Infection

 

Soothes Cold Symptoms
The "common cold" is caused by any of a large group of viruses, most commonly rhinoviruses. There are 99 known serotypes of rhinovirus alone that infect humans, and when the seven additional genera of viruses implicated in causing colds are factored in, there are over 200 viruses responsible for causing what is commonly called "a cold."

Antibiotics are entirely ineffective against viruses, and doctors who prescribe them for a cold not only are not helping their patients but are actually contributing to the erosion of antibiotic effectiveness in general and risking adverse side effects in the patient without any possibility of gain. Furthermore, no currently known antiviral drugs have shown effectiveness against the various viruses responsible for colds.

Consequently, treatment of a cold is limited to providing symptomatic relief rather than combating the infectious agent directly. Medications which soothe cold symptoms don't have any effect on the disease's severity or duration, but help the patient feel better. Most cold medicines provide basic pain relief for aches, fever-breakers like acetaminophen (commonly paracetamol in the EU) or ibuprofen, decongestants, and cough suppressants.

Despite wishful thinking, scientific studies have shown no other treatments with statistically-provable effects on colds, including various vitamin and mineral supplements, foods, spices, and alternative medicines.

Learn more at Wikipedia or the ICD

Antibiotic
Effective against bacterial infections only, true antibiotics are used to either kill bacteria outright or at least inhibit their reproduction. Antibiotics interfere with processes key in cellular reproduction, inhibiting the manufacture of critical compounds (such as folate) or the copying of DNA or RNA. While antibiotic effects have been noted in some materials since antiquity, modern science was able to identify and isolate the anti-microbial compounds and produce them in quantity.

Antibiotics fall into two classes. Biological antibiotics are typically isolated from molds and soil bacteria which secrete them to reduce competition in their native environments. Ernest Duchesne was the first to identify the inhibitory action of molds against bacteria, but was unable to pursue his research because he was enlisted in the French army at the time. Duchense would die at the age of 38 from tuberculosis - a disease which would be defeated by antibiotics in 1939. Thirty-two years after Duchese's discovery, in 1928, Alexander Fleming succeeded in isolating the secretion of a common mold, Penicillium chrysogenum, and proving its effectiveness in combating certain bacteria. Oral phenoxymethylpenicillin soon followed, but its efficacy was low and spectrum of action limited (it could not affect many bacteria). Further development and processing of penicillin produced the first members of the penicillin family of antibiotics and labeling penicillin a "wonder drug." Synthetic antibiotics are typically derived from dyes and stains, including arsenic. While early synthetic antibiotics had toxicity issues, these issues were corrected in the late 1930s.

Today, there are over 100 antibiotics in use, however they are derived from only a handful of sources. Over-prescription of antibiotics, particularly the practice of prescribing antibiotics in cases where they are known to be ineffective (such as viral infections), and the misuse of prescribed antibiotics by failing to take the complete course of medication has prompted the emergence of resistant bacteria. The efficacy of antibiotics varies from bacterium to bacterium, with some more resistant than others. A course of antibiotics is designed to last for a certain duration at a certain serum concentration to ensure that even more resistant microbes are destroyed. Stopping antibiotic therapy early allows these more resistant bacteria to survive and reproduce, giving rise to a strain that is not as easily affected by the original antibiotic. Perhaps the best-known resistant strain is MRSA - Methicillin-resistant Staphylococcus aureus.

The development of new antibiotics is of critical concern to health organizations like the WHO, CDC, and NHS; current antibiotics are rapidly losing effectiveness, and few are in the development pipeline to replace them.

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Antimalarial
Malaria is not a microbial disease in the common sense; rather than being the result of bacterial or viral infection, malaria is caused by infection with a parasitic protozoan of the genus Plasmodium. These parasites have a life cycle that always involves two hosts: an insect in which the parasite reproduces sporozoites which are transmitted to a vertebrate host where the parasite takes up residence in the liver and produces gametocytes. These are picked up when another mosquito feeds on the infected vertebrate, starting the cycle over again.

As a parasitic protozoan, malaria is notoriously difficult to treat. There are thirteen families of drugs that have been developed in the ongoing war against malaria, but each is not universally effective and has significant side effects. Two classes of antimalarial drugs exist: prophylactics, which seek to prevent infection, and treatments, which combat existing infection. Antimalarial drugs seek either to disrupt the disease's ability to take root in the liver or to deny it the use of red blood cells for proliferation, often by toxifying cellular chemistry. Unfortunately, this also interferes with the cells' ability to perform their normal bodily functions.

Common side effects of antimalarial drugs include headache, fever, severe and persistent rashes, hallucination, tinnitus, impaired balance, suicidal or otherwise bizarre ideation, impaired judgment, alteration of heart rhythm, vomiting, and cramps. In the US, nearly all animalarials carry a "boxed warning," the highest level of medical warning that the FDA can apply. Some medications can only be used for a very limited span of time as the side effects can become permanently damaging or even lethal with longer exposure.

In addition to the problems inherent in current antimalarial drugs, there is great interest by the health organizations of the world in the development of new treatments as the malaria-causing protozoan is developing resistance to many of the current drugs. However, as malaria is considered to be a relatively low profit disease by the larger pharmaceutical industry, research efforts are not highly focused.

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Combats AIDS
Despite popular misconception, Acquired Immuno-Deficiency Syndrome is itself not a disease, but a syndrome resulting from a disease. The Human Immunodeficiency Virus (HIV) has several stages of progression, the last of which is AIDS.

AIDS is characterized by the presence of an HIV infection combined with a low CD4 count in the blood. CD4 cells, properly called CD4+ T-helper cells, are both the primary means by which the immune system combats infection and the way by which HIV reproduces. As the disease progresses, more and more CD4 cells are destroyed and the body's ability to replace them is degraded, leading to diminished CD4 blood count. A healthy adult has a CD4 count of between 500 and 1,500; persons in advanced AIDS have a count of 200 or lower. While the effects of the loss of CD4 cells are not seen for months or years, the bulk of CD4 destruction from HIV infection occurs in the first 2-4 weeks of infection as T cells in the intestinal mucosa are destroyed en masse as the virus replicates exponentially.

As the immune system loses its ability to fight infection, the body becomes more susceptible to infection from other diseases. These infections, called opportunistic illnesses, are able to attack the body effectively because the immune system is no longer able to keep them at bay. Opportunistic illnesses are a characteristic sign of AIDS and indicate the HIV infection has progressed beyond control. Ultimately, persons that succumb to AIDS are not killed by the HIV organism but rather by the combined effects of these opportunistic illnesses.

Curing the AIDS condition is effectively impossible, so treatment plans focus on two primary goals. First, the reproduction of HIV must be curtailed as much as possible to preserve what CD4 cells can be produced. Second, opportunistic diseases must be kept in check to help the weakened immune system. Barring a cure for HIV, the root cause of AIDS cannot be directly attacked. Consequently, supportive care for AIDS is the only means to prolong a patient's life.

Cures HIV
First isolated in 1983, strong evidence suggests that Human Immunodeficiency Virus first entered the human population as early as the 1800s. HIV is a retrovirus - a virus that carries not DNA as its nuclear material but RNA. Once the virus gains access to a suitable host cell, a transcriptase enzyme carried by the virus copies the RNA into DNA, whereupon a integrase enzyme also carried by the virus installs the viral DNA into the host cell's DNA, effectively hijacking the cell.

Back-tracing the spread and genetic drift of HIV has resulted in the identification of the likely original source of the virus. Simian Immunodeficiency Virus, or SIV, has existed in chimpanzee populations in Central Africa for a substantial span of time. It is currently believed that a mutant form of SIV came into contact with humans who were hunting and butchering chimpanzees for food. This mutant form made the species jump to become HIV. Species jumps of diseases are not uncommon and have given rise to some of the most dangerous diseases known, such as swine flu, bubonic plague, Ebola, polio, anthrax, and SARS.

HIV operates by using the body's own immune system as its means of reproduction, infecting and incapacitating CD4 helper-T cells. These cells, which are normally responsible for identifying pathogens previously unknown to the body and initiating an immune response, form a critical link in the body's immune response chain. To make matters worse, as additional HIV particles exit the infected CD4 cells, they are cloaked in CD4 antigens, causing the immune system to ignore them as they carry the correct marker proteins to be identified as "friendly" cells. The virus is so effective at commandeering CD4 cells that the bulk of the body's CD4 cells are deactivated and/or destroyed within the first two to four weeks of infection.

Current medical state of the art does not include a cure, but multiple treatments to keep HIV in check are available. With proper and daily treatment, a person infected with HIV can have almost the same lifespan as someone not infected. Current treatment protocols rely heavily on CCR5 antagonists, which block the CCR5 receptor on T cells, preventing HIV virions from entering the cell and beginning the replication process.

Cure research is focusing on several avenues of attack against the virus. One weak link is the integrase enzyme; only retroviruses use this enzyme, and it is critical in installing the viral DNA into the host cell's nuclear material. If the integrase can be inactivated or inhibited, the viral DNA cannot be bonded to the cell's DNA and viral replication cannot occur. Stem cell transplantation has also shown promise where the stem cells used possess a CCR5-Δ32 mutation, but shortage of potential donors and ongoing political issues have stymied further research.