202 The Philippine Journal of Science 1919 
I, fig. 3). The muscles of the thigh were all normally arranged, 
but the muscles having their insertion at the proximal end of 
the tibia and the fibula were attached to the end of the femur by 
fibrous connective tissue. At the distal end, and lying slightly 
anteriorly and laterally, a single cartilaginous mass was found— 
apparently the patella. The patella was attached to the end 
of the femur by fibrous connective-tissue bands. 
On careful examination I also discovered that the pig had 
a cleft palate. This extended from the posterior part of the 
alveolar process throughout the entire soft and hard palate 
(see Plate I, fig. 2). The length of the cleft was 27 milli- 
meters; its width was 3 millimeters anteriorly and 7.5 milli- 
meters posteriorly. The nasal septum and various parts of 
the roof of the nasal cavity can be easily made out. The tongue 
appears normal in size, but on the median line is a ridge which 
fits into the cleft palate. This ridge serves as a palate for ins- 
piration and expiration. 
In this interesting specimen two abnormalities were found; 
namely, the missing legs and the cleft palate. It is reasonable to 
assume that the underlying cause producing the pathological con- 
ditions was identical for both anomalies. Both show an inter- 
rupted growth very early in the development of the pig. What 
the influence was that inhibited the growth of the legs and the 
palate is not definitely known, though everything points toward 
a physicochemical interference with growth. Mall: discusses 
this question in great detail and in part says: 
It would have been quite simple to conclude that the poison produced by 
an inflamed uterus should be viewed as the sole cause, but when it is recalled 
that the pathological ova occur far more commonly in tubal than in uterine 
pregnancy, such a theory becomes untenable. Moreover, monsters are 
frequently observed in swine and other animals without any indication of an 
inflammatory environment. For this reason I have sought the primary 
factor in a condition buried in the non-committal term faulty implantation. 
It would seem to be apparent that lesions occurring in the chorion as the 
result of faulty implantation, can and must be reflected in the embryo. 
He further states: 
It is perfectly clear that monsters are not due to germinal and hereditary 
causes, but are produced from normal embryos by influences which are to 
be sought in their environment. Consequently, if these influences are 
carried to the embryo by means of fluids which reach it either before or 
after the circulation has become established, it would not be very far amiss 
to attribute these conditions to alterations in the nutrition of the embryo. 
*On the frequency of localized anomalies in human embryos and infants 
at birth, Am. Journ. Anat. (1917), 22, 69. 
