CODIT

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CODIT was initially an acronym for C ompartmentalization O f D ecay I n T rees ( compartmentalization of rot in trees ).

In 1977 the American forest pathologist and tree biologist Alex Shigo published a paper together with Harold Marx that described how trees defend themselves against fungal attack after an injury. Above all, the spatial extent of a fungal attack and the resulting isolation of the tree were considered.

It was later found out that immediately after being injured, the tree did not react to rot, but initially to the ingress of air. Since the air embolism significant influence on the immune functions of trees has is under CODIT today " C ompartmentalization O f Damage I n T rees" (partitioning against damage in trees understood) and closes the penetration of the air with a.

The CODIT model

In the CODIT model, the tree is represented as a chambered organism, these chambers are divided by four structural walls. As a result of damage, these are closed one after the other, which in combination causes the injury to be sealed off.

Fig. 1: The four walls of the CODIT model

The four walls of the CODIT model

Wall 1 (axial)

The first wall is formed by plugging the normally conductive vascular tissue above and below the wound. This slows down the fungal attack of the tissue and the penetration of air in the vertical direction.

In deciduous trees, blockage occurs primarily through so-called Verthyllen , i.e. H. Parenchyma cells (living cells) form bulges in the conductive tissue and close it. In contrast to deciduous trees, the wood fibers of conifers are connected to one another by pits . These can be actively closed by the trees, killed and then lignified (lignified). This wall seals off the weakest of all four, but ensures that the negative pressure prevailing in the trees is maintained despite the ingress of air. Without this negative pressure, liquid transport inside the tree would not be possible.

Wall 2 (radially inwards)

The second wall is formed by the thick-walled, lignin-rich cells of the latewood growth ring towards the center of the trunk, which slows down the radial spread of the decay. This wall seals off the second weakest.

Wall 3 (tangential)

The third wall is made up of ray cells. More precisely from groups of these cells, which are aligned horizontally to the trunk axis and divides it into segments. These groups of cells are discontinuous and vary in length, height and thickness, creating a labyrinthine barrier against tangential spread of decay. After being wounded, some radiation cells are also chemically altered and thus become toxic to some microorganisms. This is the strongest wall at the time of the wounding before the fourth wall grows and is often sufficient to prevent the spread of an infestation in the long term. The fungus, however, usually stays alive.

Wall 4 (radially outwards)

The fourth wall is created by new growth of specialized wood tissue (wound xylem) on the outside of the tree, isolating tissue present at the time of infection from subsequent growth. This is the strongest wall and often the only one that can completely prevent the infection from spreading by closing the wound with new wood, killing the fungus.

Fig. 2: Wall 3 was able to withstand the spread of the infestation for many years. The tree remained in phase 3 of the CODIT principle, phase 4 was not reached until it was felled
Fig. 3: Failed overflow - phase 4 of the CODIT principle could not be reached, the fungus has spread inside the tree

The CODIT principle

The CODIT principle complements today's view of the wound reaction of trees. In addition to the structural classification, the destruction of wood as a result of an injury is divided into four phases:

Phase 1

  1. Air penetrates the tissue.
  2. The tissue near the wound dies on the surface.
  3. The bark, or more precisely the bast, begins to form a wound periderm , while the cambium near the wound forms a callus to the outside and a barrier zone to the inside. This barrier zone then delimits the cambium from the wood on the inside near the wound. Thus, the cambium can form overburden more efficiently and does not have to actively defend itself. Antifungal substances are often stored in this area .

Phase 2

  1. Penetration of harmful pathogens (e.g. wood-destroying fungi)
  2. A bulging bulge begins to form from the callus (formation of wall 4). This is formed from the sides of the wound, which typically results in an elliptical overhang of the wound (Fig. 6).

Phase 3

  1. Pests spread when the barrier zone is breached, after which trees can form a new one and try again to prevent them from spreading. In this area, trees also store antifungal substances.
  2. The overburden ridges continue to grow towards each other.

Phase 3 usually lasts the longest, e.g. B. when cambial tissue is removed over a large area (Fig. 2). This is typical for approach and back damage (see wound types). However, the phase can also be very short and even skipped, which often happens with minor injuries.

Phase 4

The pests are encapsulated by the overburden ridges. As a result of the encapsulation, they die and cannot spread any further, so the encapsulation is the survival strategy of trees after injuries!

Types and effectiveness of foreclosure

Active defense

According to the CODIT model, trees are able to actively defend themselves in the event of an injury. However, this can only take place via living cells in the sapwood area or in the bast .

The wood area tries to “overwhelm” the injury and thus encapsulate it. In addition, antifungal , mostly phenolic substances are stored.

In the bast, parenchymal (living) cells near the wound die within a few days. Here is often suberin (Korkstoff) in Oberflächenperiderm stored, which can be difficult or impossible degraded by fungus.

In both cases, these deposits separate the dead from the living tissue.

Passive defense

In the case of obligatory (real) color core formers , such substances are stored in the wood before they are damaged. They usually lead to discoloration of the heartwood (dead tissue inside the trunk), which is then difficult to break down by wood-destroying fungi .

This passive defense is z. B. to be observed with: oak , cherry , larch , walnut , or elm.

Existing vertifications (cell occlusion), the size of the vessels and the type of vascular perforation can also influence how well a tree can defend itself against injury. With regard to these influencing factors, a distinction is made between:

  1. Weak compartmentalizers : (e.g. birch , ash , poplar , willow and spruce )
  2. effective compartmentalizers : (e.g. beech , oak , hornbeam , linden , plane and pine )

Wound types

Fig. 5: so-called T-error after cambial injury - the cambium was injured in several places. Overflows occurred between injuries. The sealed off areas are darkly colored and have a T-shape typical of the injury (cross-section was taken about 3 years after the injury).
Fig. 4: Asting wound: Successful partitioning and encapsulation - the fungus could not spread any further

Asting wounds and broken crowns

Here an injury occurs across the grain. Often there is older tissue in the middle of the wound, which does not seal well. With such injuries, the wound remains for a long time, or for the rest of the tree's life in phase 3 according to the CODIT principle. Often in a short time is pith of the branch concerned closed, as this leads to the tree inside and pests so provides an attractive entry point.

Trunk drilling

Trunk drilling is usually done to determine whether the tree is already rotten or to measure the number of growth zones . Since the beginning of the 1990s, the resistance that the wood offers to a long and thin (Ø approx. 2 mm) drill has been measured. These holes lead to slight discolouration, the holes are usually covered over within a year, which is why the tree only remains in phase 3 for a short time.

Collision and back damage

Fig. 6: Successful encapsulation after a branch wound in a Japanese pagoda tree (Sophora japonica)

In this type of injury, living cambial tissue is usually removed over a large area. The injury is sealed off very tightly (barrier zone). As usually only young, living tissue is injured, the tree can defend itself well. However, the wound is not covered, a so-called surface callus is formed. Exposed paranchyma cells are specifically killed by the tree and the corresponding substances are stored. The sealing off of such injuries can be supported by the application of special wound closure agents or foils, which can occasionally be seen in trees at the roadside. These injuries were most likely caused by traffic accidents.

Root truncations

Root truncations are comparable to branching wounds, but roots contain considerably more parenchymatic cells. For this reason, although they can defend themselves well against injuries, a fungus can still infect the whole tree from there . Since such injuries are often caused by civil engineering work near the road, the traffic safety of trees can be severely impaired. In this context, therefore, in DIN 18 920, 2002; RAS-LP 4, 1999 summarized: “When digging trenches, roots with a diameter ≥ 2 cm must not be cut. Injuries should be avoided and should be treated immediately if necessary.

Animal feed

Animals such as wood-destroying insects can also pave the way for pests to get inside a tree. Wood breeding insects (xylophagous) as the eastern subterranean termite ( Reticulitermes flavipes ), the carpenter ant ( Camponotus formicidae ) or the Common wood wasp (Sirex juvencus) enable, for example by their insect holes in the wood various fungi a good breeding ground. The danger posed by beavers can also be underestimated; they usually injure trees over a large area or even kill them.

literature

Individual evidence

  1. ↑ (Tyree & Sperry 1988, Liese and Dujesiefken 1989, Rayner 1993, Dujesiefken et al. 1997)
  2. ↑ a b c D. Dujesiefken, W. Liese: The CODIT principle - learning from the trees for professional tree care. 2008.
  3. ↑ (Biggs 1985, 1987, 1990, Trockenbrodt 1991, 1994)
  4. ↑ (Matthek & ´Breloer 1993; Eckstein & Sass 1994; Rust & Weihs 2007)
  5. ↑ (Schwarze & Heuser 2005)