Thursday, October 31, 2013

CDC Recommends Hepatitis C Testing For All Boomers

Listen up, baby boomers. The government wants every one of you to get tested for the hepatitis C virus.

The Centers for Disease Control and Prevention made a sweeping recommendation official amid growing concern about the estimated 2 million boomers infected with the virus, which can cause cirrhosis and liver cancer. The in the latest Morbidity and Mortality Weekly Report.
CDC officials say most of these people don't know they are infected and will develop liver disease unless they get treatment that clears the virus from the body.
The agency decided to target people born from 1945 through 1965 because they are five times more likely than other adults to carry the hepatitis C virus. About 1 in 30 boomers is infected and thousands die each year of cirrhosis and liver cancer.
One reason so many boomers are infected is that more than a few used injected drugs much earlier in their lives, says , who runs the CDC's viral hepatitis division.
"We had an epidemic of hepatitis C transmission in the '70s and '80s, and we're now seeing an epidemic of hepatitis C disease," he says
The virus hepatitis C virus can be transmitted through sharing needles. It was also spread through blood transfusions and organ transplants before widespread screening of the blood supply began in 1992.
Ward says a blood test is the only way for a person to know if they have hepatitis C.
"Even at the time of infection, it often does not cause any symptoms," he says. Over years or even decades the infection causes scarring in the liver. But by the time symptoms appear, he says, "they may have already have developed cirrhosis or even liver cancer."
Until now, the CDC recommended testing only for people with known risk factors. That meant relying on patients to reveal to a doctor that they were at risk. "I felt we were battling this problem with one arm tied behind our back," Ward says.
One problem is that many patients don't want to talk about behavior that could have caused their infection, says director of hepatology at Duke University.
"A lot of the people that I meet who have been diagnosed with hepatitis C did use injection drugs many years ago," he says. "But many of them have moved on and are at a very different place in their lives," he says.
Unfortunately, reluctance to talk about things like drug use can have major health consequences, Muir says.
"When I meet a patient who shows up with a liver cancer or shows up at the point where they need a liver transplant it's especially poignant, because I know that if we'd identified them a few years ago we could have treated them and prevented this from happening," Muir says.
Muir hopes more people will be treated now that screening extends to everyone in a specific age group. And thanks to new drugs, he says, up to three-quarters of people who finish treatment completely clear the virus from their body.
But Muir says treatment remains expensive and gruelling.
It can cost $100,000, which can be beyond the reach of people without health insurance, Muir says. And having hepatitis C can make it hard to get insurance.
CDC officials acknowledged that health insurance is a problem for people with hepatitis C infection when they published a draft of the current recommendation several months ago. The agency likes to showing that it's cheaper for insurers to pay for treatment that eliminates the virus than pay for the care of patients who get sick.
Another concern about treatment involves its lengthy course and unpleasant side effects. Treatment regimens can take up to 48 weeks, although many patients are able to finish in half that time. And the drugs can cause fevers, chills, muscle aches, vomiting and depression.
But there are dozens of new hepatitis C drugs in the pipeline, Muir says. That should mean that treatment will becomes more effective, quicker and less arduous, he says.


Hepatitis E

From Wikipedia, the free encyclopedia

Hepatitis E
Classification and external resources
Hepatitis E virus.jpg
ICD-10 B17.2
ICD-9 070.4
DiseasesDB 5794
eMedicine med/995
MeSH D016751
Hepatitis E is a viral hepatitis (liver inflammation) caused by infection with a virus called hepatitis E virus (HEV). HEV is a positive-sense single-stranded RNA icosahedral virus with a 7.5 kilobase genome. HEV has a fecal-oral transmission route. It is one of five known hepatitis viruses: A, B, C, D, and E. Infection with this virus was first documented in 1955 during an outbreak in New Delhi, India.[1] A preventative vaccine (HEV 239) is approved for use in China.
The incidence of hepatitis E is highest in juveniles and adults between the ages of 15 and 40. Though children often contract this infection as well, they less frequently become symptomatic. Mortality rates are generally low, for hepatitis E is a "self-limiting" disease, in that it usually goes away by itself and the patient recovers. However, during the duration of the infection (usually several weeks), the disease severely impairs a person’s ability to work, care for family members, and obtain food. Hepatitis E occasionally develops into an acute, severe liver disease, and is fatal in about 2% of all cases. Clinically, it is comparable to hepatitis A, but in pregnant women the disease is more often severe and is associated with a clinical syndrome called fulminant hepatic failure. Pregnant women, especially those in the third trimester, suffer an elevated mortality rate from the disease of around 20%.[2]

Signs and symptoms

Acute infection

The incubation period of hepatitis E varies from 3 to 8 weeks. After a short prodromal phase symptoms lasting from days to weeks follow. They may include jaundice, fatigue and nausea. The symptomatic phase coincides with elevated hepatic aminotransferase levels.[3]
Viral RNA becomes detectable in stool and blood serum during incubation period. Serum IgM and IgG antibodies against HEV appear just before onset of clinical symptoms. Recovery leads to virus clearance from the blood, while the virus may persist in stool for much longer. Recovery is also marked by disappearance of IgM antibodies and increase of levels of IgG antibodies.[3]

Chronic infection

While usually an acute disease, in immunocompromised subjects—particularly in solid organ transplanted patients—hepatitis E may cause a chronic infection.[4] Occasionally this may cause liver fibrosis and cirrhosis.



There is only one serotype of the virus and classification is based on the nucleotide sequences of the genome.[5] Genotype 1 has been classified into five subtypes. The number of genotype 2 can be classified into two subtypes. Genotypes 3 and 4 have been into ten and seven subtypes respectively.
Differences have been noted between the different genotypes. For genotype 1, the age at which incidence peaks is between 15 and 35 years and mortality is about 1%. Genotype 3 and 4—the most common in Japan—are more common in people older than 60 years and the mortality is between 5 and 10%.[6]


Genotype 1 has been isolated from tropical and several subtropical countries in Asia and Africa. Genotype 2 has been isolated from Mexico, Nigeria, and Chad. Genotype 3 has been isolated almost worldwide including Asia, Europe, Oceania, North and South America. Genotype 4 appears to be limited exclusively to Asia.
Genotypes 1 and 2 are restricted to humans and often associated with large outbreaks and epidemics in developing countries with poor sanitation conditions. Genotypes 3 and 4 infect humans, pigs and other animal species and have been responsible for sporadic cases of hepatitis E in both developing and industrialized countries.
In the United Kingdom the Department for Environment, Food and Rural Affairs (DEFRA) said that the number of human hepatitis E cases increased by 39% between 2011 and 2012.[7]


Hepatitis E is prevalent in most developing countries, and common in any country with a hot climate. It is widespread in Southeast Asia, northern and central Africa, India, and Central America. It is spread mainly through fecal contamination of water supplies or food; person-to-person transmission is uncommon.
The incubation period following exposure to the hepatitis E virus ranges from three to eight weeks, with a mean of 40 days.[8] Outbreaks of epidemic hepatitis E most commonly occur after heavy rainfalls and monsoons because of their disruption of water supplies. Major outbreaks have occurred in New Delhi, India (30,000 cases in 1955–1956), Burma (20,000 cases in 1976–1977), Kashmir, India (52,000 cases in 1978), Kanpur, India (79,000 cases in 1991), and China (100,000 cases between 1986 and 1988).
DEFRA said that there was evidence that the increase in hepatitis E in the UK was due to food-borne zoonoses, citing a study that found 10% of pork sausages on sale in the UK contained the virus. Some research suggests that food must reach a temperature of 70°C for 20 minutes to eliminate the risk of infection. An investigation by the Animal Health and Veterinary Laboratories Agency found hepatitis E in 49% of pigs in Scotland.[7]

Animal reservoir

Domestic animals have been reported as a reservoir for the hepatitis E virus, with some surveys showing infection rates exceeding 95% among domestic pigs.[9] Replicative virus has been found in the small intestine, lymph nodes, colon and liver of experimentally infected pigs. Transmission after consumption of wild boar meat and uncooked deer meat has been reported as well.[10] The rate of transmission to humans by this route and the public health importance of this are, however, still unclear.[11]
A number of other small mammals have been identified as potential reservoirs: the lesser bandicoot rat (Bandicota bengalensis), the black rat (Rattus rattus brunneusculus) and the Asian house shrew (Suncus murinus).[12] A new virus designated rat hepatitis E virus has been isolated.[13]
A rabbit hepatitis E virus has also been described.[14]
An avian virus has been described that is associated with hepatitis-splenomegaly syndrome in chickens. This virus is genetically and antigenically related to mammalian HEV, and probably represents a new genus in the family.

Molecular biology

Although it was originally classified in the Caliciviridae family, the virus has since been classified into the genus Hepevirus, and has been reassigned into the Hepeviridae family. The virus itself is a small non-enveloped particle.
The genome is approximately 7200 bases in length, is a polyadenylated single-strand RNA molecule that contains three discontinuous and partially overlapping open reading frames (ORFs) along with 5' and 3' cis-acting elements, which have important roles in HEV replication and transcription. ORF1 encode a methyltransferase, protease, helicase and replicase; ORF2 encode the capsid protein and ORF3 encodes a protein of undefined function. A three-dimensional, atomic-resolution structure of the capsid protein in the context of a virus-like particle has been described.[15] An in vitro culture system is not yet available.
As of 2009 there are approximately 1,600 sequences of both human and animal isolates of HEV available in open-access sequence databases.
Species of this genus infect humans, pigs, boars, deer, rats, rabbits and birds.[16]



Improving sanitation is the most important measure in prevention of hepatitis E; this consists of proper treatment and disposal of human waste, higher standards for public water supplies, improved personal hygiene procedures and sanitary food preparation. Thus, prevention strategies of this disease are similar to those of many others that plague developing nations, and they require large-scale international financing of water supply and water treatment projects.


A vaccine based on recombinant viral proteins was developed in the 1990s and tested in a high-risk population (military personnel of Nepal) in 2001.[17] The vaccine appeared to be effective and safe, but development stopped for economical reasons, since hepatitis E is rare in developed countries.[18] There is no licensed hepatitis E vaccine for use in the US.
Although other HEV vaccine trials, including trials conducted in populations in southern Asia, have shown candidate vaccines to be effective and well-tolerated, these vaccines have not yet been produced or made available to susceptible populations. The exception is China. After more than a year of scrutiny and inspection by China's State Food and Drug Administration (SFDA), a hepatitis E vaccine developed by Chinese scientists was available at the end of 2012. This vaccine—called HEV 239 and sold as Hecolin by its developer Xiamen Innovax Biotech—was approved for prevention of hepatitis E in 2012 by the Chinese Ministry of Science and Technology, following a phase 3 trial on two groups of 50,000 people each from Jiangsu Province where none of the vaccinated became infected during a 12-month period, compared to 15 in the group given placebo treatment.[19] The first vaccine batches came out of Innovax' factory in late October 2012, and will be sold to Chinese distributors.[18]


Although prednisolone has been used in the treatment of this condition, because large scale studies have not yet been reported the role of this drug in treatment is not yet clear.[citation needed]

Chronic infection

The use of low doses, 600 to 800 milligrams per day, of ribavirin over a three-month period has been associated with viral clearance in about two-thirds of chronic cases. Other possible treatments include peginterferon or a combination of ribavirin and peginterferon. In one thirds of patients with solid-organ transplantation viral clearance can be achieved by temporal reduction of the level of immunosuppression.[3]


The hepatitis E virus causes around 20 million infections a year. These result in around three million acute illnesses and as of 2010 57,000 deaths annually.[20] It is particularly dangerous for pregnant women, who can develop an acute form of the disease that is lethal in 20 per cent of cases. The virus (HEV) is a major cause of illness and of death in the developing world and disproportionate cause of deaths among pregnant women.

Recent outbreaks

In 2004, there were two major outbreaks, both of them in sub-Saharan Africa. There was an outbreak in Chad in which, as of September 27, there were 1,442 reported cases and 46 deaths. The second was in Sudan with, as of September 28, 6,861 cases and 87 deaths. Increasingly, hepatitis E is being seen in developed nations, with reports of cases in the UK, US and Japan. The disease is thought to be a zoonosis in that animals are thought to be the source. Both deer and swine have been implicated.
In October 2007, an epidemic of hepatitis E was suspected in Kitgum District of northern Uganda where no previous epidemics had been documented. This outbreak has progressed to become one of the largest hepatitis E outbreaks in the world. By June 2009, the epidemic had caused illness in >10,196 persons and 160 deaths.[21]
In 2011, a minor outbreak was reported in Tangail, a neighborhood of Dhaka, Bangladesh.[22]
In June 2012, an outbreak was reported in city of Ichalkaranji, Maharashtra, India. As of June 14, 2012, 3232 cases were reported and 18 died.[23] and 3 died in Shirol taluka of Kolhapur Maharashtra, India in June 2012. Officials in the Indian state of Maharashtra India suspect that contaminated water from the Panchganga river was responsible for the hepatitis E outbreak in Ichalkaranji.
In July 2012, an outbreak was reported in South Sudanese refugee camps in Maban County near the Sudan border. South Sudan's Ministry of Health reported over 400 cases and 16 fatalities as of September 13, 2012.[24] Progressing further, as of February 2, 2013, 88 have died due to the outbreak. The "Medical charity Medecins Sans Frontieres (MSF) said it had treated almost 4,000 patients."[25]


The most recent common ancestor of Hepatitis E evolved between 536 and 1344 years ago.[16] It diverged into two clades—an anthropotropic and an enzootic form—which subsequently evolved into genotypes 1 and 2 and genotypes 3 and 4 respectively. The divergence dates for the various genotypes are as follows: Genotypes 1/2 367–656 years ago; Genotypes 3/4 417–679 years ago. For the most recent common ancestor of the various viruses themselves: Genotype 1 between 87 and 199 years ago; Genotype 3 between 265 and 342 years ago; and Genotype 4 between 131 and 266 years ago. The anthropotropic strains (genotype 1 and 2) have evolved more recently than the others suggesting that this virus was originally a zooenosis.
The use of an avian strain confirmed the proposed topology of the genotypes 1–4 and suggested that the genus may have evolved 1.36 million years ago (range 0.23 million years ago to 2.6 million years ago).[16] The use of a rat sequence also confirmed this topology and estimated date of divergence from the swine/human strains was 7.44×104 years ago (range 2.1×104 to 1.4×105 years ago). Since this date is approximately coincident with the advent of agriculture it may be that this virus originally infected rats and subsequently spread to pigs and then to humans. Additional work is required to support or refute this possibility as very few sequences have been isolated from species other than humans and suids.
Genotypes 1, 3 and 4 all increased their effective population sizes in the 20th century.[16] The population size of genotype 1 increased noticeably in the last 30–35 years. Genotypes 3 and 4 population sizes began to increase in the late 19th century up to 1940–1945. Genotype 3 underwent a subsequent increase in population size until the 1960s. Since 1990 both genotypes' population sizes have been reduced back to levels last seen in the 19th century.
The overall mutation rate for the genome has been estimated at ~1.4×10−3 substitutions/site/year.[16]

Viral hepatitis

Viral hepatitis is a silent epidemic in the United States. Although it is a leading infectious cause of death and claims the lives of 12,000–15,000 Americans each year, viral hepatitis remains virtually unknown to the general public, at-risk populations, and policymakers; even health-care providers often lack knowledge and awareness about these infections. As a consequence, most of the 3.5–5.3 million Americans living with viral hepatitis do not know that they are infected, placing them at greater risk for severe, even fatal, complications from the disease and increasing the likelihood that they will spread the virus to others. Viral hepatitis is a major cause of liver cirrhosis and liver cancer in the United States; persons living with viral hepatitis are at increased risk for both conditions.

Hepatitis outbreak linked to semi-dried tomatoes

VICTORIAN health authorities have renewed their warnings over links between semi-dried tomatoes and an outbreak of hepatitis A following a further 23 cases of the infectious disease diagnosed in the past week.
Victoria's chief health officer Dr John Carnie said that so far this year there had been 200 notifications of hepatitis A, compared to 74 at the same time last year.
A study into the increase of cases indicates that more than two thirds of people that have become ill recalled eating semi-dried tomatoes, he said.
"Because the incubation period for hepatitis A could be as long as two months, trying to get people who fell ill to accurately pin down what and where they actually ate this product can be difficult," Dr Carnie said.
"We still are unclear as to why there has been a recent spike in cases in Victoria.
"However, we are continuing to work with the manufacturers and suppliers of semi-dried tomatoes to try and identify the source."
Local producers had promised the Department of Human Services they were doing their best to reduce the risk, while importers of the tomatoes had also been instructed to ensure appropriate quality control measures were in place, he said.
Bottled semi-dried tomatoes in supermarkets were pasteurised and considered safe along with any of the cooked product such as in pizzas or quiches.
The greatest risk would appear to be at restaurants and cafes, where semi-dried tomatoes are served in foods such as salads and sandwiches.
Hepatitis A involves inflammation of the liver and is spread when traces of faecal matter containing the virus contaminates hands, objects, water or food and is then taken in through the mouth.
Symptoms include abdominal pain, nausea, fever and chills and jaundice.

multi-state outbreak of Hepatitis Townsend Farms Organic Antioxidant Blend

The U.S. Food and Drug Administration and the Centers for Disease Control and Prevention (CDC) and state and local officials are investigating a multi-state outbreak of Hepatitis A illnesses potentially associated with a frozen food blend. We are moving quickly to learn as much as possible and prevent additional people from becoming ill. We recognize that people will be concerned about this outbreak, and we will continue to provide updates and advice. 

What is the Problem and What is Being Done About It?

The FDA, the CDC, and state and local officials are investigating a multi-state outbreak of Hepatitis A illnesses potentially associated with Townsend Farms Organic Antioxidant Blend, a frozen blend containing pomegranate seed mix.
The CDC reports that as of September 20, 2013, 162 people have been confirmed to have become ill with Hepatitis A after eating Townsend Farms Organic Antioxidant Blend.  The illnesses have been reported from 10 states: Arizona, California, Colorado, Hawaii, Nevada, New Hampshire, New Jersey, New Mexico, Utah, and Wisconsin.  The cases reported from Wisconsin resulted from exposure to the product in California, the cases reported from New Hampshire reported fruit exposure during travel to Nevada, and the case reported in New Jersey was a household contact of a confirmed case from Colorado.
The CDC reports that the outbreak strain of hepatitis A virus, belonging to genotype 1B, was found in clinical specimens of 117 people in nine states: AZ, CA, CO, HI, NH, NJ, NM, NV and WI.  This subtype is rarely seen in the Americas but circulates in North Africa and the Middle East.
On June 4, 2013, Townsend Farms, Inc. of Fairview, Oregon, recalled certain lots of its frozen Organic Antioxidant Blend, because it has the potential to be contaminated with Hepatitis A virus.  No other Townsend Farms products, frozen or fresh, are covered by this voluntary recall or linked to the illness outbreak at this time.
The product was sold at Costco warehouse stores under the product name Townsend Farms Organic Antioxidant Blend, 3 lb. bag and UPC 0 78414 404448. The recalled codes are located on the back of the package with the words “BEST BY”; followed by the code T012415 sequentially through T053115, followed by a letter. All of these letter designations are included in this recall for the lot codes listed above.
The product was also sold at Harris Teeter stores from April 19 until May 7, 2013, under the product name Harris Teeter Organic Antioxidant Berry Blend, 10 oz. bag and UPC 0 72036 70463 4, with Lot Codes of T041613E or T041613C and a “BEST BY” code of 101614.
On June 28, 2013, Townsend Farms, Inc. expanded its recall to include Townsend Farms Organic Antioxidant Blend, 3 lb. bag with UPC number 0 78414 40444 8. The recall codes are located on the back of the package with the words “BEST BY” followed by the code T122114 sequentially through T053115, followed by a letter. All letter designations are included in the recall.
On June 14, 2013, the Jackson County Oregon Health Department warned customers of Evo’s Coffee Lounge, in Ashland, Oregon, that they may have been exposed to Hepatitis A in the coffee shop's "Radically Free" smoothie served between May 17 and June 12, 2013.  The coffee shop used Townsend Farms Organic Antioxidant Blend to produce this menu item. The Jackson County Health Department also alerted those who may have been exposed in the last 14 days of the availability of Hepatitis A vaccine in the local area.
On June 19, 2013, the Mendocino County Public Health Department warned customers of A Frame Espresso in Fort Bragg Calif. that they may have been exposed to Hepatitis A in the coffee shop's "Mixed Berry" smoothie served between March 4 and June 8, 2013.  The smoothies may have contained Townsend Farms Organic Antioxidant Blend.
On June 26, 2013, Scenic Fruit Company of Gresham, Oregon recalled specific lots of Woodstock Frozen Organic Pomegranate Kernels because they have the potential to be contaminated with the Hepatitis A virus.

Woodstock Organic Pomegranate Kernels are sold in eight-ounce (227 gram) resealable plastic pouches (see image) with UPC Code 0 42563 01628 9. Specific coding information to identify the product can be found on the back portion of these pouches below the zip-lock seal. The following lots are subject to this recall:
  1. C 0129 (A,B, or C) 035 with a best by date of 02/04/2015
  2. C 0388 (A,B, or C) 087 with a best by date of 03/28/2015
  3. 0490 (A,B, or C) 109 with a best by date of 04/19/2015
The recalled Scenic Fruit products  were shipped from February 2013 through May 2013 to United Natural Foods, Inc. (UNFI) distribution centers in California, Colorado, Connecticut, Florida, Georgia, Indiana, Iowa, New Hampshire, Pennsylvania, Rhode Island, Texas, and Washington State. UNFI distribution centers may have further distributed products to retail stores in other states.
The FDA has finalized a protocol to test berries for the Hepatitis A virus (HAV), and is testing samples related to the outbreak for the presence of HAV. 
On June 29, 2013, the U.S. Food and Drug Administration (FDA) announced that it will detain shipments of pomegranate seeds from Goknur Gida Maddeleri Ithalat Ihracat Tic (Goknur Foodstuffs Import Export Trading) of Turkey when they are offered for import into the United States. There have not been any importations of these products since that time.
By combining information gained from the FDA’s traceback and traceforward investigations and the CDC’s epidemiological investigation, the FDA and CDC have determined that the most likely vehicle for the Hepatitis A virus appears to be a common shipment of pomegranate seeds from Goknur used by Townsend Farms to make the Townsend Farms and Harris Teeter Organic Antioxidant Blends that were recalled in June.   These seeds were also used by Scenic Fruit Company to make their recently recalled Woodstock Frozen Organic Pomegranate Kernels.
The FDA reviewed records and determined that the pomegranate seeds from this shipment were the only ingredient common to all of the recalled Townsend Farms and Harris Teeter Organic Antioxidant Blend.
FDA worked with the recalling firms that received pomegranate seeds from this shipment from Turkey and continues to oversee the necessary recalls.
As of July 15, 2013, the FDA has placed Goknur Gida Maddeleri Ithalat Ihracat Tic [Goknur Foodstuffs Import Export Trading] of Turkey on two separate Import Alerts (Import Alert 99-23 and Import Alert 99-35).  The epidemiological and trace back evidence developed in this investigation supported placement of pomegranate products produced by Goknur on both alerts. The firm will remain on these import alerts until the FDA has confidence that future shipments will be in compliance. To satisfy the requirements for removal from both Import Alerts, the firm will have to submit documentation to the FDA demonstrating that it has made all relevant corrections to address contamination issues.
The FDA is working closely with the CDC and state and local agencies and will provide updates as soon as they become available. 

Health Officials Warn of Hepatitis A Outbreak at Bronx Restaurant

Customers at New Hawaii Sea restaurant in the Bronx are urged to get vaccinated

Monday, Sep 23, 2013  |  Updated 9:48 AM EDT
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NBC 4 New York
The Health Department is urging customers who ate food from a Bronx restaurant to get a vaccine for hepatitis A as soon as possible. Checkey Beckford reports.
The Health Department is urging customers who ate food from a Bronx restaurant to get a vaccine for hepatitis A as soon as possible.
Officials say a worker and four customers at New Hawaii Sea, a Chinese and Japanese eatery in the Westchester Village section, have been infected with hepatitis A. 
Customers who've eaten food from the restaurant between Sept. 7 and Sept. 19 are urged to get a hepatitis A vaccine as soon as possible. People typically develop symptoms of hepatitis A about one month after they're exposed, but can prevent the disease if they're vaccinated within 14 days of exposure. 
Hepatitis A is spread by eating food that has been contaminated by an infected person. Symptoms include jaundice, fatigue, abdominal pain, nausea and diarrhea. 
The restaurant is closed while workers get vaccinated, leaving some regular customers who showed up Friday worried.
"We came here like two weeks ago. You hear that, you get scared," said Chrissy England. 
John Niccolls said he never expected the restaurant to be the center of an outbreak.
"It's pretty popular around here," he said. 
England says the restaurant had recently renovated and "cleaned it up a lot." 
New Hawaiian Sea received a B grade in its last Health Department inspection in May, but received critical contamination violations as recently as last year. 
Checkey Beckford contributed to this report. 

NBC New York

Nevada doctor sentenced to life over hepatitis outbreak

Posted at 10/31/2013 5:57 PM | Updated as of 10/31/2013 5:57 PM
Some of the victims were Pinoys

LAS VEGAS - Former Las Vegas endoscopy owner Dipak Desai was found guilty in 27 criminal charges, including a second-degree murder, in the 2007 Southern Nevada viral outbreak, one of the largest in the United States.
Officials traced the outbreak to Desai's clinics.
In 2007, 40,000 Nevadans were contacted by the Southern Nevada Health District that they may have been exposed to HIV and hepatitis after a surgical procedure at the endoscopy center Desai used to own.
The transmission of hepatitis and HIV from one patient to another is through the re-use of the same syringe and multi-use vials of anesthesia injected into the patient’s IV.
Although the needle is new for the next patient, the use of the same syringe and the same vials from previous patients could be the means of carrying the disease.
Dr. Noel Fajardo, the only Fil-Am gastroenterologist in southern Nevada said that there are significant number of Pinoy patients who went to Desai's clinic at the time of the viral outbreak.
"The practice of Dr. Depak Desai is composed of 16 gastroenterologist so it's the biggest practice in Las Vegas back then, so majority of the Filipinos were sent to their practice so as percentage wise I would say a lot of Filipinos were sent there. Since they're the only big practice during that time," said Dr. Fajardo.
A Filipino, who declined to be identified, said that she contracted Hepatitis-C during her trip to Desai's clinic.
"My children knows and they felt so bad they cried everyday. I have to face it. I can't do anything about it, Asawa ko di makatulog gabi-gabi ako lagi ang iniisip nya, sabi ko i don’t know when my time is up,” she said.
After six years of argument and some delays in trial, members of the jury at the Clark County District Court found Desai guilty of 27 criminal charges, including second degree murder. This is believed to be one of the largest viral outbreaks in the nation.
One of Desai's convictions is the death of 77-year old retired Philippine Army Colonel Rodolfo Maena in April of 2012. Authorities report that Maena was the second person infected in the viral outbreak case.
Desai now faces lifetime imprisonment, with eligibility for parole after having served 18 years in Nevada prison.
Dr. Fajardo said that although Desai made an extreme negative impact to the medical community in terms of standard of care, he assures patients that getting a colonoscopy is safe and will be beneficial for early detection of colon cancer.

Deadly Hawaii Hepatitis Outbreak Possibly Tied to Supplements

By ABC News
Oct 9, 2013 5:15pm
A dietary supplement may be the common link in a rash of hepatitis cases in Hawaii that has sickened 29 people, leaving two in need of a liver transplant and one dead, federal health officials said.
The only thing investigators have found in common between the cases so far, officials said, is that roughly four out of five of them took OxyElite Pro, marketed to burn fat, within 60 days of becoming sick.
The epidemiologic data linking the use of the dietary weight-loss supplements with liver failure and death is “compelling,” said Dr. Sarah Park, head of Hawaii’s Department of Health Disease Outbreak Control.
“We are actively soliciting more cases, and we are investigating what it is about this product,” Park told ABC News.
Park’s involvement with the cases of hepatitis began early in September, when the state’s transplant center notified her of an unusual case in which a young, previously healthy individual required a liver transplant. No infectious cause of the liver failure could be identified, she said. More cases soon followed, which led Park to release a medical advisory across the state of Hawaii.
For now, nobody knows for sure what is causing the outbreak. The company that makes OxyElite Pro is USPlabs. Company officials have said they do not believe their product is at fault.
“The ingredients have been studied for safety, are consumed in the food supply and widely used in dietary supplements,” the company said in a statement. “Out of an abundance of caution, the company has ceased domestic distribution of OxyElite Pro with the Purple Top and OxyElite Pro Super Thermo Powder until the investigation has been completed. The company continues to believe these versions are safe and are not the cause of the cluster of liver toxicity that has occurred in Hawaii.”
The company previously marketed a product that contained an ingredient known as 1,3 dimethylamylamine, or DMAA. In 2012, the Food and Drug Administration began sending warning letters to companies manufacturing DMAA-containing products demanding that they remove these products from the shelves. More recently, the Department of Defense issued a report on a safety review of DMAA after a number of adverse events and two deaths were reported in military service members who reported taking supplements containing the ingredient. In its statement, USPlabs said that the DMAA-containing version of its products has not been marketed or distributed since early in the year.
Regardless of the cause, hepatitis is a serious condition. The liver is the primary filter for toxins in the body, and hepatitis — which is essentially inflammation of the liver — shuts it down. Symptoms include yellowing skin and eyes and abdominal pain.
For now, both the CDC and FDA are investigating whether there could be more cases of this hepatitis in the mainland U.S.
Park said she is concerned that there could be. And she said that she feels the government shutdown could complicate the matter of catching them early. “Standard disease surveillance is not set up for this,” Park said. “Since this is not an infectious disease, the investigation is much tougher.”
Dr. Natalie Stavas contributed to this story.

 ABC News

Hepatitis from Wikipedia

From Wikipedia, the free encyclopedia

Classification and external resources
Alcoholic hepatitis.jpg
Alcoholic hepatitis evident by fatty change, cell necrosis, Mallory bodies
ICD-10 K75.9
ICD-9 573.3
DiseasesDB 20061
MedlinePlus 001154
MeSH D006505
Hepatitis (plural: hepatitides) is a medical condition defined by the inflammation of the liver and characterized by the presence of inflammatory cells in the tissue of the organ. The name is from the Greek hepar (ἧπαρ), the root being hepat- (ἡπατ-), meaning liver, and suffix -itis, meaning "inflammation" (c. 1727).[1] The condition can be self-limiting (healing on its own) or can progress to fibrosis (scarring) and cirrhosis.
Hepatitis may occur with limited or no symptoms, but often leads to jaundice, anorexia (poor appetite) and malaise. Hepatitis is acute when it lasts less than six months and chronic when it persists longer. A group of viruses known as the hepatitis viruses cause most cases of hepatitis worldwide, but hepatitis can also be caused by toxic substances (notably alcohol, certain medications, some industrial organic solvents and plants), other infections and autoimmune diseases.

Signs and Symptoms


Initial features are of nonspecific flu-like symptoms, common to almost all acute viral infections and may include malaise, muscle and joint aches, fever, nausea or vomiting, diarrhea, and headache. More specific symptoms, which can be present in acute hepatitis from any cause, are: profound loss of appetite, aversion to smoking among smokers, dark urine, yellowing of the eyes and skin (i.e., jaundice) and abdominal discomfort. Physical findings are usually minimal, apart from jaundice in a third and tender hepatomegaly (swelling of the liver) in about 10%. Some exhibit lymphadenopathy (enlarged lymph nodes, in 5%) or splenomegaly (enlargement of the spleen, in 5%).[2]
Acute viral hepatitis is more likely to be asymptomatic in younger people. Symptomatic individuals may present after convalescent stage of 7 to 10 days, with the total illness lasting 2 to 6 weeks.[3]
A small proportion of people with acute hepatitis progress to acute liver failure, in which the liver is unable to clear harmful substances from the circulation (leading to confusion and coma due to hepatic encephalopathy) and produce blood proteins (leading to peripheral oedema and bleeding). This may become life-threatening and occasionally requires a liver transplant.


Chronic hepatitis often leads to nonspecific symptoms such as malaise, tiredness and weakness, and often leads to no symptoms at all. It is commonly identified on blood tests performed either for screening or to evaluate nonspecific symptoms. The occurrence of jaundice indicates advanced liver damage. On physical examination there may be enlargement of the liver.[4]
Extensive damage to and scarring of liver (i.e. cirrhosis) leads to weight loss, easy bruising and bleeding tendencies, peripheral edema (swelling of the legs) and accumulation of ascites (fluid in the peritoneal cavity). Eventually, cirrhosis may lead to various complications: esophageal varices (enlarged veins in the wall of the esophagus that can cause life-threatening bleeding) hepatic encephalopathy (confusion and coma) and hepatorenal syndrome (kidney dysfunction).
Acne, abnormal menstruation, lung scarring, inflammation of the thyroid gland and kidneys may be present in women with autoimmune hepatitis.[4]

Study: Bat-to-Human Leap Likely for SARS-Like Virus

Updated Oct. 30, 2013 7:07 p.m. ET
A decade after SARS swept through the world and killed more than 750 people, scientists have made a troubling discovery: A very close cousin of the SARS virus lives in bats and it can likely jump directly to people.
The findings create new fears about the emergence of diseases like SARS, or severe acute respiratory syndrome. The virus spread quickly from person to person in 2003 and had a mortality rate of at least 9%. Worries of a severe pandemic led the World Health Organization to issue an emergency travel advisory.
While bats have previously been fingered as a host for SARS, it was believed that the virus jumped from there to weasel-like mammals known as civets, where it went through genetic changes before infecting people. Operating on that belief, China cracked down on markets where bats, civets and other wildlife were sold for food.
A Chinese horseshoe bat. SARS-like coronaviruses were found in a colony of these animals in Yunnan province in southwest China. Dr. Libiao Zhang, Guangdong Entomological Institute/South China Institute of Endangered Animals
The new bat-to-human discovery suggests that the control tactic may have limited effectiveness because a SARS-like virus remains loose in the wild and could potentially spark another outbreak.
"It changes the equation" for public health, said Peter Daszak, a senior author of the study and president of EcoHealth Alliance, a group involved in conservation and global health. "We can close all the markets in China and still have a pandemic."
The latest findings, published in the journal Nature on Wednesday, may also help scientists grapple with a more immediate worry. About a year ago, a novel SARS-like virus was reported in the Middle East. It has since killed more than 50 people, and some preliminary research suggests that it also may have originated in bats.
A decade after SARS swept through the world and killed more than 750 people, scientists have made a troubling discovery: A very close cousin of the SARS virus lives in bats and it can likely jump directly to people. Gautam Naik reports. Photo: AP.
SARS is caused by a germ known as a coronavirus. First discovered in 2003 in southern China, SARS went on to sicken more than 8,000 people in more than two dozen countries in North America, South America, Europe and Asia, before it was contained. No known cases have been reported anywhere since 2004.
But a key puzzle remained. No one ever found a live SARS virus in bats found in southern China's wildlife markets, making it unclear that those bats were the source. So where did it come from?
Dr. Daszak and his colleagues chose to study a horseshoe bat colony in Yunnan province in southwest China—hundreds of miles from the big wildlife-for-food markets of Guangdong province, where SARS was first reported. The researchers took hundreds of samples from the horseshoe bats. A genetic analysis revealed at least seven different strains of SARS-like coronaviruses circulating in that single group of animals.
Crucially, the scientists were also able to isolate and culture a live virus that binds to a receptor on a human cell. That suggests that direct bat-to-human infection would likely occur.
"This paper indicates that the bat is the origin and that the virus can be directly transmitted to humans," said Charles Calisher, a virologist at Colorado State University who wasn't involved in the study. "It practically rules out the possibility" of an intermediate host.
Dr. Daszak described a potential scenario where close contact between bats and humans—such as when the animals are captured for food—could increase the risk of viral transmission. "They are bringing wildlife in from new areas. They are going to Yunnan where bats are still common."
Dr. Calisher said the finding was important because researchers will now be able to get clues about the danger these novel SARS-like coronaviruses pose. For example, if a bat carries a high load of the virus, it indicates that the potential for transmission to humans is also high.
The U.S. Agency for International Development has a project that tries to identify emerging infectious diseases that may pose a threat to human health. One target: bats. Not much is known about the flying mammals, because they are nocturnal and often hard to find. But there is strong evidence that bats are a natural reservoir for a host of dangerous viruses, including Ebola, Nipah and SARS.
A year ago, scientists reported the emergence of a novel coronavirus, called Middle East Respiratory Syndrome, or MERS. It has since been reported in people in several countries, including Saudi Arabia, Germany, France, Italy, Britain and other parts of the Persian Gulf. Oman reported its first case on Wednesday, according to local reports.
In July, a WHO committee concluded that while MERS was of "serious and great concern," it wasn't a global health emergency. Research has suggested local bats may be a host for MERS, though the findings aren't definitive.
Nonetheless, the authors of the Nature study noted that the outbreak in the Middle East "suggests that this group of viruses remains a key threat and that their distribution is wider than previously recognized."

Monday, October 28, 2013

Woman Injured in Shark Attack off Australian Coast

A woman received serious injuries to her arm when she was mauled by a small shark on Monday as she snorkeled off Australia's remote northwest coast, officials said.
The 60-year-old woman was attacked by a 1-meter (39-inch) reef shark at Turquoise Bay, a picturesque tourist spot south of the coastal town of Exmouth, the Fisheries Department said.
She had been snorkeling with her partner about 40 meters (yards) from the beach when she was bitten, it said.
"The couple have reported the shark initially showed signs of aggression toward him, then turned and bit the woman on the arm," the department's Shark Response Unit manager, Lisa Clack, said in a statement.
The woman would be flown from Exmouth hospital more than 1,200 kilometers (740 miles) to the Western Australia state capital, Perth, for surgery on her right arm, Royal Flying Doctor Service spokeswoman Joanne Hill said.
Hill described her injuries as serious but not life threatening.
The beach was closed to the public following the attack and will likely remain closed Tuesday as rangers assess the shark danger, the Fisheries Department statement said.
Earlier this month, a 55-year-old professional diver was seriously injured by a suspected great white shark near the town of Esperance on the Western Australia southern coast.
It was the second time diver Greg Pickering found himself in the jaws of a shark. In 2004, he was bitten on the leg while spearfishing near Cervantes, north of Perth.
Sharks are common in Australian waters, though the nation has averaged just more than one fatal attack per year over the past 50 years.

 ABC News

Sunday, October 27, 2013

Fertilizers Are (Nearly) Forever

Scientific American

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Without industrially created fertilizer, a third of the world's population would starve to death. Since Fritz Haber and Carl Bosch came up with a way a century ago to wrest nitrogen from the air and turn it into fertilizer for plants, food supplies have exploded.
But a lot of fertilizer applied to cropland simply washes off and fertilizes blooms of algae instead. When the bloom dies, other microbes move in to feast, in the process sucking all the oxygen out of the surrounding waters. The result: dead zones that lay waste to any sea life that could not flee. And such dead zones are proliferating.
Now research shows that a vast store of nitrogen is waiting in the soil to create new dead zones for decades to come. French scientists traced nitrogen fertilizer and found that roughly 15 percent of the nitrogen applied in 1982 was still sitting in the soil today. Their report is in the Proceedings of the National Academy of Sciences.
The research suggests that existing soil nitrogen could continue to flow to the sea for decades. A good reminder that our actions today have environmental consequences that our grandchildren will have to deal with.
--David Biello