Hammondia hammondi

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Hammondia hammondi
Scientific classification OOjs UI icon edit-ltr.svg
Domain: Eukaryota
Clade: Diaphoretickes
Clade: SAR
Clade: Alveolata
Phylum: Apicomplexa
Class: Conoidasida
Order: Eucoccidiorida
Family: Sarcocystidae
Genus: Hammondia
Species:
H. hammondi
Binomial name
Hammondia hammondi
Frenkel & Dubey 1975

Hammondia hammondi is a species of obligate heteroxenous parasitic alveolates of domestic cats (final host). Intracellular cysts develop mainly in striated muscle. After the ingestion of cysts by cats, a multiplicative cycle precedes the development of gametocytes in the epithelium of the small intestine (each oocyst of the species averaging 11×13 μm). Oocyst shedding persists for 10 to 28 days followed by immunity. Cysts in skeletal muscle measure between 100 and 340 μm in length and 40 and 95 μm in width. Some of the intermediate hosts (e.g. guinea pigs, hamsters) develop low levels of antibody and some cross-immunity against Toxoplasma . [1]

Contents

Background

Hammondia hammondi is an apicomplexan parasite with cat as its definitive host. It was discovered in 1975 and named after the eminent protozoologist D. M. Hammond. The parasite is obligate intracellular by nature and closely resembles Toxoplasma gondii , another zoonotic parasite of cats. After bradyzoites (in tissue cysts) are ingested by cats, just like T. gondii, H. hammondi also multiplies both asexually and sexually in the intestines of cats and in about 1–3 days, stages of parasites can be found in sections of the cat's small intestine. Subsequently, oocysts are excreted in the faeces. [2]

Relation to Toxoplasma gondii - very similar although H. hammondi has a smaller group of hosts that it can infect. This group is cats, rats, mice, other small rodents, goats, and roe deer. Mice were used to test the differences between T. gondii and H. hammondi, telling scientists that H. hammondi infections in mice can only be caused by oocysts and not the tachyzoites or bradyzoites. The different stages (tachyzoite, bradyzoites and sporozoites) are virtually indistinguishable from T. gondii under light microscopy. [3]

Earlier, the validity of H. hammondi as a separate organism was under question. However, detailed studies have conclusively proved that H. hammondi is structurally, biologically, antigenically, and genetically distinct from T. gondii. Though they appear similar under light microscopy, under electron microscopy, there are two consistent differences between their tachyzoites and sporozoites. Rhoptries in H. hammondi tachyzoites are electron-dense whereas those of T. gondii tachyzoites are electron-lucent. The crystalloid body present in sporozoites of H. hammondi and other coccidia is absent in T. gondii. Unlike T. gondii, H. hammondi does not multiply 'luxuriously' in cell culture. Tissue cysts are formed within a few days of culture and the parasite is soon 'outgrown' by the host cells. With T. gondii, all stages can set up infection in both definite and intermediate hosts, whereas only the oocysts of H. hammondi are infective to mice and cats get patent infection only on consuming tissues containing the bradyzoite cysts. [4]

Subsequent studies have clearly shown molecular differences between H. hammondi and T. gondii using the PCR (polymerase chain reaction). Primers can differentially diagnose the parasites even in a tissue sample with mixed infection of both parasites, which was not possible previously. [5]

As an experiment, oocysts were given to eight dogs while cysts were given to four dogs. Between the period of 16–101 days, all of the experimented dogs died and did not shed oocysts. The intestines of the dogs were given to cats which then shed oocysts after 8–10 days. The scientists found out that there were no lesions in any of the twelve dogs that were given the parasite. Dogs, along with the other rodents, are intermediate hosts and cats are the final host. [6] That means cats are don't experience the symptoms of the disease. [7] [8]

TA cat from Iowa was infected, along with a cat from Germany and three out of 1,604 cats from Hawaii. Over a thousand cats were killed by the Humane Society in Ohio and their feces were examined for intestinal issues. H. hammondi was discovered along with some other parasites. There was a wide range of the disease. [9] In Australia, 1978, another scientist discovered feeding his laboratory-raised cats infected mice and rats. The result was the cats shed oocysts. In Japan, scientists discovered that feeding muscles from infected goats to cats lead to patent infections. The cat from Germany was fed roe deer muscles and shed oocysts, proving that there are many intermediate hosts and cats being the final host. [10]

Related Research Articles

<span class="mw-page-title-main">Toxoplasmosis</span> Protozoan parasitic disease

Toxoplasmosis is a parasitic disease caused by Toxoplasma gondii, an apicomplexan. Infections with toxoplasmosis are associated with a variety of neuropsychiatric and behavioral conditions. Occasionally, people may have a few weeks or months of mild, flu-like illness such as muscle aches and tender lymph nodes. In a small number of people, eye problems may develop. In those with a weak immune system, severe symptoms such as seizures and poor coordination may occur. If a woman becomes infected during pregnancy, a condition known as congenital toxoplasmosis may affect the child.

<i>Toxoplasma gondii</i> Type of protozoan parasite

Toxoplasma gondii is a parasitic protozoan that causes toxoplasmosis. Found worldwide, T. gondii is capable of infecting virtually all warm-blooded animals, but felids are the only known definitive hosts in which the parasite may undergo sexual reproduction.

<span class="mw-page-title-main">Isosporiasis</span> Human intestinal disease

Isosporiasis, also known as cystoisosporiasis, is a human intestinal disease caused by the parasite Cystoisospora belli. It is found worldwide, especially in tropical and subtropical areas. Infection often occurs in immuno-compromised individuals, notably AIDS patients, and outbreaks have been reported in institutionalized groups in the United States. The first documented case was in 1915. It is usually spread indirectly, normally through contaminated food or water (CDC.gov).

<span class="mw-page-title-main">Coccidia</span> Subclass of protists

Coccidia (Coccidiasina) are a subclass of microscopic, spore-forming, single-celled obligate intracellular parasites belonging to the apicomplexan class Conoidasida. As obligate intracellular parasites, they must live and reproduce within an animal cell. Coccidian parasites infect the intestinal tracts of animals, and are the largest group of apicomplexan protozoa.

Coccidiosis is a parasitic disease of the intestinal tract of animals caused by coccidian protozoa. The disease spreads from one animal to another by contact with infected feces or ingestion of infected tissue. Diarrhea, which may become bloody in severe cases, is the primary symptom. Most animals infected with coccidia are asymptomatic, but young or immunocompromised animals may suffer severe symptoms and death.

<i>Eimeria</i> Genus of single-celled organisms

Eimeria is a genus of apicomplexan parasites that includes various species capable of causing the disease coccidiosis in animals such as cattle, poultry and smaller ruminants including sheep and goats. Eimeria species are considered to be monoxenous because the life cycle is completed within a single host, and stenoxenous because they tend to be host specific, although a number of exceptions have been identified. Species of this genus infect a wide variety of hosts. Thirty-one species are known to occur in bats (Chiroptera), two in turtles, and 130 named species infect fish. Two species infect seals. Five species infect llamas and alpacas: E. alpacae, E. ivitaensis, E. lamae, E. macusaniensis, and E. punonensis. A number of species infect rodents, including E. couesii, E. kinsellai, E. palustris, E. ojastii and E. oryzomysi. Others infect poultry, rabbits and cattle. For full species list, see below.

<i>Neospora caninum</i> Species of Conoidasida in the apicomplex phylum

Neospora caninum is a coccidian parasite that was identified as a species in 1988. Prior to this, it was misclassified as Toxoplasma gondii due to structural similarities. The genome sequence of Neospora caninum has been determined by the Wellcome Trust Sanger Institute and the University of Liverpool. Neospora caninum is an important cause of spontaneous abortion in infected livestock.

<span class="mw-page-title-main">Rhoptry</span>

A rhoptry is a specialized secretory organelle. They are club-shaped organelles connected by thin necks to the extreme apical pole of the parasite. These organelles, like micronemes, are characteristic of the motile stages of Apicomplexa protozoans. They can vary in number and shape and contain numerous enzymes that are released during the process of host penetration. The proteins they contain are important in the interaction between the host and the parasite, including the formation of the parasitophorous vacuole (PV).

Besnoitia bennetti is a parasite that can cause besnoitiosis infections in donkeys. The range of this organism ranges from Africa to the United States. B. bennettii shares similar characteristics with Toxoplasma, Neospora, and Sarcocystis genera. Lab work onB. bennetti is conducted at biosafety level 1.

<span class="mw-page-title-main">Gregarinasina</span> Subclass of protists

The gregarines are a group of Apicomplexan alveolates, classified as the Gregarinasina or Gregarinia. The large parasites inhabit the intestines of many invertebrates. They are not found in any vertebrates. Gregarines are closely related to both Toxoplasma and Plasmodium, which cause toxoplasmosis and malaria, respectively. Both protists use protein complexes similar to those that are formed by the gregarines for gliding motility and for invading target cells. This makes the gregarines excellent models for studying gliding motility, with the goal of developing treatment options for both toxoplasmosis and malaria. Thousands of different species of gregarine are expected to be found in insects, and 99% of these gregarine species still need to be described. Each insect species can be the host of multiple gregarine species. One of the most-studied gregarines is Gregarina garnhami. In general, gregarines are regarded as a very successful group of parasites, as their hosts are distributed over the entire planet.

<i>Sarcocystis</i> Genus of protists in the apicomplex phylum

Sarcocystis is a genus of protozoan parasites, with many species infecting mammals, reptiles and birds. Its name is dervived from Greek sarx = flesh and kystis = bladder.

<i>Neospora</i> Genus of single-celled organisms

Neospora is a single celled parasite of livestock and companion animals. It was not discovered until 1984 in Norway, where it was found in dogs. Neosporosis, the disease that affects cattle and companion animals, has a worldwide distribution. Neosporosis causes abortions in cattle and paralysis in companion animals. It is highly transmissible and some herds can have up to a 90% prevalence. Up to 33% of pregnancies can result in aborted fetuses on one dairy farm. In many countries this organism is the main cause of abortion in cattle. Neosporosis is now considered as a major cause of abortion in cattle worldwide. Many reliable diagnostic tests are commercially available. Neospora caninum does not appear to be infectious to humans. In dogs, Neospora caninum can cause neurological signs, especially in congenitally infected puppies, where it can form cysts in the central nervous system.

<span class="mw-page-title-main">Toll-like receptor 11</span>

Toll-like receptor 11 (TLR11) is a protein that in mice and rats is encoded by the gene TLR11, whereas in humans it is represented by a pseudogene. TLR11 belongs to the toll-like receptor (TLR) family and the interleukin-1 receptor/toll-like receptor superfamily. In mice, TLR11 has been shown to recognise (bacterial) flagellin and (eukaryotic) profilin present on certain microbes, it helps propagate a host immune response. TLR11 plays a fundamental role in both the innate and adaptive immune responses, through the activation of Tumor necrosis factor-alpha, the Interleukin 12 (IL-12) response, and Interferon-gamma (IFN-gamma) secretion. TLR11 mounts an immune response to multiple microbes, including Toxoplasma gondii, Salmonella species, and uropathogenic E. coli, and likely many other species due to the highly conserved nature of flagellin and profilin.

<span class="mw-page-title-main">Apicomplexan life cycle</span> Apicomplexa life cycle

Apicomplexans, a group of intracellular parasites, have life cycle stages that allow them to survive the wide variety of environments they are exposed to during their complex life cycle. Each stage in the life cycle of an apicomplexan organism is typified by a cellular variety with a distinct morphology and biochemistry.

The genus Schellackia comprises obligate unicellular eukaryotic parasites within the phylum Apicomplexa, and infects numerous species of lizards and amphibians worldwide. Schellackia is transmitted via insect vectors, primarily mites and mosquitoes, which take up the parasite in blood meals. These vectors then subsequently infect reptilian and amphibian which consume the infected insects. The parasites deform erythrocytes of the host into crescents, and can be visualized using a blood smear.

Hammondia is a genus of parasitic alveolates in the phylum Apicomplexa.

Behavior-altering parasites are parasites with two or more hosts, capable of causing changes in the behavior of one of their hosts to enhance their transmission, sometimes directly affecting the hosts' decision-making and behavior control mechanisms. They do this by making the intermediate host, where they may reproduce asexually, more likely to be eaten by a predator at a higher trophic level which becomes the definitive host where the parasite reproduces sexually; the mechanism is therefore sometimes called parasite increased trophic facilitation or parasite increased trophic transmission. Examples can be found in bacteria, protozoa, viruses, and animals. Parasites may also alter the host behaviour to increase protection of the parasites or their offspring; the term bodyguard manipulation is used for such mechanisms.

<i>Cystoisospora belli</i> Species of single-celled organism

Cystoisospora belli, previously known as Isospora belli, is a parasite that causes an intestinal disease known as cystoisosporiasis. This protozoan parasite is opportunistic in immune suppressed human hosts. It primarily exists in the epithelial cells of the small intestine, and develops in the cell cytoplasm. The distribution of this coccidian parasite is cosmopolitan, but is mainly found in tropical and subtropical areas of the world such as the Caribbean, Central and S. America, India, Africa, and S.E. Asia. In the U.S., it is usually associated with HIV infection and institutional living.

Cystoisospora canis, previously known as Isospora canis, is a microscopic, coccidian parasite that causes an intestinal tract infection in dogs. The intestinal tract infection is coccidiosis caused by a protozoa called coccidia.

<span class="mw-page-title-main">Heteroxeny</span> Several-host parasitic lifestyle

Heteroxeny, or heteroxenous development, characterizes a parasite whose development involves several host species. Heteroxeny has been used as the basis for splitting genera.

References

  1. Frenkel, J. K.; Dubey, J. P. (1975). "Hammondia hammondi gen. nov., sp.nov., from domestic cats, a new coccidian related to Toxoplasma and Sarcocystis". Zeitschrift für Parasitenkunde. 46 (1): 3–12. doi:10.1007/BF00383662. ISSN   0044-3255. PMID   807048. S2CID   6970694.
  2. Dubey, Jitender P.; Ferguson, David J. P. (May 2015). "Life Cycle of Hammondia hammondi (Apicomplexa: Sarcocystidae) in Cats". Journal of Eukaryotic Microbiology. 62 (3): 346–352. doi: 10.1111/jeu.12188 . PMID   25312612. S2CID   25363165.
  3. Frenkel, J. K.; Dubey, J. P. (2000-09-22). "The taxonomic importance of obligate heteroxeny: distinction of Hammondia hammondi from Toxoplasma gondii - another opinion". Parasitology Research. 86 (10): 783–786. doi:10.1007/s004360000261. ISSN   0932-0113. PMID   11068808. S2CID   31899029.
  4. Dubey, J.P.; Sreekumar, C. (2003). "Redescription of Hammondia hammondi and its differentiation from Toxoplasma gondii". International Journal for Parasitology. 33 (13): 1437–1453. doi:10.1016/S0020-7519(03)00141-3. PMID   14572507.
  5. Sreekumar, C.; Vianna, M.C.B.; Hill, D.E.; Miska, K.B.; Lindquist, A.; Dubey, J.P. (January 2006). "Differential detection of Hammondia hammondi from Toxoplasma gondii using polymerase chain reaction". Parasitology International. 54 (4): 267–269. doi:10.1016/j.parint.2005.06.008. PMID   16153883.
  6. Bowman, Dwight D. (2001). Feline Clinical Parasitology. Hendrix, Charles M., Lindsay, David S. Hoboken: John Wiley & Sons. ISBN   9780470376591. OCLC   609847424.
  7. Mehlhorn, Heinz (December 2016). Animal parasites : diagnosis, treatment, prevention. Cham, Switzerland. ISBN   9783319464039. OCLC   967775544.{{cite book}}: CS1 maint: location missing publisher (link)
  8. Dubey, J.P. (November 1975). "Experimental Hammondia hammondi Infection in Dogs". British Veterinary Journal. 131 (6): 741–743. doi:10.1016/S0007-1935(17)35147-3. PMID   1212613.
  9. Chistie, Emanuel; Dubey, J. P.; Pappas, P. W. (October 1977). "Prevalence of Hammondia hammondi in the Feces of Cats in Ohio". The Journal of Parasitology. 63 (5): 929–931. doi:10.2307/3279915. JSTOR   3279915. PMID   410914.
  10. Dubey, J. P.; Tilahun, G.; Boyle, J. P.; Schares, G.; Verma, S. K.; Ferreira, L. R.; Oliveira, S.; Tiao, N.; Darrington, C. (August 2013). "Molecular and Biological Characterization of First Isolates of Hammondia hammondi from Cats from Ethiopia". Journal of Parasitology. 99 (4): 614–618. doi:10.1645/12-51.1. ISSN   0022-3395. PMID   23517380. S2CID   16046497.

Further reading