Clinical Case Study 1: Fever 6 months after a visit to Pakistan

A 44-year-old man is seen at a physician’s office in the United States, during a week-end, for suspected malaria.

The patient was born in Pakistan but has lived in the United States for the past 12 years. He travels frequently back to Pakistan to visit friends and relatives. His last visit there was for two months, returning 11 months before the current episode. He did not take malaria prophylaxis then.

Five weeks ago, he was diagnosed with malaria and treated at a local hospital. The blood smear at that time was reported by the hospital as positive for malaria, species undetermined. He was then treated with 2 days of IV fluids (nature unknown) and tablets (nature unknown), and recovered.

The patient now presents with a history of low grade fever for the past few days, with no other symptoms. A blood smear is taken and examined at a hospital laboratory by the technician (no pathologist is available on this week-end). Through a telephone discussion, the technician states that she sees 4 parasites per 1000 red blood cells, with rings, “other forms with up to four nuclei,” and that some of the infected red blood cells are enlarged and deformed.

Question 1: What is your most probable diagnosis?

Not Malaria

That is incorrect. Please, try another answer.

Plasmodium falciparum

Plasmodium vivax

That is correct.

This is the most probable diagnosis. The reported microscopic findings are compatible with P. vivax: some infected red cells are enlarged and deformed, and the “other forms with four nuclei” are compatible with the presence of schizonts. Plasmodium vivax does occur in Pakistan, where it is found in slightly more than 50% of malaria cases.

The history suggests a relapse of P. vivax malaria, following an earlier episode five weeks ago. The earlier treatment apparently did not include primaquine, thus allowing the persistence of hypnozoites which caused this relapse.

An alternate explanation would be that the earlier infection was caused by chloroquine-resistant P. vivax (which has been reported in Pakistan), with recrudescence of blood-stage parasites occurring after an unsuccessful earlier treatment (if indeed the earlier treatment included chloroquine). However, recrudescences usually occur within 28 days of the intial episode, rather than at five weeks as described here.

The other species are less likely:

  • While P. falciparum does occur in Pakistan (slightly less than 50% of malaria cases), this patient reportedly did not develop symptoms until 10 months after departure from the exposure area: most cases of P. falciparum would have become symptomatic earlier.
  • P. ovale occurs mainly in Africa and has been found only occasionally in Asia (in the western Pacific).
  • P. malariae occurs worldwide, but its distribution is spotty, and its frequency in Pakistan is low to negligible.
  • Babesia would not fit with the microscopic description; in addition, babesiosis has not been reported in Pakistan, although admittedly the disease might have escaped detection.

Plasmodium ovale

Plasmodium malariae

Question 2: What treatment approach would you recommend, based on this clinical history and on the fact that the microscopy findings will not be confirmed by a pathologist for at least 24 hours?

Do not start treatment until a formal microscopic diagnosis is made (in 12-24 hours)

Treat as if chloroquine-sensitive Plasmodium falciparum malaria

A reasonable option, signifying that in the absence of definitive microscopic diagnosis, you prefer to play it safe and treat the patient for the most dangerous and rapidly progressing infection possible.

The safest course of action is to initially admit all cases of proven or suspected P. falciparum to the hospital until one can begin treatment and ensure that they are improving clinically and parasitologically.

However in this case, if the patient is only minimally symptomatic, one might elect against hospitalization and instead treat as an outpatient provided that close follow-up can be arranged. Once the definitive microscopic diagnosis is made the following day, you can always switch treatment.

Treat as if chloroquine-resistant Plasmodium falciparum malaria

Treat as if Plasmodium vivax malaria

Plasmodium vivax schizont

P. Vivax schizont

The diagnosis of P. vivax malaria is later confirmed by review of a blood smear available from the first episode (Figure), and by a PCR positive for P. vivax on blood collected during the current episode.

The microscopic diagnosis  of P. vivax is based on the following:

  • The infected red cells are enlarged and deformed;
  • The schizont shown contains 20 merozoites (schizonts of P. malariae and P. ovale have fewer merozoites; and in P. falciparum , schizonts are not usually seen in the peripheral blood);
  • The round gametocyte shown, contained in an enlarged red cell. (In this case, the typical Schüffner’s dots were not visible, probably due to staining problems.)

Question 3. To prevent further relapses from dormant liver stages, what would you recommend?

No further measures needed

A lab test to determine if the patient has dormant liver stages

Treatment immediately with a drug that kills dormant liver stages

A lab test, followed by treatment with a drug that kills dormant liver stages

You should exclude G6PD deficiency first, then give the patient primaquine, 30 mg per day for 14 days.

In case of G6PD deficiency, consultation with an expert in infectious diseases or tropical medicine is advised to discuss options for relapse prevention. For some patients with partial G6PD deficiency, an alternative regimen of primaquine 45 mg weekly for 8 weeks can sometime be used. Alternatively, weekly chloroquine prophylaxis may also be considered. Treatment with primaquine is justified because this patient probably has already had a relapse, and is at risk for further relapses. No test exists to detect the presence of liver stage parasites.

Question 4. Should this patient have taken preventive measures against malaria for his visit to Pakistan, considering that he was born there?

Even to visit friends and relatives, preventive measures must be taken. Chloroquine-resistant Plasmodium falciparum occurs in Pakistan, and thus the drugs recommended would be atovaquone-proguanil (Malarone®), doxycycline or mefloquine. Other preventive measures against mosquito bites also apply. Even though the patient was born in Pakistan, whatever acquired immunity he has developed would most likely have waned; negligence of preventive measures often occurs in individuals visiting friends and relatives , a situation that needs to be remedied.

Main Points

Travelers to Pakistan (including those visiting friends and relatives) need to take prophylaxis (atovaquone-proguanil [Malarone®], doxycycline or mefloquine).

Clinical history and travel history, and careful microscopic examination, probably would have directed the diagnosis toward P. vivax during the earlier episode, so that the relapse could have been prevented.

P. vivax malaria should be treated with chloroquine, except when acquired in Papua New Guinea and Indonesia, areas with high prevalence of chloroquine-resistant P. vivax . After a normal G6PD test, patients should get a radical cure with primaquine (30 mg per day for 14 days).

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Patient Presentation

Differential diagnosis, examination, investigations, final outcome.

  • Evaluation - Questions & answers

A 2 year old boy presented to a district hospital with decreased oral intake, listlessness and fever. On arrival he was adequately resuscitated but continued to have spiking fevers and a depressed level of consciousness.

Acknowledgement This case study was kindly provided by Barclay Stewart, Medical University of South Carolina, Fogarty International Clinical Research Scholar, Nairobi, Keny a

Six months ago the patient presented to the hospital with a two day history of irritability, decreased appetite, discomfort on lying down, recurrent fever, profuse sweating and diarrhea, no vomiting. On admission he was lethargic and dehydrated which worsened over a few hours and culminated in a seizure. He had no prior history of seizures. He was then diagnosed with severe malaria. He was treated appropriately and discharged 2 weeks later with no residual effects.

Past medical and surgical history

  • There is no additional significant medical or surgical history.
  • Road to health card shows all growth parameters to be within normal limits, with all vaccinations up to date.

Family and social history

  • He lives with his mother, father, and two older siblings who are all healthy.
  • His mother was recently tested and is HIV negative; his father has not been tested.
  • Their home, which has electricity and water, is located in a low-lying area near Musina, a town in South Africa’s Limpopo province. This is the country’s most northerly located town, with a seasonal high rate of malaria transmission from October through May.

Travel History No travel outside of Musina since birth.

  • Encephalitis
  • Gastroenteritis with severe dehydration
  • Toxic Shock Syndrome
  • Typhoid Fever
  • Brucellosis
  • Relapsing Fever
  • Katayama Fever
  • Urinary tract infection
  • Bacteraemia

On appearance the child is miserable and toxic looking.

  • Pulse – 166
  • Respiratory Rate – 34
  • Temperature – 39.8
  • Pulse-Oxygen – 95%

Height and weight were in the 65 percentile

  • Eyes were sunken and jaundiced.
  • No lymphadenopathy
  • Erythematous, non bulging tympanic membranes.
  • Non-inflamed nasal passage, no discharge.
  • Pale oral mucosa
  • No papilloedema
  • No retinal heamorrhages
  • Midline trachea
  • Chest shape normal in appearance, tachypnoea present
  • Mild subcostal retractions.
  • Clear on auscultation bilaterally.


  • Tachycardia with a regular rhythm.
  • Normal S1 and S2 with a 2/6 mid systolic murmur best auscultated over the upper left sternal border with minimal radiation.
  • Bounding pulses felt radially, femorally and dorsalis pedis
  • Capillary refill within 2 seconds.
  • Normal on inspection.
  • Bowel sounds diminished but present.
  • No hepatomegaly.
  • 4cm splenomegaly.


  • Child listless though attempts to follow commands.
  • Not resisting or crying in response to aggravating stimuli.


Human malaria infection is caused by four protozoa species of the genus Plasmodium. These are P.falciparum, P. malariae, P. vivax, and P. ovalae , of which the preponderance of severe malaria and mortality is due to P.falciparum . Children living in endemic areas typically have a primary malaria episode during their first few years of life and most toddlers and juveniles develop some degree of acquired immunity against severe disease but still experience periodic clinical episodes. Those who survive to adulthood are often clinically immune, however, low grade parasitaemia is often present but causes few symptoms. Adults in endemic areas maintain low-grade infections throughout the transmission season. Endemicity is typically defined as parasitaemia rates or palpable spleens in children aged 2-9 years. The categories include holoendemic where the rate is >75% (transmission of infection is year round and the bulk of mortality is seen in infants), hyperendemic where the rate is 51-75% (mortality is also mostly seen in infants), mesoendemic where the rate is 11-50% (regular seasonal transmission affecting infants, toddlers and adults who develop chronic ill health) and hypoendemic which is <10% (occasional epidemics, whole population is susceptible to severe and fatal disease). Clinical immunity also fails if a person moves away from an endemic area and during pregnancy.

plasmodium falciparum

The female Anopheles mosquito inoculates the host with 10 to 100 malaria sporozoites from her salivary glands during a blood meal. These microscopic motile forms of the malaria parasite are carried via the bloodstream to the liver. Within 30 minutes, those sporozoites not bound by previously formed antibodies, invade and begin replicating in hepatocytes. Parasites not destroyed by cytotoxic T lymphocytes in the liver replicate for 2-10 days creating merozoites. Tens of thousands of merozoites are released into the bloodstream as the hepatocyte bursts. Each merozoite is then able to bind, invade, and infect erythrocytes. After red blood cell (RBC) infection, each merozoite matures to form a highly metabolically active trophozoite, which replicates asexually to become multinucleate schizonts. As the schizonts enlarge they rupture erythrocytes 48 hours after their formation which results in 20-30 new merozoites which continue the cycle. Some sexual forms of the parasite develop during this erythrocytic stage; these gametocytes are responsible for infecting the salivary glands of female Anopheles mosquitoes. The gametes mature into ookinetes then into an oocyst. The oocyst ruptures and releases sporozoites which can then infect another host during a blood meal.


A person’s first infection usually creates no symptoms for 7-10 days, which is followed first by nonspecific symptoms such as headache, fatigue, abdominal discomfort and muscle aches. This is then followed by fever. During this latent period, parasite maturation occurs in the liver and parasites undergo a cycle of blood stage replication. Symptoms begin when the parasites undergoing an asexual blood cycle, reach threshold density sufficient to initiate the host’s pathogenic immune response process. Fever, malaria’s hallmark, is due to parasite-derived molecules released from ruptured host cells. These molecules activate host inflammatory cells, such as macrophages, which secrete pro-inflammatory pyrogenic cytokines such as interleukin (IL)-1 and tumor necrosis factor (TNF)–α. As parasites synchronise their replication cycles the fever becomes periodic. Although childhood febrile convulsions can occur, generalised seizures are typically associated with P.falciparum infections and may herald cerebral malaria. Splenomegaly results from massive reticuloendothelial system activation to clear parasitised erythrocytes. Mild hepatomegally is common in young children, while mild jaundice is more common in adults. Anaemia is also common and is partly due to the phasic rupture of RBCs by mature schizonts, splenic sequestration of red blood cells and ineffective erythropoiesis.


Cerebral Malaria Onset may be gradual or sudden following a convulsion. Features include obtundation, delirium, abnormal behaviour and coma. Focal neurologic signs and meningism do not typically occur. Fifteen percent of children who survive cerebral malaria, especially when associated with hypoglycaemia, coma and anaemia will have some residual neurologic deficit.

Hypoglycaemia Common complication that is associated with a poor prognosis, particularly in children and pregnant women. Hypoglycaemia is due to a failure of hepatic gluconeogenesis and an increase in glucose consumption by host and parasite. This may manifest as an added complication during treatment as Quinine is also a potent stimulator of insulin secretion.


Haematologic Pathology Anaemia due to increased destruction and removal or red blood cells and dyserythropoesis. Mild thrombocytopaenia Mild coagulation abnormalities Bleeding and DIC in more severe cases

Renal pathology Interference in microcirculation resulting in tubular necrosis and acute renal failure, more common in adults.

Host Response-Immunology


  • Antibody responses are induced during the sporozoite stage. Antibody bound sporozoites are prevented from invading hepatocytes.
  • CD8 + T cells have been shown to be cytotoxic against maturing sporozoite infected liver cells.
  • Both of these responses are potentially able to terminate the infection before the onset of clinical disease caused by the release of merozoites from hepatocytes and subsequent RBC invasion and rupture.
  • CD4 + T cells are a requisite for the production of merozoite neutralising antibodies by B cells and the activation of macrophages which secrete interferon (INF) –γ to enhance parasitized RBC.
  • The host is also able to develop transmission-blocking antibodies directed to gametocyte specific antigens. These antibodies hinder the development of the parasite within the mosquito vector, thereby preventing further infections. Though this immune response is not particularly valuable to the infected host, it does assist in reducing population level transmission.


Download images for this case

Plasmodium falciparum malaria.

It is recommended that patients receive prompt and effective treatment. Ideally, treatment should be initiated in a hospital setting. The choice of chemotherapy for malaria is dependent on the severity of disease, the known or suspected resistance pattern of the parasite in the area where the malaria infection was acquired, the species of parasite, patient characteristics (age, pregnancy, co-morbidity, allergies, other medications) and the presence or absence of vomiting. In South Africa, malaria treatment varies in the different provinces due to differences in the resistance patterns. These treatment guidelines may not be appropriate for infections contracted in other countries with high levels of multi-drug resistance.

The patient was treated with IV artesunate and anti-pyretics for 3 days. IV antibiotics were started on admission as there was no confirmatory diagnosis at the time and culture results were not yet available. On the third day the child was markedly improved. He was started on a full course of mefloquine on receiving laboratory results which confirmed infection with P.falciparum. Upon discharge there were no neurologic sequelae. He and his family were counseled on the use of insecticide-treated bed nets and indoor residual spraying.

Guerin, P.J., et al. (2002). Malaria: current status of control, diagnosis, treatment, and a proposed agenda for research and development. Lancet Infect Dis. 2(9): p. 564-73.

Link to Abstract Ferreira, M.U et al. (2004). Antigenic diversity and immune evasion by malaria parasites. Clin Diagn Lab Immunol. 11(6): p. 987-95.

Link to Abstract May, J. et al. (1999). High rate of mixed and subpatent malarial infections in southwest Nigeria. Am J Trop Med Hyg. 61(2): p. 339-43.

Link to Abstract Rosenberg, R. et al. (1990). An estimation of the number of malaria sporozoites ejected by a feeding mosquito. Trans R Soc Trop Med Hyg. 84(2): p. 209-12.

Link to Abstract Ponnudurai, T. et al. (1982). Mosquito transmission of cultured Plasmodium falciparum. Trans R Soc Trop Med Hyg. 76(2): p. 278-9.

Link to Abstract Ferreira, M.U et al. (1998). The IgG-subclass distribution of naturally acquired antibodies to Plasmodium falciparum, in relation to malaria exposure and severity. Ann Trop Med Parasitol. 92(3): p. 245-56.

Link to Abstract Nardin, E.H et al. (1993). T cell responses to pre-erythrocytic stages of malaria: role in protection and vaccine development against pre-erythrocytic stages. Annu Rev Immunol. 11: p. 687-727.

Link to Abstract Nardin, E.H. et al. (1982). Circumsporozoite proteins of human malaria parasites Plasmodium falciparum and Plasmodium vivax. J Exp Med. 156(1): p. 20-30.

Link to Abstract Inselburg, J. (1983). Gametocyte formation by the progeny of single Plasmodium falciparum schizonts. J Parasitol. 69(3): p. 584-91.

Link to Abstract Aitman, T.J. et al. (2000). Malaria susceptibility and CD36 mutation. Nature. 405(6790): p. 1015-6.

Link to Abstract Jenkins, N. et al. (2007). Plasmodium falciparum intercellular adhesion molecule-1-based cytoadherence-related signaling in human endothelial cells. J Infect Dis. 196(2): p. 321-7.

Link to Abstract McCormick, C.J. et al. (1997). Intercellular adhesion molecule-1 and CD36 synergize to mediate adherence of Plasmodium falciparum-infected erythrocytes to cultured human microvascular endothelial cells. J Clin Invest. 100(10): p. 2521-9.

Link to Abstract

Miller, L.H. et al. (2002). The pathogenic basis of malaria. Nature. 415(6872): p. 673-9.

Abdel-Latif, M.S. et al. (2003). Antibodies to Plasmodium falciparum rifin proteins are associated with rapid parasite clearance and asymptomatic infections. Infect Immun. 71(11): p. 6229-33.

Good, M.F. et al. (1998). Pathways and strategies for developing a malaria blood-stage vaccine. Annu Rev Immunol. 16: p. 57-87.

Hoffman, S.L. et al. (1998). Sporozoite vaccine induces genetically restricted T cell elimination of malaria from hepatocytes. Science. 244(4908): p. 1078-81.

Link to Abstract Snewin, V.A et al. (1995). Transmission blocking immunity in Plasmodium vivax malaria: antibodies raised against a peptide block parasite development in the mosquito vector. J Exp Med. 181(1): p. 357-62.

Link to Abstract Hisaeda, H. et al. (2005). Malaria: immune evasion by parasites. Int J Biochem Cell Biol. 37(4): p. 700-6.

Link to Abstract Qari, S.H. et al. (1998). Predicted and observed alleles of Plasmodium falciparum merozoite surface protein-1 (MSP-1), a potential malaria vaccine antigen. Mol Biochem Parasitol. 92(2): p. 241-52.

Link to Abstract Burns, J.M. et al. (1989). A protective monoclonal antibody recognizes a variant-specific epitope in the precursor of the major merozoite surface antigen of the rodent malarial parasite Plasmodium yoelii. J Immunol. 142(8): p. 2835-40.

Link to Abstract Smith, J.D. et al. (1995). Switches in expression of Plasmodium falciparum var genes correlate with changes in antigenic and cytoadherent phenotypes of infected erythrocytes. Cell. 82(1): p. 101-10.

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Link to Abstract Williamson, W.A. et al. (1978). Impairment of the immune response to vaccination after acute malaria. Lancet. 1(8078): p. 1328-9.

Link to Abstract Takeda, K. et al. (2003). Toll-like receptors. Annu Rev Immunol. 21: p. 335-76.

Link to Abstract Urban, B.C. et al. (1999). Plasmodium falciparum-infected erythrocytes modulate the maturation of dendritic cells. Nature. 400(6739): p. 73-7.

Link to Abstract Ocana-Morgner, C. et al. (2003). Malaria blood stage suppression of liver stage immunity by dendritic cells. J Exp Med. 197(2): p. 143-51.

Link to Abstract Omer, F.M et al. (2003). Differential induction of TGF-beta regulates proinflammatory cytokine production and determines the outcome of lethal and nonlethal Plasmodium yoelii infections. J Immunol. 171(10): p. 5430-6.

Link to Abstract Shevach, E.M. (2002). CD4+ CD25+ suppressor T cells: more questions than answers. Nat Rev Immunol. 2(6): p. 389-400.

Hisaeda, H. et al. (2004). Escape of malaria parasites from host immunity requires CD4+ CD25+ regulatory T cells. Nat Med. 10(1): p. 29-30.

Evaluation – Questions & answers

What is the diagnosis?

With regards to parasitized erythrocytes which endothelial receptors do they bind to resulting in occlusion of microvessels?

What are the three ways that infected erythrocytes can bind to occlude microvessels?

What is the benefit of occlusion of microvessels?

Which organs are most affected by occlusion of microvessels?

Describe the immune response required to neutralize malaria parasites at each stage during their development.

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Congenital Malaria in a 2-Day-Old Neonate: A Case Report and Literature Review

Dickson kajoba.

1 Department of Paediatrics and Child Health, Faculty of Clinical Medicine and Dentistry, Kampala International University, Kampala, Uganda

Walufu Ivan Egesa

Habonimana jean petit, muhiadin omar matan, goretty laker, william mugowa waibi, daniel asiimwe.

2 Department of Surgery, Faculty of Clinical Medicine and Dentistry, Kampala International University, Kampala, Uganda

Congenital malaria is the presence of malaria parasites in a blood smear obtained from a neonate usually within 24 hours to 7 days of life. It has for long been regarded a rare condition. However, recent data indicate that congenital malaria complicates around 35.9% of live births globally, 0–37% in Sub-Saharan Africa and about 4–6.1% in Eastern Uganda. We present a 2-day-old neonate who presented with fever, irritability, and failure to breastfeed. Laboratory tests indicated that the neonate had a positive Giemsa-stained peripheral smear for Plasmodium falciparum , with a positive malaria rapid diagnostic test (MRDT) for P . falciparum malaria. The mother had a negative peripheral film for malaria and a negative MRDT. The neonate was managed with intravenous artesunate with improvement.

1. Introduction

Uganda remains a highly malaria-endemic country, one of the 6 most affected countries contributing 5% to the global malaria burden [ 1 ]. Children under 5 years and pregnant women are the most affected with children under 5 years contributing an estimated 70% of malaria-related deaths in the country [ 2 ].

Congenital malaria (CM) is defined as a positive blood smear for malaria in a neonate from 24 hours to 7 days of life. This is usually due to maternofoetal transfer of malaria parasites. On the other hand, neonatal malaria is defined by the presence of malaria parasites in peripheral blood within 28 days of life, usually attributable to mosquito bites [ 3 , 4 ]. The maternofoetal transfer of malaria parasites can be reduced if mothers routinely take their intermittent presumptive treatment of malaria during pregnancy with sulfadoxine/pyrimethamine which reduces neonatal mortality by approximately 60% [ 5 ].

CM presents with nonspecific signs and symptoms of fever, anaemia, jaundice, vomiting, lethargy, convulsions, irritability, tachypnoea, respiratory distress, and hepatosplenomegaly which overlap with sepsis syndrome [ 6 ]. Due to a low index of suspicion and nonspecific presentations, it is often wrongly managed as neonatal sepsis, which contributes to mortality and morbidity among neonates [ 7 ].

Neonates have some level of protection from malaria due to passive immunisation from maternal antibodies, presence of foetal haemoglobin, and low iron levels which do not favour growth of plasmodium [ 3 ]. However, as maternal IgG and HbF wane, there is a surge in malaria parasitaemia among the infants [ 8 , 9 ]. The prevalence of congenital malaria may be under-reported due to its nonspecificity in presentation and delay in onset of symptoms. Only 34% of affected neonates become symptomatic within 72 hours of life, while others may present after 3 weeks of life [ 8 ].

Currently, it is estimated that there is a 33.7% global burden of congenital malaria [ 10 ] with Sub-Saharan Africa having a prevalence of 0 to 37% [ 11 ] and a prevalence of 4–6.1% in Eastern Uganda [ 12 , 13 ]. In order to reduce the malaria case incidence and death rate to at least 90%, the World Health Organisation (WHO) came up with Global Technical Strategy for Malaria, 2016–2030. The program launched in 2015 was geared towards eliminating malaria in at least 35 countries and to prevent its reintroduction in all countries that eliminated it [ 14 ].

2. Case Report

We report a case of a male neonate delivered at term by spontaneous vaginal delivery from a lower level health centre, with a birthweight of 3.7 kg. Apgar score was not documented, but the neonate cried immediately after birth. Labour lasted about 8 hours and membranes ruptured just before delivery. Breastfeeding was initiated within the 1 st hour of life and the neonate was suckling well. He passed meconium and urine within the first 24 hours of life.

The neonate was born to a 29-year-old G2P1 + 0 who attended antenatal care 6 times, starting at 3 months. She had been screened for HIV, syphilis, hepatitis B, and urinalysis, and all were negative, with a blood group of A Rhesus D negative. She received tetanus toxoid, Fansidar for malaria prophylaxis, haematinics, and deworming. She reported that the pregnancy was uneventful.

About 36 hours after delivery, the neonate developed a high-grade fever, irritability, poor breastfeeding, and yellowing of eyes and skin. The neonate was managed with unknown oral medication before referral to Jinja Regional Referral Hospital for further management.

At admission, the neonate was conscious, with an axillary temperature of 38.0°C, and jaundice (Kramer stage 2). There was no respiratory distress, no pallor, no dehydration, and no dysmorphic features noted. The systemic physical examination was unremarkable.

Investigations done were as follows:

  • Malaria rapid diagnostic test (MRDT) for P . falciparum was positive; thin blood smear showed P . falciparum malaria species with 1.846 ∗ 10 3 malaria-infected red blood cells.
  • Complete blood count was normal with Hb of 15.2 g/dl, white blood cells 11.79 ∗ 103/ul, and platelet count 244 ∗ 103/ul.
  • Blood group was A Rhesus D negative.
  • Total serum bilirubin was 200.33 umol/l with direct bilirubin 7.48 umol/l.
  • The rapid diagnostic test for P . falciparum was negative, and no haemoparasites were seen on the peripheral smear of maternal blood.

The neonate was initiated on intravenous artesunate at admission, 12 hr and 24 hr later, then once a day for 5 days. Intravenous empiric antibiotics (cloxacillin and cefotaxime) for presumed neonatal sepsis were also administered. After 48 hours of antibiotics, C-reactive protein (CRP) was done and it was nonreactive, and the antibiotics were stopped. Blood culture and sensitivity was not performed for this patient. A peripheral blood smear done on day 5 of antimalarial treatment revealed no malaria parasites. The neonate was discharged after 5 days of artesunate with great improvement. We were not able to follow up the patient after discharge.

3. Discussion

Malaria is a parasitic disease that is transmitted by an infectious female Anopheles mosquito during a blood meal. This is caused by a parasitic protozoan of the genus plasmodium which has 5 different species, with P . falciparum being the most predominant in the Sub-Saharan region [ 1 ]. In this case report, the neonate had P . falciparum as the causative plasmodium species.

In 2019, there were 229 million cases of malaria, with over 94% of an estimated 409,000 deaths globally. More than 94% of all cases and deaths occurred in Sub-Saharan Africa. Children under 5 years are the most vulnerable, and in 2019, they accounted for 67% (274000) of all malaria deaths worldwide [ 15 ].

Congenital malaria is defined as the presence of malarial parasites in the peripheral blood smear of the new born from 24 hours to 7 days of life. However, it can occur beyond 28 days of life confounding with neonatal malaria [ 3 , 6 ]. CM is acquired from the mother, while neonatal malaria is by mosquito inoculation [ 6 ]. Unfortunately, due to its nonspecific presentations and low index of suspicion, CM is often managed as neonatal sepsis, which unwittingly increases hospital stay and neonatal morbidity and mortality [ 7 ].

Babies are believed to have partial protection from malaria in the first few months of life, owing to passively acquired maternal IgG antibodies, the predominance of haemoglobin F (HbF) in their erythrocytes, and the low levels of iron and para-amino benzoic acid (both required for parasite growth) in breast milk [ 3 ]. Despite these factors, newborns and infants less than 12 months of age are one of the most vulnerable groups affected by malaria [ 16 ].

Globally, there is a 33.7% prevalence of congenital malaria with Africa having 39.5%. Furthermore, it is estimated that 40 neonates per 1000 live births will experience clinical malaria during the first 7 days of life [ 10 ]. In Sub -Saharan Africa, the prevalence is estimated to be between 0 and 37% [ 4 ], while in Eastern Uganda, the prevalence of CM is reported to range from 4 to 6.1% [ 12 , 13 ].

The true burden of congenital malaria may be underestimated due to absence of routine screening of newborns with fever, low index of suspicion, absence of specific signs, and symptoms, coupled with the late symptom presentation. Only one-third (34%) of the affected neonates present within 72 hours of life [ 9 , 13 ]. This was the case with our patient who presented with CM within 48 hours of life. On the other hand, delayed presentation of CM has been reported up to 2 months after delivery [ 3 ]. A case report by Rai and colleagues documented a 21-day-old neonate with congenital malaria in Burundi [ 17 ]. This is because transplacentally acquired maternal antibodies delay the onset of symptoms, with symptom occurrence coinciding with half-life of maternal IgG antibodies [ 17 ].

It is recommended therefore that malaria parasite testing be included in the routine screening of febrile babies with suspected septicaemia in malaria-endemic regions [ 18 ]. To maximise the chances of detection, some authors suggest malaria screening irrespective of clinical presentation at delivery, followed by weekly follow up with repeated blood smear up to 4 weeks if the mother was known to have malaria 7 days before delivery [ 9 ]. Neonates with severe illness and parasitaemia should have blood samples taken for culture and, in any case, should be treated with antibiotics as well as antimalarial drugs [ 3 ].

Use of peripheral blood smear with microscopy is the routinely used diagnostic modality for diagnosis of malaria in developing countries [ 13 ], but with the introduction of malaria rapid diagnostic testing (MRDT), there has been found a useful alternative with good sensitivity and specificity for malaria diagnosis including pregnant women and newborns. Polymerase chain reaction (PCR) may have a higher sensitivity for CM. However, it is not readily available in developing countries, except in research settings [ 19 ]. In this case, the MRDT and blood smear for maternal and neonatal blood were negative and positive for P . falciparum, respectively. PCR could have been useful in differentiating between congenital or neonatal malaria since it is very sensitive compared to MRDT and peripheral smear.

Malaria due to P . falciparum should be treated, be it symptomatic or asymptomatic because it is associated with high mortality and morbidity [ 20 ]. However, there are no clear guidelines for treatment of CM [ 9 , 10 ]. Artemisinin-based combination therapy (ACT) is the regimen by WHO, yet there are limited clinical trials particularly in neonates for ACT, and many carry labels restricting its use [ 9 ]. WHO recommends use of same dosages for neonates below 5 kgs as the dosage for neonates weighing 5 kgs [ 16 ]. This however caries a risk of drug over dose in these neonates. Additionally, there is no well-established pharmacokinetics and pharmacodynamics of these antimalarial drugs in neonates with still rapidly evolving physiology. Therefore, parenteral treatment is preferred in neonates and young infants [ 9 ], as was the case in this neonate, where parenteral artesunate was considered.

The prognosis of congenital malaria is variable, depending on when intervention is initiated. In Burkina Faso, Nagalo and colleagues reported that 11.8% of CM-related deaths occurred within an average of 4.8 days from admission, of which 55% of these deaths occurred within 24 hours of admission [ 21 ]. However, timely intervention of the newborn may prevent neonatal morbidity and mortality [ 17 ], as was the case in this neonate.

4. Conclusion

Congenital malaria should be considered as a differential for sepsis in neonates presenting with unexplained fever and failure to breastfeed. There is need to raise awareness of this condition so as to increase diagnostic suspicion and investigatory habit among patients suspected for neonatal sepsis.

Conflicts of Interest

None of the authors have any conflicts of interest.

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  • Case report
  • Open access
  • Published: 20 April 2018

Neonatal and congenital malaria: a case series in malaria endemic eastern Uganda

  • Peter Olupot-Olupot 1 , 2 , 3 ,
  • Emma I. E. Eregu 1 ,
  • Ketty Naizuli 1 ,
  • Julie Ikiror 1 ,
  • Linda Acom 1 &
  • Kathy Burgoine 1 , 2  

Malaria Journal volume  17 , Article number:  171 ( 2018 ) Cite this article

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Congenital malaria is the direct infection of an infant with malaria parasites from their mother prior to or during birth. Neonatal malaria is due to an infective mosquito bite after birth. Neonatal and congenital malaria (NCM) are potentially life-threatening conditions that are believed to occur at relatively low rates in malaria endemic regions. However, recent reports suggest that the number of NCM cases is increasing, and its epidemiology remains poorly described. NCM can mimic other neonatal conditions and because it is thought to be rare, blood film examinations for malaria are not always routinely performed. Consequently, many cases of NCM are likely to be undiagnosed. A retrospective chart review for all neonates admitted with suspected sepsis between January and July 2017 was conducted and noted four cases of NCM since routine malaria testing was introduced as part of standard of care for suspected sepsis at Mbale Regional Referral Hospital Neonatology Unit. This description highlights the need to conduct routine malaria diagnostic testing for febrile neonates in malaria endemic areas, and supports the urgent need to undertake pharmacological studies on therapeutic agents in this population.

Case presentation

Four cases (two congenital malaria cases and two neonatal malaria cases) are described after presenting for care at the Mbale Regional Referral Hospital Neonatal Unit (Mbale RRH-NNU). The maternal age was similar across the cases, but both neonatal malaria cases were born to primigravidae. At presentation three cases had fever and history of fever, but one was hypothermic (34.8 °C) and no history of fever. One case of congenital malaria had low birth weight, while the other was born to an HIV positive mother. Both cases of congenital malaria presented with poor feeding, in addition one of them had clinical jaundice. The neonatal malaria cases presented in the third week compared to the congenital malaria cases that presented within 48 h after birth. All of the cases of NCM were treated with intravenous artesunate. The admitting clinicians also instituted a course of antibiotics empirically to cover against possible bacterial co-infections. All four cases recovered and were discharged alive.

At the Mbale RRH-NNU, the finding of cases of NCM was not expected, therefore, neonates presenting with features of suspected sepsis in malaria endemic settings should be routinely screened for NCM. There is currently a lack of appropriate guidelines for treatment of NCM in the era of artemisinin-based combination therapy (ACT), therefore, efforts to establish the safety profile and efficacy of ACT anti-malarials in neonates to guide development of evidence-based treatment guidelines for NCM are needed.

Uganda remains a malaria high burden country, with eastern Uganda experiencing perennial high malaria transmission with > 100 infective bites per person per year [ 1 , 2 ]. In endemic areas where mothers have acquired considerable immunity to malaria, infection with Plasmodium falciparum during pregnancy does not always cause symptomatic illness [ 3 ]. Congenital malaria results from transplacental transmission of malaria parasites from the mother to the baby in utero or during delivery. Its diagnosis is based upon detection of asexual forms of malaria parasites on a blood smear of the peripheral blood of the newborn, or later if there is no possibility of postpartum infection through infective mosquito bites [ 4 ]. However, these definitions are not precise if time is not tagged to them to enable differentiate congenital from neonatal malaria. Furthermore, precision of definitions would be achieved by using temporal relationship with PCR testing for malaria in the mother and their neonate. The reported incidence of congenital malaria in endemic regions varies widely from 0 to 37% [ 5 , 6 , 7 ]. It is widely believed that the placenta acts as an effective barrier preventing transfer of malaria parasites. However, even in the absence of congenital malaria, placental malaria significantly increase the risk of perinatal morbidity and mortality including low birth weight, intrauterine growth restriction, preterm labour and intrauterine fetal death [ 8 ]. Malaria in pregnancy is estimated to account for 100,000 neonatal deaths annually [ 3 ]. Maternal malaria can be prevented during pregnancy with intermittent presumptive treatment of malaria in pregnancy (IPTp) using sulfadoxine–pyrimethamine, and can reduce neonatal mortality by up to 61% [ 9 ].

It is also possible that maternal immunity to malaria may confer protection to the fetus through transmission of immunoglobulin G antibodies (IgG) against malaria [ 10 ]. The presence of fetal haemoglobin (HbF) in the neonate also prevents high parasitaemia [ 11 ]. However as maternal IgG and HbF in infants diminish with age, the infant’s susceptibility to P. falciparum increases. It is possible that this passive immunity may delay the onset or modify severity of symptoms by up to 6 weeks after birth making it hard to differentiate between congenital and neonatal malaria [ 12 ]. To maximize the chances of early detection of congenital malaria, neonates born to mothers with malaria in the last 7 days before delivery should be investigated with a blood film for malaria parasites irrespective of the clinical picture and weekly thereafter for the first month.

In the eastern region of Uganda, despite perennial malaria transmission, NCM is a rarely reported condition presumably because of low index of suspicion among clinicians, and greater emphasis on the diagnosis and treatment of neonatal sepsis (NS). Although it is recommended that neonates be routinely tested if mother was known to suffer from malaria in the 7 days before delivery, in practice it is often not routine to test neonates for malaria and, therefore, many cases may be missed. In neonates, the historical and most common symptom of malaria is fever [ 13 ]. Other symptoms and signs differ from those in older children with malaria, the clinical features of neonatal and congenital malaria overlap with sepsis syndromes [ 14 ]. Other symptoms can include anaemia, jaundice, diarrhoea, vomiting, lethargy, convulsions, irritability, tachypnoea, respiratory distress, hepatosplenomegaly [ 14 ]. Clinical descriptions and outcomes of NCM remain poorly documented even in malaria endemic areas where descriptions in infants, older children and adults have over the times progressed. More comprehensive descriptions inclusive of NCM are needed, especially from areas with intense transmission, and serially over time.

At Mbale Regional Referral Hospital IPTp is routinely administered to pregnant mothers, however, not all pregnant mothers in the region served by this hospital attend antenatal care. At the hospital NNU there are estimated 200 admissions per month. During the study period June–December 2017 routine blood slides for malaria for all neonates admitted with fever had been introduced. This report is on four cases of NCM that highlight the presenting clinical features and their outcomes in a perennially malaria high transmission area in eastern Uganda. This has shown that malaria is a potentially missed diagnosis or co-morbidity in neonatal illnesses in malaria endemic areas.

In this study congenital was differentiated from neonatal malaria based on the time of presentation from birth. Congenital malaria, as was previously defined, was used to classify cases 1 and 2 (Table  1 ). However, this description modified the definition for neonatal malaria that was applied by Runsewe-Abiodun et al. in Nigeria [ 15 ]. Therefore, for cases 3 and 4 (Table  1 ), this study considered symptoms attributable to malaria with evidence of ring forms of malaria parasite in the erythrocyte of an infant within the 8th–28th days of life. The maternal age was similar across all the 4 cases, range 24–28 years. The two neonatal malaria cases (3 and 4) were born to primigravidae who had no recent history of fever in the 14 days to delivery. Three of the cases presented with fever or history of fever, while one of the congenital cases was hypothermic (34.8 °C), possibly due to the concurrent prematurity. This same infant was also born to an HIV+ mother. Whereas there are many risk factors for preterm deliveries, it is possible that in this mother either the HIV [ 16 ], or antiretroviral drugs [ 17 ], may have contributed to both prematurity and susceptibility to malaria in this baby. The other congenital malaria case had clinical jaundice and pyogenic meningitis. The jaundice in this case 1 was attributed to a number of possible factors including neonatal jaundice, sepsis, malaria or a combination of these. Poor breastfeeding was noted in both congenital cases. All of the cases of NCM were treated with intravenous artesunate 4 mg/kg at 0, 12, 24 h then daily for 7 days. Since sepsis could not be excluded due to lack of laboratory investigative capacity, the admitting clinicians also instituted a course of broad-spectrum antibiotics empirically to cover against possible bacterial infections. All cases recovered and were discharged alive.

Discussion and conclusions

In this case series, a description is made of both congenital and neonatal malaria in a setting that introduced routine neonatal malaria testing in a malaria endemic area. This case series shows that NCM malaria is more common than previously thought [ 18 ]. It is also a reminder that NCM still exists despite IPTp and other malaria preventive measures, and its diagnosis may be missed especially when malaria screening measures are not put in place in NNUs in malaria endemic areas. Other reports suggest that the incidence of NCM may be increasing. Proper descriptions of NCM are important to ensure more comprehensive understanding of the clinical spectrum and outcomes of malaria in neonates. Malaria endemicity has been suggested to play a role in the prevalence of NCM. There are reports suggesting in hyperendemic areas the prevalence of NCM is higher [ 5 , 15 ], while others are contrary [ 7 ]. It is however, plausible epidemiologically that in settings of intense perennial transmission the mothers have developed herd immunity, their newborn babies have protective antibodies to the disease, and therefore the prevalence is negligible [ 10 ]. Some underlying factors may be responsible for the equipoise observed in this case series. For instance, primigravidae are known to have a high risk for malaria compared to multigravidae [ 19 ]. In addition, the role of maternal malaria in congenital malaria infections has been traced to infections in the third trimester [ 15 ]. It is also possible that co-morbidity that damages the placenta in utero may contribute to the risk of the congenital malaria. HIV co-infected pregnant women may have impaired antibody response and have been shown to have a significantly increased risk of placental malaria [ 20 ]. This is consistent with some reports suggesting that HIV increases the chances of vertical transmission of malaria [ 16 , 20 ]. Maternal low age has been reported to influence congenital malaria [ 19 ]. In this series, all the mothers were within the same age range, but their parities differed.

Although rapid malaria tests have been used for the diagnosis of NCM, the gold standard for the diagnosis of NCM is the detection of parasites in the Giemsa-stained peripheral blood smear [ 21 ]. The Mbale RRH-NNU recently introduced routine testing for malaria using blood smears in neonates reporting with signs of sepsis. Consequently, all cases identified with NCM were managed with good outcomes.

On treatment, amodiaquine, chloroquine and sulfadoxine–pyrimethamine have all been successfully used in Nigeria to treat neonates with malaria [ 22 ]. Although artemisinin-based combination therapy (ACT) is the recommended treatment for uncomplicated malaria in infants, the neonates have been largely excluded from ACT clinical trials. There are, therefore, limited data available on the use of ACT in neonates and many of them carry label restrictions for neonates [ 23 ]. For infants weighing less than 5 kg with uncomplicated P. falciparum , the World Health Organization (WHO) recommends treatment with ACT at the same mg/kg body weight dose as for children weighing 5 kg. The WHO acknowledges too that most anti-malarials lack infant formulations, which can lead to either under or over dosing. In addition, infants can deteriorate rapidly therefore there should be a low threshold for parenteral treatment. Many anti-malarials are frequently used off-label based on the dosing schedule for older children [ 24 ], but have not reported evidence of serious toxicity [ 23 ].

Due to the physiological immaturity and rapid changes that occur in neonates, the pharmacokinetic and dynamic (PK/PD) profiles of anti-malarial drugs are likely to be different to older children. Slow gastric emptying, villous formation and intestinal motor activity, which do not mature until week 20 of life, affect the enteral absorption of most medications [ 25 ]. Parenteral treatment is preferable for neonates and young infants. Differentiating congenital from neonatal malaria based on temporal relationship to birth may be strengthened by inclusion of DNA PCR for both the mother and her newborn to determine the source of the infection. But in resource limited areas there are no routine DNA PRC testing services due to prohibitive capital, running and maintenance costs, except in research settings. The temporal characteristic would help interpret the role of physiological immaturity in neonates for future PK/PD studies on anti-malarial drugs in this age group, and how these determine treatment outcomes.


This is only a case series with case definitions based on temporal relationships from birth to case presentation. A larger study with capacity to conduct molecular, parasite count and PK/PD testing, and long term follow up would help better refine definitions, outcomes and interpretation of these findings. Nonetheless, this report has been able to demonstrate that NCM still exists. The definitions used have set pace in appropriate description of the spectrum of disease in this age group and will strengthen interpretation of anti-malarial PK/PD studies in this population in relation to the physiological immaturity.

In summary, NCM is an important diagnosis to consider in any newborn with clinical features of NS to a mother in a malaria-endemic area. It is possible that in the absence of routine malaria testing many neonates are dying before malaria is diagnosed. In areas with malaria endemicity the burden of NCM may be underestimated. Malaria test should be incorporated as routine test in neonates with suspected sepsis so as not to miss NCM. Early and correct diagnosis of NCM is crucial as infants are at increased risk of rapid disease progression, severe malaria and death. Additional efforts are needed to establish the safety profile and efficacy of ACT in neonates to guide the development of evidence-based treatment guidelines for NCM. Furthermore, for pregnant mothers who test malaria positive in their late gestational period weekly malaria testing of their babies as follow up mechanism for surveillance of NCM should be done.

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Authors’ contributions

EIEE, KN, JI, LA and KB—collected the data and participated in writing the manuscript; P-OO—conceived the idea and wrote the manuscript. All authors read and approved the final manuscript.


The authors acknowledge Mbale Regional Referral Hospital, Mbale Clinical Research Institute and all staff at the Mbale RRH-NNU for their various contributions to this work.

Competing interests

The authors declare that they have no competing interests.

Availability of data and materials

The study data is available on personal request to the corresponding author.

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The Mbale Clinical Research Institute (MCRI, ), a research entity affiliated to the Uganda National Health Research Organization (UNHRO), permits the publication of this manuscript.

Ethics approval and consent to participate

The Mbale Regional Referral Hospital Research & Ethics Committee (MRRH-REC) approved the study and local permission to conduct the study was obtained from Mbale Regional Referral Hospital.

This study was conducted within the provisions of ethical standards in Uganda.

This study was not funded.

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Olupot-Olupot, P., Eregu, E.I.E., Naizuli, K. et al. Neonatal and congenital malaria: a case series in malaria endemic eastern Uganda. Malar J 17 , 171 (2018).

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