pg-1 Report on Etiology, Epidermiology, pathogenesis, clinic, dd, (typhoid bilious including), the treatment & prophylaxis of malaria 1) Ethiology: Caused by one

of 4 species of plasmoidium: P. Vivax, P. Ovale, P. Falciparum, P. Malariae. Transmitted by Anopheles Mosquito vector. The parasite can be transmitted also by blood transfusion, transplacentally or injections. 2- Epidemiology: Endemics, Epidemics occurs, Malaria is PO disease of hot, humid contries where conditions are ideal for breeding of the mosquito vector. In SriLanka only P. Vivax & P. Falciparum. Endemic in India, Africa, South America 3- Life Cycle – 2 Stages a) Sexual Cycle (Sporogony) – In mosquito b) Asexual Cycle (Schizogony) – In human A) Sexual Cycle (Sporogony) – occurs in the mosquito, it sucks blood from the infected persons where the gametocytes are ingested, the gametocytes are released from RBC in mosquitos stomach there by the gametocyts are transformed in to gamest→fertilysation→zygote→ookinete→oocyte→sporozoites develop withen the oocyte→the sporozoites are released in to mosquitos salivary glands→mosquito bytes humans→sporozoites are released in to human blood. B)Asexual cycle (Schizogony)- occures in the human and devided in to 3 main stages. 1. pre erythrocytic (primary exoerythrocytic cycle) 2.erythrocytic 3 secondary exoerythrocytic cycle 1. pre erythrocytic – sporozoites circulate in humans blood enters hepatocytes & multiply withen them→Merozoites→come out of them after 1 wk and invade RBC to cause the erythrocytic cycle. 2.Erythrocytic cycle- after ingestion of merozoites in to the RBC→ring from early trophozoites→late trophozoites by binary fussion →schizont(immature)→mature schizont(schizont contains many merozoites→RBC rupture→release merozoites in plasma→some reenter and repeat the cycle→after 2-3 wks→merozoites develop in to ♀ & ♂ gametocytes→gametocytes are ingested by mosquitos. 3. Erythrocytic cycle- after release from hepatocye some merozoites→reenter hepatocytes and cause further multiplication of merozoites. They usually stay latent in hepatocytes and are called hypnozoites they are responsible for persistant of infection or late relapses. This secondary exoerythrocytic cycle occurs in P.malariae, P vivax, P.ovale In falciparum this does not occur they have no hypnozoites. Differance in the 4 types of malaria parasite Characteristics P.falciparum P.vivax I.P 10-14 days 10-14 days Duration of Aprox 1wk Aprox 1wk intrahepatic cycle Erythrocytic 48 hrs 48 hrs cycle Red cells Younger cells reticulocytes prferance Stage of Rings + All stages paracyte seen in gametocytes peripheral blood Relapses No yes Main Cerebral relapses complications malaria,black water fever P.ovale 10-14 days Aprox 1wk 48 hrs reticulorcytes All stages P.malariae 18 days-6wks Aprox 2wk 72 hrs Older cells All stages

yes relapses

Some times Nephroti syndrome

W-17-pg-2 Clinical features of malaria 1. fever –every 24hrs in Vivax,ovale,falciparum and 72hrs in malriae due to rupture of RBC and release ofmerozoites in to plasma, fever in malariae has 3 charactoristic stages. (i) cold stage-due to vasicostriction patient feels cold and shivering lasts 30 mins – 1hr-temp rises rapidly. (ii) Hot stage- lasts 2-6 hrs feels hot,restless & has head ache and rapid pulse. (iii) sweating stage- temp rapidly goes down and the pulse becomes normal, pateint becomes exausted and falls a sleep and when waking up feels normal again. 2. Anaemia 3. hepatosplenomegaly. Complications in malaria-common complications ●Hypoglycemia, ●Anemia, ●acute renal failure, ●ARDS and pulmonary edema, ● Circulatory shcok-may be due to pulmonary edema,GIT heamorrhages, spleen rupture, ●DIC, ●Acidosis, ●Tropical splenomegaly syndrome-occures in hyperendemic regions. Charactorised by 1. massive hepatosplenomegaly,2.↑IgM in serum,3.Malaria paracyte are not seen in spleen or peripheral blood,4.splenomegaly response to antimalarial therapy. Complications perticular to specific kindof malariaa) P.falciparum- causes pernicious malaria, the infected Rbc adher to blood vesseles→cause vascular occlusion→damage in kidney, brain,liver GIT ●cerebral malaria, ●black water fever-occures due to heamolysis of adhered RBC intravascularly b)P.malariae- Nephrotic syndrome- develops because immune complex depossition. Diagnosis of malaria ●Typical clinic eg- periodic fever etc.●peripheral blood taken for thick and thin film- to spot the parasite and to identify the species.●F.B.C-leukocytes law or normal,thrombocyte law, ↑CRP,↑ESR, PT and APTT is prolonged.●Blood biochem- if complicated HCO3-,Na+,glucose,Ca2+ will be decreased due to acidosis.●U.F.R – If complicated ARF- BUN ↑,creatinnr↑, craetinine clearance↓. Treatment and management ●correct dehydration due to vomiting,diarrhoea-give i.v saline, glucose ●reduce fever by giving PCM, removing clothing etc ●check for hypoglycemia specially in young children and in pregnant women. ●ask about previous treament with anti malarial drugs ●ask about previous history of G6PD defficiency leading to heamolysis when giving premiquine. Drug tharapy- ●Quinine- slow i.v infusion drug of choice, Quinine dehydrochloride 20mg/kg i.v over 24 hrs fallowed by 100mg/kg infused over 4hrs at 8 hourly intervals until patient is able to tolarate oral therapy. ●Chloroquine 4:4:2→then single dose of 3 tab of fansidar. Fansidar 1 tab contains sulfadoxine 500mg+pyramethamine 25mg (quinine is usually given in severe complicated malaria) Prophylaxis of malaria ●mosquito repellants,● protective clothing, ●sleeping under nets, ●avoiding outdoor exposure at nights. ●Chemoprophylaxis- chloroquin 300 mg forone week before entering malarious areas→continue during the stay and →after returning for another 4wks. D/D of malaria- Hepatitis, meningitis,septicaemia, Arbo virus infection, Leptospirosis, Typhoid, Gastroenteritis.

Report on Etiology, Epidermiology, pathogenesis, clinic, dd, (typhoid bilious including), the treatment & prophylaxis of malaria Report prepared by 1. Dr. Sajid Mahmood, MD (EU), Accident & Emergency Department, NHS Royal infirmary Liverpool United Kingdom. 2. Dr. Adnan Akram, MD (EU), Department of Infectious Diseases. University Hospital Riga Latvia. 3. Dr. Aftab Ahmed, MD (EU), Infection Control Department, Kaunas Medical University Clinic. Lithuania. Contact: publications [at]