Saethre- Chotzen Syndrome

                             Saethre- Chotzen Syndrome

   Saether-Chotzen syndrome is a rare type of craniosynostosis- the early closing of one or more of the soft, fibrous seams(sutures) between the skull bone. When a suture closes too early, a baby skull cannot grow correctly.

  Saethre-Chotzen syndrome is a genetic condition characterized by the premature fusion of certain skull bones. This early fusion prevents the skull from growing normally and affects the shape and symmetry of the head and face.  Other features may include webbing of certain fingers or toes, small or unusually shaped ears, short stature, and abnormalities of the bones in the spine (the vertebrae). The signs and symptoms of Saethre- Chotzen syndrome vary from the TWIST1 gene cause most cases of Saethre- Chotzen syndrome. The condition is inherited in an autosomal dominant pattern. In some cases, an affected person inherits the mutation from one affected parent. Other cases may result from new mutations in the gene. 

   Treatment is aimed at addressing the symptoms found in each individual and may require the coordinated efforts of a team of specialists. Surgery is often needed to prevent or correct early closure of the cranial sutures and correct certain craniofacial abnormalities, syndactyly, and/or skeletal defects. 

Causes:

  Most cases of Saethre-Chotzen syndrome are caused by mutations in the TWIST1 gene. The TWIST1 gene provides instructions for making a protein that plays an important role in early development.

   This protein is a transcription factor, which means that it attaches to a specific region of DNA and helps control the activity of particular genes. The TWIST1 protein is active in cells that give rise to bones, muscles, and other tissues in the head and face. It is also involved in the development of the limbs. Mutations in the TWIST1 gene prevent one copy of the gene in each cell from making any functional protein. A shortage of the TWIST1 protein affects the development and maturation of cells in the skull, face, and limbs. These abnormalities underline the signs and symptoms of Saethre- Chotzen syndrome, including the premature fusion of certain skull bones. 

    A small number of cases of Saethre-Chotzen syndrome have resulted from a structural chromosomal abnormality, such as a deletion or rearrangement of genetic material, in the region of chromosome 7 that contains the TWIST1 gene. When Saethre-Chotzen syndrome is caused by a chromosomal deletion instead of a mutation within the TWIST1 gene, affected children are much more likely to have intellectual disability, developmental delay, and learning difficulties. 

Signs and Symptoms: 

  SCS presents in a variable fashion. The majority of individuals with SCS are moderately affected, with uneven facial features and a relatively flat face due to underdeveloped eye sockets, cheekbones, and lower jaw. In addition to the physical abnormality, people with SCS also experience growth delays, which results in relatively short stature. Although most individuals with SCS are of normal intelligence, some Individuals may have mild to moderate mental delays. More Severe Cases of SCS, with more serious facial deformities, occur when multiple cranial sutures close prematurely. 

Cranial defects: 

- Flat, asymmetric head and face

- Head is typically cone-shaped (acrocephaly) or flat (brachycephaly) but can also be long and narrow (Dolichocephaly). 

- Head is short from front to back

- Lopsided face 

- Low set hairline causing the forehead to appear tall and wide 

Defects of the hands and feet:

 - Webbing between the second and third finger and between the second and third toes

- Short fingers and toes

- Broad thumb and or a broad hallux with a valgus deformity. 

- Hands have a single palmar flexion crease

Ocular defects:

- Unevenly positioned eyes that may be crossed(strabismus) or wide-set(hypertelorism) 

- Vision problems due to abnormal facial anatomy, which causes mechanical disturbances of the extraocular muscles, resulting in strabismus(crossed eyes)

- Tear duct stenosis(narrowing of the tear duct)

- Drooping eyelids

- Downward slanting palpebral fissures(separation between upper and lower eyelids)

- Nearsightedness

- Epicanthal folds (skin folds of the upper eyelid covering the inner corner of the eye)

- Blepharophimosis(bilateral ptosis with reduced size of the eye)

- Optic atrophy

- Refractory errors 

Ear, Nose, and mouth defects:

 -Small, low-set ears that may be rotated somewhat backward and has a prominent(bulging) pinna.

- Beaked nose(slightly bent downward at the tip) that is slightly off-center and contains a deviated septum

- Malocclusion is associated with dental abnormalities including enamel hypoplasia(thin enamel due to incomplete formation), Hyperdontia (extra teeth), and peg teeth(small, abnormality shaped teeth)

- Cleft palate with a high arch

Less common defects:

- Short stature

- Vertebral fusion

- Congenital heart problems

- Speech problems

- Anal atresia (malformed rectum)

- Undescended testes (cryptorchidism)

- Renal kidney abnormality

- Personality disorders 

Inheritance:

 Saethre-Chptzen syndrome is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In some cases, an affected person inherited the mutation from one affected parent. Other cases may result from new mutations in the end. These cases occur in people with no history of the disorder in their families. Each child of an individual with Sarthre- Chotzen syndrome has a 50% chance of inheriting the mutation. 

Diagnosis:

      Making a diagnosis for a genetic or rare disease can often be challenging. Healthcare professionals typically look at t person's medical history, symptoms, physical exam, and laboratory test results in order to make a diagnosis. The following resources provide information relating to diagnosis and testing for this condition. If you have questions about getting a diagnosis, you should contact a healthcare professional. 

Testing:

 The genetic testing registry(GTR) provides information about the genetic tests for this condition. The intended audience for the GTR is health care providers and researchers. Patients and consumers with specific questions about a genetic test should contact a health care provider or a genetic professional. 

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Nipah Virus(Nipah Henipavirus)

                                                Nipah Virus

       Nipah virus (NiV) is a zoonotic virus it is transmitted from animals to humans and can also be transmitted through contaminated food or directly between people. In infected people, it causes a range of illnesses from asymptomatic infection to acute respiratory illness and fatal encephalitis. The virus can also cause severe disease in animals such as pigs, resulting in significant economic losses for farmers. 

      Nipah virus, scientific name Nipah Henipavirus, is a bat-borne virus that causes Nipah Virus infection in humans and other animals, a disease with a high mortality rate. Numerous disease outbreaks caused by the Nipah virus have occurred in south and southeast Asia. Nipah Virus belongs to the genus Henipavirus along with the Hendra virus, which has also caused disease outbreaks. 

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

Transmission:

     During the first recognized outbreak in Malaysia, which also affected Singapore, most human infections resulted from direct contact with sick pigs or their contaminated tissues. Transmission is thought to have occurred via unprotected exposure to secretions from the pigs, or unprotected contact with the tissue of a sick animal. 

    In subsequent outbreaks in Bangladesh and India, consumption of fruits or fruit products contaminated with urine or saliva from infected fruit bats was the most likely source of infection. 

    During the later outbreaks in Bangladesh a d India, Nipah virus spread directly from Human - to humans through close contact with people's secretions and excretions. Transmission of the virus was also reported within a healthcare setting, where 75% of cases occurred among hospital staff or visitors. Around half of reported cases in Bangladesh were die to the human-to-human transmission through providing care to infected patients. 

Signs and symptoms:

      Human infections range from asymptomatic infection to acute respiratory infection (mild, severe) and fatal encephalitis. 

     Infected people initially develop symptoms including fever, headaches, myalgia, 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 is believed to range from 4 to 14 days. However, an incubation period as long as 45 days have been reported.  

     Most people who survive acute encephalitis make a full recovery, but long-term neurological conditions have been reported in survivors. Approximately 20% of patients are left with residential 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%. This rate can vary by outbreak depending on local capabilities for epidemiological surveillance and clinical management. 

 - Fever

- Headache 

- Muscle Pain(Myalgia)

- Vomiting

- Sore Throat

 These symptoms can be followed by more serious conditions including: 

 - Dizziness

- Altered consciousness

- Acute encephalitis

- Atypical Pneumonia

- Severe Respiratory

- Seizures

Diagnosis:

  Initial signs and symptoms of Nipah virus infection are nonspecific, and the diagnosis is often not suspected at the time of presentation. This can hinder accurate diagnosis and creates challenges in outbreak detection, effective and timely infection control measures, and outbreak response activities. 

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

    Nipah virus infection can be diagnosed with clinical history during the acute and convalescent phases of the disease. The main tests used are real-time polymerase chain reaction from bodily fluids and antibody detection via enzyme-linked immunosorbent assay (ELISA). Other tests used include polymerase chain reaction (PCR) assay and virus isolation by cell culture. 

Treatment:

  There are currently no drugs or vaccines specific for Nipah virus infection although WHO has identified Nipah as a priority disease for the WHO research and development Blueprint. Intensive supportive care is recommended to treat severe respiratory and neurological complications. 

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Vitamin D

                                                          Vitamin D

  Vitamin D is a group of fat-soluble secosteroids responsible for increasing intestinal absorption of calcium, magnesium, and phosphate, and many other biological effects. In humans, the most important compounds in this group are vitamin D3 and D2. 

 Vitamin D obtained from sun exposure, foods, and supplements are biologically inert and must undergo two hydroxylations in the body activation. The first hydroxylation, which occurs in the liver, converts vitamin D to 25- hydroxyvitamin D also known as "Calcidiol". 

   Vitamin D promotes calcium absorption in the gut and maintains adequate serum calcium and phosphate concentrations to enable normal bone mineralization and to prevent hypocalcemic tetany (involuntary contraction of muscles, leading to cramps and spasms). It is also needed for bone growth and bone remodeling by osteoblasts and osteoclasts, without sufficient vitamin D, bones can become thin, brittle, or misshapen. Vitamin D also helps protect older adults from osteoporosis. 

Types:

 Several forms (Vitamers) of vitamin D exist. The two major forms are vitamin D2 or ergocalciferol, and vitamin D3 or cholecalciferol. Vitamin D without a subscript refers to either D2 or D3, or both, and is known collectively as calciferol. 

   Vitamin D2 was chemically characterized in 1931. In 1935, the chemical structure of vitamin D3 was defined and shown to result from the ultraviolet irradiation of 7- dehydrocholesterol. A chemical nomenclature for vitamin D forms was recommended in 1981 but alternative names remain in common use. 

   Chemically, the various forms of vitamin D are secosteroids, that is steroids in which one of the bonds in the steroid rings is broken. the structural difference between vitamin D2 and vitamin D3 is in the side chain, which contains a double bond, between carbons 22 and 23, and a methyl group on carbon 24 in vitamin D2. 

Vitamin D deficiency:

 

  People can develop vitamin D deficiency when usual intakes are lower over time than recommended levels, exposure to sunlight is limited, the kidneys cannot 25(OH)D to its active form or absorption of vitamin D from the digestive tract is inadequate. Diets low in vitamin D are more common in people who have a milk allergy or lactose intolerance and those who consume a non-vegetarian or vegan diet. 

 In children, vitamin D deficiency is manifested as rickets, a disease characterized by a failure of bone tissue to become properly mineralized, resulting in soft bones and skeletal deformities. In addition to bone deformities and pain, severe rickets can cause failure to thrive, developmental delay, hypocalcemic seizures, tetanic spasm, cardiomyopathy, and dental abnormalities. 

 

 The incidence rate of rickets in children younger than 3 years in the decade beginning in 2000 was 24. 1per 100,000. Rickets occurred mainly in black children who were breastfed longer, were born with low birth weight, weighed less, and were shorter than other children.  The incidence rate of rickets in infants and children are seen by 2325 pediatricians throughout Canada was 2.9 per 100,000, and almost all patients with rickets had been breastfed.  

  In adults and adolescents, vitamin D deficiency can lead to osteomalacia, in which existing bone is incompletely or effectively mineralized during the remodeling process, resulting in weak bones. Signs and symptoms of osteomalacia are familiar to those of rickets and include bone deformities and pain, hypocalcemic seizures, tetanic spasms, and dental abnormalities. 

  Screening for vitamin D status is becoming a more common part of the routine laboratory bloodwork ordered by primary-care physicians, irrespective of any indications for this practice. No studies have examined whether such screening for vitamin D deficiency results in improved health outcomes. 

Symptoms:

 Being sick it getting infections often:

 

 One of vitamin D most important roles is keeping your immune system strong so you're able to fight off viruses and bacteria that cause illness. It directly interacts with the cells that are responsible for fighting infection. If you often become sick, especially with colds or the flu, low levels of vitamin D may be a contributing factor. 

Fatigue and tiredness:

 Feeling tired can have many causes, and vitamin D deficiency may be one of them. Unfortunately, it's often overlooked as a potential cause. case studies have shown that very low blood levels of vitamin D can cause fatigue that can have a severe negative effect on the quality of life. 

 Bone and back pain:

 Vitamin D helps maintain bone health in a number of ways. for one, it improves your body's absorption of calcium. Bone pain and lower back pain may be signs of inadequate vitamin D levels in the blood. large observational studies have found a relationship between a deficiency and chronic lower back pain. 

Bone Loss:

 Vitamin D plays a crucial in calcium absorption and bone metabolism. Many older people who are diagnosed with bone loss believe they need to take more calcium. However, they may be deficient in vitamin D as well. Low bone mineral density is an indication that your bones have lost calcium and other minerals. This places older adults, especially women, at an increased risk for fractures. 

Hair loss:

 Hair loss is often attributed to stress, which is certainly a common cause. However, when hair loss is severe, it may be the result of disease or nutrient deficiency. Hair loss in women has been linked to low vitamin D levels, though there is very little research on this to date. In particular, research suggests that low vitamin D levels are linked to alopecia areata and may be a risk factor for developing the disease. 

Muscle pain:

 The causes of muscle pain are often difficult to pinpoint. There is some evidence that vitamin D deficiency may be a potential cause of muscle pain in children and adults. in one study, 71% of people with chronic pain were found to be deficient. The vitamin D receptor is present in nerve cells nociceptors, which sense pain. 

 Groups at risk of vitamin D inadequacy:

 

  Obtaining sufficient vitamin D from natural food sources alone is difficult. For many people, consuming vitamin- D fortifies foods and exposing themselves to some sunlight are essential for maintaining a healthy vitamin D status. 

Breastfeed Infants:

  

 Consumption of human milk alone does not ordinarily enable infants to meet vitamin D requirements, because it provides less than 0.6 to 2.0 mcg/L. The vitamin D content of human milk is related to the mother's vitamin D status, studies suggest that the breastmilk of mothers who take daily supplements containing at least 50 mcg (2,000IU) vitamin D3 have higher levels of the nutrient. 

Older Adults:

 Older adults are at increased risk of developing vitamin D insufficiency, partly because the skin's ability to synthesize vitamin D decline with age. In addition, older adults are likely to spend more time than younger people indoors and might have an inadequate dietary intake of the vitamin. 

People with limited sun exposure: 

 Homebound individuals, people who wear long robes, dresses, or head coverings for religious reasons, and people with occupations that limit sun exposure are among the groups that are unlikely to obtain adequate amounts of vitamin D from sunlight. 

People with dark skin:

 

 Greater amounts of the pigment melanin in the epidermal layer of the skin result in darker skin and reduce the skin's ability to produce vitamin D from sunlight. Black Americans, for example, typically have lower serum25(OH) D levels than white Americans. However, whether these lower levels in persons with dark skin have significant health consequences is not clear. 

People with conditions that limit fat absorption:

   Vitamin D is fat-soluble, its absorption depends on the Ability of dietary fat. Fat malabsorption is associated with medical conditions that include some forms of liver disease, cystic fibrosis, celiac disease, Crohn's disease, and ulcerative colitis. In addition to having an increased risk of vitamin D deficiency, people with these conditions might not eat certain foods, such as dairy products or eat only small amounts of these foods. 

People who are obese or have undergone gastric bypass surgery: 

  Individuals with a body mass index(BMI) of 30 or more have lower serum 25(OH)D levels than nonobese individuals. Obesity does not affect the skin's capacity to synthesize vitamin D. Obese individuals who have undergone gastric bypass surgery can also become vitamin D deficient. In this procedure, part of the upper small intestine, where vitamin D is absorbed, is bypassed, and vitamin D that is mobilized into the bloodstream from fat stores might not rise 25(OH) D to adequate levels over time. 

Other Conditions: 

 Diabetes: 

  A systematic review of 2014 concluded that the available studies show no evidence of vitamin D3 supplementation having an effect on glucose homeostasis or diabetes prevention. A review article of 201 reported that while there is increasing evidence that vitamin D deficiency may be a risk factor for diabetes, overall evidence regarding vitamin D levels and diabetes mellitus is contradictory, requiring future studies. 

ADHD: 

  a  meta-analysis of observational studies showed that children with ADHD have lower vitamin D levels and that there was a small association between low vitamin D levels at the time of birth and later development of ADHD. Several small randomized controlled trials of vitamin D supplementation indicated improved ADHD symptoms such as impulsivity and hyperactivity. 

Depression: 

 

 Clinical trials of vitamin D supplementation for depressive symptoms have generally been of low quality and show no overall effect, although subgroup analysis showed supplementation for participants with clinically significant depressive symptoms or depressive disorder had a moderate effect. 

 Cognition and dementia:

 

 A systematic review of clinical studies found an association between low vitamin D levels with cognitive impairment and a higher risk of developing Alzheimer's disease. However, lower vitamin D concentrations are also associated with poor nutrition and spending less time outdoors. Therefore, alternative explanations for the increase in cognitive impairment exist and hence the direct causal relationship between vitamin D levels and cognition could not be established. 

 Pregnancy: 

  Low levels of vitamin D in pregnancy are associated with gestational diabetes, pre-eclampsia, and small infants. Although taking vitamin D supplements during pregnancy raises blood levels of vitamin D in the mother at term, the full extent of benefits for the mother or baby is unclear. 

 

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Intermittent explosive disorder

                        Intermittent explosive disorder

     Intermittent explosive disorder is a lesser-known mental disorder marked by episodes of unwarranted anger. 

It is commonly described ad "Flying into a rage for no reason". In an individual with intermittent explosive disorder, the behavioral outbursts are out of proportion to the situation.

It is estimated that between one to seven percent of individuals will develop intermittent explosive disorder during their lifetime. Usually begins in the early teens, but can be seen in children as young as six. It is most common in people under the age of 40.

Causes:

 The cause of intermittent explosive disorder is unknown, but some contributing factors have been identified. Include:

 - A genetic component (occurs in families)

- Being exposed to verbal and physical abuse in childhood

- Brain chemistry can contribute to the disorder.

- Having experienced one or more traumatic events in childhood 

- A history of mental health disorders, including attention deficit hyperactivity disorder (ADHD), antisocial disorder have a borderline personality disorder. 

- Nearly 82% of those with the intermittent explosive disorder have also had depression, anxiety, or substance abuse disorder. 

Signs:

 Intermittent explosive disorder manifests itself in what seems like adult temper tantrums. Throwing objects, fighting for no reason, road rage and domestic abuse are examples of intermittent explosive disorder. The outbursts typically last less than 30 minuteS. After an outburst, an individual may feel a sense of relief- followed by regret and embarrassment. 

Symptoms: 

 Individuals experiencing intermittent explosive disorder may display one or more of the following symptoms: 

- Rage

-Irritability 

- An increasing sense of tension

- Racin thoughts

- Increased energy

- Tremors

- Palpitations

- Temper tantrums

- Chest tightness

- Shouting

- Being argumentative

- Getting into fights

- Threatening others

- Assaulting people or animals

- Damaging property 

Diagnosis:

 Diagnosis begins with taking the individual's general medical history, psychiatric history and conducting a physical and mental status exam. To be diagnosed with intermittent explosive disorder, an individual must display a failure to control aggressive impulses as defined by either of the following:

- Verbal aggression or physical aggression toward property, animals, or individuals, occurring twice weekly, on average for a period of 3 months. The aggression does not result in physical harm to individuals or animals or the destruction of property. 

- Three episodes involving damage or destruction of property and or physical assault involving physical injury against animals or other individuals occurring within a 12-months period. 

 The degree of aggression displayed during the outbursts is greatly out of proportion to the situation. In addition, the outbursts are not pre-planned, they are impulse and or anger-based. Also, the outburst is not better explained by another mental disorder, medical condition, or substance abuse. 

Complications: 

 The intermittent explosive disorder can have a very negative impact on an individual's health and life. It can lead to trouble in personal relationships and marriages. It can negatively impair a person's relationships and judgment at work and school. Individuals with intermittent explosive disorder are more likely to have other psychiatric disorders, abuse drugs, and school, and engage in self-harm. 

 They also are at a higher risk of some medical conditions including stroke diabetes, chronic pain, ulcer, and high blood pressure. For these reasons, it is important to seek medical attention if you think you or someone you know has intermittent explosive disorder. 

Prevention: 

People diagnosed with intermittent explosive disorder will learn a variety of coping techniques in therapy. These can help prevent episodes. They include:

- Relaxation techniques

- Changing the ways you think 

- Communication skills

- Learning to change your environment and leaving stressful situations when possible

- Avoiding alcohol and recreational drugs

Prognosis: 

 Having intermittent explosive disorder can predispose an individual to depression, anxiety, and alcohol and drug abuse. It can also lead to serve personal and relationship problems. For that reason, it is essential to seek medical help if you feel you or a family member has intermittent explosive disorder. With cognitive therapy and medication, the condition can be successfully managed. However, according to studies, it is thought that intermittent explosive disorder is a long-term condition, lasting from 12 years to 20 years or even a lifetime. 

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Sudden Infant Death Syndrome (SIDS)

      Sudden Infant Death Syndrome (SIDS)

 Sudden infant death syndrome is the sudden and unexplained death of a baby younger than 1-year-old. A diagnosis of SIDS is made if the baby's death remains unexplained even after a death scene investigation, an autopsy, and a review of the clinical history. 

   SIDS is part of a large category of unexpected infant deaths called SUDI (sudden unexpected death in infancy). Babies who die suddenly but the cause of death are later explained (infection, brain abnormality, cardiac dysfunction) also fall into this SUDI category. 

  Sudden infant death syndrome usually during sleep, of a seemingly healthy baby less than a year old. SIDS is sometimes known as crib death because infants often die in their cribs. Although the cause is unknown, it appears that SIDS might be associated with defects in the portion of an infant's brain that controls breathing and arousal from sleep. 

  Researchers have discovered some factors that might put babies at extra risk. They've also identified measures you can take to help protect yourself from SIDS. Perhaps the most important is placing your baby on his or her back to sleep. 

Causes:

 A combination of physical and sleep environmental factors can make an infant more vulnerable to SIDS. These factors vary from child to child. 

SIDS is a mysterious syndrome, and by its very definition, the cause cannot be determined. Children's researchers have uncovered strong evidence that SIDS has a biological basis, and are continuing to work towards determining the underlying causes and identifying at-risk babies. 

Physical factors:

 - Brain defects: Some infants are born with problems that make them more likely to die of SIDS. In many of these babies, the portion of the brain that controls breathing and arousal from sleep hasn't matured enough to work properly. 

- Low birth weight: Premature birth or being part of multiple births increases the likelihood that a baby's brain hasn't matured completely, so he or she has less control over such automatic processes as breathing and heart rate. 

- Respiratory infection: Many infants who died of SIDS had recently had a cold, which might contribute to breathing problems. 

Sleep environmental factors: 

The items in a baby's crib and his or her sleeping position can combine with a baby's physical problems to increase the risk of SIDS. Examples include: 

- Sleep on the stomach or side: Babies placed in these positions to sleep might have more difficulty breathing than those placed on their backs. 

- Sleeping on a soft surface: Lying face down on a fluffy comforter, a soft mattress, or a waterbed can block an infant's airway. 

- Sharing a bed: While the risk of SIDS is lowered if an infant sleeps in the same room as his or her parents, the risk increases if the baby sleeps in the same bed with parents, siblings, or pets. 

- Overheating: being too warm while sleeping can increase a baby's risk of SIDS. 

Risk factors:

 SIDS is a mysterious syndrome since by its very definition the cause cannot be determined, but certain risk factors do exist. About 2,300 babies in the united states die of SIDS each year. Some babies are more at risk than others. SIDS is more likely to affect a baby who is between 1 and 4 months old, it is more common in boys than girls, and most deaths occur during the fall, winter, and early spring months. 

Factors that may place a baby at higher risk of dying from SIDS include the following: 

- Sex: Boys are slightly more likely to die of SIDS.

- Age: Infants are most vulnerable between the second and fourth months of life.

- Race: Reasons that aren't well-understood, nonwhite infants are more likely to develop SIDS. 

- Family history: Babies who've had siblings or cousins die of SIDS are at higher risk of SIDS. 

Secondhand smoke: Babies who live with smokers have a higher risk of SIDS. 

- Being premature: Both being born early and having a low birth weight increase your baby's chances of SIDS. 

Maternal risk factors: 

During pregnancy, the mother also affects her risk of SIDS, especially if she: 

- Smokes cigarettes.

- Uses drugs or alcohol.

- Has inadequate prenatal care.

Prevention:

 There's no guaranteed way to prevent SIDS, but you can help your baby sleep more safely by following these tips: 

Back to sleep: Place your baby to sleep on his or her back, rather than on the stomach or side, every time you, or alone else, put the baby to sleep for the first year of life. This isn't necessary when our baby's awake or able to roll over both ways without help. 

Don't assume that others will place your baby to sleep in the correct position, insist on it. Advise sitters and child care providers not to use the stomach position to calm an upset baby. 

Keep the crib as bare as possible: Use a mattress and avoid placing your baby on thick, fluffy padding, such as lambskin or a thick quilt. Don't leave pillows, fluffy toys stuffed animals in the crib. These can interfere with breathing if your baby's face presses against them. 

Don't overheat your baby: To keep your baby warm, try a sleep sack or other sleep clothing that doesn't require additional covers. Don't cover your baby's head. 

Have your baby sleep in your room: Ideally, your baby should sleep in your room with you, but alone in a crib, bassinet, or other structure designed for infant sleep, for at least six months, and if possible up to a year. 

 Adult beds aren't safe for infants, A baby can become trapped and suffocate between the headboard slats, the space between the mattress and the bed frame, or the space between the mattress and the wall. A baby can also suffocate if a sleeping parent accidentally rolls over and covers the baby's nose and mouth. 

- Breast-feed baby, if possible: Breastfeeding for at least six months lowers the risk of SIDS. 

Other theories about why SIDS occurs?

 While the cause of SIDS is unknown, many clinicians and researchers believe that SIDS is associated with problems in the ability of the baby to arouse from sleep, to detect low levels of oxygen, or a buildup of carbon dioxide in the blood. When babies sleep face down, they may re-breathe exhaled carbon dioxide. Normally, rising carbon dioxide levels activate nerve cells in the brainstem, which stimulate the brain's respiratory and arousal centers. The baby then wakes up, turns his head, and breathes faster to get more oxygen. SIDS babies, however, may fail to rouse. 

The "Triple-risk model" for SIDS has been proposed to explain how SIDS occurs. The model holds that SIDS occurs when three conditions exist simultaneously:

 - Infant has an underlying abnormality that makes him unable to respond to low oxygen or high carbon dioxide blood levels. 

- The infant is exposed to a triggering event such as sleeping face down on its tummy. 

- These events occur during a vulnerable stage in the infant's development i.e. the first 6 months of life. 

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Green Fungus

                                         Green Fungus (Aspergillosis)

      Aspergillosis is an infection caused by Aspergillus, a common mold that lives indoors and outdoors. Most people breathe in Aspergillus spores every day without getting sick. However, people with weakened immune systems or lung disease are at a higher risk of developing health problems due to Aspergillus. The types of health problems caused by Aspergillus include allergic reactions. Lung infection, and infections in other organs. 

 Aspergillosis is a fungal infection that most commonly affects the lung AIIMS director, informed in his press conference, as early as May.  

Can people get infected:

 People can get infected with green fungus by breathing in microscopic Aspergillus spores from the environment. According to the US Center for Disease Control and Prevention (CDC), most people breathe in Aspergillus spores every day without getting sick. However immune system or lung disease puts one at a higher risk of catching the infection. 

Risk: 

 People with weakened immune systems, such as Covid-19 survivors, or those who have lung diseases, are at a greater risk of developing health issues due to infection, says CDC, those who have 

- Cystic fibrosis or asthma

- Tuberculosis, chronic obstructive pulmonary disease (COPD), or sarcoidosis. 

Symptoms of Aspergillosis:

 

 According to CDC, different types of infection have different symptoms

-Allergic bronchopulmonary aspergillosis (ABPA):

- Wheezing

- Shortness of breath

- Cough

- Fever in some cases

Allergic Aspergillus sinusitis: 

- Stiffness

- Runny nose

- Headache 

- Reduced ability to smell

Aspergilloma(''Fungus ball'):

- Cough

- Coughing up blood

- Shortness of breath

Chronic pulmonary aspergillosis:

- Weight loss

- Cough

- Coughing up blood

- Fatigue

- Shortness of breath

Invasive aspergillosis:

- Fever

- Chest pain

- Cough

-Coughing up blood

- Shortness of breath 

Other symptoms can develop if the infection spreads from the lungs to other parts of the body. 

Is it Contagious:

 No, Aspergillosis cannot spread between people or between people and animals. 

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Yellow Fungus

                                                      Yellow Fungus

    

           The second wave of coronavirus is finally slowing down with daily cases in India dipping to below 2 lakhs, but new fungal infections have followed in its aftermath, the most recently reported one being the deadly "Yellow Fungus".

     A patient recovering from Covid-19 in UP was recently diagnosed with yellow fungus, while he was already infected with both black and white fungal infections. Yellow fungus is even more dangerous as it originates internally, which makes it more difficult to identify and treat the disease. 

Yellow Fungus:

  Yellow fungus, also called mucor septic, is a fungal infection, which as per experts does not generally occur in humans but in lizards. The treatment for Covid-19 includes steroids and immunosuppressants that leave the body with weak immunity. 

  Yellow fungus is a fungal infection that spreads via contaminated environments or when a patient inhales moulds that grow in the environment. It is different from black fungus and white fungus infections in its manner of spreading. The yellow fungus attacks the body's internal organs and disturbs vital bodily processes, whereas black fungus starts spreading with distinct facial disfiguration. Damage caused by yellow fungus is much more severe. Hence, people should start to observe its symptoms from day 1 and consult their doctor. 

Yellow Fungus spread:

  

 The yellow fungus spreads when a person inhales molds that are in the environment. It can also spread through the presence of contaminated or old food unsanitary conditions, poor hygiene, and a high level of humidity from the spread of the infection. Yellow fungus isn't contagious, hence, it cannot spread from person to person. 

Is yellow fungus more dangerous than white and black fungus:

 The yellow fungus can be treated easily when detected on time, but because it arises within the body, the detection and treatment are often delayed. It can even cause organ failure in many people. Though there is yet no clear study or data by experts to give an exact figure on the mortality rate. 

White fungus:

 

  As compared to black fungus, fewer cases of white have been detected. Symptoms of white fungus are similar to that of covid-19 infection. People who have compromised immunity and not following proper hygiene are more prone to catching the infection. Delay in the treatment can be dangerous. White fungus is more lethal because of the way it spreads, which can cause damage to vital organs. It can impact the brain, digestive system, respiratory organs, kidneys, and even private parts.

Black fungus:

 So far, more than 10,000 cases of black fungus have been reported. The fungus affects the eyes, nose, face, lungs, and even brain in some severe cases. As per experts, misuse of steroids can be a reason behind the rise in black fungus cases. People who are given steroids for a long time, have other comorbidities, or are on oxygen support for a long time are more at risk of contracting the infection. If not treated in time, it can turn fatal. 

 Symptoms: 

 Symptoms of yellow fungus include weight loss, lethargy, and loss of appetite or no appetite. Other symptoms could be the formation and leakage of pus and sunken eyes. Due to the yellow fungus, the healing of wounds gets hindered and prolonged. It can also result in malnutrition, organ failure, and necrosis in extreme cases. 

Risk factors: 

 Yellow fungus might occur as a primary or secondary infection, depending on an individual's health and risk factors. So far, it has been observed that people with compromised immunity and suffering from pre-existing conditions such ad high cholesterol and uncontrolled diabetes are at higher risk of getting infected with yellow fungus. 

 The infection could also occur by the fungus entering the skin through cuts, burns, scrapes, or any other skin trauma. Other individuals at high risk of fungal infections also include: 

- Individuals who were in the ICU for a long time. 

- Individuals who have an organ transplant recently and have low WBC or immune complications

- Individuals on steroid or antibacterial use for long duration.

- Individuals who have kidney damage or are on dialysis. 

 Yellow fungus more dangerous! 

 Yellow fungus is more dangerous as compared to other fungal infections because it spreads internally and causes more internal damage. 

Precautions: 

 Here are some precautions that one must take to protect themselves from yellow fungus:

- Keep your house and surroundings clean

- Do not consume stale food

- Keep the humidity in the room in check Too much humidity can promote the growth of the fungus. Try to maintain cross ventilation.  

- Covid-19 patients should start their treatment as soon as possible so that complications like yellow fungus do not arise. 

  

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