INCOMPLETE TREATMENT OF MALARIA AND SPECIAL CONCERNS IN PREGNANCY

Presenter : Siti Azliza Binti Yaacob 030.08.304

INTRODUCTION
A round the world, the malaria situation is serious and getting worse. Malaria threatens the lives of 40% of the worlds population over 2 200 million people. Each year, there are an estimated 300-500 million clinical cases. Malaria is a major public health problem in Indonesia with 6 million clinical cases and 700 deaths each year (Laihad, 2000). It has been estimated that malaria during pregnancy is responsible for 512% of all low birth weight and 35% of preventable low birth weight and contributes to 75 000 to 200 000 infant deaths each year. (Steketee et al., 2001)

OUTCOMES
Incomplete of previous treatment. Recurrency of malaria infection. The infecting Plasmodium species The clinical status of the patient The drug susceptibility of the infecting parasites as determined by the geographic area.

PATIENT IDENTITY
Name Place/born/age Address : Mrs.H :Sukabumi / 5 September 1974 /38 yo :Kp. Sukamarah RT 02/01 Taman Sari Bogor Religion :Moeslim Occupation :Housewife Marital status :Married Education :SMA MR Number : 229575 Date of admission : 23 January 2013 Date of examination :1 February 2013 Consultant :Dr. Adi Wijaya Sp PD

HISTORY TAKING
An autoanamnesis in ward on 1 February 2013 at 20.00 pm. Chief complaint : Increasing fatigue since 1 weeks ago before admitted to the hospital.

Additional complaint:
A week history of remitten fever along with shaking chills

nausea, vomite that contain fluid

abdominal discomfort.

headache

loss of appetite

arthralgia

History of present illness:

16 January 2013 Return to Java from Papua in fatigue condition, nausea and arthralgia. Progresively instable condition increasing fatigue, a sudden onset of flue-like symptoms sustained recurrent severe attacks of fever + shaking chills sometimes with sweating arthralgia almost every day.

Admitted to the hospital

23 January 2013 Fatigue High fever (39.3c) nausea, vomite that contain fluid abdominal discomfort. headache loss of appetite arthralgia

A week before admitted to the hospital

HISTORY OF ILLNESS
February 2012 she had an abortion.

Disember 2012 3rd diagnosed of Malaria Admitted in the hospital in Papua. In a pregnancy (G4 P2 A1) HPHT : 16 Disember 2012

September 2011 frequently travel from Papua to Java she was employed in an oil palm plantations in Papua. 1st admitted to hospital in Papua on Disember 2011 with the diagnosed of malaria: malaria tertian (P.Vivax and P.Ovale). admitted in the hospital for only 7 days remained controlled at Polyclinic for the next 14 days totally recovered. Unexpectedly pregnancy (G3 P2 A0)

November 2012 2nd diagnosed of Malaria Admitted to the hospital in Papua. Recovered without controll to docter.

16 January Return to Java uneventfully condition Progresively instable condition. 23 January 2013 : she was admitted to the Marzoeki Mahdi Hospital, Bogor

Past medical history Varicella (+) Measles (+) Influenza (+) Malaria (+) Gastritis (+) Appendicitis (+) *malaria : 4 times already Family history Father : HT Mother : HD + DM

History of habitual: rarely do the excersice Smoke (-) drink coffee and tea (-) routine medication or herbs.(-) History of diet: Present diet : frequent of meal is 2x/day, with portion and variation of food. Apetite : loss of apetite.

NUTRITIONAL STATUS
WEIGHT : 53 kg HEIGHT: 155 cm

BMI: 53kg / (1.15)2 m = 22.06

EFFECT: Normal weight.

PHYSICAL EXAMINATION
General condition : Mrs. H appears alert, oriented and cooperative.
Consciousness: conscious Vital signs: Blood pressure Pulse rate Respiration rate Temperature :100/70 mmHg :90x/m :20x/m :39.3c

GENERAL PHYSICAL EXAMINATION

Head : Normocephalic, atraumatic head, normal distribution of hair. : cervical and supraclavicula lymph nodes is not palpable enlarged.

Lymph node Eyes

:conjunctival pallor (+/+), sclera icterus (-/-),isochoric pupils, pupils equally round, 3 mm of diameter, direct pupillary light reflex (+/+), indirect papillary light reflex (+/+). : Normotia, secrete -/-, serumen -/-, intact timpany membrane+/+ :septum deviation (-), secrete -/-, concha is normal, mucosa not hyperemic

Ears Nose

Mouth : Dirty mouth (-), dry mouth (+), normal papil, mucosa hyperemic(-), sianosis (-)

Throat Neck

: Tonsils T1/T1 calm, pharynx hyperemic (-) : trachea is palpable in the midline and thyroid gland is normal without masses, jugular veins pressure is normal 5-2mmHg. Shape : Chest is of regular shape and size,symetrical with prominent ribs and well-defined intercostal spaces. Breast : atrophic and symmetric, nontender, no masses or discharges Inspection:Chest expands symmetrically and bilaterally on inhalation, breathing pattern is thoracoabdominal, there is no expansion of intercostals. Palpation : tactile vocal fremitus is symmetrical bilaterally, Percussion Auscultation :resonant, No apparent dullness or hyperresonance upon percussion of the chest. : vesicular breath sounds, with no apparent crackles, wheezes (-/-), ronchi (-/-).

Thorac :

Heart

Inspection : puctum maximum of ictus cordis is not visible. Palpation : Point of puctum maximum is located at the left fifth intercostal space on the mid-clavicular line. No palpable heaves or thrills.

Percussion :

Left upper border : second left intercostal space on parasternal line. Left lower border: fourth left intercostal space lateral to mid-cavicular line. Right upper border: third right intercostals space on sternal line.
Right lower border : third-fourth right intercostal space on sternal line.

Auscultation : S1 and S2 is regular, murmur sound (-), gallop (-).

Abdominal

Inspection

: bulging, symmetrical, smiling umbilical (-), caput medusa (-), spider nevi (-).

Palpation

: tenderness (+), and no palpable masses. The spleen and the lower edge of the liver are not palpable, and there is no evidence of hernia.
: tympanic

Percussion

Auscultation

: bowel sound (+) normal.

Blood vessel Temporal artery : pulse is palpable

Carotid artery
Brachial artery Radial artery

: pulse is palpable
: pulse is palpable : pulse is palpable.

Femoral artery
Popliteal artery Posterior tibial artery Dorsalis pedal artery

: pulse is palpable
: pulse is palpable : pulse is palpable : pulse is palpable

Extremities Upper limb

Right Left

Lower limb Wound : Varises Tone Joint ::normotonic normotonic :normal -

Muscle :normotrophic normotrophic Tone :normotonic normotonic

normal

Joint

:normal

normal
active active scor : 5 -

Movement
Power 5 Sensoric Edema Warm acral

:active
: scor : 5 :normal ::+

active
scor : normal +

Movement :

Power :scor : 5 Edema : -

Warm acral:

 23 January 2013 (In Emergency Room)

Hematology

LABORATORY TEST
Result
9.7 6.810 73.000 29

Test performed
Hemoglobin Leukocyte Thrombocyte Hematocrit Serologic Widal test

Unit
g/dl /mm3 mm3 %

Recommended
13-18 4000-10000 150000-400000 40-54

Interpretation

Negative (-)

Chemistry blood count SGOT SGPT BUN 36 26 15.0 U/l U/l mg/dl <42 <47 10-50 N N N

Creatinine

0.65

mg/dl

0.67-1.36

Laboratory test : 24 January 2013 Test / 12 hours

Hematology 1st Test performed Hemoglobin Leukocyte Thrombocyte Hematocrit Result 8.7 7.620 59.000 27 Unit g/dl /mm3 mm3 % Recommended 13-18 4000-10000 150000-400000 40-54 N Interpretation

Hematology 2nd Test performed Result Unit Recommended Interpretation

Hemoglobin
Leukocyte Thrombocyte Hematocrit

8.4
6.870 52.000 26

g/dl
/mm3 mm3 %

13-18
4000-10000 150000-400000 40-54 N

Laboratory test : 25 January 2013

Hematology 1st Test performed Hemoglobin Leukocyte Thrombocyte Hematocrit Result 7.9 6.620 64.00 24 Unit g/dl /mm3 mm3 % Recommended 13-18 4000-10000 150000-400000 40-54 N Interpretation

Hematology 2nd Test performed Hemoglobin Leukocyte Thrombocyte Hematocrit Hematology Test performed Malaria Result Unit Recommended Interpretation Result 7.5 5.690 47.000 20 Unit g/dl /mm3 mm3 % Recommended 13-18 4000-10000 150000-400000 40-54 N Interpretation

In a sample was found the plasmodium Early Vivax in a

trophozoite

shape

(ring form)

Laboratory test: 26 January 2013

Hematology Test performed Hemoglobin Leukocyte Thrombocyte Hematocrit Result 7.2 5.740 53.000 22 Unit g/dl /mm3 mm3 % Recommended 13-18 4000-10000 150000-400000 40-54 N Interpretation

Laboratory test: 27 January 2013.

Hematology Test performed Hemoglobin Result 7.4 Unit g/dl Recommended 13-18 Interpretation

Leukocyte
Thrombocyte Hematocrit

4.580
64.000 22

mm3
mm3 %

4000-10000
150000-400000 40-54

Laboratory test : 28 January 2013.

Hematology 1st Test performed Hemoglobin Leukocyte Thrombocyte Hematocrit Hematology 2nd Test performed Hemoglobin Leukocyte Thrombocyte Hematocrit Result 10.2 8.890 91.000 31 Unit g/dl /mm3 mm3 % Recommended 13-18 4000-10000 150000-400000 40-54 N Interpretation Result 10.1 9.910 95.000 30 Unit g/dl /mm3 mm3 % Recommended 13-18 4000-10000 150000-400000 40-54 N Interpretation

Laboratory test : 29 January 2013.

Hematology Test performed Hemoglobin Leukocyte Thrombocyte Result 10.1 8.000 123.000 Unit g/dl /mm3 mm3 Recommended 13-18 4000-10000 150000-400000 N Interpretation

Hematocrit Chemistry blood count SGOT SGPT BUN Creatinine

Blood glucose

30

40-54

25 30 41.1 0.51
143

U/l U/l mg/dl mg/dl

mg/dl

<42 <47 10-50 0.67-1.36

<140

N N N

Electrolyte Test performed Natrium Na+ Sodium K+ Chloride ClHEMOSTASIS Test performed Result Unit Recommended Interpretation Result 139 4.5 96 Unit Recommended 136-146 3.5-5.0 95-115 Interpretation N N N

APTT
Protrombin time Fibrinogen

26.8
12.2 214

Dtk
Dtk mg/dl

25.9-39.5
11.8-14.4 200-400

N
N N

Laboratory test : 30 January 2013

Blood Gas Analysis Test performed Ph PCO2 Result 7.50 30 Unit Recommended 7.35-7.45 30-50 N Interpretation

PO2
BE TCO2 HCO3 BE act SO2 O2 CT Temp FlO2 Hematology Test performed D-Dimer

74
0.0 23.9 23.0 0.7 97 16.6 35.6 0.21

70-700
-2-+3.0 22-29 18-23 -2.0- +3.0 95-98 15.0-23.0

N
N N N N N N N

Result 6,809.36

Unit ng/mL FEU

Interpretation

Laboratory test : 31 January 2013

Hematology Test performed Hemoglobin Leukocyte Thrombocyte Hematocrit Result 10.1 7.580 217.000 31 Unit g/dl /mm3 mm3 % Recommended 13-18 4000-10000 150000-400000 40-54 N N Interpretation

Laboratory test : 1 February 2013.

Hematology Test performed Malaria Result Positive (+) Malaria found Vivax) parasite was Unit Recommended Interpretation -

(Plasmodium

Another examination ECG Normal ECG

RESUME
HISTORY TAKING :
A women, 35 years old was admitted to dr. H. Marzoeki Mahdi Hospitals ER on 23 January that was complain increasing fatigue since a week before admitted to the hospital. She was had a history of sustained fever a long with shaking chills. The additional complaint was nausea, vomite that contain fluids, headache, loss of appetite, arthralgia and abdominal discomfort. She had instable condition with increasing fatigue, with a sudden onset of flue-like symptoms and sustained recurrent severe attacks with the highest temperature is 39.6c with shaking chills and sometimes with sweating and arthralgia almost every day. All of this complains have become progressively worst within a last week before admitted to the hospital.

In the past history patient often frequently travel from Papua to Java since September 2011.She was 3 times diagnosed of malaria in Papua. 1st diagnosed on Disember 2011 malaria tertian (P.Vivax and P.Ovale). she was in pregnancy, G3 P2 A0 (aborted on February 2012.) Admitted in the Hospital Totally recovered 2nd diagnosed on November 2012 Admitted in the hospital not sure recovered 3rd diagnosed on Disember 2012 She had a 4 weeks gestation in pregnancy. (G4 P2 A1). admitted discharged instable condition. Then she was decided to going back to Java.

PHYSICAL EXAMINATION General condition : Mrs. H appears alert, oriented and cooperative. Consciousness: conscious Vital signs: Blood pressure :100/70 mmHg Pulse rate :90x/m Respiration rate :20x/m Temperature :39.3c Eyes :conjunctival pallor (+/+) Abdomen: palpitation : tenderness (+).

LABORATORY TEST (23 Jan 2013) Hemoglobin 9.7g/dl 3 Thrombocyte 73.000mm Hematocrit 29%

Anemia Thrombocytopenia

24 Jan Hemoglobin -8.7 (g/dl) -8.4 Hematocrit % -29 -26

25 Jan -7.9 -7.5 -24 -20

26 Jan -7.2 -22

27 Jan -7.4 -22

28 Jan -10.1 -10.2 -30 -31

29 Jan 30 31 Jan 1 Feb Jan 10.1 39 10.1 31 -

Thrombocyt -59.000 e (mm3) -52.000

Microscopic of malaria

-64.000 -47
P.vivax in a Early trophozoite Shape (ring form) -

53.00 64.00 0 0
-

91.00 0
-

123.00 0
-

217.00 0
(+) P.viva x

Chemistry blood count Electrolyte Hemostasis Blood gas analysis D-Dimer (ng/ml FEU)

N N N -

N 6,8 09. 36

PROBLEMS
Sustained recurrent high fever Fatigue Dyspepsia (Nausea,vomit,abdominal discomfort), Loss of apetite Arthralgia Anemia , Thrombositopenia Recurrent malaria infection. Pregnancy Most probably she was infected from the high transmission area that is Papua New Guinea.

History taking : 3x diagnosed of malaria in papua, return to Java instable condition Temp : 39.3c(febris) , Eyes: conjunctival pallor (+/+)

History of past medical record

Pregnant reported

Working Diagnose : Incomplete treatment of Malaria infection with pregnancy and anemia.
Microscopic examination : P.vivax in a Early trophozoite Sha pe (ring form)

Anemia, thrombositopeni a

Differential diagnosis : Relapse of malaria. Thyphoid fever Dengue hemorrhagic fever.

THERAPY
Medicamentosa IVFD RL /8hrs Oxygen canul 2L/m Antipyretic : Paracetamol 3x1g H2 Blocker : Ranitidine 2x1 Planning for transfusion of PRC 200cc. Planning for giving of anti-malaria drugs.

DISCUSSION
Diagnosed of malaria Complain (symptom), PE, laboratory test Microscopic examination : p.vivax

3x diagnosed of malaria (in Papua) 1st (malaria tertiana) totally recoreved Incomplete of 2nd and 3rd ??? previous She could not recall the medication taken. treatment (in Return to Java in unventually condition. Papua)

relapse, recrudescence, or reinfection? Relaps : p.vivax hypnozoite forms that remain dormant in the liver and can cause a relapsing infection. Reinfection : usually occurs after day 14 of treatment and in endemic areas. Recurrency of Most probably :Recrudescence recurrence of malaria within days or weeks of malaria apparent cure, without new infection caused incomplete or inadequate treatment infection. since in Papua.

The clinical status of the patient

Pregnancy History of abortion in 1st diagnosed of malaria in Papua 4 weeks of gestation Problem in planning teratment. Anemia (complication )

Infecting parasites

Patient was acquiring P. vivax infections which is most probably from Papua New Guinea. Chloroquine (or hydroxychloroquine) remains an effective choice for all P. vivax infection. High prevalence of chloroquine-resistant P. vivax in Papua New Guinea should initially be treated with a regimen recommended for chloroquine-resistant P. vivax infections.

objective of treating malaria

blood stage infection liver stage infections primaquine CI to be used during pregnancy. Big Problem

RESOLUTION AND THERAPY

Blood transfusion 500cc of PRC in low-transmission area: a threshold of 20% (haemoglobin 7 g/100 ml) is recommended to transfusion of blood. In 4th day hospitalization : hemoglobin : 7.4g/dl and hematocrite : 22% 1st : chloroquine was given in 3 days with dose : I day : chloroquine 250mg 4 units, II day : chloroquine 250mg 4 unit and III day: chloroquine 250mg 2 unit. parenteral artesunate: Day I : Artesunat (D5% 100cc) 1x drip, Day II : Artesunate (D5% 100cc) 1x1 ampul drip. Day III: Artesunate (D5% 100cc) 1x1 ampul drip.

Anemia

Blood stage treatment

Liver stage infection

the preventive primaquine Primaquine 0.250.5 mg base/kg body weight in two divided daily doses should be given for 14 days, primaquine phosphate should not be given during pregnancy. maintained on prophylaxis for the duration of their pregnancyAfter deliverytreated with primaquine. Consult to Obstetric and Gynecology specialist the paediatricians alerted, and blood glucose checked frequently. Severe malaria present immediately following delivery. Postpartum bacterial infection is a common complication in these cases.

Pregnancy

use of antibiotics

supervening bacterial infection enteric bacteria (notably Salmonella) have predominated in most trial series. Ceftriaxon 2x2gr drip -Dexamethason 2x1gr

Monitoring therapeutic efficacy for vivax malaria

needs monitoring to track and respond to emerging resistance the sensitivity of P. vivax to ACTs must also be routinely monitored. vivo test for P. vivax

In 9th hospitalization On 1 February 2013 patient was ask to discharge by her on dicision and there is no provided any anti-malarial drugs during she was discharged. Condition : Conscious, mild illness. Mild headache Nausea (+),vomit(-), Apetite is good Arthralgia(+). BP: 110/60mmHg Pulse: 80x/m RR: 20x/m Temp: 36 c Hb : 10.1 g/dl Ht : 31% Throm : 217,000 mm3

DEFINITION AND EPIDEMIOLOGY

Malaria is caused by infection of red blood cells with protozoan parasites of the genus Plasmodium . The four Plasmodium species that infect humans are P. falciparum, P. vivax, P. ovale and P. malariae. Increasingly, human infections with the monkey malaria parasite, P. knowlesi, have also been reported from the forested regions of South-East Asia.(1) The World Health Organization estimates that malaria caused approximately 655,000 deaths in 2010. Most are in young children in sub-Saharan Africa. Malaria can also cause dangerously low birth weights and permanent disability

LIFE CYCLE OF MALARIA PARASITES

PHATOFISIOLOGY
The incubation period : Malaria bite until clinical symptoms appear 7 days (1-2 weeks). Symptom due to the cycling parasitemia in the bloodstreams. symptoms every 2 to 3 days depending on the type of Plasmodium with which they are infected.

Blood stage

BODYS INFLAMMATORY RESPONSE

 Repeated malarial infections lead to some immunity. learned immunity In fact, in areas where malaria incidence is episodic rather than endemic, patients will present with more severe forms of the disease, as their previously learned immunity appears to fade over time. It is not surprising, therefore, that malaria-naive and immunocompromised patients are prone to more severe infection. This puts pregnant women, children, travelers to endemic regions, and persons with coexisting HIV infection at highest risk for morbidity and mortality secondary to malarial infection.(9)

CLINICAL DISEASE
Caused by the asexual erythrocytic or blood stage parasites. When the parasite develops in the erythrocyte, substances such as : hemozoin pigment and other toxic factors accumulate in the infected red blood cell. These are dumped into the bloodstream when the infected cells lyse and release invasive merozoites. The hemozoin and other toxic factors such as glucose phosphate isomerase (GPI) stimulate macrophages and other cells to produce cytokines and other soluble factors which act to produce fever and rigors and probably influence other severe pathophysiology associated with malaria.

Pregnancy-malaria and intensity of transmission:

Complication High Transmission Low transmission

Hypoglycemia
Severe Anemia Pulmonary oedema ARF Hyperpyrexia Placental malaria LBW babies Abortions Congenital malaria

+++ + +++ +++ -

++
+++ ++ ++ +++ +++ +++ +++ +++

Fever: Patient may have different patterns of fever

Others Complications:Acute pulmonary edema, hypoglycemia and anemia are more common in pregnancy. Jaundice, convulsions, altered sensorium, coma, vomiting / diarrhoea and other complications may be seen.

Atypical manifestations of malaria are more common in pregnancy, particularly in the 2nd half of pregnancy.

Anemia

Splenomegaly

PATENT PARASITEMIA FOR MALARIA CAUSED BY P.VIVAX

When a parasitemia reappears after blood schizonticidal therapy, it may be a relapse from the liver, a reinfection by a mosquito, or a recrudescence originating from asexual blood-stage parasites that survived therapy. The emergence of CQ-resistant P. vivax favors the last possibility.

REINFECTION

RELAPSE New parasitemia originating from hypnozoites (dormant liver stages) may occur at relatively short intervals or after long period (8-24 weeks). characterized by an asymptomatic latency period measured in months or years Primaquine prevent relapse by killing the stages of the organism in the liver. usually due to: primaquine resistance incomplete response or inadequate primaquine treatment.

RECRUDESENCE New parasitemia originating from the original parasitemia recurrence of malaria within days or weeks of apparent cure, without new infection May be due : incomplete or inadequate treatment as a result of drug resistance or improper choice of medicate an antigenic variation multiple infection by different strains.

New parasitemia originating from new infectious mosquito bite can occur at any time after 2 weeks of the 1st attack. may be due to : persistent source of infection such as an asymptomatic carrier or persistent malaria in the neighbourhood household because of high endemicity

DIAGNOSIS
The diagnosis of malaria is based on : - clinical suspicion -the detection of parasites in the blood ( parasitological or confirmatory diagnosis).

CLINICAL DIAGNOSIS
patient's symptoms fever, chills, sweats, headaches, muscle pains, nausea and vomiting and often not specific and are also found in other diseases (such as the "flu" and common viral infections).

physical findings : often not specific (elevated temperature, perspiration, tiredness).

If possible, clinical findings should always be confirmed by a

laboratory test
for malaria.

In severe malaria (caused by Plasmodium falciparum), clinical findings (confusion, coma, neurologic focal signs, severe anemia, respiratory difficulties) are more striking and may increase the index of suspicion for malaria.

Microscopic examination : "gold standard"

Drug Resistance Tests

Antigen Detection

Laboratory Test

Serology

Molecular Diagnosis

 Ring-form trophozoites of P. vivax in thin blood smears

Trophozoite of P. vivax in a thick blood smear

TREATMENT OF MALARIA INFECTION

Treatment should be guided by three main factors :

The drug susceptibility of the infecting parasites as determined by the geographic area where the infection was acquired and the previous use of antimalarial medicines

The infecting Plasmodium species

The clinical status of the patient

TREATMENT OF MALARIA CAUSED BY P.VIVAX

Classes and representative antimalarial drugs

Type of drug Blood schizontocide Target Trophozoite in blood Clinical application Treatment of acute malaria Prophylaxis Suppressive Licensed drug(s) Experimental drug(s) Chloroquine, Tafenoquine, quinine, ACTs mefloquine, doxycycline, AVPG, DH-PP

Primary tissue schizontocide

Hypnozoitocide

Active schizont in liver

Dormant hypnozoite in liver

None

Causal

Primaquine

Tafenoquine

Prevention of relapse Prevention of transmission Prevention of transmission

None

Primaquine

Tafenoquine, elubaquine Tafenoquine, artesunate, artemether Tafenoquine

Gametocytocide Gametocyte in blood Sporontocide Forms in mosquito including sporozoite

None

Primaquine

Causal prophylaxis

Primaquine

Deterioration of chloroquine (CQ) efficacy between 1945 (green line) and 1995 (red line) among tropical Asian strains of P. vivax relative to natural relapse of the same strains following quinine (QN) therapy (blue line). The suppression of relapse by chloroquine in 1945 is due to lingering levels of drug in blood up to day 35, and the 1995 data suggest not only failure to suppress relapse but also failure to clear primary asexual parasitemia. Data were derived from various sources

 Plot of the cumulative incidence of recurrent parasitemia after chloroquine therapy of vivax malaria in western Indonesian Borneo and eastern Indonesian New Guinea

A regimen recommended for chloroquineresistant P. vivax infections.

P. vivax infections Liver stage treatment 14-day course of primaquine phosphate

blood stage treatment

initially be treated with chloroquine.

The 3 treatment regimens for chloroquine-resistant P. vivax infections are quinine sulfate + doxycycline/ tetracycline QS + Atovaquone-proguanil QS + mefloquine.

45 mg (base) orally one time per week for 8 weeks

Primaquine must not be used during pregnancy. does not respond to chloroquinechloroqu ine-resistant P. vivax? one of the two regimens recommended for chloroquine-resistant P. vivax infections.

Artemisinin-based combination therapy (ACTs)

Recent studies have also demonstrated the efficacy of the recommended ACTs in the treatment of vivax malaria. ACTs based on either amodiaquine, mefloquine or piperaquine, rather than monotherapy, are the recommended treatment of choice. The exception to this is artesunate plus sulfadoxinepyrimethamine. P. vivax has developed resistance to sulfadoxinepyrimethamine. (study from Afghanistan reported)

TREATMENT DURING PREGNANCY

Determine whether malaria is uncomplicated or complicated MANAGEMENT OF UNCOMPLICATED MALARIA IN PREGNANCY First Trimester :Oral Quinine or a combination of oral quinine and clindamycin shall be used for seven days 2nd line drugs :Artesunate plus clindamycin for seven days is indicated if this treatment fails.

Second and Third Trimesters : Oral Quinine or the combination of Artesunate-Amodiaquine or Artemether -Lumefantrine shall be used.

 Parenteral artesunate is preferred over quinine in the second and third trimesters, because quinine is associated with recurrent hypoglycaemia. In the first trimester, the risk of hypoglycaemia is lower and the uncertainties over the safety of the artemisinin derivatives are greater. However, weighing these risks against the evidence that artesunate reduces the risk of death from severe malaria, both artesunate and quinine may be considered as options until more evidence becomes available. Treatment must not be delayed; so if only one of the drugs artesunate, artemether or quinine is available, then it should be started immediately ????????????

PRIMAQUINE IN PREGNANCY
For P. vivax or P. ovale infections, primaquine phosphate for radical treatment of hypnozoites should not be given during pregnancy. Pregnant patients with P. vivax or P. ovale infections should be maintained on chloroquine prophylaxis for the duration of their pregnancy. The chemoprophylactic dose of chloroquine phosphate is 300mg base (=500 mg salt) orally once per week. After delivery, pregnant patients with P. vivax or P. ovale infections should be treated with primaquine. Pregnant women di agnosed with severe malaria should be treated aggressively with parenteral anti malarial therapy .(10)

Facts about Malaria and Pregnancy

30 million African women are pregnant yearly Malaria is more frequent and complicated during pregnancy In malaria-endemic areas, malaria during pregnancy may account for: Up to 15% of maternal anemia 514% of low birthweight 30% of preventable low birthweight

Prevention and Control of Malaria during Pregnancy

78

Awareness of risk

Diagnosis and treatment which must be prompt

The ABCD of Malaria prevention Formula

Bite prevention

Chemopro phylaxis

Chemoprophylaxis
Remind women that there is no malaria prophylaxis regimen that is 100% protective.

Chemoprophylaxis for long-term travellers

Long-term travellers are defined as those travelling through or visiting malaria-endemic countries for over six months. Chloroquine and proguanil are the only drugs licensed for long-term use but there effectiveness is reduced in some areas, due to resistance. Mefloquine is licensed for up to one year (although it has been used for up to three years without problems). Doxycycline can be used for up to two years. Malarone is licensed for up to 28 days but can be safely used for up to three months (and possibly six months or longer).

CLONCLUSION
Malaria in a pregnant woman increases the risk of maternal death, miscarriage, stillbirth and low birth weight with associated risk of neonatal death. Pregnant women should be advised to avoid travelling to areas where malaria transmission occurs. When travel cannot be avoided, it is very important to take effective preventive measures against malaria, even when travelling to areas with transmission only of vivax malaria. Pregnant women should seek medical help immediately if malaria is suspected. There is very limited information on the safety and efficacy of most antimalarials in pregnancy, particularly during the first trimester. However, inadvertent exposure to antima -larials is not an indication for termination of the pregnancy.