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Tropical Biomedicine 32(4): 699–703 (2015)

Gigantic amoebic liver abscess in pregnancy: A case report

Chiam, K.H.1, Yvonne AL Lim2, Rohela Mahmud3, Romano Ngui4 and Lee Lee Low5*

1Department of Internal Medicine, Hospital Keningau, Sabah, Malaysia2,3,4Department of Parasitology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia5Department of Internal Medicine, Hospital Sultanah Bahiyah, Alor Setar, Kedah, Malaysia*Corresponding author email: lowleelee@yahoo.comReceived 22 March 2015; accepted in revised form 25 July 2015; accepted 26 July 2015

Abstract. Amoebic liver abscess in pregnancy is genuinely rare in its presentation. Yet, themain issue surrounding this agenda is the diagnostic challenge that it poses especially whensymptomatology is vague and clues are subtle which altogether evades the diagnosis proper.We would like to dwell mainly on these issues in hopes of enlightening clinicians towardsthese diagnostic dilemmas. We report an extremely rare case of amoebic liver abscessoccurring in the third trimester of pregnancy in a 29-year-old lady living in an interior villagein Sabah. It was a combination of biochemical, radiographic and molecular investigationsthat ultimately led to the final diagnosis. In lieu of the high risk of mortality amongst pregnantmothers afflicted with amoebic liver abscess, the inherent need for early diagnosis requiringa high index of suspicion is vital. Elevated alkaline phosphatase alongside neutrophilia appearsto be the most consistent liver parameters in guiding clinicians towards the presence of liverabscess.

INTRODUCTION

Amoebic liver abscess (ALA) is one of thecommonest sequelae of invasive amoebiasis,which is caused by an intestinal protozoa,Entamoeba histolytica. Prevalence tends tovary, but a local study reported that as highas 44.1% of liver abscess in patients werecaused by ALA (Goh et al., 1987). Howeverdata of ALA occurring in pregnancy, areconfined to case reports from endemicregions due to its paucity of incidence andnone has been reported from Malaysia. Inaddition to this lack of information, ALA inpregnancy poses diagnostic and treatmentdilemmas (Read et al., 2001).

CASE REPORT

A 29-year-old pregnant woman gravida 6para 4 + 1 at 30-weeks gestation came to thehospital with complains of four days of fever,

lethargy and flu like symptoms. There wereno known comorbidities. She was initiallygiven a course of Amoxicillin by her GeneralPractitioner but to no avail and wassubsequently admitted to the hospital. Uponpresentation to the hospital, she was referredto the Internal Medicine Unit by the Obstetricsand Gynaecology team; whereupon she wastreated for pneumonia. She appeared pale,mildly tachypneic with a blood pressure of107/63 mmHg, heart rate of 120-140 bpm,temperature of 37.5ºC and a SpO2 of 98%on nasal prong 2 L/min. Examination of hercardiovascular system was unremarkable.Respiratory examination revealed mildbibasal fine inspiratory crepitation’sattributed to over-hydration. Abdominalexamination revealed mild upper abdominaltenderness. Organomegalies were difficultto appreciate in view of the gravid uterus.

Laboratory investigations showed anelevated erythrocyte sedimentation rate at140 mm/hr, total white count of 30-40 x 109/L,

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elevated alkaline phosphatase at 346 U/Lwith borderline increment in alaninetransaminase at 40-50 IU/L, raised lactatedehydrogenase at 1200-1300 U/L withpersistently low albumin at 18 g/L. Bilirubinwas normal. Her blood cultures, tuberculosisworkup and viral hepatitis were negative.Likewise, her transthoracic echocardio-graphy was normal while her Chest X-rayrevealed interstitial edema in keeping withthe clinical findings of over-hydration. Thepossibility of liver pathology was given dueconsideration and a subsequent abdominalultrasonography revealed a huge non-liquefied abscess at the right lobe of livermeasuring 13.6 cm x 15.9 cm x 20.2 cm indimension. Antibiotics were changed tointravenous Meropenem 500 mg 8 hourlyalongside intravenous Metronidazole 500 mg8 hourly to cover for potential pyogenic andamoebic liver abscess.

Upon further questioning she revealedfactors of poor personal hygiene andsanitation coupled with overcrowded livingconditions. There was no history of dysentery,no history to suggest immunosuppressionand her HIV screen was negative. Her travelhistory was insignificant. Ultrasound guidedpercutaneous liver abscess drainage wasdone upon transfer to a subspecializedtertiary center in which 2.3 liters of odorlessbrownish pus (anchovy sauce pus) wasdrained over time (Figure 1).

Subsequently, pus from the abscess, bloodserum and stool samples from the patientwere sent to the Department of Parasitology,Faculty of Medicine, University of Malaya forfurther confirmatory diagnosis.

The patient’s serum was analysed forIgG antibody against E. histolytica using acommercial enzyme linked immunosorbentassay (ELISA) kit (Diagnostic Automation,Inc., USA). Briefly, a 1:64 dilution of patientserum was made using a dilution buffer andadded into the microwells coated with E.

histolytica antigen as in accordance to themanufacturer’s instructions. The microwellswere then finally read at 450 nm with areference filter of 620 nm. An absorbancereading greater than 0.4 O.D unit was obtainedin which indicated that the patient may be

infected by E. histolytica. Given that thepositive ELISA reactions would notunequivocally prove current active infectionand could rather result from a persisting levelof antibody from a past infection, subsequentconfirmation using a nested polymerasechain reaction (PCR) was carried out.

Briefly, total genomic DNA was extractedfrom the pus drained from the liver abscessusing Tissue DNA Isolation kit (Macherey-Nagel, Neumann-Neander, Duren, Germany)following the manufacturer’s guideline andused as template DNA for further specific-species confirmation. The pus digested andincubated at 56ºC overnight in an incubatorshaker with proteinase K for complete celllysis followed by genomic DNA extraction.The extracted DNA was subjected to a nestedPCR targeting the 16S-like ribosomal RNAgene of Entamoeba genus (i.e., E. histolytica,

E. dispar and E. moshkovskii) accordingto previously published protocol with somemodifications (Khairnar et al., 2007). Thefirst PCR was carried for the detection ofEntamoeba genus. Subsequently, the primaryPCR product was then subjected to secondary

Figure 1. Anchovy sauce-like pus being drainedfrom the liver abscess.

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PCR for Entamoeba species-specificcharacterization. Control samples withoutDNA (negative control) and with E.

histolytica as template DNA were includedin each PCR run. DNA amplificationproduced an approximately 439 bp specificamplicon which corresponded to the specificPCR product of E. histolytica (Figure 2).Clinicoserological and molecular findingsuggested the final diagnosis of E. histolytica

infection occurring in this third trimesterpregnant woman.

In addition, faecal sample was examinedvia microscopy for the presence of E.

histolytica. However, it was negative for bothE. histolytica cysts and trophozoites.

Meanwhile, she completed two weeks ofintravenous Metronidazole with no untowardcomplications and the pregnancy progressednormally to term. She delivered a healthybaby girl weighing 3.0 kg at 38th week ofgestation. Unfortunately, luminal amoebicidewas not available locally. She remained welland was last followed up a week after herdelivery. Repeated ultrasonography showedprogressive size reduction of the liverabscess cavity.

DISCUSSION

Amoebic liver abscess is a disease oftropical and sub-tropical countries. It isrelatively uncommon in women and is a rarecomplication of pregnancy (de Silva et al.,1990; Mabina et al., 1998). ALA previouslyreported in Malaysia were from males andnon-pregnant females (Jamaiah & Shekhar,1999). We believe this patient to be the firstreported case in pregnancy in Malaysia.Amoebiasis occurs in people from the lowersocio-economic groups. It is associated withpoverty, improper sanitation, contaminatedfood and water. This patient came from apoor socio-economic background and sheis exposed to the associated factors foramoebiasis including poor sanitation andover crowding living condition.

ALA carries significant morbidity ifdiagnosis is delayed. Clinicians in endemiccountries need to be aware of its possibilitywhen pregnant women present with fever,abdominal pain, and upper abdominaltenderness even if they have no bowel relatedsymptoms. Not all of the classic features ofhepatic amoebiasis were present as in our

Figure 2. The PCR results. Lane M: 100 marker; Lanes 1-2: No template (negative controls);Lane 3: E. histolytica DNA (positive control); Lane 4: Patient’s sample.

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case. Pregnancy increases the susceptibilityto amoebiasis due to a defective immuneresponse and to raised progesteronelevels and thus patients with sub-clinicalinfections may develop clinical symptomsduring pregnancy (Cowan & Houltan, 1978;Constantine et al., 1987).

Fever, right upper quadrant pain andhepatomegaly are the commonest presentingfeatures of ALA. The difficulties and the delayin diagnosing this patient was due to the vaguesymptomatology and the gravid uterus, whichobscured clinical findings. With literaturedocumenting 60-80% of ALA patientsdeveloping abnormally high alkalinephosphatase levels; this finding together withleukocytosis help in guiding towards thediagnosis of liver abscess (Petri & Singh,1999; Mathur et al., 2002). Though serumbilirubin was normal in this patient, it shouldbe noted that hyperbilirubinaemia isassociated with a grave outcome (Mathuret al., 2002).

Abdominal ultrasonography carried outin this patient revealed a huge liver abscessin the right lobe which could either bepyogenic or ALA. Serological test carried outfor this patient was positive for amoebiasis.Serological tests are positive in about 90–95% of patients with an ALA. Antibody titerscan confirm E. histolytica infection butmay persist for 6 months or more making itimpossible to differentiate acute from pastinfections in residents from areas with a highprevalence of infection. This report alsohighlighted the usefulness of advancedmolecular technique such as polymerasechain reaction in the diagnosis by detectingthe presence of the DNA of E. histolytica inthe pus from the liver abscess. Similarly, thishas been reported in North India by Khan(2006).

In the treatment of amoebic liverabscess; antibiotics remain the cornerstoneof therapy. Metronidazole is highly effectiveagainst invasive amoebiasis. When ultra-sonography confirms a liver abscess andwhile awaiting serologic and molecularconfirmation of an amoebic etiology as in thiscase, treatment with Metronidazole shouldbe initiated. However drainage of liverabscess measuring more than 10 cm has been

recommended to prevent its potentialrupture. Such complementary managementaids in preventing rupture of the abscessand expedites recovery (Mathur et al.,2002). There have been cases reported ofintraperitoneal rupture, rupture after birthand rupture during birth (Jamaiah & Shekhar,1999). ALA may extend and /or rupture intothe abdomen or chest. Ultrasonography ishelpful in the long term follow-up of patients.It is assessed by patterns of resolution ofthe abscess cavity. Liver abscesses usuallydisappear within 8 months to 2 years afterdrainage.

Control of amoebiasis is via adequatesanitation, safe food and water and goodpersonal hygiene of the population.

CONCLUSION

A high index of suspicion in the presence ofconfounding symptoms is vital to come to thelikely diagnosis. Serum alkaline phosphataseis probably the most common and consistentbiochemical indicator of amoebic liverabscess. Laboratory tests should includemolecular techniques. This case serves toillustrate the importance of combining andinterpreting the relevant laboratory andmolecular investigations in order to clinchthe diagnosis early and prevent fatalcomplications.

Acknowledgements. We would like to extendour gratitude to Dr Tan Li Fen and Ms JenniferChong for aiding us in retrieving vital recordsof the patient. This work was supported bythe University of Malaya HIR-MOHE Grant(H-20001-00-E000061).

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