Serological Picture Research Articles

Liver damage in children and adolescents with newly diagnosed celiac disease: clinical and anamnestic, serological and morphological patterns

To analyze the frequency of hypertransaminasemia, clinical and anamnestic, serological and morphological picture in children in the active period of celiac disease. The study included 272 children with celiac disease aged from 8 months to 17 years. The patients were divided into two groups: the first - children with hypertransaminasemia, the second - without hypertransaminasemia. Hypertransaminasemia was detected in 55.9% of children with celiac disease. The age of manifestation of the disease in the first group was 1.0 [0.5; 2.0] years, in the second group - 1.9 [0.5; 4.0] years (p=0.0004). Children of the first group were diagnosed at 2.5 [1.7; 4.9] years, the second group - at 4.9 [3.0; 10.8] years (p<0.001). The duration of the latency period in children of the first and second groups was 1.4 [0.6; 3.1] years and 2.4 [0.9; 4.3] years, respectively (p=0.002). The average values of IgA anti-tTG antibodies in children of the analyzed groups did not differ, and the indicators of IgG anti-tTG antibodies in the first group were 1.6 (p=0.04) times higher. The level of EMA in children with hypertransaminasemia was 2 times higher than in children without hypertransaminasemia. Hypertransaminasemia is more often detected in young children with early manifestation of the disease, increases with the deepening of atrophy in the mucous membrane of the small intestine. Higher titers of celiac-specific antibodies were detected in children with hypertransaminasemia.

DIFFUSE ALVEOLAR HEMORRHAGE AS A CONSEQUENCE OF MICROSCOPIC POLYANGIITIS DUE TO COVID-19

SESSION TITLE: Fellows' COVID-19 SESSION TYPE: Fellow Case Reports PRESENTED ON: October 18-21, 2020 INTRODUCTION: Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is a small vessel vasculitis of which microscopic polyangiitis (MPA) is a subset. They are known to cause life threatening renal failure and/or pulmonary hemorrhage. Viruses are a known trigger of vasculitis, including MPA. (1) We present a case of MPA caused by COVID-19 presenting as diffuse alveolar hemorrhage (DAH) CASE PRESENTATION: 55 year old female with a past medical history of hemorrhagic stroke, hypertension & asthma who presented with respiratory distress & severe hypoxemia. At the time of intubation, a moderate amount of blood was suctioned from her endotracheal tube. She was profoundly hypoxemic & required 100% FiO2 and PEEP 18 cmH2O. A SARS CoV2 PCR test was positive. Other admission laboratory values were significant for a creatinine of 4.9 mg/dL (baseline: 0.8mg/dL), hemoglobin of 8 g/dL (baseline: 11.8g/dL), ferritin 569 ng/mL, D-dimer 3.18 ug/mL, CRP 62.8 mg/L, ESR 118 mm/hr. Chest X-ray showed dense bilateral airspace opacities. A CT scan showed extensive bilateral consolidations with air bronchograms that were not typical for a COVID-19 pneumonia (Image 1) except in the apices where these dense consolidations had a peripheral pattern. She was admitted to the medical ICU where she continued to have bleeding into her endotracheal tubing. Bronchoscopy showed blood in the airways diffusely with no focality to the bleeding. A bronchoalveolar lavage was performed of two separate lobes, and was notable for progressively bloody aliquots consistent with DAH. Because of concern for a pulmonary-renal syndrome, rheumatologic testing was performed. She was empirically treated with high dose intravenous steroids and plasmapheresis. Unfortunately, profound hypoxia persisted and family elected to withdraw life-sustaining therapies. Two days after her death, serologies revealed a mildly positive ANA and a strongly positive anti-MPO ANCA, suggesting the diagnosis of MPA. DISCUSSION: While the primary signs and symptoms of COVID-19 are fever, cough, and dyspnea, other reported manifesations include kawasaki-like disease in children (2) and cutaneous manifestations such as livedo reticularis (3). We believe that in our case the patient’s infection with COVID-19 & its subsequent increased inflammatory state led to her developing MPA vasculitis with subsequent pulmonary-renal syndrome complicated by diffuse alveolar hemorrhage, rapidly progressive renal failure and ultimately death. Her clinical and serologic picture were consistent with a diagnosis of microscopic polyangiitis. It is unclear whether our patient had a smoldering vasculitis that was triggered by the hyper-inflammatory nature of COVID-19 or whether this virus caused a vasculitis de novo. CONCLUSIONS: With vasculitis potentially being one of COVID-19's presenting symptoms, prompt diagnosis and intervention is essential in improving outcomes. Reference #1: Yates M, Watts R. ANCA-associated vasculitis. Clin Med (Lond). 2017;17(1):60-64. doi:10.7861/clinmedicine.17-1-60 Reference #2: Viner RM, Whittaker E. Kawasaki-like disease: emerging complication during the COVID-19 pandemic [published online ahead of print, 2020 May 13]. Lancet. 2020;10.1016/S0140-6736(20)31129-6. doi:10.1016/S0140-6736(20)31129-6 Reference #3: Sachdeva M, Gianotti R, Shah M, et al. Cutaneous manifestations of COVID-19: Report of three cases and a review of literature [published online ahead of print, 2020 Apr 29]. J Dermatol Sci. 2020;S0923-1811(20)30149-3. doi:10.1016/j.jdermsci.2020.04.011 DISCLOSURES: no disclosure on file for Christopher Damiano; No relevant relationships by Elie Fares, source=Web Response no disclosure on file for Catherine Kuntz; No relevant relationships by Kriti Pathak, source=Web Response

FRI0565 PREVALENCE AND SIGNIFICANCE OF ANTIBODIES AGAINST CITRULLINATED ALPHA-ENOLASE (ANTI-CEP1) IN CONNECTIVE TISSUE DISEASES.

Background:Anti-cyclic citrullinated peptide (anti-CCP) auto-antibodies represent the current gold standard for the diagnosis of rheumatoid arthritis (RA). However, growing evidence suggests that a variety of other citrullinated self-proteins may act as autoantigens and lead to the production of autoantibodies (1). Furthermore, autoantibodies believed to be RA-specific have been detected also in patients with connective tissue diseases (CTDs). We recently demonstrated that antibodies against citrullinated alpha-enolase (anti-CEP1) are a biomarker of erosive disease and RA-associated interstitial lung disease (2).Objectives:The purpose of this study was to investigate the prevalence and possible prognostic value of anti-CEP-1 in patients with CTDs.Methods:Two hundred and twelve consecutive patients with CTDs (51 systemic lupus erythematosus (SLE), 85 primary Sjogren’s syndrome (pSS) and 76 systemic sclerosis (SSc)) were studied and compared to 97 sex and age matched normal controls (NC) and 267 patients with RA. Anti-CEP1 IgG were detected in serum samples with a commercial ELISA kit (Euroimmun).Results:The overall prevalence of anti-CEP1 in CTDs was 7% (15/212 patients). In detail, these antibodies were detectable in 4 out of 85 pSS (5%), 5 out of 51 SLE (10%) and 6/76 SSc (8%). The prevalence and the titer of anti-CEP1 in CTDs was significantly higher compared to NC and significantly lower compared to RA. Anti-CEP1 positive patients did not display a specific clinical and serological picture. Unlike in RA, anti-CEP1 did not correlate with CTD-associated ILD.Conclusion:This is the first study assessing anti-CEP1 in a large cohort of patients with CTDs. We demonstrated that the association of these autoantibodies with ILD is specific for RA since it is not observed in SLE, pSS and SSc. Furthermore, although being significantly more prevalent and at higher titer compared to NC, anti-CEP1 do not allow to discriminate different patient subsets displaying peculiar clinical or serological phenotypes. Based on our results, the application of anti-CEP1 in CTDs is not advisable, however larger studies may possibly identify correlations not evident in our cohort.

Cytokine Milieu in Undifferentiated Connective Tissue Disease: a Comprehensive Review.

Undifferentiated connective tissue disease (UCTD) is a unique clinical entity, a potential forerunner of well-established systemic autoimmune/rheumatic diseases. UCTD is characterized by the presence of various clinical symptoms, as well as a diverse repertoire of autoantibodies, resembling systemic autoimmune diseases. Since approximately one third of these patients consequently transform into a full-blown systemic autoimmune/rheumatic disease, it is of major importance to assess pathogenic factors leading to this progression. In view of the fact that the serological and clinical picture of UCTD and systemic autoimmune diseases are very similar, it is assumed that analogous pathogenic factors perpetuate both disease entities. In systemic autoimmune conditions, a quantitative and qualitative impairment of regulatory T cells has been shown previously, and in parallel, a relative dominance of pro-inflammatory Th17 cells has been introduced. Moreover, the imbalance between regulatory and Th17 cells plays a pivotal role in the initiation and propagation of UCTD. Additionally, we depict a cytokine imbalance, which give raise to a biased T cell homeostasis from the UCTD phase throughout the fully developed systemic autoimmune disease stage. The levels of interleukin (IL)-6, IL-12, IL-17, IL-23, and interferon (IFN)-γ were pathologically increased with a parallel reduction of IL-10. We believe that the assessment of Th17/Treg cell ratio, as well as the simultaneous quantitation of cytokines may give a useful diagnostic tool at the early UCTD stage to identify patients with a higher chance of consecutive disease progression toward serious systemic autoimmune diseases. Moreover, the early targeted immunomodulating therapy in these patients may decelerate, or even stop this progression, before the development of serious autoimmune conditions with organ damage.

Molecular detection of hepatitis B virus (HBV) among voluntary ELISA positive blood donors in Almadinah Almunawwarah

Abstract Objective Hepatitis B virus is considered as one of the most common viruses spreading through blood transfusion and organ transplants. This usually results in more considerable cases of disease and mortalities; so it is necessary to perform tests for viral infection in all blood donors. The present study aimed at highlighting the serological picture of blood donors and HBV suspected patients reported to the hospitals in Al-Madina Al-Mounawara; using standard PCR technique. Methods The present study is conducted on 17,131 samples (blood donors and suspected patients reported to the Central Blood Bank the achievement of conformation tests in Al-Madina Al-Mounawara Saudi Arabia). Virus was detected by two techniques: PCR and ELISA. COBAS TagMan V2.0 was used as PCR test to measure HBV-DNA in human plasma or serum. Three different ELISA tests had been used to detect HBV antigen and antibody: HBsAg, HBcAb and HBsAb. Results The overall prevalence of hepatitis B surface antigen (HBsAg) was (9.02%), hepatitis B core antibody (HBcAb) was (9.02%), hepatitis B surface antibody (HBsAb) was approximately (7.93%) and hepatitis B DNA (HBVDNA) was the highest one (9.29%). Conclusion Comparison of PCR positive results with those of the ELISA positive indicates that the PCR technique is more sensitive and reliable than the ELISA technique, as not all ELISA positive cases confirmed HBV infection.

Drug-induced lupus: simvastatin or amiodarone? A case report in elderly

Reports of systemic lupus erythematosus (SLE) seen during treatment with amiodarone are rare in the literature. SLE or immunological abnormalities induced by treatment with statins are more frequent. In this issue we report a case of a 81-year-old male who, after a 2-year therapy with amiodarone, developed a clinical and serologic picture of drug-induced SLE (DILE). He was admitted for congestive heart failure in mechanical aortic valve prosthesis, permanent atrial fibrillation (anticoagulation with warfarin), hypercholesterolaemia, and hypothyroidism. Amiodarone was started two years earlier for polymorphic ventricular tachycardia, statin and L-thyroxine the following year. At admission he presented pleuro-pericardical effusion detected by CT-scan (also indicative of interstitial lung involvement) and echocardiography. Serological main indicative findings were: elevation of inflammatory markers, ANA (Anti-Nuclear Antibodies) titers = 1:320 (indirect immune-fluorescence – IIF – assay on HEp-2), homogeneous/fine speckled pattern, anti-dsDNA titers = 1:80 (IIF on Crithidia luciliae), negative ENA (Extractable Nuclear Antigens) and antibodies anti-citrulline, rheumatoid factor = 253 KU/l, normal C3-C4, negative HbsAg and anti-HCV, negative anticardiolipin antibodies IgG and IgM, negative anti-beta2GPI IgG and IgM. Amiodarone was discontinued and methylprednisolone was started, since the patient was severely ill. At discharge, after a month, the patient was better and pleuro-pericardical effusion was reduced. Readmitted few weeks later for bradyarithmia and worsening of dyspnoea, pericardial effusion was further reduced but he died for refractory congestive heart failure and pneumonia. Clinical picture (sierositis, neither skin nor kidney involvement), other typical side effects of amiodarone (hypothyroidism and lung interstitial pathology) and serological findings are suggestive of amiodarone-induced SLE.

Celiac disease and giardiasis

When investigating a patient with suspected celiac disease (CD), several other conditions must be considered, including potential infection with Giardia lamblia. Although giardiasis is rare, its histopathological and serological picture may resemble that of CD. We report the case of a young man with diabetes mellitus and a family history of CD referred to our hospital because of diarrhoea and weight loss. Investigation showed, among other factors, partial villous atrophy in duodenal biopsies and elevated immunoglobulin A antitissue transglutaminase antibodies. The patient was diagnosed with CD and recommended a gluten-free diet. At the same time, faecal tests were conducted, indicating the presence of G. lamblia. The patient was treated and improved, even after discontinuing the gluten-free diet. Subsequent follow-up after 6 months showed total regression of mucosal histopathology and a normal antitissue transglutaminase antibodies level.

Specific IgA antibodies in Mycoplasma pneumoniae infections

Mycoplasma pneumoniae is the prevalent cause of community acquired pneumonia (CAP), especially in pediatric age. M. pneumoniae infection may presents a severe pulmonary disease whose clinical picture is undistinguishable from that of other pneumotropic agents.A rapid and suitable laboratory diagnosis mainly lies on serological test investigations. A total of 37 consecutive CAP pediatric and adult patients, and 102 subjets with suspected respiratory tract infections (SIR) were enrolled and examined for specific IgA-, IgG-, IgM anti-M. pneumoniae antibodies using a rapid ELISA test (Mycoplasma Chorus-Diesse), and a two step ELISA test (MYP test-Savyon). Agreement of IgA, IgG, and IgM values were 96%, 64%, 100%, respectively. Among CAP patients, IgM was the prevalent marker (23/37); in this population, 12/23 pediatric patients were both IgM and IgA positives. Conversely, among adults, IgA antibodies were the most prevalent infection marker. Pediatric patients of both CAP and SIR population showed a similar serological picture; instead, all adult patients resulted as IgM negatives; IgA and IgG antibodies showed high positive values in 4/8, and in four old patients IgA was the alone infection marker. Although specific IgM antibodies detection remains the main serological sign of recent infection in pediatric age, the presence of IgA antibodies is a suitable tool to revealing the etiology of clinical picture in both pediatric and adult patients.

Origins of syphilis and management in the immunocompetent patient: Facts and controversies

Despite the continued efficacy of penicillin since the 1940s, many aspects of the natural history, diagnosis, and management of syphilis remain controversial. A key factor among the numerous factors explaining the persistence of significant areas of controversies is the absence of a gold standard direct method for distinguishing between the different stages of syphilis and appraising treatment response. This contribution presents an overview of some of the most debated aspects of the origins, diagnosis, and management of syphilis in immunocompetent patients. The two main current hypotheses on the origins of Treponema pallidum are the “Columbian” and the “Pre-Columbian” hypotheses. Strong evidence supports that Columbus' crew brought T pallidum to Europe at the time of discovery of the New World. Because T pallidum culture and inoculation to animals are not readily available methods, the gold standard method for the diagnosis of syphilis is the direct identification of T pallidum by dark field microscopy or direct fluorescent antibody tests. These methods, however, are inapplicable in many patients, and thus the diagnosis of syphilis is usually based on the clinical and serologic picture. Serologic tests should only be considered as surrogate markers of the disease and do not provide definite distinction between syphilis stages. The optimal combination of serologic tests is still undefined. Other areas of controversy include the identification of patients who would benefit from a lumbar puncture, the diagnostic criteria of neurosyphilis, and the most relevant markers of treatment response.

Seroepidemiology of EBV and interpretation of the “isolated VCA IgG” pattern

The presence of VCA IgG in the absence of VCA IgM and EBNA-1 IgG antibodies makes classifying EBV infection more difficult as this serological picture can be seen in the case of past infection with EBNA-1 IgG loss or non-appearance, or acute infections with the early disappearance or delayed onset of VCA IgM. The aim of this study was to assess the prevalence of this pattern in 2,422 outpatients with suspected EBV infection examined in 2005-2006, and to interpret its significance by means of immunoblotting. One hundred and seventy-seven (7.3%) of the patients were VCA IgG-positive, VCA IgM-negative and EBNA-1 IgG-negative, 15 of whom (8.5%) presented with heterophile antibodies. Analysis by age class showed that the prevalence of isolated VCA IgG ranged from 4.5% in the subjects aged 1-10 years to 9% in those aged >60 years. Immunoblotting allowed 18.9% of the cases to be classified as acute and 81.1% as past infections, the latter being observed in about 37% of the patients aged less than 10 years and in 100% of those aged >30 years. Therefore, in our case series, the presence of isolated VCA IgG was associated usually with past infection, particularly among adults. In children aged less than 10 years, it was associated mainly with acute infection but as past infection may be present in about one-third of such children, this possibility should not be overlooked.

Primary Sjogren's syndrome associated with inclusion body myositis

To describe three new patients with inclusion body myositis (IBM) associated with primary Sjögren's syndrome (pSS) and summarize the clinical and serological picture for all six patients reported so far. Three out of 518 (0.6%) pSS patients followed in our department over a period of 15 yr (1985-2000) also presented IBM. The diagnosis was based on histological criteria. Previous reports described four more patients with IBM associated with pSS. Five out of six were females; the mean age of IBM onset was 53.3+/-14.0 yr and the disease duration 8.0+5.8 yr. Four out of six patients presented IBM several years after the onset of pSS. Four out of six patients presented extraglandular manifestations, such as arthralgias, vitamin B12 deficiency, interstitial kidney disease and biliary cirrhosis. The serological picture did not differ significantly from that observed in pSS alone. Although rare, IBM may be seen in patients with pSS and it affects predominantly women. The clinical and pathological pictures do not differ from those observed in idiopathic IBM. A common autoimmune pathway in these two diseases, but no definite conclusions can be drawn.

Lack of correlation between sensitivity characteristics of the tests for hepatitis C virus antibodies estimated with serially diluted and natural low-reactive control specimens

Sensitivity characteristics of seven commercial ELISA test systems for the detection of antibodies to hepatitis C virus were assessed using control panels consisting of: (i) serial dilutions of pooled sera highly reactive for anti-HCV; (ii) serial dilutions of RIBA 3.0 HCV SIA positive control; and (iii) natural (non-diluted, non-spiked) sera low-reactive for anti-HCV. ?Dilutional sensitivity? values estimated with these two kinds of highly reactive samples did not coincide and were not found to correlate with the proportion of natural low-reactive specimens detected by each test. Thus, laboratories assessing sensitivity of anti-HCV ELISAs should take into consideration the nature and properties of the control material used. Natural low-reactive control specimens are preferable because they adequately reflect the real serological picture of early stage of HCV infection.

74-Year-Old-Woman With Cough and Proptosis

74-Year-Old-Woman With Cough and Proptosis

Hepatitis B virus strains in Thailand: Genomic variants in chronic carriers

Genetic heterogeneity of the hepatitis B virus (HBV) has been shown to influence the serological pattern and clinical picture in HBV infection. Thailand has a high transmission rate of HBV, but the molecular epidemiology of HBV strains circulating in this region was hitherto unknown. In this study, the HBV strains from 34 Thai HBsAg-positive patients were investigated. In a proportion of these samples, an antigenically important region of the S gene (n = 18), and the pre-S2 and precore genes (n = 15) were sequenced after PCR amplification. Four strains had in-frame deletions of an upstream region of the pre-S2 gene, with all deletions ending at the same nucleotide. In one of three anti-HBe positive strains without a translational stop at codon 28 of the precore gene, there was a one nucleotide insertion in the precore gene. This insertion would cause a frame shift and result in a nonsense protein being expressed, thus providing one explanation for the lack of HBeAg in this patient. Several rare or unique amino acid changes in the region between residues 120 and 161 of the S protein were found. Glycine 145 was changed to alanine in one strain, and this position showed an apparent mixture of glycine and arginine in another. In total, 10 strains displayed unexpected changes that were not related to the normal variability between subtypes or genetic subgroups. It is concluded that there is considerable heterogeneity in HBV strains in Thailand and that this could have clinical and epidemiological importance in a region with high HBV transmission rates.

HLA-B15: a widespread and diverse family of HLA-B alleles.

HLA-B15 embraces a multiplicity of antigenic specificities which vary in their distribution amongst human populations. To correlate B15 molecular structure with the serological picture we have sequenced alleles encoding the various subspecificities of the B15 antigen: B62, B63, B75, B76 and B77, and a number of "variants" of these antigens including the 8w66 split of B63. HLA-B63 (B*1517) and 8w66 (B*1516) heavy chains have sequence identity to B17 in the alpha 1 helix correlating with the antigenic crossreactivity of these molecules. HLA-B77(B*1513) and B75 (B*1502) heavy chains differ solely in segments determining the Bw4 and Bw6 public epitopes, consistent with the serological description of the B77 and B75 antigens. One allele encoding the B76 antigen (B*1512) appears to be the product of gene conversion between the HLA-A and -B loci and differs from B*1501 in codons 166 and 167. In contrast, a second allele encoding the B76 antigen (B*1514) differs from B*1501 by an unrelated substitution in codon 167 which confers similarily with B45, an antigen crossreactive with B76. A third allele encoding B76, B*1519, differs from B*1512 by a unique point substitution in exon 4. Three alleles encoding variant B15 and B62 antigens (B*1508, B*1511 and B*1515) differ from B*1501 by localized clusters of substitutions that probably result from interallelic conversion. The B15 sequences described in this paper, in combination with those previously determined, define a family of 22 alleles, including those encoding the B46 and B70 antigens. Within this family the patterns of allelic substitution are analogous to those of other HLA-A and -B families, in that pairwise differences almost always involve functional positions of the antigen recognition site and recombination is the major agent of diversification.

Failure to detect a prozoning anti-Fya in the serum of a chronically transfused patient

Abstract A 78-year-old white male presented to our facility with vascular occlusion. He was Group A, D-positive, with a negative indirect antiglobulin test (antibody screen). Records at our facility, 4 years prior to this admission, indicated a history of anti-Fya, and Fy(a−) units were provided. A referring hospital had transfused the patient for “chronic anemia” (1-3 units weekly for 2 years), and he had received eight units (untested for Fya) immediately prior to his transfer to our facility for acute hemorrhage. Only the presence of anti-IH in the serum was documented. To detect possible immune red cell destruction, the patient was monitored by our facility at 24-hour intervals with a direct antiglobulin test and antibody screen. On day 4, a 4+ anti-Fya was identified in the serum and the DAT was negative. Three days later anti-K was also identified. The serologic picture remained unchanged for 10 days, when the DAT became positive. Concurrently, a mixed-field Fya typing (on the patient’s chloroquinediphosphate-treated cells) was detected. Repeat Fya typing of all units transfused at our facility confirmed their Fy(a-) status. From the day of admission, eluates on every sample, using a low pH technique, showed anti-Fya specificity. Titration of the anti-Fya but not in neat serum. Although a prozoning phenomenon is uncommon, thi in the sample drawn on admission reacted from a dilution of 4 through 2,048 s case study suggests that a prozoning anti-Fya present in the patient’s serum may have been a contributing factor to his “chronic anemia.” Intmunobenurtology 1992;8:44–46.

Cryoglobulinemia in autoimmune rheumatic diseases. Evidence of circulating monoclonal cryoglobulins in patients with primary Sjögren's syndrome.

The incidence and nature of cryoglobulins, as well as their correlation with the clinical and serologic picture of Sjögren's syndrome (SS), were studied in the sera of 30 consecutive primary SS patients. Sera from 29 patients with systemic lupus erythematosus, 58 patients with rheumatoid arthritis, and 125 healthy blood donors were also studied. It was shown that one-third of the patients with SS had cryoglobulinemia. These cryoglobulins were mixed monoclonal IgM immunoglobulins, whereas those observed in systemic lupus erythematosus and rheumatoid arthritis patients were mixed polyclonal. The nature of the cryoglobulins was demonstrated using high-resolution electrophoresis combined with immunofixation. The presence of cryoglobulins in the sera of SS patients correlated with extraglandular disease and with antibodies to Ro (SS-A) and IgM rheumatoid factor. SS patients with cryoglobulins had lower serum C4 levels than did patients without cryoglobulins. These findings suggest that SS expresses, in addition to polyclonal B cell hyperreactivity, a monoclonal process in the absence of lymphoid neoplasia. Further, they show that the extraglandular manifestations of the syndrome may be due to an immune complex-mediated pathology.

Opisthorchis viverrini: pathogenesis of infection in immunodeprived hamsters.

Opisthorchis viverrini infections were established in immunologically intact and T cell deprived hamsters. T cell deprivation appeared to have no effect on worm establishment or egg production. Histopathologically, intact and deprived animals showed similar degrees of bile duct hyperplasia and periductular fibrosis, though there was a marked reduction in the intensity of the periportal inflammation in the majority of T cell deprived animals. Serum transaminase levels were significantly raised in intact animals by 25 days after infection, whilst levels remained within normal limits throughout the infection period for the majority of the T cell deprived animals. The antibody response to parasite antigens as determined by immunoelectrophoresis, was impaired in T cell deprived animals. Attempts to correlate the serological picture with transaminase levels at three time points after infection and also with the extent of periductular inflammation seen on killing, proved largely unsuccessful. These results indicate that T cell deprivation of the hamster host ameliorates the periductular inflammatory response provoked by O. viverrini in this species. It is suggested that such inflammatory responses are evoked by parasite antigens which gain access to portal tract and surrounding areas, and that such reactions are immunopathological in their outcome to the host, resulting in liver cell death and subsequent replacement of resolving inflammatory and necrotic areas with fibrotic tissue.

Serological response of turkey hens to vaccination with Salmonella hadar and its effect on their subsequently challenged embryos and poults

An inactivated Salmonella hadar vaccine was administered to parent turkey stock and the progeny were subjected to challenge with S hadar. There was some evidence that eggs from vaccinated birds were more resistant to growth of the organism. When compared with similarly infected poults from unvaccinated parents, a markedly different serological picture and pattern of salmonella excretion was seen. It appeared that the passive immunity induced by the vaccine encouraged the faster establishment of other gut Enterobacteriacae, even in the presence of large numbers of S hadar.

The Patient With Multiple Alloantibodies-Reply

In Reply.— We are grateful for the interest that Mr Issitt and Dr Tomasulo have taken in our report and welcome the opportunity to respond to their letter. The patient presented a complex serological picture, which was abbreviated in the case report. She was studied by two American Association of Blood Banks reference laboratories during a period of several months in 1978. There was a difference of opinion as to whether the presence of anti-Jk b could be proved conclusively. The high-frequency antibody was thought initially to be anti-Joseph, but ultimately its specificity could not be determined. Anti-Lewis a , anti-Lewis b , and an additional unidentified antibody were suspected. Two months after the delayed hemolytic transfusion reaction, an IgG autoantibody, reacting less strongly with Rh mull cells, developed. The exact cause of the delayed hemolytic transfusion reaction could not be determined, and the reference laboratory recommended that transfusion be restricted to