Hemolytic uremic syndrome may complicate infections with Shigella species and Escherichia coli, and it carries a mortality rate greater than 50%.
-In vivax and oval infection the merozoites reinvade the liver cells (exoerythrocytic phase) leading to what is called relapse, but in plasmodium falciparum exoerethrocytic phase do not present but the persistance of infection may be due to reinfection 0r persistence of erythrocyte phase (recrudescence).
(2)Chronic amebic colitis:*Bouts of abdominal discomfort.*Alternating diarrhea and constipation.*The colon usually distended with gas.*Sigmoid and even caecum may be palpable.Investigations:(1)Stool examination: detect the trophozoite or cyst form.(2)Sigmoidoscopic examination : to show amebic ulcers.(3)Serological test: IHA and complement fixation test.
Complications:A. Intestinal:(1)Perforation of the bowel: lead to localized peritonitis orgeneralized peritonitis.(2)Hemorrhage: from erosion of blood vessels or ulcer.(3)Intussusception: usually occur in caeco-colic part.(4)Ameboma: mass like tumor in the course of the colon.(5)Amebic appendicitis and cholecystitis.B. Extra-intestinal:(1) Hepatic amebiasis.(2) Cutaneous amebiasis.(3) Amebic lung abscess.(4) Amebic brain abscess.
Hepatic amebiasis(amebic hepatitis & amebic liver abscess)*It is caused by Entameba histolytica carried from the colonvia the portal vein to the liver.Clinical picture:(A) Symptoms:*Fever, rigors, sweating and malaise.*Pain:- Site: in the right hypochondrium.- Radiation: right shoulder and back.- Character: dull aching, stabbing or throbbing.- Aggravated by: coughing or straining.- Relieved by: leaning to the left side.
(B) Signs:*Fever, usually remittent or hectic.*Marked toxemia.*Mild jaundice in 10% of cases.*Liver is enlarged mainly upwards than downwards.*Tenderness over the right intercostal spaces, andover the right lower ribs posteriorly.*Edema of chest wall is a late sign.Investigations:(1)Stool examination and sigmoidoscopic examination.(2)Serological test: IHA and complement fixation test.(3)Blood examination: Leucocytosis (12,000-20,000).
(4)Therapeutic test with dehydroemetine: usually dramaticresponse occurs after few injections.(5)Radiological examination:a- screen show localized bulging and diminishedmovement of the right cupola of the diaphragm.b- X-ray: show raised right cupola of the diaphragm.(6)Liver scanning using radioactive gold, US and CT scanshelp in localization of the abscess.(7)Diagnostic aspiration: chocolate-brown fluid (anchovysauce) will come out cases of amebic liver abscess.Complications:(1)Rarely becomes chronic.(2)Secondary infection lead to pyogenic abscess.
(3)Rupture of amebic liver abscess may lead to :*Subphrenic abscess. *Amebic lung abscess.*Pleural effusion or empyema.*Generalized peritonitis. *Amebic skin ulcer.Treatment:(1) Treatment of amebic dysentery:*Metronidazole 800 mg TID for 5 days with or withoutdiloxanide furoate 0.5 g TID for 5 days.(2) Treatment of hepatic amebiasis:*Metronidazole 400 mg TID for 10 days with diloxanidefuroate 0.5 g TID for 10 days.*If medical treatment failed, aspiration of the abscessmust be done, through the right 9th intercostalspace in the mid axially line.*Open drainage may be done in chronic cases.
MALARIADefinition:*A disease characterized by recurrent attacks of fever withrigors, enlargement of the spleen and anemia.Geographical distribution:*The disease occurs throughout the tropics and subtropicsand can occur also in temperate climates.Causative organism:*Human malaria is caused by any of the following plasmodia:- P. falciparum (malignant malaria).- P. vivax (benign tertian malaria).- P. ovale (ovale tertian malaria).- P. malariae (quartan malaria).*In Egypt, P. vivax is the commonest type and the femaleanopheles (pharoensis or sergenti) is the commonest vector.
Life cycle of malaria:(1)Asexual phase: (cycle in man)*If infected mosquito bites man, the sporozoites rapidlydisappear form the blood stream.*They invade the liver cells and start what is known as pre-erythrocytic phase.*During this time sporozoites change to trophozoiteschizot schizot filled with merozoites.*The diseased liver cells are destroyed merozoites.*When the merozoites invade the R.B.Cs it give the ringform trophozoite schizont schizontfilled with merozoites .*The diseased R.B.Cs are destroyed merozoites.*After several generations gametocyte formation occurswith production of male microgametocytes and femalemacrogametocytes.
(2)Sexual phase: (cycle in mosquito)*The female mosquito ingests microgametocytes andmacrogametocytes from infected man, which unite, inthe stomach to form zygote ookinte,penetrate the gastric wall to form oocystsporocyst sporocyst contain many sporozoites, then thesporozoites migrate to the salivary gland.Incubation period:*About 10- 14 days.Clinical picture:(1)Prodromal symptoms:*In the last 2 days of the incubation period.*Headache, generalized aches, malaise and anorexia.
(2)The paroxysm:*Typical attack occurs every:* 48 hours in P. vivax and P. ovale (tertian),* 72 h in P. malariae (quartan), and* 36 h in P. falciparum (subtertian).*It passes into three stages:A-Cold stage:*Lasting from 15 minutes to one hour.*The patient feels cold, shivering, and then rigors.*Rapid rise of temperature sometimes reaching 40oC.*Nausea and vomiting are common.B-Hot stage:*Lasting from 2 to 6 hours .*The rigor stop and feeling of cold disappear.
*Hotness and the body temperature is still high.*Headache, dry flushed face, thirst and tachypnea.*Nausea and vomiting are still present.C-Sweating stage:*Lasting from 2 to 3 hours.*Profuse sweating with rapid fall of temperature.*Vomiting stop and patient feels well, the patientusually passes into an exhausted sleep.(3)Spleen:*The spleen always enlarged, fragile and is easilyruptured by an blow on the abdomen.(4)Liver:*Liver may become enlarged and tender.(5)Anemia: Hemolysis and bone marrow suppression.
Complications:*Relapse (in P. vivax and P. ovale).*Anemia.*Rupture spleen.*Nephrotic syndrome (in P. malariae).Malignant malaria (complicated P. falciparum):*Complicated P. falciparum malaria may take a number ofclinical forms:(1)Cerebral malaria:*Headache, drowsiness, fits and if untreated passesinto coma and death.(2)Hyperpyrexia:*May occur in association with cerebral malariawhere the body temperature is more than 41C.*Hot dry skin, and the patient passes into coma.
(3)Bilious Remittent fever:*Attacks of epigastric pain, nausea, vomiting, diarrhea andjaundice due to severe liver damage.(4)Dysenteric malaria:*Stools containing blood and mucous with nausea andvomiting.(5)Choleric malaria:*Profuse watery diarrhea, vomiting and dehydration.*Shock or acute renal failure may occur.(6)Black-water fever:*Acute intravascular hemolysis and hemoglobinuria as acomplication of P. falicparum infection.* Fever with rigor, heavy sweating, nausea, vomiting,jaundice, loin pain and dark urine.*Mortality rate 20 - 30 %.
Investigations:(1)Demonstration of the parasite by blood film.(2)Therapeutic test where the fever responds to anti-malarial drugs.(3)Enzyme-linked immunosorbent assay (ELISA).Treatment:*Chloroquine: 4 tables (600mg) orally then 2 tablets after 6hours then 2 tablet once daily for 2 days.*Quinine: 2 tablets (650mg) three times daily for 10 days.*To prevent relapse in P. vivax and P. ovale primaquine ina dose of 7.5 mg twice daily for 10 days is added toany of the above regimen.*In severe malignant malaria (e.g. cerebral malaria) IVquinine is the drug of choice.
*In chloroquine resistant P. falciparum infection, acombination of quinine and fansidar should be used.Prophylaxis of malaria for travelers:*Chloroquine 300 mg once weekly.*Pyrimethamine 25-50 mg twice a week.*The drug should start one week before travel and continuefor at least 4 weeks after leaving the endemic area.*If chloroquine resistant P. falciparum is expected fansidarone tablet weekly should be added to any of theabove regimen.