Diseases with Discoloured Urine & Anaemia

Disease
Aetiology:

Babesiosis

Babesia bigemina

B. bovis (small but more potent)

Descriptions:

Epidemiology:
Source &
Transmission:

Pathogenesis:

Clinical signs:

Pathology:

Diagnosis:

Treatment:

Remark:

Signs in 7 - 20 d (incubation period)

Anaemia, jaundice
Fever, anorexia
Rumen stasis (unknown mechanism)
Haemoglobinuria, increased HR & RR
Abortion
CNS signs (not common - only B. canis) convulsion, hyperexcitability, opisthotomus,
posterior paresis, coma, death
Hypotensive shock & DIC
Generalised jaundice, enlarged spleen,
swollen dark kidney, brown red urine, tick
granular bile
Thin watery blood & excessive serous fluid
in body cavity
Thin blood smear + Giemsa (ear tip smear)
Splenectomy of suspected dog to enhance
multiplication of protozoa to increase chances
of isolating it
Serology

Chemoprophylaxis: (Imizol) chosen because it

can remain in blood at effective level for a long time
(20 - 30d). Drug will kill the tick during blood
feeding but Ag will be injected slowly during every
tick bite (can't multiply) - stimulate premunity
Immunity:

Zebu (high) vs Temperate (low/nil)

Innate resistance

Premunity (low Babesia burden stimulate

immunity b4 major challenge) - presence of
Ag in the population to keep immunity in
balance

Cross immunity (only to some extent - not full

immunity)

Trypanosomiasis

Trypanosoma congolense, T. vivex,

T. brucei (all are potent)

T. rhodenci, T. gumbiense (in human)

T. evansi (from. T. brucei)

In India, Malaysia & Middle East - T.

evansi cause a disease known as Surra

Cattle, buffaloes, horses

In Africa

Glossina (tsetse flies). Cyclical

transmission for T. congolense & other
(Tabanid too)

Mechanical transmission for T. evansi

First 3 spp - Lymphoid tissue & RBC

Last 2 spp - RBC only (in various shape rod, ring, oblong, coma shape) (benign no haemolysis or rupture of RBC)
East Coast Fever

High mortality up to 90% in clinical case

Inappetance, listless, depression

High T0C (fever), emaciation

Enlarged lymph nodes

Exudate from eyes, nose

T. orientalis & T. mutans (dark brown red
urine)

Depression, muscle tremors, fever, weak,

anorexia, reduced milk, increased RR,
pale/icteric mm, swelling of lymph nodes

Pale/icteric organs

Centrolobular necrosis in liver

Hemosiderin in Kupffer cells in kidney,

spleen, lymph nodes (hypertrophy)

Diminazene aceturate (Berenil) 2 mg/kg

(yellow powder)
Imidocarb (Imizol) 5 mg/kg
Avoid excitement
Fluid therapy
Hematinic (things that help/stimulate RBC
multiplication e.g. iron, Vit. B12)
Blood transfusion
Control of tick population (spray, dip, race)
Vaccination (live vaccine)
Pasture management (spell according to tick
life cycle)

Tick-borne
Rhiphicephalus appendiculatus (3-hosttick)
Haemaphysalis & Boophilus - for T.
orientalis & T. mutans

Poor prognosis after cerebral involvement

Control &
Prevention:

Febrile tick borne disease characterised by

breakdown of RBC, haemolytic anaemia,
jaundice & haemoglobinuria
Common in imported breed
Tick-borne
Boophilus microplus (one-host-tick)
Transovarian (more important)
Transtadial
Mechanical (can but not important)
Injected into blood & enter RBC & multiply
RBC rupture (intravascular haemolysis) &
infect other RBC

Theileriosis

Theileria parva, T. annulata, T. lawrencei

(all cause East Coast Fever in Africa)

T. orientalis & T. mutans (not so severe) in

this region

Blood smear + Giemsa of biopsy of

enlarged lymph node
As spheroid piroplasm in some RBC or
Meronts (Koch's blue bodies in Giemsastained smear) in lymphocytes in spleen &
lymph nodes
Serology: IFT

Oxytetracycline (the only protozoa species

that is able to be killed by antibiotic)
Primaquine diphosphate (Primaquine )
5 mg/kg PO 3 d (to remove piroplasms
from the blood)

Tick control

Surra

Severe in horses. Cattle & buffaloes as

carriers

Recurrent high fever (due to VSG)

Anaemia (no direct haemolysis but

secrete VSG (Ag) that coat the RBC become foreign to body

Progressive emaciation

Oedema (hypoproteinaemia due to

utilisation by Trypanosome)

Death

High mortality due to lymphoid

destruction
Ddx: Leptospira, Babesiosis,
Anaplasmosis

Show diurnal periodicity

Blood film (wet mount smear - can see

RBC moving) use buffy coat
Direct smear + Giemsa
Lymph nodes smear
Mice inoculation intraperitoneal 1ml
(acute - can detect low parasitemia)
Mercuric chloride test
Serology - ELISA
Diminazene aceturate (Berenil)
2 - 3 mg/kg
Suramin 7 - 10 mg/kg
Naganol
Isometamidium chloride 25 mg/kg

Detect & remove infected animal

Control stock movement
Remove susceptible animal from
infected area
Trypanotolerance breed: N'Dama,
West African Shorthorn

Vaccine is not practical due to VSG

During mass importation of cattle from New

Zealand/Australia, blood vaccine was used to induce
immunity (no full protection & short shelf life)
Diseases with Discoloured Urine & Anaemia
Disease
Aetiology:
Descriptions:
Epidemiology:

Urolithiasis

Disease of exclusively male (ram, buck, steer),

Kept intensively (feed lot, concentrate diet, less water intake/water
deprivation)

Source &
Transmission:

Cereal based diet (ammonium, calcium, magnesium & phosphate

calculus)
Struvite calculi (in renal medulla) - Mg, NH3, phosphate
Grass (silica, oxalate)
In more anabolic state (young animal) oestrogen enhance
mucoprotein (denuded cells) act as nidus & cement (all
colloid/mineral will settle down & stick to mucoprotein)

Predispose factor: trauma (ascending infection)

Calculus at sigmoid flexure (bull) & urethral process (ram)

Factors contributing to calculus formation:
Genotype: varying degree in ability to absorb & secrete phosphorus
Mineral content of diet (P-cereal, Ca, Mg- concentrate, etc)
The nature of diet (e.g. roughage - more mineral is excreted via
faeces, more mineral in concentrate is excreted via urine)
Mucoprotein content (animal in anabolic state)
Urinary volume (water intake)
Urinary pH (depend on diet)

Necrosis of renal papillae

Calyces & renal pelvis dilated
Ureters filled with debris (pressure atrophy)
Pus filled sac (pyelonephrosis)
Renal failure

Acute: dull pyrexic, anorexia, arched back, shifting stance, periodic

kick of abdomen, straining to urinate, little urine + blood + pus +
debris
Chronic: loss of condition, straining, turbid urine + pus + debris +
clots

Pathogenesis:

1)
2)
3)
4)
5)
6)

Clinical signs:

Calculogenic crystalloid becomes concentrated to a point when the

solution become unstable -- precipitate
With the presence of urinary protein (mucoprotein) which act as
nidus & cement -- calculi formation

Usually subclinical. Show signs when there is obstruction

Abdominal pain, kicking at abdomen

Shift its weight, switches its tail

Frequent attempt to urinate

Teeth grinding,

"sand" at prepuce
From rectal examination:

Distended bladder & urethra. This condition can lead to rupture of

bladder/perforation of urethra - oedema (cool) in surrounding tissue

Pathology:

Diagnosis:

Treatment:

Control &
Prevention:

Pyelonephritis

Corynebacterium renale in urinary passage of cows

Inflammation of renal pelvis, parenchyma kidney

Sporadic, in mature cattle (cows)

Occasionally acute, commonly chronic

Sequele: urethral perforation & rupture, urethral stricture, bladder

rupture, ureteral rupture, hydronephrosis
Cytology, urinalysis
X-ray

Prognosis (long term) = poor

Muscle relaxant (ease dislodge) e.g. aminopromazine
Antispasmodic (ease dislodge) e.g. promazine, acepromazine to
relaxes retractor penis muscle to straighten the sigmoid flexure
Retrograde flushing
Snip the urethra process (early case)
Cystotomy
Urethrostomy (short term as salvage operation - use to stabilise the
animal/stop uraemia b4 slaughter) - can't breed the animal anymore
Affected animal has poor anaesthetic risk (metabolically unstable) use epidural instead of GA
Urine acidifiers to increase solubility of salt ammonium chloride
(steer 45 gm/d, sheep 10 gm/d). Only if urine is alkaline
Correct diet imbalance
Maintain Ca : P ration 1: 1 or 2 : 1
Alfa-alfa roughage - high calcium
Sodium chloride - 300 g/d (increase water intake, reduce deposition
of magnesium ammonium & phosphate around nidus, chloride
binds mucoprotein
Adequate water supply - reduce phosphate binding

During rectal examination: enlarged kidney & ureters (painful), loss of

normal lobulation of kidney

Examination of urine (Gram +ve diphtheroid organism)

Rectal examination
Ultrasound: dilated renal calyces, enchogenic, flocculent material
within renal pelvic, abnormal renal shape, enlarged kidney

Penicillin (disease will relapse after recovery)

- 22000 - 44000 IU/kg i.m. BID x 3w

Hygiene
Remove clinical cases?

Remark:

Postpone early castration to allow complete development of urethra

(7 - 8m)

lith = stone

Diseases with Discoloured Urine & Anaemia

Note:
Spleen is a lymphoid tissue (when splenectomised - not enough lymphoid cells e.g. macrophages to engulf Babesia (enhance multiplication))
Role of spleen in Babesiosis: remove parasites from infected cells by "pitting", site of phogocytosis & site of antibabesial Ab production
Premunity: persistence of solid immunity to clinical Babesiosis depends on continuous maintenance of causative agent in the blood
Neurological signs in Babesiosis are caused by brain anoxia from severe anaemia &/or RBC blockage of cerebellar capillaries
Source: Diseases of Cattle in the Tropics pg. 460