Unit 1- Clostridiums Flashcards
Clostridiums
Rods, produce identifying endospores, cultures emit putrid odor due to peptide catabolism, anaerobic, catalase negative, oxidase negative, motile, fastidious
Saprophytes
Part of normal flora
Neurotoxic Clostridia
Clostridium tetani and botulinum
Clostridium tetani
TeNT antigenically uniform for vaccine, serology based on flagellar antigens, present in soil, terminal drumstick shaped spores
Tetanus Cause
Clostridium tetani introduced into traumatized tissue
Tetanus
Neuroparalytic intoxication and tonic-clonic convulsions due to a protein neurotoxins
Tetanus Toxin
Tetanospasmin binds to neurons, releasing GABA and glycine, also hydrolyzes docking proteins and prevents vesicles to fuse with the synapse and release neurotransmitters
Tetanus Pathogenesis
Spores germinate in anaerobic environment, toxins diffuse, toxins attach to cholinergic receptors and are internalized, vesicles travel to the ventral horns of the spinal cord and cause sustained spasm in affected muscles
Spastic Paralysis
Continuous excitatory stimulation from ACH release causes continuous spasm
Tetanus Clinical Signs
Retraction of third eyelid, erect ears, grinding teeth, stiff tail, bloat, lockjaw, sawhorse
Tetanus Immunology
Acquired resistance depends on circulating antitoxin, reinfection possible, vaccination with toxin possible
Tetanus Diagnosis
Gram stain, blood agar in anaerobic culture, injection into antitoxin dosed mouse, PCR
Clostridium botulinum
Neuroparalytic intoxication and flaccid paralysis, 7 protein neurotoxins, affects ruminants, horses, mink, and fowl
Botulinum Neurotoxins
Act in the neuromuscular junction, binds cholinergic nerve cells and decreases the release of acetylcholine
Botulism Pathogenesis
Ingested and toxins absorbed in GI, circulates in blood stream, attaches to neuro-muscular junction of cholinergic nerves, hydrolyzes a SNARE protein, synapse degenerates
Botulism Clinical Signs
Muscular incoordination, no changes in consciousness, normal temperature, recumbency, flaccid paralysis
Limberneck
Initial clinical sign of botulism
Botulism Diagnosis
Demonstration in toxin by injecting into a mouse
Botulism Prevention
Stomach purging, antitoxin, vaccination with toxoids, antiserum
Histotoxic Clostridia
Enteropathogenic, exotoxins induce necrosis and lethal systemic effects, present as latent spores
Nagler Test
Egg yolk agar is used, alpha toxin breaks down agar, antibody binds toxin and prevents lecithin breakdown
Black Leg
Clostridium chauvoei causes muscle necrosis and air bubbles
Malignant Edema
Clostridium perfringens, nobyi, chauvoei, and sordelli cause edema, hemorrhage, and fibrin in the pericardium
Braxy
Clostridium septicum causes hemorrhagic mucus in the abomasum of sheep
Black Disease
Clostridium novyi associated with liver parasites causes air bubbles in liver
Bacillary hemoglobinuria
Clostridium haemolyticum causes jaundice and hemoglobinuria
Enteropathogenic Clostridia Diagnosis
Immunofluorescence of tissue, strict anaerobic conditions, liver in culture, PCR
Enteropathogenic Clostridia Prevention
Vaccination, change of pasture
Enterotoxemia Type A
Enterotoxin destroys membrane and connective tissue causing yellow lamb disease, hemorrhagic enteritis, necrotic enteritis, and food poisoning
Enterotoxemia Co-infection
Clostridia in chickens
Enterotoxemia Type B
Beta toxin causes lamb dysentery because proteolytic enzymes destroy colostrum proteins, also causes hemorrhagic enteritis in small intestine
Enterotoxemia Type C
Absence of established normal flora in neonates and protease inhibitors favor Beta toxin and cause hemorrhagic enteritis
Sheep Struck
Type C enterotoxemia in older sheep, gives the impression the animal has been struck by lightning
Enterotoxemia Type D
Epsilon toxin causes overeating and pulpy kidney disease in older lambs after an upset in the gut flora
Epsilon Toxin
Increases intestinal permeability, causes vascular damage and fluid loss, encephalomalacia in CNS, and activated by trypsin so has a predilection for older animals
Pulpy Kidney
Acute death and rapid kidney breakdown with glycosuria caused by enterotoxemia type D
Immunity
Antibodies correlate with anti-toxin levels
Lab Diagnosis
Non motile, polysaccharide capsule, spores rare, isolation in blood agar in anaerobic environment, alpha toxin, gram positive rods
Growth on blood agar
Small, grey, translucent colonies surrounded by double zone hemolysis
Double Zone Hemolysis
Consists of an inner clear zone and outer hazy zone
Stormy Fermentation
Clotting of milk followed by gaseous disruption
Treatment
Usually too acute, some antitoxin
Immunization
Active immunization with bacteria and toxins to induce immune response
Clostridium difficile
Gram positive, motile, encapsulated, spore-forming, anaerobic rod causing diarrhea
Toxin A
Produced by C. difficile, breaks down cytoskeletal components, disrupting tight junctions in epithelial cells, stimulates polymorphonuclear cell influx
C. difficile Pathogenesis
Trigger event disrupts normal flora and C. difficile adheres to large intestine, causing intense inflammatory response including diarrhea
C. difficile Treatment
Metronidazole, no vaccines, hand washing
C. piliforme
Acute fatal diarrhea disease with liver necrosis: Tyzzer’s disease
C. sordellii
Fatal myositis and hepatic disease in ruminants and horses
C. colinum
Causes ulcerative enteritis and necrotizing hepatitis of fowl
C. spiroforme
Mucoid enteritis and antibiotic induced enteritis in rabbits
