Abstract
Platynosomum fastosum is a small fluke found in the biliary ducts and gallbladder of cats. Its lifecycle includes the snail Sublima octona as intermediate host, and lizards, toads and geckos as paratenic hosts. Affected cats are usually adult and acquire the parasite by feeding on infected lizards. This parasite occurs across the world but is more frequent in tropical areas. The clinical signs range from none to obstruction of the biliary tract, with hepatic failure and death, reinforcing the necessity of including the liver fluke Platynosomum fastosum in the differential diagnosis of hepatic diseases in cats. This report describes an unusual case of a cat with a polycystic hepatic disease and a severe infestation by Platynosomum fastosum and presents a review of the literature.
Paty, an 11-year old cat of undefined breed was admitted to the São Francisco Veterinary Clinic (Piracicaba city, State of São Paulo, Brazil) for intermittent inappetence/anorexia and occasional episodes of apathy and vomiting over the preceding 3 months. The cat presented with similar signs 1 year earlier and was presumptively treated for haemobartonellosis. Two months before the current admission, the animal developed jaundice, progressive increase of the abdominal volume, and weight loss. According to the owner's report, the cat frequently chased and ingested geckos. Two other cats living in the same house were asymptomatic.
At admission, the cat was in poor condition, showing moderate to severe dehydration, jaundice and an enlarged abdomen with no palpable masses. Its vital signs were normal.
The red blood cell (RBC) counts were within normal range, but white blood cell (WBC) count showed lymphopenia (230/mm3; reference range: 1200–9000/mm3). There was an increase of serum concentration of the hepatic enzymes alanine transaminase (ALT: 892 U/l; reference range: up to 50 U/l), aspartate transaminase (AST: 453 U/l; reference range: up to 40 U/l), as well as an increase in alkaline phosphatase (339 U/l; reference range: up to 70 U/l). Serum bilirubin was also increased (10.2 mg/dl; reference range 0.05–1.0 mg/dl), as well as direct bilirubin (8.6 mg/dl; reference range: lower than 0.15). Serum protein levels were within normal range (6.5 g/dl; reference range: 5.5–8.5 g/dl), but albumin levels were decreased (0.6 g/dl; reference range: 2.7–4.6 g/dl) and globulins were increased (5.9 g/dl; reference range: 2.1–4.1 g/dl). There was an increase in blood urea concentration (185 mg/dl; reference range: 30–65 mg/dl) and serum creatinine (3.9 mg/dl; reference range: 0.5–2.0 mg/dl). Blood glucose levels showed a mild decrease (65 mg/dl; reference range: 70–100 mg/dl). Stool analysis for ova and parasites was negative.
Abdominal ultrasound revealed an enlarged liver with regular boundaries and heterogeneous echogenicity, with cavitary lesions spread diffusely in the parenchyma. These lesions were spherical, heterogeneous in size, well-defined, and filled with anechoic content, suggesting the presence of cysts or abscesses. The gallbladder had anechoic content and thin wall.
After rehydration, an exploratory laparotomy was performed. Hepatomegaly with diffusely distributed small cysts throughout the liver was confirmed. Three larger cystic lesions (two lesions with 3 cm of diameter and one with 10 cm – Fig. 1) were also present, causing compression of adjacent structures. No extrahepatic obstruction was observed. Sampling of the cystic content was performed for analysis and revealed a serous brownish liquid with presence of bilirubin pigments (++), 100–300 mg/dl of protein and a large number of live parasites. The liquid was characterised as a transudate and the parasites were classified as Platynosomum fastosum (Fig. 2).
Photograph of the laparotomy procedure, evidencing a large hepatic cyst, among many other smaller, cystic structures.
Photomicrography of identified Platynosomum fastosum.
Despite treatment with fluids and support therapy, the clinical condition of the animal deteriorated and euthanasia was performed at the owner's request.
A complete necropsy was performed. Histopathological analysis of the liver showed dilated and hyperplasic biliary ducts, periportal fibrosis, and predominantly periductal lymphoplasmocytic inflammatory infiltrate, with deposits of hemosiderin and the presence of biliary casts. Cystic structures of different sizes were surrounded by variable amounts of fibrous tissue (Fig. 3A). Hepatocytes were vacuolated and enlarged. These findings were compatible with the presence of chronic cholangiohepatitis (Fig. 3B).
Photomicrography of the liver, showing (A) cystic area (arrow) surrounded by dense fibrotic tissue (H&E − 250 mm scale bar) and (B) centrolobular fibrosis with biliary duct hyperplasia (arrow) (H&E–25 μm scale bar).
Infection caused by Platynosomum fastosum (Dicrocoeliidae family), also known as Dicrocollium concinum, Platynosomum concinnum and Platynosomum plancipidus, was first reported in cats in 1901 (Ferreira et al 1999). Since then, it has been detected in wild and domestic cats in several countries, mainly in tropical and subtropical areas (Bielsa and Greiner 1985, Ferreira et al 1999, Rodriguez-Vivas et al 2004). In Brazil there is a prevalence of up to 45% in the state of Rio de Janeiro and up to 5.6% in the city of Sao Paulo (Salomão et al 2005). In the USA (Hawaii and Florida) its prevalence reaches up to 70%, where it is referred to as ‘lizard poisoning’ (Soulsby 1982, August 2001). P fastosum is the most common liver parasite of domestic cats and is usually located in the biliary ducts and gallbladder, but can also be found in the small intestine, pancreas and lungs (Barriga et al 1981, Ferreira et al 1999).
This parasite belongs to the Dicrocoeliidae family of flatworms, with adult trematodes ranging from 4 to 8 mm long, by 1.2 to 2.5 mm wide (Soulsby 1982). Miracidia-containing eggs range from 34 to 50 μm long, by 20 to 35 μm wide, and are eliminated with the faeces of the infected animal (Bielsa and Greiner 1985). The primary intermediate host, the snail Sublima octona, ingests the eggs, which form the sporocyst-containing cercariae, that are subsequently eliminated to the environment (O'Sullivan et al 1976, Ferreira and Almeida 2003). The sporocyst-containing cercaria is then ingested by arthropods, such as beetles, in which maturation occurs, leading to the generation of metacercariae. Some authors suggest that cockroaches are also intermediate hosts (Retnasabapathy and Prathap 1971). The isopoda is subsequently ingested by a third intermediate host, reptile or amphibian (lizards, geckos and toads), and the metacercariae form cysts in the gallbladder and biliary ducts of these animals (Ferreira and Almeida 2003). Lifecycle is completed when the intermediate hosts are ingested by cats (Center 1996). The metacercariae migrate to biliary ducts and gallbladder, reaching maturity in 8–12 weeks, and then eliminate fertilised eggs into the intestines through bile (Soulsby 1982, Center 1996).
Platynosomum fastosum infection generally causes mild disease, but clinical findings may vary with the severity of infestation, the number of adult parasites, the time of infection, and the individual reaction to parasite invasion (Salomão et al 2005). Clinical signs include jaundice, anorexia, depression, lethargy, weight loss, mucous diarrhoea, vomiting, hepatomegaly, abdominal distension, ascites, gallbladder and biliary duct distension (O'Sullivan et al 1976, Barriga et al 1981, Ferreira and Almeida 2003, Rodriguez-Vivas et al 2004). Eosinophilia, high alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, and hyperbilirubinaemia are found in severe infections (Center 1996). Liver carcinoma also has been observed in parasitised cats (Santos et al 1981, Foley 1994, Ferreira and Almeida 2003).
Two reports of cystic liver disease and severe fluke infestation by Platynosomum fastosum are found in the literature (Robinson and Ehrenford 1962, Jenkins et al 1988). In both acquired or congenital disease, the cystic structures are derived from ductular epithelium (Center 1996). The congenital disease is usually polycystic (Center 1996, Johnson 2000), with Persian and Persian crossbred cats over-represented; the polycystic form may be associated with cystic lesions in other organs, mainly kidneys (Center 1996, Bosje et al 1998) with a clear cyst content (Center 1996, Crawford 2005). The acquired disease is commonly solitary, with blood or bilirubin cyst content and may be produced by inflammation, trauma or neoplasia (Center 1996). Therefore, the chronic inflammation and obstruction induced by severe platynosomiasis caused by retained glandular and biliary secretion can result in an acquired hepatic cystic disease.
Diagnosis can be made based on history, clinical findings, and by detecting eggs in stool (Ferreira and Almeida 2003). The formalin–ether centrifugation method is the most effective procedure for coprologic diagnosis of platynosomiasis (Barriga et al 1981, Bielsa and Greiner 1985). However, the diagnosis is often difficult as the eggs are only sporadically found on faecal examination and they will not be present in faeces in cases with complete biliary obstruction (Willard and Fossum 2000). Complementary examinations such as ultrasound can also be helpful. Evidence of tortuous, distended gallbladder, and dilated biliary ducts may indicate large numbers of parasites in these sites (Salomão et al 2005).
The most common histopathological findings include diffuse portal congestion, hepatic sinusoid dilation, hepatocyte degeneration, mild centrolobular fatty change that may involve the whole lobule, polymorphonuclear inflammatory infiltrate and an abundant collection of mononuclear cells around biliary ducts (Ferreira et al 1999, Ferreira and Almeida 2003). Hyperplasia of the biliary duct epithelium, periductal inflammation and fibrosis, are also observed, and may lead to obstructive disorders or terminal liver disease (Ikede et al 1971, Center 1996, Ferreira et al 1999). Bile duct distension increases with growth of adult flukes (Bielsa and Greiner 1985, Center 1996). Chronicity of the inflammatory process results in proliferation of a dense and hyaline connective tissue, leading to an enhancement of the lobular tissue pattern, along with moderate inflammation and mild congestion (Ferreira et al 1999). Adult parasites are occasionally seen in tissue samples. P fastosum infestation can be included as one of the disorders associated with biliary obstruction and non-suppurative colangitis-colangiohepatitis in the cat (Center 1996).
Despite being reported for over a century, the efficacy of available treatment protocols is still controversial (Neer 1992, Center 1996), probably because of the relative rarity of these cases in the world (August 2001). Different treatment regimens have been employed. Praziquantel (20 mg/kg parenterally, once a day for 3 days) (Willard and Fossum 2000) is suggested as the most effective agent (Foley 1994). Nevertheless, prognosis for severe conditions is guarded (Neer 1992, Willard and Fossum 2000).
This report described a case of a cat presenting with severe polycystic hepatic disease and infestation by P fastosum. In this case, the hepatic failure may have been a result of a combination of the chronic disease induced throughout the biliary system over time by the flukes, as well as the presence of numerous cystic structures compressing the hepatic parenchyma. Comparing the literature on the major characteristics of the congenital polycystic entity and excluding those of neoplasia or traumatic origin, the cystic disease in this case could be due to chronic inflammation and biliary obstruction induced by platynosomiasis or a combination of congenital and acquired disease. Salomão et al (2005) described the fluke-induced obstruction of bile ducts, especially in cases of ductal fibrosis initiated by adult parasites.
Unfortunately, due to the severity of the obstructive hepatobiliar disease, and unsatisfactory response to treatment, euthanasia was performed. Despite possible limitations for the diagnosis of P fastosum infection, veterinary practitioners should consider infection by this parasite in animals that chase and ingest geckos or other putative hosts, even if asymptomatic, particularly in regions with high prevalence of P fastosum. As described here, chronic progression of this condition, with non-specific signs, leading to a recurrent, progressive, and fatal outcome is also possible in an area not previously considered at great risk.
Footnotes
Acknowledgements
We are in debt to Dr Luciana Neves Torres, DVM, MSc, from the Department of Pathology, School of Veterinary Medicine, University of São Paulo, for the histopathogical analyses, and to the Laboratory of Parasitic Diseases, Department of Preventive Veterinary Medicine and Animal Health, School of Veterinary Medicine, University of São Paulo, for the identification of P fastosum.