BRD is the most economically important disease in the beef cattle industry and one of the highest-yield topics on the NAVLE. Know the pathogens, know the scoring system, know when to use tulathromycin versus florfenicol, and know what metaphylaxis means. That's most of what the exam tests here.
The disease is a synergistic process. Viral pathogens hit first — damaging the mucociliary escalator, suppressing local immunity, and priming the lung for bacterial invasion. The bacteria that follow are the ones that kill. Understanding that two-step sequence explains most of the clinical picture and most of the exam questions.
The Pathogens
BRD involves a predictable cast of bacterial and viral agents. The exam expects you to know each one's specific niche in the disease complex.
| Pathogen | Type | Role in BRD | NAVLE Clue |
|---|---|---|---|
| Mannheimia haemolytica A1 | Bacterial | Primary bacterial killer; shipping fever | Leukotoxin + cranioventral fibrinonecrotic pneumonia |
| Pasteurella multocida | Bacterial | Secondary invader; milder fibrinopurulent pneumonia | Less fibrin, less necrosis than Mannheimia |
| Histophilus somni | Bacterial | Vasculitis → TME + myocarditis + pleuritis | Neurological signs + chest = think H. somni |
| Mycoplasma bovis | Bacterial | Chronic caseonecrotic pneumonia + arthritis + otitis | No cell wall — beta-lactams don't work |
| BHV-1 (IBR) | Viral | Upper respiratory viral primer; latency in trigeminal ganglia | "Red nose," nasal plaques, abortion after reactivation |
| BRSV | Viral | Severe interstitial pneumonia in calves <6 months | Subcutaneous emphysema + syncytial cells on histo |
| BVDV | Viral | Immunosuppression; no specific respiratory lesion alone | PI cattle are persistent shedders; erosive mucosal lesions |
| Parainfluenza-3 (PI-3) | Viral | Mild disease alone; sets up bacterial secondary invasion | Damages mucociliary escalator — key primer |
Pathogenesis: Why Shipping Fever Kills
Calves arrive already stressed from weaning, transport, and commingling. Stress elevates cortisol, which hammers neutrophil and macrophage function. Viral pathogens (most commonly PI-3, BRSV, or BHV-1) damage the respiratory epithelium and further suppress local defenses. This leaves the lower airway open to colonization by Mannheimia haemolytica, which normally lives as a commensal in the upper respiratory tract.
Once Mannheimia reaches the lung, it produces leukotoxin (LktA) — an RTX-family pore-forming toxin specific to bovine ruminant leukocytes. At high concentrations, LktA lyses neutrophils and alveolar macrophages. Those dying cells dump lysosomal enzymes and reactive oxygen species into lung tissue. The result is the classic pathology: cranioventral fibrinonecrotic bronchopneumonia with distended, gelatinous interlobular septa and fibrinous pleuritis.
BRD Scoring: The DART System
BRD scoring systems allow pen riders to flag cattle for treatment without needing a thermometer on every animal. The most commonly referenced system on the NAVLE is based on scoring depression, appetite, respiratory signs, and temperature — often remembered as DART.
| Sign | Score 0 | Score 1 | Score 2 |
|---|---|---|---|
| Depression | Alert, responsive | Mildly dull | Recumbent/unresponsive |
| Appetite | Normal | Off feed slightly | Not eating |
| Respiratory | Normal rate/effort | Increased RR or cough | Labored, open-mouth |
| Temperature | <39.5°C (103.1°F) | 39.5–40.0°C | ≥40.0°C (≥104°F) |
| Total score ≥4 → pull and treat. Score 5–8 → high severity, consider additional NSAIDs. | |||
No single parameter has adequate sensitivity. The combination of depression + fever ≥40°C + abnormal respiration gives the best sensitivity for catching BRD in pen-riding scenarios. The exam has tested this directly — single-sign scoring misses too many cases.
Antibiotic Selection
The exam tests antibiotic choices for both treatment and metaphylaxis. Know the drug classes, their mechanisms, and when each one is appropriate.
| Drug | Class | Mechanism | Route / Dosing | Notes |
|---|---|---|---|---|
| Tulathromycin | Macrolide (triamilide) | 50S ribosomal inhibition | 2.5 mg/kg SC, single dose | #1 for metaphylaxis; long t½; 18-day WDT |
| Florfenicol | Phenicol | 50S ribosomal inhibition (bacteriostatic) | 40 mg/kg SC single, or 20 mg/kg IM q48h | Active vs. macrolide-resistant strains; 38-day WDT |
| Enrofloxacin | Fluoroquinolone | DNA gyrase inhibition (bactericidal) | 7.5–12.5 mg/kg SC once | Critically important antimicrobial — use judiciously |
| Ceftiofur (CCFA) | 3rd-gen cephalosporin | Cell wall synthesis inhibition (bactericidal) | 6.6 mg/kg SC single (CCFA) | Use when macrolide resistance documented |
| Gamithromycin | Macrolide | 50S ribosomal inhibition | 6 mg/kg SC single | Cross-resistance with tulathromycin expected |
| Oxytetracycline | Tetracycline | 30S ribosomal inhibition | 11 mg/kg IV/IM | Older option; increasing resistance; oral form unreliable in ruminants |
Metaphylaxis
Metaphylaxis means treating an entire group of high-risk animals at arrival, before most of them develop clinical disease. It is not prophylaxis — it targets animals already likely incubating infection. The classic population: newly arrived feedlot calves that are recently weaned, transported long distances, commingled from multiple sources, and not preconditioned.
Tulathromycin is the agent of choice by network meta-analysis. Single SC injection at 2.5 mg/kg. Its long half-life gives sustained tissue concentrations across the highest-risk period (first 45 days post-arrival). Gamithromycin is an acceptable alternative. Oral medications (oxytetracycline in feed or water) perform poorly in this context because sick animals don't eat or drink, and ruminant oral bioavailability for tetracyclines is poor.
Distinguishing the BRD Pathogens on the NAVLE
Most BRD questions give you a signalment and a cluster of findings. Here's how to rapidly sort them:
Mannheimia haemolytica: 7–14 days post-arrival. Acute, high fever (40.5–41.5°C). Cranioventral consolidation with marbled interlobular septa. Fibrinous pleuritis. The leukotoxin question answers itself.
Histophilus somni: 40–60 days post-arrival. Watch for the multi-organ hit: bronchopneumonia plus myocarditis plus thrombotic meningoencephalitis (ataxia, blindness, opisthotonus). Fibrinous pleuritis over relatively normal lung. Vasculitis is the mechanism — not leukotoxin, but direct endothelial adhesion and thrombosis.
Mycoplasma bovis: Chronic, relapsing. Resistant to multiple antibiotics. The classic triad is caseonecrotic pneumonia + polyarthritis + otitis media. Round, white caseous foci in the lung at necropsy. No cell wall = beta-lactams are useless. Macrolides and fluoroquinolones have the best activity, though resistance is rising. PCR from deep nasopharyngeal swab is the fastest diagnosis.
BRSV: Calves under 6 months. Severe interstitial pneumonia, subcutaneous emphysema, failure of lungs to collapse at necropsy, rubbery texture. Syncytial cells on histopathology. Inactivated vaccines can cause vaccine-enhanced disease through a Th2-biased response on subsequent natural infection — the exam has asked about this.
BHV-1 (IBR): Upper respiratory, not lower. "Red nose" — inflamed, crusty nares. Nasal mucosal plaques (necrosis). Conjunctivitis. High fever. Latency in trigeminal ganglia — stress reactivates it. BHV-1 in a pregnant cow = abortion risk 15–60 days later. IBR seropositive animals shed virus on stress even without clinical signs.
Diagnostics
Culture from nasal swabs is not specific — Mannheimia, Pasteurella, and Histophilus all live in the upper respiratory tract of healthy cattle. Transtracheal wash (TTW) or bronchoalveolar lavage (BAL) samples the lower airway directly and is the most specific antemortem bacterial culture technique.
For rapid multi-pathogen ID, multiplex PCR panels beat everything else. One nasopharyngeal sample, same-day results, identifies viral and bacterial agents simultaneously. Paired serology (0 and 21 days) is retrospective — useless for acute management, useful for outbreak investigation.
Thoracic ultrasound shows lung consolidation as hypoechoic, hepatized tissue replacing the normally echogenic, artifact-rich aerated lung. Useful for following response to treatment and identifying chronic non-responders.