الفهرس 
Aim of the workOnly 14 pages are availabe for public view
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Abstract
Mice were immunosuppressed by oral administration of synthetic
corticosteroid (Dexazone tablets 0.5 mg, Al Kahira Pharmaceutical and Chemical
Industries Company, Egypt ) at a dose of 25μg/ gm body weight /day for 14
successive days before oral inoculation with Cryptosporidium oocysts. Treatment
with NTZ, AZB or both were given to prophylactic and theraputic groups.
Fresh faecal pellets were collected from each mouse separately and
examined by MZN staining method to calculate Cryptosporidium oocyst shedding
on the last day of the experiment (30th dpi). Mice were sacrificed at 30th dpi.
The peripheral blood was aseptically collected and the serum was separated
after centrifugation and stored at -20 ºC for immunological analysis. The terminal
one cm of the ileum and the whole lung tissues were taken from each mouse, then
fixed in 10% neutral formalin for histopathological examination and
immunohistochemical staining of CD3 and iNOS.
Parasitological results
The lowest mean number of oocyst shedding in mice stool (310± 7.45) was
observed in the prophylactic subgroup GIIc (received AZB+NTZ) in comparison
with control positive subgroup GIb (8008.571± 7.48) (P>0.001).
In the therapeutic subgroup GIIIc (received AZB+NTZ), reduction was
recorded with a mean of 1508±7.15, then therapeutic subgroup GIIIb (NTZ treated)
with a mean of 2007.78±5.65. In the therapeutic GIIIa (AZB treated) mean number
of oocyst shedding (4508.13± 5.94) was not as low as in the other groups. In
desending order, the reduction percent of oocyst was 96.13%, 89.89%, 81.17%,
74.93, 62.45% in GIIc, GIIb, GIIIc, GIIIb and GIIa, respectively. while the lowest
reduction percent of oocyst was 43.71% in the therapeutic subgroup GIIIa (AZB
treated).
Histopathological results:
Intestine
Histopathological examination of ileal sections from mice of GIa (control -
ve) showed normal structure with average length and width of villi without any
pathological changes in the mucosa or the lamina propria, while GI b (control + ve)
showed loss of villous architecture, shortening, broadening of the villi and even
villous atrophy. Additionally, there were mucosal ulceration, edema, low-grade
dysplasia, and goblet cells depletion in the covering epithelium and inflammatory
cellular infiltrate observed mainly in the core of the villi and extending into the
submucosa. Cryptosporidum oocysts appeared along the brush border of the villi
and in the intestinal lumen as rounded to oval bodies and purple-stained.
Improvement of ileal tissue samples appeared in groups GIIc and GIIIc
(receive combined treatment with AZB and NTZ either prophylactic or
therapeutic), in the form of mild inflammation with intact mucosa, intestinal villi,
and crypts. In addition, Cryptosporidium endogenous developmental stages have
hardly been seen and the epithelium of these groups showed preserved polarity and
were devoid of any cytological atypia. While GIIa, GIIb, and GIIIb showed partial
improvement in the histopathological changes with mild to moderate inflammatory
infiltrate in the core of villi with intact mucosa and mild blunting, shortening and
ulceration of villi.
Summary