NAVLE Cardiovascular

Camelidae and Cervidae Pericarditis and Epicarditis – NAVLE Study Guide

Pericarditis (inflammation of the pericardium) and epicarditis (inflammation of the epicardium/visceral pericardium) represent important cardiovascular conditions in camelids and cervids.

Overview and Clinical Importance

Pericarditis (inflammation of the pericardium) and epicarditis (inflammation of the epicardium/visceral pericardium) represent important cardiovascular conditions in camelids and cervids. While relatively uncommon compared to cattle, these conditions carry significant clinical importance for veterinary practitioners working with llamas, alpacas, deer, and elk. The pericardium consists of two layers: the fibrous pericardium (outer layer) and the serous pericardium, which is divided into the parietal layer (lining the fibrous pericardium) and the visceral layer (epicardium, covering the heart surface). Inflammation of these structures leads to fluid accumulation, fibrin deposition, and potentially life-threatening cardiac tamponade.

In camelids, pericarditis most commonly occurs as part of polyserositis associated with septicemic bacterial infections, particularly Streptococcus equi subspecies zooepidemicus (alpaca fever). In cervids, pericardial disease is less well documented but can occur secondary to systemic infections, trauma, or as part of multisystemic disease processes.

Parameter Alpaca (Normal) Llama (Normal)
Heart Rate 50-110 bpm 60-90 bpm
Rhythm Sinus arrhythmia common (87.5%) Sinus arrhythmia common
Fractional Shortening Greater than or equal to 25% Greater than or equal to 25%
Echo Window 4th-5th ICS, right side 4th-5th ICS, right side

Anatomical Considerations

Camelid Cardiac Anatomy

The alpaca heart is located in the middle mediastinum with a craniocaudal extension from the third to the sixth rib. Unlike domestic ruminants, no ligament connects the fibrous pericardium to the sternum or diaphragm in alpacas, which may have implications for pericardial mobility and disease presentation. The Purkinje fiber network in camelids penetrates completely through the ventricular wall from endocardium to epicardium (similar to sheep), resulting in distinctive ECG patterns that differ from dogs and cats.

Normal Camelid Cardiac Parameters

High-YieldThe prevalence of congenital heart disease is higher in camelids than in other domestic species. Complex defects involving the great vessels are more frequently encountered in llamas and alpacas than in other species. Always perform cardiac auscultation and consider echocardiography when evaluating sick camelids.

Cervid Cardiac Anatomy

Cervids (deer, elk, moose) share cardiac anatomical features with domestic ruminants. The heart is located in the thoracic cavity with similar positioning to cattle. Sarcocysts in the myocardium are commonly found in wild deer populations (affecting up to 42% of free-living deer in some studies) and may be associated with interstitial cellularity and myocardial changes. Cardiovascular disease in cervids can include aortic lesions ranging from lipid streaking to massive calcium deposits, coronary artery changes, and pericardial involvement.

Type Characteristics Common Causes
Fibrinous Fibrin strands cover epicardium; "bread and butter" appearance; small fluid volume Septicemia, bacterial infections, polyserositis syndromes
Serous/Effusive Clear to straw-colored fluid accumulation; can cause tamponade Heart failure, hypoproteinemia, early infection
Suppurative/Purulent Purulent exudate up to 4 liters; foul odor; severe ventricular constriction Pyogenic bacteria (Staphylococcus, Streptococcus), foreign body
Hemorrhagic Blood-tinged to frank hemorrhage in pericardial sac Trauma, neoplasia, coagulopathy, clostridial disease
Constrictive Fibrous thickening and adhesions; chronic progression from acute forms End-stage chronic pericarditis, organized fibrin

Etiology and Pathophysiology

Classification of Pericarditis

Etiologies in Camelidae

Alpaca Fever (Streptococcus equi ssp. zooepidemicus)

The most clinically important cause of pericarditis in camelids is Streptococcus equi subspecies zooepidemicus septicemia, commonly called "alpaca fever." This gram-positive, beta-hemolytic, Lancefield group C organism causes characteristic fibrinosuppurative polyserositis affecting the pericardium, pleura, and peritoneum. The disease was first described in Peru, where morbidity in some herds reaches 5-10%, with mortality rates of 50-100% in untreated cases.

Alpaca Fever: Key Features

NAVLE TipWhen you see a recently transported alpaca or llama with acute fever, depression, and recumbency, think "alpaca fever" (S. equi ssp. zooepidemicus polyserositis) first. Remember the mnemonic: "STRESS" = Streptococcus, Transport, Recumbency, Effusions (polyserositis), Septicemia, Sudden death

Other Causes in Camelids

  • Clostridial infections: C. perfringens can cause enterotoxemia with hydropericardium and pulmonary edema
  • Lymphoma: Most common cardiac tumor in camelids; heart involved in 25-40% of camelids with lymphoma; can cause pericardial effusion/tamponade
  • Heart failure: Secondary mild pericardial effusion can occur with severe heart failure or hypoproteinemia
  • Endocarditis extension: Mural endocarditis (more common in camelids than valvular) can extend to epicardium

Etiologies in Cervidae

Pericardial disease in cervids (deer, elk, moose) is less well documented than in camelids or cattle. Potential causes include:

  • Septicemic infections: Histophilus somni, Pasteurella multocida, Mannheimia haemolytica can cause polyserositis similar to bovine disease
  • Parasitic myocarditis: Sarcocysts commonly affect wild deer myocardium (up to 42% prevalence) and may involve the epicardium
  • Traumatic pericarditis: Less common than in cattle due to different feeding behavior, but can occur in farmed cervids fed processed feeds containing wire or metal
  • Cardiovascular degeneration: Aortic lesions and coronary artery changes have been documented in wild red deer
Feature Description
Predisposing Factors Stress (transport, overcrowding), contact with horses, immunosuppression
Clinical Signs Fever, depression, anorexia, recumbency, sudden death
Gross Pathology Fibrin strands on pleura and pericardium, serofibrinous thoracic effusion, epicardial ecchymoses, hydropericardium
Histopathology Fibrinocellular polyserositis with fibrin, macrophages, lymphocytes, plasma cells, neutrophils, and gram-positive cocci
Zoonotic Potential Yes - can cause meningitis, endocarditis in humans; associated with unpasteurized dairy and horse contact

Clinical Signs and Presentation

Acute Pericarditis

The clinical presentation of pericarditis depends on the underlying cause, rate of fluid accumulation, and presence of concurrent disease. Acute pericarditis, particularly as part of septicemic polyserositis, typically presents with:

Cardiac Tamponade

Cardiac tamponade occurs when pericardial fluid accumulation raises intrapericardial pressure sufficiently to impair cardiac filling. Right-sided heart failure signs predominate because right atrial and ventricular diastolic pressures need to increase only from 5 mmHg to 10-15 mmHg to cause clinical signs, while left-sided pressures must exceed 20 mmHg.

Classic findings of tamponade:

  • Muffled/distant heart sounds
  • Jugular venous distension with or without pulsation
  • Hypotension or weak arterial pulses
  • Pulsus paradoxus (exaggerated decrease in arterial pressure with inspiration)
  • Tachycardia
High-YieldRemember "Beck's Triad" for cardiac tamponade: (1) Muffled heart sounds, (2) Jugular venous distension, (3) Hypotension. While described in human medicine, these findings apply to veterinary patients as well.
System Clinical Signs
General/Constitutional Fever, depression, anorexia, weight loss, lethargy, recumbency
Cardiovascular Tachycardia, muffled heart sounds, pericardial friction rub (early fibrinous stage), jugular distension, jugular pulsation
Respiratory Tachypnea, dyspnea, decreased lung sounds (pleural effusion)
Edema/Effusions Ventral/brisket edema, submandibular edema, ascites
Pain Signs Elbow abduction, reluctance to move, grunting, arched back, extended neck

Diagnostic Approach

Laboratory Findings

Laboratory abnormalities in pericarditis are often nonspecific but support the presence of inflammation and may indicate organ dysfunction secondary to compromised cardiac output:

Echocardiography

Echocardiography is the gold standard for diagnosing pericardial disease and assessing hemodynamic impact. In camelids, standard echocardiographic examination is performed from the right parasternal window at the 4th-5th intercostal space using a low-frequency (2-3.5 MHz) transducer for adults or higher frequency (5-7.5 MHz) for crias.

Echocardiographic Findings in Pericarditis

Pericardiocentesis

Ultrasound-guided pericardiocentesis may be performed diagnostically or therapeutically through the 4th intercostal space on either side, taking care to avoid the heart. Analysis of pericardial fluid includes:

  • Gross appearance: Color, turbidity, odor (septic pericarditis often has foul odor)
  • Cytology: Cell count, differential, presence of bacteria (intracellular or extracellular)
  • Culture: Aerobic and anaerobic bacterial culture with sensitivity testing
  • Protein/specific gravity: Distinguishes transudate from exudate

Electrocardiography

Important limitation: ECG in camelids provides limited information about cardiac chamber size due to extensive Purkinje fiber penetration throughout the myocardium. However, ECG may show:

  • Sinus tachycardia
  • Decreased QRS voltage (with significant effusion)
  • Electrical alternans (varying QRS amplitude with cardiac swinging)
  • Premature complexes or arrhythmias
High-YieldUnlike small animals where ECG changes are diagnostically valuable in pericardial disease, the extensive Purkinje fiber network in camelids limits ECG utility. Echocardiography is essential for definitive diagnosis.
Test Expected Finding Significance
CBC Leukocytosis with neutrophilia; or leukopenia with degenerative left shift (septicemia) Acute inflammatory response; leukopenia suggests overwhelming infection
Fibrinogen Hyperfibrinogenemia Indicator of inflammation (positive in more than 90% of cattle with TP)
Total Protein Hyperproteinemia (hyperglobulinemia) or hypoalbuminemia Inflammatory response; protein loss with effusions
Liver Enzymes Elevated GGT, AST Hepatic congestion secondary to right heart failure
Cardiac Biomarkers Elevated cTnI, CK-MB, LDH Myocardial damage; useful prognostic indicator
Blood Culture May isolate causative organism Confirms septicemia; guides antibiotic selection

Treatment and Management

Antimicrobial Therapy

For septic pericarditis and polyserositis (particularly S. equi ssp. zooepidemicus), aggressive antimicrobial therapy is essential. Antimicrobial selection should ideally be guided by culture and sensitivity, but empirical therapy is often initiated while awaiting results:

Supportive Care

  • Fluid therapy: IV crystalloid fluids for dehydration and cardiovascular support; avoid fluid overload in animals with significant effusion
  • NSAIDs: Flunixin meglumine (1 mg/kg IV q 12-24h) for anti-inflammatory and analgesic effects
  • Analgesia: Butorphanol (0.1 mg/kg SC) for additional pain control
  • Diuretics: Furosemide (1-2 mg/kg) may provide short-term relief of congestive signs; use cautiously
  • Nutritional support: Partial parenteral nutrition if anorexic; maintain hydration and caloric intake

Pericardiocentesis and Surgical Options

Pericardiocentesis can relieve cardiac tamponade and provide diagnostic samples. However, results in septic pericarditis are often disappointing as fibrinous/purulent material may be too thick for needle drainage. For valuable animals, options include:

  • Repeated pericardiocentesis: May be performed daily with indwelling catheter for drainage and local antibiotic infusion
  • Pericardiotomy: Fifth rib resection approach; allows evacuation and lavage of pericardial sac
  • Pericardiectomy: Partial or subtotal removal of pericardium; may be considered for constrictive pericarditis
NAVLE TipFor NAVLE, remember that treatment of traumatic pericarditis in ruminants is generally unrewarding with poor prognosis. In contrast, septic pericarditis secondary to polyserositis in camelids (alpaca fever) may respond favorably to aggressive antimicrobial therapy if treated early, with rapid clinical improvement often seen within 24 hours of initiating appropriate antibiotics.
Finding Description and Significance
Pericardial Effusion Anechoic (clear fluid) to echogenic (fibrin, cellular material) space between epicardium and pericardium
Fibrin Strands Echogenic strands or deposits on epicardial surface; indicates fibrinous pericarditis
Cardiac Swinging Heart swinging within large effusion; causes electrical alternans on ECG
Chamber Collapse RA collapse (diastolic), RV collapse (diastolic); indicates tamponade physiology
Ventricular Compression Ventricles compressed by effusion; reduced diastolic filling
Pleural Effusion Often concurrent with pericardial disease in polyserositis; seen as anechoic space in thorax

Prognosis

Prognosis varies significantly based on the underlying etiology and stage of disease at presentation:

Drug Dose Route/Frequency Notes
Ceftiofur sodium 5 mg/kg IV q 12h First-line for S. equi ssp. zooepidemicus
Ceftiofur crystalline free acid 6.6 mg/kg SC (neck) Long-acting; off-label in camelids; used for herd treatment
Ampicillin sodium 12 mg/kg IV q 12h Alternative for gram-positive coverage
Penicillin G 22,000-44,000 IU/kg IM q 12h Effective against streptococci
Chlortetracycline (feed) 2.2 mg/kg/day PO in feed Herd prophylaxis; empirical use during outbreaks

Prevention and Herd Management

Prevention strategies focus on reducing stress and limiting exposure to infectious agents:

  • Minimize transport stress: Adequate rest periods, appropriate climate control, minimize commingling
  • Quarantine new arrivals: Isolate new animals for 2-4 weeks; monitor for clinical signs
  • Separate species: Avoid housing camelids with horses (potential S. equi ssp. zooepidemicus reservoir)
  • Reduce overcrowding: Adequate space reduces stress and disease transmission
  • Biosecurity: Fomite disinfection, clean equipment, limit visitors
  • Feed management (cervids): Use magnets in feed systems if feeding processed feeds; inspect hay and feed for metal contamination

Memory Aid - "ALPACA HEARTS":

A = Alpaca fever (S. equi ssp. zooepidemicus)

L = Lymphoma (most common cardiac tumor)

P = Polyserositis (pericardium + pleura + peritoneum)

A = Anechoic effusion on echo

C = Ceftiofur is first-line treatment

A = Acute onset with stress/transport

Etiology Prognosis Notes
S. equi ssp. zooepidemicus (early) Guarded to Fair Rapid response to antibiotics if treated early; 50-100% mortality without treatment
S. equi ssp. zooepidemicus (advanced) Poor Meningitis, severe organ damage indicate poor outcome
Cardiac lymphoma Poor Palliative care; no curative treatment
Traumatic pericarditis (if present) Poor Treatment generally unrewarding in ruminants/camelids
Constrictive pericarditis Guarded May require pericardiectomy; surgical risk significant

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