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Malaria Malaria Presentation Transcript

  • Malaria By Dr. Osman Sadig
    • Malaria:
    • - is a m ajor health problem in developing tropical countries:
    • 1- Annual incidence of 300– 500 x 1000 000
    • 2- 1% mortality , mainly in under 5 years ,
    • pregnant ladies & non immune
    • 3- 80% of cases & 90% of deaths in AFRICA.
    • - In Sudan :-
    • 1- 250/ 10 000 population/ year (7.5 million/
    • year
    • 2- 35 000 deaths every year
    • 3- 20—40% of health institute attendance
    • 4- 20—30% of total hospital admissions
    • 5- 15—20% of total deaths
    • 6- 22% loss of working hours
    • Organism:-
    • - Plasmodium falciparum ( 95% in Sudan)
    • - P. vivax
    • - P. ovale
    • - P. malariae
    • ** P. falcip is endemic in the tropics , has no
    • hypnozoites to sustain transmission which
    • depends on the presence of vector all za year.
    • ** P.f invades RBC of all ages, multiple
    • RBC infection is common & mature trophoz
    • are absent in the peripheral
    • blood.
    • ** P.f is the only sp. of malaria associated with
    • life threatening complications & is often
    • drug resistant
    • ** P.v. & P.o. are endemic in the temperate
    • zones, invade reticulocytes & cause relapsing
    • malaria.
    • ** P.m. produces chronic low parasitaemia.
    • ** 5—7% of infections are multiple with more
    • than one sp.
    • ** Light microscopy of stained BF is used to
    • diagnose malaria & identify the sps.
    • Transmission
    • 1- Female anopheles mosquito (A. gambiensis
    • and A. arabiensis). Transmission depends on
    • the presence of gametocytes in the peri blood
    • 2- BT & sharing needles . No relapse with this
    • mode of transmission
    • 3- Transplacental Congenital malaria
    • Epidemiology
    • Transmission of malaria depends on the presence of:-
    • 1- Infected reservoir
    • 2- Susceptible human being
    • 3- Competent vector
    • 4- Multiple opportunities for contact between
    • the vector & human host.
  •  
    • Endemicity of malaria
    • - Endemicity is the amount & severity of malaria
    • in an area or community.
    • - Prevalence of malaria = to estimate the preval
    • of malaria a large No of people, sp infants and
    • children must be examined by:
    • 1- Spleen rate : this is the proportion of
    • children (2-10 years) in a community
    • who have enlarged spleen:
    • - hypoendemic= spleen rate of 0-10%
    • - mesoendemic= spleen rate of 11-50%
    • - hyperendemic= spleen rate of over 50%
    • - holoendemic= spleen rate over 75%
    • 2- Parasite rate = it is the proportion of persons in a given community who show parasites in the peripheral blood.
    • Immunity
    • 1- Natural resistance depends on cellular factors
    • that prevent penetration & development of
    • parasites in the RBCs (G6PD def & HbC) and
    • the susceptibility of parasitized cells to
    • removal from circulation by lymphoid macrop
    • system (Hb AS, Hb F, Hb C), the later
    • protects against severe complicated malaria.
    • P.v can not invade RBCs with duffy blood
    • group
    • 2- Acquired resistance is either passive transplacental which persists for 6/12 OR
    • active resistance which is sp & stage specific.
    • Humoral immunity deals with extracellular
    • parasites & cellular immunity deals with intracell
    • parasites. The Spleen traps & removes parasitized cells.
    • Pathogenesis
    • - Invasion of RBCs by malaria parasites is comm
    • to all sp. causing hemolysis, fever & splenome
    • - P.f is the only sp. that causes microvascular dis. With maturation of P.f the parasitized RBCs become spherical and knobs appear on the surface facilitating cytoadherance to
    • endoth cells of capillaries & post capillary venules of vital organs. Cytokines (TNF alpha) increases cytoadherance and microvascular obstruction, tissue anoxia and wide spread organ failure.
  •  
    • 1- Fever is due to rupture of the schizonts
    • releasing toxic substances stimulating
    • macrophages to release endogenous pyrogen
    • raising temp. via the hypothalamus
    • 2- Anaemia : rapidly developing anaemia is a
    • feature of P.f in children < 5y & pregn ladies
    • - hemolysis of parasitized & unparasitized
    • RBCs
    • - dyserythropoiesis - TNF alpha.
    • - haemodilution from sequestration of RBCs
    • in the spleen
    • - depletion of folate stores
    • 3- Hypoglycemia :- related to the degree of
    • parasitaemia
    • - depletion of glycogen stores from low intake
    • - Increased Glucose consumption by the large
    • numbers of parasites.
    • - Hypoglycemic effect of TNF
    • - Quinine therapy & release of insulin
    • - Suppression of gluconeogenesis
    • 4- Black water fever wz severe intravas hemolys
    • causing anaemia, Hb uria & renal failure
    • 5- Immune thrombocytopenia & coagulopathy
    • 6- Liver :- congested & enlarged with centrilobular necrosis in severe cases
    • 7- Jaundice : either hemolytic or hepato cellular.
    • Hepato renal syndrome can occur.
    • 8- Spleen : there is R/E hyperplasia with congestion, hage & thrombosis. Spleen is tender & may rupture. Hypersplenism.
    • 9- Kidneys : Ischemic pre renal failure may occur
    • as well as immune complex nephritis
    • 10- CNS : congested meningeal & cerebral capill
    • with parasitized RBCs with ring hage & mild reversible peri vascular inflammation.
    • 11- Lungs : pulm edema
    • 12- GIT : micro vascular dis causes mucosal
    • edema, hage & ulceration causing D & V
    • 13- Adrenals : congestion & hage
    • 14- Placenta : may be heavily parasitized sp. In
    • PG & may cause abortion & low birth Wt.
    • Uncomplicated malaria
    • Case definition :
    • 1- Suspected malaria : Malaria is suspected when
    • a pat presents with fever (or history of fever
    • in za last 24 hours) and other S & S suggestive
    • of malaria after exclusion of other common
    • causes of fever in the area.
    • 2- Confirmed malaria : Malaria is confirmed by
    • demonstration of asexual forms of za parasite
    • in za thick or thin peri BF or by rapid diagnost
    • test in the presence of fever
    • * When malaria is suspected & there is no
    • facilities for lab. diagnosis., assume that the pat has malaria when there is no other
    • obvious cause for za fever.
    • * Incubation period is 9—14 days in P.f
    • * Periodic fever is the hallmark of malaria and
    • coincides with rupture of RBCs & release of
    • new merozoites.
    • - Tertian wz P.v & P.o
    • - Quartan wz P.m
    • - Contin. wz irregular intermittent spikes
    • wz P.f, sometimes quotidian or sub tertian
    • * Paroxysms :
    • - Cold stage —15 min to hours
    • - Hot stage –2—6 hours
    • - Sweating stage —2—4 hours
    • * Anaemia & splenomegaly are other signs
    • * Herpes labialis is common
    • * Natural history of falciparum malaria varies
    • from rapidly fatal in the non immune to no
    • symptom in semi immune even with significa
    • parasitaemia. In non immune hyperparasit
    • with double infection (>5%) may lead to fatal
    • outcome in za absence of skilled management.
    • Lab diagnosis of malaria
    • 1- Thick BF stained with Giemsa is examined
    • microscopically for:
    • - presence of infection
    • - Stage of parasite
    • - parasite count
    • + 1—10 parasites/ 100 fields
    • ++ 11—100 parasites/ 100 fields
    • +++ 1—10 parasites/ one field
    • ++++ 11—100 parasites/ one field * Thin BF is used where sp other than P.f
    • coexist
  •  
    • 2- Rapid diagnostic tests e.g. ICT. This is not
    • good in areas of high transmission where
    • asymptomatic parasitaemia & antigenaemia
    • is common. High cost but can be used by
    • unskilled personale , used in emergency and epidemic situations & where the cost of malaria TR is high to avoid unnecessary use of drugs.
    • Other investigations include: CBC, urine exam
    • BUN & E, blood sugar & serum bilirubin.
    • Management of uncomplicated malaria
    • 1-1 st line TR :- Artsunate + sulfadoxine- pyremeth
    • - Artsunate (AS)= tabs of 50, 100 & 200 mg
    • SE = transient rise in transaminases & transien
    • reduction in reticulocytes
    • - Sulfadoxine- pyremethamine (SP)= fixed dose
    • schozonticidal combination against P.f
    • SP= 500 mg sulfadoxine + 25 mg pyremeth
    • in tab & injection forms.
    • SE = GIT, visual disturbance & cutaneous
    • reactions
    • * Dose regimens :-
    • - 1 st day= 4 mg/ kg BW AS + 25 mg/kg BW
    • sulfadoxine + 1.25 mg/kg BW pyremeth
    • - 2 nd day= 4 mg/ kg BW AS 24 h after 1 st dose
    • - 3 rd day= 4 mg/ kg BW AS 24 h after 2 nd dose
    • * TR failure is not always due to parasite resist?
    • If BF or RDT is +ve go to:
    • 2- 2 nd line TR : Artemethe r (ARM) 20 mg- lumef
    • antrine (LF) 120 mg fixed dose comb. wz high
    • clinical & parasitological cure rate & rapid gametocyte clearance
    • SE = GIT, dizziness, fatigue, palpitation, headache skin rash, arthralgia,& myalgia. No serious cardiotoxicity
    • ** Dose regimens : 4 tabs 1 st , repeated after 8h
    • then 4 tabs M & E 2 nd & 3 rd day, better taken
    • with fatty meal or milk.
    • 3- 3 rd line TR : Quinine (Q) dihydroCL, Q CL or
    • Q SO4 used if no response ARM/ LF (lab+ve)
    • ** Dose regimens : Oral= 10mg/kg 8 hrly x 7 D
    • - Injectable Q diluted IM or IV infusion 10mg/
    • kg & shift to oral as soon as possible
    • Severe malaria ( SM)
    • - SM is defined as malaria due to P.f infection
    • sufficiently serious to be an immediate threat to
    • life. It is med emergency & require hospitalizati
    • - A pat is regarded as having severe malaria if
    • he or she has one or more of the following:
    • 1- Impaired level of consciousness (cerebral mal
    • 2- Resp distress (acidotic breathing)
    • 3- Repetitive convulsions
    • 4-Circulatory collapse
    • 5- Pulm edema
    • 6- Abn bleeding (DIC)
    • 7- Jaundice
    • 8- Hb uria
    • 9- Prostration
    • 10- Severe anaemia (Hb < 5gm/dl)
    • 11- Hypoglycemia ( BS < 40mg/dl)
    • 12- Acidosis
    • 13- Hyperlactinaemia ( lactic acidosis)
    • 14- Hyperparasitaemia ( >5% RBCs wz ring
    • stage)
    • 15- Renal impairment
    • 16- Electrolyte imbalance (hyponatraemia)
    • *** TSS is a chronic complication of malaria
    • Differential diagnosis of malaria
    • - Fever : infections ( viral, bacterial, protozoal)
    • - Rigors : UTI, septicemia, gall stones & cholecy
    • pneumonia, amoebic liver abs
    • - Cerebral malaria : meningitis, stroke, encephalit
    • metabolic in comatosed pats,
    • heat stroke
    • - Other causes of anaemia & splenomegaly
    • e.g typhoid, brucellosis
    • 1- General management of SM(8+8+4)
    • * * Immediate measures :
    • 1- Start resuscitation- ABC
    • 2- IV line
    • 3- Thick BF for immediate parasite count
    • 4- Assess degree of dehydration, fluid requirem
    • and correct accordingly
    • 5- Control fever if axillary temp 38.5 or above
    • by tepid sponge & fanning, paracetamol
    • 15mg/kg 4—6 hourly
    • 6- Control convulsion by diazepam. Correct hypogly 7- Detect & TR hypoglycemia which can recur specially in pregnant women & children
    • Give 1 ml/kg of 50% dextrose IV diluted in
    • equal volume of NS over 3-5 min. followed by
    • 10% dextrose infusion
    • 8- Start Q IV or ARM IM. Q IM or AS supposit
    • can do the job.
    • ** Look & deal with following complications :
    • 1- Shock, algid malaria: if SBP < 80mmHg
    • suspect septicemia & take blood samples for
    • cultures. Give parentral broad spectrum
    • antibiotics, saline infusion & O2
    • 2- Consider the need for BT: transfuse if there
    • is cardiopulm symptoms, PCV <20% or Hb<5
    • 3- Metabolic acidosis: exclude & TR hypoglycem
    • hypovolaemia & gm –ve septicemia.
    • 4- Spontaneous bleeding & coagulopathy: fresh
    • screened whole BT or clotting factors, Vit K
    • 10mg IV daily for adults
    • 5- Acute renal failure: exclude dehydr, maintain
    • strict fluid balance. Dialysis if indicated
    • 6- Black- water fever (malarial Hb uria): suitable
    • antimalarial & screened fresh BT
    • 7- Acute pulm edema: prevent by avoiding
    • overload. IV frusemide & O2 8- Exclude common infections that mimic malaria
    • e.g. WBC, L/P & CXR
    • ** Monitor the patient :
    • 1- level of consciousness by Glasgow scale 6 hrly to
    • assess the progress until the pat regains
    • full consciousness
    • 2- Fluid input/ output: detect dehydr & TR but avoid
    • overload e.g pulm edema
    • 3- Monitor vital signs every 6 hrs to detect
    • compl of SM
    • 4- level of parasitaemia: monitor parasite count
    • daily to monitor therapeutic effect
    • 2- Specific treatment of SM
    • ** Pre referral TR : Q IM or AS suppositories
    • 10mg/kg rectal caps. Then refer to hospital
    • ** Hospital TR:
    • 1- Q IV infusion or IM if IV is not feasible & shift to oral as soon as possible. Total of 10mg/kg 8 hrly for 7 days
    • 2- Q for 3 days & shift to 1 st line therapy if the
    • patient can take oral medication & can not tolerate oral Q.
    • SE = N, V & tinnitus. Over dose cause HA, dizzi,
    • CNS dist & delerium, hypoglycemia, hypotn
    • 3- ARM injections ( 40mg & 80mg/ml) as
    • monotherapy should only be used for SM
    • - 1.6 mg/kg initially, repeated after 12 hrs
    • and then daily for 6 days (total of 8 amp)
    • - 1.6 mg/kg initially, repeated after 12 hrs
    • and then daily in za 2 nd & 3 rd day (4 amp)
    • followed by the 1 st line TR if the pat can
    • take orally.
    • - SE of ARM are mild= HA, abd pain, vomiting
    • itching, non specific ST changes & 1 st
    • degree A/V block.
    • Malaria in pregnancy (MIP)
    • 1-The manifestation of malaria in preg , specially
    • in the 2 nd half, include:
    • - fever - anaemia
    • - splenomegaly - acute pulm edema
    • - hypoglycemia - 2ndry infections
    • 2- Management of MIP : TR malaria & compl,
    • manage labour
    • - 1 st trimester = oral Q is safe 10mg/kgx3x7
    • - 2 nd & 3 rd trimester = oral Q for 7 days OR
    • oral Q for 3 days followed by SP in full dose
    • OR use 1 st line TR
    • 3- Management of SM during preg :
    • - Q 10mg/kg x3x7 days through out preg
    • - Start wz IV infusion or IM & shift to oral OR
    • - Start wz Q IV or IM for at least for 3 days OR
    • then shift to 1 st line TR in 2 nd & 3 rd trim OR
    • - ARM injections for 7 days
    • - Management of pulm edema, hypoglycemi
    • anaemia wz packed cell transfusion, renal F
    • and septicaemic shock or algid malaria by
    • 3 rd generation cephalosporin, monitoring of
    • vital signs & fluids if required (SBP< 90)
    • 4- Intermittent preventive TR (IPT):
    • - recommended only in high transmission
    • areas
    • - SP= 1 st dose in za 1 st ANC visit after quickening (16-20W)
    • - 2 nd dose 4W later
    • TR of Vivax malaria
    • - malaria other than P.f constitute 5—15% in
    • Sudan, mainly in eastern borders. Death is
    • rare & relapse expected wz P.v & Po.
    • - Still sensitive to CQ & susceptible to ARM/LF
    • - Primaquine used following TR of asexual forms
    • to clear exsoerythrocytic phase 15mg/d x14 d.
    • CI in preg, during lactation & children < 1year
    • Malaria prophylaxis & prevention
    • - The following are at higher risk for malaria:
    • 1- travelers from malaria free areas
    • 2- preg women, sp primigravida
    • 3- SS dis
    • 4- splenectomized individuals
    • 5- children on steroids & immunosupp drugs
    • 6- expatriates & sudanese returning from
    • non malarious areas
    • - Mefloquine 250mg weekly, starting one week
    • before entering the area & for 4W after
    • leaving za area.
    • Mefloquine not recommended in children < 3/12
    • - atovaquine 250mg + proguanil 100mg begin
    • one day before entering the area & for 7 days
    • after leaving the area in those can not take
    • Mefloquine.
    • Tropical splenomegaly (TSS)
    • - Results from abn immunological response to
    • malaria
    • - Occurs in malaria endemic areas in the
    • indigenous inhabitants. Parasites not present
    • - There is high malarial Ab titre wz over- produc
    • of IgM & reduced C3
    • - Massive splenomegaly >10cm which is firm
    • - Hepatic sinusoidal dilatation, infilt wz lymphocy
    • and Kupffer cell hyperplasia
    • - Pancytopeni a with normocytic normochromic
    • anaemia & reticulocytosis
    • - The condition is reversible
    • - Increased susceptibility to infection & there is
    • wasting in advanced cases
    • - Criteria for diagn of TSS : exclusion of other
    • causes of massive splenomegaly, immunity to
    • malaria, raised IgM, hepatic sinusoidal
    • lymphocytosis & IgM on immunofl & the
    • response to anti malarial prophylaxis
    • - TR for symptomatic pats with anaemia & large
    • spleen- -- Chemoprophylaxis + F acid
    • Splenectomy wz permanent malaria chemoprophylaxis in those who fail to respond.