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The Journal of allergy1964; 35; 322-330; doi: 10.1016/0021-8707(64)90095-4

Observations on Heaves: An Asthma-Like Syndrome in the Horse.

Abstract: Observations in six horses with heaves established a clear relationship between attacks of heaves and the feeding of hay. Severe acute attacks were accompanied by striking changes in the eosinophil count and the sedimentation rate. The variation in the severity of heaves in relation to the feeding and withholding of hay is accounted for by assuming that attacks result from a transient, obstructive lesion in the bronchial tree or lung caused by hypersensitivity to some component of hay. The observations strongly suggest that heaves is a respiratory allergic disease in the horse. The relation of heaves to pulmonary emphysema in the horse is discussed.
Publication Date: 1964-07-01 PubMed ID: 14193184DOI: 10.1016/0021-8707(64)90095-4Google Scholar: Lookup
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  • Journal Article

Summary

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This study followed six horses with heaves and found that attacks consistently occurred after feeding hay, alongside spikes in inflammatory blood markers. The authors conclude that heaves is a hay-related allergic airway disease that causes transient bronchial obstruction and can lead to emphysema over time.

What the researchers set out to understand

  • Determine whether feeding hay precipitates attacks of heaves (an asthma-like respiratory condition in horses).
  • Assess whether measurable systemic changes accompany attacks, focusing on eosinophil counts and erythrocyte sedimentation rate (ESR).
  • Explain the pattern of worsening and improvement with exposure versus withholding of hay.
  • Clarify how recurrent heaves relates to structural lung damage such as pulmonary emphysema.

How the study was conducted (as described in the abstract)

  • Observational follow-up of six horses clinically diagnosed with heaves.
  • Comparison of periods when hay was fed versus when hay was withheld.
  • Monitoring of clinical attacks in relation to feeding timing.
  • Measurement of blood eosinophil counts and ESR during severe acute attacks.

Key observations

  • Attacks of heaves showed a clear temporal relationship with the feeding of hay.
  • Withholding hay reduced the severity of clinical signs, indicating reversibility with removal of the exposure.
  • Severe acute attacks were accompanied by marked increases in eosinophil counts and an elevated ESR, signaling an inflammatory and likely allergic response.
  • The variability in attack severity tracked closely with exposure intensity (feeding) versus cessation (withholding).

Authors’ interpretation and proposed mechanism

  • Heaves episodes stem from a transient, obstructive lesion in the bronchial tree or lung, consistent with airway narrowing and/or plugging.
  • The trigger is hypothesized to be hypersensitivity to components of hay—likely inhaled particulates such as dust, molds, or other allergens present in hay.
  • The combination of exposure-linked attacks and eosinophilia supports an allergic pathophysiology.
  • Thus, heaves is characterized as a respiratory allergic disease in horses, analogous to human asthma.

Relation to pulmonary emphysema

  • Repeated, severe airway obstruction increases expiratory effort and promotes air trapping (dynamic hyperinflation).
  • Over time, this can contribute to structural changes in the lung parenchyma consistent with emphysema.
  • The paper discusses heaves as a functional airway disease that, when recurrent, may lead to or exacerbate emphysematous changes.

Why these findings mattered at the time

  • They established a practical, modifiable exposure (hay feeding) as a key driver of attacks, shifting attention to environmental management.
  • They linked clinical events to biological markers (eosinophils, ESR), reinforcing the concept of an immunologically mediated process rather than solely mechanical or infectious causes.
  • They offered a unifying explanation for the on–off pattern of disease in relation to stable practices.

Strengths and limitations

  • Strengths:
    • Clear temporal association between hay exposure and attacks.
    • Physiological corroboration via changes in eosinophils and ESR during acute episodes.
    • Consistency of the pattern across multiple horses.
  • Limitations:
    • Small sample size (n=6) and observational design limit generalizability and causal inference.
    • “Hay” bundles multiple potential triggers (dust, molds, endotoxin, spores); the specific allergen(s) were not identified.
    • Eosinophil counts and ESR are nonspecific markers and can be influenced by other conditions.
    • No quantitative exposure assessment or blinded outcome evaluation is described in the abstract.

Clinical and management implications (inferred from the findings)

  • Reducing or modifying hay exposure is central:
    • Consider hay alternatives (pelleted/cubed forage) or dust-reducing strategies (soaking/steaming hay).
    • Improve stable ventilation and reduce dust sources (low-dust bedding, wet down aisles, clean feeding areas).
    • Maximize outdoor turnout when feasible.
  • Medical approaches for symptomatic control (not tested in the described study but consistent with the mechanism):
    • Anti-inflammatory therapy (e.g., corticosteroids) to suppress airway inflammation.
    • Bronchodilators to relieve reversible bronchospasm.
    • Monitoring clinical response to environmental changes to guide long-term management.

How these observations fit with later knowledge

  • Heaves is now encompassed under the term “equine asthma,” with severe equine asthma showing strong links to barn dust and hay-derived particulates (including molds and endotoxin).
  • Environmental control remains the cornerstone of management, validating the study’s central inference about hay exposure.
  • While this study highlighted eosinophil changes, later work often finds neutrophilic airway inflammation in severe equine asthma; nonetheless, allergic/mixed inflammatory mechanisms still underpin disease expression.
  • The paper’s emphasis on reversible airway obstruction with exposure provides a foundation for understanding exacerbations and preventing progression to chronic structural lung changes.

Bottom line

  • In six horses, hay feeding reliably precipitated heaves attacks accompanied by inflammatory blood changes, supporting an allergic, exposure-driven airway obstruction.
  • This work helped establish environmental (hay/dust) control as first-line management and framed heaves as an asthma-like disease that can lead to emphysema with repeated exacerbations.

Cite This Article

APA
LOWELL FC. (1964). Observations on Heaves: An Asthma-Like Syndrome in the Horse. J Allergy, 35, 322-330. https://doi.org/10.1016/0021-8707(64)90095-4

Publication

ISSN: 0021-8707
NlmUniqueID: 1305603
Country: United States
Language: English
Volume: 35
Pages: 322-330

Researcher Affiliations

LOWELL, F C

    MeSH Terms

    • Animals
    • Asthma
    • Food Hypersensitivity
    • Horse Diseases
    • Horses
    • Pulmonary Emphysema
    • Research
    • Rhinitis, Allergic, Seasonal

    Citations

    This article has been cited 10 times.
    1. Klier J, Fuchs S, Winter G, Gehlen H. Inhalative Nanoparticulate CpG Immunotherapy in Severe Equine Asthma: An Innovative Therapeutic Concept and Potential Animal Model for Human Asthma Treatment. Animals (Basel) 2022 Aug 16;12(16).
      doi: 10.3390/ani12162087pubmed: 36009677google scholar: lookup
    2. Lau N, Norman A, Smith MJ, Sarkar A, Gao Z. Association between Traffic Related Air Pollution and the Development of Asthma Phenotypes in Children: A Systematic Review. Int J Chronic Dis 2018;2018:4047386.
      doi: 10.1155/2018/4047386pubmed: 30631772google scholar: lookup
    3. Kehrli D, Jandova V, Fey K, Jahn P, Gerber V. Multiple hypersensitivities including recurrent airway obstruction, insect bite hypersensitivity, and urticaria in 2 warmblood horse populations. J Vet Intern Med 2015 Jan;29(1):320-6.
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    4. Bosshard S, Gerber V. Evaluation of coughing and nasal discharge as early indicators for an increased risk to develop equine recurrent airway obstruction (RAO). J Vet Intern Med 2014 Mar-Apr;28(2):618-23.
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    5. Toussaint M, Fievez L, Desmet CJ, Pirottin D, Farnir F, Bureau F, Lekeux P. Increased hypoxia-inducible factor 1α expression in lung cells of horses with recurrent airway obstruction. BMC Vet Res 2012 May 23;8:64.
      doi: 10.1186/1746-6148-8-64pubmed: 22621400google scholar: lookup
    6. Lavoie JP, Lefebvre-Lavoie J, Leclere M, Lavoie-Lamoureux A, Chamberland A, Laprise C, Lussier J. Profiling of differentially expressed genes using suppression subtractive hybridization in an equine model of chronic asthma. PLoS One 2012;7(1):e29440.
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    8. Patel AC, Brett TJ, Holtzman MJ. The role of CLCA proteins in inflammatory airway disease. Annu Rev Physiol 2009;71:425-49.
    9. Vanarsdel PP Jr, Thune R. Infiltrative lung disease and hypersensitivity to organic dusts. Yale J Biol Med 1968 Apr-Jun;40(5-6):501-6.
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