28 July 2010

Salmonella paratypi b Version 1.0

The hadoscan can pick up Salmonella paratypi b and frequencies can be determined from infected individuals. This strain of Salmonella is particularly bad as it can cause typhoid fever. Frequencies are available to subscribers.

Salmonella paratyphi b

Today, the Hawaii Department of Health announced a Salmonella paratyphi b outbreak linked to ahi tuna.  Interestingly, the ten illnesses in Hawaii appear to be linked to 13 other illnesses nationally, and possibly even linked to an outbreak of illnesses linked to the same product two years ago.  (We reported on this phase of the outbreak in February 2008).  Was it a frozen product that was held at the manufacturer or distributor's facilities for two years, and finally released now?  Or is there a persistent source of the paratyphi b strain at the manufacturer's facilities?
The paratyphi b strain of salmonella is different from those that we see most frequently in foodpoisoning outbreaks.  There are well over 2,000 individual strains of salmonella, but not all of them cause typhoid fever.  Paratyphi b, however, does cause typhoid fever. 
Typhoid fever is the most serious form of enteric fever, with humans being the sole reservoir of the bacteria. Based on a recent survey, the global number of typhoid cases in 2000 exceeded 21,000,000, with more than 200,000 deaths [1]. Enteric fever, that is typhoid and paratyphoid fevers, is the common name for infections caused by Salmonella enterica serotypes typhi and paratyphi. Of the three types of S. paratyphi (A, B, and C), B is the most common.
http://casesjournal.com/content/1/1/403.  Salmonella typhi and paratyphi are also more likely than other salmonella serotypes to cause enteric fever, as well as the chronic carrier state.
Typhoid fever, or enteric fever, differs from the typical salmonella gastrointestinal illness in that typhoid fever does not always cause severe gastrointestinal symptoms. 
The syndrome of enteric fever is characterized by prolonged sustained fever, relative bradycardia, hepatosplenomegaly, rose spots, and leucopenia and neutropenia [3]. After an incubation period of 5 to 21 days (generally 7 to 14 days), fever and malaise develop, often associated with cough. A small proportion of patients may have diarrhea during the incubation period. The fever tends to rise in stepwise fashion over the first few days to a week and then becomes sustained, usually at 39.4 to 40°C (103 to 104°F) or higher. After 2 weeks of illness, the severe complications of intestinal hemorrhage or perforation may be observed. The illness usually resolves by the end of the fourth week in an untreated patient. Relapse may occur in untreated as well as treated patients, but the illness is milder than the original episode. Rarely, some of the following complications may occur: pancreatitis, cholecystitis, infective endocarditis, pneumonia, hepatic or splenic abscess, orchitis, or focal infection at virtually any site [6].

14 July 2010

Polio Virus Version 1.0

The lyme complex has hundreds of viruses and as ongoing research determines the actual pathogen corresponding to certain frequency sequences we discover that organisms like polio virus are there in lyme infections. The virus is latent in individuals exposed to polio, even though they may have been vaccinated several times so researchers should check for the present of this virus, particularly if they have been exposed to lyme.

The virus is embedded in the lyme virus program. It is broken out on the Frequency Foundation subscribers blog so that researchers can give it special attention.


Pathogenesis


Electron micrograph of poliovirus.
The primary determinant of infection for any virus is its ability to enter a cell and produce additional infectious particles. The presence of CD155 is thought to define the animals and tissues that can be infected by poliovirus. CD155 is found (outside of laboratories) only on the cells of humans, higher primates, and Old World monkeys. Poliovirus is however strictly a human pathogen, and does not naturally infect any other species (although chimpanzees and Old World monkeys can be experimentally infected).[31]
Poliovirus is an enterovirus. Infection occurs via the fecal-oral route, meaning that one ingests the virus and viral replicaion occurs in the alimentary tract.[32] Virus is shed in the feces of infected individuals. In 95% of cases only a primary, transient presence of viremia (virus in the bloodstream) occurs, and the poliovirus infection is asymptomatic. In about 5% of cases, the virus spreads and replicates in other sites such as brown fatreticuloendothelialtissue, and muscle. The sustained viral replication causes secondary viremia and leads to the development of minor symptoms such as fever, headache and sore throat.[33] Paralytic poliomyelitis occurs in less than 1% of poliovirus infections. Paralytic disease occurs when the virus enters the central nervous system (CNS) and replicates in motor neurons within the spinal cordbrain stem, or motor cortex, resulting in the selective destruction of motor neurons leading to temporary or permanent paralysis. In rare cases, paralytic poliomyelitis leads to respiratory arrest and death. In cases of paralytic disease, muscle pain and spasms are frequently observed prior to onset of weakness and paralysis. Paralysis typically persists anywhere from days to weeks prior to recovery.[34][35]
In many respects the neurological phase of infection is thought to be an accidental diversion of the normal gastrointestinal infection.[15] The mechanisms by which poliovirus enters the CNS are poorly understood. Three non-mutually exclusive hypotheses have been suggested to explain its entry. All theories require primary viremia. The first hypothesis predicts that virions passes directly from the blood into the central nervous system by crossing the blood brain barrier independent of CD155.[36] A second hypothesis suggests that the virions are transported from peripheral tissues that have been bathed in the viremic blood, for example muscle tissue, to the spinal cord through nerve pathways via retrograde axonal transport.[37][38][39] A third hypothesis is that the virus is imported into the CNS via infected monocytes or macrophages.[8]
Poliomyelitis is a disease of the central nervous system. However, CD155 is believed to be present on the surface of most or all human cells. Therefore receptor expression does not explain why poliovirus preferentially infects certain tissues. This suggests that tissue tropism is determined after cellular infection. Recent work has suggested that the type I interferon response (specifically that of interferon alpha and beta) is an important factor that defines which types of cells support poliovirus replication.[40] In mice expressing CD155 (through genetic engineering) but lacking the type I interferon receptor, poliovirus not only replicates in an expanded repertoire of tissue types, but these mice are also able to be infected orally with the virus.[41]

This frequency set is available on the Frequency Foundation subscribers blog.

02 July 2010

Parasites Rule the World - Toxoplasma gondii


Landon Donovan Needs a CatCould a brain parasite found in cats help soccer teams win at the World Cup?

Ghana player Kevin-Prince Boateng. Click image to expand.What if I told you that last week I predicted all eight winners of a round of the World Cup? And that instead of rankings or divination all I did was look up how many people in each team's home country had a tiny parasite lurking in their amygdalas? Would you believe me? A decade ago,Discover Magazine concluded that parasites ruled the world, and now I'm going to try to tell you that, at the very least, parasites rule the World Cup.
First, a quick primer on the organism in question, a single-celled parasite called Toxoplasma gondii.

Toxoplasmosis


Diagram of Toxoplasma gondiistructure
T. gondii infections have the ability to change the behavior of rats and mice, making them drawn to rather than fearful of the scent of cats. This effect is advantageous to the parasite, which will be able to sexually reproduce if its host is eaten by a cat.[11] The infection is highly precise, as it does not affect a rat's other fears such as the fear of open spaces or of unfamiliar smelling food.
Studies have also shown behavioral changes in humans, including slower reaction times and a sixfold increased risk of traffic accidents among infected males, as well as links to schizophrenia including hallucinations and reckless behavior[13]. Additionally, studies of students and conscript soldiers in the Czech Republic in the mid-1990s highlighted the fact that infected people showed different personality traits to uninfected people—and that the differences depended on sex. Infected women were more likely to become more outgoing and showed signs of higher intelligence, while men became aggressive, jealous and suspicious.
The prevalence of human infection by Toxoplasma varies greatly between countries. Factors that influence infection rates include diet (prevalence is possibly higher where there is a preference for less-cooked meat) and proximity to cats. It has been suggested that climate change will also influence Toxoplasma gondii prevalence in some regions of the world.
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