Материал: Oxford American Handbook of Urology ( PDFDrive )

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Investigations

•Urine: At least 3 early morning urines (EMUs) are required, but often many more EMU specimens will be needed before a positive culture for TB is obtained. A typical finding is sterile pyuria (leukocytes, but no growth). Ziehl–Neelsen staining will identify these acidand alcoholfast bacilli (cultured on Lowenstein–Jensen medium).

•CXR and sputum

•Tuberculin skin test

•IVP or CT urogram: Findings include renal calcification (nephrocalcinosis), irregular calyces (“moth-eaten kidney”), infundibular stenosis, cavitation, pelviureteric and vesicoureteric obstruction, and a contracted, calcified bladder.

•Cystoscopy and biopsy

Treatment

Treatment is with 6 months of isoniazid, rifampicin, and pyrazinamide. Regular follow-up imaging with IVP is recommended to monitor for ureteric strictures, which may need stenting, nephrostomies, or ureteric reimplantation.

Severe bladder disease may require surgical augmentation, reconstruction, or urinary diversion.

178 CHAPTER 5 Infections and inflammatory conditions

Parasitic infections

Schistosomiasis (bilharziasis)

Urinary schistosomiasis is caused by the trematode (or fluke) Schistoma haematobium. It is endemic in Africa, Egypt, and the Middle East. Fresh water snails release the infective form of the parasite (cercariae), which can penetrate skin, and migrate to the liver (as schistosomules), where they mature. Adult flukes couple, migrate to vesical veins, and lay eggs (containing miracidia larvae), which leave the body by penetrating the bladder and entering the urine.

The disease has two stages: active (when adult worms are actively laying eggs) and inactive (when the adult has died, and there is a reaction to the remaining eggs). The development of squamous cell carcinoma of the bladder is result of the chronic inflammation.

Presentation

The first clinical sign is “swimmer’s itch”—a local inflammatory response. Other early manifestations include Katayama fever, a generalized allergic reaction, which includes fever, urticaria, lymphadenopathy, hepatosplenomegaly, and eosinophilia. Active inflammation results in hematuria, frequency, and terminal dysuria.

Investigation

•Midday urine specimen; bladder and rectal biopsies may contain eggs (distinguished by having a terminal spine).

•Serology tests (ELISA).

•Cystoscopy identifies eggs in the trigone (“sandy patches”).

•IVP or CT urogram may show a calcified, contracted bladder, and obstructive uropathy.

Treatment

Give praziquantel 40 mg/kg in 2 divided doses 4–6 hours apart. Alternative medications include metrifonate or niridazole.

Complications

Chronic infection can lead to obstructive uropathy, ureteric stenosis, renal failure, and bladder contraction, or ulceration. The most significant and concerning complication is the development of squamous cell carcinoma of the bladder that often presents at an advanced stage.

Hydatid disease

Infection occurs after ingestion of the dog parasite Echinococcus granulosus (tapeworm). Sheep are the intermediate hosts. Cases occur in the Middle East, Australia, and Argentina, with 3% affecting the kidneys. Large cysts form, which can be asymptomatic or present with flank pain. A peripheral eosinophilia is seen with a positive hydatid complement-fixation test. X-rays and CT scans show a thick-walled, fluid-filled spherical cyst with a calcified wall.

Medical treatment is with albendazole. Where surgical excision is indicated, cysts can be first sterilized with formalin or alcohol. Praziquantel is also recommended preoperatively or if cyst contents are spilt (which can provoke systemic anaphylaxis).

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Genital filariasis

Lymphatic filariasis is caused by Wuchereria bancrofti nematode infection and is common in the tropics. Manifestations include funiculoepididymitis, orchitis, hydrocele, scrotal and penile elephantiasis, and lymph scrotum (edema).

Diagnosis is made on capillary finger-prick, or venous blood is used for thick blood microscopic thick film and serology.

Medical treatments include diethylcarbamazine, ivermectin, and albendazole.

180 CHAPTER 5 Infections and inflammatory conditions

HIV in urological surgery

Human immunodeficiency virus (HIV)

HIV disease results from the acquired deficiency of cellular immunity caused by the human immunodeficiency virus (HIV). The signature hallmark of the disease is the reduction of the helper T-lymphocytes in the blood and the lymph nodes, the development of opportunistic infections (Pneumocystis carinii pneumonia, cytomegalovirus (CMV) infections, tuberculosis, candida infections, cryptococcosis, others), and the development of malignancy such as lymphoma and Kaposi sarcoma.

The spectrum HIV infections range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS). HIV-1 is pandemic and accounts for significant mortality in developing countries.

HIV-2 has less pathogenicity and is predominant in West Africa. Transmission is via sexual intercourse, contaminated needles, mother-to- fetus transmission, and infected blood and blood products (blood transfusion risks are now minimal).

Urological manifestations of HIV/AIDS include bacterial and nonbacterial infections, urolithiasis, increased risk of malignancy, renal impairment, and voiding dysfunction.

Pathogenesis

HIV is a retrovirus. It possesses the enzyme reverse transcriptase that enables viral RNA to be transcribed into DNA, which is then incorporated into the host cell genome. HIV binds to CD4 receptors on helper T-lymphocytes (CD4 cells), monocytes, and neural cells. After an extended latent period (8–10 years), CD4 counts decline.

AIDS is defined as HIV positivity and CD4 lymphocyte counts <200 x 106/L. The associated immunosuppression increases the risk of opportunistic infections and tumors.

Diagnosis

Screening HIV-1 antibody titer, if positive, is confirmed by Western blot or immunofluorescence. Separate consent for HIV testing is required. Informed consent is required for the test.

Urological sequelae

•Urinary tract infections: Common bacterial pathogens are most common in HIV: E. coli, Enterobacter (enterococci), Pseudomonas aeruginosa, Proteus spp, Klebsiella, Acinetobacter, Staphylococcus aureus, group D streptococcus, Serratia, and Salmonella spp. If UTI is suspected and C&S are negative, consider atypical organisms such as fungi, parasites, or viruses

•Kidneys: cytomegalovirus, Aspergillus, Toxoplasma gondii infections, which can cause acute tubular necrosis and abscess formation; renal failure; HIV-associated nephropathy (HIVAN): nephrotic disease with proteinuria >3.5 g/day and edema, hypertension. Progresses to dialysis in <10 months; renal stones (secondary to indinavir treatment). Up to 8-fold risk of renal cell carcinoma.

•Ureters: calculi associated with indinavir therapy

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•Bladder: voiding dysfunction and retention (hypoand hyperreflexia, acontractile hypoactive bladder, and detrusor-sphincter dyssynergia); UTI (opportunistic organisms); squamous cell carcinoma

•Urethra: Reiter syndrome (urethritis, conjunctivitis, arthritis); bacterial urethritis

•Prostate: bacterial prostatitis and abscesses (opportunistic organisms)

•External genitalia: chronic or recurrent genital herpes; atypical syphilis; opportunistic infections of testicle and epididymis (Salmonella epididymitis); scrotal and penile Kaposi sarcoma; Fournier gangrene. Testicular tumors are up to 50 times more common, usually seminoma.

Needle stick injury

The risk of seroconversion following needle stick injury from a seropositive patient is ~0.3%. Risks are increased if the patient has terminal ARC illness and if the needle is hollow bore with visible blood contamination, inserted deeply or directly into a vein.

The seroconversion rate after cutaneous exposure to HIV-infected blood is 0.09%. Immediately wash the area well, report to occupational health, and where appropriate, commence antiviral prophylaxis as soon as possible.

Health care workers exposed to infected blood from non-AIDS or acute HIV should be given zidovudine plus lamivudine.

For increased-risk exposure use a three-drug regimen including a protease inhibitor (lopinavir and ritonavir).

Further reading

Cohen MS, Hellmann N, Levy JA, DeCock K, Lange J (2008). The spread, treatment and prevention of HIV-1: evolution of a global pandemic. J Clin Invest 118:1244–1254.

Lebovitch S, Mydlo JH (2008). HIV-AIDS: urologic considerations. Urol Clin North Am 35(1):59–68.