MALARIA IN PREGNANCY BY DR. NYENGIDIKI DEPARTMENT OF OBSTETRICS & GYNAECOLOGY, U.P.T.H. PORT HARCOURT
MALARIA IN PREGNANCY INTRODUCTION EPIDEMIOLOGY AETIOPATHOGENESIS EPIDEMIOLOGICAL CLASSIFICATION MODE OF TRANSMISSION EFFECT OF PREGNANCY ON MALARIA EFFECT OF MALARIA ON PREGNANCY
GENERAL INTRODUCTION Malaria –
Malaria – Sporozoa of the genus plasmodium-pigment producing ameboid intracellular parasite of vertebrates . Parasite transmitted –Female Anopheles mosquito. Found in all parts of the world in the last centurylatitude 640 North – latitude32 0 south -Russian Siberia –Northern U.S.A With improvement in living standards/effective preventive measures –change in geographical preponderance –latitude 300N and 200 south. (malaria belt-Tropics and Sub-Tropical areas.) With repeated infections, immunity was acquired by the non pregnant female which is considerably reduced during pregnancy thus making malaria a serious public health and obstetrics problems.
EPIDEMIOLOGY Over 300millions cases of malaria reported annually- 90% in Africa. 2-3 million deaths annually-90% in Africa 2.8billion cases in indigenous malaria areas. Prevalence of malaria in pregnancy differ from location to location. -lle-lfe – 16% -UPTH – 14% Incidence during protected pregnancy -8% More amongst primigravidae and secundigravidae.
AETIOPATHOGENESIS Four species of plasmodium -plasmodium falciparum-found in Africa, south East Asia, Papua New Guinea -P. Vivax –central America, the indian subcontinent and China. -P. Malaria –Wide spread in distribution -P. Ovale – west Africa In Nigeria malaria infections are caused by: -P.Falciparum- 95% -Pure P.malaria – 4% -P. Ovale - 1% Mixed infection of P.falciparum /malaria -15% , increased in dry season to 35% P. Vivax infection –Not present in Nigeria b/c of the absence of Duffy blood group.
EPIDEMIOLOGICAL CLASSIFICATION OF MALARIA ENDEMIC - Risk of getting malaria present all year round EPIDEMIC -Risk of getting the disease may disappear or remain insignificant for a long time with sudden reappearance with bouts of disease HOLODEMIC -intense all year transmission of malaria parasite with high population immunity. High spleen rates > 75%. HYPERENDEMIC -Seasonal transmission which do not provide adequate immunity .spleen rates of 51-75% MESODEMIC -some malaria transmission with occasional epidemics providing low immunity. Spleen rates of 11-50% HYPOENDEMIC -Limited malaria transmmission, with little or no immunity Spleen rates of <10%
MODE OF TRANSMISSION NATURAL -Transplacental – 20% of neonates(congenital malaria) -bite of an infected female anopheles mosquito UNNATURAL -Blood transfusion -needle shared amongst addicts infected with the malaria parasite. The above method of transmission is devoid of exoerythrocystic phase hence no relapse.
EFFECT OF PREGNANCY ON MALARIA PARTIALLY IMMUNED -Presence of antibodies from repeated infections prior to pregnancy. In pregnancy: -Increased cortisol production,higher in 1st pregnancies. -Formation of anti-adhesive antibodies by the multigravidae. NON-IMMUNED This includes: -Indigenes who had lost their immunity -patients from unstable malarious zones -prolonged chemoprophylaxis These groups are more susceptible to malaria attacks and likely to suffer from serious complications of malaria
EFFECTS OF MALARIA ON PREGNANCY
jMATERNAL Worst amongst non-immuned 1.Anaemia worst during the 16th-24th weeks Mechanism .hemolysis of parasitized/non parasitized cells .sequestration in the spleen .depletion of folate 2.Cerebral malaria 3.Gastrointestinal malaria .abdominal pains, distension, vomiting and diarrhoea 4.Hypoglycaemia 5.Acute pulmonary oedema 6.Acute renal failure 7.Hyperparasitaemia - Asexual forms >250,000 per microlitre of blood 8.Hyperpyrexia 9.Premature labour 10.prostration,acidiosis and circulatory collapse
FETUS Protected by three mechanisms -Immunoglobulin G -Placenta barrier -Haemoglobin F However despite these, -abortions, -intrauterine growth restriction -intrauterine fetal death -low birth weight Severe birth asphyxia -congenital /neonatal malaria
EFFECTS OF MALARIA IN PREGNANCY CONT. PLACENTA About 50% of women have placental parasitaemia without peripheral parasitaemia -Highly vascular and favourable site of sequestration -Initiates microvillous destruction by chemical mediators – cytokines -Fibrinoid degeneration -Reduced tissue perfusion and barrier ability of the placenta -producing intrauterine growth restirction,congenital malaria and intrauterine fetal death Placenta binding is made possible by: .presence of endothelial receptors CD36 .Unique receptors chondrotin sulphate A developed by primigravidae increasing their susceptibility to placenta parasitization -Subsequent pregnancies develop immunity against these receptors.