Concurrent Helminth Infection Research Articles

Impact of helminth infections on clinical and epidemiological features of microbial infections, and vaccine responses in ruminants: a systematic review.

Abstract Helminth infections are ubiquitous in animal populations, and their interactions with concurrent or subsequent microbial infections can alter clinical and epidemiological features of infectious diseases and outcomes of vaccines. We used the PRISMA 2009 guidelines to conduct a systematic review of helminth-microbial-pathogen interactions and their impact on epidemiology and clinical outcomes of microbial infections in ruminants. Of the 1,375 probable studies identified through Google Scholar and PubMed databases, 20 studies met our inclusion criteria and were qualitatively analysed. Fourteen studies were on domestic ruminants, while six were on African buffaloes. Individual helminths investigated were Fasciola hepatica (six studies) Haemonchus contortus (three studies), Ostertagia ostertagi (one study) and Dicrocoelium dendriticum (one study), while the rest looked at gastrointestinal nematodes in general. Thirteen studies evaluated interactions between helminths and bovine tuberculosis (BTB), trypanosomes and theileria pathogens while four focused on responses to vaccination against rabies, bovine respiratory pathogens and Bacillus of Calmette-Guérin. Helminths interacted with Trypanosoma spp , Mycobacterium bovis , Theileria parva synergistically to aggravate clinical anaemia as measured by PCV and mortality. Furthermore, concurrent helminth infections were reported to lower the sensitivity of BTB diagnostic tests, but they did not appear to affect antibody responses to vaccines. We envision that helminths may interact with microbial pathogens in a number of ways, but primarily through immune pathways to modify clinical and epidemiological features of infections in ruminants. The implications of these interactions include missed diagnosis, underestimation of disease burden and increased severity of disease outcomes.

Helminth Parasite Prevalence in the Endangered Ethiopian Wolf (Canis simensis) in Web Valley, Bale Mountains National Park, Ethiopia.

Ethiopian wolves (EWs), Canis simensis, are the rarest canids in the world and Africa's most endangered carnivore, found in only six isolated habitat fragments in the highlands of Ethiopia. Previous reports on the prevalence of parasites in the EW in Bale Mountains National Park (BMNP) are limited, with little information on their helminth fauna. This study seeks to understand the prevalence of helminth parasites in the EW in BMNP, Ethiopia. In this study, fecal samples were collected from 43 EWs in Web Valley (WV), BMNP, from June to October 2020, and the presence of helminth eggs was assessed using fecal sedimentation and centrifugal floatation methods with microscopy. Forty-two out of 43 fecal samples from wolves (98%) contained eggs from two taxonomic groups of helminths. Eggs from Capillaria spp. and Trichuris vulpis were found most frequently, followed by Toxocara canis, Diphyllobothrium spp., Toxascaris leonina, and Capillaria aerophila. One EW (2%) was recorded for harboring the cestode Moniezia expansa. About 9 of the 43 EWs (21%) presented monospecific infection: 9 EWs (21%) harbored 2 parasite species, 9 EWs (21%) hosted 3 parasite species, 11 EWs (26%) had infection involving 4 parasite species, 2 EWs (5%) were infected with 5 parasite species, 1 EW (2%) presented 6 parasite species, 1 EW (2%) harbored 7 parasite species, and 1 EW (2%) was diagnosed without parasite species. Concurrent helminth infection was highly associated with female EW. Megeti 3 was associated with a low level of concurrent helminth infection. The prevalence of helminth parasites found in wolves in the study area suggests that the environment is highly contaminated with intestinal parasites. Regular control of parasite transmission in EW, domestic dogs, and humans in and around BMNP, public education, and further parasite epidemiological studies must be conducted.

Immunological Responses to Helminths and HIV-1 CoInfections

Aim: Helminth infections result from poor sanitation. We evaluated the effect of helminth infections on HIV disease progression through the monitoring of 2 outcomes: (1) plasma HIV-1 RNA Viral load (V/L) and (2) Cluster of Differentiation (CD4+) T-lymphocyte count amongst helminth-HIV-1 co-infected persons. We hypothesized that (1) concurrent helminth infections compromise immune control, resulting in rising VL and reduced CD4+ T-lymphocyte count (2) and that, subject to successful treatment, a decrease in plasma VL could slow down disease progression. Methods: We reviewed 2032 citations, evaluated 432 abstracts, and included 10 articles according to the PRISMA diagram. The methodologies were appraised using a Mixed Method Appraisal Tool (MMAT). Results: At enrolment, plasma VL was significantly higher in individuals with helminths (5.01 log10 vs. 3.41 log10, p < 0.001). The effective range was 5.28 log10 copies/mL at baseline and 4.67 log10 copies/mL, (p < 0.05) after treatment and a trend for 0.61 log10 lower VL. Significant interactions were seen in the successfully treated groups (p < 0.001). CD4+ T-lymphocyte count values were not significantly different in the co-infection groups relative to those with HIV infection alone.
 Conclusion: Helminths and HIV-1 co-infections are associated with an increase in HIV-1 RNA levels that accelerate the progression of the sub-clinical disease to symptomatic AIDS.

Immunological Responses to Helminths and HIV-1 Co-Infections

Helminth infections result from either ingestion or contact with contaminated fecal matter. To date, there is insufficient evidence as to whether helminths have influence on HIV-1 specific immune responses as literature results are indeterminate. We evaluated the effect of helminth infections on HIV disease progression through the monitoring of 2 outcomes: (1) plasma HIV-1 RNA Viral load (V/L) and (2) Cluster of Differentiation (CD4+) T-lymphocyte count amongst helminth-HIV-1 co-infected persons. We hypothesized that (1) concurrent helminth infections may damage immune control, resulting in escalating VL and reduced CD4+ T-lymphocyte count (2) and that, subject to successful treatment, a decrease in plasma VL could slow down disease progression. We reviewed 2032 citations, evaluated 432 abstracts, and read 10 articles (See PRISMA diagram). The methodologies were appraised using a Mixed Method Appraisal Tool (MMAT). At enrolment, plasma VL were significantly higher in individuals with helminths (5.01 log10 vs. 3.41 log10, p < 0.001). The magnitude of effect ranged from 5.28 log10 copies/mL at baseline and 4.67 log10 copies/mL, (p < 0.05) after treatment and a trend for 0.61 log10 lower VL. All but one RCT reported decline in plasma VL and significant interactions were seen in the successfully treated groups (p < 0.001). CD4+ T-lymphocyte count values were not significantly different in the co-infection groups relative to those with HIV-infection alone. This evidence supports that WaSH and HIV/AIDS co-programming could promote health of PLWHA. We suggest large scale trials for future studies. This systematic review registration number is CRD42022364296.

Immunological Responses to Helminths and HIV-1 Co-Infections

Helminth infections result from either ingestion or contact with contaminated fecal matter. To date, there is insufficient evidence as to whether helminths have influence on HIV-1 specific immune responses as literature results are indeterminate. We evaluated the effect of helminth infections on HIV disease progression through the monitoring of 2 outcomes: (1) plasma HIV-1 RNA Viral load (V/L) and (2) Cluster of Differentiation (CD4+) T-lymphocyte count amongst helminth-HIV-1 co-infected persons. We hypothesized that (1) concurrent helminth infections may damage immune control, resulting in escalating VL and reduced CD4+ T-lymphocyte count (2) and that, subject to successful treatment, a decrease in plasma VL could slow down disease progression. We reviewed 2032 citations, evaluated 432 abstracts, and read 10 articles (See PRISMA diagram). The methodologies were appraised using a Mixed Method Appraisal Tool (MMAT). At enrolment, plasma VL were significantly higher in individuals with helminths (5.01 log10 vs. 3.41 log10, p < 0.001). The magnitude of effect ranged from 5.28 log10 copies/mL at baseline and 4.67 log10 copies/mL, (p < 0.05) after treatment and a trend for 0.61 log10 lower VL. All but one RCT reported decline in plasma VL and significant interactions were seen in the successfully treated groups (p < 0.001). CD4+ T-lymphocyte count values were not significantly different in the co-infection groups relative to those with HIV-infection alone. This evidence supports that WaSH and HIV/AIDS co-programming could promote health of PLWHA. We suggest large scale trials for future studies. This systematic review registration number is CRD42022364296.

Pre-existing helminth infection impairs the efficacy of adjuvanted influenza vaccination in mice.

The world health organization estimates that more than a quarter of the human population is infected with parasitic worms that are called helminths. Many helminths suppress the immune system of their hosts to prolong their survival. This helminth-induced immunosuppression “spills over” to unrelated antigens and can suppress the immune response to vaccination against other pathogens. Indeed, several human studies have reported a negative correlation between helminth infections and responses to vaccinations. Using mice that are infected with the parasitic nematode Litomosoides sigmodontis as a model for chronic human filarial infections, we reported previously that concurrent helminth infection impaired the vaccination-induced protection against the human pathogenic 2009 pandemic H1N1 influenza A virus (2009 pH1N1). Vaccinated, helminth-infected mice produced less neutralizing, influenza-specific antibodies than vaccinated naïve control mice. Consequently helminth-infected and vaccinated mice were not protected against a challenge infection with influenza virus but displayed high virus burden in the lung and a transient weight loss. In the current study we tried to improve the vaccination efficacy using vaccines that are licensed for humans. We either introduced a prime-boost vaccination regimen using the non-adjuvanted anti-influenza vaccine Begripal or employed the adjuvanted influenza vaccine Fluad. Although both strategies elevated the production of influenza-specific antibodies and protected mice from the transient weight loss that is caused by an influenza challenge infection, sterile immunity was not achieved. Helminth-infected vaccinated mice still had high virus burden in the lung while non-helminth-infected vaccinated mice rapidly cleared the virus. In summary we demonstrate that basic improvements of influenza vaccination regimen are not sufficient to confer sterile immunity on the background of helminth-induced immunosuppression, despite amelioration of pathology i.e. weight loss. Our findings highlight the risk of failed vaccinations in helminth-endemic areas, especially in light of the ongoing vaccination campaign to control the COVID-19 pandemic.

GAS6 signaling tempers Th17 development in patients with multiple sclerosis and helminth infection.

Multiple sclerosis (MS) is a highly disabling neurodegenerative autoimmune condition in which an unbalanced immune response plays a critical role. Although the mechanisms remain poorly defined, helminth infections are known to modulate the severity and progression of chronic inflammatory diseases. The tyrosine kinase receptors TYRO3, AXL, and MERTK (TAM) have been described as inhibitors of the immune response in various inflammatory settings. We show here that patients with concurrent natural helminth infections and MS condition (HIMS) had an increased expression of the negative regulatory TAM receptors in antigen-presenting cells and their agonist GAS6 in circulating CD11bhigh and CD4+ T cells compared to patients with only MS. The Th17 subset was reduced in patients with HIMS with a subsequent downregulation of its pathogenic genetic program. Moreover, these CD4+ T cells promoted lower levels of the co-stimulatory molecules CD80, CD86, and CD40 on dendritic cells compared with CD4+ T cells from patients with MS, an effect that was GAS6-dependent. IL-10+ cells from patients with HIMS showed higher GAS6 expression levels than Th17 cells, and inhibition of phosphatidylserine/GAS6 binding led to an expansion of Th17 effector genes. The addition of GAS6 on activated CD4+ T cells from patients with MS restrains the Th17 gene expression signature. This cohort of patients with HIMS unravels a promising regulatory mechanism to dampen the Th17 inflammatory response in autoimmunity.

Morbidity associated with Schistosoma mekongi and concurrent helminth infection in Lao People's Democratic Republic

In 2006, some 7 years after the halt of a multi-year schistosomiasis control programme, a study was conducted in the southern part of Lao People's Democratic Republic to determine the morbidity associated with Schistosoma mekongi and concurrent helminth infection. In two S. mekongi-endemic districts, Khong and Mounlapamok, 640 individuals aged 9–40 years were randomly selected. Two stool samples were obtained from each participant and subjected to the Kato–Katz technique for helminth diagnosis. Morbidity was assessed by clinical examination and abdominal ultrasonography. Multiple logistic regression analysis was employed to relate S. mekongi infection with morbidity indicators. In Khong district, S. mekongi prevalence was 13-fold higher than in Mounlapamok district (57.7% vs. 4.4%, p < 0.001). Likewise, we observed significantly more often palpated hepatomegaly (15.5% vs. 5.4%) and splenomegaly (9.6% vs. 0.4%). Abdominal ultrasonography revealed that, in Khong district, liver and spleen morbidity occurred more frequently (e.g., enlarged left liver lobe: 89.2% vs. 68.7%, p < 0.001). Single species infection with S. mekongi was associated with enlarged peri-portal vein (adjusted odds ratio (aOR) 47.7, 95% confidence interval (CI) 4.2–85.7, p = 0.002), as was S. mekongi-Opisthorchis viverrini co-infection (aOR 2.2, 95% CI 1.1–4.5, p = 0.020). In conclusion, our study shows that in 2006, several years after the halt of the Lao schistosomiasis control programme that emphasised preventive chemotherapy, S. mekongi infection again had reached high prevalence rates. Infection with S. mekongi was associated with substantial hepatosplenic morbidity. Schistosomiasis control measures were re-instigated in 2010. In view of the ultimate goal to eliminate schistosomiasis, rigorous surveillance and public health responses tailored to the social-ecological settings and long-term programme commitment are warranted.

Helminth Infections Suppress the Efficacy of Vaccination against Seasonal Influenza

Helminth parasites infect more than a quarter of the human population and inflict significant changes to the immunological status of their hosts. Here, we analyze the impact of helminth infections on the efficacy of vaccinations using Litomosoides sigmodontis-infected mice. Concurrent helminth infection reduces the quantity and quality of antibody responses to vaccination against seasonal influenza. Vaccination-induced protection against challenge infections with the human pathogenic 2009 pandemic H1N1 influenza A virus is drastically impaired in helminth-infected mice. Impaired responses are also observed if vaccinations are performed after clearance of a previous helminth infection, suggesting that individuals in helminth-endemic areas may not always benefit from vaccinations, even in the absence of an acute and diagnosable helminth infection. Mechanistically, the suppression is associated with a systemic and sustained expansion of interleukin (IL)-10-producing CD4+CD49+LAG-3+ type 1 regulatory Tcells and partially abrogated by invivo blockade of the IL-10 receptor.

Helminthiasis Epidemiology and Control: Scoring Successes and Meeting the Remaining Challenges.

Parasitic helminth infections remain a significant challenge to global health. These arehighly prevalent diseases, affecting over 1 billion persons worldwide. Their prevalence is closely linked to the presence of severe poverty and its associated sub-standard housing and sanitation. The last decade has seen a remarkable increase in our understanding of the true disease burden of helminth infections, and there has been increasing momentum on the part of national and non-governmental developmental organizations for prevention and control of these diseases. The expansion in mass treatment programmes for their control has yielded some significant successes. However, challenges remain in terms of ecological heterogeneity in transmission, incomplete drug uptake, and the likelihood of emerging drug resistance. The development of new, more-sensitive diagnostics is now broadening our knowledge of infection prevalence and of the risk of reinfection and has enhanced our knowledge of the prevalence of concurrent helminth infections. Adoption of these new diagnostic techniques for large-scale screening and surveillance will require adaptation of current mass treatment guidelines for control as programmes move from initial morbidity control objectives toward coordinated interventions aimed at local elimination.

Correction: Cutting Edge: Helminth Coinfection Blocks Effector Differentiation of CD8 T Cells through Alternate Host Th2- and IL-10-Mediated Responses.

Concurrent helminth infection potently inhibits T cell immunity; however, whether helminthes prevent T cell priming or skew clonal recruitment and effector differentiation is not known. Using coinfection with two natural mouse pathogens, Heligmosomoides polygyrus and Toxoplasma gondii, to investigate the negative impact of helminthes on the CD8 T cell response, we demonstrate helminth-induced suppression of IL-12–dependent differentiation of killer-like receptor G1 + effector CD8 T cells and IFN-γ production. Nevertheless, reversal of helminth suppression of the innate IL-12 response of CD8α + dendritic cells, which occurred in STAT6-deficient mice, was not sufficient to normalize CD8 T cell differentiation. Instead, a combined deficiency in IL-4 and IL-10 was required to reverse the negative effects of helminth coinfection on the CD8 T cell response. Monoclonal T. gondii –specific CD8 T cells adoptively transferred into coinfected mice recapitulated the spectrum of helminth-induced effects on the polyclonal CD8 T response, indicating the lack of requirement for clonal skewing.

Toxoplasma Co-infection Prevents Th2 Differentiation and Leads to a Helminth-Specific Th1 Response.

Nematode infections, in particular gastrointestinal nematodes, are widespread and co-infections with other parasites and pathogens are frequently encountered in humans and animals. To decipher the immunological effects of a widespread protozoan infection on the anti-helminth immune response we studied a co-infection with the enteric nematode Heligmosomoides polygyrus in mice previously infected with Toxoplasma gondii. Protective immune responses against nematodes are dependent on parasite-specific Th2 responses associated with IL-4, IL-5, IL-13, IgE, and IgG1 antibodies. In contrast, Toxoplasma gondii infection elicits a strong and protective Th1 immune response characterized by IFN-γ, IL-12, and IgG2a antibodies. Co-infected animals displayed significantly higher worm fecundity although worm burden remained unchanged. In line with this, the Th2 response to H. polygyrus in co-infected animals showed a profound reduction of IL-4, IL-5, IL-13, and GATA-3 expressing T cells. Co-infection also resulted in the lack of eosinophilia and reduced expression of the Th2 effector molecule RELM-β in intestinal tissue. In contrast, the Th1 response to the protozoan parasite was not diminished and parasitemia of T. gondii was unaffected by concurrent helminth infection. Importantly, H. polygyrus specific restimulation of splenocytes revealed H. polygyrus-reactive CD4+ T cells that produce a significant amount of IFN-γ in co-infected animals. This was not observed in animals infected with the nematode alone. Increased levels of H. polygyrus-specific IgG2a antibodies in co-infected mice mirrored this finding. This study suggests that polarization rather than priming of naive CD4+ T cells is disturbed in mice previously infected with T. gondii. In conclusion, a previous T. gondii infection limits a helminth-specific Th2 immune response while promoting a shift toward a Th1-type immune response.

Cutting Edge: Helminth Coinfection Blocks Effector Differentiation of CD8 T Cells through Alternate Host Th2- and IL-10-Mediated Responses.

Concurrent helminth infection potently inhibits T cell immunity; however, whether helminthes prevent T cell priming or skew clonal recruitment and effector differentiation is not known. Using coinfection with two natural mouse pathogens, Heligmosomoides polygyrus and Toxoplasma gondii, to investigate the negative impact of helminthes on the CD8 T cell response, we demonstrate helminth-induced suppression of IL-12-dependent differentiation of killer-like receptor G1+ effector CD8 T cells and IFN-γ production. Nevertheless, reversal of helminth suppression of the innate IL-12 response of CD8α+ dendritic cells, which occurred in STAT6-deficient mice, was not sufficient to normalize CD8 T cell differentiation. Instead, a combined deficiency in IL-4 and IL-10 was required to reverse the negative effects of helminth coinfection on the CD8 T cell response. Monoclonal T. gondii-specific CD8 T cells adoptively transferred into coinfected mice recapitulated the spectrum of helminth-induced effects on the polyclonal CD8 T response, indicating the lack of requirement for clonal skewing.

Ostertagia spp., rumen fluke and liver fluke single- and poly-infections in cattle: An abattoir study of prevalence and production impacts in England and Wales

This study aims at investigating the occurrence, risk factors and production impacts on beef carcass parameters of three of the most important cattle helminth infections in England and Wales. Abomasa, reticulorumens and livers from healthy cattle were collected and examined post-mortem quarterly over a one year period in an abattoir in South-West England. Specific viscera from 974 cattle were collected, examined and scored for Ostertagia spp., adult rumen fluke and liver fluke lesions/presence. A total of 89%, 25% and 29% of the carcasses had lesions/presence of Ostertagia spp., rumen fluke and liver fluke, respectively, and 39% had presence of helminth co-infection. Animal demographic and carcass parameters associated with helminth infections were investigated using multilevel multinomial and multilevel linear mixed models respectively. After adjusting for other factors, significant differences in the distribution of helminth infections were observed among cattle by type of breed, animal category (cow, heifer, steer and young bull), age, season and concurrent helminth infections. Compared to carcasses free of helminths, carcasses presenting solely Ostertagia Spp. lesions or adult rumen fluke had significantly lower cold carcass weight (coef.: −30.58 [−50.92;−10.24] and −50.34 [−88.50;−12.18]) and fat coverage (coef.: −3.28 [−5.56;−1.00] and −5.49 [−10.28;−0.69]) and carcasses presenting solely liver fluke lesions had significantly lower conformation grade (coef.: −3.65 [−6.98;−0.32]). Presence of helminth poly-infections was negatively associated with cold carcass weight.

Cytokine and chemokine profile of the innate and adaptive immune response of Schistosoma haematobium and Plasmodium falciparum single and co-infected school-aged children from an endemic area of Lambaréné, Gabon.

BackgroundHelminths and malaria are among the most prevalent infectious diseases in the world. They both occur in tropical area where they often affect the same populations. There are studies suggesting an effect of helminths on malariometric indices. For example, malaria attacks as well as disease severity has been shown to be influenced by a concurrent chronic helminth infection. However, there are also studies that show no effect of concurrent helminth infections on malarial outcomes. To start addressing this issue, the effect of chronic Schistosoma haematobium infection on both the innate and adaptive immune response of Plasmodium falciparum-infected subjects was assessed in an area endemic for both these infections in Gabon.MethodSubjects infected with S. haematobium and or P. falciparum, as well as a control group with neither of these infections, were recruited. For innate immune response, heparinized blood was obtained and cultured for 24 hours with a panel of TLR ligands. For adaptive immune response, PBMC was isolated and stimulated with SEB for 72 hours. Cytokines and chemokines were measured in supernatants using a multiplex beads array immunoassay. Principal Component analysis was used to assess pattern of cytokine and chemokine responses representing the innate and adaptive components of the immune system.ResultsOverall it was observed that the presence of P. falciparum infection was marked by an increase in innate and adaptive immune responsiveness while S. haematobium infection was characterized by an increased chemokine profile, with at the same time, lower pro inflammatory markers. When the study subjects were split into single infected and co-infected groups no effect of S. haematobium on the immune response of P. falciparum infected subjects was observed, neither for the innate nor for the adaptive component of the immune response.ConclusionThis study provides original information on the cellular immune response of S. haematobium and/or P. falciparum in infected subjects. It rules out an effect of S. haematobium on the cytokine profile of subjects co-infected with P. falciparum.

Helminths and their implication in sepsis - a new branch of their immunomodulatory behaviour?

The prevalence of autoimmune and allergic disorders has dramatically increased in developed countries, and it is believed that our ‘cleaner living’ reduces exposure to certain microorganisms and leads to deviated and/or reduced regulation of the immune system. In substantiation of this health hygiene hypothesis, multiple epidemiological studies and animal models have characterized the protective immune responses induced by helminths during auto-inflammatory disorders. The beneficial effects of such helminths, like schistosomes and filariae, are thought to lie in their immunomodulatory capacity, which can be induced by different life-cycle stages or components thereof. In addition to suppressing autoimmunity recent evidence indicates that concurrent helminth infections also counterbalance exacerbated pro-inflammatory immune responses that occur during sepsis, improving survival. As with allergy, epidemiological studies have observed a steady rise in severe sepsis cases and although this may have resulted from several factors (immunosuppressive drugs, chemotherapy, transplantation, increased awareness and increased surgical procedures), it is tempting to hypothesize that the lack of helminth infections in Western countries may have contributed to this phenomenon. This review summarizes how helminths modulate host immunity during sepsis, such as manipulating macrophage activation and provides an overview about the possible implications that may arise during overwhelming bacterial co-infections.This well written review gives a comprehensive overview on the immunopathology of sepsis and the modulation of immune responses by helminths. It provides evidence that helminths or components thereof may improve the outcome of severe infections. This will allow the development of therapeutic strategies to fight infections and sepsis.

Corprological and haematological parameters of albino mice (Mus musculus) concurrently infected with Heligmosomoides bakeri and Trypanosoma brucei

The effect of concurrent infection with Trypanosoma brucei (T. brucei) and Heligmosomoides bakeri (H. bakeri) was investigated in this study. Thirty adult male albino mice were used for the study. The mice were divided into six groups of five mice each. Group 1 served as uninfected control, Groups 2 and 3 were infected with H. bakeri and T. brucei respectively, Group 4 received both T. brucei and H. bakeri on the same day, Group 5 was experimentally infected with H. bakeri three days after T. brucei infection, while Group 6 was infected with T. brucei three days after H. bakeri infection. Blood and faecal samples were collected and analyzed weekly to determine the faecal egg counts (FEC), packed cell volume (PCV) and level of parasitaemia (LP). Weekly body weights (BW) were also recorded. FEC and parasitaemia increased in all the infected groups during the study, but these were significantly (p&lt;0.05) higher in the multiple-infection (groups 4, 5 and 6) than those with the single infection (groups 2 and 3). The same trend was also observed in the BW and PCV (p&lt;0.05). The level of infection produced by single infection with T. brucei and H. bakeri respectively were similar (p&lt;0.05). All treatment groups were significantly (p&lt;0.05) different from the control group. From the results, it was concluded that concurrent helminth and protozoan parasite infections produced more deleterious effect on the host when compared with single infection with either parasite. However, the pathology produced by concurrent infection was more severe when the host was exposed to the protozoan parasite before the helminth parasite.

The immune response to tuberculosis infection in the setting ofHelicobacter pyloriand helminth infections

We screened 176 healthy, adult (aged 18-55 years) US refugees from tuberculosis (TB)-endemic countries to evaluate whether cytokine responses to latent TB infection (LTBI) are modified in the setting of concurrent H. pylori and helminth infection. As measured by the Quantiferon-TB GOLD interferon-γ release assay, a total 38 (22%) subjects had LTBI, of which 28 (74%) also were H. pylori seropositive and/or helminth infected. Relative to ten subjects with LTBI only, 16 subjects with concurrent H. pylori infection had significantly elevated levels of IFN-γ, and nine subjects with both H. pylori and helminth infection had significantly elevated levels of IFN-γ, IL-2, IL-13, and IL-5. H. pylori is associated with enhanced IFN-γ responses to TB, even in the setting of concurrent helminth infection. Efficacy of TB vaccines may vary with the co-existence of these three infections in the developing world.

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Concurrent gastro-intestinal nematode infection does not alter the development of experimental cerebral malaria

Concurrent helminth infections have been suggested to be associated with protection against cerebral malaria in humans, a condition characterised by systemic inflammation. Here we show that a concurrent chronic gastro-intestinal nematode infection does not alter the course of murine cerebral malaria. Mice infected with Heligmosomoides polygyrus, and co-infected with Plasmodium berghei ANKA 14 days later, developed malaria parasitemia, weight loss and anemia, at the same rate as mice without nematode infection. Both groups developed cerebral malaria around the same time point. The data suggest that a chronic helminth infection does not affect the development of cerebral malaria in a murine model.