CODIT
(Compartmentalisation of decay in trees)
Compartmentalisation is a three-dimensional concept that occurs in two stages:
Stage 1
The first part occurs immediately, at the time of wounding. The tree attempts to
confine the pathogen to a small compartment (localisation). This may be successful or
the pathogen may eventually spread through and digest all the tissues present at the
time of wounding until a cavity forms. A cavity indicates that some boundary must
separate the tissues present at the time of wounding from new tissues that continue to
form. At one extreme, this first stage may be a localisation process or, at the other
extreme, a complete breakdown of all boundaries (see Figure 7).
Stage 2
This part occurs after wounding and includes the formation of a barrier zone that
usually localises the compartment for the first stage and protects the cambium.
Closure of wounds by callus takes place after wounding as new cells are generated in
new spatial positions. (Callus is new phloem, xylem and other tissues produced by the
cambium but not arranged in as organised a way as ‘natural’ growth.)
The process of compartmentalisation can be explained more fully by examining a
conceptual model that describes the changes in the infected tissues. The model is
CODIT, an acronym for ‘Compartmentalisation of Decay in Trees’. Shigo and others
use the concept of ‘walls’ being formed to explain how the tree responds.
Stage 1 of CODIT
This occurs at the time of wounding. When a wound occurs, parenchyma cells in the
phloem, cambium and/or xylem are broken and their contents are exposed to the air.
Oxygen combines with a number of cell contents, some of which react to produce
compounds which break down living materials, and cells may die. In nearby living,
but injured, cells some energy reserves are converted to phenols. These phenols either
oxidise or combine with proteins. The products of these reactions become
antimicrobial substances, or at least resist microbial breakdown. Ions accumulate in
the injured cells and the pH of the cells change. All of these chemical processes are
part of the tree’s response to rapidly convert energy reserves into antimicrobial
products and into products that cannot be used as food by the microorganisms.
During this stage, three ‘walls’ are produced by the tree to localise the injury. (The
term ‘wall’ relates to the CODIT model and not to an actual anatomical structure.)
Figure 8 summarises the process of compartmentalisation.
The three walls that are formed during the first stage of compartmentalisation have
the following functions:

Wall 1 resists vertical spread. It does not exist as an anatomical entity before
infection but is formed after injury by the plugging of xylem vessels. There are
several ways in which the xylem can be plugged:
* gums, tyloses and other extractives can plug xylem vessels;
* companion parenchyma cells can balloon into the vessels through pits in the
walls;
* granular or crystalline materials can fill the vessels;
* pits between vessels can close;
* air bubbles may develop, impeding transport of liquids.
The parenchyma cells which surround the non-living vessels play an important role in
Wall 2 resists inward spread and is moderately strong. After each flush of growth or
each season’s growth, sets of highly lignified cells are formed (annual rings). Most
micro-organisms do not have the enzymes to digest lignin; hence, Wall 2 is already in
place in the tree. When shallow wounds kill the cambium, Wall 2 resists inward
spread of pathogens behind the wound. As deeper wounds are inflicted, the injuries
approach older sheaths of xylem and the resisting power of Wall 2 diminishes. When
Wall 2 fails to the pith, inward spread ends.
Wall 3 resists lateral spread and is the strongest wall produced at the time of
wounding. Wedge-shaped sections defined by ray cells provide a living cell
communication between the older, inner xylem and the newer outer xylem and
phloem. The rays form a screen of small groups of living cells which are capable of a
short-term response to invasion. This response includes many of the chemical
reactions already mentioned in the discussion of Stage 1 of CODIT: that is, the
production of oxidised phenols and other antimicrobial substances. Because they
maintain a living connection with the cambium of a vigorous tree, the rays may be
continually re-supplied with energy reserves for extended response and containment
of invasion by decay fungi. Hollows or cavities will form if this wall fails over time
and the boundaries open as a fan.
While the walls are operating or failing in Stage 1, the undamaged cambium is
generating new cells in new positions: that is, the rest of the tree continues to grow.
These new cells are protected from the infected tissues in the second part of the
process of compartmentalisation. In the CODIT model, only Stage 1 is present at the
time of wounding. Stage 2 may not begin to form for many months, depending upon
the time of wounding and in relation to the next surge of cambial activity. Figure 11
illustrates the walls.
Stage 2 of CODIT
This occurs after the wounding. Wall 4, also known as the barrier zone, is formed.
This is a protective tissue or boundary that is formed by living cambium in response
to mechanical wounding and infection. It serves to isolate or separate the infected
wood from the healthy wood that continues to form after the zone is completed. Have
a look a Figure 2; in this example only a small section of the cambium has been
damaged the rest of the cambium continues to divide and produce new phloem and
xylem. These new tissues produced by the cambium after wounding, and the cambium
itself, are protected by Wall 4. After wounding, the cambium produces cells which
differentiate to form a protective boundary. Some of these cells convert their contents
to antimicrobial substances.
The barrier zone is usually non-conducting and, in some trees (oaks), suberin is
present in the cell walls of such tissue. In some species of trees, the cambial zone
responds to wounding by producing ducts of defensive materials. For example,
Eucalypts produce kino veins (kino is a polyphenol), conifers produce resin ducts and
Liquidambar styraciflua produces storax veins.
The barrier zone may be extensive and encircle the stem or it may be only localised.
Factors affecting the extent of barrier zone formation are poorly understood.
Wall 4 is produced by trees when the cambium is active, so a tree wounded during a
dormant period will not form a barrier zone until after growth resumes in spring.
Have you ever cut and split firewood and noticed that sometimes the timber falls out
in rings, or that the wood is most easily split around a ring? If you have, then you
have observed a characteristic of Wall 4. The barrier zone is a very strong protective
boundary against pathogens, but a very weak structural boundary. As wood dries, or
after felling, cracks often start along the barrier zone; if they are around the tree they
are usually referred to as ‘ring shakes’. ‘Ray shakes’-separations along the rays which
radiate outwards-usually start from a ring shake and hence originate from old wounds
and may also form where new callus begins to roll inward from the sides of the
wound.
While we are discussing cracks in trees, shallow vertical cracks may also form in the
bark as a result of rapid growth-these are often referred to as ‘growth splits’. They do
not affect the growth of the tree and require no treatment.
Figure 6.
Figure 7: Wall 1, 2, 3 formed at time of wounding
Note that:

in this example, no decay has developed and Walls 1, 2 & 3 have held

the tissues surrounding the wound are likely to be discoloured as a result of the
chemical changes that occur during the wound response.
Figure 8: Wall 1 is the weakest wall
Figure 9: Walls in the CODIT model
Figure 10: Wall 4 formed after wounding
Figure 11: Wall 4 after wounding.
Figure 12 gives another view of compartmentalization.
Depending on the severity of the wound, there will be varying degrees of alteration,
discolouration and decay.
Compartmentalisation is not always effective; sometimes micro-organisms kill the
tree before compartmentalisation commences. Some individual trees are more
effective than others.
Examples of compartmentalisation
Roots
Compartmentalisation also occurs in response to wounds in roots and to root diseases.
An example of this is in jarrah dieback. It has been reported that compartmentalisation
of the pathogen Phytophthora cinnamoni in the secondary phloem of Eucalyptus
marginata (jarrah) is temporary. The fungus is contained during winter and spring but
outbreaks occur in summer and new areas of phloem are invaded in winter.
This type of breakout pattern is common in perennial canker and also in root
infections such as those by Armillaria mellea. Alternating breakout and
compartmentalisation in stems results in a concentric pattern of canker, but in the
roots the breakout results in more and more root death until a threshold is reached and
the tree dies.
Whether the tree has time to regain its capacity to resist further invasion depends on
when the pathogen is compartmentalised. If environmental conditions do not favour
the tree, the advantage may go to the pathogen.
Branches
As a branch dies, the tree forms a boundary within the branch base. This boundary
contains materials that usually inhibit the growth of decay-causing fungi. The
boundary usually functions effectively and the branch falls out of the socket. The tree
compartmentalises the decayed wood in the socket. This protective boundary zone is
the ‘branch collar’.
Figure 13: Pruning to the branch collar