Detecting the Landmines on the Path Ahead!A Season of Celebration and Thanksgiving!Friday, November 8, 2013Dear Advancing Saints:I am back from ministering in Browning, Montana on the Blackfeet Reservation for a NativeMinisters Leadership Meeting with Apostle Jay Swallow and Roy Wolf Tail. Getting here was along journey, but the presence of God moved powerfully! There were sovereign encounters thatonly the Lord could have orchestrated. The meeting is still continuing in Browning, so keeppraying for our Host Peoples to be renewed and revived by Holy Spirit! Below are pictures ofour team entering the reservation (the first with Anne Tate, Rebekah Faubion and RavenVincent) and the second with James Vincent. The third picture is of Richard and Vicki Aznoe,faithful webcasters from Montana who were also attending the gathering.
•This genus contains many species ofgrampositive, anaerobic and sporeformingrods.•Some of them are pathogenic for humansand animals.
The human pathogens in genusClostridium may be categorized asfollows:1. The gas gangrene group, the most important ofwhich is Clostridium perfringens.2. Clostridium botulinum, the cause of botulism.3. Clostridium difficile, the cause of toxicenterocolitis.4. Clostridium tetani, the cause of tetanus.
The speciesClostridium tetani• C. tetani requires strict anaerobic conditions.• Because of its motility, it spreads over thesurface of anaerobic blood agar in a thin veil ofgrowth.• Some strains can grow in small spidery colonies.• They weakly hemolyse on blood agar.• They do not form acids from sugars.• Aminoacids serve as main sources of energy.
The speciesClostridium tetani• All C. tetani strains share a common somatic(O) antigen.• The 10 types of C. tetani can be distinquishedby specific flagellar (H) antigens. Antigenictypes I and III most often cause tetanus inhumans. However, this serotyping has not asignificance for epidemiological practise.
The speciesClostridium tetani• C. tetani spores remain viable in soil for manyyears.• The spores are heat-stable.• The spores of some strains are resistant to boilingin water for up to 3 hours. They are killed byautoclaving at 121 °C for 15 minutes. They mayresist to 5% phenol for 10 hours or more.• Vegetative cells of C. tetani are heat-labile.
The speciesClostridium tetani• C. tetani produces an oxygen-labile hemolysin -tetanolysin. This toxin has only a negligiblesignificance for the pathogenesis of tetanus. The mostimportant product of C. tetani is neurotoxic exotoxin tetanospasmin.• The tetanospasmin production appears to be undercontrol of plasmid gene.• Vegetative cells produce tetanospasmin during thestationary phase and release it mainly when they lyse.
The speciesClostridium tetani• Tetanospasmin is a heat-labile antigenic proteinrapidly destroyed at 65 °C and by intestinalproteases.• It is toxic to man and various animals when injectedparenterally, but it is not toxic by the oral route.• The LD 50of the toxin for mice is 0.0001 mg, lessthan 1 mg is lethal to humans.
The speciesClostridium tetani• C. tetani is not an invasive microorganism.• The infection remains strictly localized in the area ofdevitalized tissue, into which the spores have beenintroduced.• Germination of the spores and development ofvegetative organisms that produce toxin are aided by: necrotic tissue, calcium salts, associated pyogenic infections.
The speciesClostridium tetani• Tetanospamin acts by blocking the release ofneurotransmitters (glycine and GABA"gamma-aminobutyric acid") on the level ofthe postsynaptic neuron junctions of theanterior horn cells of the spinal cord.• Incubation: approximatelly 5 to 15 days.
Symptoms of tetanus• Sudden difficulties with mastication due to rigidityof masticatory muscles.• Elevated temperature.• The patient cannot open his mouth, this effect isnamed as trismus.• Risus sardonicus is another sign in which trismus iscombined with facial spasm.• In severe cases, spasms of the back musclesproduce the opisthotonus.• The patients are fully conscious, and pain may bevery intensive.
Symptoms of tetanus• In a later stage of the disease, high temperature isusually present.• Tachycardia.• Generalized tonic spasms are more and more frequent,prolonged and intensive.• Breathlesness and cyanosis are expressed when therespiratory muscles are affected by spasms.• Laryngospasmus can be also present.• In fatal cases death results from exhaustion andrespiratory or circulatory failures.• Tetanus of newborns follows infections of the umbilicalstump.• Others.
• Localized tetanus is another form of C. tetanidisease. It remains confined to the muscles atthe site of primary wound and infection. Thisform has a good prognosis.• Another variant of localized tetanus is socalled cephalic tetanus. The incubation ofthis variant is very short and its prognosis isconsiderably poor.
There are two basic types of tetanus:• The most often C. tetani infection in humans is of adescendent type which spreads through lymphaticand blood routes to nerve fibres. It begins withspactic symptoms on the face. This type has ashorter incubation and worse prognosis.• The less frequent form is an ascendent type oftetanus. Spasm begin in the environment of awound. This type has a longer incubation andbetter prognosis.
The tetanus• The mortality caused by the generalizeddisease represents more than 50%.• Mortality is the highest in the neonates, eldersand in the patients with cardiac diseases.• Tetanus of newborns has the highest mortality,even more than 90%.
The tetanus- treatment• Surgical wound treatment is vitally importantbecause it removes the necrotic tissue that isessential for proliferation of the C. tetani strains.• Tetanus antitoxin of human origin.• Penicillin (or other antibiotics) strongly inhibitsthe growth of C. tetani and stops further toxinproduction. Antibiotics may also controlassociated pyogenic infection.
The tetanus- treatmentExamples of antibiotic therapy:• penicillin G 4x5-10 mil. IU, 10 days• gentamicin 3x80 mg (or 1x240 mg) +clindamycin 4x900 mg, 10 days• others (like metronidazol)Prevence:Application of toxoid
The tetanusEpidemiology:• Sources: exogenous, endogenous.• Transmission: Direct contact of wound with sources. Perforation of the intestinal wall after injuries,operations or during pathological processes.
Clostridium botulinum• C. botulinum is a strictly anaerobic grampositivebacillus. It is motile with peritrichous flagella. Itsspores are oval and subterminal. It is a widelydistributed saprophyte occuring in soil, vegetables,fruits, and others.• The widespread occurrence of C. botulinum innature, its ability to produce a potent neurotoxin infood, and the resistance of its spores to inactivationcombine to make it a formidable pathogen of manand range of animals and birds.
Clostridium botulinum• Botulinal toxins are among the mostpoisonous natural substances known.• Seven main types of C. botulinum designatedA-G produce antigenically distinct toxinswith pharmacologically identical actions.
Clostridium botulinum• Botulism is a severe, often fatal, form of foodpoisoning characterized by pronounced neurotoxicefects.• The preformed toxin in the food is absorbed fromthe intestinal tract. Although it is protein, it is notinactivated by the intestinal proteolytic enzymes.• The toxin primarly affects the cholinergic systemand seems to block release of acetylcholine, chieflyat points in the peripheral nervous system.
Clinical presentation• Descending symmetrical paralysis beginning with cranial nerveinvolvement, induced by botulinum toxin. Onset begins with blurryvision, followed by ocular muscle paralysis, difficulty speaking andinability to swalow. Respiratory paralysis may occur in severe cases.Mental status in unaffected.• Usual incubation period is 10 12 hours. Incubation is shortest fortype E strain (hours), longest for type A strains (up to 10 days), andis inversely proportional to the quantity of toxin consumed (foodbotulism).• Wound botulism (types A or B) may follow C. botulinum entry intoIV drug abuser injection site, surgical or traumatic wounds.• Infant (less then 1 year) botulism (most commonly type A or B) isacquired from C. botulinum containing honey.
Therapy of botulism• Application of antitoxin antitoxin neutralizes only free toxin, and does notreverse toxin-induced paralysis botulism is toxic-mediated infection and antibiotictherapy (wound botulism) is adjunctive• Prognosis: good if treated early, before respiratory paralysis
Clostridia that produceinvasive infections• Many different toxin-producing clostridia canproduce invasive infections (including myonecrosisand gas gangrene) if introduced into damagedtissue.• About 30 species of clostridia may produce such aneffect, but the most common in invasive disease isClostridium perfringens (90%).
Clostridium difficile• This organism has a direct relationship withpseudomembranous colitis, usually is association withbroad-spectrum antibiotic therapy.• Pseudomembranous colitis is diagnosed by endoscopicobservation of pseudomembranes or microabscesses inpatients who have diarrhea and have been givenantibiotics. The diarrhea may be watery or bloody, andthe patient frequently has associated abdominal cramps,leukocytosis, and fewer.
Clostridium difficile -pseudomembranous colitis• Administration of antibiotics results inproliferation of drug-resistant C. difficile, thatproduce two toxins (toxin A, toxin B). Bothtoxins are found in the stools of patients withpseudomembranous colitis.• Treatment:metronidazol 3-4 x 250-500 mg p.osvancomycin 2x1 g p.os