scholarly journals Effect of Various Stabilizers on Viability of Lyophilized Pasteurella multocida B:3,4 for Use as Hemorrhagic Septicemia Vaccine

2021 ◽  
Vol 25 (03) ◽  
pp. 567-574
Author(s):  
Sajid Mahmood Sajid
Keyword(s):  
Cell Viability ◽  
Vaccine Strain ◽  
Pasteurella Multocida ◽  
Live Vaccine ◽  
Live Vaccine Strain ◽  
Suitable Temperature ◽  
Effective Stabilizer ◽  
Skimmed Milk ◽  
Subsequent Storage ◽  
Storage Temperatures

Hemorrhagic septicemia (HS) is a devastating disease of cattle and buffaloes. The live aerosol vaccine is the best option to control HS. However, stability and viability of live vaccine is an issue. The present study was conducted to investigate the effect of three extraneous stabilizers trehalose, skimmed milk and lactalbumin on the viability of the live vaccine strain Pasteurella multocida B:3,4. The viability of the strain was evaluated using various concentrations (5, 10, 15 and 20%) of these three stabilizers. Moreover, viability of P. multocida B:3,4 was also determined at four different storage temperatures (-20, 4, 25 and 37°C). The duration of lyophilization cycle was also standardized for highest survival of cells. The data showed that trehalose and lactalbumin ensued percentage of viability as 91.89±0.08 and 80.38±2.57 respectively. Skimmed milk as stabilizer did not prove to defend cells during lyophiliztion and subsequent storage and exhibited cell viability approximately 0.47±0.009%. The study indicated that most effective stabilizer for lyophiliztion of P. multocida B:3,4 was trehalose at 15% concentration and was most suitable temperature for storage of lyophilized P. multocida B:3,4. © 2021 Friends Science Publishers

Differentiation of Field Isolates of Pasteurella multocida Serotype 3,4 from Live Vaccine Strain by Genotypic Characterization

1990 ◽  
Vol 34 (2) ◽  
pp. 419 ◽  
Author(s):  
Kurt P. Snipes ◽  
Dwight C. Hirsh ◽  
Rick W. Kasten ◽  
Tim E. Carpenter ◽  
David W. Hird ◽  
...  
Keyword(s):  
Vaccine Strain ◽  
Pasteurella Multocida ◽  
Live Vaccine ◽  
Live Vaccine Strain ◽  
Field Isolates ◽  
Genotypic Characterization

scholarly journals TolC-Dependent Modulation of Host Cell Death by the Francisella tularensis Live Vaccine Strain

2014 ◽  
Vol 82 (5) ◽  
pp. 2068-2078 ◽  
Author(s):  
Christopher R. Doyle ◽  
Ji-An Pan ◽  
Patricio Mena ◽  
Wei-Xing Zong ◽  
David G. Thanassi
Keyword(s):  
Cell Death ◽  
Immune Responses ◽  
Host Cell ◽  
Francisella Tularensis ◽  
Vaccine Strain ◽  
Live Vaccine ◽  
Live Vaccine Strain ◽  
Type I ◽  
Content Type ◽  
Host Cell Death

ABSTRACTFrancisella tularensisis a facultative intracellular, Gram-negative pathogen and the causative agent of tularemia. We previously identified TolC as a virulence factor of theF. tularensislive vaccine strain (LVS) and demonstrated that a ΔtolCmutant exhibits increased cytotoxicity toward host cells and elicits increased proinflammatory responses compared to those of the wild-type (WT) strain. TolC is the outer membrane channel component used by the type I secretion pathway to export toxins and other bacterial virulence factors. Here, we show that the LVS delays activation of the intrinsic apoptotic pathway in a TolC-dependent manner, both during infection of primary macrophages and during organ colonization in mice. The TolC-dependent delay in host cell death is required forF. tularensisto preserve its intracellular replicative niche. We demonstrate that TolC-mediated inhibition of apoptosis is an active process and not due to defects in the structural integrity of the ΔtolCmutant. These findings support a model wherein the immunomodulatory capacity ofF. tularensisrelies, at least in part, on TolC-secreted effectors. Finally, mice vaccinated with the ΔtolCLVS are protected from lethal challenge and clear challenge doses faster than WT-vaccinated mice, demonstrating that the altered host responses to primary infection with the ΔtolCmutant led to altered adaptive immune responses. Taken together, our data demonstrate that TolC is required for temporal modulation of host cell death during infection byF. tularensisand highlight how shifts in the magnitude and timing of host innate immune responses may lead to dramatic changes in the outcome of infection.

scholarly journals Intranasal Interleukin-12 Treatment for Protection against Respiratory Infection with the Francisella tularensis Live Vaccine Strain

2005 ◽  
Vol 73 (4) ◽  
pp. 2306-2311 ◽  
Author(s):  
Nathalie S. Duckett ◽  
Sofia Olmos ◽  
Douglas M. Durrant ◽  
Dennis W. Metzger
Keyword(s):  
Respiratory Infection ◽  
Francisella Tularensis ◽  
Vaccine Strain ◽  
Live Vaccine ◽  
Interleukin 12 ◽  
Live Vaccine Strain ◽  
Wild Type ◽  
Intranasal Infection ◽  
Ifn Γ

ABSTRACT Francisella tularensis is a gram-negative intracellular bacterium that can induce lethal respiratory infection in humans and rodents. However, little is known about the role of innate or adaptive immunity in protection from respiratory tularemia. In the present study, the role of interleukin-12 (IL-12) in inducing protective immunity in the lungs against intranasal infection of mice with the live vaccine strain (LVS) of F. tularensis was investigated. It was found that gamma interferon (IFN-γ) and IL-12 were strictly required for protection, since mice deficient in IFN-γ, IL-12 p35, or IL-12 p40 all succumbed to LVS doses that were sublethal for wild-type mice. Furthermore, exogenous IL-12 treatment 24 h before intranasal infection with a lethal dose of LVS (10,000 CFU) significantly decreased bacterial loads in the lungs, livers, and spleens of wild-type BALB/c and C57BL/6 mice and allowed the animals to survive infection; such protection was not observed in IFN-γ-deficient mice. The resistance induced by IL-12 to LVS infection was still observed in NK cell-deficient beige mice but not in CD8−/− mice. These results demonstrate that exogenous IL-12 delivered intranasally can prevent respiratory tularemia through a mechanism that is at least partially dependent upon the expression of IFN-γ and CD8 T cells.

scholarly journals O-Antigen-Deficient Francisella tularensis Live Vaccine Strain Mutants Are Ingested via an Aberrant Form of Looping Phagocytosis and Show Altered Kinetics of Intracellular Trafficking in Human Macrophages

2011 ◽  
Vol 80 (3) ◽  
pp. 952-967 ◽  
Author(s):  
Daniel L. Clemens ◽  
Bai-Yu Lee ◽  
Marcus A. Horwitz
Keyword(s):  
Vaccine Strain ◽  
Intracellular Trafficking ◽  
Live Vaccine ◽  
Live Vaccine Strain ◽  
Complement Components ◽  
Content Type ◽  
Human Macrophages ◽  
O Antigen ◽  
Kinetics Of ◽  
Terminal Complement

We examined the uptake and intracellular trafficking ofF. tularensisLive Vaccine Strain (LVS) and LVS with disruptions ofwbtDEFandwbtIgenes essential for synthesis of the O antigen of lipopolysaccharide. Unlike parental bacteria, O-antigen-deficient LVS is efficiently killed by serum with intact complement but not by serum lacking terminal complement components. Opsonization of O-antigen-deficient LVS in serum lacking terminal complement components allows efficient uptake of these live bacteria by macrophages. In the presence of complement, whereas parentalF. tularensisLVS is internalized within spacious pseudopod loops, mutant LVS is internalized within tightly juxtaposed multiple onion-like layers of pseudopodia. Without complement, both parental and mutant LVSs are internalized within spacious pseudopod loops. Thus, molecules other than O antigen are important in triggering dramatic pseudopod extensions and uptake by spacious pseudopod loops. Following uptake, both parental and mutant LVSs enter compartments that show limited staining for the lysosomal membrane glycoprotein CD63 and little fusion with secondary lysosomes. Subsequently, both parental and mutant LVSs lose their CD63 staining. Whereas the majority of parental LVS escapes into the cytosol by 6 h after uptake, mutant LVS shows a marked lag but does escape by 1 day after uptake. Despite the altered kinetics of phagosome escape, both mutant and parental strains grow to high levels within human macrophages. Thus, the O antigen plays a role in the morphology of uptake in the presence of complement and the kinetics of intracellular growth but is not essential for escape, survival, altered membrane trafficking, or intramacrophage growth.

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