Malaria

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MALARIA : 

MALARIA DR SS BUX

BRIEF OUTLINE : 

BRIEF OUTLINE INTRODUCTION ETIOLOGY LIFE CYCLE EPIDEMIOLOGY PATHOGENESIS CLINICAL FEATURES DIAGNOSIS TREATMENT PROPHYLAXIS

INTRODUCTION : 

INTRODUCTION Malaria is a protozoan disease transmitted by the bite of infected female anopheles mosquito. One of the most important parasitic diseases of humans. No-1 cause of death among parasitic diseases.

DISEASE BURDEN:GLOBAL : 

DISEASE BURDEN:GLOBAL

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40% of the world population 170 countries 3 billion infections 1-3 million deaths………per yr. Resurgence of malaria in many parts of the world. Emergence of drug resistance.

ETIOLOGY : 

ETIOLOGY

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Caused by the bite of female anohiline mosquito Inoculation of sporozoites from the salivary gland occur during the blood meal. Four species Plasmodia cause human infections. P.vivax , P.falciparum ,P.ovale , P.malariae .

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1 Plasmodium vivax – Benign Tertian, Tertian Malaria 2 P.ovale - Ovale tertian Malaria 3 P.malariae – Quartan malaria 4 P.falciparum – Falciparum malaria or Malignant Tertian malaria.

LIFE CYCLE : 

LIFE CYCLE Asexual cycle: Man Sexual cycle: Mosquito. Man: Intermediate host Mosquito: Definitive host. Infective form: sporozoite.

HUMAN CYCLE : 

HUMAN CYCLE PRE ERYTHOCYTIC SCHIZOGONY ERYTHOCYTIC SCHIZOGONY EXOERYTHOCYTIC SCHIZOGONY

LIFE CYCLE : 

LIFE CYCLE

INDIVIDUAL CHARACTERISTICS : 

INDIVIDUAL CHARACTERISTICS

PATHOGENESIS : 

PATHOGENESIS Host –Parasite interaction. Effects of parasite on host. RBC lysis Cytoadherance, Rosette formation, Aglutination. Nondefomability of the RBC.

RBC LYSIS N TOXIN RELEASE : 

RBC LYSIS N TOXIN RELEASE Rupture of RBCs at the end of erythocytic cycle Realase of putative toxins and cytokines IL1,TNF,IL8,IL12,IL18 Responsible for various manifestations like,fever,malaise,organ dysfunctions,reduced hemopoesis n gluconeogenesis,cytoadherance. Higher level of mediators are responsible for pathogenesis,whereas lower levels are protective.

SEQUESTRATIONS : 

SEQUESTRATIONS CYTOADHERENCE ROSETTE FORMATION AGGREGATION PfEMP1 expressin on erythrocytic membrane. Endothelial ligands:ICAM,CD36,CSA Responsible for organ dysfunction and severe malaria.

CLINICAL FEATURES : 

CLINICAL FEATURES UNCOMPLICATED MALARIA COMPLICATED/SEVERE MALARIA

UNCOMLICATED MALARIA : 

UNCOMLICATED MALARIA A poor general condition, feeling unwell and having headaches like influenza. Diarrhea, nausea and vomiting often occur as well. Fever and shivering. The attack begins with fever, with the temperature rising as high as 40ºC and falling again over a period of several hours

CONTD…. : 

CONTD…. Classically described as having 3 stages. COLD STAGE HOT STAGE SWEATING STAGE Rarely seen in the present day practice Except for some degree of anemia n splenomegally few signs are seen.

SEVERE MALARIA : 

SEVERE MALARIA

CONTD…. : 

CONTD….

CEREBRAL MALARIA : 

CEREBRAL MALARIA The most dreaded complication Defined: Unarousable coma/coma lasting>30min after Conv. Any level of sensorium to b taken seriously Extreme agitation is poor prognostic sign

Signs…. : 

Signs…. Diffuse symmetric encephalopathy; focal signs are unusual. Fever, Altered sensorim Passive resistance to neck flexon but not like meningitis. EYE: divergent,retinal hge,opacity,papilloedema. Musle tone, DTR, Plantar reflex-variable. Corneal reflex preserved till late. Pout reflex may b present;no other primitive reflex found.

Signs…. : 

Signs…. Neurological sequelae : <3% adults Common in children:upto 15% Especially those with sev anemia,hypoglycemia, repeated seizures,deep coma. Hemiplegia,cerebral palsy, cortical blindness, deafness, impaired cognition n learning-variable duration. Epilepsy; incidence increased, life expectancy decreased.

HYPOGLYCEMIA : 

HYPOGLYCEMIA Important common complication. Associated with poor prognosis, particularly in children and pregnat women. Causes: Failure of hepatic gluconeogenesis Increased consumption by both host n parasite. Quinine induced hyper insulinemic hypo. Reduced intake. Increased peripheral req. due to anaerobic glyco(PASTEUR EFFECT)

ACIDOSIS : 

ACIDOSIS One of the imp cause of death Manifest as acidotic breathing Leads to refractory circulatory failure Casuses: Lactacidemia Anaerobic glycolysis Reduced lactate clearance Lactate production by the parasite 2 Ketoacidosis(CHILDREN)

NON CARDIOGENIC PE : 

NON CARDIOGENIC PE Carries hihest risk of death:80% Common in adults Can develop even after several days of treatment Pathogenesis is poorly understood May be precipitated by overzealous fluid admin. One serious comlication that can develop in otherwise uncomlicated vivax malaria also.

RENAL FAILURE : 

RENAL FAILURE Common among adults. Erythrocyte seqestration leading to impairment of microcircultory flow and metabolism. Acute tubular ncrosis Urine flow resumes in a median of 4 days and creat level normalizes in median of 17 days.

HEMATOLOGIC ABNORMALITIES : 

HEMATOLOGIC ABNORMALITIES ANEMIIA is one of the poor prog. Factors Causes: Obligatory rbc destruction by the parasite Splenic seqestration Ineffective erythropoesis. Stress induced gasrtritis-hematemesis Other hematologic complications include: Coagulopathy Thrombocytopenia DIC <5%

LIVER DYSFUNCTION : 

LIVER DYSFUNCTION Jaundice in malaria may b due to several causes Hemolytic jaundice Hepatocellular Cholestatic Liver dysfunction also contributes to several other prob Nausea vomiting Hypoglycemia Lactacidemia Reduced drug clearance

MALARIA IN PREGNANCY : 

MALARIA IN PREGNANCY Leads to fetal n maternal complications In endemic areas –LBW, fetal n infant mortality In nonendemic areas-fetal distress,prem labour,still birth,and maternal death. HIV infection predisposes preg women to malaria

CHRONIC COMPLICATIONS : 

CHRONIC COMPLICATIONS TROPICAL SPLENOMEGALLY(HMS) QUARTAN MALARIAL NEPHROPATHY BURKIT’S LYMPHOMA

TROPICAL SPLENOMEGALLY(HMS) : 

TROPICAL SPLENOMEGALLY(HMS) Hyper gama-globulinemia,normocytic normochromic anemia, splenomegally Marked titres of IgM antimalarial antibody,hepatic sinusoidal lymphocytosis,peripheral B-cell lymphocytosis. IgM antibody against CD8+T lymho,CD5+T lympho Increased ratio of CD4+to CD8+ lympho Uninhibited Bcell production of IgM-cryoglobulin Rediculoendothelial hyperplasia is a cconequence

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Manifest :Mass abdomen ,anemia, pancytopenia ,susceptbility to infection. Antimalarial chemoprophylaxis for endemic areas and antimalarial treatment for non endemic areas Refractory: Malignant lympho proliferative disorder.

QUARTAN MALARIAL NEPHROPATHY : 

QUARTAN MALARIAL NEPHROPATHY Chronic n repeated infection with P. malariae leads to soluble immune comlex injury to renal glomeruli LM:Focal segmental glomerulonephritis EM:Subendothelial dense deposit IFM: Coarse granular pattern(IgG3)-Selective protinuria Fine granular pattern(IgG2)-Non-selective protinuria Poorly responds to treatment.

DIAGNOSIS : 

DIAGNOSIS CLINICAL FEATURES INVESIGATIONS Demonstration of parasite Hematology Biochemistry

DEMO OF PARASITE : 

DEMO OF PARASITE THICK SMEAR THIN SMEAR RAPID ANTIGEN FLOURESCENT MICROSCOPY

BLOOD COLLECTION : 

BLOOD COLLECTION

MAKING OF A SMEAR : 

MAKING OF A SMEAR

RAPID ANTIGEN METHOD : 

RAPID ANTIGEN METHOD Antigen Detection Various test kits are available to detect antigens derived from malaria parasites. Such immunologic ("immunochromatographic") tests most often use a dipstick or cassette format, and provide results in 2-15 minutes. These "Rapid Diagnostic Tests" (RDTs) offer a useful alternative to microscopy in situations where reliable microscopic diagnosis is not available. Malaria RDTs are currently used in some clinical settings . PfHRP2 BASED-specific for PF LDH BASED-NONSPECIFIC

MICROTUBE METHOD : 

MICROTUBE METHOD The QBC Malaria method is the simplest and most sensitive method for diagnosing the following diseases. Malaria Babesiosis Trypanosomiasis (Chagas disease, Sleeping Sickness) Filariasis (Elephantiasis, Loa-Loa) Relapsing Fever (Borreliosis)

PRICIPLE OF QBC : 

PRICIPLE OF QBC

SEROLOGY : 

SEROLOGY Serology detects antibodies against malaria parasites, using either indirect immunofluorescence (IFA) or enzyme-linked immunosorbent assay (ELISA). Serology does not detect current infection but rather measures past experience.

MOLECULAR DIAGNOSIS : 

MOLECULAR DIAGNOSIS Parasite nucleic acids are detected using polymerase chain reaction (PCR). This technique is more accurate than microscopy. However, it is expensive, and requires a specialized laboratory (even though technical advances will likely result in field-operated PCR machines).

OTHER LAB TESTS : 

OTHER LAB TESTS Normocytic normochromic anemia Raised ESR, CRP, Plasma viscosity Platelet slightly reduced PT, PTT may b prolonged in severe infection AT3 reduced LFT-impaired RFT-impaired Hypergamaglobulinemia Blood glucose

TREATMENT : 

TREATMENT

TREATMENT…… : 

TREATMENT……

MANAGEMENT OF COMPLICATIONS : 

MANAGEMENT OF COMPLICATIONS ANEMIA: Blood transfusion Hyperparasitemia: Exchange transfusion Hypoglycemia: Dextrose infusion ARF:RRT ARDS:O2 supplementation,mech ventilation,diuretics Convulsion: Anticonvulsant IV antimicrobials

PREVENTION : 

PREVENTION CHEMOPROPHYLAXIS BEHAVIOURAL PROPHYLAXIS IMMUNOPROPHYLAXIS

CHEMOPROPHYLAXIS : 

CHEMOPROPHYLAXIS

BEHAVIURAL PROPHYLAXIS : 

BEHAVIURAL PROPHYLAXIS

IMMUNO PROPHYLAXIS : 

IMMUNO PROPHYLAXIS This degree of protection would be extremely difficult to achieve and might not be technically feasible with current vaccinology art and science. Many vaccine developers have therefore focused their efforts on creating a vaccine that limits the ability of the parasite to successfully infect large numbers of red blood cells. This would not prevent infection but would limit the severity of the disease and help prevent malaria deaths.…Vaccine Challenges

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This degree of protection would be extremely difficult to achieve and might not be technically feasible with current vaccinology art and science. Many vaccine developers have therefore focused their efforts on creating a vaccine that limits the ability of the parasite to successfully infect large numbers of red blood cells. This would not prevent infection but would limit the severity of the disease and help prevent malaria deaths.…Vaccine Challenges

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The most successful candidate developed to date is the RTS,S recombinant vaccine. The RTS,S/AS02A, one of the key vaccines produced using this technique, has been used in field trials in The Gambia. Three repeat doses were administered in the 6 months leading up to the period of highest malaria transmission. The vaccine efficacy was reported at approximately 71% (with 95% confidence intervals spanning from 46 to 85%) during the first 2 months of follow-up, but falling to 0% in the last 6 weeks in 250 male volunteers.