Escherichia coli: Part 2 PDF

Escherichia coli: Part 2 ENTEROBACTERIACEAE Escherichia coli EPEC: Enteropathogenic E. coli Attaching and effacing E. coli lesions (AEEC group) EPEC in humans (carry EAF in plasmid) (a)EPEC piglets, lambs, calves, rabbits and pups Pathogenicity island: locus of enterocyte effacement (LEE) chromosoma...

Escherichia coli: Part 2 ENTEROBACTERIACEAE Escherichia coli EPEC: Enteropathogenic E. coli Attaching and effacing E. coli lesions (AEEC group) EPEC in humans (carry EAF in plasmid) (a)EPEC piglets, lambs, calves, rabbits and pups Pathogenicity island: locus of enterocyte effacement (LEE) chromosomal Etcheverria et al., 2016 ENTEROBACTERIACEAE Escherichia coli EPEC: Enteropathogenic E. coli Pathogenesis 1. 2. 3. 4. 5. 6. EPEC contact gut epithelial cells In some EPEC strains, BFP pili to adhere EPEC expresses T3SS and translocates receptor (Tir) and adhesin (intimin) Cascade of intracellular reactions in host cells to form a pedestal beneath E. coli Effacement of microvilli follows Other effectors affect Ca2+ and Cl- concentrations, tight junctions and recruitment of neutrophils ENTEROBACTERIACEAE Escherichia coli EPEC: Enteropathogenic E. coli Piglets Rarer than ETEC Diarrhea (PWD) Colonization small and large intestines Rabbits RPEC (EPEC with eae) Specific sero/biotypes: suckling and weaned dep. The only important class of pathogenic E. coli One of the principal infectious agents in diarrheic (25–40% losses). High mortality! Lesions all length of small and large intestines (suckling rabbits). In weaning rabbits, mostly in cecum. Calves Not a common infection 1-8 weeks old calves Mucoid diarrhea +/-blood Mainly in large intestine Pups Not clear association as primary etiological agent of diarrhea ONT:H16 serotype* Typical lesions in the small intestine support its association ENTEROBACTERIACEAE Escherichia coli EPEC: therapy Treatment (idem as ETEC) 1. 2. 3. 4. 5. 6. 7. Hydration! Oral electrolytes; in shock (IV: HCO3-, KCl) Antimicrobial therapy - controversial Prevention (reducing predisposing factors) Vaccination Separation of sick animals Antibodies p.o. (anti- lipid A) ENTEROBACTERIACEAE Escherichia coli STEC/VTEC/EHEC: Enterohemorragic E. coli (Shiga-toxigenic E. coli) STEC Shiga-toxigenic E. coli Shiga toxin (cytotoxin): Inhibit protein synthesis in host cells following interaction with the 60S ribosomal subunit resulting in cell death Edema (oedema) disease in pigs is the only animal disease for which the role of Shiga toxin (Stx2e) is clear E. coli O139 and O141 strains are usually hemolytic and produce Stx Some strains produce attaching and effacing AE lesions Subtype Stx2e is associated with oedema disease in pigs Stx1, Stx2, Stx2c and Stx2d are associated with haemorrhagic enteritis in humans. ENTEROBACTERIACEAE Escherichia coli STEC: Shigatoxigenic E. coli The toxin Stx2e is produced in the intestine but is absorbed and carried via the bloodstream to the target cells, usually endothelial cells of the small arteries. STEC E. coli are normally present in the large intestine of pigs, but they appear to multiply rapidly under conditions of stress, particularly a change of diet ENTEROBACTERIACEAE Escherichia coli STEC: Shiga-toxigenic E. coli Disease appears around 5-14 days after weaning (F18 receptor) Edema disease may also appear during the fattening period, as the introduction of pigs into the feedlot is a critical point in its development (STRESS) Exotoxin Stx2e: necrosis (blood vessels!) Endotoxin: acute mortality ENTEROBACTERIACEAE Escherichia coli STEC/VTEC: Enterohemorragic E. coli (Shiga-toxigenic E. coli) Sudden death (*infarction of brain) Edema in head and internal organs Neurological signs (ataxia, convulsions, paralysis) Anorexia Diarrhea is rare Multiple piglets affected ENTEROBACTERIACEAE Escherichia coli STEC: Shiga-toxigenic E. coli ENTEROBACTERIACEAE Escherichia coli STEC: Shiga-toxigenic E. coli Therapy Affected animals: Fasting (elimination of toxin & increase of intestinal peristaltic) Antimicrobial therapy (perform AST!) parentally Not yet affected animals: Antimicrobial therapy and acidifiers orally Incubation time of toxin 2-3 days (so you may see still symptoms after treatment) Prevention Reduce stress Vaccination Selection of F18r- animals Feed composition ENTEROBACTERIACEAE Escherichia coli STEC/VTEC/EHEC: Enterohemorragic E. coli in humans Carried by bovines, humans affected: EHEC/STEC/VTEC => cattle are reservoirs Zoonotic importance Intimin gene (eae) + Shiga toxin gene (stx1 or stx2) O157:H7 best known In 1982, E. coli O157:H7 was initially identified as the cause of bloody diarrhea from eating undercooked or raw hamburger meat that was contaminated with the bacteria ENTEROBACTERIACEAE Escherichia coli STEC/VTEC: Enterohemorragic E. coli (Shiga-toxigenic E. coli) O157:H7 in humans: Shiga toxins blocks ribosomal peptide elongation, disrupting protein synthesis leading to cell death. Intestinal damage permits Shiga toxins and other bacterial factors to gain entrance to the circulation. These may reach multiple host tissues including the kidneys where damage to the microvasculature results in the potentially lethal hemolytic uremic syndrome (HUS). HUS is defined by the triad: acute renal failure, thrombocytopenia, and microangiopathic hemolytic anemia ENTEROBACTERIACEAE Escherichia coli STEC/VTEC: Enterohemorragic E. coli (Shiga-toxigenic E. coli) HUS: rarely described in dogs HUS occurs occasionally in young dogs: Thrombocytopenia Microangiopathic hemolytic anemia Anuric acute renal failure Bloody diarrhea Kidneys of affected dogs show: Renal proximal tubular necrosis and hemorrhage Glomerular lesions Dell´Orco et al., 2005; Vet. Clin. Path. ENTEROBACTERIACEAE Escherichia coli Extraintestinal pathogenic E. coli (ExPEC) Commensals 1. Uropathogenic (UPEC) 2. Septicemic (SEPEC) 3. Necrotoxigenic (NTEC) 4. Avian Pathogenic (APEC) 5. Mammary Pathogenic (MPEC) E. coli Diarrheagenic/ Intestinal (DEC or InPEC) Extraintestinal (ExPEC) ENTEROBACTERIACEAE Escherichia coli UPEC: Uropathogenic E. coli E. coli most important pathogen in UTI in warm-blooded animals Originates mostly from intestine Predisposing factors: Hygiene Water intake Obstipation Age Individual (anatomical) differences Symptoms Anorexia Stranguria, hematuria, dysuria, anuria, and pollakiuria Vaginal exudate General malaise (sometimes) Bacteriology (semi-quantitative from 10e3 - 10e5) UTI classification according the site of infection: cystitis (the bladder) pyelonephritis (the kidney) bacteriuria (the urine) ENTEROBACTERIACEAE Escherichia coli UPEC: Uropathogenic E. coli 1st agent causing UTI (14% of all dogs) Cystitis, urethritis, pyelonephritis and prostatitis UPEC 1. Fimbriae (adhesins) Type 1 (mannose receptor) F12 F13 (human UTI) P fimbrae Urinary infections affect mainly adult animals 2. Afimbrial adhesins 3. Specific serotypes (O2, O4, O6, O83) Not as common as in dogs: Higher osmolarity of urine is antibacterial (but it occurs! Being E.coli the most common infection) Older animals more affected 4. 50% α-hemolytic (hemolysin, HlyA) 5. Other toxins: tissue damage 6. Other VFs: capsule, aerobactin (siderophore) Associated with catheterization or parturition in females. Urolithiasis in males Horses and other small ruminants may present UTIs too. ENTEROBACTERIACEAE Escherichia coli UPEC: Uropathogenic E. coli Pathogenesis 1. 2. 3. 4. 5. Adherence to urethral mucosa Internalization (intracellular shelter) Release of hemolysins (damage red blood cells and other cells) Cellular destruction by E. coli toxins and by the immune response Ascendent through the upper tract (may occur) causing pyelonephritis and possibly septicemia. ENTEROBACTERIACEAE Escherichia coli UPEC: Uropathogenic E. coli Treatment Depends on the animal affected Check for underlaying causes (bladder stone, tumor…) In general: broad-spectrum antibiotics with renal excretion In dogs: administrate at night Ancillary treatment: cranberries contain proanthocyanidins, which can inhibit the adhesion of E.coli to the uroepithelium Sporadic vs recurrent (≥ 3 episodes of UTI in 1 year): recurrent is more common in large animals Subclinical bacteriuria: culture positive in the absence of clinical signs FYI ENTEROBACTERIACEAE Escherichia coli UPEC: Uropathogenic E. coli – In reproductive tract Pyometra is a secondary infection that occurs as a result of hormonal changes in the female's reproductive tract. Pyometra (in bitches) same UPEC E. coli strains as cystitis Treatment frequently surgery + antibiotics E. coli is the bacterium most frequently implicated in pyometra (isolated from 58% to 88% of cases) ENTEROBACTERIACEAE Escherichia coli SEPEC: Septicemic E. coli (“colisepticemia”) Occurs during first few days of life Invasion through intestinal epithelium or the umbilicus May be acquired by fecal contamination after caudectomy Peracute disease: petechial hemorrhages on the epicardium and serosal surfaces and pulmonary edema and hemorrhage and enlargement of the spleen Acute: generalized infection, sometimes with diarrhea (terminal stage), signs of shock and sudden death in 3-8 hours (48h of birth). Mortality up to 100% Chronic cases: fibrinous polyarthritis and meningitis Bacteria are excreted in nasal secretions & urine Navel infection is a common port of entry Navel ill (Omphalitis/Omphaloplebitis) Septicemia by E. coli may result in internal abscesses in the liver or kidneys, abdomen, or other places in the body. Polyarthritis is a common result in a chronic infection. Usually, signs are observed until the third week of life “Watery mouth disease” (E. coli endotoxemia) ENTEROBACTERIACEAE Escherichia coli SEPEC : Septicemic E. coli Virulence factors Capsule: The most important determinant of resistance to phagocytosis and serum resistance P fimbriae and certain O antigens: ability to avoid phagocytosis LPS: symptoms of shock associated with septicemia Type 1 fimbriae: bacterial adhesion to phagocytic cells by lectin– carbohydrate interactions Siderophores: iron-acquisition system. Iron scavenger. NOTE: All other pathogenic E. coli types may progress to systemic infections SEPEC from calves and pigs: Fimbrial adhesins F17, P, S, F1C, F165, CS31A Afimbrial AfaE-VIII adhesin Some hemolytic and often produce colicin V, CNF1, CNF2, and CDT and HPI. ENTEROBACTERIACEAE Escherichia coli NTEC: necrotoxigenic E. coli Originally defined as strains of E. coli producing a toxin called cytotoxic necrotizing factor (CNF) CNF1: all mammals (cattle, dogs, cats, pigs) CNF2: in cattle & sheep (SEPEC, INPEC, UPEC) CNF3: sheep & goats (not clinically associated) Virulence factors (VF): Cytotoxic necrotizing factors (CNF1-3) Cytolethal distending toxin (CDT) Hemolysins Other VF associated: F17, Afa, aerobactin Related to cases of: 1. Diarrhea and septicemia (SEPEC) 2. Urinary tract infection (UPEC) ENTEROBACTERIACEAE Escherichia coli MPEC: mammary pathogenic E. coli Bovines: Coliform mastitis (environmental mastitis) Environmental origin – fecal contamination of udders Clinical signs Classically a peracute disease Range: subclinical infection to a severe systemic disease Fever Anorexia Depression Sunken eyes Severe mastitis: may result in death due to endotoxic shock or culling due to agalactia No specific virulence factors known Sequential milk samples collected from 6 to 36 hours after E coli infection in a quarter of a cow Erskine R., 2022; MERCK MANUAL ENTEROBACTERIACEAE Escherichia coli MPEC: mammary pathogenic E. coli Bovines: Coliform mastitis Pathogenesis ENTEROBACTERIACEAE Escherichia coli MPEC: mammary pathogenic E. coli Bovines: Coliform mastitis Therapy Fluoroquinolones, cephalosporins, oxytetracycline: with scientific evidence of beneficial effects for MPEC In severe mastitis: primary concern is LPS-induced shock. Treatment with fluid, electrolytes and anti-inflammatory drugs NSAIDs PREVENTION! ENTEROBACTERIACEAE Escherichia coli MPEC: mammary pathogenic E. coli (?) PIGS (sows & gilts): Metritis-Mastitis-Agalactiae (MMA) Post Partum Dysgalactiae Syndrome (PPDS) Clinical signs (more common than lesion in udders): Pyrexia Reluctance to allow nursing Anorexia Constipation Thickened white vaginal discharge Increased respiratory rate Reluctance to rise Signs of insufficient caloric intake in piglets Lower weight gain in piglets Etiology of the syndrome is multifactorial No commonly defined phenotype To be continue…