1058 
ANIMAL RESOURCES 
Table IV. — Neutralizing Antibody to SDA Virus in 
Sera of WAG-RIG Rats — Retired Breeders 
No. 
No. 
Time of Collection 
Tested 
Positive 
Pre epizootic 
28 
0 
Post epizootic 
34 
33 
ocular studies realize that serious damage to 
that organ may be associated with this 
disease. Table IV clearly demonstrates sero- 
conversion in a closed WAG/RIG inbred rat col- 
ony infected with SDA. This evidence was 
accompanied by clinical, pathological, and viro- 
logical evidence of SDA infection. 
Simian tuberculosis is a constant threat to re- 
search primate colonies the world over. Suspi- 
cion that this disease is present in a colony 
should immediately activate strenuous control 
measures. Therefore, its improper diagnosis 
could be most costly. Pulmonary nocardiosis" 
in nonhuman primates was unreported until 
1966 when our laboratory described this condi- 
tion in two unrelated Macaca mullata. The simi- 
lar gross appearance of the pulmonary lesion 
along with the presence of fragmented, par- 
tially acid fast organisms could prompt an in- 
correct presumptive diagnosis of tuberculosis. 
Differential features of these diseases are listed 
Table V. — Differential Features of Pulmonary Nocard- 
iosis versus Tuberculosis in the Non-Human Primate 
Nocardiosis 
Tuberculosis 
Similar except media- 
Radiology stinal widening should not 
be expected. 
Gram +, beaded fila- 
mentous rods, partially 
Bacteriology acid fast. May fragment. 
Aerobic, grows well on 
Lowenstein agar. 
Necrotizing bronchopneu- 
monia identical to T.B. 
No Gohn's complex. No 
extrathoracic lesions seen 
to date. 
Pleomorphic infiltrates, 
giant cells not observed. 
Brown-Brenn stains may 
reveal individual beaded 
filaments or colonies of 
organisms. Partially acid 
fast. Fibrosis may be 
present. 
Epizootiology Sporadic, not considered 
highly infectious. 
Gross 
Pathology 
Histopath 
Dense infiltrates with fre- 
quent widening of media- 
stinum due to lymph node 
involvement. 
Acid fast, thin, slightly 
curved rods; best site for 
in vivo smear and culture 
is LARYNX. 
Necrotizing, granuloma- 
tous bronchopneumonia. 
Invariably Gohn's com- 
plex present. Extratho- 
racic lesions common. 
Usually mononuclear in- 
filtrates predominate, ac- 
companied by many giant 
cells. Acid-fast techniques 
reveal typical rods with- 
in cytoplasm of giant 
cells. Fibrosis usually not 
seen. 
Highly infectious, may 
spread rapidly through 
colony. 
in Table V and are now recognized by other lab- 
oratories. This example further amplifies the 
positive role that adequate diagnostic labora- 
tory support can play in defining disease prob- 
lems and directly effecting disease control. 
Finally, I would like to mention the facilities 
of these diagnostic laboratories as resources in 
recognizing and characterizing potential animal 
model systems. The cat is frequently found to 
have medial hypertrophy and hyperplasia of 
pulmonary arteries (PA) (1.3%-68%).i2 Our 
experience places this figure at approximately 
20-30%. Contrary to recently published work 
by Rogers et al.,^^ we have found significant el- 
evations of pulmonary vascular resistance 
(PVR) in 2 cats with natural disease. Pathoge- 
netic studies of this disease indicated that oral 
inoculation of embryonated Toxocara cati eggs 
or infective larvae of Aelurostrongylus abstru- 
sus resulted in production of pulmonary vascu- 
lar lesions and moderate elevation of PVR.^* 
Preliminary findings suggest this inducible vas- 
cular disease resulting in elevated PVR could be 
an exciting animal model system to: study (1) 
pathogenic mechanisms of vascular smooth 
muscle changes, and (2) changes in pulmonary 
hemodynamics not secondary to vascular occlu- 
sion or destruction of the vascular bed follow- 
ing parenchymal disease (Figures 3 and 4). 
Other systems studied in our laboratory in- 
clude a fascinating and controversial intestinal 
70 r 
- -s; 60 - 
t- E 50 - 
- 40 h 
>■ UJ 
cc cc 
<t 
o to 20 
_i cr 
=) Q- 
a. 
30 - 
10 - 
9128 
pH =7.47 
PO2 = 132 
pCOa = 13 
_L 
.1 .2 .3 .4 .5 .6 .7 .8 .9 1.0 1.1 
CARDIAC OUTPUT (L/min) 
Figure 8. — Pressure flow curve from uninoculated cat 
with lesions of PA medial hyperplasia. Lower curve 
is from a normal control cat. 
0 — Flow rate of 125 ml/kg/min. 
1 = Eange within ± 1 S.D. for normal control data 
calculated at a flow rate of 125 ml/kg/min. 
