Bacteriology exam prep Clostridium, Enterobacteriaceae ,Escherichia, Salmonella
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Questions and Answers

What is the optimal environment for the growth of Clostridium species on enriched media?

  • 15-25% CO2
  • 5-15% CO2
  • 10-20% O2
  • 2-10% CO2 (correct)

    • What differentiates neurotropic Clostridium species from other types?

  • Exogenous infections via respiratory contamination
  • Production of endotoxins specific to the intestinal tract
  • Non-invasive action with neurotoxin targeting neuronal cells (correct)
  • Invasive properties with high-potency exotoxins

    • Which species of animal is most susceptible to Tetanus?

  • Horses (correct)
  • Birds
  • Sheep
  • Carnivores

    • How does Tetanus toxin (TeNT) travel to the CNS?

    <p>Retrograde axonal transport (C)</p> Signup and view all the answers

    Where are Clostridium species commonly found causing exogenous infections?

    <p>In soil via wound contamination (D)</p> Signup and view all the answers

    What characterizes spastic paralysis caused by Tetanus toxin?

    <p>Hyperactivity of voluntary muscles leading to rigidity (D)</p> Signup and view all the answers

    What is a common mode of Tetanus infection in animals?

    <p>Poor management practices leading to wound contamination (D)</p> Signup and view all the answers

    Which statement is true about Clostridium tetani?

    <p>It is ubiquitous in soils globally (D)</p> Signup and view all the answers

    Why do Clostridium endospores bulge the mother cell?

    <p>From the pressure of endospore formation inside the cell (A)</p> Signup and view all the answers

    What is the primary route for Tetanus spore entry into the body?

    <p>Wound contamination (D)</p> Signup and view all the answers

    What is a characteristic clinical sign of systemic tetanus?

    <p>Rigidity of masseter and temporal muscles (C)</p> Signup and view all the answers

    Which of the following mechanisms is primarily inhibited by botulinum toxin, resulting in paralysis?

    <p>Inhibition of acetylcholine release (A)</p> Signup and view all the answers

    Opisthotonus, seen in systemic tetanus, is best described as what?

    <p>An abnormal, extremely arched posture caused by muscle spasms (C)</p> Signup and view all the answers

    In local tetanus, what type of autonomic nervous system symptoms can be observed?

    <p>Tachycardia, hypertension, and sweating alternating with bradycardia and hypotension (C)</p> Signup and view all the answers

    Which animal is considered a natural reservoir for botulism?

    <p>Birds (D)</p> Signup and view all the answers

    What is a significant predisposing factor for toxico-infection botulism in animals?

    <p>Abrupt changes to the intestinal microbiota (C)</p> Signup and view all the answers

    Foals with Shaker Foal Syndrome predominantly exhibit what symptom?

    <p>Weakness &amp; tremors of muscles in the limbs (D)</p> Signup and view all the answers

    How does botulism primarily cause respiratory failure?

    <p>By causing diaphragmatic, laryngeal, and respiratory muscle spasms (A)</p> Signup and view all the answers

    Botulism in animals is primarily characterized by which of the following signs?

    <p>Progressive, symmetrical, flaccid paralysis and limb weakness (C)</p> Signup and view all the answers

    Why does botulism affect only the motor systems and not the sensory systems?

    <p>Because the toxin selectively inhibits neurotransmitter release at motor neuron endings (B)</p> Signup and view all the answers

    What is the primary source of clostridial infections?

    <p>Fecal shedding (B)</p> Signup and view all the answers

    What is the primary effect of the toxins produced by Clostridioides difficile?

    <p>Inhibition of actin polymerization (D)</p> Signup and view all the answers

    What is the primary route of transmission of Clostridioides difficile?

    <p>Fecal-oral route (A)</p> Signup and view all the answers

    What is the characteristic histopathological finding in Clostridioides difficile infections?

    <p>Necrotizing and hemorrhagic typhlocolitis (B)</p> Signup and view all the answers

    What is the primary factor that predisposes to enteric clostridial infections?

    <p>All of the above (D)</p> Signup and view all the answers

    What is the primary mode of action of pore-forming toxins?

    <p>Acting on the cell surface (C)</p> Signup and view all the answers

    What is the primary effect of toxins produced by C. perfringens?

    <p>Acute severe hemorrhagic and necrotic enteritis (A)</p> Signup and view all the answers

    What is the characteristic clinical sign of Clostridioides difficile infections in horses?

    <p>Mesocolic edema (B)</p> Signup and view all the answers

    What is the primary mechanism of action of the toxins produced by Clostridioides difficile?

    <p>Causing cell rounding and death (A)</p> Signup and view all the answers

    What is the primary difference between Clostridioides difficile and C. perfringens?

    <p>Mode of action (D)</p> Signup and view all the answers

    Which proteins are essential for membrane fusion and docking of vesicles involved in neurotransmission?

    <p>VAMP, SNAP25, Syntaxin (A)</p> Signup and view all the answers

    What is the primary result of Botulinum toxin's action at motor neuron endings?

    <p>Flaccid paralysis (D)</p> Signup and view all the answers

    Which protein involved in neurotransmission is anchored specifically to the synaptic vesicle membrane?

    <p>VAMP (D)</p> Signup and view all the answers

    What mechanism allows clostridial neurotoxins to block exocytosis of neurotransmitters?

    <p>Cleavage of SNARE complex proteins (B)</p> Signup and view all the answers

    Where is SNAP25 anchored in the process of neurotransmission?

    <p>Plasma membrane (D)</p> Signup and view all the answers

    How do Botulinum and Tetanus toxins become active neurotoxins?

    <p>Proteolytic activation (C)</p> Signup and view all the answers

    Which structure links the light and heavy chains in active clostridial neurotoxins?

    <p>Disulfide bridge (B)</p> Signup and view all the answers

    What is the primary effect of Tetanus toxin on central inhibitory interneurons?

    <p>Causes spastic paralysis (A)</p> Signup and view all the answers

    Which vesicle docking protein is anchored to the plasma membrane?

    <p>Syntaxin (B)</p> Signup and view all the answers

    What role do the L chains of clostridial neurotoxins play in their mechanism of action?

    <p>Cleaving SNARE complex proteins (C)</p> Signup and view all the answers

    Which Clostridium species is associated with abomasitis and enterotoxemia in sheep when they feed on frozen grass during winter?

    <p>C. septicum (D)</p> Signup and view all the answers

    What is the role of cytotoxin CctA produced by C. chauvoie in infected animals?

    <p>Forms pores and causes lesions (D)</p> Signup and view all the answers

    What triggers the dormancy of Clostridium spores in infected tissues until favorable conditions arise?

    <p>Lowering oxygen tension (A)</p> Signup and view all the answers

    Which Clostridium species produces alpha and beta toxins that are lethal and necrotizing, as well as pore-forming cytolysins?

    <p>C. septicum (B)</p> Signup and view all the answers

    Which feature is characteristic of C. chauvoie infection concerning tissue lesions?

    <p>Lesions in skeletal muscles, diaphragm, tongue, or heart (B)</p> Signup and view all the answers

    Which condition is necessary for the spores of C. septicum to germinate and cause malignant edema?

    <p>Anaerobic environment (D)</p> Signup and view all the answers

    How are the toxins produced by enteropathogenic Clostridium species absorbed and what do they cause?

    <p>Absorbed in bloodstream causing generalized toxemia (A)</p> Signup and view all the answers

    What event can trigger the germination of Clostridium perfringens endospores in an animal's GI tract?

    <p>Biliary acids (B)</p> Signup and view all the answers

    What is the clinical presentation of animals affected by blackleg caused by C. chauvoie?

    <p>Difficulty walking and recumbency before death (C)</p> Signup and view all the answers

    Why do pathogens of Clostridium species remain highly persistent in the environment?

    <p>Endospores are heat-resistant and aerotolerant (C)</p> Signup and view all the answers

    What is the primary characteristic of the Enterobacteriaceae family?

    <p>Gram negative enteric rods (D)</p> Signup and view all the answers

    What is the arrangement of flagella in motile Enterobacteriaceae species?

    <p>Peritrichous (C)</p> Signup and view all the answers

    What is the primary habitat of Enterobacteriaceae species?

    <p>All of the above (D)</p> Signup and view all the answers

    What is the term for species that ferment lactose in the Enterobacteriaceae family?

    <p>Coliforms (A)</p> Signup and view all the answers

    Which of the following is not a characteristic of the genus Escherichia?

    <p>Oxidase positive (A)</p> Signup and view all the answers

    What is the concentration of E. coli in the large intestine?

    <p>10^8-10^9 organisms per gram of feces (B)</p> Signup and view all the answers

    What is the primary disease caused by E. coli in neonates?

    <p>Septicemia (B)</p> Signup and view all the answers

    Which of the following is not a pathogenic species in the Enterobacteriaceae family?

    <p>Pseudocitrobacter (C)</p> Signup and view all the answers

    What is the primary difference between pathogenic and opportunistic pathogens in the Enterobacteriaceae family?

    <p>Disease severity (B)</p> Signup and view all the answers

    How do Enterobacteriaceae species reduce nitrates?

    <p>By reducing nitrates to nitrites (B)</p> Signup and view all the answers

    What is the primary cause of shock in enteric colibacillosis?

    <p>Lipid A portion of lipopolysaccharides (B)</p> Signup and view all the answers

    Which epithelial cells are affected by enterotoxins produced by ETEC strains?

    <p>Jejunal and ileal epithelial cells (B)</p> Signup and view all the answers

    What is the primary route of entry for E. coli in enteric colibacillosis?

    <p>Oral route (C)</p> Signup and view all the answers

    What is the primary role of adhesins produced by ETEC strains?

    <p>To promote attachment to epithelial cells (C)</p> Signup and view all the answers

    What is the characteristic clinical sign of enteric colibacillosis?

    <p>Watery, non-bloody diarrhea (B)</p> Signup and view all the answers

    Why are fimbrial adhesins F4, F5, F6, and F41 host and species specific?

    <p>Because they are regulated by the age of the animal (A)</p> Signup and view all the answers

    What is the primary mechanism of action of enterotoxins produced by ETEC strains?

    <p>Promotion of water and electrolyte secretion into the intestinal lumen (C)</p> Signup and view all the answers

    What is the primary result of enteric colibacillosis complicated by shock?

    <p>Dehydration and metabolic acidosis (B)</p> Signup and view all the answers

    What is the primary difference between enteric colibacillosis and uncomplicated enteric colibacillosis?

    <p>Presence of shock (A)</p> Signup and view all the answers

    What is the primary role of lipopolysaccharides in enteric colibacillosis?

    <p>To cause shock (D)</p> Signup and view all the answers

    What is the primary critical virulence factor of EHEC?

    <p>Shiga toxin (B)</p> Signup and view all the answers

    What is the characteristic clinical presentation of pigs affected by edema disease?

    <p>Depression, swelling of eyelids, and peculiar squealing (A)</p> Signup and view all the answers

    What is the primary mechanism of Shiga toxin action in endothelial cells?

    <p>Inhibition of protein synthesis (A)</p> Signup and view all the answers

    What is the primary receptor for Shiga toxin on erythrocytes?

    <p>GB4 (B)</p> Signup and view all the answers

    What is the primary predisposing factor for STEC infections in pigs?

    <p>Weaning (B)</p> Signup and view all the answers

    What is the primary site of Shiga toxin absorption in pigs?

    <p>Small intestine (A)</p> Signup and view all the answers

    What is the primary consequence of Shiga toxin action on endothelial cells?

    <p>Cell death and vascular leakage (B)</p> Signup and view all the answers

    What is the primary difference between EHEC and STEC?

    <p>EHEC produces Shiga toxin, while STEC does not (C)</p> Signup and view all the answers

    What is the primary consequence of edema disease in pigs?

    <p>Severe edema and hemorrhage in specific tissues (A)</p> Signup and view all the answers

    What is the primary site of Shiga toxin binding in the body?

    <p>Erythrocytes (A)</p> Signup and view all the answers

    Which animal experiences diarrhea caused by Enteropathogenic E.coli within 3-12 days of birth with a mortality rate of up to 100%?

    <p>Suckling rabbits (A)</p> Signup and view all the answers

    What is the primary cause of diarrhea in animals affected by Enteropathogenic E.coli?

    <p>Malabsorption due to destroyed microvilli (A)</p> Signup and view all the answers

    Which protein interaction is crucial for creating intimate contact between Enteropathogenic E.coli and host cells?

    <p>Tir and intimin (C)</p> Signup and view all the answers

    What type of lesions are primarily seen under the microscope in cases of Enteropathogenic E.coli infection?

    <p>Light to moderate inflammation and mild ulceration (B)</p> Signup and view all the answers

    What role does the Type III secretion system (T3SS) play in Enteropathogenic E.coli infections?

    <p>Secretes proteins into the enterocyte leading to cytoskeletal rearrangement (A)</p> Signup and view all the answers

    In Enteropathogenic E.coli pathogenesis, what structure forms as a result of cytoskeletal rearrangement?

    <p>Cup-like pedestals (D)</p> Signup and view all the answers

    In Enteropathogenic E.coli infections, which cellular structure is reabsorbed, leading to the effacement of microvilli?

    <p>Actin (A)</p> Signup and view all the answers

    Which animals are commonly associated with Enteropathogenic E.coli induced diarrhea in pet stores and kennels?

    <p>Dogs between the ages of 1.5-3 months (D)</p> Signup and view all the answers

    What is the primary reason Enteropathogenic E.coli does not produce typical enterotoxins?

    <p>They use attaching and effacing lesions to disrupt host cells (B)</p> Signup and view all the answers

    What type of intestinal changes cause diarrhea in Enteropathogenic E.coli infections?

    <p>Loss of absorptive microvilli (A)</p> Signup and view all the answers

    What is the primary function of siderophores in ExPEC?

    <p>To acquire iron from host tissues (C)</p> Signup and view all the answers

    How do ExPEC strains gain access to the body?

    <p>Via conjunctival, umbilical or intestinal tissues (A)</p> Signup and view all the answers

    What is the result of insufficient passive immunity in animals?

    <p>Increased susceptibility to ExPEC infections (D)</p> Signup and view all the answers

    What is the outcome of ExPEC proliferation in lymphatics and bloodstream?

    <p>Endotoxemia (D)</p> Signup and view all the answers

    What is the role of adhesins in ExPEC pathogenesis?

    <p>To facilitate adherence to host cells (D)</p> Signup and view all the answers

    What is the outcome if antibacterial therapy and immune system are unable to remove ExPEC?

    <p>Death of the host (C)</p> Signup and view all the answers

    Which of the following is NOT a virulence factor of ExPEC?

    <p>Flagella (A)</p> Signup and view all the answers

    What is the mechanism of ExPEC entry into lymphatics?

    <p>Via endocytotic process (A)</p> Signup and view all the answers

    What is the outcome of ExPEC infection in animals?

    <p>All of the above (D)</p> Signup and view all the answers

    What is a characteristic of Septicemic E. coli (SEPEC)?

    <p>Causes septicemia (B)</p> Signup and view all the answers

    Which characteristic is most commonly associated with Uropathogenic E.coli (UPEC) infections in dogs?

    <p>Prostatitis (D)</p> Signup and view all the answers

    What is a notable histopathological feature in ruminants affected by coli strains in their early days of life?

    <p>Inflammatory changes in liver, spleen, joints, and meninges (C)</p> Signup and view all the answers

    What predisposing factor is commonly associated with cystic endometrial hyperplasia in bitches during UPEC infections?

    <p>High progesterone levels (D)</p> Signup and view all the answers

    Which clinical syndrome is NOT commonly associated with Avian Pathogenic E.coli (APEC) infections?

    <p>Cystitis (C)</p> Signup and view all the answers

    What is a common presentation of E.coli mastitis in dairy cattle two weeks post parturition?

    <p>Environmental contamination (B)</p> Signup and view all the answers

    Which factor commonly affects the nature of E.coli mastitis developed in dairy cattle?

    <p>Genetic makeup (A)</p> Signup and view all the answers

    Which description best fits the pathogenesis of Uropathogenic E.coli (UPEC) in dogs?

    <p>Colonization of periurethral area and migrating up the urethra (C)</p> Signup and view all the answers

    Which systemic effect is primarily attributed to absorbed E.coli lipopolysaccharide (LPS) in UPEC infections?

    <p>Renal damage and dysfunction (C)</p> Signup and view all the answers

    Which effect is commonly seen during the periparturient period in cows with E.coli mastitis?

    <p>Delayed PMN leukocyte response (C)</p> Signup and view all the answers

    What distinguishes Uropathogenic E.coli strains causing pyometra in canines?

    <p>Often have same characteristics as UPEC (D)</p> Signup and view all the answers

    What is the primary purpose of serotyping in E. coli differentiation?

    <p>To perform epidemiological investigations (D)</p> Signup and view all the answers

    What is the primary role of adhesins in E. coli?

    <p>To mediate attachment to host tissues (C)</p> Signup and view all the answers

    Which of the following is NOT a type of adhesin in E. coli?

    <p>F7 (A)</p> Signup and view all the answers

    What is the primary association of F4 adhesin in E. coli?

    <p>Piglets (B)</p> Signup and view all the answers

    What is the primary role of fimbrial antigens in E. coli?

    <p>To facilitate identification and characterization of strains (C)</p> Signup and view all the answers

    How many virulence factors are associated with E. coli?

    <p>7 (B)</p> Signup and view all the answers

    What is the primary association of F17 adhesin in E. coli?

    <p>Calves (A)</p> Signup and view all the answers

    What is the primary role of enterotoxins in E. coli?

    <p>To cause diarrhea (C)</p> Signup and view all the answers

    What is the primary association of F165 adhesin in E. coli?

    <p>Pigs (B)</p> Signup and view all the answers

    What is the primary characteristic of F6 adhesin in E. coli?

    <p>Causes diarrhea in piglets that are less than 1 week old only (D)</p> Signup and view all the answers

    Which type of toxin causes disturbances in the intestinal fluid metabolism without causing morphological lesions in the mucosa?

    <p>Heat-Stable enterotoxins (D)</p> Signup and view all the answers

    What is the mechanism of action of Shiga toxin in endothelial cells?

    <p>Inhibits protein synthesis and induces apoptosis (C)</p> Signup and view all the answers

    Which enterotoxin opens enterocyte calcium channels leading to an influx of Ca2+?

    <p>STb (A)</p> Signup and view all the answers

    Which heat-labile enterotoxin causes permanent activation of adenylyl cyclase?

    <p>LT1 (B)</p> Signup and view all the answers

    What is the primary effect of heat-labile enterotoxin on enterocytes?

    <p>Decreased reabsorption of Na+ and secretion of Cl- &amp; HCO3- (A)</p> Signup and view all the answers

    Which toxin does not cause diarrhea on its own and requires the secretion of other toxins?

    <p>EAST1 (D)</p> Signup and view all the answers

    Which cyclomodulin is known to inhibit the cell cycle?

    <p>CDT (A)</p> Signup and view all the answers

    Which of the following is a common result of hemolysins' action on red blood cells?

    <p>Obtaining iron by damaging RBCs (B)</p> Signup and view all the answers

    What is the primary consequence of shiga toxin upregulating proinflammatory cytokines in monocytes?

    <p>Induce proinflammatory response (B)</p> Signup and view all the answers

    What is the primary impact of high intracellular cAMP concentration caused by heat-labile enterotoxins?

    <p>Inhibition of Na+ reabsorption and increased diarrhea (A)</p> Signup and view all the answers

    What is the primary purpose of serotyping in E.coli?

    <p>To differentiate pathogenic and non-pathogenic strains of E.coli (D)</p> Signup and view all the answers

    What type of antigens is used for identification and characterization of E.coli strains?

    <p>Fimbrial antigens (D)</p> Signup and view all the answers

    What is the role of adhesins in E.coli?

    <p>To mediate attachment to host tissues (D)</p> Signup and view all the answers

    Which adhesin is commonly found in E.coli strains that cause urinary tract infections (UTIs)?

    <p>F1 (C)</p> Signup and view all the answers

    Which of the following adhesins is associated with E.coli strains that cause colibacillosis in animals?

    <p>F4 (D)</p> Signup and view all the answers

    What is the primary function of enterotoxins produced by E.coli?

    <p>To cause diarrhea (C)</p> Signup and view all the answers

    How are enterotoxins encoded in E.coli?

    <p>On plasmids (A)</p> Signup and view all the answers

    What is the primary characteristic of F6 adhesin?

    <p>Causes diarrhea in piglets less than 1 week old (D)</p> Signup and view all the answers

    Which adhesin is associated with E.coli strains that cause septicemia in calves?

    <p>F17 (A)</p> Signup and view all the answers

    What is the primary difference between F4 and F5 adhesins?

    <p>F4 is associated with pigs, while F5 is associated with cattle, swine and sheep (C)</p> Signup and view all the answers

    What is the main effect of heat-stable enterotoxins (STa) on enterocytes?

    <p>Induction of fluid secretion (B)</p> Signup and view all the answers

    Which factor is NOT directly associated with the mechanism of Shiga toxins?

    <p>Increase in intracellular cAMP levels (C)</p> Signup and view all the answers

    How does heat-labile enterotoxin LT1 primarily cause diarrhea?

    <p>Through activation of adenylyl cyclase (A)</p> Signup and view all the answers

    Which enterotoxin is noted for increasing the permeability of the intestinal epithelium and causing loss of villous epithelial cells?

    <p>STb (B)</p> Signup and view all the answers

    Regarding the stability of enterotoxins under heat, which statement is MOST accurate?

    <p>Heat-stable toxins are inactivated at 100ºC after 15 minutes. (D)</p> Signup and view all the answers

    What is the role of hemolysins in bacterial infections?

    <p>Forming pores in red blood cells (B)</p> Signup and view all the answers

    Which confirmatory sign of epithelial cell damage is linked to Shiga toxin's action?

    <p>Actin and microtubule rearrangement (A)</p> Signup and view all the answers

    Which component is common between East1 and STa toxins?

    <p>Inhibition of Na+ reabsorption (D)</p> Signup and view all the answers

    What effect does STb (T2) have on intracellular processes in enterocytes?

    <p>Activation of intracellular enzymes (D)</p> Signup and view all the answers

    Which condition is primarily caused by the action of heat-labile enterotoxins resulting in metabolic acidosis and death?

    <p>Irreversible high cAMP concentration (D)</p> Signup and view all the answers

    What is the primary reason why neonates under 1 week of age are more susceptible to E. coli infection?

    <p>The normal intestinal flora not being fully established (C)</p> Signup and view all the answers

    Which of the following is NOT a method of controlling and preventing E. coli infection?

    <p>Administering broad-spectrum antibiotics prophylactically (B)</p> Signup and view all the answers

    What is the primary function of commercially produced preparations containing monoclonal antibodies to ETEC adhesins?

    <p>To reduce the severity and mortality of E. coli infections (A)</p> Signup and view all the answers

    What is the primary characteristic of the genus Salmonella?

    <p>It is a facultatively anaerobic, motile bacterium (D)</p> Signup and view all the answers

    What is the primary reservoir for Salmonella species?

    <p>The intestinal tract of warm-blooded and cold-blooded animals (C)</p> Signup and view all the answers

    What is the primary reason why Salmonella species are important?

    <p>They are a common cause of gastroenteritis in humans and young animals (C)</p> Signup and view all the answers

    What is the primary difference between S. enterica subsp. enterica and other subspecies of Salmonella?

    <p>S. enterica subsp. enterica includes over 2600 serotypes (D)</p> Signup and view all the answers

    What is the primary method of prevention and control of E. coli infections?

    <p>Practicing sound husbandry practices (B)</p> Signup and view all the answers

    What is the primary reason why E. coli infections are more common in intensive husbandry practices?

    <p>Due to the rapid spread of E. coli strains (D)</p> Signup and view all the answers

    What is the primary reason why E. coli bacteria can survive for weeks to months in moist, shaded environments?

    <p>Due to their ability to survive in a variety of environments (B)</p> Signup and view all the answers

    In what environmental conditions can Salmonellae survive for nine months or more?

    <p>Moist soil, water, fecal particles, and food (A)</p> Signup and view all the answers

    Which host factor does NOT affect the outcome of salmonellosis?

    <p>Genetic makeup (A)</p> Signup and view all the answers

    Which serotype of Salmonella affects cattle specifically?

    <p>S. Dublin (C)</p> Signup and view all the answers

    What pathologic change is seen in the septicemic form of salmonellosis?

    <p>Fibrinoid changes in blood vessels in various organs (B)</p> Signup and view all the answers

    What is the primary method of transmission for Salmonella?

    <p>Fecal-oral route (B)</p> Signup and view all the answers

    Which factor primarily influences the severity of a Salmonella infection?

    <p>Host's immune response (A)</p> Signup and view all the answers

    What clinical sign is typically observed in acute enteritis with septicemia caused by salmonellosis?

    <p>Depression and high fever (B)</p> Signup and view all the answers

    What host cell interaction is crucial for the pathogenesis of Salmonella?

    <p>Adhesion to the M cells in the gut-associated lymphatic tissue (B)</p> Signup and view all the answers

    Which of the following is a common clinical sign of salmonellosis in young ruminants?

    <p>Pneumonia and neurologic signs (A)</p> Signup and view all the answers

    What is a typical feature of acute enteritis without septicemia in salmonellosis?

    <p>Severe watery diarrhea followed by dysentery (D)</p> Signup and view all the answers

    Which of the following serovars is less virulent in chicks, but can colonize the intestine and cause human food poisoning?

    <p>S.Heidelberg (B)</p> Signup and view all the answers

    What is the primary mode of transmission of S.Pullorum?

    <p>Vertical transmission from infected breeding stock (B)</p> Signup and view all the answers

    What is the primary clinical sign of Fowl typhoid caused by S.Gallinarum?

    <p>Acute septicemia (C)</p> Signup and view all the answers

    What is the outcome for birds that survive Pullorum disease?

    <p>They become lifelong carriers (B)</p> Signup and view all the answers

    What is the primary route of infection for S.Gallinarum?

    <p>Fecal-oral transmission (B)</p> Signup and view all the answers

    What is the primary difference between Pullorum disease and Fowl typhoid?

    <p>Pullorum disease is caused by S.Pullorum, while Fowl typhoid is caused by S.Gallinarum (D)</p> Signup and view all the answers

    What is the primary effect of S.Pullorum infection in breeding stock?

    <p>Vertical transmission of the organism to offspring (B)</p> Signup and view all the answers

    What is the primary consequence of S.Gallinarum infection in adult birds?

    <p>Acute septicemia (A)</p> Signup and view all the answers

    Study Notes

    Genus Clostridium

    • Widely distributed in soil, freshwater, and marine sediments globally
    • Many pathogenic strains are normal inhabitants of intestinal tracts and cause endogenous infections
    • Others are present in soil and cause exogenous infections via wound contamination
    • 14 species are significant in veterinary medicine
    • Most produce ≥1 exotoxins with varying potency

    Characteristics

    • Gram +’ve
    • Large rods
    • Anaerobic
    • 2-10% CO2 is optimal environment for growth on enriched media
    • Endospore producing
    • Endospores usually bulge the mother cell

    Classification of Clostridia

    • Based on potency and the invasive ability of the toxins
    • Three different classifications:
      • Neurotropic

    Clostridium Tetani

    • Produces potent non-invasive neurotoxins
    • Colonizes hosts to a limited extent
    • Toxins specifically target neuronal cells in animals and humans
    • Causes spastic paralysis
    • Acts at inhibitory interneurons
    • Tetanus toxin only produced by C.tetani
    • Ubiquitous organism in soils globally
    • Horses are most susceptible species, carnivores less-so, and birds are resistant
    • Tetanus in animals is mostly seen in horses and sheep, and is almost always fatal
    • Wound contamination from spores in the soil, feces, dust, contaminated equipment
    • Sporadic infections most stemming from poor management practices
    • Tetanus only occurs through wound contamination

    Tetanus Infection

    • Spores germinate into vegetative cells where they begin to multiply and produce the neurotoxin
    • Toxin (TeNT) enters peripheral nerve endings and proceeds to the CNS via retrograde axonal transport
    • Once it reaches the CNS it inhibits the release of inhibitory neurotransmitters causing spastic paralysis
    • Characterized by hyperactivity of voluntary muscles leading to rigidity and tetanic spasms
    • Tonic, involuntary, and prolonged muscle contractions
    • Spasms- shorter lasting muscle contractions triggered by sensory stimuli (light, touch, noise)

    Clinical Signs of Tetanus

    • Can present locally or systemically
    • Systemic tetanus:
      • Increased spasticity of masticatory muscles followed by progressively more spastic paralysis of the trunk and limb muscles
      • Rigidity of masseter and temporal muscles→ inability to open mouth
      • Spastic paralysis of extensors of the back and neck are accompanied by Opisthotonus (abnormal, extremely arched posture caused by muscle spasms)
    • Local tetanus:
      • Muscles of affected limb or region become painful and eventually spastic
      • Seen in animals that are more resistant to tetanus toxin (dogs, cats, etc.)
    • Autonomic nervous system is affected and causes tachycardia, hypertension, sweating, and then alternates with bradycardia, hypotension due to respiratory failure
    • Respiratory failure caused by diaphragmatic, laryngeal, and respiratory muscle spasms

    Clostridium Botulinum

    • Produces potent non-invasive neurotoxins
    • Acts at motor neuron endings
    • Causes flaccid paralysis
    • Botulinum toxin is also produced by C.butyricum and C.baratii
    • Widespread in soils, lake, and sea sediments
    • Toxins are divided into 9 types based on antisera and biological effects (A, B, C, D, E, F, G, H, J, X) and 40 subtypes
    • Variations may affect biological functions
    • Recognition, invasion efficiency, persistence, enzymatic activity
    • Most common in cattle, horses, and birds
    • Birds are considered botulism reservoirs in nature

    Botulism

    • Botulism in animals has 3 forms:
      • Toxico-infection (intestinal infection)
      • Food-borne intoxication
      • Wound Contamination
    • Botulism is not contagious but can occur in groups of animals that are exposed to the same environments
    • Botulism clinical signs usually present in animals affected by botulinum toxin types C and D
    • No fever (afebrile)
    • Progressive, symmetrical, flaccid paralysis and limb weakness
    • Recumbency
    • Respiratory difficulty
    • Death occurring due to respiratory arrest
    • Sensory nervous systems are unaffected, only motor
    • No visible pathological changes

    Clinical Signs of Botulism

    • Cattle and Horses:
      • Dysphagia
      • Hypersalivation
      • Decreased tongue tone
      • Anorexia
      • Constipation or Diarrhea
      • Colics
    • Foals (Shaker Foal Syndrome):
      • Weakness and tremors of muscles in the limbs

    Botulinum and Tetanus Toxins

    • Share a common structure and are released from the bacterium
    • Synthesized as a precursor, activated by proteolytic activity of Clostridium proteases or exogenous proteases (intestinal)
    • Consist of a light chain and heavy chain linked by a disulfide bridge

    Neurotransmission at the Neuromuscular Junction

    • Peptide neurotransmitters are synthesized in the endoplasmic reticulum of neurons and stored in synaptic vesicles
    • Vesicles move to the active zone (presynaptic) and dock close to calcium channels, ready for membrane fusion and release of neurotransmitters
    • Three critical proteins involved in calcium-mediated exocytosis: VAMP, SNAP25, and Syntaxin, which form the SNARE Complex
    • SNARE Complex brings the plasma membrane and vesicle into close contact for fusion and release of neurotransmitters

    Mechanism of Action of Clostridial Neurotoxins

    • Light chains of clostridial neurotoxins drive intracellular activity in target neurons
    • Light chains cleave one of the three SNARE complex proteins, blocking exocytosis of neurotransmitters by impairing fusion of vesicles to the plasma membrane
    • Botulinum toxins act at motor neuron endings, resulting in flaccid paralysis
    • Tetanus toxin acts at central inhibitory interneurons, causing spastic paralysis

    Histotoxic Clostridium (Gas Gangrene)

    • Produce less potent but invasive toxins, causing histotoxic infections that destroy living tissues
    • Enzymes and toxins cause damage

    C.chauvoie (Blackleg)

    • Causes disease in cattle between 2-24 months globally
    • Rapid progression and high mortality
    • Animals found dead without clinical signs
    • May present with difficulty walking, recumbency before death
    • Bacteria produce cytotoxin CctA, which is pore-forming and causes lesions
    • Lesions typically in skeletal muscles in the leg or neck, can also develop in the diaphragm, tongue, or heart

    C.septicum (Malignant Edema/Gas Gangrene/Braxy)

    • Affects cattle, sheep, pigs, horses, and other animals of different ages
    • Sheep: Abomasitis (braxy) and Enterotoxemia after feeding on frosted root crops and frozen grass during winter months
    • Damage to mucosal epithelium of the abomasum allows for colonization and causes abomasitis and enterotoxemia
    • Malignant edema (myositis): Introduction of the pathogen to an open wound, requiring an anaerobic environment
    • Lesions begin with rapid swelling at the wound site, becoming distended by gas
    • Swelling caused by inflammation and bloody subcutaneous edema fluid
    • Gas caused by fermentation of sugars and compounds by Clostridium
    • Diseased animals will become systemically ill and die within 36 hours of first lesion development, especially if left untreated

    Other Clostridium Species

    • C.novyi (Types A & B)
    • C.haemolyticum
    • Paeniclostrium sordellii
    • C.perfringens (Type A)

    Pathogenesis

    • Spores are ingested and begin to colonize the intestinal tract
    • Spores are carried from the intestine to tissues through the bloodstream or lymphatic system
    • Spores remain dormant in tissues until conditions change, activating germination into vegetative cells
    • Proliferation occurs in tissues as long as the environment remains anaerobic

    C.perfringens

    • Found in nature, present in soil, sewage, and contaminated foods
    • Normal intestinal habitant, aerotolerant
    • Can survive on aerobic surfaces and oxygen-exposed tissues, facilitating interhost transmission
    • Highly persistent in the environment due to aerotolerance and heat-resistant endospores
    • Germination triggered by biliary acids in the GI tract of mammals
    • Secondary bile acids produced by resident commensal bacteria inhibit germination, proliferation, and colonization

    Virulence Factors

    • Toxins and non-toxin tissue-degrading enzymes with strain variations
    • Toxins: Alpha (CPA), Beta (CPB) & Beta2 (CPB2), Enterotixin (CPE), Epsilons (ETX), Iota (ITX), Perfringolysins O (PFO)
    • Enzymes: Sialidase, collagenase, proteases, hyaluronidase, etc.
    • Three major classes based on their mode of action: Enzymes acting on cell surface, pore-forming toxins, and toxins acting in the cytoplasm (locally or systemically)

    Predisposing Factors

    • Enteric clostridial infections usually require predisposing conditions modifying the GI environment
    • Nutrition (protein-rich, high digestible carbohydrate concentration in diet)
    • Enhanced availability of nutrients through malabsorption or intestinal damage by other microorganisms
    • Use of antibiotics
    • Environmental contamination
    • Increased gastric intestinal pH

    Other C.perfringens Caused Diseases

    • Fecal shedding is the main source of clostridial infections
    • Bacterium can survive in the environment for years
    • Acute severe hemorrhagic and necrotic enteritis in young animals, often fatal

    Clostridioides difficile (formerly Clostridium difficile)

    • Strict anaerobe, highly resistant spores
    • Widespread in the large intestine of humans, animals, and fecally contaminated environments
    • Transmission: Fecal-oral route, infections associated with antibiotic treatment
    • Typhlocolitis: common hospital-acquired infections in humans
    • Caused by the absence of microbial competition due to antibiotic treatments
    • Two toxins (TcdA and TcdB) cause cell rounding and death, interfere with actin polymerization, causing fluid loss and diarrhea

    Other Clostridioides difficile Caused Diseases

    • Infections typically characterized by diarrhea, dehydration, toxemia, severe inflammation of the colon and cecum
    • Especially occurs in animals with expanded and large intestines (horses)
    • Mesocolic edema is characteristic in piglets
    • Histopathologically, necrotizing and hemorrhagic defocalitis

    Family Enterobacteriaceae

    • 33 genera, 140 species
    • Distributed in soil, water, on plants, insects, and intestinal tracts
    • Some species cause significant intestinal or extraintestinal disease in most animals and humans
    • Extraintestinal infections usually involve urinary tract, respiratory tract, systemic circulation, and wounds
    • Species that ferment lactose are called Coliforms
    • Important pathogenic species include Citrobacter, Cronobacter, Enterobacter, Escherichia, Klebsiella, Kluyvera, Raoultella, Salmonella, and Shigella

    Characteristics of Enterobacteriaceae Family

    • Gram negative, medium-sized rods
    • Peritrichous arrangement of flagella if motile
    • Facultatively anaerobic, glucose fermenters
    • Catalase +ve, Oxidase -ve
    • Capable of reducing nitrates to nitrites
    • Grows on non-enriched media (e.g., Nutrient agar)

    Genus Escherichia

    • Gram negative enteric rod
    • Family of Enterobacteriaceae
    • 6 species (type genus of family with type species of genus)
    • Only pathogenic species of importance in animals
    • Dominant organism recovered facultatively anaerobic bacterium in most animal intestinal tracts
    • Present at a level of 10^7-10^9 organisms per gram of feces
    • Exception is birds, where E. coli is recovered in very low percentage of healthy birds
    • Concentration of E. coli increases progressively from small to large intestine with the largest concentration being in large intestines

    E. coli

    • Causes septicemia in neonates in most species, especially in cows, dogs, kittens, pigs, lambs, and foals
    • Causes opportunistic septicemia in older, immunocompromised animals
    • In avian species, it causes sacculitis, omphalitis, and other systemic infectious manifestations
    • Classification of E. coli: pathogenic strains are classified into pathotypes based on virulence factors and disease-causing mechanisms

    Diarrheagenic E. coli

    • Diarrheagenic strains (DEC) are economically important in porcine, cattle, and sheep industries
    • E. coli causes septicemia in neonatal piglets, cows, and lambs
    • Post-weaning diarrheal infections are most important in piglets
    • Enterotoxigenic E. coli (ETEC) causes diarrheal disease in neonatal and weanling piglets, calves, lambs, dogs, and horses
    • Most common E. coli strain in farm animals (enteric colibacillosis)

    Pathogenesis of ETEC

    • Entrance via oral route
    • Colonize in small intestine once sufficient number is reached
    • Proliferation occurs rapidly
    • Enterotoxins produced and stimulate water and electrolyte secretion into the intestinal lumen
    • Excess fluid in small intestine and lack of absorption in large intestine → Diarrhea

    Enteric Colibacillosis

    • Severe, watery, non-bloody diarrhea
    • Requires treatment and correction of electrolyte and fluid imbalances to avoid fatalities due to dehydration and metabolic acidosis
    • Infection may progress so rapidly that death may occur before clinical signs of diarrhea develop
    • Especially in pigs
    • Rarely microscopic lesions
    • In uncomplicated cases, bacteria will be observed histologically coating the villi of mid-distal portions of the small intestines

    Enteropathogenic E. coli (EPEC)

    • Causes diarrhea in all animal species and humans
    • Reservoirs: healthy cattle, sheep, pigs, dogs, and cats
    • Most affected species: rabbits
      • Suckling rabbits: diarrhea at 3-12 days of age (mortality up to 100%)
      • Weanling rabbits: diarrhea at 5-14 days after weaning (mortality 5-50%)
    • Pigs and dogs are also affected

    Pathogenesis of EPEC

    • Bacterial colonization of small and large intestines by formation of attaching and effacing lesions
    • Lesions develop in 3 stages:
      • Initial adherence: interaction between adhesins and host epithelial cells
      • Type III secretion system (T3SS): secretion of several proteins into the enterocyte
      • Host cell undergoes substantial cytoskeletal rearrangement and forms cup-like pedestals
    • Microvilli are effaced, and bacteria are intimately attached to the apical plasma membrane of host cells
    • Loss of absorptive microvilli leads to diarrhea due to malabsorption

    Microscopic Lesions

    • Light to moderate inflammation of lamina propria
    • Enterocyte desquamation and mild ulceration
    • Light-moderate villous atrophy in small intestine
    • Extensive multifocal bacterial colonization of surface epithelium

    Shiga Toxin-producing E. coli (STEC) and Enterohemorrhagic E. coli (EHEC)

    • Greater virulence due to ability to produce attaching and effacing lesions plus Shiga toxin
    • STEC that produce intimin and other LEE products are called EHEC (enterohemorrhagic E. coli)
    • Shiga toxin (Stx) is the critical virulence factor

    EHEC Infections

    • Can cause hemolytic uremic syndrome (HUS) in dogs, which occurs occasionally as a consequence to bloody diarrhea in young dogs
    • Bloody diarrhea is followed by thrombocytopenia, hemolytic anemia, and acute anuric renal failure
    • Renal proximal tubular necrosis, hemorrhages, glomerular lesions, fibrin thrombi, and fibrinoid necrosis of blood vessels

    Edema Disease in Pigs

    • Caused by STEC
    • Affected pigs become depressed, develop swelling of eyelids and forehead, peculiar squealing due to laryngeal edema, incoordination, and respiratory distress
    • Some pigs may die before presentation of clinical signs
    • Form of shiga toxemia that results in severe edema in specific sites in pigs where the toxin has been absorbed
    • Causative strains: certain serotypes expressing α-hemolysin, F18ab fimbria

    Gross Lesions in Edema Disease

    • Subcutaneous tissues of eyelids and forehead
    • Greater curvature of the stomach
    • Cerebellum (infarction of brain and brainstem)
    • Mesenteric lymph nodes
    • Colonic mesentery

    Predisposing Factors for Edema Disease

    • Intestinal colonization aided by environmental and host factors
    • Weaning: intestinal epithelial cells undergo changes, receptors for F18 fimbriae (found in STECs) are expressed
    • High protein diets: optimal STEC proliferation environment
    • Fastest growing pigs in a litter are most susceptible

    ExPEC (Extraintestinal Pathogenic Strains)

    • Found in normal intestinal microbiota
    • Possess multiple virulence factors, including:
      • Siderophores
      • Capsule
      • 𝛼-hemolysin
    • Commonly cause infections in:
      • Urinary tract
      • Umbilicus
      • Lungs
      • Blood
      • Wounds
    • Strains are increasingly resistant to antimicrobials
    • Includes E. coli, which is implicated in various infections, such as septicemia, urogenital infections, respiratory infections, and mammary gland infections

    Pathogenesis

    • Insufficient passive immunity leaves animals susceptible
    • Strains enter the body via conjunctival, umbilical, or intestinal tissues
    • Adherence and self-induced uptake via endocytosis allow for infiltration of intestinal epithelial cells
    • After traversing epithelial surface, expression of adhesins is repressed, reducing binding with host phagocytic immune cells
    • Subsequent entry into lymphatics and bloodstream, where they proliferate, leading to endotoxemia
    • Death of host if antibacterial therapy and immune system are unable to remove the organism

    Septicemic E. coli (SEPEC)

    • Causes septicemia in pigs, usually in neonates and less frequently in suckling animals
    • Characterized by acute, generalized infection, sometimes with diarrhea at the terminal stage
    • Signs of shock, often fatal within 3-8 hours, with a mortality rate of up to 100%
    • Also occurs in ruminants, typically in the first few days of life in calves and within the first 2-3 weeks in lambs
    • Histopathological changes include inflammatory changes in liver, spleen, joints, meninges, and hemorrhages on the pericardium, peritoneal surfaces, and adrenal cortices

    Uropathogenic E. coli (UPEC)

    • Frequently implicated in UTIs in dogs, cats, and humans
    • Infections often manifest as:
      • Cystitis
      • Urethritis
      • Pyelonephritis
      • Prostatitis
    • Rarely ascends to the kidneys
    • Isolated from 58-88% of canine pyometra cases (accumulation of pus in the uterus)
    • Bitches are most susceptible during early stages of metestrus when serum progesterone levels are high
    • Cystic endometrial hyperplasia caused by high progesterone is a predisposing factor
    • E. coli recovered from cases are usually hemolytic and have the same characteristics as UPEC
    • Systemic effects are attributed to absorbed E. coli lipopolysaccharide (LPS)
    • Renal damage and dysfunction have been documented

    Pathogenesis of UPEC

    • UPEC from feces colonizes the periurethral area and migrates up the urethra
    • Adheres to bladder epithelial cells, triggering a strong neutrophil response
    • Damage to bladder epithelium leads to systemic effects

    Avian Pathogenic E. coli (APEC)

    • Invasive extraintestinal strains of E. coli that are usually specific serotypes
    • Disease-causing in fowl
    • Colibacillosis has various clinical forms depending on the age of the host and mode of infection
    • Egg infections occur when bacteria penetrate the egg shell and infect the yolk sac, leading to embryo death or death within 3 weeks of hatching
    • Respiratory and septicemic disease can be rapidly fatal or chronic, with clinical signs including debilitation, diarrhea, and respiratory distress
    • Common presentations include air sacculitis and pneumonia

    Mammary Pathogenic E. coli (MPEC)

    • E. coli mastitis can develop in any host species, but most commonly in dairy cattle two weeks post-parturition
    • Environmental mastitis pathogens
    • Host factors impact the nature of developed mastitis, including:
      • Nutritional status
      • Immune status
      • Genetic makeup
      • Parity
      • Lactation stage
    • Pathogenesis involves:
      • E. coli from the environment contaminating the teat orifice
      • Bacteria ascending into the teat canal to the gland lumen
      • Dry period: robust immune response often leads to elimination of the organism with little to no disease
      • Periparturient period: cows are immunosuppressed, with low levels of lactoferrin, delayed PMN leukocyte response, and LPS-induced local inflammatory response and toxemia
      • Mastitis presentation

    Serotyping of E. coli

    • Serotyping is used to differentiate between pathogenic and non-pathogenic E. coli strains and for epidemiological investigations.
    • It is based on the presence of O or H antigens in the lipopolysaccharide layer and flagellar antigens.
    • Cells may also express a Capsular (K antigen), flagella (H antigen), adhesins, and fimbrial antigens.

    Virulence Factors of E. coli

    • There are over 7 virulence factors associated with E. coli, including:

    Adhesins

    • Mediate attachment to host tissues.
    • Can be assembled into organelles such as pili and fimbriae or consist of a single outer membrane protein.
    • Types of adhesins include:
      • F1: most E. coli produce type Fimbriae 1 (F1), plays a role in UTIs by binding to uroplakin and uroepithelium.
      • F4, F5, F6, F11, F17, F18, F41, and F165: associated with E. coli that cause colibacillosis in animals.

    Toxins

    • Some pathogenic strains produce one or more enterotoxins, which are protein exotoxins encoded by genes on transmissible plasmids.

    E. coli Enterotoxins (ETEC)

    • Cause disturbances in intestinal fluid metabolism, but do not cause morphological or pathological lesions in the mucosa.

    Heat-Stable Toxins

    • Low molecular weight, poorly antigenic, and inactivated at 100°C after 15 minutes.
    • Include:
      • STa (ST1): causes release of Cl- and HCO3- into the intestinal lumen, inhibits Na+ reabsorption, and triggers fluid secretion by enterocytes.
      • STb (T2): opens enterocyte calcium channels, triggers fluid secretion, and increases permeability of intestinal epithelium.
      • EAST1: same mechanism of action as STa, but does not induce diarrhea alone.

    Heat-Labile Toxins

    • Produced and secreted in the small intestine only, increase intestinal epithelium permeability, and have immunomodulatory effects.
    • Include:
      • LT1 and LT2: cause permanent activation of adenylyl cyclase, increased secretion of Cl- and HCO3- into the intestinal lumen, and decreased reabsorption of Na+.

    Shiga Toxins

    • Also known as verotoxins, belong to a large family of ribosome-inactivating toxins, and are associated with STEC and EHEC groups.
    • Include:
      • Stx 1 and Stx 2: inhibit protein synthesis, induce host cell apoptosis signaling pathways, and cause vascular damage.

    Hemolysins

    • Pore-forming protein toxins that damage RBCs to obtain iron and impair leukocyte functions.
    • Include:
      • α-hemolysin, Enterohemolysin (EHEC toxin), Cytolysin A.

    Cyclomodulins

    • Family of bacterial toxins and effector proteins that interfere with the eukaryotic cell cycle.
    • Include:
      • CNF: stimulates cellular proliferation.
      • CDT: inhibits cell cycle.
      • Cif: inhibits cell cycle.
      • Colibactin: causes cell death or impaired cell function by interfering with the cell cycle.

    Serotyping of E. coli

    • Serotyping is used to differentiate between pathogenic and non-pathogenic E. coli strains and for epidemiological investigations.
    • It is based on the presence of O or H antigens in the lipopolysaccharide layer and flagellar antigens.
    • Cells may also express a Capsular (K antigen), flagella (H antigen), adhesins, and fimbrial antigens.

    Virulence Factors of E. coli

    • There are over 7 virulence factors associated with E. coli, including:

    Adhesins

    • Mediate attachment to host tissues.
    • Can be assembled into organelles such as pili and fimbriae or consist of a single outer membrane protein.
    • Types of adhesins include:
      • F1: most E. coli produce type Fimbriae 1 (F1), plays a role in UTIs by binding to uroplakin and uroepithelium.
      • F4, F5, F6, F11, F17, F18, F41, and F165: associated with E. coli that cause colibacillosis in animals.

    Toxins

    • Some pathogenic strains produce one or more enterotoxins, which are protein exotoxins encoded by genes on transmissible plasmids.

    E. coli Enterotoxins (ETEC)

    • Cause disturbances in intestinal fluid metabolism, but do not cause morphological or pathological lesions in the mucosa.

    Heat-Stable Toxins

    • Low molecular weight, poorly antigenic, and inactivated at 100°C after 15 minutes.
    • Include:
      • STa (ST1): causes release of Cl- and HCO3- into the intestinal lumen, inhibits Na+ reabsorption, and triggers fluid secretion by enterocytes.
      • STb (T2): opens enterocyte calcium channels, triggers fluid secretion, and increases permeability of intestinal epithelium.
      • EAST1: same mechanism of action as STa, but does not induce diarrhea alone.

    Heat-Labile Toxins

    • Produced and secreted in the small intestine only, increase intestinal epithelium permeability, and have immunomodulatory effects.
    • Include:
      • LT1 and LT2: cause permanent activation of adenylyl cyclase, increased secretion of Cl- and HCO3- into the intestinal lumen, and decreased reabsorption of Na+.

    Shiga Toxins

    • Also known as verotoxins, belong to a large family of ribosome-inactivating toxins, and are associated with STEC and EHEC groups.
    • Include:
      • Stx 1 and Stx 2: inhibit protein synthesis, induce host cell apoptosis signaling pathways, and cause vascular damage.

    Hemolysins

    • Pore-forming protein toxins that damage RBCs to obtain iron and impair leukocyte functions.
    • Include:
      • α-hemolysin, Enterohemolysin (EHEC toxin), Cytolysin A.

    Cyclomodulins

    • Family of bacterial toxins and effector proteins that interfere with the eukaryotic cell cycle.
    • Include:
      • CNF: stimulates cellular proliferation.
      • CDT: inhibits cell cycle.
      • Cif: inhibits cell cycle.
      • Colibactin: causes cell death or impaired cell function by interfering with the cell cycle.

    Predisposing Factors to Infection

    • Insufficient passive immunity from colostrum in neonates can lead to infection
    • Factors that contribute to infection include:
      • Quantity or quality of colostrum
      • Age of neonates (under 1 week)
      • Normal intestinal flora not fully established
      • Naive immune system
      • Presence of receptors for specific adhesins
      • Intensive husbandry practices with rapid spread of E. coli strains
      • Poor hygiene
      • Stress (environmental changes, weaning, rapid diet change, etc.)

    Control & Prevention

    • Enterobacteriaceae family is susceptible to killing via:
      • Sunlight
      • Drying
      • Pasteurization
      • Common disinfectants (chlorine, phenol, and quaternary ammonium-based compounds)
    • Bacteria can survive for weeks to months in:
      • Moist, shaded environments
      • Pastures
      • Manure
      • Litter
      • Bedding
    • Sound husbandry practices are key in prevention and control of E. coli related infections
    • Commercially produced preparations containing monoclonal antibodies to ETEC adhesins can be given to neonatal animals to reduce severity and mortality

    Genus Salmonella

    • Gram-negative bacilli belonging to the family Enterobacteriaceae
    • Motile, non-spore forming, and facultatively anaerobic
    • Three species: S. subterranea, S. bongori, and S. enterica
    • S. enterica is divided into six subspecies, with S. enterica subsp. enterica being the most important
    • S. enterica subsp. enterica includes over 2600 serotypes/serovars
    • Natural habitat is the intestinal tract of warm-blooded and cold-blooded animals
    • Salmonellae can survive for nine months or more in the environment in sites such as:
      • Moist soil
      • Water
      • Fecal particles
      • Animal feed
      • Foods

    Epidemiology of Salmonellosis

    • Some serotypes are relatively host-specific, while others affect a wide host range
    • Clinical outbreaks are correlated with:
      • Depressed immune system
      • Newborn animals
      • Stressed adult animals
      • Parturient cows
      • Equine surgical patients
      • Swine with systemic viral disease
    • Risk increases if intestinal microbiota is disrupted (e.g., from stress or use of antibiotics)

    Pathogenesis of Salmonellosis

    • Transmission occurs through the fecal-oral route, often through ingestion of contaminated food and water
    • Outcome of the interaction between the host and Salmonella depends on:
      • Host factors (state of colonization resistance, immune status, age, concurrent disease)
      • Infectious dose
      • Serotype of Salmonella
    • Adhesion to target cells occurs in the distal small intestine and upper large bowel
    • Salmonellae are internalized, leading to apoptosis of target cells, and inflammatory response
    • Diarrhea is thought to result from prostaglandin synthesis and activation of different signaling pathways

    Salmonellosis: Clinical Signs and Pathologic Changes

    • Clinical signs include:
      • Depression
      • Fever
      • Diarrhea
      • Tenesmus
      • Mortality may reach 100%
    • Pathologic changes include:
      • Fibrinosuppurative, necrotizing, and hemorrhagic inflammation of the distal small intestine and large bowel
      • Multifocal necrotizing hepatitis
      • Fibrinoid changes in blood vessels, vasculitis, thromboembolism, hemorrhages, and infarcts in the septicemic form

    Salmonellosis in Ruminants and Other Animals

    • Affects young and adult animals, causing enteritis, enterocolitis, or septicemia
    • Abortions may follow septicemia
    • S. Dublin, S. Typhimurium, and S. Newport are commonly isolated serotypes from cattle
    • S. Typhimurium is the main serotype affecting sheep
    • In pigs, the disease can present as acute, fulminating septicemia or chronic debilitating intestinal disease
    • In horses, diarrhea, but occasionally septicemia, can occur
    • In dogs and cats, salmonellosis is uncommon and usually associated with a common source

    Salmonellosis in Poultry

    • Salmonellosis in poultry is a major threat to bird health, welfare, and the local economy, caused by non-motile strains S.Gallinarum and S.Pullorum.
    • Other serovars, such as S.Enteritidis and S.Typhimurium, can cause clinical salmonellosis in very young birds, especially in high ambient temperatures and low biosecurity conditions.
    • Serovars like Heidelberg, Seftenberg, Infantis, Motevideo, and Menston are less virulent in chicks but can colonize the intestine and cause human food poisoning.

    Sources of Infections

    • Poultry themselves can be a source of infection.
    • Feed can also be a source of infection.
    • The environment can be a source of infection.
    • Vertical transmission occurs in the case of S.Gallinarum and S.Pullorum.

    Pullorum Disease

    • Pullorum disease is caused by S.Pullorum.
    • It infects the ova of turkeys and chickens, and the embryos are already infected when the eggs are hatched.
    • Environmental contamination occurs as a result.
    • Mortality is highest in the 2nd-3rd weeks of life and is due to septicemia.
    • Surviving birds become carriers and shed the organism in feces only periodically.
    • The organism circulates in the spleen despite high numbers of antibodies, and it is not eliminated for months.
    • When hens become sexually active, the organism multiplies and spreads to other tissues like the reproductive tract and ovaries, where eggs become infected.

    Fowl Typhoid

    • Fowl typhoid is caused by S.Gallinarum.
    • It is either an acute septicemic or chronic disease of domesticated adult birds, mainly chickens.
    • Horizontal transmission occurs through the fecal-oral route.
    • The organism colonizes the gut poorly but multiplies in monocytes and macrophage cell lineage in the spleen and liver.
    • This leads to ensuing bacteremia and localizes in the wall, causing sterile necrosis in the myocardium.

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    Bacteriology exam prep Clostridium, Enterobacteriaceae ,Escherichia, Salmonella

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