26. Malaria Flashcards
What is malaria, and what causes it (most common, uncomplicated etc.)?
What are the routes of transmission?
Distinguish between stable and unstable transmission.
Systemic tropical parasitic infection of RBC by plasmodium spp (protozoa) transmitted by female anopheles mosquitos. P. falciparum (most common, complicated). P. vivax, P. ovale (uncomplicated, relapsing). P. malariae (uncomplicated, doesn’t relapse). P knowlesi (zoonotic malaria (macaques); certain parts of SE Asia only).
Bite, congenital (in utero), blood transfusion. Incubation 7-30d.
Stable: populations continuously exposed to malaria, high bkground immunity (mainly adults), young children suffer acute illness and high parasite densities, epidemics less likely. Sub-Saharan Africa and parts of Oceania.
Unstable: fluctuating rates, low bkground immunity, both adults and children suffer acute malaria and its complications, epidemics likely to occur due to sudden increase in mosquito vector densities. Asia and Latin America.
Why has there been a decrease in malaria death rate since 2000?
What is the main risk for acquiring malaria in tropical travellers?
Describe the life cycle of malaria.
Which Plasmodium spp. enter a dormancy stage “hypnozoites” and may cause relapses later?
Insecticides, bed nets, improved dx and tx.
Failing to take effective prophylaxis.
(pic)
P. vivax, P. ovale.
How do infected erythrocytes cause damage in malaria?
What can you see in this histology from the brain?
Differentiate between ‘benign’ and falciparum malaria.
Adhere to host endothelium (b/c one of parasites genes changes RBC -> more deformable and sticky) causing: microvascular occlusion, metabolic derangement and acidosis (due to parasite metabolism), intravascular RBC haemolysis
Cerebral malaria caused by P. falciparum - brain capillary clogged with infected parasite cells.
Falciparum infects RBC of all ages, can lead to far greater parasitaemias and sequestrates. Vivax, malariae and ovale do not, and have preference for early RBC (smaller number so infection milder). Most deaths due to falciparum.
What is the gold standard for malaria dx and how does it work?
Differentiate between thick and thin blood films.
What Plasmodium spp do these films show and why?
Light microscopy: parasites visualised on thick and thin blood smears stained with Giemsa stains. (pic)
Thick: sensitive, allows exam of a greater volume of RBCs, concentrates parasites as RBCs are lysed.
Thin: useful for spp ID and determination of level of parasitaemia, less sensitive than thick.
P. falciparum. Numerous fine ring forms, double chromatin dots, multiple parasitization of cells, schizonts rare in peripheral blood, red cells not enlarged. 2nd pic down on L = schizont.
What Plasmodium spp do these films show and why?
L = ***P. vivax***. Developing and thick (signet) ring forms, trophozoites have **amoeboid** appearance, **enlarged red cells**. R = ***P.ovale***. Oval-shaped trophozoite, **comet-like** RBC, **enlarged red cells**.
What Plasmodium spp do these films show and why?
L: P. malariae. Broad band form of Plasmodium. Red cells not enlarged. Schizonts look like daisies.
R: P. knowlesi. Ring stages resemble P. falciparum, same size and few have multiple parasites. Mature stages indistinguishable from P. malariae. Molecular methods needed to confirm dx + travel hx.
Detection of antigens or enzymatic activities associated with the malaria parasites is important. How is this done?
How might someone with malaria present?
Why is it important to ask when enquiring about foreign travel?
What else would you want to ask?
RDTs - rapid diagnostic tests (apply blood to strip):
Detection of antigen (histidine rich protein-2, HRP-2) associated with P. falciparum.
Detection of a plasmodium-assocaited lactate dehydrogenase (pLDH).
Hx: fever, headache, muscle-ache, diarrhoea, vomiting.
When: last 12m -> falciparum (longer for others)
Where: likely malaria risks
Malaria prophylaxis (drugs, duration, compliance), pregnancy status (high complication risk), immunocompetence status (HIV, cancer, transplant recipients), drug history (previous prophylaxis, allergies, potential drug-drug interactions).
In examination of malaria, what do the vital signs ABCDEFG stand for?
What are some signs of severe malaria?
How does the presentation of adults and children differ with severe malaria?
What does this image show?
Airway, Breathing, Circulation, Disability (neuro assessment), Exposure, Fluids, Glucose. Give O2, position pt, call for help, establish IV if not present +/- fluids.
Impaired consciousness/seizures. Renal impairment (if sequestration in kidneys - oliguria <0.4ml/kg/hr or creatine >265 mmol/l). Acidosis (pH <7.3). Hypoglycaemia (<2.2mmol/l). Pulmonary oedema (due to leaky capillaries)/ARDS (pic). Hb 80g/L. Spontaneous bleeding/DIC. Shock. Haemoglobinuria (without G6PD deficiency). Parasitaemia >10% (RBC infected with ≥1 parasites).
Mainly kids - severe anaemia, hypoglycaemia worse. Adults - renal failure much worse.
A child with cerebral malaria, exhibiting severe opisthotonic (extensor) posturing
Why do you avoid anti-inflammatories like ibuprofen when managing malaria?
How is malaria managed (uncomplicated P .falciparum, non-falciparum, and severe/complicated falciparum)?
What are some indications for IV therapy?
Can exacerbate renal failure.
Anti-pyretics as appropriate. Non-falciparum cases may be managed in outpatients. Notify public health team.
Uncomplicated falciparum: oral tx with either Malarone (atovaquone-proguanil), Riamet (artemether-lumefantrine; artemisinin combination therapy - ACT), or quinine and doxy/clinda (older, not used much)
Non-falciparum: Chloroquine followed by primaquine - check G6PD status.
Severe/complicated falciparum: IV Artesunate (preferred) OR IV Quinine (cardiac and BG monitoring - can cause arrhythmias and exacerbate hyperglycaemia). Once improved switch to oral therapy as for uncomplicated (above). Check blood film daily.
Parasitaemia >2% or presence of schizonts (pic). Vomiting. Pregnancy.
What is the ABCD of malaria prevention?
What are some global control measures for malaria?
Awareness of travel risk, Bite prevention (repellent, nets, clothing etc.), Chemoprophylaxis (travel clinics etc.), prompt Dx and tx.
- *1) Vector control:** insecticide treated nets, indoor residual spray, GM mosquitos
- *2) Immunisation:** vaccine development, vaccine against P. falciparum