Plasmodium - Morphology | Medical Science Optional Notes for UPSC PDF Download

Introduction

Nearly all cases of malaria in humans are attributed to six species within the Plasmodium genus. These include P. falciparum, P. vivax, two morphologically identical sympatric species of P. ovale (curtisi and wallikeri), P. malariae, and, in Southeast Asia, the simian malaria parasite P. knowlesi.

Man-Intermediate host
Female anopheles mosquito-Definitive host
Infective stage to man-Sporozoite
Infective stage to mosquito-Gametocytes
Relapse-Hypnozoites
Clinical manifestations-merozoites

Plasmodium - Vertical Transmission

• Merozoites are responsible for the vertical transmission of malaria.
• Variances in the life cycle include:
  (a) Absence of a liver stage (exoerythrocytic stage)
  (b) Non-production of hypnozoites
  (c) Lack of relapse
  (d) No requirement for Primaquine

Plasmodium - Pathogenicity

Why Falciparum is dangerous?

It invades all stages of red blood cells (RBCs) at notably high parasite densities. P. vivax and P. ovale exhibit a distinct preference for young RBCs, while P. malariae tends to infect older cells. These species result in a parasitemia level that rarely surpasses 2%.

The pathogenesis of falciparum is intricately linked to the central mechanisms of cytoadherence, resetting, and agglutination.

Plasmodium - Complications

The majority of severe or complicated malaria cases are caused by P. falciparum; however, there is a growing number of recent reports indicating severe disease attributed to P. vivax.

Falciparum Malaria complications:
CHAPLIN
C - Cerebral malaria
H - Hypoglycemia
A - Anemia
P - Pulmonary edema
L - Lactic acidosis
I - Infections
N - Necrosis of renal tubules

Cerebral Malaria

High-grade fever with stupor - Differential Diagnosis:

1. Encephalitis (HSV)
2. Bacterial meningitis
3. Brain abscess
4. Pontine hemorrhage
5. Cerebral malaria
6. Heat exhaustion/heat stroke
7. Malignant neuroleptic syndrome
8. Malignant hyperthermia
9. Prion diseases

It presents as a diffuse symmetric encephalopathy, with uncommon occurrence of focal neurologic signs.
The onset can be either gradual or sudden, often following a convulsion.
Convulsions typically manifest as generalized tonic-clonic and may be recurrent.
Symptoms of meningeal irritation are generally not observed.
Muscle tone may exhibit either an increase or decrease.

Neurological impairments such as hemiplegia, cerebral palsy, cortical blindness, deafness, and cognitive and language deficits are predominantly reported in children.

Severe Malaria - Management

Management
Managing severe malaria requires supportive measures, ideally administered in a critical care unit. This entails addressing elevated body temperatures and potential seizures. Additionally, monitoring for inadequate respiratory effort, low blood sugar, and diminished blood potassium levels is crucial.

Antimalarials
Severe Falciparum Malaria:

• Administration of Artesunate (2.4 mg/kg as a one-time intravenous dose, followed by 2.4 mg/kg at 12 and 24 hours, and subsequently daily if needed). If unavailable,
• Utilization of Artemether (3.2 mg/kg as a one-time intramuscular dose, followed by 1.6 mg/kg once daily). If unavailable,
• Alternative use of Quinine dihydrochloride (20 mg of salt/kg infused over 4 hours, followed by 10 mg of salt/kg infused over 2-8 hours every 8 hours). If unavailable,
• Consideration of Quinidine (10 mg of base/kg infused over 1-2 hours, followed by 1.2 mg of base/kg per hour with electrocardiographic monitoring).

Hyperpyrexia - Employ tepid sponging, fanning, and paracetamol to facilitate defervescence. Avoid the use of aspirin and other NSAIDs due to the potential risk of gastrointestinal bleeding.

Cerebral malaria:

• Position the patient laterally, rotate every 2 hours, implement continuous nasogastric aspiration, maintain an open airway, and irrigate and patch the eyes.
• In the event of convulsions: Rule out hypoglycemia and hyperthermia; manage seizures with a slow intravenous push of diazepam, midazolam, or lorazepam; if seizures persist, administer a phenytoin loading dose of 15-20 mg/kg.
• Consider a CT scan for intracerebral bleed, cerebral edema, or herniation if there is a decline in consciousness or the appearance of new neurological abnormalities.
• For elevated intracranial pressure, position the patient with the head propped up and in a midline position; control seizures; address hypoglycemia; consider hyperventilation; the use of mannitol is debatable, and corticosteroids do not play a role.

Anemia - Administer packed cell transfusion if hemoglobin is <5 g/dl or in the presence of impaired consciousness, hyperparasitemia, respiratory distress, or metabolic acidosis. If fluid overload is present, use diuretics and transfuse slowly; perform exchange transfusion in patients with overt congestive cardiac failure.

Hypoglycemia - Administer 1 ml/kg of 50% glucose slowly intravenously, followed by infusion of 10% dextrose; closely monitor blood sugar levels; consider octreotide and glucagon if intravenous fluids are restricted.

Metabolic acidosis - Correct hypovolemia, hypoglycemia, and anemia; provide oxygen; slowly administer sodium bicarbonate if pH is <7.

Disseminated Intravascular Coagulation (DIC) - Administer Vitamin K, fresh frozen plasma, and/or cryoprecipitate; consider exchange transfusion in the presence of fluid overload.

Renal failure - Perform a careful fluid challenge with 20 ml/kg of normal saline, followed by furosemide 1 mg/kg (max 5 mg/kg) if no response is noted; restrict fluid intake; consider dialysis if refractory hyperkalemia or metabolic acidosis, fluid overload, and a rapid rise in serum creatinine are present.

Hemolysis - Consider artemisinin derivatives as antimalarial drugs; transfuse packed cells to maintain hematocrit; monitor urine output and renal function for the need for dialytic support.

Acute respiratory distress syndrome - Caused by pulmonary capillary leak and, less commonly, fluid overload; administer oxygen; position the patient in a propped-up position; restrict fluid intake; use loop diuretics if necessary; severe cases may require mechanical ventilation with high peak end-expiratory pressure.

Shock - Obtain blood cultures and administer broad-spectrum antibiotics (e.g., cefotaxime and amikacin); monitor central venous pressure; replace fluids; administer vasopressors and respiratory support as required.

Hyperparasitemia - Consider exchange transfusion.

Plasmodium - Lab diagnosis

If a patient from a malaria-endemic region or exhibiting fever is encountered, prompt preparation and examination of thick and thin blood smears are crucial to confirm the diagnosis and determine the infecting parasite species. Typically, if an experienced microscopist finds the blood smear negative, it suggests the absence of malaria. In cases where reliable microscopy is unavailable, conducting a rapid test is recommended.

Demonstration of the parasite-Peripheral Blood Smear

The primary and crucial approach for diagnosing malaria involves detecting the presence of the parasite in the blood.

Note:

• Prior to considering a thick smear as negative, a thorough examination of 100-200 fields should be conducted under oil immersion.
• In infections with P. vivax, P. ovale, and P. malariae, all asexual erythrocytic stages as well as gametocytes are observable in peripheral blood. However, in P. falciparum infection, only the ring form and gametocytes are visible.
• Parasite concentration is highest in peripheral blood a few hours after the fever peaks. Consequently, blood smears should ideally be collected during this period.

Quantitative Estimation

Newer approaches to diagnosis of Malaria-Rapid Diagnostic tests (RDT)

Plasmodium - Repeats

• Explore the laboratory diagnosis of malaria, with a particular focus on new diagnostic approaches (2009).
• How is malaria diagnosis confirmed? Detail the presumptive and radical treatment for severe malaria (2009).
• Identify malaria parasites and outline complications associated with malaria. Describe the methods for confirming and treating malaria (2012).
• An 18-year-old boy in a stuporous state is brought to the casualty with a 3-day history of high-grade fever. List potential causes and elaborate on the management of cerebral malaria (2013).
• Discuss the challenges in the epidemiology of malaria and the measures for its control. Delve into the laboratory diagnosis of malaria (2017).
• Provide details on the laboratory diagnosis and complications associated with Plasmodium falciparum infection (2018).