Hepatitis A outbreaks among illicit drug users and their contacts in Queensland, 1997.

OBJECTIVE: To describe five outbreaks of hepatitis A virus (HAV) infection associated with illicit drug use during a statewide outbreak of HAV infection in Queensland. DESIGN: Risk factor prevalence survey. PATIENTS AND SETTING: All 875 cases of HAV infection notified to Public Health Units in Queensland in the 12 months to 30 November 1997. MAIN OUTCOME MEASURE: Type and prevalence of illicit drug use. RESULTS: Risk factor assessment was completed for 804 cases (91.9%). We identified five outbreaks of HAV infection linked to illicit drug use. These outbreaks accounted for 24.6% (215/875) of all notified cases and 39% (190/482) of notified cases in the 15-34 years age group. The main type of illicit drug use in four of the five outbreaks was injecting drug use (74%; 118/160), while in the other outbreak it was sharing of smoking implements for marijuana (38%; 21/55). CONCLUSION: Illicit drug use may be an under-recognised risk factor for HAV infection, particularly in young people. Faecal-oral transmission through poor personal hygiene, including sharing of implements for smoking marijuana, is the most probable route of transmission in these drug-linked outbreaks. The role of contaminated drug and needle-sharing remains to be clarified.

Two contiguous outbreaks of dengue type 2 in north Queensland.

OBJECTIVES: To investigate two outbreaks of dengue type 2 in north Queensland, one in the Torres Strait beginning in late 1996, the other in a Cairns suburb in early 1997. DESIGN: Epidemiological investigation of all laboratory-confirmed cases of dengue, entomological investigation of the local environment, and laboratory analysis of the isolated dengue viruses. MAIN OUTCOME MEASURES: Numbers of confirmed and of locally acquired cases; virus serotype; comparison of nucleotide sequences between viruses isolated from the two outbreaks; and Breteau Index (BI = number of containers with larvae of the mosquito vector Aedes aegypti found per 100 houses investigated) on the affected islands and in the Cairns suburb. RESULTS: There were 201 confirmed cases of dengue in the Torres Strait outbreak, which lasted nearly seven months, and seven confirmed cases in the Cairns outbreak, which lasted about nearly 11 weeks. Most (190) were confirmed as dengue type 2. Nucleotide sequencing of viruses isolated from the two outbreaks showed they were identical. Ae. aegypti breeding sites were very common on the five Torres Strait islands surveyed (BIs, 73-219--high risk), but less so in the Cairns suburb (BI, 23). The most common breeding sites were water storage reservoirs, particularly rainwater tanks, on the outer Torres Strait islands, discarded containers (such as plastic containers, buckets and tyres) on Thursday Island, and garden items (such as flowerpot bases and jars) in Cairns. CONCLUSIONS: The virus responsible for the Cairns outbreak was most probably introduced from the Torres Strait, whereas the virus responsible for the Torres Strait outbreak was imported from Papua New Guinea. Preventive strategies tailored to specific locations are needed to reduce breeding of Ae. aegypti in north Queensland, and the consequent risk of future outbreaks of dengue.

An amylase-producing serous cystadenocarcinoma of the ovary.

A patient with an amylase-producing serous cystadenocarcinoma of the ovary had elevated serum and urine amylase levels and high levels of amylase in pleural and ascitic fluids. Serum and urine amylase levels reflected both surgical removal of tumor mass and response to chemotherapy. Tumor homogenates had pronounced amylase activity. Salivary type amylase isozyme patterns were found in electrophoresis of samples from all sources. Ascites tumor cells were successfully cultured and salivary type amylase was found in the culture media throughout 5 passages. The tumor was classified by light microscopy as poorly differentiated serous cystadenocarcinoma. Ultrastructural studies on the tumor were consistent with that diagnosis. Amylase was detected in the cells of the tumor examined by the immunoperoxidase technique.

Linkage relationships and multipoint mapping of the human parotid salivary proteins (Pr, Pa, Db).

Based on data from 76 informative families, linkages between Pa and Pr and between Pr and Db have been established by two-point linkage analysis. In both pairs of loci, there were no significant sex heterogeneity in recombination fractions. Linkage between Pa and Db cannot be established based on two-point analyses, but a significant sex difference in the recombination fraction between Pa and Db was observed. Strong confirming evidence was obtained from three-point analysis to place Pa, Pr, and Db in one linkage group. The most likely order is Pa-Pr-Db, but the relative odds over second order Pr-Pa-Db are small. Haplotype frequencies of Pr, Pa, and Db were obtained based on the phenotypes of the 685 random Caucasians, providing evidence for marked linkage disequilibrium among the three loci.

Heritable salivary proteins and dental disease.

A sample consisting of 92 black subjects was examined in this study. According to results of preliminary statistical tests there is a significant relationship between certain genetically determined salivary factors and individual susceptibility to dental disease in the racial group studied. These findings are been validated by the examination of data from several additional studies involving large samples.

Human salivary proline-rich (Pr) proteins: a posttranslational derivation of the phenotypes.

The acidic proline-rich proteins (Pr) showing genetic polymorphism were purified from human parotid salivas by gel filtration and ion exchange chromatography. Molecular weight determinations, amino acid composition analyses, and polypeptide mapping experiments indicate that the Pr 3 protein is a fragment of the Pr 1 protein. Studies of a parotid saliva factor capable of converting Pr 1 to Pr 3 and Pr 2 to Pr 4 indicate that Pr 3 and Pr 4 are generated from Pr 1 and Pr 2, respectively. Evidence suggests that the converting factor is a protease capable of posttranslationally cleaving Pr 1 and Pr 2, the primary or derived products of alleles Pr1 and Pr2.

Urinary pepsinogen isozymes: a highly polymorphic locus in man.

A genetic analysis of human urinary pepsinogen isozymes is presented. Nine discrete phenotypes were identified in a population survey of 215 unrelated Caucasian individuals. The phenotypes were characterized by differences among the staining intensities of the activated group I pepsinogens, Pg 5, Pg 4, Pg 3, and Pg 2. The genetic studies demonstrated that the codominant expression of four alleles, PgA, PgB, PgC and PgD, at a single genetic locus determined the nine phenotypes identified. Linkage analysis excluded close linkage of the Pg locus with the chromosome 6 markers HLA, GLO1, and Bf.

Genetic control of the eighth component of complement.

Using isoelectric focusing in polyacrylamide gel and a hemolytic assay for development of patterns, extensive, structural polymorphism in human C8 has been delineated. Two alleles, C8A and C8B, have been identified in orientals, with gene frequencies of 0.655 and 0.345. In blacks, what appears to be a third common allele was found, so that frequencies were 0.692, 0.259, and 0.049 for C8A, C8B, and C8A1. In whites, C8A1 was rare with a frequency of 0.003, and frequencies for C8A and C8B were 0.649 and 0.349. Inheritance was autosomal codominant in family studies and the distribution of types in random unrelated populations fit the Hardy-Weinberg equilibrium in all groups. C8 allotypes have been determined for two previously studied families, each with a homozygous C8-deficient propositus. This study suggests that C8 deficiency is a silent or null allele of the C8 structural locus, and that half normal levels of C8 cannot be used as a single criterion for the establishment of heterozygous C8 deficiency. C8 allotypes, as well as 18 other autosomal markers, were also determined for 24 families. The C8 structural locus is not closely linked to these markers, including the human histocompatibility loci complex.

Hyperamylasemia in diabetic ketoacidosis: sources and significance.

The origins and clinical significance of hyperamylasemia during diabetic ketoacidosis are unclear. We have therefore correlated important clinical and laboratory indices of diabetic ketoacidosis with sequential determinations of serum and urine amylase concentrations, amylase/creatinine clearance ratios, and specific amylase isozyme types. Hyperamylasemia occurred in 79% of our patients with diabetic ketoacidosis, often after admission to the hospital. Among these patients, 48% had pancreatic-type, 36% salivary-type, and 16% mixed-type (pancreatic and salivary) hyperamylasemia. There were no correlations between the presence, degree, or isozyme type of hyperamylasemia and most laboratory or clinical characteristics, including gastrointestinal symptoms. Patients with pancreatic-type hyperamylasemia tended to have higher amylase/creatinine clearance ratios, but it was not possible to unequivocably diagnose acute pancreatitis during diabetic ketoacidosis with current routine clinical or laboratory procedures.

Human pancreatic alpha-amylase: phenotypic codominance and new electrophoretic variants.

The genetic heterogeneity of human pancreatic alpha-amylase (alpha-1,4-glucan 4-glucanohydrolase, E.C. 3.2.1.1) has been better defined through the development of an asparagine buffered electrophoretic gel system. Three alleles had been identified for the pancreatic amylase locus, AMY2, with two variant alleles as autosomal dominant traits on Tris HCl buffered sheet gels. The asparagine buffered sheet gel now allows the differentiation of the genotypes AMY2B/AMY2B,AMY2B/AMY2A, and AMY2B/AMY2C, thus classifying these three alleles as codominants. Asparagine buffered polyacrylamide gels and thin layer polyacrylamide isoelectric focusing aided in the identification of three new pancreatic amylase variants: AMY2D,AMY2E, and AMY2F. AMY2E has been identified only in AMY2B and AMY2E individuals. This allele is proposed as a quantitative activity variant with essentially the same electrophoretic mobility as AMY2A. The other new autosomal variants have each been identified in single white families. AMY2D is dominant and AMY2F is a codominant trait as shown on thin layer polyacrylamide isoelectric focusing gels.

Autosomal dominant "spheroid body myopathy".

A slowly progressive autosomal dominant neuromuscular disease--termed spheroid body myopathy--is described in four successive generations and documented by muscle biopsies in five patients of two generations. With an onset in adolescence, the disease proceeds to some motor incapacitation, but life span is apparently not shortened. The salient morphologic feature is the presence of spheroid bodies, chiefly occurring in type 1 myofibers. Ultrastructurally, these spheroid bodies are composed of tiny filaments but are devoid of organelles; in some cases they resemble cytoplasmic bodies. "Smearing in the 1-band" is a frequent and early finding. At a later age, signs of denervation are also present, both clinically and in muscle biopsies. The clinical and morphologic features justify the designation of this neuromuscular condition as a distinct entity.