ُيعؤشفهخى

1. Diseases of the bladder,
ureters and urethra
Dr.Karima Al Salihi

2. (1) Cystitis
•It is the inflammation of the bladder,
usually caused by bacterial infection and is
characterized clinically by frequent painful
urination as well as presence of blood,
inflammatory cells and bacteria in the urine.

3. Etiology
(1) Sporadic cases due to the introduction of infection into the
bladder when trauma to the bladder has occurred or when
there is stagnation of the urine.
(2) Secondary to bacterial infection (E. coli, Streptococci and
Diphtheroid bacilli are common) associations with:
1) Cystic calculus
2) Difficult parturition
3) Contaminated catheterization
4) Late pregnancy as a sequel to paralysis of the bladder.
5) A special case of bladder paralysis occurs in horses
grazing Sudax or Sudan grass.
6) Pyelonephritis, endometritis, vaginitis occur in cattle
and horses. Enlargement of the kidney is the characteristic
sign.
7) Certain drugs for long period as turpentine oil.

4. Pathogenesis
(1) Bacteria frequently gain entrance to the
bladder but are usually removed by the
flushing action of voided urine before
they invade the mucosa.
(2) Mucosal injury facilitates invasion but
stagnation of urine is the most important
predisposing cause.
(3) Bacteria usually enter the bladder by
ascending from urethra or descending
infection from kidney.

5. Clinical findings
(1) Frequent urination with small urine volume. It is accompanied
by pain and sometimes grunting; the animal remains in the
urination posture (for some minutes after the flow has ceased)
and arched back (as if it wants to urinate with presence of pain).
(2) In very acute cases, moderate abdominal pain (baddling of
the hind feet, kicking at the belly and raising the tail) and a
moderate fever may occur.
(3) Acute retention may develop if the urethra blocked with pus
or blood.
(4) In acute cases no palpable abnormality but pain may be
evidenced.
(5) Chronic cases show less marked signs, the bladder wall
may feel thickened on rectal examination and, in horses, a
calculus may be present.
(6) The presence of calculi in the bladder is detected by rectal
ultrasonographic or radiographic examination in small animals.

6. Clinical pathology
l) Blood and pus in the urine is typical of
acute cases and die urine may have a strong
ammonia odor.
(2) In less severe cases the urine may only
turbid and in; chronic cases there may be no
abnormality on gross inspection.
(3) Microscopic examination of urine
sediment reveal erythrocytes, leukocytes
and desquamated epithelial cells.
(4) Bacterial culture is necessary for diagnosis
and treatment.

7. Necropsy findings
(1) Acute cystitis is manifested by hyperemia,
hemorrhage and edema of the mucosa.
(2) The urine is cloudy and contain mucous.
(3) In subacute and chronic cases the wall is grossly
thickened and the mucosal surface is rough and granular.
(4) Highly vascular papillary projection may have
eroded causing the urine to be blood stained or contain
large clots of blood especially at the end of urination.

8. Differential diagnosis
(1) Pyelonephritis: Lesions in the kidney.
{2} Thickening of the bladder wall occurs in
cystitis, enzootic hematuria and in poisoning
by the yellow-wood tree (Terminalia oblongate)
in cattle and by sorghum in horses.
(3) Urethral obstruction causes frequent
attempts at urination but the urine flow is
greatly restricted, usually only drops are
voided and the distended bladder can be feel
on rectal examination.

9. Treatment
(1) Antimicrobials for 7 -1 4 days to avoid relapse.
(2) Free access to water at all times to increase flow of
urine.
(3) Hexamine or sulfonamide to alter urine pH.
(4) Irrigate urinary bladder with mild antiseptic (Lotagin or
Lugal).
(5) Surgical for calculi.
NB: Diuretic is contraindicated in cases of urine
retention to avoid rupture of urinary bladder.
NB: The prognosis in chronic cases is poor because of
difficulty of completely eradicating the infection and the
common secondary involvement of the kidney.

10. (2) Paralysis of the bladder
Paralysis of the bladder is uncommon in
large animals,
Causes:
(1) Spinal cord degeneration following
consumption of sorghum can lead to bladder
paralysis and posterior ataxia.
(2) Idiopathic bladder paralysis and overflow
incontinence may occur sporadically in the
absence of other neurological or systemic
signs.

12. Symptoms
(1) Bladder is markedly distended with urine.
(2) Constant or intermittent drippling of urine.
(3) The bladder is enlarged on per rectum examination and
urine can be easily expressed by manual compression.
(4) Chronic distension of the bladder leads to
accumulation of calcium carbonate crystals.
(5) Urine stasis produces cystitis.
Treatment:
the supportive aimed at relieving bladder distension by
regular catheterization and lavage as well as antibiotics to
avoid cystitis.
Prognosis
Depends on the primary disease. Paralysis in the absence of spinal cord
disease has a poor prognosis.

13. (3) Rupture of the bladder
(Uroperitoneum
Etiology
(1) Obstruction of the urethra by calculi.
(2) Rare cases occur due to difficult or
normal parturition, due to
compression of a full bladder during
birthing.
(3) Congenital rupture.

15. Pathogenesis
(1) After the bladder ruptures, uroperitoneum results
in a series of abnormalities that arise from failure of
the excretory process combined with solute and
fluid redistribution between the peritoneal fluid and
extracellular fluid.
(2) Urine is usually hypertonic especially in
animals whose water intake is decreased by uremia.
(3) Osmotic pressure from hypertonic urine
promotes movement of extracellular water into
the peritoneal cavity.
If this movement combined with reduced water
intake, it results in clinical dehydration.

16. (4) Urine usually has a lower concentration of
sodium and chloride and higher concentrations of
urea, creatinine, potassium and phosphates than
plasma.
Diffusion along this concentration gradient
across the peritoneal membrane results in a
general pattern of azotemia with hyponatremia,
hypochloremia, hyperkalemia and
hyperphosphatemia.
(5) Bladder rupture leads to gradual
development of ascites from uroperitoneum,
ruminal stasis, constipation and depression.
(6) In cattle, uremia may take 1-2 weeks to develop

17. Clinical signs
(1) Sudden disappears of
previously severe colic.
(2) Depression, anorexia, colic,
abdominal distension
(3) Uremia develop within 1-2 days
following rupture.
(4) Thrilling per rectum and
abdominal wall.

18. Clinical pathology
(1) Increase urea and creatinine
concentrations in plasma.
(2) The ratio of urea in peritoneal fluid to
that in serum is a good guide in the early
stages, but after 40 hours the ratio of the
peritoneal to serum creatinine greater
than 2:1 is diagnostic of uroperitoneum.
Treatment:
Surgical with a goal of bladder repair or
slaughter

19. (4)Urinary bladder neoplasms
It is common only in cattle where bracken
poisoning, very rare in horses.
!Angioma,
!transitional epithelial carcinoma,
!vascular endothelioma more common than
papillomas,
!adenomas,
!hemangiomas
!and transitional cell tumors.
Clinical signs included hematuria, weight loss,
stranguria and the secondary development of
cystitis.

21. (5)Urolithiasis in ruminants
Urolithiasis is common as a subclinical disorder
among ruminants, 50% of animal fed primarily
of grain or where animals graze certain types of
pasture, especially the castrated male. It is
characterized by complete retention of urine,
frequent unsuccessful attempts to urinate and
distension of the bladder. Mortality rate is high.
Etiology
organic and organic urinary solutes are precipitated around a nidus as
crystals or as amorphous deposit in a prolonged period. There are three
main factors contribute to urolithiasis:

23. (1) Nidus formation
1) A nidus may be a group of
desquamated epithelial cells or
necrotic tissues from local infection in
urinary tract. The nidus favors the
deposition of crystals about itself.
2) Deficiency of vitamin A or the
administration of estrogen and or
using of stilbosterol (a growth
promoting) favor the nidus formation.

24. (2) Precipitation of urinary solutes on the nidus: It
occurs for several reasons, including:
(1) Increased phosphate or carbonate calculi formation
in the alkaline urine of herbivores
(2) Increased concentration of urine solutes as a result
of water deprivation in cold weather.
(3) Heavy fluid loss, which may occur in hot weather.
(4) Excessive mineral intake (which often occurs in
feedlots), particularly with respect to a high phosphate
intake.
(5) Diet high in magnesium (some calf milk replaces) and
phosphate (Heavy concentrated diets) which prevented by
supplementation by calcium.
(6) Ingestion of plant with high oxalic acid content
causing calcium carbonate calculi in sheep.

25. In the urine act as cementing agents to
solidify the solutes that have precipitated
around the nidus.
Heavy-concentrate and low-roughage feeding
and the pelleting o f rations (common in
most feedlot feeding) increase mucoproteins
in the urine and consequently calculi
formation.
NB: Cattle usually have single, hard,
discrete calculi, but there can be up to200
calculi present in an individual animal's urinary
tract.

26. Types of calculi
(1)Magnesium ammonium phosphate calculi: They are
common in feedlot cattle and sheep fed high-concentrate
low-roughage rations. These calculi are highly insoluble
in alkaline urine (pH of 8.5-9.5); thus, precipitate readily
in the normally alkaline urine of herbivores. These calculi
are usually small, smooth, and soft, with a high
recurrence because there are many salts.
(2) Silicate calculi occur in animals grazing on mature
grasses or wheat or oat (which contains up to 2% silica).
Water in these areas also high in silicates. Silicate calculi
are rough and hard, usually forming only a single calculus.
A high level of silica in both diet and water, causing
outbreaks of calculi at any time of the year in any age.

27. Composition of calculi(1)
Animal grazing in pasture grasses have a
high content of silica form siliceous
calculi.
(2) Calcium, ammonium and magnesium carbonate re common
constituents of calculi in cattle and sheep grazing clover-rich pasture.
(3) Magnesium ammonium phosphate calculi in lambs fed high
concentrations of magnesium in feedlot rations.
(4) Oxalate calculi are rare in ruminants.
(5) Estrogenic subterranean clover causes soft, moist, yellow
calculi. Feedlot lambs receiving a supplement of stilboestrol (1 mg/kg
of feed or 2 mg per lamb daily) developed urolithins calculi causing
urethral obstruction due to plugs formation of mucoprotein and
enlargement of accessory sex glands.

28. Miscellaneous factors favor the
development of urolithiasis:
(1) Stasis of urine.
(2) Certain feed such as cottonseed meal and milosorghum.
(3) In feedlots a combination of high mineral feeding and high
level of mucoprotein in the urine.
(4) In large animals a high intake of mineralized water, or oxalate
or silica in plants
Risk factors for obstructive urolithiasis:
(1) Size of calculi.
(2) Diameter of the urethra. Wethers (castrated lambs) and
steers (castrated cattle) are more affected due to the relatively
small diameter of the urethra.
(3) Bulls pass calculi which are twice in size of those which could
be passed by an early castrated steer.

29. Occurrence
It is mainly seen in castrated males and is particularly common in
feedlot and range-fed steers or withers. Although bulls cows, heifers,
ewes, and rams, also form urinary calculi, however:
(1) The female urethra is shorter and more able to pass urethral calculi
than the male urethra.
(2) In bulls, the urethra is up to 40% larger in diameter than in a similarly
aged steer; so bulls are less likely to become obstructed by urolith.
(3) It may occur at any site. It is more common at the sigmoid flexure in
steers, and in the vermiform appendage (urethral process) or at the
sigmoid flexure in wither or ram.
(4) It is highest during the early part of the feeding period (fed roughage
and grain) and during cold weather when the consumption of water may
be decreased. It may occur as outbreaks in large number of animals.
(5) It is common in old age and less common in lambs young as 1 month.
Outbreaks may occur affecting a large number of animals in short-time
especially in feeder steer and withers (castrated lamb) being fed heavy
concentrate ration and animal in pasture containing large quantities of
oxalate, estrogen or silica.

30. Clinical findings
Vary with the site and completeness of
urinary tract obstruction.
(1) Partial incomplete obstruction
Urine dribbling from the prepuce (dribblers)
with blood tinged urine surrounding the
prepuce may be evident with white, powdery
crystals precipitating around the preputial
orifice. These animals have prolonged
painful urination and may tramp or tread
when attempting to pass urine.

31. (2) Complete urethral obstruction
Bladder rupture occurs after 18-72 hours if the obstruction is not
relieved.
(1) Inappetence, depression, and colic signs (with kicking at the
abdomen).
2) Treading: Steers shift their weight to opposing hind limbs (i.e.,
treading) and appear restless, getting up and down frequently.
3) Tenesmus may also be present, with palpable pulsations of
the urethra and straining sufficient to prolapse the rectum.
(4) The preputial orifice hairs are dry.
(5) Sheep may also exhibit tail wriggling.
(3) Other signs
Can include grunting and grinding of the teeth.
(4) Rectal palpation
May reveal a large and tightly distended urinary bladder.

32. Sequelae of urolithiasis
(1) Urethral rupture
The calculus lodges in the penile urethra, and
causes pressure necrosis of the urethral wall.
Urine leaks into the subcutaneous tissue around
the penis and accumulates in the subcutaneous
connective tissue along the prepuce, resulting in
extensive edema along the abdominal floor
(extending from the sigmoid flexure to the
umbilicus). Usually, the leakage of fluid relieves
the acute pain of urinary bladder distention,
toxemia and tissue necrosis with sloughing of the
skin of the ventral abdomen.

33. (4) Bladder rupture
Sudden disappearance of abdominal
pain, bilateral fluid filled distended of the
abdomen (pear-shape abdomen). In
contrast to urethral rupture, there is little
or no detectable ventral edema in the
preputial or umbilical region. On rectal
examination, the bladder is not palpable.

34. Diagnosis of urolithiasis
(1) Clinical examination and history.
(2) Urine analysis in its early when the calculi are present in
kidney or bladder. The urine usually contains erythrocytes
and epithelial cells, crystals (Sand, sabulous deposit and or
bacteria may be present in secondary invasion of the
traumatic cystitis and pyelonephritis).
(3) abdominocentesis to detect uroperitonium after rupture
of the bladder or needle aspiration from the subcutaneous
swelling associated with urethral rupture.
(5) Ultrasonography: The kidneys are examined from the
paralumber fossa for enlargement, and urethra for dilatation.
(6) Necropsy findings: For calculi unilateral ureteral
obstruction is usually accompanied by dilatation of the ureter
and hydronephrosis.

35. 1) Bilateral obstruction causes fatal uremia.
2) Calculi in the bladder are usually accompanied by
varying degrees of chronic cystitis.
3) The urethra or urethral process may be obstructed by
one or more stones, or may be impacted for up to 35 cm
with fine sabulous deposit.
4) When rupture of the urethra has occurred the urethra
eroded at the site of obstruction and extensive cellulitis and
accumulation of urine are present in the ventral abdominal
wall.
5) When the bladder as ruptured, the peritoneal cavity s
distended with urine and there is mild to moderate
chemical peritonitis.
(7) Determine the chemical composition of the calculi in
areas where urolithiasis is a problem.

36. Differential diagnosis
(1) Urethral rupture
1) The ventral abdominal edematous swelling
that is associated with the prepuce caudally to
the level of the scrotum, accompanied by pain
at the sigmoid flexure.
2) In sheep and goats, Examination of the penis
tip often reveals a turgid cyanotic vermiform
appendage. Blockage further proximal in the
penile urethra is usually present.

37. (2) Bladder rupture
1) Abdominal swelling (fetus, false fetus, fibroma,
fat, fluid, food, feces and flatus). A fluid wave can
usually be balloted across the abdomen, and
centesis of the abdomen with a large-bore needle
yields a large amount of clear, non-cellular fluid.
2) Palpation of the penis at the sigmoid flexure
may identify the site of obstruction, with pain
induced on manipulation of the region.
3) On rectal palpation, the urinary bladder is
usually nonpalpable. Although the abdomen is
filled with fluid, this cannot be determined by per
rectum palpation.

38. (3) Dilatation of the urethral process in young cattle is
characterized by a midline perineal swelling and may
resemble pulsation of the perineal urethra in obstructive
urolithiasis. The urethral recess arises from the junction
of the pelvic and spongy parts of the urethra at the level
of the ischial arch.
A fold of urethra mucosa proximal to the recess acts as
a valve to prevent the retrograde flow of the urine into
the pelvic urethra. In dilatation of the urethral recess,
during urination the proximal urethra pulses and the
swelling may enlarge slightly. There is no urethral
obstruction and urine flows passively from the penis for
several minutes after the urethral pulsation ceases. The
dilatation can be radiographed using contrast media.

39. Treatment
(1) Slaughter of cattle or lambs that are near the end of
their feedlot-feeding period.
(2) Metal catheterization (For mare, cow, and female
buffaloes) and rubber catheterization for male equines.
(3) In early stages of the disease or in cases of
incomplete obstruction, treatment with:
1) Urinary antiseptic (Antibiotic, sulphonamide or others)
to prevent secondary infection.
2) Analgesic (Novalgin 10 ml/100 KgBW, IV) to relief
pain.
3) Smooth muscle relaxants (Depropanx or Prostagmine
or Neurazine or Neuril) to relax the urethral muscle and
permit passage of the obstructing calculus.

40. 4) IV glucose 5% (After or with muscle relaxant) as diuretic,
increase urine flow and facilitate calculi passage.
5) Ammonium chloride at 200 mg/kg BW orally twice/ daily
and decreased at biweekly intervals until a dosage of 60
mg/ Kg BW is reached to maintain the pH below 7.0.
NB: Animals treated medically should be observed for
urination and that obstruction does not recur.
(5) If there is no urine passage within 6 hours of treatment,
but surgery may be required.

41. (6) Surgical
1) Urethrotomy or cystotomy to remove the calculi.
2) Amputation of the urethral process in ram, then applied
local antiseptic then massage of urinary bladder and slight
exercise.
Prevention
(1) Clean water intake all times.
(2) Adequate intake of vitamin A (Berseem or Berseem
hay).
(3) Ca: P ratio of ration should be 1.2: 1 or (1.5-2.0:1) to
avoid precipitation of excess phosphorus in the urine.

42. (4) Sodium chloride 3-5 % of total ration helps to prevent urolithiasis by
decreasing the rate of deposition of magnesium and phosphate around the
nidus of a calculus.
(5) For yearling (300 kg steers the daily consumption of 50g of salt does not
prevent he formation of siliceous calculi; at 200 g daily intake the occurrence of
calculi is significantly reduced, and at 300g daily calculus formation is almost
eliminated. This effect is due to the physical diluting effect of increased water
intake promoted by salt supplementation. The salt concentration be gradually
increased to 10 % in several weeks and incorporate it in pellets to facilitate
mixing.
(6) Feeding of ammonium chloride (45 g/day to steers and 10 daily to sheep) to
prevent urolithiasis due to phosphate calculi.
(7) Ammonium chloride or phosphoric acid added to the of steers increases the
acidity of urine and reduce A Incidence of calculi except silicic acid which
prevented by feeding of sodium chloride, which reduce the concentration of
silicic acid in the urine and maintaining it below the saturation concentration.
(8) Limitation of the oxalate supplies.
(9) The control of siliceous calculi in cattle by increasing the water intake (to
increase urine flow) and feeding of alfalfa hay (it contains less silica).
(10) Castration may increase urethral dilatation and reduce the incidence of
urolithiasis.

43. Prognosis
The survival rate for urethral rupture is 90% and is 50%
for bladder rupture.

44. Urolithiasis in horses
Urolithiasis occurs sporadically in horses, with
low prevalence (0.04-0.5%) and occur mainly in
older age 5-15 years and commonly affected male
(75%) than female. The urolith are most commonly
in the bladder. It is composed of calcium carbonate.
Urine from healthy adult horses is characterized by a
substantial quantity of mucoprotein, a high
concentration of minerals considerable insoluble
materials, and alkalinity. Nephrolithiasis may arise a
sequel to degenerative or inflammatory processes in
the kidney in which inflammatory debris serves as a
nidus for calculus formation.

45. Clinical finding and diagnosis
(1) Stranguria (straining to urinate).
(2) Pollakiuria (frequent passage of small
amounts of urine, hematuria, and dysuria
(difficult urination).
(3) Incontinence resulting in urine scalding of
the perineum in females or of the medial
aspect of the hind limbs in males.
(4) Painful urination with hematuria
associated with cystitis.

46. (5) Bacterial infection is common.
(6) The bladder wall may be thickened and large calculi
may be palpable per rectum just as the hand enters the
rectum.
(7) In males, urethral calculi may present with signs of
complete or partial obstruction that may be confused with
colic of gastrointestinal origin. Horses with urethral
obstructions make frequent attempts to urinate but pass
only small amounts of blood-tinged urine.
(8) Urinalysis reveals evidence of erythrocytes,
leucocytes, protein, amorphous depress, and calcium
carbonate crystals.
(9) Renal calculi are frequently bilateral and lead to
chronic renal failure resulting in chronic weight loss and
colic.

47. Congenital defects of the urinary tract
Congenital defects of the urinary tract are not common in farm
animals. Most common is uroperitoneum in foals following
leakage from the urinary bladder.
1. Patent urachus: See diseases of newborn.
2. Rupture of the bladder: The cause is unclear. It may be
traumatic origin during the birth process or defective closure of
the bladder wall, clinical signs develop due to urine
accumulation in the peritoneal cavity and ruptured bladder. For
treatment surgical repair of the bladder defect is necessary with
IV normal saline to correct dehydration and electrolyte
abnormalities.
3. Urethral atresia: It is a congential obstruction of urethral
opening. It is manifested by failure to pass urine and distension
of the patent portion of the urethra.

48. 4. Ureteral defect: (Unilateral and or bilateral). It is similar to
rupture of the urinary bladder.
5. Polycystic kidneys: It is a common congenital defect. If it is
extensive and bilateral the affected animal is usually stillborn or
dies soon after birth.
6. Hypospadias: It is an imperfect closure of the external male
urethra in a series of newborn lambs is recorded with other
neonatal defects including atresia ani and diaphragmatic hernia
7. Ectopic ureter: It occurs in cattle and horses. It may be
unilateral or bilateral with urinary incontinence resent since birth
as the major clinical manifestation. The ectopic ureter opens
into the urogenital tract at a place other than the bladder such
as the cervix, urethra or vagina. The condition is often
complicated by ascending infections, hydronephrosis and
dilatation of the ureter.
Definite diagnosis is done by radiology or endoscopy.