Date of Award

Winter 1982

Project Type


Program or Major


Degree Name

Doctor of Philosophy


American beech (Fagus grandifolia Ehrh.) in forest stands of North America are threatened by a destructive disease commonly known as the beech bark disease. Investigations on bark structure and on response of bark tissues to mechanical injury and pathogen invasion would increase our understanding of the etiology of this disease. The objectives of this investigation were to provide descriptions of the development and anatomy of bark of American beech, with emphasis on bark periderms. Investigations were made of the ontogeny of the first exophylactic periderm, and on characteristics and development of the necrophylactic periderms resulting from the beech bark disease and from experimentally inflicted wounds.

The phellogen of the first exophylactic periderm in current year shoots was initiated within one week after budbreak in late April. This phellogen developed from the cortical cell layer immediately below the epidermis. A phellem of five or six cell layers in thickness and a phelloderm of up to two cell layers in thickness were present by the end of the first growing season. First year periderm development was complete ten weeks after budbreak.

Nectria coccinea var. faginata was capable of inducing cankers on beech stems when applied to wounds made by the removal of only the first exophylactic periderm. Wounds inflicted and inoculated in the fall resulted in more cankers than those inflicted and inoculated in any other season. All cankers became delimited by a necrophylactic periderm within two years after injury.

When beech trees susceptible or apparently resistant to the beech bark disease were wounded and inoculated during the fall, initiation of the necrophylactic periderm did not occur until at least 30 weeks later. No differences were noted between susceptible and apparently resistant trees in rate of necrophylactic periderm development. Amounts of total bark phenolics during the development of delimited cankers was also investigated.

Anatomical evidence is presented which supports an hypothesis that the necrophylactic periderm which delimits naturally and experimentally induced cankers is generated from recent derivatives of the vascular cambium, as well as from living cells of the bark tissues present at the time of wounding or infection.