Urinary tract infection (UTI):

Urinary tract infection (UTI) can be divided into the following:

1- Upper UTI: Pyelonephritis and Ureteritis.

2- Lower UTI: Cystitis, Urethritis, and Prostatitis in men.

Urinary tract infection is more common in females due to the following factors:

1-The short urethra, and proximity of the urethral opening to the anus.

2-Lack of antibacterial prostatic secretions.

3-Facilitation of bacterial migration by sexual intercourse.

Other risk factors for UTI:

1- Poor personal hygiene.

2-The insertion of contaminated catheters.

Physical and chemical barriers that protect human urinary tracts:

Human urinary tracts are protected from infectious microbes by :1-The frequent flushing action of urination.

2- The acidity of urine ( pH from 4.5 to 8 ).

3- The prostatic secretions (lysozyme and IgA).

Factors that play a role in establishment of UTI:

1-The microbial virulence.

2-The pathogenic dose.

3-The antibiotic resistance ability (Hospital-dwelling bacteria).

4-The immune system (weakness of Humoral immunity in urinary

tracts).

Pyelonephritis:

Pyelonephritis: (Pyelum: Renal pelvis, Nephro: kidney) : is an urinary tract infection that has reached the pelvis of the kidney. Severe cases of pyelonephritis leads to pyonephrosis (accumulation of Pus in kidney pelvis).

Etiology of Pyelonephritis: 1- Escherichia coli. 2- Staphylococcus saprophyticus.

3- Other genera of Enterobacteriaceae : Klebsiella, Enterobacter, Proteus, and Serratia.

4- Pseudomonas aeruginosa ( Hospital-acquired infection).5- Enterococcus faecalis ( Hospital-acquired infection).

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Escherichia coli: E.coli:- The most common cause of UTI ( 70-95%).- Complicated UTI (Pyelonephritis) mainly caused by nonuropathogenic strains of E.coli.- Source of bacteria: Fecal contamination.

Staphylococcus saprophyticus: - It considered as a second causative agent of UTI (5-20%). - Frequent cause of urinary bladder infection in female due to its occurrence as part of normal vaginal flora.

Others microbes : Enterobacteriaceae: -Species of Enterobacteriaceae form the other percentage of infection.

Microbial Pathogenesis :

Pyelonephritis is established according to the following arranged Consequences: 1-The bacterial lower urinary tract infection.2-PMNs influx from lower urinary bladder to ureter and kidney. 3-Reflux of infected urine up the ureters into the renal pelvis due to: A-Congenital abnormality ( short intravesical ureter). B- Obstruction of ureters ( ureter stone or carcinoma).- If PMN cell proliferation occurs in Renal Pelvis; Pyelonephritis will be established.

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3- Bacterial entry through the papillae into the renal parenchyma. 4- adhesion of microbes to interstitial tissue surrounding the tubules in kidney medulla. 5- Activation of PMN cells, infiltration of interstitial tissue by B, and T -lymphocytes, and eosinophils, proliferation of cells, inflammation .6- Tubulointerstitial nephritis.

Microbial pathogenesis:n

Tubulointerstitial nephritis ( TIN):Types:1-Acute TIN: - involves an inflammatory infiltrate and edema affecting the renal interstitium that often develops over days to months. - Over 95% of cases result from infection or an allergic drug reaction.

- interstitium abscesses : necrosis contains neutrophils, fibrin, cell debris and central germ colonies (hematoxylinophils). -Tubules are damaged by exudate and may contain neutrophil casts. - In the early stages, the glomerulus and vessels are normal.

Acute Tubulointerstitial nephritis:a

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2- Chronic TIN: - Gradual interstitial infiltration and fibrosis, tubular atrophy and dysfunction, and a gradual deterioration of renal function, usually over years. - Glomerular involvement is much more common in CTIN than in ATIN. - Causes: immunologically mediated disorders, infections, obstructive nephropathy, and drug interaction.

-A perinephric abscess (infection around the kidney) and/or pyonephrosis may be developed in chronic pyelonephritis (chronic TIN).

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Chronic TIN:

Normal, and Destroyed Glomeruli with cellular infiltration.

Fibrosis, cellular infiltration, tubules could be absent or atrophied.

Signs and Symptoms of Pyelonephritis:

The symptoms of acute bacterial pyelonephritis are summarized as :1- High fever ( Pyrogenic infection) , flank pain, and pain in the joints and muscles including flank pain.

2- Burning sensation during urination (dysuria: Difficult and painful urination) , and increased frequency of urination (polyuria).

3- Pyuria (pus in urine; pyogenic infection).

4- As the kidney becomes more inflamed, pain, loss of appetite, and headache could be present.

Diagnosis of Urinary tract infection:

Urine analysis:1- Physical properties: -Appearance: turbidity or milky: suggested pus in urine or others. -Color: white color: Pus in urine: Pyuria :infection?

Red color: RBCs in urine: (Hematuria): kidney stones, infections , or tumors?

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2-Chemical properties: -Glucose in urine: (Glycosuria) : In Diabetes mellitus patients. : considered as a risk factor for bacterial infection; because bacteria utilize glucose during binary fission. -Nitrite in urine: (Nitrituria): : indicates the presence of Coliform bacteria in urine. : Note: Enterobacteriaceae species reduce Nitrate to Nitrite.

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Protein in urine: Proteinuria: Albuminuria: - In Pyelonephritis, and lower UTI: Proteinuria (trace from pus or bacterial origin) and Pyuria. - In interstitial nephritis and Glomerulonephritis: Proteinuria , Hematuria, lower number of Pus in urine.

3-Microscopic properties: -WBCs: Normal : 2-3 /HPF. -RBCs: Normal : 3-4 cells/HPF. - Casts: A- Granular and fatty cast: in tubulointerstitial nephritis, glomerular disease.

B- Hemoglobin and RBCs cast: Acute Glomerulonephritis due to immune system response. C- WBCs cast: acute pyelonephritis, acute tubulointerstitial nephritis due to infection.

Microscopic appearance of Pus, RBCs, and Casts in urine: a

Glomerulonephritis: GN:GN: is the inflammation of the Glomeruli of the nephron. Causes:1- Insoluble antigen: trapped in the glomerulus; antibodies attack the structural components of the kidney and antigen.

2- Soluble antigen: in blood stream: antibodies react with soluble antigen: Immune- complexes formation: precipitation in glomeruli. Both antigen-antibodies reactions cause GN or TIN.

Types of soluble antigen:

1- Exogenous: A-Drugs, toxoid, or serum. B-Infectious agent antigen: - Post-Streptococcal glomerulonephritis: Anti-Streptolysin-O- Ag complexes. -Other infections: Bacterial: Staphylococci, Streptococcus pneumoniae, Klebsella, Yersinia enterocolitica, Treponema, Salmonella. Parasites: Malaria, Schistosoma, and Toxoplasma. Viral : Hepatitis, and E.B.V. Fungal: Candidiasis. 2- Endogenous: Self antigen.

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Proliferative Post-Infectious Glomerulonephritis.

Diagnosis of GN of immune-complexes origin.