Quail Disease in the United States* 
A PRELIMINARY REPORT BY GEORGE BYRON MORSE, 
M. D.j V. S. 
Assistant in Bacteriology and Pathology, Division of 
Pathology in Bureau of Animal Industry. 
A highly contagious and rapidly fatal disease 
has recently prevailed among quail in this coun¬ 
try. New to the United States, or at least 
hitherto unrecognized, its enzootic character, 
already manifest in some localities, makes it a 
matter of grave concern to naturalists, ornitholo¬ 
gists, members of Audubon societies, sportsmen, 
and owners of hunting preserves. 
English sportsmen know too well the gloom 
cast over grouse hunting by the dreaded grouse 
disease. It is hardly possible with the data at 
hand to claim identity of the British disease of 
grouse with the fatal malady now attacking the 
quail of this country. However, the near re¬ 
lationship of the birds—all being members of 
the same family Tetraomdce the close resemb¬ 
lance in several essential features of the two 
diseases; the fact that Klein’s bacillus of grouse 
disease ( Bacillus scoticus Migula) and the bacillus 
incriminated in this report, are if not identical, 
closely related members of the same group of 
bacteria ( Bacillus coti), all combine to make a 
brief review of the history of grouse disease ex¬ 
ceedingly appropriate. 
Quail disease ( Colibacillosis tetraonidarum ) is 
an infectious disease of the grouse family, caused 
by a microbe of the B. coli group, and character¬ 
ized by congestion of the lungs, focal necroses of 
the liver, and intestinal ulceration. 
On April 3, 1906, three dead Bobwhites were 
received from a dealer in Washington. Accom¬ 
panying the birds was the statement that these 
were among the last of a large number that had 
been steadily dying off. At night the whole flock 
would appear well; in the morning several would 
be dead. Upon necropsy these birds showed the 
alterations described later under “post mortem 
appearances.” Bacteriologic investigation _ re¬ 
sulted in the isolation and cultivation of a viru¬ 
lent Bacillus coli, whose high percentage of gas 
formation in dextrose and lactose_ bouillons gave 
it a marked resemblance to Klein’s bacillus of 
grouse disease as studied by Theobald Smith. 
Some time later this dealer received from 
Wichita, Kans., two dozen blue quail. Nearly 
all the birds were dead on arrival. Although no 
post mortem work was attempted, the dealer,, a 
most competent man, of thorough scientific train¬ 
ing, avers that he was able to recognize the 
disease by the characteristic odor of the drop¬ 
pings. He further states that the previous year 
he "had received shipments from Birmingham, 
Ala., one of which had a mortality of 100 per 
cent. 
In May, 1906, this office received a letter from 
Boston, Mass., regarding disease among quail 
there. This letter contained an inclosure from 
an eminent Boston pathologist noting the same 
findings that are described below. On account 
of decomposition no bacteriologic work was at¬ 
tempted. It was stated, however, that no ameba 
could be found. 
On Jan. 2, 1907, a letter was received from 
Worcester, Mass., in which the writer deplored 
the fact that disease was the great hindrance 
to the rearing of ruffed grouse in that section. 
Further investigation revealed the fact that Bob- 
whites were also included in this complaint. The 
birds with which breeding work had been under¬ 
taken were obtained from Alabama. 
On Feb. 11, 1907, the Washington dealer sent 
to this laboratory two dead Bobwhites with the 
statement that of sixty-five just received from 
Alexander City, Ala., thirty-four were dead. 
Post mortem examination was made of not only 
the thirtv-four, but of nearly all the others that 
died. The same lesions were revealed. 
On Feb. 23, 1907, there were received from the 
same person fifteen birds—eight Kansas Bob- 
whites and seven scaled quail (“cotton-top” or 
blue quail of Texas). These quail had been for 
several months on the place and had appeared 
perfectly well. The infected shipment of Feb. 
11 was brought to the entrance of the building 
where the fifteen were kept. In ten days the 
disease broke out among them and in two days 
all were dead. 
On Feb. 25, 1907, two crates of live Bobwhites 
were received from this gentleman. This rep¬ 
resented a shipment of five dozen birds from 
Alexander City, Ala., to take the place of the 
other five dozen that had died. Upon arrival 
in the city two were dead. These were examined 
by Dr. John R. Mohler, Chief of the Division of 
Pathology, and pronounced by him to be cases 
of quail disease. The shipment was immediately 
transferred to this laboratory. Within eight days 
all had died except three, which three, removed 
to fresh cages, continue at the present writing 
apparently perfectly free from disease. 
On Feb. 26, 1907, another dealer in Washing¬ 
ton received a shipment of fifty-three Bobwhites 
from Indian Territory, but which had come by 
way of Wichita, Kans. There exists some un¬ 
certainty as to whether or not they were re¬ 
crated at Wichita, but, as will be recognized 
later, this question is of no moment, for the 
disease is in Indian Territory. On arrival twelve 
of this lot were dead and four died subsequently. 
These birds showed the lesions of quail disease. 
The rest of the birds were sent to Mr. H. H. 
Dodge, custodian at Mount Vernon, Va. Mr. 
Dodge has since sent to this laboratory four of 
these birds, dead from the same disease. 
Another shipment of Bobwhites from Marlow, 
I. T., consigned to the first mentioned dealer, 
arrived March 4, 1907. Of this lot twenty-six 
were dead, and post mortem examination of 
twenty of them proved the existence of _ the 
disease and the presence of the causative bacillus. 
March 5, 1907, there was received for examina¬ 
tion one female California quail, forwarded from 
Elizabeth, Pa. Putrefactive changes had ad¬ 
vanced too far to permit bacteriologic examina¬ 
tion, but the lesions pointed strongly to quail 
disease. However, it is of interest, to note that 
the lesion-complex was that which is peculiar to 
grouse disease rather than the disease among 
quail in this country, namely, pneumonia, super¬ 
ficial necroses of the liver, and congestion of the 
intestines. 
March 17, 1907, the second mentioned Wash¬ 
ington dealer received from Wichita, Kans., a 
lot of forty-eight Bobwhites. Upon arrival six 
were found dead of quail disease. The balance 
were shipped to Mount Vernon, whence two have 
been returned to this laboratory for autopsy. 
March 21, 1907, a sharp-tailed grouse was re¬ 
ceived for autopsy from the first mentioned 
Washington dealer. A most perfect picture of 
quail disease was presented by this bird. The 
next day two more sharp-tailed grouse died with 
the same lesions, and another is reported sick. 
Word has also been received of the disease 
occurring at Yarmouth, Nova Scotia. These 
Bobwhites came from Alabama. 
The facts recorded in the previous section 
constitute all that we know at present concerning 
the geographical distribution of quail disease. . It 
is certain, however, that the disease is occurring 
wherever shipments of Bobwhites or other quail 
are being received from those distributing centers 
which have become infected. For instance, if we 
hear of a person receiving quail from one of the 
infected points in Alabama, we shortly after¬ 
ward hear of his lot of birds dying with disease 
which proves to be quail disease. 
According to the above recorded facts, quail 
disease exists or has occurred in Alabama, Kan¬ 
sas, Indian Territory, Washington, D. C., Mount 
Vernon, Va., Elizabeth, Pa.„ Boston and Worces¬ 
ter, Mass., and Yarmouth, Nova Scotia. 
By this is meant collecting and distributing- 
points which have been proved infected by the 
fact of birds shipped from those points having 
died en route or immediately after arrival and 
the presence of the disease demonstrated by post 
mortem examination. Such centers of infection 
are Alexander City and Dadeville, Tallapoosa 
county, and Birmingham, Jefferson county, Ala.; 
Wichita, Kans., and Marlow, Chickasaw Nation, 
I. T. 
Post mortem examination has up to the present 
time demonstrated the presence of quail disease 
in the common Bobwhite ( Colinus virginianus ), 
the California quail ( Lopliortyx californicus valli- 
cola ), the Gambel quail (Lopliortyx gambcli ), 
the mountain quail (Oreortyx pictus), the scaled 
quail, called also “cotton-top” or blue quail 
(Callipepla squamata), and the sharp-tailed grouse 
(Pedioccetcs phasianellus campestris). 
Had the disease remained limited to the quail 
only it would have been serious enough, but the 
recent demonstration of its transmissibility to 
sharp-tailed grouse is nothing less than appalling 
in its suggestion of widespread fatality among 
game birds. This fact calls for the most ener¬ 
getic action on the part of all lovers of sport and 
all who appreciate the economic importance of 
these birds, in noting and reporting every out¬ 
break of the disease, and, if possible, tracing its 
origin. 
The period of incubation appears to be about 
ten days. The disease first manifests itself by 
dullness and a tendency to sit in the corner of 
the cage with feathers fluffed. The food is neg¬ 
lected, and generally in two or three days (be¬ 
fore diarrhea has developed or emaciation made 
its appearance) the bird is dead. Sometimes the 
disease runs a more chronic course, and, though 
diarrhea is rarely very marked, emaciation be¬ 
comes extreme. 
On picking the birds one is surprised to find 
them presenting, as a rule, such a fine appear¬ 
ance. Their plump, meaty breasts of perfectly 
normal hue contrast strongly with what is seen 
upon opening the body cavity. There are ex¬ 
ceptional cases, however, exhibiting great emacia¬ 
tion. Upon exposing the viscera, the note that 
is made usually reads: “Fungs slightly con¬ 
gested ; liver congested and presenting a few 
small areas of superficial necrosis; intestines 
studded with minute ulcers.” These may be 
called the salient features of the disease, the 
characteristic lesions that, immediately on open¬ 
ing the carcass, attract the attention of the ob¬ 
server, be he layman or scientist. 
Sometimes, though rarely, the lungs exhibit 
areas of consolidation, represented by small, dark 
red spots. Often the liver presents no necrotic 
areas, is merely congested; on the other hand, 
sometimes the destruction of tissue will involve 
a large portion of a lobe, in depth as well as 
in extent of surface. The spleen is always con¬ 
gested, sometimes enlarged, sometimes quite 
dark. The constant feature, however, is the in¬ 
testinal lesion. This may be recognized, gener¬ 
ally, by the presence here and there, throughout 
the length of the intestine, of minute to large 
pin head sized areas of necrosis which are seen 
through the wall of the intestine as small, yel¬ 
lowish spots. Sometimes there is merely what 
Klein has described in his report on grouse disease 
as “patchy redness.” Again there may be dis¬ 
tinct, minute erosions; also, as first mentioned, 
there may be focal necroses covered with a croup- 
'ous exudate. Quite often the necrotic process 
has gone on until a true ulcer is formed, some¬ 
times even penetrating the wall of the gut. In 
the event of this last condition obtaining we 
may expect to find little yellowish masses of 
necrotic material coating the intestines or the 
walls of the abdominal cavity. 
