Things I’m learning at med school: Malaria
Protozoan disease of the genus Plasmodium.
Transmitted only by female Anopheles mosquitos.
4 main species: P. falciparum, P. vivax. P. ovale and P. malariae (P. knowlesi may also infect humans but rarely does so, more commonly affecting monkeys).
When inside RBCs the parasite consumes intracellular proteins (particularly haemoglobin). As haem is potentially toxic, plasmodium detoxifies it to a biologically inert form (haemozoin), which can be seen as a coloured pigment.
Plasmodium alters the RBC membrane, making it irregular in shape, more antigenic and less deformable.
Mosquito inoculates plasmodial sporozoites from its salivary glands during a blood meal and motile forms of the parasite are carried rapidly in the bloodstream to the liver where they invade hepatic cells and begin a period of asexual reproduction. An amplification process produces 10,000 – 30,000 daughter merozoites.
Infected liver cells swell and burst, discharging motile merozoites into the bloodstream. RBCs are then invaded and the merozoite takes a ring form known as a trophozoite. The trophozoite multiplies, consumes haemoglobin and fills the RBC; the RBC is now known as a schizont (shown in the image above). When the RBCs rupture, daughter merozoites are released, capable of invading more RBCs and repeating the cycle.
Some parasites may develop into longer-lived gametocytes that can transmit malaria. These may be ingested by another mosquito, which forms a zygote in the insect. It matures and migrates to the salivary glands where it can be transmitted to another human host.
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In P. vivax and P. ovale, a proportion of the intrahepatic forms remain dormant from 3 weeks – 1 year (or more) before reproduction begins (hypnozoites). These are the cause of relapses that characterise infection with these two species.
In P. falciparum, protuberances appear on the surface of RBCs; a specific type of adhesion protein that mediates attachment to receptors on venular and capillary endothelium (cytoadherence). This can lead to blockage and sequestration of RBCs in vital organs. May also adhere to other infected RBCs (agglutination) or non-infected RBCs (rosetting = decreased deformability). Sequestration allows parasites to develop out of reach of splenic processing and filtration, therefore only younger ring forms of asexual parasites are seen circulating in peripheral blood in P. falciparum, so peripheral parasitsaemia is an underestimated value.
Splenic filtration is accelerated (becomes enlarged in later stages).
When schizont ruptures interleukin-1 is released, which causes a fever.
Temperatures exceeding 40◦C damage mature parasites, which synchronise the malarial cycle and if left untreated will present as a tertian fever (except in P. malariae which is quartan).
First symptoms: Fever, malaise, headache, fatigue, abdominal discomfort, muscle aches, nausea, vomiting, orthostatic hypertension. May have: mild anaemia, palpable spleen, slightly enlarged liver, mild jaundice.
Severe P. falciparum: Cerebral malaria due to sequestration and agglutination. May cause coma. ~20% adult mortality.
Acidosis due to accumulation of organic acids (e.g. lactic acid released from RBCs).
Hypoglycaemia as the liver is not maintaining adequate glucose levels due to failure of hepatic gluconeogenesis. There is also increased glucose consumption by host and parasite.
Other symptoms include anaemia, renal failure, pulmonary oedema, hypotension/shock, haemorrhaging, haemoglobinuria and jaundice.
Relies on asexual parasite forms in peripheral blood smears (thick and thin; x1000 oil immersion).
Parasitsaemia expressed as number of parasitised erythocytes per 1000 RBCs.
Antibody stick or card tests can also be used using finger prick blood samples.
Quinidine – Trophozoite stage. Kills gametocytes of P. v, P. o and P. m.
Chloroquine – As above but earlier in the asexual cycle.
Others include amodiaquine, mefloquine, tetra/doxycycline, halofantrine.
Prophylaxis – malarone, chloroquine, doxycycline (these will reduce the incidence of P. f infection but cannot treat it once infected).
Biological Illustration by Sarah Faris, assistant professor in the Communication Arts program. Interested in work like this? Check out the VCU Scientific Illustrators Society.
ANATOMY OF OUR GENES: The Human Body
The human body is made of some 50 trillion to 100 trillion cells, which form the basic units of life and combine to form more complex tissues and organs. Inside each cell, genes make up a “blueprint” for protein production that determines how the cell will function. Genes also determine physical characteristics or traits. The complete set of some 20,000 to 25,000 genes is called the genome. Only a tiny fraction of the total genome sets the human body apart from those of other animals.
Most cells have a similar basic structure. An outer layer, called the cell membrane, contains fluid called cytoplasm. Within the cytoplasm are many different specialized “little organs” called organelles. The most important of these is the nucleus, which controls the cell and houses the genetic material in structures called chromosomes. Another type of organelle is mitochondrion. These “cellular power plants” have their own genome and do not recombine during reproduction.
Chromosomes carry hereditary, genetic information in long strings of DNA called genes. Humans have 22 numbered pairs of chromosomes and a single pair of sex chromosomes—XX in females and XY in males. Each chromosomal pair includes one inherited from the father and one from the mother. If unwound, the microscopic DNA strands in one cell’s nucleus would stretch to over six feet (two meters) in length.
DNA (deoxyribonucleic acid) is the set of genetic instructions for creating an organism. DNA molecules are shaped like a spiral staircase called a double helix. Each stair is composed of the DNA bases A, C, T, and G. Some segments of these bases contain sequences, like A-T-C-C-G-A-A-C-T-A-G, which constitute individual genes. Genes determine which proteins individual cells will manufacture, and thus what function particular cells will perform.
read more, photos and info from Nat Geo
Biro and ink heart
An Unexpected Choir with a Powerful Message
The audience at the São Paolo’s Museum of Art was waiting to listen to the famous São Paulo University choir. Instead, a choir of 12 laryngectomy patients went on stage and performed All You Need is Love by the Beatles using esophageal voice, prosthesis and electronic larynx. Most of the singers lost their voice due to larynx cancer, as a result of smoking. At the end of the performance, they displayed the sign: LISTEN TO THIS CHOIR’S VOICE: DON’T SMOKE
The development of the human brain
First the embryonic spinal chord is formed along common sequences and patterns then the nervous system develops from a simple elongated neural tubes. The cranial region then differentiates into several clusters of cells which produce the forebrain, midbrain and hindbrain portions.
Do you know about Chiari malformation?
Unless you know someone personally affected by this condition, or conduct research in this area, your answer is likely ‘no.’ But the rate of occurrence of Chiari malformation (CM) is not entirely rare!
We would like to help raise awareness of this neurological condition that is thought to affect 1 in 1000 people, the predominance of whom are females.
In this condition, brain tissue descends into the spinal canal at the base of the skull and can cause any number of symptoms that are often attributed to other sources or simply not properly traced back to the underlying cause. Some people with CM are entirely asymptomatic while others experience a range of severity of symptoms such as headaches, unsteady gait, neck pain, dizziness, vision problems, numbness and tingling of hands and feet or difficulty swallowing, among others.
There are three types of CM that are classified based on the severity of the case and the parts of the brain that protrude from the skull. Causes of CM range from congenital deformations of the skull that form in utero to excessive drainage of lumbar or thoracic spinal fluid that can occur from injury or infection later in life.
So what can be done about CM? In some cases, pain management is all that is required if headaches or pain are the primary symptoms. Other patients with more severe cases must undergo surgery to reduce pressure on the cerebellum and spinal cord and restore the normal flow of spinal fluid.
Here are a few links where you can learn more about CM:
NIH (US) Fact Sheet: http://goo.gl/lck0Ia
NHS (UK): http://goo.gl/ZkI9QQ
Conquer Chiari (C&S Patient Education Foundation): http://goo.gl/tpw9vF
This post is inspired by a member of this NRT community who is recovering from recent CM surgery.
Pictured: MRI of human patient with Tyoe 1 Arnold-Chiari Malformation. The cerebellum has descended 7mm into the foramen magnum.
Main image source: Wikimedia Commons. Inset image source: Conquer Chiari
20 inspirations of skull nails - click for more http://www.skullspiration.com/skull-nail-designs/