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Clinical case: Platynosomum fastosum Kossack, 1910 infection in a cat: First reported case in Trinidad and Tobago



School of Veterinary Medicine, Faculty of Medical Sciences, The University of the West Indies, St. Augustine, TRINIDAD AND TOBAGO

*Corresponding author:

This study is the first recorded case of Platynosomum fastosum infection in a cat, resident in Trinidad and Tobago. The history, clinical signs (strong emaciation, anorexia and chronic pain) coupled to marked dilated gallbladder evidenced by abdominal echography as well as haematological and biochemical findings indicating severe inflammation and hepatic / gallbladder injury have led to suspicion of cholangiohepatitis or cholecystitis. Histological findings have confirmed the diagnosis and parasites (adults and eggs) were identified in the bile at necropsy.

Cas Clinique : infection par Platynosomum fastosum Kossack, 1910 chez un chat: premire observation Trinid et Tobago Cette tude de cas prsente la premire description dune infection par Platynosomum fastosum chez un chat de Trinid et Tobago. Les commmoratifs recueillis et les signes cliniques (amaigrissement important, anorexie, douleur chronique) associs la mise en vidence par chographie abdominale dune forte dilatation de la vsicule biliaire et aux rsultats hmatologiques et biochimiques indiquant une inflammation svre et des lsions du foie et du systme biliaire ont conduit une suspicion de cholangiohpatite ou de cholcystite. Lexamen histopathologique a confirm le diagnostic et de nombreux parasites (adultes et ufs) ont t identifis dans la bile lautopsie.

Keywords : cat, Platynosomum gallbladder, inflammation, Trinidad.



Mots-cls : chat, Platynosomum fastosum, foie, vsicule biliaire, inflammation, Trinid.

Infection of cats by the gallbladder fluke, Platynosomum fastosum, the cause of Lizard poisoning in cats [4], is usually found in tropical and sub-tropical regions [12]. It has been reported in several countries such as Illinois, USA [7], The Bahamas [8], Puerto Rico, British Guyana [1], Mexico [2], Venezuela [13], Brazil [14] and Colombia [9]. This parasite, however, has not been previously recorded in Trinidad and Tobago. According to MALDONADO [10] the life cycle of the fluke involves two intermediate hosts: first the land snail, Sublina octona and second the lizard, Anolis cristellus. The cat becomes infected after ingestion of the second intermediate host containing the metacercaria. The cercariae are released into the upper digestive tract, enter the biliary tree and complete their life cycle [14]. Mature flukes are found in the gallbladder, bile ducts and after 8 to 12 weeks fluke eggs start to be shed with the faeces into the environment.

Case report
A ten-year old male domestic short haired cat from Chaguanas, Trinidad, was brought to the Veterinary Teaching Hospital (VTH), University of the West Indies, St. Augustine, with the complaint of anorexia for one week, recent weight loss and continuous crying. The cat was also known to roam a lot. The cat lived his entire life in Trinidad with no known exposure to any imported cat. On physical examination, mucosae were icteric. There was a slight mucus discharge from both eyes. The animal was emaciated (body condition score: 1.5/ 5) and approximately 8% dehydrated. All other parameters (heart rate, respiratory rate and temperature) were within usual values. Abdominal echography revealed a severely distended gallbladder (38.7 mm). The walls were thickened (2.71 mm) and at one point folded inward. The hepatic parenchyma appeared coarse and hyperechoic. Fine needle aspirate of the gall bladder produced a pale yellow, blood tinged and cloudy fluid. These findings were highly suggestive of cholangiohepatitis or cholecystitis. Haematological analysis

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(Table I) showed a neutrophilia with significant left shift and toxic neutrophils, indicating severe inflammation coupled to lymphopenia suggesting stress. Throughout biochemistry (Table II) hyperproteinemia, hypernatremia, hyperphosphatemia, hypercholesterolemia and high urea and creatinine concentrations were evidenced and were associated with increased serum alanine transaminase (ALT), alkaline phosphatase (ALP), g-glutamyl transferase (GGT) and creatine kinase (CK) activities. The hospitalised cat was placed on intravenous fluids with multivitamins as well as being force fed. He was dewormed


with ivermectin at a dose rate of 0.4 mg/kg subcutaneously once (as it is routinely used at this hospital since most cats are not up-to-date with their deworming and are also exposed to heartworm) and amoxicillin-clavulanic acid orally at 10 mg/kg twice daily since treatment with amoxicillin has been shown to be effective in cats with cholangitis/ cholangiohepatitis [6]. The cat, however, subsequently died and necropsy was performed. Necropsy revealed an extremely emaciated cat (body condition score: 1/5) with a ruffled coat. There was mild icterus of the carcass. The liver parenchyma appeared normal but there was dilation of the intrahepatic ducts on the cut surface. The gall bladder was Patient value 33 25.74 5.61 0.99 0.33 7.76 2+ 106 0.388 50 13.7 273 368 Usual values1 5.5-19.5 2.5-12.5 0.0-0.3 1.5-7.0 0.00-0.85 5-10 80-150 0.24-0.45 39-55 13-17 300-360 300-700

Parameter WBC (109/L) Seg. (109/L) Bands (109/L) L (109/L) M (109/L) RBC (1012/L) Toxic change Hb (g/L) Ht (L/L) MCV (fL) MCH (pg) MCHC (g/L) Platelets (109/L)

WBC: White blood cells; Seg.: Segmented neutrophils; Bands: Immature neutrophils; L: lymphocytes; M: Monocytes; RBC: Red blood cells; Toxic changes: morphologic abnormalities acquired during maturation; Hb: Haemoglobin; Ht: haematocrite; MCV: Mean corpuscular volume; MCH: Mean corpuscular haemoglobin content; MCHC: Mean corpuscular haemoglobin concentration.1University laboratory values.

Table I: Haematological results determined in the 10 year old male cat suspected for cholangiohepatitis or cholecystitis. Values indicated in bold were outside usual ranges.

Parameter TP (g/L) Alb. (g/L) A/G Na (mmol/L) K (mmol/L) Na/K Cl (mmol/L) Ca (mmol/L) P (mmol/L) TBil (mmol/L) Cholesterol (mmol/L) Glucose (mmol/L) Urea (mmol/L) Creatinine (mmol/L) CK (U/L) ALT (U/L) ALP (U/L) GGT (U/L)

Patient value 87 36 0.7 165 4.3 38.3 130 2.54 2.74 2.32 7.42 4.6 25.7 202 840 468 704 33

Usual values1 57-75 29-42 137-155 3.7-4.9 110-131 2.0-2.7 1.4-2.5 0-10 1.0-4.0 3.7-6.1 4.6-9.2 62-169 50-450 10-80 20-150 0-10

TP: Total protein; Alb: Albumin; A/G: Albumin / globulins; TBil: Total bilirubin; CK: creatine kinase; ALT: alanine aminotransferase; ALP: alkaline phosphatase; GGT: g-glutamyl transferase. 1University laboratory values.

Table II: Biochemical results determined in the 10 year old male cat suspected for cholangiohepatitis or cholecystitis. Revue Md. Vt., 2013, 164, 1, 9-12



a ventral sucker, both male and female reproductive organs and prominent vitelline glands were present. Numerous brown, operculated and oval eggs measuring in average 37.5 x 25.0 m were also recorded in the bile. The parasites were identified as Platynosomum fastosum Kossack, 1910 (figure 3).

Figure 1 : Macroscopic aspect of liver (arrow) and gallbladder (arrowhead) from the 10 year old male cat suspected for cholangiohepatitis or cholecystitis.

grossly enlarged (figure 1) and the wall markedly thickened. The common bile duct was dilated and tortuous. By histology dilation of the hepatic biliary ducts with thickened walls was observed. The liver parenchyma showed areas of normal architecture with a central vein and portal tract. There were also areas of nodular regeneration that were separated from areas of normal architecture by dissecting fibrosis. A peribiliary inflammation involving mononuclear cells was seen (figure 2). There were also multiple biliary ducts in the portal tract indicating chronic inflammation and hyperplasia of the biliary ducts. The mononuclear infiltration was found

Figure 3 : Adult Platynosomum fastosum found in the gallbladder from the 10 year old male cat suspected for cholangiohepatitis or cholecystitis. No stain, X 10.

The P. fastosum infection is usually asymptomatic and animals can harbour parasites without any important clinical abnormalities. The clinical signs range from none to obstruction of the biliary tract, with hepatic failure and death [15]. VIEIRA et al. [14] also indicate that the clinical signs of P. fastosum are very unspecific and even absent in many cases. When present, clinical signs may include: emaciation, anorexia, depression, vomiting, diarrhoea, and progressive jaundice. Clinical manifestation and severity of the disease is thought to be dependent on the severity of fluke infestation. With a heavy fluke burden in the biliary tree, significant irritation and inflammation occurs leading to fibrosis and possibly biliary obstruction. Cirrhosis occurs due to chronic inflammation and obstruction. According to RATNASABAPATHY and PRATHAP [11] cats clinically in good condition were found to have Platynosomum infection with lesions such as mottling and enlargement of liver. Histological lesions of the bile ducts observed in the reported case are corroborated with other findings [11, 14]. Ultrasound showed a severely distended gall bladder with a thickened wall. Similar observations were reported by SALOMAO et al. [12]. In parallel, laboratory findings have also evoked liver and bile duct tree damage; indeed, severe inflammation was sustained by neutrophilia with left shift and toxic neutrophils whereas strong increases in serum ALT and ALP activities have indicated hepatocellular injury and stress and the marked increase in serum GGT activity was highly compatible with bile duct lesions observed in cholangiohepatitis or cholecystitis [3, 15]. It is also believed

Figure 2 : Histological section of liver from the 10 year old male cat suspected for cholangiohepatitis or cholecystitis. Note the thickened and dilated bile ducts (arrow). Haematoxylin and eosin, X 10.

to specifically contain lymphocytes and plasmocytes. In summary there was peribiliary portal fibrosis, chronic lymphocytic and plasmocytic cholecystitis and chronic inflammation of the liver with dissecting fibrosis coupled to nodular regeneration. The gall bladder contained yellow mucoid bile with myriad of ovoid, flattened dark brown helminth parasites measuring in average 4.1 mm x 1.7 mm. Microscopic examination of the parasite showed a smooth, thin, external cuticle. A sub terminal oral sucker along with
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that the uraemia, phosphataemia and creatininemia resulted from a prerenal azotaemia as the cat was not drinking or eating for at least a week before presentation, these biochemical findings were similar to those found in another report [15]. The slight increase in serum protein could have been due to a hyperglobulinaemia which can be a common finding in these cases [5]. In spite of its occurrence in many other Caribbean islands, platynosomosis has not been reported earlier from Trinidad and Tobago. This study is the first recorded case of P. fastosum infection in a cat resident in Trinidad and Tobago. The heavy infection with Platynosomum in this resident cat reveals the presence of the parasite in Trinidad and Tobago. But the absence of any clinical sign until heavy worm burden leading to death might be the cause of unnoticed occurrences.


10. MALDONADO J.F.: The life history and biology of P. fastosum. Puerto Rico J. Pub. Health Trop. Med., 1945, 21, 17-39. 11. RETNASABAPATHY A., PRATHAP K.: The liver-fluke Platynosomum fastosum in domestic cats. Vet. Rec., 1971, 88, 62-65. 12. SALOMAO M., SOUZA-DANTAS L.M., MENDESDE-DANTAS L.M., MENDES-DE-ALMEIDA F., BRANCO A.S., BASTOS O.P.M., STERMAN F., LABARTHE N.: Ultrasonography in hepatobiliary evaluation of domestic cats (Felis catus, L.,1758) infected by Platynosomum Looss, 1907. Intern. J. Appl. Res. Vet. Med., 2005, 3, 271-279. 13. SOTO J.A., VILLALOBOS A., ARRAGA DE ALVARADO C.M., CHIRINOS A.R.: Obstructive biliary cirrhosis in a cat due to Platynosomum fastosum infection. Rev. Cient., FCV de LUZ, 1991, 1, 16-19. 14. VIEIRA A.L.S., ECCO R., LIMA W.S., GUEDES R.M.C.: Platynosomum fastosum infection in two cats in Belo Horizonte, Minas Gerais State-Brazil. Brazil J. Vet. Pathol., 2009, 2, 45-48. 15. XAVIER F.G., MORATO G.S., RIGHI D.A., MAIORKA P.C., SPINOSA H.S.: Cystic liver disease related to high Platynosomum fastosum infection in a domestic cat. J.Fel. Med. Surg., 2007, 9, 51-55.

1. BIELSA L.M., GREINER E.C.: Liver flukes (P. concinnum) in cats. J. Am. Vet. Med. Assoc., 1985, 21, 269-274. 2. CARDENAS L.F., AGUIRRE M.M., VIDAL V., DOMINGUEZ A.J., RODRIGUEZ V.R.I.: Prevalencia, caracterizacion morfometrica y hallazgicos de un trematodo de higado y vesicula biliar de gatos (Felis catus) de la ciudad de Merida. Proceedings of the 12th Pan American Congress of Veterinary Science. La Habana, Cuba, July 31 to August 4, 1990, pp.: 79. 3. CARRIERA V., VIEIRA F.F.C., MACHADO G.F., LUVIZOTTO M.C.R.: Feline cholangitis / cholangiohepatitis complex secondary to Platynosomum fastosum infection in a cat. Rev. Bras. Parasitol. Vet., 2008, 17 (supl.1), 184-187. 4. CATCOTT E.J.: Feline Medicine and sugery, Catcott E.J. (ed.), American Veterinary Publications, Santa Barbara, 1964, pp.: 129. 5. DAY D.G.: Feline cholangiohepatitis complex. Vet. Clin. North Am.: Small Anim. Pract., 1995, 25, 375-385. 6. EDWARDS M.: Feline cholangiohepatitis. Comp. Cont. Educ. Pract. Vet., 2004, 26, 855-862. 7. GREVE J.H., LEONARD P.O.: Hepatic flukes in a cat from Illinois. J. Am. Vet. Med. Assoc., 1966, 149, 418-420. 8. LEAM G., WALKER I.E.: The occurrence of Platynosomum fastosum in domestic cats in the Bahamas. Vet. Rec., 1963, 75, 46-48. 9. LENIS C., FERNANDO NAVARRO J., VALEZ I.: First case of platinosomosis from Colombia: Platynosomum illiciens (Digenea: Dicrocoeliidae) in Felis catus, Turbo, Antioquia, Rev. Colom. Cienc. Pecuda., 2009, 22, 659663.

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