These SNPs were also inferred in Sanger sequencing
These SNPs were also inferred in Sanger sequencing. The average rate of mutation of the bacteria was also gathered. This can be estimated by getting the number of variations that have transpired in a genome over a value of organisms. In vivo, unlike vitro, which is faster, the mutation degree in an average of hours between 17-241 hours by use of polymorphism given by Whole Genome Sequencing.
The article concluded that the mutations occur at similar rates despite the level of the infection. The SNPs showed the rate of mutation in the bacterium during its life, and the number of mutations is assumed to be the right way of calculating the mutation rate in the cell. The results show the significance of drug opposition challenges and keen nursing of patients with such an infection. It was also concluded that the use of one type of antibiotic increases the risk of developing Mtb resistant strains. Moreover, after the administration of antibiotics, the drugs only kill the susceptible bacteria, leaving the mutated ones. The process reactivates the mutation process resulting in more severe infections. Mtb strain has in vivo mutation, which is consistent in terms of the number of mutations. Hence, based on epidemiologic studies, external factors like chemicals will have no influence on the mutation process. It was also concluded that there is a strong connection between Mtb resistant strain and HIV+ individuals due to suppressed immunity. Such patients are at high risk of having resistant strains of Mtb.
The data collection involved the generation of two read lengths of 2 by 75 base pairs were than snipped to ensure the purity of bases, later to go under filtration. To ensure all the base pairs were known, all the chromosomes containing unknown bases were discarded. Eight million reads were left after the process of filtering. The processing of the filtered reads was done with Edena v2.1.110, that permitted for the detection and insertion of nitrogenous bases in the chromosomes. The change in genetic makeup within the chromosome was then established. Counting the number of newly formed was done using statistical analysis of WGS data. The selection of scientific statistical data should be able to detect the changes in Mtb after sequencing the newly formed chromosome after mutations.
The comparison of the number of chromosomal mutations during the latent and active disease stages showed that Mtb is prone to mutations which creates the resistance to antibiotics. The Ford et al. hypothesis was evident after the end of the study which proved that Mtb has a similar number of mutations during the latency stages and active disease stages. Statistical analysis of WGS data helped the researchers to account for all the base pairs formed after the research. The research, therefore, explained the reason for Mycobacterium tuberculosis antibiotic resistance.
μ=m[N*tg]
(2)
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3562 words (14 pages) Essay
18th May 2020 Biology Reference this
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PPID is a disease commonly seen in the equine population with an increase occurrence found in older horses as it is a degenerative condition associated with ageing (McGowan et al, 2013). Once thought to be a rare condition of geriatric horses, it is a condition that is now found in a large section of horses and ponies 15yrs and over .This is thought to be due to the increase in the number of aged horses and owners seeking veterinary attention and guidance for older horses as they have a better understanding of the disease than before (Sojka-Kritchevsky and Johnson, 2014).
The prevalence of equine gastric ulceration syndrome remains high particularly in competitive horses. This is predominantly due to some modern management practices that go against the evolution of the horse as a grazing, free moving non ruminant herbivore. These include limited opportunity to free movement, high grain low forage diets, intensive training and stressful environments which all contribute to a poorly buffered and acidic stomach leading to gastric ulcers (Luthersson et al, 2009). There is a greater understanding of preventative measures such as increased turnout, ad lib forage, reduced training intensity and reduce stress but these are not always possible or effective in some horses and combined with the high cost of antiulcer treatment, the frequency of EGUS in horses remains relatively high (Nadeu and Andrews, 2009).
2.
Equine dysautonmia otherwise known as equine grass sickness (EGS) is a polyneuronopathy that affects the central and peripheral nervous system. It is a condition that primarily affects grazing horses and has varying severity of clinical signs but all cases will show signs of neural degradation in the autonomic and enteral nervous system. The acute and subacute cases tend to be fatal but milder chronic cases may recover with intense nursing. The disease is linked with the bacteria Clostridium botulinum which is found in the soil; however the exact aetiology of the disease is unknown but is thought to be caused by neurotoxicosis (Hunter et al, 1999). The clinical signs usually present as increased heart rate, muscle tremors, patchy sweating, difficulty swallowing, mild colic symptoms, gut ileus, abdominal distention, oesophageal ulceration, drooping eyelids, rhinitis sicca (dry nose) weight loss or sudden death (Hedderson and Newton, 2004). There is no treatment currently available for EGS so the most effective way to prevent the disease is to minimise the risks. A study in Scotland in the 1970’s which was then matched in by a study conducted by the Animal Health Trust in 1998 identified the major risk factors as; horses grazing 24/7, younger animals aged 2-7yrs, previous occurrence of the disease on the premises, recent changes to pasture or premises with risk decreasing as time passed and absence of hay supplementation (Pirie, 2006). A study by Woods et al suggested there is also climate associated risk factors as cases where identified after cooler, dryer weather and irregular ground frosts. The findings from previous studies link the condition to a ingested soil borne agent that under certain conditions produces neurotoxins in the horse therefore preventative measures should be taken to reduce the chance of this agent being taken in by the horse. Measures that can be taken include; avoid previous infected paddocks, introduce horses to new paddocks gradually and not during period of high risk e.g after cold, dry period and provide hay supplementation and avoid soil disturbance (Pirie et al, 2014).
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Sweet Itch is an allergic skin reaction to predominantly midge (cullicoides) bites but reactions can also be caused by mosquitoes and black fly. The condition has been found to affect 5% of the equine population with a high prevalence amongst native breeds. It is the saliva of the biting insects that causes a localised skin reaction and the actual bite can also be painful. The hypersensitivity to the insect varies between horses which will impact on the clinical signs but the majority of cases will show some degree of pruritus that is concentrated on the mane, neck and tail (Pilsworth and Knottenbelt, 2004). At the affected areas hair loss is usually the first clinical sign to appear but due to the self-inflicted trauma from scratching, over time the area can become sore, bleeding and the skin becomes thickened. Irritability and restlessness can also be present in some horses and in severe cases the distress can lead to weight loss. There is no cure available for sweet itch and it is a disease that usually gets increasingly worse with time therefore it the best control of the condition is to try and limit the exposure of the horse to midges – the allergic reaction. These measures include: wearing fly rugs that cover the whole body 24hrs a day, use of fly repellents containing pyrethroid or permethrin based ingredients and stable horses when insects are most active which tends to be dawn and dusk. There are treatments available to control skin irritation but none can cure. These methods include the use of; steroids, antihistamines, anti-itch shampoos, providing essential fatty acids, immunotherapy. A hypersensitivity vaccine is being developed which may be available in the next couple of years will hopefully provide an effective treatment for owners (Chapman, 2019).
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Modern equine management practices may increase the susceptibility of horses developing colic as they go against how the horse has evolved. Horses are forage grazing hindgut fermenters that are designed to eat little and studies suggest that diet and management has an important influence on the risk of colic (Scantlebury et al, 2015). Horses on a high grain/low forage diet are at greater risk of colic because the intestine has evolved to process a high fibre diet which is essential for gut mobility. The horse has a relatively small stomach which can process effectively small amounts of grain but horses that have large grain or concentrate feeds have an increased risk of colic as some of the concentrate feed may remain unprocessed and pass through into the large intestine causing gastrointestinal upset (). Any changes to diet must be gradually, over 10-14 days, to enable the gut microflora to adjust to the new food that has been introduced. Horses that have a sudden change to their diet are at a great disposition of colic as the sudden change can cause imbalances to the microflora which negatively affects how food is digested. Clean, fresh water must always be available as water is essential in equine digestion as it is consistently secreted into and then reabsorbed by the gastrointestinal tract. Horses with an inadequate water supply are at a higher risk of impaction colic. Other management factors such as limited access to grazing, poor worm control (high worm burden), no routine dental checks and stress are also predisposing risk factors for colic (Hillyer et al, 2002).
Recurrent airway obstruction (RAO) or otherwise known as severe equine asthma is the name given to nonseptic airway inflammation that is usually induced by an immunological response to organic dust and moulds. The most predisposing factor in the development of the disease is housing and the challenge it causes to the horse’s respiratory tract. There are many contributing factors that are associated with stabling that increases the risk of RAO but they all lead to poor air hygiene as they cause irritantants or allergens to be suspended in the air that are then breathed in and enter the lungs. Forage and in particular dry hay that has been baled with higher than desired moisture content has been associated with RAO due to the high amount if organic particles it produces and in particular the aspergillus fumigatus spores. Horses that are fed from a haynet are more predisposed to RAO compared to being fed off the floor as the nostrils remain in the source of the particles (Ivester et al, 2014). Straw bedding is also linked to the development of RAO due to the high dust content and has been used in studies to induce clinical signs of RAO. Horses kept in poorly ventilated stabling have an increase risk of RAO because respirable particles remain in the air for long periods if there is no or very little through air. A study by McGorum et al (1998) found that respirable particulate and endotoxin levels in the breathing zone where significantly less as pasture than a horse stabled in a low dust environment. Therefore horses that are stabled for any significant time even with low dust management practices are at a higher risk of developing RAO than compared to horses kept at grass.
Pasture associated laminitis the most common form of laminitis seen in the equine population. There are management factors that may predispose horses to this disease. Overweight horses and ponies on unlimited pasture with grass species containing high levels of non-structural carbohydrates are at the greatest risk. Turning horses out onto paddocks when the grass is actively photosynthesising (lush grass) or when the condition for growth is not optimal (stressed grass) is a common predisposing factor as it is thought that there is more storage carbohydrates in the grass at these times which are thought to be a trigger of laminitis (Harris et al, 2006). Also horses that are not exercised or spend very little time moving around the paddock also have an increased predisposition due to the likelihood of them being or becoming overweight. As study by Alford et al, found a significant higher proportion of acute limits cases happened in the no regular exercise category compared to the control group.
4.
Nutrition has a key role in the development of laminitis and although the exact mechanism is still not clearly determined there is evidence to suggest that a metabolic or digestive disturbance is a contributing factor. If the horse ingests a large amount of poorly digested but highly fermentable food that particularly contains a large amount of starch or fructose (storage forms of carbohydrates) then there is a change to the gut bacterial flora and mucosal permeability (Secombe and Lester, 2012). Studies have suggested that like other mammals, horses do not have the necessary enzymes to digest fructans directly within the small intestine so they therefore pass into the hindgut where they are easily fermented; in a way similar to starch that avoids digestion in the small intestine. This causes some bacteria to die releasing endotoxins which eventually leads to the reduced blood flow to the foot which develops into laminitis (Kronfeld and Harris, 2003).
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5. One possible cause of the ponies symptoms is Equine Hyperadrenocorticism / Pituitary pars intermedia dysfunction (PPID) otherwise called equine cushings ‘s disease. It is an endocrine disorder of aged horses and ponies that results in the loss of dopaminergic inhibition of the pars intermedia of the pituitary gland which leads to the overproduction of hormones that exert endocrine effects which result in the clinical symptoms of the disease (McGowen et al, 2012). The signs associated with PPID include; delayed coat shedding, hirsutism, weight loss, increased thirst (polydipsia), increased urination (polyuria) and laminitis and some of these symptoms have been described by the owner. There may be other effects leading to the clinical signs such as insulin dysregulation or equine metabolic syndrome (EMS). This is often a condition linked to the predisposition of PPID however the exact relationship between the two conditions is unknown. EMS increases the likely hood of laminitis due to the excessive hyperinsulinemic response to glucose in the horses’ diet (Krichevsky and Johnson, 2014).
Alongside the presence of clinical signs, the diagnostic test most commonly used is an assay of resting plasma ACTH concentration. a high concentration supports the diagnosis of PPID but it is important that they are interpreted with seasonally adjusted reference ranges in order to gain accurate results. Horses and ponies with unclear results ( when they have suggestive clinical signs with normal ACTH results) or in the grey zone ( these are clinically normal horses with mildly elevated ACTH levels) should either be resampled during autumn or undergo a TRH stimulation test. Thyrotropin releasing hormone stimulation test is deemed the most precise test for the identification of PPID. The test relies on an extreme pituitary response to the administration of Thyrotropin-releasing hormone (TRH) in horses with PPID when compared to normal horses.
6.
Simple Mendelian diseases are inherited diseases that involve single genes. The inheritance pattern of single gene diseases is called Mendelian after Gregor Mendel who first observed the different patterns of gene segregation for selected traits in garden peas and was able to determine probabilities of recurrence of a trait for subsequent generations. These diseases are predictable in inheritance as the causative DNA is usually identified in distinct individuals. They can be characterised in groups as dominant, co – dominant or recessive depending on the expression of the mutated allele compared to the normal allele (Finno and Bannasch, 2014). Complex diseases involve the interaction of multiple genes as well as environmental factors. Unlike single gene diseases, complex diseases have a more unpredictable outcome as there is no clear cut pattern of inheritance. Not all horses in the same family will develop the disease but those that do have the right combination of genetic mutation and environmental factors and in some cases the disease will develop regardless of the environmental conditions. This makes it challenging to determine the risk of inheriting or passing on these disorders. Compared to single gene diseases, complex disorders are tough to study and treat because the precise factors that cause most of these disorders have still not be found (Genetics Home Reference, 2019).
Hyperkalaemic periodic paralysis (HYPP) is a Mendelian autosomal dominant genetic disease that is seen in quarter horse breeds. The disease emerged as a natural occurring genetic mutation that has been passed on through selective breeding (for desirable pronounced musculature) as HYPP can be traced back to a single breeding sire. The most common clinical signs of the disease are muscle twitching and tensing. In mild attacks they remain standing and the recovery can be spontaneous but in severe cases the horse can display weakness by swaying, buckling at the knees, paralysis of hindquarters and involuntary collapse. The symptoms are usually accompanied by sweating, slightly increased heart and respiratory rate and decreased tendon reflexes. The disease can be indicated by high potassium levels in serum which can help in the diagnostic testing for the disease. The episodes of HYPP are unpredictable and very in severity but can occur; after sleep, rest after exercise, during or after a period of stress, traveling or surgery. Usually horses that are homozygous are more severely affected than heterozygotes and as the disease is autosomal dominant there is no gender difference in developing HYPP. The most effective treatment is controlling the potassium contractions in the serum which is can managed through diet and medication using acetazolamide a potassium wasting diuretic and carbonic anhydrase inhibitor (Meyer et al, 1999).
Osteochondritis dissecans (OCD) is a complex developmental disease in horses that affects the bones and cartilage of joints and is a cause of lameness and decreased performance in young athletic horses. The disease causes the cartilage in the joints to form abnormally causing the cartilage and the bone underneath to become irregular and thickened and forms bone and cartilage flaps that either are partially attached to the bone or break off and float in the joint space (Bates et al, 2015). This then causes an inflammatory response in the area which overtime may develop into arthritis. Studies have found there is a genetic component to the development of the disease but environmental factors such as; nutrition leading to high growth rate, exercise, trauma and hormone imbalance are also key in the disease formation. Alongside lameness, the most common clinical sign is swelling at the joint and it is most commonly seen in the hock, fetlock and stifle joints (Weeren and Olstad, 2015).
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2028 words (8 pages) Essay
18th May 2020 Biology Reference this
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Alexander Ogston was a surgeon and bacteriologist most famous for his discovery of Staphylococcus aureus in the year 1880. With a great admiration for Joseph Lister and his value of antisepsis, Ogston rejected the belief that the formation of pus was a natural part of the healing process. Since post-operative patients of Lister did not show any signs of inflammation in their wounds, Ogston sought out to find the reason. After successfully isolating S. aureus from pus, he would go on to publish his clinical observations and laboratory studies describing diseases caused by it and its role in the formation of suppuration (Orenstein, n.d.).
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Some physical characteristics of the bacteria Staphylococcus aureus can be determined from its name. Staphylococcus is derived from the Greek root staphyle, which translates to a bunch of grapes (Golden Staph, 2015). This refers to the arrangement of the bacteria when looking at them through a microscope after a gram staining process. Gram staining also reveals that the bacteria are Gram-positive, meaning it has a thick peptidoglycan layer. They are facultative anaerobes that have evolved to thrive in harsh environments such as human skin, which is dry and salty.
At some point in everyone’s life, these bacteria can be found in their nostrils. Roughly one out of three healthy adults are considered long term carriers of S. aureus (one year or more) and about 60% will be colonized at some time during a given year (Taylor, 2019). Once inside the nose, the bacteria can spread to other parts of the body.
S. aureus can colonize nearly any part of the body given its opportunistic nature. The bacteria will exploit of broken skin or other entry points to cause disease in other areas. Infections have been known to cause systematic complications. Once it can grow inside a wound, S. aureus will spread through the bloodstream forming abscesses in the heart, the bones, the brain, or other tissues.
In a vast majority of cases, S. aureus is a harmless bacterium found in our microbial flora. However, after a successful invasion through a cut, a person can experience an infection that ranges from mild to severe. Some cases have even documented death as a result of infection from this bacterium. Minor skin infections include pimples, impetigo, boils, cellulitis, folliculitis, carbuncles, scalded skin syndrome, and abscesses. Abscesses are generally caused by infections of the skin and form as a result of your body’s inflammatory response to defend itself. They are filled with pus, bacteria, and other debris (Rayner & Munckhof, 2015). Treatment typically involves drainage of the infected site and the use of antibiotics. Life-threatening diseases include: pneumonia- infection of one or both lungs; meningitis- infection of the membranes lining the brain; osteomyelitis – infection of the bone and bone marrow; endocarditis – infection of the heart valves; toxic shock syndrome, bacteremia, and sepsis. Sepsis is also result of your body’s response to an infection. In the fight against invading pathogens, your body will naturally release chemicals. If your body’s response is out of balance when this happens, sepsis will result. The imbalance will bring about changes that are harmful to the organ systems.
Treating S. aureus infections can be problematic in some cases because many strains have developed a resistance to commonly used antibacterial medications. This type of bacteria is known as Methicillin-resistant Staphylococcus aureus (MRSA). According to the CDC, around two in every 100 people carry MRSA. Even though so many people carry MRSA bacteria in their nostrils, most will not develop serious MRSA infections (MRSA, n.d.) Methicillin-susceptible Staphylococcus aureus (MSSA) is a strain of staphylococcus that responds well to the medicines used to treat them because they are not resistant to certain antibiotics.
Staph infections are a concern for the medical community because it is especially dangerous for those who are immunocompromised, which is common for patients staying in a hospital setting. Some states, such as California, require by law that patients get tested for MRSA once admitted to the hospital for surgery and are considered susceptible for such an infection (MRSA Testing, n.d.). Some hospitals also screen patients for MRSA upon discharge from the hospital to make sure they do not take a MRSA strain home with them. Employees are tested periodically, as they are most likely to be carriers of the bacteria. This is important as it will help to prevent the spread of the bacteria.
The mannitol salt agar (MSA) test required the following materials: one Mannitol salt agar plate, a permanent marker/wax pencil, two sterile cotton swabs, and a parafilm. Using a permanent marker or wax pencil, the MSA plate was divided into two sections. One half was labeled ear while the other half was labeled nose to indicate the environments we swabbed. One sterile cotton swab was carefully removed from its wrapping, so it would not come into contact with any other object. It was then used to swab the mucous membranes inside the nostrils. The cotton swab was then rubbed over the surface of the agar plate labeled nose. Those same steps were repeated, only this time the ear was swabbed and placed over the section labeled ear. Used swabs were discarded in the waste bin and lids for the agar plates are secured on with the use of parafilm. The agar plate was placed in a 37 degrees Celsius room for 48 hours. The following lab day, the plates were examined for color and quality of growth.
The mannitol salt agar plate contains the sugar mannitol, sodium chloride, and the pH indicator phenol red. Phenol red turns yellow below a pH of 6.8, red at a pH between 7.4 and 8.4, and pink at a pH of 8.4 and above. Mannitol provides the substrate for fermentation and makes the medium differential. Sodium chloride makes the medium selective because its concentration is high enough to kill most bacteria. Staphylococci thrive on MSA because the environment is similar to that of the human skin, a place S. aureus adapted to survive. Phenol red serves as an indicator that will change color in the presence of fermentation with an acid end-product. While most staphylococci are able to grow on MSA, not all are able to ferment mannitol. The MSA plate will remain unchanged in those cases. S. aureus is capable of fermenting mannitol, so we can expect the pH on the medium to decrease, resulting in a yellow color change (Vital Source, n.d.).
I tested positive for S. aureus colonization in my ears indicated by a yellow color change on the MSA plate. I tested negative for S. aureus in my nose indicated by the lack of color change on the MSA plate. Since the color did not change, it is safe to say there were no bacteria present capable of fermenting the mannitol resulting in an acid end-product. The likely bacteria were Staphylococcus epidermis, since they thrived on the MSA plate but were unable to ferment the mannitol the way S. aureus can.
Nose and Ear Swab for S.
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