Effect of experimental infection of Trypanosoma congolense on the packed cell volume of Dutch belted rabbits and its implication

doi:10.21203/rs.3.rs-2106175/v1

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Effect of experimental infection of Trypanosoma congolense on the packed cell volume of Dutch belted rabbits and its implication

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Effect of Trypanosoma congolense infection on Packed Cell Volume (PCV) of Dutch belted (does) rabbits was investigated. Sixteen Dutch belted rabbits weighing between 1.6 and 1.8 kg were grouped into two of eight each. Following intraperitoneal inoculation with T. congolense, PCV, total leucocyte count (TLC), rectal temperature (RT), heart rate (HR), body weight (BW) were assessed, as well as the level of parasitaemia. Mean PCV of infected rabbits were 36.0 ± 0.53%, 35.3 ± 0.19%, and 28.0 ± 0.89% while that for uninfected were 40.8 ± 0.11%, 41.8 ± 0.19%, and 41.3 ± 0.08% at days 18, 25 and 58 post inoculation (PI) respectively. Mean TLC of infected group were 5.5 ± 0.08 x10⁹/L, 3.9 ± 0.08 x10⁹/L and 3.4 ± 0.09 x10⁹/L while that for uninfected were 5.9 ± 0.05, 4.2 ± 0.08, and 3.5 ± 0.09 at days 18, 25 and 58 respectively. Mean RT of infected were 38.3 ± 0.07⁰C, 39.2 ± 0.09⁰C and 39 ± 0.10⁰C while that for uninfected were 38.0 ± 0.12⁰C, 38.2 ± 0.11⁰C and 38.8 ± 0.08⁰C at days 18, 25 and 58 PI respectively. Mean HR of infected were 141 ± 0.96/bpm, 143 ± 1.22/bpm and 144 ± 1.13/bpm while that for uninfected were 149 ± 0.59/bpm, 144 ± 0.94/bpm and 149 ± 1.27/bpm at days 18, 25 and 58 respectively. Mean BW of infected were 1.7 ± 0.07kg, 1.5 ± 0.07kg and 1.6 ± 0.06kg while that for uninfected were 1.6 ± 0.07kg, 1.6 ± 0.07kg and 1.80 ± 0.07kg at days 18, 25 and 58 PI respectively. PCV of infected was significantly (P < 0.05) lower as compared to uninfected group at days 18, 25 and 58 of the study. Parasitaemia was detected at 6th day PI and remained high to the end of the study. The study suggest use of haematinics and anti-pyrexia in the disease management for rabbits.

Trypanosoma congolense

packed cell volume

Dutch belted

Rabbits

Africa

African Trypanosomes are protozoan parasites transmitted by various species of the genus Glossina. They cause devastating medical, veterinary, and socioeconomic disorders that have a negative impact on Sub-Saharan Africa's economic development (Aksoy et al. 2017). Each parasite species is adapted to certain climatic and ecological parameters that correspond to the habitat of the tsetse fly vector (Glossina spp.), often known as the "belt" of tsetse flies (Shaw et al. 2014). In humans, the disease is known as "sleeping sickness" or human African trypanosomiasis (HAT) and "nagana" or animal African trypanosomiasis (AAT) in domestic animals (Courtin et al. 2008). HAT is caused by two distinct Trypanosoma brucei subspecies: Trypanosoma brucei gambiense (chronic form) found in western and central Africa, and Trypanosoma brucei rhodesiense (acute form) prevalent in eastern and southern Africa (Ruiz et al. 2015). T. congolense, T. brucei, and T. vivax are the most common trypanosomes that cause disease in domestic animals in Sub-Saharan Africa (Morrison et al. 2016). The camel trypanosome, Trypanosoma evansi, and the horse trypanosome, Trypanosoma equiperdum, have both been linked to animal diseases (Morrison et al., 2016). The bovidae and suidae families of game animals are major reservoirs of infections with minor clinical indications, but the disease in domestic animals is severe often with high fatality (Yaro et al. 2016). Tsetse flies inoculate metacyclic trypanosomes into the skin of the susceptible host, infecting the animal. Anemia is the most prevalent immunopathological disease-related characteristic and the leading cause of death among Nagana patients (Naessens 2006).

The severity of infection with various species of trypanosomes is dependent on the parasite’s highly sophisticated immune escape mechanisms, which allow them to manipulate the entire host immune response to evade elimination via antigenic variation of the variant surface glycoprotein (VSG) (Stijlemans et al. 2016). This antigenic polymorphism allows the parasite to evade the immune system of the host and generate long-term infections. The disease condition is exacerbated by the fact that each species has a vast number of strains capable of disclosing diverse stocks of changeable antigens. They are extracellular hemoprotozoa that use a variety of evasion mechanism to stay alive in the host's bloodstream, such as antigenic variation of the variable surface glycoprotein (VSG), immunosuppression, and polyclonal B cell activation (Henry et al., 2004). The most common pathogen in livestock is Trypanosoma congolense (Henry et al. 2004). Studies have demonstrated phagocytosis of T. brucei or T. congolense by macrophages in the presence of immunological sera in- vitro using Giemsa stain or electron microscopy (Henry et al. 2004). The parasite was discovered to be eliminated from the circulation by VSG – specific antibody in mice experimentally infected with T. brucei, and the liver was determined to be the major organ of clearance (Henry et al. 2004).

In Africa, trypanosomiasis is a serious threat to livestock production causing severe debilitation on animals presenting mainly as rough hair coat, loss of weight and emaciation. The infection has been identified as the largest impediment to livestock development in tropical Africa due to lack of productive animals in terms of meat/milk production and draft power (WHO 2001). Report indicates that roughly forty African countries impacted by the disease are underdeveloped, destitute, deeply indebted, and food-deficient, resulting in an annual economic loss of about $5 billion US dollars (Giordani et al. 2016). Similarly, in both humans and animals, various haematological disorders have been linked to trypanosomiasis. Immune complex responses, red cell fragmentation (Suliman and Feldman 1989), and haemodilution (Egbe – Nwiyi et al. 2005) are among them. However, several investigations have used Trypanosoma vivax or Trypanosoma brucei, and have been carried out in rats, cattle, sheep, and goats but scanty work exists in rabbits.

In Nigeria, rabbit is a non-traditional meat source in many households and its husbandry is becoming increasingly important for a variety of reasons, including its low initial investment and high fecundity, trypanotolerant rabbits would result in increased rabbit production and more protein available to the population. Therefore, this study aimed to assess effect of experimental infection with Trypanosoma congolense on the packed cell volume (PCV) of Dutch belted rabbits.

1.2.1 Source of trypanosome

The Trypanosoma congolense (Kaura strain) used for the study was isolated from cattle in Kaduna State. It was frozen in liquid nitrogen and thawed at Faculty of Veterinary Medicine, University of Abuja. It was passage in mice. These mice's samples were separated and re-passage into other mice, where they were allowed to develop for thirteen days before infection.

1.2.2 Animals and experimental infection

Sixteen Dutch belted rabbits (does) between the ages of 7 and 12 months were purchased from the experimental animal unit of the Faculty of Veterinary Medicine, University of Abuja. The experiment was guided by the principles of the Laboratory Animal Care (CACC 1993). The rabbits were housed in fly-proof conventional rabbit cages in the laboratory animal house of Department of Parasitology and Entomology, University of Abuja. Commercial layers pelletized poultry feed (guinea feed®) was fed to them and fresh water was available ad libitum. The rabbits were acclimatized for two weeks, during which time they were given normal health checks that included packed cell volume (%), total leucocyte count (x10ᶺ3/L), rectal temperature (⁰C), heart rate (/min) and body weight (g). The rabbits were divided into two groups of eight rabbits each, infected (T) and control (C) groups. The rabbits were inoculated via intra-peritoneal with 1 ml Trypanosoma congolense suspension equivalent to 4 x10⁹ trypanosomes in diluted mouse blood used as a donor as described by Eisler et al. (2001).

1.2.3 Preparation and analysis of samples

A clinical thermometer and a stethoscope were used to assess rectal temperature and heart rate respectively on a daily basis. Parasitaemia was confirmed by wet mount of blood collected from the rabbits' ear veins on alternate days (Herbert and Lumsden 1976). On days 18, 25, and 58 post infection, blood was taken from the rabbits' ear veins into ethylene diamine tetra acetic acid (EDTA) tubes to determine Packed Cell Volume (PCV) using the microhaematocrit method and total leucocyte count (TLC) was assessed using haemocytometer (Schalm et al. 1975). A suspended scale and sac were used to weigh all of the rabbits on days 18, 25, and 58 post infection. Wet mount was used to estimate parasitaemia on a weekly basis. Parasitaemia was graded by number of parasites/field.

= zero parasites/field

+ = 1-10/field

++ = 11-50/field

+++ = 51-100/field

++++ = >100/field

1.2.4 Data analysis

Data collected were analyzed using the T-Test (independent samples test) in SPSS version 23 and the difference was regarded significant at P < 0.05 (Bamgboye 2002). Data are presented as Mean ± Standard Error of Mean (SE).

The parameters monitored during the 2 weeks stabilization of the rabbits recorded mean values of Packed Cell Volume (41.3±0.03% - 42.3±0.04%), Total Leucocyte Count (5.2±0.05 x10⁹/L - 5.3±0.03 x10⁹/L) Rectal temperature (38.4±0.06⁰C–38.6±0.06⁰C), Heart rate (143.0±0.71/bpm –145.0±56/bpm), and Body weight (1.7±0.04kg – 1.7±0.03kg) respectively. The clinical parameters evaluated showed the values were within the normal range, an indication that the rabbits used in the study were in good health (Table 1).

The mean PCV of the infected rabbits were 36.0±0.53%, 35.3±0.19% and 28.0±0.89% while mean the mean PVC of the control were 40.8±0.11%, 41.8±0.19% and 41.3±0.08% at days 18, 25 and 58 respectively. There was a significant (P< 0.05) decrease in the PCV of the rabbits on day 18, 25 and 58 post infection until the end of the trial (Table 2).

The mean TLC of the treated rabbits were 5.5±0.08 x10⁹/L, 3.9±0.08 x10⁹/L and 3.4±0.09 x10⁹/L while the mean TLC of the control were 5.9±0.05x10⁹/L, 4.2±0.08x10⁹/L, and 3.5±0.09x10⁹/L for days 18, 25 and 58 respectively. The mean TLC did not show any significant difference (P< 0.05) between the infected rabbits and control rabbits post inoculation (Table 3).

The mean RT of the infected showed 38.3±0.07⁰C, 39.2±0.09⁰C, and 39±0.10⁰C while the mean RT for the control are 38.0±0.12⁰C, 38.2±0.11⁰C and 38.8±0.08⁰C at days 18, 25 and 58 respectively. The rectal temperature of rabbits fluctuated post inoculation with the infected rabbits showing higher values at day 25 post infection, however, there was no significant difference recorded (Table 4).

The mean HR of the infected rabbits were 141±0.96/bpm, 143±1.22/bpm, and 144±1.13/bpm, while the mean HR of the control were 149±0.59/bpm, 144±0.94/bpm, and 149±1.27/bpm, at days 18, 25 and 58 respectively. There was no significant difference (P>0.05) recorded between the mean HR of the infected and control rabbits (Table 5).

The BW of the infected rabbits were 1.7±0.07kg, 1.5±0.071kg and 1.6±0.06kg while the control were 1.6±0.07k1.6±0.07kg and 1.80±0.07kg at days 18, 25 and 58 respectively. The mean body weights of the control rabbits were higher than that of the infected group at days 25 and 58 post inoculation, however, no significant difference (P> 0.05) was recorded between (Table 6).

Six days post inoculation, trypanosomes were found in the blood samples of infected animals. From the day of parasite inoculation to the 5^th day, no parasite was found in the blood. The parasites multiplied as the disease progressed and was observed from the 6^th day post inoculation until the end of the trial. Wet mount revealed nucleated red cells, while mature red cells in infected samples lost their peripheral redness. Fragments of red blood cells were found. The level of parasitaemia was represented based on the number of trypanosomes found in the microscopic field (Table 7).

Anemia is a common pathological features associated with trypanosomiasis as was observed under the current study. This corresponds to the findings of (Toma et al. 2008). Anemia developed in Typanosoma congolense-infected rabbits, as shown by lower PCV levels all through the investigation. This is consistent with the findings of Egbe – Nwiyi et al. (2005), who reported that the PCV levels in all infected rats reduced significantly (P<0.05) when compared with the values in uninfected control rats. According to Leigh and Fayemi (2010), our base line results were within the typical PCV range of rabbits. Anemia became more severe when PCV levels dropped. Toma et al. (2008), found anemia in rabbits infected with T. congolense as demonstrated by pale mucous membranes. In rats infected with T. congolense, anemia has also been recorded (Egbe- Nwiyi et al. 2005; Henry et al. 2004). RBCs from infected mice had increased osmotic fragility and a different fatty acid membrane composition than RBCs from non-infected mice, according to studies (Cnops et al. 2015). It was also observed that the change in RBC fragility was not caused by interferon (IFN), but rather by host-derived factors such as tumor necrotic factors (TNF), which M1 cells produced (Balogun et al. 2014; Szempruch et al. 2016). Additionally, parasite-derived substances such as sialidases in T. congolense infections and extracellular vehicles (EVs) in T. brucei infections may contribute to RBC alteration and hence facilitate elimination (Nok and Balogun 2003; Szempruch et al. 2016). Anemia is one of the most prominent symptoms of Trypanosoma congolense infection, a vascular parasite (Losos and Ikede 1972). The mechanisms by which the parasite causes anemia are complex and not fully understood, but they most likely include differences in erythropoietic potential and hemodilution (Naessens 2006), factors involved in erythrolysis (Rifkin and Landsberger 1990), eryhtrophagocytosis (Habila et al. 2012), the regulation of erythropoietin homeostasis, the host's potential to raise neutralizing antibodies against secreted trypanosome virulent factors (Authié et al. 2001), and the general mechanism involved in inflammation control such as the regulation of the interferon-gamma and interleukin (IFNγ/IL-10) balance, as well as other cytokines (Stijlemans et al. 2018). Infection-induced erythropoiesis deregulation as well as the participation of stress-induced acute phase responses associated to T. congolense-associated anemia have been identified in mouse gene expression profiling investigations (Thompson et al. 2010). The hallmarks of anemia are arguably the most well-known and well-described features of AT (African trypanosomiasis) to date. Anemia is frequently used to indicate disease severity once fresh surveillance efforts result in the detection of new infection foci. This is true for T. evansi, T. congolense, and T. vivax, regardless of infection location or host species. T. evansi-induced anemia was associated to infection-related iron metabolism deregulation, just as T. congolense-induced anemia was (da Silva et al. 2013).

In the present study, rectal temperature of the infected rabbits showed fluctuating pyrexia as trypanosomiasis has been linked to pyrexia in animals (Ogwu and Njoku 1986), and chronic pyrexia has negative effect on spermatogenesis.

Low body weight, loss of body condition, anaemia and stress associated with immune complex reactions of the animal could cause anoestrus in the females resulting to poor reproductive performance and low production output. The presence of flagellated trypanosomes in the blood samples of infected animals was initially noticed six days after infection, which is consistent with previous studies which reported that Trypanosoma congolense prefers the capillary bed (Losos and Ikede 1972). Trypanosoma congolense has a seven-day incubation period (Losos 1978). By the eighth day after inoculation with Trypanosoma congolense, rabbits became parasitaemic (Toma et al. 2008). The phagocytosis of trypanosomes by kupfer cells, mediated by actively produced antibodies, was first noticed on day 5 post infection in mice infected with T. congolense, and was greatly increased on day 6 post infection (Henry et al., 2004). Given the 6 days incubation duration we observed in our work and Toma et al. (2008), report of an 8-day incubation period in rabbits, this report of a 7-day incubation period for T. congolense may be considered an average incubation period for T. congolense. Henry et al. (2004), found a 6-day incubation period in mice, which was identical. As a result, the length of the incubation time may not be determined by the animal species involved but the species of the trypanosomes. As the condition worsened, the parasites multiplied, according to the findings (Table VI). Wet mount revealed nucleated red cells, indicating regenerative anaemia, but mature red cells in infected samples lost their peripheral redness. There were red cell fragments present. This is consistent with Suliman and Feldman (1989) findings on red cell fragmentation. All of these characteristics would reduce the output of T. congolense-infected rabbits. As the parasites multiplied, the PCV level dropped and remained low, resulting in pale mucous membranes, chronic anemia, and pyrexia. The infected rabbits began to lose weight. Rabbits' reproductive performance would be affected by a reduction in relative weight and boldly condition. Rabbits infected with T. congolense had significantly reduced ejaculate characteristics (Leigh and Fayemi 2010). As a result, T. congolense infection would reduce the output of Dutch – belted rabbits.

This study has revealed that T. congolense induced severe anemia in infected rabbits, as seen by pale mucous membranes. It was therefore recommended that, in addition to trypanocides and antipyretics, haematinic therapy be given priority in the treatment of rabbits infected with T. congolense.

Acknowledgements

The authors express their appreciation to the Technologists of Parasitology and Entomology, and that of Theriogenology Laboratories, Faculty of Veterinary Medicine, University of Abuja for their support and technical assistance.

Funding: No funding was received for conducting this study.

Conflict of Interest/Competing interests: The authors have no competing interests to declare that are relevant to the content of this article.

Availability of data and material - Data sharing not applicable to this article as no datasets were generated or analysed during the current study.

Author’s Contributions

Sylvester Sunday Obeta - Conceptualization, Simon Azubuike Ubah – Supervision, Charles Ejike Ejiofor - Edited manuscript, Adikpe Oluwa Agbonu – Investigation, Columbus Philemon Kwinjoh - Resources, Kenneth Owoicho Abah – Resources, Alapa Baba Ikpe – Resources, Samuel Bankole Abayomi – Resources, Prisca Adaoma Ezinwo – Resources, Joy Iyojo Itodo – Resources, Isaac Oluwatobi Akefe - Drafted Original manuscript, Charles Amaechi Ubah – Review the manuscript, Samuel Mailafia – Review the manuscript, All authors reviewed and approved the manuscript

Ethics approval

Approval was obtained from the University of Abuja Ethical Committee on Animal Use (UAECAU) (UAECAU/2022/008). The procedures used in this study adhere to the tenets of the Declaration of UAECAU.

Consent to participate – Not applicable

Consent for publication – Not applicable

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Table 1: Mean (±SEM) of PCV, TLC, HR, RT, and BW of Rabbits before inoculation with Trypanosoma congolense

Parameters	T	C
PCV (%)	41.3±0.03	42.3±0.04
TLCx10ᶺ3/L	5.2±0.05	5.3±0.03
RT (⁰C)	38.4±0.06	38.6±0.06
HR (bpm)	143.0±0.71	145.0±56
BW (g)	1.7±0.04	1.7±03

MV = Mean Value, T=Inoculated group, C=Control group

Table 2: Mean (±SEM) Packed cell volume PCV (%) of Infected (T) and Control (C) Rabbits at days 18, 25 and 58 post inoculation with Trypanosoma congolense.

Days PI	T	C

18	36.0±0.53	40.8±0.11
25	35.3±0.19	41.8±0.19
58	28.0±0.89	41.3±0.08

P-value =0.001

T=Infected group, C=Control group

There was a significant (P< 0.05) difference in the mean PCV of the rabbits on day 18, 25 and 58 PI

Table 3: Mean (±SEM) Total Leucocytes Count (TLCx10⁹/L) of the Infected and Control Rabbits at day 18, 25 and 58 post inoculation with Trypanosoma congolense.

Days PI	T	C
18	5.5±0.08	5.9±0.05
25	3.9±0.08	4.2±0.08
58	3.4±0.09	3.5±0.09

P-value = 0.44

Mean TLC did not show any significant difference (P< 0.05) of the rabbits on day 18, 25 and 58 PI

Table 4: Mean (±SEM) rectal temperature (⁰C) of the infected (T) and control (C) Rabbits at day 18, 25 and 58 post inoculation with Trypanosoma congolense.

Days PI	T	C
18	38.3±0.07	38.0±0.12
25	39.2±0.09	38.2±0.11
58	39±0.10	38.8±0.08

P-value = 0.14

Mean RT did not show any significant difference (P< 0.05) of the rabbits on day 18, 25 and 58 PI

Table 5: Mean (±SEM) Heart Rate (HR/bpm) of the Infected (T) and Control (C) Rabbits at day 18, 25 and 58 post inoculation with Trypanosoma congolense

Days PI	T	C
18	141±0.96	149±0.59
25	143±1.22	144±0.94
58	144±1.13	149±1.27

P-value = 2.94

Mean HR did not show any significant difference (P< 0.05) of the rabbits on day 18, 25 and 58 PI

Table 6: Mean (±SEM) Body Weight (kg) of Infected (T) and Control (C) Rabbits at day 18, 25 and 58 post inoculation with Trypanosoma congolense

Days PI	T	C
18	1.7±0.07	1.6±0.07
25	1.5±0.07	1.6±0.07
58	1.6±0.06	1.80±0.07

P- Value – 2.44

Mean BW did not show any significant difference (P< 0.05) of the rabbits on day 18, 25 and 58 PI

Table 7: Shows levels of Parasitaemia of eight infected rabbits Post-infection with Trypanosoma congolense

Days PI	Number of Parasites/Field
0-5	-
6-14	+
14-18	++
18-25	+++
25- 58	++++

Key: P1 = Post inoculation.

No competing interests reported.

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Effect of experimental infection of Trypanosoma congolense on the packed cell volume of Dutch belted rabbits and its implication

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Abstract

1.1 Introduction

1.2 Materials And Methods

1.3 Results

1.4 Discussion

1.5 Conclusion

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