Protopolystoma xenopodis (Monogenea) primary and secondary infections in Xenopus laevis

Parasitology ◽  
2001 ◽  
Vol 123 (5) ◽  
pp. 455-463 ◽  
Author(s):  
J. A. JACKSON ◽  
R. C. TINSLEY
Keyword(s):  
Xenopus Laevis ◽  
Primary Infection ◽  
Protective Immunity ◽  
Egg Production ◽  
Secondary Infection ◽  
Reproductive Rate ◽  
Secondary Infections ◽  
Kinetics Of ◽  
Patent Infection

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.

scholarly journals Profiles of Th1 and Th2 Cytokines after Primary and Secondary Infection by Schistosoma mansoni in the Semipermissive Rat Host

1999 ◽  
Vol 67 (6) ◽  
pp. 2713-2719 ◽  
Author(s):  
Catherine Cêtre ◽  
Christine Pierrot ◽  
Cécile Cocude ◽  
Sophia Lafitte ◽  
André Capron ◽  
...  
Keyword(s):  
Lymph Nodes ◽  
Mrna Expression ◽  
Primary Infection ◽  
Protective Immunity ◽  
Egg Production ◽  
Secondary Infection ◽  
Mouse Strains ◽  
Th2 Response ◽  
Ifn Γ ◽  
Predominant Expression

ABSTRACT In contrast to most mouse strains, rats eliminate the primary schistosome burden around 4 weeks postinfection and subsequently develop protective immunity to reinfection. In rat schistosomiasis, we have shown predominant expression of a Th2-type cytokine response at the mRNA level after primary infection. In the present study, we showed a significant increase in interleukin-4 (IL-4) mRNA expression in inguinal lymph nodes early after a secondary infection. IL-5 mRNA expression showed a significant increase at days 2 and 4 postreinfection in the spleen and lymph nodes, respectively. We did not detect any gamma interferon (IFN-γ) mRNA after a challenge infection. Analysis of cytokine secretion by stimulated spleen cells after a primary infection showed predominant expression of IL-4 with maximum production on day 21, accompanied by production of IL-5 from day 11 to day 67. A significant increase in IFN-γ secretion was detected at day 21. Analysis of immunoglobulin G2b (IgG2b) and IgG2c (Th1-related isotypes) showed undetectable levels of IgG2b, but detectable levels of specific IgG2c antibodies were observed from day 42. The analysis of Th2-related isotypes showed high specific IgG1 and IgG2a antibody titers from day 29. After a secondary infection, only IL-4 and IL-5 secretion was sustained. This is supported by the increased production of Th2-related isotypes. These findings showed that S. mansoni infection can drive Th2 responses in rats in the absence of egg production which is required to induce a Th2 response in mice and are in favor of the role of Th2-type cytokines in protective immunity against reinfection.

scholarly journals Distinct Roles of CD28- and CD40 Ligand-Mediated Costimulation in the Development of Protective Immunity and Pathology during Chlamydia muridarum Urogenital Infection in Mice

2009 ◽  
Vol 77 (7) ◽  
pp. 3080-3089 ◽  
Author(s):  
Lili Chen ◽  
Wen Cheng ◽  
Pooja Shivshankar ◽  
Lei Lei ◽  
Xiaoyun Zhang ◽  
...  
Keyword(s):  
Primary Infection ◽  
Protective Immunity ◽  
Gene Knockout ◽  
Secondary Infection ◽  
Cd40 Ligand ◽  
Wild Type ◽  
Chlamydia Muridarum ◽  
Urogenital Infection ◽  
Costimulatory Signals ◽  
Deficient Mice

ABSTRACT Infection with Chlamydia muridarum in the mouse urogenital tract can induce both protective immunity and inflammatory pathologies, which has been used as a model for understanding the immune and pathogenic mechanisms of C. trachomatis infection. We compared the roles of CD28- and CD40 ligand (CD40L)-mediated costimulation in C. muridarum infection. Mice with CD28 or CD80/CD86 gene knockout (KO) displayed an infection course similar to that of wild-type mice during both primary and secondary infection, suggesting that CD28-mediated costimulation is not required for protection against C. muridarum infection. However, mice deficient in CD40L or CD40 displayed a prolonged infection course after primary or secondary infection, suggesting that CD40-CD40L costimulation plays an essential role in the development of anti-C. muridarum immunity. Interestingly, the CD28- or CD80/CD86-deficient mice displayed significantly lower levels of inflammatory pathologies in the upper genital tracts after primary infection, although the attenuation in inflammation was no longer significant during secondary infection. However, the CD40L or CD40 KO mice developed inflammatory pathologies as severe as those in wild-type mice following either primary or secondary infection despite the obvious deficits in adaptive immunity in these KO mice. The resistance of CD28 or CD80/CD86 KO mice to chlamydial infection correlated with production of gamma interferon, while the development of inflammatory pathologies in CD40L or CD40 KO mice correlated with the production of other proinflammatory cytokines in mouse urogenital tracts during the early stages of the infection. These observations together suggest that C. muridarum-induced protective immunity and inflammatory pathologies can be mediated by distinct costimulatory signals.

scholarly journals Estimation of Dengue Virus IgM Persistence Using Regression Analysis

2011 ◽  
Vol 18 (12) ◽  
pp. 2183-2185 ◽  
Author(s):  
Harry E. Prince ◽  
Jose L. Matud
Keyword(s):  
Regression Analysis ◽  
Dengue Virus ◽  
Primary Infection ◽  
Secondary Infection ◽  
Disease Onset ◽  
Decay Rates ◽  
Point Index ◽  
Infection Group ◽  
Secondary Infections

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.

Strongyloides ratti: 1. Parasitological observations on primary and secondary infections in the small intestine of rats

1977 ◽  
Vol 51 (4) ◽  
pp. 301-308 ◽  
Author(s):  
R. Moqbel ◽  
D. A. Denham
Keyword(s):  
Small Intestine ◽  
Primary Infection ◽  
Secondary Infection ◽  
Secondary Infections

ABSTRACTAdult Strongyloides ratti were expelled from the small intestine of rats starting 14—18 days after a primary infection. In a secondary infection very few adult worms developed and most of these were expelled before day 14. At the time of expulsion the worms migrated posteriorly in the intestine and their size decreased.

scholarly journals Protective Immunity against Secondary Poxvirus Infection Is Dependent on Antibody but Not on CD4 or CD8 T-Cell Function

2006 ◽  
Vol 80 (13) ◽  
pp. 6333-6338 ◽  
Author(s):  
Vijay Panchanathan ◽  
Geeta Chaudhri ◽  
Gunasegaran Karupiah
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Primary Infection ◽  
Protective Immunity ◽  
Cell Function ◽  
Secondary Infection ◽  
Cd8 T Cell ◽  
Ectromelia Virus ◽  
T Cell Function

ABSTRACT Renewed interest in smallpox and the need for safer vaccines have highlighted our lack of understanding of the requirements for protective immunity. Since smallpox has been eradicated, surrogate animal models of closely related orthopoxviruses, such as ectromelia virus, have been used to establish critical roles for CD8 T cells in the control of primary infection. To study the requirements for protection against secondary infection, we have used a prime-challenge regime, in which avirulent ectromelia virus was used to prime mice that were then challenged with virulent ectromelia virus. In contrast to primary infection, T cells are not required for recovery from secondary infection, since gene knockout mice deficient in CD8 T-cell function and wild-type mice acutely depleted of CD4, CD8, or both subsets were fully protected. Protection correlated with effective virus control and generation of neutralizing antibody. Notably, primed mice that lacked B cells, major histocompatibility complex class II, or CD40 succumbed to secondary infection. Thus, antibody is essential, but CD4 or CD8 T cells are not required for recovery from secondary poxvirus infection.

Hymenolepis microstoma: a change in susceptibility to resistance with increasing age of the parasite

Parasitology ◽  
1977 ◽  
Vol 75 (2) ◽  
pp. 241-249 ◽  
Author(s):  
R. J. Howard
Keyword(s):  
Bile Duct ◽  
Primary Infection ◽  
Secondary Infection ◽  
Similar Rate ◽  
Rate Of Growth ◽  
Secondary Infections ◽  
Hymenolepis Microstoma

Hymenolepis microstoma from secondary infections in mice were found to grow initially more slowly than H. microstoma from primary infections. Eventually a similar rate of growth was attained by both kinds of worm. After transplantation, young worms (≤4 days old) grew more slowly in previously infected than in naive mice. In contrast, 10-day-old worms grew equally well in naive or resistant mice. The administration of cortisone to mice during a secondary infection of H. microstoma inhibited the stunting of growth in young worms which were able to grow as well as those in a primary infection. The effects of the cortisone persisted for less than 4 days. Worms in a secondary infection given 4days after cortisone treatment were stunted in growth. These experiments suggest that the susceptibility of the worms to the resistance of the mouse applies to the first 4 days within the host. The loss or reduction of this susceptibility might be associated with the worms' entry into the bile duct which occurs 3–4 days after infection.

scholarly journals Primary infection with dengue or Zika virus does not affect the severity of heterologous secondary infection in macaques

2019 ◽  
Author(s):  
Meghan E. Breitbach ◽  
Christina M. Newman ◽  
Dawn M. Dudley ◽  
Laurel M. Stewart ◽  
Matthew T. Aliota ◽  
...  
Keyword(s):  
Zika Virus ◽  
Primary Infection ◽  
Rhesus Macaques ◽  
Secondary Infection ◽  
Denv Infection ◽  
The Other ◽  
Sample Type ◽  
Zikv Infection ◽  
Secondary Infections ◽  
Cynomolgus Macaques

AbstractZika virus (ZIKV) and dengue virus (DENV) are genetically and antigenically related flaviviruses that now co-circulate in much of the tropical and subtropical world. The rapid emergence of ZIKV in the Americas in 2015 and 2016, and its recent associations with Guillain-Barré syndrome, birth defects, and fetal loss have led to the hypothesis that DENV infection induces cross-reactive antibodies that influence the severity of secondary ZIKV infections. It has also been proposed that pre-existing ZIKV immunity could affect DENV pathogenesis. We examined outcomes of secondary ZIKV infections in three rhesus and fifteen cynomolgus macaques, as well as secondary DENV-2 infections in three additional rhesus macaques up to a year post-primary ZIKV infection. Although cross-binding antibodies were detected prior to secondary infection for all animals and cross-neutralizing antibodies were detected for some animals, previous DENV or ZIKV infection had no apparent effect on the clinical course of heterotypic secondary infections in these animals. All animals had asymptomatic infections and, when compared to controls, did not have significantly perturbed hematological parameters. Rhesus macaques infected with DENV-2 approximately one year after primary ZIKV infection had higher vRNA loads in plasma when compared with serum vRNA loads from ZIKV-naive animals infected with DENV-2, but a differential effect of sample type could not be ruled out. In cynomolgus macaques, the serotype of primary DENV infection did not affect the outcome of secondary ZIKV infection.Author summaryPre-existing immunity to one of the four DENV serotypes is known to increase the risk of severe disease upon secondary infection with a different serotype. Due to the antigenic similarities between ZIKV and DENV, it has been proposed that these viruses could interact in a similar fashion. Data from in vitro experiments and murine models suggests that pre-existing immunity to one virus could either enhance or protect against infection with the other. These somewhat contradictory findings highlight the need for immune competent animal models for understanding the role of cross-reactive antibodies in flavivirus pathogenesis. We examined secondary ZIKV or DENV infections in rhesus and cynomolgus macaques that had previously been infected with the other virus. We assessed the outcomes of secondary ZIKV or DENV infections by quantifying vRNA loads, clinical and laboratory parameters, body temperature, and weight for each cohort of animals and compared them with control animals. These comparisons demonstrated that within a year of primary infection, secondary infections with either ZIKV or DENV were similar to primary infections and were not associated with enhancement or reduction in severity of disease based on the outcomes that we assessed.

Immune responses of the argasid tick Ornithodoros moubata moubata induced by infection with the filarial worm Acanthocheilonema viteae

2000 ◽  
Vol 74 (3) ◽  
pp. 233-239 ◽  
Author(s):  
D. Hutton ◽  
A.P. Reid ◽  
S. Townson
Keyword(s):  
Survival Rate ◽  
Primary Infection ◽  
Secondary Infection ◽  
Post Secondary ◽  
Ornithodoros Moubata ◽  
Secondary Infections ◽  
Acanthocheilonema Viteae ◽  
Tick Survival ◽  
Argasid Tick

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.

scholarly journals Serological and virological features of dengue fever and dengue haemorrhagic fever in Thailand from 1999 to 2002

2005 ◽  
Vol 133 (3) ◽  
pp. 503-507 ◽  
Author(s):  
S. ANANTAPREECHA ◽  
S. CHANAMA ◽  
A. A-NUEGOONPIPAT ◽  
S. NAEMKHUNTHOT ◽  
A. SA-NGASANG ◽  
...  
Keyword(s):  
Dengue Fever ◽  
Primary Infection ◽  
Secondary Infection ◽  
Age Distribution ◽  
Dengue Haemorrhagic Fever ◽  
Haemorrhagic Fever ◽  
Female Ratio ◽  
Male Ratio ◽  
Secondary Infections ◽  
Almost All

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.

In vitro oncospheral agglutination given by immune sera from mice infected, and rabbits injected, with eggs of Hymenolepis nana

Parasitology ◽  
1975 ◽  
Vol 71 (3) ◽  
pp. 465-473 ◽  
Author(s):  
Akira Ito
Keyword(s):  
Salt Solution ◽  
Primary Infection ◽  
Protective Immunity ◽  
Secondary Infection ◽  
Hymenolepis Nana ◽  
Intravenous Injections

Oncospheral agglutination given by sera immunized with Hymenolepisnana eggs is described as a new way of assessing H. nana infection. All sera of mice which possessed acquired protective immunity against reinfection by H. nana eggs had the potency to induce oncospheral agglutination in vitro. Only oncospheres, which had been hatched, agglutinated, no agglutination occurred in sera from uninfected mice. Oncospheral agglutination was carried out by mixing 0·1 ml of serial two-fold dilutions of serum and 0·1 ml of Hanks' balanced salt solution containing about 600 hatched oncospheres. Titre of agglutinins was indicated as a reciprocal of the final dilution capable of giving agglutination clusters made of three or more oncospheres. Agglutinins developed within 14 days after a primary infection with 500 shell-free eggs. There was no rapid increase of agglutinins within 4 days following a secondary infection. The titre increase coincided with the increase in dosages of eggs. Agglutinins were thought to be immunoglobulins, because the potency of the serum to agglutinate oncospheres was extinguished after absorption of globulins with rabbit anti-mouse globulin serum.Agglutinins were produced in rabbits by intravenous injections of shell-free eggs. The titres of the rabbit sera were much higher than those of mouse sera.

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