Hammondiapardalis Hendricks, Ernst, Courtney, and Speer, 1979

ETYMOLOGY:Hammondia after Dr. D.M. Hammond and pardalis for the species name of the ocelot, Felispardalis.

SYNONYMS:Toxoplasmapardalis (Hendricks, Ernst, Courtney, and Speer, 1979) Levine and Ivens, 1981. Oocysts of this species closely resemble those of Isosporafelis and misidentification is possible.

HISTORY: This coccidium was first described in 1979 from the feces of an Ocelot housed at the Air Force Survival School Zoo, Albrook Air Force Station, Panama Canal Zone (Hendricks et al., 1979). It has recently been isolated from domestic cats fed heart, skeletal muscles and uterus tissues from cattle that had aborted (Abbitt et al., 1993), but its causal relationship to these abortions is not clear at present.

GEOGRAPHIC DISTRIBUTION: Panama Canal Zone, Panama, the Cockscomb Basin of Belize, Central America and northeastern Mexico (Hendrix et al., 1979; Patton et al., 1986; Abbitt et al., 1993).


Feline definitive hosts: The number of asexual stages (if any) and location of developmental sexual stages within the feline definitive host is not known. However, it is likely that they occur within th eenterocytes of the intestinal tract.

Intermediate hosts: Asexual stages are present in the mesenteric lymph nodes. lungs, and intestinal mucosa of experimentally inoculated mice.

PARASITE IDENTIFICATION: Oocysts are ovid, and measure 36-46 by 25-35 _m (mean, 40.8 by 28.5 _m). A micropyle is present at the small end of the oocyst while a suture line is present in the larger end of the oocyst. A small granule is often attached to the inner portion of the oocyst wall. Sporulated oocysts contain two ellipsoid sporocysts each with 4 sporozoites. Sporocysts measure 19-25 by 14-19 _m (mean, 22.2 by 16.4 _m), lack a Stieda body, and contain a sporocyst residuum composed of a single refractile globule or several small globules. The sporozoites lIe lengthwise within the sporocyst had have no refractile bodies.

The presence of a micropyle and suture line in the oocyst wall differentiates the oocysts of H. pardalis from I. felis which is similar in size but lacks these structures in its oocyst wall. The large size of H. pardalis oocysts differentiates it from H. hammondi, I. rivolta, T. gondii, and Besnoitia species, all of which have smaller oocysts.

Identification of H. pardalis stages in intermediate hosts is difficult. The original description of these stages was not comprehensive enough to allow for the identification of clear cut diagnostic features. Groups of merozoites (tachyzoites?) were present in the alveolar septa, mesenteric lymph nodes and lymphoid tissue in the colon. Individual merozoites measured 6 by 3 _m.

LIFE CYCLE: The type host is the Ocelot, Felispardalis. Other natural hosts are the jaguar (Pantheraonca) and the puma (Felisconcolor) (Patton et al., 1986). Experimental definitive hosts are the domestic cat, Feliscatus and the jaguarundi, Felisyagouaroundi. Raccoons, Procyonlotor, are not suitable definitive hosts (Hendrixs et al., 1979). The life cycle is obligatorily heteroxenous, meaning that there must be one host containing one set of stages, the sexual stages, and one host containing another set of stages, the asexual stages. Cattle are natural intermediate hosts and mice are experimental intermediate hosts. Tissue feeding studies indicate that infectious stages are present in the heart, skeletal muscles, and uterus of infected cows.

No life cycle stages have been identified in the cat. The prepatent period was 6 to 7 days in seven domestic cats, two ocelots, and a jarguarundi fed infective mice, and the patent period was 5 to 13 days (Hendricks et al., 1979). The prepatent period in eight domestic cats fed naturally infected bovine tissues was 6 to 11 days, and the patent period was 5 to 11 days (Abbitt et al., 1993). Sporulation occurs at room temperature within 7 days, however no properly conducted studies have been done on this, and it is likely that sporogony is completed within 2 to 3 days. Sporulated oocysts do not produce patent infections in recipient cats. It is not known if tissues from cats fed oocysts contain stages that induce oocyst excretion in other cats. The parasite can not be passed from mouse to mouse by the inoxculation of infected tissues.

CLINICAL PRESENTATION AND PATHOGENESIS: Clinical signs of infection in cats have not been reported. Oocysts induced infections in mice can cause clinical disease and death (Hendricks et al., 1979).

TREATMENT: There has been no attempt to stop the shedding of Hammondiapardalis oocysts by infected cats. It is possible that the shedding of oocysts might be prevented by the treatment of cats with sulfonamides or the other products used for feline coccidiosis (Table 4)

EPIZOOTIOLOGY: Cats are not commonly infected with this parasite.

HAZARDS TO OTHER ANIMALS: None known. Hammondiapardalis oocysts have been isolated from cats fed tissues from cattle suffering from abortions from a drylot dairy in northeastern Mexico (Abbitt et al., 1993). None of the cattle were clinically ill prior to abortion and the role of H. pardalis in inducing the abortions is not clear.

HAZARDS TO HUMANS: It is possible that humans could serve as intermediate hosts. No recorded cases of human infection exist.


Abbitt B, Craig TM, Jones LP, Huey RL, Eugster AK. 1993. Protozoal abortion in a herd of cattle concurrently infected with Hammondiapardalis. JAVMA 203:444-448.

Hendricks LD, Ernst JV, Courtney CH, Speer CA. 1979. Hamondiapardalis sp. n. (Sarcocystidae) from the ocelot, Felispardalis, and experimental infection of other felines. J Protozool. 26:39-43.

Patton SP, Rabinowitz A, Randolph SS, Johnson SS. 1986. A coprological survey of parasites of wild neotropical felidae. J Parasitol 72:517-520.