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Biomedical subjects

T Poon-King

Publications and source records attributed to T Poon-King.

At least 19 recordsLinked to original sources

Ciguatera fish poisoning in industrial ship crewmembers: a retrospective study in a seaport general practice in Trinidad and Tobago.

The objective of this study was to outline the epidemiology of Ciguatera fish poisoning as seen in a general practice serving two industrial seaports in Trinidad and Tobago, in order to highlight the potential public health implications. A retrospective study was undertaken of all the cases of Ciguatera fish poisoning identified between November 1, 1992 and October 31, 1998 in a seaport general practice to identify signs, symptoms and treatment. An investigation of one outbreak was undertaken. Four outbreaks affecting 42 male ship crewmembers were identified. The suspect fish were caught in northern Caribbean waters en route to Trinidad and Tobago. The most common early symptoms were diarrhoea, vomiting, abdominal cramps, pruritus and tiredness. In the third outbreak, dysaesthesia was common. Progression to muscular weakness, ataxic gait, unsteadiness and other neurotoxic signs were seen in moderate to severe disease. Hypotension was an important prognostic sign in the initial case. Treatment was symptomatic and supportive and included vitamins B12 and BCO, folic acid, prostigmine, steroids and antihistamines as indicated. In the investigation of the second outbreak, the relative risk of 'eating fish meat' was 5 (95% CI 1.45, 17.27, p < 0.0001). Abdominal symptoms, pruritus, and muscle weakness with a history of consuming a fish-meal were diagnostic indicators of 'ciguatera fish poisoning.' All cases were industrial ship crewmembers. It is suggested that increased clinician awareness with early and appropriate treatment, and focussed public health intervention may help limit the potential public health impact of ciguatera poisoning in industrial ship crewmembers and other fish-consuming communities in the future.

Adult↗

Genetic variation at the immunoglobulin allotype loci in Creoles of Trinidad.

The sera of a sample of 204 Creoles from Trinidad were tested for the presence of polymorphic gene complexes occurring on immunoglobulin light- and heavy-chain molecules including the allotypic markers IGKC 1, IGHA2 1 and 2, IGHG1 A, X, F, and Z, and IGHG3 G, G5, B0, B1, B3, B4, B5, C3, C5, S, and T. Nine IGHG (GM) haplotypes occur in polymorphic frequencies (greater than .01) in this population, including known African, Asian, Caucasian, and Amerindian marker haplotypes. Significant differences (P less than .01) were found in the frequency distributions of three IGHG (GM) haplotypes and the frequency of IGKC*1 in these data and data from Creole populations of Belize and St. Vincent. The Creoles of Trinidad and St. Vincent are more similar in IGHG (GM) haplotype distributions than are Trinidad and Belize populations. Previous testing has revealed no significant differences between St. Vincent and Belize Creoles at the Ig allotypic loci. Analysis of migration patterns in the Caribbean suggests that different rates of Asian migration have maintained regional diversity at these loci, while continuous gene flow from the eastern Caribbean to Trinidad has had a relative homogenizing effect on the gene pools of this area.

Chi-Square Distribution↗

Streptococcal serotypes newly associated with epidemic post-streptococcal acute glomerulonephritis.

The increasing incidence of reported scabies in Trinidad, from 24.2/100,000 population in 1984 to 59.5/100,000 in 1985, led to a careful monitoring in 1986 of all patients with post-streptococcal acute glomerulonephritis (PSAGN). There were 181 cases of PSAGN; 84 beta-haemolytic streptococcal isolates from 72 patients were sent to the Central Public Health Laboratory, Colindale, for grouping and serotyping. The PSAGN epidemic of 1986 was bimodal. Streptococci of M-type 73 appeared to be associated with the first phase (March-May) and comprised 20% of the isolates serotyped. New to Trinidad, streptococci of M-type 48 (4% of the isolates serotyped) preceded the first phase of the epidemic and were isolated from two patients with PSAGN. Provisional type (PT) 5757, also new to Trinidad, had been previously identified only among serotypes from the United Kingdom and the Federal Republic of Germany. This type was isolated from seven patients, in six from skin lesions and in one from the throat. PT 5757 occurred during the first wave of the epidemic and comprised 14% of the strains serotyped. Thus, the first wave of the bimodal epidemic involved serotypes M73, M48 and PT 5757. The more intense second phase (July-October) was associated with the previously documented nephritogenic M-type 55.

Acute Disease↗

Presence of a non-HLA B cell antigen in rheumatic fever patients and their families as defined by a monoclonal antibody.

Numerous investigators have suspected that there is a genetic predisposition to rheumatic fever (RF). In this context we have recently produced a series of monoclonal antibodies directed against B cells obtained from RF patients one of which, labeled D8/17, identifies a B cell antigen present in 100% of all RF patients studied. While the highest percentage of positive cells were exhibited by RF probands (33.5% +/- SE), the percentage of cells in unaffected siblings and parents was 14.6 and 13%, respectively. The percentage of positive cells in APSGN probands, unaffected siblings, and parents was 2.96, 3.86, and 2.8%, respectively. A low level of B cells (5-7%) bearing the D8/17 marker was seen in control patients. The segregation pattern of the phenotypes defined by the percentage of D8/17 positive cells within HLA-typed RF families are consistent with an autosomal recessive mode of inheritance not associated with the human MHC system. We postulate that these phenotypes indicate the presence of at least one necessary genetic factor for susceptibility to RF.

Analysis of Variance↗

Leucocyte suppression in treatment of 72 patients with paraquat poisoning.

72 patients who had ingested more than 10 ml 20% or 24% liquid paraquat concentrate were treated for 2 weeks with high doses of dexamethasone and cyclophosphamide, forced diuresis with liberal potassium supplements, and, to eliminate paraquat from the gut, Fuller's earth suspension, activated charcoal, and magnesium sulphate. 52 patients (72%) survived. Serum paraquat concentrations were measured retrospectively in samples from 25 patients. 18 had levels of 2-76 mg/l; 6 survived and 12 died. The other survivors were a patient with a serum level of 0.5 mg/l at 24 h and 6 with positive urine tests but no measurable paraquat in serum collected 8-16 h after admission.

Adolescent↗

Antibodies to basement membrane collagen and to laminin are present in sera from patients with poststreptococcal glomerulonephritis.

Sera from patients with poststreptococcal glomerulonephritis (PSGN) known to have antibodies to proteoglycans were studied for the presence of antibodies against other basement membrane (BM) components. BM collagen (type IV) was isolated in the native state by extracting bovine anterior lens capsule (ALC) with 0.5 M acetic acid. The 7-S (collagenous) domain and the NC-1 (noncollagenous) domain of type IV collagen were obtained after bacterial collagenase digestion of ALC followed by gel filtration. Laminin was isolated from the mouse EHS tumor and fibronectin from human plasma. Immunologic studies, using an ELISA and electroimmunoblot, revealed the presence of antibodies that reacted with intact, native type IV collagen and the 7-S collagenous domain of this molecule. Reaction with the NC-1 (noncollagenous) domain was minimal, and not higher than that obtained with control sera. Laminin reaction strongly with the patients' sera, but fibronectin did not. Unlike sera from patients with Goodpasture syndrome, which contain antibodies primarily against the NC-1 (noncollagenous) domain of type IV collagen, sera from patients with acute PSGN contain antibodies against all the major macromolecular components of BM. This difference in immunologic reactivity may account for the observed differences in the pathologic picture at the glomerular level.

Anti-Glomerular Basement Membrane Disease↗

Serial studies on the cellular immune response to streptococcal antigens in acute and convalescent rheumatic fever patients in Trinidad.

Acute rheumatic fever (ARF) has the characteristics of an autoimmune disease, triggered by cross-reactive antigens shared by the group A streptococcus and a variety of tissues including the heart, endothelium, and basal ganglia. Using two parameters of cellular reactivity, migration inhibition and blastogenic transformation, ARF patients from Trinidad show significant lymphocyte reactivity to streptococcal antigens, particularly those from an ARF associated streptococcal strain. This reactivity, studied over a 2-year period, peaked at 1 to 6 months after the acute onset and remained significantly elevated for at least 2 years. The reactivity is directed mainly toward a nonionic detergent extractable material in the cell membrane. These studies suggest a possible streptococcal strain specificity in ARF and demonstrate persistent sensitization, which explains the increased susceptibility to recurrences in the 2 years following the acute episode.

Antigens, Bacterial↗

Sera from patients with poststreptococcal glomerulonephritis contain antibodies to glomerular heparan sulfate proteoglycan.

Antibodies, found in human sera from patients with poststreptococcal glomerulonephritis, against proteoglycans (PG) derived from bovine and human glomeruli were investigated. PG were isolated by 4 M guanidine-HCl extraction of whole glomeruli, followed by DEAE-Sepharose CL-6B ion exchange chromatography. The anionic fractions were further purified by chromatography on Sepharose CL-4B. Biochemical analysis of the two resulting peaks revealed the presence of high molecular weight anionic material containing protein, uronic acid, glucosamine, and galactosamine. Enzymatic and chemical susceptibilities indicated the presence of heparan sulfate PG and a galactosamine-containing PG. Immunologic studies revealed the presence of anti-PG antibodies to both PG peaks of the Sepharose CL-4B column in glomerulonephritis sera. Inhibition studies using an ELISA demonstrated that heparan sulfate was a major antigenic determinant. Cross-reactivity with both mammalian and streptococcal hyaluronate was noted. Inhibition studies also indicated the presence of a second antigenic site containing N-acetylgalactosamine, possibly representing chondroitin or dermatan sulfate PG.

Acute Disease↗

Group G streptococci in healthy school-children and in patients with glomerulonephritis in Trinidad.

The group G streptococcus has generally not been considered a prominent pathogen. In a 1982 study of the colonization rate by beta-haemolytic streptococci in apparently healthy children, age 5-11 years, 25 of 69 isolates belonged to group G. This surprisingly high rate of group G colonization (14.3%) led to a retrospective study of school surveys in 1967 which showed that the colonization rate with this organism was 2.3% (range 1.3-3.5%). A review of bacitracin-sensitive streptococcal isolates from hospital admissions of patients with acute glomerulonephritis (AGN), rheumatic fever, and their siblings, between January 1967 and July 1980, was conducted. Of 1063 bacitracin-sensitive isolates, 63 were group G, and 52 of these were isolated from AGN patients and their siblings, i.e. 7 from skin lesions of AGN patients, 40 from the throats of siblings and only 5 from the skins of the siblings. The other 11 group G isolates were from rheumatic-fever patients and their siblings. Thus, the group G colonization rate fluctuates in the population. The isolation of only group G streptococci from skin lesions of patients with AGN suggests a possible association between group G streptococcal pyoderma and acute post-streptococcal glomerulonephritis.

Acute Disease↗

Suppression of cellular reactivity to group A streptococcal antigens in patients with acute poststreptococcal glomerulonephritis.

Lymphocyte reactivity to group A streptococcal antigens was studied in patients with acute poststreptococcal glomerulonephritis (AGN) in Trinidad. When compared with controls, patients with AGN had significantly lower responses. This finding was most prominent in the patients who were greater than 10 years of age at onset of disease. The total number of T lymphocytes was found to be decreased in patients with AGN, and in particular, the percentage of cells bearing Fc receptors for IgG (T gamma) was low. Removal of the T gamma-cell population abrogated the lymphocyte response to streptococcal antigens. However, removal of the adherent cells resulted in enhancement of the response to the level of the normal control population. The presence of suppressor activity in the adherent cell population of older patients with AGN may be an important factor in progression of AGN to chronic disease.

Adolescent↗

Immunological studies of post-streptococcal sequelae: serological studies with an extracellular protein associated with nephritogenic streptococci.

Using the Ouchterlony double diffusion and the crossed-immunoelectrophoresis techniques the reactivity to a purified extracellular product of nephritogenic group A streptococci (NASP) was examined with both acute and convalescent sera obtained from patients with documented post-streptococcal glomerulonephritis and patients with documented acute rheumatic fever. The streptococcal antigen utilized in these studies was first purified on SDS gels and then eluted from the gel, resulting in a single protein band on SDS electrophoresis. Double diffusion studies revealed that only nephritis patients reacted to this extracellular product associated with nephritogenic strains, whereas rheumatic fever sera produced no line of precipitation. An assay of serial bleedings from nephritis patients suggested that the antibody reactive to the NASP was in higher titre in the acute phase of the disease and decreased with convalescence. In confirmation of these findings, crossed-immunoelectrophoresis experiments were conducted with a battery of sera from acute nephritic and non-nephritic patients against the NASP antigen. A striking increase was detected in the reactivity of nephritis patients (96%) compared to non-nephritis sera (15-20%). Comparison between acute and convalescent sera using this technique confirmed the finding of decreasing antibody titre with resolution of disease. These findings of a specific humoral response in patients with acute post-streptococcal nephritis to the NASP of nephritogenic strains further implicates an aetiological function to this protein.

Adolescent↗

Skin infections and immunoglobulin A in serum, sweat, and saliva of patients recovered from poststreptococcal acute glomerulonephritis or acute rheumatic fever and their siblings.

Differences in hygienic habits and base-line secretory immunoglobulin (Ig) A which might have contributed to the prevalence of skin infections and/or absence of increased serum IgA values were sought in patients with poststreptococcal acute glomerulonephritis (nephritis) in contrast to patients with acute rheumatic fever in Trinidad by studying patients and their siblings after the patients had recovered from these diseases. The overall history of skin infections was similar at this time in all groups, although they had been much more common in patients with nephritis and their families at the time of acute illness. The recovered nephritis patients bathed slightly less often than the other individuals, used a cream or lotion after bathing rather than coconut oil, and tended to sweat less than the others, but none of these differences was statistically significant. Neither were significant differences demonstrated in amounts of IgA and IgG in serum and saliva of recovered nephritis patients and their siblings compared to recovered rheumatic fever patients and their siblings, while only small amounts of IgA and IgG were present in any sweat, and probably had been transuded rather than secreted. These studies suggest that the lower serum IgA titers in patients with nephritis compared to patients with rheumatic fever in Trinidad do not reflect basic differences in serum IgA or secretory IgA as measured in saliva, and that IgA is not secreted by the eccrine glands.

Adolescent↗

Serum immunoglobulin A and antibody to M-associated protein in patients with acute glomerulonephritis or rheumatic fever.

Serum immunoglobulin A (IgA) was markedly increased in 80% of 50 patients with acute rheumatic fever in Trinidad in contrast to 20% of 63 patients with acute glomerulonephritis, whereas serum IgG was increased in nearly all of both groups. Since total antibody to M-associated protein (MAP) (assessed by complement fixation) is the only antibody as yet consistently found to be of higher titer in patients with acute rheumatic fever than in patients with acute glomerulonephritis in Trinidad, it was measured and the titers were related to serum levels of IgA. The titers of total antibody to MAP were greater than or equal to 40 in 58% of the rheumatic fever patients, 43% of the nephritis patients, and 8% of well school-children. However, its presence in rheumatic fever patients did not correlate directly with amounts of serum IgA present (r = 0.0507). Moreover, titers of total antibody to MAP related equally well to enzyme-linked immunosorbent assay indicated amounts of IgG antibody (r = 0.3939) and IgA antibody (r = 0.3054) to MAP in rheumatic fever patients but not in nephritis patients (r = 0.0301 for IgA antibody and 0.6909 for IgG antibody to MAP), whereas they related best to IgM antibody to MAP in the school-children (r = 0.4204).

Acute Disease↗

Streptococcal neuraminidase and acute glomerulonephritis.

We examined the hypothesis that streptococcal neuraminidase may alter host serum immunoglobulin G so that autoantibodies are formed which lead to immune complexes and acute glomerulonephritis. We confirmed the observation that T-type 4 and T-type 12 streptococci (both associated with acute glomerulonephritis) are the most likely of many types studied to produce neuraminidase. However, we did not find this enzyme to be produced by any of 23 streptococcal strains isolated from patients with nephritis, whereas it was produced by two strains from patients with rheumatic fever and by one strain from a patient with scarlet fever. Also, we were unable to find direct or indirect evidence of increased neuraminidase activity in the sera of six patients with acute glomerulonephritis when they were compared with the sera of six patients with acute rheumatic fever and with those of six normal subjects.

Acute Disease↗