Journal articles: 'Primary and secondary infections'

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JACKSON, J. A., and R. C. TINSLEY. "Protopolystoma xenopodis (Monogenea) primary and secondary infections in Xenopus laevis." Parasitology 123, no. 5 (November 2001): 455–63. http://dx.doi.org/10.1017/s0031182001008745.

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The reproductive kinetics of Protopolystoma xenopodis primary and secondary infections in Xenopus laevis were monitored in a 3-year study. Thirty-five naïve, lab-raised, full-sib X. laevis from 1 spawning were each exposed to 30 P. xenopodis eggs. The course of infections at 20 °C was monitored by screening isolated hosts for parasite egg production. Ninety-four percent of toads supported the development of gravid parasites. Infections became patent 9–19 weeks p.i., lasted 3–30 months and produced estimated totals of 1–7152 eggs/host. Variation in primary infection characters was discontinuous: a subgrouping of hosts (16%) was characterized by extended infection duration and low reproductive rate. In order to test the effect of long-term infection history on a subsequent challenge, each host was re-exposed to P. xenopodis infective stages (30 eggs/host) 6 months after the loss of its original infection. Establishment of patent infection was significantly lower (15%), and pre-patent period (12–28 weeks) longer, than in primary infections of the same hosts, and than in concurrently exposed naïve controls (contemporary full-sibs of the primary/secondary infection group, maintained in parallel; n = 28). There was no relationship between primary infection characteristics and secondary infection outcome. Overall reproductive output per initial infective stage for the primary exposure exceeded that for the secondary exposure by a ratio of 15[ratio ]1. Results suggest that primary infection with P. xenopodis can elicit strong, long-term protective immunity against re-infection in X. laevis.

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Prince, Harry E., and Jose L. Matud. "Estimation of Dengue Virus IgM Persistence Using Regression Analysis." Clinical and Vaccine Immunology 18, no. 12 (October 26, 2011): 2183–85. http://dx.doi.org/10.1128/cvi.05425-11.

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ABSTRACTDengue virus IgM persistence was estimated using follow-up sera from 98 patients (60 with primary infections and 38 with secondary infections) whose first-specimen IgM index was strongly positive, suggesting recent disease onset. Regression analysis of the follow-up IgM index versus days between samples yielded a trend line that reached the cut-point index (1.10) at 179 days for the primary infection group and 139 days for the secondary infection group. This difference reflected significantly higher first-sample IgM indices in primary infections than in secondary infections rather than differences in IgM decay rates.

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Alghali, Sidit O. "Immunity to tapeworms: acquired resistance toHymenolepis citelliin the mouse." Journal of Helminthology 60, no. 3 (September 1986): 219–33. http://dx.doi.org/10.1017/s0022149x00026146.

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AbstractThe dynamics of secondary infections withHymenolepis citelliin mice are described. A primary infection of one and six cysticercoids for 21 days sensitized CFLP male mice against homologous challenge infections. Acquired resistance was manifested mainly as stunting/destrobilation of secondary worms. The severity of stunting depended on the intensity of the primary infection. Secondary worms were not expelled more rapidly than primary worms but the protective response retards growth early in challenge infections. Sensitization of mice for seven days with six or 24 cysticercoids did not confer a measurable protective response, whereas priming by the same regime for 21 days induced a significant Protective response. Acquired resistance to challenge waned with time in the absence of the primary Worms. The growth and survival of a six-cysticercoid primary infection was enhanced by the administration of the immunosuppressant drug cortisone acetate. Worms from cortisone-treated mice Were heavier than those from untreated controls. Acquired resistance to homologous challenge was also Partially ablated in cortisone-treated mice. It is suggested that rejection of primary infections and stunting/destrobilation of secondary worms may be immunologically mediated.

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Drazin, Doniel, Jens R. Chapman, Andrew Dailey, and John Street. "Introduction. Primary and secondary infections of the spine." Neurosurgical Focus 46, no. 1 (January 2019): E1. http://dx.doi.org/10.3171/2018.10.focus18588.

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Lewis, Ariane, Amol Raheja, and Ian E. McCutcheon. "Introduction. Primary and secondary infections of the brain." Neurosurgical Focus 47, no. 2 (August 2019): E1. http://dx.doi.org/10.3171/2019.5.focus19390.

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Prince, Harry E., Cindy Yeh, and Mary Lapé-Nixon. "Utility of IgM/IgG Ratio and IgG Avidity for Distinguishing Primary and Secondary Dengue Virus Infections Using Sera Collected More than 30 Days after Disease Onset." Clinical and Vaccine Immunology 18, no. 11 (August 31, 2011): 1951–56. http://dx.doi.org/10.1128/cvi.05278-11.

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ABSTRACTDengue virus (DV) IgM/IgG ratio and IgG avidity value (AV) can reliably distinguish between primary and secondary DV infections using sera collected within 30 days of disease onset, but little is known about their efficacies using sera collected >30 days after onset. To investigate this issue, we analyzed specimens submitted to our reference laboratory for DV antibody testing. We first classified patients as having primary (n= 55) or secondary (n= 58) infections based on seroconversion patterns in a comparison of two sera collected <30 days apart. We then evaluated IgM/IgG ratios and IgG AVs of the second specimens by using receiver operating characteristic curve analysis. The IgM/IgG ratio that best discriminated primary from secondary infection was 1.32; 95% of 55 primary infections exhibited ratios of >1.32, whereas 93% of 58 secondary infections exhibited ratios of ≤1.32. The discriminatory AV was 0.39; 95% of 41 primary infections exhibited AVs of ≤0.39, whereas 95% of 38 secondary infections exhibited AVs of >0.39. We then evaluated the IgM/IgG ratios and AV for primary-infection patients whose second serum samples were collected ≥30 days after the first serum samples; only 56% of 27 sera exhibited ratios of >1.32, whereas 81% of 21 sera exhibited AVs of ≤0.39. Assuming that the first specimens were collected within a week after symptoms appeared, these findings indicate that IgG AV is superior to the IgM/IgG ratio for distinguishing primary from secondary DV infections when using samples collected more than 5 weeks after disease onset.

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Stout-Delgado, Heather, Anushree Shirali, Richard Jaramillo, and Kevin Harrod. "Impaired NLRP3 inflammasome activity in elderly hosts contributes to the prevalence of primary and secondary Streptococcus pneumoniae infection. (114.4)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 114.4. http://dx.doi.org/10.4049/jimmunol.188.supp.114.4.

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Abstract Lethal pneumonia has become a serious problem in elderly populations. Although influenza infection alone may lead to pneumonia, secondary bacterial infections, such as Streptococcus pneumoniae, during and shortly after recovery from influenza infections are more common. Previous work has demonstrated that the NLRP3 inflammasome is activated in the lung during influenza viral infection by the M2 ion channel as well as during S. pneumoniae bacterial infection by pneumolysin; however, the impact of aging on inflammasome function during primary or secondary S. pneumoniae infection has not been examined. Here, we show that elderly mice infected with S. pneumoniae alone or shortly after influenza infection produced lower levels of IL-1β and IL-18 during infection when compared to young mice. Further, elderly mice had increased morbidity, decreased cellular infiltration to the lung, and higher bacterial titers in lung during both primary and secondary bacterial infections. Examination of whole lung tissue collected from elderly mice exhibited decreased expression of ASC, NLRP3, TXNIP, and capase-1, but similar expression of pro-IL-1β and pro-IL-18, when compared to young, similarly infected mice during both primary and secondary bacterial infections. Taken together, our study demonstrates that during primary and secondary S. pneumoniae infections, elderly mice have impaired NLRP3 inflammasome activity which may contribute to increased susceptibility for developing pneumonia.

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Waskito, Langgeng A., Paulus B. Notopuro, and Pepy Dwi Endraswari. "ANTIBODY ANTI-DENGUE PROFILE IN DENGUE HEMORRHAGIC FEVER PATIENTS AT DR. SOETOMO HOSPITAL, SURABAYA." Folia Medica Indonesiana 51, no. 3 (November 2, 2016): 173. http://dx.doi.org/10.20473/fmi.v51i3.2830.

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Dengue hemorrhagic fever is one infectious diseases that have high case fatality rate in Indonesia. The aim of this study was to descibe the antibody anti-dengue profile in dengue hemorrhagic fever patients at Dr. Soetomo Hospital Surabaya. This study was epidemiological descriptive study to aims prevalence primary and secondary infection of dengue hemorrhagic fever and its clinical appearances. This study used 85 samples by taking medical record data of IgM and IgG anti-dengue serologic test from Internal Medicine Department, Dr. Soetomo Hospital, Surabaya, between January to December 2010. The data were collected and analyzed in diagrams and tables. Result of this study showed 25 (29,4%) patients had positive IgM serologic test, 14 (16,4%) patients had positive IgG serologic test and 46 (54,2%) patients had positive IgM and IgG serologic test. In primary infections, the history of fever was 3.8±1.2 days; platelet counts 58,6±21,4/ml and bleeding sign 37% of 25 patients. In secondary infections, the history of fever was 4.28±1.15 days; platelet count was 44,17±24,2/ml and bleeding sign 52% of 60 patients. In conclusion, patients with secondary infection have higher prevalence than primary infection. Then in secondary infection had more severe clinical appearance than primary infection.

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Büyüktuna, Seyit Ali, Rabin Saba, Mustafa Gökhan Gözel, Özge Turhan, Dilara İnan, Zahide Aşık, and Adem Köse. "Secondary infections after cytotoxic chemotherapy in patient with hematological malignancies." Journal of Infection in Developing Countries 11, no. 07 (July 31, 2017): 521–26. http://dx.doi.org/10.3855/jidc.8530.

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Introduction: This study was initiated to investigate the risk factors of secondary infections in febrile neutropenic patients following chemotherapy, and to evaluate the clinical, microbiological, and mortality outcomes of these infections. Methodology: An evaluation was done on all patients with hematological malignancy who developed a febrile neutropenic episode (FNE) after cytotoxic chemotherapy in the Department of Hematology, Akdeniz University Faculty of Medicine, between January 2007 and December 2008. Results: A total of 294 primary FNEs that responded to the initial empirical or targeted treatment were included in the study, and secondary infections developed after 72 (24.5%) of 294 primary FNEs. Risk factors for secondary infections were determined as acute leukemia as the underlying disease, salvage chemotherapy for refractory/relapse diseases, prolonged neutropenia (10 days and over), Multinational Association of Supportive Care in Cancer (MASSC) score < 21, and fungal infection during the primary episode. The mortality rate of patients who developed secondary infections was significantly higher compared to patients without secondary infections (27.8% and 5.4%, respectively; p = 0.001). Conclusions: The development of secondary infections in patients with hematological malignancy was not very rare. Greater concern should be shown for these infections to increase patient survival rates.

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Gilligan, Christopher A., and Adam Kleczkowski. "Population dynamics of botanical epidemics involving primary and secondary infection." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 352, no. 1353 (May 29, 1997): 591–608. http://dx.doi.org/10.1098/rstb.1997.0040.

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In this paper we study the dynamical properties of models for botanical epidemics, especially for soil–borne fungal infection. The models develop several new concepts, involving dual sources of infection, host and inoculum dynamics. Epidemics are modelled with respect to the infection status of whole plants and plant organs (the G model) or to lesion density and size (the SW model). The infection can originate in two sources, either from the initial inoculum (primary infection) or by a direct transmission between plant tissue (secondary infection). The first term corresponds to the transmission through the free–living stages of macroparasites or an external source of infection in certain medical models, whereas the second term is equivalent to direct transmission between the hosts in microparasitic infections. The models allow for dynamics of host growth and inoculum decay. We show that the two models for root and lesion dynamics can be derived as special cases of a single generic model. Analytical and numerical methods are used to analyse the behaviour of the models for static, unlimited (exponential) and asymptotically limited host growth with and without secondary infection, and with and without decay of initial inoculum. The models are shown to exhibit a range of epidemic behaviour within single seasons that extends from simple monotonic increase with saturation of the host population, through temporary plateaux as the system switches from primary to secondary infection, to effective elimination of the pathogen by the host outgrowing the fungal infection. For certain conditions, the equilibrium values are shown to depend on initial conditions. These results have important consequences for the control of plant disease. They can be applied beyond soil–borne plant pathogens to mycorrhizal fungi and aerial pathogens while the principles of primary and secondary infection with host and inoculum dynamics may be used to link classical models for both microparasitic and macroparasitic infections.

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Warren, Rachel, William Domm, Min Yee, Andrew Campbell, Jane Malone, Terry Wright, Margot Mayer-Pröschel, and Michael A. O’Reilly. "Ataxia-telangiectasia mutated is required for the development of protective immune memory after influenza A virus infection." American Journal of Physiology-Lung Cellular and Molecular Physiology 317, no. 5 (November 1, 2019): L591—L601. http://dx.doi.org/10.1152/ajplung.00031.2019.

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Ataxia-telangiectasia (A-T), caused by mutations in the A-T mutated ( ATM) gene, is a neurodegenerative disorder affecting ∼1 in 40,000–100,000 children. Recurrent respiratory infections are a common and challenging comorbidity, often leading to the development of bronchiectasis in individuals with A-T. The role of ATM in development of immune memory in response to recurrent respiratory viral infections is not well understood. Here, we infect wild-type (WT) and Atm-null mice with influenza A virus (IAV; HKx31, H3N2) and interrogate the immune memory with secondary infections designed to challenge the B cell memory response with homologous infection (HKx31) and the T cell memory response with heterologous infection (PR8, H1N1). Although Atm-null mice survived primary and secondary infections, they lost more weight than WT mice during secondary infections. This enhanced morbidity to secondary infections was not attributed to failure to effectively clear virus during the primary IAV infection. Instead, Atm-null mice developed persistent peribronchial inflammation, characterized in part by clusters of B220+ B cells. Additionally, levels of select serum antibodies to hemagglutinin-specific IAV were significantly lower in Atm-null than WT mice. These findings reveal that Atm is required to mount a proper memory response to a primary IAV infection, implying that vaccination of children with A-T by itself may not be sufficiently protective against respiratory viral infections.

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Fakae, B. B., L. J. S. Harrison, and M. M. H. Sewell. "The intensity and duration of primary Heligmosomoides polygyrus infection in TO mice modify acquired immunity to secondary challenge." Journal of Helminthology 74, no. 3 (September 2000): 225–31. http://dx.doi.org/10.1017/s0022149x00000329.

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AbstractThe effect of dose and duration of immunizing infections of Heligmosomoides polygyrus on protection against homologous challenge was studied in female TO mice. Primary infections were terminated at various levels with pyrantel embonate (adult infections) or ivermectin (larval infections) and mice were then challenged with 500 infective larvae (L3). The level of protection to secondary challenge positively correlated with the intensity of the primary immunizing infection but truncation of larval infection produced significantly better protection than termination of the adult nematode infection. The duration of the primary larval infection (1–6 days) positively correlated with the level of protection to secondary challenge, antibody responses and the proportion of circulating eosinophils. Histological changes in the gastrointestinal tract, peripheral leucocytic changes and antibody responses of the mice to H. polygyrus adult somatic antigens indicate both a cellular and humoral basis of host immunity to secondary challenge. Although the TO mice are slow responders in that they harbour chronic infections, immunization by intramucosal killing of the larval stage produced strong protection against secondary challenge infection. The presence of dead immunogenic larval stages within the intestinal wall may well be an important factor, since it exposes the host to stage specific antigens at an appropriate location. The implications of the findings for the control of gastrointestinal nematode infections are also discussed.

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Wormley, Floyd L., Joseph Chaiban, and Paul L. Fidel. "Cell Adhesion Molecule and Lymphocyte Activation Marker Expression during Experimental Vaginal Candidiasis." Infection and Immunity 69, no. 8 (August 1, 2001): 5072–79. http://dx.doi.org/10.1128/iai.69.8.5072-5079.2001.

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ABSTRACT Cell-mediated immunity by Th1-type CD4+ T cells is the predominant host defense mechanism against mucosal candidiasis. However, studies using an estrogen-dependent murine model of vaginal candidiasis have demonstrated little to no change in resident vaginal T cells during infection and no systemic T-cell infiltration despite the presence of Candida-specific systemic Th1-type responses in infected mice. The present study was designed to further investigate these observations by characterizing T-cell activation and cell adhesion molecule expression during primary and secondary C. albicans vaginal infections. While flow cytometry analysis of activation markers showed some evidence for activation of CD3+ draining lymph node and/or vaginal lymphocytes during both primary and secondary vaginal Candida infection, CD3+ cells expressing the homing receptors and integrins α4β7, αM290β7, and α4β1 in draining lymph nodes of mice with primary and secondary infections were reduced compared to results for uninfected mice. At the local level, few vaginal lymphocytes expressed integrins, with only minor changes observed during both primary and secondary infections. On the other hand, immunohistochemical analysis of vaginal cell adhesion molecule expression showed increases in mucosal addressin cell adhesion molecule 1 and vascular cell adhesion molecule 1 expression during both primary and secondary infections. Altogether, these data suggest that although the vaginal tissue is permissive to cellular infiltration during a vaginal Candida infection, the reduced numbers of systemic cells expressing the reciprocal cellular adhesion molecules may preempt cellular infiltration, thereby limitingCandida-specific T-cell responses against infection.

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ANANTAPREECHA, S., S. CHANAMA, A. A-NUEGOONPIPAT, S. NAEMKHUNTHOT, A. SA-NGASANG, P. SAWANPANYALERT, and I. KURANE. "Serological and virological features of dengue fever and dengue haemorrhagic fever in Thailand from 1999 to 2002." Epidemiology and Infection 133, no. 3 (January 14, 2005): 503–7. http://dx.doi.org/10.1017/s0950268804003541.

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Serological and virological features of dengue fever (DF) and dengue haemorrhagic fever (DHF) in Thailand were analysed in 2715 patients from 1999 to 2002. The illness was caused by DEN-1 in 45%, DEN-2 in 32%, DEN-3 in 18% and DEN-4 in 5% of patients. Almost all of the DHF cases caused by DEN-2 and DEN-4 were in secondary infection, while approximately 20% of the DHF cases caused by DEN-1 and DEN-3 were in primary infection. Male[ratio ]female ratio and age distribution were not different among four serotypes in primary and secondary infections. These results indicate that DEN-1 and DEN-3 induce DHF in both primary and secondary infections, and suggest that DEN-2 and DEN-4 in Thailand are less likely to cause DHF in primary infections.

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van Boven, Michiel, Frits R. Mooi, Joop F. P. Schellekens, Hester E. de Melker, and Mirjam Kretzschmar. "Pathogen adaptation under imperfect vaccination: implications for pertussis." Proceedings of the Royal Society B: Biological Sciences 272, no. 1572 (July 6, 2005): 1617–24. http://dx.doi.org/10.1098/rspb.2005.3108.

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Mass vaccination campaigns have drastically reduced the burden of infectious diseases. Unfortunately, in recent years several infectious diseases have re-emerged. Pertussis poses a well-known example. Inspired by pertussis, we study, by means of an epidemic model, the population and evolutionary dynamics of a pathogen population under the pressure of vaccination. A distinction is made between infection in immunologically naive individuals (primary infection) and infection in individuals whose immune system has been primed by vaccination or infection (secondary infection). The results show that (i) vaccination with an imperfect vaccine may not succeed in reducing the infection pressure if the transmissibility of secondary infections is higher than that of primary infections; (ii) pathogen strains that are able to evade the immunity induced by vaccination can only spread if escape mutants incur no or only a modest fitness cost and (iii) the direction of evolution depends crucially on the distribution of the different types of susceptibles in the population. We discuss the implications of these results for the design and use of vaccines that provide temporary immunity.

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Milosevic, Drago, Danijela Ristic, Slobodan Kuzmanovic, and Mira Starovic. "Potato cv. Romano reaction to primary and secondary infection with potato necrotic strain Y virus (PVYNTN)." Pesticidi i fitomedicina 30, no. 1 (2015): 17–24. http://dx.doi.org/10.2298/pif1501017m.

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Primary and secondary infections with PVYNTN were investigated on forty plants of the potato cv. Romano inoculated in a greenhouse in Serbia in 2012 and 2013. PVY isolates were collected from the potato growing region of Cacak and identified by ELISA and RT-PCR methods. The sequence of the Serbian isolate 3D (Acc. No. KJ946936) showed 100% match with seven PVY isolates deposited in GenBank and described as NTN. A significant difference was detected between PVYNTN symptoms exibited on leaves of the cv. Romano under primary and secondary infections. The findings are significant because they are based on symptoms observed, so that it is clear that there are two distinct types of infection: primary and secondary. Symptoms of primary and secondary infection were the same on potato tubers and had the form of necrotic rings.

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Sharma, Vishal, and HarshalS Mandavdhare. "Differentiating primary and secondary dengue infections: Why and how?" Medical Journal of Dr. D.Y. Patil University 9, no. 5 (2016): 594. http://dx.doi.org/10.4103/0975-2870.192145.

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Alsharifi, Mohammed, Arno Müllbacher, and Matthias Regner. "Interferon type I responses in primary and secondary infections." Immunology & Cell Biology 86, no. 3 (January 8, 2008): 239–45. http://dx.doi.org/10.1038/sj.icb.7100159.

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Gomes, Brenda P. F. A., Francisco Montagner, Rogério Castilho Jacinto, Ericka Tavares Pinheiro, Alexandre A. Zaia, Caio Cezar Randi Ferraz, and Francisco J. Souza-Filho. "Gemella morbillorum in primary and secondary/persistent endodontic infections." Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 105, no. 4 (April 2008): 519–25. http://dx.doi.org/10.1016/j.tripleo.2007.10.005.

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Vázquez, S., A. B. Pérez, D. Ruiz, R. Rodríguez, M. Pupo, N. Calzada, L. González, et al. "Serological markers during dengue 3 primary and secondary infections." Journal of Clinical Virology 33, no. 2 (June 2005): 132–37. http://dx.doi.org/10.1016/j.jcv.2004.10.013.

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Gujarati, Tanvi P., and G. Ambika. "Virus antibody dynamics in primary and secondary dengue infections." Journal of Mathematical Biology 69, no. 6-7 (January 4, 2014): 1773–800. http://dx.doi.org/10.1007/s00285-013-0749-4.

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Dioguardi, Mario, Vito Crincoli, Luigi Laino, Mario Alovisi, Diego Sovereto, Lorenzo Lo Muzio, and Giuseppe Troiano. "Prevalence of Bacteria of Genus Actinomyces in Persistent Extraradicular Lesions—Systematic Review." Journal of Clinical Medicine 9, no. 2 (February 7, 2020): 457. http://dx.doi.org/10.3390/jcm9020457.

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Actinomyces are anaerobic, rod-shaped, Gram-positive bacteria. They are associated with persistent extraradicular endodontic infections, with possible involvement of the soft tissues of the maxillofacial district. Many studies reported conflicting data on the presence of bacteria of the genus Actinomyces in endodontic infections. The aim of this systematic review of the literature was to determine the real prevalence of such bacteria in primary and/or secondary endodontic infections and in cases of persistence with extraradicular involvement. This systematic review was performed according to the PRISMA protocol. A search was carried out through the Scopus and PubMed databases of potentially eligible articles through the use of appropriate keywords. The literature research resulted in preliminary 2240 records which, after the elimination of overlaps and the application of inclusion and exclusion criteria, led to the inclusion of 46 articles focusing on three outcomes (primary outcome: number of teeth with the presence of a persistent extraradicular infection in which the presence of Actinomyces was ascertained; secondary outcome: number of teeth with endodontic infection in which the presence of Actinomyces was assessed; tertiary outcome: difference in the prevalence of bacteria of the genus Actinomyces between primary endodontic infections and secondary endodontic infections). Results of the meta-analysis show how bacteria of the genus Actinomyces are present in primary and secondary intraradicular infections and in those with persistence with a prevalence (ratio between teeth with actinomyces and teeth with infection) ranging from 0.091 up to 0.130 depending on the subgroups analyzed.

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Sharker, Yushuf, and Eben Kenah. "Estimating and interpreting secondary attack risk: Binomial considered biased." PLOS Computational Biology 17, no. 1 (January 20, 2021): e1008601. http://dx.doi.org/10.1371/journal.pcbi.1008601.

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The household secondary attack risk (SAR), often called the secondary attack rate or secondary infection risk, is the probability of infectious contact from an infectious household memberAto a given household memberB, where we define infectious contact to be a contact sufficient to infectBif he or she is susceptible. Estimation of the SAR is an important part of understanding and controlling the transmission of infectious diseases. In practice, it is most often estimated using binomial models such as logistic regression, which implicitly attribute all secondary infections in a household to the primary case. In the simplest case, the number of secondary infections in a household withmsusceptibles and a single primary case is modeled as a binomial(m,p) random variable wherepis the SAR. Although it has long been understood that transmission within households is not binomial, it is thought that multiple generations of transmission can be neglected safely whenpis small. We use probability generating functions and simulations to show that this is a mistake. The proportion of susceptible household members infected can be substantially larger than the SAR even whenpis small. As a result, binomial estimates of the SAR are biased upward and their confidence intervals have poor coverage probabilities even if adjusted for clustering. Accurate point and interval estimates of the SAR can be obtained using longitudinal chain binomial models or pairwise survival analysis, which account for multiple generations of transmission within households, the ongoing risk of infection from outside the household, and incomplete follow-up. We illustrate the practical implications of these results in an analysis of household surveillance data collected by the Los Angeles County Department of Public Health during the 2009 influenza A (H1N1) pandemic.

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Tang, Biao, Yanni Xiao, Beate Sander, Manisha A. Kulkarni, RADAM-LAC Research Team, and Jianhong Wu. "Modelling the impact of antibody-dependent enhancement on disease severity of Zika virus and dengue virus sequential and co-infection." Royal Society Open Science 7, no. 4 (April 2020): 191749. http://dx.doi.org/10.1098/rsos.191749.

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Human infections with viruses of the genus Flavivirus , including dengue virus (DENV) and Zika virus (ZIKV), are of increasing global importance. Owing to antibody-dependent enhancement (ADE), secondary infection with one Flavivirus following primary infection with another Flavivirus can result in a significantly larger peak viral load with a much higher risk of severe disease. Although several mathematical models have been developed to quantify the virus dynamics in the primary and secondary infections of DENV, little progress has been made regarding secondary infection of DENV after a primary infection of ZIKV, or DENV-ZIKV co-infection. Here, we address this critical gap by developing compartmental models of virus dynamics. We first fitted the models to published data on dengue viral loads of the primary and secondary infections with the observation that the primary infection reaches its peak much more gradually than the secondary infection. We then quantitatively show that ADE is the key factor determining a sharp increase/decrease of viral load near the peak time in the secondary infection. In comparison, our simulations of DENV and ZIKV co-infection (simultaneous rather than sequential) show that ADE has very limited influence on the peak DENV viral load. This indicates pre-existing immunity to ZIKV is the determinant of a high level of ADE effect. Our numerical simulations show that (i) in the absence of ADE effect, a subsequent co-infection is beneficial to the second virus; and (ii) if ADE is feasible, then a subsequent co-infection can induce greater damage to the host with a higher peak viral load and a much earlier peak time for the second virus, and for the second peak for the first virus.

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Arnason, A. N., T. A. Dick, and D. L. Wassom. "A model to assess survival mechanisms of parasites in a genetically defined host system." Parasitology 92, no. 2 (April 1986): 253–67. http://dx.doi.org/10.1017/s0031182000064039.

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SUMMARYWe examined a host system (Peromyscus maniculatus) in which a single autosomal gene controls susceptibility or resistance to infection by the cestode parasite Hymenolepis citelli. Parasite deaths of both primary and secondary (challenge) infections were examined, using a probabilistic model, to see if deaths were random and uncorrelated within each genotype. Within susceptible hosts, post-patent survival of primary worms was not random and heterogeneity was due to among-host effects rather than parasite-age effects, suggesting a second genetic or immunological process. Secondary infections in susceptible hosts appear to be lost randomly, independent of primary infection age or burden. The loss rate is similar to that for primary worms. The lack of correlation or alteration in (susceptible) host response to primary and secondary infections suggests that the latter are eliminated by a process that differs from that acting on primary worms. In resistant hosts, parasite survival rates suggest that the immunological process elicited by the primary infection also acts to eliminate the secondary infection more rapidly. Suggestions are made for improving experimental methods when dealing with mixed genotype populations. Experiments should permit direct estimation of genotype frequency and of parasite death rates within each genotype. This separation of host type is particularly important when studying correlation of successive worm burdens since any host or treatment mixture (genotype, age, sex, size or infection dose) may induce correlations that could be mistakenly interpreted.

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Dernbach, Paul D., Heldo Gomez, and Joseph Hahn. "Primary Closure of Infected Spinal Wounds." Neurosurgery 26, no. 4 (April 1, 1990): 707–9. http://dx.doi.org/10.1227/00006123-199004000-00028.

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Abstract Although postoperative infections of spinal wounds are uncommon, when they occur, they cause considerable morbidity. The classic treatment for deep infected wounds of the spine involves opening the wound, packing it, and permitting secondary closure to occur through granulation. A combined total of 10 patients with infected postoperative spinal wounds (two cervical and eight lumbar) from the Lahey Clinic and the Cleveland Clinic were treated by primary closure. Infection was diagnosed, usually within 2 weeks of operation (average, 10.9 days), by increasing back pain, purulent drainage from the incision, cultures, and subfascial extension of the process. In one patient, an associated disk space infection was observed. Causative organisms were Staphylococcus aureus in five patients and Staphylococcus epidermidis in five patients. At the second operation, the wounds were opened and radically debrided, irrigated, and closed primarily over one or two large drains. Treatment with intravenously administered antibiotics was continued postoperatively; the duration of treatment varied from 10 days to 6 weeks, depending on the presence or absence of involvement of bone or disks. Complete resolution of the infections and primary healing of the wounds occurred in all patients. This technique offers advantages over the traditional technique of secondary wound closure by decreasing the amount of wound care and length of hospitalization and is recommended as the treatment of choice for patients with postoperative spinal wound infections.

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Isaieva, H. O., M. M. Mishyna, Y. A. Mozgova, M. O. Gonchar, O. L. Logvinova, and M. A. Basiuk. "Ability of Microorganisms, Causing Respiratory Infections in Children, to Form Biofilms in vitro." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 6, no. 1 (February 26, 2021): 177–83. http://dx.doi.org/10.26693/jmbs06.01.177.

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The purpose of the study was to detect ability to form biofilms by microorganisms that cause respiratory tract infections. Materials and methods. The study involved 97 strains of microorganisms. Microorganisms were isolated from children with respiratory tract infections. All strains, isolated from patients, were able to form biofilms. There were 44 strains of S. aureus (from patients with pneumonia – 13 strains, from patients with other respiratory diseases – 31), 34 strains of S. pneumoniae (pneumonia – 27 strains, other respiratory diseases – 7), 13 strains of K. pneumoniae (pneumonia – 6 strains, other respiratory diseases – 7), 6 strains of P. aeruginosa (pneumonia – 5 strains, other respiratory diseases – 1). Children were treated at the pulmonary department and intensive care unit in Kharkiv Regional Children's Clinical Hospital. Results and discussion. The optical density of primary biofilms formed by Gram-positive microorganisms was 1.33±0.24 Units of OD, and their secondary biofilms was 0.32±0.10 Units of OD. In patients with pneumonia optical density of primary biofilms of Gram-positive microorganisms was 1.48±0.21 Units of OD and of secondary biofilms was 0.30±0.08 Units of OD. Optical density of primary biofilms of Gram-positive microorganisms in patients with other respiratory infections was 1.18±0.15 Units of OD, of secondary biofilms was 0.35±0.12 Units of OD. The optical density of primary biofilms formed by Gram-negative microorganisms was 2.01±1.03 Units of OD, optical density of secondary biofilms was 1.06±0.42 Units of OD. In patients with pneumonia optical density of primary biofilms of Gram-negative microorganisms was 2.57±0.87 Units of OD, of secondary biofilms was 1.21±0.50 Units of OD. Optical density of primary biofilms of Gram-negative microorganisms in patients with other respiratory infections was 1.24±0.66 Units of OD, of secondary biofilms was 0.84±0.11 Units of OD. Conclusion. Gram-negative microorganisms in general formed more massive biofilms compared with Gram-positive microorganisms. Among all microorganisms P. aeruginosa formed the thickest primary and secondary biofilms. Strains of P. aeruginosa isolated from patients with pneumonia formed the thickest primary and secondary biofilms. Strains of S. aureus isolated from patients with other respiratory infections formed most massive primary biofilms, strains of K. pneumoniae formed the hardest secondary biofilms in this group

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Hutton, D., A. P. Reid, and S. Townson. "Immune responses of the argasid tick Ornithodoros moubata moubata induced by infection with the filarial worm Acanthocheilonema viteae." Journal of Helminthology 74, no. 3 (September 2000): 233–39. http://dx.doi.org/10.1017/s0022149x00000330.

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AbstractInvestigations were undertaken to determine whether the tick Ornithodoros moubatamoubata mounted a detectable immune response to primary and secondary infections with Acanthocheilonema viteae. Uninfected control tick survival rate was 70%, but only 45% in the primary infection group. Post-secondary infection survival rate (82%) was comparable to controls, indicating that these selected ticks had some protective advantage. Mean A. viteae infective larvae recovery from ticks with secondary infections was 31.4% lower than expected, suggesting the development of immunity. SDS–PAGE of haemolymph for proteins induced post-primary infection yielded a stronger signal at 45 kDa than controls, which was further elevated post-secondary infection. Proteins at 48, 22 and 16 to 18 kDa were detected in haemolymph from infected ticks but not seen from controls. The direct effect of haemolymph on microfilarial viability was examined using a novel in vitro assay; in these preliminary trials no differences were observed in parasite viability when exposed to haemolymph from infected or uninfected groups of ticks.

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Falcone, Marco, Alessandro Russo, Federica Iraci, Paolo Carfagna, Paola Goldoni, Vincenzo Vullo, and Mario Venditti. "Risk Factors and Outcomes for Bloodstream Infections Secondary to Clostridium difficile Infection." Antimicrobial Agents and Chemotherapy 60, no. 1 (October 19, 2015): 252–57. http://dx.doi.org/10.1128/aac.01927-15.

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ABSTRACTWe determined the incidence, risk factors, and outcomes of bloodstream infections (BSI) subsequent toClostridium difficileinfection (CDI). We performed a retrospective study of all patients with definite diagnosis of CDI admitted from January 2014 to December 2014 in two large hospitals in Rome. Two groups of patients were analyzed: those with CDI and subsequent BSI (CDI/BSI+) and those with CDI and no evidence of primary BSI (CDI/BSI−). Data about clinical features, microbiology, treatments, and mortality were obtained. Overall, 393 cases of CDI were included in the final analysis: 72 developed a primary nosocomial BSI, while 321 had CDI without microbiological and clinical evidence of BSI. Etiologic agents of BSI wereCandidaspecies (47.3%),Enterobacteriaceae(19.4%), enterococci (13.9%), and mixed infections (19.4%). In multivariate analysis, ribotype 027 status (odds ratio [OR], 6.5), CDI recurrence (OR, 5.5), severe CDI infection (OR, 8.3), and oral vancomycin at >500 mg/day (OR, 3.1) were recognized as factors independently associated with the development of nosocomial BSI. Thirty-day mortality from CDI diagnosis was higher for patients of the CDI/BSI+group than for the controls (38.9 versus 13.1%;P< 0.001). Among patients of the CDI/BSI+group, mortality attributable to primary BSI was as high as 57%. Our findings suggest that severe CDI is complicated by the development of nosocomial BSI.Candidaspecies and enteric bacteria appear to be the leading causative pathogens and are associated with poor outcomes.

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Vaughn, David W., Ananda Nisalak, Siripen Kalayanarooj, Tom Solomon, Nguyen Minh Dung, Andrea Cuzzubbo, and Peter L. Devine. "Evaluation of a Rapid Immunochromatographic Test for Diagnosis of Dengue Virus Infection." Journal of Clinical Microbiology 36, no. 1 (1998): 234–38. http://dx.doi.org/10.1128/jcm.36.1.234-238.1998.

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A rapid (<7-min) immunochromatographic test for immunoglobulin M (IgM) and IgG antibodies to dengue viruses was evaluated by using hospital admission and discharge sera from 124 patients. The reference laboratory diagnosis was based on the results of virus isolation, hemagglutination-inhibition assay (HAI), and enzyme immunoassay (EIA). By the standard assays, patients experienced primary dengue virus infection (n = 30), secondary dengue virus infection (n = 48), Japanese encephalitis (JE) virus infection (n = 20), or no flavivirus infection (n = 26). The rapid test demonstrated 100% sensitivity in the diagnosis of dengue virus infection and was able to distinguish between primary and secondary dengue virus infections through the separate determinations of IgM and IgG. For all patients with primary dengue virus infection a positive test for IgM to dengue virus and a negative test for IgG to dengue virus were obtained, whereas for 46 of 48 patients (96%) with secondary dengue virus infection, a positive test for IgG to dengue virus with or without a positive test for IgM to dengue virus was obtained. The remaining two patients with secondary dengue virus infection had positive IgM test results and negative IgG test results. Furthermore, the rapid test was positive for patients confirmed to be infected with different dengue virus serotypes (12 infected with dengue virus serotype 1, 4 infected with dengue virus serotype 2, 3 infected with dengue virus serotype 3, and 2 infected with dengue virus serotype 4). The specificity of the test for nonflavivirus infections was 88% (3 of 26 positive), while for JE virus infections the specificity of the test was only 50% (10 of 20). However, most patients with secondary dengue virus infection were positive for both IgM and IgG antibodies to dengue virus, while no patients with JE virus infection had this profile, so cross-reactivity was only a concern for a small proportion of patients with secondary dengue infections. The rapid test demonstrated a good correlation with the reference EIA and HAI and should be useful for the rapid diagnosis of dengue virus infections.

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SA-NGASANG, A., S. ANANTAPREECHA, A. A-NUEGOONPIPAT, S. CHANAMA, S. WIBULWATTANAKIJ, K. PATTANAKUL, P. SAWANPANYALERT, and I. KURANE. "Specific IgM and IgG responses in primary and secondary dengue virus infections determined by enzyme-linked immunosorbent assay." Epidemiology and Infection 134, no. 4 (December 22, 2005): 820–25. http://dx.doi.org/10.1017/s0950268805005753.

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IgM- and IgG-capture ELISAs are widely used as diagnostic tests for confirmation of dengue virus infection. The positive rate of anti-dengue IgM and IgG detection was examined in primary and secondary dengue virus infections in the setting of a provincial hospital using IgM- and IgG-capture ELISAs. Disease day 1 was defined as the day of onset of symptoms. In total, 232 plasma samples were collected from 106 confirmed dengue cases consisting of 12 primary and 94 secondary infections. In primary infection, anti-dengue IgM was detected in 4 out of 5 samples collected on disease day 5 and in all the 21 samples collected on disease day 6 or later. Specific IgG was detected in 2 out of 5 samples collected on day 12, and in 5 out of 6 samples collected on disease days 13–15, but was not detected in samples collected on disease day 10 or earlier. In secondary infection, IgM was not detected in the samples on disease days 2 and 3, but detected in 20 out of 79 samples collected on days 4–6, in 44 out of 65 on disease days 7–11 and in 40 out of 51 samples on disease days 12–14. In contrast, specific IgG was detected in 21 out of 60 samples on disease days 4 and 5, in 13 out of 19 on disease day 6, in 62 out of 65 on disease days 7–11 and in all the samples collected on disease day 12 or later. The result indicate that seroconversion rates of IgM and IgG are different between primary and secondary infections, and suggest that detection of specific IgM and IgG is necessary for determining dengue virus infection and for differentiating primary and secondary dengue infections.

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Shaabani, Namir, Nadine Honke, Marco Prinz, Klaus-peter Knobeloch, Dong-Er Zhang, and John R. Teijaro. "The pro-bacterial effect of Type 1 Interferon signaling requires its own negative regulator USP18." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 117.2. http://dx.doi.org/10.4049/jimmunol.200.supp.117.2.

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Abstract Elevated Type 1 interferon (IFN-I) production following bacterial and viral infections has been causally linked with promoting host susceptibility to primary and secondary bacterial infections, some which can result in severe morbidity and Mortality. Using a Listeria monocytogenes (L.m.) model system, we found that among the many Interferon-induced genes (ISGs), USP18 is a central ISG that increases susceptibility to primary and secondary L.m. infection downstream of IFN-I signaling. Knocking out Usp18 specifically in DCs enhanced bacterial control, despite an elevated IFN-I gene signature compared to WT mice. Moreover, Usp18 pro-bacterial effect hinges on the ability of Usp18 to inhibit TNF-α signaling. We extended our findings to demonstrate that Usp18 expression also regulates IFN-I sensitive Staphylococcus aureus infection, suggesting that Usp18 may regulate many IFN-I-sensitive bacterial infections. In summary, we identify a single downstream ISG responsible for promoting primary and secondary bacterial infection – a significant conceptual advance. Targeting host USP18 will have the distinct advantage of exerting less selective pressure on bacterial populations and thus likely attenuate the rate at which resistance develops.

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Bateman, Caroline M., Alison Kesson, Madeleine Powys, Melanie Wong, and Emily Blyth. "Cytomegalovirus Infections in Children with Primary and Secondary Immune Deficiencies." Viruses 13, no. 10 (October 5, 2021): 2001. http://dx.doi.org/10.3390/v13102001.

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Cytomegalovirus (CMV) is a human herpes virus that causes significant morbidity and mortality in immunosuppressed children. CMV primary infection causes a clinically mild disease in healthy children, usually in early childhood; the virus then utilises several mechanisms to establish host latency, which allows for periodic reactivation, particularly when the host is immunocompromised. It is this reactivation that is responsible for the significant morbidity and mortality in immunocompromised children. We review CMV infection in the primary immunodeficient host, including early identification of these infants by newborn screening to allow for CMV infection prevention strategies. Furthermore, clinical CMV is discussed in the context of children treated with secondary immunodeficiency, particularly paediatric cancer patients and children undergoing haematopoietic stem cell transplant (HSCT). Treatments for CMV are highlighted and include CMV immunotherapy.

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Thai, Khoa T. D., Hiroshi Nishiura, Phuong Lan Hoang, Nga Thanh Thi Tran, Giao Trong Phan, Hung Quoc Le, Binh Quang Tran, Nam Van Nguyen, and Peter J. de Vries. "Age-Specificity of Clinical Dengue during Primary and Secondary Infections." PLoS Neglected Tropical Diseases 5, no. 6 (June 21, 2011): e1180. http://dx.doi.org/10.1371/journal.pntd.0001180.

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Ugonna, Kelechi, Konstantinos Douros, Colin D. Bingle, and Mark L. Everard. "Cytokine responses in primary and secondary respiratory syncytial virus infections." Pediatric Research 79, no. 6 (February 16, 2016): 946–50. http://dx.doi.org/10.1038/pr.2016.29.

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St. John, Ashley L., and Abhay P. S. Rathore. "Adaptive immune responses to primary and secondary dengue virus infections." Nature Reviews Immunology 19, no. 4 (January 24, 2019): 218–30. http://dx.doi.org/10.1038/s41577-019-0123-x.

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Waickman, Adam T., Gregory D. Gromowski, Tao Li, Hayden Siegfried, Kaitlin Victor, Caitlin Kuklis, Edgar Davidson, et al. "Transcriptional and clonal characterization of B cell plasmablast diversity following primary and secondary natural DENV infection." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 247.5. http://dx.doi.org/10.4049/jimmunol.204.supp.247.5.

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Abstract Antibody-mediated humoral immunity is thought to play a central role in mediating the immunopathogenesis of acute DENV infection, but limited data are available on the molecular-level diversity, specificity, and functionality of the antibody response elicited by primary or secondary DENV infection. In order to close this functional gap in our understanding of DENV-specific humoral immunity, we utilized high-throughput single cell RNA sequencing to investigate B cells circulating in both primary and secondary natural DENV infections. We captured full-length paired immunoglobulin receptor sequence data from 9,027 B cells from a total of 6 subjects, including 2,717 plasmablasts. Unexpectedly, we found a high proportion of the DENV-elicited plasmablasts expressing IgA, principally in individuals with primary DENV infections. These IgA class-switched cells were extensively hypermutated and appeared to be derived from memory B cells, even in individuals with a serologically confirmed primary DENV infection. Utilizing a combination of conventional proteomics and high-throughput shotgun mutagenesis, we determined that DENV-reactive IgA class-switched antibodies represent a significant fraction of DENV-reactive and DENV-neutralizing Igs generated in response to DENV infection, and that they exhibit a comparable epitope specificity to DENV-reactive IgG antibodies. These results identify a heretofore unappreciated role for DENV-reactive IgA in the humoral response to DENV infection, and may offer insight into the differential pathogenesis associated with primary and secondary DENV infections.

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BLEAY, C., C. P. WILKES, S. PATERSON, and M. E. VINEY. "The effect of infection history on the fitness of the gastrointestinal nematode Strongyloides ratti." Parasitology 136, no. 5 (March 5, 2009): 567–77. http://dx.doi.org/10.1017/s0031182009005617.

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SUMMARYHosts in nature will often acquire infections by different helminth species over their lifetime. This presents the potential for new infections to be affected (particularly via the host immune response) by a host's history of previous con- or hetero-specific infection. Here we have used an experimental rat model to investigate the consequences of a history of primary infection with either Nippostrongylus brasiliensis, Strongyloides venezuelensis or S. ratti on the fitness of, and immunological response to, secondary infections of S. ratti. We found that a history of con-specific, but not hetero-specific, infection reduced the survivorship of S. ratti; the fecundity of S. ratti was not affected by a history of either con- or hetero-specific infections. We also found that a history of con-specific infection promoted Th2-type responses, as shown by increased concentrations of total IgE, S. ratti-specific IgG1, rat mast cell protease II (RMCPII), IL4 (but decreased concentrations of IFNγ) produced by mesenteric lymph node cells in response to S. ratti antigen. Additionally, S. ratti-specific IgG1 was positively related to the intensity of both primary and secondary infections of S. ratti. Hetero-specific primary infections were only observed to affect the concentration of total IgE and RMCPII. The overall conclusion of these experiments is that the major immunological effect acting against an infection is induced by the infection itself and that there is little effect of prior infections of the host.

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Harada, Yuichi, Masamichi Muramatsu, Toshikatsu Shibata, Tasuku Honjo, and Kazumichi Kuroda. "Unmutated Immunoglobulin M Can Protect Mice from Death by Influenza Virus Infection." Journal of Experimental Medicine 197, no. 12 (June 9, 2003): 1779–85. http://dx.doi.org/10.1084/jem.20021457.

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To elucidate the role of class switch recombination (CSR) and somatic hypermutation (SHM) in virus infection, we have investigated the influence of the primary and secondary infections of influenza virus on mice deficient of activation-induced cytidine deaminase (AID), which is absolutely required for CSR and SHM. In the primary infection, AID deficiency caused no significant difference in mortality but did cause difference in morbidity. In the secondary infection with a lethal dose of influenza virus, both AID−/− and AID+/− mice survived completely. However, AID−/− mice could not completely block replication of the virus and their body weights decreased severely whereas AID+/− mice showed almost complete prevention from the reinfection. Depletion of CD8+ T cells by administration of an anti-CD8 monoclonal antibody caused slightly severer body weight loss but did not alter the survival rate of AID−/− mice in secondary infection. These results indicate that unmutated immunoglobulin (Ig)M alone is capable of protecting mice from death upon primary and secondary infections. Because the titers of virus-neutralizing antibodies were comparable between AID−/− and AID+/− mice at the time of the secondary infection, a defect of AID−/− mice in protection of morbidity might be due to the absence of either other Ig classes such as IgG, high affinity antibodies with SHM, or both.

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Finkelman, F. D., K. B. Madden, A. W. Cheever, I. M. Katona, S. C. Morris, M. K. Gately, B. R. Hubbard, W. C. Gause, and J. F. Urban. "Effects of interleukin 12 on immune responses and host protection in mice infected with intestinal nematode parasites." Journal of Experimental Medicine 179, no. 5 (May 1, 1994): 1563–72. http://dx.doi.org/10.1084/jem.179.5.1563.

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The cytokine interleukin (IL) 12 stimulates T cell and natural killer cell production of interferon (IFN) gamma and inhibits T cell production of IL-4. We investigated the effects of IL-12 on cytokine gene expression, immunoglobulin (Ig)E, mucosal mast cell, and eosinophil responses, and the course of infection in mice inoculated with the nematode parasite Nippostrongylus brasiliensis, as well as the IFN-gamma dependence of these effects. IL-12 stimulated IFN-gamma and IL-10 gene expression during primary and secondary N. brasiliensis infections and inhibited IL-3, IL-4, IL-5, and IL-9 gene expression during primary infections but had little inhibitory effect during secondary infections. IL-12 inhibited IgE, mucosal mast cell, and blood and tissue eosinophil responses during primary infections, but only eosinophil responses during secondary infections. IL-12 enhanced adult worm survival and egg production during primary, but not secondary infections. IL-12 needed to be administered by day 4 of a primary infection to inhibit IgE and mucosal mast cell responses, and by day 6 to strongly inhibit eosinophil responses and to enhance worm survival and fecundity. Anti-IFN-gamma mAb inhibited the effects of IL-12 on IgE secretion, intestinal mucosal mastocytosis, and parasite survival and fecundity, but did not affect IL-12 inhibition of eosinophilia. These observations indicate that IL-12, if administered during the initiation of eosinophilia. These observations indicate that IL-12, if administered during the initiation of an immune response, can change the response from one that is characterized by the production of T helper (Th)2-associated cytokines to one characterized by the production of Th-1 associated cytokines. However, IL-12 treatment has less of an effect once the production of Th2-associated cytokines has become established. In addition, our results provide evidence that Th2-associated responses protect against, and/or Th1-associated responses exacerbate, nematode infections.

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Nolz, Jeffrey C., and John T. Harty. "Multiple antigen encounters decrease memory CD8 T cell-mediated protection against chronic viral infection (132.8)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 132.8. http://dx.doi.org/10.4049/jimmunol.182.supp.132.8.

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Abstract While multiple studies demonstrate the enhanced protective capacity of primary memory compared to naive CD8 T cells, much less is known about the function and properties of memory CD8 T cells that have received multiple antigen exposures through either recurring infections or from booster immunizations. Therefore, we analyzed the ability of primary and secondary memory CD8 T cells to protect against a variety of pathogens expressing a common antigen. Our findings demonstrate that secondary memory CD8 T cells provide better per cell protective capacity than primary memory CD8 T cells against acute infections with both LCMV Armstrong and Listeria monocytogenes. In contrast, while primary memory CD8 T cells were able to effectively prevent a chronic infection with LCMV clone 13, an equal number of secondary memory T cells were unable to clear virus and became functionally exhausted. Delayed re-expression of CD62L on the secondary memory CD8 T cell population affected control of LCMV clone 13, as sorted CD62Lhi primary and secondary memory CD8 T cells were equally capable in preventing chronic infection. Overall, these studies demonstrate that multiple antigen encounters impact the ability of memory CD8 T cells to protect against different pathogens, information that should be considered during vaccine design. Supported by NIH (RO1-AI42767 to JTH and T32-AI07343 to JCN)

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Intansari, Umi S., Usi Sukorini, and Shanti Ika Sari. "FCγII (CD32) MONOSIT DI INFEKSI DENGUE PRIMER DAN SEKUNDER {FcγRII (CD32) Monocytes in Primary and Secondary Dengue Infection}." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 22, no. 1 (April 14, 2018): 42. http://dx.doi.org/10.24293/ijcpml.v22i1.1221.

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Dengue infection is a major health problem in the world, including Indonesia. Clinical manifestations of dengue infection varywidely, from asymptomatic until dengue shock syndrome (DSS). Antibody Dependent Enhancement (ADE) hypothesis that states thatnon-neutralizing antibodies in secondary dengue infection may enhance dengue infection via Fcγ receptors is still controversial. Clinicalresearch shows that not all secondary infections manifest as DHF/DSS, but nearly all DHF/DSS cases are caused by secondary infection.Allegedly, the expression of Fcγ has an effect on this incident. This study is an observational analytical study with a cross sectional designto determine the expression of FcγRII (CD32) monocytes in patients with primary and secondary dengue infection. CD32 of monocyteswas measured using FACS Calibur with lyse no wash technique. Primary and secondary dengue infection were determined by IgM/IgGoptical density ratio using ELISA capture method. The ratio of IgM/IgG ≥1.2 was considered as primary infection, while the ratio <1.2was considered as secondary infection. Twenty primary and 32 secondary dengue infection patients in acute phase of dengue infectionpartisipated in this study. Expressions of Fcγ RII (CD32) monocytes were significantly lower in primary than secondary dengue infection(187.825±31.584 vs 218.598±43.414 MFI; p=0.008). CD32 expressions were higher in day 3 compared to day 4 of fever.

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Shu, Pei-Yun, Li-Kuang Chen, Shu-Fen Chang, Yi-Yun Yueh, Ling Chow, Li-Jung Chien, Chuan Chin, Ting-Hsiang Lin, and Jyh-Hsiung Huang. "Comparison of Capture Immunoglobulin M (IgM) and IgG Enzyme-Linked Immunosorbent Assay (ELISA) and Nonstructural Protein NS1 Serotype-Specific IgG ELISA for Differentiation of Primary and Secondary Dengue Virus Infections." Clinical Diagnostic Laboratory Immunology 10, no. 4 (July 2003): 622–30. http://dx.doi.org/10.1128/cdli.10.4.622-630.2003.

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ABSTRACT We have found that NS1 serotype-specific immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA) can be used to differentiate primary and secondary dengue virus infections. This is due to the fact that the NS1-specific IgG antibody cannot be detected before day 9 of illness for primary infection, so the NS1-specific IgG antibodies measured in acute-phase sera must come from previous infection. Comparison of NS1 serotype-specific IgG ELISA with envelope- and membrane-specific capture IgM and IgG ELISA in the differentiation of primary and secondary dengue virus infections showed good correlation (95.90% agreement). Most important, we have found that the serotype of the dengue virus from the majority of patients with primary infection could be correctly identified when convalescent-phase or postinfection sera were analyzed by NS1 serotype-specific IgG ELISA. These findings suggested that NS1 serotype-specific IgG ELISA could be reliably applied for serodiagnosis and seroepidemiological study of dengue virus infection.

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Dioguardi, Mario, Mario Alovisi, Vito Crincoli, Riccardo Aiuto, Giancarlo Malagnino, Cristian Quarta, Enrica Laneve, et al. "Prevalence of the Genus Propionibacterium in Primary and Persistent Endodontic Lesions: A Systematic Review." Journal of Clinical Medicine 9, no. 3 (March 9, 2020): 739. http://dx.doi.org/10.3390/jcm9030739.

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Propionibacterium are anaerobic/aero-tolerant rod Gram-positive bacteria, and numerous studies are associated with primary and secondary endodontic infections. The data in the literature on the prevalence of Propionibacterium are conflicting, and there are studies that report conflicting data on the prevalence in primary and secondary endodontic infections. This review aims to clarify the prevalence of bacteria of the genus Propionibacterium in endodontic lesions. The present systematic review work was performed on the basis of the Prisma protocol. A search was carried out on the PubMed and Scopus databases with the use of keywords. The research produced 410 records, which, after the elimination of the overlaps and the application of the inclusion and exclusion criteria, led to a number of 36 included articles divided by the three outcomes. The first outcome concerns prevalence of bacteria of the genus Propionibacterium in primary and secondary endodontic lesions. The secondary outcome, differences in the prevalence of bacteria of the genus Propionibacterium between primary endodontic infections and secondary endodontic infections. The tertiary outcome, differences in the prevalence of Propionibacterium Acnes compared to Propionibacterium propionicum in endodontic infections. The results of the meta-analysis show that the genus Propionibacterium bacteria are more prevalent in secondary endodontic infections and that P. acnes has a higher prevalence than P. propionicum.

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Nasser, Mouhamad, and Vincent Cottin. "Alveolar Hemorrhage in Vasculitis (Primary and Secondary)." Seminars in Respiratory and Critical Care Medicine 39, no. 04 (August 2018): 482–93. http://dx.doi.org/10.1055/s-0038-1668533.

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AbstractDefined by the accumulation of red blood cells into the alveolar space, diffuse alveolar hemorrhage (DAH) is a severe and potentially fatal medical condition requiring careful attention. In contrast to simple extravasation of erythrocytes facilitated by impaired hemostasis or hemodynamic causes, DAH in vasculitis is due to capillaritis, that is, inflammation of capillaries. Dyspnea, hemoptysis, chest infiltrates, and abrupt fall of blood hemoglobin level represent the cardinal features of DAH; yet, hemoptysis is lacking in one-third of cases. Bronchoalveolar lavage, retrieving bright red fluid, is the best diagnostic clue, also excluding infection and other causes of hemoptysis. Although not recommended, lung biopsy is the gold standard for the diagnosis of DAH and pulmonary capillaritis. Pulmonary capillaritis may be primary as in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis or secondary to drugs (especially antithyroid drugs such as propylthiouracil), infections, connective tissue diseases especially systemic lupus erythematosus, or other small vessel vasculitides. Newer toxic causes of drugs of abuse may be difficult to diagnose. Granulomatosis with polyangiitis and microscopic polyangiitis are the most common causes of capillaritis and DAH, whereas DAH is extremely rare in eosinophilic granulomatosis with polyangiitis. When pulmonary capillaritis is not secondary to underlying systemic vasculitis, idiopathic pauci-immune pulmonary capillaritis may be considered, with or without ANCA. Supportive treatment strategy is mandatory in all cases of DAH. Mechanical ventilation and extracorporeal membrane oxygenation may be used in severe cases. Early identification and removal of the putative drug is crucial in drug-induced vasculitis/DAH and may obviate the need for immunosuppressive therapy. High-dose corticosteroids, intravenous cyclophosphamide, and recently rituximab are the mainstay of treatment in vasculitis. Plasma exchange is recommended in anti–glomerular basement membrane disease and in severe DAH associated with systemic lupus erythematosus and is used in selected cases in ANCA-associated vasculitis.

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Subramaniam, Nathiya, Suneel Mundkur, Pushpa Kini, Nalini Bhaskaranand, and Shrikiran Aroor. "Clinicohematological Study of Thrombocytosis in Children." ISRN Hematology 2014 (January 29, 2014): 1–4. http://dx.doi.org/10.1155/2014/389257.

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Introduction. Primary thrombocytosis is very rare in children; reactive thrombocytosis is frequently observed in children with infections, anemia, and many other causes. Aims and Objectives. To identify the etiology of thrombocytosis in children and to analyze platelet indices (MPV, PDW, and PCT) in children with thrombocytosis. Study Design. A prospective observational study. Material and Methods. A total of 1000 patients with thrombocytosis (platelet > 400×109/L) were studied over a period of 2 years. Platelet distribution width (PDW), mean platelet volume (MPV), and plateletcrit (PCT) were noted. Results. Of 1000 patients, 99.8% had secondary thrombocytosis and only two children had primary thrombocytosis (chronic myeloid leukemia and acute myelogenous leukemia, M7). The majority of the children belonged to the age group of 1month to 2 years (39.7%) and male to female ratio was 1.6 : 1. Infection with anemia (48.3%) was the most common cause of secondary thrombocytosis followed by iron deficiency alone (17.2%) and infection alone (16.2%). Respiratory infection (28.3%) was the predominant infectious cause observed. Thrombocytosis was commonly associated with IDA among all causes of anemia and severity of thrombocytosis increased with severity of anemia (P=0.021). With increasing platelet count, there was a decrease in MPV (<0.001). Platelet count and mean PDW among children with infection and anemia were significantly higher than those among children with infection alone and anemia alone. None were observed to have thromboembolic manifestations. Conclusions. Primary thrombocytosis is extremely rare in children than secondary thrombocytosis. Infections in association with anemia are most commonly associated with reactive thrombocytosis and severity of thrombocytosis increases with severity of anemia.

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Mizuki, Mayuko, Akio Nakane, Kenji Sekikawa, Yoh-ich Tagawa, and Yoichiro Iwakura. "Comparison of Host Resistance to Primary and Secondary Listeria monocytogenes Infections in Mice by Intranasal and Intravenous Routes." Infection and Immunity 70, no. 9 (September 2002): 4805–11. http://dx.doi.org/10.1128/iai.70.9.4805-4811.2002.

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ABSTRACT There have been no studies on the susceptibility and host immune responses to an intranasal infection with Listeria monocytogenes. In this study, we compared the susceptibilities and cytokine responses between intranasal and intravenous infections with L. monocytogenes in mice. Moreover, we compared efficiency of acquisition of host resistance to L. monocytogenes infection between intranasally and intravenously immunized mice because an intranasal immunization of vaccines is reportedly available for induction of adaptive immunity against various infectious pathogens. The susceptibility to an intranasal infection with L. monocytogenes was markedly lower than that to the intravenous infection. The bacterial growth in the lungs, spleens, and livers was substantially similar between intranasally and intravenously infected mice. Titers of endogenous gamma interferon (IFN-γ) and tumor necrosis factor-α (TNF-α) in the spleens, livers, and lungs were parallel to bacterial numbers in each organ of mice during intranasal infection and intravenous infection. IFN-γ-deficient mice and TNF-α-deficient mice were highly susceptible to intranasal infection as well as intravenous infection. Susceptibilities to intranasal and intravenous L. monocytogenes infection were the same in these cytokine-deficient mice. These results suggest that both IFN-γ and TNF-α play critical roles in host resistance to intranasal L. monocytogenes infection as well as the intravenous infection. Acquisition of host resistance to intravenous and intranasal L. monocytogenes infection was induced in intranasally immunized mice as well as intravenously immunized mice, suggesting that intranasal immunization is effective for prevention of a systemic infection with L. monocytogenes.

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Chandola, Dr Iva, Dr Brahmnish Sitara, Dr Nidhi Negi, and Dr V. K. Kataria. "Biomarkers as a diagnostic tool in primary and secondary dengue Infections." Tropical Journal of Pathology and Microbiology 5, no. 1 (January 31, 2019): 37–42. http://dx.doi.org/10.17511/jopm.2019.i01.07.

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Jula, Alma, Matti Waris, Kalle Kantola, Ville Peltola, Maria Söderlund-Venermo, Klaus Hedman, and Olli Ruuskanen. "Primary and Secondary Human Bocavirus 1 Infections in a Family, Finland." Emerging Infectious Diseases 19, no. 8 (August 2013): 1328–31. http://dx.doi.org/10.3201/eid1908.130074.

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Cheng, Liping, Kathleen R. Rasmussen, Mark C. Healey, and Shiguang Yang. "Primary and Secondary Infections with Cryptosporidium parvum in Immunosuppressed Adult Mice." American Journal of Tropical Medicine and Hygiene 55, no. 3 (September 1, 1996): 324–29. http://dx.doi.org/10.4269/ajtmh.1996.55.324.

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Journal articles on the topic 'Primary and secondary infections'

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