Tick Time

The Associated Press reports that Lone Star ticks have been spotted in Maine and New Hampshire.

The ticks, which are named for a small white spot on their backs, used to be found only in the Southeast, but they have been reported in growing numbers in Rhode Island, Connecticut and Cape Cod in recent years.
Scientists don't believe they are established in Maine and New Hampshire yet: The few that have been found are probably straying travelers, and there's no clear evidence yet that they are surviving the winter and living out their entire life cycle in northern New England.

Should you meet a migrant or a local tick, the CDC has illustrated instructions for safe tick removal.

Johne's Disease in Western Australia

The Australian reports an outbreak of Johne's Disease in Western Australian cattle after a twelve year lull:

Bovine Johne's Disease was confirmed yesterday [July 10th] in a beef herd near Albany, about 400km south of Perth.
It is the first case of its kind in Western Australia since 1994, but Animal Health Australia said the disease was known to have infected about 1350 cattle herds in NSW, Victoria, South Australia and Tasmania.
The highly infectious disease, which is most common in dairy cows, wastes the animal's intestines, preventing the absorption of minerals and proteins.

Johne's Disease is caused by Mycobacterium avium paratuberculosis and is suspected of causing Crohn's Disease in humans. The University of Wisconsin School of Veterinary Medicine has a webpage devoted to the controversy:

The triggering event for Crohn's disease is thought to occur early in life and then be followed by a 15-30 year incubation or latency period. Johne's disease also has a long interval between infection with M. paratuberculosis and onset of clinical signs (2-10 years). Clinical signs in both diseases are seldom seen before sexual maturity. Interestingly, a strong inverse relationship was found between Crohn's disease and gastric cancer using data from 26 countries.

PARA, the Paratuberculosis Awareness & Research Association, has more information on the bacterial theory:

In the early 1900's, the disease we call today "Crohn's disease" was characterized as an infectious disease, specifically intestinal tuberculosis. However, by the early 1930's, definitive classification (proof) that this disease was infectious was not forthcoming. More specifically, when Dr. Burrill B. Crohn failed to prove an infectious cause in 1932, the disease became formally known as "Crohn's disease" (named after Dr. Crohn) and the search for an infectious cause was largely discontinued.

Kuru in the 21st Century

Via ProMED-mail: A paper in The Lancet [registration required even to see the abstract] establishes the incubation period for Kuru, the famous cannibal prion disease, and makes some ominous predictions about the future of mad cow disease:

We identified 11 patients with kuru from July 1996, to June 2004, all living in the South Fore. All patients were born before the cessation of cannibalism in the late 1950s. The minimum estimated incubation periods ranged from 34 to 41 years. However, likely incubation periods in men ranged from 39 to 56 years and could have been up to 7 years longer. PRNP [the prion protein gene] analysis showed that most patients with kuru were heterozygous at polymorphic codon 129, a genotype associated with extended incubation periods and resistance to prion disease.

Interpretation

Incubation periods of infection with human prions can exceed 50 years. In human infection with BSE prions, species-barrier effects, which are characteristic of cross-species transmission, would be expected to further increase the mean and range of incubation periods, compared with recycling of prions within species. These data should inform attempts to model variant CJD epidemiology.

Another paper in PNAS also indicates that many more people than the current victims may eventually come down with a new and unknown variant of mad cow disease:

All neuropathologically confirmed cases of variant Creutzfeldt-Jakob disease (vCJD), characterized by abundant florid plaques and type 4 disease-related prion protein (PrP^Sc) in the brain, have been homozygous for methionine at polymorphic residue 129 of PRNP. The distinctive neuropathological and molecular phenotype of vCJD can be faithfully recapitulated in Prnp-null transgenic mice homozygous for human PrP M129 but not V129, where a distinct prion strain is propagated. Here we model susceptibility of 129MV heterozygotes, the most common PRNP genotype, in transgenic mice and show that, remarkably, propagation of type 4 PrP^Sc was not associated with characteristic vCJD neuropathology. Depending on the source of the inoculum these mice can develop four distinct disease phenotypes after challenge with bovine spongiform encephalopathy (BSE) prions or vCJD (human-passaged BSE) prions. vCJD-challenged mice had higher attack rates of prion infection than BSE-challenged recipients. These data argue that human PRNP 129 heterozygotes will be more susceptible to infection with vCJD prions than to cattle BSE prions and may present with a neuropathological phenotype distinct from vCJD.

Attack of the Killer Tomatoes

New Scientist reports on genetically modifying tomatoes with viral DNA to create cheap, edible vaccines for hepatitis B and HIV:

Mice fed a solution containing the tomatoes in powdered form developed high levels of antibodies in their blood to both viruses. Equally important, the researchers found antibodies on mucosal surfaces, where the viruses can gain entry to the body through sexual contact. "That's where you want it to be protective," says Rose Hammond of the US Department of Agriculture's Agricultural Research Service in Beltsville, Maryland, which is collaborating with the Russian researchers.