University of Babylon



3rd lecture

LOWER URINARY TRACT INFECTION AND CYSTITIS:

Isolated infection

A single episode of lower tract infection occurs frequently in females and is rarely complicated.

Recurrent infection

Recurrent infection may be associated with an underlying predisposing cause or may be a result of bacterial resistance.

Repeated attacks of UTI in women, or a single attack in a man or a child of either sex, should always be followed by investigation to discover and treat the cause; sometimes, however, no cause can be found. Asymptomatic bacteriuria is common and investigation may fail to demonstrate any underlying cause.

Predisposing causes of urinary tract infection

• Incomplete emptying of the bladder, secondary to bladder outflow obstruction, a bladder diverticulum, neurogenic bladder dysfunction or decompensation of the detrusor muscle.

• A calculus, foreign body or neoplasm.

• Incomplete emptying of the upper tract, dilatation of the ureters associated with pregnancy, or vesicoureteric reflux.

• Oestrogen deficiency, which may give rise to lowered local resistance.

• Colonisation of the perineal skin by strains of Escherichia coli expressing molecules that facilitate adherence to mucosa.

• Diabetes.

• Immunosuppression.

Avenues of infection

Ascending infection from the urethra is the most common route. The organisms originate in the bowel, contaminate the vulva and reach the bladder. The passage of urethral instruments may cause infection in either sex, especially when the bladder contains residual urine.

Other routes are less common and include descending infection from the kidney(tuberculosis), haematogenous spread, lymphogenous spread and spread from adjoining structures (fallopian tube, vagina or gut).

Bacteriology

Bacterial virulence factors affect the ability of a pathogen to infect the host. The possession of pili (rod-shaped structures) that project from the outer membrane increases adhesiveness.The type of pilus can be used to classify the pathogen involved.

Escherichia coli is the most common organism followed by Proteus mirabilis, Staphylococcus epidermidis and Streptococcus faecalis. Infection with other organisms or infection with mixed organisms is found in patients with neurogenic bladder dysfunction or those with a longstanding indwelling urethral catheter. These organisms include Pseudomonas, Klebsiella, Staphylococcus aureus and various streptococci.

Sterile pyuria: presence of pus cells without organisms calls for examination for:

1-Tuberculous infection( Mycobacterium tuberculosis).

2-Neisseria gonorrhoeae.

3-abacterial cystitis.

4- CIS.

5- renal papillary necrosis.

6-stones.

7- incomplete treatment of a urinary infection.

Clinical features

These include frequency, pain, haematuria and pyuria. Pyrexia and rigors are not associated with a simple UTI but are a sign of upper tract infection or septicaemia.

Examination

1-On examination/ there is tenderness over the bladder.

2-GUE/ Initial and midstream urine specimens should be collected in a male as acute prostatitis may be present , which will lead to threads in the initial specimen. The midstream specimen must be subjected to microscopy and culture, and the sensitivity of any organisms assessed.

Treatment

Treatment should be commenced immediately and modified if necessary when the bacteriological report is to hand. The patient is urged to drink. Appropriate first-line antibiotics depend on ocal likely sensitivities but would include trimethoprim or one of the quinolones. Failure to respond indicates the need for further investigation to exclude predisposing factors. It is important to

check for associated allergies or other drugs or conditions that might preclude the use of some antibiotics [e.g. concomitant administration of methotrexate and trimethoprim (both inhibit

tetrahydrofolate reductase)].

Investigation

Investigation may be needed in the male or when recurrent infection occurs. This includes measurement of urinary flow rates and post-void residual urine. IVU, ultrasound scan or CT scanning will usually be carried out together with cystoscopy. Difficult cases may require urodynamic investigation.

SPECIAL FORMS OF LOWER URINARY TRACT INFECTION

Acute abacterial cystitis (acute haemorrhagic cystitis)

The patient presents with severe UTI. Pus is present in the urine

but no organism can be cultured. It is commonly sexually acquired but tuberculous infection and CIS must be ruled out.

The underlying causative organism may be Mycoplasma or herpes

simplex virus. Cyclophosphamide can also cause this problem.

Frequency–dysuria syndrome (urethral syndrome)

This consists of symptoms of lower tract infection but with negative urine cultures. CIS, tuberculosis and interstitial cystitis

should be excluded. Most urologists advise patients to adopt general measures such as wearing cotton underwear, using simple

soaps, adopting general perineal hygiene measures and voiding

after intercourse. Other treatments include cystoscopy and urethral dilatation, although the benefits remain doubtful.

Tuberculous urinary infection

Tuberculous urinary infection is secondary to renal tuberculosis.

Early tuberculosis of the bladder commences around the ureteric

orifice or trigone, the earliest evidence being pallor of the mucosa

due to submucous oedema. Subsequently, tubercles may be seen

and, in longstanding cases, there is marked fibrosis and the capacity of the bladder is greatly reduced.

Treatment

Tuberculous infection usually responds rapidly to anti-tuberculous

drugs but occasionally the involved kidney and ureter have to be

removed. If the bladder remains of low capacity, patients will have

severe symptoms and the upper tracts are at risk because of high

filling pressures and vesicoureteric reflux. Such patients, after

appropriate chemotherapy, respond well to bladder augmentation.

The ureters may need reimplantation.Bladder augmentation by ileocystoplasty or caecocystoplasty The fibrosed supratrigonal bladder is removed and the bladder augmented with a segment of bowel. This may consist of intact caecum, a detubularised segment of ileum or a detubularised ileocaecal segment.

Interstitial cystitis (Hunner’s ulcer)

For practical purposes, this is confined to women. The first symptom is increased frequency; pain, relieved by micturition and

aggravated by jarring and overdistension of the bladder, is another characteristic symptom. In most patients pyuria and urinary infection are absent. Haematuria also occurs. The aetiology remains as obscure as it was when Guy Hunner described the ondition in 1914. It consists of a chronic pancystitis, often with marked infiltration with lymphocytes and macrophages. Fibrosis of the vesical musculature and areas of avascular atrophy of the epithelium occur. Ulceration of the mucosa occurs in the fundus of the bladder. In severe cases the bladder capacity is reduced to 30–60 ml. The characteristic linear bleeding ulcer is caused by splitting of the mucosa when the bladder is distended under anaesthesia. Inflammation of all coats of the bladder is present with granulation tissue in the submucosa underlying the ulcer.

Treatment is difficult and unsatisfactory. Hydrostatic dilatation under anaesthesia may give relief for some months. Instillation of dimethylsulphoxide results in improvement Patients with severe symptoms may well require cystectomy and orthotopic bladder substitution.

SCHISTOSOMIASIS OF THE BLADDER

Geographical distribution

The disease is endemic in Egypt, parts of Africa, Israel, Syria, Saudi Arabia, Iran, Iraq and the shores of China’s great lakes. Dwellers of the Nile valley have suffered for centuries. Marshes or

slow-running fresh water provide the habitat for the freshwater snail (Bulinus truncatus) that is the intermediate host.

Mode of infestation

The disease is acquired through exposure of the skin to infected

water, which usually occurs while bathing. The free-swimming, bifid-tailed embryos (cercariae) of the trematode Schistosoma

haematobium penetrate the skin. Shedding their tails, they enter

blood vessels and are swept to all parts of the body but they flourish in the liver where they live on erythrocytes and develop into male and female worms. Sexual maturity having been attained, the nematodes leave the liver and enter the portal vein. The male worm bends into the shape of a gutter (the gynaecophoric canal) into which a female worm nestles, and the

pair makes its way towards the inferior mesenteric vein. Schistosoma haematobium has an affinity for the vesical venous plexus, which it reaches through the portosystemic anastomotic channels. Having reached the bladder the female worm eventually

enters a submucous venule which is so small that she completely blocks it. She now proceeds to lay about 20 ova in a chain; each ovum is provided with a terminal spine that penetrates the vessel wall. A heavily infected subject passes hundreds of ova a day. If the ova reach fresh water, the low osmotic pressure causes rupture and the ciliated miracidium emerges. To survive, it must reach and penetrate the intermediate snail host within 36 hours.

Within the snail’s liver, the miracidium enlarges and gives rise to myriads of daughter cysts, which are set free on the death of the

snail. A single miracidium begets thousands of cercariae to complete the life cycle.

Clinical features

After penetration of the skin, urticaria lasting about 5 days can

occur (swimmer’s itch). Following an incubation period of 4–12

weeks, a high evening temperature, sweating and asthma, together with leucocytosis and eosinophilia, occur. Usually, an asymptomatic period of several months supervenes before the ova are released, causing the typical early sign and symptom of intermittent, painless, terminal haematuria. Men are affected three times more frequently than women.

Examination of the urine

The last few millilitres of an early-morning urine specimen are

collected and centrifuged. Examination on several consecutive

days may be required, but a negative result does not exclude bilharziasis,especially in patients no longer resident in bilharzial districts.Antibody detection by enzyme-linked immunoabsorbent

assay (ELISA) using Schistosoma mansoni adult microsomal antigen (MAMA) can be performed. The test is positive 1 month

after infection and is specific for Schistosoma mansoni and

Schistosoma haematobium.

Cystoscopy

Depending on the length of time for which the disease has

remained untreated, cystoscopy will reveal one or more of the

following:

1Bilharzial pseudotubercles are the earliest specific appearance of

the disease.

2 Bilharzial nodules are caused by the fusion of tubercles.

3 ‘Sandy patches’ are the result of calcified dead ova with degeneration of the overlying epithelium .

4 Ulceration is the result of sloughing of the mucous membrane

containing dead ova.

5 Fibrosis is mainly the result of secondary infection.

6 Granulomas. Bilharzial masses are caused by the aggregation of

nodules.

7 Papillomas are more pedunculated.

8 Carcinoma is a common end result in grossly infected bilharziasis

of the bladder that has been neglected for years.

Treatment

Safe and effective drugs are available for the treatment of

schistosomiasis, including praziquantel taken in three doses of

20 mg kg–1 (total 60 mg kg–1) 4 hours apart. It takes many months for dead ova to be expelled and, even after repeated courses and healing of the bladder lesion, living bilharzial worms have been found at necropsy in the portal system. Other complications, requiring specific treatment, include the following:

• urinary calculi;

• stricture of the ureters;

• prostatoseminal vesiculitis;

• fibrosis of the bladder and bladder neck

• bilharzial urethral strictures;

• squamous bladder cancer.

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