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Anti-vaccination is a factor in the spread of diseases!
More info here:

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4 Reasons Why Parents Are Refusing To Vaccinate Their Children, And 4 Reasons Why They (Really) Shouldn't - World Innovation Summit for Health

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By Maha El Akoum, Head of content, WISH The WHO has recently named vaccine hesitancy as one of the world's top 10 global health threats of 2019. Yes, 2019. Vaccine hesitancy [...]

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Is it a disease? A virus?
Most people have heard of tetanus but don't know what it actually is. The CDC states that "Tetanus is an infection caused by a bacterium called Clostridium tetani.". Clostridium tetani exists in the environment as spores.

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Made by a bad artist(me)

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4 available:

DT (diphtheria and tetanus) used for <7yrs

DTaP(diphtheria, tetanus, and pertussis) used for <7yrs

TD (tetanus and diphtheria)

Tdap (Tetanus, diphtheria, and pertussis)

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The Tetanus vaccine is a toxoid vaccine, a vaccine that uses a toxin produced by the bacteria. This makes a person immune to the toxin as opposed to the bacteria. For the pharmacology information go here:

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PRECAUTIONS

GENERAL

Care is to be taken by the health-care provider for the safe and effective use of Tetanus Toxoid (tetanus (tetanus toxoid) toxoid) .

EPINEPHRINE INJECTION (1:1, 000) MUST BE IMMEDIATELY AVAILABLE SHOULD AN ACUTE ANAPHYLACTIC REACTION OCCUR DUE TO ANY COMPONENT OF THE VACCINE.

There is an increased incidence of local and systemic reactions to booster doses of tetanus toxoid (tetanus (tetanus toxoid) toxoid) when given to previously immunized persons. (Refer to DOSAGE AND ADMINISTRATION section for timing of booster injections.) Prior to an injection of any vaccine, all known precautions should be taken to prevent adverse reactions. The physician should have a current knowledge of the literature concerning the use of the vaccine under consideration, including the nature of the adverse reactions that may follow its use. The patients medical history should be reviewed with respect to possible sensitivity and any previous adverse reactions to the vaccine or similar vaccines, possible sensitivity to dry natural latex rubber, previous immunization history, and current health status (see CONTRAINDICATIONS section).

Persons who have a history of Guillain-Barré syndrome (GBS) may be at increased risk of recurrent GBS after subsequent doses of Tetanus Toxoid (tetanus (tetanus toxoid) toxoid) vaccines. However, in a study in which an estimated 1.2 million doses of tetanus (tetanus toxoid) -containing toxoid were administered to persons >18 years of age, two cases of GBS were expected by chance alone during the 6 weeks after vaccination, and only one case was reported. This finding suggests that the risk of GBS after administration of tetanus toxoid (tetanus (tetanus toxoid) toxoid) is extremely low. The decision to administer tetanus (tetanus toxoid) -toxoid-containing vaccine to persons who have had GBS within 6 weeks after receiving tetanus toxoid (tetanus (tetanus toxoid) toxoid) should be based on the benefits of subsequent vaccination and the risk of the recurrence of GBS. 9

The expected immune response to Tetanus Toxoid (tetanus (tetanus toxoid) toxoid) may not be obtained in immunosuppressed patients. Administration of Tetanus Toxoid (tetanus (tetanus toxoid) toxoid) is not contraindicated in patients with HIV infection. 10

Special care should be taken to ensure that the injection does not enter a blood vessel.

Immunosuppressive therapies including radiation, corticosteroids, antimetabolites, alkylating agents, and cytotoxic drugs may reduce the immune response to vaccines. Therefore, routine vaccination should be deferred, if possible, while patients are receiving such therapy. 2 If Tetanus Toxoid (tetanus (tetanus toxoid) toxoid) has been administered to persons receiving immunosuppressive therapy, or having an immunodeficiency disorder, an adequate antibody response may not be obtained. 5 When possible, immunosuppressive treatment should be interrupted when immunization is required due to a tetanus (tetanus toxoid) - prone wound.

It is advisable to use DT (For Pediatric Use 6 years of age and younger) or Td (For Adult Use 7 years of age and older) in wound prophylaxis instead of tetanus toxoid (tetanus (tetanus toxoid) toxoid) alone in order to maintain adequate levels of diphtheria immunity. 5

A separate, sterile syringe and needle or a sterile disposable unit must be used for each patient to prevent transmission of hepatitis or other infectious agents from person to person. Needles should not be recapped and should be properly disposed.

Caution: The stopper of the vial contains dry natural latex rubber, that may cause allergic reactions.
CARCINOGENESIS, MUTAGENESIS, IMPAIRMENT OF FERTILITY
No studies have been performed to evaluate carcinogenicity, mutagenic potential, or impact on fertility.
PREGNANCY REPRODUCTIVE STUDIES PREGNANCY CATEGORY C
Adequate immunization by routine boosters in non-pregnant women of child-bearing age can obviate the need to vaccinate women during pregnancy (see DOSAGE AND ADMINISTRATION section).

Animal reproduction studies have not been conducted with Tetanus Toxoid (tetanus (tetanus toxoid) toxoid) . The risk to the fetus from tetanus toxoid (tetanus (tetanus toxoid) toxoid) is unknown. The ACIP recommends that an appropriate tetanus toxoid (tetanus (tetanus toxoid) toxoid) -containing preparation be given to inadequately immunized pregnant women because it affords protection against neonatal tetanus (tetanus toxoid) . 10 Waiting until the second trimester is a reasonable precaution to minimize any theoretical teratogenic concern. 5

It has been reported that Tetanus Toxoid (tetanus (tetanus toxoid) toxoid) administered to pregnant women prevents neonatal tetanus (tetanus toxoid) in newborns. 14,15 However, the data reported on the safety of Tetanus Toxoid (tetanus (tetanus toxoid) toxoid) when so used is inconclusive because the incidence of neonatal deaths in New Guinea was significantly higher than in the US.A prospective study in the US has not been done to confirm these reports. 14
NURSING MOTHERS PEDIATRIC USE SAFETY AND EFFECTIVENESS OF TETANUS TOXOID (tetanus (tetanus toxoid) toxoid) IN INFANTS BELOW THE AGE OF SIX WEEKS HAS NOT BEEN ESTABLISHED. HOWEVER, THIS VACCINE IS NOT INDICATED FOR CHILDREN UNDER 7 YEARS OF AGE. GERIATRIC USE
Tetanus Toxoid (tetanus (tetanus toxoid) toxoid) should only be used in geriatric patients known to have received a primary series (at least 2 doses) of tetanus (tetanus toxoid) -containing vaccine, since many such persons have no prior immunity. 16 Clinical studies of Tetanus Toxoid (tetanus (tetanus toxoid) toxoid) did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients.
REFERENCES
2. Recommendations of the Immunization Practices Advisory Committee (ACIP). Diphtheria, Tetanus (tetanus toxoid) , and Pertussis: Recommendations for vaccine use and other preventive measures. MMWR 40:No. RR-10, 1991

5. Report on the Committee of Infectious Diseases, ed 25. Elk Grove Village, IL. American Academy of Pediatrics, 2000

9. CDC. Update:Vaccine Side Effects, Adverse Reactions, Contraindications, and Precautions (ACIP). MMWR 45:No. RR-12, 1996

10. ACIP. General recommendations on immunization. MMWR 43:No. RR-1, 1994

15. Newell KW, et al. The use of toxoid for the prevention of tetanus (tetanus toxoid) neonatorum. Bull WHO 35:863-871, 1966

16. Ruben FL, et al. Antitoxin responses in the elderly to tetanus (tetanus toxoid) -diphtheria (TD) immunization. Am J Epidemiol 108:145-149, 1978

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tetanus tetanus toxoid drug description chemical structure black box warning medications drugs generic fda approved patient labeling reviews professionals clinicians clinical

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Tetanus (Tetanus Toxoid): Uses, Dosage, Side Effects, Interactions, Warning

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GENERAL Care is to be taken by the health-care provider for the safe and effective use of Tetanus Toxoid (tetanus (tetanus toxoid) toxoid) . EPINEPHRINE INJECTION (1:1, 000) MUST BE IMMEDIATELY AVAILABLE SHOULD AN ACUTE ANAPHYLACTIC REACTION OCCUR DUE TO ANY COMPONENT OF THE VACCINE.

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Email: jacob.vondrasek@my.tccd.edu

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Rust and tetanus are often associated because items left to nature tend to rust and accumulate Clostridium tetani bacteria

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This kind of model is known as a

"Ribbon Diagram"

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There are "...at least 209 species" of clostridium

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Gram positive

Obligate anaerobe

Saprophytic

Spore-former

Extremely environmentally resilient

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Pathophysiology

Tetanus is caused by the toxin (tetanospasmin) produced by C. tetani, a spore-bearing anaerobic bacillus. The spores are resistant to most sporicidal agents and can remain viable for years. The organisms may be found in soil and are common in the feces of many species. Bacteria gain access to the animal's tissues through open wounds, proliferate, and produce the toxin. Deep wounds with poor oxygenation are most susceptible. The toxin is composed of a heavy (H) and light (L) chain. The H chain is responsible for binding to gangliosides on nerves and subsequent internalization. The toxin ascends via retrograde transport within the axons of nerves to the spinal cord where it transsynaptically invades the inhibitory interneurons and then disseminates throughout the central nervous system (CNS). The L chain is a metalloprotease, which cleaves synaptobrevin, a membrane protein in synaptic vesicles necessary for the release of neurotransmitters. Ultimately, tetanus toxin blocks the release of the inhibitory neurotransmitters glycine and GABA. Glycine is the neurotransmitter for primary inhibitory interneurons such as the Renshaw cell; GABA is the inhibitory transmitter for descending pathways. The result is an uninhibited firing of the LMN. Tetanus toxin can also block sympathetic preganglionic neurons resulting in autonomic dysfunction. Finally, tetanus toxin may bind directly at neuromuscular junctions and cause neuromuscular facilitation. Although all domestic animals are susceptible to tetanus, horses are most sensitive whereas dogs and ruminants are more resistant. Cats appear to be very resistant.

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Pathogenesis

Clostridium tetani produces two exotoxins, tetanolysin and tetanospasmin. Tetanolysin is an oxygen-sensitive hemolysin related to streptolysin and the θ-toxin of Clostridium perfringens. It may play a part in establishing infection at the site of inoculation, but it has no other known role in pathogenesis of the disease. Tetanospasmin, referred to as tetanus toxin, is the neurotoxin that causes the manifestations of tetanus. The toxin is a protein produced intracellularly during the logarithmic phase of bacterial growth and released on autolysis. The genes for tetanus toxin and its transcriptional regulator are present on a plasmid. Observed differences in C. tetani reference-strain toxigenicity are related to heterogeneity in the strains' constituent clones; lower toxigenicity results when there are mixtures of organisms with and without the plasmid.

Tetanus toxin has an approximate molecular weight of 150,000 kDa and is synthesized as a single polypeptide prototoxin chain. When released by cell death, the prototoxin is cleaved by bacterial or tissue proteases into its active form, consisting of a 50,000-kDa light chain, the toxic domain, and a 100,000-kDa heavy chain with two domains related to membrane binding and translocation. The light and heavy chains are held together by a single disulfide bond; a second disulphide bond connects two heavy chain sites. The three distinct domains of the toxin are related to the separate steps of neuron receptor binding, internalization, intra-axonal transport, membrane translocation, and target enzymatic activity. The carboxy-terminal end of the heavy chain (HC, or fragment C) binds to receptor sites and is required for internalization by endocytosis; the amino-terminal end (HN) of the heavy chain mediates intra-axonal transport and, in central interneurons, the translocation of the toxin molecule into the neuronal cytosol. The light chain is an endopeptidase that is responsible for tetanospasm's specific toxic properties (discussed later).

Tetanus toxin is one of the most potent known poisons on a weight basis because of its absolute neurospecificity and enzymatic function at the site of action. As little as 1 ng/kg will kill a mouse; 0.3 ng/kg will kill a guinea pig. The estimated minimum human lethal dose is less than 2.5 ng/kg. Various species have different levels of responsiveness to the toxin: cats, dogs, birds, and poikilotherms are relatively resistant to its effects; mice, guinea pigs, monkeys, sheep, goats, and particularly horses are sensitive. Humeau and coworkers described evidence that these differences are the result of specific differences in toxin binding and neurotransmitter blocking activity.

Infection usually begins with the inoculation of spores into wounds, accompanied by tissue injury, necrosis, and the anaerobic conditions necessary for spore germination and bacterial replication. Ionic calcium appears to increase local necrosis and the likelihood of C. tetani infection; its presence in soil contaminating wounds may enhance spore germination and bacterial replication.

Transport of toxin from the infected site into the CNS is complex (Figure 33-2). After extracellular release, toxin diffuses to neuromuscular junctions of α-motor neurons in adjacent muscle tissue or to the lymphatic system, which transports the toxin to the bloodstream, leading to systemic dissemination and widespread uptake. The toxin gains entry into α-motor neurons via a double-receptor sequential binding process involving specific polysialgangliosides, and possibly glycoproteins, in lipid raft microdomains, followed by internalization by clathrin-mediated endocytosis. Once internalized, toxin is transported by a specific retrograde axonal transport system to the motor neuron cell body at a rate of 3 to 13 mm/hr. The mechanism of its release into contiguous synaptic junctions is unclear. Entry into adjacent inhibitory interneurons in the CNS occurs via synaptic vesicle reuptake (recycling), whereby the toxin binds to synaptic vesicle membrane protein SV2 and is endocytosed in the synaptic vesicle lumen.

Once inside an inhibitory neuron, the light chain is transferred to the neuronal cytosol by membrane translocation through a channel created in the vesicle membrane by the amino-terminal of the HC portion of the toxin molecule. In the cytosol, the disulphide bond between the heavy and light chains is broken, freeing the light chain to begin its toxic enzymatic activity. The light chain is a zinc endoprotease that cleaves peptide bonds in synaptobrevin, a synaptic vesicle protein necessary for vesicle fusion with the plasma membrane. Without intact synaptobrevin, synaptic vesicles accumulate at the nerve ending, unable to release their contents of the inhibitory neurotransmitters glycine or γ-aminobutyric acid (GABA). With inhibition blocked, increased excitatory neuron baseline firing rates lead to muscle rigidity, followed by multiplication of unchecked excitatory reflexes that cause characteristic tetanic spasms, and, less commonly at the cerebral level, convulsions.

Tetanus toxin does not cross the blood-brain barrier; neuronal transport is the sole means of entry into the CNS. Transynaptic transport of intact toxin allows transfer to inhibitory neurons in the spinal cord and wider dissemination in the CNS. Recovery may depend on new functional connections or toxin degradation.

Tetanospasmin can act at the peripheral neuromuscular junctions, the spinal cord, the brain, and the sympathetic nervous system., With local tetanus, transport of toxin is from the neuromuscular junction of the affected muscle without hematogenous dissemination; the predominant effect is on spinal glycinergic inhibitory neurons. In generalized tetanus, hematogenous dissemination of toxin allows more widespread uptake at neuromuscular junctions; the predominant effect is on the GABAergic supraspinal inhibitory neurons. The clinical syndrome appears almost identical to strychnine poisoning, which acts by competitively binding to postsynaptic glycine receptors at the motor neurons. Tetanospasmin has also been shown to interfere with release of a variety of other neurotransmitters, including acetylcholine in peripheral somatic and autonomic nerves. This accounts for autonomic dysfunction in cases of severe disease, flaccid cranial nerve palsy in cephalic tetanus, and peripheral muscle weakness, which often is masked by the more dramatic manifestations of the central inhibitory blockade. More detailed information on tetanus toxin can be found in recent reviews.

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Abstract

Tetanus occurs when spores from Clostridium tetani release the tetanospasmin, which binds to the axons of α motor and autonomical neurons, affecting the function of central inhibitory interneurons. This leads to excessive muscle activity, rigidity, and autonomical hyperactivity. Inoculation of spores can occur after any trauma. Tetanus is still important in developing countries, with 300 000 reported cases worldwide/year. Prevention by appropriate wound care (cleaning and antibiotics) and immunization is vital. If tetanus is suspected clinically, human tetanus immune globulin should be given intramuscularly, preferably near the wound site. Combined intramuscular and intrathecal immune globulin is more effective than intramuscular injection.

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Tetanus.

Tetanus is a spastic paralytic disease caused by the neurotoxin called tetanospasmin produced by Clostridium tetani. Similar to Clostridium botulinum, the bacterium is a ubiquitous Gram-positive spore-forming anaerobe commonly found in soil. Tetanospasmin is synthesized in anaerobic wounds and first binds at myoneural junctions and/or sensory receptors. It is transported via retrograde axoplasmic flow within the axon and across synaptic junctions until it reaches the CNS (see Fig. 4-28). In the CNS the toxin is transferred across synapses until it becomes fixed to gangliosides in the presynaptic inhibitory motor neuron. Tetanospasmin blocks the release of inhibitory neurotransmitters such as glycine and GABA. Inhibitory neurotransmitters act to dampen the actions of excitatory nerve impulses from upper motor neurons that are imposed on lower motor neurons. If these impulses cannot be dampened by normal inhibitory mechanisms, the generalized muscular spasms characteristic of tetanus ensue. Tetanospasmin appears to act by selective cleavage of a protein component of synaptic vesicles, thus preventing the release of neurotransmitters by the cells. Once toxin is bound to synapses, the administration of antitoxin is useless.

This disease is most common in horses but may also occur in lambs castrated in areas contaminated with spores of C. tetani. Tetanus also has been reported in cows, pigs, dogs, and cats. Except for the anaerobic wound, there are no macroscopic and microscopic tissue lesions in tetanus. Infected horses initially show signs of colic and muscle stiffness involving muscle groups of the lips, nostrils, ears, jaw (lockjaw), and tail. Horses are hyperesthetic and rapidly have a spastic and tetanic paralytic syndrome develop.

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Tetanus

Infection with Clostridium tetani results in the release of an exotoxin, tetanospasmin. This is carried up the axons of peripheral nerves to the anterior horn cells and medulla, where it blocks the normal inhibitory input to the motor neurons. This leads to increased muscle tone and an exaggeration of any movement into uncontrollable, painful spasms. Respiratory failure can develop as a direct result of frequent generalized spasms, or secondary to laryngeal edema, and inhalation of secretions. In addition to specific therapy for the infection, paralysis and mechanical ventilation is required while recovery occurs over 1−2 weeks.

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Definition

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Tetanus is a nervous system disease caused by a toxin (tetanospasmin) produced by Clostridium tetani.

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Tetanus is divided into four clinical types: generalized, localized, cephalic, and neonatal.

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Acute injury and injection drug use are risk factors for tetanus.

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Tetanus is rare in developed countries due to the availability of effective vaccines.

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In developing countries, neonatal tetanus can occur when there is failure of aseptic technique and mothers are inadequately immunized.

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In the United States, tetanus is more common in people older than 60 years, likely due to waning immunity.

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C. tetani is an obligately anaerobic bacillus.

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Tetanus produces two toxins: tetanospasmin and tetanolysin.

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It develops a terminal spore that is extremely stable in the environment, retaining the ability to germinate and cause disease indefinitely.

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The airway must be secured at the time of presentation.

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Benzodiazepines provide the mainstay of symptomatic therapy.

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Passive immunization with human tetanus immune globulin (HTIG) shortens the disease course and may lessen disease severity.

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Antibiotic therapy with metronidazole (Flagyl) may improve outcomes.

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All children should be vaccinated against tetanus through DTaP vaccine series.

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Adults should receive a tetanus booster (Td) every 10 years. One of the Td doses should be replaced with Tdap.

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Wound management of minor, clean wounds should include completion of tetanus immunization if incomplete, or a booster dose of vaccine (Td), if the last dose was given more than 10 years before. Patients with serious contaminated wounds should also receive HTIG.

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Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780123704696000131 Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780323052603500447 Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B978012417044500010X Tetanus is caused by the toxin (tetanospasmin) produced by C. tetani, a spore-bearing anaerobic bacillus. The spores are resistant to most sporicidal agents and can remain viable for years.

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Tetanospasmin is a nerve toxin that "...impairs the nerves that control your muscles (motor neurons)." More specifically it "interfer[es] with the release of neurotransmitters (glycine and γ-aminobutyric acid)".

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From Proteopedia

3D structures of tetanus toxin

Updated on 23-November-2020

References

1. ↑ Hatheway CL. Toxigenic clostridia. Clin Microbiol Rev. 1990 Jan;3(1):66-98. PMID:2404569

2. ↑ Bizzini B. Tetanus Toxin. Microbiological Reviews.1979 June;43(2):224-236.[1]

3. ↑ Mechanism of Action of Tetanospasmin (Dr. Arnab K Rana) [image on the internet]. 2005[updated 2005 Dec 26; cited 2011 Apr 20]. Available from: http://en.wikipedia.org/wiki/File:Mechanism_of_action_of_tetanospasmin.gif

4. ↑ Lalli G, Schiavo G. Analysis of retrograde transport in motor neurons reveals common endocytic carriers for tetanus toxin and neurotrophin receptor p75NTR. J Cell Biol. 2002 Jan 21;156(2):233-9. Epub 2002 Jan 21. PMID:11807088 doi:10.1083/jcb.200106142

5. ↑ Mocchetti I. Exogenous gangliosides, neuronal plasticity and repair, and the neurotrophins. Cell Mol Life Sci. 2005 Oct;62(19-20):2283-94. PMID:16158191 doi:10.1007/s00018-005-5188-y

6. ↑ Chen C, Fu Z, Kim JJ, Barbieri JT, Baldwin MR. Gangliosides as high affinity receptors for tetanus neurotoxin. J Biol Chem. 2009 Sep 25;284(39):26569-77. Epub 2009 Jul 14. PMID:19602728 doi:10.1074/jbc.M109.027391

7. ↑ Fotinou C, Emsley P, Black I, Ando H, Ishida H, Kiso M, Sinha KA, Fairweather NF, Isaacs NW. The crystal structure of tetanus toxin Hc fragment complexed with a synthetic GT1b analogue suggests cross-linking between ganglioside receptors and the toxin. J Biol Chem. 2001 Aug 24;276(34):32274-81. Epub 2001 Jun 19. PMID:11418600 doi:10.1074/jbc.M103285200

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Updated on 23-November-2020 ↑ Hatheway CL. Toxigenic clostridia. Clin Microbiol Rev. 1990 Jan;3(1):66-98. PMID:2404569 ↑ Bizzini B. Tetanus Toxin. Microbiological Reviews.1979 June;43(2):224-236.[1] ↑ Mechanism of Action of Tetanospasmin (Dr. Arnab K Rana) [image on the internet]. 2005[updated 2005 Dec 26; cited 2011 Apr 20]. Available from: http://en.wikipedia.org/wiki/File:Mechanism_of_action_of_tetanospasmin.gif ↑ Lalli G, Schiavo G.

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What does Tetanus actually do to the body?

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What does Tetanus actually do to the body?

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Once Clostridium tetani has actually gotten a foothold in the body it produces a toxin called " tetanospasmin" that interferes with the communication between your nervous system and your muscles.

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Click me!

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Clostridium tetani is a common soil bacterium and the causative agent of tetanus. When growing in soil, C. tetani are rod-shaped and up to 2.5 micrometers long. However, when forming spores C. tetani becomes substantially enlarged at one end, resembling tennis rackets or drumsticks. C.

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Video link : Click pop out

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Tetanus is also known as lockjaw

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I'm interactive!

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New tetanus infections per 100,000 people

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An interactive visualization from Our World in Data.

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Tetanus can be prevented. The WHO states that "Tetanus can be prevented through immunization with tetanus-toxoid-containing vaccines (TTCV)"

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"Studies have linked neonatal tetanus to neurological disabilities"

One study compared 40 patients to 40 controls and found "significantly more muscle fatigue and cramps, nervousness, decreased mental capacity and difficulties in balance, speech and memory" in the patients.

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Treatments for lockjaw include:

antibiotics to kill the bacteria

muscle relaxers

a tetanus vaccine

wound care

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Tetanus is usually diagnosed through "...physical exam, medical and immunization history" as opposed to laboratory tests.

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We've already discussed one of the virulence factors: Tetanospasmin; One other is "Tetanolysin" which causes "a local necrotizing effect" allowing for increased spread.

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Jaw cramping

muscle spasms

painful muscle stiffness

trouble swallowing

seizures

headache

fever

changes in blood pressure

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The CDC notes that tetanus "...bacteria are usually found in soil, dust, and manure and enter the body through breaks in the skin"