Inbred Strains
of Mice: BALB
Albino:
A,b,c. Origin: Stock acquired by H.Bagg in 1913, to MacDowell,
to Snell in 1932 (who added the /c). Now widely distributed and among
the top 2-3 most widely used inbred strains. The strain is particularly
well known for the production of plasmacytomas on injection with mineral
oil. These tumours form the basis for the production of monoclonal antibodies.
Used as a general-purpose strain in many different disciplines. Good breeding
performance and long reproductive life-span. Normally has low mammary
tumour incidence but can be infected with the mammary tumour virus by
fostering to C3H (which carries the virus), and it then gets a high incidence
of mammary tumours.
The history and characteristics of the strain have been reviewed by Potter
(1985). Three major substrains trace back to
before 1940, and are listed separately below. Data on genetic markers
suggest that these substrains have diverged largely through mutation or
residual heterozygosity rather than genetic contamination. Hilgers et
al (1985) have shown that the substrains
differ as a result of mutations at the Raf1 locus (controlling
the expression of alpha-fetoprotein), the Qa2 locus (governing
cell surface antigens), the Gdc1 locus (governing L-glycerol
3-phosphate dehydrogenas activity in the liver) and the PR1 repetative
sequence. There is no evidence for genetic contamination during the early
history of the strain. A fourth substrain, BALB/cWt is also listed as
it has a high incidence of hermaphroditism.
BALB/cHeAn
Inbr ?.To Snell circa 1932, to He circa 1935. Now widely distributed (including
the By, AnN, HeA and AnPt substrains). This substrain is much less aggressive
than the J substrain. Maint. by A, N.
BALB/cJ
Inbr 150 +?.Snell to Jackson Laboratory after 1940. Males of this substrain
are extremely aggressive and will fight if housed together once mature.
The Lac substrain separated in 1952 is non-aggressive. Maintained by J,
Ola (JLac substrain).
BALB/cRl
Inbr ?. Snell to Green circa 1937, to W.L. and L.B.Russell c1948.
BALB/cWt
Inbr. ?. Has about a 3% incidence of true hermaphroditism, which significantly
distorts the sex ratio (
Eicher et al 1980)
Behaviour
High intrastrain aggression (4/14), low open-field activity (12/14), high
tail rattling but low social grooming (14/14) during aggressive encounters
(
Southwick and Clark, 1966,1968). Low
open-field activity (13/15) (
Thompson, 1953).
High spontaneous locomotor activity (7/9) (
Nikulina
et al 1991). Long time of immobility in a forced swimming test (1/9)
(
Nikulina et al 1991). Short latency
to cross barrier in maze (2/7), high urination (2/7) and defaecation (1/7)
in test apparatus (
McClearn et al., 1970.,
1970). Low wheel activity (
Messeri et al.,
1972., 1972). Low avoidance conditionability (9/9) (
Royce,
1972) and low shock avoidance learning in males (6/6) (
Royce et al., 1971., 1971). Poor shock avoidance learning
(7/8) (
Wahlsten, 1973). Low alcohol preference
ratio (4/5) (
McClearn, 1965), (13/18) (
Rodgers, 1966). High social dominance of males
in competition for females (2/6) (
DeFries
and McClearn, 1970). High balsa-wood gnawing activity (14/16) (Fawdington
and Festing 1980). Exhibit hypersecretion of corticosterone and marked
brain catecholamine alterations and disruption of Morris water maze performance
following stressors such as foot-shock. However, performance deficits
were prevented by cross fostering to C57BL/6 foster mothers (
Zaharia et al, 1996).
Life-span and spontaneous disease
Life-span intermediate in both sexes in conventional conditions (12/22
= 539 days in males, 11/22 = 575 days in females) (Storer,
1966). Life-span intermediate in males (7/17 = 509 days) and short
in females (4/17 = 561 days) in SPF fostered conditions (Festing and Blackmore, 1971). Life-span 648 _ 20.6 days
in females and 816 32.4 days in males (Goodrick,
1975). Life-span 20 months in females and 13 months in males. Amyloidosis
40% in males. Reticular neoplasms 23% females and 3% males (Ebbesen,
1971). Primary lung tumours 32% in males, 30% in breeding females
and 14% in virgin females in Scott substrain. Leukaemia 5% (Myers et al., 1970., 1970). Zero incidence of lymphatic
leukaemia. Mammary adenocarcinomas zero in males, 5% in breeding females
and 1% in virgin females (Hoag, 1963). Mammary
tumours 30% at 2 years (3/7) (Bentvelzen
et al., 1970., 1970). Mammary tumours 20% in females at 16.7 months,
but 100% at 7.1 months in BALB/cfC3H (Heston
and Vlahakis, 1971). Mammary tumours 10% at 14 months (Schlom et al., 1973., 1973). Low gross tumour incidence
in males (20/22) (Storer, 1966). Renal tumours
25-48%, mammary tumours 3-13%, reticuloendothelial tumours 11-20%, lung
tumours 10-16%, synoviomas 2-8%, depending on substrain (Sass et al., 1976., 1976). Low incidence of virus-like
particles in chemically induced sarcomas (5/6) (Liebelt
et al., 1970., 1970). Frequency of rhabdomyosarcomas was calculated
to be 2.4/100,000 mice retained as breeders, and 10/14 mice found with
these tumours were of the BALB/cJ substrain (Sundberg et al 1991). Rare
spontaneous myoepitheliomas arising from myoepithelial cells of various
exocrine glands have been observed in the J and ByJ substrains (Sundberg
et al 1991)
Gross tumour incidence in germ-free mice 43%, with lung tumours 21%, angiomas
6%, lymphosarcomas 5% and other tumour types less than 3% each (Smith and Pilgrim, 1971). Pulmonary tumours 26-29% (Heston, 1968).
Left auricular thrombosis occurs in 66% of older breeding females. This
is associated with reduced levels of the prothrombin complex factors such
as factor IX (40% of normal), factor XIII (60% of normal), factor X (50%
of normal) and prothrombin (about 33% of normal). These deficiencies occur
slightly before parturition (Meier and Hoag,
1966). High incidence of epicardial mineralisation (11% in males,
4% in females), which increases slightly with age (Frith et al., 1975., 1975). Heart defects, including cardiac
calcinosis 17-62% (Festing and Blackmore,
1971). Spontaneous myocardial lesions of right ventricle found in
60% of females and 30% of males. These macroscopically visible degenerative
fibrosclerotic lesions may represent a last phase of myocarditis of the
inflammatory type found in apparently normal mice (Bellini et al., 1976., 1976).
Carry a single recessive gene different from that found in C57BL/6J and
WB/ReJ, causing age-related hearing loss (Willott
et al, 1995).
Zero incidence of spontaneous congenital malformations (cf. 2/9) in GrKt-tk
substrain (Kalter, 1968).
Normal physiology and biochemistry
High Na/K ratio in erythrocytes (2/9) (Waymouth,
1973). Low levels of serum ceruloplasmin in males (26/26) (Meier and MacPike, 1968). Low serum haptoglobin level (9/11)
(Peacock et al., 1967., 1967). High systolic
blood pressure (2/19) (Schlager and Weibust,
1967). Low mean heart rate (6/7) but high heart rate adaptation (3/7)
(Blizard and Welty, 1971). Low plasma
cholinesterase activity in females (19/22) (Angel
et al., 1967., 1967). High plasma cholesterol levels (9/11) (Jiao et al 1990). High erythrocyte catalase level (1/18)
(Hoffman and Rechcigl, 1971). Low intra-ocular
pressure (4/4) (John et al, 1997).
High peripheral nerve conduction velocity (1/6) (Hegmann,
1972). High brain L-glutamic acid decarboxylase (GAD) and choline
acetyltransferase and catechol-O-methyltransferase (1/7 in all cases);
low brain acetylcholinesterase (5/7) and monoamine oxidase activity (7/7)(Tunnicliff et al., 1973., 1973). High
brain tyrosine hydroxylase activity (1/5) (Ciranello
et al., 1972., 1972). High brain plasmalogen (1/5) (Sampugna et al., 1975., 1975). High proportion of time
spent sleeping (1/6) with a high percentage of slow-wave sleep (2/6) and
low proportion of paradoxical sleep (6/6) (Valatx
and Bugat, 1974). Short tau DD, the endogenous (free-running) period
of the circadian pacemaker measured in constant environmental darkness
(1/12) (Schwartz and Zimmerman 1990).
High hypoxanthene-guanine phosphoribosyl transferase in the thalamus (1/7)
(Suran 1973). Low N-methylnicotinamide oxidase
activity (5/7 males, 6/7 females) (Huff and
Chaykin, 1967). Low rectal (9/9) and tail (8/9) temperature (Shepard and Habas, 1967). High kidney arylsulphatase activity
(2/12) (Daniel, 1976). Low basal level of serum
prolactin (5/6) (Sinha et al., 1975., 1975).
Low spermatazoal beta-glucuronidase activity (8/9) (Erickson,
1976). Urine has high osmolality (1/7) (Silverstein,
1961). High basal levels of kidney catalase (1/4), and superoxide
dismutase (1/4) but low basal level of kidney glutathione peroxidase (4/4)
and kidney glutathione (4/4) (Misra et al 1991).
High level of alpha-fetoprotein in amniotic fluid and neonatal plasma
(1/6) (Adinolfi et al 1990). Low hepatic
microsomal coumarin hydroxylase activity in males (8/8) (Van Iersel et al, 1994).
Secretory group II phospholipase A2 gene has very high expression in small
intestine (contrast 129/Sv and C57BL/6) (Kennedy
et al, 1995).
Anatomy
Large brain weight (1/18 in both sexes) (
Storer,
1967), (2/25) (
Roderick et al, 1973
, 1973), (1/6) (
Wahlsten et al., 1975.,
1975). Large brain to body weight ratio (2/20). Large spinal cord (5/25)
(
Roderick et al., 1973., 1973). Large
relative kidney weight (2/21) (
Schlager, 1968).
Large forebrain (1/9) and hippocampus (1/9) volume (
Wimer et al., 1969., 1969). Large number of A10 dopaminergic
neurons in midbrain region (1/4) (Bernardini et al 1991). Corpus callosum
absent in 39% of animals (1/6) (
Wahlsten, 1974).
This is associated with slow growth of the medial septum subadjacent to
the cavum septi. See also strains I/LnJ and CXBG (
Wahlsten and Bulman-Fleming, 1994). Absence of corpus callosum
related to retarded formation of the hippocampal commissure in this strain
and in 129/J mice (
Livy and Wahlsten, 1997).
Low bone density of femur (9/11) (
Beamer et
al, 1996).
Anatomy of Ammon's horn (hippocampus and dentate gyrus) different from
that of seven other strains (Barber et al.,
1974., 1974). High erythrocyte count (2/18 J substrain, 5/18 An substrain),
high haematocrit (3/18 J substrain, 5/18 An substrain), high haemoglobin
(1/18 J substrain, 4/18 An substrain) (Russell
et al., 1951., 1951). Large spleen at all ages (3/9 to 1/9) (Albert et al., 1966., 1966). Accessory spleens in about
21% of animals, and number of nipples commonly exceeds five pairs (Hummel et al., 1966., 1966). Occasional (less
than 2%) cases of visceral inversion (Hummel
and Chapman, 1959). Small pituitary (5/6) (Sinha
et al., 1975., 1975). Large proportion of sperm-head abnormalities
(1/5, 44%) (Styrna et al 1991). Low level
of spontaneous sister chromatid exchange (1/4) (Nishi
et al, 1993). Provides a sensitive and reproducible model of focal
and global brain ischemia (Barone et al, 1993).
Drugs
Susceptible to skin ulceration by 7,12-dimethylbenz(a)anthracene (DMBA)
(cf. 13/23) (
Thomas et al., 1973., 1973).
Sensitive to the development of uterine tumours following treatment with
DMBA at 4-weeks of age (cf 3/6) (
Tsubura
et al, 1993). Sensitive to the induction of skin tumours by methylnitrosourea
in methanol (1/4) (
Lijinsky et al 1991).
Susceptible to tumour induction by 3-methylcholanthrene (3/12) (
Whitmire et al., 1971., 1971). Susceptible to induction
of leukaemia (1/6) but resistant (6/6) to induction of liver tumours by
neonatally administered DMBA (
Flaks, 1968). High
incidence of interstitial tumours of testis induced by stilboestrol, high
incidence of haemangioendotheliomas, particularly in interscapular fat
pad and lung in mice treated with O-aminoazotoluene (
Heston,
1963). High incidence of lung tumours after administration of methycholanthrene
by gavage (1/5) (Akamatsu and Barton, 1974). Injection of mineral oil
i.p. induces a high incidence of transplantable plasmacytomas (myelomas).
Bence Jones proteins include kappa and lamda light chains and the two-chain
IgA protein. 60% of tumours are of the IgA type (
Potter,
1972). Susceptibility appears to be mediated by two genes on chromosome
4 (
Potter et al, 1994). Susceptible (2/8)
to daunomycin-induced nephorsis (
Kimura et
al 1993).
Sensitive to X-irradiation (26/27) (Roderick, 1963),
(10/10) (Storer, 1966); low LD50
to X-irradiation (9/9) (Yuhas and Storer, 1969).
Nicotine increases shock avoidance learning (3/9) (Bovet
et al., 1966., 1966). Sensitive to insulin (3/9) (Brown,
1965). Poor ovulatory response to PMS at both 3 IU (6/6) and 7 IU
(5/6), but response increased by exposure to males (Zarrow et al., 1971., 1971). Low locomotor excitation after
treatment with D-amphetamine (6/6) (Babbini
et al., 1974., 1974). Resistant to hyperbaric oxygen (16/18) (Hill et al., 1968., 1968). Insensitive (eosinophil response)
to cortisone acetate (cf. 3/6) (Wragg and Speirs,
1952). Low sensitivity to induction of malformed ribs and vertebrae
by hypoxia on ninth day of gestation (5/5) (Dagg,
1966). Sensitive to chloroform toxicity (cf. 5/10) (Christensen et al., 1963., 1963). Resistant to toxic effects
of isoniazid (1/10) (Taylor, 1976b). Resistant (3/3) to neurotoxic effects
of monocrotophos (Rao et al 1991). High transient
increase in renal lipid peroxidation following treatment with nickel (1/4)
(Misra et al 1991). Resistant to biliary
tract injury following oral dosing with 500 micrograms of the fungal toxin
sporidesmin (3/4), but the injury is much more persistent than in SJL
and was accompanied by periductal fibrosis and occasionally by obliteration
of ducts typical of sclerosing cholangitis (Bhathal
et al 1990). High LD50 following injection of butylated hydroxytoluene
(BHT) (1/4) (Kehrer and DiGiovanni 1990).
High histamine release from peritoneal mast cells induced by compound
48/80, a calcium dependent histamine releaser (1/8) (Toda et al 1989). High histamine release from peritoneal mast
cells induced by Ca2+ ionophore A23187 ( c.f. 7/8, contrast C57BL/6) (Toda et al 1989). Cultured mast cells grow
more slowly and release less histamine and TNF-alpha following anti-DBN
IgE antibody treatment than those of strain SJL (Bebo
et al, 1996). Highly sensitive to the induction of catalepsy by haloperidol
(1/8) associated with midbrain dopamine D2 receptor density levels (Kanes et al, 1993). Resistant to both acute
and chronic cadmium toxicity (contrast NFS) (Abshire
and Waalkes, 1994). However, cadmium can induce hematopoetic and suppress
pulmonary tumours in these mice (Waalkes
and Rehm, 1994). Resistant to weight loss induced by cocaine (1/7)
(Shimosato et al, 1994). Clonidene
induces a strong aggressive behavioural response (1/9) (Nikulina and Klimek, 1993). More resistant to acute toxic
effects of aflatoxin B-1 than C57BL/6 (Almeida
et al, 1996).
The IgE response following topical application has been used to predict
which chemicals may have the potential to cause sensitization of the respiratory
tract (Hilton et al, 1996). More susceptible
to the development of micronuclei than C57BL/6 or DBA/2 following treatment
with clastogenic base analogues and nucleosides (Sato
et al, 1993). Estrogen does not induce an increase in VLDL and LDL-cholesterol
(like C3H contrast C57BL/6 and C57L)) (Srivastava,
1995).
Immunology
Resistant to experimental allergic encephalomyelitis (EAE) (cf. 7/18) (
Levine and Sowinski, 1973). Resistant to
EAE (9/10) with short duration (10/10) but moderate mortality (
Lindsey,
1996). High lymphocyte phytohaemagglutinin response (14/43) (
Heiniger et al., 1975., 1975). Good immune response to
type III pneumococcal polysaccharide (1/5) (
Braley
and Freeman, 1971). Good splenic PFC immune response to pneumococcal
polysaccharide (1/9) (
Amsbaugh et al., 1972.,
1972). Poor primary immune response to bacteriophage fd (7/7 in Str substrain,
5/7 in Ho substrain) (Kolsch
et al., 1971). Poor immune response
to synthetic double-stranded RNA (7/7) (
Steinberg
et al., 1971., 1971). Responder to synthetic polypeptide (cf. 3/7)
(
Pinchuck and Maurer, 1965) and Glu
60,
Ala
30, Tyr
10 (2/10) (
Dorf
et al., 1974., 1974). Very good immune response to cholera A and B
antigens (1/9) (
Cerny et al., 1971., 1971).
Good immune response to dextran -1,3-glucosyl linkages (cf. 4/10) (
Blomberg et al., 1972., 1972). Good primary
immune haemolysin and haemagglutinin response (1/6 at various dose levels)
(
Ghaffar and James, 1973). Poor immune
response to
Salmonella anatum and
S. senftenberg lipopolysaccharide
(5/5) (
Di Pauli, 1972). Good immune response to
Vi antigen (1/5) (
Gaines et al., 1965.,
1965). Precipitating and skin-sensitising antibodies have fast electrophoretic
mobility (1/6) (
Fahey, 1965). Non-discriminator
between `H' and `L' sheep RBC (cf. 6/18) (
McCarthy
and Dutton, 1975). Low anti-DNP antibody concentration (6/7) (
Paul et al., 1970., 1970). Poor immune response to
Salmonella
strasbourg lipopolysac-charide (6/7) (
Di Pauli,
1972). High PHA-stimulated lymphocyte blastogenic response (1/6) (
Hellman and Fowler, 1972). Poor primary
immune response to bacteriophage fd (5/7 and 7/7, depending on substrain)
(
Klsch et al., 1971l., 1971). Erythrocytes
have a low agglutinability (cf. 11/25) (
Rubinstein
et al., 1974., 1974). High responder to dextran (cf. 4/10) (
Blomberg et al., 1972., 1972).
Resistant to induction of experimental autoimmune thyroiditis (cf. 2/5)
(Vladutiu and Rose, 1971a). Resistant (5/5) to induction of autoimmune
prostatisis (contrast C57BL/6) (Keetch et
al, 1994).
Immunization by intraperitoneal injection of fetal human (but not calf)
proteoglycan depleted of chondroitin sulphate together with complete or
incomplete Freund's adjuvent produces progressive polyarthritis and ankylosing
spondylitis. Clinical assessment suggests that affected mice have many
similarities to human rheumatoid arthritis and ankylosing spondylitis.
Eventually, the joints become stiff and deformed. Antibodies against collagen
type II were detected in approximately 25% of arthritic mice, but only
following cartilage degradation. Sublines differed in their response,
but 9 other mouse strains and 5 F1 hybrids were resistant. See Glant et
al (1993) for a review.
Resistant to induction of anaphylactic shock by ovalbumin (cf. 6/13) (Tanioka and Esaki, 1971). Anti-BPO IgE
monoclonal antibody failed to produce potent systemic sensitization sufficient
for provocation of lethal shock in most aged (6 to 10 months) mice (c.f.
5/8) (Harada et al 1991). Low immunological
response to Salmonella typhi porins (4/4) (Gonzales et al, 1995).
Resistant to immunosuppression of contact hypersensitivity by ultraviolet
B light (cf 4/18) (Noonan and Hoffman, 1994).
Low neutrophil response to thioglycolate broth and killed bacteria (contrast
C57BL/10) (Marley et al, 1994). Pristance
induces immune complex glomerulonephritis in association with autoantibodies
typical of lupus erythematosus, though the strain is not normally considered
to be susceptible to the disease (Satoh et
al, 1995).
The IgE response following topical application has been used to predict
which chemicals may have the potential to cause sensitization of the respiratory
tract (Hilton et al, 1996). Diminished
expression of neutral glycosphingolipid GgOse(4)Cer in concanavalin A
stimulated T lymphoblasts (cf 3/6) (Muthing, 1997).
Infection
Highly susceptible to infection by
Salmonella typhimurium strain
C5 (1/7) (
Plant and Glynn, 1974), (2/5)
(
Robson and Vas, 1972). Relatively resistant
to a natural intestinal helminth infection (1/10), (
Eaton,
1972). High susceptibility to BALB/Tennant leukaemia virus (1/12)
(
Tennant, 1965). Transmission of murine leukaemia
virus (Scripps) through three successive generations 100% (cf. 2/5) (
Jenson et al., 1976., 1976). Highly susceptible
to development of leukaemia on infection with Friend virus (cf. 5/11)
(
Dietz and Rich, 1972). Susceptible to
Mycobacterium marinum (3/9) and good plateau harvest of M.
leprae
8 months after infection (2/9) (
Shepard
and Habas, 1967). Susceptible to infection with
Mycobacterium
paratuberculosis, and develops a chronic infection (
Chiodini and Buergelt, 1993). Susceptible to infection
with
Mycobacterium avium, but resistance is enhanced by Freund's
incomplete adjuvent (
Castro et al, 1993).
Susceptible to infection with
Yersinia enterocolitica associate
with a poor interferon gamma response (contrast C57BL/6) (
Autenrieth et al, 1994). Susceptible to the induction of
chronic pyelonephritis with
Escherichia coli after introduction
of the bacteria by the ascending route (
Gupta
et al, 1995). Relatively resistant to infection with
Helicobacter
felis (contrast C57BL/6) (
Mohammadi
et al, 1996). Resistant to infection by
Helicobacter felis
with only mild gastritis in the antrum and no atrophy seen over time (cf
CBA, contrast 4 other strains) (
Sakagami
et al, 1996).
Susceptible to mouse hepatitis virus type 3 (cf. 5/14) (Le Prevost et al., 1975., 1975). Resistant to mouse adenovirus
type 1 (contrast C57BL/6) (Guida et al, 1995).
Resistant to induction of diabetes mellitus by encephalomyocarditis virus
(cf. 7/14) (Boucher et al., 1975. See also Hirasawa et al, 1995l, 1995). Resistant to measles
virus induced encephalitis, which correlates with a low cytotoxic T-lymphocyte
response (contrast C3H, C57BL/6) (Niewiesk
et al, 1993).
Highly susceptible to the Leishmania tropica parasite, with the
local disease being uncontrolled and with the development of metastases
and fatal visceralization (Howard et al 1980i0
1980). Supported sustained growth of six strains of Leishmania mexicana
mexicana (contrast C57BL/6) (Monroy-Ostria
et al, 1994). Highly susceptible to Leishmania major, with
the parasites disseminated within 10-24 hrs. from the site of subcutaneous
footpad injection into the popliteal lymph node, spleen, lung, liver and
bone marrow in contrast to resistant C57BL/6, CBA/J and C3H/HeJ (Laskay et al, 1995, Scott et
al, 1996).
Susceptible (1/4) to infection with the helminth worm Angiostrongylus
costaricennsis (Ishii and Sano 1989).
Susceptible (6/7) to the induction of dental caries due to infection with
Streptococcus mutans (Kurihara
et al 1991). Resistant to infection with Pseudomonas aeruginosa
in contrast with susceptible DBA/2 mice (Morissette
et al, 1995). Resistance is associated with a quicker inflamatory
response and earlier initiation of bacterial clearance (Morisette et al,
1996). Develop mycotic mastitis following inoculation of the mammary gland
with Candida krusei isolated from bovine mastitis (Guhad et al, 1995).
Susceptible (1/7) to the development of chronic Chagas' cardiomyopathy
in postacute Trypanosoma cruzi infection (Rowland et al 1992). Susceptible to infection with Trypanosoma
congolense with unrestrained parasite growth to the time of death
about 12 days later (contrast C57BL/6) (Ogunremi
and Tabel, 1995). Resistant to lethal and body weight effects of Toxacaria
canis, but high larval brain levels (1/5) (Epe
et al, 1994). Infection with larval Echinococcus multilocularis
by transportal injection of hyatid homogenate results in a multivesiculation
form of hyatid development (cf 4/9) (Nakaya
et al, 1997).
Susceptible to Streptococcus suis type 2 including the type strain,
two isolates from meningitis in pigs and two isolates from tonsils of
clinically healthy pigs (c.f. 2/5) (Kataoka
et al 1991). Resistant to street rabies virus (SRV) injected via the
intraperitoneal route (Perry and Lodmell 1991).
Following administration of murine cytomegalovirus, BALB/c, BALB.B, and
BALB.K mice develop persistent myocarditis regardless of age at infection,
and age-related cardiopathy is frequent and severe in infected and uninfected
mice (contrast C57BL/10 and C3H) (Price et
al 1991). Susceptible to the lethal effects of murine hepatitis virus
strain 3 (contrast A/J) (Fingerote et al,
1995). The mouse hepatitis virus JHM strain induces a biphasic retinal
disease (Wang et al, 1996). Susceptible
to infection with the tick-born Thogoto virus, with severe symptoms and
death after a few days. The congenic strain carrying the Mx1 gene from
strain A2G is resistant (Haller et al, 1995).
Susceptible to herpes simplex virus-1 (contrast C67BL/6) (Brenner et al, 1994).
Develop carditis on infection with Lyme borreliosis (Borrelia burgdorferi)
(Barthold et al 1990), but develop only
mild arthritis (contrast C3H/HeJ) (Matyniak
and Reiner, 1995). Hepatic amoebiasis can be induced by introducing
Entamoeba histolytica-infected hamster liver tissue in between
the adjacent liver lobes of these mice. (Bhol
et al 1990). Resistant to intra-vaginally innoculated Neisseria
gonorrhoeae (c.f. 5/5) (Johnson et al
1989). Susceptible (2/10) to infection with Ehrlichia risticii
(Williams and Timoney, 1994)
Widely used in study of Plasmodium berghei infections, though
much less sensitive than C57BL/6 (Scheller
et al, 1994). Infection with P. berghei results in high peripheral
blood parasitemia and death within 22-24 days, but without neuological
complication, in contrast with the more susceptible C57BL/6 (Moumaris et al (1995).
Susceptible (1/4) to disseminated Cryptococcus neoformans
(Irokanulo et al, 1995). Nippostrongylus
brasiliensis normally rejected by 14 days postinfection. However,
this pattern of self-cure was not observed in a "putative" BALB/c substrain
from the University of Texas (Mayberry et
al, 1993). Susceptible, with high amylase response to the fungus Paracoccidioides
brasiliensis (cf 6/12) (Xidieh et al,
1994). Susceptible to the protozoan parasite Neospora canium
following subcutaneous inoculation with tachyzoites of the NC-1 strain
(Lindsey et al, 1995). May develop mite-associated ulcerative dermatitis
with an allergic reaction to parasite-derived substances following infection
with Mycoptes musculinus (Jungmann
et al, 1996)
Reproduction
Good breeding performance (8/25). Colony output 1.18 young/female/wk, litter
size at weaning 5.2 (15/25) (Festing, 1976a). Good breeding performance,
mean 3.24 young/female/month (1/24) (
Hansen
et al., 1973., 1973). Intermediate breeding performance (5/8), litter
size 5.1 _ 0.3, sterility 32% (
Nagasawa
et al., 1973., 1973). Low litter size (6/6) (
Verley
et al., 1967., 1967). Low pre-implantation loss of embryos (1/8),
but high post-implantation losses (8/8) (
Leonard
et al., 1971., 1971). Embryos subject to the 2-cell block and only
grow successfully in culture from the late 2-cell stage (
Sekirina and Neganova, 1995).
Miscellaneous
Recommended host for transplantable tumours: melanoma HP and pleomorphic
sarcoma 5180 (although the latter is not host-specific) (Kaliss, 1972).
Low mortality after neonatal thymectomy (2/6) (
Law,
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INBRED STRAINS OF MICE
Updated 9 Apr. 1998
Michael FW
Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester,
UK
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