Bovine Thromboembolic Meningoencephalitis – NAVLE Study Guide

Overview and Clinical Importance

Thromboembolic meningoencephalitis (TEME), also known as thrombotic meningoencephalitis (TME) or colloquially as "Brainers," is a severe neurological disease primarily affecting feedlot cattle between 6 to 12 months of age. The condition is caused by Histophilus somni (previously known as Haemophilus somnus), a Gram-negative opportunistic coccobacillus belonging to the family Pasteurellaceae.

TEME represents a significant cause of economic loss in the cattle industry, particularly in intensive beef production systems. The disease is characterized by vasculitis, thrombosis, and multifocal hemorrhagic infarcts in the central nervous system. Understanding this condition is critical for NAVLE success, as it frequently appears in questions related to bovine neurological diseases, differential diagnosis of "downer" cattle, and treatment protocols for bacterial CNS infections.

Etiology

Causative Agent

Histophilus somni is a pleomorphic, non-motile, non-encapsulated, Gram-negative coccobacillus. Key microbiological characteristics include:

• Facultative anaerobe with capnophilic tendencies (enhanced growth in CO2)
• Normal commensal of bovine respiratory and reproductive tract mucosae
• Fastidious organism requiring specialized culture conditions and thiamine supplementation
• Fragile outside host making sample collection and transport critical for diagnosis

Epidemiology

Risk Factors and Predisposing Conditions

Board Tip - Memory Aid: "TEME = STRESS" T = Transportation stress E = Entry to feedlot (1-4 weeks post-arrival) M = Mixing/commingling cattle E = Environmental cold stress = STRESS compromises immunity and allows H. somni invasion

Pathogenesis

Mechanism of Disease

The pathogenesis of TEME involves a complex interplay between bacterial virulence factors and host responses. The key virulence factor is lipooligosaccharide (LOS), which is responsible for the hallmark vasculitis and thrombosis characteristic of this disease.

Pathogenesis Sequence:

• Colonization: H. somni colonizes the upper respiratory tract mucosa following stress-induced immunosuppression
• Bacteremia: Organism enters bloodstream and disseminates hematogenously
• Endothelial Adherence: H. somni adheres to vascular endothelium, particularly in small venules of the CNS
• LOS-Mediated Damage: Lipooligosaccharide activates TLR-4, induces caspase-3 mediated apoptosis of endothelial cells
• Platelet Activation: H. somni and LOS activate bovine platelets, enhancing tissue factor activity and pro-coagulant state
• Vasculitis and Thrombosis: Mural thrombi form in small vessels, causing hemorrhagic infarction of neural tissue

Key Virulence Factors

Clinical Signs

Clinical presentation reflects the multifocal nature of CNS lesions. Disease onset is typically acute to peracute, with death possible within 24-36 hours of clinical sign onset. The disease is characterized by low morbidity but high case fatality rate.

Neurological Signs

Other Manifestations of H. somni Disease Complex

H. somni can cause disease in multiple organ systems beyond the CNS:

• Respiratory: Fibrinosuppurative bronchopneumonia, pleuritis (component of BRD)
• Cardiovascular: Necrotizing myocarditis (especially left ventricular papillary muscle)
• Musculoskeletal: Fibrinopurulent polyarthritis
• Reproductive: Abortion, endometritis, vulvovaginitis, orchitis
• Ocular: Chorioretinitis with retinal hemorrhages (causes blindness)

Diagnosis

Antemortem Diagnosis

Antemortem diagnosis of TEME is challenging due to the rapid disease course. CSF analysis is helpful when feasible:

Gross Pathology

Necropsy findings are characteristic and often diagnostic. The hallmark lesions are multifocal hemorrhagic infarcts in the CNS:

• Brain: Multiple red-brown hemorrhagic foci (1-10 mm) at gray-white matter junction; particularly in cerebrum, thalamus, and brainstem
• Meninges: Congestion, hemorrhage, and fibrinous exudate
• Spinal cord: Similar hemorrhagic foci may be present
• Heart: Myocardial infarcts, especially papillary muscles (concurrent myocarditis)

Histopathology

Classic microscopic findings:

• Necrotizing vasculitis: Primarily phlebitis (venule inflammation) with fibrinoid necrosis of vessel walls
• Thrombosis: Poorly organized fibrin thrombi rich in neutrophils occluding small vessels
• Hemorrhage and necrosis: Perivascular hemorrhage with parenchymal necrosis
• Bacterial colonies: Gram-negative coccobacilli visible in thrombi and vessel walls
• Inflammatory infiltrate: Neutrophils and macrophages in affected parenchyma

Differential Diagnosis

Differentiating TEME from other bovine neurological diseases is critical for both clinical practice and NAVLE questions:

Exam Focus - Differential Diagnosis Mnemonic: "PLR TBS" P = Polioencephalomalacia (responds to thiamine) L = Listeriosis (unilateral CN deficits, silage history) R = Rabies (ALWAYS consider!) T = TEME (feedlot, fever, multifocal hemorrhagic infarcts) B = BHV-5 encephalitis (viral, trigeminal ganglionitis) S = Salt poisoning (water deprivation history)

Treatment

Treatment success depends heavily on early detection and intervention. Once recumbent, prognosis is grave. Even with optimal treatment, a 50% recovery rate is considered good.

Antimicrobial Therapy

Effective antibiotics must cross the blood-brain barrier. H. somni is susceptible to multiple antimicrobials:

Supportive Care

• Anti-inflammatory therapy: NSAIDs (flunixin meglumine 1.1-2.2 mg/kg IV) to reduce inflammation; corticosteroids controversial
• Fluid therapy: IV fluids for dehydration correction
• Nursing care: Soft bedding, frequent repositioning for recumbent animals
• Monitoring: Close observation of penmates during outbreaks for early detection

Prevention and Control

Vaccination

Killed whole-cell bacterins are commercially available:

• Two doses required, 2-4 weeks apart
• Annual revaccination recommended
• Best administered at weaning or before feedlot entry
• NOT effective in the face of an outbreak
• Efficacy is variable and may be compromised by stress at time of vaccination

Management Strategies

• Reduce stress: Minimize transportation time, avoid overcrowding, provide adequate ventilation
• Metaphylaxis: Consider antibiotic treatment of all high-risk cattle upon feedlot arrival
• Control viral infections: Vaccination against BHV-1, BVDV, BRSV, PI-3 to reduce predisposing respiratory infections
• Isolation: Separate sick animals promptly during outbreaks
• Early detection: Close monitoring of newly arrived cattle for respiratory and neurological signs

Prognosis

Guarded to poor. Key prognostic factors:

• Ambulatory animals treated early: 50% recovery rate possible
• Recumbent animals: Near-universally fatal; treatment typically unrewarding
• Recovered animals: May have permanent neurological deficits; often uneconomical to continue treatment