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Results for “BALB/c mouse model”

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PubMed1993

Antibody responses of BALB/c mice to salivary antigens of hematophagous black flies (Diptera: Simuliidae).

The humoral antibody responses to salivary antigens of Simulium vittatum Zetterstedt were investigated in a BALB/c mouse laboratory model. Production of antisera was stimulated by intraperitoneal immunization with salivary gland extract or by feeding flies directly on depilated mice. Antibody responses in these two groups of mice were compared by western blotting, thus characterizing "true" salivary immunogens present in salivary gland extract. Immunized mice developed IgG, IgM, and IgE antibodies which recognized several salivary gland components, ranging in molecular weight between 26 and 67 kDa. Sera from bitten mice recognized fewer antigens, indicating that some components of the salivary gland extract were poorly immunogenic or absent from the saliva secreted during blood feeding. Antisera raised against S. vittatum also were used to identify cross-reactive immunogens and allergens in salivary gland extracts from other New World simuliids (Simulium argus Williston, S. metallicum Bellardi, and S. ochraceum Walker). SDS-PAGE protein profiles indicated a high degree of similarity between salivary gland extract of S. vittatum and S. argus, and several cross-reacting antigens were identified by western blotting. In contrast, protein profiles of S. ochraceum and S. metallicum differed from the former species, both qualitatively and quantitatively. Antisera demonstrated a low degree of cross-reactivity against salivary gland extract of S. ochraceum, whereas no cross-reactivity was detected against S. metallicum. These observations were confirmed using a monoclonal antibody raised against S. vittatum salivary gland extract (designated SVSG.1.F10), which showed cross-reactivity against S. argus but failed to recognize salivary gland components of either S. ochraceum or S. metallicum.

Animals↗

PubMed2006

Inhibition of phosphoinositide 3-kinase delta attenuates allergic airway inflammation and hyperresponsiveness in murine asthma model.

P110delta phosphoinositide 3-kinase (PI3K) plays a pivotal role in the recruitment and activation of certain inflammatory cells. Recent findings revealed that the activity of p110delta also contributes to allergen-IgE-induced mast cell activation and vascular permeability. We investigated the role of p110delta in allergic airway inflammation and hyperresponsiveness using IC87114, a selective p110delta inhibitor, in a mouse asthma model. BALB/c mice were sensitized with OVA and, upon OVA aerosol challenge, developed airway eosinophilia, mucus hypersecretion, elevation in cytokine and chemokine levels, up-regulation of ICAM-1 and VCAM-1 expression, and airway hyperresponsiveness. Intratracheal administration of IC87114 significantly (P<0.05) attenuated OVA-induced influx into lungs of total leukocytes, eosinophils, neutrophils, and lymphocytes, as well as levels of IL-4, IL-5, IL-13, and RANTES in a dose-dependent manner. IC87114 also significantly (P<0.05) reduced the serum levels of total IgE and OVA-specific IgE and LTC(4) release into the airspace. Histological studies show that IC87114 inhibited OVA-induced lung tissue eosinophilia, airway mucus production, and inflammation score. In addition, IC87114 significantly (P<0.05) suppressed OVA-induced airway hyperresponsiveness to inhaled methacholine. Western blot analyses of whole lung tissue lysates shows that IC87114 markedly attenuated the OVA-induced increase in expression of IL-4, IL-5, IL-13, ICAM-1, VCAM-1, RANTES, and eotaxin. Furthermore, IC87114 treatment markedly attenuated OVA-induced serine phosphorylation of Akt, a downstream effector of PI3K signaling. Taken together, our findings implicate that inhibition of p110delta signaling pathway may have therapeutic potential for the treatment of allergic airway inflammation.

Adenine↗

PubMed1987

Prolonged survival of cultured keratinocyte allografts in the nonimmunosuppressed mouse.

The effect of in vitro culture on the survival of allografts of epidermal keratinocytes has been examined using a mouse model. Female BALB/c tail epidermal cells were cultured from single cell suspensions to form confluent sheets that were grafted onto male CBA recipients using a transplantation technique that ensured separation of donor graft from host skin. Animals were killed at defined intervals, and the status of the grafts determined histologically. Full thickness skin allografts rejected at 13-15 days. Allografts of epidermis (obtained by enzymatic cleavage at the dermoepidermal junction) rejected at 19-20 days. Cultured keratinocyte allografts were not rejected at least within 70 days and had a histological appearance identical to syngeneic controls. The expression of MHC class I and class II determinants and the leukocyte common (Ly5) surface marker on the donor cells before and after culture were examined using indirect immunofluorescence and monoclonal antibodies. These and other cytochemical studies showed that freshly dissociated tail epidermal cells contained 0.3% of cells that expressed membrane-bound ATP-ase activity, Ia antigens, and the Ly5 surface antigen. These are the Langerhans' cells of the epidermis. In culture, these cells decrease so that by day 8 of culture, no such cells can be detected. At confluence, there are no Ia positive cells, but all cells express MHC class I antigens and stain with an antikeratin antibody. The loss of Ia expression on culture correlates with a decreased stimulation of the class II H-2d-restricted T cell clone D7.1 by cultured keratinocytes compared with freshly dispersed epidermal cells. Furthermore, cultured keratinocytes fail to prime allogeneic mice as determined by the survival of whole thickness skin grafts, whereas freshly dispersed cells induce an accelerated rejection. The results suggest that the survival of cultured keratinocyte allografts is due to the elimination of cells expressing Ia antigens and supports the passenger leukocyte theory of graft rejection.

Animals↗

PubMed2006

Compaction of islets is detrimental to transplant outcome in mice.

BACKGROUND: Despite recent progress in clinical islet transplantation, the cumulative world experience remains small. Optimizing protection of islets throughout the isolation, purification, and peritransplant period remains critical to outcome. We herein investigate the potential detrimental impact of maintaining islets in a pelleted state for periods preceding implantation. We hypothesize that periods of islet compaction lead to impairment if islet function in vivo. METHODS: In this study, 250-islet marginal mass transplants were conducted in the BALB/c syngeneic mouse model using islets either preincubated as an islet pellet or suspended in culture during the 30 min immediately preceding transplant. Nonfasting blood glucose, intraperitoneal glucose tolerance test, graft histology, and graft insulin content were all used to monitor graft function up to four weeks posttransplant. RESULTS: Maintaining islets in a compact pellet for 30 min prior to transplantation significantly reduces the proportion of transplant recipients that achieve normoglycemia (from 100% to 38%, P=0.026) and increases the proportion of apoptotic beta-cells. CONCLUSION: Our findings confirm that damage induced by sustained islet compaction results in poor graft outcome in mice. These findings raise concerns relating to potential damage to human islets prior to clinical transplantation, and this will be explored in further studies.

Animals↗

PubMed2001

Failure of Mycoplasma pneumoniae infection to confer protection against Mycoplasma genitalium: observations from a mouse model.

Mycoplasma pneumoniae and M. genitalium are genomically distinct but share antigens that induce some serological cross-reactivity. Therefore, the possibility that M. pneumoniae infection of the human respiratory tract might provide immunity to M. genitalium infection of the genital tract was considered. Because of the difficulty of assessing this proposition in man, it was evaluated experimentally in a mouse model. Female BALB/c mice were susceptible to infection of the vagina with M. pneumoniae, whereas those infected previously in the oropharynx with M. pneumoniae were completely immune to infection of the vagina with this mycoplasma. However, all mice with such a respiratory tract infection were susceptible to infection of the vagina with M. genitalium. The findings suggest that an M. pneumoniae infection of the human respiratory tract is unlikely to influence infection of the genital tract by M. genitalium.

Animals↗

PubMed2005

Nasal exposure to Staphylococcal enterotoxin enhances the development of allergic rhinitis in mice.

BACKGROUND: Staphylococcal enterotoxins (SEs) appear to play a role in the pathogenesis of allergic disease. However, little is known whether the nasal exposure to SE affects the development of allergic rhinitis (AR). OBJECTIVE: We sought to determine the in vivo effect of nasal exposure to SE on the development of AR using mouse model. METHODS: BALB/c mice were intranasally sensitized with Schistosoma mansoni egg antigen (SmEA) in the presence or absence of staphylococcal enterotoxin B (SEB). Control mice were intranasally sensitized with either SEB or SmEA alone. The production of antigen-specific antibodies including IgE, nasal eosinoplilia and cytokines by nasal mononuclear cells was compared among mice that had or had not received SEB treatment. RESULTS: Nasal exposure to SEB enhanced the development of AR in SmEA-sensitized mice, as manifested by SmEA-specific IgE production, nasal eosinophilia, and IL-4 and IL-5 production by nasal mononuclear cells after Ag challenge. This treatment also elicited IFN-gamma production by SmEA-primed cells. In addition, these mice produced SEB-specific IgE whereas mice treated with SEB without SmEA sensitization did not produce SEB-specific IgE or demonstrate nasal eosinophilia. CONCLUSION: These results suggest that the nasal exposure to SEB enhances susceptibility to AR although the exposure to SE solely does not induce AR.

Allergens↗

PubMed1994

The modulation of tumour necrosis factor-alpha, interleukin-1 alpha and glucose levels with GMDP and other analogues of muramyl dipeptide.

Immunomodulatory agent muramyl dipeptide (MDP) and seven of its analogues were tested for ability to counteract the toxic actions of lipopolysaccharide (LPS) in experimental mouse models. Female BALB/c mice were presensitized with Corynebacterium parvum (P. acnes) and given MDP or equimolar doses of one of its analogues after 2 weeks, followed by intravenous challenge with LPS 18 h later. This treatment produced a sharp increase in blood cytokine (TNF-alpha, IL-1 alpha) levels 4 h after LPS administration followed by a decline to control values after 6 h. Four analogues, GMDP, threonylMDP, GMDPBenz and GMDPOBut, were able to reduce the level of cytokines induced with LPS. For most of the analogues, the higher doses reduced the levels of TNF-alpha but slightly increased the concomitant IL-1 alpha levels. GMDP was the most effective compound tested in terms of reduction of TNF-alpha and IL-1 alpha levels, as well as for reduction of the hypoglycaemia caused by the administration of LPS.

Acetylmuramyl-Alanyl-Isoglutamine↗

PubMed2001

Expression analysis of the yersiniabactin receptor gene fyuA and the heme receptor hemR of Yersinia enterocolitica in vitro and in vivo using the reporter genes for green fluorescent protein and luciferase.

The enteropathogenic Yersinia enterocolitica strains have several systems for scavenging iron from their environment. We have studied the expression of the fyuA gene, which encodes the outer membrane receptor for the siderophore yersiniabactin (Ybt), and the hemR gene, which encodes the receptor for heme, using the reporter genes gfp (encoding green fluorescent protein) and luc (encoding firefly luciferase). To study gene expression in vitro as well as in vivo, we have constructed several translational reporter gene fusions to monitor simultaneously expression of fyuA and hemR or expression of one gene by a gfp-luc tandem reporter. Results of the in vitro expression analysis (liquid media) indicated that fyuA and hemR are strongly derepressed under iron starvation conditions, resulting in strong fluorescence and/or luminescence at 27 degrees C. In the in vivo BALB/C mouse infection model, tissue-specific expression of fyuA and hemR reporter fusions was observed. Surprisingly, fyuA and hemR reporter constructs were weakly expressed by yersiniae located in the liver and intestinal lumen, whereas strong expression was found for yersiniae in the peritoneal cavity and moderate expression was found in the spleen. Strikingly, yersiniae carrying fyuA or hemR reporter fusions exhibited threefold-stronger signals when grown in the peritoneal cavity of mice than those growing under iron derepression in vitro. This hyperexpression suggests that besides Fur derepression, additional activators may be involved in the enhanced expression of fyuA and hemR under peritoneal growth conditions. Differential expression of the fyuA and hemR reporter fusions could not be observed, suggesting similar regulation of fyuA and hemR in the mouse infection model.

Animals↗

PubMed1997

Identification of a T-helper cell epitope on the rotavirus VP6 protein.

In this work, we have studied the T-helper (Th)-cell response against rotavirus, in a mouse model. Adult BALB/c mice were inoculated parenterally with porcine rotavirus YM, and the Th-cell response from spleen cells against the virus and two overlapping fragments of the major capsid protein VP6 (VP6(1-192) and VP6(171-397)) were evaluated in vitro. The Th cells recognized the YM virus and the two protein fragments, suggesting that there are at least two Th-cell epitopes on the VP6 molecule. To study the specificity of Th cells against VP6 at the clonal level, we established two Th-cell hybridomas cross-reactive for the VP6 protein of rotavirus strains YM and SA11. Both hybridomas recognized the VP6(171-397) polypeptide, and a synthetic peptide comprising the amino acids 289 to 302 (RLSFQLVRPPNMTP) of YM VP6 in the context of the major histocompatibility complex class II IEd molecule. The Th-cell hybridomas recognized rotavirus VP6 in a highly cross-reactive fashion, since they could be stimulated by eight different strains of rotavirus, including the murine rotavirus EDIM, that represent five G serotypes and at least two subgroups. The amino acid sequence of the VP6 epitope is highly conserved in most group A rotavirus strains sequenced so far. On the other hand, it was found that Th cells specific for the VP6 epitope may constitute an important proportion of the total polyclonal Th-cell response against rotavirus YM in spleen cells. These results demonstrate that VP6 can be a target for highly cross-reactive Th cells.

Animals↗

PubMed1989

A deficiency in chromatin repair, genetic instability, and predisposition to cancer.

This review traces steps leading to malignant neoplastic transformation of rodent and human cells in culture and in vivo. Emphasis is placed on an abnormal response characterized by persistent chromatid damage following irradiation of cells in culture with X-rays or fluorescent light during G2 phase of the cell cycle. Evidence is presented that deficient or unbalanced DNA repair during G2 accounts for the abnormal response. This G2 repair deficiency can be inherited or acquired by normal tissue cells during the process of or following attainment of infinite lifespan. It appears as an early, possibly initiating step in neoplastic transformation. It characterizes all human tumor cells examined irrespective of histopathology or tissue of origin. It has a genetic basis. In an animal model, the BALB/c mouse, this phenotype is associated with genes on chromosomes 1 and 4. It characterizes skin fibroblasts and blood lymphocytes from individuals with genetic or familial conditions predisposing to cancer and can be used to identify clinically normal family members carrying a gene(s) for any one of the three cancer-prone genetic disorders studied to date. Furthermore, it can provide the basis of a test for carriers of genes predisposing to a high risk of cancer. We conclude that the G2 repair deficiency, whether inherited or acquired, is a prerequisite for cancer development and that it accounts for the genetic instability of the cancer cell.

Animals↗

PubMed1992

Inoculated mouse model of Pneumocystis carinii infection.

A transtracheally inoculated mouse model of Pneumocystis carinii has been developed using BALB/c mice. The advantage of this strain of mice include that they are widely available, inexpensive, and were not infected with Pneumocystis before inoculation. Inoculated mice that were not treated had a mean infectivity score of 4.1 compared with inoculated mice treated with the effective anti-Pneumocystis drug combination of trimethoprim plus sulfamethoxazole, which had a mean infectivity score of 0.1, an approximately 4 log difference. The inoculated BALB/c mouse provides a model to serve as a valuable addition to rat models currently used, providing a source of organisms from a different host for cross-species comparisons and for studies of drug efficacy for therapy and prophylaxis. The inoculated mouse is especially cost effective and allows testing of compounds in short supply.

Aminoquinolines↗

PubMed2005

Sand fly specificity of saliva-mediated protective immunity in Leishmania amazonensis-BALB/c mouse model.

Immune response of BALB/c mice to the salivary antigens of sand flies was found to vary with different species used, i.e. Phlebotomus papatasi, Phlebotomus sergenti and Lutzomyia longipalpis. Exposure of mice to bites of these sand flies elicits production of antibodies, which are largely specific to different saliva antigens previously identified as unique to the respective fly species. When immunized intradermally (i.d.) with salivary gland lysates (SGL) of L. longipalpis, BALB/c mice developed partial protective immunity against challenges in the contralateral ears with Leishmania amazonensis plus the gland lysates. Preimmunization of these mice with the lysates from the other two species was ineffective, further indicative of the specificity of saliva-mediated immune response. The partial protective immunity observed is significant, although it is not as dramatic as reported previously in a different sand fly-mouse model. There is a correlation of this immunity with a lower number of mononuclear and polymorphonuclear phagocytes at the site of parasite inoculation. Vector species-specificity of this immunity implies its elicitation by unique saliva antigen-an issue which requires attention when designing saliva-based vaccines against leishmaniasis.

Animals↗

PubMed1989

T cell-dependent induction of antibody against foot-and-mouth disease virus in a mouse model.

Nude and normal BALB/c mice were primed by intravenous inoculation of purified, infectious foot-and-mouth disease virus (FMDV) type A24, strain Cruzeiro. Frequency estimation of antigen-specific antibody-secreting cells (ASC) and Thy 1+ T cells in the spleens of immunized mice identified that the IgM response was similar for both nude and normal mice, whereas substantial numbers of both IgG ASC and Thy 1+ cells were present in normal mice only. In contrast, nude and normal mouse sera both contained IgG although the nude mouse serum was deficient in IgG1. Antigen-specific antibody could not be induced in spleen cell cultures from C57BL/6 mice after depletion of T cells with monoclonal antibody plus complement. However, the antibody response could be reconstituted if either a source of exogenous lymphokines or T cells from primed but not unprimed mice were added. Similarly, polyclonal stimulation or unprimed T cells could restore the in vitro response and thus complemented the finding of a low frequency of helper T cells in unprimed mice. Taken together, these data identify that the induction of IgG in FMDV-immunized mice is T cell-dependent and regulated by lymphokines. Furthermore, in nude mice a site other than the spleen must be responsible for the synthesis of the observed serum IgG.

Animals↗

PubMed2000

Chemokine expression by central nervous system resident cells and infiltrating neutrophils during experimental autoimmune encephalomyelitis in the BALB/c mouse.

The active role of chemokines in the central nervous system (CNS) during the pathogenesis of experimental autoimmune encephalomyelitis (EAE) has been clearly established. In this study the expression pattern of several chemokines and cytokines was elucidated using reverse transcription-PCR and immunohistochemistry in a recently established EAE model of the BALB/c mouse that is characterized by CNS infiltration of polymorphonuclear neutrophils. Elevated mRNA levels of the chemokines MIP-1alpha, MIP-2 and MCP-1 were detected in the CNS of diseased mice, whereas no chemokine expression could be measured in asymptomatic mice. Activated astrocytes were shown to be the main source of MIP-1alpha and MIP-2 before and during cellular CNS infiltration. Among the infiltrating immune cells the neutrophils secreted MIP-1alpha and MCP-1. These results suggest involvement of ordered chemokine expression during the process of neutrophil attraction into the CNS, which may play an important role in the initiation and perpetuation of autoimmune CNS inflammation in the BALB/c mouse. This is the first EAE model to describe CNS expression of the C-X-C chemokine MIP-2, corresponding to an observed neutrophil accumulation in the CNS.

Animals↗

PubMed2004

Chronic Helicobacter pylori infection with Sydney strain 1 and a newly identified mouse-adapted strain (Sydney strain 2000) in C57BL/6 and BALB/c mice.

The mouse model of Helicobacter pylori-induced disease using Sydney strain 1 (SS1) has been used extensively in Helicobacter research. Herein we describe the isolation and characterization of a new mouse-colonizing strain for use in comparative studies. One strain capable of persistent mouse colonization was isolated from a total of 110 clinical isolates and is named here SS2000 (Sydney strain 2000). Genome typing revealed a number of differences between SS1 and SS2000 as well as between them and the respective original clinical isolates. In particular, SS2000 lacked the entire cag pathogenicity island, while SS1 contained all 27 genes of the island. C57BL/6 and BALB/c mice were infected with SS1 or SS2000 or were treated with broth medium (controls). After 6 months host-specific effects were evident, including lower colonization levels in the BALB/c animals. Few pathological differences were observed between SS1- and SS2000-infected animals. However, by 15 months postinfection, SS1-infected C57BL/6 mice had developed more severe gastritis than the SS2000-infected animals. In contrast SS2000-infected BALB/c mice showed increased accumulation of mucosa-associated lymphoid tissue compared to those infected with SS1. This improved comparative model of H. pylori-induced disease allowed dissection of both host and strain effects and thus will prove useful in further studies.

Animals↗

PubMed2005

Short-term administration of 17-beta estradiol to outbred male CD-1 mice induces changes in the immune system, but not in reproductive organs.

The magnitude of an immune response to many foreign and/or self-antigens is known to be gender-dependent and influenced by sex hormones. While the immune consequences of long-term exposure (3 to 5 months) to natural 17-beta estradiol in an inbred mouse model (e.g., C57BL/6, Balb/c) are relatively well-documented, the immunological effects of shorter-term 17-beta estradiol exposure in an outbred mouse model (CD-1) have not been thoroughly evaluated. The male outbred-CD-1 mouse is considered to be less 17-beta estradiol-responsive (in terms of reproductive changes) compared to the inbred mouse. In the present study, CD-1 male mice were dosed with vehicle, or 17-beta estradiol at 2 or 4 micrg/100 g body weight on alternate days over a 7-day period. The immune changes in the developmental organ (thymus) and mature lymphoid organ (spleen) were determined. Thymic organ weight/body weight ratio and thymocyte cellularity decreased with increasing dose of 17-beta estradiol, reaching significance at the 4 microg dose. Although 17-beta estradiol decreased thymocyte numbers, no differences were noted in the relative percentages of major thymocyte subsets (CD4+CD8-, CD4-CD8+, CD4+CD8+, CD4- CD8-) and no evidence of enhanced apoptosis was found. In contrast to the diminished thymocyte numbers, 17-beta estradiol increased splenic lymphocyte cellularity, especially in mice given 4 microg 17-beta estradiol dose. The functionality of splenocytes from mice exposed to 17-beta estradiol was also altered. Supernatants from Con-A activated splenocytes from 17-beta estradiol-treated mice had increased IFN-gamma and decreased IL-4 levels (p < 0.05 at the 4 microg dose). This increase in IFN-gamma in 17-beta estradiol-treated mice was not due to an increase in the relative percentages of T cells, since they were comparable to relative percentages of T cells from oil-treated control mice. In addition, supernatants from cultured splenocytes (both Con A-activated and unstimulated) also had significantly higher levels of nitric oxide activity, especially at the 4 microg 17-beta estradiol dose. These results indicate that short-term 17-beta estradiol treatment in outbred mice, at relatively modest doses (2-4 microg/100 g body weight), altered both thymocytes and splenocytes. These 17-beta estradiol-induced immune changes are compelling, since in these mice, post-17-beta estradiol exposure did not demonstrate robust changes in the male reproductive system (testicular and seminal vesical weights to body weight ratios).

Animals↗

PubMed2003

Airway fibrosis in a mouse model of airway inflammation.

BALB/c mice were sensitized to ovalbumin by systemic injection and then exposed for up to 8 weeks to ovalbumin aerosols in whole body chambers. A pattern of airway inflammation, mucous cell hypertrophy and hyperplasia, and airway remodeling with submucosal fibrosis was observed as lesions evolved over time. Larger conducting airways were removed from the lungs by microdissection. Airway fibrosis was quantified by direct assay for collagen content, which was significantly increased after 4 and 8 weeks of exposure to ovalbumin aerosol. Based upon PCR analysis of mRNA levels in the airways, most of the newly synthesized collagen was Type I. Relaxin, administered by continuous infusion over the second half of a 4-week exposure to ovalbumin, was able to inhibit the accumulation of collagen in the airways of exposed mice. Thus, stimulation of collagen degradation by an activator of collagen breakdown by matrix metalloproteinases appears to be an effective therapeutic strategy in prevention of airway fibrosis in this animal model. Whole body plethysmography of unrestrained mice indicated functional changes in airway reactivity in the lungs of exposed animals occurring in conjunction with the reported structural changes. This result indicates that the ovalbumin-exposed mouse may be a suitable model for examining structure-function relationships in the lungs of animals with a predictable time course of airway inflammation, remodeling, and fibrosis and for testing potential new drugs for treatment of asthma or chronic bronchitis at a mechanistic level.

Aerosols↗

PubMed2002

Beta-lactam modification of the bacteraemic profile and its relationship with mortality in a pneumococcal mouse sepsis model.

A sepsis BALB/c mice model was used to investigate the relationship between mortality and the bacteraemic profile produced by a serotype 6B Streptococcus pneumoniae clinical isolate (MIC/MBC of amoxicillin 4/4 mg/L and of cefotaxime 2/4 mg/L). Animals were treated subcutaneously with doses of amoxicillin or cefotaxime ranging from 6.25 to 50 mg/kg tds for 48 h, starting 1 h after intraperitoneal inoculation (2 x 10(7) cfu/mouse). Blood cultures were carried out daily over 15 days. A survival rate of 100% was obtained with amoxicillin 25 mg/kg and of 60% with cefotaxime 50 mg/kg. A statistically significant (P = 0.012) relationship was found between the maximum cfu/mL in blood and mortality. A maximum log cfu/mL of 6.5 was associated with an 84% probability of death.

Animals↗