Cerebral Malaria And Malaria ,TB And Buruli Ulcer Flashcards
What is malaria
About 20% fever in travellers from Africa presenting to UK hospitals is due to malaria.
•Plasmodium falciparium is the most prevalent parasite in Africa and responsible for most malaria deaths worldwide.
True or false
• Which region of Ghana has the highest prevalence of malaria in the country
Malaria is an acute febrile illness caused by Plasmodium parasite, which are spread to people through the bites of infected female Anopheles mosquitoes.
True
Volta
State five causative organisms of malaria and theee other causes of malaria
Causative organisms of malaria are as follows:
•Plasmodium falciparum (commonest and responsible for most of the deaths and morbidity associated with malaria in Ghana)
•Plasmodium malariae
•Plasmodium ovale
•Plasmodium vivax
•Plasmodium knowlesi
bite from an infected female Anopheles mosquito
•Congenital transfer from mother to child
•Transfusion of infected red blood cells
•Infected organ transplantation
•Sharing infected needle
How many stages are in the pathophysiology of malaria
Explain the first stage
In Which two causative organisms of malaria are the sporozoites dormant in the hepatocytes over the next few months to years? What is the name of the sporozoites at that stage ?
Two stages
Exoerythrocytic (occurs in liver)
Erythrocytic stage(occurs in RBC)
Exo:
Plasmodium ( the development stage of sporozoite in the salivary gland of a mosquito) is released into the blood stream when an infected female Anopheles mosquito feeds on human blood.
•Sporozoites head to the liver and engage in asexual reproduction called schizogony
•Over 1 to 2 weeks, sporozoites from P. falciparium, P. malariae or P. knowlesi will mature to merozoites. Infected hepatocytes will rupture and release merozoites into the blood stream.
•Exorythrocytic phase is generally asymptomatic
P ovale and P vivax infections
Hypnozoites
Explain the second stage in malaria infection
What is a schizont?
Erythrocytic phase
Merozoites will invade the RBC and undergo asexual reproduction and transformational changes which last 2 to 3 days and matures into trophozoites.
•Trophozoites will mature by digesting the haemoglobin and leaving hemazoin called schizont.
•Schizont is the replication phase where the parasite undergoes mitosis and differentiates into lot of merozoites.
RBCs rupture to release merozoites into the blood stream.
•The rupture of the RBCs recruits TNF and other inflammatory cytokines which accounts for fever in the patients and the other malaria symptoms found in the patient.
Merozoites infect further cells (erythrocytic schizogony or erythrocytic asexual reproduction)
• merozoites undergo gametogony where they give rise to gametocytes (male and female).
•Gametocyte remain in RBCs and
will be sucked up by female Anopheles mosquitoes.
The gametocyte reaches the mosquito’s gut where they undergo sexual reproduction (sporogony) to form a zygote.
•Zygote develops in to ookinete and later into oocyst the ruptures in to sporozoites into the salivary gland of the mosquitoes
Which people are won’t susceptible to malaria and why?
group of people below are not susceptible to malaria;
•Sickle cell trait (HbAS):This is because the parasite-infected HbAS red blood cells tend to sickle, a process that may result in their premature destruction of the red blood cells by the spleen.
•Thalassemia :Protection against malaria by abnormalities in red blood cell surface antigens and cytoskeletal proteins.
G6PD deficiency : It increases oxidative stress in RBCs which has negative influence on the parasite. As such, individuals who possess this mutation have some protection against malaria.
State four signs and six symptoms of
Malaria
Symptoms: Fever •Chills •Rigor •Sweating •Headache •Generalized body and joint pains •Nausea and or vomiting •Loss of appetite •Diarrhoea •Abdominal pain (especially in children) •Irritability and refusal to feed (infants)
Signs:
Warm to touch •Pallor •Jaundice •Abdominal tenderness •Splenomegaly
State four ddx of malaria and three ddx that are mostly seen in kids
Typhoid fever •Urinary tract infection •Septicaemia •Pneumonia •Meningitis
Note that the following medical conditions can also be differentials of malaria mostly in children:
- Measles
- Otitis media
- Tonsillitis
State four investigations done in malaria
What are the objectives of treatment ?
- Malaria Rapid Diagnostic Test to detect parasite antigen
- Blood film for malaria parasites to quantify the number of malaria parasites in the blood
- Microscopy – thick and thin blood film for malaria parasites
- Full Blood Count
- Widal test to rule out enteric fever
To avoid progression to severe malaria or complications of malaria
•To limit the duration of the illness
•To minimize the development of drug resistant parasites
How is malaria treated
Non pharma: In children, it is advisable to tepid sponge them to reduce body temperature in order to prevent seizures from occurring.
Artesunate + Amodiaquine or,
•Artemether + lumefantrine or
•Dihydroartemisinin + Piperaquine
For exact doses go to the slides
State four complications of malaria
Cerebral malaria •Severe anaemia •Hypoglycemia •Liver failure •Acute respiratory distress syndrome •Pulmonary edema •Acute renal failure
What is cerebral malaria
It is caused by only P falciparum true or false
State five ddx
According to World Health Organization (WHO), cerebral malaria is defined as a severe form of Plasmodium falciparum malaria that causes cerebral manifestations.
False
P falciparum is the most common cause but the other types can cause it
Pyogenic meningitis(Pyogenic meningitis, also referred as bacterial meningitis, is a life-threatening CNS infectious disease affecting the meninges, with elevated mortality and disability rates. Three bacteria (Haemophilus influenzae, Streptococcus pneumoniae, Neisseria meningitidis) account for the majority of cases )
•Hepatic coma or hepatic encephalopathy
•Hypoglycemic coma
•Uraemia-raised level in the blood of urea and other nitrogenous waste compounds that are normally eliminated by the kidneys.
•Encephalitis: Inflammation of the brain, often due to infection.
Meningitis is an infection of the meninges, the membranes that surround the brain and spinal cord. Encephalitis is inflammation of the brain itself.
What is the pathophysiology of cerebral
Malaria
RBCs infected with P. falciparum trophozoites synthesize a protein called plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1).
•PfEMP1 will be expressed on the surface of the RBCs.
•Receptors of the PfEMP1 are located on the endothelial cells of blood vessels which enables PfEMP1 to bind to blood vessels narrowing the lumen of the blood vessels. Also, A-antigen and Complement receptor one on other healthy RBCs helps the PfEMP1 to bind to them causing the RBCs to clump up within the lumen.
This partially blocks blood vessels causing brain tissues to suffer hypoxia.
•This activates macrophages which will cause the release of interleukin 1, IL 6, TNF, ROS & RNS. These cause inflammation and cell injury.
• the inflammation & the cell injury leads to the pathological manifestations of cerebral malaria.
State five signs and five symptoms of CM
While decorticate posturing is still an ominous sign of severe brain damage, decerebrate posturing is usually indicative of more severe damage at the rubrospinal tract, and hence, the red nucleus is also involved, indicating a lesion lower in the brainstem.
True or false
Symptoms:
Coma •Headache •Drowsiness •Confusion •Disorientation
•Delirium: Serious disturbance in mental abilities that results in confused thinking and reduced awareness of surroundings.
- Agitation
- Seizures
Signs:
Sustained ocular deviation, usually upward or lateral
•Abnormal posturing
1.Decerebrate or extensor rigidity: Decerebrate posturing is caused by damage to deeper brain structures, including the midbrain, pons, and diencephalon. Upper pontine damage. Decerebrate posture is an abnormal body posture that involves the arms and legs being held straight out, the toes being pointed downward, and the head and neck being arched backward.
Arms are straight and extended and hands are curled
2.Decorticate rigidity: Decorticate posture is an abnormal posturing in which a person is stiff with bent arms, clenched fists, and legs held out straight.(arms are adducted and flexed) and toes are internally rotated or they’re turned inward . Arms are flexed against the chest
3.Opisthotonos: spasm of the muscles causing backward arching of the head, neck, and spine, as in severe tetanus, some kinds of meningitis, and strychnine poisoning.
4.Neck rigidity
•Disconjugate gaze
•Nystagmus:involuntary movement You may feel like your eyes have a mind of their own. They move up and down, side to side, or in a circle. This is called nystagmus or “dancing eyes.
State five investigations in CM
Rapid diagnostic test •Blood film for malaria parasites •Full blood count •Sickling test •Random blood glucose •BUE and creatinine •Lumber puncture in the convulsing or comatose patient to exclude meningitis or encephalitis
How is CM managed
- To ensure rapid clearance of parasitaemia
- To provide urgent treatment for life threatening complications or conditions such as convulsion and hypoglycaemia
- To provide appropriate supportive care
Place patients who are unconscious or having seizures in an appropriate position to prevent aspiration
•Artesunate, IM, adults and children > 20kg 2.4 mg/kg
< 20kg 3 mg/kg or
•Artemether, IM, Adults and children 3.2 mg/kg or
•Quinine, IM, Artesunate, rectal, 10 mg/kg (preferred in children under 6 years)
•Artesunate, rectal, 10 mg/kg (preferred in children under 6 years)
Complications of CM and how it’s prevented
Renal failure •Pulmonary edema •Shocks •Spontaneous bleeding •Repeated generalized convulsions •Acidosis •Hypoglycemia
Prevention
Using mosquito repellent lotion
•Drain the water reservoir regularly
•Close the water reservoir
•Burn used goods
•Use mosquito repellent spray to spray the room
•Using the bed net that has been smeared with insecticide.
Both tuberculosis and buruli ulcer are caused by a family of microorganism called mycobacteriaceae. True or false
Why are they called acid fast
•
•Tuberculosis and buruli ulcer are caused by?
True
Members of this group have a unique property of resisting decolourisation by acids hence described as acid fast bacilli.
mycobacterium tuberculosis and mycobacterium ulceran respectively.
What is TB Which areas of the body does it involve Which centers undergo caseous necrosis? Refer to pathology card for what that type of necrosis is How is TB transmitted
Child and adolescent TB is often overlooked by health providers and can be difficult to diagnose and treat.
TB is curable and preventable
True or false
- Tuberculosis is a communicable chronic granulomatous disease caused by Mycobacterium tuberculosis.
- It usually involves the lungs but may affect any organ or tissue in the body such as the skin, brain and spine.
- Typically, the centers of tubercular granulomas undergo caseous necrosis
It is transmitted from person to person through droplets from the throat and lungs of people with active respiratory disease.
Pathogenesis of TB and pathophysiology of TB
Tuberculosis is caused by mycobacterium tuberculosis which is a rod-shaped bacterium also called Koch’s bacilli.
MTB is an aerobic bacterium, meaning needs only oxygen to survive. For this reason , during active tuberculous disease, MTB complexes are always found in the upper air sacs of the lungs. The bacterium is a facultative intracellular parasite, usually of macrophages and has slow generation time, 15-20 hours, that contribute to it virulence
Inhalation of MTB leads to one of the following:
•Immediate clearance of the organism
•Latent infection
•Primary tuberculosis(onset of active disease)
•Post primary tuberculosis(reactivation disease)
Explain latent TB(most common thing that occurs in TB when a person gets exposed)
- Latent TB occurs when a person has the TB bacteria within their body but the bacteria are small in number.
- They are kept under control by the body’s immune system and do not cause any symptoms.
- The lifetime risk for the reactivation for a person with documented latent TB infection to be 5-10% with majority developing TB disease within first 5years after initial infection
