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Health Surveillance Program
A rodent disease surveillance (RDS) program has been established
as part of the overall health assessment and control program through
the Comparative Pathology Laboratory (CPL) of the Animal Resources
Service (ARS) at UC Davis.
What is rodent disease surveillance (RDS)?
Rodent disease surveillance programs are systematic laboratory
investigations that employ a panel of tests (microbiology, parasitology,
serology, and pathology) for the purpose of defining the pathogen
and health status of an animal population. These programs are
crucially important in rodent disease prevention; they provide
data, the only reliable basis for rodent pathogen staus or health
quality assurance.
Why should I, the principal investigator, participate in
a RDS?
Most natural infections of laboratory rodents, which include
strong pathogens, weak pathogens, opportunists, and commensals,
are subclinical. Some of those pathogens may also have a zoonotic
potential as a public health hazard. Thus, clinical manifestations
of pathogen infections have only limited diagnostic value. Also,
it cannot be overemphasized that aberrations in research results
due to natural infections often occur in the absence of clinical
disease. Thus, prevention of infection, not merely prevention
of clinical disease, is essential.
What type of test procedures are being employed?
Just as research objectives can differ greatly, health surveillance
requirements may also vary. The basic health screen involves a
complete gross necropsy with histopathologic examination of any
observed lesions, microbiological evaluation for respiratory and
gastrointestinal pathogens, evaluation for endo- and ectoparasites,
and serologic profiles.
Who is paying for this extra service?
Costs of the RDS program related to the testing procedures
will be the responsibility of the CPL (ARS). In addition, the
sentinal animals (animals ordered with study animals to be used
in the RDS program, usually a breeding pair) that are housed in
ARS vivaria will be purchased by ARS and per diem charges will
be paid from ARS animal health funds. However, sentinal animals
in satellite facilities will be purchased by the facilities home
department.
How do I, the PI, get on the RDS program?
For all information regarding ordering animals, type of animals,
husbandry and frequency of surveillance examinations etc. please
call the CPL at 752-2832 or Dr. Rick Ermel directly at 752-5836.
In conclusion, this is an excellent opportunity to get information
about the health status of your animals, what pathogens you are
dealing with, how those pathogens potentailly may interfere with
your research, and what you can do about it.
Participation in the RDS is strongly encouraged by the American
Association for Accreditation of Laboratory Animal Care (AAALAC).
INDEX
MOUSE ROTAVIRUS (EPIZOOTIC DIARRHEA OF
INFANT MICE)
SIGNIFICANCE
Low.
AGENT
Double-stranded RNA virus, family Reoviridae, genus Rotavirus,
group A. It is unstable at -24, 4, and 37oC.
ANIMALS AFFECTED
Mice.
EPIZOOTIOLOGY
MRV or EDIM is generally held to be a widely prevalent important
pathogen of mice. EDIM virus is highly contagious. Rotaviruses
are shed copiously in feces and transmission is by the orofecal
route and by airborne infection in which contaminated dust and
bedding from adjacent cages probably play key roles. All ages
of mice are susceptible to infection; however, disease is limited
to mice less than 2 weeks of age. Mice are most susceptible to
infection from birth to about 17 days of age. Virus selectively
infects terminally differentiated enterocytes of villi and surface
mucosa of the small and large intestine, respectively. These cells
are most plentiful and widespread in the neonatal bowel and diminish
in number, distribution, and degree of terminal differentiation
as mucosal proliferative kinectics accelerate with the acquistion
of intestinal microflora. Infected neonates shed high concentrations
of virus in the feces from about 2 days to 8-10 days post infection.
Transient viremia and viruria can occur. It is not known whether
there is persistent infection in euthymic mice, however, scid/scid
mice become persistently infected and shed the virus in feces
for many months, perhaps for life.
CLINICAL
Clinical signs of EDIM may occur in naive breeding populations,
but once infection is enzootic within the colony, EDIM disease
is no longer apparent, although EDIM virus remains. The duration
of EDIM virus infection in an individual mouse has not been definitely
determined. Diarrhea during the first two weeks of life is considered
the only consistent sign of disease. Watery yellow stools persist
for about one week. It accumulates around the anus and base of
the tail, and soil the coats of neonates and dams. Neonates may
have distended abomens. Usually there is no mortality.
PATHOLOGY
Susceptibility to infection and disease (diarrhea) due to MRV
is age dependent (birth to 17 days of age). During this time enterocytes
in the small intestine are particularly susceptible and support
maximal cytoplasmic replication of the virus, possibly due in
part to the high pinocytotic activity of enterocytes or availability
of viral receptors on enterocytes. EDIM virus causes hydropic
change and vacuolation of enterocytes at the tips of villi and
large intestinal surface mucosa. The major pathologic change is
mild villous atrophy; regeneration occurs rapidly. Malabsorption
and osmotic diarrhea, with overgrowth of E. coli, appear
to be major components of the disease process.
DIAGNOSIS
Detection of anti-rotaviral antibodies can be accomplished
by ELISA, IFA, or other serological tests.
CONTROL
Cesarean derivation followed by barrier maintenance probably
would be necessary for scid/scid mice that are known to
become persistently infected, but it is not known whether this
approach is necessary to eliminate EDIM from immunocompetent euthymic
mice. For immunocompetent mice, it may be that the virus is shed
for only a few weeks after the acute infection. If so, this would
permit the isolation and quarantine of individual breeding pairs
with subsequent selection of EDIM seronegative progeny for breeding.
This type of control method has been successfully used with certain
other agents. The use of filter-top cage systems can be beneficial
in controlling transmission between subpopulations in the same
room.
INTERFERENCE WITH RESEARCH
EDIM infection alters intestinal absorption and intestinal
enzyme profiles. Infection can alter results of studies with infant
mice. Infected infant mice often have severe transient thymic
necrosis of unknown pathogenesis that can potentially cause immunological
aberrations.
INDEX
MYCOPLASMOSIS (MRM)
SIGNIFICANCE
The significance of Mycoplasma pulmonis infection or
murine respiratory mycoplasmosis (MRM) is very high, particularly
in long term studies. This has been primarily due to the chronicity
of the disease, which often manifests itself only after months
of infection.
AGENT
Mycoplasma pulmonis is a gram-negative bacterium lacking
a cell wall.
ANIMALS AFFECTED
Rats and mice.
EPIZOOTIOLOGY
Infection and disease are common in conventional reared rats
and mice. Sites of predilection for the organism in the host are
the nasopharynx and the middle ears. M. pulmonis has also
been reported from up to 40% of genital tract infections in conventionally
reared LEW rats. Subclinical infection occurs in some cesarean-derived,
barrier-maintained stocks. Transmission is thought to be by the
intrauterine route and by aerosol between cagemates, including
from dam to offspring and between adjacent cages.
CLINICAL
Infections are usually subclinical with the organism carried
in the upper respiratory tract and uterus. The acquisition of
primary viral or bacterial respiratory pathogens activate subclinical
mycoplasmal infections. Early signs of overt disease may include
a red (porphyrin) oculonasal discharge, nasal mucous sounds, and
otitis media. As the organism travels down the respiratory tract,
labored breathing, ungroomed hair coat, anorexia, chattering and
coughing, and hunched posture may be observed. Chronic uterine
infections may result in decreased litter size, but usually no
clinical reproductive disorder is noticed.
PATHOLOGY
M. pulmonis is an extracellular parasite that preferentially
colonizes the luminal surface of the respiratory epithelium. Organisms
and lesions, if present, tend to decrease from proximal to distal
airways. Under ideal conditions for the host, the organism probably
is a commensal. However, under less than ideal conditions, such
as intracage ammonia concentrations of 19 ug/liter of air or greater,
MRM is exacerbated by increased growth of M. pulmonis in
the respiratory tract. Other influencing factors include concurrent
infection with Sendai virus, sialodacryoadenitis virus or cilia-associated
respiratory bacillus; a deficiency of vitamins A or E; genetic
susceptibility of the host; and, possibly, virulence of the M.
pulmonis strain. Characteristic changes at any level in the
respiratory tract include neutrophils in the airways, hyperplasia
of the mucosal epithelium, and a lymphoid response in the submucosa.
Lesions include rhinitis, otitis media, laryngitis, tracheitis,
bronchitis, bronchiectasis, pulmonary abscesses, and alveolitis.
Hyperplasia of bronchus-associated lymphoid tissue is characteristic
in rats. MRM is the single most important disease of rats. Although
the disease may be acute, it is usually chronic. MRM shortens
the lifespan of the rat, and leads to experimental results of
dubious value.
DIAGNOSIS
An ELISA is commercially available for serological screening
for M. pulmonis infections in rat colonies. Retired breeders
greater than 6 months old are preferable since weanlings are often
serologically negative. Detection of subclinical infection is
a major problem; ELISA seropositivity might occur only sporadically,
the number of ELISA-positive animals might be very small, and
seropositive animals might become negative again. The best results
are obtained when only adults are tested, sample size is increased,
and testing is done repeatly. FA can also be used to identify
the organism on tracheobronchial histologic sections.
CONTROL
Cesarean-derivation and barrier-maintenance programs appear
to have reduced the prevalence of disease; however, since intrauterine
infection can occur, infection may persist. The major emphasis
should be on selecting mycoplasma-free breeding stocks. Definitive
information on eliminating M. pulmonis from clinically
or subclinically infected stocks is lacking. Administration of
antimicrobial agents might help to control clinical signs; however,
such agents are not curative and can introduce variables if used
in animals on experimental protocols.
INTERFERENCE WITH RESEARCH
Morbidity and mortality caused by MRM can disrupt long-term
studies. MRM alters ciliary function, cell kinetics, and immunity
in the respiratory tract and changes the response to carcinogens.
Infection in LEW rats delays the onset and reduces the severity
of adjuvant arthritis, reduces the incidence of experimental collagen-induced
arthritis, and reduces antibody response to collagen. Genital
infection alters genital tract histology. Mycoplasmas produce
lymphokine-like substances that are mitogenic for B and T lymphocytes
in vitro. M. pulmonis is a frequent contaminant of rodent
cell cultures. In mice infection can activate natural killer cells,
contaminate transplantable tumors, and cause arthritis in the
recipients.
INDEX
CILIA-ASSOCIATED RESPIRATORY BACILLUS
(CAR)
SIGNIFICANCE
The significance of CAR bacillus infection in laboratory rodents
is uncertain.
AGENT
A gram-negative, argyrophilic, filamentous, rod-shaped bacillus.
Presently it is not classified, but possibly belongs to the group
called gliding bacteria.
ANIMALS AFFECTED
Laboratory rats and mice, wild rats, African white-tailed rats,
and rabbits.
EPIZOOTIOLOGY
Unknown.
CLINICAL
Clinical manifestations in rats are similar to those of severe
murine respiratory mycoplasmosis (MRM) and can include hunched
posture, ruffled coat, inactivity, head tilt, and accummulation
of porphyrin pigment around the eyes and external nares. No description
of clinical disease in mice has been published.
PATHOLOGY
In those instances in which CAR bacillus has been found in
rats with natural disease, Mycoplasma pulmonis also was
present. It is possible that M. pulmonis was the primary
pathogen and the CAR bacillus increased disease severity. It is
not known whether the CAR bacillus alone can cause natural clinical
disease.
The predominant lesions in rats are those of advanced MRM due
to M. pulmonis with some additional distinctive features.
Severe bronchiectasis and bronchiolectasis, pulmonary abscesses,
and atelectasis are associated with accummulation of purulent
or mucopurulent exudate in airways. An abundance of mucus often
is present in peribronchiolar alveoli. Multifocal necrosis and
acute inflammation of bronchiolar and bronchial epithelia often
progress to severe granulamatous inflammation in airway walls
and abscess formation in airway lumens. The ciliated border of
respiratory epithelium in affected airways often appears quite
dense in hematoxylin and eosin stained sections because of the
large numbers of CAR bacilli present between the cilia.
DIAGNOSIS
Enzyme-linked immunosorbent assays (ELISA) for CAR bacillus
infection are used and an indirect immunofluorescence test (IFA)
has been developed. Recognition of the CAR bacillus in Warthin-Starry
silver-stained histiologic sections of affected lungs are also
diagnostic.
CONTROL
Uncertain. The infection can probably be eliminated by cesarean
derivation, but definitive studies have not been done.
INTERFERENCE WITH RESEARCH
Uncertain. The organism might be an important contributor to
the morbity and mortality caused by MRM in rats.
INDEX
FUR MITES
SIGNIFICANCE
Moderate.
AGENT
Myobia musculi, Myocoptes musculinus, and Radfordia
affinis are common fur mites.
ANIMALS AFFECTED
Mice and rarely rats and other laboratory rodents.
EPIZOOTIOLOGY
Transmission is by direct contact. Fur mites are usually host
specific. The dynamics of mite populations on a host are very
complex and are influenced by factors that include grooming, strain
susceptibility, and host immune responses. Athymic and other furless
mice are not susceptible to infestation.
CLINICAL
Infestations are commonly subclinical. Clinical signs include
scruffiness, pruritis, patchy alopecia, self-trauma, ulceration
of the skin, and pyoderma. Black haired mice (C57BL strains and
their congenic sublines) are thought to have an allergic sensitivity
to the mites.
PATHOLOGY
Lesions vary from mild to severe. Initially there is mild hyperkeratosis,
but this often progresses to severe hyperkeratosis with fine bran-like
material on the skin over virtually all of the body but particularly
abundant over the dorsum, head, and shoulders. Secondary bacterial
infection commonly leads to suppurative and granulomatous inflammation.
Hyperplasia of regional lymph nodes, splenic lymphoid hyperplasia,
and increased serum immunoglobulins are common.
DIAGNOSIS
Diagnosis requires demonstration and identification of mites.
Mites can be demonstrated by using a steroscopic microscope or
hand lens to examine the pelage, particularly over the back and
head. If the pelt from a recently killed mouse is cooled to room
temperature, the mites will crawl up to the tips of the hairs,
looking like white specks.
CONTROL
Cesarean derivation and barrier maintenance are the most effective
methods for eradication of mite infestations. A vapona strip (No
Pest, Dichlorvos) placed above the cage or in the room will control
infestations. The adults and weanlings can be dusted with silica
dusts, pyrethrin dusts, or can be dipped in a 2% malathion solution.
Ivermectin diluted with water can also be used to mist adults
and weanlings. Regular examinations and treatments may eventually
rid the colony of mites.
INTERFERENCE WITH RESEARCH
Infestations of M. musculi have been found to cause
secondary amyloidosis. In addition, mite-infested mice should
be considered undesirable for behavioral studies because behavioral
patterns are likely to be altered by hypersensitivity to the mites.
INDEX
Klebsiella pneumoniae
SIGNIFICANCE
Low.
AGENT
Gram-negative, nonmotile, capsulated bacillus, family Enterobacteriaceae.
ANIMALS AFFECTED
Mice, rats, humans, and others.
EPIZOOTIOLOGY
Klebsiella pneumoniae is presumably a normal inhabitant
of the gastrointestinal tract in man and animals, including mice
and rats. It is an opportunistic pathogen. Transmission is by
feces, air, and water.
CLINICAL
Nonspecific signs of dyspnea, sneezing, cervical lymphadenopathy,
inappetence, hunched posture, and rough hair coat have been observed
in diseased mice. In the reported outbreaks in rats, there were
a few deaths, and some rats had abscesses in the cervical and
inguinal lymph nodes with fistulous tracts to the adjacent skin
surface.
PATHOLOGY
Mice with natural disease have cervical lymphadenitis; cervical,
pharyngeal, renal, and hepatic abscesses; empyema; and granulomatous
pneumonia. Rats with natural disease had submaxillary, parotid,
or inguinal lymph node abscesses, often with fistulous tracts
draining to the skin; abscesses in mesenteric nodes; and renal
abscesses. Respiratory lesions either were not observed or were
considered a minor part of the disease. Like other opportunistic
pathogens, host factors probably are extremely important determinants
of disease caused by this organism.
DIAGNOSIS
Diagnosis is by culture of the organism.
CONTROL
Uncertain. The organism is presumably a part of the normal
gastrointestinal flora of mice and rats.
INTERFERENCE WITH RESEARCH
Klebsiella pneumoniae is an opportunistic pathogen that
may complicate studies in which host defenses are compromised.
INDEX
KILHAM RAT VIRUS (KRV)
SIGNIFICANCE
There are few reports of natural disease or interference with
research due to this virus, but its high prevalence in rats and
propensity for damaging populations of replicating cells in vivo
and in vitro make it a significant pathogen.
AGENT
KRV is a single-stranded DNA virus, family Parvoviridae, genus
Parvovirus. KRV is the type species of the genus.
ANIMALS AFFECTED
Laboratory and wild rats are the natural hosts.
EPIZOOTIOLOGY
KRV is a common infection in wild and laboratory rats; prevalence
exceeds 50% in some populations. Transmission is primarily by
the horizontal route, either through direct contact or fomites.
Virus is shed in urine, feces, milk, and nasal secretions. Transplacental
infection is not considered important. Persistent infection can
last up to 14 weeks. KRV is a frequent contaminant of cultured
cell lines and transplantable tumors.
CLINICAL
Natural infections nearly always are subclinical. Clinical
disease is a rare event, and few examples have been reported.
Signs in the few instances of overt disease that have been reported
include increased numbers of uterine resorption sites in pregnant
dams and runting, ataxia, cerebellar hypoplasia, and jaundice
inntheir pups.
PATHOLOGY
Parvoviruses attack rapidly dividing cells. In newborn and
young rats, KRV can cause jaundice, hemorrhagic infarction with
thrombosis in multiple organs (including brain, spinal cord, testes,
and epididymis), and cerebellar hypoplasia. Amphophilic intranuclear
inclusions occur in the endothelium and other cells of affected
organs. Focal necrosis, hypertrophy and vacuolar degeneration
of hepatocytes, cholangitis, and biliary hyperplasia also occur.
DIAGNOSIS
The enzyme-linked immunosorbent assay (ELISA) and the indirect
fluorescent antibody (IFA) test are considered most sensitive,
but do not discriminate between infections due to different serotypes
of parvoviruses in rats.
CONTROL
The most practical approach to controlling infection is to
obtain animals demonstrated free of KRV by serological monitoring.
Biological materials should be tested for KRV infection by the
mouse antibody production (MAP) test. Cesarean section should
be successful for rederiving valuable breeding stocks of rats
because transplacental transmission is not considered important.
INTERFERENCE WITH RESEARCH
KRV can contaminate transplantable tumors and rat cell cultures,
suppress the development of Moloney virus-induced leukemia, and
alter in vitro lymphocyte responses and cytotoxic lymphocyte activity.
KRV also has been reported to induce interferon production. Immunosuppression
can cause clinical disease in inapparently infected rats.
INDEX
MOUSE HEPATITIS VIRUS (MHV)
SIGNIFICANCE
The significance of mouse hepatitis virus (MHV) infection is
very high, especially when considering the extremely large number
of reported effects of MHV on mice and their biologic responses
to experimental treatments.
AGENT
The term MHV is used to designate a large group of single-stranded
RNA viruses belonging to the family Coronaviridae, genus Coronavirus.
Approximately 25 different strains or isolates of MHV have been
described. Of that number, six have been studied most extensively
and are generally considered the prototype strains: MHV-1, MHV-2,
MHV-3, JHM (MHV-4), A59, and S.
ANIMALS AFFECTED
Mice.
EPIZOOTIOLOGY
MHV is extremely contagious. Infection of the majority of mice
housed under conventional conditions in multipurpose facilities
is the norm. It is one of the most ubiquitous infections of laboratory
mice worldwide, with reported prevalence rates frequently exceeding
80%. Numerous factors such as virus strain and mouse strain are
known to influence the pathogenesis of MHV infection and may be
important determinants of its epizootiology. However, current
evidence indicates that in immunocompetent mice the infection
runs its course within 2-3 weeks, and there is no carrier state.
During active infection virus is shed in the feces and by aerosol.
Direct contact, fomites, and airborne particles are all probably
very important in transmission. Transplacental transmission is
of doubtful importance in natural infections. MHV is a frequent
contaminant of transplantable tumors and cell lines.
CLINICAL
In immunocompetent mice, MHV infections are usually subclinical
(enzootic infection). Infant mice of naive breeding populations
can show diarrhea and high mortality when infected with the more
virulent enterotropic MHV strains (epizootic infection). Athymic
(nu/nu) mice show progressive emaciation leading to debility
and death (wasting syndrome in athymic mice).
PATHOLOGY
Strains of MHV differ greatly in virulence and tissue tropism,
and mouse strains differ greatly in susceptibility to MHV. These
factors interact with host age and route and dose of virus inoculation
to determine the outcome of infection. There are two major disease
patterns: the respiratory pattern and the enteric pattern. In
the respiratory pattern, infection involves the nasal passages
and lungs; intestinal involvement is minimal. Lesions in immunocompetent
mice are present for only about 7-10 days and are usually nonspecific
and subtle. In the enteric pattern, infection is primarily restricted
to the bowel,with variable spread to other abdominal organs such
as the liver and abdominal lymph nodes. Lesions are most severe
in neonatal mice because of their relatively slow kinetics of
mucosal epithelium turnover. Varying degrees of epithelial lysis
and blunting of villi occur in the small intestine. In more severe
cases, there can be ulceration of the mucosa. A similar lytic
process occurs in the ascending colon and cecum. Occasionally,
there is multifocal necrotizing hepatitis and/or encephalitis.
MHV infection in athymic or neonatally thymectomized mice becomes
progressively more generalized, severe, and chronic, with involvement
of many organs, including brain, liver, lungs, bone marrow, lymphoreticular
organs, vascular endothelium, and intestine.
DIAGNOSIS
The enzyme-linked immunosorbent assay (ELISA) is the test of
choice for routine serological monitoring. An immunofluorescent
antibody (IFA) test also is available and is about equal to the
ELISA in sensitivity.
CONTROL
Strict adherence to barrier protocol, regular health surveillance,
and testing of biological materials from mice are necessary to
prevent MHV infection. Once MHV infection has been diagnosed in
a facility, the affected population should be either promptly
eliminated or quarantined in an area or facility completely away
from pathogen-free mice as MHV is highly contagious. Cesarian
derivation followed by barrier maintenance has traditionally been
recommended for rederivation of breeding stocks. However, recent
evidence suggests that MHV infections in immunocompetent mice
may have an acute course, with complete elimination of the virus
in about 2 weeks. Thus, a practical alternative to cesarean derivation
is the isolation of individual breeding pairs of mice from MHV-infected
populations in seperate containment devices such as filter-top
cage systems, with subsequent selection of seronegative progeny
as breeders.
INTERFERENCE WITH RESEARCH
MHV has been reported to alter many experimental results. Examples
are alterations in immune function and hepatic enzyme activities;
inhibition of lymphocyte proliferative responses in mixed lymphocyte
cultures and mitogen-stimulated cells; alteration of phagocytic
and tumorcidal activity; increase of hepatic uptake of injected
iron; increase of susceptibility to other indigenous pathogens;
activation of natural killer cells and production of interferon;
and occurrence of anemia, leukopenia, and thrombocytopenia. In
athymic mice, the virus can also cause spontaneous differentiation
of lymphocytes bearing T-cell markers, alter IgM and IgG responses
to sheep erythrocytes, enhance phagocytic activity of macrophages,
cause rejection of xenograft tumors, impair liver regeneration
after partial hepatectomy, and cause hepatosplenic myelopoiesis.
Subclinical infections are exacerbated by thymectomy; whole-body
irradiation; reticuloendothelial blockade by iron salts; and administration
of cortisone, cyclophosphamide, antilymphocyte serum, chemotherapeutic
agents, or halothane anesthesia.
INDEX
MINUTE VIRUS of MICE (MVM)
SIGNIFICANCE
The significance of minute virus of mice (MVM) is uncertain.
It has little significance for most studies, but may be highly
significant for studies involving mouse transplantable tumors,
leukemias, and in vitro immunoassays.
AGENT
MVM is a single-stranded DNA virus, family Parvoviridae, genus
Parvovirus.
ANIMALS AFFECTED
Wild and laboratory mice.
EPIZOOTIOLOGY
Wild mice serve as reservoir hosts. Enzootic infection is common
in barrier-maintained and conventional breeding colonies of mice.
MVM is highly contagious. Virus is shed in the urine and feces,
thus transmission occurs by direct contact and by urine and fecal
contamination. Fomites such as contaminated food and bedding are
particularly important because the virus is very resistant to
environmental conditions. Airborne and transplacental infection
are not considered important. In infected colonies, maternal antibodies
are protective until the young are 6-8 weeks of age; however,
most mice become infected and seroconvert by 3 months of age.
CLINICAL
Natural infections are inapparent.
PATHOLOGY
Natural infections of MVM are not known to produce disease.
Experimental infections of MVM in fetal and neonatal mice, rats,
and hamsters produce lesions such as runting, cerebellar hypoplasia,
and peridontal disease.
DIAGNOSIS
Serological methods are used for routine health surveillance.
The enzyme-linked immunosorbent assay and the immunofluorescent
antibody test are considered most sensitive. Transplantable tumors
and other biological materials from mice can be screened by the
mouse antibody production (MAP) test and/or virus isolation.
CONTROL
Infection can be eliminated from stocks of mice by cesarian
derivation, but elimination of infected mice followed by replacement
with MVM-free mice is often more practical. Strict adherence to
barrier procedures is required to maintain the MVM-free state.
Wild mice must be excluded. Transplantable tumors, virus stocks,
and other biological materials should be monitored before admission
to a facility.
INTERFERENCE WITH RESEARCH
Direct evidence that wild type MVM in contemporary mouse stocks
interferes with research is lacking. However, evidence that MVM
can interfere with research has come from studies of MVM(i), a
single variant of the virus that may or may not occur as a natural
infection in contemporary mice. MVM(i) grows lytically in cytotoxic
T-lymphocyte clones, abrogates cytotoxic T-lymphocyte responses,
suppresses T-lymphocyte mitogenic responses, and suppresses T-helper-dependent
B-lymphocyte responses in vitro.
INDEX
ORPHAN PARVOVIRUS (OPV)
SIGNIFICANCE
Little is known about the in vivo effects of OPV infections
on the host. In vitro studies suggest that OPV infections
may be immunosuppressive. OPV can be a troublesome contaminant
of many different mouse tissues, including tumors.
AGENT
OPV is a single-stranded DNA virus, family Parvoviridae, genus
Parvovirus. Over the past few years, considerable evidence
has accumulated suggesting the existence of multiple rodent parvovirus
strains that are distinct from the prototypic parvovirus strains,
Kilham's Rat Virus (KRV), Toolan's H-1 (H-1), and Minute Virus
of Mice (MVM). Isolates that are serologically distinct from prototypic
isolates have been designated as OPVs.
HOSTS
Mice and rats.
EPIZOOTIOLOGY
Little is known about the epizootiology of OPV at this time
- research is currently being conducted and new information should
be published soon. OPV should be considered highly contagious.
Current research results implicate a role for urinary, fecal,
and perhaps respiratory excretion of virus, depending on host
genotype and route of virus exposure. Researchers also suggest
that evaluation of pancreatic and immune function during acute
infection is warranted.
CLINICAL
Like natural infections with MVM, OPV infections appear to
be subclinical. Neonatal animals are more susceptible to infection
than are weanling or adult animals.
PATHOLOGY
Natural infections of OPV are not known to produce disease,
however, little is known about the pathology of OPV infections.
In vitro studies suggest that OPV infections may be immunosuppressive
- suggesting sometype of pathologic or functional change within
the tissues of the immune system.
DIAGNOSIS
Definitive diagnosis of OPV infections has been problematic,
in part due to the difficulties associated with growing the OPVs
in vitro and to the limited cross-reactivity between OPVs
and prototypic parvovirus species. Previously, OPV infections
were diagnosed serologically by detecting limited amounts of cross-reactive
serum antibody with ELISAs and IFAs in which prototypic parvovirus
were used as antigens. Recently, a new parvovirus ELISA has been
developed which utilizes a nonstructural parvovirus protein, NS1,
as the antigen. The NS1 protein is conserved among all known rodent
parvoviruses, including a variety of poorly defined OPVs from
mice and rats. The major advantage of this new test is the increased
sensitivity in detecting OPV antibody in sera from infected rodents.
To determine the specific parvovirus species involved, sera that
are positive on the NS1-based ELISA can be tested by HAI assays
for prototypic and OPVs.
CONTROL
OPV most likely could be eliminated from stocks of mice by
cesarean derivation, but elimination of infected mice followed
by replacement with OPV-free mice would probable be more practical.
Adherence to strict barrier procedures is considered essential,
along with careful attention to the exclusion of wild mice and
prompt elimination or depopulation of OPV-infected stocks of laboratory
mice.
INTERFERENCE WITH RESEARCH
In vitro studies suggest that OPV infections may be immunosuppressive.
Since these viruses may alter the immune response of the animal,
identification of infected animals is crucial. OPVs can also be
troublesome contaminants of many different rodent tissues and
tumors.
INDEX
Proteus mirabilis
SIGNIFICANCE
The significance of Proteus mirabilis is low for most
studies.
AGENT
Proteus mirabilis is a gram-negative opportunistic pathogen.
ANIMALS AFFECTED
Several species of animals and humans.
EPIZOOTIOLOGY
Proteus mirabilis is can remain latent in the respiratory
and intestinal tracts of mice. P. mirabilis has been isolated
from the intestinal tract of both clinically affected and asymptomatic
animals, but the nasopharynx may be another important portal of
entry. Transmission is via contact and environmental contamination.
The agent is common, however, disease is rare.
CLINICAL
Clinical disease can occur following stress or immunosuppression.
P. mirabilis has been associated with ulcerative lesions
in the gastrointestinal tract of mice that have been chemically
immunosuppressed. In spontaneous cases in severe combined immunodeficient
(SCID) mice, clinical signs were characterized by weight loss,
hunched posture, and dehydration.
PATHOLOGY
Suppurative pyelonephritis and septicemia may occur, and there
is some evidence that the renal lesions are hematogenous in origin.
The renal cortex is commonly affected. Proteus nephritis
is characterized by abscessation and scarring. In immunodeficient
mice, splenomegaly and multifocal hepatic lesions are typical
macroscopic findings. In some cases, fibrinopurulent exudate is
present in the peritoneal cavity. Multifocal areas of coagulation
necrosis are present in the subcapsular regions of the liver and
around the central veins. Pulmonary lesions, when present, are
characterized by alveolar flooding and mobilization of alveolar
macrophages.
DIAGNOSIS
Diagnosis is by histological lesions consistent with bacterial
sepsis and the recovery of large numbers of P. mirabilis
from sites such as liver, peritoneal cavity, and intestine.
CONTROL
Meticulous sanitation practices and reduced population densities
should help to alleviate the problem. Minimize stress, immunosuppression,
and concurrent infections in mice colonies.
INTERFERENCE WITH RESEARCH
Infections with P. mirabilis may cause significant mortality
in colonies of SCID mice and immunodeficient/immunosuppressed
animals.
INDEX
Pseudomonas aeruginosa
SIGNIFICANCE
Low, except in immunosuppressed hosts.
AGENT
Gram-negative bacterium, family Pseudomonadaceae.
ANIMALS AFFECTED
Mice, rats, humans, and numerous other species.
EPIZOOTIOLOGY
P. aeruginosa is ubiquitous, occurring widely in soil,
water, sewage, and air. It is widely distributed in conventional
stocks of rodents and is transmitted by fomites or by contact
with infected humans or rodents.
CLINICAL
The organism is sometimes part of the normal flora in the digestive
tract, and clinical signs are not present. Fulminating septicemia,
resulting in death with few clinical signs, can occur in immunosuppressed
animals. There are a few reports of "circling" or "rolling"
in mice associated with otitis media and interna caused by this
organism.
PATHOLOGY
Gross and histopathologic lesions are nonspecific. Occassionally
there is suppurative otitis media with extension into the inner
ears and to the adjacent meninges or brain. Animals subjected
to severe immunosuppression can develop fulminant septicemia with
hemorrhage and multifocal necrosis in multiple organs.
DIAGNOSIS
Diagnosis of P. aeruginosa infection is made by isolation
and identification of the organism and exclusion of other possible
causes of disease.
CONTROL
Control is only necessary for immunosuppressed rodents. Cesarean
derivation followed by maintenance under gnotobiotic conditions
completely eliminates the organism. P. aeruginosa can be
eliminated from animal facilities by rigorous sanitation measures
coupled with acidification and/or hyperchlorination of the water.
INTERFERENCE WITH RESEARCH
Indigenous infections are of little importance except when
the research involves immunosuppressed animals. Mice and rats
naturally infected with P. aeruginosa typically die eariler
than do noninfected controls when exposed to lethal doses of whole-body
irradiation, cyclophosphamide, cortisone, or other immunosuppression.
INDEX
PNEUMONIA VIRUS of MICE (PVM)
SIGNIFICANCE
The significance of pneumonia virus of mice (PVM) is low for
most studies.
AGENT
PVM is an RNA virus, family Paramyxoviridae, genus Pneumovirus.
It is antigenically distinct from other members of the paramyxoviridae.
ANIMALS AFFECTED
Mice, rats, and hamsters.
EPIZOOTIOLOGY
PVM is a very common infection of labatory rodents worldwide,
the general prevalence rates being >50% of colonies of mice,
rats, and hamsters. Prevalence rates within colonies vary greatly
but tend to be higher in rats and hamsters than in mice. Thus,
the virus has relatively low infectivity for mice and tends to
cause focal enzootics of infection within mouse colonies. Active
infection in mice (and presumably rats and hamsters) is short
lived, lasting only about 9 days. Persistent infections do not
occur in euthymic mice. Transmission is exclusively horizontal
via the respiratory tract, mainly by direct contact and aerosol.
Fomites are probably not important in transmission.
CLINICAL
Natural infections are subclinical in euthymic rodents.
PATHOLOGY
No pathological lesions have been associated with natural infections
in immunocompetent hosts. Chronic pneumonia has been reported
to occur in naturally infected athymic (nu/nu) mice.
DIAGNOSIS
Serological methods are used for routine health surveillance.
The enzyme-linked immunosorbent assay is the most sensitive, but
the hemagglutination inhibition test is highly reliable. With
either of these tests, serumantibody is first detected around
day 9 post infection. The mouse antibody production (MAP) test
may be used for testing biological specimens for the presence
of the virus.
CONTROL
Cesarean derivation and barrier maintenance are effective methods
of controlling infection. Since the normal pattern of PVM infection
within mouse populations is focal enzootics and active infection
is present in the individual mouse for only about 9 days, it is
possible to control the spread of the agent by eliminating the
exposure of susceptible animals so the infection can "burn
itself out". This is most easily accomplished by a quarantine
period of 2-4 weeks wherein no new animals are introduced either
as adults or through breeding. This way the infection runs its
course and the virus is eliminated naturally.
INTERFERENCE WITH RESEARCH
PVM conceivably could alter the experimental results of some
studies involving the respiratory tract in euthymic mice but,
no examples have been reported. Athymic mice with natural infections
of PVM develop chronic pneumonia and emaciation with deaths.
INDEX
REOVIRUS-3
SIGNIFICANCE
Natural infections due to this virus have little significance
for most studies with mice and rats but can interfere with studies
involving transplantable tumors and in vitro test systems that
use cells from these animals.
AGENT
The reoviruses are double-stranded RNA viruses, family Reoviridae,
genus Reovirus.
ANIMALS AFFECTED
Mice, rats, hamsters, and guinea pigs.
EPIZOOTIOLOGY
Reovirus-3 is prevalent in contemporary rodents. Transmission
is by fecal-oral route and probably by aerosol. Infected fomites
may be important because reoviruses are relatively resistant to
environmental conditions.
CLINICAL
Natural infections are subclinical.
PATHOLOGY
There are no pathologic changes associated with natural infections.
DIAGNOSIS
The ELISA is the most sensitive method. Transplantable tumors
and cell lines can be screened for reoviruses by using tissue-culture
methods or the MAP test.
CONTROL
Cesarean derivation and barrier maintenance appear to be effective
methods of control.
INTERFERENCE WITH RESEARCH
Reovirus-3 is an occasional contaminant of and may interfere
with research involving transplantable tumors and cell lines.
INDEX
SIALODACRYOADENITIS VIRUS (SDAV)
SIGNIFICANCE
High.
AGENT
RNA virus, family Coronaviridae, Genus Coronavirus.
ANIMALS AFFECTED
Rats. Mice are susceptible to experimental infection, but natural
infection has not been reported for this species.
EPIZOOTIOLOGY
SDAV is one of the most common viruses in laboratory rats.
It is highly contagious, spreading rapidly within rooms of susceptible
rats by contact and aerosol. Transmission is primarily by infected
nasal secretions or saliva. It is not transmitted vertically.
The virus is present in tissues of infected rats for only about
7 days, and there is no carrier state. Tissues affected by SDAV
infection are mixed (submaxillary) and serous (parotid) salivary
glands, lacrimal glands (Harderian, intraorbital, and exorbital),
cervical lymph nodes, thymus, and the mucosa of the respiratory
tract. LEW, WAG/Rij, and SHR rats are more susceptible than other
strains. Less susceptible rat strains include WI, SD, LE, and
F344.
CLINICAL SIGNS
Natural infections usually take one of two forms:
Enzootic disease: Adults are immune because of previous
infection. Suckling rats have a mild, transient (1 week or less)
conjunctivitis accompanied by blinking. Occasionally, exudate
causes the eyelids to adhere together. Signs of this form of disease
usually are mild and subtle, escaping detection by most observers.
If clinical signs are present, they usually disappear by weaning.
Epizootic disease: Overt disease. Signs include cervical
edema; sneezing; photphobia; serous to seropurulent, often porphyrin-stained
nasal and ocular discharge; corneal ulceration; and keratoconus.
Characteristically, there is high morbidity and no mortality.
Most clinical signs disappear in a week, but the eyes might be
more prominent than normal for 1-2 weeks because of inflammation
of retroorbital tissues.
PATHOLOGY
SDAV has a positive tropism for serous or mixed serous-mucous
tubuloalveolar glands. There are also mild changes in the cervical
lymph nodes, thymus, and respiratory tract. Characteristically,
by 5 days postinfection, there is diffuse necrosis of alveolar
and ductal epithelium in the salivary and lacrimal glands, and
polymorphonuclear leukocytes quickly infiltrate the necrotic debris
and interstitium accompanied by interstitial edema. The ductal
epithelium is rapidly repaired, becoming hyperplastic and squamous
in appearance by 10 days postinfection. Complete restoration of
normal glandular architecture requires about 30 days. Eye lesions
include interstitial keratitis, corneal ulcerastion, keratoconus,
synechia, hypopyon, hyphema, and conjunctivitis. Sequelae of infection
include megaloglobulus with lenticular and retinal degeneration.
Thymic lesions are limited to focal areas of necrosis. Focal necrosis
and lymphoid hyperplasia occur in cervical lymph nodes.
DIAGNOSIS
The ELISA and the IFA test are more sensitive than the CF test.
Presumptive diagnosis often can be based on characteristic histological
changes in affected glandular tissue. The virus can be isolated
by culture techniques using primary rat kidney cells or by intracerebral
inoculation of neonatal mice.
CONTROL
Control requires very strict adherence to preventative measures,
including procurement only of SDAV-free rats and adherence to
strict barrier housing procedures. Prompt elimination of infected
populations is essential to prevent spread of infection to other
rodents. A less effective alternative is to place infected animals
under strict quarantine, remove all young and pregnant females,
suspend all breeding, and discontinue adding other susceptible
animals for a period of 6-8 weeks until the infection has run
its course and the virus has been eliminated naturally.
INTERFERENCE WITH RESEARCH
SDAV can seriously complicate studies involving the eyes, salivary
glands, lacriminal glands, or respiratory tract. It is reported
to reduce reproductive rate in breeding populations and slow growth
rate of young rats. It inhibits phagocytosis and interleukin-1
production by pulmonary macrophages. SDAV infection exaberates
concurrent Mycoplasma pulmonis infection.
INDEX
SENDAI VIRUS (SV)
SIGNIFICANCE
The significance of Sendai Virus (SV) infection is very high
primarily because the virus is extremely contagious.
AGENT
SV is an RNA virus, family Paramyxoviridae, genus Paramyxovirus,
species parainfluenza 1 (Sendai). All known strains of SV are
antigenically homologous.
ANIMALS AFFECTED
Mice, rats, hamsters, and possibly guinea pigs.
EPIZOOTIOLOGY
SV is extremely contagious, one of the most contagious infections
of laboratory rodents. First time infections usually are epizootic
within rooms, but can become epizootic throughout entire facilities
or institutions. The virus is highly prevalent in laboratory mice
and rats worldwide. Natural infection occurs via the respiratory
tract. Transmission is by direct contact and fomites and is highly
efficient. Viral replication is thought to be limited to the respiratory
tract and occurs for only about 1 week postinfection.
CLINICAL
Natural SV infection in rats is usually subclinical. In pregant
rats, the infection can cause fetal resorptions, retarded embryonic
development, and mortality of neonates. Clinical disease caused
by natural SV infection in mice falls into one of two patterns.
Enzootic (subclinical) infection commonly occurs in breeding populations.
Adults have active immunity due to prior infection, and newborn
mice are passively protected by maternal antibody until around
4-8 weeks of age, when they become infected. Recovery is prompt
and usually without morbidity or mortality. Epizootic (clinically
apparent) infection occurs when a mouse population is first infected.
Infection quickly spreads through the entire population. Signs
are variable but may include chattering; mild respiratory distress;
and prolonged gestation in adults, deaths in neonates and sucklings,
and poor growth in weanling and young adults. Breeding colonies
return to normal productivity in 2 months and thereafter maintain
the enzootic pattern of infection. Epizootics of disease that
exceed these general patterns in clinical severity should arouse
suspicion of complication by other agent(s), particularly Mycoplasma
pulmonis and cilia-associated respiratory bacillus.
PATHOLOGY
There are few gross lesions in uncomplicated SV infections.
The lungs can appear focally reddened or atelectatic, and serous
fluid can be visible in the pleural and pericardial cavities.
The most serious lesions are seen in mice that are infected as
sucklings or weanlings and in mice of the more susceptible strains.
Severe necrotizing bronchitis and bronchiolitis often cause intense
inflammatory injury to terminal bronchioles, resulting in scarring
with severe distortion of the smaller airways and formation of
polypoid outgrowths into bronchiole lumens. There is also pronounced
hyperplasia of airway epithelium resulting in peribronchiolar
adenomatous hyperplasia that can persist throughout life. In aged
mice the air spaces in these lesions are often filled with mucus,
large macrophages, and cellular debris.
DIAGNOSIS
The enzyme-linked immunosorbent assay (ELISA) is the test of
choice for routine serological monitoring. The mouse antibody
production (MAP) test may be used in testing transplantable tumors
and other biologic materials for contamination by SV.
CONTROL
Exclusion of SV is extremely difficult in most institutions
that receive rodents from outside sources. Ordinarily, exclusion
requires very strict adherence to systematic measures for preventing
entrance of the infection into an entire facility or institution.
Only animals known to be free of SV should be obtained and animals
should be maintained under strict barrier conditions. In addition,
all biological materials, such as transplantable tumors, should
be pretested and shown to be free of the virus. If SV infection
is detected, prompt elimination of infected subpopulation(s) is
essential to prevent spread of the infection to other rodents
on the premises. A less effective alternative is to place the
infected animals under strict quarantine, remove all young and
pregnant females, suspend all breeding, and prevent addition of
other susceptible animals for a period of 6-8 weeks until the
infection has run its course and the virus has been eliminated
naturally. Because of this alternative, cesarean derivation of
infected stocks usually is not justified.
INTERFERENCE WITH RESEARCH
Experimental SV infection alters the phagocytic function of
pulmonary macrophages. It has been reported (but not confirmed)
that infected mice have deficiencies in T- and B-cell function
that persist throughout life, but most of the evidence indicates
that such deficiencies are transient, lasting only a few weeks.
SV infection inhibits in vitro mitogenesis of lymphocytes, increases
natural killer cell-mediated cytotoxicity, and increases cytotoxic
lymphocyte responses after in vivo stimulation with SV-coated
syngeneic cells. Isograft rejection is altered and the neoplastic
response to respiratory carcinogens can be increased or decreased.
Wound healing is delayed. SV infection alters host responses to
transplantable tumors.
INDEX
Syphacia spp. (PINWORMS)
SIGNIFICANCE
Syphacia obvelata (mouse pinworm) and Syphacia muris
(rat pinworm) are among the more common endoparasites of contemporary
rodents, including stocks that have been derived by cesarean section
and maintained in barrier facilities.
AGENT
Roundworms, order Ascarida, suborder Oxyurina.
ANIMALS AFFECTED
Laboratory mice, rats, hamsters, gerbils, and wild rodents.
EPIZOOTIOLOGY
Adults are found primarily in the cecum and colon of infected
hosts. Eggs are efficiently disseminated from the perianal area
of the host into the cage and room environments. The eggs can
survive for weeks under most animal room conditions. Transmission
is by ingestion of embryonated eggs.
CLINICAL
Infections caused by Syphacia spp. alone are subclinical.
PATHOLOGY
Pinworms of laboratory rodents are generally not considered
pathogens. Pinworm burden in an infected rodent population is
a function of age, sex, and host immune status. In enzootically
infected colonies, weanling animals develop the greatest parasite
loads, males are more heavily parasitized than females, and Syphacia
numbers diminish with increasing age of the host. Athymic
(nu/nu) mice have increased susceptibility to pinworm infection.
DIAGNOSIS
Diagnosis is made by demonstrating eggs on the perianal region
using the cellophane tape technique or by finding adult worms
in the cecum and colon at necropsy.
CONTROL
Cesarean derivation and barrier maintenance are effective methods
of control. Hygenic methods, including frequent cage and room
sanitation, can aid in controlling Syphacia in an infected
rodent population. Cage-to-cage transmission can be prevented
by using filter-top cages. Several anthelminthics are effective
in eliminating a high percentage of adult worms but are inefficient
in clearing immature worms or eggs. Thus, treatment must be repetitive
and is not generally recommended, except in special circumstances.
INTERFERENCE WITH RESEARCH
Pinworm infections in rats have been reported to reduce the
occurrence of adjuvant-induced arthritis.
INDEX
Bordetella bronchiseptica
SIGNIFICANCE
Low in rats, usually an opportunistic pathogen. High in guinea
pigs, epizootic respiratory disease with high mortality.
AGENT
Small, motile, gram-negative bacillus that grows readily on
conventional laboratory media, producing small blue-gray colonies.
ANIMALS AFFECTED
Guinea pigs, rats, rabbits, birds, cats, dogs, swine, primates,
and humans.
EPIZOOTIOLOGY
B. bronchiseptica is a relatively common inhabitant
of the upper respiratory tract of species such as the guinea pig
and domestic rabbit. The organism tends to colonize on the apices
of respiratory epithelial cells, resulting in impaired clearance
by ciliated epithelial cells. Transmission of B. bronchiseptica
is by direct contact with clinically affected animals, carrier
hosts, contaminated fomites, and respiratory aerosols. Interspecies
transmission is likely. Although most surviving animals eventually
develop immunity and eliminate the infection, subclinical infections
and carrier animals are common, and B. bronchiseptica can
be cultured from the upper respiratory tract and trachea of clinically
normal animals.
CLINICAL
Clinical signs of B. bronchiseptica infection in guinea
pigs are usually associated with pneumonia and vary from no signs
to anorexia, inappetence, nasal and ocular discharge, dyspnea,
and death. High mortality, abortions, and stillbirths are noted
in guinea pigs during epizootics.
B. bronchiseptica is a bone fide opportunistic pathogen
in the laboratory rat. When isolated from the respiratory tract
in rats with lesions, it is likely that there are concurrent infections
with other pathogens, such as mycoplasmal or viral agents.
Rabbits frequently harbor B. bronchiseptica in their
upper respiratory passages, including the paranasal sinuses. The
usual consequence, through ciliary and epithelial damage, is a
predisposition to other infections, particularly pasteurellosis.
PATHOLOGY
The most common necropsy finding is a discrete anteroventral
consolidation of a portion of a lobe, of an entire lobe, or of
several lobes of the lung. The affected lung is firmer than normal
and dark red or reddish-tan to gray. Mucopurulent exudate with
otitis media, rhinitis, and tracheitis may be seen independently
or may accompany bronchopneumonia. Additionally, there may be
marked purulent bronchitis.
DIAGNOSIS
The isolation of B. bronchiseptica in large numbers
from affected tissues is required.
CONTROL
Good husbandry, purchase of clean stock, and seperation of
possible carrier animals from healthy guinea pigs are essential.
Antibiotic therapy has limited value.
INTERFERENCE WITH RESEARCH
Lesions due to B. bronchiseptica in the resiratory tract
can interfere with research involving these organs and can lead
to an animal predisposed to other infections.
INDEX
Streptococcus pneumoniae
SIGNIFICANCE
Low.
AGENT
Streptococcus pneumoniae, an encapsulated, gram-positive,
lancet-shaped diplococcus with the following synonyms: Diplococcus
pneumoniae, Pneumococcus pneumoniae.
ANIMALS AFFECTED
Disease has been reported occasionally in rats, guinea pigs,
and monkeys. Only subclinical infection has been reported in mice.
Humans are the main natural hosts.
EPIZOOTIOLOGY
Transmission is by aerosol and direct contact. The incidence
of infection in rats is low. Host sites of greatest predilection
for infection are nasal passages and middle ears. The carrier
state is common in infected colonies.
CLINICAL
Signs are non-specific. Dyspnea, weight loss, hunched posture,
snuffling respiratory sounds, and abdominal breathing have been
reported. Clinical onset can be sudden, and young rats are affected
most often.
PATHOLOGY
Predominant lesions in rats are suppurative rhinitis and otitis
media. The disease often extends into distal airways, causing
acute tracheitis and fibrinous lobar pneumonia, and into organs
adjacent to the lungs, causing fibrinous pleuritis or empyema,
fibrinous pericarditis, and/or acute mediastinitis. The fibrinopurulent
nature of the exudate is characteristic of the bacterial infection.
Lesions associated with severe bacteremia include suppurative
arthritis, meningitis, hepatitis, splenitis, peritonitis, and
orchitis. Splenic and testicular infarcts can occur. Abdominal
lesions are frequently the primary cause of death.
DIAGNOSIS
Isolation of the organism from sites with characteristic lesions
and excluding other possible causes and contributors to the disease.
Histological examination of lungs and other tissues.
CONTROL
Cesarean derivation and barrier maintenance are extremely effective
methods of control. The basic practices of good husbandry apply
in controlling the disease. Oxytetracycline at 0.1 mg/ml in the
drinking water for 7 days has controlled mortality in epizootics
but has not eliminated the carrier state.
INTERFERENCE WITH RESEARCH
S. pneumoniae -induced septicemia alters hepatic metabolism,
serum biochemistries, blood pH and electrolytes, and thyroid function.
Studies involving the rat respiratory tract can be jeopardized.
INDEX
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