Fine Structure of the Oocyst Walls of \u3ci\u3eIsospora serini\u3c/i\u3e and \u3ci\u3eIsospora canaria\u3c/i\u3e and Excystation of \u3ci\u3eIsospora serini\u3c/i\u3e From the Canary, \u3ci\u3eSerinus canarius\u3c/i\u3e L.

Oocysts of Isospora serini and Isospora canaria, from the canary Serinus canarius, were broken, added to a cell suspension, fixed in Karnovsky\u27s fluid, and studied in the electron microscope. The oocyst wall of each species had an electron- lucent inner layer, a more osmiophilic middle layer and an outer layer of electron-lucent (I. serini) or electron-dense material interspersed with some electron-lucent material (I. canaria). A few, relatively large lipid-like bodies were present in the outer or middle layer of the oocyst wall of I. canaria. As many as 9 membranes were present in the oocyst wall of I. canaria and 3 in that of I. serini. When exposed to a trypsin-sodium taurocholate fluid, sporozoites of I. serini excysted from 5-month-old sporocysts in vitro, but not from sporocysts stored for more than 6 months. No excystation occurred in l5-month-old I. canaria sporocysts. Similarities and differences in excystation between I. serini and other Isospora, Eimeria, and Sarcocystis species are discussed

Proteção de camundongos atímicos BALB/c (Nu/Nu) contra Plasmodium berghei por esplenócitos oriundos de camundongos normais BALB/c (Nu/+)

Camundongos atímicos BALB/c (Nu/Nu) sucumbem entre 7-13 dias após a inoculação (DAI) da cepa NK65 de Plasmodium berghei. Todavia, seus singenêicos heterozigotos (Nu/+) morrem em 7-8 DAI. Camundongos nude (Nu/Nu) reconstituídos com 2xl0(7) esplenócitos de camundongos heterozigotos singenêicos normais não infectados (Nu/+) 20 dias antes da inoculação a (DBI) do parasita, sucumbem 2 dias antes que os animais controles. Camundongos nude reconstituídos 10 ou 2 DBI, vivem 2-4 dias a mais que os animais controles e alguns deles sobrevivem. Esses achados indicam que a cepa NK65 de P. berghei induz, no mínimo, dois imunofenômenos dependentes de linfócitos T; um supressivo e outro estimulatório. A reconstituição de camundongos nude com células T de camundongos BALB/c (Nu/+) parece reduzir ou "By-pass" a atividade supressora das células T, o qual leva à formação de uma resposta imune protetora por alguns dos camundongos nude.Athymic BALB/c (Nu/Nu) mice died at 7-13 days after inoculation (DAI) of Plasmodium berghei NK65, whereas their heterozygous (Nu/+) littermates died at 7-8 DAI. Nude (Nu/Nu) mice, reconstituted with 2 x 10(7) splenocytes from uninfected heterozygous (Nu/+) littermates at 20 days before parasite inoculation (DBI), died about 2 days earlier than control nude mice; nude mice reconstituted at 10 or 2 DBI lived 2 to 4 days longer than control nudes; and nude mice reconstituted 2 DAI lived even longer and some survived. These findings indicate that P. berghei NK65 induces at least two T-cell dependent immune phenomena, one suppressive and the other stimulatory. Reconstitution of nude mice with T-cells from BALB/c (Nu/+) mice appeared to reduce or bypass suppressive T-cell activities which allowed the formation of a protective immune response by some of the nude mice

Scanning and Transmission Electron Microscopy of the Oocyst Wall of \u3ci\u3eIsospora lacazei\u3c/i\u3e

The oocyst wall of Isospora lacazei from sparrows was studied with scanning (SEM) and transmission (TEM) electron microscopy. In TEM, t he oocyst wall consisted of four distinct layers (Ll-4). The innermost layer, Ll, was moderately electron-lucent and 240-285 nm thick; L2 was electronJense and 210-240 nm thick; L3 was moderately electron-lucent and 15-150 nm thick; L4, the outer most layer, was discontinuous and consisted of electron-dense discoid bodies which measured 180-220 nm x 320-840 nm. The discoid bodies of L4 as seen by TEM appeared spheroid in shape when observed by SEM. One or two membranes were situated on or between various layers of the oocyst wall. One such membrane occurred on the inner margin of Ll, two closely applied membranes were interposed between LI and L2, one membrane occurred between L2 and L3, and one membrane on the outer margin of L3

Ultrastructure of the Sporocyst Wall during Excystation of \u3ci\u3eIsospora endocallimici\u3c/i\u3e

Sporocysts of Isospora endocallimici, a parasite of marmosets, were exposed to minimal essentials medium (MEM) or a trypsin-bile salt solution (TBS) and then fixed and prepared for trans- mission electron microscopy. Excystation occurred in TBS but not MEM. The sporocyst wall has 2 layers, a thin outer layer (15 to 110 nm thick) and a thick inner layer (65 to 180 nm thick), which is composed of 4 separate curved plates. The outer layer consists of 1 to 3 membranes interspersed with lipid droplets. In the inner layer, a thin layer of material connects the peripheral margins of 2 apposing plates. Immediately beneath this layer, a thin strip of material is interposed between the 2 apposing plates. Ultrastructural changes preparatory to excystation occur primarily in the inner layer of the sporocyst wall. The TBS acts upon the site of apposition between 2 plates causing the interposed strip to swell and separate from the margin of each plate which leads to collapse of the sporocyst. As the sporocyst collapses, the margins of each curved plate curl inward toward the center of the sporocyst

Efeito do Mycobacterium bovis BCG, lipopolissacarideo bacteriano e hidrocortisona no desenvolvimento de imunidade ao Plasmodium berghei em camundongos

Mycobacterium bovis (BCG) aumenta significantemente o desenvolvimento da imunidade nos camundongos CFW, C57BL/6, C57BL/l0ScN e BALB/c (Nu/+) para os estágios eritrocitos do Plasmodium berghei. Camundongos tratados com BCG requerem menos ciclos de infecção com P. berghei e cura pelo Fansidar (pirimetamina + sulfadoxina) para desenvolverem imunidade sólida a este parasita do que os controles. Contudo, os animais que receberam BCG 30 dias antes do início da imunização evidenciaram uma perda precoce da imunidade adquirida para o P. berghei, quando comparado com os animais que receberam BCG 14 dias antes ou que não receberam BCG. Assim, sendo, o BCG aumentada a indução na resposta imune do hospedeiro ao P. berghei no curso de infecções subseqüentes. O tratamento de camundongos CFW, BALB/c e C57BL/6 com lipopolissacarídeo bacteriano ou hidrocortisona faz com que os animais requeiram um número maior de ciclos de infecção e cura para tornarem-se imunes ao P. berghei que os controles. O tratamento dos camundongos C57BL/10ScN com hidrocortisona aboliu completamente a sua habilidade de sobrevida subseqüentes a ciclos de infecção com P. berghei e cura pelo Fansidar

Effects of mycobacterium bovis BCG, bacterial lipopolysaccharide and hydrocortisone on the development of immunity to Plasmodium berghei

Mycobacterium bovis (BCG) significantly enhanced the development of immunity by CFW, C57BL/6, C57BL/10ScN and BALB/c (Nu+) mice to the erythrocytic stages of P. berghei. Mice treated with BCG required fewer cycles of infection and Pansidar (pyrimethamine + sulfadoxine) cure in order to develop solid immunity than untreated, immunized mice. However, those, mice treated with BCG at 30 days before the initiation of immunization showed an earliear loss of immunity to P. berghei than those mice which received BCG at 14 days or no BCG. Thus, BCG enhanced the host immune response to P. berghei during an initial infection, but shortened the length of immunity so that mice were more susceptible to P. berghei during subsequent infections. Treatment of CFW, BALR/c and C57BL/6 mice with bacterial lipopolysaccharide or hydrocortisone acetate (HDC) caused the animals to require more cycles of infections and drug cure in order to attain immunity than controls. Treatment of immunized C57BTV lOScN mice with hydrocortisone completely abolished their ability to survive a P. berghei infection.Mycobacterium bovis (BCG) aumenta significantemente o desenvolvimento da imunidade nos camundongos CFW, C57BL/6, C57BL/l0ScN e BALB/c (Nu/+) para os estágios eritrocitos do Plasmodium berghei. Camundongos tratados com BCG requerem menos ciclos de infecção com P. berghei e cura pelo Fansidar (pirimetamina + sulfadoxina) para desenvolverem imunidade sólida a este parasita do que os controles. Contudo, os animais que receberam BCG 30 dias antes do início da imunização evidenciaram uma perda precoce da imunidade adquirida para o P. berghei, quando comparado com os animais que receberam BCG 14 dias antes ou que não receberam BCG. Assim, sendo, o BCG aumentada a indução na resposta imune do hospedeiro ao P. berghei no curso de infecções subseqüentes. O tratamento de camundongos CFW, BALB/c e C57BL/6 com lipopolissacarídeo bacteriano ou hidrocortisona faz com que os animais requeiram um número maior de ciclos de infecção e cura para tornarem-se imunes ao P. berghei que os controles. O tratamento dos camundongos C57BL/10ScN com hidrocortisona aboliu completamente a sua habilidade de sobrevida subseqüentes a ciclos de infecção com P. berghei e cura pelo Fansidar

Prevalence of chloroquine-resistant falciparum malaria in the Brazilian Amazon

The prevalence of chloroquine-resistant falciparum malaria was determined for humans living at 28 different sites in the Brazilian Amazon. Blood samples obtained from each patient were defibrinated, placed in vials containing 0.5% glucose and or chloroquine and incubated for 24 hours at 39-40°C without agitation. In vitro sensitivity of the parasite to four different concentrations of chloroquine was determined for each sample. After 24 hours of incubation, trophozoites of Plasmodium falciparum developed to schizonts in all control cultures (no chloroquine) as well as in 80.6, 48.4, 11.8 and 7.5% of the cultures containing 0.5, 1.0, 2.0, and 3.0 nmol chloroquine/ml blood, respectively. Chloroquine-resistant P. falciparum was found in blood samples from all 28 locations, indicating that such resistance is widely spread in the Brazilian Amazon