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Biomedical subjects

J E Maynard

Publications and source records attributed to J E Maynard.

At least 199 records · Page 11Linked to original sources
PubMed1970

A study of growth, morbidity and mortality among Eskimo infants of western Alaska.

One of the most serious problems affecting the American Eskimo is that of disease and death in infants. A study undertaken to inquire into the growth and development components and the nutritional components of this morbidity and mortality and to verify and amplify the inadequate health statistics relating to this group revealed an infant mortality rate 4 times that for the USA as a whole, with a 16% under-registration of infant deaths. The majority of infant deaths occurred in the post-neonatal period, with respiratory infections constituting the most frequent cause of morbidity and mortality. There was a significant inverse association between infant haemoglobin level and frequency of respiratory and total illness, providing one of the few specific epidemiological confirmations of a synergistic nutritional interaction between anaemia and infection.

Adult↗
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Hepatitis delta virus infection and Labrea hepatitis. Prevalence and role in fulminant hepatitis in the Amazon Basin.

To define more exactly the epidemiology of delta virus infection and confirm its role in causing fulminant Labrea hepatitis in the Amazon Basin, we studied the prevalence of delta virus infection among persons with acute and chronic hepatitis B virus infection in the Boca do Acre district of the southern Amazon Basin. Delta virus infection was found in 24% of asymptomatic hepatitis B virus carriers, 29% of acute nonfulminant hepatitis B cases, 74% of fulminant hepatitis B cases, and 100% of chronic hepatitis B cases. Chronic delta virus infection occurred primarily in older children and adults, while acute and fulminant delta virus infection occurred in young children as well. In fulminant hepatitis cases, delta virus superinfection of hepatitis B virus carriers was the most common serological pattern; histopathologic examination showed features identical to those described in fulminant hepatitis cases of similar etiology in Colombia and Venezuela. Delta virus infection is highly endemic in the southern Amazon Basin and is the principal cause of Labrea hepatitis.

Acute Disease↗
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Specific histologic features of Santa Marta hepatitis: a severe form of hepatitis delta-virus infection in northern South America.

Stimulated by observations in an outbreak of hepatitis delta-virus infection among Yucpa Indians in Venezuela, in which unusual histologic features were found, we studied 100 cases of fatal hepatitis from Colombia, South America, which had been obtained by autopsy or viscerotomy. These cases were considered to be "Santa Marta hepatitis," or "hepatitis of the Sierra Nevada de Santa Marta," which has been observed in this region for more than 40 years. Of the 100 cases, 19 had a variety of histologic lesions or were normal, and hepatitis delta-virus antigen was not demonstrated immunocytochemically in any of them. By contrast, 81 cases had a characteristic histologic picture with intense microvesicular steatosis associated with conspicuous eosinophilic necrosis of the hepatocytes, which apparently were sluggishly removed by cytolysis. Hepatitis delta-virus antigen was detected in 70% of the 81 cases, and the absence of detection of this antigen was often associated with poor tissue preservation and more extensive hepatocyte necrosis. A smaller percentage of patients had hepatitis B virus antigens detectable in liver tissue. The characteristic lesion in these 81 cases could be distinguished from other causes of microvesicular steatosis by the extensive eosinophilic necrosis. Other variable accompanying features included intraacinar, mainly macrophagic, scavenger cell inflammation, intense portal inflammation, a parenchymal regeneration, and ductular and arteriolar proliferation. Santa Marta hepatitis as a severe form of hepatitis delta-virus infection differs markedly from fulminant delta-hepatitis in Europe and the United States in which the microsteatosis with marked eosinophilic degeneration is not found. The causes for these differences are unknown but may relate to nutritional factors or environmental toxins.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, Viral↗
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Epidemiologic aspects of Santa Marta hepatitis over a 40-year period.

"Santa Marta" hepatitis has been recognized as an unusual type of severe hepatitis occurring in northern Colombia since 1930. Liver specimens from a historic viscerotomy series, used by Gast-Galvis to identify cases and describe epidemiologic features of this disease, were available for review and histopathologic staining for delta-virus. Of 86 liver specimens examined from cases of fulminant Santa Marta hepatitis, 81 showed a distinct histopathologic picture, in various stages of progression, with features of eosinophilic necrosis, microvesicular fat infiltration of the liver parenchyma and morula cells; 69% were positive for delta-antigen by immunoperoxidase staining. This disease occurred predominantly in several small towns within 50 km of Santa Marta, with mortality reaching 1.25 per 1,000 inhabitants per year during the 1940's. Children under age 15 were most commonly affected and males affected twice as frequently as females. Liver specimens obtained from children, or within 15 hr of death, or which showed early histologic stages of disease were most likely to be positive for delta-antigen. This and the accompanying study confirm the existence of a distinct type of fulminant hepatitis in Colombia for over 50 years. The epidemiologic and histopathologic features are comparable to severe hepatitis in Venezuela Indians and in the Amazon basin of Brazil, suggesting that all are caused by delta-superinfection of hepatitis B virus carriers.

Adolescent↗
PubMedDate not supplied

The epidemiology and clinical outcome of hepatitis D virus (delta) infection in Jordan.

The epidemiology and clinical outcome of hepatitis D viral infection in HBsAg-positive acute hepatitis, chronic liver disease, primary hepatocellular carcinoma and the symptomless carrier state was studied in Jordan. The prevalence of hepatitis D viral infection was significantly higher in patients with chronic liver disease (18/79, 23%) and acute hepatitis (17/108, 16%) than in symptomless HBsAg carriers (2/136, 2%). The highest prevalence of hepatitis D viral infection was found in patients with primary hepatocellular carcinoma (10/15, 67%) who were also significantly older than such patients without hepatitis D viral infection. Antihepatitis D virus IgM was detected persistently in 83% of patients with antihepatitis D virus-positive chronic liver disease and transiently in 41% of patients with acute hepatitis. A trend to increased mortality was observed in acute hepatitis D viral superinfection (25%) compared to hepatitis D viral coinfection (0%) and to antihepatitis D virus-negative HBsAg-positive acute hepatitis (4%). In patients with established chronic liver disease, however, neither survival nor histological parameters of disease activity were significantly different in the antihepatitis D virus-positive and antihepatitis D virus-negative groups. While the early stage of hepatitis D viral superinfection is associated with increased mortality, it appears that in patients with late-stage chronic liver disease, severe histological activity subsides, and survival is no longer influenced by the factor of hepatitis D viral infection. However, primary hepatocellular carcinoma appears to complicate the course of those antihepatitis D virus-positive patients surviving beyond this stage.

Acute Disease↗
PubMedDate not supplied

Global control of hepatitis B through vaccination: role of hepatitis B vaccine in the Expanded Programme on Immunization.

Hepatitis B is a disease that affects people throughout the world, and over 200 million are persistent carriers of the hepatitis B virus (HBV). The chronic sequelae of this infection include chronic active hepatitis, cirrhosis, and primary hepatocellular carcinoma. The development of safe and highly effective hepatitis B vaccines now provides the means by which HBV infection, including the HBV chronic carrier state, can be prevented and the related mortality significantly reduced. The cost of these vaccines has significantly decreased and will soon approach levels at which the cost-effectiveness (cost per death prevented) of hepatitis B vaccine will be similar to that of other childhood vaccines. Integration of hepatitis B vaccine into the Expanded Programme on Immunization for mass vaccination of infants in areas where HBV infection is endemic and morbidity is high would be the most effective means of providing the coverage necessary for effective control and prevention.

Carrier State↗
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Review of infectivity studies in nonhuman primates with virus-like particles associated with MS-1 hepatitis.

Using the technique of immune electron microscopy we have conducted hepatitis A infectivity studies in marmoset monkeys and chimpanzees. Marmosets inoculated with human serum containing the MS-1 strain of hepatitis A virus have developed hepatitis and seroconverted to 27 nm virus-like particles isolated from stools of humans in the early acute stages of hepatitis. Similar results have been observed through several marmoset subpassages, and the virus-like particles have been recovered from the liver of animals in the acute phase of hepatitis. Chimpanzees inoculated with stool filtrates containing the virus-like particles develop hepatitis with concomitant excretion of the particles in early acute phase stools and subsequent development of serum antibody to the particles. These studies provide evidence that the above particles constitute the virus of hepatitis A of the MS-1 prototype.

Acute Disease↗
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Viral hepatitis, type B, in experimental animals.

Evidence of natural infection with hepatitis B virus (HBV) in chimpanzees was followed by demonstration that this species provides a highly sensitive animal model system for experimental type B hepatitis. With rare exceptions, inoculation of sero-negative chimps with materials containing infectious HBV produces serologic evidence of infection including appearance of circulating hepatitis B surface antigen (HBs Ag) and subsequently development of antibody to HBs Ag and hepatitis B core antigen. Serum enzyme elevations indicative of liver damage occurred in 31 of 46 aminals infected to date. The antigenic subtypes of HBV in the inocula breed true in the infected animals, and HBV titers of sera containing the adw and ayw subtypes have been established as 10(7.5) infectious units/ml. Rhesus monkeys also provide a valuable animal model for type B hepatitis, but they appear to be less sensitive than chimps, and they do not develop evidence of liver damage.

Animals↗
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Immunofluorescent localization of hepatitis B antigens in chimpanzee tissues.

Three chimpanzee chronic carriers of hepatitis B surface antigen (HBs Ag) were examined by immunofluorescent techniques to determine the localization of HBs Ag and hepatitis B core antigen (HBc Ag) in their tissues. All specimens were quick-frozen in liquid nitrogen and stored at -70degrees until sectioned. Frozen sections were prepared and stained for examination by fluorescent microscopy. For staining, anti-HBs and anti-HBc labeled with fluorescein isothiocyanate were used. HBs Ag was found in the liver of all three animals. In two animals which were necropsied, HBs Ag was detected in other tissues, e.g., lymph nodes, spleen, and kidney. Specificity of these tests was demonstrated by blocking with purified HBs Ag. Examination of various tissues revealed HBc Ag only in the liver. 32 samples of liver, from different sites from one chimpanzee, were examined and all were positive for both HBs Ag and HBc Ag. The finding of HBc Ag only in the liver further supports the assertion that the liver is the sole site of replication of hepatitis B virus in chronic carriers.

Adrenal Glands↗