PARASITIC INFECTIONS IN UROLOGYS

PARASITIC INFECTIONS IN UROLOGYS

1. Parasitic infestations in Urology
Dept of Urology
Govt Royapettah Hospital and Kilpauk Medical College
Chennai
1

2. Moderators:
Professors:
•Prof. Dr. G. Sivasankar, M.S., M.Ch.,
•Prof. Dr. A. Senthilvel, M.S., M.Ch.,
Asst Professors:
•Dr. J. Sivabalan, M.S., M.Ch.,
•Dr. R. Bhargavi, M.S., M.Ch.,
•Dr. S. Raju, M.S., M.Ch.,
•Dr. K. Muthurathinam, M.S., M.Ch.,
•Dr. D. Tamilselvan, M.S., M.Ch.,
•Dr. K. Senthilkumar, M.S., M.Ch.
Dept of Urology, GRH and KMC, Chennai. 2

3. UROLOGICAL PARASITES
•Schistosomahaematobium,
•Filarial roundworms of the genera Wuchereria,
Brugia,and Onchocerca
•Hydatid
•Amebiasis
•Strongyloides
•Trichomonas
•Gnathostomiasis
•Enterobiasis
•Malaria
3Dept of Urology, GRH and KMC, Chennai.

4. Schistosomiasis
•Snail fever disease / Katayama disease
•Schistosome:A parasitic trematodeworm
(helminth) contracted from infested water that is
capable of causing liver, gastrointestinal tract
and bladder disease.
•Schistosomiasisor bilharziaafter the German
physician Theodor Bilharz(1825-1862).
•Nickname “Bill Harris” by British soldiers serving
in Europe during WWI.
4Dept of Urology, GRH and KMC, Chennai.

5. DISCOVERY OF THE SCHISTOSOMIASIS PARASITE
Bilharzin 1852 described trematodeworms recovered
from postmortems in Egypt, demonstrated relationship
to hematuria and eggs with terminal spine in the urine.
He also described terminal and lateral spine eggs in the
same female worm and concluded that only one species
Infected man. This was S. hematobium.
Manson later described schistosomiasisin patients in
the West Indies and this was called S.mansoni.
Parajáda Silva in Brazil in1908 described schistosomes
which produced lateral spine eggs and showed that the
adults were also different from S. hematobium, and thus
showed that S.mansoniwas a different species. 5Dept of Urology, GRH and KMC, Chennai.

6. Etiology :
Schistosomiasisis caused by, Schistosomahematobium.
The male and female worms always go in pair and live in
the blood vessels of the pelvis.
Other species:
S. mansoni
S. mekongi
S. japonicum
S. intercalatum
6Dept of Urology, GRH and KMC, Chennai.

7. Sites of infection
Gastrointestinal tract:inhabiting the portal vein.
•S. mansoni, S. japonicum
S. mekongi, S. intercalatum
Urinary tract: veins of the urinary bladder
•S. haematobium
7Dept of Urology, GRH and KMC, Chennai.

8. Incidence
Species Geographical distribution
IntestinalS. S. mansoni Africa, Middle East,
Caribbean,Brazil,
Venezuela, Suriname
S. japonicum China, Indonesia,
Philippines
S.mekongi Cambodia, Lao
S. intercalatum Rainforestsof central
Africa
UrogenitalS. S. haematobium Africa, Middle East
Mainly anyone in contact/sustained with infested waters.
ie. Farmers, women washing clothes, and
children
8Dept of Urology, GRH and KMC, Chennai.

9. 9Dept of Urology, GRH and KMC, Chennai.

10. *Definitive Host/ Intermediate Host*
•Definitive host: Human
•Intermediate host: Snail
Bulinus(S. haematobium)
Biomphalaria(S. mansoni)
Oncomelania(S.japonicum)
•Reservoirs: monkeys, rodents, cats, dogs, cattle,
horses, swine, wild mammals.
10Dept of Urology, GRH and KMC, Chennai.

11. LIFE CYCLE
80 –120 days
11Dept of Urology, GRH and KMC, Chennai.

12. 1.5 cm in length
reside in vesicaland pelvic venulesand lay eggs
within the venules.
Male and female worms pair and attach to the blood
vessel endothelia
Depositing 200 to 500 eggs per day.
mean life span of 3 to 6 years.
12Dept of Urology, GRH and KMC, Chennai.

13. 13Dept of Urology, GRH and KMC, Chennai.

14. Pathogenesis
•Granulomatous host response to schistosome
eggs -T cell dependent
•Four factors: intensity, duration, activity, and
focality
•Determines morbidity and mortality
•Egg laying occurs chiefly in the pelvic lower
urinary tract, thus leading to its pathologic
manifestations
•S. haematobiumdeposits eggs in groups, rather
than singly, and thus produces composite
granulomas rather than uniovalgranulomas
14Dept of Urology, GRH and KMC, Chennai.

15. Requires
▪Viable adult worm pairs,
▪sustained egg laying,
▪vigorous granulomatous host response
15Dept of Urology, GRH and KMC, Chennai.

16. Chronic phase
•As egg laying then ceases, entrapped eggs are
destroyed or calcified and the inflammation
wanes, being supplanted by fibrous tissue to
produce the sandy patches characteristic of
chronic urinary schistosomiasis
•Inactive urinary schistosomiasis, which occurs
after adult worms have died, is characterized by
the absence of viable eggs in tissues or urine and
the presence of “sandy patches”—relatively flat,
tan mucosal lesions of various depth, often not
sharply defined
16Dept of Urology, GRH and KMC, Chennai.

17. Schistosomalobstructive uropathy
•2 components -obstruction and its effect on the
proximal ureter
•Bilaterally asymmetrical
•ureteral meatus (1%),
•interstitial ureter (10% to 30%),
•juxtavesicalureter (20% to 60%),
•lower third (pelvic) of the ureter (15% to 50%),
•or a contiguous combination of these areas (30%
to 60%)
17Dept of Urology, GRH and KMC, Chennai.

18. Three types of hydroureterare associated with
schistosomalobstruction: Segmental (i.e.,
cylindrical or fusiform), Tonic, and Atonic.
•Segmental ureteral dilatations constitute 25%
of schistosomalobstructive uropathy; nearly
80% of these are in the lower ureter and are
accompanied by concentric ureteral muscular
obliteration by fibrosis and sandy patches.
Segmental lesions are rarely associated with
important hydronephrosis.
18Dept of Urology, GRH and KMC, Chennai.

19. Tonic Hydroureter,
found in 25% to 30% of patients with schistosomal
obstructive uropathy,
Dilated, tortuous, thick-walled, and trabeculatedureter
with marked ureteralmuscle hypertrophy and retarded
peristaltic action.
It involves the entire ureterproximal to an obstructive
lesion, often a functional stenosis,
Often accompanied by significant hydronephrosis, which
usually resolves after relief of obstruction.
19Dept of Urology, GRH and KMC, Chennai.

20. Atonichydroureter, seen in 35% of patients with
schistosomalobstructive uropathy, is a markedly
dilated, very tortuous, thin-walled ureter, without
peristalsis and with atrophic fibrotic ureteral
muscle
20Dept of Urology, GRH and KMC, Chennai.

21. Bladder cancer
•Final pathologic sequelaof schistosomiasis.
•Bladder cancer in the setting of S. haematobiumhas an early onset
(40 to 50 years) and a high frequency of squamous cell carcinomas
(60% to 90%), with 5% to 15% adenocarcinomas.
•More than 40% of schistosomiasisassociated SCC are
welldifferentiatedor verrucouscarcinomas that are exophyticand
carry an overall good prognosis.
•Tumors are found on the posterior wall about 50% of the time and
on the lateral wall roughly 30% of the time.
•Exophytictumors constitute about two thirds of schistosomal
bladder cancers, while one third are ulcerative endophytictumors.
•Mass schistosomiasistreatment campaigns in Egypt are associated
with an overall reduction of all bladder cancers (27.6% to 11.7%)
and a shift to more transitional cell carcinoma from squamous cell
carcinoma
21Dept of Urology, GRH and KMC, Chennai.

22. Clinical Presentation
Acute schistosomiasis/ katayamafever :
•first, and presumably heavy, exposure of a noninfected
individual that leads to fever, lymphadenopathy,
splenomegaly, eosinophilia, urticaria, and other
manifestations of a serum sickness–like disease
•Acute schistosomiasisgenerally occurs 3 to 9 weeks
after infection, coinciding with the onset of egg-laying,
but may be delayed for up to 4 months
•Hematuria is the first sign often appearing 10 to 12
weeks after infection
22Dept of Urology, GRH and KMC, Chennai.

23. Chronic schistosomiasis
EARLY CHRONIC ACTIVE PHASE
•The most typical presentation of active
schistosomiasisis hematuria with terminal
dysuria.
•This hematuria can be sufficient to induce anemia
•Early polypoidlesions of the bladder that result in
urethral or ureteral obstruction or develop heavy
bleeding, enough to produce clot retention.
23Dept of Urology, GRH and KMC, Chennai.

24. •Childhood Exposure –common
•Male -the egg load is higher in genital regions
–SV & ED
•Females 30% of genital infection –
VAGINITIS / CREVICITIS
•May be asymptomatic
24Dept of Urology, GRH and KMC, Chennai.

25. LATE, CHRONIC, ACTIVE STAGE
•Develops when egg burdens in the tissue are at their
highest.
•Clinically constant, deep lower abdominal and pelvic pain
with associated urinary urgency, frequency, and
incontinence are noted with the “schistosomalcontracted
bladder” .
•Anatomically, the trigoneappears normal or minimally
hyperemic and edematous, while the detrusor muscle is
indurated and thickened, along with the entire bladder
wall.
•The bladder lumen is reduced to as little as 50 mL of
functional capacity.
25Dept of Urology, GRH and KMC, Chennai.

26. QUIESCENT PHASE
•Egg deposition and excretion continue at a lower rate and
symptoms are diminished.
•Over 30% of light infections “resolve” spontaneously in
some endemic areas
•The painful presentations of acute schistosomiasisare
typically absent at this point.
•However, silent obstructive uropathymay develop
throughout this phase as fibrosis replaces polypoidlesions
and the bladder and ureters undergo irreversible damage.
•A slow, insidious evolution may result in enormous
hydrouretersand hydronephrosiswith few symptoms
26Dept of Urology, GRH and KMC, Chennai.

27. CHRONIC INACTIVE PHASE
•Viable eggs are no longer detected in urine or
tissues.
•Signs and symptoms at this stage are caused by
sequelaeand complications of the immune
reaction to the eggs rather than the schistosomal
infection itself.
•40% to 60% present to urologists at this stage of
their disease.
•Salmonella organisms -reside in the apical
invaginations of the schistosometegument
27Dept of Urology, GRH and KMC, Chennai.

28. Bladder ulcers
•Two types
•Acute schistosomalulcers will rarely present in the active
stage, when a necrotic polyp sloughs into the urine.
•The more common chronic schistosomalulcer is a late
sequelaof heavy infection.
•This lesion is associated with a constant “burning”
micturition and intense pelvic and suprapubicpain.
•Over 90% of these patients have a history of previous
urinary schistosomiasis, 20% have histories of previous
sequelaeand complications, and 10% have had previous
surgical intervention for urinary schistosomiasis.
•Gross hematuria and gross pyuriaare found in more than
half of these patients.
28Dept of Urology, GRH and KMC, Chennai.

29. DIAGNOSIS
•Urine / fecal –terminal spine eggs
(intercalatum)
•Rectal Bx> bladder Bx
•FAST ELISA + WB
•Real time PCR under evaluation
29Dept of Urology, GRH and KMC, Chennai.

30. Radiology
•Calcification
•The classic presentation of a calcified bladder, which may even
look like a fetal head in the pelvis, is pathognomonic of chronic
urinary schistosomiasis.
•The seminal vesicles, prostate, posterior urethra, distal ureters,
and, in rare instances, the colon may also show calcified lesions.
•The earliest radiographic changes appear to be striations in the
ureters and renal pelvis
•Ureteral calcification is typically mural, and the ureter is dilated.
•This differs from the calcification seen in tuberculosis, which
forms a cast of a nondilatedureter
•Xray–CT > IVU USG
•VCU (25% VUR) 30Dept of Urology, GRH and KMC, Chennai.

31. 31Dept of Urology, GRH and KMC, Chennai.

32. MNG
•Praziquantelis the drug of choice for all schistosoma
species
•active against all clinical forms and stages of the disease
after the first 3 to 4 weeks of infection, because it works
better in the presence of antibodies against schistosomal
organisms.
•Praziquantelinterferes with the ion transport in the
schistosometegument, resulting in calcium and sodium
fluxes, metabolic alterations, and sudden contraction of the
parasite’s musculature.
•Cure rates for S. haematobiuminfections are 73% to 100%
•2 oral doses of 20 mg/kg (or a single 40 mg/kg dose) in 1
day
32Dept of Urology, GRH and KMC, Chennai.

33. Surgery
•Surgery –not responded to adequate medical treatment
within a reasonable follow-up time, or for those settings
where immediate surgical intervention is necessary.
•Obstructive uropathy-MC chronic condition requiring
surgery
•Severe bladder hemorrhage –MC cause for urgent surgical
intervention.
•clinical studies -report cystoscopic, urodynamic , and
postvoidresidual urine, which are evidence of functional
bladder outlet obstruction that occasionally requires
surgical intervention in patients with severe inactive
urinary schistosomiasis
33Dept of Urology, GRH and KMC, Chennai.

34. Bladder
•Chronically contracted bladder -vesical
denervation, urinary diversion, ileocystoplasty,or
hydrodistention.
•Any treatment, however, must be done in
conjunction with medical chemotherapy.
•Chronic deep bladder ulcers may necessitate a
partial cystectomy, because fulguration rarely
produces either symptomatic relief or healing of
the ulcer.
•Schistosomalbladder cancer -cystectomy
34Dept of Urology, GRH and KMC, Chennai.

35. Ureteric schistosomiasis
•Anatomic ureteral stenosis, with or without calculi -80% of obstructions.
•residual ureteral stenosis after successful chemotherapy
•Depending on the extent and location of the stricture, procedures
involving excision or dilatation have been used.
•Balloon dilatation has reportedly proved effective with anatomic stenosis
but mechanical dilatation is frequently followed by repeat stenosis
•When the ureteral meatus, intermural ureter, ureterovesicaljunction, or
lower ureter is involved, a variety of plastic operations to reconstruct a
functional valve are available.
35Dept of Urology, GRH and KMC, Chennai.

36. •Variants of the Leadbetter-Politano.
•In long or multisegmentallesions, excision of the
affected portion leaves an inadequate residual
ureter for reimplantation-Boari-Ockerblad
bladder flap, Boari-Küssflap, ilealconduit,
suprapubicintravesicalureterostomy, and
ureteroileocystostomy, taking care to have an
isoperistalticdirection of the ilealsegment
•When a ureter is hopelessly obstructed, long-
term nephrostomy drainage or creation of an ileal
ureter can provide relief.
36Dept of Urology, GRH and KMC, Chennai.

37. Filariasis
•Wuchereriabancrofti
•Brugimalayi
•India –40% of infected
•W. bancrofti-periaortic, iliac,
inguinal,intrascrotallymph
vessels.
•B. malayi-inguinal and more
distal lymphangioles.
•Lifecycle –human →mosquito
→human
37Dept of Urology, GRH and KMC, Chennai.

38. •Early -(funiculoepididymitis, orchitis, filarial
lymphangitis, filarial abscess), in their
lymphatic distribution (e.g., hydrocele,
lymphadenitis, genital edema), or both.
•Tissue eosinophilia is a useful diagnostic hint
but may be absent.
38Dept of Urology, GRH and KMC, Chennai.

39. •Late
•Lymphangiographicstudies reveal that the
initial obliteration of lymphatic vessels is
bypassed by collateral formation. As these
collaterals become progressively obstructed,
lymph dilatation follows
•chyluriaand filarial hydrocele
•elephantiasis and lymphedematousscrotum
39Dept of Urology, GRH and KMC, Chennai.

40. Presentations
•Asymptomatic Infection
•Filarial Fevers –amicrofilaremic
•Chronic Filariasis-funiculoepididymitis,
hydrocele, orchitis, scrotal and penile
elephantiasis, lymph scrotum, and chyluria
40Dept of Urology, GRH and KMC, Chennai.

41. Funiculoepididymitis
•Fourth decade.
•The attack -isolated, with remission, or may be repetitive and
progressive.
•Pain radiating to the testis and simulating ureteral colic.
•Palpable cordlike swelling may mimic an intrascrotaltumor or torsion
of the cord and be accompanied by hydrocele or soft tissue edema.
•Eosinophilia is common
•Varicocele, or thrombosis of the pampiniformplexus, may complicate
inflammation, increasing pain and swelling.
•Bacterial superinfectionof acute filarial corditis, is a rare but often
lethal complication, with exquisite pain and septic thrombophlebitis as
a contributing cause.
•The disease frequently simulates malignancy, and many patients
ultimately undergo operations including orchiectomy.
•Even in severe filarial funiculitis, the spermatic cord is usually intact
and patent.
•Sterility and orchitisdue to filariasisare rare.
41Dept of Urology, GRH and KMC, Chennai.

42. Hydrocele
•milky or sediment-rich hydrocele fluid
suggests a filarial origin.
•Discovery of a thick, fibrous tunica, especially
with cholesterol or calcium deposits, should
also suggest a diagnosis of filariasis.
•Tunicalcalcification is very rare in idiopathic
hydrocele.
•Penis --
42Dept of Urology, GRH and KMC, Chennai.

43. Chyluria
•Chyluriaoccurs with or without microfilaremia, usually
in young adults.
•Early age of presentation.
•Dying worms provoke lymphatic obstruction with
proximal lymphangiolardilatation.
•Rupture of a lymphatic varixinto the urinary collecting
system has been demonstrated by lymphangiography.
•Chyluriamay initially alarm patients but often is
disregarded and may result in severe protein loss,
leading to hypoalbuminemiaand anasarca.
•Chyluriais usually intermittent and may spontaneously
remit with bed rest.
43Dept of Urology, GRH and KMC, Chennai.

44. Mng
•Ivermectin
•Albendazole
•Doxycycline (wolbachia)
•Surgery
44Dept of Urology, GRH and KMC, Chennai.

45. Onchocerciasis
•Onchocercavolvulus is the agent of river blindness and
of severe, debilitating, chronic dermatitis.
•“hanging groin” or scrotal elephantiasis.
•Histology demonstrates atrophy and fibrosis of the
inguinal lymph nodes with subcutaneous edema and
fibrosis superimposed on the typical onchocercal
dermatitis
•Large inguinal lymphadenopathy
•A single oral dose of ivermectin(150 μg/kg) repeated
every 2 to 6 months until the patient is asymptomatic.
•DEC -allergy
45Dept of Urology, GRH and KMC, Chennai.

46. Enterobiusvermicularis
•intestinal pinworm, ubiquitous worldwide.
•Migrates from the anus to upward into the vagina, reaching
the peritoneal cavity through the uterus and fallopian tubes.
•inflammation of the pelvic peritoneum
•Pain, fever, simulated acute appendicitis, or other lesions.
•Dead worms and eggs incite granulomas and adhesions.
•Careful searching for enterobiasiseggs in vaginal secretions
may properly diagnose a persistent vaginal discharge that was
originally thought to be caused by more typical organisms.
•Treatment of pelvic enterobiasisis with pyrantelpamoate,
mebendazole, or albendazole
46Dept of Urology, GRH and KMC, Chennai.

47. HYDATID DISEASE
•Renal hydatid–2%
•The hydatidis the larval form of Echinococcusgranulosus,
whose definitive host is the dog, and whose principal
intermediate host is the sheep.
•Cysts by accidentally eating eggs excreted in the feces of dogs
or alternative feral hosts.
•Cysts can reach over 20 cm in diameter.
•A host fibrous shell with scant inflammatory reaction envelops
the cyst.
•They often enlarge 1 to 2 cm per year.
•MC -chronic dull flank or lower back discomfort from cystic
pressure.
•The cysts seldom affect renal function
47Dept of Urology, GRH and KMC, Chennai.

48. 48Dept of Urology, GRH and KMC, Chennai.

49. MNG
•Albendazole400 mg twice daily for 1 to 6
months
•Surgical excision of their cysts because of the size
or location of the lesions .
•Praziquanteland albendazolehave been
recommended preoperatively for 7 to 10 days to
minimize or prevent secondary seeding by
daughter cysts if they accidentally contaminate
the operative field
•Metastases / anaphylaxis
49Dept of Urology, GRH and KMC, Chennai.

50. Trichomoniasis
•Flagellate protozoal-sexually transmitted
•Vagina or the Preputialskin or the urethral mucosa
•Cowperor Skeneglands.
•In women, the prevalence is estimated to be 3% to 48%
•Vaginitis is the most frequent manifestation
•Male -asymptomatic
•Men may experience urethritis, epididymitis,
prostatitis, and infertility, probably through infection of
the seminal vesicles.
•Diagnosis -microscope -highly active motile flagellum
•Management –T.Flagyl
50Dept of Urology, GRH and KMC, Chennai.

51. 51Dept of Urology, GRH and KMC, Chennai.

52. Amebiasis
•E. histolyticais a rare cause of renal abscess
•Liver abscesses invariably accompany the abscess.
•The right kidney is more frequently involved.
•Hematuriamay be a prominent manifestation,
especially if the abscess induces renal vein thrombosis.
•Medical therapy (metronidazole or tinidazole) must be
promptly instituted .
•Surgery, if necessary, should be delayed until drug
therapy has been initiated; otherwise, disastrous
spread of amebic infection is likely.
52Dept of Urology, GRH and KMC, Chennai.

53. Malaria
•Plasmodium falciparum
•The urogenital manifestation is through the
phenomenon of black water fever due to
hemoglobinuria
•This is a rare manifestation involving a complement
mediatedimmune reaction found in patients who
have resided 2 to 3 months in endemic areas, and
who have also been treated with inadequate doses
of antimalarial medication.
•The treatment includes appropriate full-course doses
of effective antimalarialstogether with supportive
medical care if the hemoglobinuriahas resulted in
acute renal tubular necrosis.
53Dept of Urology, GRH and KMC, Chennai.

54. Strongyloidiasis
•Strongyloidesstercoralisis the fourth most important
intestinal nematode infection in the world, with
distribution throughout the tropical and temperate
world.
•Auto reinfection -perpetuates infection for decades
after exposure.
•Strongyloideshyperinfectioncan develop with
dissemination of the larvae to extraintestinalorgans
with mortality rates as high as 85%.
•Genitourinary infection is extremely rare and is
usually an indication of disseminated disease.
54Dept of Urology, GRH and KMC, Chennai.

55. •Motile larvae are rarely visible on urinalysis
•The migrating worms carry gram-negative
bacteria on their coat
•Diagnosis -blood serology
•T. Ivermectin-200 μg/kg daily for 2 days
•Thiabendazoleshould no longer be used due to
its prominent gastrointestinal and
neuropsychologicside effects.
•Albendazolehas some activity but a lower cure
rate than ivermectin
55Dept of Urology, GRH and KMC, Chennai.

56. Gnathostomiasis
•Food-borne zoonotic nematode.
•Gnathostomaspinigerumis the most common species
to infect humans.
•Diseaseis acquired by consumption of infected fish
when eaten raw or undercooked.
•Accidental host
•It wanders through tissues resulting in local symptoms,
depending on location, and typically a very
predominant eosinophilia (often greater than 50%).
•Very rare genitourinary cases have been reported
•The definitive treatment is surgical excision when
possible.
•Albendazole
56Dept of Urology, GRH and KMC, Chennai.

57. 57Dept of Urology, GRH and KMC, Chennai.