Bovine Mycotoxicosis Study Guide

Overview and Clinical Importance

Mycotoxicosis refers to diseases caused by ingestion of toxic secondary metabolites (mycotoxins) produced by fungi growing on grains, forages, and other feedstuffs. In cattle, mycotoxicosis represents a significant cause of multisystemic disease with effects ranging from subtle production losses to acute toxicity and death. Over 400 mycotoxins have been identified, but only a handful cause clinically significant disease in cattle.

The six major mycotoxins of concern in bovine practice include aflatoxins (hepatotoxic, carcinogenic), ergot alkaloids (vasoconstriction, gangrene), trichothecenes (DON and T-2 toxin causing immunosuppression), zearalenone (estrogenic effects), fumonisins (hepatotoxicity), and ochratoxin A (nephrotoxicity). Understanding these toxins is critical for NAVLE success as they frequently appear in questions involving multisystemic disease, production losses, and public health concerns.

Pathophysiology and Toxin Classification

Mycotoxins are produced by fungi primarily of genera Aspergillus, Fusarium, Penicillium, and Claviceps. Toxin production occurs in the field (pre-harvest) or during storage (post-harvest) depending on environmental conditions including temperature, moisture, and substrate availability.

Major Mycotoxins and Their Characteristics

Aflatoxicosis

Etiology and Pathogenesis

Aflatoxin B1 is the most potent and prevalent aflatoxin. After ingestion, AFB1 is metabolized in the liver by cytochrome P450 enzymes to the reactive aflatoxin-8,9-epoxide, which binds to DNA and proteins causing cellular damage. The major metabolite aflatoxin M1 (AFM1) is excreted in milk, representing a significant public health concern. The carryover rate from feed to milk averages 1-2% but can reach 6% in high-producing cows.

Clinical Signs

Pathologic Findings

Gross findings: Enlarged pale or yellow liver with rounded edges, distended gallbladder, congested kidneys, icterus, petechial hemorrhages, ascites

Histopathology: Centrilobular hepatocyte necrosis, fatty degeneration, bile duct proliferation, hepatocyte megalocytosis, fibrosis in chronic cases

Diagnosis and Regulatory Limits

Feed testing: FDA action level is 20 ppb AFB1 for lactating dairy cattle feed. Aflatoxin M1 in milk must be less than 0.5 ppb (US FDA) or less than 0.05 ppb (EU).

Laboratory findings: Elevated AST, GGT, SDH, and ALP; increased bilirubin; prolonged PT/aPTT; hypoalbuminemia

Treatment

Ergotism and Fescue Toxicosis

Etiology and Pathogenesis

Ergot alkaloids are produced by Claviceps purpurea (infecting grain heads forming sclerotia) and Epichloë coenophiala (endophyte in tall fescue). The primary toxic alkaloid in fescue is ergovaline, which accounts for approximately 90% of ergopeptides in infected grass. These alkaloids are structurally similar to dopamine, serotonin, and norepinephrine, allowing them to bind neurotransmitter receptors and cause potent vasoconstriction.

Clinical Syndromes

Diagnosis

Feed analysis: Ergovaline levels greater than 200-400 ppb are associated with toxicosis. Grain with greater than 0.1-0.3% ergot sclerotia by weight can cause clinical disease.

Pasture testing: Endophyte testing of fescue tillers. Greater than 90% of Kentucky 31 (K-31) fescue in unimproved pastures is endophyte-infected.

Treatment and Management

Trichothecene Toxicosis (DON and T-2 Toxin)

Etiology and Pathogenesis

Trichothecenes are produced primarily by Fusarium species and contain a 12,13-epoxytrichothecene core structure responsible for their toxicity. They are classified as Type A (T-2 and HT-2 toxin) and Type B (deoxynivalenol/DON/vomitoxin). These mycotoxins are potent protein synthesis inhibitors and affect rapidly dividing cells, particularly the GI epithelium, bone marrow, and immune tissues.

Clinical Signs

Key point: Ruminants are more resistant to trichothecenes than monogastrics due to ruminal de-epoxidation. However, pre-ruminal calves and stressed animals (fresh cows) are more susceptible. DON is considered a marker mycotoxin - its presence indicates conditions favorable for multiple mycotoxin production.

Zearalenone Toxicosis

Etiology and Pathogenesis

Zearalenone (ZEA) is a non-steroidal mycoestrogen produced by Fusarium graminearum. It has high affinity for estrogen receptors and mimics 17?-estradiol, causing hyperestrogenism. In the rumen, ZEA is converted to ?-zearalenol, which has 4 times greater estrogenic activity than the parent compound. Cattle are more resistant than swine due to extensive ruminal metabolism.

Clinical Signs

Heifers (most susceptible): Vulvovaginitis with vulvar swelling and vaginal secretions, mammary gland enlargement in virgin heifers, irregular estrous cycles, anestrus, decreased conception rates, pseudopregnancy

Mature cows: Reduced fertility, early embryonic death, ovarian cysts, decreased corpus luteum size

Males: Testicular atrophy, decreased libido, reduced sperm production in young bulls (mature bulls relatively resistant)

Diagnosis and Treatment

Feed limits: No FDA guidelines exist for ZEA in cattle. Suggested limits are less than 2-4 ppm for dairy cattle and less than 5-10 ppm for beef cattle.

Treatment: Remove contaminated feed. Effects are generally reversible once exposure stops. ZEA is poorly bound by clay binders; modified adsorbents or enzymatic products may be more effective.

Fumonisin Toxicosis

Fumonisin B1 is produced by Fusarium verticillioides primarily in corn. It disrupts sphingolipid biosynthesis by inhibiting ceramide synthase, leading to accumulation of sphinganine and sphingosine. While cattle are relatively resistant compared to horses (leukoencephalomalacia) and swine (pulmonary edema), fumonisin can cause hepatotoxicity and nephrotoxicity.

Clinical Signs in Cattle

Reduced feed intake, decreased milk production, liver damage (elevated GGT, AST), mild kidney damage in calves. Young calves without fully developed rumens are more susceptible. At concentrations greater than 100 ppm, reduced performance and hepatotoxicity occur.

FDA Guidelines

Breeding ruminants and dairy cattle: Less than 15 ppm total fumonisin in corn products, not exceeding 50% of diet

Ruminants for slaughter: Less than 30 ppm total fumonisin

Diagnostic Approach to Mycotoxicosis

Feed Sampling and Testing

Mycotoxins are distributed heterogeneously in feed - 'hot spots' can exist with high concentrations next to areas with none. Proper sampling is critical: collect at least 10-20 probes from different locations, mix thoroughly, and submit at least a 2-pound sample.

Key Diagnostic Principles

• Presence of mold does NOT equal presence of mycotoxin (and vice versa)
• Clinical signs are often nonspecific - comprehensive differential diagnosis essential
• Multiple mycotoxins often co-occur with additive or synergistic effects
• Submit feed that was being fed when problems began, not just current feed
• Fresh/transition cows are most susceptible due to stress and immunosuppression

Prevention and Treatment Strategies

Mycotoxin Binders

Mycotoxin binders work by adsorbing toxins in the GI tract, preventing absorption. No products are FDA-approved for this use in the US, but they are widely employed.

Prevention Strategies

• Proper harvest timing: Avoid harvesting wet or damaged grain
• Storage conditions: Maintain grain moisture less than 14%, ensure adequate ventilation
• Silage management: Rapid packing, proper sealing, maintain anaerobic conditions
• Regular testing: Monitor high-risk commodities (corn, cottonseed) especially during drought years
• Grain cleaning: Remove screenings and damaged kernels (concentrates mycotoxins)