INFECTIOUS DISEASES II.pptx

INFECTIOUS DISEASES II MALARIA IN CHILDREN DR UGOLEE JERRY INTRODUCTION • Malaria is an infectious disease caused by the parasite of the genus Plasmodium • Five species cause infection in humans • P. falciparum Most common/deadly • P. vivax • P. ovale • P. malariae • P. knowlesi INTRODUCTION •...

INFECTIOUS DISEASES II MALARIA IN CHILDREN DR UGOLEE JERRY INTRODUCTION • Malaria is an infectious disease caused by the parasite of the genus Plasmodium • Five species cause infection in humans • P. falciparum Most common/deadly • P. vivax • P. ovale • P. malariae • P. knowlesi INTRODUCTION • Transmission may follow • Bites from infected female anopheles mosquito  The main method of transmission. Bites occur between dusk and dawn • Parenteral Blood transfusion, needle stick injury INTRODUCTION • Mother to Child • Through the placenta • Animal to Man • From close interaction with the Macaques EPIDEMIOLOGY  According to WMR(2018), in 2017, there were an estimated 435 000 deaths from malaria globally, with children <5 years accounting for 61%.  Endemic in tropic & subtropics regions both north and south of the equator, as far as latitudes 64°N & 32°S  Annual cases of malaria in Nigeria = 53 million cases (1 in 4 persons).  Nigeria accounts for 25% of global malaria burden.  Annual deaths from malaria in Nigeria is put at 81,640(9 deaths per hour) while Nigeria accounts for 19% of global malaria death. EPIDEMIOLOGY EPIDEMIOLOGY • Everyone in malaria belt is at risk • Most especially children (Under the age of 5 years) • Pregnant women • Non-immune adults • Immigrants • Travellers EPIDEMIOLOGY •P. falciparum accounts for 80-90% of infection, either alone, or in combination with one or more of the other species •Endemicity of malaria describes the amount and severity of malaria in a community or a region •There are 2 systems of classification based on :  Spleen and parasite rates in children 2-10 years; and  Transmission rates EPIDEMIOLOGY  Hypoendemic : Spleen and parasite rates 1–10%  Mesoendemic : Spleen and parasite rates 11–50%.  Hyperendemic : Spleen and parasite rates constantly > 50% (with adult spleen rate >25%).  Holoendemic : Spleen and parasite rates constantly > 75% ( with low adult spleen rates). EPIDEMIOLOGY • Low(Unstable) transmission: (<1 case per 1000 population)  Intermittent transmission that may be annual, bi-annual or variable.  Low immunity and prone to occurrence of malaria epidemics. High(Stable) transmission (>1case per 1000 pop). Transmission is all year round, but there may be seasonal variation. Partial immunity in older children and adults who may be less likely to get severe LIFE CYCLE OF MALARIA PARASITE Oocyst Sporozoites Mosquito Salivary Gland Zygote Gametocytes Liver stage Red Blood Cell Cycle Hypnozoites AETIOLOGY Feature P.falciparum P. malariae P. vivax P. ovale Pre erythrocytic cycle(days) 5½-7 13-16 7-8 9 Incubation period(days) 9-14 18-37 12-17 16-18 Erythrocytic cycle(hours) 36-48 72 48 48 Relapse - - Yes yes Parasitaemia Up to (cu. ml.) 2,000,000 Up to 20,000 Up to 50,000 Up to 30,000 Dev. period in mosquito(da ys) 28 10-12 10 14 PATHOGENESIS • P. falciparum has the ability to invade RBCs of all ages and with repeated cycles of development within the red cells, the parasite numbers grow exponentially into high parasite burdens if infection is not inhibited by host or with drugs. • Infected red cells adhere to the wall of vessels(cytoadherence), to each other and sometimes to uninfected erythrocytes(rosetting).Adherence causes (sequestration) of rbc’s containing mature parasites PATHOGENESIS • Cytoadherence: increased adhesiveness of RBCs infected with late stages of the P. falciparum that adhere to the post capillary venular endothelium in the deep microvasculature. • Sequestration: of parasites in various organs such as brain, heart, placenta, kidney, adipose tissues etc following cytoadherence. • Rosetting : adherence of uninfected RBCs to infected red cells CLASSIFICATION UNCOMPLICATED MALARIA & SEVERE MALARIA CLASSIFICATION UNCOMPLICATED MALARIA Symptomatic infection with malaria parasitaemia without evidence of vital organ dysfunction. CLINICAL FEATURES: • Symptoms • The main manifestation is FEVER • Cold Chills / Rigor • Headaches and other body aches • Malaise, bitter aftertaste, flu-like symptoms • Nausea /Vomiting/poor appetite • Joint weakness/pains Signs • Fever , hepatosplenomegally, pallor, lethargy CLASSIFICATION SEVERE MALARIA • Acute febrile illness with demonstrable with evidence of asexual P. Falciparum infection and lifethreatening signs and/or symptoms or vital organ dysfunction OR • Patient with P. falciparum asexual parasitaemia and presence of one or more of the clinical or laboratory features listed below SEVERE MALARIA WHO 2015 Feature Description Cerebral malaria unarousable coma score lasting > 30mins,exclude other encephalopathies & show evidence of P. falciparum (blood ,marrow or brain smear) Prostration Generalized weakness so that the person is unable to sit, stand or walk without assistance Multiple convulsions More than two episodes within 24 h Acidosis A base deficit of > 8 mEq/L or, if not available, a plasma bicarbonate level of < 15 mmol/L or venous plasma lactate ≥ 5 mmol/L. Severe acidosis manifests clinically as respiratory distress (rapid, deep, laboured breathing) SEVERE MALARIA WHO 2015 Feature Description Including recurrent or prolonged bleeding Significant from bleeding (DIC) the nose, gums or venepuncture sites; haematemesis or melena Blood or plasma glucose < 2.2 mmol/L (< 40 Hypoglycaemia mg/dL) Severe malarial anaemia Haemoglobin concentration ≤ 5 g/dL or a haematocrit of ≤ 15% in children < 12 years of age (< 7 g/dL and < 20%, respectively, in adults) with a parasite count > 10 000/uL Renal impairment Plasma or serum creatinine > 265 μmol/L (3 mg/dL) or blood urea > 20 mmol/L SEVERE MALARIA WHO 2015 Feature Jaundice Pulmonary oedema Shock Description Plasma or serum bilirubin > 50 μmol/L (3 mg/dL) with a parasite count > 100 000/ μL Radiologically confirmed or oxygen saturation < 92% on room air with a respiratory rate > 30/min, often with chest in-drawing and crepitation on auscultation Compensated shock is defined as capillary refill ≥ 3 s or temperature gradient on leg (mid to proximal limb), but no hypotension. Decompensated shock is defined as systolic blood pressure < 70 mm Hg in children or < 80 mmHg in adults, with evidence of impaired perfusion (cool peripheries or prolonged capillary refill) DIAGNOSIS • Malaria is a diagnosis of exclusion. The predominant parasite specie causing over 95% of severe malaria is P. falciparum • Take a good history, ask general information such as age, place of residence, travel, use of LLIN • Ask about previous treatment with antimalarial drug • Explore specific features of uncomplicated disease fever, chills / rigor, head aches and other aches in the older patient and features of severe disease in˂5yr’s DIAGNOSIS • Physical Examination: • body temperature. • Pallor (children/pregnant women) • Check state of hydration • Pulse and BP • Enlarged spleen or liver,especially in children DIAGNOSIS • Exclude signs of severe disease  CNS : Assess level of consciousness using an objective coma scale; brain stem abnormalities; posturing.  Fundoscopy-Posterior chamber findings: Retinal whitening & haemorrhage, papilloedema (cotton wool spot) is pathognomonic.  Respiratory system: check for respiratory distress  CVS: rate, volume of pulse, BP  Abdomen: Feel for the spleen and liver DIAGNOSIS DIAGNOSIS • All suspected cases of malaria should have a parasite based confirmation before the institution of antimalarial treatment at all levels of health care delivery in the country; except in extraordinary circumstances where diagnostic facility is not accessible • For routine services, diagnosis of malaria should be by microscopy or mRDT or a combination of both methods DIAGNOSIS MICROSCOPY BASED TESTS: Require direct visualisation of the parasite under the microscope Blood(giemsa stained thick & thin) film light microscopy Quantitative Buffy Coat(QBC) method, Benzothiocarboxypurine(BCP) procedure. DIAGNOSIS DIAGNOSIS NON MICROCSOPY TESTS Involves identification of the parasitic antigen or the anti-plasmodial antibodies or the parasitic metabolic products.  RDTs: • P. falciparium histidine rich protein-2(PfHRP-2) antigens • parasite lactate dehydrogenase(pLDH) enzyme OTHER TESTS • PCR (Mandatory in Research) • Detection of antibodies by Radio immuno assay, immunofluorescence or enzyme immuno assay. PfHRP2 • This is a dip stick antigen capture assay, using a monoclonal antibody against P. falciparum histidine rich protein-2 (PfHRP-2) pLDH DIAGNOSIS Unlike with microscopy, the number of parasites present cannot be determined using RDTs. The result is given as the presence or absence of the parasite  Some RDTs detect parasite antigens that can remain in circulation in the blood for up to 2 weeks after a patient has received treatment Other RDTs ( e.g pLDH and aldolase) detect antigens that disappear from the blood rapidly and so will usually be negative a few days after effective treatment. Correct storage is critical. Remove RDT from its sealed packet only when ready to used as it may be impaired by heat or humidity giving an invalid result TREATMENT ANTI MALARIA COMBINATION THERAPY(ACT) • Simultaneous use of two or more blood schizonticidal drugs with -independent modes of action and - different biochemical targets in the parasite • The concept is based on the synergistic or additive potential of 2 or more drugs to:  Improve treatment efficacy  Retard the development of resistance to the individual components of the combination • come as fixed-dose formulations or co-administrated therapy TREATMENT TREATMENT OF UNCOMPLICATED MALARIA • Preferred Treatment is Anti-malarial Combination Therapy • Artemisinin derivatives such as Artemether or Artesunate are combined with one other anti-malarial medicine to form various types of ACTs. • DO NOT USE ARTEMISININ DERIVATIVES AS SINGLE OR MONOTHERAPY. If misused, the parasites can potentially develop resistance to them. • • • • • TREATMENT Artemether – Lumefantrine (AL) Artesunate – Amodiaquine (AA) Artesunate – Mefloquine (AM) Di-hydroartemisinin – Piperaquine (DHP) Artesunate -Pyronaridine (AP) • In Nigeria, AL is the 1st ACT of choice while AA is the 2nd choice TREATMENT • Artemether-lumefantrine • 1.5/9 mg/kg twice daily for three days • Artesunate-Amodiaquine •Artesunate 4 mg/kg once dly for 3 days + • Amodiaquine 10mg base/kg on days 1, 2, & 3 • Artesunate+Mefloquine • Artesunate 4 mg/kg once daily for 3 days + mefloquine 25 mg base/kg (mefloquine 8.3mg/kg daily for 3 days) TREATMENT TREATMENT OF SEVERE MALARIA This comprises of four main steps • clinical assessment of the patient, • specific anti-malarial treatment; • Treatment of complications and • Supportive care. • CLINICAL ASSESSMENT:  Rapid evaluation  To make a clinical diagnosis of severe malaria  Identify life threatening complications TREATMENT TREATMENT OF SEVERE MALARIA • If artesunate injection is not available.. • Artemether 3.2 mg/kg IM given on admission then 1.6mg/kg per day; or • Quinine 20 mg salt/kg on admission (in IV infusion of 10mls/kg of 10% Dextrose) then 10 mg/kg in same infusion to run over 4hrs, 8 hrly x 3doses. • Parenteral antimalarials used in the treatment of severe malaria should be given for a minimum of 24hours, once started (irrespective of the patient's ability to tolerate oral medication earlier), and, thereafter, complete treatment with a full course of the recommended ACT . TREATMENT FAILURE • Said to occur If fever and parasitaemia fail to resolve or recur within 2 weeks of treatment • Treatment failure must be confirmed parasitologically • May result from drug resistance, poor adherence, under-dosing, poor quality drugs & unusual pharmacokinetic properties in that individual. • Drug resistance is defined as the ability of a parasite to survive in a concentration of a drug equal to or higher than that obtained by the recommended dosage. TREATMENT FAILURE MANAGEMENT Artesunate + Amodiaquine (10mg/Kg/ dose daily for 3 days) Artesunate (4mg/Kg/dose –Day 1; then 2mg/Kg/dose daily for 6 days)+ Clindamycin (10 – 20mg/Kg/ per day 12 hourly for 7 days) Quinine (10mg per Kg per dose 8 hourly for 7 days) + Clindamycin (10 – 20mg/Kg/ per day 12 hourly for 7 days) PREVENTION General health protection Health education, appropriate sanitary measures, good ANC, Specific protection Use of LLIN, IPT, chemoprevention, IRS, insect repellants Early diagnosis & prompt Rx Use of parasite based test and ACT within 24hrs of onset of symptoms Limitation of disability Rx of severe malaria with parenteral antimalarials for at least 24hrs, pre-referral Rx of suspected severe malaria with stat dose of IM antimalarials, specific & supportive Rx of life threatening conditions Rehabilitation Physiotherapy, speech therapy, special need school, CHEMOPREVENTION FOR SPECIAL RISK GROUPS • In malaria endemic regions, malaria chemoprophylaxis is recommended in the following category of children only  SCDx  Visitors to or those who are non-indigenous residents of malarious regions.  Those born to mothers who are known to be non immune to malaria.  Those who are immunodeficient due to dx or drugs.