CEREBERAL MALARIA 🦟🦟

What is Cereberal Malaria?

Cerebral malaria is one of the complications of malaria which is a severe systemic infection characterized by recurrent fevers, accompanied by rigors, enlargement of the spleen and anaemia. The disease is mostly in the tropics and sub-topics and caused by the four (4) protozoan parasite of the plasmodium family; namely: Plasmodium falciparum, Plasmodium malarae, Plasmodium vivax, Plasmodium ovale.

AETIOLOGY

It is caused by a protozoan of the genus plasmodium. The plasmodium is carried by the female anopheles mosquitoes. 

MODE OF TRANSMISSION 

Malaria is transmitted through the bite of the infected female anopheles mosquito an (intermediate host).Malaria has also been transmitted via blood transfusions and from the use of shared contaminated needles and syringe by drug abusers. 

INCIDENCE 

The disease occurs in all age groups irrespective of the blood group. It is most severe in children and pregnant women. It is most prevalent in the tropics, sub-tropics and temperate zones. Malaria is the most common cause of fever and morbidity in the tropics.

INCUBATION PERIOD

The incubation period for malaria is about one to two weeks (that is, 10-15days) depending on the type of plasmodium.

PATHOPHYSIOLOGY OF MALARIA

The life cycle of plasmodium goes through two stages: 

The Sexual stage 

The Asexual stage 

THE SEXUAL STAGE

This takes places in the intestines of the female anopheles mosquito. When the male and female mate, they produce sprozoites which are discharged and deposited into the saliva of the female anopheles mosquitoes. When it bites, it injects the saliva containing the sprozoites into blood stream.

THE ASEXUAL STAGE 

This occurs in the human body after the saliva has been injected into the blood stream. This covers the pre-erythrocyte, erythrocyte and gametocyte phases.

PRE- ERYTHROCYTE PHASE

In this phase, the sprozoites in the blood stream are carried to the liver, where they invade the hepatocytes. They form cyst-like structures which rupture upon maturity to release merozoites into the blood stream. Other sprozoites remain in the liver in the latent form as hypnotizes.

ERYTHROCYTE PHASE 

Here, the merozoites invade the red blood cells (R B Cs) or erythrocytes. Inside the erythrocytes, they feed on the haemoglobin leaving the ferrous part and develop into trophozoites. The trophozoites grow into schizonts which sexually segment into numerous merozoites again. The red blood cells then rapture releasing the merozoites which re-invade other red blood cells.Clinical signs such as headache, anaemia, muscular pains and enlargement of the spleen are seen as a result of the haemolytic effects of the parasite.

GAMETOCYTE PHASE

In this phase, the merozoites develop into sexual form of the parasites known as gametocytes. At this stage, the parson is infective. The fertilized parasite move into the stomach walls and become encysted (oocyst) and divide into small spindle shaped sporozoites or parasites. The cyst rupture and the parasite are injected into the blood when the mosquito bites.

HOW MALARIA COMPLICATES INTO CERREBRAL MALARIA/SEVERE FORM

This complicated form of malaria occurs as a result of the parasite gaining access to the brain through the blood. There are a number of theories that try to explain this transfer of the parasite to the brain. Some of the theories are hyperparasitaemia and agglutination.From the erythrocyte phase, when each schizonts ruptures, thousands of the merozoites are released, which invade the red blood cells. Parasitized red blood cells attach themselves to non-parasitized erythrocytes and this is called rostte formation or cytoadherance. The parasitized erythrocytes again attach themselves to other parasitized erythrocytes and this is known as agglutination. When these happen, it leads to haemolysis of both intravascular and extra vascular. While some of the merozoites are in the circulation, some remain the latent form in the liver which in two weeks or more becomes matured and are released into the circulation resulting to hyperparasitemia and relapse. In plasmodium falciparum malaria, these erythrocytes containing schizonts are transported to the brain where they adhere to the lining of capillaries in the brain as well as causing mechanical obstruction. The schizonts in the brain capillaries rupture, releasing toxins and stimulating further cytokine release. Clinical signs such as diminished consciousness, confusion, and convulsions often progressing to coma are seen as a result of sequestration (adherence). Obstruction and the toxins released, deprives the brain of adequate nutrients and oxygen hence, malaria of the brain/cerebral malaria.

TYPES OF MALARIA

There are four main clinical types of malaria including;

• Benign Tertian
• Malaria Quartan Malaria 
• Malignant  Tertian Malaria
• Mild Tertian Malaria

BENIGN TERTIAN MALARIA 

This is caused by plasmodium vivax. This type gives rise to chronic relapsing malaria. It is common in people suffering from malnutrition. Relapse occurs within 42-48hours. Its incubation period ranges from 12-17 days.It is characterized by recurrent bouts of fever every three days. This pyrexia is accompanied by severe rigors, and the patient’s teeth charter, profuse sweating, headache, vomiting and malaise. Hepatomegaly may also be present on physical examination

QUARTAN MALARIA

This is caused by plasmodium malariae. The incubation period is about 30-40 days and relapse occurs in 72 hours. It most commonly occurs in children, but pre-dominantly seen in male adult.It is characterized by fever occurring every four days. Rigors are more common and severe and splenomegaly is frequent and may be pronounced.The liver is less affected and the anaemia is pronounced. Jaundice is less severe and splenomegaly is frequent and may be pronounced. The liver is less affected and the anaemia pronounced. Jaundice is less pronounced.

MALIGNANT TERTIAN MALARIA

This is the most dangerous of all the types of malaria. It is caused by plasmodium falciparum. Incubation period is 9-14days, with an average of 12 days. The relapse period is 48 hours.This plasmodium falciparum causes cerebral malaria in children. Children can deteriorate rapidly over1-2 days, going into coma. The clinical features include herpes labialis and herpes simplex. Rigor is less marked or absent, however, if present the hot and sweating stages are prolonged. The primary signs include chills. This is followed by vomiting, intestinal irritation and diarrhoea. There is pyrexia, headache, anorexia, supra-orbital neuralgia, and delirium, irritability (convulsion, coma, stupor, and confusion). Altered consciousness and focal neurological deficit or psychosis and generalized weakness. This denotes cerebral malaria. There is also marked haemolytic anaemia and patient complains of pain in the joints and bones.

MILD TERTIAN MALARIA

This type of malaria is caused by plasmodium ovale. It resembles the benign tertian, but it has a relapse period of 50 hour its incubation period is 14 days.The clinical features of this type of malaria and its attacks are slider, short and mild. Relapses are less common. Rigors are often present in the evenings. Rheumatoid pains especially in the lumbar region are characteristic signs.

GENERAL CLINICAL FEATURES OF CEREBRAL MALARIA

1. Rigors which is the body’s homeostatic mechanism to retain heat.
2. Fever and headache which is brought by the infection.
3. Altered sensorium because of the spread of the infection to the cerebrum of the brain.
4. Vomiting as a result of disturbance of the chemoreceptor trigger zone.
5. Neurological signs, altered consciousness made up of the following,Confusion, delirium, stupor, coma, convulsion (50% generalized), focal neurological deficit and psychosis, brain stem signs, irritability.
6. Severe hemolytic anemia which comes about when the bacterial feed on the red blood cells.Jaundice as a result of the end product of the destructed red blood cells by the bacterial.
7. Hypoglycemia due to reduced blood which is unable to transport the required glucose to the body cells 
8. Black water fever-due to the widespread intravascular haemolysis, affecting both parasitized and unparasitized erythrocytes giving rise to dark urine.

DIAGNOSTIC INVESTIGATIONS

• Blood film for malaria parasite which should be negative. 
• Full blood count which should be within the normal range  
• Blood for haemoglobin level estimation which should be within the normal range Blood for sickle test which suppose to be negative.  
• Cerebrospinal fluid examination (Lumbar puncture) to exclude bacterial meningitis (children with unrousable coma for no obvious cause)

SPECIFIC MEDICAL TREATMENT (ANTI-MALARIA DRUGS)

The most common anti-malarial used include; 

1. artesunate-amodiaquin 
2. arthemeter-lumefantrine
3. quinine
4. fansider (sulphadoxine-pyrimethamine)
5. artesonate
6. arthemeter etc.

SUPPORTIVE MANAGEMENT 

1. Intravenous fluids and electrolytes such as dextrose
2. Transfusion of whole blood or plasma or parked cells in case of anaemia

 ANALGESICS/ ANTI-PYRETICS

Analgesics and antipyretics for relieving pain and reducing temperature include paracetamol, brufen, aspirin and diclofenac.

Prevention of Cereberal Malaria 

1. Primary Prevention Level 

• Ensure good environmental sanitation example weeding of the surroundings, draining all stagnant waters, choked gutters, and proper means of disposal of refuse.
• Regular spraying of breeding places of mosquitoes.
• Use of mosquito repellents or coils.
• Sleep under treated mosquito nets.
• Use mosquito proof doors, and windows (trap doors)
• Encourage chemoprophylaxis.

Secondary prevention Level

• Early detection of malaria by screening for those with malaria and tracing their contacts keeping & surveillance.
• Treat those who have malaria

Tertiary Prevention Level 

1. Rehabilitation example getting adult back to works. Children being taught by hospital school teachers. Currently, there is also roll back malaria as a primary prevention of malaria. Here when a country is treated, its neighbouring countries are also treated to prevent spread between boundaries or different geographical locations.

COMPLICATIONS 

1. Hemiparesis or paralysis of limbs
2. Speech disorders such as poverty of speech
3. Cortical blindness
4. Mental retardation and mental confusion
5. Diffused cerebral dysfunction with unrousable coma, altered senszorium.
6. Spastic limbs
7. Hypothermia, acidosis and respiratory distress.
8. Gastro intestinal tract infection
9. Abortion, premature delivery, still birth and low birth weight infants
10. Hemolytic anemia
11. Septicemia secondary to shock 
12. Oliguria and 
13. Uremia jaundice and black water fever
14. Pulmonary 
15. Edema
16. Renal failure