Pathogenesis of acute pyelonephritis

Pathogenesis of acute pyelonephritis

Pathogenesis of acute pyelonephritis

1 ascending infection

About 95% of the urinary tract infection is caused by the passage of the urethra through the bladder and ureter to the kidneys. Under normal circumstances, there are a small number of bacteria at the upper end of the urethra 1 ~ 2cm, only when the body's resistance to reduce or damage to the urethra mucosa, bacteria can invade, multiply. The flushing of urine, urinary IgA, lysozyme, organic acids, the integrity of the mucosa, and the anti adhesion factor (Muein) secreted by the bladder transitional epithelium can resist the invasion of pathogens. Electron microscopy confirmed that in recent years, the Escherichia coli surface has many P fimbriae, they can specifically recognize and bind to the corresponding receptor surface urothelial cells, which was closely attached to the urothelial cells, avoid urine wash away. Escherichia coli (K) antigen (O) antigen, H antigen and K antigen can inhibit the bactericidal activity of phagocytic cells, which is directly related to its pathogenicity. Proteus has no P pili and K antigen, which is not easy to adhere to the transitional epithelium of the bladder, but can adhere to the epithelial cells of the external genitalia. Indwelling catheter, urinary calculi, trauma, tumor, benign prostatic hypertrophy, congenital urinary tract malformation (including bladder sphincter, ureteral hypoplasia caused by vesicoureteral reflux), neuronal bladder are risk factors for ascending infection.

2 hematogenous infection

Hematogenous infection accounted for only 3% of urinary tract infection. The renal blood flow accounted for 20% to 25% of the cardiac output, and the bacteria in the circulating blood reached the renal cortex. Diabetes mellitus, polycystic kidney disease, kidney transplantation, urinary tract obstruction, renal vascular stenosis, the use of analgesics or sulfa drugs increased the vulnerability of renal tissue. The common pathogens are Staphylococcus aureus, Salmonella, Pseudomonas and Candida albicans.

3 the chance of direct infection is rare, and the infection has not been confirmed.

(1) urinary tract obstruction: urinary tract obstruction caused by various reasons, such as kidney and ureteral stones, urethral stricture, urinary tract tumor, prostatic hypertrophy, etc. can cause urinary retention, so that bacteria easy to reproduce and produce infection. Uterine compression of the uterus, kidney prolapse or hydronephrosis can make the urine excretion of the disease.

(2) abnormalities of the urinary system or function: such as renal hypoplasia, polycystic kidney, sponge kidney, horseshoe kidney, double renal pelvis or ureter and ureter, and so on. Reflux of the urinary bladder from the bladder to the renal pelvis, thereby increasing the chance of illness. Dysfunction of the urinary bladder, leading to urinary retention and bacterial infection.

(3) urethral catheterization and instrument examination: urethral catheterization, cystoscopy, urinary tract surgery can cause local mucosal damage, the anterior urethra pathogenic bacteria into the bladder or upper urinary tract infection. According to statistics, the incidence of persistent bacteriuria after catheterization was 1% ~ 2%, and more than 4 days after indwelling catheterization, the incidence of persistent bacteriuria was more than 90%, and the risk of severe pyelonephritis and gram negative bacterial septicemia.

(4) anatomical and physiological characteristics of female urinary tract: female urethral length is only 3 ~ 5cm, straight and wide, urethral sphincter weakness, bladder urethra bacteria easily along the rise to the urethra and anus, and to provide the conditions for bacterial invasion of urethra. Local irritation around the urethra, menstruation vulva is susceptible to bacterial contamination, vaginitis, cervicitis and other gynecological diseases, sex hormones, and postpartum sexual life during pregnancy, can cause vaginal and urethral mucosa changes to pathogen invasion. Therefore, the incidence of urinary tract infection in adult women is 8 to 10 times higher than that of men.

(5) the body resistance weakened: systemic diseases such as diabetes, hypertension, chronic kidney disease, chronic diarrhea, long-term use of corticosteroids, decreased body resistance, urinary tract infection rate was significantly higher.

4 virulence factors of bacteria

Urinary tract infections are mostly caused by a single strain, E. coli, which accounts for the majority of urinary tract infections, can cause asymptomatic bacteriuria to cystitis and pyelonephritis. Invade the urinary Escherichia coli is not only the most common fecal strains, but they have some special strains. These strains have various virulence characteristics, they settled in the intestinal tract, urinary tract upward intruded into the normal anatomy. When there is foreign body in the urinary tract, VUR or obstruction, it is more likely to be infected.

The Escherichia coli antigen O antigen (hapten or cell surface antigen), H antigen and K antigen (flagellin) (membrane antigen), although the relationship between Escherichia coli serotype specific and symptomatic urinary tract infection has not been fully elucidated, but studies have found that Escherichia coli serotype, and its pathogenicity in addition. Distinguish serotype O is helpful in the differential diagnosis of infection or re infection recurrence. It has about 170 different types of O antigen in 8 (O1, O2, O4, O5, O7, O16, O18 and O75) Escherichia coli strains caused by the strain of pyelonephritis in 80%, more than 70% of the pathogenic bacteria isolated from pyelonephritis with K antigen (K1, K2, K5, K12 and K13 or K51). In contrast, H antigens do not appear to be associated with virulence alone. May not be the Escherichia coli O antigen caused by these Escherichia coli strains of uropathogenic, specifically, O antigen gene and determine structure closely linked genes with these bacterial strains pathogenic related closely

In conclusion, the pathogenesis of urinary tract infection is a rather complex process, which can be summarized in the following steps;

(1) bacterial colonies with P pili are spread around the intestine and urethra and spread to the urethra.

(2) through the turbulent flow in the urine of the ureter, the bacteria will go up to the kidney, if the inflammation is not controlled in time, it can cause kidney damage.

(3) by reverse flow of urine, the bacteria in the urinary tract and the urinary tract of the epithelial cells of the corresponding receptor, local reproduction of renal inflammation. When the pathogen enters the body, it can produce antibodies against the bacteria, which is beneficial to the removal of bacteria, but also can lead to kidney damage.

In acute pyelonephritis, renal tubular damage can release tubular antigen into the blood circulation, induce antibody mediated tubulointerstitial disease. However, a number of studies have not demonstrated the presence of anti renal antibodies in sera of patients with bacterial pyelonephritis or in animals with locally synthesized IgG and IgM in experimental pyelonephritis. But in animal or human pyelonephritis, by immunofluorescence microscopy or granular deposits of IgG and complement (suggesting that the immune complex type tubular disease), and no linear deposition (suggesting that anti tubular basement membrane disease). However, Losse was found to have antibodies against E.coli antigens in experimental rabbit pyelonephritis, which could also react with antigens from liver and kidney tissues.

5 pathological changes

The pathogenic bacteria reached the renal pelvis from the lower urinary tract through the ascending infection pathway, and there were special bacterial clones in the kidney, urinary system, renal tubule and renal parenchyma. Congestion and edema of the kidney results in an enlarged kidney, but the lesion is not homogeneous. The infiltration of white blood cells in the renal papilla rapidly spread to the renal cortex. As the disease progresses, many small abscesses are formed in the kidney. The glomerulus is generally not affected, unless a severe necrosis or whole kidney infection occurs.

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