Author: Nora Grenager

Rhodococcus equi is the primary bacterial cause of severe bronchopneumonia in 1 to 5-month-old foals, and NAVLE^® questions frequently test your ability to quickly identify it. The disease often has a recognizable pattern of presentation that emerges before culture results are available. If you understand how to read the clinical signs and clinicopathology clues, you will consistently and confidently identify R. equi in various exam scenarios.

How to Recognize R. equi Before Culture Results

Most foals develop clinical pneumonia between 1 and 5 months, but classic R. equi cases cluster around 3-4 months as passive immunity wanes.

R. equi infections can quickly become life-threatening once the affected foal crosses a threshold into decompensation. Early clinical signs are nonspecific (e.g., anorexia, fever, lethargy). As the disease progresses, however, affected foals struggle with progressive respiratory compromise, presenting with nostril flare and abdominal breathing. Cough and nasal discharge are less consistent findings.

Use thoracic ultrasound and radiography to identify pulmonary consolidation and/or abscessation. Mediastinal lymphadenopathy and nodular lung lesions in a foal 1 to 5 months of age are classic clinical signs of R. equi pneumonia.

Inflammatory Markers That Narrow Your Differential

The NAVLE^® frequently tests your ability to interpret CBCs and acute phase proteins. Affected foals have:

• Neutrophilic leukocytosis 
• Dramatically elevated fibrinogen, increased globulins 
• Serum amyloid A (SAA) increases are variable and nonreliable

Viral pneumonia, intestinal parasitism, and equine proliferative enteropathy (caused by Lawsonia intracellularis) may affect the same age group and at first have similar signs of lethargy/anorexia (+/- fever), but these clinicopathologic lab findings are not consistent with those differentials. Tracheal wash is a key diagnostic, revealing pleomorphic gram-positive coccobacilli, an immediate signal that R. equi is the top differential in a young foal.

Submit the sample for both culture/sensitivity and PCR for the virulence-associated protein A (VapA) gene. Because R. equi is ubiquitous in the environment, and subclinical infections may not require treatment, the VapA gene proves any cultured R. equi is actually causing the infection.

Therapy that Targets the Source

Most foals require combination therapy with a macrolide antibiotic (best: clarithromycin) and rifampin, which work synergistically, plus supportive care, and anti-inflammatories as needed. This regimen targets intracellular bacteria and penetrates abscesses, which are common in R. equi pneumonia. Treat until consistent improvement of abnormalities on radiographs, and resolution of hematology/proteins and clinical signs (treatment regimen lasts 4-12 weeks). Hyperthermia, diarrhea, and tachypnea are possible side effects of these antibiotics.

Successful treatment of R. equi pneumonia requires ongoing evaluation.

Watch for Extrapulmonary Manifestations

R. equi can concurrently (or solely) affect the GI tract, mesenteric lymph nodes, abdominal organs, synovial structures, and bone (from most to least common) although infection or inflammation is possible anywhere. Up to 50% of foals show intestinal involvement at necropsy without any specific clinical signs. Prognosis with extrapulmonary manifestations is worse than for bronchopneumonia.

See the Pattern, Make the Diagnosis

R. equi pneumonia is a pattern-recognition disease: the age, clinical signs, tracheal wash cytology, and clinical pathology findings (+ diagnostic imaging, when possible) point strongly toward the correct diagnosis before confirmatory tests return. Strengthen your ability to connect these clinical and clinicopathologic clues, and you will move through NAVLE^® questions with greater speed, accuracy, and confidence.

More from Zuku:

• Master NAVLE^® concepts
• Subscribe to the Question of the Day to receive a NAVLE^® question delivered to your inbox daily
• View the Study Strategy video series
• Review the Equine ECG Made Simple: How to Recognize Second-Degree AV Block and Differentiate from Atrial Fibrillation blog
• Review The Productivity Trap: Why More Studying Can Hurt Your NAVLE^® Score blog

Interpreting ECGs in horses can feel intimidating at first, but the truth is there are a few main arrhythmias to remember. Understanding equine physiology is one of the easiest ways to correctly identify arrhythmias and score points on the NAVLE^®. In this guide, you’ll learn to recognize a classic and common physiologic arrhythmia (second-degree atrioventricular (AV) block), differentiate it from the most common pathologic arrhythmia (atrial fibrillation), and build a structured approach to equine ECGs.

Don’t Panic Over Dropped Beats

Horses are athletes by design. Their massive size and impressive cardiovascular efficiency allow them to maintain low resting heart rates, normally between 28-44 bpm. This is the slowest heart rate among common domestic species.

Horses (especially fit ones) also frequently display physiologic arrhythmias at rest due to high vagal tone when relaxed. This leads to common identification of second-degree AV block, as well as sinus arrhythmia and first-degree AV block.

The ability to recognize physiologic arrhythmias allows you to know when auscultatory or ECG abnormalities are significant.

Focus on the Big Three Equine Cardiac Principles

If you understand these three fundamentals, equine ECGs are straightforward:

1. Bigger Animals have Slower Heart Rates

Massive stroke volume allows horses to circulate blood with a slower resting rate.

2. Athletic Horses Display High Vagal Tone

Relaxed, athletic horses often develop normal physiologic arrhythmias (e.g., sinus arrhythmia, second-degree AV block) that are normal at rest and disappear with light exercise. The most common example is second-degree AV block, where there is a P wave without an associated QRS complex. The rhythm is normal between dropped beats, and resting heart rate might be slightly low (22-28 bpm). This is a physiologic (normal) arrhythmia seen in healthy athletes and should not warrant worry or intervention.

3. Atrial Fibrillation is the Most Common Pathologic Arrhythmia

It is critical to distinguish second-degree AV block from atrial fibrillation (Afib), the most common pathologic arrhythmia causing poor performance in horses.

How to Interpret Equine ECGs

Veterinary students benefit from using a systematic, repeatable ECG interpretation strategy, as outlined below:

Interpret the ECG, Recognizing Normal Sinus Rhythm

Start by identifying the P wave, QRS complex, and T wave. Ask yourself:

• Is there a P wave for every QRS complex?
• Is there a QRS complex for every P wave? 
• Are the R-R intervals regular or irregular?
• Do the QRS complexes all look similar?

Identify Second-Degree AV Block

In second-degree AV block, the ECG strip shows mostly normal P-QRS-T complexes, with occasional “dropped” beats (i.e., AV block):

• Normal P wave
• No QRS, instead a pause
• The next P wave is when you would expect it (consistent P-P interval)
• Normal rhythm between dropped beats

Distinguish Normal from Abnormal

Second-degree AV block is considered physiologic when:

• The horse is calm or resting
• The dropped beat is infrequent (i.e., not >2 dropped beats in succession)
• Resting heart rate is normal (or often a bit low, 22-28)
• Exercise or sympathetic stimulation causes sinus rhythm

Look for Red Flags

Escalate concern if you observe:

• High-grade AV block (i.e., >2 blocked P-waves in a row)
  • Persistent AV block during exercise
• Syncope, weakness, or collapse
• Atrial fibrillation
• Identification of additional/other arrhythmias (e.g., atrial or ventricular premature contractions, ventricular tachycardia) 

These may signal structural or inflammatory heart disease that warrant a full cardiac workup.

Study Habits that Build ECG Confidence

ECG interpretation improves with repetition, not memorization. Try these habits:

• Review normal and abnormal ECGs side-by-side
• Practice identifying second-degree AV block and atrial fibrillation
• Create your own ECG flashcards labeled only with waveforms and key clues

Students who recognize the normal patterns more confidently identify arrhythmias, allowing them to succeed quickly.

Your NAVLE^®-Friendly ECG Interpretation Framework 

Use this framework for every equine ECG question:

1. Classic Case Pattern

• Second-degree AV block: healthy/athletic adult horse, low resting HR with regularly irregular rhythm, occasional dropped beat (P wave not followed by QRS)
• Afib: Adult horse presenting for poor performance (most often a racehorse), irregularly irregular heart rhythm, no P waves, and irregular R-R intervals

2. Test of Choice

Careful auscultation followed by light exercise (when safe) and repeat auscultation. Physiologic arrhythmias resolve with increased heart rate. Use ECG to confirm when needed.

3. First-Line Response

Second-degree AV block is a physiologic arrhythmia that does not require treatment. Treatment of Afib varies depending on the cause and horse’s intended use: use exercising ECG and echocardiography to determine the best recommendation (i.e., to cardiovert or not).

Master the Normal to Recognize the Abnormal

Second-degree AV block represents one of the most common physiologic arrhythmias in horses and is not a cardiac emergency. A calm, methodical approach—identify the P wave, confirm the missing QRS, and evaluate the horse’s demeanor and clinical signs—allows you to move through NAVLE^® questions with confidence. Remember the main rule-out is Afib, which usually presents differently and has different ECG findings. Master the normal patterns first, and both the exam and clinical practice become much more manageable.

More from Zuku:

• Master NAVLE^® concepts
• Subscribe to the Question of the Day to receive a NAVLE^® question delivered to your inbox daily
• View Zuku Review’s Sample Lecture Videos
• Review the No Zebras: How to Triage your NAVLE^® Study for Maximum Points blog
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Pregnancy toxemia ranks as the top “can’t-miss” metabolic condition in late gestation for small ruminants. The syndrome combines ketosis with hepatic lipidosis and develops when fetal glucose demand exceeds maternal supply. As blood glucose drops, the dam experiences hypoglycemic encephalopathy, progressive depression, and, without timely intervention, death.

Why Late Gestation is the Danger Zone

Most fetal growth happens in the final trimester. The dam ramps up gluconeogenesis and mobilizes fat reserves to meet rising glucose demands of the enlarging fetus. When this overwhelms hepatic capacity, triglycerides accumulate, impairing hepatic function and triggering ketosis. Multiple fetuses, poor body conditioning (too thin or obese), and any cause of inappetence increase the risk for pregnancy toxemia during this period.  

The Classic Case Pattern You Can’t Miss

Typical early signs include going off grain, separation from the flock, and bruxism in late gestation. As the disease progresses, the dam may pace, show facial tremors, develop opisthotonos or central blindness, and become recumbent. Most affected animals are either over- or under-conditioned (BCS 1/5 or 5/5, ideal is 3/5). The presence of multiple fetuses greatly increases glucose demand and therefore risk.

Field-Testing: What to Test First

In the field, clinical signs are diagnostic clues. Confirm the diagnosis by checking urine ketones or measuring blood BHBA with a stall-side meter.

• Urine ketones are the quickest and most accurate diagnostic tool, as they provide a more sensitive and specific result than blood alone
• BHBA > ~1.0 mmol/L supports ketosis; many clinical cases run higher
• Blood chemistry may reveal hypoglycemia, low calcium, magnesium, and potassium; and elevated liver enzymes

Treatment Priorities (And What to Avoid)

Focus on three goals: restore energy, reduce pain, and correct deficits

• Administer propylene glycol PO and limit duration/frequency to protect rumen flora and avoid worsening anorexia
• Offer highly palatable feed away from flockmates to encourage intake
• Provide calcium (SQ or PO) if levels are borderline or low
• Use NSAIDs (e.g., flunixin) to manage pain and improve both dam and fetal outcomes
• Deliver oral or IV fluids as needed to correct dehydration and potassium imbalances

When to Induce Parturition vs. Wait

Getting the fetuses out is not always the answer. Consider induction when:

• The dam is valuable
• The fetuses are alive and within ~3 days of due date

If the fetuses are dead or far from term, induction with steroids and dexamethasone may still protect the dam. Evaluate the need for a C-section on a case-by-case basis.

Herd-Level Prevention

• Maintain a BCS of 2.5–3.5/5; avoid thin or obese dams 
• Implement good feeding management: provide enough space at feeders and group animals by gestation size, age, or BCS
• Ensure adequate bunk space, minimize social stress, address parasitism, and correct dental issues that reduce intake
• In large herds, consider performing late-gestation BHBA screening to identify subclinical disease early

When you detect disease early and the dam remains ambulatory, the prognosis is favorable with prompt supportive care. Recumbent or comatose animals face much poorer outcomes, and fatalities can approach ~40% in severe presentations. Rapid field testing and decisive intervention make all the difference.

More from Zuku:

• Master NAVLE^® concepts
• Subscribe to the Question of the Day to receive a NAVLE^® question delivered to your inbox daily
• View Zuku Review’s Sample Lecture Videos
• Review the Listeriosis in Ruminants: Fast Clues, Field Diagnostics, & Prevention Methods blog
• Review the Parelaphostrongylus tenius in Camelids: Why Prevention Beats Treatment blog