                               RAT
                       BACTERIAL DISEASES 
                                
                                 
                                
                        STREPTOCOCCOSIS 

OCCURRENCE 

The organism is ubiquitous among humans & animals but is not
considered to be zoonotic.  It is frequently recovered from
respiratory tract lesions in guinea pigs, nonhuman primates, and
some domestic animals.  URI of conventionally raised rats has been
reported to be common.  However, it is seldom present in
barrier-maintained, commercial rat sources.  

ETIOLOGY 

The causative organism, Streptococcus pneumoniae, is a
gram-positive coccus.  A number of serological types have been
associated with respiratory disease in rats.  

TRANSMISSION 

Via aerosol droplets.  

PREDISPOSING FACTORS 

Poor husbandry and general stress factors predispose to
streptococcal infections.  Biting facilitates transmission, as does
the traumatic effect of overgrown teeth.  

PATHOGENESIS 

The infection often remains localized in the nasopharynx without
the development of overt disease.  A shift in the host-parasite
balance due to stress or concurrent infection with another pathogen
may result in bronchopneumonia and bacteremia.  

CLINICAL SIGNS 

The most common signs disease are serous to mucopurulent nasal and
ocular discharge and "red tears" due to porphyrin pigments secreted
from the Harderian glands, ruffled fur, anorexia, weight loss,
dyspnea, rales, hematuria, and depressed activity.  Torticollis may
exist if the inner ear is affected, and abortions are associated
with both general and uterine infections.Young animals are more apt
to be clinically affected.  Transmission is by aerosol droplet. 
Animals often die within a few days after onset of pneumonic signs.



MORBIDITY & MORTALITY 

High in the acute phase.  Variable in prolonged epizootics.  

LESIONS 

Gross: The most characteristic gross lesions are pulmonary
consolidation and fibrinopurulent pleuritis and pericarditis.  An
extensive fibrinopurulent peritonitis, otitis media and interna,
metritis, orchitis, or meningitis may occur as well.  If a
bacteremia occurs early, the disease may be acute with few gross
lesions.  

Histo.: Streptococcus pneumoniae induces an outpouring of exudate
rich in fibrin, neutrophils, and erythrocytes into the alveoli. 
Bronchioles are filled with neutrophils.  Embolic lesions may occur
in multiple tissues which include the spleen, liver, kidneys,
joints, and brain.  

DIAGNOSIS 

Clinical signs and lesions.  Recovery of S.  pneumoniae on blood
agar culture in the presence of 10% carbon dioxide confirms the
diagnosis.  The organism is alpha hemolytic and bile soluble and is
inhibited by ethylhydrocupreine (optochin), an antibiotic.  S. 
pneumoniae ferments inulin.  

PREVENTION 

There is no effective means to control S.  pneumoniae infection
once it is enzootic in the colony.  Antibiotics will not eliminate
the organism from rat colonies.  Hysterectomy rederivation of
breeding stock from infected colonies is an effective method of
initiating new stock free from pneumococcal infection.  

TREATMENT 

Benzathine penicillin (30,000 units/200 gm BW) or Oxytetracycline
(0.1 mg/ml in drinking water) for 7 days may be helpful in reducing
the severity of the disease and as an aid in limiting infections to
a subclinical mode in some animals.  Selection of an antobiotic is
based on sensitivity testing.  A carrier state often develops
following treatment, and rats may experience a relapse during a
subsequent period of stress.  

SIGNIFICANCE TO RESEARCH 

Carrier animals are prone to clinical disease following
experimental manipulations, e.g., peritonitis following
intraperitoneal injections of any kind, encephalitis following
placement of intracranial implants, and pleuritis following cardiac
puncture.  

ZOONOSIS 

Streptococcus pneumoniae can cause respiratory and meningeal
disease in man, esp.  in the elderly and in people lacking spleens,
and in some cases the serotypes that affect animals may also affect
humans.  

         PSEUDOTUBERCULOSIS (CORYNEBACTERIOSIS) 

OCCURRENCE 

Epizootics of pseudotuberculosis may occur in conventionally raised
breeding colonies.  Epizootics often can be retrospectively
associated with an environmental stress (e.g., fluctuation in
ambient temperature or ventilation).  Mice & rats are affected. 
Rare isolations have been reported in the guinea pig.  

ETIOLOGY 

The causative agent is the gram-positive, nonmotile, diphtheroid
bacillus, Corynebacterium kutcheri.  After 48-hour aerobic
incubation on 5% blood agar, colonies are circular, 1 to 4 mm in
diameter, translucent, gray to yellow, smooth, and non-hemolytic. 
On occasion, other Corynebacterium species can cause similar
syndromes in rats.  

TRANSMISSION 

Little is known concerning how C.  kutscheri is carried or
transmitted within a colony.  It has been suggested that the
organism is transmitted via aerosol droplet, fecal-oral, or direct
contact.  

PREDISPOSING FACTORS 

Corynebacterium kutsheri infections in mice and rats are more often
inapparent or latent and become overt disease following stressful
manipulations.  Nutritional deficiencies, concomitant infections,
cortisone injections, and radiation exposure are predisposing
stresses.  Rats are more resistant to the spontaneous disease than
mice.  

PATHOGENESIS 

The organism is an opportunistic pathogen uncommonly resident in
the intestine and, possible, the upper respiratory tract.  Once
rats are infected, a hematogenous spread may be involved, since
lung lesions are initially interstitial and not bronchial.  

CLINICAL SIGNS 

Typically, the organism causes inapparent infections in rats, with
exacerbation of respiratory disease under conditions of stress. 
When clinically ill, the most commonly seen signs include serous
oculonasal discharge, rough hair coat,abnormal gait, swollen
joints, lethargy, dyspnea, anorexia, and loss of weight or retarded
growth.  In cutaneous infections the skin is abscessed, ulcerated,
and underlaid with fistulous tracts.  Most rats will have
inapparent infections in which C.  kutscheri cannot be isolated
from internal organs.  

MORBIDITY & MORTALITY 

High in the acute clinical disease.  Low in chronic infecton.  

LESIONS 

Gross: Lesions are characterized by a variable number of
grayish-yellow foci surrounded by red zones, particularly in the
lung.  In longer standing cases, individual foci coalesce into
raised lesions 1 cm or larger in diameter and become caseous, hence
the term "pseudotuberculosis".  Occasionally, fibrous adhesions
occur between the lungs and thoracic walls.  Similar lesions may be
seen in other organs, including the liver, heart,skin, brain, and
kidneys.  The hepatic lesions resemble tubercles and have caseous
centers and fibrous capsules.  Prepucial adenitis, arthritis, and
otitis media may also be caused by C.  kutscheri.  

Histo.: The lesions in various target organs appear to be due to
septic emboli.  Pulmonary lesions initially consist of a
polymorphonuclear cell and macrophage infiltrate of the bronchioles
and interstitial tissue with a round cell infiltrate occurring
later.  Bronchi become impacted with PMN cells and necrotic
leukocytes.  Giemsa or Gram staining of infected tissues will
reveal the rod-shaped C.  kutscheri organisms.  

DIAGNOSIS 

Clinical signs, gross & microscopic lesions, serology (ELISA) and
isolation of the bacterium from infected tissues.  Corynebacterium
kutscheri is easily recovered from lesions and upper respiratory
tract exudates by culturing on blood agar plates incubated
aerobically at 37 degrees C.  

DIFFERENTIAL DIAGNOSIS 

1.  Mycoplasma pulmonis- The rapidity with which C.  kutscheri
clinically affected rats succumb helps differentiate it from
Mycoplasma.  Whereas peribronchial lymphoid hyperplasia is a
dominant lesion in Mycoplasmosis, it is unremarkable in C. 
kutscheri infections.  

2.  Streptococcosis- Fibrinopurulent pericarditis, peritonitis, and
pleural effusion are not seen in Pseudotuberculosis.  

3.  Salmonellosis- There are usually no splenic lesions in
Pseudotuberculosis.  

PREVENTION 

Culling of ill animals will not eliminate C.  kutscheri from
animals remaining in a colony.  Isolation of the organism from
animals with subclinical infections is not usually successful.  For
this reason, cortisone administration (10mg SC) has been advocated
as a means for surveillance of infection in colonies prior to
necropsy and culturing for C.  kutscheri.  Hysterectomy derivation
is an effective means to establish a C.  kutscheri-free colony.  

TREATMENT 

Antibiotic therapy will not eliminate C.  kutscheri from a colony. 
The organism is sensitive to ampicillin (2-10 mg/100g BW PO bid),
CHPC (20 mg/100g BW PO tid), or tetracycline (450-643 mg/L drinking
water).  

SIGNIFICANCE TO RESEARCH 

Since C.  kutscheri infection is, in most cases, inapparent and
manifests itself whenever the host is sufficiently stressed, it can
be a significant problem in experimentally stressed rats.  

ZOONOSIS 

Corynebacterium kutscheri is a rodent pathogen, but a case of
chorioamnionitis has been observed in man.  

              TYZZER'S DISEASE 

OCCURRENCE 

The number of species susceptible to infection by Bacillus
piliformis continues to increase and presently includes mice, rats,
hamsters, gerbils, rabbits, guinea pigs, horses, rhesus monkeys,
cats, dogs, several wildlife species, and others.  Tyzzer's disease
is probably the most common disease of gerbils.  It is also common
in rabbits, foals, mice, and hamsters.  It occurs occasionally in
conventially raised rat colonies.  It is widely distributed
geographically.  The acute, highly fatal disease is most often seen
in weanling animals.  

ETIOLOGY 

Tyzzer's disease is caused by the gram-negative, spore-forming rod,
pleomorphic, PAS-positive nonacid-fast Bacillus piliformis.  This
organism, which is not a true Bacillus, is an intracellular
pathogen that has not been cultivated on artificial media, and is,
as yet, taxonomically undefined.  In the laboratory, B.  piliformis
is propagated on the yolk sac of embryonated chick eggs.  

TRANSMISSION 

Transmission is thought to be by the fecal-oral route.  Infectious
spore-like bodies may survive a year or more in bedding, soil, or
contaminated feed.  In utero transmission to the fetus has been
demonstrated experimentally.- 

PREDISPOSING FACTORS 

Poor environmental sanitation, stress of shipping, and
immunosuppressors such as radiation, corticosteroids, concurrent
disease, thymectomy, and crowding contribute to the development of
clinical disease.  

PATHOGENESIS 

The pathogenesis of the disease is believed to involve a primary
intestinal infection with spread to the liver via the portal
circulation.  

CLINICAL SIGNS 

Clinical signs associated with Tyzzer's disease are not
particularly distinctive and, accordingly, only suggestive in
making a diagnosis.  Tyzzer's disease in weanling or stressed
animals is an acute, enzootic disease causing rough hair coat,
lethargy, and death within 48 to 72 hours.  Chronically infected
animals, in which hepatic lesions are more pronounced, exhibit
weight loss, rough hair coat, distended abdomen and eventually
death.  Diarrhea is not a common sign in rats with B.  piliformis
infection.  

MORBIDITY & MORTALITY 

Animals displaying clinical signs generally die within several
weeks.  

LESIONS 

Gross: The most consistent lesion of B.  piliformis infection is an
enlarged liver with few to numerous gray, white, or yellow foci, 1
to 2 mm in diameter on the surface or within the parenchyma.  In
more acute cases there may be edema, congestion, hemorrhage, and
focal ulceration of the intestine, particularly around the
iliocecal-colonic junction.  The intestinal lesion has been termed
"megaloileitis" due to a segmental dilatation and inflammation of
the ileum.  However, ileal distension is not always present.  The
gut is often atonic and filled with a yellowish fluid.  Pale,
circumscribed, gray myocardial foci have been noted in rabbits,
rats, and hamsters with Tyzzer's disease.  There are usually no
splenic lesions.  

Histo.: Intracellular organisms are demonstratable in epithelium of
crypts and villi.  The necrotic foci in the liver are most often
present near vessels.  Surrounding these foci are varying numbers
of leukocytes, macrophages, and fibroblasts.  Intracytoplasmic
bacteria may be seen in hepatocytes at the periphery of the
lesions, but may be present in very small numbers and thus be hard
to find.  Organisms are also found in myocardium around foci of
necrosis.  The filamentous organisms may be seen within the
cytoplasm of cells adjacent to the necrotic area, often in a "pile
of sticks" arrangement.  

DIAGNOSIS 

A presumptive diagnosis can be made by the gross lesions, but a
definitive diagnosis is dependent upon observation of the organism
within hepatocytes, intestinal epithelium, or myocardium. 
Impression smears of liver taken at necropsy and stained with Gram,
PAS, silver staining, Giemsa, or methylene blue stains may be
useful for a rapid diagnosis.  However, formalin-fixed specimens
stained by Giemsa or Warthin-Starry methods are usually performed
to confirm a diagnosis.  Even with special stains, organisms in
tissues may be difficult to find because of their paucity.  Suspect
material inoculated into cortisonized, susceptible strains of mice
from a Tyzzer's-free colony may aid in detecting the disease. 
Similarly, cortisonizing suspect animals may aid in establishing
the disease.  Indirect fluorescent antibody tests are also a
diagnostic aid.  A CF test is widely used for screening in Japan. 
An intradermal skin test has been described in the United States
but, as yet, does not appear to be widely used.  

DIFFERENTIAL DIAGNOSIS 

Chloral hydrate-induced lesions- causes ileal distension.  

PREVENTION 

Prevention of Tyzzer's disease in a colony is dependent upon a
barrier that excludes entry of the agent by contaminated cages,
equipment, and infected animals.  Routine cage sanitation probably
is ineffective in killing the spores of B.  piliformis, but
exposure of spores to 80 degree Centigrade for 30 min has been
shown to inactivate them.  Sodium hypochlorite (0.3%) and peracetic
acid are effective disinfectants.  Spores are resistant to ethanol
and quaternary ammonia compounds.  Filter cage covers aid in
reducing transmission.  

TREATMENT 

The acute (1 to 4 day) course of the disease and the intracellular
location of the organism reduce the effectiveness of treatment. 
Oxytetracycline in the drinking water at 0.1g/L for 30 days has
reportedly suppressed an outbreak.  Tetracycline at 10 mg/kg BW for
5 days "on-off-on" or at 400 mg/L for 10 days has also been used. 
Bacillus piliformis infection is also sensitive to penicillin,
streptomycin, and erythromycin.  Sulfonamides and CHPC appear not
to affect the agent.  

SIGNIFICANCE TO RESEARCH 

Clinically evident Tyzzer's disease is usually associated with
experimentation that compromises the immunocompetence of rats.  

ZOONOSIS 

No public health significance is known, but the report of B. 
piliformis infection in a rhesus monkey should be noted. 
Antibodies to B.  piliformis have been found in pregnant women. 
Because B.  piliformis affects such a wide spectrum of animal
species, man may very well be susceptible to clinical disease under
certain circumstances.  

              PASTEURELLOSIS 

 OCCURRENCE 

Rats, mice, and occasionally hamsters are susceptible to this
disease.  Only a relatively few reports document Pasteurella
pneumotropica as a primary pathogen in cases of pneumonia, otitis
media, and conjunctivitis.  

ETIOLOGY 

Pasteurella pneumotropica is a gram-negative, nonmotile,
pleomorphic coccobacillus of very low virulence.  It has been
suggested that Pasteurella pneumotropica is essentially an
enterotropic rather than a pneumotropic organism.  

TRANSMISSION 

Pasteurella pneumotropica often exists in a latent, carrier state
in the upper respiratory or gastrointestinal or reproduction
tracts, and may be disseminated by respiratory aerosol or fecal
contamination, biting, licking, and intrauterine contamination. 
The intestinal tract is probably the primary site for localization
of the organism in subclinical infections.  

PREDISPOSING FACTORS 

Since P.  pneumotropica is an opportunistic pathogen, circumstances
that lower a host's resistance, particularly other infections, may
precipitate the clinical disease.  P.  pneumotropica may complicate
Mycoplasma pulmonis infection in rats.  

CLINICAL SIGNS 

Pasteurella pneumotropica is widespread as a latent infection, but
the bacterium causes clinical disease only sporadically.  Signs
associated with P.  pneumotropica infection include chattering,
labored respiration, weight loss, skin abscesses, conjunctivitis,
panophthalmitis, mastitis, infertility, abortion, and internal and
subcutaneous abscesses.  

LESIONS 

Gross & Histo.: Well-demarcated, red foci of consolidation in the
lungs, with occasional scattering of abscesses.  Suppurative
reactions may also occur in the middle ears, orbital glands,
uterus, skin, mammary gland, lymph nodes, accessory sex glands, and
the urinary system.  

DIAGNOSIS 

Culture.  On 24-hour incubation on blood agar the colonies are
small (1 mm), circular, convex, smooth, and surrounded by a zone of
slight greenish discoloration.  Blood agar medium is satisfactory
for primary isolation from nonenteric sites.  However, for recovery
from the intestinal tract, enrichment in a medium such as GN broth
is recommended before isolation is attempted on blood agar plates. 


DIFFERENTIAL DIAGNOSIS 

Mycoplasma pulmonis- Pasteurella pneumotropica may have scattered
areas of abscesses.  

PREVENTION 

Elimination of murine respiratory infection from a colony requires
a known disease-free stock placed into a clean and
barrier-sustained colony.  Newly arrived animals should be
quarantined until the microbial status of the rat has been
determined.  Caesarean derivation should be done with the knowledge
that Pasteurella pneumotropica is a relatively common uterine
inhabitant, as is M.  pulmonis.  

TREATMENT 

Pasteurella pneumotropica is sensitive to several antibiotics. 
Among specific antibiotic regimens used with this organism are CHPC
in the drinking water (0.25 mg/ml) for 2 weeks; ampicillin (9 mg
daily for 5 days); oxytetracycline in the water at 3.5 mg per day,
and streptomycin, although many isolants are resistant to the last
2 and streptomycin can be toxic for rodents.  

SIGNIFICANCE TO RESEARCH 

Since Pasteurella pneumotropica is frequently carried in the
uterus, vertical transmission can occur, and, accordingly, this can
compromise the microbial status of axenic and gnotobiotic colonies.



ZOONOSIS 

A strain of Pasteurella pneumotropica can infect man, the
possibility of rodent-to-man transmission is unlikely.  

              SALMONELLOSIS 

OCCURRENCE 

Salmonellae are widespread in nature and affect a wide range of
vertebrates.  Guinea pigs are highly susceptible and develop severe
clinical disease; mice and rats are also very susceptible and may
carry subclinical infections for long periods.  Rabbits, hamsters,
and gerbils are less often infected, but severe outbreaks have
occurred in these species.  Infection in an immunologically naive
colony typically results in an epizootic of clinically affected
rats and a varying proportion of animals with inapparent infection.

These latter animals act as subclinical carriers to render the
infection as enzootic in a colony.  However, salmonellosis is
rarely reported today.  

ETIOLOGY 

Salmonella species that infect rats include Salmonella enteritidis,
S.  typhimurium, S.  dublin, and S.  meleagridis.  Salmonella
typhimurium and S.  enteritidis are the species most often isolated
from laboratory animal species.  

TRANSMISSION 

Transmission is by the fecal-oral route through ingestion of feces
or fecal-contaminated feed or bedding.  The organism can exist in
the carrier state in the intestinal tract and be continually shed
into the environment.  

PREDISPOSING FACTORS 

Among the factors predisposing to salmonellosis are youth or old
age, nutritional deficiencies, concomitant diseases, genetic
predisposition, serotype of organism involved, and environmental
and experimental stresses.  

 PATHOGENESIS 

Salmonellae penetrate the intestinal mucosa at the level of the
ileum and cecum.  The earliest lesions occur in this locale.  In
some infected animals, a bacteremic state occurs that results in
the demise of the host before the development of further lesions. 


CLINICAL SIGNS 

Salmonellosis in laboratory animals is an enteric and systemic
infection that may be enzootic or epizootic.  Specific signs, when
present, include anorexia, depressed activity, rough hair coat,
weight loss, light soft feces, ocular discharge, small litters,
dyspnea, and abortions.  A colony of affected rats had
conjunctivitis, anorexia, weight loss, and sporadic deaths. 
Chronic carriers exist and make elimination of the infection
difficult.  

MORBIDITY & MORTALITY 

Affected animals die within 1 to 2 weeks.  

LESIONS 

Gross: Lesions that occur in salmonellosis differ depending on the
stage of the disease.  The earliest lesions occur in the intestinal
mucosa of the ileum and cecum due to penetration of the organism. 
The lesions consist of mild dilatation, thickened intestinal walls,
and a granular mucosal surface.  Involvement of the
reticuloendothelial system is reflected by enlarged Peyer's
patches, mesenteric lymph nodes, and spleen.  In some infected
animals, a bacteremic state occurs that results in the demise of
the host before the development of further lesions.  However, in
animals not succumbing to septicemia, ulceration of the ileal,
colonic, and cecal mucosa occurs.  Histo.: The villus epithelium of
the ileum is markedly degenerated, and the lamina propria is
infiltrated with neutrophils and macrophages.  Concomitant with
intestinal lesions is the development of focal necrosis and
granulomas in the spleen and liver due to hematogenous spread of
the organism.  

In rats who are intermittent or chronic shedders of salmonella, the
most remarkable lesions are lymphadenitis of the mesenteric lymph
nodes and ulceration of the cecal mucosa.  Rats from which
salmonella is chronically shed have more advanced lesions than do
intermittent shedders of the organism.  

DIAGNOSIS 

While necropsy signs may be suggestive of salmonellosis, culture of
feces or cecum is the method of choice for confirming an outbreak
or a carrier state of salmonellosis.  However, in asymptomatic
carriers, organisms will be shed intermittently in the feces and
recovery from tissues is difficult.  The agents do not hydrolize
urea and usually do not use lactose.  Standard bacteriologic media
are used in culture.  These media may include selenite F or
tetrathionate broth to selectively enhance growth of salmonella
from fecal samples followed by culture on MacConkey's (MC),
brilliant green (BG), agars, XLD, and HE.  From these media,
possible salmonella colonies are inoculated into triple-sugar-iron
slants.  A battery of additional biochemical tests is used to
identify suspect cultures further.  Suspected salmonella isolants
must by confirmed by serology because several nonpathogenic enteric
bacteria may have similar biochemical reactions.  A final
determination of serotype is best performed in a reference
laboratory.  

PREVENTION 

Rigid, high husbandry standards and the screening of new arrivals,
existing animals, especially dogs and subhuman primates, and animal
care personnel will reduce the possibility of outbreaks.  Birds,
wild rodents, and contaminated feed must be excluded.  Elimination
of the infection from conventional colonies is extremely difficult;
killing, disinfection, and restocking are more practical
approaches.  

TREATMENT 

Treatment of salmonellosis may suppress an epizootic to an enzootic
infection, but elimination of carriers is difficult.  Because of
the major public health concern, colonies infected with Salmonella
should be eliminated, premises are sanitized, and clean animals are
used for restocking.  

One therapeutic regiment that has been followed with some success
is the additon of oxytetracycline to the drinking water at 10 g/L
for 10 days or 250 mg/kg body weight per day.  Treated rats may be
isolated, the remainder of the colony killed, the room disinfected,
and first litters monitored for Salmonella.  Thus, infection in
valuable rodents by minimally pathogenic strains of Salmonella may
be controlled or eliminated by intense culture, isolation, and
treatment.  

ZOONOSIS 

Salmonellosis occurs in man and can be contracted from, or given
to, laboratory animals.  Animal care personnel should be
periodically inspected for latent infections of Salmonella.  

              PSEUDOMONIASIS 

OCCURRENCE 

This ubiquitous bacteria found in soil and water, colonizes plants,
insects, animals, and humans.  

ETIOLOGY 

Pseudomonas aeruginosa is a gram-negative bacterium.  

TRANSMISSION 

Transmission in laboratory rodents occurs primarily by direct
contact and contaminated water bottles and automatic watering
systems.  

PREDISPOSING FACTORS 

Infection with this organism in immunocompetent rats is nearly
always inapparent.  However, when rats are immunosuppressed,
Pseudomonas aeruginosa invades the upper respiratory mucosa and
cervical lymph nodes.  

PATHOGENESIS 

When rats are immunosuppressed, Pseudomonas aeruginosa invades the
upper respiratory mucosa and cervical lymph nodes causing
bacteremia and induces an acute, lethal disease.  

CLINICAL SIGNS 

In some cases, rats develop facial edema, conjunctivitis, and nasal
discharge.  In genetically thymic-deficient rats (nude),
retro-orbital abscesses may occur prior to bacteremia.  

DIAGNOSIS 

Diagnosis of pseudomoniasis is based upon a history of
immunosuppression associated with an epizootic of acute disease and
isolation of Pseudomonas aeruginosa from the blood and organs of
affected rats.  

Pseudomonas aeruginosa grows well on blood agar and most other
standard laboratory media.  Most strains are B-hemolytic and
produce a bluish-green pigment, pyocyanin, as well as fluorescein. 
The use of specialized media (Pseudomonas P agar) enhances pigment
production.  The organism derives energy from carbohydrates via
oxidation rather than fermentative metabolism.  Identification of
isolates as Pseudomonas aeruginosa is easily made by the above
characteristics and appropriate biochemical reactions.  

DIFFERENTIAL DIAGNOSIS 

Facial edema in affected rats must be differentiated from viral
sialodacryoadenitis.  

PREVENTION 

Phenolics are usually effective disinfectants, but quaternary
ammonium compounds may actually support its growth.  Infection can
be relatively well controlled in a colony by hyperchlorinating
drinking water at 12 ppm or by acidification of water to a pH of
2.5-2.8.  In a closed colony, it is advisable to remove rats that
remain culturally positive after water treatment has been
instituted.  In studies requiring pseudomonas-free rats, isolators
are useful in which a gnotobiotic environment can be achieved. 
Alternatively, laminar flow units may suffice if supplies and
equipment are sterilized and personnel wear sterile garments.  

SIGNIFICANCE TO RESEARCH 

In most research applications, Pseudomonas aeruginosa-free rats are
not necessary for the conduct of the work.  It is a major problem,
however, in rats used for burn research and in studies in which
drugs or radiation induce immunosuppression.  

             STREPTOBACILLOSIS 

OCCURRENCE 

Streptobacillus moniliformis is considered a commensal of low
pathogenicity for rats but is capable of producing disease in mice,
guinea pigs, and humans.  

ETIOLOGY 

Streptobacillus moniliformis, a pleomorphic, gram negative rod or
filamentous bacterium.  

PATHOGENESIS 

Streptobacillus moniliformis is a commensal bacterium often present
in the nasopharynx of conventially raised rats.  It may be involved
occasionally as a secondary invader within inflammatory lesions of
the rat.  

DIAGNOSIS 

Culture- media requires blood, serum, or ascites fluid and growth
is enhanced with 10% carbon dioxide.  

PREVENTION 

Gnotobiotic derivation and segregation from infected animals and
proper management of air and personnel flows.  

ZOONOSIS 

The chief importance of S.  moniliformis is that it is the
principal agent causing rat-bite fever in humans.  The other
bacterium associated with this clinical syndrome is Spirillum
minus.  Clinical signs in humans usually occur within 10 days of a
rat bite and consist of headache, weakness, fever, a generalized
rash, and arthritis.  Often clinical signs subside in several days
but then recur at irregular intervals for weeks or months.  

             MYCOPLASMAL DISEASES 

        MURINE RESPIRATORY MYCOPLASMOSIS (MRM) 

OCCURRENCE 

Rats and mice are the principal hosts of Mycoplasma pulmonis and M.

arthritidis.  Rabbits, guinea pigs, and other rodents may carry the
organism, but they are not clinically affected.  The disease has
many synonyms: murine pneumonitis, infectious catarrh, enzootic
bronchietasis, chronic respiratory disease (CRD), endemic murine
pneumonia , viral pneumonia of rats, labyrinthitis, and chronic
murine pneumonia.  By far, this is the most common disease of
laboratory rats.  

ETIOLOGY 

Mycoplasmas are very small pleomorphic organisms with no
distinctive cell wall and a diameter between 0.2 and 1.0 um. 
Mycoplasma pulmonis, which may accompany Sendai virus or bacterial
infections, is a mucosal pathogen responsible for the clinical
signs and lesions of murine mycoplasmosis.  The bacteria that may
accompany M.  pulmonis in respiratory disease include Pasteurella
pneumotropica, Actinobacillus spp, Streptococcus pnemoniae,
Bordetella bronchiseptica, and Corynebacterium kutscheri.  Mice,
like rats, may carry the agent as an inapparent infection.  

TRANSMISSION 

Transmission of the extremely contagious mycoplasmal infections is
by direct contact between mother and young, respiratory aerosol
over short distances, sexual transfer, animal carriers, and in
utero passage.  Some of the unexplained appearances of
mycoplasmosis in established, isolated, pathogen-free colonies may
arise from infections acquired in utero and undetected, minute foci
of infection in a few individuals.  There is little evidence to
indicate that transmission occurs thru fomites such as caging
equipment and garments worn by personnel.  

PREDISPOSING FACTORS 

Agents that damage the protective capacity of the respiratory
epithelium predispose to M.  pulmonis infection.  Such agents
include ammonia, sulfur dioxide, and Sendai virus.  

Ammonia gas in an animal colony is generated from urine and feces
by urease-positive bacteria.  Factors involved in ammonia
accumulation include poor ventilation and sanitation, cage
crowding, bacterial growth, and excessive populations.  The
metaplastic and ciliary inhibiting effects of ammonia can extend an
innocuous upper respiratory infection into a bronchopneumonia.  

Older animals and animals of certain strains with diminished immune
function are more susceptible to the clinical manifestations of the
chronic disease.  Lewis strain rats are, for example, more
susceptible to clinical murine respiratory mycoplasmosis than F344
rats.  Vitamin A or E deficiencies may also be predisposing
factors.  

PATHOGENESIS 

The basis for the pathogenicity of M.  pulmonis is not well
understood.  Mycoplasma pulmonis adsorbs to the cell membrane of
the ciliated, columnar or cuboidal epithelia in the respiratory
tract.  It has been suggested that adsorption is a means by which
mycoplasmas damage host cells by uptake of essential cellular
metabolites; release of cytotoxic products, such as hydrogen
peroxide; or cross reaction of antibody with cell membrane
components that are antigenically similar to or altered by
mycoplasmas.  Infection severely distorts or ablates ciliary
structures, interfering with mucociliary clearance mechanisms.  

Unilateral or bilateral otitis interna occurs because of an
extension of the infection up the eutachian tube into the middle
ear and then to the inner ear.  

The disease is usually slowly progressive, with young animals only
mildly affected but clinical signs becoming more severe in older
animals.  

CLINICAL SIGNS 

Clinical signs are typically not evident until an advanced stage of
disease is reached.  Acute death is usually the result of secondary
bacterial infections.  

The upper respiratory disease, involving the nasal passages and
middle ears, is indicated by sniffling, occasional squinting, rough
hair coat, serous or mucopurulent oculonasal discharge, and
sneezing.  If the inner ear becomes involved, torticollis may
occur.  When rats with labrinthitis are held by the tail in a
vertical position, they typically rotate their bodies rapidly;
whereas rats without inner ear involvement remain rigidly
suspended.  

The bronchopulmonary syndrome, initiated or exacerbated by ammonia,
bacterial infections, or Sendai virus infection, is characterized
by lethargy, rough hair coat, hunched posture, chattering, weight
loss, labored breathing, and eventually death.  Unless the
respiratory infections are complicated by bacteria, the terminal
clinical stages of mycoplasmosis may last weeks or months.  

LESIONS 

Gross: In the earliest stage, pulmonary lesions are limited to
peribroncholar lymphoid hyperplasia, visible only on microcopic
exam.  As the disease progresses, the upper respiratory infection
is characterized by serous to purulent inflammation in affected
tissues.  In murine mycoplasmosis unilateral or bilateral otitis
media is a common finding, often the only gross abnormality.  The
pulmonary lesions in the early stages of the disease are
well-demarcated foci of firm red or gray atelectasis and
consolidation or lymphoid aggregation.  As the disease progresses,
inflammatory debris accumulates in the air passages, resulting in
bulging, mucopurulent areas of bronchiectasis.  The content of
these lumps is viscid to caseous and yellow-gray.  

Histo.: Microscopically, the inflammatory response is characterized
by a lymphocyte and plasma cell infiltrate in the submucosa and
neutrophilic leukocyte response within the lumina of the nasal
cavity, eustachian tubes, middle ears, and tracheobronchial tree. 
A consistent and prominent lesion in the lung is the peribronchial
lymphoid hyperplasia that often becomes quite massive.  Within the
lumina of the bronchi and bronchioles, mucin and neutrophil
exudation increases during the course of the disease to the point
of bronchiectasis.  

DIAGNOSIS 

Diagnosis is based on gross and microscopic lesions and on the
isolation of M.  pulmonis from the nasal pharynx, tympanic bullae,
trachea, uterus, or lungs.  The organism may be carried in the
upper respiratory passages in the absence of clinical disease. 
Culture of M.  pulmonis requires special media enriched with yeast
extract and 10% swine or horse blood.  The plates are incubated at
37 degrees C in an atmosphere of normal or reduced oxygen and
increased humidity.  Mycoplasma pulmonis spp require sterols for
growth.  Mycoplasma arthritidis requires arginine.  In mycoplasma
broth media, moderate to heavy growth is reflected by pH and color
of the broth.  In broth cultures in which the titer is low, a
perceptable pH change may not occur.  Tissue and washing samples
should be placed in broth rather than agar media, since recovery of
the organism is more likely in those samples containing few
mycoplasmas.  Samples from broth cultures are transferred to agar
media when a pH change is readily evident or at 7-10 days if no pH
change occurs.  Mycoplasma colonies are evident in 3-4 days by
observation with 40X stereoscopic microscopy.  

ELISA tests for detecting mycoplasmal infections has eliminated
some of the uncertainty associated with the diagnosis of
mycoplasmosis by cultural means, e.g., culture negatives, but false
positives and cross reactions with other Mycoplasma do occur.  

DIFFERENTIAL DIAGNOSIS 

1.  Streptococcosis-nasal exudate is also present in this disease. 


2.  Sialdacryoadenitis-causes reddish porphyrin deposition around
the nares which can be confused with exudate.  

3.  Water deprivation- same as 2.  

4.  Pseudotuberculosis-lung lesions may mimic each other.  

5.  Sendai-often superimposed on MRM.  Histo.  and serology will
differentiate the two from each other.  

6.  Unknown filamentous bacterium-recently a filamentous bacterium
has been associated with bronchietasis in wild and laboratory rats.

However, the causal relationship of this organism with lesions is
undefined .  This filamentous bacterium has not been successfully
grown on artificial media, and its presence is best verified by
either histology, using the Warthin-Starry Stain, or electron
microscopy.  

Although a definitive diagnosis of MRM is made by isolation of M. 
pulmonis from involved tissues, it is evident that the existence of
other agents must be evaluated to determine if copathogens are
contributory to lesions.  

PREVENTION 

Prevention of murine mycoplasmosis involves placing Mycoplasma-free
rodents into a barrier-sustained facility.  Strict husbandry
standards, exclusion of wild rodents, serologic and postmortem
monitoring, good ventilation, and low population densities in cage
and room contribute to the maintenance of a Mycoplasma-free colony.



Hysterectomy derivation is the only means of establishing an M. 
pulmonis-free breeding colony from a previously infected stock. 
Due to the frequent localization of this microorganism in the
uterus, it is necessary to ensure that neonates taken by
hysterectomy have not been infected in utero.  

Rats used in research animal facilities are obtained from various
commercial and institutional sources.  Accordingly, it is essential
that the mycoplasma status of these sources is known and that the
rats are housed by vendor or in groups with a similar microbial
status.  For assessment of whether a group of rats is M. 
pulmonis-free, the best sites for isolation in animals without
gross lesions are the nasal cavity, middle ear, trachea, and
uterus-oviduct.  

Localized, low level infections with Mycoplasma spp may be more
common than suspected.  Such infections are very difficult to
detect and constitute a continuous source of the organism in a
colony.  

TREATMENT 

Elimination of a mycoplasmal infection from affected rats and mice
is, for all practical purposes, impossible.  Antimicrobials placed
in the drinking water, however, may suppress infection and clinical
signs.  Bacterial culture and sensitivity testing are necessary to
determine the most appropriate choice of antibiotics.  Tetracycline
hydrochloride at 2 to 5 mg/ml given fresh daily for 5 days in
deionized, sweetened drinking water (5% sucrose) often suppresses
clinical signs if rats drink the concentrated solution.  Some
tetracycline solutions at this concentration in tap water form a
scale that blocks the sipper tube.  Lower levels of tetracycline
may have an effect on secondary bacterial complications.  

Sulfamerazine at 0.02% in the drinking water or 1 mg/4 g feed;
tylosin at 66 mg/L (2.5 g/10 gal) for 21 days, and CHPC at 30 mg/kg
BW for 5 days are other treatment suggestions, but the prognosis
for recovery remains poor, and treatment should never be advocated
as a method to eliminate Mycoplasma from a colony.  

Labyrinthitis does not usually respond to treatment, but animals
with pronounced head tilt will often survive for months.  

SIGNIFICANCE TO RESEARCH 

Of all the pathogens occurring in laboratory rats, M.  pulmonis has
had the greatest negative impact on studies.  Long-term studies in
areas of toxicology, carcinogenesis, nutrition, and gerontology, in
particular, are affected.  

Mycoplasma pulmonis and arthritidis may contaminate transmissible
tumors and caution should be exercised to ensue transplanted
tissues are not contaminated.  

ZOONOSIS 

Mycoplasma pulmonis does not affect man, although the organism may
be carried in the human nasal passage.  

           MURINE GENITAL MYCOPLASMOSIS 

OCCURRENCE 

Mycoplasma pulmonis recently has become recognized as an important
pathogen in the female genital tract of rats.  Genial mycoplasmosis
in the male rat has not been well documented.  However, it is known
that experimental inoculation can include an inflammatory response
in the ductus efferens and epididymis.  Moreover, it is known that
M.  pulmonis is capable of adherence to spermatozoa in an in vitro
system.  

ETIOLOGY 

Same as MRM.  

TRANSMISSION 

Same as MRM.  

PATHOGENESIS 

Infection of the oviduct and uterus occurs frequently in rats who
have respiratory mycoplasmosis.  It is unknown whether localization
in the genital tract occurs due to a hematogenous spread or to an
ascending infection of the genital tract.  It has been shown that
subsequent to intravenous inoculation, M.  pulmonis almost
invariably localizes in the female oviduct-uterus.  

CLINICAL SIGNS 

Infertility, embryonic resorptions, and small litters occur.  

LESIONS 

Gross: The genital infection, which may exist independently of the
respiratory infection, is an ascending process that can involve the
entire reproductive tract.  Older females are more often affected. 
The LEW strain is particularly prone to develop gross lesions. 
Metritis, pyometra, and purulent oophoritis and salpingitis
characterize the serious genital infection.  The lesions in the
ovarian bursa include edema and inflammation.  Uterine lesions can
vary from a mild inflammatory change to pyometra.  

Histo.: M.  pulmonis adsorbs to the epithelial cells in the genital
tract in a manner similar to that seen in the respiratory tract. 
Salpingitis occurs most frequently and is characterized by
exudation of neutrophils into the lumen, hyperplasia of oviductal
epithelium, and a lymphoidal response in the submucosa.  

DIAGNOSIS 

Same as MRM.  

DIFFERENTIAL DIAGNOSIS 

1.  Pasteurella pneumotropica- induces similar lesions in the
female rat.  

2.  Neoplasia- caseous lesions in the ovary and oviduct can be
mistaken for neoplasia if microscopy is not done.  

PREVENTION 

Same as MRM.  

TREATMENT 

Same as MRM.  

SIGNIFICANCE TO RESEARCH 

Same as MRM.  

ZOONOSIS 

Same as MRM.  

            MYCOPLASMAL ARTHRITIS 

OCCURRENCE 

This mycoplasma species colonizes the pharynx, middle ears, and
lungs of rats, although few studies have been done to document the
relative frequency of this mycoplasma in rat sources.  Although it
is often considerd to be the principal agent involved in arthritis
in rats, the disease has been rarely reported.  

ETIOLOGY 

Mycoplasma arthritidis.  

PREDISPOSING FACTORS 

It has been suggested that poor cage sanitation and abrasions of
the extemities are involved in entry of the organism to the joints
by hematogenous spread or extension from surrounding tissues. 
Since the organism appears to be of low virulence, the
immunocompetence of the host may be a major factor in the outcome
of infection.  

CLINICAL SIGNS 

Arthritic animals limp and move with difficulty due to pain
associated with the polyarthritis.  Affected joints are hyperemic
and swollen.  Any of the joints in the limbs and vertebrae can be
affected, but the tibiotarsal and radiocarpal joints are most often
involved.  

LESIONS 

Within the respiratory tract, M.  arthritidis colonization is
thought to induce negligible lesions, and it has been shown to
coexist with M.  pulmonis.  

Gross: Incised joints reveal a purulent exudate in both articular
and periarticular tissues.  

Histo.: There is exudation of neutrophils into the synovial spaces,
and lymphocyte and plasma cell infiltration in the synovial
membranes.  Destruction of the articular cartilage occurs
subsequent to the inflammatory response.  

DIAGNOSIS 

Same as MRM.  

DIFFERENTIAL DIAGNOSIS 

Pseudotuberculosis- polyarthritis can occur subsequent to
septicemias associated with other bacteria, particularly C. 
kutscheri.  

TREATMENT 

Same as MRM.  

SIGNIFICANCE TO RESEARCH 

Same as MRM.  

             RICKETTSIAL DISEASES 

             HEMOBARTONELLOSIS 

OCCURRENCE 

The rarity of reported cases would indicate H.  muris is no longer
a significant problem in barrier-maintained colonies.  However,
conventionally maintained colonies may be exposed to infected wild
rats and P.  spinulosa (see "Transmission") and, accordingly, the
disease still is of importance in the laboratory rat.  

ETIOLOGY 

The causative agent of this rickettsial disease is Hemobartonella
muris.  This organism is an extracellular parasite of erythrocytes
and induces inapparent infections that may persist for long
periods.  

TRANSMISSION 

Transmission of H.  muris involves the blood-sucking louse, Polypax
spinulosa.  Transmission can occur during a blood meal or when rats
crush infected lice and are inoculated via pruritis-induced
abrasions.  The organism can also be transmitted inadvertantly with
transplantable tumors and other biological products.  PREDISPOSING
FACTORS 

 PATHOGENESIS 

The ability of the host to restrict the infection to a subclinical
mode rests with the integrity of the retculoendothelial system.  

CLINICAL SIGNS 

H.  muris infections in rats are almost always inapparent unless an
animal is splenectomized or splenic function is otherwise impaired.

Evidence of infection is usually limited to splenomegaly and
laboratory findings of mild parasitemia and reticulocytosis.  

DIAGNOSIS 

Diagnosis of hemobartonellosis is dependent upon identification of
the organism in the peripheral blood of infected animals.  However,
in the latent state, organisms are not seen in peripheral blood. 
The usual method of detection is by splenectomizing rats suspected
of harboring the organism.  In these rats, severe parasitemia with
hemolytic anemia, reticulocytosis and frequently hemoglobinuria and
death occurs within 2 weeks after surgery.  Hemobartonella muris
can be visualized on the surface of erythrocytes in
Romanowsky-stained blood smears as coccoid bodies arranged singly,
in clusters, or chains.  

TREATMENT 

None.  

SIGNIFICANCE TO RESEARCH 

The disease has had a negative impact on investigations of various
types, but principally with those in which the host's immune
competence has been impaired.  

Infection with H.  muris can alter host response to transplantable
tumors, generally making rats more resistant to tumor growth. 
Latent infection causes marked elevation in serum levels of
immunoglobulin.  Infection causes severe alteration in the RE
system.  The phagocytic index of experimentally infected rats is
markedly elevated.  In mice, infected animals show an almost
completely blocked response to interferon induction.  Experimental
plasmodium infection in rats is alterd by coincidental infection
with hemobartonella.  

Concurrent infection with eperythrozoon potentiates the virulence
of ectromelia virus, lymphocytic choriomeningitis virus and mouse
hepatitis virus.  The effect appears to be related to altered
phagocytic activity.  

              FUNGAL DISEASES 

              ASPERGILLOSIS 

OCCURRENCE 

Pulmonary aspergillosis is occasionally observed in rats and mice. 


ETIOLOGY 

Aspergillus sp.  

PREDISPOSING FACTORS 

Immunocompromisation due to stress, debilatation, ammonia,
cortisone treatment, etc.  

CLINICAL SIGNS 

Dyspnea.  

LESIONS 

Gross: Pulmonary lesions consist of miliary granulomas are the
primary lesions.  However, other organs such as liver and kidney
may be affected due to hematogenous spread.  

Histo.: Granulomas contain Langhans giant cells, macrophages,
epitheloid cells, and eosinophils in areas with characteristic
uniformly branched, septate hyphae.  Congestion, microscopic
hemorrhage, and septal thickening occurs in surrounding parenchyma.



DIAGNOSIS 

Aspergillus can be readily isolated or observed in affected lung
tissue with selected histochemical techniques.  Sabouraud's agar
with bacterial inhibitors (CHPC, penicillin, and streptomycin) is
satisfactory for this purpose, but care must be used to avoid
modern media designed for isolation of dermatophytes, since the
cycloheximide used as inhibitor will prevent growth by
"contaminants" such as Aspergillus.  Isolated Aspergillus cultures
should be speciated according to the critieria outlined in the
"Manual of Medical Microbiology" by Austwick, which emphasizes
subculture on Czapek-Dox medium for optimal growth of differential
features useful in speciation.  

Aspergillus is seen quite distinctly in hematoxylin and eosin
stained material, but Gridley's fungus stain or Gomori-Grocott
should be used for careful study.  

DIFFERENTIAL DIAGNOSIS 

Phycomycosis- The Aspergillus species may be differentiated in
tissue from those causing phycomycosis by the more uniform and
smaller hyphae (2.5 um in diamter), regular branching at 45 degree
angles, and prominant septae.  In contrast, phycomycotic fungi in
tissue have thicker hyphae (10-15 um in diameter), irregular
branches, and are nonseptate.  

           PHYCOMYCOTIC ENCEPHALITIS 

OCCURRENCE 

Phycomycotic encephalitis has been reported as a natural disease in
2 to 4 week old rats.  The disease is quite rare.  

ETIOLOGY 

Fungi of the group Phycomycetes, including species of Absidia,
Mucor, Rhizopus, Hyphomyces, Basidiobolus, Entomophora, and
Mortierella.  

PREDISPOSING FACTORS 

The disease has most often been reported in association with
primary conditions lowering resistance , e.g., diabetis mellitus,
cortisone treatment.  

LESIONS 

Gross: Lesions present as purulent, necrotizing foci.  

Histo.: Phycomycotic fungi have thick, irregularly branched,
nonseptate hyphae (10-15 um in diameter) in tissue.  An acute
inflammatory response will be present.  

              DERMATOMYCOSIS 

 OCCURRENCE 

Dermatomycosis is probably more likely to be encountered than deep
mycosis, but is also rare in laboratory rats.  Dermatophytes affect
a wide range of animals.  

ETIOLOGY 

Trichophyton mentagrophytes.  Occasionally, Microsporum.  

TRANSMISSION 

Although clinical infections are uncommon, asymptomatic carriers of
the dermatophyte are not and pose a continuing threat to both
animals and caretakers.  Dermatophytes are transmitted easily by
direct contact with spores on hair coats, bedding, and soil.  

PREDISPOSING FACTORS 

Husbandry, nutritional, and environmental or internal stress
factors that increase exposure or reduce resistance predispose to
dermatophytoses.  Genetic background, overcrowding, heat and
humidity, ectoparasitism, youth, old age, and pregnancy have all
been implicated as predisposing factors.  

CLINICAL SIGNS 

Infected rats can be lesionless carriers or display patchy alopecia
and erythema with scale, papule, or pustule formation.  Lesions are
generally over the back as opposed to mice which have tail lesions.



LESIONS 

Fungal elements are visable within the stratum corneum and hair
follicles.  Ecothrix spore formation in hair shafts can be present.



DIAGNOSIS 

The disease can be diagnosed by examination of skin scrapings
treated with 10% potassium hydroxide, histological sections of skin
prepared with fungal stains (periodic acid Schiff or silver), or
isolation.  Dermatophyte test medium can be used.  

PREVENTION 

Maintenance of high-level husbandry standards, particularly with
the young, aged, pregnant, or otherwise stressed, is a protective
measure.  Cultural screening for dermatophytes, proper adjustment
of temperature and humidity, removal of ectoparasites, culling
carriers, and sterilization of contaminated equipment are other
preventive measures.  

TREATMENT 

Successful treatment of ringworm involves elimination of the
organism, not just the lesions.  In the case of T.  mentagrophytes
infection, treatment is more a textbook exercise than a practical
enterprise.  Topical and systemic antifungal agents are available,
but treatment should be undertaken only after consideration of the
public health significance of the fungus and the probably
ineffective but prolonged therapeutic regimen.  

Topical antifungal creams are applied twice daily for a minimum of
4 weeks.  Griseofulvin is administered at 25 mg/kg BW daily in the
water or feed (0.375 g/lb feed) for 14 days.  Animals may also be
dipped in a mixture of 67 g of 25% tetraethylthiuram monosulfide in
alcohol made to 1 liter in water.  The animals are dipped at 3-week
intervals.  A single local application of 10% polyyvinyl iodine
solution may be effective.  Another reported treatment is 1.5%
griseofulvin in DMSO applied topically SID or BID for 5 to 7 days. 


ZOONOSIS 

Trichophyton mentagrophytes may infect the caretakers before it is
noticed on the animals.  The fungus is highly infectious for man,
particularly children and the infirm.  

               REFERENCES 

Holmes, D.D.  1984: Clinical Laboratory Animal Medicine.  Iowa
State University Press, Ames.  

Baker, H.J., Lindsey, J.R., & Weisbroth, S.H.  1979: The Laboratory
Rat.  Academic Press, New York.  

Fox, J.G., Cohen, B.J., & Loew, F.M.  1984: Laboratory Animal
Medicine.  Academic Press, New York.  

Harkness, J.E., Wagner, J.E.  1983: The Biology and Medicine of
Rabbits & Rodents.  Lea & Febiger, Philadelphia.  

VanHoosier, Jr., G.L.  1977: The Laboratory Rat.  ACLAM.  

 