A. M. JONAS 
1057 
colony normally experiences almost no mortal- 
ity in sucklings, with litter size frequently ex- 
ceeding 10 animals. Sendai virus was isolated 
from sick mice during all stages of the out- 
break. Serologic studies of the colony indicated 
low sporadic levels (5-10%) of antibodies 
(1:10-1:20) to Sendai from 1969 onward; but 
during and following the outbreak, seroconver- 
sion occurred rapidly and resulted in titres up 
to 1:320 with over 80% of samples positive as 
seen in Table II. Epizootologic studies (Figure 
2) indicated a rapid rise in numbers of litters 
with some mortality during the first days of the 
outbreak. A sharp drop then occurred with an 
end of mortality at 24 days after the first 
deaths. This pattern correlated inversely with a 
rise in antibody titres to Sendai virus. Lesions 
were confined to pulmonary tissues and were 
compatible with experimental studies of Sendai 
infection in mice.^ The sudden occurrence of 
mortality in an endemic Sendai virus-infected 
Table II. — Hi Antibodies for Sendai Virus in Sera of 
Retired Breeders from Nucleus Colony 
Date 
HI Antibody Titers 
Total No. of 
Samples 
<1:10 
1:10 
>1:10 
1970 
60 
0 
3 
63 
Pre-Feb. 1971 
24 
0 
2 
26 
Outbreak Jan. 19, 
1971 
Post Feb. 11, 1971 
10 
2 
69 
81 
PERCENTAGE 
OF 
LITTERS WITH 
SOME 
MORTALITY 
IN COLONY 
AVE 
RAGED 
DURING 
4 DAY 
PERIODS 
3 - 
% 2 - 
1 - 
1-4 5-8 9-12 13-16 17-20 21-24 
DAYS 
Figure 2. — Calculated as litters with one or more 
deaths out of susceptible litters in colony. 
colony is unusual* and places new importance 
on interpretation of low levels of Sendai H.l. 
antibodies in colonies of mice. 
During the course of attempting to isolate an 
agent associated with lesions of interstitial ne- 
phritis from high leukemia strain II guinea 
pigs, a Herpes virus was isolated in our labora- 
tory. This agent was also isolated in another 
laboratory by Hsiung and Kaplow.^ Further 
work by our group,'' however, revealed that this 
agent was widespread not only in strain II, but 
also in low leukemic strains such as Hartley and 
random source guinea pigs. Preliminary trials 
did not demonstrate any causal relationship be- 
tween this virus and nephritis. The significance 
of this agent is at present not known, but its 
possible presence as a latent agent in guinea 
pigs must be considered in evaluating research 
data from that species. 
Sialodacryoadenitis (SDA) is a highly infec- 
tious agent of rats that is associated with a 
high morbidity but minimal mortality, and 
which primarily effects the submaxillary sali- 
vary and Harderian glands, anterior uveal tract 
of the eye, and less commonly the parotid and 
exorbital glands. Jonas et al.'^ studied the path- 
ogenesis of this lesion by light and electron mi- 
croscopy after infecting germfree rats with 
crude suspensions of infected salivary tissue. A 
virus was isolated by Bhatt et al.^ after inocu- 
lating 1-day-old mice intracerebrally and inocu- 
lating kidney cell monolayers derived from DA 
inbred rats. Characterization studies indicate 
that it is a corona virus, which cross reacts with 
mouse hepatitis virus (MHV) and is possibly 
different from Parker's rat corona agent.^ This 
disease is widespread in many commercial 
breeding facilities as shown in Table III. It is of 
extreme importance that workers using rats for 
Table III. — Prevalence Neutralizing Antibody to SDA 
Virus in Sera * of Rats Obtained from Commercial 
Sources 
No. 
No. 
Source 
Tested 
Positive 
A 
12 
12 
B 
12 
12 
C 
12 
12 
D 
12 
12 
E 
12 
11 
F 
12 
12 
contributing cross-reacting antibodies. 
