Keywords
visceral larva migrans - eosinophilia - parasitic infections of the liver - toxocariasis - albendazole - eosinophilic abscess
Introduction
Visceral larva migrans (VLM) is a systemic zoonotic parasitic disease caused by migrating second-stage larva of Toxocara canis or Toxocara catis through the viscera of human beings. The eggs of these ascarids are common environmental contaminants of human habitation, and humans ingest embryonated eggs by accident.[1] Larvae, after hatching, fail to mature in the aberrant host; instead, they wander and reach different parts of the body, including the liver, lungs, eyes, brain, or heart. In these organs, the worm larvae cause varying degrees of local inflammation leading to nonspecific symptoms.[2] There are two forms of clinical expressions visceral and ocular. The liver is the most common visceral organ to be involved due to its blood supply. Despite being a public health problem, it remains neglected, and diagnosis is delayed and challenging. Secondly, it is predominantly considered a disease of children; hence, most adult patients with VLM are initially treated as a liver abscess or neoplastic mass in the liver. Here, we describe a case series of four adults with hepatic VLM
Case Series
Case 1
A 23-year-old female presented with right upper quadrant dull aching abdominal pain of 15 days' duration and low-grade intermittent fever with nausea and decreased appetite. Hemogram revealed mild anemia and leukocytosis with predominately peripheral eosinophilia (eosinophil count 34%). Computed tomographic (CT) abdomen showed an ill-defined heterogeneous solid cystic lesion in segments VI and VII, multiple lymph nodes at the porta, para-aortic, and aortocaval region. Liver biopsy is suggestive of the eosinophilic abscess.
Case 2
A 45-year-old female had a low-grade fever, decreased appetite, and weight loss of 10 kg in the last 2 months, and mild, dull aching upper abdominal pain for the last month. Hemogram revealed a total leucocyte count of 12,750 with peripheral eosinophilia (eosinophil count of 39%). CT abdomen was suggestive of multiple hypodense, hypovascular lesions in the right lobe of the liver, with few showing central necrotic area. Her liver biopsy was suggestive of the eosinophilic abscess.
Case 3
A 26-year female presented with high-grade, intermittent fever, and right upper quadrant pain of 3 months. Magnetic resonance imaging (MRI) of the upper abdomen showed multiple ill-defined, lobulated, and communicated rounded and elongated lesions in the liver with the postcontrast enhancement of lesions. Investigations revealed a total leucocyte count of 8,660 with an eosinophil count of 35%.
Case 4
A 64-year-old diabetic male presented with high-grade intermittent fever for the last 2 months, initially treated for a liver abscess with an attempt to drain it percutaneously with no improvement. CT scan of the abdomen revealed multiple variable-sized clusters of coalescing fluid density lesions along the adjoining surfaces of the right and left lobe, caudate lobe, and segment V of the liver. The clinical, laboratory parameters and imaging studies of all these patients are summarized ([Table 1]).
Table 1
Demographic, clinical, and laboratory investigations of all four patients at presentations
|
Name of investigation
|
Case I
23 years, female
Student hails from semiurban background
No H/O contact with Pets
|
Case II
47 years, female
Housewife from rural background.
H/O Contact with pets during childhood
|
Case III
28 years, female
In private job from urban background. No H/O contact with pets
|
Case IV
64 years, male
Retired from Job staying in urban areas for last many years. No H/O contact with pets
|
|
Presenting symptoms
|
RUQ pain for 15 days, low-grade intermittent fever
Nausea and Decreased appetite
|
Low-grade fever, decreased appetite, weight loss of 10 kg in last 2 months, and mild dull aching upper abdominal pain for the last 1 month
|
High-grade, intermittent fever and RUQ pain of 3 months duration
|
High-grade intermittent fever, decreased appetite for last 2 months,
known diabetic
|
|
Hemoglobin
|
10.4
|
11.4
|
10.4
|
8.3
|
|
Total leucocytes
|
11,110
|
12,750
|
8,660
|
27,940
|
|
Differential leucocytes
|
P-42; L-21; E-33; M-4
|
P-41; L-16; E-39; M-4
|
P-32; L-27; E-35; M-4; B-2
|
P-94,L-2,M-4 E-3
|
|
Platelets
|
3.52
|
4.69
|
1.50
|
4.81
|
|
Serum bilirubin (mg%)
|
0.29
|
0.36
|
0.29
|
0.81
|
|
AST (SGOT) IU
|
15
|
43
|
86
|
25
|
|
ALT (SGPT) IU
|
16
|
36
|
123
|
22
|
|
SAP
|
94
|
90
|
287
|
289
|
|
GGT
|
29
|
|
86
|
490
|
|
Serum proteins (gm%)
|
8.0
|
8.1
|
7.7
|
7.1
|
|
Serum albumin (gm%)
|
3.8
|
3.6
|
3.6
|
3.2
|
|
INR
|
1.19
|
1.07
|
1.34
|
1.35
|
|
Serum creatinine (mg%)
|
0.53
|
0.55
|
0.5
|
0.94
|
|
Hydatid serology
|
Positive
|
Negative
|
Negative
|
Negative
|
|
Amoebic serology
|
Negative
|
Negative
|
Borderline positive 12.3 (normal up to 12)
|
Negative
|
|
AFP
|
4.0
|
2.24
|
–
|
4.84
|
|
Sonography of upper abdomen
|
A heteroechoic lesion with cystic area and thick walls in right lobe measures 8 × 6.5 × 6.8cms with enlarged peripancreatic nodes measuring about 2 cm
|
Multiple small cystic lesions seen in right lobe of liver suggestive of pyogenic abscess
|
Heterogenous hyperechoic to hypoechoic lesion in right lobe of liver
|
There are multiple hypoechoic areas in right and left lobe of liver suggestive of multiple abscess
|
|
Cross-sectional imaging of upper abdomen
|
CECT: Ill-defined heterogenous solid cystic lesion in seg VI & VII measuring 9.5 × 6.6 × 5.5 cm having an attenuation of 14–16 HU. multiple LN at porta, para-aortic and aorto-caval with largest LN measuring 1.9 × 1.0cm
|
CECT: Multiple hypodense hypovascular lesion in right lobe with few showing central necrotic area
|
MRI: A cluster of multiple ill-defined intercommunicated rounded to elongated lesion within hepatic parenchyma with thrombotic occlusion of posterior and inferior segmental branches of right portal vein
|
Multiple variable-sized cluster of coalescing fluid density lesions along the adjoining surfaces of right and left lobe of liver, in caudate lobe and in segment of V of liver
|
|
Liver biopsy
|
Eosinophilic micro abscesses, epithelioid cell granuloma with central necrosis, cellular debris and retractile hook-lets, bile duct loss with ductular proliferation, patchy intra-hepatocytic cholestasis. No larval were identified
|
Portal tracts are infiltrated with polymorphonuclear and eosinophilic infiltrate and PAS positive Charcot-Leyden crystals suggestive of parasitic infestation
|
Distorted lobular architecture with eosinophilic abscesses. An ill formed granuloma with necrosis is seen. Few Charcot-Leyden crystals are seen
|
Not done
|
Abbreviations: AFP, Alpha fetoprotein; ALT, alanine aminotransferase; AST, aspartate aminotransferase; CECT, contrast-enhanced computed tomography; GGT, gamma glutamyltransferase; HU, Hounsfield unit; INR, international normalized ratio; LN, lymph node; MRI, magnetic resonance imaging; PAS, periodic acid-Schiff; PETS,—; RUQ, right upper quadrant; SGOT, serum glutamic-oxaloacetic transaminase; SGPT, serum glutamic-pyruvic transaminase.
Three of these patients, who were further evaluated with liver biopsy, were found to have an eosinophilic abscess ([Fig. 1]). The fourth patient, an elderly diabetic, did not consent to a biopsy. The blood and urine cultures sent in all these patients showed no evidence of bacterial infection. All four patients responded to oral albendazole.[3] With this albendazole treatment, there was a complete resolution of fever and pain and a significant reduction in the size of liver space-occupying lesions (SOL). Post-treatment eosinophil count decreased to normal in all three patients who had high eosinophil count before starting treatment. All patients on follow-up were asymptomatic with no pain in the abdomen and fever.
Fig. 1 Liver biopsy from patient 1 showing eosinophilic abscess along with an ill formed granuloma with necrosis (H & E stain, 400X.zip)
Discussion
VLM is a disease described predominantly in children due to accidental ingestion of embryonated eggs of Toxocara canis or Toxocara catis, but of late, many adults with VLM have been reported. All these patients present with fever, significant abdominal pain, and SOL of the Liver.[4] Most of these patients are initially treated like liver abscesses because of fever and SOL within the liver for a few weeks without any improvement. Some of these patients have aspiration, which sometimes lead to secondary infection. Occasionally VLM may be complicated by vascular injuries such as portal vein thrombosis, or arterial pseudoaneurysm. Sometimes these SOLs are interpreted as neoplastic. None of these patients responded to initial treatment done with antibiotics and antiamoebic drugs. On evaluation, we found that these patients had significant peripheral eosinophilia. On contrast-enhanced computerized tomography, these lesions within the liver appear as a conglomerate of heterogeneous solid cystic nodular lesions, which are hypodense, and hypovascular ([Figs. 2] and [3]). Contrast-enhanced MRI of the upper abdomen showed a cluster of low attenuating, nonspherical small nodular lesions with fuzzy margins. These lesions enhance on the hepatic arterial phase with no washout on equilibrium and delayed phases ([Fig. 4]). Another feature seen on this MRI is a T1 hypointense rim around the abscess cavity, which is a layer of granulation tissue that favors an infective origin more than a malignant origin. These lesions may show a change in morphology and position on follow-up imaging, a finding consistent with the migration of larvae. Sometimes, linear tracts are also seen, which could be a very useful imaging feature that raises a suspicion of VLM. Another important differentiating feature and a clue to the diagnosis in these patients is the “presence of significant peripheral eosinophilia” with a “cluster of coalescing lesions which appears as solid cystic lesions in the liver on imaging.”[5] Liver biopsy of these lesions typically shows eosinophilic abscesses suggestive of parasitic infestation ([Fig. 1]). The majority of these patients respond very well to oral albendazole therapy.[6] However, hepatic segmental resection may also be required in some cases.
Fig. 2 Triple-phase computed tomographic abdomen plain (A) and arterial phase (B) from patient 2, showing a large cluster of multiple rounded heterogenous irregular hypodense lesions with subtle peripheral enhancement in the right lobe.
Fig. 3 Triple-phase computed tomographic abdomen plain (A) and arterial phase (B) from patient 4, showing a conglomerate of multiple hypodense, hypovascular lesions in the left lobe of the liver with few showing central necrotic area.
Fig. 4 Contrast-enhanced axial magnetic resonance imaging arterial phase (A), and delayed phase (B) from patient 3 showing cluster of multiple hypointense nonspherical lesions with peripheral rim enhancement on delayed scan.
Conclusion
VLM must be considered in patients with prolonged fever, heterogenous, hypovascular space-occupying liver lesions, and peripheral eosinophilia.
