Agent Article: Onchocerca Volvulus

The causative agent of Onchocerciasis, also known as “River blindness”, is a by a parasitic worm Onchocerca volvulus. It is a filarial nematode worm that is transmitted to humans by blackflies of the genus Simulium.  They are tissue-dwelling nematode parasites that live as adults in the circulatory system or connective tissues of vertebrate hosts. Female worms produce live microfilariae (pre-larvae) instead of laying eggs. They have indirect life-indirect life cycles which consist of  the transmission of larvae by arthropod intermediate hosts (blood or tissue feeding insect vectors). A key reason of why the worm is so virulent to humans is its ability to circumvent the innate immune response. The microfilariae that the filariae produce are capable of arresting complement action in the innate immune response. The microfilariae that the filariae produce are slow down complement action in the innate immune response. This inhibits the innate immune response and also disrupts the adaptive immune response allowing the parasite to continue to thrive.

The microfilariae develop in the fly over a period of two weeks and then migrate to its mouthparts. The infectious larvae are then transmitted to a new human host during the next blood meal.The incubation varies from host to host and by the amount of bites from infected vectors. The generally accepted incubation period ranges from 3 months-2 years. This is considered the time from initial infection to the time that the mature filariae produce larvae. The larvae then form nodules and begin maturing into adult world. This process can take up to a year. Nodules may contain various male and female worms where they live coiled up mating together.. Normally nodules only contain 3-5 adult worms, but in extreme cases there has been up to 50 adult worms found inside a single nodule.  Females measure 33 to 50 cm in length and 270 to 400 μm in diameter, while males measure 19 to 42 mm by 130 to 210 μm.  Once inside the nodules of the skin the adult , the female worms produce progeny microfilariae in numbers of up to 1000 per day for a lifespan of 15 years. The microfilariae, measuring 220 to 360 µm by 5 to 9 µm and unsheathed, have a life span that may reach 2 years. The microfilariae migrate throughout the body. The death of the microfilariae in sensitive organs leads to the major symptoms of Onchocerciasis. Major symptoms generally appear nine months to two years after initial infection. The worms are normally found in the skin and in the lymphatics of connective tissues but also sometimes found in peripheral blood, urine, and sputum.

Onchocerciasis manifests into three different forms; subcutaneous nodule formation; dermatitis; and blindness. These nodules tend to form in subcutaneous tissues over bony areas as a form of protection from the immune system. These areas include areas such as the hips, pelvis, ribs, shoulder blades, and skull. If ruptured it is possible that these nodules will trigger a very painful immune response.

Blindness is the most well-known system of Onchocerciasis .  As the microfilariae try to make it towards the skin in order to continue the life cycle, some of the organisms make it into the cornea of the eye. The microfilariae cannot survive in the eye and end up dying. The corpses of the microfilariae trigger an inflammatory response that leaves scar tissue in the eye. This makes blindness very gradual but also inevitable without proper treatment. Since blindness take a while to develop, to see anyone under the age of 30 to exhibit serious ocular deficiency. This scar tissue causes multiple issues within the eye including punctate (snowflake) keratitis, sclerosing keratitis, and iridocyclitis.




Schistosomiasis Agent Article Summary


Schistosomiasis is a parasitic infection that afflicts hundreds of millions, and kills hundreds of thousands every year. Despite a strong immune response, the parasitic worms live and reproduce in the body for years. There are two diagnosis for schistosomiasis depending on the severity of the immune response: acute or chronic schistosomiasis. Acute schistosomiasis is characterised by a debilitating fever that can occur before the peak of the infection at 6-8 weeks caused by an intense immune response. This acute response is uncommon in natives to endemic areas as a result of in-utero sensitization to the disease. Testing in mice has revealed that without this harmfull over-reaction by the immune system, patients would be more likely to die.

On the other hand, chronic schistosomiasis leads to fibrosis. Those affected by this variation of the disease are more likely to have a genetic predisposition to it, built up over generations of life in infected regions. Even if genetics play a role, the intensity of infection still varies from person to person regardless of which variety of the disease is present. Studies of mice have shown that the intensity of infection, which corresponds to survival rates, is also genetic, but tied to a different gene. The relevant gene, surprisingly, doesn’t relate to the Schistosome itself, but to dampening the inflammatory response. It isn’t tied to lymphocytes though. Right now, no one knows the impact of B-Cells on the disease.

Interestingly, Schistosomes don’t have the capacity to grow in labs. They can only live in live humans, which hints that they take subtle biological cues from their hosts to stay alive. By infecting immunodeficient mice with schistosomiasis, the disease died off quickly without input from the T Cells and MHC molecules of the mice. This relationship has been hard to explore, given as to how the difficulty of growing these flukes has led to few insights into how they interface with us on a molecular level. We have found one lead: a receptor on Schistosomes that can bind to our cytokines, hinting at further connection between their survival and our immune responses.

Since schistosomiasis is endemic to areas commonly afflicted with other tropical diseases, we need research to find out what the correlation between schistosomiasis’s effect on our immune system and susceptibility to other diseases is. From testing mice, it seems like infection with schistosomiasis makes the acquisition of malaria, hepatitis, and toxoplasmosis more likely. Dealing with schistosomiasis and AIDS at the same time would kill you, even if the signals mentioned above wouldn’t work for the schistosomiasis. It does seem that having an ongoing immune reaction to schistosomiasis is similar to having allergies, and that helminth infections and allergies are inversely proportional.

Since schistosomiasis affects primarily children, researchers have looked into the high infection and reinfection rate in children contrasted to adults and found that IgE works as a good protector against Schistosomes. Researching this further on mice has proved difficult due to our differing biologies. Currently the body only triggers an immune response when the Schistosomes lay an egg. Because we can’t attack their adult forms, it takes even longer to start a fight against these invaders. We can’t even use Toll-like Receptors on them because they can’t toll the sugars on the eggs, even if our T Cells can.

Right now, we have developed a working vaccine for schistosomiasis in mice, with plans to scale it up in the future, even if making a vaccine for such an ancient and resilient pathogen is a challenge. While the working rodent vaccine is meant for killing cercariae(a larval stage of Schistosomes), another in development has shown promise if we’re capable of mass production. This vaccine is different from almost all others: it seeks to prevent the symptoms of the disease rather than the infection itself. This vaccine would disrupt the immune response to the schistosomiasis, keeping your body from fighting itself, and keeping the disease from spreading with the right host input.

In summary, Schistosomes are a complicated species that we don’t know enough about. We don’t understand how they evade the immune system, we don’t understand how the body can react to them without dying most of the time, and we don’t understand how interconnected we get as pair of species. If we want to eliminate schistosomiasis, then we need to continue our research, and figure these worms out.


Article: The Immunobiology of Schistosomiasis, by Edward J. Pearce and Andrew S. MacDonald


Agent Article: The Life Cycle of Trypanosoma Cruzi

Two major Neglected Tropical Diseases are Leishmaniasis and Chagas disease. They are parasites belonging to the Trypanosomatidae family and as such they have very similar tactics when it comes to avoiding the body’s immune response. Immune response comes about as a result of the host’s recognition of disease specific antigens. These two Neglected Tropical Diseases possess a complex series of ways to avoid detection and cause the persistence of disease. Chagas disease is among a group of parasites able to avoid immune detection by hiding within the body’s own cells. This is called an intracellular infection. Furthermore, Chagas is capable of infecting different hosts and progresses through several stages of its life cycle in various vertebrate and invertebrate hosts.

The two relevant life cycles are the trypomastigote stage and the amastigote stage. Chagas disease is present in the Trypomastigote stage within its primary vector, the kissing bug. This stage possesses a single flagellum and is non-dividing. Within human hosts, Trypanosoma Cruzi takes the amastigote form which is an intracellular, actively dividing stage with no obvious flagellum, as well as the trypomastigote form in the blood.

Molecular Basis for Infection

Metacyclogenesis, the process by which these parasites differentiate between their dividing and non-dividing stages, is vital for their success as parasites. Once inside a host’s gut, T. Cruzi parasites transform from an epimastigote stage into metacyclic trypomastigotes in order to reproduce. Early in host infection, neutrophils are recruited by the immune system to rush to the area of the bite. Neutrophils are phagocytic cells: one of the body’s most common white blood cells. Neutrophils attempt to attack the parasite through the release of reactive oxygen species which serve to dissolve foreign things, through the release of an enzyme called Neutrophil Elastase (NE) which destroys pathogens and host tissues alike, and the use of Neutrophil Extracellular Traps (NETs).

The Continuing Challenges of Leprosy: A Summary

Leprosy, better explained as a combination of two diseases over time that have become conjoined, is curable, but not preventable. The first disease of the combination is a chronic mycobacterial infection, eliciting a surprising amount of immune responses in human beings. The second is a peripheral neuropathy that begins after the first infection sets in, and accompanies the immunological events that transpire. Leprosy, unfortunately, remains at the forefront of global health and has done so for decades. The agent itself, Mycobacterium Leprae, is elusive; uncultivable, the agent presents challenges in the fields of microbiology, pathology, immunology, and genetics. The article I’m writing about focuses in on the current understanding of M. Leprae, and the host cell responses to the pathogen, especially related to “molecular identification of M. leprae, knowledge of its genome, transcriptome, and proteome, its mechanisms of microbial resistance, and recognition of strains by variable-number tandem repeat analysis.”

Leprosy is not going to be eradicated within the clear future, there is no path towards prevention. The exact method of transmission of Leprosy is still a vast unknown. As of now, there has been no highly effective vaccine, nor have there been any practical tools for early diagnosis developed. With that said, however, the full genome (the complete set of genes or genetic material present in a cell or organism) has been sequenced, and in labs across the world, this knowledge is beginning to open up pathways. In the field of molecular microbiology, the reason behind M. Leprae seemingly fastidious nature has begun to be unearthed.

  1. Leprae itself is a nonmotile (incapable of being moved), non-spore-forming, microaerophilic (requiring oxygen because they cannot ferment or respire anaerobically, but too much oxygen will poison them), acid-fast-staining bacterium that usually forms slightly curved or straight rods (seen below, the slim red fiber-looking rods).Screen Shot 2017-04-26 at 10.02.37 AM
  2. M. leprae has never been grown on artificial media due to its elusive nature, but can be maintained in axenic cultures in what appears to be a stable metabolic state for a few weeks. As a result, propagation of M. leprae has been restricted to animal models, including the armadillo and normal, athymic, and gene knockout mice (genetically modified mice to better exhibit, in this case, the effects and results of M. Leprae). The growth of the specific agent M. Leprae has been known to vary greatly depending on certain conditions (temperature, medium in which the bacterium was preserved), and so in this study, the metabolism of the bacterium was studied at great length in order to determine whether or not there could be steps taken to provide the world with a prevention method. While the study proved to be relatively inconclusive, the previously thought-to-be-true hypothesis that M. Leprae held remarkable similarities to M. Tuberculosis was disproved. There are many very important differences between the two Mycobacteria, as “M. leprae has many fewer enzymes involved in degradative pathways for carbon and nitrogenous compounds than M. tuberculosis. This is reflected in the [scarcity] of oxidoreductases (the enzyme that catalyzes the transfer of electrons from one molecule, the reductant, also called the electron donor, to another, the oxidant, also called the electron acceptor) [among other enzymes]. In addition, other major problems associated with metabolism for M. leprae are that the bacilli have lost anaerobic and microaerophilic electron transfer systems and that the aerobic respiratory chain is severely curtailed, making it impossible for M. leprae to generate ATP from the oxidation of NADH.”

Reductive evolution, the process by which a genome shrinks in length or size as compared to an ancestral genome, is the exact process M. Leprae went through. M. Leprae “…possesses 1,133 inactivated genes (genes lost through mutation, or pseudogenes), compared to six pseudogenes in M. tuberculosis. In addition, a large number of genes apparently have been entirely deleted from the genome. The result of this massive gene loss leaves M. leprae with less than 50% of its genome encoding functional genes, compared to M. tuberculosis, in which 90% of the genome encodes functional genes, and 34% of M. leprae‘s proteins identified in silico appear to be the products of gene duplication events or share common domains. Downsizing of the genome has resulted in the elimination of several metabolic pathways, leaving a pathogen with very specific growth requirements, as discussed above (Metabolism). The largest functional groups of genes in M. leprae are those involved in gene regulation, metabolism and modification of fatty acids and polyketides, cell envelope synthesis, and transport of metabolites.”

In summation, Leprosy as a disease poses major challenges to the world’s understanding in microbiology, immunology, pathology, treatment, and prevention. “The genome of M. leprae has been sequenced, and this organism has been shown to be able to synthesize far fewer proteins than the other major human-pathogenic mycobacteria, M. tuberculosis. Thus, although M. leprae still cannot be cultivated axenically, the new molecular ability to assess its ability to transcribe and synthesize various proteins in response to different environments and stresses will likely provide valuable information about its mechanisms of pathogenicity in the near future.” In addition, “Genetic influences on immunity to M. leprae in humans appear to operate at two levels: some mechanisms act at the level of overall susceptibility, and others function at the level of acquired immunity. One leprosy susceptibility gene has been identified, and several genes possibly influencing adaptive immunity have also been described.”

At this point in time, with failed efforts to reach global immunity by the years 2000 and 2005, the main goal of the Leprosy community is focusing in on early detection. Because early detection would be treating those who are asymptomatic, the challenges presented by this are great; “in many areas with endemic leprosy, even patients with overt disease are finding that resources for diagnosis and treatment are being systematically reduced.” Another possible answer for the cure of leprosy has to do with all patients living with leprosy who contract the infection, but rendering it harmless.


Sources cited: (all quotations and diagrams are taken from this link)

Agent Article: Trachoma

Bacterial diseases had a great impact on the health of the human population in the world since the dawn of time. Especially in times of great war, it is able to spread through unsanitary and unclean conditions to other hosts, infecting them. Trachomaurl.jpg, a bacterial disease that blinds its hosts, is no different. With time and study within this disease, it is possible to spread the therapy used to prevent and stop the spread of this disease.


This article describes the etymology of the bacteria, the impact it had on the world, its classification, and the therapies available to treat the disease. Mohammadpour, Abrishami, Masoumi, and Hashemi, all from Tehran, Iran, recognized the significance and impact the disease can have, if allowed to have hosts. They were able to use the World Health Organization reports to understand the disease more and explain in depth ways to treat Trachoma.

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Article Summery

Leishmaniasis is caused by 17 unique and different species of protozoan parasites. These parasites are able to be transmitted between

mammals (and namely humans)  from a phlebotomine sandflies when they bite. It effects a fairly large number of people with an estimated 12 million humans infected. There are about .5 million cases of the visceral form and 1.5-2 million of the cutaneous form. It is predominately located in Central and south America, southern Europe, North and East Africa, the Middle East, and the Indian subcontinent.

The treatment situation thus far has been promising and the chemotherapy of Leishmaniasis is aided by new drugs and new formulations of older drugs. The immune systems of the patients themselves are vital in judging the probable efficacy of drug treatments. When people have human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS), it is much less likely that commonly used drugs will be effective in treating their form of Leishmaniasis. Oftentimes, people who have HIV/AIDS lack an adequate T-cell mediated immune response which greatly limits their ability to fight infections such as Leishmaniasis. There are some Leishmaniasis drugs that are T cell dependent, such as pentamidine, but some are t cell independent, such as amphotericin B and miltefosine. In addition to people who express both HIV/AIDS, Idiopathic CD4+ lymphocytopenia patients are also more susceptible to prolonged Leishmaniasis. When people have too few  CD4+ T lymphocytes, a specific type of white blood cell, they generally have a weakened immune system. Not only would it be weakened, and thus more susceptible to Leishmaniasis, but people with either of these conditions would be more susceptible to any type of infection.

There are over 17 known species of Leishmania that can infect humans, so, logically, each species has biochemical/molecular differences between each other. Because of these distinct differences, each species has a different level of sensitivity to several drugs and some may be more receptive to a certain drug over another. According to a number of previous studies, L. donovani and L. brasiliensis were found to be three to fivefold more sensitive to sodium stibogluconate (a common drug used to fight Leishmaniasis) than L. major, L. tropica, and L. mexicana. In addition to the species variation of certain Leishmaniasis causing agents, there has also been an increasing level of clinical resistance to Leishmaniasis fighting drugs.


Rabies Article


Rabies, which collectively includes the lyssavirus and all strains of bat lyssviruses, is a collective group of virus strains in the Rhabdoviridae family. In addition to the rabies virus, the genus lyssavirus includes the Australian bat virus, Mokola virus, Duvenhage virus, European bat viruses 1 and 2, ant the Lagos bat virus. Rabies only affects mammals, and does not affect other fauna. In an infected creature, the rabies virus is found only in the nervous tissue or in the saliva of that creature, meaning that transmission occurs primarily through scratches, bites, or through saliva entering an open wound.


Once inside the body, the virus follows a specific course of actions:

  1. Travels through the muscle tissue to enter nervous tissues.
  2. Travels up spinal nervous tissue toward brain.
  3. Once inside brain, begins to multiply rapidly, beginning the distinct and easily recognizable symptoms.
  4. The onset of encephalitis occurs in the brain, which is followed by a prolonged, painful death.

The incubation period of the virus from initial contraction to the onset of the first symptoms can last anywhere from a few days to a couple of months. This is determined by the amount of rabies virus transmitted by the bite or scratch, the severity and size of the wound, and the location of the wound on the body. While no initial symptoms occur, other than slight pain or itching around the bite or scratch wound, symptoms reminscent of a fever soon follow. An elevated body temperature, coughing and sneezing, headaches, dizziness, confusion, are all common symptoms. As the virus multiplies in the brain, the symptoms become more painful and more sever, with more symptoms like loss of balance, trouble breathing, muscle spasms, and agitation. In humans, hydrophobia and aerophobia are common, as the virus causes severe and painful muscle spasms in the throat, rendering the victim unable to drink water. After the onset of symptoms, death is almost surely imminent.





Dengue is becoming an escalating problem in the world. Right now the world is seeing more and more cases each year. More than ⅖ of the world population live in areas at risk for the dengue fever. Travelers are also at risk if they visit these areas, and one relatable area that all would know is the Caribbean. Now I will talk about the epidemiology. There are four different dengue viruses that are recognized and once infected with one of the viruses, you will have a lifelong immunity to that specific dengue virus. Mosquitos will carry the disease for the rest of their life but humans will not. Mosquitos are believed to contract the disease from forest in tropical regions through vertical transmission in a mosquito.

The Dengue virus in the past 60 years has increased in clinical severity. The Dengue virus cases have risen in part to uncontrolled urbanization in the tropics. Urbanization results in inadequate management of water and waste. This leads to large water disposal areas which are in large non biodegradable containers that become homes for the larvae. Also, air travel has been another way for the take off of this disease because an infected human can take the disease back to their homeland and thus the disease can spread. These are the more important reasons of why the disease is increasingly becoming a problem.

The pathology of Dengue is distinguished by the presence of increased vascular permeability. Vascular permeability is the capacity of blood vessel wall to allow the flow of small molecules like water in and out of the vessel. The dengue virus is mostly found in the liver and reticuloendothelial (involved in the immune response and are most commonly found in liver) systems.

The clinical features of dengue can vary from patient to patient. There are five different presentations of this disease. The five different presentations are as followed: nonspecific febrile illness, classic dengue, dengue haemorrhagic fever, dengue haemorrhagic fever with dengue shock syndrome, and other unusual symptoms such as liver failure. Young children under the age of 15 dengue infections are asymptomatic or minimally symptomatic. A study in Thailand showed that only 13% of children under the age of 15 missed school for more than one day with the dengue virus.

Classic dengue is most common in people above the age of 15 and these are less likely to be asymptomatic. This dengue is very abrupt that will bring a high fever accompanied by a high fever. The recovery for this disease will take a long day and may even include depression.

Dengue haemorrhagic fever is most common in children under the age of 15 in hyperendemic areas. These types of areas are in climate where the temperature is above 80 degrees all year round. Black populations are at a decreased risk of contracting this disease. Black populations are at a decreased risk of contracting the disease because the disease is increased by the capillary permeability and haemostatic changes. If plasma leakage occurs then victims can experience effusions and ascites with bleeding. There will also be an development of enlargement or tenderness of the liver that occurs in 40% of patients. Death can be in up to 20% of patients with this specific type of dengue fever. Only .2% of hospitals know how to deal with type of dengue fever. Dengue shock can be very deadly in patients because if shock occurs, then 50% of patients with shock will die. Dengue shock brings symptoms of vomiting, changing in level of consciousness, a decrease in platelet count, and sustained abdominal pain.  

Dengue can be transmitted back to your homeland even though you may not live in a dengue present region. Travellers can unknowingly contract dengue because transmission is maintained between the epidemics. For example, a test conducted in Germany and Australia showed that 8% of travellers returning with a febrile illness were found to have dengue. The incubation period of dengue can vary from 3 to 14 days and the viraemia can persist up to 12 days. Dengue can be ruled out if the symptoms begin more than 2 to 3 weeks after a patient has left an epidemic area. Dengue haemorrhagic and dengue shock is very rare in travellers.

As of right now their is no specific treatment for dengue. A medical professional would be trained to run different assessments in order to see how serve and how to improve the dengue virus in you. Different assessments they would run is testing a patient’s packed cell count, platelet count, liver function tests, prothrombin time, partial thromboplastin time, electrolytes, and blood gas analysis. This would allow the doctor to determine how to treat the certain affected region of your body. Since there is no treatment for dengue, the doctor would just treat the affected part of the body with drugs proven to improve that affected body part. For example: If a patient is experiencing a fever the doctor would give that patient Paracetamol. Aspirin or other non inflammatory rugs would be avoided because these drugs can increase your risk of Reye’s syndrome and haemorrhage. To avoid dengue or completely wipe out dengue would be to kill or contain all mosquitos which is close to impossible.

Prevention and Control of Taeniasis and Cysticercosis in Peru

There is currently an effort to eliminate Taeniasis, a tapeworm disease, or helminth, found in most parts of the world, which is currently hyperendemic in Northern Peru. Taeniasis is a gateway disease to Cysticercosis, as the Taeniasis solium tapeworm can cause the buildup of cysts in the brain, causing epilepsy, drastically decreasing quality of life. Funded by the Bill and Melinda Gates Foundation, ways of eliminating this disease from this region and eventually the world are being researched, and various options are being considered as steps toward eradication. These options include types of chemotherapies in humans as well as pigs, which are vital to the life cycle of this helminth. This disease is prevalent in poorer parts of the world due to its propensity to occur as a result of poor conditions on pig farms. The main source of the continuation of this disease’s life cycle is farmers allowing their pigs to roam in the open and find their own food. This aids in continuing the part of the disease’s life cycle where the tapeworm’s eggs, found in human feces, are consumed by the pig. This occurs with much ease as this disease is endemic in places where open-air defecation is popular. A person infected with the Taeniasis solium tapeworm can excrete up to 100,000 Taenia Unknowneggs in their stool, which can spread far and wide in open air.

Many of the ways in which Taeniasis can be tested for using modern technology require heavy funding in efforts to eliminate the disease in neglected tropical areas. ELISA tests, ELISA reading machines, and trained operators in such an area are expensive, and CT and MRI imaging for diagnosis of Cysticercosis are by no means cheap or accessible methods for screening in this part of the world. Therefore, the financial backing of the Bill and Melinda Gates foundation proves paramount. With capital, the most practical method of treatment of this disease would be to properly screen for infected individuals and give them treatment in the form of one of two drugs that have proven highly effective in treating the disease: praz1472579078181.pngiquantel and niclosamide. Niclosamide is the preferred drug as it does not e
ntail absorption through the intestines, which can lead to the onset of intensified neurological symptoms if the person has already acquired Cysticercosis along with their tapeworm infection. Both are relatively expensive and not readily available in Peru.

Other possible methods of treatment include mass treatment of pigs, new measures to be taken during pork preparation, and mass, nonspecific treatment of humans. As for the pigs, a drug called oxfendazole is capable of killing the larvae-filled cysts (pictured below) form pigs’ muscles, making them clean for their eventual consumption. The proposition for mass treatment with this drug has been made as well, however the negative aspect of this is that the desired results of the drug, complete destruction of larvae-filled cysts, the direct source of the tapeworm growing inside the human after consumption, manifest after about three months of therapy. Other precautionary measures concerning the pigs are being considered as well, ones that are environmental rather than drug-related. Slaughterhouse control and the examination of meat post-slaughter is being considered as a method for vetting pork being sold in Peru, however carcass examination is not foolproof. Cysts not easily detected during inspection are bound to be passed over. The requirement for containment of pigs in a corral has been considered as well. However, this would force villagers to feed their pigs on their own, which they most likely cannot afford. The appealing aspect TAE_002of allowing the pigs to roam freely is that they are then capable of finding their own food. This, as previously mentioned, is a main cause of the continuation of Taeniasis’ life cycle, as this is when eggs are consumed by pigs. One final proposition for the treatment of this disease is mass, nonspecific treatment of humans, which would entail mass chemotherapy of all people in an endemic area using praziquantel and niclosamide. This has been done in other neglected tropical areas, and results were positive. Mass treatment is less costly as less engagement with patients in diagnosis and individual care is required, but it does nothing to prohibit the presence of Taenia eggs already in the environment. These tapeworm eggs can last for several years in soil, and may outlast the effect of the mass treatment performed. New people may move into the environment during that time, or children born after the time of the treatment may be vulnerable. Thus, the life cycle of the disease would resume after a short period of elimination. Another concern would be the possibility of giving praziquantel to a patient who is already suffering from Cysticercosis, thus heightening their neurologic disorder, causing more seizures.

The effort in Northern Peru is still a work in progress, but these options are being weighed, and a combination of these courses of action may lead to the eventual elimination of this disease. Elimination will improve the quality of life in this area, as well as make pork consumption safer. Thanks to the Bill and Melinda Gates Foundation, funding for the procedures being pursued has been easier to come by.



Source article:

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Article Review

This article talks about an experiment testing two new drugs on Trypanosomiasis, or sleeping sickness. Sleeping Sickness is caused by the bite of the Tsetse fly, which injects the Trypanosoma parasite, of which there are a three different known kinds. However, this experiment focused exclusively on Trypanosoma Brucei, which is not toxic to humans, but is found in animals in the same region of sub saharan africa, mostly livestock. The two new drugs tested are both alkaloids derived from plants: emetine and homoharringtonine. The study tested the effectiveness of these drugs in five different ways: through testing the level of protein synthesis, through testing the mitochondrial membrane of the parasite itself inside of cells, through testing to see if the cell cycle was arrested, as well as testing DNA intercalculation (mutations in parasite genetic formula) and finally the drugs ability to inhibit an enzyme specific to the Trypanosoma Brucei. Cell cultures were soaked in a solution containing either of these drugs in different concentrations. After two hours in the soak and forty eight to rest, the growth rate of the parasites were reduced by fifty and thirty percent, in the highest concentration of the emetine and homoharringtonine respectively. After four hours at any concentration of emetine, the growth was slowed by sixty, seventy, and eighty percent at intervals of a day. The homoharringtonine was more effective in stopping protein synthesis, slowing the parasites by fifty percent, while the comparable concentration of emetine only slowed by twenty. However, neither drug was effective compared to the control at weakening the mitochondrial membrane after four hours. Homoharringtonine was slightly effective after twenty four hours of a soak.  After a four hour soak, homoharringtonine arrested cells in between the G0 and G1 phases. However, after twenty four hours, the effect was diminished. Emetine stopped the cell cycle in the G2 and M phases, but only after a twenty four hour soak. Neither drug incubation could do anything to reduce the level of the enzyme concentration. Emetine could intercalate DNA, but the homoharringtonine was unable to. All in all, it seems as if homoharringtonine is more effective than emetine at fighting the parasite. However, the most important thing to keep in mind about the study is that these alkaloids are not healthy for humans to have in their systems. Therefore, no matter what, it is best that these drugs would be used in moderation. The writer of the article says that because sleeping sickness is life threatening, the benefits outweigh the costs. Either way, human subjects would knowingly be injecting bleach into their bodies. Also important is these drugs even if they did become widespread, would only be used to treat stage one of the disease. Once the parasite crosses the blood brain barrier, it would require an entirely new treatment. This second stage is also one that we are under equipped to deal with. Of the few medicines we have for treatment, only two are available for the second stage. Therefore, despite how promising this study might be, it is far better to focus our efforts on prevention, namely education and eradication of the tsetse fly.