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TAR Syndrome Month Awareness

Apr26

Thrombocytopenia-absent radius (TAR) syndrome is a rare disorder that is present at birth (congenital). It is characterized by low levels of platelets in the blood (thrombocytopenia) and absence (aplasia) of the long, thin bones of the forearms (radii) but with presence of thumbs.

Other abnormalities are often present including additional skeletal defects such as absence or underdevelopment of the other bone of the forearm (ulna), structural malformations of the heart (congenital heart defects) and kidney (renal) defects. Affected individuals may be short for their age (short stature) and have cow’s milk intolerance.

Thrombocytopenia is congenital or develop within the first few weeks to months of life. Usually, platelet counts remain low during the first two years of life; then, they increase but do not normalize. Additional recurrent manifestations include: cardiac anomalies (atrial and/or ventricular septal defect, patent foramen ovale), gastro-intestinal involvement (cow’s milk allergy, increased susceptibility to gastro-enteritis), genitourinary anomalies (kidney agenesis or malrotation, horseshoe kidney, hydronephrosis, pyelectasis). Other rare manifestations include Mayer-Rokitansky-Kuster-Hauser syndrome, rib and vertebral anomalies, Langerhans cell histiocytosis, transient leukemoid reaction, acute myeloid or lymphoblastic leukemia. Cognitive development is usually normal.

The prevalence of thrombocytopenia-absent radius (TAR) syndrome is estimated at around 1/100,000-200,000 people.

Cause of TAR-Thrombocytopenia Absent Radius Syndrome:

TAR syndrome is inherited as an autosomal recessive genetic disorder and caused by deletion and/or variants in the RBM8A gene.

TAR syndrome is caused by compound heterozygosity for a null (most often a 1q21.1 deletion including RBM8A) and a hypomorphic RBM8A allele.  It was demonstrated that Rbm8a is an essential neurogenesis regulator in embryonic cortical development.  Most people with TAR syndrome have a mutation in one copy of the RBM8A gene and a deletion of genetic material from chromosome 1 that includes the other copy of the RBM8A gene in each cell.

Diagnosing TAR-Thrombocytopenia Absent Radius Syndrome:

It has been reported that TAR syndrome can be accompanied by craniofacial, cardiac, digestive, urogenital, and psychiatric abnormalities, as well as by lactose intolerance(4). The diagnosis of TAR syndrome is based on ultrasound findings and fetal blood sampling by cordocentesis to determine the number of platelets.

Suggestive Findings. Thrombocytopenia absent radius (TAR) syndrome should be suspected in individuals with: Bilateral absence of the radii with the presence of both thumbs. Thrombocytopenia, usually <50 platelets/nL (normal range: 150-400 platelets/nL)

Management and Treatment of TAR-Thrombocytopenia Absent Radius Syndrome:

There is no curative treatment for TAR syndrome. Symptomatic treatment of manifestations and prevention of complications include: early detection of thrombocytopenia, prevention of bleeding and hemorrhage, platelet transfusions in case of severe thrombocytopenia, surgical interventions if required to manage cardiac, urinary or skeletal malformations, avoidance of cow’s milk.

Prognosis of TAR-Thrombocytopenia Absent Radius Syndrome:

Prognosis is variable and mainly conditioned by the severity of thrombocytopenia and its complications (intracranial, digestive hemorrhage). Cardiac defects, renal malformations, acute complications of cow’s milk intolerance, acute leukemia can also affect the prognosis.

If a patient survives the initial 2 years of life, life expectancy is normal, MedLinePlus.com states.

Affected children who survive this period and do not have damaging hemorrhages in the brain usually have a normal life expectancy and normal intellectual development. The severity of skeletal problems in TAR syndrome varies among affected individuals.

 

QUOTE FOR THURSDAY:

Apr25

“Cotard’s syndrome is a relatively rare condition that was first described by Dr. Jules Cotard in 1882. Cotard’s syndrome comprises any one of a series of delusions that range from a belief that one has lost organs, blood, or body parts to insisting that one has lost one’s soul or is dead.”

NIH National Library of Medicine (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695744/)

Cotard’s syndrome

Apr25

Cotard delusion, also known as or nihilistic delusion or walking corpse syndrome or Cotard’s syndrome , is a rare mental disorder in which the affected person holds the delusional belief that they are already dead, do not exist, are putrefying, or have lost their blood or internal organs.

Signs and Symptoms: 

One of the main symptoms of Cotard delusion is nihilism. Nihilism is the belief that nothing has any value or meaning. It can also include the belief that nothing really exists. People with Cotard delusion feel as if they’re dead or rotting away. In some cases, they might feel like they’ve never existed.

While some people feel this way about their entire body, others only feel it in regard to specific organs, limbs, or even their soul.

Depression is also closely related to Cotard delusion. A 2011 review of existing research about Cotard delusion notes that 89% of documented cases include depression as a symptom.

Other symptoms include:

  • anxiety
  • hallucinations
  • hypochondria
  • guilt
  • preoccupation with hurting yourself or death

Researchers aren’t sure what causes Cotard delusion, but there are a few possible risk factors. Several studies indicate that the average age of people with Cotard delusion is about 50. It can also occur in children and teenagers. People under the age of 25 with Cotard delusion tend to also have bipolar depression. Women also seem to be more likely to develop Cotard delusion.

In addition, Cotard delusion seems to occur more often in people who think their personal characteristics, rather than their environment, cause their behavior. People who believe that their environment causes their behavior are more likely to have a related condition called Capgras syndrome. This syndrome causes people to think their family and friends have been replaced by imposters. Cotard delusion and Capgras syndrome can also appear together.

Other mental health conditions that might increase someone’s risk of developing Cotard delusion include:

  • bipolar disorder
  • postpartum depression
  • catatonia
  • depersonalization disorder
  • dissociative disorder
  • psychotic depression
  • schizophrenia

Cotard delusion also seems to be associated with certain neurological conditions, including:

  • brain infections
  • brain tumors
  • dementia
  • epilepsy
  • migraines
  • multiple sclerosis
  • Parkinson’s disease
  • stroke
  • traumatic brain injuries

QUOTES FOR WEDNESDAY:

Apr24

1-“Since 1996, evidence has been increasing for a causal relationship between the outbreak in Europe of a disease in cattle, called bovine spongiform encephalopathy (BSE, or “mad cow disease”), and a disease in humans, called “variant” Creutzfeldt-Jakob disease (vCJD).

Both disorders are invariably fatal brain diseases with unusually long incubation periods measured in years, and are caused by abnormally folded proteins in the brain called “prions” (pree-ons).  ”

Cattle affected by BSE experience progressive degeneration of the nervous system. Signs usually don’t appear until about 3–6 years after initial infection.

The highest quality beef comes from animals that are under 36 months of age. Old cows produce highly acceptable beef if properly fattened and processed but know there is testing cows for it before making it food on our table.

Know this BSE belongs to a family of diseases known as transmissible spongiform encephalopathies that includes, among others, scrapie in sheep and goats; chronic wasting disease in deer, elk, and moose; and classic and variant Creutzfeldt-Jakob disease in people.”

1-Centers for Disease Control and Prevention-CDC (https://www.cdc.gov/prions/index.html)

*****

2-CHICAGO (Reuters) states – On May 19,2023 they stated “The U.S. Department of Agriculture (USDA) announced on Friday an atypical case of Bovine Spongiform Encephalopathy (BSE), commonly called mad cow disease, in an older beef cow at a slaughter plant in South Carolina.

USDA stated “the animal never entered slaughter channels and the agency did not expect any trade impacts as a result.
It was the seventh detection of BSE in the United States since 2003 and all but one have been atypical”
Animal and Plant Health Inspection Service said in a statement “This finding of an atypical case will not change the negligible risk status of the United States and should not lead to any trade issues,”.
2-Reuters (https://www.reuters.com/world/us/us-reports-case-atypical-mad-cow-disease-2023-05-19/)

*****

3-“We know that the earliest point at which current tests can accurately detect BSE is 2-to-3 months before the animal begins to show symptoms. The time between initial infection and the appearance of symptoms is about 5 years. Since most cattle that go to slaughter in the United States are both young and clinically normal, testing all slaughter cattle for BSE might offer misleading assurances of safety to the public.

The carcasses from the tested animals are held and not allowed to enter the human food chain until test results show the samples are negative for Bovine spongiform encephalopathy (BSE or Mad Cow Disease).”

3-U.S.D.A  US Dept of Agriculture (https://www.usda.gov/topics/animals/bse-surveillance-information-center)

“Currently, there is no test to detect the disease in a live animal or in muscle meat products. BSE can only be confirmed by microscopic examination of brain tissue from the animal after its death using sophisticated laboratory techniques.”

3-U.S.D.A (https://ask.usda.gov/s/article/how-do-cattle-get-bovine-spongiform-encephalopathy)

Their is no standard testing before each cow including other wild life animals listed at the top that go on our plate sold in stores for food? Another thought, In the United States and the European Union, cows are typically slaughtered for beef between the ages of 18 months and 30 months. In the United States, most cows are slaughtered at around 24-30 months of age, although some may be slaughtered as young as 18 months; cows are about 5 yrs old when symptoms start showing. No regular testing on all cows used for meat for BSE no matter how low the incidence in US due to spreading can occur; really?  Quite interesting but know based on statistics you have a 1 in a million chance getting this & it seems by history you have more of a chance in the mid to mid west area of US.

Part II MAD COW DISEASE=bovine spongiform encephalopathy. BSE in humans called Creutzfeldt-Jakob disease (vCJD).

Apr24

        

Brain Results that were exposed to Mad Cow Disease making the brain a  spongy like appearance.  This is how it got the name BSE.

U.S. Drug and Food Administration states, “People can get a version of BSE called variant Creutzfeldt-Jakob disease (vCJD). As of December 4, 2017, 231 people worldwide are known to have become sick with vCJD according to the University of Edinburgh’s National CJD Research & Surveillance Unit. It is thought that they got the disease from eating food made from cows sick with BSE. Most of the people who have become sick with vCJD lived in the United Kingdom at some point in their lives. Only four lived in the U.S., and most likely, these four people became infected when they were living or traveling overseas.

Neither vCJD nor BSE is contagious. This means that it is not like catching a cold. A person (or a cow) cannot catch it from being near a sick person or cow. Also, research studies have shown that people cannot get BSE from drinking milk or eating dairy products, even if the milk came from a sick cow.”

Unfortunately, there are currently no treatments for prion diseases, brain-wasting diseases that are invariably fatal. The most common human prion disease is Creutzfeldt-Jakob disease (CJD), better known as mad cow disease.  This disease is rare in humans.

Symptoms of Creutzfeldt-Jakob disease (CJD) can resemble those of other dementia-like brain disorders, such as Alzheimer’s. But Creutzfeldt-Jakob disease usually progresses much more rapidly.

CJD captured public attention in the 1990s when some people in the United Kingdom developed a form of the disease — variant CJD (vCJD) — after eating meat from diseased cattle. However, “classic” Creutzfeldt-Jakob disease hasn’t been linked to contaminated beef.

Although serious, CJD is rare, and vCJD is the least common form. Worldwide, there is an estimated one case of CJD diagnosed per million people each year, most often in older adults.

Creutzfeldt-Jakob disease (CJD) is marked by rapid mental deterioration, usually within a few months. Initial signs and symptoms typically include:

  • Personality changes
  • Anxiety
  • Depression
  • Memory loss
  • Impaired thinking
  • Blurred vision or blindness
  • Insomnia
  • Difficulty speaking
  • Difficulty swallowing
  • Sudden, jerky movements

As the disease progresses, mental symptoms worsen. Most people eventually lapse into a coma, first dementia to death. Heart failure, respiratory failure, pneumonia or other infections are generally the cause of death. Death usually occurs within a year.

In people with the rarer vCJD, psychiatric symptoms may be more prominent in the beginning, with dementia — the loss of the ability to think, reason and remember — developing later in the illness. In addition, this variant affects people at a younger age than classic CJD does and appears to have a slightly longer duration — 12 to 14 months.

Creutzfeldt-Jakob disease & its variants belong to a broad group of human & Sanimal diseases known as transmissible spongiform encephalopathies (TSEs). The name derives from the spongy holes, visible under a microscope, that affect the brain tissue.

How its transmitted?  The risk of CJD is low. The disease can’t be transmitted through coughing or sneezing, touching, or sexual contact.

1-Heredity: 15 percent of people with CJD have a family history of the disease or test positive for a genetic mutation associated with CJD. This type is referred to as familial CJD.

2-Exposure to contaminated tissue. People who’ve received human growth hormone derived from human pituitary glands or who’ve had grafts of tissue that covers the brain (dura mater) may be at risk of iatrogenic CJD. .

3-The low risk of contracting vCJD from eating contaminated beef.

Regulating potential sources of vCJD

Most countries have taken steps to prevent BSE-infected tissue from entering the food supply, including:

  • Tight restrictions on importation of cattle from countries where BSE is common
  • Restrictions on animal feed
  • Strict procedures for dealing with sick animals
  • Surveillance and testing methods for tracking cattle health
  • Restrictions on which parts of cattle can be processed for food

 

QUOTE FOR TUESDAY:

Apr23

“The word BSE is short but it stands for a disease with a long name, bovine spongiform encephalopathy. “Bovine” means that the disease affects cows, “spongiform” refers to the way the brain from a sick cow looks spongy under a microscope, and “encephalopathy” meaning that it is a disease of the brain. BSE is commonly called “mad cow disease.

Cattle affected by BSE experience progressive degeneration of the nervous system. Signs usually don’t appear until about 3–6 years after initial infection.

Here’s what to look for:

  • Changes in temperament (nervousness or aggression)
  • Abnormal posture
  • Coordination problems and difficulty in rising
  • Weight loss
  • Decreased milk production
  • Loss of condition without noticeable loss of appetite

After signs appear, the animal’s condition deteriorates until it dies. This usually takes anywhere from 2 weeks to 6 months.”

U.S.D.A. US Dept or Agriculture (https://www.aphis.usda.gov/livestock-poultry-disease/cattle/bse)

 

 

 

Part I MAD COW DISEASE=bovine spongiform encephalopathy (BSE) & in humans called Creutzfeldt-Jakob disease (vCJD).

Apr23

Mad Cow Disease (Spongiform Encephalopathy or BSE)

Mad cow disease, or bovine spongiform encephalopathy (BSE), is a disease that was first found in cattle. It’s related to a disease in humans called variant Creutzfeldt-Jakob disease (vCJD). Both disorders are universally fatal brain diseases caused by a prion. A prion is a protein particle that lacks DNA (nucleic acid). It’s believed to be the cause of various infectious diseases of the nervous system. Eating infected cattle products, including beef, can cause a human to develop mad cow disease.

What is mad cow disease?

Mad cow disease is a progressive, fatal neurological disorder of cattle resulting from infection by a prion. It appears to be caused by contaminated cattle feed that contains the prion agent. Most mad cow disease has happened in cattle in the United Kingdom (U.K.), a few cases were found in cattle in the U.S. between 2003 and 2006. There were 4 more reported up to 2018.  Feed regulations were then tightened.

In addition to the cases of mad cow reported in the U.K. (78% of all cases were reported there) and the U.S., cases have also been reported in other countries, including France, Spain, Netherlands, Portugal, Ireland, Italy, Japan, Saudi Arabia, and Canada. Public health control measures have been implemented in many of the countries to prevent potentially infected tissues from entering the human food chain. These preventative measures appear to have been effective. For instance, Canada believes its prevention measures will wipe out the disease from its cattle population by 2017.

What is variant Creutzfeldt-Jakob Disease (vCJD)?

Creutzfeldt-Jakob Disease (CJD) is a rare, fatal brain disorder. It causes a rapid, progressive dementia (deterioration of mental functions), as well as associated neuromuscular disturbances. The disease, which in some ways resembles mad cow disease, traditionally has affected men and women between the ages of 50 and 75. The variant form, however, affects younger people (the average age of onset is 28) and has observed features that are not typical as compared with CJD. About 230 people with vCJD have been identified since 1996. Most are from the U.K. and other countries in Europe. It is rare in the U.S., with only 4 reported cases since 1996 until May of 2023 in Chicago found in baby cow.

What is the current risk of acquiring vCJD from eating beef and beef products produced from cattle in Europe?

Currently this risk appears to be very small, perhaps fewer than 1 case per 10 billion servings–if the risk exists at all. Travelers to Europe who are concerned about reducing any risk of exposure can avoid beef and beef products altogether, or can select beef or beef products, such as solid pieces of muscle meat, as opposed to ground beef and sausages. Solid pieces of beef are less likely to be contaminated with tissues that may hide the mad cow agent. Milk and milk products are not believed to transmit the mad cow agent. You can’t get vCJD or CJD by direct contact with a person who has the disease. Three cases acquired during transfusion of blood from an infected donor have been reported in the U.K. Most human Creutzfeldt-Jakob disease is not vCJD and is not related to beef consumption but is also likely due to prion proteins

The Risk of getting Mad Cow Disease in the US, based on CDC-Centers for Disease Prevention and Control show the following statistics:

On December 23, 2003, the U.S. Department of Agriculture (USDA) announced a presumptive diagnosis of the first known case of BSE in the United States. It was in an adult Holstein cow from Washington State. This diagnosis was confirmed by an international reference laboratory in Weybridge, England, on December 25. Trace-back based on an ear-tag identification number and subsequent genetic testing confirmed that the BSE-infected cow was imported into the United States from Canada in August 2001.

Because the animal was non-ambulatory (a “downer cow”) at slaughter, brain tissue samples were taken by USDA’s Animal and Plant Health Inspection Service as part of its targeted surveillance for BSE. However the animal’s condition was attributed to complications from calving. After the animal was examined by a USDA Food Safety and Inspection Service (FSIS) veterinary medical officer both before and after slaughter, the carcass was released for use as food for human consumption. During slaughter, the tissues considered to be at high risk for the transmission of the BSE agent were removed.

On December 24, 2003, FSIS recalled beef from cattle slaughtered in the same plant on the same day as the BSE positive cow.

On June 24, 2005, the USDA announced receipt of final results from The Veterinary Laboratories Agency in Weybridge, England, confirming BSE in a cow that had conflicting test results in 2004. This cow was from Texas, died at approximately 12 years of age, and represented the first endemic case of BSE by a cow in the United States.

On March 15, 2006, the USDA announced the confirmation of BSE in a cow in Alabama. The case was identified in a non-ambulatory (downer) cow on a farm in Alabama. The animal was euthanized by a local veterinarian and buried on the farm. The age of the cow was estimated by examination of the dentition as 10 years old.

It had no ear tags or distinctive marks; the herd of origin could not be identified despite an intense investigation.

In August 2008, several ARS investigators reported that a rare, genetic abnormality that may persist within the cattle population “is considered to have caused” BSE in this atypical (H-type) BSE animal from Alabama.

On April 24, 2012, the USDA confirmed a BSE case in a dairy cow in California. This cow was tested as part of the USDA targeted BSE surveillance at rendering facilities in the United States. The cow was 10 years and 7 months old and was classified as having the L-type BSE strain.

On July 18, 2017, the U.S. Department of Agriculture (USDA) announced the confirmation of the fifth case of bovine spongiform encephalopathy (BSE) in an 11-year-old cow in Alabama. The cow was found through USDA’s routine surveillance. The cow was found to be positive for an atypical (L-type) strain of BSE. Atypical BSE usually occurs in older cattle and seems to arise spontaneously in cattle populations.

On August 29, 2018 the U.S. Department of Agriculture (USDA) announced a confirmed atypical, H-type case of bovine spongiform encephalopathy (BSE) in a six year old mixed-breed beef cow in Florida. USDA reported that this animal never entered the food supply and at no time presented a risk to human health.

How does the cow even get Mad Cow Disease?

The parts of a cow that are not eaten by people are cooked, dried, and ground into a powder. The powder is then used for a variety of purposes, including as an ingredient in animal feed. A cow gets BSE by eating feed contaminated with parts that came from another cow that was sick with BSE. The contaminated feed contains the abnormal prion, and a cow becomes infected with the abnormal prion when it eats the feed. If a cow gets BSE, it most likely ate the contaminated feed during its first year of life. Remember, if a cow becomes infected with the abnormal prion when it is one-year-old, it usually will not show signs of BSE until it is five-years-old or possibly older.

Learn more tomorrow in Part II on Mad Cow Disease.

 

 

QUOTE FOR MONDAY:

Apr22

“Meningitis is an inflammation of the membranes that cover the brain and spinal cord. It can be caused by a number of infectious agents including viruses and bacteria. The type of meningitis and its cause can only be determined by conducting laboratory tests.

Viral meningitis (also called aseptic meningitis) is the most common type of meningitis and is less severe than bacterial meningitis. In Illinois, an average of 600 cases of aseptic meningitis is reported annually, with most occurring in late summer and early autumn. The majority of cases of aseptic meningitis are due to viruses called enteroviruses that can infect the stomach and small intestine. A small number of cases are caused by different viruses, which can be transmitted by infected mosquitoes; these are called arboviruses. Fatal cases of viral meningitis are rare and complete recovery is the rule.

Bacterial meningitis is often more severe than aseptic meningitis, particularly in infants and the elderly. Before antibiotics were widely used, 70 percent or more of bacterial meningitis cases were fatal; with antibiotic treatment, the fatality rate has dropped to 15 percent or less. Bacterial meningitis is most common in the winter and spring. Three bacteria cause the majority of cases: Haemophilus influenzae, Neisseria meningitidis or Streptococcus pneumoniae.”

Illinois Dept. Public Health-IDPH (https://dph.illinois.gov/topics-services/diseases-and-conditions/diseases-a-z-list/meningitis.html)

 

Meningococcal Meningitis

Apr22

 

Meningococcal meningitis is a form of meningitis caused by a specific bacterium known as Neisseria meningitidis. Meningitis is characterized by inflammation of the membranes (meninges) around the brain or spinal cord. This inflammation can begin suddenly (acute) or develop gradually (subacute).

Meningococcal meningitis is a form of meningitis caused by a specific bacterium known as Neisseria meningitidis. Meningitis is characterized by inflammation of the membranes (meninges) around the brain or spinal cord. This inflammation can begin suddenly (acute) or develop gradually (subacute). Symptoms may include fever, headache, and a stiff neck, sometimes with aching muscles. Nausea, vomiting and other symptoms may also occur. Skin rashes occur in about half of all individuals with meningococcal meningitis.

Meningococcal meningitis is still associated with a high mortality rate and persistent neurological defects, particularly among infants and young children. Meningococcal meningitis without antibiotic therapy is uniformly fatal.

Meningococcal meningitis evolves when the bacteria, Neisseria meningitidis (N.meningitidis) progresses from initial adherence to the nasopharyngeal (nose and throat) mucosa to invasion of the deeper mucosal layers (the submucosa). These bacteria rapidly multiply, and can lead to a mild (subclinical) infection. However, in approximately 10-20% of cases, the N.meningitidis enters the bloodstream (meningococcemia). This systemic form of the disease, meningococcemia, usually precedes the development of meningococcal meningitis by 24-48 hours.

Key facts

  • Meningitis is a devastating disease with a high case fatality rate and leading to serious long-term complications (sequelae).
  • Meningitis remains a major global public-health challenge.
  • Epidemics of meningitis are seen across the world, particularly in sub-Saharan Africa.
  • Many organisms can cause meningitis including bacteria, viruses, fungi, and parasites.
  • Bacterial meningitis is of particular concern. Around 1 in 10 people who get this type of meningitis die and 1 in 5 have severe complications.
  • Safe affordable vaccines are the most effective way to deliver long-lasting protection

4 main causes of acute bacterial meningitis:

  • Neisseria meningitidis (meningococcus)
  • Streptococcus pneumoniae (pneumococcus)
  • Haemophilus influenzae
  • Streptococcus agalactiae (group B streptococcus)

The WHO World Health Organization states that these bacteria are responsible for more than half of the deaths from meningitis globally and they cause other severe diseases like sepsis and pneumonia; including other bacteria e.g., Mycobacterium tuberculosis, Salmonella, Listeria, Streptococcus and Staphylococcus, viruses such as enteroviruses and mumps, fungi especially Cryptococcus, and parasites like Amoeba are also important causes of meningitis.

Those at Risk:

Although meningitis affects all ages, young children are most at risk. Newborn babies are at most risk from Group B streptococcus, young children are at higher risk from meningococcus, pneumococcus and Haemophilus influenzae. Adolescents and young adults are at particular risk of meningococcal disease while the elderly are at particular risk of pneumococcal disease.

People all over the world are at risk of meningitis. The highest burden of disease is seen in a region of sub-Saharan Africa, known as the African Meningitis Belt, especially recognised to be at high risk of epidemics of meningococcal but also pneumococcal meningitis.

Higher risk is seen when people are living in close proximity, for example at mass gatherings, in refugee camps, in overcrowded households or in student, military and other occupational settings. Immune deficiencies such as HIV infection or complement deficiency, immunosuppression, and active or passive smoking can also raise the risk of different types of meningitis.

 

 

 

 

QUOTE FOR THE WEEKEND:

Apr20

“With the onset of spring in the Northern Hemisphere, animals that hibernate are waking up from a long-period of deep sleep. They spent the winter hibernating to conserve energy when food was scarce. Animals that hibernate include bats, black bears, Arctic ground squirrels, and common poorwill birds. Many other species such as raccoons and skunks go into a state of torpor during the cold weather, which is a type of light hibernation. Most hibernators wake up during the months of March and April, but some do so as late as May.”

Earth Sky (https://earthsky.org/earth/spring-means-these-4-hibernators-are-waking-up/)