||De Kock, V.E.
||The articles have been scanned in colour with a HP Scanjet 5590; 300dpi.
Adobe Acrobat XI Pro was used to OCR the text and also for the merging and conversion to the final presentation PDF-format.
||1. Fowl glioma has erroneously been classified as astrocytoma.
2. Two chief variants occur, more rarely astroblastoma and much more
commonly a glioma closely related structurally to glioblastoma
(spongioblastoma) multiforme of man, but in general more slowly
growing. This commoner type must either be identified for purposes
of classification with low-grade glioblastoma multiforme or assessed
as intermediate between astroblastoma and glioblastoma.
3. "Microcystic degeneration" leading to cystic cavitation of avian gliomas
is associated with the secretory ability of neoplastic glia cells. This
secretion is often of demonstrably mucinous nature. The question is
raised whether this phenomenon may perhaps be merely an exaggeration
of the normal physiology of glia.
4. The growth of avian gliomas occurs overwhelmingly by conversion
of neighbouring (adult) astrocytes to tumour cells.
5. The histopathology of a non-purulent disseminated perivascular encephalitis
of fowls has been closely studied and is identical with that of the
brain tissue at the spreading margin of glioma.
6. Very commonly these focal inflammatory lesions exist side by side with
glioma in the same brain.
7. All possible gradations occur between these inflammatory foci and
glioma. The earliest gliomas of fowls have been shown to be nothing
but encephalitic foci in which glia proliferation becomes exaggerated
and predominant over haematogenous cellular infiltrative changes.
8. The reacting marginal brain tissue around fowl glioma is identical in
all details of its histopathology with this chronic perivascular
encephalitis. Thus not only does glioma arise from encephalitis, but
its continued growth and spread are similarly due to conversion of
chronically inflamed brain tissue at its periphery into tumour tissue.
9. The very common occurrence of multiplicity of avian gliomas is
explained as due to the progression of multiple scattered pre-existent
encephalitic foci to tumours.
10. The characteristic lobulation of avian glioma is explained as due to
an initial concentration of encephalitic foci which fuse as they become
converted into gliomas.
11. Multiplicity of avian glioma should not be thought of as a secondary
multiplicity Although gliomas may break into the ventricles, there
is no evidence whatever of a spread by transplantation of tumour
cells transported by the C.S.F., or by any other means. On the other
hand, each of the multiple tumours is primary and bas arisen from
a pre-existent focus of encephalitis.
12. The protrusion of gliomas into the ventricles is due to prior location
in or near the ventricular walls of encephalitic foci which later become
converted to gliomas.
13. The ependymal cells lining such stimulated ventricles readily de-differentiate
into ependymal spongioblasts, but such cells have not been
observed to participate in neoplasia in birds.
14. All gradations exist between the non-purulent encephalitic foci mentioned
and purulent encephalitis including cerebral abscess.
15. All gradations occur between non-purulent encephalitic (and especially
meningo-encephalitic) foci and lymphocytoma of the C.N.S.- or in
cases where it is the plasma cell transformation of lymphocytes which
becomes predominant- between encephalitis and plasmacytoma.
16. The occurrence of haemangioblastoma of the brain of the fowl is
reported. The idea is entertained that these tumours also are related
to glioma in the sense that they too may arise as encephalitic foci.
17. The proliferation of haematogenous infiltrating cells in gliomas as well
as in disseminated meningo-encephalitis may reach neoplastic grade
Thus from foci of leptomeningitis, lymphocytoma may arise and invade
the brain. Neoplastic proliferation of lymphocytes in glioma lead
to a variant designated glioma lymphomatosum. Neoplastic proliferation of the emigrated haematogenous monocytes gives rise to other
mixed tumours designated glioma monoblastomatosum.
18. In four cases of avian glioma [three of the present author's and one
of Fox (1912)] there have been concomitant liver tumours of a peculiar
type. These - as might have been anticipated - are not metastatic
gliomas in the liver(!) In my own cases they were cholangiocellular
adenocarcinoma, cholangiocellular carcinoma, or mixed hepatocellular
and cholangiocellular adenoma or adenocarcinoma; in all cases
admixed with myelocytomatous neoplasia. It is suspected that these
unusual findings are to be explained by the assumption that an
unknown factor causing glioma (or encephalitis) may in some cases
operate simultaneously on the liver, and that much more constantly
in the liver than has above been mentioned in the C.N.S., this factor
tends to evoke simultaneous neoplastic proliferation of emigrated
19. The relationship of a spectacular case of diffuse gliosis of the brain to
glioma has been discussed.
20. Avian glioma (as well as the related lesions of non-purulent and purulent
encephalitis, lymphocytomatous tumours and solid haemangioblastomas
of the C.N.S., and the peculiar concomitant liver neoplasms) is characterised
by the presence of an iron-containing pigment responsible for
a peculiar orange to yellow coloration of all these lesions. The author
believes this pigment to be of great significance, indeed that it is derived
from a parasitic agent present in these lesions.
21. The theory of origin of gliomas from embryonal cells which recapitulate
their ontogenetic ancestry by differentiation towards adult types is
false in the case of gliomas of birds. These gliomas on the contrary
arise from previously adult cells which de-differentiate into more
primitive cells - a " recapitulation in reverse order" of their embryonic
22. A suggested pathogenesis of avian glioma and related lesions has been
developed in considerable detail.
23. The histopathological, histogenetic, and pathogenetic observations
suggested strongly that avian glioma is a response to some noxa which
continues to spread in the brain in advance of the tumour. This led
to a search for the presence of a visible agent associated with glioma
and related lesions of the fowl and also later in. human gliomas.
Preliminary accounts of the results of this search have been published
and fuller reports are in preparation.
||Jackson, C 1954, 'Studies in comparative neuropathology. I. Gliomas of the domestic fowl: their pathology with special reference to histogenesis and pathogenesis; and their relationship to other diseases’, Onderstepoort Journal of Veterinary Research, vol. 26, no. 4, pp. 501-597.
||Published by The Government Printer, Pretoria
||© 1954 ARC - Onderstepoort and Faculty of Veterinary Science, University of Pretoria (original). © 2016 University of Pretoria. Dept. of Library Services (digital).
||Veterinary medicine -- South Africa
||Studies in comparative neuropathology. I. Gliomas of the domestic fowl: their pathology with special reference to histogenesis and pathogenesis; and their relationship to other diseases