PERINATAL�MALARIA, TYPHOID, TUBERCULOSIS

Dr Furqan Saleem

MBBS. FCPS Pediatrics. FCPS Neonatology

Consultant Neonatologist/Pediatrician PAF Hospital Lahore

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• Malaria is a mosquito transmitted infection caused by 1 of 5 parasite Plasmodium species:
• P falciparum
• P vivax
• P ovale
• P malariae
• P knowlesi

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Transmission to fetus

• During pregnancy or at delivery

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• direct penetration of parasitized red blood cells through the chorionic villi or through premature separation of the placenta

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• Transmission of malaria by breastfeeding is not known to occur.

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Maternal effects during pregnancy

• Anemia
• Disease itself(fever, headache, nausea, vomiting, muscle aches, respiratory distress, severe anemia, RF, PE ,cerebral malaria and death

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• Pregnant persons are at higher risk of P falciparum infection compared to their nonpregnant
• Placental dysfunction and altered vasculature
• Risk of placental malaria decreases with increasing gravidity

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Effects on fetus

• Based on trimester of infection and on whether the pregnant person receives appropriate medical treatment
• Highest in PG and 1^st trimester
• Preterm delivery
• LBW & IUGR/both
• Miscarriage/Still birth

Newborn period

• Minimal to no clinical symptoms in first couple of months
• transplacental passage of antibodies
• hemoglobin F
• Preterms have early symptoms
• Poor growth
• Anemia
• Poor neurodevelopment ??
• Increased risk of non malarial infections(measles, streptococcus, tetanus)??
• Reduce response to immunizations??

Congenital Malaria

• Presence of Plasmodium parasites in the cord blood or in the peripheral blood during the first week of life.

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• Fever
• Anemia
• Hepatosplenomegaly
• Hemolysis
• hyperbilirubinemia
• Thrombocytopenia
• Poor feeding
• Respiratory distress

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Severe Malaria

• Parasitemia greater than 5% of red blood cells
• Central nervous system or other end-organ involvement
• Shock
• Acidosis
• Severe anemia
• Hypoglycemia

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Neonatal Malaria

• Presence of Plasmodium parasites in the peripheral blood from 8 to 30 days of life

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Diagnosis

• light microscopy (Thick and thin blood films)
• rapid immune- chromatographic diagnostic tests (RDTs)
• PCR
• loop-mediated isothermal amplification
• Congenital Malaria—both baby and mother tested

Placental Malaria

• placental histopathology

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Treatment in pregnancy

• In all trimesters, ACTs are the first-line treatment for uncomplicated falciparum malaria
• But in first trimester AL (artemether with lumefantrine) is preferred
• ACTs(artemisinin-combination therapies)
• Artemisinin with piperaquine, lumefantrine, or mefloquine.

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Treatment for Neonates

• Supportive: Maintain normoglycemia, fluid management, treat acidosis, anemia and fits as per local guidelines
• Uncomplicated Malaria
• First-Line:
• Artemisinin-Based Combination Therapies (ACTs):
• (Artemether-lumefantrine for P. falciparum in regions without resistance).
• Chloroquine: Used for P. vivax or P. ovale in chloroquine-sensitive areas.
• Alternative:
• Quinine + Clindamycin: Preferred in settings where ACTs are contraindicated or unavailable. Quinine requires 7-day treatment with strict monitoring for hypoglycemia and cardiac effects.

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Severe Malaria�

• Intravenous Artesunate: First-line for severe cases
• Dose: 3 mg/kg at 0, 12, and 24 hours, then daily until oral therapy can resume.
• Transition to ACT: Once oral intake is possible, complete treatment with a full ACT course.

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Special Considerations�

• Drug Resistance: Tailor treatment to local resistance patterns.
• Exchange Transfusion: Rarely used, reserved for extreme parasitemia with organ failure( > 10% paracitemia)
• Follow-Up: Monitor for relapse (especially in P. vivax) and adverse drug reactions.�

Prevention

• ITNs (insecticide-treated bed net )
• IRS (Indoor residual sprays) maybe unsafe in neonates
• Chemoprevention in high risk areas(Sulfadoxine- pyrimethamine)
• Mefloquine(Travelling)

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Maternal- Neonatal typhoid

• Rare in neonatal population

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• Clinical Suspicion:

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• Consider typhoid in neonates with non-specific symptoms (fever, lethargy, poor feeding, jaundice) in endemic areas or with maternal exposure.

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Transmission

Vertical Transmission (Rare):

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• In Utero: Placental transmission is rare but possible, particularly if the mother has severe bacteremia. Case reports document isolated instances of congenital typhoid.

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• During Delivery: Neonates may acquire infection if exposed to maternal fecal matter or contaminated fluids during birth, leading to early-onset neonatal typhoid.

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Pregnancy Complications:�

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• Preterm Birth/Low Birth Weight: 

Severe maternal illness (high fever, dehydration, malnutrition) increases risks of preterm labor and intrauterine growth restriction.

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• Miscarriage/Stillbirth: 

Rare, but possible with untreated high-grade fever or septicemia.

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Neonatal Risks�

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• Neonatal typhoid is uncommon but can be severe due to immature immunity. Symptoms include

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• Fever
• Vomiting
• Diarrhea
• Hepatosplenomegaly

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Diagnosis

• Blood Culture: Gold standard for diagnosis.

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• Stool/Urine Cultures: Less reliable but may supplement diagnosis.

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• PCR: Emerging role for rapid detection, especially in culture-negative cases.

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• Maternal Screening: Test mothers with recent typhoid or exposure history.

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Treatment

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• Delivery Hygiene: Strict infection control during birth minimizes neonatal exposure to contaminated secretions.

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• Breastfeeding: Generally safe if the mother is on treatment and practices hand/nipple hygiene.

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No evidence of S. Typhi transmission via breast milk.�

Treatment

• Supportive Care

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• Hydration/Nutrition: IV fluids for dehydration; encourage breastfeeding if possible.

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• Complication Management: Monitor for sepsis, meningitis, or ileus. Consider neonatal intensive care for severe cases.�

Treatment�

•  Empiric Antibiotics:
• Third-Generation Cephalosporins (e.g., Ceftriaxone): First-line due to rising resistance to

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ampicillin and cotrimoxazole. Neonatal dosage: 50–75 mg/kg/day IV/IM; monitor for bilirubin

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displacement in preterm infants.

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• Azithromycin: Alternative in areas with ceftriaxone resistance. Limited neonatal safety data; use

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under specialist guidance (10–20 mg/kg/day orally/IV).

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• Meropenam : XDR cases with dose of (60-120 mg/kg/day IV)

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• Adjust Based on Susceptibility: Tailor therapy once sensitivity results are available.
• Duration: Typically 10–14 days, extended if complications (e.g., sepsis) arise.�

Prevention�

• Maternal Measures:
• Treat maternal typhoid during pregnancy with safe antibiotics (e.g., ceftriaxone).
• Ensure hygiene to reduce vertical transmission risk.
• Breastfeeding: Generally safe; emphasize hand hygiene to prevent fecal-oral transmission.

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• Vaccination:
• Typhoid Conjugate Vaccine (TCV): Recommended for children ≥6 months in endemic areas; not for neonates.
• Maternal Immunization: Not standard but under investigation for indirect neonatal protection.

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Infection Control�

• Isolation: Practice contact precautions in hospital settings.
• Sanitation: Ensure sterile procedures and safe water in neonatal units.

Emerging Concerns

• Antimicrobial Resistance: Monitor for XDR strains (resistant to ceftriaxone, fluoroquinolones). Azithromycin or meropenem may be needed in resistant cases.
• Research Gaps: Limited neonatal-specific data; prioritize culture-guided therapy.

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Congenital Tuberculosis

• Congenital tuberculosis (TB) refers to the acquisition of Mycobacterium tuberculosis either in utero or during the intrapartum period
• Transmitted
• Umbilical vein
• In utero aspiration/ingestion of contaminated amniotic fluid of placenta or endometrium
• ingestion of infected amniotic fluid or secretions from maternal genital lesions during delivery
• Risk of congenital tuberculosis in infants born to women with tuberculosis is very low (underreported, endometrial TB)

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Pathogenesis of congenital Tuberculosis

Perinatal TB

• When acquired in the immediate postpartum period, known as perinatal TB, the bacteria are spread to the neonate via

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• Ingestion or inhalation of infected droplets
• Direct contact with the infected maternal genital tract, traumatized skin/ mucous membrane
• Infected persons

Transmission via breast milk has not been documented, unless mother has tuberculous breast abscess

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Complications of tuberculous pregnancy

• Prematurity
• Stillbirth
• Recurrent abortion
• Infertility

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Neonatal Presentation

• Symptoms can occur at birth and even up to several days to weeks after birth (20 days)

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• Earlier presentation>>severe disease

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• Manifestation is just sepsis

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• Suspicion for congenital TB increased if an ill-appearing infant did not improve with broad-spectrum antibiotics

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• Initially appearing well to severe respiratory distress and abdominal symptoms

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Neonatal Presentation

• Prematurity
• Respiratory distress
• Lethargy/irritability
• Fever
• Hepatosplenomegaly
• Lymphadenopathy
• Abdominal distention
• Ascites
• Persistent diarrhea

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• Jaundice
• Otitis media(presenting sign Cong TB)
• FTT
• Skin lesions
• Spine
• Septic shock
• DIC
• Hemophagocytic syndrome
• TB Meningitis

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Laboratory findings

• Laboratory abnormalities among infants with congenital TB are also nonspecific
• Leukocytosis (63.8%),
• Thrombocytopenia (80%),
• elevated inflammatory markers such as CRP (94.7%) or erythrocyte sedimentation rate (60.8%)
• Elevated liver function tests (76.4%)

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Diagnosis of congenital TB

• The infant must have proven tuberculous lesions and at least one of the following

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• Primary hepatic complex (caseating granuloma) on biopsy
• Lesions from any source (pulmonary, hepatic, skin) in the first weeks after birth
• TB infection of maternal genital tract and/or placenta
• Exclusion of postnatal transmission by thorough investigation of contacts

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Diagnosis Radiology

• CXR
• (Miliary (46.8%) , multiple pulmonary nodules (11.1%), lobar pneumonia (11.8%), bronchopneumonia (9.7%), and interstitial pneumonia (9%). Mediastinal adenopathy was also reported in 9.7% of infants
• CT chest
• adenopathy suggestive of TB or confirm miliary disease.
• Ultrasound/ CT Abdomen
• Enlargement of the liver, spleen, or both, possibly with areas of abscesses
• Necrotic retroperitoneal of intra-abdominal lymphadenopathy
• Ascites

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Diagnosis Microscopy and Immunology

Evaluation of mother

• The mother of a newborn in whom congenital tuberculosis is suspected is often asymptomatic or has subclinical disease
• In the series of congenitally infected infants reported by Hageman et al. majority of mothers (16 of 26) did not have a diagnosis until after the disease became apparent in their infants
• Cantwell et al. found that 50% of the mothers of infected infants were not ill at the time their newborns exhibited clinical signs of disease
• TST
• CXR
• Sputum for microbiology
• Pathologic examination and culture of the placenta (if available)
• Endometrial biopsy can confirm the diagnosis of genital transmission.
• Culture of amniotic fluid should aslo be performed when genital involvement is suspected.
• ✷ All mothers with tuberculosis should be tested for HIV infection and, if the mother is seropositive, the infant should be evaluated for perinatally acquired HIV infection.

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Management of infant whose mother has positive TST

• Pyridoxine should be provided to breastfeeding infants receiving INH
• Corticosteroids tuberculosis meningitis
• Endobronchial obstruction
• Pericardial/pleural disease.
• Duration
• pulmonary disease ---6 months
• Meningitis ---9 to 12 months.
• Drug resistant disease -----24 months or longer
• Monitoring
• LFTs
• Eye

• Mother should be treated as per guidelines
• Separation of the infant and mother
• Infectious mother at the time of delivery
• Nonadherent to medication
• Has drug-resistant disease, or who has not been on at least 2 weeks of treatment
• Isolations practices are recommended for airborne precautions in sick hospitalized infants with
• AFB +
• Intubated Infants
• Extensive pulmonary disease
• Laryngeal involvement
• Breastfeeding should be continued
• Except in mother with an active tuberculous breast lesion( pumped & discarded )

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References

• Neo reviews February 2023
• Avery’s diseases of Newborn
• Fanaroff & Martins perinatal medicine
• WHO guidelines

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THANK YOU

Transmission�

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• Transmitted when an infected female Anopheles mosquito takes a human blood meal and releases Plasmodium into the bloodstream of another human host.

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Plasmodium

Pathogenesis