Hammondia hammondi

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]

Hammondia hammondi
Scientific classification
Clade: SAR
Infrakingdom: Alveolata
Phylum: Apicomplexa
Class: Conoidasida
Order: Eucoccidiorida
Family: Sarcocystidae
Genus: Hammondia
Species:
H. hammondi
Binomial name
Hammondia hammondi
Frenkel & Dubey 1975

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]

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.
  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.
  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.
  4. Dubey, J.P.; Sreekumar, C. (2003). "Redescription of Hammondia hammondi and its differentiation from Toxoplasma gondii". International Journal for Parasitology. 33: 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.
  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.
  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. doi:10.2307/3279915. JSTOR 3279915.
  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.

Further reading
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