Saudi Journal of Gastroenterology
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CASE REPORT Table of Contents   
Year : 2000  |  Volume : 6  |  Issue : 1  |  Page : 51-55
Hepatic fascioliasis; A cause of pyrexia of unknown origin and persistant eosinophilia


1 Department of Internal Medicine, King Fahd Hospital of the University, Al Khobar, Saudi Arabia
2 Department of Pathology, King Fahd Hospital of the University, Al Khobar, Saudi Arabia
3 Arabian Oil Company Hospitals, Saudi Arabia

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Date of Submission18-Jul-1998
Date of Acceptance03-Apr-1999
 

How to cite this article:
Saeed I, Satti MB, Khamis A, Al Muhanna F. Hepatic fascioliasis; A cause of pyrexia of unknown origin and persistant eosinophilia. Saudi J Gastroenterol 2000;6:51-5

How to cite this URL:
Saeed I, Satti MB, Khamis A, Al Muhanna F. Hepatic fascioliasis; A cause of pyrexia of unknown origin and persistant eosinophilia. Saudi J Gastroenterol [serial online] 2000 [cited 2019 Jul 23];6:51-5. Available from: http://www.saudijgastro.com/text.asp?2000/6/1/51/33506


Human fascioliasis is a world wide problem that is mainly caused by Fasciola hepatica and to a lesser extent by Fasciola gigantica[1]. Infection is contracted by ingestion of the encysted forms of the fluke attached to edible aquatic plants such as watercress. The larvae exist in the duodenum, migrate through the intestinal wall, pass into the peritoneal cavity, penetrate the liver capsule and finally reach the bile ducts, where they mautre. Occasionally larvae may migrate to and mature in ectopic locations including subcutaneous tissue, chest cavity or brain. The disease usually manifests as epigastric pain, diarrhea, jaundice, urticaria, pruritis, arthralgia and eosinophilia. Fever is not a common presentation. Fibrosis of the liver may appear after prolonged residence of many adult worms in the bile ducts. Obstruction of the bile ducts occurs frequently. Human Fascioliasis is becoming a public health problem in some countries such as Egyp[2], Spain[3] and other Mediterranean countries. In fact an outbreak of acute fascioliasis was reported among Aymara Indians in the Bolivian Altiplano[4], but to our knowledge no cases of Fasciola infestation have been reported among people living in Saudi Arabia. This report illustrates a patient presented primarily with pyrexia of unknown origin (PUO). The latter was defined by Petersdorf and Beeson as temperature more than 38.3°C (101°F) on several occasions with a duration of fever more than three weeks and failure to reach a diagnosis despite one week of inpatient investigations[5].


   Case report Top


A 43 years old male Egyptian Dermatologist living in Kingdom of Saudi Arabia for the last sixteen years, presented in July 1995 with two months history of fever and rigors, 3-4 hours each early evening associated with sweating. During day time he used to perform his normal activities. He also noticed poor appetite with central upper abdominal pain. His initial examination showed mild hepatomegaly, which was firm, non tender, with no bruit and no other organ enlargement. There were two spider nevei noticed on the right shoulder. Chest and heart were clinically free and CNS examination was unremarkable. His initial investigations showed total white cell count of 2.7xl09/L, polymorphs were 24%, Lymphocytes 50%, eosinophils 20%, basophils 1% and Monocytes 5%. ESR was 16 mm in the first hour and 48 mm in the second hour (Westergren). Urine, stool analysis by concentration method and cultures were negative as well as repeated blood cultures for both aerobic and anaerobic organisms. His initial LFT were: total bilirubin 22 tmol/l, ALT 20u/L, AST 27 u/L, Alkaline phosphatase 122 U/l, LDH 158 U/1, GGTP 92 U/1.  Brucella More Details and  Salmonella More Details agglutination tests were negative and so were blood malaria films. Tuberculin test was 11 mm after 48 hours. Chest X­ray was normal and abdominal ultrasound showed fatty infiltration of the liver. Ten days after admission, fever was continuous and associated with increasing sensation of itching, weakness, mild jaundice, nausea, vomiting and few bouts of loose bowel motion. Later on attacks of transient palmer erythema were noticed by the treating physician. Tests for hepatitis A, B and C were negative. Epstein-Barr virus as well as schistosoma antibodies were also negative. Total bilirubin increased up to 68 µmol/l with a direct fraction of 54 µmol/l. AST and ALT were mildly elevated but alkaline phosphatase and GGT were approximately five folds elevated. Antinuclear antibody test and other serologic markers were negative while Alpha feto­protein was normal.

Because of the persistent upper abdominal pain and repeated vomiting, upper G.I., endoscopy was performed and revealed marked hyperaemia of the gastric mucosa but duodenal aspirate was free of parasites or significant bacterial growth. Repeated blood count showed hemoglobin 11.2 gm/dl and a total white cell count of 9.8 with Polymorphs 11%, stabs 3%, lymphocytes 35%, monocytes 3%, basophils 1% and eosinophils 47%. His IgE level was >457 units normal (-120 units).

In view of the persistent fever, hepatomegaly, eosinophilia and high IgE levels, serologic tests for a variety of parasites were requested. These included tests for amoeba, toxocara, trichinella, filaria, fasciola, schistosoma and hydatidosis. On the 28th day of admission, CT scan of the abdomen showed moderate hepatomegaly with multiple cystic leions in the left lobe [Figure - 1] which were interpreted by the radiologist as intraductal lesions. Liver biopsy under CT guidance was attempted and the histologic examination revealed a granuloma with necrotic areas and marked eosinophilic infiltration in and around the granuloma [Figure - 2]. The serologic tests for parasites were all negative except for the indirect hemagglutination test for fasciola hepatica which was reported as positive with a titre of 1/2560. Upon requestioning the patient, he could remember ingesting watercress on several occasions.

The patient was treated with praziquantel 75mg/kg daily for 5 days. The response was dramatic; fever subsided gradually and disappeared in one week. Itching, palmer erythema, jaundice and abdominal pain disappeared and the liver was back to normal size in about two weeks. Repeated Fasciola antibody titre after one month from therapy was 1/40 and repeated CT scan showed complete resolution of the cystic lesions [Figure - 3].


   Discussion Top


Pyrexia of unknown origin (PUO) was first defined by Petersdorf and Beeson in 1961[5]. They studied 100 cases of classic PUO in 1952-57 in adults. 36% were due to infections, 19% neoplasms, 13% collagen vascular disease, 25% miscellaneous causes and 7% left undiagnosed. Durack and Stree[6] have proposed a new system of classification of PUO: classical PUO, nosocomialPUO, neuotropenic PUO and PUO associated with human immunodeficiency virus (HIV) infection. Jacoby and Swartz[7]studied 128 cases of PUO during 1957-71, 40% were due to infections, 20% neoplasm, 15% collagen vascular disease, 17% miscellaneous and 8% undiagnosed. Howard et al[8] studied 100 cases of PUO during 1969-76, 37% of cases were caused by infections, 31% neoplasms, 19% collagen vascular disease, 8% miscellaneous causes and 5% undiagnosed. Larson and Featherstone[9] studied 105 cases of PUO in 1970­80. They found that 30% of cases were caused by infections, 31% neoplasm, 16% collagen vascular disease, 10% miscellaneous causes and still 12% of cases were undiagnosed. Knockaert and Vanneste[10],[11] studied 199 cases in 1980-89, 22.5% were due to infections, 7% neoplasm, 21.5% collagen vascular diseases, 26.5% miscellaneous and 2.5% undiagnosed. Infections especially extrapulmonary tuberculosis remain the leading cause of PUO. Prolonged mononucelous infection caused by Epstein-Barr virus, cytomegalic virus or human immunodeficiency viruses are included in the list. Intraabdominal abscesses and renal, retroperitoneal and paraspinal abscesses continue to be difficult to diagnose. Prostatitis, dental abscesses, sinusitis, endocarditis and cholangitis continue to be sources of occult fever[12]. Eosinophilia is one of the most common hematologic abnormalities in patients in tropical and subtropical countries. Normally eosinophilic count ranges from 0-350 cell/mm3. Among other helmenthic infestations, eosinophilia usually accompanies Fascioliasis especially in the acute phase when the juvenile worms migrate from the intestine to the liver[13],[14] In a previous study on 30 cases of fascioliasis[15], all cases showed eosinophilia which ranged from 770 to 10560 cell/mm3. Makled et al (1988)[16]reported that eosinophilia was present in 100% of clinically suspected fascioliasis cases with an eosinophilic count ranging from 540 to 7200 cell/mm3. In a study carried out by Stork et al, eosinophilia was noticed in only 59% of cases passing fasciola eggs in their stool[13], while Osman (1991) observed that a normal eosinophilic count was present in 35.2% of patients passing fasciola eggs[2]. This indicates that eosinophilia although may be an indicator of fasciola infestation yet it is not a constant feature in chronic fascioliasis and if present it is usually of a higher level in the acute migratory phase. Eosinophilia was mentioned in a study by Arjona et al as the most frequent laboratory abnormality[17] Chauvin et al reported similar results[18]

A definite diagnosis of Fasciola hepatica may be established by the identification of parasite ova in the feces, but most cases may be diagnosed by serologic methods[17]. In our patient, repeated stool analysis by concentration methods was negative for Fasciola ova, but low sensitivity of stool examination is well known in Fasciola cases. De Weil et al attributed this low sensitivity to difficulty in finding Fasciola eggs during acute and even chronic fascioliasis[19]. The sole dependence on stool examination will result in false negative diagnoses as was reported by Makled et at[16]. The reference to serologic tests is of remarkable value in many cases[20] as it was the case in establishing the diagnosis of fascioliasis in our patient.

Schistosomiasis was ruled out both clinically and by a negative schistosoma antibody titre, since cross reactions between schistosomiasis and fascioliasis were reported by many workers using ELISA technique[21],[22]

Radiology may play a role in diagnosis. CT scan has become a useful technique in the diagnostic work-up. Recently a report concerning MR (Magnetic Resonance) in human fascioliasis, stated that there are findings that suggest various changes associated with traumatic hepatitis caused by the migration of the worm in the liver and that these changes can be helpful in diagnosing Fascioliasis[23]

The obstructive jaundice in our patient is a rare presentation. A middle aged woman presented with obstructive jaundice of 6 months duration was described by Kumar et al in 1995[24]. Radiologic investigations revealed multiple pyogenic liver abscesses with the possibility of choledocholithiasis. Exploration of common bile duct revealed that Fasciola hepatica was responsible for the illness. The case was reported because of its rarity. In addition these liver flukes were found to be responsible for destruction of liver tissue during an early migratory phase of several weeks duration which is responsible for elevation of liver enzymes[25], as was observed in our patient. Infestation of the biliary tract by adult helminths or their ova may produce a chronic, recurrent pyogenic cholangitis with or without multiple abscesses, ductal stones or biliary obstruction. This condition is relatively rare but does occur in inhabitants of Southern China and elsewhere in South-East Asia[26].

The organisms most commonly involved are trematodes or flukes, including Clonorchis sinensis, Opisthorchis felineus and Faciola hepatica. The biliary tract may be involved by intraductal migration of adult Ascaris lumbricoides from the duodenum or by intrabiliary rupture of hydatid cysts of the liver produced by Echinococcus species. In such circumstances cholangiography including Endoscopic Retrograde Cholangiopancreatography (ERCP) plays a role in the diagnosis [26] . It should be emphasized that in the orient, one also see cholangiohepatitis associated with pigment lithiasis, which may in fact, be more common than cholangitis due to parasites[26].

Triclabendazole and bithionol are reported to be the most effective drugs against Fasciola hepatica[17],[27],[28]. Although the efficacy of praziquantel was questioned by Arjona et al[17] there are other reports which encourage the use of praziquantel and focus on its therapeutic value[29]. A very useful retrospective study was carried out by Moreau et al on twenty five patients with Fasciola hepatica, all of them were treated with praziquantel (75 mg/kg/day orally) for 5 days and they concluded that the drug is both effective and well tolerated[30]. They also recommended praziquantel as a first choice drug for distomatosis due to Fasciola hepatica in human.

In conclusion, an Egyptian patient, resident in Saudi Arabia who presented primarily with fever, eosinophilia and jaundice was confirmed serologically to have hepatic fascioliasis. The patient showed a dramatic response to specific therapy. The unusual presentation of this case should widen our scope when investigating patients with P.U.O.


   Acknowledgment Top


Our gratitude goes to Mr. Ramesh Kumar for typing the manuscript and to Mr. Gordon Ntow for photographic assistance.

 
   References Top

1.Hardman EW, Jones RLH, Davis AH. Fascioliasis a large outbreak. BMJ 1970;3:502.  Back to cited text no. 1    
2.Osman MM. Evaluation of Fasciola antigenic fractions in the diagnosis of human fascioliasis. Ph.D. Thesis. Alexandria University, Egypt 1991.  Back to cited text no. 2    
3.Luzon-Pena M, Rojo-Vazquez FA, Gomez-Bautista M. Seasonal availability of Fasciola hepatica metacercaria in a temperate Mediterranena area (Madrid, Spain). Zentralbl­Veterinarmed-B 1995;42(10):577-85.  Back to cited text no. 3    
4.Bjorland J, Bryan RT, Strauss W, Hillyar GV, McAuley JB. An outbreak of acute fascioliasis among Aymara Indians in the Bolivian Altiplano. Clin Infect Dis 1995;21:1228-33.  Back to cited text no. 4    
5.Petersdord RC. Fever of unknown origin: An old friend revisited (Editorial). Arch Intern Med 1992;152:21.  Back to cited text no. 5    
6.Durack DT, Street AC. Fever of unknown origin-reexamined and redefined. In: Current Clinical Topics in Infectious Diseases. Remington JS, Swartz MN (Eds). Cambridge, MA, Blackwell, 1991.  Back to cited text no. 6    
7.Jacoby GA, Swartz MN: Fever of undetermined origin. N Engl J Med 1974;298:1407.  Back to cited text no. 7    
8.Howard PJR, et al. Fever of unknown origin: A prospecctive study of 100 patients. Tex Med 1977;73:56.  Back to cited text no. 8    
9.Larson FB, Featherstone HJ. Fever of undertemined origin. Diagnosis and Follow-up of 105 cases, 1970-80. Medicine 1982;61:269.  Back to cited text no. 9    
10.Knockaert DC, Vanneste LJ. Fever of unknown origin in the 1980. Arch Intern Med 1992;152:51.  Back to cited text no. 10    
11.Knockaert DC, et al. Fever of unknown origin in elderly patients. J Am Geriatr Soc 1993;41:1187.  Back to cited text no. 11    
12.Dinarello CA, Wolff SM. Fever of unknown origin. In: Principles and Practice of Infectious Disease, 3 rd Ed. Mandell G, et al (Eds). New York, Willey 1990;468-79.  Back to cited text no. 12    
13.Stork MG, Venables GS, Jennings SMF, Beesley JR, Bendezu P, Capron A. Investigations of endemic fascioliasis in peruvian village children. J Trop Med Hyg 1973;76:231-5.  Back to cited text no. 13    
14.Beaver PC, Jung RC, Cupp EW. Clinical value of eosinophil count. Clinical parasitology. 9 th Ed. Philadelphia, Lee and Rebiger 1984.  Back to cited text no. 14    
15.Lobna AZ, Suzanne FN, Mervat ZA, Iman FN, Mona MT, Helen NA. A study on patients with eosinophilia of suspected parasitic origin. J Egypt Soc Parasitol 1995;25:245-55.  Back to cited text no. 15    
16.Makled MK, Khalil HM, El Sibae MM, Abdalla HM, El­Zayyat EA. Fascioliasis and hepatic affection. J Egypt Soc Parasitol 1988;18:1-9.  Back to cited text no. 16    
17.Arjona R, Riancho JA, Aguado JM, Salesa R, Gonzalez­Macias J. Fascioliasis in developed countries, a review of classic and aberrant forms of the disease. Medicine Baltimore 1995;74:13-23.  Back to cited text no. 17    
18.Chauvin A, Bouvet G, Boulard C. Humoral and cellular immune response to Fasciola hepatica experimental primary and secondary infection in sheep. Int J Parasitol 1995;25:1227-41.  Back to cited text no. 18    
19.De Weil NS, Hillyar GV, Phacheco E. Isolation of Fasciola hepatica genus specific antigens. Int J Parasitol 1984;14:197-206.  Back to cited text no. 19    
20.Hillyer GV, De Weil NS. Serodiagnosis of fascioliasis by immunorecipitation tests. Int J Parasitol 1981;11:71-8.  Back to cited text no. 20    
21.Khalil HM, Abdel-Aal TM, Makled MK, Abdalla HM, Fahmy IA, El-Zayyat EA: Specificity of crude and purified Fasciola antigens in immunodiagnosis of human fascioliasis. J Egypt Soc Parasitol 1990;20:87-94.  Back to cited text no. 21    
22.Osman MM, Helmy MH, Molecular weight determination of Fasciola antigens specific for diagnosis of acute fascioliasis. J Egypt Soc Parasitol 1994;24:471-8.  Back to cited text no. 22    
23.Han JK, Han D, Choi BI, Han MC. MR findings in human fascioliasis. Trop Med Int Health 1996;1:367-72.  Back to cited text no. 23    
24.Kumar A, Gautam A, Chaturvedi S. Obstructive jaundice due to Fasciola hepatica. Indian J Gastroenterol 1995;14:97-80.  Back to cited text no. 24    
25.Seitz HM. Parasitic diseases of the liver. Verb Dtsch Ges Pathol 1995;79:241-8.  Back to cited text no. 25    
26.Norton JG, Kurt JI. Diseases of the gall bladder and bile ducts. In: Harrison's Principles of Internal Medicine, 14 th Ed. Fauci, et al (Eds). New York: McGraw Hill 1998;1735-6.  Back to cited text no. 26    
27.Apt W, Augilera X, Vega F, Miranda C, Zulantay I, Perez C, Gabor M, Apt P. Treatment of human chronic fascioliasis with triclabendazole, drug efficacy and serologic response. Am J Trop Med Hyg 1995;52:532-5.  Back to cited text no. 27    
28.Abdul-Hadi S, Contreras R, Tombazzi C, Alvarez M, Melendez M. Hepatic fascioliasis, case report and review. Rev Inst Med Trop Sao-Paulo 1996;38:69-73.  Back to cited text no. 28    
29.Torresi J, Richards MJ, Taggart GJ, Smallwood RA. Fasciola hepatica liver infection in Victorian diary farmer (Letter). Med J Aust 1996;164:511.  Back to cited text no. 29    
30.Moreau JA, Fernandez J, Recco P, Seguela JP, Frexinos J: Efficacy and tolerance of praziquantel in the treatment of distomatosis caused by Fasciola hepatica. Gastroenterol Clin Biol 1995;19:514-9.  Back to cited text no. 30    

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Correspondence Address:
Ibrahim Saeed
P.O. Box 40032, Al Khobar 31952
Saudi Arabia
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