Corticotomy-facilitated orthodontics.
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Biomedical subjects
Publications and source records attributed to R Hoff.
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A cross-sectional study of morbidity associated with Schistosoma mansoni infection in an area in North-East Brazil where the disease is endemic was carried out in 1974. The survey was repeated in 1977, before mass treatment with oxamniquine, providing a cohort of 210 individuals who had both examinations. The high prevalence of hepatomegaly (over 80%) and of splenomegaly (over 15%) contrasted with rates of 10% and 1%, respectively, in a non-endemic area. Over the 3-year period hepatomegaly spontaneously regressed in 13% of patients, and splenomegaly regressed in 56%, a phenomenon most common in older individuals with light infections. Those with heavy infections--ie, 500 or more eggs per g faeces, had an excess risk of splenomegaly of 19.6% and, of its persistence, of 61.5%. Thus, intensity of infection was a critical factor in liver and spleen involvement, and programmes of chemotherapy that reduce infection should mitigate the risk of schistosomal morbidity.
We previously observed that mice bearing the autoimmune associated lpr gene exhibit increased susceptibility to challenge with Trypanosoma cruzi, the causative agent of Chagas' disease. We have now tested two other autoimmune prone strains of mice, BXSB and NZB, and found that these animals also show increased sensitivity to acute T. cruzi infection. When challenged with a standard dose (10(2)) of Y strain trypomastigotes, BXSB males (BXSB-YSB), which develop early onset autoimmune disease, suffered high mortality, while late onset autoimmune BXSB females and minimally autoimmune male BXSB mice whose Y chromosome was derived from C57BL/6J mice (BXSB-YB/6) also recover. NZB mice were found to be highly susceptible to challenge while NZW and NZB/W were resistant. A finding common to all groups of susceptible autoimmune mice was increased plasma levels of T. cruzi specific antibody, especially IgM. The data indicate that in two of the three autoimmune prone strains examined, increased T. cruzi susceptibility appears to be linked to restricted genetic elements (i.e. lpr gene and the YSB associated factor) which also influence the rapidity of onset of autoimmunity.
We studied the association between human incidence of Trypanosoma cruzi infection and household infestation density of Panstrongylus megistus in Castro Alves, Bahia, Brazil. During a 9-year period, 19 persons seroconverted; 17 were children, 17 lived in nonplastered houses, and 13 lived in houses infested with triatomines. Although 6 seroconverting persons lived in houses where triatomines could not be found, the risk of seroconversion was significantly greater in infested houses and 16 times greater in densely infested houses (greater than 15 bugs/person-hour of search). The highest rate of seroconversion (6/100 person-years exposure) occurred in houses containing the greatest number of bugs infected with T. cruzi (greater than 6 infected bugs/person-hour). These observations suggest that vector control measures could have a dramatic impact on transmission of T. cruzi by P. megistus.
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The relationship of infection with Trypanosoma cruzi to ECG abnormalities was studied in a defined population in rural Bahia, Brazil. Of 644 individuals 10 years of age or older who had complement fixation tests for antibodies to T. cruzi and ECGs, 53.7% were seropositive. ECG abnormalities were more common in seropositive individuals than in seronegative individuals, and more common in men than in women. The peak prevalence rate of abnormal ECGs occurred among seropositive individuals between 25 and 44 years of age; in this age group ECG abnormalities occurred 9.6 times more frequently among seropositive individuals than among seronegative individuals. The most common abnormalities were ventricular conduction defects, and right bundle branch block with or without fascicular block occurred in 10.7% of the infected population. PR intervals were longer in seropositive individuals than in seronegative individuals. Ventricular extrasystoles were slightly more common in seropositive individuals. A declining prevalence rate of abnormal ECGs among older seropositive individuals suggested selective mortality due to Chagas' heart disease.
There is evidence that autoimmune aberrations may contribute to the immunopathological consequences of Chagas' disease and because of this we sought to determine whether four inbred strains of mice bearing the single autosomal recessive gene, lpr (lymphoproliferation), which controls certain autoimmune manifestations, are particularly susceptible to acute infection with the Y strain of Trypanosoma cruzi. MRL/MpJ-lpr/lpr, C57Bl/6J-lpr/lpr, AKR/J-lpr/lpr, C3H/HeJ-lpr/lpr showed parasitaemias 2-10 times higher when compared to their congenic partners. Mortality was significantly higher in three of the four lpr strains. The results indicate that a single autosomal recessive gene which is associated with autoimmunity can influence susceptibility to acute T. cruzi infection in mice.
We compare results of one Bell and one Kato-Katz examination performed on each of 315 stool specimens from residents in an area in north-eastern Brazil endemic for schistosomiasis mansoni. The prevalence of Schistosome infection detected by the Bell technique was 76% and by the Kato-Katz technique was 63%. 81% (44/54) of the infections missed by a Kato-Katz smear were light infections (one of 50 epg range by Bell examination). Over, all, 55% (44/80) of stools in this egg count range by the Bell technique were negative on a single Kato-Katz smear. This implies that five Kato-Katz smears per stool would ensure a 95% probability (0.55(5) X 100) of detecting such light infections. However, a single Kato-Katz smear detected eggs in 97% (124/128) of stools with a Bell count greater than 100 epg. For stools positive by both methods the egg counts per gram of stool were higher (p less than 0.001) by Kato-Katz examination. Geometric mean egg counts for the infected population were 199 epg by the Kato-Katz and 92 epg by the Bell methods. 64% (59 v. 36) more persons were classified as heavily infected (greater than 400 epg) by the Kato-Katz method than by the Bell method. The differing measurements of schistosome infection obtained with the Bell and Kato-Katz methods must be considered when comparing data on morbidity-infection relationships.
For an exploration of the effects of interferon-inducible resistance mechanisms in acute American trypanosomiasis, the synthetic interferon inducer tilerone hydrochloride was administered to mice of the C57BL/6J strain, which is highly resistant to Trypanosoma cruzi, 18 to 24 h before infection with a potentially lethal dose of bloodstream trypomastigotes. Although all of the control mice died within 30 days of the acute infection, approximately 50% of the tilerone-treated animals were able to survive indefinitely (P less than 0.05). The tilerone-treated mice demonstrated significant levels of serum interferon and splenic natural killer cells at the time of infection. Macrophages isolated from the peritoneal cavities of tilerone-treated C57BL/6J mice appeared to kill significant numbers of trypanosomes during 2 to 3 days of in vitro culture, indicating that activated macrophages may contribute to the enhanced resistance to T. cruzi infection in these mice. Beige mice treated with tilerone did not survive T. cruzi infection as well as tilerone-treated heterozygotes did, suggesting a role for natural killer cells in interferon-induced resistance. These results suggest that interferon or effector mechanisms enhanced by interferon induction can play a significant role in influencing resistance to T. cruzi infection.
The relationship between parasitemia, seroreactivity to Trypanosoma cruzi, and electrocardiographic abnormalities was studied in 115 individuals from a rural community in northeast Brazil where Chagas' disease is endemic. Vector control measures were introduced, and after 3 years 106 of the original participants were located and re-examined. Serum antibodies to T. cruzi were measured by complement fixation and indirect fluorescent antibody tests and parasitemia by xenodiagnosis and blood cultures. On both examinations more seropositive children than seropositive adults showed parasitemia, and parasitemia was more likely to persist over the 3-year period in younger individuals. Electrocardiographic (ECG) abnormalities were seen more frequently in seropositive individuals without parasitemia. However, ECG abnormalities, as expected, were more prevalent in older individuals and therefore no specific inverse relationship between ECG findings and parasitemia could be shown. The decreased prevalence of infection noted in younger individuals following the introduction of vector control measures indicates that this approach limited transmission.
Oral oxamniquine was tested as a control strategy for endemic schistosomiasis in a rural area of Bahia, Brazil. Adults were treated with a single dose (12.5 to 15 mg per kg) and children (less than 12 years old) with a total of 20 mg per kg in two doses. The 191 (infected) persons treated represented 69% of the infected population in the study area. Follow-up stool examinations (Kato-Katz method) at one, 3, 6, 13, 25 and 33 months showed the cure rate declining from 80% at three months to 46% at 33 months. Over one half of those not cured showed a decrease in egg counts throughout the follow-up which, after 33 months, remained 66% below the pre-treatment levels. Stool examinations conducted on all study area residents during three years before chemotherapy showed the prevalence and intensity of Schistosoma mansoni infection to be high and stable. 33 months after the chemotherapy the prevalence was 41% and for infected individuals the geometric mean egg count was 121 epg, a decline of respectively 35% and 40% from pre-treatment levels for each index. Chemotherapy of infected persons with oxamniquine protected the community as a whole from high worm burdens for almost three years, although at this point the prevalence began to rise towards pretreatment levels.
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The effect of BCG and levamisole on the course of established murine leishmaniasis was examined. C3H mice infected subcutaneously in the perinasal region with 10(5) L. mexicana promastigotes produced chronic non-ulcerating, non-healing lesions and demonstrated positive humoral and delayed hypersensitivity responses to leishmanial antigens. Infected animals were treated during months 3-5 of infection with either live BCG or with levamisole. Neither treatment resulted in resolution of lesions or in production of a hyperallergic form of infection; similarly, neither immune responses to leishmanial antigens nor histopathological features of lesions were significantly altered. BCG treatment resulted in accelerated growth of primary leishmanial lesions and in the appearance of metastases in some animals. Levamisole treatment of uninfected animals resulted in low levels of antibodies reacting with promastigote antigens, but not in positive delayed intradermal responses. BCG induced delayed intradermal sensitivity to PPD in both infected and control animals; significantly increased delayed reactions to leishmania, were observed in treated uninfected mice.
Following reports of an unusually high incidence of acute Chagas's disease and the appearance of large numbers of Triatoma infestans in the southwestern region of the State of Bahia, triatomine bugs (Hemiptera: Reduviidae) and domestic animals in one of the affected communities were surveyed and examined for infection with Trypanosoma cruzi. Triatoma infestans was prevalent in houses and was also found in peridomestic habitats. T. sordida and T. pseudomaculata occupied peridomestic and sylvatic habitats and T. brasiliensis was found only among rocks far from houses. Panstrongylus megistus, formerly present in the region, was not found. Trypanosoma cruzi was detected in 19.5% of Triatoma infestans, 11.5% of T. sordida, 19% of dogs, 29% of cats and 100% of rats examined. A disproportionate number of early instar bugs were infected with Trypanosoma cruzi, suggesting that a rapid increase in the rate of transmission had recently occurred. The history of the domestic triatomine fauna of the region since 1912 is reviewed, and it is proposed that the relatively recent arrival of Triatoma infestans initiated a domestic cycle linked to peridomestic and sylvatic cycles of Trypanosoma cruzi transmission. Increased human mobility, the use of DDT for malaria control, and drought conditions are considered as factors which might have contributed to the outbreak of human infection.
Age-specific prevalence rates of parasitemia and seroreactivity to Trypanosoma cruzi were determined in a rural area endemic for Chagas' disease in Northeast Brazil. Parasitemia was detected by blood cultures and xenodiagnosis, and serum antibodies to the parasite were measured by the complement fixation (CF) and indirect immunofluorescence (IFA) tests. Of the 116 persons examined, 39 (33.7%) had antibodies and 23 (19.8%) had parasitemia. Ninety-six percent of parasitemic individuals were seropositive and 56% of seropositive individuals were parasitemic. The percentage of seropositive individuals with detectable parasitemia declined with age; all seropositive children in the 1- to 4-year age group and two-thirds of seropositive persons 5-19 years old had parasitemia while only one-third of seropositive adults above 19 years had parasitemia. CF and IFA tests were equally sensitive in detecting persons with parasitemia. Xenodiagnosis was more sensitive than culture for detecting parasitemia, but the two methods together were more sensitive than either method alone. Using the age-dependent relationship of parasitemia to seropositivity determined in this study, the prevalence rate of T. cruzi parasitemia was estimated in a much larger adjacent population in which seropositivity rates and the demographic structure were already known.
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In the Nordeste de Amaralina suburb of Salvador Bahia, Brazil, 47 of 285 pregnant women surveyed had complement fixing antibodies to Trypanosoma cruzi. At delivery T. cruzi was detected in one of 17 placentas from the sero-positive women. The offspring of this case were premature twins and T. cruzi was detected in the peripheral blood of each before death. At autopsy the gastro-intestinal tract and urinary bladder of both were severely affected. Immunofluorescence tests on cord sera, including the single case with T. cruzi in the placenta, were negative for IgM antibodies to T. cruzi. The mother of the infected twins and three of her living children, who were born and have resided in the city, were also infected with T. cruzi. Although the children had visited an area endemic for Chagas's disease for short periods, the mode of transmission in this family may have been transplacental. The value of the immunofluorescence test in the diagnosis of congenital Chagas's disease is discussed.
Household distribution of seroreactivity to Trypanosoma cruzi in inhabitants was analyzed in relation to house construction and the distribution of Panstrongylus megistus, the principal domestic vector of Chagas' disease in a rural area in northeast Brazil. No children residing in mud-brick houses were seroreactive to T. cruzi. The highest rates of seroreactivity occurred in residents of unplastered mud-stick houses, and were twice as high as those found in persons living in mud-brick houses or plastered mud-stick houses. Two-thirds of seroreactive children in this area resided in unplastered mud-stick houses. Over 90% of the P. megistus infestations were found in mud-stick houses. Mud-brick houses had the lowest infestation rates of P. megistus and the lowest household rates of seroreactivity to T. cruzi.