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Subclinical Infection (subclinical + infection)
Selected AbstractsTemporal cytokine gene expression patterns in subjects with trachoma identify distinct conjunctival responses associated with infectionCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 2 2005N. Faal Summary Ocular chlamydial disease is clinically diagnosed by the appearance of characteristic inflammatory changes and development of lymphoid follicles in the conjunctiva. Nucleic acid amplification tests and relatively non-invasive methods of sampling the conjunctival surface can be used to quantify the expression of chlamydial and host genes. Using quantitative real-time polymerase chain reaction to detect the presence of Chlamydia trachomatis (CT) 16S rRNA and human interleukin (IL)-1,, IL-10, IL-12p40, interferon (IFN)-, and tumour necrosis factor (TNF)-, transcripts we examined the immune response at the conjunctival surface in a cohort of children living in a trachoma-endemic village in The Gambia. Elevated cytokine transcript levels were associated with the presence of CT 16S rRNA. Subclinical infection (CT infection without clinical signs of disease) elicited an immune response that is proinflammatory in nature, with elevations in the transcription of IL-1,, IFN-, and IL-12p40. Clinically apparent infections were associated with the elevation of mRNA for the multi-functional cytokine TNF-, (fibrotic, type 1 inflammatory and regulatory) and the counter regulatory cytokine, IL-10, in addition to the other proinflammatory cytokines. A positive correlation between IFN-, transcript levels and the amount of CT 16S rRNA expressed in conjunctiva was found. [source] Faecal shedding and serological cross-sectional study of Lawsonia intracellularis in horses in the state of Minas Gerais, BrazilEQUINE VETERINARY JOURNAL, Issue 6 2009C. V. Guimarăes-Ladeira Summary Reason for performing the study: Proliferative enteropathy, caused by the intracellular bacterium Lawsonia intracellularis, has been described in horses in Australia, the USA, Canada and European countries but has not been reported in Latin America. The prevalence of the disease in horses worldwide is unknown. Objective: To evaluate the presence of subclinical L. intracellularis infection in horses in the state of Minas Gerais, Brazil. Methods: A longitudinal study using serology and PCR for detecting antibodies (IgG) and shedding of L. intracellularis in faecal samples, respectively, was conducted using a total of 223 horses from 14 different horse farms in Minas Gerais, and from the Veterinary School of UFMG equine herds in Minas Gerais. The immunoperoxidase technique in glass slides was used as the serological test. Results: Twenty-one horse sera had immunoglobulin G titres of 1:60 and were considered positive. The PCR technique in faeces for L. intracellularis DNA identified 7 horses as faecal shedders. Horses shedding the organism appeared healthy, indicating that subclinical infection of L. intracellularis occurred in the horses. Conclusion: Seropositivity and detection of faecal shedding of L. intracellularis indicates the presence of the agent in the equine population in Minas Gerais. Potential relevance: Results of this study should alert clinicians in countries where proliferative enteropthy in horses has not been reported to consider this disease as a possible cause of enteric disease. [source] Severe pulmonary haemorrhage accompanying hepatorenal failure in fulminant leptospirosisINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 1 2007B. Dursun Summary Leptospirosis is a re-emerging spirochetal zoonosis with a worldwide distribution affecting both animals and humans. The clinical syndromes may vary from a subclinical infection to a severe illness. Although it may potentially have a fulminant and fatal course, leptospirosis usually remains as an underdiagnosed cause of multiorgan failure. In this study, we report a patient with leptospirosis who presented with a fulminant course of diffuse alveolar haemorrhage and hepatorenal failure. His clinical condition deteriorated, despite appropriate antibiotic therapy and haemodialysis. However, he showed prompt clinical improvement when corticosteroids and plasma exchange were instituted in addition to the original therapy. We conclude that leptospirosis should be considered in any case presenting with pulmonary haemorrhage and hepatorenal failure. Plasma exchange and corticosteroids may be a choice of treatment in selected patients unresponsive to conventional therapy. Potential benefits of plasma exchange and corticosteroids may be based on a toxin- and/or cytokine-mediated pathogenesis of the disease. [source] Nitric oxide metabolite levels in preterm laborJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 5 2007Sandeep Chadha Abstract Aim:, To investigate the role of nitric oxide metabolites as markers of infection in subjects with preterm labor or preterm premature rupture of membranes (PTPROM). PTPROM means that there was spontaneous rupture of fetal membrane before the onset of labor and gestational age was <37 weeks. This occurs because of imbalance between matrix metalloproteinase and tissue inhibitor of matrix metalloproteinase. The cause of this imbalance that leads to degradation of collagen causing PTPROM is infection. The bactericidal, fungicidal, viricidal and tumoricidal activities of macrophages are determined in part by elaboration of nitric oxide, hence nitric oxide levels have been found to be increased in infections Methods:, During an 18-month period 50 women with preterm labor or PTPROM and 50 controls were enrolled prospectively. Blood and urine samples were obtained for analysis of nitric oxide metabolites. Patients with known causes of preterm labor were excluded. Result:, The nitric oxide metabolites, which included both nitrite levels and citrulline levels were significantly higher both in blood as well as urine in patients with preterm labor and PTPROM compared to controls. Serum nitrite levels in subjects with preterm labor were 376.5 ± 345 nmol/L while in subjects with PTPROM they were 295.7 ± 161.1 nmol/L and in controls the levels were 62.7 ± 33.9 nmol/L. Serum citrulline levels in subjects with preterm labor were 5293.8 ± 2916.7 nmol/L; in PTPROM they were 6536.6 ± 609.91 nmol/L and in controls they were 949.8 ± 67.1 nmol/L. On comparing patients with preterm labor, those in whom preterm labor could not be inhibited had statistically significant higher levels of nitrite in both serum and urine (482.9 ± 387.7 nmol/L and 754.5 ± 336.5 nmol/L, respectively) compared to patients in whom labor could be inhibited (172.2 ± 61.9 nmol/L and 401.8 ± 236.9 nmol/L, respectively). The citrulline levels were also higher among the group who delivered preterm for both serum and urine (5355.4 ± 3229.7 nmol/L and 11 482.8 ± 2541.4 nmol/L, respectively) compared to patients in whom labor could be inhibited (5260.2 ± 2897.08 nmol/L and 10 651.4 ± 1502.7 nmol/L, respectively) but this did not reach statistical significance. Conclusion:, Higher nitric oxide metabolites in women with preterm labor are marker of subclinical infection. [source] Rhesus monkey model for Leishmania major transmitted by Phlebotomus papatasi sandfly bitesMEDICAL AND VETERINARY ENTOMOLOGY, Issue 1 2001R. J. Probst Summary Leishmaniasis research needs a near-human model for investigations of natural infection processes, immunological responses and evaluation of treatments. Therefore, we developed a reproducible system using Leishmania major Yakimoff & Schokhor (Trypanosomatidae: Kinetoplastida), the cause of Old World zoonotic cutaneous leishmaniasis (ZCL), transmitted to rhesus monkeys Macaca mulatta (Zimmerman) (Primates: Cercopithecidae) by sandfly bites of experimentally infected Phlebotomus papatasi (Scopoli) (Diptera: Psychodidae). Eight monkeys of presumed Indian origin (Leishmania naïve) were exposed to bites of female sandflies that had been infected with L. major by membrane-feeding on human blood seeded with amastigotes isolated from hamster footpad lesions. Infection rates of membrane-fed sandflies averaged >,85% seven days after the infective feed, with uniformly high numbers of promastigotes in the stomodaeal valve region of the sandfly gut. Nodules and ulcerating dermal lesions developed on 7/8 monkeys 2,4 weeks post-bite and persisted for 3,7 months. Monkeys also developed satellite lesions beyond the area of sandfly bites on the head, but not on the chest. Three re-challenged monkeys developed lesions that healed faster than lesions from their primary challenges. After infection, monkeys developed delayed type hypersensitivity (DTH) responses to a panel of Leishmania skin test antigens (LSTA) and, when tested by ELISA and IFA, showed significant post-infection antibody titres which typically rose for ,170 days and then gradually receded during the next 100 days following the first challenge. After the second challenge, antibody titres spiked higher within ,50 days and receded more rapidly. In contrast, four rhesus macaques of Chinese origin developed no lesions following infected sandfly bites, although they raised antibodies and LSTA reactions, indicating subclinical infection. [source] Variant Creutzfeldt-Jakob Disease: implications for the health care systemAUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH, Issue 4 2005R. A. Dunstan The recognition of the first cases of variant Creutzfeldt-Jakob Disease in the United Kingdom (UK) in 1996 and the realisation that this new disease represented the human form of the cattle disease BSE has prompted a considerable investment in research, particularly in the UK, Europe and the United States (US). Much has been learnt about this disease but much is still unknown. Infectivity is not destroyed by conventional sterilisation and disinfection treatment methods. This, combined with the widespread distribution throughout the lymphoid system as well as the central nervous system, raises the spectre of transmission through both surgical and ophthalmological procedures. Reports in 2004 of two likely transfusion-transmitted cases of vCJD suggest the probability of infection through blood transfusion and tissue transplantation. The risk of hospital-based and community-based transmission has not been quantified. To complicate matters even further, there is no suitable ante-mortem screening test or effective treatment for this fatal disease. The incubation period prior to onset of clinical disease is many years and there is good evidence for the existence of subclinical infection and infectivity during this stage. The extent of under-diagnosis and misdiagnosis is probably significant, adding to the risk of human-to-human transmission. [source] | ||||||||||