Bacterial Infections of the Nervous System

Tetanus is a disease caused by the bacterium Clostridium tetani. The bacteria are gram-positive, anaerobic, and spore-forming, making them highly difficult to kill. They are a normal part of the gut flora of horses, leading to their ubiquitous spread across the globe. C. tetani spores can persist on surfaces indefinitely and are found in all types of soils, especially those that have been enriched with manure. In order to cause infection, C. tetani spores must be deposited in tissue away from oxygen, which typically happens with puncture wounds. Hence, folk wisdom says tetanus infections result from stepping on a rusty nail. In reality, any object can be a source of tetanus infection if the surface is contaminated with C. tetani spores. Other infection sites, if Clostridium tetani is present, include crush injuries and burns. Tetanus symptoms typically begin between 3 and 21 (usually 14) days after infection. The bacteria produce a toxin called tetanospasmin, which is responsible for the symptoms of tetanus. The toxin affects the central nervous system and results in symptoms including generalized muscle stiffness and spasms marked by clenched fists, a clenched jaw, and an arched back. Severe infections lead to paralysis of the diaphragm or heart muscles, causing breathing problems or rapid heartbeat, respectively. In a minority of cases, death can result from such extreme infections. However, recovery is possible even without treatment. Treatment for tetanus begins with vaccination prior to injury. The vaccine lasts between 5 and 10 years and is recommended for everyone. Following an injury, the wound should be washed and bled to remove spores that may have been deposited. For people who have suffered a wound and who have not been immunized, treatment of the wound site with antitoxin may prevent symptoms. Treatment with antibiotics may also be effective. Following treatment, the patient should be immunized against further infection.

Botulism is a disease caused by the bacterium Clostridium botulinum, which is a gram-positive, anaerobic, spore-forming bacterium. Thus, like Clostridium tetani, it is difficult to kill and can persist in spore form on surfaces despite antimicrobial attempts. Its dormant, asexual, nonreproductive endospores are tremendously heat-resistant and are also resistant to freezing and irradiation. C. botulinum releases a potent toxin, botulinum toxin, a form of which has use as a cosmetic enhancement for the reduction of the appearance of wrinkles. Additionally, the medical applications of botulinum toxin have been applied to cervical dystonia, where the toxins have an effect on where the nerves and muscles meet. It has also been used in the treatment of chronic migraine headaches. Botulism can be acquired by eating contaminated foods, in which case the disease is an intoxication rather than an infection. It can also be acquired via wounds or from proliferation of C. botulinum in the gastrointestinal tract of an infant. Wound botulism and infant botulism both involve the growth of bacteria that release botulinum toxin and are thus infections in addition to intoxications.

Botulinum toxin interrupts the junctions between neurons and muscle cells. This leads to blurred vision, slurred speech, drooping eyelids, difficulty speaking and swallowing, and difficulty breathing. The toxin is the most potent known to exist. Untreated, botulism is fatal. Thus, treatment must begin immediately when symptoms present, without waiting for a positive diagnosis, which can take up to 96 hours. Treatment with an antitoxin and mechanical breathing assistance are the preferred courses of action. For foodborne botulism, antibiotics are of no use, because the bacteria are not present in the patient.

Meningitis is an inflammation of the meninges, tissues that surround and protect the brain and spinal cord. Meningitis can cause decreased blood flow to the brain; swelling within the cranium due to accumulation of fluid, called edema, leading to pressure on the brain; decreased flow of cerebrospinal fluid, which protects the brain and spinal cord; and impaired neurological function. In some cases meningitis can be fatal if untreated. Symptoms of meningitis include severe headache, fever, stiff neck, nausea and vomiting, rash, sensitivity to light, and cognitive changes, including confusion and difficulty concentrating. Meningitis may be caused by a number of pathogens. The most common causes are bacteria and viruses, although occasionally fungi, parasites, or amoebae can cause meningitis. Bacteria that cause meningitis are transmitted through respiratory secretions to the mucous membranes and include Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae, and Listeria monocytogenes. N. meningitidis and H. influenzae are gram-negative bacteria, while S. pneumoniae and L. monocytogenes are gram-positive. Meningitis caused by N. meningitidis is commonly called meningococcal meningitis and produces a characteristic petechial rash, which appears as tiny purple, red, or brown spots on the skin. Without treatment, meningococcal meningitis is fatal in over 50% of cases, but with treatment the infection is usually not fatal. A vaccine against this pathogen is available for adults and children over age 3, although endurance of the vaccine is diminished for children under age 11. Pneumococcus refers to Streptococcus pneumoniae, a bacteria that causes pneumonia, an infection in the lungs, and pneumococcal meningitis, an infection of the meninges. Bacterial meningitis is readily treatable with antibiotics. Penicillin is effective against all of the bacteria that cause meningitis. In addition, a bacteriophage—that is, a virus that infects bacteria—can be used to treat meningitis caused by L. monocytogenes. Prevention via vaccination is highly recommended, however, in order to control the spread of infection and avoid potential complications. Motor neuron disease refers to a group of disorders leading to motor neuron death and may be caused by genetics or environmental factors, such as infection by cyanobacteria. The cyanobacteria produce a toxin called β-methylamino-L-alanine (BMAA), which the body mistakes for the amino acid serine. BMAA is then incorporated into proteins in place of serine, leading to a buildup of damaged protein in nerve cells and eventual cell death. This results in extensive paralysis. The condition has no known treatment or cure.