The bradyzoites are primarily found in brain and muscle tissue, whereas the tachyzoites tend to be in reticuloendothelial cells.
The tissue phase of the infection can also be transmitted congenitally to offspring and to other intermediate hosts through carnivorism. Ingestion of an infected animal will release the bradyzoites from the tissue cysts which then infect cells in the new host.
Possibly all mammals, including humans, can become infected with Toxoplasma. As in the case of acquiring the infection through the ingestion of oocysts, the parasites will go through an acute phase characterized by rapid replication followed by a chronic phase characterized by dormant tissue cysts.
Ingestion of an infected intermediate host by the cat will initiate the intestinal stage of the life cycle involving merogony and gamogony in the intestinal epithial cells. Cats can also support the tissue stage of the infection. Obviously humans are not a natural part of the predator-prey life cycle and represent an accidental host that does not participate in the continuation of the transmission cycle.
One source of infection is the ingestion of material contaminated with sporulated oocysts excreted by cats. This implies some association with cats. However, since the oocysts need to mature in the environment before becoming infectious, transmission will include features of soil transmission similar to Isospora and Cyclospora. For example, children of crawling and dirt-eating ages are believed to be at higher risk for infection.
Oocysts can also be acquired through gardening activities or unwashed fruits or vegetables. In addition a few water-borne outbreaks have been documented. The high prevalence of toxoplasmosis in South and Central America is believed to be due to high levels of contamination of the environment with oocysts. Ironically, contact with dogs is more of a risk factor for becoming infected with Toxoplasma than contact with cats. This is likely due to dogs seeking out cat feces and becoming contaminated with the feces and then transferring the sporulated oocysts to the clothes and hands of their owners.
Interestingly, a waterborne outbreak associated with kittens living on top of a municipal water reservoir in Brazil was reported de Moura et al, , Emerg. Toxoplasmosis can also be acquired through the ingestion of undercooked meat containing tissue cysts or tachyzoites. Presumably livestock acquire the infection through grazing in areas contaminated with cat feces. The ability of the parasite to transfer between intermediate hosts may be a relatively recent evolutionary adaptation of the parasite that coincides with the domestication of the cat and the expansion of agriculture see Box.
In fact, most infections in the United States and Europe among adults are probably acquired from undercooked meat. Mutton and pork are more common sources than beef. There have also been a few isolated reports of Toxoplasma being transmitted via tachyzoites in unpasteurised goat's milk. Toxoplasma can also be transmitted from mother to fetus, often with dire consequences see below.
Congenital transmission can only occur during an acute infection ie, tachyzoites acquired during pregancy. Mothers with a chronic infection acquired before the pregnancy are not at a risk for transmitting Toxoplasma. Tranmission of Toxoplasma as a result of organ transplants is also possible. Tissue cysts from a chronically infected organ donor may reactivate when transplanted into a previously uninfected organ recipient.
In addition, the immunosuppressive therapy could also reactivate a latent infection in the recipient. Acquisition of tachyzoites from an acutely infected person via blood transfusion is also possible. Transmission by transplantation or transfusion are now rare, though. Recent expansion of Toxoplasma? The three Toxoplasma genotypes also exhibit differences in virulence 2. For example, type I parasites are highly virulent in mice.
Similarly, type I is disproportionately associated with severe atypical ocular toxoplasmosis in immunocompetent individuals and severe congenital toxoplasmosis. Fortunately though, type II infections tend to dominate, especially in the U. However, there is some evidence suggesting that Toxoplasma exhibits more diversity in South America. Improvements in our knowledge about Toxoplasma population biology may help resolve these issues and lead to better control and treatment.
Toxoplasmosis in adults and children past the neonatal stage is usually benign and asymptomatic. Acquisition of the infection via either oocysts or tissue cysts results in an acute infection in which tachyzoites are disseminated throughout the body via the lymphatics and hematogenously.
This acute stage will persist for several weeks as immunity develops. Antibody production requires weeks and cellular immunity occurs weeks post-infection. Both humoral and cellular immunity are important, but the cellular response appears critical for the conversion from acute ie, tachyzoites to chronic ie, bradyzoites infection.
See life cycle for explanation of tachy- and bradyzoites. In particular, a strong Th1 response characterized by the production of proinflammatory cytokines including interleukin, interferon-gamma, and tumor necrosis factor-alpha are associated with Toxoplasma infection. When symptoms do occur they are generally mild and typically described as mononucleosis-like with chills, fever, headache, myalgia, fatigue and swollen lymph nodes.
These symptoms are self-limiting and resolve within weeks to months. A chronic lympadenopathy without fever persisting or recurring for up to a year has also been noted as a symptom of toxoplasmosis. Rarely do immunocompetent individuals exhibit severe symptoms and the acute infection almost always progresses to the chronic stage.
This latent infection probably persists for the life of the patient without producing any progressive pathology. Toxoplasmosis has been long noted as an opportunistic infection in regards to reactivation of latent infections due to immunosuppression associated with organ transplants and certain cancer treatments.
During the 's toxoplasmic encephalitis emerged as a common complication associated with AIDS. Reactivation of the infection typically occurs when CD4 cells drop below cells per microliter. Early symptoms of toxoplasmic encephalitis can include headache, fever, lethargy, and altered mental status with progression to focal neurological deficits and convulsions. The disease is almost always due to a reactivation of a latent infection see Box and tends to remain confined to the CNS.
In other words, the tissue cysts are rupturing and the released bradyzoites are transforming into tachyzoites. The focal lesions are caused by the destruction of host cells in the immediate vicinity.
Other forms of the reactivated disease, especially retinochoroiditis, pneumonitis, myocarditis and myositis, may occasionally occur in conjunction with immunosuppression. Carlos S. Toxoplasma can also be transmitted congenitally i. Congenital ie, transplacental infections are more likely to be symptomatic than postnatal infections and can be particularly severe see Outcomes Box. Some of the salient features are:.
A retinochoroiditis, inflammation of the retina and choroid thick vascular area at back of eye , is another clinical manifestation of Toxoplasma infection. Retinochoroiditiis can result from congenital infections or from acute or reactivated infections acquired postnatally. Originally the ocular manifestations were more often associated with congenital infections or a late manifestation due to the reactivation of a congenital infection.
However, ocular toxoplasmosis is being reported with increasing frequency in association with acute infections. It has been suggested that different genotypes exhibit different levels of virulence especially in regards to the expression of ocular disease.
In the case of congenital infection, the retinochoroiditis can develop weeks to years after birth. The lesions are focal in nature and generally self-limiting.
They are believed to be the result of cyst rupture in the retina in reactivated cases or tachyzoites in acute cases. The cells of the retina closely resemble those of the central nervous system. Granulomatous lesions may also be present in the choroid.
The lesions are usually bilateral in congenital infections and unilateral if acquired postnatally. Animal studies provide evidence that the retinal necrosis associated with the lesion is attributable to proliferation of parasites, while hypersensitivity responses to toxoplasmic antigens are responsible for the accompanying inflammation.
Symptoms can include blurred vision or other visual defects. Vision may improve with the resolution of the inflammation. Recurrences of the disease have been noted, but the frequency and factors influencing the recurrence are not clear. The disease is rarely progressive in immunocompetent individuals, but can scar the retina. However, the disease can be quite severe in AIDS patients and continue to progress.
In contrast to most other protozoan infections, diagnosis is rarely made through the detection or recovery of organisms, but relies heavily on serologic procedures. Parasites can be detected in biopsied specimens, buffy coat cells, or cerebral spinal fluid.
However, detecting tachyzoites from these materials may be difficult. These specimens can also be used to inoculated mice or tissue culture cells or analyzed by PCR. The results can be misleading though, since many individuals have been exposed to Toxoplasma and harbor tissue cysts bradyzoites.
Therefore, serologic tests are a recommended component of diagnosis. The serologic diagnosis of Toxoplasma is also complex because of the prevalence of sero-positive individuals. High antibody titers by themselves are not definitive evidence of an acute infection. Congenital infections are similarly difficult to diagnose serologically because maternal IgG crosses the placenta and persists for several months.
Treatment indications and duration :. The prognosis for acute toxoplasmosis in immunocompetent adults is excellent. Acute infections in the fetus or young children may be followed by repeated attacks of retinochoroiditis.
Treatment does appear to reduce the frequency of these attacks. If begun early enough, treatment of immunosuppressed patients usually results in improvements, but recrudescences are common. Control measures for toxoplasmosis focus on avoiding the two major sources of infection: raw meat and contaminated cat feces.
Preventive activities Box include: avoiding the ingestion of sporulated oocysts or tissue cysts, destruction of the infective forms eg.
Prevention is especially important during pregnancy when the consequences of infection are most severe. Neospora caninum. Babesiosis is a rare zoonotic infection transmitted by ticks. The etiological agents, Babesia species, are blood parasites which infect a wide variety of wild and domestic animals throughout the world.
Babesia and Theileria form a group called the piroplasms, in reference to intraerythrocytic forms that are pear-shaped in some species. Piroplasms cause tremendous losses of livestock in endemic areas. Is has been speculated that the plague of the Egyptians' cattle described in the biblical book of Exodus may have been red water fever caused by B.
The two piroplasm genera are usually distinguished by the lack of a pre-erythrocytic cycle in Babesia and the lack of transovarial transmission in Theileria see life cycle below. Molecular data indicate that Babesia and Theileria species do not form respective monophylogenic groups. In particular, many Babesia species, which had been informally grouped as 'small' Babesia , are more closely related to Theileria.
Consistent with this molecular data, none of the small Babesia-- in contrast to the 'large' Babesia --appears to be transmitted transovarially in ticks, suggesting a need for some re-evaluation of piroplasm classification.
Many species of Babesia have been reported to infect humans. The three most predominant species infecting humans are B. Infections with other species have either been poorly documented or limited to a few isolated cases.
The initial cases were associated with splenectomy or other immuno-compromising conditions. However, immuno-competent persons infected with Babesia and not exhibiting clinical symptoms have been described. Furthermore serological surveys suggest that the infection may be under diagnosed.
The largest focus of human infections in the U. Infection in Europe is apparently rarer then in the U. Most of these infections have been associated with individuals who have frequent contact with cattle. Babesia exhibits a typical apicomplexan life cycle characterized by merogony, gametogony, and sporogony Figure.
Many species are highly pathogenic to their host including human and domestic animals and from medical perspective represent the most important eukaryotic parasites. Coccidians are omnipresent in vertebrates, e.
The phylum Apicomplexa includes morphologically and ecologically diverse protists, such as the gregarines, cryptosporidia, coccidia, haemosporidia, and piroplasms. The life cycle of majority of Apicomplexa involves sexual and asexual multiplication in the parasitized host and an environmentally resilient cyst forms.
Transmission strategies are diverse, from direct transmission to intricate cycles in trophic webs between predators and their prey or involving arthropod vectors. The phylum is highly successful, thanks to morphological and molecular adaptations. The name is derived from two Latin words, apex top and complexus infolds , and refers to a set of organelles composed from spirally arranged microtubules, polar ring s , and secretory bodies, such as rhoptries and micronemes.
Apical complex structures mediate entry of the parasite into the host cells, where they usually survive inside a parasitophorous vacuole. Most apicomplexans possess a unique organelle called the apicoplast, which is a highly reduced non-photosynthetic plastid, which retains few functions essential for a parasite survival. The phylum evolved from a photosynthetic flagellate, and core apicomplexans form a sister group to a free-living marine and freshwater protists Chromera , Vitrella , and Colpodella.
Skip to main content. This service is more advanced with JavaScript available. Advertisement Hide. Reference work entry First Online: 01 August This is a preview of subscription content, log in to check access. Adl, S. The revised classification of eukaryotes. Journal of Eukaryotic Microbiology, 59 , — Allen, P. Recent advances in biology and immunobiology of Eimeria species and in diagnosis and control of infection with these coccidian parasites of poultry.
Clinical Microbiology Review, 15 , 58— CrossRef Google Scholar. Al-Olayan, E. Complete development of mosquito phases of the malaria parasite in vitro. Science, , — PLoS Pathogens, 11 , e Baum, J. Host-cell invasion by malaria parasites: Insights from Plasmodium and Toxoplasma.
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The blastogregarine Siedleckia was strongly related to the archigregarine Selenidium pygospionis. Gregarine apicomplexans sensu lato including blastogregarines but excluding Digyalum ; see below and eugregarines were both monophyletic, in contrast to most interpretations based on ribosomal RNA genes rDNA Cavalier-Smith, ; Leander, ; Rueckert et al.
The resulting trees had congruent topologies with all internal branches fully supported except for two eugregarine subclades and the position of cryptosporidians Figure 1—figure supplement 1B. The relationship of cryptosporidians therefore requires additional support, although their sister position to gregarines, which was unambiguously recovered in all trees including the ten PhyloBayes runs, is a preferred hypothesis.
Two apicomplexan-like parasites branched outside the main apicomplexan clade Figure 1A,B. Digyalum oweni , a formally described archigregarine was fully resolved as a sister lineage to all apicomplexans and chrompodellids. Thus, apicomplexan parasites in the traditional sense are polyphyletic see Discussion. We next explored the existence of plastids in gregarines, Digyalum , and other parasites, where none have been known.
Digyalum , Selenidium, Siedleckia, rhytidocystids, and Eleutheroschizon all contain near-complete plastidial biosynthesis of isoprenoid precursors, heme, and fatty acids, ferredoxin redox system, iron-sulfur cluster synthesis, and plastid genomes Figure 2A. The eugregarine Lankesteria unusually contains fatty acid biosynthesis as the only plastidial pathway, whereas Symbiont X contains only the isoprenoid pathway, similar to piroplasms Lizundia et al.
The distribution of control, signature plastid genes involved in polypeptide import, folding, and DNA replication in the plastid cpn60 , sDer-1 , PREX , matches the presence of plastid metabolism and genomes Figure 2A. Maximum likelihood phylogenies of all individual proteins allowed us to readily distinguish the apicomplexan sequences from bacteria and other contaminants in the datasets Materials and methods. In most phylogenies, the apicomplexan sequences cluster with algal plastid forms, confirming that they came from the plastid endosymbiont rather than the eukaryotic host.
The phylogeny is different in several genes that are either derived by horizontal gene transfer from bacteria or in fact localize outside of the plastid in Plasmodium in heme biosynthesis; see below. N-terminal regions of plastid sequences from our new transcriptomes often carry signal peptides typical for targeting to the plastid the other have incomplete N-termini or lack targeting signatures by default, such as most triose phosphate translocators. The signal peptides are often followed by transit peptide-like regions, although these are more difficult to predict computationally Supplementary file 5.
In Digyalum , transit peptides have a net positive charge similar to other plastid leaders they are low in acidic and high in basic residues; Figure 2—figure supplement 1A.
Digyalum transit peptides are compositionally similar to transit peptides in Plasmodium , and likewise lack the phenylalanine motif at the first position after the signal peptide cleavage site Figure 2—figure supplement 1B Patron and Waller, Predicted localizations for plastidial proteins and mitochondrial ALAS correspond closely to experimental evidence in Plasmodium and Toxoplasma Figure 2A.
The only exceptions to this pattern are the last three enzymes in heme biosynthesis, which are predicted to be plastidial in some parasites see Discussion. The reconstructed plastid pathways also reflect known dependencies between their modules Figure 2B. Iron-sulphur cluster assembly and ferredoxin system are widely required as co-factors for isoprenoid and fatty acid synthesis, whereas heme biosynthesis can be lost independently of other modules — likely the case in Lankesteria and Symbiont X.
SufA was not identified in the Chromera genome. Pyruvate dehydrogenase and fatty and lipoic acid synthesis protein sequences in Digyalum are notably divergent, including three that are more closely related to bacterial than plastid sequences Figure 2A.
The cytosolic mevalonate pathway for isoprenoid precursor synthesis is absent in all species, but the mitochondrial cysteine desulphurase IscS and cytosolic fatty acid synthase FASI and elongase ELO pathways are present, as expected Materials and methods Dellibovi-Ragheb et al.
No plastid genes were identified in five eugregarine lineages other than Lankesteria , including in the draft genome of Gregarina Figure 2A ; see Discussion about the PREX fragment in Ascogregarina. This result is suggestive of at least two losses of plastids in eugregarines, which were independent of the one in Cryptosporidium Discussion.
A Presence of genes and pathway modules top; abbreviations in Supplementary file 4 in representative genomes G and transcriptomes left. Each gene box is color-coded as to its evolutionary origin, as determined by a maximum likelihood phylogeny plastid-encoded rps , rpl , rpo , trn genes were not analyzed. Empty boxes indicate gene absence in completed genomes and blank spaces indicate absence in transcriptomes.
Intracellular localization of corresponding proteins is shown by a circle inside the box and summarizes known experimental data Supplementary file 4 or de novo prediction in silico by SignalP v4.
B Dependence network of plastid protein modules for the biosynthesis of key metabolites — isoprenoid precursors IPP and DMAP, fatty acids and heme — which underlie dependency on the plastid organelle in Apicomplexa. Colored regions contain modules specific to one pathway: fatty acid pink , isoprenoid precursor pale green and heme biosynthesis yellow. Plastid 16S rDNA transcripts of newly sequenced species are shown in red.
Note that sequences in the tree vary greatly in their AT content and substitution rates, which can induce a misleading topology - deep relationships in the tree should therefore be interpreted with caution. The fast-evolving sequences of peridinin dinoflagellates were not included. B Extremely high AT content in rhytidocystid plastid genomes arrows.
AT content of representative species from part A and Balanophora laxiflora and B. Plastid genomes in the newly sequenced species are only partially reconstructed from transcripts red color; see Supplementary file 7. Altered genetic codes are indicated. C Euler diagram of plastid genome contents in apicomplexans, dinoflagellates ancestral gene sets for each , Digyalum , Chromera, and Vitrella. Genes on the green background are associated solely with photosynthesis.
Small RNA genes are not shown. Instead, the five genera have some of the fastest-evolving and most AT-rich 16S rDNAs of all apicomplexans, and they cluster with compositionally similar sequences of the more distantly related hematozoans compare Figure 1A and Figure 3A. Such artificial grouping of highly divergent sequences is a well-known phylogenetic artifact, and deep-level relationships in the tree thus ought to be interpreted with caution.
The 16S rDNAs of Digyalum , Eleutheroschizon , Siedleckia , Selenidium or Rhytidocystis were recovered among a set of AT-rich transcriptomic contigs, which encode other genes typical of apicomplexan plastid genomes Supplementary file 7 ; Materials and methods.
Digyalum , Siedleckia , Selenidium , and Rhytidocystis sp. The Digyalum plastid encodes six genes never identified in apicomplexan plastids and lacks nine genes they do contain; only one gene rps18 was relocated to the nucleus in parallel in both lineages Figure 3C.
To test if the plastids in Digyalum , chrompodellids and apicomplexans are likely derived from a common source we searched for shared innovations in their plastid genes.
PREX protein contains N-terminal primase and helicase domains, which are homologous to the mitochondrial primase-helicase Twinkle and fused with an Aquifex -type exonuclease-polymerase downstream. Phylogeny of the polymerase unit confirms that it was acquired from an unknown bacterial source related to Aquifex before the Digyalum -apicomplexan split Figure 4A,C.
The gene subsequently fused with the Twinkle gene and the product became targeted to the plastid the N-terminus of PREX is incomplete in most species including Digyalum but contains a signal peptide in Chromera ; Supplementary file 5. Another unusual fusion took place in 4-hydroxymethylbutenyl diphosphate reductase IspH , the last enzyme in the plastid isoprenoid precursor biosynthesis. A canonical plastid ispH gene of a cyanobacterial origin, which is also present in dinoflagellates and Perkinsus , was replaced by a Chlamydiae-like variant in the ancestor of Digyalum and Apicomplexa and fused with the plastid gene for sedoheptulose-1,7-bisphosphatase form 3 SBP3 Figure 4B,C.
The fusion is absent in Toxoplasma , Plasmodium and piroplasms, which lack SBP3 , and has been interpreted as a derived characteristic in Chromera Petersen et al. Apicomplexans, chrompodellids and Digyalum are highlighted in orange, and other eukaryotes in gray. Characterized enzymes are highlighted in bold.
C Predicted gain, loss, fusion and fission events in the evolution of five plastid-associated and two cytosolic genes. Note that the ferrochelatase HemH is mitochondrial in Plasmodium but probably plastidial in Chromera and some apicomplexans. Another unique evolutionary event in apicomplexan plastids is a fission in a non-conserved region of the plastid-encoded rpoC2 gene. The unprecedented split was once interpreted as a read-through frame shift in Plasmodium or read-through STOP codons in Toxoplasma and Eimeria in a continuous rpoC2 Cai et al.
We instead find that all apicomplexan rpoC2 genes are split within the same region, including those in the deep-branching Selenidium and Siedleckia Figure 4C and Figure 4—figure supplement 1. Both frame shifting and STOP codon read-through would be required for continuous rpoC2 translation in Eleutheroschizon Figure 4—figure supplement 1.
Such variable gene arrangements are incongruent with the expression of the apicomplexan rpoC2 as a single protein. Indeed, the downstream rpoC2 moiety almost unequivocally possesses an ATG start codon near the split site allowing it to be translated independently Figure 4—figure supplement 1.
The evidence altogether points to a fission event in rpoC2 , which is absent in all other plastids, including those of Digyalum and chrompodellids, and thus represents a defining ancestral characteristic of the apicomplexan plastid.
Two additional plastid-associated proteins in apicomplexan and chrompodellid plastids derive from horizontally acquired genes. The first is Alphaproteobacteria-like ferrochelatase HemH , which is localized to mitochondria in Plasmodium but likely targeted to plastids in Chromera and possibly in some apicomplexans see Discussion Koreny et al.
Digyalum encodes the same alphaproteobacterial HemH but it has an unusual FabG, which is related to other bacteria Figure 4C , Figure 4—figure supplement 2 and Figure 4—figure supplement 3. Finally, genes of two well-known cytosolic proteins Huang et al. Generating transcriptomes from uncultured apicomplexans across their evolutionary diversity provides the first comprehensive insights into relationships between major apicomplexan groups. Two species with apicomplexan-like morphology either described as apicomplexans Digyalum or yet unclassified Symbiont X are not members of Apicomplexa sensu stricto.
This shows that apicomplexan-like parasites are polyphyletic and evolved at least three times independently. Specifically, large trophont stages attached to intestines of marine invertebrates by specialized apical structures are products of convergent evolution. The trophonts of Digyalum , for example, parasitize the gut epithelium of Littorina snails and their attachment structure contains an apical complex with a protruded polar ring, which provides a gateway for rhoptry-mediated secretion — a combination of traits typical for gregarine apicomplexans Dyson et al.
Symbiont X is known only from light microscopy data but would be also readily classified as an apicomplexan based on crude characteristics: it parasitizes the gut of Scoloplos armiger polychaetes being attached to the host epithelium by its apical end unpublished data.
Tracing the evolution of such parasite characteristics, however, indicates that the basis for convergence lies in evolution acting on similar preconditions. Such broad distribution points to a single origin of the apical complex in the ancestor of apicomplexans and dinoflagellates in a non-parasitic context Figure 1A.
Because the apical complex mediates secretion often associated with cell-to-cell interactions, it is likely an important precondition in multiple origins of parasitism in both apicomplexans and dinoflagellates. In similar host environments the structure may have also promoted convergent parasite morphologies. The use of the apical complex in extracellular attachment and secretion in the gut epithelium of animal hosts, for example, may have triggered convergent expansion in the cell size of gregarine, Digyalum and Symbiont X trophonts.
Unsurprisingly, convergent similarities in the three lineages are accompanied by considerable differences in detailed morphology: Digyalum and Symbiont X do not glide or twist but they pulsate, and detailed ultrastructure of their apical complex and pellicle Dyson et al. Similar divergence characterizes their molecular make-ups: apicomplexans are well-known auxotrophs for purines, but Digyalum contains a pathway for their synthesis data not shown and, despite that both lineages lost photosynthesis, their plastid genomes have been reduced in different ways Figure 3C.
The convergent morphologies of Digyalum , Symbiont X and apicomplexans are therefore rather superficial similarities, but the possibility that they were driven by the presence of shared ancestral traits such as the apical complex in similar host habitats highlights the importance of preconditions in the origin of parasites Janouskovec and Keeling, Key findings of multiprotein phylogenies are that eugregarines and gregarines are unequivocally monophyletic Figure 1 and Figure 1—figure supplement 1.
Indeed, protein sequences allow for building larger phylogenetic matrices and have more even substitution rates than rDNAs, some of which are notoriously divergent and phylogenetically unstable. Although the sampling of eugregarine diversity is incomplete, our phylogeny contains six of their seven main lineages at the superfamily level Simdyanov et al. The eugregarine monophyly provides the first unambiguous phylogenetic support for their two candidate synapomorphies: the ultrastructure of the epimerite, and the ultrastructure of epicytic crests Simdyanov et al.
It also partially resolves the little understood relationships between eugregarine superfamilies Cavalier-Smith, ; Simdyanov et al. The blastogregarine Siedleckia groups strongly with the archigregarine Selenidium. Both lineages also feed by myzocytosis, which is known in some relatives of apicomplexans Foissner and Foissner, ; Mylnikov and Mylnikova, but not in eugregarines, cryptosporidians or coccidiomorphs.
Because the blastogregarine ultrastructure and life cycle share additional similarities with coccidians Simdyanov et al. The monophyly of gregarines sensu lato in our trees Figure 1 and Figure 1—figure supplement 1 provides phylogenetic support for a tentative synapomorphy of this group, the forming of a gametocyst during the life cycle Simdyanov et al. The position of cryptosporidians is still not fully resolved, but the group is consistently recovered next to gregarines Figure 1 and Figure 1—figure supplement 1.
The most serious disease is East Coast fever of cattle, caused by T. Another species, T. Cryptosporiidiosis is a serious emerging human pathogenic disease. Since , it has been a debilitating illness causing enteritis in humans, and various Cryptosporidium species infect other animals primarily mammals causing a waterborne diarrheal disease.
Ingestion of infective oocysts leads to the disease, which may range from asymptomatic to relatively mild cases of diarrhea in immunocompetent individuals to potentially life-threatening profuse watery diarrhea in patients who have weakened immune systems, such as those with AIDS.
There are no drugs coccidostats that completely get rid of the disease, but some, like Alinia nitazoxanide , may help slow down the progression. In hosts with healthy immune systems, the disease is self-limiting in a few days.
Another pathogenic apicomplexan of humans perhaps also in other primates as well is Cyclospora cayetanensis. The first human cases of C. Infection leads to a gastrointestinal disease, usually from foodborne outbreaks, called cyclosporiasis that can range from asymptomatic to debilitating. Restaurant-associated cases have been reported in the United States, linked to salad mixes that contained contaminated iceberg and romaine lettuce, red cabbage, carrots, and cilantro.
Most people who have healthy immune systems will recover without treatment, although the illness may last for a few days to a month or longer. To date, no highly effective alternative antibiotic regimen has been identified for patients who do not respond to the standard treatment or have an allergy to sulfa drugs. Cystoisosporiasis is an intestinal disease of humans caused by the coccidian parasite Cystoisospora belli formerly Isospora belli. It is most common in tropical and subtropical areas of the planet.
The parasite can be spread by ingesting contaminated food or water. In immune-competent people, C. The most common symptom is a profuse watery diarrhea. However, the infection is treatable with Bactrim. Malaria is a mosquito-borne usually from female Anopheles infectious disease caused by apicomplexans in the genus Plasmodium that affects humans and other animals. Typical symptoms include fever, malaise, vomiting, and headaches. In severe cases it can cause jaundiced skin, seizures, coma, or death.
Most deaths are caused by P. Symptoms usually begin ten to fifteen days after a bite from an infected mosquito. If not properly treated, people may have recurrences of the disease months later.
In those who have recently survived an infection, reinfection usually causes milder symptoms. This partial resistance disappears over months to years if the person has no continuing exposure to malaria. Interestingly, in the s and s, Arkansas had more malaria deaths than any other state.
However, the protist Plasmodium is no longer a threat in Arkansas, as the last malaria cases except for rare cases in travelers or immigrants, mostly from sub-Saharan Africa and South Asia in the state was in There are several drugs including chloroquine and antibiotics used in treatment against the parasitic forms in the blood the form that causes disease , and most are used in combination with quinine.
Another pathogenic coccidian that causes the disease toxoplasmosis and affects humans worldwide is Toxoplasma gondii. It is capable of infecting nearly all mammals, and almost a third of the human global population has been exposed to and may be chronically infected with the parasite. However, in immunocompetent humans, no symptoms at all may be present, or a mild, flu-like illness can occur during the first few weeks following exposure.
In infants, AIDS patients, and others who are immunocompromised, infection can lead to serious health problems and sometimes death. Wild and domestic cats are considered the final hosts of T. There are at least four routes of infection in humans and other warm-blooded animals: 1 by consuming raw or undercooked meat containing T. Treatment with pyrimethamine Daraprim and the antibiotic sulfadiazine is recommended.
Another apicomplexan, Neospora caninum , is closely related to T. It does not affect humans; rather, it infects several domestic animals and is a major cause of abortions and stillbirth in domestic cattle worldwide. The definitive hosts are dogs, which exhibit neuromuscular disease. Dogs become infected after ingestion of infected tissues from intermediate hosts. The infection can also be transmitted congenitally, and the parasite is readily maintained in cattle and dogs by vertical transmission.
A sylvatic cycle involving white-tailed deer Odocoileus virginianus and coyotes Canis latrans has also been reported. The study of various apicomplexans in Arkansas has become more popular in the last four decades than in all years prior combined. However, several groups are yet to be studied, such as the gregarines, as none have yet been reported from any Arkansas host. Hematozoans such as Haemogregarina and Hematozoon have been reported from erythrocytes of turtles and snakes in Arkansas, respectively.
There has also been an explosion in the description of new and previously described species of coccidians from various animals surveyed in the state such as amphibians salamanders, frogs, and toads , reptiles turtles, lizards and snakes , and mammals particularly bats. For additional information: Barta, John R. Dubey, Jitender P. Weiss and Kami Kim. New York: Elsevier, Duszynski, Donald W.
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