Category Archives: Ailmemts & Remedies

Dysphagia

Description:

Dysphagia is the medical term for the symptom of difficulty in swallowing. or it takes more time and effort to move food or liquid from your mouth to your stomach. Dysphagia may also be associated with pain. In some cases, swallowing may be impossible . It may be a sensation that suggests difficulty in the passage of solids or liquids from the mouth to the stomach, a lack of pharyngeal sensation or various other inadequacies of the swallowing mechanism. Dysphagia is distinguished from other symptoms including odynophagia, which is defined as painful swallowing, and globus, which is the sensation of a lump in the throat. A person can have dysphagia without odynophagia (dysfunction without pain), odynophagia without dysphagia (pain without dysfunction) or both together. A psychogenic dysphagia is known as phagophobia.

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Occasional difficulty swallowing, which may occur when you eat too fast or don’t chew your food well enough, usually isn’t cause for concern. But persistent dysphagia may indicate a serious medical condition requiring treatment. Dysphagia can occur at any age, but it’s more common in older adults. The causes of swallowing problems vary, and treatment depends on the cause.

Sign & Symptoms:
Signs and symptoms associated with dysphagia may include:
* Having pain while swallowing (odynophagia)
* Being unable to swallow
* Having the sensation of food getting stuck in the throat or chest or behind breastbone (sternum)
* Drooling
* Being hoarse
* Bringing food back up (regurgitation)
* Having frequent heartburn
* Having food or stomach acid back up into the throat
* Unexpectedly losing weight
* Coughing or gagging when swallowing
* Having to cut food into smaller pieces or avoiding certain foods because of trouble swallowing

Causes:
Swallowing is complex, and a number of conditions can interfere with this process. Sometimes the cause of dysphagia can’t be identified. However, the causes of dysphagia generally falls into one of the following categories.
1.Esophageal dysphagia
Esophageal dysphagia refers to the sensation of food sticking or getting hung up in the base of our throat or in our chest after we started to swallow. Some of the causes of esophageal dysphagia include:
* Achalasia. When our lower esophageal muscle (sphincter) doesn’t relax properly to let food enter our stomach, it may cause us to bring food back up into our throat. Muscles in the wall of our esophagus may be weak as well, a condition that tends to worsen over time.
* Diffuse spasm. This condition produces multiple high-pressure, poorly coordinated contractions of our esophagus, usually after we swallow. Diffuse spasm affects the involuntary muscles in the walls of our lower esophagus.
* Esophageal stricture. A narrowed esophagus (stricture) can trap large pieces of food. Tumors or scar tissue, often caused by gastroesophageal reflux disease (GERD), can cause narrowing.
* Esophageal tumors. Difficulty swallowing tends to get progressively worse when esophageal tumors are present.
* Foreign bodies. Sometimes food or another object can partially block our throat or esophagus. Older adults with dentures and people who have difficulty chewing their food may be more likely to have a piece of food become lodged in the throat or esophagus.
* Esophageal ring. A thin area of narrowing in the lower esophagus can intermittently cause difficulty swallowing solid foods.
* GERD. Damage to esophageal tissues from stomach acid backing up into our esophagus can lead to spasm or scarring and narrowing of our lower esophagus.
* Eosinophilic esophagitis. This condition, which may be related to a food allergy, is caused by an overpopulation of cells called eosinophils in the esophagus.
* Scleroderma. Development of scar-like tissue, causing stiffening and hardening of tissues, can weaken our lower esophageal sphincter, allowing acid to back up into our esophagus and cause frequent heartburn.
* Radiation therapy. This cancer treatment can lead to inflammation and scarring of the esophagus.

2. Oropharyngeal dysphagia
* Certain conditions can weaken our throat muscles, making it difficult to move food from our mouth into our throat and esophagus when  we  start to swallow.  we may choke, gag or cough when  we  try to swallow or have the sensation of food or fluids going down  our windpipe (trachea) or up  our nose. This may lead to pneumonia.

Causes of oropharyngeal dysphagia include:
*Neurological disorders. Certain disorders — such as multiple sclerosis, muscular dystrophy and Parkinson’s disease — can cause dysphagia.
* Neurological damage. Sudden neurological damage, such as from a stroke or brain or spinal cord injury, can affect  our ability to swallow.
* Pharyngoesophageal diverticulum (Zenker’s diverticulum). A small pouch that forms and collects food particles in our throat, often just above  our esophagus, leads to difficulty swallowing, gurgling sounds, bad breath, and repeated throat clearing or coughing.
* Cancer. Certain cancers and some cancer treatments, such as radiation, can cause difficulty swallowing.

Risk Factors &  complications

* The following are risk factors for dysphagia

* Aging. Due to natural aging and normal wear and tear on the esophagus and a greater risk of certain conditions, such as stroke or Parkinson’s disease, older adults are at higher risk of swallowing difficulties. But, dysphagia isn’t considered a normal sign of aging.

* Certain health conditions. People with certain neurological or nervous system disorders are more likely to experience difficulty swallowing.

The Complecations can be as follows:

  • Malnutrition, weight loss and dehydration. Dysphagia can make it difficult to take in adequate nourishment and fluids.
  • Aspiration pneumonia. Food or liquid entering your airway when you try to swallow can cause aspiration pneumonia, because the food can introduce bacteria to the lungs.
  • Choking. When food becomes impacted, choking can occur. If food completely blocks the airway, and no one intervenes with a successful Heimlich maneuver, death can occur.

Diagnosis:

The gold-standard of diagnosing dysphagia is to perform an instrumental evaluation, as the area of interest is not visible to the eye, and the person may not accurately sense the dysphagia or localize where the problem is.

One of the gold-standards for diagnosing oropharyngeal dysphagia is the modified barium swallow study (MBSS), also known as the videofluoroscopic swallow study (VFSS/fluoroscopy). This is a lateral and anterior-posterior (AP) view of a motion x-ray that provides objective information on the structure and physiology of the swallow. The oral, pharyngeal and esophageal phases of the swallow are analyzed. Oral phase components that are evaluated are: lip closure, bolus control, initiation of lingual movement, mastication, bolus transport, and oral residue after the swallow. Pharyngeal phase issues that are examined are: velopharyngeal closure, initiation of the pharyngeal swallow, laryngeal elevation, anterior hyoid movement, epiglottic inversion, laryngeal vestibule closure and reaction times, tongue base retraction, pharyngeal constriction or stripping wave, and pharyngeal residue after the swallow. The esophagus is analyzed for clearance versus retention of food, liquids and a barium pill. Any retention is monitored to see if it returns to the upper esophagus or back to the pharynx and airway. The clinician tests a variety of foods, liquids, and potentially a barium tablet. It is important to test a variety of viscosities and volumes. Typically the test involves a thin/regular liquid, a mildly thick/nectar thick liquid, a moderately thick/honey thick liquid, a pudding/puree, a cracker or cookie, a mixed consistency, and a barium pill taken with liquid or with a puree (depending on the person’s baseline method). The clinician determines if the swallow is safe (lack of aspiration) and efficient (lack of residue). The goal is to figure out why the person is having difficulty swallowing and to figure out what can be done to improve safety and efficiency. Sometimes regular liquids can easily cause aspiration, and the clinician can test various maneuvers, postures, and safe swallow strategies to prevent aspiration depending on that person’s specific anatomy and physiology. One method to potential improve the safety of the liquid bolus is to alter the consistency of bolus (i.e., thickening the liquid to mildly thick/nectar thick liquid, moderately thick/honey thick liquid, or extremely thick/pudding thick liquid). If there is a lot of residue after the swallow, there are also techniques that will be tested to reduce this. See treatment section below for more on compensatory strategies versus rehabilitation techniques for the swallow.

Another gold-standard for diagnosing dysphagia is the Fiberoptic Endoscopic Evaluation of Swallowing (FEES). This involves similar testing of foods and liquids, along with implementation of strategies to find out why the dysphagia is occurring and what can be done about it. The duration of the examination is not limited by radiation exposure; therefore, the person could be watched in a more natural environment over the course of a meal. The endoscope is very thin and usually well tolerated even without numbing the nose.

A barium swallow study/esophagram/upper GI study can best evaluate the entire esophagus. The barium is given in large volumes to fully distend and evaluate the esophageal lumen. This study can also evaluate for reflux, unlike the VFSS. A Zenker’s diverticulum can be seen on the VFSS and on an esophagram. The, barium may fills the pouch and then overflow, with food/liquid returning to the pharynx with risk for aspiration after the swallow. Achalasia is best evaluated on the barium swallow/esophagram, and it shows “bird-beak” tapering of distal esophagus, this is also described as a “rat’s tail” appearance. In esophageal strictures, liquid barium may remain above the stricture and then gradually trickles down. Strictures can sometimes be seen on a VFSS if the clinician suspects stricture or esophageal dysmotility. The clinician can scan down the esophagus after giving solid foods like cookie or bread. It is helpful to scan the esophagus on the VFSS as this is the exam that can test a full array of solids. The barium swallow/esophagram typically only tests barium liquids and a barium tablet.

* Esophagoscopy and laryngoscopy can give direct view of lumens.

* Chest radiograph may show air-fluid level in mediastinumPott’s disease and calcified aneurysms of aorta can be easily diagnosed.

* Esophageal motility study is useful in cases of achalasia and diffuse esophageal spasms.

* Exfoliative cytology can be performed on esophageal lavage obtained by esophagoscopy. It can detect malignant cells in early stage.

* Ultrasonography and CT scan are not very useful in finding cause of dysphagia; but can detect masses in mediastinum and aortic aneurysms.

* FEES (Fibreoptic endoscopic evaluation of swallowing), sometimes with sensory evaluation, is done usually by a Medical Speech Pathologist or Deglutologist. This procedure involves the patient eating different consistencies as above.

* Swallowing sounds and vibrations could be potentially used for dysphagia screening, but these approaches are in the early research stages.

Differential diagnosis:

All causes of dysphagia are considered as differential diagnoses. Some common ones are:

Esophageal dysphagia is almost always caused by disease in or adjacent to the esophagus but occasionally the lesion is in the pharynx or stomach. In many of the pathological conditions causing dysphagia, the lumen becomes progressively narrowed and indistensible. Initially only fibrous solids cause difficulty but later the problem can extend to all solids and later even to liquids. Patients with difficulty swallowing may benefit from thickened fluids if the person is more comfortable with those liquids, although, so far, there are no scientific study that proves that those thickened liquids are beneficial.

Dysphagia may manifest as the result of autonomic nervous system pathologies including stroke.  and ALS,   or due to rapid iatrogenic correction of an electrolyte imbalance.

Treatments:

There are many ways to treat dysphagia, such as swallowing therapy, dietary changes, feeding tubes, certain medications, and surgery. Treatment for dysphagia is managed by a group of specialists known as a multidisciplinary team. Members of the multidisciplinary team include: a speech language pathologist specializing in swallowing disorders (swallowing therapist), primary physician, gastroenterologist, nursing staff, respiratory therapist, dietitian, occupational therapist, physical therapist, pharmacist, and radiologist.  The role of the members of the multidisciplinary team will differ depending on the type of swallowing disorder present. For example, the swallowing therapist will be directly involved in the treatment of a patient with oropharyngeal dysphagia, while a gastroenterologist will be directly involved in the treatment of an esophageal disorder.

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Prevention:

Although swallowing difficulties can’t be prevented, you can reduce your risk of occasional difficulty swallowing by eating slowly and chewing your food well. Early detection and effective treatment of GERD can lower your risk of developing dysphagia associated with an esophageal stricture.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

 

Resources:

https://www.mayoclinic.org/diseases-conditions/dysphagia/symptoms-causes/syc-20372028

https://en.wikipedia.org/wiki/Dysphagia

 

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Nipah virus (NiV)

Description:
Nipah virus (NiV) infection is a newly emerging zoonosis that causes severe disease in both animals and humans. The natural host of the virus are fruit bats of the Pteropodidae Family, Pteropus genus.

NiV was first identified during an outbreak of disease that took place in Kampung Sungai Nipah, Malaysia in 1998. On this occasion, pigs were the intermediate hosts. However, in subsequent NiV outbreaks, there were no intermediate hosts. In Bangladesh in 2004, humans became infected with NiV as a result of consuming date palm sap that had been contaminated by infected fruit bats. Human-to-human transmission has also been documented, including in a hospital setting in India.

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NiV infection in humans has a range of clinical presentations, from asymptomatic infection to acute respiratory syndrome and fatal encephalitis. NiV is also capable of causing disease in pigs and other domestic animals. There is no vaccine for either humans or animals. The primary treatment for human cases is intensive supportive care.

Symptoms:
Human infections range from asymptomatic infection, acute respiratory infection (mild, severe), and fatal encephalitis. Infected people initially develop influenza-like symptoms of fever, headaches, myalgia (muscle pain), vomiting and sore throat. This can be followed by dizziness, drowsiness, altered consciousness, and neurological signs that indicate acute encephalitis. Some people can also experience atypical pneumonia and severe respiratory problems, including acute respiratory distress. Encephalitis and seizures occur in severe cases, progressing to coma within 24 to 48 hours.

The incubation period (interval from infection to the onset of symptoms) is believed to range between from 4-14 days. However an incubation period as long as 45 days has been reported.

Most people who survive acute encephalitis make a full recovery, but long term neurologic conditions have been reported in survivors. Approximately 20% of patients are left with residual neurological consequences such as seizure disorder and personality changes. A small number of people who recover subsequently relapse or develop delayed onset encephalitis.

The case fatality rate is estimated at 40% to 75%; however, this rate can vary by outbreak depending on local capabilities for epidemiological surveillance and clinical management.

Causes:
Nipah virus is an RNA virus that is part of the Paramyxovidae family that was first identified as a zoonotic pathogen after an outbreak involving severe respiratory illness in pigs and encephalitic disease in humans in Malaysia and Singapore in 1998 and 1999.

Nipah virus can cause a range of mild to severe disease in domestic animals such as pigs.

Nipah virus infection in humans causes a range of clinical presentations, from asymptomatic infection (subclinical) to acute respiratory infection and fatal encephalitis.

Nipah virus can be transmitted to humans from animals (bats, pigs), and can also be transmitted directly from human-to-human.

Fruit bats of the Pteropodidae family are the natural host of Nipah virus:-

Nipah virus (NiV) is an emerging zoonotic virus (a virus transmitted to humans from animals). In infected people, Nipah virus causes a range of illnesses from asymptomatic (subclinical) infection to acute respiratory illness and fatal encephalitis. NiV can also cause severe disease in animals such as pigs, resulting in significant economic losses for farmers.

Nipah virus is closely related to Hendra virus. Both are members of the genus Henipavirus, a new class of virus in the Paramyxoviridae family.

Although Nipah virus has caused only a few outbreaks, it infects a wide range of animals and causes severe disease and death in people, making it a public health concern.

Transmission:

NiV is a zoonotic virus (a virus transmitted to humans from animals). During the initial outbreaks in Malaysia and Singapore, most human infections resulted from direct contact with sick pigs or their contaminated tissues. Transmission is thought to have occurred via respiratory droplets, contact with throat or nasal secretions from the pigs, or contact with the tissue of a sick animal.

In the Bangladesh and India outbreaks, consumption of fruits or fruit products (e.g. raw date palm juice) contaminated with urine or saliva from infected fruit bats was the most likely source of infection.

Limited human to human transmission of NiV has also been reported among family and care givers of infected NiV patients. During the later outbreaks in Bangladesh and India, Nipah virus spread directly from human-to-human through close contact with people’s secretions and excretions. In Siliguri, India, transmission of the virus was also reported within a health-care setting (nosocomial), where 75% of cases occurred among hospital staff or visitors. From 2001 to 2008, around half of reported cases in Bangladesh were due to human-to-human transmission through providing care to infected patients.

Natural host: Fruit bats
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Fruit bats of the family Pteropodidae – particularly species belonging to the Pteropus genus – are the natural hosts for Nipah virus. There is no apparent disease in fruit bats.

It is assumed that the geographic distribution of Henipaviruses overlaps with that of Pteropus category. This hypothesis was reinforced with the evidence of Henipavirus infection in Pteropus bats from Australia, Bangladesh, Cambodia, China, India, Indonesia, Madagascar, Malaysia, Papua New Guinea, Thailand and Timor-Leste.

African fruit bats of the genus Eidolon, family Pteropodidae, were found positive for antibodies against Nipah and Hendra viruses, indicating that these viruses might be present within the geographic distribution of Pteropodidae bats in Africa.

Nipah virus in domestic animals:
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Nipah outbreaks in pigs and other domestic animals (horses, goats, sheep, cats and dogs) were first reported during the initial Malaysian outbreak in 1999.

Nipah virus is highly contagious in pigs. Pigs are infectious during the incubation period, which lasts from 4 to 14 days.

An infected pig can exhibit no symptoms, but some develop acute feverish illness, labored breathing, and neurological symptoms such as trembling, twitching and muscle spasms. Generally, mortality was low except in young piglets. These symptoms are not dramatically different from other respiratory and neurological illnesses of pigs. Nipah should be suspected if pigs also have an unusual barking cough or if human cases of encephalitis are present.

Diagnosis:
Initial signs and symptoms of NiV infection are non-specific and the diagnosis is often not suspected at the time of presentation. This can hinder accurate diagnosis and creates challenges in outbreak detection and institution of effective and timely infection control measures and outbreak response activities.

In addition, clinical sample quality, quantity, type, timing of collection and the time necessary to transfer samples from patients to the laboratory can affect the accuracy of laboratory results.

NiV infection can be diagnosed together with clinical history during the acute and convalescent phase of the disease. Main tests including real time polymerase chain reaction (RT-PCR) from bodily fluids as well as antibody detection via ELISA. Different tests include:

*Enzyme-linked immunosorbent assay (ELISA)
*Polymerase chain reaction (PCR) assay
*Virus isolation by cell culture.

Treatment:
There is no treatment or vaccine available for either people or animals. The primary treatment for humans is supportive care.

Prevention:
Nipah virus in domestic animals

Nipah outbreaks in pigs and other domestic animals (horses, goats, sheep, cats and dogs) were first reported during the initial Malaysian outbreak in 1999.

Nipah virus is highly contagious in pigs. Pigs are infectious during the incubation period, which lasts from 4 to 14 days.

An infected pig can exhibit no symptoms, but some develop acute feverish illness, labored breathing, and neurological symptoms such as trembling, twitching and muscle spasms. Generally, mortality was low except in young piglets. These symptoms are not dramatically different from other respiratory and neurological illnesses of pigs. Nipah should be suspected if pigs also have an unusual barking cough or if human cases of encephalitis are present.

Reducing the risk of bat-to-human transmission: Efforts to prevent transmission should first focus on decreasing bat access to date palm sap and to other fresh food products. Keeping bats away from sap collection sites with protective coverings (e.g., bamboo sap skirts) may be helpful.Freshly collected date palm juice should be boiled and fruits should be thoroughly washed and peeled before consumption.

Reducing the risk of animal-to-human transmission: Gloves and other protective clothing should be worn while handling sick animals or their tissues, and during slaughtering and culling procedures. As much as possible, people should avoid being in contact with infected pigs.

Reducing the risk of human-to-human transmission: Close unprotected physical contact with Nipah virus-infected people should be avoided. Regular hand washing should be carried out after caring for or visiting sick people.

Controlling infection in health-care settings:
___________________________________________________________

Health-care workers caring for patients with suspected or confirmed NiV infection, or handling specimens from them, should implement standard infection control precautions for all patients at all times.

As human-to-human transmission in particular nosocomial transmission have been reported, contact and droplet precautions should be used in addition to standard precautions.

Samples taken from people and animals with suspected NiV infection should be handled by trained staff working in suitably equipped laboratories.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.who.int/csr/disease/nipah/en/
https://en.wikipedia.org/wiki/Henipavirus
http://www.who.int/news-room/fact-sheets/detail/nipah-virus

Dysthymia

Other Name: Persistent Depressive Disorder (PDD)

Description:
Dysthymia is a serious state of chronic depression, which persists for at least two years (one year for children and adolescents). Dysthymia is less acute and severe than major depressive disorder. As dysthymia is a chronic disorder, sufferers may experience symptoms for many years before it is diagnosed, if diagnosis occurs at all. As a result, they may believe that depression is a part of their character, so they may not even discuss their symptoms with doctors, family members or friends.

Dysthymia often co-occurs with other mental disorders. A “double depression” is the occurrence of episodes of major depression in addition to dysthymia. Switching between periods of dysthymic moods and periods of hypomanic moods is indicative of cyclothymia, which is a mild variant of bipolar disorder.

In the DSM-5, dysthymia is replaced by persistent depressive disorder. This new condition includes both chronic major depressive disorder and the previous dysthymic disorder. The reason for this change is that there was no evidence for meaningful differences between these two conditions.

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Symptoms:
Dysthymia characteristics include an extended period of depressed mood combined with at least two other symptoms which may include insomnia or hypersomnia, fatigue or low energy, eating changes (more or less), low self-esteem, or feelings of hopelessness. Poor concentration or difficulty making decisions are treated as another possible symptom. Mild degrees of dysthymia may result in people withdrawing from stress and avoiding opportunities for failure. In more severe cases of dysthymia, people may even withdraw from daily activities. They will usually find little pleasure in usual activities and pastimes.

The main symptoms of PDD are similar to those of depression. However, the key difference is that PDD is chronic, with symptoms occurring on most days for at least two years.

These symptoms include:

*Persistent feelings of sadness and hopelessness
*Sleep problems
*Low energy
*A change in appetite
*Difficulty concentrating
*Indecisiveness
*A lack of interest in daily activities
*Decreased productivity
*Poor self-esteem
*A negative attitude
*Avoidance of social activities

The symptoms of PDD often begin to appear during childhood or adolescence. Children and teens with PDD may appear to be irritable, moody, or pessimistic over an extended period. They may also display behavior problems, poor performance at school, and difficulty interacting with other children in social situations. Their symptoms may come and go over several years, and the severity of them may vary over time.

Causes:
There are no known biological causes that apply consistently to all cases of dysthymia, which suggests diverse origin of the disorder. However, there are some indications that there is a genetic predisposition to dysthymia: “The rate of depression in the families of people with dysthymia is as high as fifty percent for the early-onset form of the disorder”. Other factors linked with dysthymia include stress, social isolation, and lack of social support.

The main causes may include:

*A chemical imbalance in the brain
*A family history of the condition
*A history of other mental health conditions, such as anxiety or bipolar disorder
*Stressful or traumatic life events, such as the loss of a loved one or financial problems
*Chronic physical illness, such as heart disease or diabetes
*Physical brain trauma, such as a concussion

In a study using identical and fraternal twins, results indicated that there is a stronger likelihood of identical twins both having depression than fraternal twins. This provides support for the idea that dysthymia is in part caused by heredity.
Diagnosis:
The Diagnostic and Statistical Manual of Mental Disorders IV (DSM-IV), published by the American Psychiatric Association, characterizes dysthymic disorder. The essential symptom involves the individual feeling depressed for the majority of days, and parts of the day, for at least two years. Low energy, disturbances in sleep or in appetite, and low self-esteem typically contribute to the clinical picture as well. Sufferers have often experienced dysthymia for many years before it is diagnosed. People around them often describe the sufferer in words similar to “just a moody person”. Note the following diagnostic criteria:

During a majority of days for two years or more, the adult patient reports depressed mood, or appears depressed to others for most of the day.

When depressed, the patient has two or more of:

*Decreased or increased appetite
*Decreased or increased sleep (insomnia or hypersomnia)
*Fatigue or low energy
*Reduced self-esteem
*Decreased concentration or problems making decisions
*Feelings of hopelessness or pessimism
*During this two-year period, the above symptoms are never absent longer than two consecutive months.
*During the duration of the two-year period, the patient may have had a perpetual major depressive episode.
*The patient has not had any manic, hypomanic, or mixed episodes.
*The patient has never fulfilled criteria for cyclothymic disorder.
*The depression does not exist only as part of a chronic psychosis (such as schizophrenia or delusional disorder).
*The symptoms are often not directly caused by a medical illness or by substances, including drug abuse or other medications.
*The symptoms may cause significant problems or distress in social, work, academic, or other major areas of life functioning.

In children and adolescents, mood can be irritable, and duration must be at least one year, in contrast to two years needed for diagnosis in adults.

Early onset (diagnosis before age 21) is associated with more frequent relapses, psychiatric hospitalizations, and more co-occurring conditions. For younger adults with dysthymia, there is a higher co-occurrence in personality abnormalities and the symptoms are likely chronic.[citation needed] However, in older adults suffering from dysthymia, the psychological symptoms are associated with medical conditions and/or stressful life events and losses.

Dysthymia can be contrasted with major depressive disorder by assessing the acute nature of the symptoms. Dysthymia is far more chronic (long lasting) than major depressive disorder, in which symptoms may be present for as little as 2 weeks. Also Dysthymia often presents itself at an earlier age than Major Depressive Disorder.

Treatments:
Often, people with dysthymia will seek out treatment not necessarily because of depressed mood, but rather due to increasing levels of stress or because of personal difficulties that may be situation-related. This is hypothesized to be because of the chronic nature of the disorder, and how depressed mood is often thought to be a characterological pattern for the individual with the condition. Thus, it is only when the person experiences increasing stress that he or she thinks to go to some sort of trained professional for symptom relief. It is usually through the administration of the Structured Clinical Interview for DSM-IV that dysthymia is first diagnosed. At this point, with the help of a trained professional, a certain line of treatment is often discussed and then selected. It is important to consider all factors in the person’s life that may be affected when deciding on a particular course of treatment. Additionally, if one method of treatment does not particularly work for a certain individual, it may be helpful to try something else.

Therapy:
Psychotherapy is often effective in treating dysthymia. Different modalities have been shown to be beneficial. Empirically-based treatments, such as cognitive-behavioral therapy, have been researched to show that through the proper course of treatment, symptoms can dissipate over time. Other forms of talk-therapy (e.g. psychodynamic psychotherapy, interpersonal psychotherapy) have also been said to be effective in treating the disorder. It may be helpful for people diagnosed with dysthymia to develop better coping skills, search for the root cause of symptoms, and work on changing faulty beliefs (such as when patients believe themselves to be worthless).

In addition to individual psychotherapy, both group psychotherapy and self-help, or support groups, can be an effective line of treatment for dysthymia as well. Through these treatment modalities, issues such as self-esteem, self-confidence, relationship issues/patterns, assertiveness skills, cognitive restructuring, etc., can be worked through and strengthened.

Medications:
The first line of pharmacotherapy is usually SSRIs due to their more tolerable nature and reduced side effects compared to the irreversible monoamine oxidase inhibitors or tricyclic antidepressants. Studies have found that the mean response to antidepressant medications for people with dysthymia is 55%, compared with a 31% response rate to a placebo. The most commonly prescribed antidepressants/SSRIs for dysthymia are escitalopram, citalopram, sertraline, fluoxetine, paroxetine, and fluvoxamine. It often takes an average of 6–8 weeks before the patient begins to feel these medications’ therapeutic effects. Additionally, multi-clinic governmental study, found that people with overall depression will generally need to try different brands of medication before finding one that works specifically for them. Research shows that 1 in 4 of those who switch medications get better results regardless of whether the second medication is an SSRI or some other type of antidepressant.

In a meta-analytic study from 2005, it was found that SSRIs and TCAs are equally effective in treating dysthymia. They also found that MAOIs have a slight advantage over the use of other medication in treating this disorder. However, the author of this study cautions that MAOIs should not necessarily be the first line of defense in the treatment of dysthymia, as they are often less tolerable than their counterparts, such as SSRIs.

Tentative evidence supports the use of amisulpride to treat dysthymia but with increased side effects.

Combination treatment:
A combination of antidepressant medication and psychotherapy has consistently been shown to be the most effective line of treatment for people diagnosed with dysthymia. Working with a psychotherapist to address the causes and effects of the disorder, in addition to taking antidepressants to help eliminate the symptoms, can be extremely beneficial. This combination is often the preferred method of treatment for those who have dysthymia. Looking at various studies involving treatment for dysthymia, 75% of people responded positively to a combination of cognitive behavioral therapy (CBT) and pharmacotherapy, whereas only 48% of people responded positively to just CBT or medication alone.

In a meta-analytic study from 2008, researchers found an effect size of ?.07 (Cohen’s d) between pharmacologic treatments and psychological treatments for depressive disorders, suggesting pharmacologic treatments to be slightly more effective, though the results were not found to be statistically significant. This small effect is true only for SSRIs, with TCAs and other pharmacologic treatments showing no differences from psychological treatments. Additionally, there have been several studies yielding results that indicate that severe depression responds more favorably to psychotherapy than pharmacotherapy.

Resistance:
Because of dysthymia’s chronic nature, treatment resistance is somewhat common. In such a case, augmentation is often recommended. Such treatment augmentations can include lithium pharmacology, thyroid hormone augmentation, amisulpride, buspirone, bupropion, stimulants, and mirtazapine. Additionally, if the person also suffers from seasonal affective disorder, light therapy can be useful in helping augment therapeutic effects.

Regular Yoga exercise with meditation under a trained & experienced teacher helps a lot to recover substantially  & sometimes permanently.

Prevention:
Though there is no clear-cut way to prevent dysthymia from occurring, some suggestions may have been made. Since dysthymia will often first occur in childhood, it is important to identify children who may be at risk. It may be beneficial to work with children in helping to control their stress, increase resilience, boost self-esteem, and provide strong networks of social support. These tactics may be helpful in warding off or delaying dysthymic symptoms.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
https://en.wikipedia.org/wiki/Dysthymia
https://www.healthline.com/health/dysthymia

Clostridium difficile (C-Diff)

Description:
Clostridium difficile infection (CDI or C-dif) is a symptomatic infection due to the spore-forming bacterium, Clostridium difficile. Symptoms include watery diarrhea, fever, nausea, and abdominal pain. It makes up about 20% of cases of antibiotic-associated diarrhea. Complications may include pseudomembranous colitis, toxic megacolon, perforation of the colon, and sepsis.

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Clostridium difficile infection is spread by bacterial spores found within feces. Surfaces may become contaminated with the spores with further spread occurring via the hands of healthcare workers. Risk factors for infection include antibiotic or proton pump inhibitors use, hospitalization, other health problems, and older age. Diagnosis is by stool culture or testing for the bacteria’s DNA or toxins. If a person tests positive but has no symptoms, the condition is known as C. difficile colonization rather than an infection.

C. difficile infections occur in all areas of the world. About 453,000 cases occurred in the United States in 2011, resulting in 29,000 deaths. Rates of disease globally have increased between 2001 and 2016. Women are more often affected than men. The bacterium was discovered in 1935 and found to be disease-causing in 1978. In the United States, health–care associated infections increase the cost of care by US$1.5 billion each year.

Symptoms:
Many people have C diff living in their intestines and the bacteria doesn’t cause any problems for them. When kept in check by other good bacteria, C diff can cause no symptoms. However, when something (most often antibiotic usage) throws off the balance of bacteria in the body then this is when a problem can occur and C diff can start growing rapidly.

C. difficile bacteria can release toxins that attack the lining of the colon by not only destroying cells, but also creating patches of inflammatory cells that cause watery diarrhea.

Symptoms of overgrowth C diff can include:
*Watery diarrhea (at least three bowel movements per day for two days or longer)
*Appetite loss
*Nausea
*Fever
*Abdominal pain and/or tenderness

Symptoms of severe C diff infection can include:

*Watery diarrhea 10 to 15 times a day
*Abdominal cramping and pain, which may be severe
*Swollen abdomen
*Nausea
*Loss of appetite
*Pus or blood in the stool
*Fever
*Rapid heart rate
*Dehydration
*Weight loss
*Increased white blood cell count
*Kidney failure

Couses:
A C diff infection is caused by C diff bacteria. C. difficile bacteria can be found in several common places including human and animal feces as well as soil, air and water. The bacteria can also be found in some foods such as processed meat. The human intestines have somewhere around 100 trillion bacterial cells and up to 2,000 different kinds of bacteria. Much of this bacteria is good because it keeps possibly problematic bacteria in check and guards the body against infection. According to Mayo Clinic, “A small number of healthy people naturally carry the bacteria in their large intestine and don’t have ill effects from the infection.”

Risk Factors:
Antibiotics:
C. difficile colitis is associated most strongly with the use of these antibiotics: fluoroquinolones, cephalosporins, and clindamycin.

Some research suggests the routine use of antibiotics in the raising of livestock is contributing to outbreaks of bacterial infections such as C. difficile.[20]

Healthcare environment:
People are most often infected in hospitals, nursing homes, or other medical institutions, although infection outside medical settings is increasing. Individuals can develop the infection if they touch objects or surfaces that are contaminated with feces and then touch their mouth or mucous membranes. Healthcare workers could possibly spread the bacteria to patients or contaminate surfaces through hand contact. The rate of C. difficile acquisition is estimated to be 13% in patients with hospital stays of up to two weeks, and 50% with stays longer than four weeks.

Long-term hospitalization or residence in a nursing home within the previous year are independent risk factors for increased colonization.

Acid suppression medication:
Increasing rates of community-acquired CDI are associated with the use of medication to suppress gastric acid production: H2-receptor antagonists increased the risk 1.5-fold, and proton pump inhibitors by 1.7 with once-daily use and 2.4 with more than once-daily use.

Elemental diet:
As a result of suppression of healthy bacteria, via a loss of bacterial food source, prolonged use of an elemental diet elevates the risk of developing C. difficile infection.

Diagnosis:
Prior to the advent of tests to detect C. difficile toxins, the diagnosis most often was made by colonoscopy or sigmoidoscopy. The appearance of “pseudomembranes” on the mucosa of the colon or rectum is highly suggestive, but not diagnostic of the condition. The pseudomembranes are composed of an exudate made of inflammatory debris, white blood cells. Although colonoscopy and sigmoidoscopy are still employed, now stool testing for the presence of C. difficile toxins is frequently the first-line diagnostic approach. Usually, only two toxins are tested for—toxin A and toxin B—but the organism produces several others. This test is not 100% accurate, with a considerable false-negative rate even with repeat testing.

Toxin ELISA:
Assessment of the A and B toxins by enzyme-linked immunosorbent assay (ELISA) for toxin A or B (or both) has a sensitivity of 63–99% and a specificity of 93–100%.

Previously, experts recommended sending as many as three stool samples to rule out disease if initial tests are negative, but evidence suggests repeated testing during the same episode of diarrhea is of limited value and should be discouraged. C. difficile toxin should clear from the stool of previously infected patients if treatment is effective. Many hospitals only test for the prevalent toxin A. Strains that express only the B toxin are now present in many hospitals, however, so testing for both toxins should occur. Not testing for both may contribute to a delay in obtaining laboratory results, which is often the cause of prolonged illness and poor outcomes.

Other stool tests:
Stool leukocyte measurements and stool lactoferrin levels also have been proposed as diagnostic tests, but may have limited diagnostic accuracy.

PCR:
Testing of stool samples by real-time polymerase chain reaction is able to pick up the disease about 90% of the time and when positive is incorrectly positive about 4% of the time. Multistep PCR testing algorithms can improve overall performance. Repeat testing may be misleading, and testing specimens more than once every seven days in patients without new symptoms is highly unlikely to yield useful information.

Treatments:
Carrying C. difficile without symptoms is common. Treatment in those without symptoms is controversial. In general, mild cases do not require specific treatment. Oral rehydration therapy is useful in treating dehydration associated with the diarrhea.

According to the CDC: “Whenever possible, other antibiotics should be discontinued; in a small number of patients, diarrhea may go away when other antibiotics are stopped. Treatment of primary infection caused by C. difficile is an antibiotic such as metronidazole, vancomycin, or fidaxomicin. While metronidazole is not approved for treating C. difficile infections by the FDA, it has been commonly recommended and used for mild C. difficile infections; however, it should not be used for severe C. difficile infections. Whenever possible, treatment should be given by mouth and continued for a minimum of 10 days.”

Another important fact that the CDC points out is that when antibiotics are used to treat a primary C diff infection, the infection ends up coming back in around 20 percent or a fifth of patients. Even worse, for some C diff patients, the infection doesn’t just come back once, but again and again. You can imagine how difficult that must be on a person’s body. When the infection comes back the first time, the same antibiotic is typically used, but if the infection comes back more than once then stronger antibiotics are employed.

Natural Treatments:
*Stop Antibiotics Whenever Possible

*Load Up On Good Bacteria
Also get lots of probiotic-rich foods from your diet that will help to balance the intestinal flora and fight C diff. Some top probiotic foods to consume regularly: cultured dairy products (such as kefir, goat milk yogurt or cultured probiotic yogurt made from raw cow’s milk), raw apple cider vinegar, fermented vegetables (sauerkraut, kimchi, kvass) and probiotic beverages (kombucha and coconut kefir). To get the most out of apple cider vinegar, make sure to buy a raw variety with the “mother” intact, which means it still contains all its beneficial compounds including probiotics.

*Avoid or Reduce Certain Foods
According to the C Diff Foundation, there are some of the foods most people find helpful to avoid during a C Diff infection. For example dairy products,greasy, fatty foods and processed foods,some foods that are definitely healthy but may cause extra bloating, gas and discomfort,raw fruits and veggies,Processed fat-free foods like Olestra,spicy foods and large quantities of caffeine.

*Thorough Hand Washing

*Consume Natural Antibiotics like manuka honey,raw garlic, and oil of Oregano.

Prevention:

Prevention is by limiting antibiotic use, hand washing, and terminal room cleaning in hospital. Discontinuation of antibiotics may result in resolution of symptoms within three days in about 20% of those infected. Often the antibiotics metronidazole, vancomycin or fidaxomicin will cure the infection. Retesting after treatment, as long as the symptoms have resolved, is not recommended, as the person may remain colonized. Recurrences have been reported in up to 25% of people. Some tentative evidence indicates fecal microbiota transplantation and probiotics may decrease the risk of recurrence.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
https://en.wikipedia.org/wiki/Clostridium_difficile_infection#Role_in_disease
https://draxe.com/c-diff/

Campylobacteriosis (Campylobacter Infection)

Description:
Campylobacteriosis is an infection by the Campylobacter bacterium, most commonly C. jejuni. It is among the most common bacterial infections of humans, often a foodborne illness. It produces an inflammatory, sometimes bloody, diarrhea or dysentery syndrome, mostly including cramps, fever and pain.

It is usually contracted through poorly handled food. Actually, it’s one reason why one should carefully handle raw meat to avoid contamination and make sure meat is cooked to proper temperatures.

The Campylobacter bacteria is commonly known as a foodborne pathogen that may also be in the feces of animals carrying the bacteria. In addition to chicken and other poultry, the pathogen has been found in cattle, pigs, sheep, ostriches, shellfish, cats and dogs.

While many people are able to ride out these relatively mild infections, young children, the elderly and those with suppressed immune systems are at a greater risk for complications and even death.

Campylobacter infections are not contagious, at least in the traditional sense of airborne germs going from one human to another.

Rather, campylobacteriosis is what’s known as a zoonosis, meaning a disease that occurs as a result of contact with contaminated animal products (meat, milk, etc.).

The only way to contract an infection caused by Campylobacter from another human or an infected live animal (such as a pet) would be to come in contact with its feces.

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Symptoms:
The prodromal symptoms are fever, headache, and myalgia, which can be severe, lasting as long as 24 hours. After 1–5 days, typically, these are followed by diarrhea (as many as 10 watery, frequently bloody, bowel movements per day) or dysentery, cramps, abdominal pain, and fever as high as 40 °C (104 °F). In most people, the illness lasts for 2–10 days. It is classified as invasive/inflammatory diarrhea, also described as bloody diarrhea or dysentery.

There are other diseases showing similar symptoms. For instance, abdominal pain and tenderness may be very localized, mimicking acute appendicitis. Furthermore, Helicobacter pylori is closely related to Campylobacter and causes peptic ulcer disease.

Causes:
Campylobacteriosis is caused by Campylobacter bacteria (curved or spiral, motile, non–spore-forming, Gram-negative rods). The disease is usually caused by C. jejuni, a spiral and comma shaped bacterium normally found in cattle, swine, and birds, where it is nonpathogenic, but the illness can also be caused by C. coli (also found in cattle, swine, and birds), C. upsaliensis (found in cats and dogs) and C. lari (present in seabirds in particular).

One effect of campylobacteriosis is tissue injury in the gut. The sites of tissue injury include the jejunum, the ileum, and the colon. C jejuni appears to achieve this by invading and destroying epithelial cells.

C. jejuni can also cause a latent autoimmune effect on the nerves of the legs, which is usually seen several weeks after a surgical procedure of the abdomen. The effect is known as an acute idiopathic demyelinating polyneuropathy (AIDP), i.e. Guillain–Barré syndrome, in which one sees symptoms of ascending paralysis, dysaesthesias usually below the waist, and, in the later stages, respiratory failure.

Some strains of C jejuni produce a cholera-like enterotoxin, which is important in the watery diarrhea observed in infections. The organism produces diffuse, bloody, edematous, and exudative enteritis. In a small number of cases, the infection may be associated with hemolytic uremic syndrome and thrombotic thrombocytopenic purpura through a poorly understood mechanism.

Complications:
Complications include toxic megacolon, dehydration and sepsis. Such complications generally occur in young children (< 1 year of age) and immunocompromised people. A chronic course of the disease is possible; this disease process is likely to develop without a distinct acute phase. Chronic campylobacteriosis features a long period of sub-febrile temperature and asthenia; eye damage, arthritis, endocarditis may develop if infection is untreated.

Occasional deaths occur in young, previously healthy individuals because of blood volume depletion (due to dehydration), and in persons who are elderly or immunocompromised.

Some individuals (1–2 in 100,000 cases) develop Guillain–Barré syndrome, in which the nerves that join the spinal cord and brain to the rest of the body are damaged, sometimes permanently. This occurs only with infection of C. jejuni and C. upsaliensis.

Other factors:
In patients with HIV, infections may be more frequent, may cause prolonged bouts of dirty brown diarrhea, and may be more commonly associated with bacteremia and antibiotic resistance. In participants of unprotected anal intercourse, campylobacteriosis is more localized to the distal end of the colon and may be termed a proctocolitis. The severity and persistence of infection in patients with AIDS and hypogammaglobulinemia indicates that both cell-mediated and humoral immunity are important in preventing and terminating infection.

Diagnosis:
Campylobacter organisms can be detected by performing a Gram stain of a stool sample with high specificity and a sensitivity of ~60%, but are most often diagnosed by stool culture. Fecal leukocytes should be present and indicate the diarrhea to be inflammatory in nature. Methods currently being developed to detect the presence of campylobacter organisms include antigen testing via an EIA or PCR.

Treatment:
The infection is usually self-limiting, and in most cases, symptomatic treatment by liquid and electrolyte replacement is enough in human infections.

Antibiotics:
Antibiotic treatment only has a marginal effect on the duration of symptoms, and its use is not recommended except in high-risk patients with clinical complications.

Erythromycin can be used in children, and tetracycline in adults. Some studies show, however, that erythromycin rapidly eliminates Campylobacter from the stool without affecting the duration of illness. Nevertheless, children with dysentery due to C. jejuni benefit from early treatment with erythromycin. Treatment with antibiotics, therefore, depends on the severity of symptoms. Quinolones are effective if the organism is sensitive, but high rates of quinolone use in livestock means that quinolones are now largely ineffective.

Antimotility agents, such as loperamide, can lead to prolonged illness or intestinal perforation in any invasive diarrhea, and should be avoided. Trimethoprim/sulfamethoxazole and ampicillin are ineffective against Campylobacter.

In animals:
In the past, poultry infections were often treated by mass administration of enrofloxacin and sarafloxacin for single instances of infection. The FDA banned this practice, as it promoted the development of fluoroquinolone-resistant populations. A major broad-spectrum fluoroquinolone used in humans is ciprofloxacin.

Currently growing resistance of the Campylobacter to fluoroquinolones and macrolides is of a major concern.

In the meantime, it can be useful to use antibacterial essential oils to fight Campylobacter infection. Thyme oil, clove oil, orange oil and bergamot oil have all been found to have bacteria-killing benefits against Campylobacter.

When using essential oils, be careful to follow safety instructions. For example, with bergamot oil, monitor your blood sugar if you have diabetes, as it may affect these levels. Clove oil shouldn’t be taken internally for more than two weeks, and thyme oil is not safe for pregnant women or people with high blood pressure or epilepsy.

Prevention:
The number one preventive measure for Campylobacter infections is to use safe food preparation methods and thoroughly cook all your food. Less than 500 Campylobacter germs are required to infect your body, which means it could happen with as little as one drop of juice from raw chicken.

Because it’s possible to contract this infection from a sick pet, do your best to adopt animals that are happy and alert. Sluggishness, abnormal eating and diarrhea can be early signs of infection in dogs and cats. See a veterinarian within a short period of time after adopting an animal to make sure the animal is in optimal health, and always keep the pet’s living area as clean as possible.

Prognosis:
Campylobacteriosis is usually self-limited without any mortality (assuming proper hydration is maintained). However, there are several possible complications.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
https://en.wikipedia.org/wiki/Campylobacteriosis
https://draxe.com/campylobacter/