scholarly journals EFFECT OF THE LESION DUE TO INFLUENZA VIRUS ON THE RESISTANCE OF MICE TO INHALED PNEUMOCOCCI

1949 ◽  
Vol 89 (1) ◽  
pp. 53-68 ◽  
Author(s):  
Carl G. Harford ◽  
Virginia Leidler ◽  
Mary Hara ◽  
Keyword(s):  
Influenza Virus ◽  
Bacterial Infection ◽  
Viral Pneumonia ◽  
Normal Lung ◽  
Type I ◽  
Apparent Effect ◽  
Secondary Bacterial Infection

1. The normal lung of the mouse possesses the power of reducing markedly its content of Type I pneumococci within 3 hours after inhalation of the organisms in the form of fine droplets. 2. Lungs with fully developed influenza viral pneumonia not only fail to reduce the pulmonary content of pneumococci administered in this manner but, on the contrary, support their growth. 3. After intrabronchial inoculation into mice, influenza virus multiplies rapidly in the lung within 24 hours. 4. Criteria have been established for distinction between true viral lesions of the lung and changes due to the inoculation of diluents as vehicles for the virus. 5. 24 hours after inoculation of virus, there are no macroscopic lesions in the lung and the microscopic changes are due to the diluent. 6. Presence and multiplication of the virus in the lung 24 hours after inoculation have no apparent effect on the power of the lung to reduce rapidly its content of inhaled pneumococci. 7. The effect of the virus in lowering resistance to secondary bacterial infection appears to be due to the presence of the lesion produced by the virus.

scholarly journals Influenza Virus-Induced Glucocorticoids Compromise Innate Host Defense against a Secondary Bacterial Infection

2010 ◽  
Vol 7 (2) ◽  
pp. 103-114 ◽  
Author(s):  
Amanda M. Jamieson ◽  
Shuang Yu ◽  
Charles H. Annicelli ◽  
Ruslan Medzhitov
Keyword(s):  
Influenza Virus ◽  
Bacterial Infection ◽  
Host Defense ◽  
Secondary Bacterial Infection

scholarly journals A Perfect Storm: Increased Colonization and Failure of Vaccination Leads to Severe Secondary Bacterial Infection in Influenza Virus-Infected Obese Mice

mBio ◽  
2017 ◽  
Vol 8 (5) ◽  
Author(s):  
Erik A. Karlsson ◽  
Victoria A. Meliopoulos ◽  
Nicholas C. van de Velde ◽  
Lee-Ann van de Velde ◽  
Beth Mann ◽  
...  
Keyword(s):  
Public Health ◽  
Influenza Virus ◽  
Virus Infection ◽  
Bacterial Infection ◽  
Antibiotic Treatment ◽  
Influenza Virus Infection ◽  
Health Concern ◽  
Obese Mice ◽  
Secondary Bacterial Infection ◽  
Perfect Storm

ABSTRACT Obesity is a risk factor for developing severe disease following influenza virus infection; however, the comorbidity of obesity and secondary bacterial infection, a serious complication of influenza virus infections, is unknown. To fill this gap in knowledge, lean and obese C57BL/6 mice were infected with a nonlethal dose of influenza virus followed by a nonlethal dose of Streptococcus pneumoniae. Strikingly, not only did significantly enhanced death occur in obese coinfected mice compared to lean controls, but also high mortality was seen irrespective of influenza virus strain, bacterial strain, or timing of coinfection. This result was unexpected, given that most influenza virus strains, especially seasonal human A and B viruses, are nonlethal in this model. Both viral and bacterial titers were increased in the upper respiratory tract and lungs of obese animals as early as days 1 and 2 post-bacterial infection, leading to a significant decrease in lung function. This increased bacterial load correlated with extensive cellular damage and upregulation of platelet-activating factor receptor, a host receptor central to pneumococcal invasion. Importantly, while vaccination of obese mice against either influenza virus or pneumococcus failed to confer protection, antibiotic treatment was able to resolve secondary bacterial infection-associated mortality. Overall, secondary bacterial pneumonia could be a widespread, unaddressed public health problem in an increasingly obese population. IMPORTANCE Worldwide obesity rates have continued to increase. Obesity is associated with increased severity of influenza virus infection; however, very little is known about respiratory coinfections in this expanding, high-risk population. Our studies utilized a coinfection model to show that obesity increases mortality from secondary bacterial infection following influenza virus challenge through a “perfect storm” of host factors that lead to excessive viral and bacterial outgrowth. In addition, we found that vaccination of obese mice against either virus or bacteria failed to confer protection against coinfection, but antibiotic treatment did alleviate mortality. Combined, these results represent an understudied and imminent public health concern in a weighty portion of the global population. IMPORTANCE Worldwide obesity rates have continued to increase. Obesity is associated with increased severity of influenza virus infection; however, very little is known about respiratory coinfections in this expanding, high-risk population. Our studies utilized a coinfection model to show that obesity increases mortality from secondary bacterial infection following influenza virus challenge through a “perfect storm” of host factors that lead to excessive viral and bacterial outgrowth. In addition, we found that vaccination of obese mice against either virus or bacteria failed to confer protection against coinfection, but antibiotic treatment did alleviate mortality. Combined, these results represent an understudied and imminent public health concern in a weighty portion of the global population.

scholarly journals Influenza “Trains” the Host for Enhanced Susceptibility to Secondary Bacterial Infection

mBio ◽  
2019 ◽  
Vol 10 (3) ◽  
Author(s):  
Kari Ann Shirey ◽  
Darren J. Perkins ◽  
Wendy Lai ◽  
Wei Zhang ◽  
Lurds R. Fernando ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Bacterial Infection ◽  
Bacterial Infections ◽  
Influenza Virus Infection ◽  
Health Concern ◽  
Type I ◽  
Lung Pathology ◽  
Chemokine Production ◽  
Content Type

ABSTRACT We previously reported that the Toll-like receptor 4 (TLR4) antagonist Eritoran blocks acute lung injury (ALI) therapeutically in mouse and cotton rat models of influenza. However, secondary (2°) bacterial infection following influenza virus infection is associated with excess morbidity and mortality. Wild-type (WT) mice infected with mouse-adapted influenza A/Puerto Rico/8/34 virus (PR8) and, 7 days later, with Streptococcus pneumoniae serotype 3 (Sp3) exhibited significantly enhanced lung pathology and lethality that was reversed by Eritoran therapy after PR8 infection but before Sp3 infection. Cotton rats infected with nonadapted pH1N1 influenza virus and then superinfected with methicillin-resistant Staphylococcus aureus also exhibited increased lung pathology and serum high-mobility-group box 1 (HMGB1) levels, both of which were blunted by Eritoran therapy. In mice, PR8 infection suppressed Sp3-induced CXCL1 and CXCL2 mRNA, reducing neutrophil infiltration and increasing the bacterial burden, all of which were reversed by Eritoran treatment. While beta interferon (IFN-β)-deficient (IFN-β−/−) mice are highly susceptible to PR8, they exhibited delayed death upon Sp3 superinfection, indicating that while IFN-β was protective against influenza, it negatively impacted the host response to Sp3. IFN-β-treated WT macrophages selectively suppressed Sp3-induced CXCL1/CXCL2 transcriptionally, as evidenced by reduced recruitment of RNA polymerase II to the CXCL1 promoter. Thus, influenza establishes a “trained” state of immunosuppression toward 2° bacterial infection, in part through the potent induction of IFN-β and its downstream transcriptional regulation of chemokines, an effect reversed by Eritoran. IMPORTANCE Enhanced susceptibility to 2° bacterial infections following infection with influenza virus is a global health concern that accounts for many hospitalizations and deaths, particularly during pandemics. The complexity of the impaired host immune response during 2° bacterial infection has been widely studied. Both type I IFN and neutrophil dysfunction through decreased chemokine production have been implicated as mechanisms underlying enhanced susceptibility to 2° bacterial infections. Our findings support the conclusion that selective suppression of CXCL1/CXCL2 represents an IFN-β-mediated “training” of the macrophage transcriptional response to TLR2 agonists and that blocking of TLR4 therapeutically with Eritoran after influenza virus infection reverses this suppression by blunting influenza-induced IFN-β.

Herpetic Whitlow of the Hand in Infants

2020 ◽  
Author(s):  
Mohammad M. Al-Qattan ◽  
Nada G. AlQadri ◽  
Ghada AlHayaza
Keyword(s):  
Bacterial Infection ◽  
Case Reports ◽  
Case Series ◽  
Individual Case ◽  
Senior Author ◽  
Secondary Bacterial Infection ◽  
Clinical Appearance ◽  
History Of ◽  
Mode Of Transmission ◽  
Time Of Presentation

Abstract Introduction Herpetic whitlows in infants are rare. Previous authors only reported individual case reports. We present a case series of six infants. Materials and Methods This is a retrospective study of six cases of herpetic whitlows in infants seen by the senior author (MMA) over the past 23 years (1995–2017 inclusive). The following data were collected: age, sex, digit involved in the hand, mode of transmission, time of presentation to the author, clinical appearance, presence of secondary bacterial infection, presence of other lesions outside the hand, method of diagnosis, treatment, and outcome. Results All six infants initially presented with classic multiple vesicles of the digital pulp. In all cases, there was a history of active herpes labialis in the mother. Incision and drainage or deroofing of the vesicles (for diagnostic purposes) resulted in secondary bacterial infection. Conclusion The current report is the first series in the literature on herpetic whitlows in infants. We stress on the mode of transmission (from the mother) and establishing the diagnosis clinically. In these cases, no need for obtaining viral cultures or polymerase chain reaction; and no medications are required. Once the vesicles are disrupted, secondary bacterial infection is frequent and a combination of oral acyclovir and intravenous antibiotics will be required.

PLASMACYTOID DENDRITIC CELLS FUNCTION IN HIV INFECTION

2008 ◽  
Vol 31 (4) ◽  
pp. 13
Author(s):  
Martin Hyrcza ◽  
Mario Ostrowski ◽  
Sandy Der
Keyword(s):  
Dendritic Cells ◽  
Influenza Virus ◽  
Hiv Infection ◽  
Gene Transcription ◽  
Sendai Virus ◽  
Plasmacytoid Dendritic Cells ◽  
Type I Interferons ◽  
Interferon Response ◽  
Type I ◽  
Type I Ifn

Plasmacytoid dendritic cells (pDCs) are innate immune cells able to produce large quantities of type I interferons (IFN) when activated. Human immunodeficiency virus (HIV)-infected patients show generalized immune dysfunction characterized in part by chronic interferon response. In this study we investigated the role of dendritic cells inactivating and maintaining this response. Specifically we compared the IFN geneactivity in pDCs in response to several viruses and TLR agonists. We hypothesized that 1) the pattern of IFN gene transcription would differ in pDCs treated with HIV than with other agents, and 2) that pDCs from patients from different stages of disease would respond differently to the stimulations. To test these hypotheses, we obtained pDCs from 15 HIV-infected and uninfected individuals and treated freshly isolated pDCs with either HIV (BAL strain), influenza virus (A/PR/8/34), Sendai virus (Cantell strain), TLR7 agonist(imiquimod), or TLR9 agonist (CpG-ODN) for 6h. Type I IFN gene transcription was monitored by real time qPCRfor IFNA1, A2, A5, A6, A8,A17, B1, and E1, and cytokine levels were assayed by Cytometric Bead Arrays forTNF?, IL6, IL8, IL10, IL1?, and IL12p70. pDC function as determined by these two assays showed no difference between HIV-infected and uninfected patients or between patients with early or chronic infection. Specifically, HIV did notinduce type I IFN gene expression, whereas influenza virus, Sendai virus and imiquimod did. Similarly, HIV failed to induce any cytokine release from pDCs in contrast to influenza virus, Sendai virus and imiquimod, which stimulatedrelease of TNF?, IL6, or IL8. Together these results suggest that the reaction of pDCs to HIV virus is quantitatively different from the response to agents such as virus, Sendai virus, and imiquimod. In addition, pDCs from HIV-infected persons have responses similar to pDCs from uninfected donors, suggesting, that the DC function may not be affected by HIV infection.

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