




































In ternationa l
Scholars
Journa ls

 

African Journal of Pig Farming ISSN 2375-0731 Vol. 8 (3), pp. 001-009, March, 2020. Available online at 
www.internationalscholarsjournals.org © International Scholars Journals 

 

Author(s) retain the copyright of this article. 

 

Full Length Research Paper 

 

Posterior paresis in pregnant gilts experimentally 
infected with Trypanosoma brucei 

 
Lushaikyaa Allam1, David Ogwu2, Rowland Ibrahim Shehu Agbede3 and Anthony 

Kojo Bedu Sackey2
 

 
1
Veterinary Teaching Hospital, Ahmadu Bello University, Zaria, Kaduna, Nigeria. 

2
Department of Veterinary Surgery and Medicine, Ahmadu Bello University, Zaria, Kaduna, Nigeria. 

3
Department of Veterinary Parasitology and Entomology, Ahmadu Bello University, Zaria, Kaduna, Nigeria. 

 
Accepted 14 October, 2019 

 
The effect of Trypanosoma brucei infection on reproductive efficiency in gilts (n=12) was conducted. 
The gilts were bought as piglets aged eight weeks from piggeries in Samaru village in Zaria, Nigeria. On 
attaining puberty, the gilts were divided into experimental and control groups, each group containing 
six animals. All the gilts were subsequently bred by fertile boars and they were confirmed pregnant. The 

pregnant gilts were then inoculated with about 1.8 × 10
6
 trypanosomes via the anterior vena cava. The 

infected gilts developed clinical trypanosomosis after a pre-patent period of 2 to 3 days. The clinical 
signs observed were intermittent fever, short and moist cough, moist rales, mucopurulent ocular 
discharges, hyperaemia of the skin, reduced feed intake, loss of body condition, recumbency, 
uncoordinated movements, posterior paresis, loss of pregnancy and death. Severe degeneration of the 
fibers of the hamstring muscles was observed along with elevated levels of serum potassium, aspartate 
amino transferase and creatine kinase. 

 
Key words: Trypanosomosis, infection, pregnant gilts. 

 
 
INTRODUCTION 

 
The physiology of animals alters when they are infected 
with trypanosomosis (Biryomumaisho et al., 2003). This is 
usually due to the wide range of biochemical changes 
that take place in the infected animals (Katunguka– 
Rwakishaya, 1996). Hematological aberrations do occur 
in animals infected with trypanosomes (Anosa and Isoun, 
1980; Singla and Juyal, 2000). The severity of the 
hematological and biochemical changes that take place in 
infected animals is determined by the strain of the 
infecting trypanosome and the host (Anosa, 1983a, b). 
The evaluation of blood indices and parameters is 
required to enable the health status of animals to be 
determined (Coles, 1986). This gives an indication of the  
 
 

 
*Corresponding author. E-mail: doclu64@gmail.com. Tel: +234-
803-701-2731. 

 
 
 
 

 
degree of degenerative changes that have occurred to 
host tissues as well as the severity of the infection 
(Otesile et al., 1991).  

Pigs like other domestic livestock are infected with 
several species of trypanosomes. The trypanosomes that 
cause infections in pigs are Trypanosoma simiae, 
Trypanosoma brucei Trypanosoma congolense and 
Trypanosoma suis (Losos, 1986; Sekoni, 1994; Seifert 
1996). Infections in pigs by T. brucei have been reported 
to cause nervous signs (Otesile, 1992; Onah and 
Ozuokwu 1991), uncoordinated movements and posterior 
paresis characterized by wobbling of the hind-legs 
(Mumah, 1996; Allam, 2004). The posterior paresis 
interfered with mating efficiency of gilts (Allam et al., 
2006). This paper intends to report the cause of the 
posterior paresis that was noticed in pregnant gilts 
infected with T. brucei along with other pathogenic effects 
of this parasitic infection. 



 
 
 

 
MATERIALS AND METHODS 
 
Experimental animals 
 
Twelve cross breed piglets aged eight weeks were bought from 
piggeries in Samaru village in Sabon gari Zaria Local Government 
Area of Kaduna State, Nigeria. They were housed in clean fly proof 
pens in the Faculty of Veterinary Medicine, Ahmadu Bello University 
Zaria, Nigeria. Base line hematological data of the piglets were 
obtained on arrival and they were screened for endo and ecto 
parasites. The piglets were subsequently ear notched for 
identification and treated for nematodes and ectoparasites with 
Ivermectin (Ivomec®), at 200 µg/kg body weight sub-cutaneously. 
The piglets were fed compounded diet of 18% crude protein 
(composition: maize 36.8%, soya bean 5%, ground nuts 23.5%, rice 
bran 30%, beniseed 2%, bone meal 2%, premix 0.2%; table salt 
0.5%) and water was provided ad libitum. 

 

Strain of T. brucei used 
 
The T. brucei used in this present study was obtained from the 
Nigerian Institute of Trypanosomiasis Research Vom, Nigeria. It 
was originally isolated from a pure natural infection in cattle in 
Federe, Kaduna State Nigeria. The parasite was inoculated into 2 
mice and transported to the Faculty of Veterinary Medicine, 
Ahmadu Bello University Zaria, Nigeria. 

 

Inoculation of animals 
 
When the gilts were 7 months old, they were randomly divided into 
two groups of 6 experimental and 6 controls. About 2 ml of the 

infected rat blood containing approximately 1.8 × 10
6
 T. brucei 

organisms were inoculated into each animal in the experimental 
group via the anterior vena cava while the ones in the control group 
were left intact. Following inoculation, all the gilts were clinically 
examined, weighed and their blood samples collected daily using 
EDTA as anticoagulant. The blood was examined for levels of 
parasitaemia, packed cell volume (PCV) and serum biochemical 
parameters. The values obtained were recorded daily along with 
their weights and rectal temperatures. This continued until all the 
infected animals were positive for trypanosomes. Subsequently, all 
the gilts were clinically examined weighed and their blood collected 
weekly to determine PCV levels, parasitaemia, and serum 
biochemical parameters until the experiment was terminated. 

 

Gross pathological examination 
 
Post mortem examination was carried out on the infected gilts that 
died during the study and also on the remaining ones that were 
sacrificed at the end of the experiment. 

 

Histo-pathological examination 
 
The samples of the heart, brain and hamstring muscles were 
obtained from all the infected pigs. They were put into appropriately 
labeled bijou bottles and fixed in 10% formalin. The tissues were 
dehydrated and processed in tissue wax embedded in paraffin and 
were subsequently cut in to 5 µm thickness on slides and stained 
with hematoxyline and eosin. The slides were eventually examined 
using a light microscope. 

 
Statistical tests used 
 
Data obtained from the study were analyzed using student t test. 

 
 
 
 

 
Values of p<0.05 were considered to be statistically significant 
(Chatfield, 1983). 
 

 

RESULTS 

 
Clinical observations 

 

All the pigs developed clinical trypanosomosis after a 
pre-patent period of 2 to 3 days. There was a steady 
increase in the levels of parasitaemia of the infected gilts 
which was followed by fluctuations. Peak parasitemia 
was recorded between days 7 and 35 post infection (pi) 
(Figure 1).  

The rectal temperatures of all the infected gilts 
increased during the course of the infection. This was 
also followed by fluctuations. The highest mean 
temperature attained by the infected gilts was 40.3ºC. 
During this period, the temperatures of the animals in the 
control group were within the normal range. The 
difference in the ranges of temperature between infected 
and the control animals was significant (p<0.05) (Figure 
2).  

There was a gradual decrease in the PCV of the 
infected gilts. This was first noticed on day 14 pi in one of 
the pigs. The lowest PCV value recorded during the 
experiment was 17%, the mean PCV values of the 
infected animals were significantly different from those of 
the control (p<0.05) (Figure 3).  

The infected animals from day 28 pi were observed to 
be gaining less weight than the ones in the control group. 
The infected animals were gaining an average of 0.71 kg 
every two weeks whereas the controls were gaining an 
average of 1.5 kg during the same period. By day 42 pi, 
the infected animals started losing weight while the 
control gained weight steadily (Figure 4). The difference 
in the weights between the infected and the control 
groups was found to be statistically significant (p<0.05).  
Other clinical signs observed in the infected gilts were 
pale mucus membranes, short and moist cough, moist 
rales, mucopurulent ocular discharges, hyperemia of the 
skin, reduced feed intake, recumbency, uncoordinated 
movements, posterior paresis, loss of pregnancy and 
death.  

During the study, the mean aspartate amino 
transferase (AST) levels of the infected pigs increased 
significantly from day 35 pi and its level remained 
elevated until the end of the study. The highest mean 
level of 60.6 I.U/L was recorded on day 91 pi (Figure 5).  

The mean serum levels of creatine kinase (CK) 
increased progressively from day 21 pi till the end of the 
experiment in the infected animals. The highest mean 
level recorded for this enzyme was 856.7 I.U/L on day 42 
pi. The values of CK were significantly different from 
those of the control animals (p < 0.05) (Figure 6).  

The mean serum values of potassium in the infected 
gilts increased progressively during the study. This 



   
 
 
 
 
 
 
 
 
 
 

 

M
e

a
n
 p

a
ra

s
it
e

m
ia

 (
+

) 

 
 
 
 
 
 
 
 
 
 
 

 
Days pre and post infection 

 
Figure 1. Mean parasitemia of T. brucei Infected gilts.  

 
 
 
 
 
 
 
 
 
 
 
 

 

T
e

m
p

e
ra

tu
re

 v
a
lu

e
s
 (

ºC
) 

 
 
 
 
 
 

 
Days pre and post infection 

 
Figure 2. Mean temperature changes of T. brucei Infected and control gilts.



  
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

 

Days pre and post infection 
 

Figure 3. Mean packed cell volume of T. brucei Infected and control gilts.  
 
 
 
 
 
 
 
 
 
 
 
 
 
 

B
o
d
y
  

w
e
ig

h
t 
 (

K
g
s
) 

 
 
 
 
 

 

Days pre and post infection 
 

Figure 4. Mean body weight changes of T. brucei Infected and control gilts. 



   
 
 
 
 
 
 

 

A
s
p

a
rt

a
te

 a
m

in
o
 t
ra

n
s
fe

ra
s
e
 l
e

v
e
l 
(i
. 
u

.)
 

 
 

 

Days pre and post infection 
 

Figure 5. Mean aspartate amino transferase levels of control and T.brucei infected gilts.  
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

 
Figure 6. Mean creatine kinase levels of control and T. brucei Infected gilts. 



 
  
 
 
 
 
 
 
 
 
 

 

P
o
ta

s
s
iu

m
 l
e
v
e

ls
 (

m
m

o
l/
L

) 

 
 
 
 
 

 

Days pre and post infection 
 

Figure 7. Mean potassium levels of control and T. brucei infected gilts. 
 
 

 

increase started on day 14 pi. The highest mean level 
recorded was 8.6 mmole/ L on day 63 pi. These levels 
were significantly different from those of the control 
animals (p < 0.05) (Figure 7). 
 

 

Histopathological lesions 

 

Severe inflammatory lesions were observed in the heart 
of the infected gilts (Figure 8). In some cases, necrosis of 
the myocardium with massive mononuclear cellular 
infiltration was observed. The blood vessels in the 
cerebrum were congested (Figure 9). The fibers of the 
hamstrings muscle were degenerated. The perimysial 
tissue of the muscles had widened and had become 
edematous (Figure 10). 
 

 

DISCUSSION 

 

The increase in AST levels noticed in this study agrees 
with the results obtained during an infection in sheep by 
T. brucei (Taiwo et al., 2003), T. vivax infection of cattle 
and sheep (Gray, 1963), T. congolense infection of goats 
(Adah et al., 1992), and also in dogs infected with T. 
brucei (Omotainse et al., 1994). However, it contradicts 

 
 
 

 

observations were made by Taiwo et al. (2003) during an 
infected of sheep with T. congolense.  

The increase in the levels of CK agrees with results 
obtained in a T. cruzi infection in mice (Cano et al., 
2000), but disagrees with results obtained by (Lunkins, 
1992; Chaudhary and Iqbal 2000), who observed no 
change in CK values in animals with trypanosomosis.  

The causes of elevation of AST levels in the serum of 
animals are necrosis of the liver, skeletal muscles and 
kidneys, whereas CK is increased in skeletal muscle 
disease, myocardial injury or necrosis and cerebral 
cortical necrosis (Lording and Friend, 1991). 
 

 

Conclusion 

 

In this study, the increase in AST and CK levels in the 
infected gilts could only have been due to the 
degeneration of skeletal muscle fibers that was observed 
histopathologically. Even though histopathological lesions 
were also observed in the heart and brain of the infected 
animals, they were not that severe as to cause the 
increase in the levels of AST and CK as was noticed in 
this experiment.  

The hyperkalemia that was noticed is suggestive of 
massive leakages of this electrolyte from the skeletal 
Days pre and post infection 
 



   
 
 
 
 
 
 
 

 

M 

 
 
 
 
 
 
 
 
 
 

 

M 

 
 
 
 
 

 
Figure 8. Photomicrograph of the heart of a T. brucei infected gilt. Note the mononuclear cellular 
infiltration (M). H and E X 303.  

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

Figure 9. Photomicrograph of the brain of a gilt infected with T. brucei. Note the congestion of the 
cerebral blood vessels (arrows). H and E X 303. 



  
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

 

F 

P
 

 
 
 
 
 
 
 
 
 
 
 

 

Figure 10. Photomicrograph of the transverse section of the Hamstrings muscle of a gilt infected with T. brucei. Note the 
degeneration of muscle fibres in the fascicule (F) with widened and edematous perimysial tissue (P). H and E X147. 

 
 

 

muscles that were damaged during this infection. The low 
levels of this electrolyte in the skeletal muscles could 
have caused the decrease in neuromuscular excitability 
of the muscles.  

The pathology in the hampstring muscles could have 
caused the posterior paresis and the wobbling that was 
observed in the infected gilts. However, whether this 
abnormality could be reversed in treated cases or how 
the trypanosomes could have caused this problem was 
not within the scope of this study. Further studies in these 
areas are therefore recommended. 
 
 
REFERENCES 
 
Adah MJ, Otesile EB and Joshua RA (1992). Changes in level of 

transaminases in goats experimentally infected with T. congolense. 
Rev d’ Elev. Me’d Vet. Pays Trop., 45 (3-4): 284-286.  

Allam L (2004). The effect of Trypanosoma brucei infection on 
reproduction in female pigs. MSc Thesis, Ahmadu Bello University 
Zaria. 

Allam L, Ogwu D, Agbede RIS and Sackey AKB (2006). Clinical and 
mating problems in gilts experimentally infected with Trypanosoma 
brucei. J. Trop. Bios., 6: 28-31.  

Anosa V0 (1983b). Mammalian blood cells in health and in 

 
 
 

 
trypanosomiasis. Trop. Vet., 1: l77- 199.  
Anosa V0 (1983a). Diseases produced by Trypanosoma vivax in 

ruminants, horses and rodents. Zent fur Vet B, 30 : 717-741.  
Anosa VO, Isoun TT (1980). Haematological studies on Trypanosoma 

vivax infection of goats and intact and splenectomised sheep. J. 
Comp. Path., 90: 155-168.  

Biryomumaisho S, Katunguka-Rwakishaya E, Rubaire-Akiiki CM (2003). 
Serum biochemical changes in experimental Trypanosoma 
congolencse and Tryapanosoma brucei infection in small east African 
goats. Vet. Arhiv., 73 (3): 167-180.  

Cano RC, Hliba E, Rubilo ER (2000). Creatine kinase and lactate 
dehydrogenase levels as potential indicators of Trypanosoma cruzi 
infectivity and histotropism in experimental Chagas' disease. 
Parasitol. Res. 86:244-252.  

Chaudhary ZI, Iqbal J (2000): Incidence, biochemical and 
haematological alterations induced by natural trypanosomosis in 
racing dromedary camels. Acta Trop., 77, 209-213.  

Coles EH (1986). Veterinary Clinical Pathology. Edition Published by 
W.B. Sounders Company Philadelphia, London, Toronto, Mexico City 
Rio de Janeiro, Sydney, Tokyo Hong Kong, 4: 1-486.  

Gray AR (1963). Serum transaminase levels in cattle and sheep 
infected with Trypanosoma vivax. Exp. Parasitol., 14: 374-381.  

Katunguka-Rwakishaya E (1996). The prevalence of trypanosomosis in 
small ruminants and pigs in a sleeping sickness endemic area of 
Buikwe country Mukono district, Uganda. Rev d’ Elev. Me’d Vet. Pays 
Trop., 49: 56-58.  

Lording PM, Friend SCE (1991). Data analyasis guide. Interpretation of 
laboratory results. Austral. Vet. Pract., 21 (4): 186-195. 



 
 
 

 
Losos GJ (1986). Infectious Tropical Diseases of Domestic Animals. 

Longman Scientific and Technical, published in Association with the 
International Development Research Centre, Canada, pp. 182-318.  

Luckins AG (1992): Protozoal diseases of camels. Proceedings of the 
First International Camel Conference Dubai, United Arab Emirate, pp. 
23-27.  

Mumah ET (1996). The Pathogenicity of Trypanosoma brucei brucei of 
Cattle origin in experimentally infected piglets. MSc thesis, Ahmadu 
Bello University Zaria.  

Omotainse SO, Anosa VO, Falaye C (1994). Clinical and biochemical 
changes in experimental Trypanosoma brucei infection of dogs. Isrl J. 
Vet. Med., 49: 36-39.  

Onah DN, Uzoukwu M (1991). Porcine cerebral Trypanosoma brucei 
brucei trypanosomiasis. Trop. Anim. Health. Prod., 23 (1): 39-44.  

Otesile EB, Akpavie SO, Fagbemi BO, Ogunremi AO (1991). 
Pathogenicity of Trypanosoma brucei brucei in experimentally 
infected pigs. Rev d’ Elev. Me’d Vet. Pays Trop., 44 (3): 279-282.  

Otesile EB, Fagbemi BO, Makinde MO, Akinboade OA (1992). The 
response of pigs experimentally infected with T. brucei to 
Isomethamedium® chloride therapy in relation to nutrition. Vet-Quart, 
14 (3): 88-91. 

  
  

 
 

 
Seifert SHH (1996). Vector born disease: Trypanosomosis. In: Tropical 

Animal Health. Edited by Kluver Academic Publishers, 152-169.  
Sekoni VO (1994). Reproductive disorders caused by animal 

trypanosomosis. A Review Therio. 42: 557-570.  
Singla LD, Juyal PD (2000). Blood cellular responses in Trypanosoma 

evansi infected and levamisole treated bovine calves. J. Vet. 
Parasitol., 14: 137-139, 2000  

Taiwo VO, Olaniyi MO, Ogunsanmi AO (2003). Comparative plasma 
biochemical changes and susceptibility of erythrocytes to in vitro 
peroxidation during experimental Trypanosoma congolense and 
Trypanosoma brucei infections in sheep. Isrl J. Vet. Med., 58 (4): 1-
10. 


