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 Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 29  |  Issue : 4  |  Page : 868-873

The histopathological effects of Trypanosoma evansi on experimentally infected mice


Department of Parasitology, Faculty of Medicine, Menoufia University, Menoufia, Egypt

Date of Submission29-Mar-2015
Date of Acceptance04-May-2015
Date of Web Publication21-Mar-2017

Correspondence Address:
Amany F. I. Atia
Meet Afia, Shebin El-Kom, Menoufia, 32511
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-2098.202492

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  Abstract 

Objectives
The objective of this study was to study the histopathological changes in different tissues in experimentally Trypanosoma evansi-infected mice.
Background
There is variation in the pathogenicity of different host species. Animals that are subjected to stress, malnutrition, pregnancy, or work are more susceptible to this disease. The pathogenesis of T. evansi is complex and the cause of death is still somewhat obscure.
Materials and methods
The T. evansi isolate used in the present study was obtained from the blood of naturally infected camels. The strain was maintained in mice, where their infected blood was used for inducing the experimental infection. Giemsa-stained blood films were prepared for detection of infection and estimation of parasitemia. A total of 64 mice were divided into two main groups as follows: group I (the infected group), which included 40 mice inoculated with T. evansi strain, and group II (the control group), which included 24 mice used as uninfected healthy controls.
Results
In the present study, trypanosomes were observed using wet blood films and Giemsa-stained blood films at 48 h after infection in infected mice (group I) and there was high parasitemia on approximately the fifth day after infection (subgroup I-b). Mice from the uninfected control group (II) remained negative for trypanosomes until their death. Gross examination of various tissues from the infected mouse subgroups (infected group I) revealed splenomegaly, hepatomegaly, and marked congestion of lungs. All degrees of inflammation were detected in these tissues. Moreover, most of the examined tissues showed trypanosomes. It was noted that these pathological changes were more obvious in subgroup I-b when the parasitemia had reached its peak.
Conclusion
Microscopic examination showed significant histopathological changes in different organs, and in most examined tissues the parasites were detected in high numbers, especially in subgroup I-b (on the fifth day).

Keywords: histopathology, parasitemia, Trypanosoma evansi


How to cite this article:
Ghaffar MA, El-Melegy M, Afifi AF, El-Aswad BW, El-Kady N, Atia AF. The histopathological effects of Trypanosoma evansi on experimentally infected mice. Menoufia Med J 2016;29:868-73

How to cite this URL:
Ghaffar MA, El-Melegy M, Afifi AF, El-Aswad BW, El-Kady N, Atia AF. The histopathological effects of Trypanosoma evansi on experimentally infected mice. Menoufia Med J [serial online] 2016 [cited 2020 Feb 27];29:868-73. Available from: http://www.mmj.eg.net/text.asp?2016/29/4/868/202492


  Introduction Top


Trypanosoma evansi is a pathogenic hemoflagellate protozoa belonging to the salivaria section, having a global distribution and affecting several animal species. The clinical, hematological, and pathological aspects of T. evansi in the host can vary according to the strain virulence, the host susceptibility, and the epizootic conditions. The transmission occurs mainly through hematophagous insects (Tabanus spp., Chrysops spp., and Hematopota spp.) [1].

T. evansi causes 'surra', which is an animal disease. Surra spreads in various geographical areas, widely distributing among domestic and wild animals, such as horses, donkeys, mules, camels, Indian elephants, cattle, buffaloes, sheep, goats, dogs, cats, pigs, tapirs, deer, tiger, capybara, foxes, jackals, hyenas, mongoose, and bears [2]. In Egypt, T. evansi is a major livestock disease causing significant losses in camels [3].

Surra should be considered when the clinical signs include anemia, weight loss, and dependent edema [4],[5]. The disease passes from acute to chronic stages with progressive weakness, emaciation, depletion, recurrent fever, enlarged lymph nodes, and finally death [4],[5]. The infiltration and dissemination of T. evansi in the central nervous system has been reported to cause severe and potentially fatal clinical symptoms in the second stage of the disease [6].

For a long time, T. evansi was not known to be pathogenic to humans [1], but in 2004 the first case of human infection with T. evansi was reported from the central part of India, in a farmer who had fluctuating trypanosome parasitemia associated with febrile episodes for several months; there is no central nervous system invasion, and the diagnosis was confirmed by parasitological, immunological, and molecular methods. The patient was successfully treated with suramin. It was suggested that the patient wound had become contaminated by an infected animal blood [7],[8].

In 2010 in Egypt, out of 30 individuals one found to be positive for T. evansi infection, as indicated by enzyme-linked immunosorbent assay and stained blood smear, but was negative on urine thymol turbidity test. The infected person was a farmer and he was successfully treated as indicated clinically, parasitologically, and serologically. This is the first reported human case in Egypt of T. evansi, a neglected zoonosis.

No doubt the presence of animal cases of T. evansi in Egypt and neighboring countries and the abundance of insect-vectors and bats must be taken into consideration [9]. However, a number of cases of atypical human T. evansi might be underestimated [10].

The pathogenicity of T. evansi varies significantly among its strains and across animal species [11]. The pathogenesis of T. evansi is complex and the cause of death is still somewhat obscure. The protozoan invades the host, multiplies rapidly in the blood and later in the central nervous system, and this requires energy, which is supplied by the host for the survival of the trypanosome [12].

The pathological changes including multiple necrotic foci in the liver and spleen, as well as generalized lymphoid tissue hyperplasia in animals suffering from surra, could be attributed to tissue anoxia, possibly caused by anemia, which results in a fall in tissue pH and vascular damage [12]. T. evansi has a preference for connective tissues of the host, where they disrupt the collagen bundles and destroy the fibroblasts, releasing large quantities of cytoplasmic and mitochondrial enzymes into the serum, thereby causing further tissue damage [13]. Also, the parasite utilizes glucose for its growth and multiplication. In addition, further changes developing in the organs are caused by toxicants released by the parasite, or due to immunological reactions [14]. Although T. evansi is a hemoprotozoa, visceral forms have been reported in the heart, optic lobes, cerebrum, liver, kidney, and lungs [15].

Post-mortem examination of T. evansi-infected hosts revealed that in the terminal stages of the disease there is enlargement of the spleen and petechial hemorrhage in the liver. Tissue sections revealed the presence of numerous trypanosomes in the blood vessels of the liver, spleen, brain, and kidneys [14].

This study aimed to study the histopathological changes in mice experimentally infected with T. evansi.


  Materials and Methods Top


Experimental animals

Female BALB/c mice (7 weeks old; weight 18 ± 5 g) were used. The animals were kept under controlled conditions of temperature 25 ± 2°C and humidity 70%. They had free access to commercial diet and water. The animals were kept before T. evansi infection for 10 days for adaptation and during this period the stool of the mice was examined to rule out the presence of parasites (animals were handled in accordance with animal rights).

Parasite

Trypomastigotes of T. evansi were separated from blood [14] drawn from infected camels in the Faculty of Veterinary Medicine, Cairo University. The strain was maintained in mice, where their infected blood was used for performing the experimental infection.

Mice groups

A total of 64 mice were divided into two main groups as follows:

Group I (the infected group): This group included 40 mice, which were inoculated with T. evansi. The group was further subdivided, according to the period of infection, into four subgroups, each containing 10 mice.

  • Group I-a: killed at day 3 after infection
  • Group I-b: killed at day 5 after infection
  • Group I-c: killed at day 10 after infection
  • Group I-d: killed at day 20 after infection.


Group II (the control group): This group included 24 noninfected mice, which served as negative controls. This group was in turn subdivided into four subgroups, each containing six mice, which were killed at the same time as the infected mice.

  • Group II-a: killed on day 3
  • Group II-b: killed on day 5
  • Group II-c: killed on day 10
  • Group II-d: killed on day 20.


Mice infection

On day 0, the number of trypanosomes per 1 ml blood was determined using a hemocytometer under a microscope. Each mouse of group I was inoculated intraperitoneally with 1 ml containing 4.5 × 105 trypomastigotes [16].

Estimation of parasitemia

The presence and degree of parasitemia were estimated daily for each infected mouse by two methods: direct blood smear from the tail vein and Giemsa-stained blood smear. The blood preparations were examined under a microscope at ×1000. T. evansi trypomastigotes were counted in 10 fields and the mean of these counts was estimated to express the level of parasitemia by the number of trypomastigotes in a high-power field [17].

Histopathological examination

The histopathological study was conducted in the Department of Pathology, Faculty of Medicine, Menoufia University. Thin sections of 5 µm thickness were cut from the spleen, liver, brain, lung, kidney, and heart from both mouse groups (I and II) and stained with routine hematoxylin and eosin stain. The degree of inflammation was categorized into four levels: free (no inflammation), mild (1–2 foci of inflammation/section), moderate (3–6 foci of inflammation/section), and severe (>6 foci of inflammation/section). Three slides were examined for each mouse and the mean of the degree of inflammation was calculated and used for analysis [18].


  Results Top


Giemsa-stained blood films of infected mice revealed the absence of trypanosomes at 12 and 24 h after infection, but they started to appear after 2 days and the parasitemia reached its peak on the fifth day after infection [Figure 1]a).
Figure 1: (a) Giemsa.stained blood film from mice infected with Trypanosoma evansi (×1000). (b) Splenomegaly. (red arrow) and hepatomegaly (blue arrow) in experimentally infected mice with Trypanosoma evansi.

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Histological examination did not reveal any pathological changes in the tissues (liver, spleen, brain, lung, kidney, and heart) of group II (the control group). Regarding group I (infected group), gross examination of their different tissues revealed splenomegaly and hepatomegaly [Figure 1]b. Microscopic examination showed significant histopathological changes in different organs, and in most examined tissues the parasite was detected in high numbers, especially in subgroup I-b [Figure 2]a, [Figure 3], [Figure 4] and [Figure 5]f).
Figure 2: (a) A section of spleen tissue from mice of subgroup I-a showing mild congestion; the red pulp is filled with red blood cells (green arrows) (H&E, ×200). (b) A section of spleen tissue from mice of subgroup I-b showing numerous scattered parasites (blue arrow) in splenic red pulp, which is stuffed with numerous lymphocytes, histiocytes, and multinucleated giant cells (red arrow) (H&E, ×400). (c) A section of spleen tissue from mice of subgroup I-d showing mild congested red pulp with a few scattered parasites (green arrow), multinucleated giant cells (blue arrow), and many histiocytes (red arrow) (H&E, ×400). H&E, hematoxylin and eosin.

Click here to view
Figure 3: (a) A section of liver tissue from mice of subgroup I-a showing a mildly dilated and congested central vein containing scattered parasites (blue arrow) surrounded by inflammatory cells (red arrow) and degenerated hepatocytes (green arrow) (H&E, ×400). (b) A section of liver tissue from mice of subgroup I-b showing a severely congested central vein containing numerous scattered parasites (red arrow) together with perivascular chronic inflammatory cells (blue arrows) (H&E, ×400). (c) A section of liver tissue from mice of subgroup I-c showing moderate perivascular lymphoplasmacytic infiltration (red arrow) and a few scattered parasites (blue arrow). The hepatocytes show vacuolar degeneration (green arrow) (H&E, ×400). H&E, hematoxylin and eosin.

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Figure 4: (a) A section of brain tissue from mice of subgroup I-b. The cerebellum shows mild mononuclear cellular infiltrate (red arrow) (H&E, ×400). (b) A section of brain tissue from mice of subgroup I-c. The cerebellum shows moderate mononuclear cellular infiltrates (H&E, ×400). (c) A section of the cerebellum from mice of subgroup I-d showing vacuolar degeneration together with mild inflammatory infiltrates (H&E, ×200). (d) A section of lung tissue from mice of subgroup I-a showing lymphoplasmacytic collection together with histiocytes surrounding a few parasites in the perivascular and peribronchial space (H&E, ×400). (e) A section of lung tissue from mice of subgroup I-b showing numerous scattered parasites (red arrow) surrounded by lymphoplasmacytic collection together with histiocytes in the perivascular and peribronchial space (H&E, ×400). (f) A section of lung tissue from mice of subgroup I-c showing a few scattered parasites in the lung tissue (red arrow) surrounded by significant lymphoplasmacytic collection (blue arrow) (H&E, ×400). H&E, hematoxylin and eosin.

Click here to view
Figure 5: (a) A section of kidney tissue from mice of subgroup I-a showing moderate renal tubules exhibiting hydropic degeneration (H&E, ×200). (b) A section of kidney tissue from mice of subgroup I-b showing renal tubules exhibiting marked cloudy and hydropic degeneration (red arrow) (H&E, ×200). (c) A section of kidney tissue from mice of subgroup I-c showing moderate perivascular mononuclear cellular infiltrates formed of lymphocytes and plasma cells (H&E, ×400). (d) A section of heart tissue from mice of subgroup I-a showing mild mononuclear cellular infiltrate in cardiac tissue (H&E, ×400). (e) A section of heart tissue from mice of subgroup I-b showing moderate to severe mononuclear cellular infiltration surrounding numerous scattered parasites and extravasculated red blood cells in the myocardium (H&E, ×400). (f) A section of heart tissue from mice of subgroup I-c showing moderate congested blood vessels together with parasites (red arrow) and perivascular lymphohistiocytic infiltrates (blue arrow) (H& E, ×400). H&E, hematoxylin and eosin.

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  Discussion Top


It is well-known that T. evansi is highly pathogenic to various laboratory animals, such as mice, rats, and rabbits [19–23]. Trypanosomes utilize glucose and oxygen of the host for their growth and multiplication, resulting in depletion of these agents and consequently to degenerative changes in the host. Also, the degenerative changes occurring during trypanosome infection might be due to toxins released by the parasite or to immunological reactions of the host against the infection [14].

In the present study, gross examination of various tissues from the infected mouse subgroups (infected group I) revealed splenomegaly and hepatomegaly. All degrees of inflammation were detected in these tissues. Moreover, most of the examined tissues showed trypanosomes, which were more obvious in subgroup I-b (fifth day) when the parasitemia reached its peak.

In our work, spleen of the infected mice showed extensive hemorrhage in the areas of red pulp, and accumulation of histiocytes and multinuclear giant cells. These initial changes in the spleen may be due to immediate hypersensitivity to T. evansi [24]. Splenomegaly observed in the present study was in agreement with other previous histopathological studies of trypanosomes [14],[22],[23],[25]. Enlargement of the spleen might be due to increased activity of the mononuclear phagocytic system, which destroys red blood cells coated with the trypanosomal antigens resulting in hemosiderosis of the spleen. Moreover, as the disease progresses, hypersplenism becomes highly pronounced [14],[15]. Aggregation of histiocytes leads to granulomatous lesions, which are seen with disease progression [20].

Liver in the infected mouse subgroups revealed mild to severe degenerative changes, and hepatocytes lost their original shape and were swollen and rounded with vacuolar spaces in the cytoplasm. These pathological changes were similar to the observations made by other workers who studied the effect of T. evansi on various animals, such as goat and buffalo [26], rat [20], goats [27], and rabbits [28]. These pathological changes affecting the liver might be due to hypoglycemia, which leads to starvation of the cells and anoxia due to anemia in T. evansi-infected animals [19],[20],[29],[30]. Further, the liberated toxins from T. evansi cause necrosis of hepatocytes [27]. Trypanosomes consume oxygen during their multiplication, leading to a hypoxemic state and consequently in degenerative changes in all vital organs [14]. Recently, hypoproteinemia in trypanosomiasis occurring in the infected animals has been proposed to cause hepatic damage [31].

Herein, the brain tissue of infected mouse subgroups showed vacuolar degeneration together with mild mononuclear cellular infiltrate in the cerebellum. The changes in the infected brain tissue were similar to those seen in the brain of Swiss albino mice infected with T. evansi [14]. It has been reported that pathological changes in the brain are due to constant irritation caused by the presence of parasites or by the toxins liberated by them [21]. Also, cell-mediated immune reaction plays a role in the degeneration of the brain and other organs [32],[33]. Mild lymphoplasmacytic meningoencephalitis has been reported from goats [27] and buffalos [26] in T. evansi infection.

In our study, the lung tissues of infected mouse subgroups showed edema, congestion, emphysema, and infiltration with inflammatory cells in addition to alveolar hemorrhage; these changes in the lung were mainly caused by vasodilatation and exudation due to inflammatory response and immune complex deposition and complement cascade reaction [19],[20]. The changes in the infected lung tissue were similar to those seen in the lung of infected animals with T. evansi, such as goat [34], rabbits [22],[35], Swiss albino mice [16] and rats, and New Zealand white rabbits [23],[25]. In contrast to our results, the lungs of rabbits infected with T. rhodesiense did not show any pathological changes [36].

Kidneys revealed tubular degeneration, congestion, and cellular infiltration, in addition to degeneration of glomeruli, in most of the T. evansi infected mice. There was dilatation of proximal and distal convoluted tubules with occasional hemorrhage. It was suggested that the toxins liberated by trypanosomes might impair the function of the kidney. The renal cast formation as well as granulomatous lesions indicated nonfunctional kidney, especially at the late stage of T. evansi infection [14],[19],[34].

The myocardium of most infected mice revealed degenerative changes, congested blood vessels, and perivascular lymphohistiocytic infiltrates. Similar changes have been reported in previous studies [14],[20].

Degenerative changes in the heart may be due to anemia and hypoglycemia [20].


  Conclusion Top


T. evansi is highly pathogenic in laboratory animals such as mice. Microscopic examination showed significant histopathological changes in different organs, and in most examined tissues the parasite was detected in high numbers, especially in subgroup I-b.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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