The clinical signs observed in the sub-clinical pregnancy toxaemic does were anorexia (100%), dullness in 10 (83%) and bruxism in 7 (58%). All the does were in a standing posture with normal carriage of head and neck and normal voiding of dung. In the clinical pregnancy toxaemic does the clinical signs observed were anorexia (100%), dullness in 10 (83%), bruxism in 7(58%), scanty dung in 12 (100%), acetone odour from mouth in 11 (92%), standing posture in 6 (50%), stargazing in 9 (67%), sternal recumbency (Fig 5) in 6 (50%) and lateral deviation of neck (Fig 6) in 5 (42%).
The body condition score (BCS) of pregnant does in control group ranged between 2.5 to 3. Among the sub-clinical pregnancy toxaemic does, eight (67%) had a BCS of 2.0 and four (33%) had 2.5, while in the clinical pregnancy toxaemic does, nine (75%) had a BCS of 2.0 and 2.5 in three (25%). The reason for the pregnancy toxaemic does to have a body condition score of 2.0 to 2.5 may be due to increased fat and protein catabolism as a result of severe under nutrition (
Rook, 2000). Body condition score should be included for effective monitoring of feeding and herd health management for the development of a healthy and productive herd (
Russel, 1984).
The BHBA concentration in blood of control group ranged between 0.2 mmol/l to 0.4 mmol/l, between 0.9 mmol/l to 1.5 mmol/l in sub-clinical pregnancy toxaemic does and between 2.1 mmol/l to 7.9 mmol/l in clinical pregnancy toxaemic does which were in accordance to
Andrews (1997). The values obtained in the portable ketone meter were immediate, reliable and highly useful in screening does for pregnancy toxaemia in field conditions. The portable human ketone meter can be successfully applied to estimate BHBA levels in field conditions due to the non-availability of other reliable spot tests
(Yadav et al., 2016).
Urinalysis of control group revealed absence of ketone bodies, glucose and protein, while presence of ketone bodies, protein and glucose are diagnostic for pregnancy toxaemia. Trace quantities of ketone bodies in the urine of 9 does (75%) and small quantities in 3 does (25%) of sub-clinical pregnancy toxaemic group, while trace in 2 (17%), moderate in 2 (17%), small in 4 (33%) and large in 4 (33%) in the urine of clinical pregnancy toxaemic group were observed. Presence of ketone bodies in urine might be due to the increased fat hydrolysis (
Cleon, 1988). Protein was completely absent in the urine sample of sub-clinical pregnancy toxaemic group, while the protein grading were 1+ in 3 does (25%), 2+ in 4 does (33%) and 3+ in 5 does (42%) in the clinical pregnancy toxaemic group. The glucose grading were trace in 6 does (50%) and 1+ grading in 6 does (50%) in the sub-clinical group, while the grading in clinical pregnancy toxaemic group were trace in 2 does (17%), 1+ in 1 doe (8 %), 2+ in 5 does (42%) and 3+ in 4 does (33%). The qualitative analysis of urine samples for the presence of ketone bodies, glucose and protein under field conditions can be carried out with accuracy and reliability using Multistix 10 SG reagent strips (
Emam and Galhoom, 2008).
The mean±SE values of haemoglobin, packed cell volume, red blood cells and white blood cells in control, sub-clinical and clinical pregnancy toxaemic groups are presented in (Table 1). Highly significant (p≤0.01) difference was observed in the haemoglobin, packed cell volume and red blood cell values between the sub-clinical and clinical pregnancy toxaemic groups compared to that of control group. The significant increase of the above values in the pregnancy toxaemic does may be due to haemoconcentration and dehydration
(Hefnawy et al., 2011).
The mean±SE values of differential count in control, sub-clinical and clinical pregnancy toxaemic groups are presented in (Table 2). Neutrophilia observed in sub-clinical and clinical pregnancy toxaemic group might be due to the increased cortisol level, which created a movement of granulocytes from the bone marrow to the peripheral blood
(Alidadi et al., 2012). The lymphopenia in sub-clinical and clinical pregnancy toxaemic group might be due to the toxic and sub-toxic concentration of BHBA and acetoacetate in blood, which inhibit the lymphocytic proliferation (
Franklin and Young, 1991) or may be due to increased cortisol level
(Alidadi et al., 2012). With respect to basophils a significant (p≤0.05) difference was observed between the sub-clinical and clinical pregnancy toxaemic group compared to that of control.
The mean±SE values of blood urea nitrogen (BUN), creatinine, aspartate aminotransferase (AST), alanine aminotransferase (ALT), glucose and total protein in control, sub-clinical and clinical pregnancy toxaemic groups are presented in (Table 3). A highly significant (p≤0.01) difference was observed between sub-clinical and clinical pregnancy toxaemic groups compared to control in BUN and creatinine levels. Elevated levels in sub-clinical and clinical pregnancy toxaemic groups concurred with
Hefnawy et al., (2011) and might be due to severe kidney dysfunction due to the elevated ketone bodies in general circulation (
El-Sayed and Siam, 1994), or reduced glomerular filtration due to fatty infiltration in tubular epithelium of kidney
(Barakat et al., 2007) or due to death and decomposition of fetuses
(Radostits et al., 2000).
A highly significant (p≤0.01) difference in AST and ALT levels was observed between sub-clinical and clinical pregnancy toxaemic groups compared to that of control. Elevated activity of the enzymes in sub-clinical and clinical pregnancy toxaemic does correlated with
Barakat et al., (2007) and might be due to the damage of the hepatic cells and release of cellular enzymes into circulation as a result of fatty infiltration of the liver due of adipolysis and hepatic ketogenesis following energy deficit
(Nassif et al., 2005).
With respect to glucose level a highly significant (p≤0.01) difference was observed between the clinical pregnancy toxaemic group and pregnant does of control group. The hypoglycemia observed in sub-clinical pregnancy toxaemic group might be due to long periods of starvation (
Andrews, 1997) or due to the increased demand for glucose by the developing twins or triplets or due to decreased hepatic gluconeogenesis and hypoglycemic effect by the increased level of BHBA level in blood, which can suppress endogenous glucose production and reduction in food intake (
Marteniuk and Herdt, 1988; Schlumbohm and Harmeyer, 2004). In the clinical pregnancy toxaemic group the glucose level was higher and equal in comparison to that of non-pregnant does. Four does (33%) of this group were presented in sternal recumbency with lateral deviation of neck and found to be >140 days pregnant with the aid of ultrasound. The fetal heart beats were absent in these four does which indicated fetal death. The blood β-hydroxybutyric acid and glucose levels monitored indicated BHBA levels >7 mmol/L (Fig 7) and abnormally high glucose levels (Fig 8). This correlated with
Lima et al., (2012), who stated hyperglycemia to occur with fetal death in advanced pregnancy toxaemia and the reason were attributed to the removal of the suppressing effect of the fetus on hepatic gluconeogenesis
(Wastney et al., 1983; Lima et al., 2012) or due to the increased serum cortisol level
(Ford et al., 1990). The mean glucose levels for the remaining eight does were 23.87±0.48 mg/dL, indicating hypoglycemia and correlated with
Rook (2000) and
Hefnawy et al., (2011).
A highly significant (p≤0.01) difference was observed in protein levels between the control and pregnancy toxaemic group. Decreased protein levels observed in sub-clinical and clinical pregnancy toxaemic does correlated with
Barakat et al., (2007) and
Hefnawy et al., (2011) and might be due to anorexia and reduction in albumin synthesis due to hepatic insufficiency and albuminuria (
Yarim and Ciftci, 2009) or malnutrition resulting in inadequate provision of amino acid substrate for general protein production
(Nasr et al., 1997).
The mean±SE values of sodium, potassium, calcium, magnesium and chloride in control, sub-clinical and clinical pregnancy toxaemic groups are presented in (Table 4). A highly significant (p≤0.01) difference in sodium levels was observed between the sub-clinical and clinical pregnancy toxaemic groups compared to that of control. Hyponatremia observed in the sub-clinical and clinical pregnancy toxaemic groups correlated with
Hefnawy et al., (2011) and might be attributed to the decrease in feed intake, dehydration or large quantity of sodium loss in the renal excretion of acetoacetate and BHBA (Judith and Thomas, 1988).
A highly significant (p≤0.01) difference in potassium levels was observed between sub-clinical and clinical pregnancy toxaemic groups compared to that of control. Hypokalemia observed in sub- clinical and clinical pregnancy toxaemic groups correlated with
Albay et al., (2014) and might be attributed to the decrease in feed intake and dehydration (
Judith and Thomas, 1988) or inadequate feed intake and incomplete renotubular absorption of potassium
(Henze et al., 1998), or lowered feed intake and loss of potassium ions in the urine as observed in human patients with ketonuria and ketoacidosis
(Lima et al., 2016).
A highly significant (p≤0.01) difference was observed in calcium levels between sub-clinical and clinical pregnancy toxaemic groups compared to the pregnant does of control. The hypocalcemia observed in pregnancy toxaemic does correlated with
Hefnawy et al., (2011) and may be due to the disturbance in the electrolytes and minerals which might be due to stress of starvation, dehydration, electrolyte imbalance or due to enhanced lipolysis (
Judith and Thomas, 1988). Alternate reasons might be due to the high demand of calcium by the developing offspring at the late stage of gestation, enhanced lipolysis as a result of high cortisol level in circulation, or fatty liver interfering with hydroxylation of Vitamin D and decreased intestinal absorption of calcium as pointed by
Andrews (1997) or anorexia and disturbance of acid base balance (acidosis) with the excretion of calcium ions in urine or might be the sequelae to renal insufficiency (
Rook, 2000).
A highly significant (p≤0.01) difference was observed in magnesium levels between sub-clinical and clinical pregnancy toxaemic groups compared to that of control. The hypomagnesemia observed in the pregnancy toxaemic does correlated with
Hefnawy et al., (2011) and may be due to the disturbance in the electrolytes and some minerals related to stress of starvation, dehydration, involvement of the kidney or due to enhanced lipolysis (
Judith and Thomas, 1988).
A highly significant (p≤0.01) difference in chloride levels was observed between sub-clinical and clinical pregnancy toxaemic groups compared to that of control. The hyperchloridemia observed in pregnancy toxaemic does correlated with
Abdallah et al., (2015) and the reasons might be due to the metabolic acidosis as a result of proportionally smaller loss of chloride than bicarbonate and improved renal reabsorption of chloride in response to decreased bicarbonate
(Kaneko et al., 1997).
The mean±SE values of serum BHBA (µmol/L), NEFA (µmol/L) and cortisol (nmol/L) concentration in control, sub-clinical and clinical pregnancy toxaemic groups are presented in (Table 5). A highly significant (p≤0.01) difference in serum BHBA concentration was observed between sub-clinical and clinical pregnancy toxaemic groups compared to that of control and correlated with
Ismail et al., (2008). Elevated levels of BHBA might be attributed to the oxidation of long chain fatty acids into ketone bodies,
viz., acetoacetate and beta hydroxy butyrate in the liver following lipolysis during periods of negative energy balance
(Nassif et al., 2005) or due to the reduction of acetoacetate produced by the liver to beta hydroxybutyrate by hydroxybutyrate dehydrogenase enzyme amounting to higher blood concentration of BHBA
(Hefnawy et al., 2011). Elevated levels of serum NEFA in the sub-clinical and clinical pregnancy toxaemic does correlated with
Ismail et al., (2008). Elevated levels of NEFA might be the result of adipolysis during periods of negative energy balance
(Vasava et al., 2016). A highly significant (p≤0.01) difference in serum cortisol concentration was observed between the sub-clinical and clinical pregnancy toxaemic groups compared to that of control. Increasing trend of cortisol concentration in pregnant and pregnancy toxaemic does correlated with
Hefnawy et al., 2011; Abdallah et al., 2015. Increase in cortisol concentration might be due to hyperactivity of the adrenal glands as a result of hypoglycemia
(Adel et al., 2005) or due to reduced hepatic metabolism of cortisol
(Radostits et al., 2000) or increasing stress in the pregnant animals (
Aly and Elshahawy, 2016).
The sub-clinical pregnancy toxaemic does responded to therapy and had a cure rate of 100%. The distribution of cases in clinical pregnancy toxaemic group is presented in (Table 6). Four does (33%) were presented in sternal recumbency with lateral deviation of neck and were found to be >140 days pregnant with the aid of ultrasound. The fetal heart beat were completely absent in these four does which indicated fetal death. The blood BHBA concentrations were >7 mmol/L (7.2 mmol/L, 7.6 mmol/L, 7.8 mmol/L and 7.9 mmol/L, respectively) and with abnormally high glucose levels (207 mg/dL, 78 mg/dL, 76 mg/dL and 132 mg/dL, respectively). The hyperglycaemia in advanced pregnancy toxaemic goats indicate fetal death and the reason were attributed to the removal of the suppressing effect of the fetus on hepatic gluconeogenesis
(Wastney et al., 1983; Lima et al., 2012) or to the increased serum cortisol level
(Ford et al., 1990). They were resorted to treatment with intravenous glucose therapy (5% Dextrose) supported with Vitamin B
1 B
6 and B
12 and antihistaminic drug chlorpheniramine maleate @ 0.5 mg/kg body weight intramuscularly on the day of presentation. The owners were advised caesarean section in order to save the dam, of which two of the owners did not accept and decided to dispose off, while the remaining two does died later in the evening before the owners decided to accept for the caesarean section. Parturition induction or caesarean section is the recommended treatment in advanced stages of pregnancy toxaemia or in pregnant does that did not respond to the treatment due to the high glucose demand or in fetal death to save the dam
(Brounts et al., 2004; Lima et al., 2012). The remaining eight does (67%) were in between 120 to 140 days of pregnancy, among which four had blood BHBA concentration of 3.6 mmol/L, 3.8 mmol/L, 5.2 mmol/L and 6.7 mmol/L, respectively. Out of these four does, two had BHBA levels above 5 mmol/L and were presented in sternal recumbency and the one with BHBA level of 6.7 mmol/L had lateral deviation of the neck in addition to sternal recumbency. Both the does had a feeble fetal heart beat and were resorted to treatment with intravenous glucose therapy (5% Dextrose) supported with parenteral Vitamin B
1, B
6 and B
12 therapy. However both the does died the next day. The remaining two had blood BHBA concentration of 3.6 mmol/L and 3.8 mmol/L, respectively, and were presented in standing posture with stargazing. They were resorted to above treatment and oral administration of glycerine for 3-4 days @ 25 ml twice daily. These two does did not show much sign of recovery even after three days of therapy and hence the owners resorted to disposal of their does.
The remaining four does of the group (between 120 to 140 days of pregnancy) had BHBA concentration of 2.1 mmol/L, 2.2 mmol/L, 3.1 mmol/L and 3.5 mmol/L, respectively and were presented in standing posture. They were resorted to standard treatment. These does showed signs of recovery from third day of treatment in the form of alertness and improved feed intake. Out of the twelve does of clinical pregnancy toxaemic group, only four does showed signs of improvement to therapy with a cure rate of 33%, while the mortality was present in four (33%). The remaining four (33%) did not show any signs of recovery to therapy and hence the owners resorted to disposal of their does.
