Neisseria meningitidis and Clumping

Neisseria meningitidis is a parasitic, aerobic, Gram-negative, non endospore forming, nonmotile (although piliated) , coccal bacterium that is responsible for causing meningitis, inflammation of the meninges layer covering the brain. Because it is an aerobic organism, like most members of the Neisseriaceae family, it also has catalase and oxidase activity. Colonies appear smooth, moist, and glistening (Rake). N. meningitidis resides primarily in humans on the surface of mucosal membranes such as those found in the respiratory tract. Progression through meningitis almost always follows after entering the blood stream (See Pathology below). Symptoms of this disease were first noted in 1805, having been described as an epidemic cerebrospinal fever (Vieusseaux) but it was not isolated until 1887 by Weichselbaum (Weichselbaum). In the U.S. every year, there are approximately 3000 to 4000 cases of N. meningitidis linked meningitis (Wong et al). Because this bacterium poses a health threat, genome sequencing has already begun for a few of these strains to enable deeper understanding of its mechanism of infection. This also provides for studies towards dealing with antibiotic resistant strains. 

Neisseria meningitidis, like most other members of the Neisseriaceae family are aerobic organisms with catalase and oxidase activity. One interesting observation made by Duong and Archibald was that in both N. gonorrhoeae and N. meningitidis, the superoxide dismutase (SOD) enzyme was not present. As a compensation for oxidative damage in a low pressure oxygen environment, N. gonorrhoeae’s natural environment, catalase activity was notably high in addition to high glutathione content (Archibald).

In terms of metabolism, N. meningitidis requires mineral salts, lactate, some amino acids such as cysteine, and glutamic acid as a carbon source (Catlin). In 2004, knock out experiments of the gdhA gene which encodes glutamate dehydrogenase in N. meningitidis, confirmed the importance of glutamic acid metabolism towards growth and virulence. In addition to organic nutrient requirements, iron is also needed as an electron acceptor as demonstrated by the increase in generation times during iron restriction (Archibald and DeVoe). In a human host, this iron is supplied from heme iron in the blood where active transport is mediated a TonB dependent receptor. 

Clumping. As mentioned in the previous section, iron reduction is a necessary part of N. meningitidis metabolism. Humans are its primary reservoir from which heme iron, along with other nutrients in the blood, satisfies its requirement for growth. The result of this is an aggregation of blood cells – clumping, a sign of infection. Although not always, it has been shown by Lappann et al that N. meningitidis is capable of forming biofilm communities in a slow flow environment. 

SAN FRANCISCO – A young research associate killed by a highly virulent strain of meningococcal disease is believed to have contracted the bacteria from the San Francisco lab where he was working on a vaccine against it, public health officials said yesterday.
United States Centres for Disease Control and Prevention experts are seeking to confirm what they already suspect: that Richard Din, 25, died Saturday in an unusual case of a scientist being fatally infected with an agent from his own laboratory.
Mr Tom Skinner, a CDC spokesman, said the CDC in Atlanta would test a biopsy sample from Din and a sample of the laboratory pathogen he was working with to create fingerprints for each.
“If the fingerprints match, you know it’s highly likely he acquired the infection from working in the lab,” he said.
“Someone getting sick and dying from the organism they’re working with in the lab is exceedingly rare,” he added.
Meanwhile, dozens of people, including relatives, close friends, medical personnel who treated Din and some of his co-workers at the research department of the San Francisco Veterans Affairs Medical Center were being given antibiotics as a precaution.
Dr Harry Lampiris, chief of infectious disease at the San Francisco VA, said it is likely Din died as a result of his work with Neisseria meningitidis, a strain of bacteria that causes meningococcal disease, which leads to meningitis and bloodstream infections.
“It’s our responsibility to assume it’s laboratory-associated until proven otherwise,” he told Reuters.
Since the 1960s, vaccines have been available for some strains of meningococcal disease. But scientists in the San Francisco lab have spent more than 20 years trying unsuccessfully to develop a vaccine against serogroup B, the strain that killed Din.
“It’s been like the Holy Grail to develop the vaccine against B,” Dr Lampiris said.
Din died of multiple organ failure caused by meningococcal infection and septic shock, said Ms Eileen Shields, a spokeswoman for the San Francisco Department of Public Health. He died less than a day after becoming ill.
The disease can come on quickly with symptoms including high fever, headache, stiff neck, vomiting, rash, confusion and fatigue.
Dr Lampiris said co-workers described Din, who began work at the lab in October, as “a very talented, hard-working and fastidious individual”.
“He was a very bright person who was probably at the beginning of a long research career,” he said.
Meningitis, an inflammation of the protective membranes covering the brain and spinal cord, commonly strikes infants and college students living in dormitories, Dr Lampiris said. He said Din had not had contact with either group.
About 1,000 Americans each year suffer from meningococcal disease, and an estimated 10 to 15 per cent die from it, Mr Skinner said. He could not say how many of the cases resulted from serogroup B.
The California Division of Occupational Safety and Health is investigating the circumstances of Din’s death, along with its federal counterpart and the CDC, the city Public Health Department and the San Francisco VA. REUTERS.

If you are able to stop the process of clumping, you would have reduced the effectiveness of the disease in causing damage and the spread of the disease, indirectly giving you time to find a 100% cure for the disease.
– Contributed by Oogle.


Developing the SRGAP2, a new generation of human intelligence

WASHINGTON – Scientists have identified the gene which may have driven the crucial step in evolution where man learned to talk.
By duplicating itself two and a half million years ago the gene could have given early human brains the power of speech and invention, leaving cousins such as chimpanzees behind.
The gene, known as SRGAP2, helps control the development of the neocortex – the part of the brain responsible for higher functions like language and conscious thought.
The duplicated gene helped our brain cells move faster and make more connections enabling the brain to grow bigger and more complex, according to researchers.
In a study published in the Cell journal, the scientists reported that the gene duplicated about 3.5 million years ago to create a “daughter” gene, and again a million years later creating a “granddaughter” copy.
Although humans and chimpanzees separated six million years ago, we still share 96 per cent of our genome and the gene is one of only about 30 which have copied themselves since that time, reported The Daily Telegraph.
The first duplication was relatively inactive but the second occurred at about the time when primitive Homo Sapiens separated from its brother Australopithecus species and began developing more sophisticated tools and behaviours.
The scientists suggest the duplication process explains how our species developed speech, complex behaviour and mastery of tools around that time.
The copy and the original gene make similar proteins, which are known to help the brain develop.
However, as the scientists found over two studies, the second version made neurons develop longer dendrites, the ‘fingers’ that pick up electrical impulses from other cells, said The Daily Mail.
Genetic scientist Evan Eichler at the University of Washington, who led the research, said the benefit of the duplication would have been instant, meaning human ancestors could have distanced themselves from rival species within a generation reported The Daily Telegraph.
Prof Eichler said: “This innovation could not have happened without that incomplete duplication. Our data suggest a mechanism where incomplete duplication of this gene created a novel function ‘at birth’.”AGENCIES