Bacteriology exam prep Clostridium, Enterobacteriaceae ,Escherichia, Salmonella

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.