African Pig Disease * *Under the title African Pig Disease The Times of September 12 1960, referred to an epidemic among pigs in Spain. The disease was believed to be the same as that described by Montgomery (1921) as East African swine fever, which is now recognized to be a separate entity. As this disease occurs in various parts of Africa and is immunologically distinct from swine fever, the original name is misleading. African pig disease would appear to be appropriate


Doyle, T.M.

British Veterinary Journal 117(6): 229-238

1961


Brit.
vet.
j.
(1
9
61),
117,
229
AFRICAN
PIG
DISEASE*
BY
T.
M.
DOYLE
Central
Veterinary
Laboratory,
Weybridge
In
1921
Montgomery
described
a
virulent
disease
of
pigs
in
Kenya
and
named
it
"East
African
swine
fever".
It
was
first
diagnosed
in
1910,
but
two
earlier
outbreaks
had
been
observed.
Fifteen
outbreaks
occurred
between
1910
and
1915;
three
were
confirmed
biologically
and
the
history,
symptoms
and
lesions
of
ten
left
no
doubt
that
they
were
the
same
disease.
Two
outbreaks
were
reported
in
1914
from
what
was
then
German
East
Africa.
The
German
veterinary
authorities
stated
that
the
disease
had
been
seen
among
wild
pigs
and
was
probably spread
by
them.
It
was
noted
that
in
every
outbreak
in
Kenya
wart-hogs
(Phacochoerus
spp.)
were
numerous
in
the
vicinity.
The
outbreaks
were
widely
scattered
and
the
movement
of
neither
domestic
pigs,
pig
products
nor
attendants
could
be
incriminated.
It
was
the
practice
on
many
farms
to
allow
pigs
free
range
during
the
day
so
that
they
came
in
contact,
directly
or
indirectly,
with
wart-
hogs
grazing
the
same
ground.
Steyn
(1928)
reported
on
an
acute
disease
of
pigs
in
the
northern
Transvaal.
Farmers
stated
it
was
so
deadly
that
breeding
was
impossible
and
that
affected
animals
rarely
recovered.
It
was
more
prevalent
among
pigs
on
free
range
than
among
those
in
sties.
Large
numbers
of
wart-hogs
were
present
on
infected
farms.
Steyn
noted
the
striking
similarity
in
the
incubation
period,
symptoms
and
lesions
of
the
Transvaal
and
the
East
African
disease.
De
Kock,
Robinson
&
Keppel
(1940)
described
outbreaks
of
disease
among
pigs
on
the
Witwatersrand
(
Johannesburg)
and
in
the
Western
Province
of
the
Cape.
Swine
fever
had
occurred
from
time
to
time
in
the
Western
Province,
but
this
disease
was
different.
It
was
believed
to
be
the
same
as
that
seen
by
Steyn
in
the
Transvaal.
Donatien
&
Lestoquard
(1940)
described
as
"pig
typhus"
a
virulent
disease
that
occurred
at
the
Pasteur
Institute,
Algiers.
It
was
believed
to
have
been
introduced
by
a
newly
purchased
pig.
It
killed
19
out
of
20
pigs
which
were
immune
to
swine
fever.
The
incubation
period,
symptoms
and
lesions
were
similar
to
those
of
the
East
African
and
the
Transvaal
disease.
Conceicao
(1947)
established
that
a
virus
disease
of
pigs
which
had
been
present
for
many
years
in
Angola
was
antigenically
distinct
from
swine
fever;
*
Under
the
title
"African
Pig
Disease"
The
Times
of
September
12
1960,
referred
to
an
epidemic
among
pigs
in
Spain.
The
disease
was
believed
to
be
the
same
as
that
described
by
Montgomery
(1921)
as
East
African
swine
fever,
which
is
now
recognized
to
be
a
separate
entity.
As
this
disease
occurs
in
various
parts
of
Africa
and
is
immunologically
distinct
from
swine
fever,
the
original
name
is
misleading.
African
pig
disease
would
appear
to
be
appropriate.
23o
BRITISH
VETERINARY
JOURNAL,
CXVII,
6
he
considered
it
to
be
the
same
disease
as
that
studied
by
Montgomery.
Velho
(1956)
had
seen
in
Angola
chronic
cases
of
the
disease
which
lasted
for
21
days
or
longer.
He
believed
the
virus
had
become
modified
from
being
endemic
in
the
country.
Rebeiro
et
al.
(1958)
reported
a
virulent
disease
near
Lisbon,
Portugal.
It
was
similar
in
all
respects
to
the
African
disease.
It
killed
pigs
hyperimmunized
against
swine
fever.
In
the
Lisbon
area
216
premises
were
infected;
of
10,731
pigs
5,222
died
and
the
remainder
were
slaughtered.
Secondary
outbreaks
occurred
in
rural
areas
through
infected
swill.
The
disease
was
present
in
Portugal
from
April
1957
to
January
1958;
16,457
premises
were
infected,
6,103
pigs
died
and
10,354
were
slaughtered.
The
origin
of
the
disease
was
not
discovered,
but
as
it
first
appeared
near
a
port,
ship's
swill
was
a
likely
cause.
The
Times
of
September
12,
1960
referred
to
an
outbreak
of
"African
pig
disease"
in
Spain.
It
stated
that
thousands
of
pigs
had
died
or
had had
to
be
slaughtered
in
the
previous
few
months
to
combat
an
epidemic
which
first
appeared
in
Badajoz
province
and
later
spread
to
Salamanca
and
Ciudad
Real.
The
Office
International
des
Epizooties
recorded
55
fresh
outbreaks
between
June
and
August
1960
in
Portugal;
and
558
outbreaks
in
August
1960
in
Spain
(Anon.,
1960).
The
most
important
outbreaks
were
those
in
East
Africa
and
the
Northern
Transvaal
because
they
pointed
to
the
wart-hog
as
the
source
of
infection.
There
was
no
swine
fever
in
East
Africa
(Walker,
1933)
so
there
was
no
possibility
of
confusing
African
pig
disease
with
it,
and
no
question
of
swine
fever
having
passed
from
domestic
to
wild
pigs
and
having
become
enhanced
by
passage.
The
Northern
Transvaal
was
far
inland
and
there
was
little
possibility
of
swine
fever
being
introduced
there
by
ship's
swill
(Geiger,
1937).
In
both
areas
wart-hogs
were
numerous
and
domestic
pigs
came
into
contact
with
them.
Geographical
distribution.
The
disease
has
been
reported
from
Kenya,
South
Africa,
South-west
Africa,
Congo,
Angola,
Nyasaland,
Northern
Rhodesia,
Mozambique,
Senegal,
Algiers,
Portugal
and
Spain.
Filtration.
The
causal
agent
of
the
disease
is
a
filterable
virus
(Montgomery,
1921;
Steyn,
5928,
1932;
Geiger,
1937;
De
Kock
et
al.,
1940;
Donatien
&
Lestoquard,
194o).
SYMPTOMS
There
is
general
agreement
among
the
various
authors
on
the
symptoms
exhibited.
Montgomery
(1921)
noted
:
"There
is
extreme
weakness
of
the
loins
and
within
24
hours
of
the
onset
of
symptoms
there
is
difficulty
in
walking.
Co-ordination
of
the
fore-limbs
remains,
but
the
hind
quarters
sway
invol-
untarily
and
in
many
cases
the
hind
legs
are
dragged
as
in
paresis.
The
temperature
varies
from
104°-107°F.
Diarrhoea
very
rarely
occurs.
Cyanosis
of
the
ears
and
thighs
is
observed,
later
the
whole
body
is
involved.
Death
almost
AFRICAN
PIG
DISEASE
231
invariably
occurs
within
48
hours
of
the
onset
of
symptoms,
often
with
con-
vulsions.
In
some
cases
the
epizootic
is
ushered
in
by
sudden
deaths.
Pigs
of
all
ages
and
breeds
are
susceptible."
Steyn
(1928)
reported
that
diarrhoea,
with
blood-stained
faeces,
frequently
occurred
and
that
a
mucopurulent
nasal
discharge
also
occurred
and
foam
issued
from
the
mouth.
Walker
(1933)
noted
that
the
faeces
were
firm
and
might
be
blood-stained.
De
Kock
et
al.
(1940)
saw
blood-stained
faeces
and
in
some
cases
blood
oozing
from
the
nose
and
anus
after
death.
Rebeiro
et
al.
(1958)
stated
that
diarrhoea,
with
blood-stained
faeces,
frequently
occurred
and
sometimes
blood
oozed
from
the
anus,
and
that
there
was
a
mucopurulent
nasal
discharge.
Walker
(1933)
and
Steyn
(1928)
observed
vomiting
in
some
cases.
MORTALITY
The
mortality
rate
from
either
artificial
or
natural
infection
is
nearly
Ioo
per
cent.
Montgomery
(1921)
mentioned
that
out
of
1,366
naturally
infected
pigs
1,352
died
(98.9
per
cent).
ARTIFICIAL
INFECTION
The
disease
can
be
transmitted
by
subcutaneous,
intramuscular,
intraperitoneal,
intravenous
and
intracutaneous
inoculation
of
virulent
material;
and
by
feed-
ing,
by
infective
faeces
and
urine,
and
by
contact
(Montgomery,
1921;
Steyn,
1928,
1932;
Geiger,
1937;
De
Kock
et
al.,
1940).
POST-MORTEM
FINDINGS
The
lesions
of
both
African
pig
disease
and
acute
swine
fever
are
character-
istic
of
a
haemorrhagic
septicaemia.
They
consist
of
petechiae,
which
occur
on
the
membranes
lining
the
thoracic
and
abdominal
cavities,
and
on
the
contained
organs.
The
lymphatic
glands
are
enlarged
and
show
on
section
either
petechiae
or
an
intense
inflammation.
Lesions
are
generally
present
in
the
cardiac
portion
of
the
stomach;
in
acute
cases
the
normal
colour
is
changed
from
pink
to
dark
red
or
purple.
The
lesions
of
African
pig
disease
are
usually
more
severe
than
those
of
swine
fever.
Spleen
Montgomery
(1921)
noted
that
the
spleen
in
African
pig
disease
was
double
the
normal
size;
it
was
thickened,
dark
and
firm.
Capsular
petechiae
were
present.
Steyn
(1928)
observed
marked
tumor
splenis
with
hyperplasia
of
the
Malpighian
bodies;
it
was
difficult
to
scrape
off
the
pulp.
Walker
(1933)
stated
that
the
spleen
was
swollen,
with
a
reddish
colour
on
section,
the
Malpighian
bodies
being
prominent
and
slightly
above
the
surface
of
the
pulp.
Geiger
(1937)
found
that
in
typical
cases
the
spleen
was
two
to
six
times
greater
than
normal.
Donatien
&
Lestoquard
(1940)
described
a
great
increase
in
the
size
of
spleen.
The
capsule
tore
easily
and
the
pulp
was
black
and
friable.
De
Kock
et
al.
(1940)
stated
that
the
spleen
might
show
little
or
no
change,
232
BRITISH
VETERINARY
JOURNAL,
CXVII,
6
but
usually
it
was
swollen
to
a
variable
extent,
occasionally
reaching
two
or
three
times
normal
size.
Velho
(1956)
observed
that
when
the
course
of
the
disease
was
longer
than
five
days
the
spleen
was
two
or
three
times
the
normal
size;
enlargement
was
particularly
noticeable
in
artificially
infected
pigs.
Rebeiro
et
al.
(1958)
described
the
spleen
as
being
three
or
four
times
normal
size,
the
capsule
a
dark
blue
colour
and
pulp
very
soft.
Contrary
to
these
findings,
De
Tray
(1957a)
stated
that
tumor
splenis
rarely
occurs:
and
Maurer,
Griesemer
and
Jones
(1958)
found
it
in
only
6
per
cent
of
83
artificially
infected
pigs.
Lungs
Montgomery
(1921)
found
interlobular
oedema
in
5o
per
cent
of
cases.
Steyn
(1932)
also
mentioned
interlobular
oedema.
Walker
(1933)
stated
that
there
was
sometimes
marked
hyperaemia
and
oedema
with
infiltration
of
the
interlobular
septa
and
Donatien
&
Lestoquard
(1940)
that
the
lungs
were
either
normal
or
oedematous.
De
Kock
et
al.
(1940)
stated
that
there
was
little
or
no
change
in
many
cases
and
in
others
interlobular
oedema
was
pronounced.
Rebeiro
et
al.
(1958)
said
that
all
cases
showed
serious
involvement
of
the
respiratory
system
with
acute
inflammation
of
the
trachea
and
bronchial
tubes
and
congestion
and
oedema
of
the
lungs.
Maurer
et
al.
(1958)
observed
inter-
lobular
oedema
in
about
25
per
cent
of
cases.
The
lesions
present
in
the
stomach,
kidneys,
heart
and
intestines
are
similar
to
but
usually
more
severe
than
those
of
swine
fever,
and
are
of
no
value
for
differential
diagnosis.
HISTOPATHOLOGY
African
pig
disease
Brain:
Walker
(1933)
found
no
perivascular
cellular
infiltration
and
no
proliferation
of
the
glia
in
African
pig
disease.
Thomas
(1940)
stated
there
was
no
perivascular
round-cell
infiltration
as
described
in
swine
fever.
The
blood
vessels
and
capillaries
of
the
brain
show
hyalinization
of
the
walls
and
karyorrhexis
of
the
endothelial
linings,
but
this
is
most
distinct
and
constant
in
the
lymphatic
glands.
Thomas
regarded
the
karyorrhexis
of
the
nuclei
of
the
large
lymphocytes
and
monocytes
of
the
spleen
and
lymph
glands
as
being
of
diagnostic
value.
Maurer
et
al.
(1958)
observed
perivascular
infil-
tration
in
most
cases
of
African
pig
disease,
although
only
a
few
vessels
might
be
affected.
The
effect
of
the
virus
on
lymphocytes
was
severe
and
their
destruction
with
karyorrhexis
is
seen
in
lymphocytic
tissue.
Maurer
et
al.
(1958)
confirmed
that
the
most
significant
difference
between
swine
fever
and
African
pig
disease
is
the
karyorrhexis
of
lymphocytes
in
the
African
disease.
Swine
fever
Brain
:
Seifried
(1931)
reported
a
more
or
less
marked
encephalomyelitis
and
meningitis
in
swine
fever.
The
encephalomyelitis
was
characterized
by
a
varying
amount
of
vascular
and
perivascular
infiltration
with
small
leucocytes
and
mononuclear
elements.
There
was
proliferation
of
the
glia.
Seifried
and
AFRICAN
PIG
DISEASE
2
33
Cain
(1932)
considered
that
the
diagnostic value
of
the
encephalitis
was
limited
as
it
occurred
in
only
6o
to
8o
per
cent
of
cases.
Helmboldt
and
Jungherr
(1950)
believed
histological
examination
of
the
brain
to
be
a
valuable
diagnostic
aid
in
the
detection
of
swine
fever.
IMMUNITY
There
is
ample
evidence
that
pigs
immune
to
swine
fever
are
susceptible
to
African
pig
disease,
and
swine
fever
immune
serum
does
not
protect
domestic
pigs
against
African
pig
disease
virus
(Montgomery,
1921;
Geiger,
1937;
De
Kock
et
al.
1940;
Donatien
&
Lestoquard,
1940).
Immune
serum
Most
attempts
to
produce
immune
serum
have
failed.
Montgomery
(1921)
and
Steyn
(1928)
failed
to
produce
a
protective
serum
from
domestic
pigs.
Mont-
gomery
failed
also
with
a
wild
pig
(Potomochoerus)
and
Walker
(1933)
failed
with
a
wart-hog.
Walker
succeeded
in
preparing
two
lots
of
sera
from
recovered
domestic
pigs.
Both
gave
protection
in
doses
of
0.2
to
1•o
ml.
per
pound
body
weight
against
the
homologous
virus.
De
Tray
(1957b)
found
that
sera
from
carrier
pigs
rarely
have
protective
properties;
but
in
two
pigs
which
survived,
antibodies
were
demonstrated
for
27
and
33
days
after
exposure
to
infection.
Vaccines
Both
De
Kock
et
al.
(1940)
and
Rebeiro
et
al.
(1958)
failed
to
protect
pigs
with
crystal
violet
vaccine.
Vaccines
killed
by
chemical
and
physical
methods
have
also
been
tried
without
success.
Serum-virus
method
Walker
(1933)
prepared
serum
from
domestic
pigs,
survivors
from
previous
experiments,
by
the
intraperitoneal
injection
of
virus.
The
serum
gave
pro-
tection
against
inoculation
with
the
homologous
virus.
The
immunity
per-
sisted
for
between
192
and
283
days.
Immunity
of
recovered
pigs
So
few
pigs
recover
that
information
on
their
resistance
to
reinfection
is
meagre.
Montgomery
(192
I)
tested
12
survivors
of
natural
outbreaks
and
only
one
was
immune.
The
others
possessed
a
variable
degree
of
resistance,
but
eventually
all
died
of
a
chronic
infection.
According
to
Walker
(1933)
pigs
which
recover
from
either
natural
or
artificial
infection
die
when
re-inoculated
with
the
homologous
virus.
Steyn
(1932)
observed
that
affected
pigs
seldom
recover,
but
those
that
do
recover
acquire
considerable
resistance,
although
they may
have
a
second
attack
which
is
less
severe
than
the
first.
Donatien
&
Lesto-
quard
(1940)
found
that
pigs
which
recovered
were
not
resistant
to
reinfection.
De
Kock
et
al.
(1940)
re-inoculated
such
a
pig
with
virus
from
a
different
source
to
that
of
the
original
inoculum
and
it
showed
no
reaction.
De
Tray
(1957b)
suggested
that
all
pigs
which
survived
became
virus
carriers,
and
these
carriers
were
the
only
pigs
capable
of
resisting
re-inoculation.
234
BRITISH
VETERINARY
JOURNAL,
CXVII,
6
Eight
domestic
pigs
which
survived
for
periods
of
86
to
456
days
after
exposure
had
a
persistent
viraemia.
De
Tray
considered
that
resistance
to
re-inoculation
may
depend
on
persistent
infection
(premunition)
rather
than
on
circulating
antibodies.
In
a
later
report
(196o)
he
modified
this
view
in
the
light
of
recent
findings.
Serial
passage
of
the
Hinde
strain
of
virus
in
kidney
monolayer
cultures
reduced
its
virulence
for
pigs.
A
considerable
percentage
of
pigs
inoculated
with
the
cultured
virus
survived.
While
most
of
the
survivors
harboured
the
virus,
in
a
few
of
them
viraemia
was
not
demon-
strated,
but
they
resisted
re-inoculation
with
the
homologous
virus.
VIROLOGY
Velho
(1956)
found
that
after
more
than
one
hundred
pig
passages
the
virus
was
infective
in
a
dilution
of
Io
1
It
was
slightly
modified
for
pigs
after
85
passages
in
rabbits
:
the
incubation
period
was
longer
and
a
more
chronic
infection
was
induced.
The
attenuation
was
insufficient
to
render
it
suitable
for
immunization
purposes.
McIntosh
(1952)
passaged
the
virus
12
times
in
8-day-old
embryonated
eggs.
Incubation
was
at
33°C.
The
embryos
usually
died
on
the
seventh
day
of
incubation.
Egg
material
of
the
third
and
sixth
passages
induced
typical
African
pig
disease
in
pigs.
Velho
(1956)
passaged
the
virus
24
times
in
embry-
onated
eggs.
The
virulence
was
diminished
for
pigs
and
a
chronic
infection
was
induced,
but
the
few
animals
that
survived
were
not
resistant
to
re-
infection.
INFECTION
OF
STIES
WITH
AFRICAN
PIG
DISEASE
VIRUS
Montgomery
(1921)
found
that
sties
remain
infective
for
three
days,
but
not
for
five
and
a
half
days.
Steyn
(1928)
confirmed
this
finding.
ABSENCE
OF
PLURALITY
OF
SWINE
FEVER
VIRUS
STRAINS
A
great
deal
of
work
has
been
carried
out
on
swine
fever
virus
in
various
countries
and
no
evidence
of
plurality
of
strains
has
been
found.
Immune
serum,
irrespective
of
its
country
of
origin,
protects
against
all
known
strains
of
the
virus.
There
is,
therefore,
no
justification
for
referring
to
"European"
or
"American"
swine
fever.
Many
strains
of
virus
obtained
from
Europe,
America
and
Britain
have
been
tested
at
Weybridge
and
all
proved
immunologically
indistinguishable.
Crystal
violet
vaccine
prepared
from
Dutch,
German,
American
and
English
viruses
has
protected
against
natural
and
artificial
infection
with
swine
fever.
Dale,
Schoening,
Cole,
Henley
&
Zinobar
(1951)
found
a
virus
in
America
which
possessed
unusual
characteristics.
Pigs
already
immunized
with
serum-
virus
were
protected
against
the
variant
virus,
but
a
number
of
susceptible
pigs
inoculated
with
it
and
with
immune
serum
either
reacted
and
recovered,
or
died,
whereas
pigs
treated
with
standard
virus
and
the
same
serum
re-
mained
normal.
By
increasing
the
dose
of
serum
the
effect
of
the
variant
could
AFRICAN
PIG
DISEASE
2
35
be
reduced
or
eliminated.
It
was
clearly
a
variant
swine
fever
virus
and
not
a
new
type.
Lucas,
Bouley,
Paraf
and
Quinchom
(1953)
reported
a
variant
virus
which
appeared
to
be
similar
to
that
found
in
America.
The
infection
in
wild
pigs
Montgomery
(1921)
stated
that
"the
case
against
the
wart-hog
is
largely
circumstantial,
but
is
in
every
way
supported
by
the
experimental
and
epi-
demiological
evidence
obtained."
During
the
outbreaks
in
1910-21
and
1954
in
Kenya,
and
in
1928
in
the
northern
Transvaal,
wart-hogs
were
numerous
in
the
vicinity.
Further
circum-
stantial
evidence
incriminating
the
wart-hog
is
that
with
closer
settlement,
the
destruction
of
vermin
and
the
provision
of
pig-proof
paddocks,
the
incidence
of
the
disease
has
been
considerably
reduced.
Montgomery
(1921)
inoculated
zo
Uganda
bush
pigs
and
one
young
wart-hog
(No.
58)
with
African
pig
disease
virus.
None
of
the
bush
pigs
reacted,
but
one
harboured
virus
in
the
blood
for
five
days.
The
wart-hog
had
an
irregular
temperature
from
the
5th
to
the
15th
day
and
then
returned
to
normal;
blood
drawn
from
it
on
the
6th,
9th,
13th
and
17th
days
infected
domestic
pigs,
while
blood
drawn
on
the
21st
day
was
avirulent.
A
second
wart-hog
(No.
59),
exposed
by
contact
to
the
disease,
died
from
lobar
pneu-
monia
on
the
3oth
day.
Its
blood
was
non-infective
on
the
1
oth
and
23rd
days
of
contact.
A
domestic
pig
in
contact
with
two
wart-hog
virus
carriers
failed
to
contract
infection.
Infected
wild
pigs
appeared
incapable
of
disseminating
the
virus
by
contact,
urine
and
faeces.
Steyn
(1932)
proved
by
inoculation
that
three
of
four
healthy
wart-hogs
from
the
northern
Transvaal
were
virus
carriers,
whereas
six
wart-hogs
from
Zululand
did
not
harbour
the
virus.
De
Kock
et
al.
(1940)
found
six
of
eleven
healthy
wart-hogs
in
the
northern
Transvaal
were
carriers.
De
Tray
(1957b)
recovered
virus
from
the
blood
of
a
wart-hog
54
days
after
inoculation.
He
confirmed
that
the
disease
was
not
readily
transmitted
by
healthy
wart-hog
carriers
to
domestic
pigs,
although
there
was,
however,
one
successful
transmission.
De
Tray
(1960)
also
reported
the
isolation
of
the
virus
from
17
of
8o
healthy
wart-hogs
(21
per
cent).
Montgomery
(1921)
suggested
that
in
nature
the
disease
is
spread
by
the
carnivorous
habits
of
pigs,
presumably
by
domestic
pigs
feeding
on
the
car-
cases
of
infected
wild
pigs.
Walker
(1933)
failed
to
transmit
the
disease
by
fleas
and
lice.
He
suggested
that
a
winged
insect
may
transmit
it
among
wild
pigs
and
and
from
wild
pigs
to
domestic
pigs.
Hammond
and
De
Tray
(1955)
thought
vultures
might
carry
infective
material
from
dead
wart-hogs
to
domestic
pigs.
Domestic
pigs
as
reservoirs
of
the
virus
Steyn
(1932)
established
that
recovered
pigs
can
harbour
the
virus
in
the
blood
for
at
least
two
months.
De
Kock
et
al.
(1940)
reported
that
six
of
ten
pigs
which
recovered
were
virus
carriers,
in
some
cases
for
ten
months.
De
Tray
(1960)
stated
that
domestic
pigs
that
survive
infection
with
virulent
African
pig
disease
virus
remain
carriers,
probably
for
life.
236
BRITISH
VETERINARY
JOURNAL,
CXVII,
6
Haemadsorption
Malmquist
&
Hay
(1960)
inoculated
cultures
of
pig
bone
marrow
and
buffy
coat
cells
(leucocytes)
with
African
pig
disease
virus.
The
virus
infected
certain
large
granular
cells
and
produced
haemadsorption
(the
adherence
of
erythro-
cytes
to
the
surfaces
of
infected
cells)
and
a
cytopathic
effect.
Immune
serum
inhibited
the
haemadsorption
reaction,
but
not
the
cytopathic
reaction,
to
a
significant
degree.
The
authors
consider
the
reaction
to
be
specific
and
that
it
can
be
used
for
the
differentiation
of
African
pig
disease
and
swine
fever
viruses.
De
Tray
(1960)
reported
that
the
existence
of
type
or
strain
differences
has
been
proved
by
the
haemadsorption-inhibition
test.
Haemadsorption
by
one
type
of
virus
was
inhibited
only
by
the
homologous
serum.
Sera
from
survivor
carriers
of
the
Hinde
strain
inhibited
haemadsorption
by
the
Hinde
virus,
but
not
by
other
strains
of
African
pig
disease
virus.
Furthermore,
serum
from
a
survivor
pig
inhibited
haemadsorption
by
the
homologous
virus,
but
failed
to
inhibit
haemadsorption
by
another
strain.
Dale
and
Sonders
(1960)
failed
to
produce
haemadsorption
or
a
cytopathic
effect
in
bone
marrow
cultures
with
swine
fever
virus.
DISCUSSION
African
pig
disease
occurs
naturally
among
wart-hogs
in
many
parts
of
Africa.
It
has
occasionally
been
observed
to
cause
mortality
among
them,
and
healthy
animals
may
be
virus
carriers.
Domestic
pigs
contract
infection
from
wart-
hogs,
but
the
method
of
transmission
has
not
yet
been
determined.
Swine
fever
was
not
present
in
East
Africa
during
the
years
1910-21
(Walker,
1933)
when
Montgomery
studied
African
pig
disease,
so
there
can
be
no
question
of
it
being
caused
by
swine
fever
virus
enhanced
by
passage
through
wild
pigs.
African
pig
disease
is
different
in
many
respects
to
swine
fever.
Pigs
immune
to
swine
fever
are
susceptible
to
African
pig
diseases
and
swine
fever
immune
serum
affords
no
protection
against
African
pig
disease
virus.
The
incubation
period,
symptoms
and
course
of
the
two
diseases
are
so
similar
that
they
are
of
little
value
for
differential
diagnosis:
African
pig
disease
is
usually
more
uniformly
acute
and
severe
than
swine
fever.
It
is
highly
infectious
and
would
appear
to
spread
more
rapidly
than
swine
fever,
but
more
evidence
is
required
on
this
point.
The
mortality
in
both
diseases
is
nearly
10o
per
cent.
In
epidemics
of
acute
swine
fever
there
is
a
tendency
for
the
mortality
rate
to
drop
gradually
and
for
chronic
cases
to
appear,
and
although
chronic
cases
of
African
pig
disease
have
so
far
been
rare
in
most
areas,
some
have
been
seen
by
Velho
(1956)
in
Angola,
where
the
disease
is
endemic.
Many
authors
(Montgomery,
1921;
Steyn,
1928,
1932;
Geiger,
1937;
De
Kock
et
al.,
1940;
Donatien
&
Lestoquard,
1940)
consider
tumor
splenis
to
be
a
characteristic
lesion
of
African
pig
disease.
In
swine
fever
the
spleen
may
or
may
not
be
slightly
enlarged
and
haemorrhagic
infarcts
frequently
occur
on
the
borders.
Interlobular
oedema
of
the
lungs
is
present
in
many
cases
of
AFRICAN
PIG
DISEASE
237
African
pig
disease.
It
is
not
a
lesion
of
swine
fever,
in
which
disease
areas
of
consolidation
are
frequently
present.
There
is
now
evidence
that
plurality
of
African
pig
disease
virus
strains
occur,
but
there
is
no
evidence
of
it
in
swine
fever.
African
pig
disease
virus
has
been
grown
in
embryonated
eggs;
it
became
slightly
attenuated
but
it
was
not
suitable
for
the
immunization
of
pigs.
Many
efforts
have
been
made
to
grow
swine
fever
virus
in
eggs,
but
with
the
exception
of
Fontanelli,
Mesance
and
D'Ascani
(1959)
no
one
has
had
any
success.
African
pig
disease
virus
is
highly
virulent,
but
appears
to
be
of
low
anti-
genicity.
Velho
(1956)
estimated
the
minimum
lethal
dose
to
be
about
10
11,
whereas
Cole,
Henley
&
Hubbard
(1946)
found
that
of
swine
fever
to
be
between
10
6
and
v5
x
in
-6
.
Swine
fever
virus
is
on
the
contrary
strongly
antigenic,
vaccines
and
immune
serum
can
be
easily
prepared
and
pigs
which
recover
are
solidly
immune.
So
far
it
has
not
been
possible
to
prepare
a
satis-
factory
immune
serum
against
African
pig
disease
but
it
would
be
an
advan-
tage
if
one
was
available
for
diagnostic
purposes.
Attempts
to
prepare
vaccine
have
not
so
far
been
successful
and
there
is
little
likelihood
of
any
being
produced
in
the
immediate
future.
The
evidence
that
plurality
of
strains
occur
will
increase
the
difficulties
of
vaccination.
Vaccination
is,
however,
merely
of
academic
interest
to
countries
with
estab-
lished
pig
industries
and
would
be
worth
consideration
only
if
the
disease
got
out
of
hand
and
became
endemic.
African
pig
disease
being
a
virulent
infectious
disease,
"stamping
out"
is
the
obvious
and
most
economic
method
of
control.
All
affected
and
in-contact
pigs
should
be
slaughtered
and
burned
or
buried
on
the
premises.
Salvaging
of
apparently
healthy
in-contacts
should
be
avoided
as
it
would
be
likely
to
spread
the
infection;
furthermore
it
is
out
of
line
with
contemporary
knowledge
of
disease
control.
CONCLUSIONS
African
pig
disease
is
a
separate
entity,
the
symptoms
and
lesions
of
which
resemble
those
of
swine
fever.
It
is
immunologically
distinct
from
swine
fever.
The
disease
may
be
brought
into
Britain
with
overseas
traffic.
It
is
signifi-
cant
that
both
the
Algiers
and
Portuguese
outbreaks
occurred
near
ports.
The
main
danger
of
introduction
would
appear
to
be
through
infected
pork
or
bacon
scraps
in
ship's
swill;
food
scraps
from
aeroplanes
might
also
be
a
source
of
infection.
The
recent
widespread
outbreaks
in
Portugal
and
Spain
emphasize
the
dangers
involved
and
the
need
for
vigilance
and
for
drastic
control
measures.
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