Indian J. Vet. Pathol., 44(2) : 101-103, 2020: DOI: 10.5958/0973-970X.2020.00019.

Histological grading of hepatic amyloidosis in ducks

RESEARCH ARTICLE

Nikhil S. Rao*, M. Pradeep, P. Hamza, K.S. Prasannna, R. Anoopraj and Ajith Jacob George
Department of Veterinary Pathology, College of Veterinary and Animal Sciences, Pookode, Kerala Veterinary and
Animal Sciences University Wayanad-673576, Kerala, India
Address for Correspondence
Dr Nikhil S. Rao, Department of Veterinary Pathology, College of Veterinary and Animal Sciences, Pookode, Kerala Veterinary and
Animal Sciences University Wayanad-673576, Kerala, India, E-mail: 12.nikhil.rao@gmail.com

Received: 21.6.2020; Accepted: 28.6.2020

ABSTRACT
Duck farming is very popular in various parts of the world. Even though ducks are highly predisposed to amyloidosis, study
on histological grading of amyloidosis and its correlation with gross findings in the visceral organs are scarce. In the current
study, we necropsied 112 duck carcasses over a period of one year and the occurrence of hepatic amyloidosis was studied and
histological scoring was made. The study revealed amyloidosis in 61.61 per cent carcasses. We analysed the livers of such ducks
histologically for the extent and pa ern of amyloid deposits. The extent of amyloid deposition was graded as mild, moderate
or severe. In severe amyloidosis without cellularity, the liver grossly showed deep yellow discolouration of the parenchyma. In
moderate amyloidosis characterised by islands of hepatocytes and erythrocytes, the liver grossly showed pale pink to brownish
discolouration. In mild amyloidosis with preserved hepatocellular architecture, the gross discolouration of the liver was minimum.
The histological severity of amyloidosis could be directly correlated with the gross features in liver tissue specimens.
Keywords: Amyloidosis, ducks, grading, histology, liver

Amyloidosis is a condition characterised by deposition of proteinaceous How to cite this article : Rao NS, Pradeep
material in the interstitium in various organs and tissues of the body. In birds, M, Hamza P, Prasannna KS, Anoopraj R, George
only AA-amyloidosis (amyloid A) has been described. Although the pathogenesis AJ. 2020. Histological grading of hepatic
of amyloidosis in birds remains obscure, the persistence of certain predisposing amyloidosis in ducks. Indian J Vet Pathol
factors such as chronic inflammation and infections cause a marked increase 44(2): 101-103.
in the serum levels of serum amyloid A (SAA), the precursor of amyloid A,
produced by the hepatocytes, leading to AA amyloidosis1. Amyloidosis develops
Representative tissue samples
spontaneously in White Pekin ducks with increasing age2. Although the exact
of liver were collected and fixed
pathogenesis of amyloidosis remains obscure, studies have shown that the
in 10 per cent neutral buffered
development of amyloidosis in the waterfowl is accelerated by the presence of
formalin for a minimum period
certain chronic inflammatory lesions due to bacteria and their endotoxins3. Even
of 48 hours. After fixation, the
though reports on amyloidosis in waterfowl such as ducks are available, studies
tissues were washed overnight
on histological grading and its correlation with gross appearance of visceral
under running tap water, paraffin
organs are scarce. The present study was aimed to grade the histological severity
embedded, sectioned and stained
of amyloidosis and to correlate it with the gross appearance of liver in ducks.
by routine haematoxylin and
eosin staining. Congo red stain
MATERIALS AND METHODS was used to demonstrate amyloid
Post mortem examination of 112 duck carcasses from different parts of Kerala, and confirm its presence wherever
India during a one-year period from the month of April 2018 to March 2019 were necessary4. Based on the observed
conducted and the gross lesions were recorded systematically. The sampled histological pa erns, the lesions
ducks were above six months of age and were of Vigova and Ku anad breeds. of hepatic amyloidosis were
Table 1. Histopathological grading of hepatic amyloidosis.
Degree of amyloidosis Grading criteria
Mild Plate architecture of hepatic chords maintained with deposition of amyloid in focal areas
and dilatation of sinusoids.
Moderate Islands of hepatocytes present in between the amyloid along with discontinuous sinusoids
containing a few erythrocytes.
Severe Complete loss of cellularity with extensive deposition of amyloid in the hepatic parenchyma
and compression of sinusoids.

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102 Rao et al.

graded depending on the cellularity of the hepatic
parenchyma and the extent of amyloid deposition as
given in Table 1. The gross appearance of the liver was
correlated with the histological grading.
RESULTS
Amyloidosis was histo-logically characterised by
deposition of homogenous, eosinophilic amorphous
material in the extracellular hepatic parenchyma and in
the walls of the portal blood vessels and central vein, in
haematoxylin and eosin stained sections. The presence
of amyloid was confirmed histologically using special
staining with Congo red which gave reddish pink colour
to the amyloid. Varying degrees of amyloid deposition
were noted and graded as mild, moderate and severe.
Amyloidosis was observed in the livers of 61.61 per cent
cases (69/112). All these birds were above one year of age.
Amyloidosis was observed only in those ducks that were
reared under intensive system of farming. Bumble foot
and pododermatitis were constant concurrent lesions
observed in all cases of hepatic amyloidosis (Fig. 1).
Mild amyloidosis was observed in 10.71 per cent
cases (12/112). Histologically, mild amyloidosis (Fig.
2) was characterised by presence of intact hepatic plate
architecture and dilated sinusoids with erythrocytes
along with focal amyloid deposits in the parenchyma.
Mild to moderate degeneration and necrosis were evident
in hepatocytes near the areas of amyloid deposition.
Grossly, there was no discernible change in the liver.
Moderate amyloidosis was observed in 7.14 per cent
cases (8/112). Microscopically, moderate amyloidosis (Fig.
3 & 4) was characterised by generalised amyloid deposits
throughout the hepatic parenchyma causing compression
of hepatocytes and islands of degenerating to atrophic
hepatocytes along with presence of discontinuous
sinusoids containing a few erythrocytes. Grossly, the
areas of the liver with moderate amyloid deposition had a
pale pink appearance with firm consistency (Fig. 5). Focal
areas of bile duct proliferation were noted in 5.36 per
cent cases (6/112) of moderate amyloidosis in this study.
Severe amyloidosis was noted in 43.75 per cent cases
(49/112). Histologically, severe amyloidosis (Fig. 6 &
7) were characterised by complete loss of cellularity in
the hepatic parenchyma and severe amyloid deposition
in the hepatic chords causing compression/complete
obliteration of the sinusoids. Grossly, severe amyloidosis
corresponded with deep yellow discolouration of the
hepatic parenchyma. Hepatomegaly was a constant
finding in all cases of severe amyloidosis.
Occasionally livers with severe amyloidosis had
focal or diffuse capsular thickening (Fig. 8). Nodular
proliferation of the liver was evident in livers of six birds
(5.36%) with severe hepatic amyloidosis. The nodules
were either single solitary (Fig. 9) or multinodular type

Fig. 1. Pododermatitis. Severe thickening and ulceration of metatarsal pad
(arrow) and smaller ulcers (arrow heads) on the digital pads; Fig. 2. Mild
amyloidosis. Focal area of amyloid deposition (arrow) with preserved
architecture of hepatocellular plates (arrow head). Liver H&E 400x; Fig. 3.
Moderate amyloidosis. Intense eosinophilic staining amyloid deposition
around central vein (CV), diffusely spreading to the entire parenchyma
with islands of compressed hepatocytes (white arrows). Liver H&E 400x;
Fig. 4. Moderate amyloidosis. Red staining of amyloid deposits with scanty
hepatocytes (arrows) in the parenchyma. Liver Congo red 400X.
INDIAN JOURNAL OF VETERINARY PATHOLOGY | Volume 44 | Issue 2 | APRIL-JUNE, 2020
Fig. 5. Pale pink liver showing severe hepatomegaly
(Moderate amyloidosis); Fig. 6. Severe hepatic amyloido-
sis. Eosinophilic homogenous staining of amyloid in the
liver parenchyma with complete absence of cellularity.
H&E 100x; Fig. 7. Severe amyloidosis. Amyloid stains red
in colour. Liver Congo red 100x; Fig. 8. Diffuse capsular
thickening (arrow) and yellow parenchyma (star) in cut
section of liver.
 Hepatic amyloidosis in ducks 103

Fig. 9. Single solitary nodule (arrow) and severe yellow discolouration of underlying parenchyma (star); Fig. 10. Multinodular prolifera-
tion (arrows) and severe yellow discolouration of underlying parenchyma (star); Fig. 11. Nodular proliferation of liver. Mild to moderate
amyloidosis with vacuolar degeneration of hepatocytes (arrow heads). H&E 400X.

(Fig. 10). Microscopically, these nodular growths majorly
contained hepatocytes with mild to moderate amyloid
deposition with occasional vacuolar degeneration and
atrophy of the hepatocytes (Fig. 11). The livers with
large nodular growths had severe hepatic amyloidosis
of the underlying parenchyma. Grossly, these nodules
were pale pink to mahogany brown in colour and
microscopically showed mild to moderate grades of
amyloid deposition with occasional degeneration and
compression of functional hepatocytes.
DISCUSSION
The present study attempted a histological grading
of amyloidosis with reference to extent of amyloid
deposition and cellularity in the liver parenchyma. A
correlation between gross and histological findings of liver
could be derived on detailed analysis. Our observations
regarding the absence of any gross discernible changes in
the liver with mild amyloidosis are in concurrence with
observations from previous reports5. In ducks, chronic
inflammatory conditions such as bumble foot have been
implicated in the development of amyloidosis6. Bile duct
proliferation of the liver has been observed in chronic
aflatoxin exposure7. Experiments have shown that the
development of hepatic amyloidosis was accelerated
by severity of lesions caused by high doses of aflatoxin
B1 administration8. However, the exact mechanisms by
which such lesions lead to development of amyloidosis
remain unknown and, hence the possible role of aflatoxin
in the induction of amyloidosis in the present study
cannot be ruled out.
A major observation in this study was that 54.46 per
cent livers examined were enlarged and firm with deep
yellow to pale pink discolouration. Similar observations
on the colour and consistencies of the liver in amyloidosis
have been observed by previous authors3. Hyperplastic
nodules of varying sizes and normal colour of the liver
have been observed in some cases of amyloid affected
livers5. Therefore, it can be deciphered that the areas of
nodular proliferation in the livers of few birds comprised
regeneration of the liver parenchyma with progressive
amyloid. The present study could make a histological
grading of amyloidosis in liver and established a
correlation between the histological grading and gross
appearance of the liver.
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