after 30 days
 C/s of myocarditis develop around day 14, resolve day 28
* Myocarditis develop 2nd to  damage and inflammation as trypomastigotes rupture from cardiomyocytes
* No echo changes, but arrhythmias may be present
 Dogs >6mo/o may not exhibit acute phase c/s

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24
Q

Chagas: latent phase

A

long 27-120 days
 Can remain asymptomatic for life
 Sudden death still possible

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25
Chagas: chronic phase feature
progressive myocardial dz over next 8-36mo  Arrhythmias, conduction disturbances: * Atrial/ventricular arrhythmias: sinus tachycardia, * 1 or 2AVB * Axis shift, RBBB, T wave inversion * ↓ R wave amplitude  Chamber enlargement and CHF * DCM occurs when fibrosis no longer permit compensatory hypertrophy * Indistinguishable from DCM
26
Chagas dx
demonstrate parasitemia o Blood smear: trypomastigote may be present in acute infection o Serology/PCR  Indirect fluorescent antibody assay  Enzyme-linked immunosorbent assay  Radioimmunoprecipitation assay  *careful cross rx w Leishmania antibodies o Culture o Serum TnI progressively increase, peak at day 21 around 10-30mg/dL
27
Chagas echo findings
o ↓LV fct w ↓ FS/EF% o ↓LVFW thickness o ↑end systolic volume
28
Pathogenesis of myocarditis and DCM phenotype in Chagas
 Immune mediated mechanism  Toxic parasitic products directed against cardiomyocytes  Microvascular dz + platelet dysfct
29
Treatment chagas
c/s o Destruction of intra form may result in severe exacerbation of host inflammatory response
30
Necropsy chagas
o Multiple pale areas in myocardium  Especially RA/RV
31
Histology Chagas
active granulomatous myocarditis o Infiltration of lymphocytes, plasma cells, macrophages o Perivasculitis o Clusters of T cruzi amastigotes (acute infection)  Parasitic pseudocysts o Fibrosis: chronically affected dogs (minimal if acute)  Often extensive in RA/RV, around conduction system
32
Prevalence of toxoplasma myocarditis
commonly reported in cats o Myocarditis rarely identified antemortem (1 reported case)  Toxoplasma organisms identified in 63% of 59 in one study, and all 21 kittens in another study  Not uncommon complication in Hu
33
Signs of toxoplasma infection
o Ocular, pulmonic, hepatic, neurological, GI, muscular abnormalites
34
Etiology toxoplasmose
Toxoplasma gondii o Can encyst in the myocardium o Chronic infection
35
Pathophys toxoplasmose
o Cyst rupture  Myocardial necrosis  Hypersensitivity reaction → myocarditis, pericarditis, CHF * Polymorphonuclear leucocytic and lymphocytic infiltrates o Infects multiple tissues  Heart  Peripheral muscles  CNS
36
Dx toxo myocarditis
o Serology → rising titers of serum antibodies (IgG, IgM) o BW: neutrophilia, lymphocytosis, monocytosis  Hypoalbuminemia in acute phase  ↑CK Echo changes
37
Echo changes toxoplasmosis myocarditis
 Pericardial effusion  ↑ myocardial echogenicity with granular appearance * Generalized, symmetric thickening of ventricular walls * Predominantly RVFW  Distorted IAS * ↑echogenicity * Nodular appearance
38
Echo changes evolution w/ toxoplasmosis
 After 3 weeks of tx: ↓ wall thickness, resolved pericardial effusion, ↓ nodularity of IAS  After 8 weeks of tx: heart appeared normal except hyperechogenic line on IAS
39
Etiology neosporosis
Neospora caninum o Obligate intracell protozoan o Worldwide distribution o Similar life cycle to toxoplasma gondii
40
Neosporosis in dogs
o Sporadic dz in dogs  Adult dogs: meningomyeloencephalitis most common, myocarditis, sudden death, polymyositis, dermatitis, pneumonia reported * Myocarditis reported in Mastiff, rare
41
Neosporosis in cattles
o Important cause of abortion in cattles
42
DX neosporosis
o Serology: antibodies o Immunohistochemestry o Electron microscopy
43
Tx neosporosis
clindamycin, potentiated sulfonamide and/or pyrimethamide
44
Necropsy findings neosporisis
1 dog (Mastiff): sudden death o Raised, mottled red and white transmural infarct in apical RVFW and LV papillary muscle  Sharply demarcated from adjacent myocardium o Multifocal, irregular, small, firm, pale, raised subendocardial lesion in RAA and RVFW o Pericardial effusion
45
Histo findings neosporosis
acute necrotizing myocarditis with myocardial infarct and intra tachyzoites o Infarct: edema +  Thick interwoven bands of fibromuscular tissue  Extensive loss of myocardial fibers o Oval intracytoplasmic vacuoles containing dozens of lunate-shaped tachyzoites o Perivascular to interstitial neutrophils, lymphocytes, plasma cells o Mild interstitial non suppurative myocarditis focally extended to endocardial surface
46
Leishmaniosis etiology
protozoal organism o Endemic in Mediterranean basin
47
Pathophys leshmaniosis myocarditis
direct action of parasite into myocardium → intense inflammatory response
48
C/s leishmaniose myocarditis
arrhythmias → 1AVB
49
Bacterial myocarditis can occur if
o Bacteremia, sepsis o Endocarditis: suppurative myocarditis  Extension of valvular lesion  Coronary circulation
50
Agents of bacterial myocarditis
o Staph/strep species, E coli: most common o Gram – in cats o Anaerobe/mycobacteria: less common o Borrelia burgdorferi
51
Most common manif of lyme disease w/ heart
 Lyme disease reported, proven cardiac sequelae rare (10% of patients in Hu)  Most common manifestation: 3AVB (1 and 2AVB reported)
52
Histo changes lyme dz myocarditis
* Multifocal myocardial necrosis * Infiltration of lymphocytes, plasma cell, macrophages, neutrophils
53
Dx lyme dz myocarditis
endomyocardial biopsies, antibody titers, necropsy
54
Pathophys of bacterial myocarditis
* Myocardial damage from bacterial toxins or immune mediated process
55
C/s bacterial myocardtis
arrhythmia mostly
56
Dx bacterial myocarditis
o Blood culture: if negative, may be secondary to Bartonella spp
57
Endocarditis incidence
0.1-1% of cases o Uncommon in cats o Male > 2x females
58
Endocarditis predisposition
o Valvular congenital defects predispose to development.  SAS → majority of dogs will not develop endocarditis  80% of dogs with endocarditis do not have any valvular lesions
59
Etiology endocarditis
o Gram + more likely vs gram – o Most common agents: staph, strept, gram – rods, enterococci, Bartonella  Bartonella: most commonly involve AoV * Absence of fever * Negative culture * Worse px, higher prevalence of CHF  Streptococcus canis: most commonly involve MV * Secondary polyarthritis  Gram - → less likely to develop CHF
60
What determine likelihood of infection
virulence factors of bacteria
61
Which agent involves most commonly AoV
Bartonella
62
Which agent involves most commonly MV
Strep canis
63
Pathophys endocarditis
o MV and AoV most commonly affected  MV: larger septal leaflet > mural leaflet o TV and ventricular wall rarely involved
64
Dx endocarditis
o BW: mild non regenerative anemia, neutrophilia w L shift and neutrophil toxicity, lymphopenia, monocytosis  Azotemia, ↑liver enzymes, mild hyperbilirubinemia  Electrolyte and acid base abnormalities: ↑anion gap, metabolic acidosis, lactic acidosis  Hyperglycemia (early septic shock), hypoglycemia if liver failure  Hypoalbuminemia: mild to severe, from * ↓ hepatic production * ↑ vascular permeability * Inflammatory response (negative acute phase protein) o UA: proteinuria, pyuria, cylindruria, microscopic hematuria, bacteriuria
65
Mycotic/fungal myocarditis features
* Extremely rare o Immunocompromised patients o Hematogenous spread
66
Mycotic/fungal myocarditis agents
o Cryptococcosis o Coccidioidomycosis o Aspergillosis o Saprophytic fongi o Blastomycosis
67
Mycotic/fungal myocarditis reports
* Cardiac compression from extra cardiac granulomas reported in 2 dogs o Myocardial, epicardial, pericardial, valvular involvement
68
Rickettsial myocarditis etiology
Ehrlichia canis, Rickettsia rickettsia, Bartonella elizabethae
69
Sarcocystis etiology
Sarcocystic neurona o Eosinophilic granulomatous reaction to degenerating cysts  Heart and skeletal muscle o Extremely rare
70
Sarcocystis histology
o Necrotizing myocarditis in RV and LV  Coalescing areas with lymphocytic infiltration  Degenerated cysts w/I foci of myocarditis  Cyst content = highly toxic o Myocardial infarcts
71
Angiostrongylosis etiology
Angiostrongylus vasorum o Metastrongyloid parasite of the R heart and PAs in dogs
72
Angiostrongylosis pathogenesis
multifocal granulomatous myocarditis centered around migrating larvae o Adult worm: live in PA vessels and R heart  Release eggs/larvae into pulmonary circulation
73
Angiostrongylosis c/s
wide spectrum o Mild respiratory signs o Severe form: coagulative, respiratory, neurologic, cardiovascular, ocular signs  Attenuated cardiac sounds, heart murmurs  Myocarditis  CHF  Periarteritis  Hematoma o Pulmonary hypertension: <5% of cases, but 1/3 of dogs referred for echo
74
Angiostrongylosis echo
o RAE, RVE o Bulging IAS o Dilated CaVC and hepatic veins o Severe TR
75
Angiostrongylosis CTX
RVE, truncated PAs, ↑VHS
76
Angiostrongylosis histo
lesions involved 20% of myocardium o Nematode larvae scattered into myocardium o Surrounded by reactive macrophages, giant  of foreign body type, lymphocytes, eosinophils o Focal degeneration of myocardiocytes o Mild multifocal interstitial fibrosis
77
Spirocercosis etiology
Spirocerca spp o Endemic in some warm climates
78
Spirocercosis pathophys
verminous arteritis o Will invade lumen/wall of arteries  Can migrate in tissues and cause vasculitis  Genera Strongylus and Ascaris o Aortic lesions can lead to Ao rupture/aneurysm  Spirocerca lupi: adventitia of thoracic Ao during part of its life cycle * Final habitat in esophagus * Migration through Ao wall to esophagus may cause o Mediastinitis, pleuritis, pyothorax
79
Spirocercosis c/s
GI, respiratory, circulatory signs
80
Transmissible myocarditis and diaphragmatitis features
* Fever in cats usually biphasic o Day 9-16 and days 17-27 after infection * Normal testing: BW, UA, CTX, AUS, FIv/FeLV/FIP
81
Transmissible myocarditis and diaphragmatitis necropsy
1-3mm pale foci w/I myocardium and diaphragm
82
Transmissible myocarditis and diaphragmatitis histo
myonecrosis with inflammatory infiltrates * No organism identified

11. Acquired heart dz (18 decks)

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