Acute Bovine Pulmonary Emphysema and Edema (ABPEE), also known as fog fever, atypical interstitial pneumonia (AIP), or bovine asthma, is a toxic interstitial pneumonia characterized by acute respiratory distress in cattle.
Overview and Clinical Importance
Acute Bovine Pulmonary Emphysema and Edema (ABPEE), also known as fog fever, atypical interstitial pneumonia (AIP), or bovine asthma, is a toxic interstitial pneumonia characterized by acute respiratory distress in cattle. This condition represents a significant cause of sudden death in adult pastured cattle and is an important topic for the NAVLE examination.
The disease occurs most commonly in late summer and fall when cattle are moved from dry, sparse pastures to lush, rapidly growing forage. The condition develops 5-10 days after pasture change and can affect up to 50% of exposed cattle, with mortality rates reaching 30% in severe outbreaks.
| Step |
Process Description |
| 1. Ingestion |
Cattle consume lush pasture with high L-tryptophan content |
| 2. Ruminal Conversion |
Lactobacillus bacteria degrade L-tryptophan to indoleacetic acid (IAA), then to 3-methylindole (3-MI/skatole) |
| 3. Absorption |
3-MI is absorbed through rumen wall into portal circulation and transported to lungs |
| 4. Bioactivation |
Cytochrome P450 (CYP) enzymes in Clara cells and Type I pneumocytes convert 3-MI to 3-methyleneindolenine (toxic electrophile) |
| 5. Cellular Damage |
Toxic metabolite alkylates cellular proteins and nucleic acids, causing lipid peroxidation, membrane damage, and necrosis |
Etiology and Pathophysiology
Primary Cause: L-Tryptophan Metabolism
The primary etiology involves the amino acid L-tryptophan found in high concentrations in lush, rapidly growing pasture grasses. The pathogenesis follows a specific metabolic pathway:
Metabolic Pathway of 3-Methylindole Toxicity
High-YieldType II pneumocytes are PROTECTED from 3-MI toxicity despite having high CYP activity because they contain high levels of glutathione and phase II detoxification enzymes. This explains why Type II pneumocyte hyperplasia (not necrosis) is a characteristic histologic finding as these cells proliferate to repair damaged alveolar epithelium.
Other Causes of Toxic Interstitial Pneumonia
| Toxin |
Source |
Clinical Notes |
| 3-Methylindole |
Lush pasture (L-tryptophan) |
Most common cause; occurs 5-10 days after pasture change |
| Perilla Ketone |
Perilla mint (Perilla frutescens) |
Flowering/seed stage most toxic; common in southeastern US |
| 4-Ipomeanol |
Moldy sweet potatoes (Fusarium solani) |
Identical clinical syndrome to ABPEE; occurs 1-2 days after exposure |
Epidemiology and Risk Factors
Key Epidemiologic Features
NAVLE TipRemember 'FOG = Fall + Old cows + Green pasture' - Fog fever occurs in FALL when OLD (adult) cattle are moved to lush GREEN pastures. Nursing calves are protected because ruminal flora has not yet adapted to convert L-tryptophan to 3-MI.
| Factor |
Details |
| Seasonality |
Late summer to fall; associated with lush regrowth after rain or frost |
| Age |
Adult cattle (greater than 2 years) most commonly affected; nursing calves are resistant |
| Timing |
5-10 days after change to lush pasture; rarely occurs after 3 weeks on pasture |
| Morbidity |
Up to 50% of herd may show signs; usually minority develop severe disease |
| Case Fatality Rate |
Approximately 30% in severely affected animals; death within 2-4 days |
Clinical Signs and Physical Examination
Clinical Presentation
Clinical signs develop acutely in animals that appeared clinically normal 12-24 hours earlier. The disease presents in acute and chronic forms:
Acute Form (Most Common)
- Severe dyspnea with rapid, shallow breathing (40-80 breaths/min)
- Open-mouth breathing with head and neck extended
- Loud expiratory grunt - pathognomonic finding
- Frothing at the mouth with tongue protrusion
- Abducted elbows (orthopneic posture)
- Coughing is UNUSUAL - distinguishes from infectious pneumonia
- Subcutaneous emphysema along the back (emphysematous crackles)
High-YieldThe ABSENCE of coughing is a key distinguishing feature of ABPEE. In bacterial pneumonia, coughing is prominent. In ABPEE, the expiratory grunt is characteristic but coughing is unusual. Mild exercise can dramatically worsen respiratory distress and precipitate death.
Chronic Form
Animals surviving the acute phase (greater than 3 days) may show:
- Persistent tachypnea with reduced severity
- Dramatic improvement in appetite by day 3
- Full clinical recovery may require 2-3 weeks
| Finding |
Description |
| Lung Collapse |
Lungs FAIL TO COLLAPSE when thorax is opened; completely fill thoracic cavity |
| Lung Texture |
Firm, rubbery, meaty consistency (not spongy as normal) |
| Rib Impressions |
Visible rib indentations on pleural surface due to overinflation |
| Interlobular Septa |
Markedly distended with edema and emphysema (gas-filled bullae) |
| Color |
Pale to red, edematous; may show checkerboard pattern of lobular variation |
| Subcutaneous Emphysema |
Air accumulation under skin from withers along dorsum |
Pathology
Gross Pathologic Findings
Histopathologic Findings
Exudative Phase (Acute, Days 1-3)
- Necrosis of Clara cells (nonciliated bronchiolar epithelial cells) - primary target
- Necrosis of Type I pneumocytes with alveolar epithelial sloughing
- Hyaline membrane formation lining alveolar surfaces
- Alveolar and interlobular edema
- Interstitial emphysema
- Vascular congestion and endothelial cell swelling
Proliferative Phase (Day 3+)
- Type II pneumocyte hyperplasia - CHARACTERISTIC finding
- Alveolar epithelialization (cuboidal epithelium lining alveoli)
- Alveolar septal fibrosis in chronic cases
- Bronchiolarization (Lambertosis) may occur
NAVLE TipRemember: Clara cells and Type I pneumocytes are DESTROYED (they have high CYP activity but lack protective mechanisms). Type II pneumocytes SURVIVE and PROLIFERATE (they have glutathione and phase II enzymes for protection). This explains the characteristic histologic pattern of Type II pneumocyte hyperplasia.
| Diagnostic Criterion |
Key Features |
| History |
Recent (5-10 days) movement to lush pasture; adult cattle; late summer/fall |
| Clinical Signs |
Acute severe dyspnea, expiratory grunt, NO coughing, multiple animals affected |
| Gross Pathology |
Non-collapsing lungs, interlobular emphysema and edema, rubbery texture |
| Histopathology |
Hyaline membranes, Type II pneumocyte hyperplasia, Clara cell necrosis |
| Rule-Outs |
PCR negative for BRSV, BHV-1, BVD, Mycoplasma bovis, coronavirus |
Diagnosis
Diagnostic Approach
Diagnosis is primarily based on history, clinical signs, and pathologic findings. No specific antemortem test exists.
Differential Diagnosis
| Differential |
Distinguishing Features |
| BRSV Pneumonia |
Syncytial cells, inclusion bodies on histology; positive PCR; younger calves |
| Pneumonic Pasteurellosis |
Cranioventral consolidation; fibrinous pleuritis; prominent coughing; positive culture |
| Perilla Mint Toxicosis |
Identical lesions; plant material in rumen; pasture inspection; 1-2 day onset |
| Moldy Sweet Potato Toxicosis |
Identical lesions; feeding history of sweet potato waste; 1-2 day onset |
| Allergic Alveolitis |
History of exposure to moldy hay; housed cattle; granulomatous inflammation |
| Dictyocaulus viviparus |
Lungworms visible in airways; eosinophilic infiltrate; first-season grazing calves |
Treatment and Management
Treatment Considerations
CRITICAL: There is NO effective treatment for ABPEE. Severely affected animals have minimal pulmonary reserve, and any handling or stress may precipitate death.
High-YieldOn the NAVLE, remember that treatment is largely SUPPORTIVE and INEFFECTIVE. The key management decision is to AVOID HANDLING severely affected animals - moving cattle is unlikely to prevent clinical signs after exposure and may cause immediate death. Mildly affected cattle often recover spontaneously within several days.
| Treatment Option |
Notes and Efficacy |
| Avoid Handling |
MOST IMPORTANT - handling precipitates death; do not move or stress animals |
| NSAIDs |
Flunixin meglumine (2.2 mg/kg IV); anti-inflammatory; aspirin also used; limited efficacy |
| Furosemide |
Diuretic to reduce pulmonary edema (0.5-1 mg/kg IV); minimal proven benefit |
| Antibiotics |
Only for secondary bacterial pneumonia; not effective for primary ABPEE |
| Corticosteroids |
Dexamethasone may reduce inflammation; use controversial; immunosuppression risk |
Prevention
Prevention Strategies
NAVLE TipRemember the ionophore timing difference: MONENSIN = 1 day pretreatment; LASALOCID = 6 days pretreatment. Ionophores work by inhibiting the ruminal bacteria (Lactobacillus) that convert L-tryptophan to 3-methylindole. They have NO benefit after clinical signs develop.
| Strategy |
Implementation Details |
| Gradual Adaptation |
Gradually increase exposure to lush pasture over 10-14 days; limit grazing time initially |
| Hay Supplementation |
Feed hay before turnout to reduce pasture intake; fill rumen with lower-risk forage |
| Pasture Management |
Cut or graze pastures before they become overly lush; use rotational grazing |
| Monensin |
200 mg/head/day; start 1 DAY before pasture exposure; inhibits Lactobacillus 3-MI production |
| Lasalocid |
Alternative ionophore; requires 6-DAY pretreatment period before pasture exposure |
| Toxic Plant Control |
Remove Perilla mint from pastures; inspect fence rows and shaded areas |
Prognosis
Prognosis depends on severity of clinical signs:
- Mild cases: Good prognosis; spontaneous recovery in several days without treatment
- Moderate cases: Guarded; improvement by day 3 if survive; full recovery in 2-3 weeks
- Severe cases: Poor to grave; death within 2-4 days; handling often precipitates death
Overall case fatality rate: Approximately 30% in severely affected animals
Memory Aids for NAVLE
ABPEE Memory Mnemonic
"3-MI = 3 Major Injuries"
- M = Membrane damage (hyaline membranes)
- I = Interstitial emphysema and edema
- 3 = Type II pneumocyte hyperplasia (the 3rd cell type survives!)
The FOG FEVER Rule
"FOG = Fall + Old cows + Green pasture"
- Fall season (late summer/fall)
- Old (adult cattle, not calves)
- Green pasture (lush, rapidly growing forage)
Treatment Memory: "DON'T MOVE THEM"
The single most important management decision is to AVOID HANDLING severely affected cattle. Movement and stress precipitate death due to minimal pulmonary reserve.