Paragonimus kellicotti Ward, 1908
(Figures 2-44 to 2-49)
ETYMOLOGY:Para = side-by-side and gonimus = gonads along with kellicotti = for Dr. Kellicott of Ohio State University who described specimens of this parasite from the lungs of a dog and sent them to Dr. Ward for further identification.
SYNONYMS: None, although initially it was thought that it might be Paragonimus westermani introduced into North America.
HISTORY: This parasite was first observed by a Mr. W.A. Kirkland of the Zoology Laboratory of the University of Michigan who found these trematodes in a cat from Ann Arbor, MI, USA. The material was passed onto Dr. Ward, who several years later (1908) described the parasite as Paragonimus kellicotti.
GEOGRAPHIC DISTRIBUTION: Distributed throughout the Mississippi and Great Lake Drainage systems of North America (Figure 2-44).
LOCATION IN HOST: In cysts in the lungs.
PARASITE IDENTIFICATION:Paragonimus adults are about a centimeter long (Figure 2-45). Specimens of Paragonimus kellicotti overall appear to be a little longer and a little more slender than specimens of Paragonimus westermani. The major distinguishing characteristic between the adults of these two species which both have single spines on the body surface is the finer branching of the ovary in Paragonimus kellicotti. The metacercariae of these two flukes also differ; the metacercariae of Paragonimus kellicotti have a thin internal cyst wall while that of Paragonimus westermani is much thicker (Ishii, 1966).
The eggs (Figure 2-46) have a brown shell, a distinct operculum, and occasionally a knob on the abopercular end; and are very similar in size and shape to those of Paragonimus westermani.
LIFE CYCLE: The eggs of Paragonimus kellicotti are in a single-celled stage when passed in the feces. Once the eggs enter fresh, aerated water, they begin to develop and ultimately, depending on temperature, produce a ciliated miracidium. The miracidium lives 1 to 3 days and seeks out and penetrates a young snail host, Pomatiopsis lapidaria, which is an amphibious and nocturnal snail. Within the snail, the miracidium develops to a sporocyst within the lymphatic system. Ultimately, first and second generation stages, rediae, are produced, the latter containing the cercariae. The cercariae emerge from the snails in the evening or at night and are capable of living in water for one to two days; the cercariae penetrate the snail in the thin chitin on the undersurface of the tail (Ameel, 1934). In fresh-water crayfish of the genera Cambarus and Orconectes, the cercariae develop into metacercariae within the pericardium. The metacercariae are somewhat resistant to environmental extremes; they have been maintained in crayfish at 7o C for 19 days and shown to be infective and can persist free in water at 12 to 20o C for 10 days.
In a cat that ingests metacercariae, the young flukes rapidly penetrate the intestinal tract and enter the peritoneal cavity (Stromberg and Dubey, 1978). The young flukes migrate about in the peritoneal cavity for a week to 10 days and then migrate through the diaphragm into the pleural cavity. Penetration of the lung begins around 10 to 14 days after infection, and most worms have succeeded in forming pairs within the lungs by 3 weeks after infection. Most of the flukes take up residence in the caudal lobes of the lung, and more flukes were found in the right lung than in the left lung. It has also been shown that if a single young fluke is present that a metacercariae ingested 2 months later is capable of finding and pairing with the fluke that is already present in the cat (Soganderes-Bernal, 1966). The cysts in the lungs of cats often contain only two flukes, however, as many as 6 flukes may be present in some cysts (According to Wallace (1931), more than two flukes per cyst is not uncommon in the natural host, the North American mink. Cats are most likely to become infected by the ingestion of metacercariae in crawfish, however, it has been shown that rats can serve as paratenic hosts of Paragonimus kellicotti (Ameel, 1934); and it is possible that cats are infected by the ingestion of infected rodents. It has also been postulated due to the appearance of possible paragonimiasis in kittens of infected queen when only a few months of age, that transmammary transmission of the juvenile flukes might be possible if the queen is infected while pregnant (Bowman et al., 1991); however, examination of 4 kittens born 67 days after the infection of the queen revealed no stages of Paragonimus kellicotti in the tissues (Dubey et al., 1978). Cats begin to shed eggs 5 to 7 weeks after infection.
CLINICAL PRESENTATION AND PATHOGENESIS: Clinical signs in experimentally infected cats are typically quite mild, occasional coughing, although bouts of paroxysmal coughing and dyspnea due to pneumothorax from rupture of lung cysts has been described (Dubey et al., 1978). Marked eosinophilias in peripheral blood has been described, especially 3 weeks after infection which is when the worms would first enter the lungs. Radiographs of early lesions will reveal indistinct nodular densities containing small air cavities and having irregular, sharply defined margins, older cysts are typical air-filled pnematocysts (Figure 2-47). Although cats often present with ill-defined interstitial nodular densities (Pechman, 1976 and 1984).
Beginning about 1 week after infection, cats develop an eosinophilic pleuritis that may be associated with areas where flukes have attempted or actually penetrated the lung tissue (Hoover and Dubey,. 1978). The young flukes within the lung are surrounded by intense eosinophilic inflammation, necrotic tissue, and cellular infiltrates. There is also hyperplasia of the bronchiolar glands, type II pneumocytes, and of the smooth muscles of the bronchioles and alveolar ducts. As the cysts continue to mature, they cause atelectasis of the adjacent tissue; the hyperplasia of the peribronchiolar glands becomes pronounced. Finally, collagenous connective tissue forms a well developed wall around the fluke containing cyst (Figure 2-48 and 2-49). This capsular wall is richly vascularized, and eggs that remain in the lung become surrounded by multinucleate giant cells (Lumsden and Soganderes-Bernal, 1970).
TREATMENT: Albendazole has been used to treat cats with experimental (50 to 100 mg per kg for 14 to 21 days) and natural (25 mg/kg twice a day for 11 to 24 days) infections (Dubey et al., 1978; Hoskins et al., 1981). In the case of the naturally infected cats, treatment was successful in 8 of the 10 treated animals. Praziquantel has been used to treat infections with Paragonimus kellicotti in experimentally-infected cats (23 mg/kg three times each day for 3 days) with excellent results (Bowman et al., 1991). There was a marked improvement in the lungs of these cats as evidenced by radiography within 11 days after treatment.
EPIZOOTIOLOGY: Numerous mammals are capable of being infected with Paragonimus kellicotti. Dogs are commonly infected. The natural host appears to be the mink. The raccoon seems to be rather refractory to infection.
HAZARD TO OTHER ANIMALS: Other animals appear likely to develop infection and disease similar to that seen in the ct, but only if they ingest the infected crayfish. Thus, the infected cat is not a direct threat to other uninfected animals.
HAZARD TO HUMANS: There has been only a single report of infection in humans with this trematode (Beaver et al., 1984). This infection occurred in a German laborer who had eaten crayfish. After returning to Germany, the infection was diagnosed.
REFERENCES:
Ameel DJ. 1934. Paragonimus, its life history and distribution in North America and its taxonomy (Trematoda: Troglotrematidae). Am J Hyg 19:279-317.
Bowman DD, Frongillo MK, Johnson RC, Beck KA, Hornbuckle WE, Blue JT. 1991. Evaluation of praziquantel for treatment of experimentally induced paragonimiasis in dogs and cats. Am J Vet Res 52:68-71.
Dubey JP, Hoover EA, Stromberg PC, Toussant MJ. 1978. Albendazole therapy for experimentally induced Paragonimuskellicotti infection in cats. Am J Vet Res 39:1027-1031.
Dubey JP, Stromberg PC, Toussant MJ, hoover EA, Pechman RD. 1978. Induced paragonimiasis in cats: clinical signs and diagnosis. JAVMA 173:734-742.
Hoover EA, Dubey JP. 1978. Pathogenesis of experimental pulmonary paragonimiasis in cats. Am J Vet Res 39:1827-1832,
Hoskins JD, Malone JB, Root CR. 1981. Albendazole therapy in naturally occurring feline paragonimiasis. J Am Hosp Assoc 17:265-269.
Ishii Y. 1966. Differential morphology of Paragonimuskellicotti in North America. J Parasitol 52:920-925.
Lumsden RD, Sogandares-Bernal. 1970. Ultrastructural manifestations of pulmonary paragonimiasis. J Parasitol 56:1095-1109.
Pechman RD. 1976. The radiographic features of pulmonary paragonimiasis in the dogs and cat. J Am Vet Radiol soc 17:182-191.
Pechman RD. 1984. newer Knowledge of feline bronchopulmonary disease. Vet Clin N Am small An Pract 14:1007-1019.
Sogandares-Bernal F. 1066. Studies on american paragonimiasis. IV. Observations on the pairing of adult worms in laboratory infections of domestic cats. J Parasitol 52:701-703.
Stromberg PC, Dubey JP. 1978. The life cycle of Paragonimuskellicotti in cats. J Parasitol 64:998-1002.
Wallace FG. 1931. Lung flukes of the genus Paragonimus in American mink. JAVMA 31:225-234.
Ward HB. 1908. Data for the determination of human entozoa II. Trans Am Micro Soc 28:177-202.
Figure 2-44. Geographical distribution of Paragonimuskellicotti in naturally infected cats in the United States.
Figure 2-45. Adult Paragonimuskellicotti recovered from the lung of a cat.
Figure 2-46. Egg of Paragonimuskellicotti in the feces of a cat.
Figure 2-47. Radiograph of young cyst of Paragonimuskellicotti in an experimentally infected cat. Note the indistinct edges to the observed parasitic opacity.
Figure 2-48. Cysts of Paragonimuskellicotti in the lungs of a naturally infected cat.
Figure 2-49. Section through s cyst of Paragonimuskellicotti in the lungs of a cat. Note the thick fibrous capsule.