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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.


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.


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).


Inbr ?. Snell to Green circa 1937, to W.L. and L.B.Russell c1948.


Inbr. ?. Has about a 3% incidence of true hermaphroditism, which significantly distorts the sex ratio (Eicher et al 1980)


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).


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).


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).


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 Glu60, Ala30, Tyr10 (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).


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)


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).


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, 1966a). Embryonic stem cell lines have been established (Kawase et al, 1994)

Abshire M. K. and Waalkes M. P. (1994) Cadmium-induced oxidative tissue damage in mice: Role of mouse strain and tissue metallothionein levels. Toxic Substances Journal 13, 141-152.

Adinolfi M., Beck S. E., Seller M. J., Fedor T., and McLaren A. (1990) Alpha-fetoprotein levels in different strains of mice during development. Exp. Clin. Immunogenet. 7, 123-128.

Albert S., Wolf P. L., Loud A. V., Pryjma I., Potter R., and Moore W. (1966) Spleen development in mice of high and low leukemic strains. J. Reticuloendothel. Soc. 3, 176-201.

Almeida R. M. A., Correa B., Xavier J. G., Mallozzi M. A. B., Gambale W., and Paula C. R. (1996) Acute effect of aflatoxin B-1 on different inbred mouse strains. Mycopathologia 133, 23-29.

Amsbaugh D. F., Hansen C. T., Prescott B., Stashak P. W., Barthold D. R., and Baker P. J. (1972) Genetic control of the antibody response to type III pneumococcal polysaccharide in mice. I. Evidence that an X-linked gene plays a decisive role in determining responsiveness. J. Exp. Med. 136, 931-949.

Angel C. R., Mahin D. T., Farris R. D., and Woodward K. T. (1967) Heritability of plasma cholinesterase activity in inbred mouse strains. Science 156, 529-530.

Autenrieth I. B., Beer M., Bohn E., Kaufmann S. H. E., and Heesemann J. (1994) Immune responses to Yersinia enterocolitica in susceptible BALB/c and resistant C57BL/6 mice: An essential role for gamma interferon. Infect. Immun. 62, 2590-2599.

Babbini M., Pong S. F., King W. T., and White C. L. (1974) Mobility of mice after amphetamine: effects of strain aggregation and illumination. Pharmacol. Biochem. Behav. 2, 803-809.

Barber R. P., Vaughn J. T., Wimer R. E., and Wimer C. C. (1974) Genetically associated variations in the distribution of dentate granule cell. Synapses upon the pyramidal cell dendrites in mouse hippocampus. J. Comp. Neurol. 156, 417-434.

Barone F. C., Knudsen D. J., Nelson A. H., Feuerstein G. Z., and Willette R. N. (1993) Mouse strain differences in susceptibility to cerebral ischemia are related to cerebral vascular anatomy. Journal of Cerebral Blood Flow and Metabolism 13, 683-692.

Barthold S. W., Beck D. S., Hansen G. M., Terwilliger G. A., and Moody K. D. (1990) Lyme borreliosis in selected strains and ages of laboratory mice. J. Infect. Dis. 162, 133-138.

Beamer W. G., Donahue L. R., Rosen C. J., and Baylink D. J. (1996) Genetic-variability in adult bone-density among inbred strains of mice. Bone 18, 397-403.

Bebo B. F., Lee C. H., Orr E. L., and Linthicum D. S. (1996) Mast cell-derived histamine and tumor-necrosis-factor - differences between SJL/J and BALB/c inbred strains of mice. Immunology and Cell Biology 74, 225-230.

Bellini O., Casazza A. M., and Di Marco A. (1976) Histological and histochemical studies of myocardial lesions in BALB/cCr mice. Lab. Animal Sci. 26, 329-333.

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Updated 9 Apr. 1998
Michael FW Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester, UK

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