PATHOPHYSIOLOGY:

Egg/Feces- Urine

Miracidium

Ascarias- penetration human skin

Portal circulation of the liver

Blood Vessel (Bladder, Intestine)

Out of the body

Laboratory Test: Conducted on April 18, 2011 Laboratory Result: (+) for Ascaris lumbricoids ova

Specimen: Stool Test Name: Total Protein Albumin Globulin AG Ratio Result 42.30 g/l 25.00g/l 17.30 g/l 1.4 g/l Normal Range 60-80 g/l 37.95-53.99 g/l 11.00-33.00 g/l 1.50-2.20 g/l

Examination: Palin abdomen Consider a dynamic ileus with retained fecal materials.

Specimen: Blood Result: (-) for COPT

Specimen: Serum Test Name Sodium Potassium Low platelet Low Hgb WBC Result 144.80 mmol/l 4.54 mmol/l 132 10.19 4.05 Normal Range

150-400 13-17 4.8-10.8

DRUG STUDY:

A. DRUG Generic Name: OMEPRAZOLE Brand Name: Transinel Class: Antisecretory Drug

DOSE: 20mg 1cap. BID ROUTE: Oral INDICATION: Short-term treatment of active duodenal cancer.Short-term treatment of active benign gastric ulcer. Eradication of Helicobacter Pylori. First-line therapy for treatment of heartburn or symptoms of GERD. CONTRAINDICATION: Contraindicated with hypersensitivity to omeprazole or its components. Use cautiously with pregnancy, lactation. ACTION: Gastric-acid pump inhibitor: suppresses gastric acid secretion by specific inhibition of the hydrogen- potassium ATPase enzyme system at the secretory surface of the gastric parietal cells; blocks the final step of acid production.

SIDEEFFECT: CNS; headache, dizziness,asthenia, vertigo, insomnia, apathy, anxiety, paresthesias, dream abnormalities Dermatologic: rash, inflammation, urticaria, pruritus, alopecia, dryskin GI: diarrhea, abdominal pain, nausea, vomiting, constipation, dry mouth, tongue atrophy Respiratory: URI symptoms, cough, epistaxis. NURSING CONSIDERATION: Assessment: 1. History: hypersensitivity to omeprazole or any of its components;pregnancy,lactation 2. Physical: skin lesions; reflexes; urinary output; abdominal examination; respiratory auscultation. Interventions: 1. Administer before meals. 2. Administer antacids with, if needed. 3. Have regular medical follow-up visits. 4. Report severe headache, worsening of symptoms, fever, chills.

B. DRUG Brand Name: TRAMADOL Class: Analgesics (centrally acting) DOSE: 50mg/2mp 1amp IVq 8hrs. PRN ROUTE: IV

INDICATION: Moderate to moderately severe pain

ACTION: Physiologic Mechanism Decreased pain. Pharmacologic Mechanism Binds to mu-opioid receptors. Inhibits reuptake of serotonin and norepinephrine in the CNS.

NURSING CONSIDERATION: Assess type, location, and intensity of pain before and 2-3 hr (peak) after administration. Assess BP & RR before and periodically during administration. Respiratory depression has not occurred with recommended doses. Assess bowel function routinely. Prevention of constipation should be instituted with increased intake of fluids and bulk and with laxatives to minimize constipating effects. Assess previous analgesic history. Tramadol is not recommended for patients dependent on opioids or who have previously received opioids for more than 1 wk; may cause opioid withdrawal symptoms. Prolonged use may lead to physical and psychological dependence and tolerance, although these may be milder than with opioids. This should not prevent patient from receiving adequate analgesia. Most patients who receive tramadol for pain d not develop psychological dependence. If tolerance develops, changing to an opioid agonist may be required to relieve pain. Tramadol is considered to provide more analgesia than codeine 60 mg but less than combined aspirin 650mg/codeine 60 mg for acute postoperative pain. Monitor patient for seizures. May occur within recommended dose range. Risk increased with higher doses and inpatients taking antidepressants (SSRIs, tricyclics, or Mao inhibitors), opioid analgesics, or other durgs that decrese the seizure threshold.

 Overdose may cause respiratory depression and seizures. Naloxone (Narcan) may reverse some, but not all, of the symptoms of overdose. Treatment should be symptomatic and supportive. Maintain adequate respiratory exchange. Encourage patient to cough and breathe deeply every 2 hr to prevent atelactasis and pneumonia. C. DRUG Generic Name: SPIRONOLACTONE Brand Name: Aldactone Class: Potassium-sparing diuretic Aldosterone antagonist DOSE: 50mg 1tab. OD ROUTE: Oral INDICATION: Diagnosis and maintenance of primary hyperaldosteronism Adjunctive therapy in edema associated with CHF, nephrotic syndrome, hepatic cirrhosis when other therapies are inadequate or inappropriate Treatment of hypokalemia or prevention of hypokalemia in patients who would be at high risk if hypokalemia occurred: Digitalized patients, patients with cardiac arrhythmias Essential hypertension, usually in combination with other drugs Unlabeled uses: Treatment of hirsutism due to its antiandrogenic properties, palliation of symptoms of PMS, treatment of familial male precocious puberty, short-term treatment of acne vulgaris.

CONTRAINDICATION: Contraindicated with allergy to spironolactone, hyperkalemia, renal disease, anuria, amiloride or triamterene use. Use cautiously with pregnancy, lactation.

ACTION: Drug-drug Increased hyperkalemia with potassium supplements, ACE inhibitors, diets rich in potassium Decreased diuretic effect with salicylates Decreased hypoprothrombinemic effect of anticoagulants Drug-food Increased absorption when taken with food Drug-lab test Interference with radioimmunoassay for digoxin; false increase in serum digoxin levels Drug-alternative therapy Decreased effectiveness if combined with licorice therapy

SIDEEFFECT:

CNS: Dizziness, headache, drowsiness, fatigue, ataxia, confusion Dermatologic:Rash,urti cari a GI: Cramping, diarrhea, dry mouth, thirst, vomiting. GU: Impotence, irregular menses, amenorrhea, postmenopausal bleeding Hematologic: Hyperkalemia, hyponatremia, agranulocytosis Other: Carcinogenic in animals, deepening of the voice, hirsutism, gynecomastia

NURSING CONSIDERATION:

Assessment History: Allergy to spironolactone; hyperkalemia; renal disease; pregnancy, lactation Physical: Skin color, lesions, edema; orientation, reflexes, muscle strength; P, baseline ECG, BP; R, pattern, adventitious sounds; liver evaluation, bowel sounds; urinary output patterns, menstrual cycle; CBC, serum electrolytes, renal function tests, urinalysis Interventions Mark calendars of edema outpatients as reminders of alternate day or 3- to 5day/wk therapy Give daily doses early so that increased urination does not interfere with sleep. Make suspension as follows: Tablets may be pulverized and given in cherry syrup for young children. This suspension is stable for 1 mo if refrigerated. Measure and record regular weight to monitor mobilization of edema fluid. Avoid giving food rich in potassium. Arrange for regular evaluation of serum electrolytes, BUN .

Schistosoma mansoni infection reduces the incidence of murine cerebral malaria

Abstract

Background Plasmodium and Schistosoma are two of the most common parasites in subtropical areas. Deregulation of the immune response to Plasmodium falciparum, characterized by a Th1 response, leads to cerebral malaria (CM), while a Th2 response accompanies chronic schistosomiasis. Methods The development of CM was examined in mice with concomitant Schistosoma mansoni and Plasmodium berghei ANKA infections. The effect of S. mansoni egg antigen injection on disease development and survival was also determined. Cytokine serum levels were estimated using ELISA. Statistical analysis was performed using t-test. Results The results demonstrate that concomitant S. mansoni and P. berghei ANKA infection leads to a reduction in CM. This effect is dependent on infection schedule and infecting cercariae number, and is correlated with a Th2 response. Schistosomal egg antigen injection delays the death of Plasmodium-infected mice, indicating immune involvement. Conclusions This research supports previous claims of a protective effect of helminth infection on CM development. The presence of multiple parasitic infections in patients from endemic areas should therefore be carefully noted in clinical trials, and in the development of standard treatment protocols for malaria. Defined helminth antigens may be considered for alleviation of immunopathological symptoms. Malaria, an infectious disease caused by the Plasmodium parasite, is a source of enormous morbidity and mortality. Cerebral malaria (CM), seen in about 7% of Plasmodium falciparum malaria cases, is characterized by the presence of neurological features, especially impaired consciousness. The simplified explanation for CM pathogenesis is adherence and sequestration of parasitized erythrocytes, immune cells and platelets to vascular endothelial cells lining the small blood vessels of the brain. Thus, parasite-triggered cerebral inflammation is a

possible cause of death from CM. The immune response is critical in determining the outcome of infection. CM is characterized by a Th1 response, with overproduction of some cytokines (e.g. interferon- , IFN ), combined with underproduction of others (e.g. interleukin-10, IL-10) . By analogy with the inhibition of autoimmune disease development by helminthic infection , it has been demonstrated, both in murine studies and in humans, that concomitant helminth infection may change the course of Plasmodium infection . Schistosomes are parasitic trematodes found in subtropical and tropical areas. Among human parasitic diseases, schistosomiasis ranks second behind malaria in terms of socio-economic and public health importance. In many areas of the world, schistosomiasis and malaria are co-endemic: shared antigens and cross-reactive antibodies to different components of the two parasites have been detected. Chronic helminthic infections are established through modulation of the host immune system. In schistosomal infection, each pair of male and female worms produces hundreds of eggs per day; egg-associated glycolipids and glycoproteins are the main target of the host humoral immune response. In schistosomiasis, the early phase of infection is characterized by Th1 immune responses, which progress to a Th2 response. This pattern of cytokine expression is also found in non-cerebral (severe anaemic) malaria. In contrast, CM results from a predominantly Th1 response. In schistosomiasis, the Th2-type responses are driven by schistosome egg antigens (SEAs) with intact carbohydrate moieties. A major secretory glycoprotein, the IL-4-inducing principle from schistosome eggs IPSE (also known as alpha-1, or IPSE/alpha-1) , was identified as the bioactive component in Schistosoma mansoni egg extracts . IPSE/alpha-1 triggers basophils to release IL-4, leading to subsequent IL-13 and additional IL-4 expression, the latter cytokine being a potential key player in Th2 biasing. Several studies in murine models demonstrate a non-consistent effect of Schistosoma infection on malaria development, which is mostly expressed as enhancement of parasitaemia . Similar conclusions concerning human malaria are based on study cases in endemic areas. This research examined the effect of a preexisting schistosomal infection on the development of murine CM, and the possible role of a main schistosomal antigen, IPSE/alpha-1, in the effect seen. The results demonstrate that IPSE/alpha-1 has a role in changing the course of malaria infection, leading to increased survival, and that a shift in cytokine expression is associated with CM reduction. Overall, this research demonstrates that CM may be alleviated by schistosomiasis.

Methods Parasites Schistosoma mansoni cercariae and schistosomula: an Egyptian strain of S. mansoni, kept in Puerto Rican Biomphalaria glabrata snails and ICR mice, was used throughout this work. Cercaria shedding was induced by subjecting infected, water-immersed snails to light for 1.5 hours. The cercariae were concentrated by cooling and low speed centrifugation. The ANKA strain of Plasmodium berghei (MRA-311, CDC, Atlanta) was maintained in vivo by serial transfer of parasitized erythrocytes from infected to naive mice. Hosts ICR HSD (Harlan-Sprague-Dawley) male mice aged six to seven weeks were used in all experiments; eight to 10 mice per group. The mice were housed under standard light and temperature conditions and were provided with unlimited access to water and food. The experiments were carried out in accordance with institutional guidelines for animal care, by a protocol approved by the Animal Ethical Care Committee of The Hebrew University of Jerusalem, AAALAC (Association for Assessment and Accreditation of Laboratory Animal Care) accreditation number #1285. The choice of genetically heterogenous mice was made in order to enable a more accurate reflection of CM susceptibility and the possible effect of coinfection in human beings. The validity of the CM model in outbred mice has previously been demonstrated. Experimental setup Mice were infected with 50 or 100 S. mansoni cercariae by subcutaneous injection. Four or seven weeks later, one group of each condition was infected with 5 104 P. berghei-parasitized red blood cells, an inoculum which leads to cerebral malaria in the majority of infected mice. Additional control groups consisted of mice infected with P. berghei or S. mansoni only. Worm burdens were determined by dissection of Schistosoma-infected mice. Alternatively, mice were first infected with P. berghei and subsequently administered complete S. mansoni egg extract (SmEA) , egg extract from which IPSE/alpha-1 was removed (SmEA IPSE/alpha-1) (45 g/mouse/day on days -7, 0, and 3 post-infection; 22.5 g/mouse on day 6 post-infection), or IPSE/alpha-1 (5 g/mouse/day from day -7 to +4 post-infection), by intravenous (iv) administration. Parasitaemia was monitored every other day by thin blood smears prepared from tail blood. These were stained with a Giemsa solution and examined under a light microscope. Blood samples were taken for subsequent cytokine analysis by ELISA (Biolegend,

Israel). The minimum detectable concentrations were 4 pg/ml, 2 pg/ml, 1 pg/ml, and 30 pg/ml for IFN , TNF, IL-4, and IL-10, respectively. The link between immune responses, death and cerebral malaria in mouse models has previously been demonstrated. Observed clinical symptoms, including an accelerated drop in temperature and death at low parasitaemia, indicate CM. Parasitaemia levels, the appearance of neurological symptoms and changes in weight, temperature, and haematocrit of infected mice were evaluated. Clinical signs, which appear one to two days before death from CM, include marked coat staring, hunching, wobbly gait and reduced locomotion, convulsions, and coma. Brain pathology observed in mice dying of CM includes haemorrhages, mononuculear cell infiltrations and the development of brain oedema . Mice that died at a parasitaemia of up to 15% with accompanying neurological symptoms, drastic weight reduction, and a body temperature of 34C or below were considered to have died of CM. Mice which did not die from CM died from severe malaria-induced anaemia and high parasitaemia, as has been reported in all other cases where mice do not succumb to P. berghei-induced CM.