There was significant depression in weekly growth and feed conversion efficiency in both the Toxin-fed groups, at all ages. The Aflatoxin-B1 (AFB1) impacted the weekly growth of Pekins, where the T
2 had higher quantum of damage compared to the T
1 in terms of morbidity and resultant growth parameters.
Variations in Body weight of ducklings
The growth of ducklings over 2 to 6 weeks underwent significant variation (p≤0.05), where the variation remained erratic between T
1 and T
2 indicating differential debilitating impact from the AFB1 on different ages of Juvenile growth (Table 1). The live weight in both the Toxin groups (T
1 and T
2) was significantly poorer than control, at most juvenile ages of measurements, especially from 2 to 4 Weeks. The differential bodyweight between the control and both- Toxin groups, remained in 200 to 300% ranges, where in continued mortality and morbidity in both toxin groups rendered them to be with highest C.V, indicating impact of AFB1 exposure, on uniformity of ducklings. In general, the reduction in bodyweight was in a
dose-dependent manner, where T
2 showed higher variation than T
1, where higher quantity of toxins consumed apparently caused the depression. To generalize, body weight was significantly (p<0.05) reduced for ducklings fed with diets containing AFB1 exceeding 200 ppb, resulting in wider Feed conversion ratio, similar to reports of earlier workers
(Han et al., 2008) where decrease in body weight of hens fed with 2.0 to 8.0 ppm levels of AFB1, were noted across juvenile stages.
Feed consumptions
There was significant (p<0.001) decrease in feed consumption (g/day) in AFB1- treated groups, throughout 1
st to 5
th week age compared to control (Fig 1). Depressing effect of toxins (AFB1) was noticeable in ducklings fed AFB1 @ 400 ppb, indicating that ducklings detested AFB1’s presence, with loss of appetite. The reduced cumulative feed consumption in both treated groups over control was probably due to impaired hepatic metabolism
(Verma et al., 2004).
Feed conversion efficiency
There was significantly-inferior feed efficiency (p≤0.05), in the toxin-treated ducklings (T
1 and T
2) during 2
nd to 6
th week of age (Fig 2). The poor feed conversion efficiency noted in both AFB1-groups in this study indicate that ducks are sensitive to mycotoxins with respect to feed efficiency that could be attributed to differences in source of contamination occurring in natural processes (
Pandey and Chauhan, 2007). The inferior feed efficiency was observed specifically in higher-toxin diet (400 ppb) which indicated the negative effect from cumulatively-higher amount of toxin on vital organs, in supporting exuberant muscle growth and metabolism, as normally due in case of meat-type ducks (Pekins). The FCR ranged from 1.23 to 4.95 during 1 to 6 weeks. The FCR of ducklings tended to remain wider, upon increase in AFB1 level in feed: T
2 (@400 ppb) as compared to T
1 (@ 200 ppb) against control. Similar findings were also reported by earlier workers (
Pandey and Chauhan, 2007;
Chen et al., 2016).
Live weight gain
The body weight gain of T
1 remained lowest, during the 2
nd week of rearing, where as the control group gained the highest live weight, during 4
th week of age (Fig 3). The T
2 remained lagging behind the other 2 groups, throughout course of study; where the growth performance remained lower in AFB1 treated groups, similar to patterns previously described by many authors
(Han et al., 2008; Khlangwis et al., 2011;
Murugesan et al., 2015;
Mahmood et al., 2017).
Serum biochemical analyses
There was significant increase (P<0.01) in levels of liver-function enzymes namely, ALT, AST and GGT for the AFB1 treated ducks, compared to control. The T
1 group’s liver enzyme status remained mid-way between control and T
2, showing a dose-dependent rise in these key enzyme’s levels in liver, probably as a sequalae to hepatocyte’s damage by Aflatoxin-B1
(Fernandez et al., 1994). Significant increases (P<0.01) in the level of Triglyceride and Cholesterolat 3
rd week and 6
th week upon impact from AFB1, was recorded (Fig 4), parallel to the findings of earlier workers
(Chen et al., 2014).
Gross and histopathology
Significant gross-pathological changes were observed (Fig 5) primarily across 3 vital organs,
i.e. liver, kidney and heart: but characteristic lesions were also visible on spleen too, which correlated well with available literature (
Madheswaran et al., 2005). There were changes in liver, signified by hepatomegaly with lesions, in ducklings fed with 400 ppb AFB1. Livers of T
1-ducklings revealed congestion with adjacent pale-patches and enlarged friable, loss of architecture with cloudy swelling and necrosis of hepatocytes; whereas in case of T
2 Liver, remarkable loss of architecture; necrosis with massive infiltration red blood cells (Fig 6) were prominent.
There was enlargement of kidney, at large, across all the specimens, with paleness evident in most samples drawn from T
1 (200 ppb) and T
2 (400 ppb). Nephrotic changes in kidney; including petechial hemorrhages, across whitish streaks (apparently from Uric acid deposits) were usual features of kidneys which were little-variant from those experienced across regular mortalities
(Monson et al., 2014). Similarly, against the normal histological factors observed in kidney from control groups, in case of T
1 kidney: slight degeneration of tubular epithelium with mild atrophy of glomerulus were noticeable and for T
2 Kidneys, distinct atrophy of glomeruli with necrosis of tubular epithelium were recorded. In T
1 spleen, mild congestion of red pulp with few nuclear debris and vacuoles were prominent; whereas across T
2 spleens, severe congestion of red pulp with Increase in Nuclear debris and vacuoles were evident.
The disturbed histopathological profiles across major necropsy specimens covering liver, spleen and kidney of the AFB1-treated pekin’s profile, as realized in this study have also been documented by many authors
(Chen et al., 2014; Peng et al., 2014), which concurs that: AFB1 at levels of 200 ppb, indeed constitutes a critical and vulnerable dose of AFB1.
Mortality and morbidity
The pattern of mortality in T
2 was in distinct contrast to that of T
1, where no mortality precipitated till 2
nd week of age. There was 25% mortality in T
2 alone in 2
nd week, apparently from poor-appetite and intense toxin-impact, which were similar to reports of Resanovic and Sinovec (2006). The mortality in T
1 occurred only after passage of 2
nd week, where the peak-mortality became visible during 5
th week of rearing. The T
1 had 10% mortality in 3
rd week, followed by a spurt in same (30%) during 5
th week, after which the mortality rate declined. Summarily, by 5
th week of age, the T
2 had suffered nearly double the mortality of T
1 (cumulative mortality: 80% versus 40%, Table 2), whereas mortality in both groups came down by 6th week of age (5% in each group), which signified rising tolerance of ducklings to AFB1 intakes to some extent. The control group did not evince any mortality, throughout the 6 weeks of dietary toxicosis.
The control group which did not shown any morbidity and had the highest uniformity in live weight, as inferred from coefficient of variation (Table 1). The T
2 remained highly morbid, with display of non-specific problems in gait (difficulty in walking), which precipitated into distinct lameness; besides poor growth; wide variation in live weight with signs of flightiness and nervousness
(Khlangwis et al., 2011). After 3
rd and 4
th week, T
1 revealed more variability compared to T
2, where Poor uniformity remained a hallmark of both AFB1-fed groups (C.V ranging: 21-29%) during morbid period. The control group maintained the best live-body weight across the entire trial period, where differences in live weight between the control and both toxin-groups remained significant (p<0.001) from 3
rd to 6
th week period
(Chen et al., 2014). The liveweight in T
1 across all ages vis a vis Control and T
2 indicated that morbidity in AFB1-fed groups acted in a dose dependent manner
(Murugesan et al., 2015). The sensitivity of ducks to AFB1, at different levels, in the diets have been reviewed by
Fouad et al., (2019), where AFB1-levels creating morbidity in ducks ranged from 20 to 1100 ppb. Our study reporting significant morbidity of ducks at 200 ppb AFB1 or above is well supported by the analogy from earlier authors
(Fouad et al., 2019), though ours varied a bit for the threshold of AFB1 @ 300 ppb reported by
Fin et al., (2012).
Aflatoxin induced leg deformities
It was observed beyond 3
rd week of growth that many surviving Pekins developed lameness, across the hock joints, in both T
1 and T
2, in varying proportion. Typically, these lame ducks continued to remain live with slower growth, but without much agility, where most deformities were irreversible, despite medical amelioration. Such lameness resulted from feeding of AFB1, could plausibly be attributed to decline in resistance of long-bones (femur and tibiotarsus) to breakage
(Maurice et al., 1983) or to changes in cholecalciferol metabolism for hepato and nephrotoxic nature of AFB1
(Huff et al., 1980), which are subject to further investigations.
