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Cystoisospora belli is an opportunistic protozoan that causes human cystoisosporiasis, an infection characterized by diarrhea, steatorrhea, abdominal pain, fever, and weight loss. The lack of animal models susceptible to C. belli, and the difficulty in obtaining clinical samples with fair amounts of oocysts have limited the research pertaining to the basic biology of this parasite. This study aimed to describe the ultrastructure of endogenous stages of C. belli in Monkey Rhesus Kidney Cells (MK2) and Human Ileocecal Adenocarcinoma cells (HCT-8). Zoites of C. belli exhibited typical morphological features of coccidia, which included a trilaminar pellicle, an apical complex formed by a conoid, polar rings, rhoptries, and micronemes, in addition to dense granules and the endoplasmic reticulum. No crystalloid body was observed but various lipid and amylopectin granules were usually present in the cytoplasm of zoites. We observed a tendency of the endoplasmic reticulum of the host cell to be located near the parasitophorous vacuole membrane. Merozoites were formed by endodyogeny and during replication, the apical complex of the mother cell remained intact. The formation of gametes or oocysts was not observed. The ultrastructural findings of C. belli are further evidence of its proximity to Sarcocystidae family members and corroborate their reclassification as Cystoisospora spp., (© 2014 Wiley Periodicals, Inc.)

Intracellular development of Cystoisospora belli was demonstrated in 4 different mammalian cell lines. Human ileocecal adenocarcinoma (HCT-8), epithelial carcinoma of lung (A549), Madin-Darby bovine kidney (MDBK), and African green monkey kidney (VERO) were exposed in vitro to C. belli sporozoites, which had been isolated from the feces of HIV-AIDS patients. Parasites invaded all the cellular types between 4 and 12h after exposure and multiplication was demonstrated after 24 h. Grater number of merozoites formed in VERO cells, followed by HCT-8. In the MDBK and HCT-8 cells, the parasitophorous vacuole was less evident and immobile merozoites were observed in the cytoplasm. In VERO cells, one or several parasitophorous vacuoles contained up to 16 mobile sporozoites. No oocysts were found in any of the cell types used. VERO cells may be suitable for studies of the interaction between parasite and host cells.

Published phylogenetic reclassifications of Pneumocystis as a fungus resulted in a nomenclatural shift from the Zoological Code to the International Code of Botanical Nomenclature. The same may be true for all microsporidians and sundry other organisms. This resulted in the invalidation of names and subsequently precipitated changes to the botanical code to accommodate Pneumocystis and microsporidian names. The repercussions following application of the 2005 Vienna Code to Pneumocystis nomenclature are detailed. Validity of the name for the human pathogen, Pneumocystis jirovecii, is re-established from its 1976 publication under the Zoological Code, contrary to interpretation of validity under earlier botanical codes. Pneumocystis jirovecii is lectotypified and epitypified. The rat parasite, Pneumocystis carinii, is neotypified, separating it from Pneumocystis wakefieldiae. The original 1909 description of Trypanosoma cruzi, type species for Schizotrypanum, and causal agent of Chagas' disease, included parts of the life cycle of Pneumocystis. Trypanosoma cruzi is neotypified by the true Trypanosoma elements, thereby completing the nomenclatural separation from Pneumocystis and ensuring that Schizotrypanum is not applicable to Pneumocystis as an earlier name. The neotypes for P. carinii and T. cruzi represent the strains currently being investigated by their two respective genome projects. They were selected in light of their medical importance, physiological characterizations, and absence of lectotypifiable materials. The classification and nomenclature of Pneumocystis is reviewed and guidelines given for the publication of new species.

Objective: To examine the relationship between antibody status and various hypothesized risk factors for Toxoplasma gondii infection among two different Amerindian populations in eastern Panama. Following up on earlier research that we conducted, we now explore the role of dogs in the natural transmission of Toxoplasma, the role that dogs play in promoting transmission, the interactive effect of cats and dogs, and the accessibility of infective material to children., Methods: In 1991, 10 Panamanian medical students conducted interviews and took blood samples from 760 Kuna and Embera children aged 2 through 12 years in the Upper Bayano River Basin and the San Blas Islands. Serologic assays were performed using direct agglutination. The data analyses in the 1990s included univariate, bivariate, and multivariate analyses, without regard to data on dogs. Further bivariate and multivariate analyses were performed in 2003 to examine the contribution of dogs., Results: In communities with high Toxoplasma antibody prevalence in children, logistic regression suggested that the factors predictive of antibody presence were: compacted soil floors of huts (P = 0.001), having a dog (P = 0.038), and the interviewer seeing a cat in the house (P = 0.049). Our results suggest that the villagers' dogs play a significant role in facilitating the transmission of Toxoplasma gondii to humans, most often in the presence of cats in the houses, and only in those communities with higher Toxoplasma seroprevalence in children., Conclusions: Dogs may act as mechanical vectors, by rolling in foul-smelling substances and by ingesting fecal material. In areas of high Toxoplasma prevalence in children and where dogs and cats are plentiful, immunocompromised individuals and pregnant women should be warned of the possibility of acquiring Toxoplasma gondii from dogs as well as from soil contaminated by cats. People should be encouraged to wash their hands after contact with soil, dogs, or cats as well as before eating.

The following heteroxenous and cyst-forming coccidian genera, Besnoitia, Cystoisospora, Frenkelia, Hammondia, Neospora, Sarcocystis and Toxoplasma have been compared biologically, and a key to determine their tissue cysts is provided.

We tested 124 isolates of Toxoplasma gondii, as determined morphologically and by their ability to elicit antibodies in the dye test with the RH strain of Toxoplasma in mice. They were compared for their capacity to immunize CF-1 mice against isolate T-1, and T-1 immune mice for their capacity to resist each of the 123 other isolates. Of the 125 isolates, 52 had been isolated in the continental USA, 33 in Central America, 15 in Europe, 9 in Hawaii, five in Japan, two in Taiwan, five in Australia, one in Indonesia, one in Tunisia, and one was of unknown origin. Complete cross-immunity was found. This suggests that only one immunotype of Toxoplasma is prevalent in the United States, and perhaps all over the earth. Vaccines are likely to immunize against most or all Toxoplasma isolates.

This report describes the presence of Isospora belli unizoic cysts in mesenteric lymph nodes and of gametocytes in the gallbladder epitelium of a 26 year-old Brazilian male patient with Acquired Immune Deficiency Syndrome. This patient had received treatment for several times with sulfamethoxazole-trimethoprim. It is discussed the significance of I. belli tissue cysts as possible foci of resistance of the parasite and their association with the infection relapse even post-treatment with anticoccidian medication.

We describe the finding of unizoic cysts of Isospora belli in lymphoid tissues of a Brazilian patient with AIDS, and discuss the possibilities of their drug resistance, they being the cause of relapses, and of being an indication for the existence of intermediary or paratenic animal hosts.

We enumerate identical and divergent findings concerning the obligate heteroxenous Hammondia hammondi and the facultatively homoxenous or heteroxenous Toxoplasma gondii. Differences exist in life-cycles, transmission, and host range, especially transmissibility to birds and mammals other than rodents, in ultrastructural morphology, immunity and serology in cats and to lesser degree in rodents, in DNA sequences and in isoenzymes. Because the recognition of obligate heteroxeny is essential to study these organisms and to recognize them as taxa, it is advantageous to give heteroxeny a generic rather than a specific value. Characterization of organisms with the life-cycle patterns of Hammondia, Sarcocystis, Frenkelia, and Toxoplasma is best achieved by means of the genera presently used.

Infection and immunity to toxoplasmosis induced by the RH strain of Toxoplasma gondii was compared in Sprague-Dawley (SD) and Wistar rats and in outbred Swiss Webster mice. All rats injected with up to 1,000,000 RH-strain tachyzoites remained clinically normal, whereas mice injected with only 1 live tachyzoite died of acute toxoplasmosis. Rats could be infected with 1 tachyzoite of the RH strain as shown by antibody development and by bioassay in mice. However, after 8 days, RH-strain organisms were recovered only inconsistently from SD and Wistar rat brains. Contrary to a report of sterile immunity to T. gondii infection in rats after immunization with live RH tachyzoites, we found infection immunity after challenge with the VEG strain. Toxoplasma gondii tissue cysts of the VEG strain could be recovered from most SD and Wistar rats, first injected with live RH-strain tachyzoites and then challenged with oocysts of the VEG strain. Our RH strain, and probably many others, passed for 50+ yr as tachyzoites has lost not only the capacity to form oocysts, but also shows a marked reduction or absence of tissue cyst (bradyzoites) formation.

We critically review and summarize information on the prevalence of Toxoplasma gondii infections in rats, mainly Rattus norvegicus, and their possible role as a source of infection for larger carnivores and omnivores. We also review information on immunology and natural resistance, contributing to the model value of rats in the analysis of human infection. Rats can be successfully infected with oocysts (sporozoites), tissue cysts (bradyzoites), and tachyzoites. Even adult rats, that are resistant to clinical toxoplasmosis, can be infected orally with a few oocysts or tissue cysts. Infections with tachyzoites of the RH strain are highly variable. Congenital transmission of T. gondii occurs at a high rate when rats are infected during pregnancy. Congenitally infected rats can harbor viable T. gondii in the absence of detectable antibodies to T. gondii and rats with low antibody titers may harbor few or no organisms. The isolation of viable T. gondii by bioassay is the only reliable means to determine persistence of chronic T. gondii infection in feral rats. No evidence was found for maintenance of T. gondii in rats by vertical transmission in the absence of cats.

Twenty-two HIV+ patients with encephalitis were studied. Of these, 7 had meningoencephalitis due to Toxoplasma gondii (MT) and 15 due to Trypanosoma cruzi (MC). Pathologic and computerized axial tomography (CAT) changes were compared. We found that focal necrotizing encephalitis due to Toxoplasma involved the cerebral cortex and the basal ganglia, whereas lesions due to Trypanosoma cruzi were centered in the white matter, sometimes extending into the cortex. Hemorrhages, myelin lesions and organisms were more pronounced in chagasic than in toxoplasmic encephalitis. These findings are consistent with the literature reviewed.

We review herein studies concerning the genomic polymorphism of Toxoplasma gondii including 3 clones (1 linked with mouse pathogenicity), 5 zymodemes, and 13 schizodemes. Because mutations occur with some frequency and several allelic configurations are present in isolates grown in the same environment, we conclude that many of the mutations may not be affected by selection pressure. However, the gametocyte-forming ability is under selection pressure from the hose and depends on the development of bradyzoites in tissue cysts. After prolonged multiplication exclusively in the tachyzoite stage in mice and, possibly, in patients the gametocyte-forming ability may be lost. To avoid this genomic change, isolates should be passed in the laboratory, permitting bradyzoite and tissue-cyst formation. Mouse pathogenicity is selected for during mouse passage. We find no major genomic instability justifying species or subspecies distinctions.

Several published biologic times for the stage conversion of Toxoplasma gondii from tachyzoite to bradyzoite in mice are critically examined. There are several reports of 3 days and many of longer times. Possible errors, related to delay from dissemination of the infection, are pointed out. The time to the appearance of the 36-kDa surface antigen, sometimes used for the diagnosis of bradyzoites, should be compared with the biologic attribute of bradyzoites, inducing the short prepatent period in cats. It is recalled that the development of acid pepsin resistance is not exclusively correlated with the biologic definition of bradyzoites. Reactivation of toxoplasmosis in mice does not necessarily follow the administration of a corticosteroid. The daily dose, the type of corticosteroid, its solubility, whether alcohol or ester, the route of administration, the host, and, probably, other factors are important in giving rise to sufficient immunosuppression for reactivation to occur. The plea is made to examine biologic measurements in the context of parasitologic and host factors.

A cohort of more than 500 children from Panama City, Panama was studied prospectively over five years for acquisition of antibody to Toxoplasma gondii. The direct agglutination test showed that 72 of 571 children seroconverted between one and six years of age, for a cumulative incidence of 12.6%. Children were examined by pediatricians quarterly, and illnesses that had occurred in the interval and their activities were noted on questionnaires. Thirty-eight variables were examined for their role as risk factors for seroconversion. There was a higher correlation between children's seroconversion and contact with dogs than with cats. Combinations of significant predictors without dogs explained only 67% of the seroconversions, but the same factors with dogs explained 90%. On the other hand, ingestion of raw or rare meat or eggs appeared to play no role in transmission. Cats were examined and 110 (45.6%) of 241 had Toxoplasma antibody on the first bleeding. Only two (0.5%) of 383 cat fecal specimens, when tested in mice, resulted in seroconversion. Ten (1.1%) of 924 soil samples resulted in seroconversion in mice that had been injected. Antibody to Toxoplasma was found in 52 (23.3%) of 226 rats (Rattus norvegicus) and two (0.035%) of 571 mice (Mus musculus). Two hundred sixteen birds of 16 different species were bled. Antibody to Toxoplasma was found in 13.4% of these birds, mostly in grackles, blue-gray tanagers, and doves. The rate of isolation of Toxoplasma was low: one of 23 in rats and three of 201 in birds. High relative risks (RRs) of transmission to children were predicted by contact histories with nursing dogs (RR = 5.8), weaned dogs (RR = 4.7), many flies (RR = 3.6), 6-12-month-old dogs (RR = 3.4), weaned cats (RR = 3.0), 6-12-month-old cats (RR = 2.7), nursing cats (RR = 2.5), much garbage (RR = 2.4), and many roaches (RR = 2.2). The high statistical correlation of dog contact with seroconversion in children suggests the possibility that dogs, by eating and rolling in cat feces, are instrumental in mechanically transmitting Toxoplasma infection. In addition, flies, and to a lesser extent, cockroaches, may have practically important roles in transmission.

We conducted a survey of 760 Amerindian children 2-12 years of age in the Bayano and San Blas areas of Panama in 1991 to determine the prevalence of serum antibodies to Toxoplasma gondii and the importance of hypothesized risk factors in human-induced native and sylvatic conditions, which have had few environmental changes, as opposed to rural and urban areas in Panama previously studied. The overall prevalence of infection ranged between 0% and 42.5%. No age curve was detected, indicative of nonconstant transmission. Only two hypothesized risk factors, floor type and having cats inside the house, were significantly associated with the presence of antibodies in some of the communities. Antibody prevalence appeared to be associated more with the community of residence than with any specific behavior. The risk factor of importance may be the level of oocyst contamination, since infection by tissue cysts in meat was excluded. On three of the nine islands studied, no antibody was detected in the children or the cats. It would appear that T. gondii is not present on these islands. Although the data did not support the importance of many of the hypothesized risk factors, the study is consistent with the theory of transmission by oocysts and the importance of cats in transmission.

We describe a variety of toxoplasmic lesions in seven patients with the acquired immunodeficiency syndrome. The first patient had multiple small-intestinal ulcers associated with Toxoplasma tachyzoites and high antibody titers; he died of disseminated histoplasmosis. The second patient, who died of tuberculosis, also had an inactive chronic Toxoplasma infection, with tissue cysts in the brain that were associated with glial nodules. A third patient died of Toxoplasma encephalitis, manifested by multiple foci of necrosis associated with Toxoplasma tachyzoites, cysts, and hypertrophic arteritis. A fourth patient had been treated for toxoplasmic encephalitis with co-trimoxozol (trimethoprim-sulfamethoxazole combination) for 3 to 4 days and showed degenerating tachyzoites associated with necrotic areas. A fifth patient, treated for toxoplasmic encephalitis with co-trimoxazol for 14 days, had necrotic lesions associated with Toxoplasma antigen and a few cysts. A sixth patient with encephalitis and Toxoplasma tachyzoites and young cysts in the biopsy showed healed brain lesions after 22 days of treatment. A seventh patient, diagnosed radiologically and serologically with Toxoplasma encephalitis, was treated for 7 months; his ring-enhancing lesions subsided, and he died of a central nervous system lymphoma. Toxoplasma could not be isolated from the brain, although toxoplasmic DNA was detected in the brain and heart by polymerase chain reaction. The pathogenesis of the range of these lesions, their diagnosis, and the possibility of terminating Toxoplasma infection by prolonged chemotherapy are discussed.

Sera from 273 wild mammals from Missouri and Kansas (USA), collected between December 1974 and December 1987, were tested for the presence of antibodies to Toxoplasma gondii using the Sabin-Feldman dye test. Sixty-five (24%) had antibodies at titers of > or = 1:8, including 38 (66%) of 58 carnivores, 14 (15%) of 94 omnivores, 13 (11%) of 117 herbivores, and none of four insectivores. The prevalence of antibodies in mice (Mus musculus and Peromyscus spp.) and rats (Rattus norvegicus and Sigmodon hispidus) was low (3%), while medium sized herbivores such as squirrels (Sciurus spp.), rabbits (Sylvilagus floridanus), and muskrats (Ondatra zibethicus) had prevalences of about 18%. Red foxes (Vulpes fulva) and mink (Mustela vison) had the highest prevalence of antibodies with frequencies of 90 and 66%, respectively. In 32 attempts to isolate Toxoplasma gondii from wild mammals with positive (> or = 1:4) titers, only six (19%) were successful: a gray squirrel (Sciurus carolinensis), a beaver (Castor canadensis), an opossum (Didelphis marsupialis), a red fox and two mink. These findings are consistent with the hypothesis that the probability of infection with Toxoplasma gondii, and therefore prevalence of antibodies in wildlife, is greatest in carnivores.

Old World psittacines experienced an acute fatal illness in outdoor breeding collections in South Florida. Toxoplasma-like organisms were found histologically in pulmonary capillaries and elsewhere. Because the organisms underwent schizogony and could not be transmitted to mice, we looked for a cause other than Toxoplasma gondii. An opossum was trapped on the premises of 1 facility and was found to be shedding sporocysts similar to Sarcocystis falcatula in its feces. Cockroaches were prevalent and suspected as transport hosts. Cockroaches that had ingested opossum feces and subsequently were fed to cockatoos induced an identical fatal illness. Obstruction of pulmonary capillaries by developing schizonts and pulmonary edema were the most important pathologic findings. The epidemic was stopped by biological insect control employing flightless chickens to reduce cockroach populations and by an electric fence restricting access of opossums to these outdoor psittacine breeding facilities.

A 24-year-old homosexual man with acquired immunodeficiency syndrome presented with intractable diarrhea and fever. Examination of a rectal biopsy specimen and stool revealed Cryptosporidium. Approximately 4 months after admission he developed respiratory failure and died. Postmortem examination revealed cryptosporidiosis involving the entire gastrointestinal tract as well as the tracheobronchial tree. To our knowledge, this is one of the rare presented cases of tracheobronchial cryptosporidiosis documented histologically.

Toxoplasmosis is a common infection of animals and man, yet remains a rare disease. The disease appears in the offspring of mothers first infected during pregnancy and by relapse of chronic infection in immunodeficient animals and man. Toxoplasmosis can be prevented by the simplest of hygienic measures, such as handwashing. Further control can be achieved by widespread education of the public about the dangers of toxoplasmosis and the methods of prevention. Education of veterinary and zoo workers would reduce transmission in an environment where it is most likely to occur because of high concentrations of cats and cat feces. Toxoplasmosis of sheep and pigs on farms may be amenable to vaccination with the ts-4 strain of Toxoplasma. Finally, the new T-263 toxoplasmosis vaccine for cats offers the possibility of drastically reducing environmental contamination with oocysts, especially on farms. The reduction in numbers of viable oocysts in the environment would eventually reduce the infection of bird and rodent intermediate hosts, and ultimately, the infection of humans.

Kittens are the principal disseminators of Toxoplasma gondii. They can shed greater than 10(8) oocysts in the feces after initial infection with bradyzoites in tissue cysts. Thereafter, most kittens develop protective immunity and do not shed oocysts again if they are reinfected. Bradyzoites of a T gondii mutant, designated T-263, were used to vaccinate kittens. Their use did not result in oocyst shedding, but successfully prevented 84% (31/37) of the kittens from shedding oocysts when challenge exposed with a normal isolate of T gondii. Vaccination of outdoor-roaming cats and kittens would be a useful public health measure to prevent transmission of toxoplasmosis near homes, on farms, and in zoos. It is anticipated that several years will be required for a lyophilized bradyzoite vaccine to be ready for licensing and possible commercial availability.

We studied Aotus lemurinus, Panamanian night monkeys, for susceptibility to Toxoplasma infection and for their capacity to develop immunity using either sufadiazine prophylaxis or the non-persistent ts-4 vaccine. The animals were highly susceptible to infection with a mouse pathogenic (T265) and a mouse nonpathogenic (T163) Toxoplasma isolate. A calculated single bradyzoite by mouth gave rise to infection which was fatal in nine to 12 days. Chemoprophylaxis with 60-300 of sulfadiazine mg per day for up to 40 days protected the animals; however this was followed by fatal reactivation of infection between 11 and 70 days after treatment was stopped. Vaccination was carried out in two or three doses subcutaneously. Challenge was performed in 26 animals using both Toxoplasma isolates. Five monkeys (19%) survived for over a year, 10 died after a prolonged illness, and 11 died as rapidly as the seven controls. Safety tests showed the vaccine to be nonpathogenic in 111 adults except for slight fever and local inflammation, although one of four juveniles died from disseminated infection. Vaccination of 25 pregnant monkeys was non-pathogenic; however two of 25 fetuses were aborted, one of which was infected and one newborn had microphthalmia, retinitis and a cataract; four of the offspring were not tested. When six lactating monkeys were vaccinated, Toxoplasma was not transmitted to the infants. The high susceptibility to Toxoplasma and the low immunizability was circumstantially attributed to absence of exposure and lack of selection by Toxoplasma of these arboreal monkeys even though about 50% of terrestrial animals from the same area were infected.(ABSTRACT TRUNCATED AT 250 WORDS)

The identification of sequence similarities in ribosome RNA subunits from Pneumocystis and certain fungi has led to the suggestion that this presumed protozoan be reclassified as a fungus. However, the absence of predictable characteristics from the fungi as a group to Pneumocystis as a genus indicates that we should wait until additional rRNA coding sequences of more organisms have been compared.

The capacity of hamster peritoneal cell populations to control viability and growth of Besnoitia and Toxoplasma organisms was assessed in vivo and in vitro. Immunized hamsters reduced the homologous organisms 100- to 10,000-fold over a 5-day period, but the heterologous infection increased 100- to 1,000-fold in numbers, similar as in the nonimmune controls. Passively administered antibody was ineffective although lytic cofactors were supplied by hamsters. In cultures, peritoneal cells from Besnoitia-immune hamsters delayed the growth of homologous parasites to an average of 38.5 h per division; however, in Toxoplasma-immune and nonimmune cells, Besnoitia divided every 12.8 h. Specificity of immunity was pronounced against both infections. With cross-infections, Toxoplasma-immune cultures did not effectively delay Besnoitia growth; however, Besnoitia-immune cultures reduced Toxoplasma growth by one-half. Co-cultivation experiments demonstrated that specifically committed lymphocytes could instruct macrophages to reduce the homologous organism 10-fold, whereas heterologous organisms were reduced only 2-fold. Lymphocyte supernatants initiated hypersensitivity as indicated by macrophage activation and giant cell formation in culture. However, these supernatants did not transfer infection immunity. Lymphokines could account for the hypersensitivity phenomena, but cell-mediated infection immunity in this model required close lymphocyte-macrophage proximity. These studies indicate that a number of distinct processes including delayed hypersensitivity, macrophage activation, and specific cellular immunity are acting simultaneously during latent Besnoitia infection of hamsters. All three processes are mediated by lymphoid cells and appear to be specifically induced. Although activated macrophages develop some heightened nonspecific capabilities, these were several orders of magnitude below the specific effects.

Toxoplasma infection in most adult animals and humans is asymptomatic because of effective protective immunity; this involves antibody acting extracellularly, and T-cell factors acting intracellularly. Whenever immunity is not acquired in a timely fashion, tachyzoites continue to multiply, destroying an excessive number of cells, producing lesions in several organs, with pneumonia and encephalitis the prominent causes of illness and death. However, immunity is insufficient to destroy the slowly multiplying bradyzoites persisting in tissue cysts in many organs - a parasite adaptation to await ingestion of one host by another. Toxoplasma cysts produce lesions when they disintegrate, because of the delayed type of hypersensitivity accompanying infections. In the presence of immunity, the released bradyzoites are destroyed, but when protective immunity fails, the bradyzoites can develop again into actively multiplying tachyzoites parasitizing and destroying cells in expanding foci, usually in the brain. In this review J.K. Frenkel discusses the complex interplay of immunological and parasite factors participating in the various lesions associated with acute and chronic Toxoplasma infections.

The disintegration of Schistosoma mansoni and their eggs was studied in the liver of mice after termination of the infection by praziquantel. Egg granulomas, which were already present at the time of treatment, attained their maximal diameter of 380 microns after 2-3 weeks. Within the following 5 weeks, granulomas very rapidly regressed in size to only 165 microns. Directly after treatment, worms were trapped in the liver where they were quickly invaded by granulocytes and subsequently phagocytosed within 3 weeks. Worm granulomas measured 700 and 900 microns after 3 and 8 weeks, respectively, but then regressed rapidly to only 550 microns after 12 weeks. Liver lesions appeared to regress more rapidly after praziquantel than after treatment with other schistosomicidal drugs.

Mice were immunized with live organisms of the different stages (i.e., tachyzoites, bradyzoites, or sporozoites) of Toxoplasma gondii, or with killed tachyzoites with or without adjuvants. The adjuvants used were liposomes, anhydrides of myristic or lauric acid, levamisole and Freund's complete or incomplete adjuvant. The following strains of T. gondii were used: RH, M-7741, the nonpersisting, temperature-sensitive mutants ts-1, ts-4, or ts-5, and the "back mutant" of ts-1 (Pfefferkorn and Pfefferkorn, 1976). The protection afforded was measured by challenge with the pathogenic M-7741 strain. Killed tachyzoites alone, or with adjuvants, offered only slight protection against challenge with M-7741 and no protection against challenge doses that were lethal to all control mice. Chronic infection and live nonpersisting vaccines conveyed a strong immunity to challenge, except strain ts-1. Because it was less pathogenic and did not require chemoprophylaxis, strain ts-4 best fulfilled the requirements for a good vaccine; its effect in hosts other than the mouse remains to be determined. The immunity induced by tachyzoites, bradyzoites, or sporozoites appeared equally strong when challenged with sporozoites.

Hammondia hammondi gen.nov.,sp.nov (Eimeriorina:Sarcocystidae) is described as an obligate heteroxenous protozoon of domestic cats (final host) and laboratory mice (experimental intermediate host). Oocysts from the final host are infectious only for the intermediate host; and cysts from the intermediate host are infectious only for the final host. Intracellular cysts develop principally in striated muscle of mice that ingest oocysts, with a few cysts in the brain and perhaps elsewhere. Cysts are without septa or radial spines; bradyzoites are slender, there is no evidence of metrocytes. Cysts are not infectious for mice. After the ingestion of cysts by cats, a multiplicative cycle precedes the development of gametocytes in the epithelium of the samll intestine. Oocysts are shed unsporulated, sporogony is outside of the host, resulting in two sporocysts with four sporozoites each. Oocysts of the species average 11 x 13 mum. The prepatent period i 5s 5 to 8 days, and oocyst shedding persists for 10 to 28 days followed by immunity. Cysts in skeletal muscle measured between 100 and 340 mum in length and 40 and 95 mu-m in width. Experimental intermediate hosts are laboratory mice, rats, hamsters, guinea pigs, Peromyscus and Mastomys. Some of the intermediate hosts develop low levels of antibody and some cross-immunity against Toxoplasma; however, this has not been observed in cats.

Development of immunity to the shedding of oocysts was examined in 75 kittens that survived infection with the three stages of Toxoplasma gondii. Of 16 kittens fed bradyzoites in cysts, 94% were immune and did not shed oocysts. Of seven injected with tachyzoites 86% were immune. Of 18 fed sporozoites only 11% were immune, but following injection, 54% of 12 were immune. After the administration of either bradyzoites or tachyzoites from nonoocyst-producing strains, only 9% of 22 were immune. Considering all inocula, immunity was present in 93% of kittens that had previously shed oocysts, 25% of those that only develop antibody, and none that had neither shed nor developed an antibody titer. After a second challenge with a different isolate, a similar percentage of immunity was observed. Infection with killed tachyzoites, alone, or together with Freund's complete or incomplete adjuvants was followed by immunity in only one of 24 kittens. Eighty-five percent of 13 kittens were immune, after they had been treated prophylactically with 200 mg/kg monensin, or 60 mg/kg cat sulfadiazine combined with 1 mg/kg cat of pyrimethamine; oocyst shedding had been suppressed in all. It is concluded that cats can be immunized against oocyst shedding by infections where oocysts are produced, or where developmental stages are suppressed by chemoprophylaxis, but not if enteroepithelial stages are absent, as in the oocyst-less strain examined.