II.1. Liver (Fig. 4)
Microscopic examination of sections of the liver from healthy control (group I) showed normal hepatic architecture divided into lobules. The hepatocellular cords were mostly one or two layers thick radiating from the central vein towards the periphery of the lobule. The normal hepatocytes were polygonal in shape with centrally placed round or oval dark violet nuclei and granulated eosinophilic cytoplasm. The cords of hepatocytes were separated by blood sinusoids lined by endothelial cells (EC). At the periphery of the lobule, the portal triads showed no inflammatory cellular infiltrates [Figure 4.1].
In the infected untreated control (group II), microscopic examination of liver tissue revealed invasive tachyzoites aggregated among the hepatocytes. Markedly dilated and congested central veins and sinusoids with evident focal necrosis and inflammation. (Fig. 4.2)
The liver sections of CS NPs treated group (III) showed pseudocysts with necrotic tachyzoites. Residual apoptotic bodies of hepatic nuclei and degenerative hepatocytes with marked dilated congested central veins and sinusoids were noticed. Moreover, there was evidence of lobular inflammation [Figure 4.3].
In the treated spiramycin group (IV), microscopic examination of the liver demonstrated that the hepatocytes were large in size with large vesicularnuclei and vacuolar degeneration of cytoplasm. Marked dilated congested central veins and dilated sinusoids surrounded by necrotic hepatocytes with obvious inflammation [Figure 4.4].
The microscopic examination of spiramycin-metronidazole treated group (V), illustrated marked dilated sinusoids surrounded by moderate inflammatory infiltrate with interface hepatitis and moderate portal fibrosis. Most hepatocytes appeared intact but some of them were necrotic [Figure 4.5].
Spiramycin- CS NPs 400 mg/kg treated group (VI) revealed dilated sinusoids and absent inflammatory infiltrate [Figure 4.6].
The liver of spiramycin-CS NPs 100 mg/kg treated group (VII) demonstrated pseudocysts with necrotic tachyzoites. There was evidence of regenerative hepatocytes. Dilatation of central veins and sinusoids were observed with minimal inflammation formed of few perivascular macrophages [Figure 4.7].
II.2. Spleen (Fig. 5)
Microscopic examination of the spleen of the healthy control (group I) revealed well-organized white pulp (W) (containing lymphocytes) and red pulp (R) differentiated by trabecular muscles (TR) [Figure 5.1].
Infected untreated control (group II) spleen section showed pseudocysts containing tachyzoites. Marked disorganized architecture and extramedullary hematopoiesis with areas of necrosis were observed. There was an obvious decrease in lymphocyte counts and increase in histiocytes [Figures5.2 and 5.3].
In CS NPs treated group (III), areas of macrophages loaded by tachyzoites were observed. Disorganized splenic architecture in addition to extramedullary hematopoiesis were evident in the red pulp [Figure 5.4].
The microscopic examination of spiramycin infected treated group (IV) illustrated pseudocysts containing necrotic tachyzoites and numerous apoptotic cells. Severe disorganized splenic architecture with enhancement of the inflammatory cells and reduction in the lymphocytes were observed [Figure 5.5].
The spleen of spiramycin-metronidazole treated group (V) demonstrated moderate disorganized architecture with extramedullary hematopoiesis and excess eosinophils [Figure 5.6].
In spiramycin-CS NPs 400 mg/kg treated group (VI), necrotic tachyzoites in pseudocysts in the red pulp and at the margin of regenerative lymphocytes of the white pulp were observed. Mild disorganized spleen architecture with evident tissue recovery and extramedullary hematopoiesis were noticed [Figure 5.7].
Spiramycin CS NPs 100 mg/kg treated group (VII) showed pseudocysts with necrotic tachyzoites. Moderate disorganized spleen architecture with regenerative white pulp forming well defined germinal centres as well as frequent epithelioid histiocytes were evident [Figure 5.8].
II.3. Brain (Fig. 6)
Examination of the brain cortex of the healthy control [group I] revealed normal architecture composed of neuroglial cells with ill-defined cytoplasm and pyramidal cells. Normal blood vessels were present [Figure 6.1].
In infected untreated control (group II), the cerebral cortex showed gliosis, apoptosis as well as perivascular and parenchymal inflammation [Figure 6.2].
The microscopic examination of CS NPs treated group (III) illustrated mild dilated blood vessels. Small pyramidal cells and others with vacuolated cytoplasm were noticed. Apoptosis and marked gliosis were observed [Figure 6.3].
In the spiramycin treated group (IV), the brain revealed the occurrence of perivascular inflammatory infiltrate, gliotic nodules and necrotic neurons [Figure 6.4].
In the brain of spiramycin-metronidazole treated group (V), no tachyzoites were detected. Mild congested blood vessels, moderate gliosis and ferrugination (mineralized bodies of necrotic neurons) were observed [Figure 6.5].
Spiramycin- CS NPs 400 mg/kg treated group (VI) revealed absence of tachyzoites with mild dilation of blood vessels. Normal neuroglial cells with no evidence of inflammation were observed [Figure 6.6].
In the brain of spiramycin-loaded CS NPs 100 mg/kg treated group (VII) spongiosis, moderate gliosis and apoptosis were seen. No inflammation was observed [Figure 6.7].