Monkeypox

by Randall Neustaedter OMD

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Attack of the lowly prairie dog

Monkeypox is usually contracted in Africa by eating rodents or monkeys, or being bitten. The first episode of monkeypox in the US occurred in May, contracted from pet rodents. Cute prairie dogs, at $100 a pop, have been traded at swap meets and sold at pet stores. They are fuzzy and adorable. But these little Tribbles have also acquired some deadly traits in the form of an African virus apparently caught from a Gambian rat.

Twenty kindergarteners were exposed to an infected pet prairie dog at their school. Now those kids are quarantined. Several families in the Midwest have contracted the disease. Monkeypox has spread, along with the infected prairie dogs, to Illinois, Indiana, Michigan, Wisconsin, Ohio, and New Jersey. The count of suspected cases is nearing the hundred mark. One child in the US has encephalitis. No one has died. Yet.

Some prairie dogs have died. They could easily be discarded in the trash. The scenario of rats in the trash dump contracting the disease and spreading deadly monkeypox through the wild rodent population is juicy enough to warrant a Hollywood movie pitch. Dust off that faded copy of Dustin Hoffman’s movie bomb, Outbreak, at your local video store.

Although monkeypox is usually contracted from infected animals, the disease will spread between people. In Africa, monkeypox infection usually stops after the first person-to-person transmission, but the disease was once tracked through four human transmissions among children. Officials expect monkeypox to spread between people in the US as well. Two health care workers now have monkeypox symptoms, and the boyfriend of one of the nurses has developed suspicious symptoms, which would represent a second-generation transmission. Not everyone with monkeypox disease has obvious symptoms. Like smallpox, this pox disease can cause inapparent infections, and those people could conceivably spread the disease.

Because the disease can spread between people, the federal government has issued guidelines for the use of smallpox vaccine to prevent this form of transmission even though the FDA has not approved the vaccine for this use. Health officials have evoked emergency powers protocols to make the vaccine available. Indiana and Wisconsin are the first states to adopt these guidelines and make the smallpox vaccine available for this purpose. One child developed encephalitis (infection of brain). Otherwise everyone with the disease has recovered, usually after a fairly mild illness.

Does the smallpox (vaccinia) vaccine work to prevent monkeypox?

Officials are claiming that the vaccine is 85 percent effective. That figure is based on one study done in the 1980s in Africa. That study evaluated 209 cases of monkeypox that occurred during a five-year period from 1980-1984 in the dense tropical rainforests of the Democratic Republic of Congo (at that time Zaire). These cases represented 125 separate episodes of disease occurrence. More than half of the cases did not spread to anyone else (only one case occurred in most episodes). The incidence of disease among vaccinated contacts of people with monkeypox was compared to the incidence in unvaccinated contacts. Both household contacts and people living in other residences were included. Over 1500 contacts of patients with the disease were identified. Only 12 cases of disease occurred in 1,099 vaccinated contacts (one percent) compared to 35 cases in 474 unvaccinated contacts (7.4 percent). The calculation (7.4-1.1 / 7.4) yields the 85 percent effectiveness conclusion. The assumption that smallpox vaccine works is based on this small sample of 47 cases, hardly a definitive answer. Many other factors, including the ability to identify and locate contacts in this environment could have altered the results.

Will monkeypox spread through a population?

That question has been evaluated in a few studies. In the study quoted above, 11 percent of household contacts contracted the disease. The majority of cases (78 percent) did not spread the disease at all in this partially vaccinated population. The longest recorded chain of human-to-human transmission of mankeypox lasted five generations, where the disease spread from one child who had eaten monkey meat with his family to four other children who had no contact with infected animals. The authors of this study constructed a mathematical model based on the transmission rate in that African setting. Based on an assumption that each individual with monkeypox would come into contact with ten other people while the individual was contagious, the authors concluded that 54 percent of cases are predicted to cause at least one subsequent case in an unvaccinated population. Theoretically, this could result in one additional case for every case of monkeypox, and the persistence of the disease in a population. However, the tactics of isolation, quarantine, and (perhaps) the vaccination of contacts would have the potential of stopping the disease’s spread. And monkeypox does tend to lose its infectous quality through transmissions in humans. The human is not considered a very good host for the disease, compared to rodents and other mammals. The spread of monkeypox from person to person is considerably less common than the spread of smallpox. Only 11 percent of unvaccinated household contacts of those with monkeypox acquired the disease compared to 40 to 97 percent of household contacts of people with smallpox (different strains of the virus having more or less virulence).

Media stories on monkeypox have repeatedly stated that vaccination within four days of exposure will prevent the disease. This figure has been estimated for smallpox prevention using the vaccinia vaccine and is erroneously attributed to monkeypox prevention. Several authorities have even questioned the veracity of this statement about smallpox prevention. In 1960, one researcher stated that smallpox vaccination given within four days of exposure still results in a 10-40 percent incidence of smallpox (Kempe, 1960).

The suspected monkeypox/vaccinia connection

In a twist on the prairie dog monkeypox story several individuals have questioned whether the monkeypox outbreak spread by these rodents could have been due to a far different source than a rat imported from Africa. Unbeknownst to many of us, veterinary health officials in several states have been distributing an oral rabies vaccine in the wild to control the spread of rabies in raccoons. This has been accomplished by dropping three-inch packets of bait containing the vaccine from airplanes. This rabies vaccine is bound to a vaccinia virus vaccine carrier. Therein lies the problem and the suspicion. Several individuals have raised concerns that the wild prairie dogs may have eaten these baits and then spread the vaccinia virus (the same virus used in the smallpox vaccine) to humans. Mary Sparrowdancer first voiced this possibility, implying that the vaccinia baits are causing monkeypox illness. She says,

“Several reports have stated that the infected prairie dogs carrying the ‘monkeypox-LIKE illness’ originated in Texas. It should be pointed out that Texas is one of the states that has been heavily involved in the above program of dropping the rabies/vaccinia biscuit baits from planes.”

This concern was published by Jeff Rense at his website. http://rense.com/general38/airc.htm

It was later picked up by Jon Rappaport and published at his website www.nomorefakenews.com. He suspects the CDC of consipiring to hide the connection between the vaccinia/rabies bait and the monkeypox outbreak.

While it is true that people have contracted the vaccinia virus from these baits (a report of such a case was published by Rupprecht in the New England Journal of Medicine), no one has proven that the bait has caused the monkeypox outbreak.

To answer this question of an association I spoke with a microbiologist at the CDC, Russ Regnery. He said that the possible connection between the vaccinia bait was discussed early on at the CDC when the monkeypox cases began appearing. They were very concerned about this possibility, but two tests have proven this is a monkeypox virus and not the vaccinia virus according to Regnery. A polymerase chain reaction DNA test was cross reactive for the monkeypox virus, and a hemagluttin gene analysis showed an exact match with the monkeypox virus gene.

Some have argued that monkeypox is just another way of disguising the return of smallpox into human populations. But monkeypox behaves much differently than smallpox. It is much less transmissible between humans, and a lot less deadly.

Rumors and suspicions spread easily. Although a healthy skepticism is always a good thing, we need to be responsible in our analysis and statements about vaccines and their association with adverse effects in order to discover the truth and have that truth recognized.

What should you do?

If you live in an area where monkeypox has been identified, begin taking supplements that boost immune function.

Adults can take vitamin C (3-4 grams), vitamin A (20,000 IU), zinc (25 mg), and colostrum (2 tspns) every day.

Children can take vitamin C (500-1000 mg), vitamin A (1,000-5,000 IU), zinc (10-20 mg), and colostrum (1/2-1 tspn). The lower dose for infants and children up to three years old, the higher dose for children four and over.

I do not recommend that people get the smallpox vaccine unless a local clinic can supply vaccinia immune globulin (VIG) in the event of severe adverse reactions to the vaccination. Most people have decided that the smallpox vaccine’s risk outweigh the risk from contracting monkeypox, which often causes relatively mild symptoms. Click here for a more detailed discussion of the smallpox vaccine from my book, The Vaccine Guide.

References

Fine PE, Jezek Z, Grab B, Dixon H. The transmission potential of monkeypox virus in human populations. Int J Epidemiol. 1988; Sep;17(3):643-50.

Jezek Z, et al. Four generations of probable person-to-person transmission of human monkeypox. Am Journal of Epidemiol 1986; 123(6):1004-1012.

Kempe CH. Studies of smallpox and complications of smallpox vaccine. Pediatrics 1960; 26:176-189

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