Hydatidosis of the brain is a rare disease. The diagnosis is usually late because of its slow progression and absence of specific symptoms. This review attempted to throw light on some aspects of cerebral hydatidosis because of deficient clinical suspicion of the disease, and imaging investigations are sometimes inadequate and biopsy reports inconclusive. Thus, the literature pertaining to parasitic causes, the incidence, the pathogenesis, the clinical picture, the diagnosis, and the management of the disease were overviewed. Our intention was to alert parasitologists and neurosurgeons concerning this morbid and rare condition, and to emphasize the fact that parasitic infection should be suspected in cystic lesions affecting the brain, especially in endemic areas of the world. Moreover, we aim to discuss or derive an answer to some amazing aspects of the disease. These include its clear abundance in children and in young age, its unusual huge size in their brains, whether the brain is an accidental or a target location, its extreme rarity in domestic animal's brains, the usual failure of serological and immunological tests used for its diagnosis, the wide range of clinical manifestations and differential diagnoses, and the recent measures used for its treatment and control.

List of contents 1. Plasmodium spp. 1.1. Introduction 1.2. Historical background 1.3. Applications 2. Leishmania spp. 2.1. Introduction 2.2. Applications 3. Trypanosoma spp. 3.1. African trypanosomiasis 3.1.1. Applications 3.2. American trypanosomiasis 3.2.1. Introduction 3.2.2. Applications 4. Toxoplasma gondii 4.1. Applications 5. Cryptosporidium spp. 5.1. Applications 6. Other protozoa 6.1. Babesia spp. 6.2. Microsporidium spp. 6.3. Giardia lamblia 6.4. Eimeria spp. 6.5. Trichomonas vaginalis 6.6. Entamoeba histolytica 6.7. Free living amoeba 6.8. Cyclospora cayetanensis 6.9. Blastocystis spp. 6.10. Theileria spp. Concluding Remarks References Abbreviations ASS: African sleeping sickness; BiP: Binding protein; BS: Bloodstream forms; CL: Cutaneous leishmaniasis; COWP: Cryptosporidium oocyst wall protein; CTL: Cytotoxic T-lymphocyte; Cy: Cytosolic; ER: Endoplasmic reticulum; GA: Geldanamycin; GP60: Glycoprotein 60; HSP: Heat shock protein; ITS: Internal transcribed spacer; KMP-11: Kinetoplastid membrane protein-11 gene; MAb: Monoclonal antibody; MCL: Mucocutaneous leishmaniasis; MHC: Major histocompatibility complexe; Mit: Mitochondrial; NO: Nitric oxide; PS: Procyclic forms; PTEX: Plasmodium translocon of exported proteins; sHSP: small heat shock protein; SSU: Small subunit; TL: Tegumentary leishmaniasis; TLR: Toll like receptor; VL: Visceral leishmaniasis; VSG: Variant surface glycoprotein.

The eicosanoid family includes prostanoids, leukotrienes, and other oxygenated derivatives. Prostanoids are a major class of the eicosanoid family derived from metabolism of arachidonic acid by the action of cyclooxygenase enzymes (COX). They are further subdivided into three main groups: prostaglandins (PGs), thromboxanes (TXs), and prostacyclins. PGs were first discovered as uterotonic substances in human seminal fluid in 1930. In the late 1950s to mid-1960s, their structures were studied and identified as being derived from unsaturated fatty acids. Prostanoids are produced by many cell types such as vascular endothelium, leukocytes, and the pathogens themselves. Prostanoid production is controlled by expression of different enzymes engaged in prostanoid biosynthesis, and by the distribution of different specific prostanoid synthases within those cells that determine their effect on the immune system. The production of prostanoids differs from one cell type to another; for example, dendritic cells predominately produce PG E ₂ (PGE ₂ ) and TXA ₂ , whereas mastocytes produce PGD ₂ . All inflammatory cells, including monocytes/macrophages, and neutrophils, are the main source of COX metabolites. Produced in response to various physiological and pathological stimuli, PGs are noted as key participants in autoimmune immunopathology, infectious diseases, and cancer. Other reports have shown that PGIs are formed by endothelial and smooth muscle cells, and TXAs are formed by platelets and lungs; PGI ₂ and some other PGs are produced by interactions between cells using enzymes in adjacent cells; for example, platelet-produced PGH ₂ is converted to PGI ₂ in the vascular epithelium. PGs secreted in the saliva of blood-sucking arthropods increase local blood flow and maintain the supply for feeding; they were also reported to increase immune suppression, allowing prolongation of attachment by ticks. Progressive studies demonstrated that, besides insects, pathogenic fungi, protozoa, and parasitic worms produce PGs. This review focuses on induced efforts to study prostanoids and their relation to different parasitic diseases. Abbreviations AA: Arachidonic acid; COXs: Cyclooxygenase enzymes; CyPG: Cyclopentanone; DC: Dendritic cell; GST: Glutathione-S-transferase; GA: Glycyrrhizic acid; MAP: Mitogen-activated protein; MIF: Macrophage migration inhibitory factor; NO: Nitric oxide; PBMC: Peripheral blood mononuclear cells; PG: Prostaglandin; PG12: Prostacyclin; PGE2: Prostaglandin E2; PL: Phospholipase; PPAR: Peroxisome proliferator-activated receptors; TGF: Transforming growth factor; TNF: Tumor necrosis factor; TP: Thromboxan receptor; TX: Thromboxane.

Background Dientamoeba fragilis was considered as a commensal amoeba that inhabits the large intestine. Later, its association with irritable bowel syndrome drew attention to its pathogenicity. Metronidazole (MTZ) is the most recommended drug for treatment of D. fragilis and other pathogenic intestinal protozoa. Many studies reported that it is not suitable for children because of its mutagenicity and carcinogenic potential. However, still more work is needed to establish new, effective, and safe therapeutic agents against D. fragilis. Aim of the work The present study aimed at evaluating the effect of different doses of the aqueous extract of Nigella sativa on D. fragilis in experimentally infected mice in comparison with MTZ as a standard drug. Materials and methods Isolates of D. fragilis were obtained from patients complaining of acute/chronic intermittent diarrhea or diarrhea alternating with constipation with/without abdominal pain. Histopathological examination of cecal tissue of experimentally infected and treated mice with three different doses of N. sativa (125, 250, and 500 mg/kg/day) was compared with that of mice infected and treated by two doses of MTZ (62.5 and 125 mg/kg/day) as the standard treatment. Infected untreated mice were used as the control group. Results Histopathological examination of cecal tissue of the infected untreated group showed different degrees of pathological changes, which completely disappeared with the highest N. sativa dose (500 mg/kg). Concentrations below 500 mg/kg produced less severe pathological changes than in untreated animals. N. sativa in high dose significantly prevented cytopathic effect in mice 1 day after infection and for five consecutive days. Conclusion N. sativa has a potential therapeutic effect against D. fragilis infection in an experimental in vivo study. We recommend double-blind controlled clinical trials in humans to assess the use of N. sativa in management of human D. fragilis infection.

Background The large-scale use of praziquantel might result in selection of drug-resistant parasites. Hence, there is an important need to develop new antischistosomal compounds. Objective This study aimed for assessment of antischistosomal properties of an antimalarial drug, mefloquine (MFQ), on juvenile and adult Schistosoma haematobium worms. Materials and methods Infected hamsters were divided into two main groups, I and II, each subdivided into (a) and (b) subgroups. Groups Ia and IIa received 200 mg/kg MFQ as single oral dose, 49 and 82 days postinfection, respectively. Groups Ib and IIb served as untreated controls, respectively. Ten days later, animals were killed. Parasitological assessment (worm burden, tissue egg load, and oogram pattern), histopathological examination, and scanning electron microscopy were performed to evaluate MFQ efficacy. Results MFQ treatment of the juvenile group Ia resulted in considerable worm burden reductions of 75.9, 69.6, and 88.6% for male, female, and coupled worms, respectively. In the treated adult group IIa, the corresponding results were 24.8 and 95% for male and coupled worms, respectively. Separate female worms were detected only in the treated groups. In group IIa treated animals, MFQ also had an observed but statistically insignificant effect on tissue egg load and oogram pattern. Schistosomal granuloma area, diameters, and numbers were insignificantly decreased. Tegumental changes of treated worms in the form of shrunken deformed tegument, loss or flattening of tubercles, furrows, and blebbing were observed. Conclusion Results concluded by this study elucidate promising MFQ antischistosomal efficacy on both juvenile and adult stages of S. haematobium with more evident effect on juvenile forms, which enforces the potential use of MFQ as an effective antischistosomal drug.

Background Leishmania major is the causative agent of cutaneous leishmaniasis in humans. It can also induce visceral or viscerotropic systemic leishmaniasis in humans. Resistance to treatment has been reported in many countries. Glibenclamide (GB) has been found to enhance treatment in resistant cases. Aim The aim of this work was to study the immunomodulatory effect of ATP inhibitor-GB on leishmaniasis caused by L. major. Materials and methods Mice were divided into three groups: group I (GI), noninfected group; group II (GII), infected with L. major; and group III (GIII), infected with L. major and treated with GB, starting 10 days postinfection till the end of the experiment. Evaluation was performed by measuring the size of cutaneous skin lesions, histopathological examination of the liver and spleen, and detection of expression of interferon γ, tumor necrosis factor α, interleukin (IL)-4, and IL-10 cytokines by reverse transcriptase real-time PCR. Transmission electron microscopic study of parasites from peritoneal exudate of GII and GIII mice was also carried out. Results The treated group showed a reduction in skin lesion size, improvement in histopathological manifestations, increased expression of interferon γ, and decreased tumor necrosis factor α, IL-4, and IL-10 expression. Transmission electron microscopic study showed vacuolation and damage of parasites in the treated group. Conclusion GB can be used effectively for the treatment of leishmaniasis.

Hydatid disease is a zoonotic infection most commonly caused by Echinococcus granulosis. Primary hydatid cysts of the skeletal muscles are extremely rare. In this paper, we present a case in which a patient had a hydatid cyst in the paraspinal muscle. A 19 years old female patient presented with a painless swelling over the left side on the back for the last two months. On local examination, a solitary, firm, non tender well defined, non movable, oval swelling was present over the left paraspinal region from T12 -L3. Provisional diagnosis of hydatid cyst was made on ultrasonography. Magnetic Resonance imaging revealed a well defined ovoid lesion measuring 4.3 × 4.54 × 2.3cm within the left erector spinae muscle. Operative intervention was planned and preoperative albendazole therapy (15 mg/kg/day) was given for two weeks. Hydatid disease is caused by the larval form of Echinococcus granulosus, It is most frequently located in the liver (75%) and lungs (15%). Musculo-skeletal involvement is secondary and uncommon. Spinal and paraspinal involvement is rare, with an incidence of less than 1%. Investigations for diagnosis include Ultrasonography, Computed tomography, Magnetic Resonance Imaging and Serologic tests. Surgical removal is the most effective treatment of hydatid cyst. Therapy with nontoxic scolocidal agents or combination chemotherapy with mebendazole is of therapeutic value. Albendazole is suggested to be given post operatively. Primary paraspinal echinococcosis must be considered in the preoperative differential diagnosis of the atypical presentation of paraspinal lesions in countries where Echinococcus infestation is endemic. Early diagnosis and radical surgery combined with antihelminthic therapy of sufficient duration are mandatory for the treatment of this disease.