Special feeding and care of senescent spontaneously hypertensive
rats. Contemporary Topics 38 (4): 7.
This study shows that as the female spontaneously hypertensive rats
(SHR) mature, special care and handling is key to maintaining body weights
and good health. They investigated the impact of feeding methods on body
weight of senescent (aged) SHRs and showed that supplementing powdered
feed was useful as they approached heart failure. SHRs are genetically
predisposed to systemic hypertension and will progress into complete heart
failure resulting in death. Close to the time of heart failure (22 to 23
months of age), some rats experienced a loss of appetite and weakness,
resulting in malnutrition and weight loss. Animals were fed commercially
available rat chow pellets until they showed persistent signs of weight
loss or a lack of interest in their food. At that time, the rats were also
given powdered rat chow in shallow bowls to facilitate the eating and the
digestion of their food. After starting the powdered chow, the rats either
maintained or gained weight and prevented malnutrition. Therefore, by supplementing
powdered food, it is possible to maintain the health of senescent SHRs
until the termination of a study or onset of heart failure.
QUESTIONS:
1) What condition can contribute to weight loss and mortality in senescentSHR
rats?
2) What feeding practice can increase viability of debilitated senescent
rats?
ANSWERS:
1) Malnutrition due to inappetence or weakness.
2) Supplementing powdered rodent chow to the diet.
The use of a percutaneous endoscopic gastrotomy (PEG) tube to reverse
fatal fasting syndrome in a cynomolgus macaque (Macaca fascicularis).
Contemporary Topics 38 (4): 12.
An aged, overweight, female cyno had an history of chronic anorexia,
weight loss, elevated serum ALP and bilirubinemia. A percutaneous endoscopic
gastrostomy (PEG) tube was inserted after one month of oral gavage. Animal
began to eat voluntarily within 2 weeks. PEG tube was removed. The animal's
weight gradually increased and stabilized at 88% of original body weigt.
One year after initial examination, liver biopsy showed the pathology was
unchanged. Almost 2 years after initial examination, the animal was found
to be SRV positive and was euthanised.
At necropsy, liver was enlarged, pale and friable. Mild hepatic lipidosis
was confirmed using Oil Red O stain.
Technique for PEG tube placement:
1. Place anesthetized animal on right lateral recumbency.
2. Pass the gastroscope into the stomach. Distend with air.
3. Insert a 18 ga needle percutaneously into the stomach (where the
endoscope light is).
4. 1-0 Silk is fed through the trochar into the stomach, grabbed by
the endoscope and pulled out through the mouth.
5. The PEG tube is tied to the suture and pulled in using the "stomach"
end of the suture.
6. A small cutaneous incision is made to allow the free end of the
PEG tube through, wedging the internal flange and mushroom tip against
the gastic wall. An external flange secured the apposition of the gastric
and abdominal walls.
7. The PEG tube was capped and protected by a primate jacket.
8. To remove the tube: exert a firm traction on the tube while applying
counter pressure on the abodomen.
Question:
1. How long did it take for clinical signs to resume, after placement
of the PEG tube ?
2. How long di it take to recover normal liver fonction ?
Answer:
1. Approx. 2 weeks to eat voluntarily.
2. Still after 2 years, liver pathology was present.
A modified cage to minimize catheter contamination in the chronically
catheterized baboon. Contemporary Topics 38 (4): 16.
The title says it all. Jacket and tether systems have been in use for
over 20 years to allow freedom of movement for nonhuman primates with chronic
instrumentation. The tether either feeds the catheters to a hole in the
side of the cage (these systems are prone to twisting with animal movement)
or to a fixed swivel which allows animals to spin without twisting the
lines. In either case, removing the animals more than 1-2 feet from the
cage requires disconnecting the catheters.
In this situation, the baboons were going to be severely immunosuppressed
for bone marrow transplantation, so catheter contamination during disconnection/reconnection
could lead to sepsis. Also, the baboons were to be frequently moved to
a remote location for irradiation. This article describes modifications
to a baboon cage that allowed frequent removal from the cage without disconnecting
the catheter. The pictures are excellent supplements to the descriptions.
In all, 10 baboons were removed an average of 30 times each and none of
them showed signs of sepsis during the course of the study. Removal was
completed by two people in an average of 2-3 minutes by two people, but
could be accomplished by a single individual when necessary.
Questions
1) What are three methods of protecting chronic instrumentation in
nonhuman primates?
2) What are two means of exiting instrumentation from a nonhuman primate
cage and the advantages/disadvantages of each?
Answers
1) chairs, jacket and tether systems, jacket and telemetry systems
2) hole in cage wall - simple to use and maintain, increased flexibility
in the number of catheters that can be used, subject to twisting
swivel - more expensive, fixed number of connectors, allow more activity
without twisting catheters
Progressive anemia in a Pig-tail Macaque with AIDS. Contemporary
Topics 38 (4): 20.
The article is a diagnostic report of progressive anemia in a pig-tailed
macaque.
A female 3.5-year of pig tail macque (Maccaca nemestrina) was used
a s part of a cohort of animals to study the pathogenesis of inmunodeficiency
caused by and HIV like virus. The animal had normal complete blood counts,
serum chemistries, and was free of any retroviruses. They only parasites
found were Balantidium coli, which was treated and resolved.
The animal was then inoculated with KUSHIV-1B. This microorganism is
a pathogenic chimeric immunodeficiency virus composed of the env, tat,
rev, and vpu of HIV-HXB2 on a background of SIVmac239. It causes severe
immunodeficiency by elimination of CD4 lymphocytes. The animal^Òs
progress of infection was monitored by examination of the attack rate of
the virus in CD4+T cells in blood. The animal became immunocompromised
beginning at week 12. At week 14 of the infection the body weight began
to decline. At week 6-post inoculation the animal began to develop anemia.
The hematocrit fell from 37% to 27% and progressively fell over the next
16 weeks to a naidir of 14.1%. The animal was euthanized at week 22 post
inoculation.
Anemias are generally described ad consumptive disorders or production
defects. Consumptive disorders include autoimmune hemolytic anemia, parasitic
infection and acute and chronic hemorrhage. Frequent blood sampling required
for doing retroviral studies can cause anemia when monthly blood volumes
exceed 20%. Production defects of ineffective hematopoiesis can be due
to iron or B12 deficiency, bone marrow intoxicants, myelophthisis or various
viral infections. The presence of giant pronormblast and inclusion bodies
in erythroid precursors on both cytology and histology preparations gave
the presumptive diagnosis of infection with a simian parvovirus. Simian
parvovirus viremia in the macaque was confirmed by dot-blot hybridization.
Human B19 and the simian parvovirus are single stranded non-enveloped
DNA viruses with tropism for erythroid precursors. Transmission of the
virus may be by aerosol of fomites, although neither rout is proven. B19
parvovirus infection in humans in a healthy person is termed "erythyema
infectiosum or fifth disease. The virus my cause inutero development of
hydrops fetalis of congenital anemia. Due to their small DNA content and
lack of a lipid envelope, parvoviruses are heat-stable and resistant to
solvent detergents. This allows them to persist in the environment and
become an opportunistic infection of animals. In summary simian parvovirus
should be considered in the differential diagnosis of anemia in the macaques
typically used in research.
[Author's note: One comment on the review below. The outcome of the
parvovirus infection is dependent on the immune status of the host (human
or non-human). The infection in the immune competent individual is transient
and resolves in several weeks. An immune deficient individual is unable
to mount an immune response and the virus replicates freely causing the
progressive anemia.]
No questions
Indirect fluorescent antibody (IFA) assay. Contemporary Topics 38
(4): 23.
This is a technology update about the Indirect Fluorescent Antibody
assay. The purpose of IFA assays is to detect antibodies to specific pathogens
indicating exposure of a host to an organism.
Briefly, the method for the assay is to adhere viral infected tissue
culture cells (or tissue sections) to a microscope slide. Diluted serum
sample (containing primary antibody) can then be incubated on the slide
and anti-viral antibodies, if present, will bind to viral proteins on the
adhered sample.
The slide is then washed to remove non-specific and unbound antibodies.
Infected cells are then incubated with a fluorescent-labeled secondary
antibody that binds specifically to the anti-viral antibodies of the infected
animal. Again unbound secondary antibodies are washed off, and the specific
fluorescence of the secondary antibody is viewed with a fluorescent microscope.
Those cells incubated with serum from infected animals will fluoresce.
Controls for this assay might include using uninfected cells adhered to
a slide and tested similarly with antibody.
Other techniques that can be used to detect specific antibodies include
Enzyme-Linked Immunosorbent Assays (ELISAs), Hemmagglutination Inhibition
Assays (HIAs), immunohistochemistry and Western blots.
The IFA tends to have a high sensitivity and a moderate to high specificity.
In addition, IFAs tend to be relatively inexpensive to perform.
However, interpretation may be subjective and depend upon the experience
of the researcher; also non-specific background fluorescence may confound
interpretation.
No questions