Platynosomum concinnum (Braun, 1901) Purvis, 1933
(Figures 2-34 through 2-
ETYMOLOGY:Platy = flat and nosomum = ????? along with concinnum = graceful or harmoniously arranged
SYNONYMS:Dicrocoelium lanceolatum var symmetricum Baylis, 1918; Concinnum concinnum (Braun, 1901) Bhalerao, 1936; Platynosomum concinnum Kossack, 1910.
HISTORY: The genus Platynosomum was described by Looss in 1907 for a species recovered from a bird (Cicaetus gallicus). A fluke from the civet cat was described by Braun (1901) as Dicrocoelium concinnum and was transferred to the subgenus Concinnum by Bhalerao (1936). Later, the subgenus Concinnum was given generic rank (Yamaguti, 1958). Kossack (1910) described a fluke from a cat, Felisminuta, that he named Platynosomum concinnum. Purvis (1931 & 1933) examined specimens of what he considered to be Platynosomum concinnum that were recovered from cats in Malaysia, and after making his observations, Purvis believed that Platynosomumconcinnum was identical with Platynosomum concinnum and Platynosomum planicipitis (Cameron, 1928). It would appear that if the species "concinnum” is the same species as that described by Kossack as Platynosomumconcinnum, that the name Platynosomum concinnum would be the name with priority because this is the name that was used as part of the original description.
GEOGRAPHIC DISTRIBUTION: The tropics, including, Malaysia, Hawaii, West Africa, South America, the Caribbean, and areas surrounding the Gulf of Mexico, including the southeastern United States and the Florida Keys (Bielsa and Greiner, 1985).
LOCATION IN HOST: Gall bladder and bile ducts; rarely in the small intestine.
PARASITE IDENTIFICATION:Platynosomum concinnum adults are about 5 mm long by 2 mm wide (Figure 2-34). The suckers are about equal in size, with the ventral sucker being about one-fourth of the body length from the anterior end. The vitellaria are located mainly at mid body and the genital opening is at or anterior to the branching point of the intestinal ceca. The testes and ovary are comparatively larger than in species of Eurytrema. The eggs are operculate and measure 34 to 50 µm by 20 to 35 µm (Figure 2-35). A comparison of diagnostic methods revealed that a formalin-ether sedimentation technique was much more sensitive than either a sugar or zinc-sulfate flotation for the diagnosis of infections with this parasite (Palumbo et al., 1976).
LIFE CYCLE: The life cycle has been incompletely described (Maldonado, 1945; Eckerlin and Leigh, 1962). Cercariae with very short tails, i.e., microcercous cercariae, develop in sporocysts within the terrestrial snail Subulina octona. The sporocysts leave the snail and are eaten by terrestrial isopods, "pill bugs." The metacercariae in the isopods are not infective to cats, but if ingested by a lizard, frog, or toad, the encysted forms are found in the common bile duct and gall bladder of these animals. Cats become infected through the ingestion of the lizard or amphibian third-intermediate host.
CLINICAL PRESENTATION AND PATHOGENESIS: Cats infected with large numbers of these parasites can present with severe disease due to the blockage of the biliary system (Robinson and Ehrenford, 1962). Clinical signs have been described in 8 infected cats in the Bahamas. The cats did not thrive and had occasional bouts of diarrhea, depression and anorexia. On examination, the cats had severe weight loss, mild jaundice of the mucous membranes, and mild hepatic enlargement. If the condition progressed to complete biliary obstruction, there was severe diarrhea and vomiting with marked jaundice. At necropsy, severe jundice was obvious, and the liver a greenish-yellow. The bile ducts were markedly dilated with thickened walls (Ikede et al., 1971). In histological sections, the trematodes could be observed within the dilated bile ducts (Figure 2-36).
Experimental infection of cats was induced by feeding of liver from infected toads, Bufo marinus (Taylor and Perri, 1977). Eggs were detected in the feces of several cats as early as two months after infection, and all cats were shedding eggs in their feces by 12 weeks after infection. No clinical signs were observed in cats given 125 metacercariae. However, in cats given about 1,000 infective stages, clinical signs were noted in number of animals. The signs included lethargy, abdominal distension, inappetence, weight loss, and an enlarged liver. There were increased numbers of circulating eosinophils in all infected cats, and increases in both alanine and aspartate aminotransferase activities. Histologically, there was severe adenomatous hyperplasia of the bile duct epithelium with periductal inflammation. The cats continued to shed eggs in their feces for a year-and-a-half after the initial exposure which was when the study terminated.
TREATMENT: Praziquantel at a dose of 20 mg per kg has markedly reduced the number of eggs shed by infected cats. Similarly, nitroscanate at 100 mg/kg also markedly reduced the numbers of eggs being shed by infected cats. Although cats often produced negative samples several weeks after treatment, they very often again shedding eggs in their feces a number of weeks after having stopped shedding (Evans and Green, 1978). It has been reported to one author (D.D. Bowman) that treatment of infected cats in Florida, USA, with severe hepatic disease using praziquantel at a dosage of 40 mg per kg resulted in the death of a compromised cat.
EPIZOOTIOLOGY: Cats are not the only hosts of this parasite. It has also been reported from opossums (Didelphis marsupialis) and from the civet (Viverra zibetha). Mice have been experimentally infected (Eckerlin and Leigh, 1962).
HAZARD TO OTHER ANIMALS: None known.
HAZARD TO HUMANS: There have been no records as to the infection of human beings with this parasite. If a person were to ingest the lizard, they could perhaps develop an infection.
CONTROL/PREVENTION: Prevent the ingestion of infected lizards, toads, and frogs.
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Bielsa LM, Greiner EC. 1985. Liver flukes (Platynosomumconcinnum) in cats. J Am Hosp Assoc 21:269-274.
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Maldonado JF. 1945. The life history and biology of Platynosomumconcinnum Kossack, 1910 (Trematoda: Dicrocoelidae). Puerto Rico J Pub Hlth trop Med 21:17-60.
Palumbo NE, Taylor D, Perri SF. 1976. Evaluation of fecal technics for the diagnosis of cat liver fluke infection. Lab An Sci 26:490-493.
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Robinson VB, Ehrenford FA. 1962. Hepatic lesions associated with liver fluke (Platynosomumconcinnum) infection in a cat. Am J Vet Res 23:1300-1303.
Taylor D, Perri SF. 1977. Experimental infection of cats with the liver fluke Platynosomumconcinnum. Am J Vet Res 38:51-54.
Yamaguti S. 1958. Systema Helminthum, The Digenetic Trematodes of Vertebrates. Interscience, New York.
Figure 2-34.Platynosomumconcinnum adult collected from the bile duct of a cat in West Hollywood, Florida, USA. Note the vitellaria along the lateral margins at midbody, the paired anterior testes in the anterior third of the body, and the extensive uterus filled with eggs.
Figure 2-35. Eggs of Platynosomumconcinnum from the feces of a naturally infected cat from the Florida Keys (photograph supplied by Dr. Robert Foley).
Figure 2-36. Section of the liver showing the presence of flukes within a dilated bile duct.