Nova Scotia Health Card (MSI)

Nova Scotia's Health Insurance Programs are designed to provide eligible residents with coverage for medically required hospital, medical, dental and optometric services with some restrictions.

The Medical Services Insurance Programs are administered by Medavie Blue Cross on behalf of the Nova Scotia government. The Department of Health provides policy direction for the programs. The Hospital Insurance Program is administered directly by the Department of Health. The cost of providing these services to Nova Scotians is met through the general revenues of the province. You pay no premiums.

Please carry your signed Nova Scotia Health Card with you at all times. You must present it to the physician and/or hospital each time you need insured hospital or physician services.

This website is designed to provide Nova Scotians with general information on the features and benefits of Nova Scotia Medical Services Insurance. Changes may be made from time to time.

What is Vibrio

Vibrio parahaemolyticus is a bacterium in the same family as those that cause cholera. It lives in brackish saltwater and causes gastrointestinal illness in humans. V. parahaemolyticus naturally inhabits coastal waters in the United States and Canada and is present in higher concentrations during summer; it is a halophilic, or salt-requiring organism.
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What type of illness is caused by V. parahaemolyticus?
When ingested, V. parahaemolyticus causes watery diarrhea often with abdominal cramping, nausea, vomiting, fever and chills. Usually these symptoms occur within 24 hours of ingestion. Illness is usually self-limited and lasts 3 days. Severe disease is rare and occurs more commonly in persons with weakened immune systems. V. parahaemolyticus can also cause an infection of the skin when an open wound is exposed to warm seawater.
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How does infection with V. parahaemolyticus occur?
Most people become infected by eating raw or undercooked shellfish, particularly oysters. Less commonly, this organism can cause an infection in the skin when an open wound is exposed to warm seawater.
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How common is infection with V. parahaemolyticus?
An estimated 4500 cases of V. parahaemolyticus infection occur each year in the United States. However, the number of cases reported to CDC is much lower because surveillance is complicated by underreporting. Laboratories rarely use the selective medium that is necessary to identify this organism, and it is likely that many cases are undetected. To improve our ability to monitor trends, infections caused by V. parahaemolyticus and other Vibrio species became nationally notifiable in 2007. State health departments report cases to CDC, and these reports are summarized annually.
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How is V. parahaemolyticus infection diagnosed?
Vibrio organisms can be isolated from cultures of stool, wound, or blood. For isolation from stool, use of a selective medium that has thiosulfate, citrate, bile salts, and sucrose (TCBS agar) is recommended. If there is clinical suspicion for infection with this organism, the microbiology laboratory should be notified so that they will perform cultures using this medium. A physician should suspect V. parahaemolyticus infection if a patient has watery diarrhea and has eaten raw or undercooked seafood, especially oysters, or when a wound infection occurs after exposure to seawater.
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How is V. parahaemolyticus treated?
Treatment is not necessary in most cases of V. parahaemolyticus infection. There is no evidence that antibiotic treatment decreases the severity or the length of the illness. Patients should drink plenty of liquids to replace fluids lost through diarrhea. In severe or prolonged illnesses, antibiotics such as tetracycline or ciprofloxicin can be used. The choice of antibiotics should be based on antimicrobial susceptibilities of the organism.
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How do oysters get contaminated with V. parahaemolyticus?
Vibrio is a naturally occurring organism commonly found in waters where oysters are cultivated. When the appropriate conditions occur with regard to salt content and temperature, V. parahaemolyticus thrives.
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How is V. parahaemolyticus infection prevented?
Most infections caused by V. parahaemolyticus in the United States can be prevented by thoroughly cooking seafood, especially oysters. Wound infections can be prevented by avoiding exposure of open wounds to warm seawater. When an outbreak is traced to an oyster bed, health officials recommend closing the oyster bed until conditions are less favorable for V. parahaemolyticus.
Timely, voluntary reporting of V. parahaemolyticus infections to state health departments and to regional offices of the Food and Drug Administration (FDA) will help collaborative efforts to improve investigation of these infections. Regional FDA specialists with expert knowledge about shellfish assist state officials with tracebacks of shellfish. When notified rapidly about cases, officials can sample harvest waters to discover possible sources of infection and may close oyster beds. Ongoing research may help us to predict environmental or other factors that increase the chance that oysters carry Vibrios.
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How can I learn more about Vibrio parahaemolyticus?
You can discuss medical concerns with your doctor or other health care provider. Your local health department can provide information about this and other public health problems. Information about problems associated with raw seafood consumption can be obtained from the FDA’s Center for Food Safety and Applied Nutrition (telephone 1-800-332-4010). At this number recorded information is available on many subjects including seafood consumption and handling. A public affairs specialist is available 12:00 p.m.-4:00 p.m. Eastern Standard Time. Seafood safety information is also available on the world wide web at http://vm.cfsan.fda.gov and http://seafood.ucdavis.edu. There is more information about other Vibrio infections, such as Vibrio vulnificus.
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* Links to non-Federal organizations found at this site are provided solely as a service to our users. These links do not constitute an endorsement of these organizations or their programs by CDC or the Federal Government, and none should be inferred. CDC is not responsible for the content of the individual organization Web pages found

What Is Pseudomonas aeruginosa

Pseudomonas aeruginosa is an opportunistic bacteria that lives in soil, water, and even in environments like hot tubs. For most healthy people, this bacteria seldom poses a problem. Occasionally people will develop conditions like hot tub rash, and swimmer’s ear, which may be due to contact with these germs. These conditions can sometimes resolve without treatment, or with minimal treatment, like antibiotic drops for swimmer’s ear.
Unfortunately, Pseudomonas aeruginosa is much more dangerous to certain populations, including those who have weak immune systems, the elderly, and those who have been hospitalized for long periods of time. People with cystic fibrosis and with full-blown AIDs frequently die from infections created by the bacteria. Those who have undergone chemotherapy, have had transplants, or have any of a variety of immunosuppressed conditions are far more at risk for developing bacterial infections due to Pseudomonas aeruginosa, and because this bacteria is relatively resistant to most antibacterial medications, infection can be deadly, particularly when it becomes infection of the lungs or bloodstream.
Doctors and medical researchers often refer to Pseudomonas aeruginosa as a blue-green pus bacteria, and/or a gram-negative bacteria. The first reference is to the pus, which can show blue to green colors, and the second refers to the Gram method for staining bacteria to determine what type it is. When samples of gram-negative bacteria, particularly those that are considered aerobic, are stained, they resist color and typically show up in slides under the microscope as a pink color. Aerobic bacteria refers to bacteria that needs oxygen to survive, which Pseudomonas aeruginosa has in ample amounts, particularly in hospital settings.
As mentioned, though Pseudomonas aeruginosa tends to live all around us, it is most dangerous to those who are in weakened physical states or have immunodeficiencies. Despite hospital cleaning and safety the bacteria may aggressively survive in basic hospital equipment, like masks used to give oxygen, breathing apparatus, or catheters for urine. Typically most common infections induced by the bacteria are of the bladder, lungs or bloodstream. Inability to produce normal immune reactions to the presence of the bacteria can mean this germ can easily result in extremely grave health conditions.
Treatment of Pseudomonas aeruginosa is usually through intravenous multiple antibiotic combinations, and it unfortunately does not always work. However, there is hope in this field, which may ultimately put an end to the suffering this bacteria may cause. Preliminary studies on a Pseudomonas aeruginosa vaccine are underway, and although these studies have not yet concluded that a currently developed vaccine is completely effective, early results do show that the vaccine can potentially reduce number of infections, as of mid-2007. These early results do not show complete protection from infection, but they are promising as to a reduction, when compared with a placebo group. Such a vaccine could indeed be a boon to the medical community and all those who are at particular risk for life-threatening infections from this bacteria

The serotonin syndrome.

Department of Psychiatry, UCLA-Neuropsychiatric Institute, Los Angeles.
OBJECTIVE AND METHOD: A review of the literature on the serotonin syndrome in animals and human beings was conducted, and 12 reports of 38 cases in human patients were then analyzed to determine the most frequently reported clinical features and drug interactions, as well as the incidence, treatment, and outcome of this syndrome. FINDINGS: The serotonin syndrome is most commonly the result of the interaction between serotonergic agents and monoamine oxidase inhibitors. The most frequent clinical features are changes in mental status, restlessness, myoclonus, hyperreflexia, diaphoresis, shivering, and tremor. The presumed pathophysiological mechanism involves brainstem and spinal cord activation of the 1A form of serotonin (5-hydroxytryptamine, or 5-HT) receptor. The incidence of the syndrome is not known. Both sexes have been affected, and patients' ages have ranged from 20 to 68 years. Discontinuation of the suspected serotonergic agent and institution of supportive measures are the primary treatment, although 5-HT receptor antagonists may also play a role. Once treatment is instituted, the syndrome typically resolves within 24 hours, but confusion can last for days, and death has been reported. CONCLUSIONS: The serotonin syndrome is a toxic condition requiring heightened clinical awareness for prevention, recognition, and prompt treatment. Further work is needed to establish the diagnostic criteria, incidence, and predisposing factors, to identify the role of 5-HT antagonists in treatment, and to differentiate the syndrome from neuroleptic malignant syndrome.
PMID: 2035713 [PubMed - indexed for MEDLINE]

International Union of Pharmacology classification of receptors for 5-hydroxytryptamine (Serotonin).

Sandoz Pharma Limited, Basel, Switzerland.
It is evident that in the last decade or so, a vast amount of new information has become available concerning the various 5-HT receptor types and their characteristics. This derives from two main research approaches, operational pharmacology, using selective ligands (both agonists and antagonists), and, more recently, molecular biology. Although the scientific community continues to deliberate about the hierarchy of criteria for neurotransmitter receptor characterisation, there seems good agreement between the two approaches regarding 5-HT receptor classification. In addition, the information regarding transduction mechanisms and second messengers is also entirely consistent. Thus, on the basis of these essential criteria for receptor characterisation and classification, there are at least three main groups or classes of 5-HT receptor: 5-HT1, 5-HT2, and 5-HT3. Each group is not only operationally but also structurally distinct, with each receptor group having its own distinct transducing system. The more recently identified 5-HT4 receptor almost undoubtedly represents a fourth 5-HT receptor class on the basis of operational and transductional data, but this will only be definitively shown when the cDNA for the receptor has been cloned and the amino acid sequence of the protein is known. Although those 5-HT receptors that have been fully characterised and classified to date (and, hence, named with confidence) would seem to mediate the majority of the actions of 5-HT throughout the mammalian body, not all receptors for 5-HT are fully encompassed within our scheme of classification. These apparent anomalies must be recognised and need further study. They may or may not represent new groups of 5-HT receptor or subtypes of already known groups of 5-HT receptor. Even though the cDNAs for the 5-ht1E, 5-ht1F, 5-ht5, 5-ht6, and 5-ht7 receptors have been cloned and their amino acid sequence defined, more data are necessary concerning their operational and transductional characteristics before one can be confident of the suitability of their appellations. Therefore, it is important to rationalise in concert all of the available data from studies involving both operational approaches of the classical pharmacological type and those from molecular and cellular biology.(ABSTRACT TRUNCATED AT 400 WORDS)
PMID: 7938165 [PubMed - indexed for MEDLINE]

:: Angiogenesis in cancer

How angiogenesis complicates cancer
Angiogenesis performs a critical role in the development of cancer. Solid tumors smaller than 1 to 2 cubic millimeters are not vascularized. To spread, they need to be supplied by blood vessels that bring oxygen and nutrients and remove metabolic wastes.

Beyond the critical volume of 2 cubic millimeters, oxygen and nutrients have difficulty diffusing to the cells in the center of the tumor, causing a state of cellular hypoxia that marks the onset of tumoral angiogenesis.

New blood vessel development is an important process in tumor progression. It favors the transition from hyperplasia to neoplasia i.e. the passage from a state of cellular multiplication to a state of uncontrolled proliferation characteristic of tumor cells.

Neovascularization also influences the dissemination of cancer cells throughout the entire body eventually leading to metastasis formation.The vascularization level of a solid tumor is thought to be an excellent indicator of its metastatic potential.

The molecular factors involved in the stimulation of blood vessel growth are described in detail in The process of angiogenesis.







Shortcomings of standard therapies


Standard therapies to combat cancer are usually aimed at interfering with the cellular replication process which is accelerated in tumors. Despite the efforts made since 1971 to fight cancer -- the year the United States declared war on the disease -- new cases of most cancers have increased significantly. Ninety percent of all cancers are solid tumors and thus depend on angiogenesis to support their growth.

Resistance to treatment is a major issue in oncology. In hormone-dependent cancer for instance, after standard anti-hormonal therapy, it is common to see a recurrence of cancer. This occurs when a malignant cell is transformed a second time, thus making its replication independent of hormones. The same phenomenon takes place with cancers treated with chemotherapy. Often a transformed cell exposed to a powerful chemical agent goes through a mutation, giving it a selective advantage for growth, such as the production of a growth factor or resistance to chemotherapeutic agents.

It has also been shown that the resection of a primary tumor is often accompanied by metastases caused by a systemic disturbance of the angiogenic balance of the body. All these standard therapies could profit from a concomitant treatment that would restrict latent tumors in a prevascular phase.


Antiangiogenesis as a strategy against cancer


As early as the 1970s, Dr. Judah Folkman of the Harvard Medical School suggested inhibiting new blood vessel formation as a way to fight cancer.

The malignant tissue would be deprived of its oxygen and nutrient supply, as well as be unable to eliminate metabolic wastes. This in turn would inhibit tumor progression and metastatic progression that accompanies most advanced cancers. These are the main steps of the angiogenic process that can be interrupted:

Inhibiting endogenous angiogenic factors, such as bFGF (basic Fibroblast Growth Factor) and VEGF (Vascular Endothelial Growth Factor)


Inhibiting degradative enzymes (Matrix Metalloproteinases) responsible for the degradation of the basement membrane of blood vessels


Inhibiting endothelial cell proliferation


Inhibiting endothelial cell migration


Inhibiting the activation and differentiation of endothelial cells
However, the challenge is to develop an antiangiogenic factor that does not affect the existing vasculature.



Neovastat is an inhibitor of angiogenesis


A number of studies have shown Neovastat to have antiangiogenic properties. The mechanisms of action include:

Inhibiting degradative Matrix Metalloproteinases,


Blocking receptor sites for the angiogenic growth factor VEGF, which prevents endothelial cells from proliferating, migrating, and organizing to form new blood vessels in vitro.
As well, clinical and pre-clinical studies show Neovastat can be used alone or in combination with other therapies. Clinical experience with 540 patients, some of whom have been administered the drug for almost four years, have confirmed Neovastat’s excellent safety and tolerability profile in monotherapy and in concomitant chemotherapy and radiotherapy.

(Angio World)

Process of Angiogenesis

Physiological and pathological angiogenesis

Almost all tissues develop a vascular network that provides cells with nutrients and oxygen and enables them to eliminate metabolic wastes. Once formed, the vascular network is a stable system that regenerates slowly.

In physiological conditions, angiogenesis occurs primarily in embryo development, during wound healing and in response to ovulation.

However, pathological angiogenesis, or the abnormal rapid proliferation of blood vessels, is implicated in over 20 diseases, including cancer, psoriasis and age-related macular degeneration.

The angiogenic sequence



The angiogenic process, as currently understood, can be summarized as follows:

A cell activated by a lack of oxygen releases angiogenic molecules that attract inflammatory and endothelial cells and promote their proliferation.


During their migration, inflammatory cells also secrete molecules that intensify the angiogenic stimuli.


The endothelial cells that form the blood vessels respond to the angiogenic call by differentiating and by secreting matrix metalloproteases (MMP), which digest the blood-vessel walls to enable them to escape and migrate toward the site of the angiogenic stimuli.


Several protein fragments produced by the digestion of the blood-vessel walls intensify the proliferative and migratory activity of endothelial cells, which then form a capillary tube by altering the arrangement of their adherence-membrane proteins.


Finally, through the process of anastomosis, the capillaries emanating from the arterioles and the venules will join, thus resulting in a continuous blood flow.




The normal regulation of angiogenesis is governed by a fine balance between factors that induce the formation of blood vessels and those that halt or inhibit the process. When this balance is destroyed, it usually results in pathological angiogenesis which causes increased blood-vessel formation in diseases that depend on angiogenesis.

More than 20 endogenous positive regulators of angiogenesis have been described, including growth factors, matrix metalloproteinases, cytokines, and integrins. Growth factors, such as vascular endothelial growth factor (VEGF), transforming growth factors (TGF-beta), fibroblast growth factors (FGF), epidermal growth factor (EGF), angiogenin, can induce the division of cultured endothelial cells thus indicating a direct action on these cells.

However, other factors have virtually no effect on the division of cultured endothelial cells or, in the case of TGF-beta and TNF-alpha, paradoxically inhibit their growth indicating that their angiogenic action is indirect.