Chisowa M.D.

MSc Animal Nutrition (UM);

ANIMAL HEALTH BSc Animal Science (UNZA);

(AAS 323) Dip Ed Agricultural Science (NRDC)

INVESTIGATING AND
REPORTING DISEASES
DIAGNOSIS- DISEASE/ILLNESS
Diagnosis
the identification of the nature of an illness or other problems by
examination of the clinical signs.
The act or process of identifying or determining the nature and cause
of a disease or injury through evaluation of patient history,
examination, and review of laboratory data.
Disease
could be defined as inability to perform physiological functions at
normal levels even though nutrition and other environmental
requirements are provided at adequate levels.
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DIAGNOSIS
clinical diagnosis 
 diagnosis based on signs, and laboratory findings.
differential diagnosis
 the determination of which one of several diseases may be
producing the same or similar clinical signs.
physical diagnosis 
diagnosis based on information obtained by inspection, palpation,
percussion, and auscultation.
serum diagnosis  serodiagnosis.
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HEALTHY STATE
Animal is able to
Drink/eat required portions
Defecate/urinate without obvious difficulties
Vital signs-temp, respiratory & heart rate,
Normal gait-locomotor system
No discharges from natural openings
Good body condition score- use of a scale

32
HEALTHY STATE
Colour of mucous membranes
Moist appearance of the muzzle
Positive stimuli to environment-response to sound/events in the
surroundings
Fur/mohair(goat fur) appears smooth and shiny

33
UNHEALTHY STATE
Animal may not be able to
Drink/eat- growths around the muzzle, loss of appetite or
complete lack of food intake due to disease
May not defecate/urinate- constipation/obstructions/UTI
infections which may present with pain

34
UNHEALTHY STATE
Abnormal heart/respiratory sounds suggestive of e.g. anaemia,
CHF, disease of the cardiovascular/respiratory system including
neoplasia (cancers)
Dysfunction of locomotor system- lameness, arthritis, wounds
affecting joints,
Poor body condition score

35
UNHEALTHY STATES
Mucous membranes appear congested (red colour from pink)
Muzzle is dry and cracky
Animal will not respond to external stimuli
 skin appears dry, loss of body fur (alopecia)
Discharges from openings-clear(nasal discharge, mucus,
purulent(pus),blood, loose stool, most times the discharges are
excessive

36
DISEASE STATES
Begin to think of body systems
Nervous system
Respiratory system
Circulatory system
Musculoskeletal system
Urogenital system
Lymphatic system
Digestive system

37
PHYSICAL/CLINICAL
EXAMINATION
is a fundamental process of animal diagnosis
It’s a systematic procedure.
Its prevents omission of important information
Easier recall of abnormal findings

38
1. SIGNALMENT /HISTORY
Signalment - Complete description of the animal
Species, Breed, Age, Sex, Reproductive status, other
distinguishing characteristics
 Always double-check client reported information (sex, age, etc)
Keep this information in mind as you examine the animal and
make clinical judgments.

41
HISTORY

History (Hx)- (see Patient History Form) Includes environment,

diet, medical history, reproductive history, vaccination status and
current medications.
Description and history of chief/presenting complaint
Reported concerns should be followed up with additional
questions to clarify nature of the complaint

42
ENVIRONMENT
Surroundings/immediate environment
Housing-open or confined
Access to water/food-nutrition
Environment temp, humidity, climate

44
CONTROL, PREVENTION AND
TREATMENT
CONTROL, PREVENTION AND
TREATMENT
Immunity:
is body's ability to resist or eliminate potentially harmful foreign materials or abnormal cells
The immune system is a functional system –NOT an organ
Complex system which includes
Skin – physical barrier
Lining of mucus membranes – physical barrier
Secretions – tears, mucus etc - antimicrobial
Blood cells and vasculature – WBCs
Bone marrow
Liver – makes complement proteins
Lymphatic system and lymphoid organs
Most tissues – have resident immune cells
IMMUNITY

consists of following activities:

Defense against invading pathogens (viruses & bacteria)
Removal of 'worn-out' cells (e.g., old RBCs) & tissue
debris (e.g., from injury or disease)
Identification & destruction of abnormal or mutant cells
(primary defense against cancer)
Rejection of 'foreign' cells (e.g., organ transplant)
Inappropriate responses:
Allergies - response to normally harmless
substances
Autoimmune diseases
THE INNATE IMMUNE SYSTEM
Innate Immune
System

External Internal
defenses defenses
Innate (non-adaptive) -first line of immune response
that relies on mechanisms that exist before infection
THE INNATE IMMUNE SYSTEM
–external defense
Anatomical Barriers – Mechanical Factors
Skin
Mucociliary escalator
Flushing action of saliva, tears, urine
Anatomical Barriers – Chemical Factors
 Antimicrobial Peptides in sweat
 HCL in stomach
 Lysozyme in tears/saliva
THE INNATE IMMUNE
SYSTEM- external defense
Anatomical Barriers – Biological Factors
Normal flora – microbes in many parts of the body
> 1000 species of bacteria
Competes with pathogens for nutrients and space
THE INNATE IMMUNE
SYSTEM- internal defense
Components of Blood
Complements of proteins
Coagulants proteins
Cytokines
WBCs
ADAPTIVE IMMUNE STYSTEM
Acquired (adaptive)
 Second line of response (if innate fails)
 relies on mechanisms that adapt after infection
 handled by T- and B- lymphocytes
 one cell determines one antigenic determinant
ADAPTIVE IMMUNITY : Second
line of response
Based upon resistance acquired during life
Relies on genetic events and cellular growth
Responds more slowly, over few days
Is specific
each cell responds to a single epitope on an antigen
Has anamnestic memory
repeated exposure leads to faster, stronger response
Leads to clonal expansion
ADAPTIVE IMMUNITY: ACTIVE AND PASSIVE
Active Immunity Passive Immunity
• induction of • the transfer of
immunity after active humoral
exposure to an immunity of ready-
antigen made antibodies
Natural clinical, sub-clinical via breast milk,
• Animal resist infection placenta
diseases without
being vaccinated
Artificial Vaccination: immune serum,
Animal has been immune cells
• Live, killed, purified
vaccinated against antigen vaccine
the disease
OTHER IMPORTANT TERMS
Premunity:
a type of immunity to a disease in which the immunity of the
animal is largely dependent upon the continued presence of the
disease organism in the body. EG Bovine Babesiosis
Tolerance:
Is a form of resistance against disease acquired by animals of an
animal population which have been in contact with a disease for
many generations. Eg N’Dama cattle are resistant to
Trypanosomiasis.
OTHER IMPORTANT TERMS
Susceptibility:
An animal is said to be susceptible to a disease when it has no
immunity, tolerance or resistance to the disease and goes down
with the disease on exposure to it.
CONTROL OF DISEASE UNDER
GOVERNMENT LEGISLATION
AND REGULATION
Appointment of veterinary and animal health laws and
regulations
Enforcement of quarantine and control of the movement of
animals.
Movement of animals to be observed only under a permit system
Animals suspected of a disease may be ordered to be slaughtered
Govern the movement of hides and skins, meat, dairy produce
and hay
Specify diseases that are notifiable (Rinderpest, FM, Anthrax,
Rabies, Sheep pox, Sheep scab, Swine Fever etc)
COMMON DISEASES IN
LIVESTOCK AND WILDLIFE
DEFINITION OF TERMS
Aetiology:
Transmission:
Pathogenesis:
Clinical Signs
Post Mortem (PM)
Treatment
Prevention
Control
Differential Diagnosis
SELECTED BACTERIAL
DISEASES
ANTHRAX
Anthrax
is a contagious and notifiable disease characterised by sudden deaths. I
 affects all warm blooded animals
Aetiology:
Bacillus anthracis. This bacterium has ability to form spores on exposure to air
which can survive for many years and is highly resistant to environmental
elements.
Transmission and occurrence:
ingestion of contaminated feed or water.
Flies are mechanical transmitters.
Outbreaks usually follow major climatic change e.g heavy rains
ANTHRAX
Pathogenesis:
Following entry, there is multiplication in lymph nodes, followed
by septicaemia, production of toxins which cause vasodilation &
tissue damage, decrease in blood pressure, shock, renal failure
and death
ANTHRAX
Clinical signs:
Incubation period of 3-7 days
death without premonitory signs (sudden deaths).
high fever up to 42oC,
 muscle tremors,
Laboured breathing,
increased heart rate,
local swelling (tongue, throat & sternum).
In pigs- inflammation and oedema of the throat, face & haemorrhages
under the skin
ANTHRAX
Postmortem findings:
 CARCASS SHOULD NEVER BE OPENED!
 Dark tarry non-clotting blood from all natural orifices.
 Lack of rigor mortis.
 Rapid gaseous decomposition.
 Enlarge spleen, enteritis, enlarged haemorrhagic lymph nodes.
 Haemorrhages in most organs with darkblood
Samples:
blood sample, blood smear on a glass slide.
ANTHRAX
Prevention & control:
Annual vaccination in susceptible areas.
Quarantine of affected areas.
Deep burial or complete burning of carcass.
Disinfecting the place where the animal died (quick lime,
formalin or caustic soda).
Suspected cases should not be opened-
NOTIFY VETERINARY AUTHORITIES
Treatment:
Usually come too late. Bacteria are susceptible to penicillin,
sulphonamides & oxytetracyclines.
ANTHRAX
Economic significance:
Deaths,
cost of control,
zoonosis
Differential diagnosis:
Lightning,
snake bite,
Black leg,
Poisoning (arsenic or copper
CONTAGIOUS ABORTION
Contagious Abortion
It is an infectious disease mainly of cattle characterised by
abortions. It is also zoonotic. Disease occurs throughout the year.
Aetiology:
Brucella abortus in cattle. B melitensis in sheep & goats, B ovis
in sheep and B suis in pigs.
Transmission:
Ingestion of contaminated feed or water
CONTAGIOUS ABORTION
Clinical signs:
Non-pregnant cows show no signs.
 In pregnant cows: Abortions in late pregnancy (7-9 months),
stillbirth or birth of weak calves, retained afterbirth,
increased incidence of metritis,
prolonged calving to conception interval.
May see swelling of the knee (hygromata)
NB** In bulls & rams orchitis & epididymitis
CONTAGIOUS ABORTION
Sample:
In cow- Blood (paired sera), milk sample
In aborted foetus- stomach contents, liver, spleen &
kidney
Treatment:
There is no effective treatment
Control:
Vaccination of heifers (4-10 months), culling of infected
cows, proper disposal of aborted foetuses.
CONTAGIOUS ABORTION
Economic significance:
Loss of production through abortions,
zoonosis
TUBERCULOSIS
Tuberculosis
It is an infectious, chronic and debilitating bacterial disease.
The disease causes considerable loss of production.
Aetiology:
Species of the genus Mycobacterium. (M tuberculosis in man, M
bovis in cattle & M avium in birds)
Transmission:
Inhalation,
ingestion of contaminated feed or water
TUBERCULOSIS
Pathogenesis:
Formation of primary focus (usually in the lungs),
bacteria get into lymphatic drainage and blood.
Causes caseous lesions in lymph nodes.
Wherever organisms localise they simulate formation of
tumour-like lesions called tubercules
.
TUBERCULOSIS
Clinical signs:
Signs depend on extent and location of lesions.
Anorexia, weakness, enlarged superficial lymph nodes,
chronic loss of body condition (emaciation),
dyspnoea (laboured breathing) and intermittent cough
TUBERCULOSIS
PM findings:
Tubercules seen in different organs (lungs, liver, lymph
nodes etc)
Control:
There is no effective treatment in cattle.
Test and slaughter is the most effective way
LEPTOSPIROSIS
Leptospirosis
It is a contagious disease of animals including man, characterised
by fever, icterus/jaundice, haemoglobinuria, abortion and death.
Aetiology:
Leptospira species (L hardjo, L pomona, L grippotyphosa, L
ictehaemorrhagiae)
Transmission:
Bacteria are shed in urine.
Direct contact with urine or intake of urine contaminated feed or
water
LEPTOSPIROSIS
Clinical signs:
The disease is characterised by a high morbidity (75-
100%) and a mortality of 5-15%.
In calves there is fever, inappetance, dyspnoea, icterus,
haemoglobinuria and anaemia.
In older cattle there is lowered milk production, milk is
thick, yellow and blood tinged.
Abortions round the 7th month.
LEPTOSPIROSIS
PM findings:
Anaemia, icterus, red urine, areas of necrosis on kidneys giving a
mottled appearance. Liver is swollen.
Samples:
Blood, bacterial isolation Treatment: Streptomycine,
Dihydrostreptomycine or Oxytetracycline
:Prevention
Annual vaccination, maintaining a closed herd, selection of
replacement stock from free herds.
LEPTOSPIROSIS
Differential diagnosis:
CA, Trichomoniasis, vibriosis
Economic significance:
Loss of production in terms of abortions, milk
production and loss of weight.
Deaths in livestock.
The disease is also zoonotic
VIBRIOSIS
Vibriosis
It is a venereal disease of cattle characterised by repeated
return to oestrus, infertility and occasionally abortions.
Aetiology:
Campylobacter fetus veneralis
Transmission:
Mainly venereal but also by artificial insemination
VIBRIOSIS
Pathogenesis:
The bacteria are deposited in the vagina and swims to reach the
uterus and fallopian tubes.
Cause endometritis which make the environment unsuitable for
embryo survival.
Salpingitis (inflammation of fallopian tubes) results in infertility.
VIBRIOSIS
Clinical signs:
Heifers affected more than mature cows.
Signs include return to serice, irregularity of the oestrus
cycle, endometritis with some vaginal discharge, vaginitis.
Abortions may occur between 4-7 months accompanied by
placental retention.
Bulls: Usually no clinical signs but remain carriers.
Samples:
Aborted foetal stomach, vaginal mucus for culture, preputial
washings, blood.
VIBRIOSIS
Control:
Vaccination is both preventive and curative.
Bulls may be treated with dihydrostreptomycine.
Use of AI and treatment of semen with penicillin and
streptomycine.
Breed to non infected bulls.
Differential diagnosis:
Bovine Trichomoniasis
QUARTER EVIL (BLACK LEG)
Quarter evil (Black leg)
It is an acute infectious disease characterised by sever myositis,
lameness and high mortality.
Aetiology:
Clostridium chauvoei, usually mixed infection with Cl septicum.
Has ability to form spores Transmission: Ingestion of contaminated
feed.
 Also contamination of wounds
Pathogenesis:
Organism proliferation and toxin production leading to toxaemia and
local necrotising myositis.
QUARTER EVIL (BLACK LEG)
Clinical signs:
Affect young cattle usually between 6 months-3 years in
good condition.
Fever of up 410C,
complete anorexia, high pulse rate, and severe depression,
lameness affecting one limb, swelling usually on the shoulder,
which is hot and painful.
Gas formation under the skin can be felt over affected area.
Death within 12-36 hrs.
QUARTER EVIL (BLACK LEG)
PM findings:
Rapid bloating and putrefaction. Blood stained froth
from nostrils and anus.
Dark discoloured muscles. Excess fluids in body
cavities.
Samples:
Pieces of muscle or spleen.
Organ smear
Treatment:
High doses of penicillin
QUARTER EVIL (BLACK LEG)
Control:
Annual vaccination of susceptible cattle.
Proper disposal of carcass (burying or burning)
Differential diagnosis:
Anthrax,
lightning,
lead poisoning
BOTULISM
Botulism
It is a rapid fatal motor paralysis. It is an intoxication rather than infection.
Aetiology:
Ingestion of a toxin of Clostridium botulinum. All species of domestic
animals and birds are susceptible. Toxin is found in decomposing bone,
animal tissue and plants.
Transmission:
Ingestion of preformed toxin
Pathogenesis:
Following ingestion, toxin is absorbed and it interferes with nerve
transmission leading to paralysis.
BOTULISM
Predisposing factors:
Phosphorus deficiency leads to pica (eating of unusual objects
including bones).
Outbreaks are common in winter
Clinical signs:
Incubation of 3-17 days.
Temperature, pulse, lymph nodes and mucous membranes are
normal. Difficulty in moving on hind limbs.
Recumbency and hind limb paralysis.
BOTULISM
Clinical Signs:
Animal looks bright and alert, eating and drinking but
remain recumbent.
Paralysis progress forward to affect fore quarters, throat
and jaw muscles.
Lead to inability to chew and swallow.
Paralysis of respiratory muscles results in difficult
breathing and death.
Course of disease is for 5-7 days.
BOTULISM
PM findings:
No specific findings. Presence of bones and unusual objects in
stomach
Samples:
No samples in a live animal can confirm disease. In a dead
animal, intestinal contents/liver sent on ice for testing of toxin.
BOTULISM
Control:
Annual vaccination of cattle.
Phosphorus supplementation in winter.
Proper carcass disposal.
Differential diagnosis:
Ephemeral fever,
Phosphorus deficiency,
Spinal injury
TETANUS
Tetanus
It is a toxaemia caused by neurotoxin from tissues infected with
Clotridium tetani
Aetiology:
Clostridium tetani Transmission: Through wounds. Usually
follows docking or open castration
Pathogenesis:
Clostridium is unable to grow in normal tissue.
Multiplication in necrotic tissue leads to toxin production.
The toxin is transported in nerves, lymphatic drainage to the
central nervous system.
TETANUS
Clinical signs:
Incubation period of 10-14 days.
Localised stiffness involving muscles of the neck, masseter
muscles, muscles of hind limb and in the region of the infected
wound.
General body stiffness become pronounced after a day.
Toni spasms, hyperaesthesia, animal become easily excitd into
violent, general spasms by sudden movement or noise. Spasm of
the head muscles lead to lock jaw.
Horses are more susceptible than other domestic animals.
Temperature may be above normal.

TETANUS
PM findings:
No specific findings
Treatment:
Combination of tetanus antitoxin and penicillin.
General good nursing care and cleaning wound with oxidising
agent.
Prevention:
Vaccination with tetanus antitoxoid annually.
Horses should be given before any surgical operation
PULPY KIDNEY
(ENTEROTOXAEMIA)
Pulpy Kidney (Enterotoxaemia)
It is an enterotaxaemia caused by a toxin produced in the gut.
It primarily affects sheep and goats, and rarely cattle
Aetiology:
Clostridium septicum type D, which is present as normal
microflora of the intestine.
It is common in young lambs.
PULPY KIDNEY
(ENTEROTOXAEMIA)
Predisposing factors:
Excessive intake of feed or milk (hence more common in single
lambs).
Deworming , high plane of nutrition (especially carbohydrates)in
young and adults
Clinical signs:
Death without premonitory signs in best conditioned lambs.
Temperature is normal, excitement, incordination, opisthotonos,
circling, pushing head against fixed objects. Convulsion and
death.
Diarrhoea may or may not be present
PULPY KIDNEY
(ENTEROTOXAEMIA)
PM findings:
 Haemorrhages on the surface of intestines and heart.
Fluid filled pericardial sac, pulmonary oedema, rapid autolysis of
the kidney is a cardinal sign hence the name Pulpy kidney.
Carcass decompose rapidly, rumen and abomasums are often
overloaded with feed.
Samples:
Small intestine contents
PULPY KIDNEY
(ENTEROTOXAEMIA)
Treatment:
No specific treatment
Control:
Lambs vaccinated at 2-4 wks.
Annual vaccination of all sheep and goats.
Vaccination of ewes before lambing so that there are adequate
antibodies in colostrum and passive immunisation of the lamb.
Sheep and goat should always be vaccinated prior to deworming.
CBPP
Contagious bovine pluera-pnuemonia
 a disease of cattle
its a bacterial disease caused by Mycoplasma mycoides
mycoides
TRANSMISSION
 CBPP is spread by inhalation of infective droplets from an
infected coughing animal to susceptible animal.
 Consequently close contact is required for transmission to
occur such as common pastures or water holes.
 Outbreaks usually begin as a result of movement of an
infected animal into a naïve herd.
CLINICAL SIGNS
Coughing
Respiratory distress
Head and neck extended
Forelimbs are apart
Animal faces direction of wind
Loss of appetite, depression
Post mortem signs-Consolidation of lung, excessive
amounts of yellowish fluid in lung
DIAGNOSIS
Laboratory diagnosis involves collection of samples
such as nasal swabs, plueral fluid and blood for culture
and serological tests

 
TREATMENT/CONTROL
In endemic areas like in north-western province of
Zambia, they may use Tylosin
In non-endemic areas no attempts at treatment are done
Test and slaughter in no endemic areas .
A ban on livestock movement is instituted from
infected areas.
CONTROL CONT’
Separate sick animals away of healthy animals farm
level
COMMON VIRAL DISEASES IN
LIVESTOCK AND WILDLIFE
ACTIVITY
Describe these diseases (Foot and Mouth, Lumpy skin, Wooden Tongue and
LumyJaws, Calf Diptheria and White Scours) basing on;
a) Aetiology:
b) Transmission:
c) Pathogenesis:
d) Clinical Signs
e) Post Mortem (PM)
f) Treatment
g) Prevention
h) Control
i) Differential Diagnosis
RICKETTSIAL, PROTOZOAL
AND FUNGAL DISEASES
HEARTWATER (COWDRIOSIS)
Heartwater (Cowdriosis)
It is an acute often fatal infectious tick-borne disease of cattle
sheep and goats. Aetiology: Cowdria ruminatum (it is a
rickettsia)
Transmission:
 It is tick-borne i.e transmitted by the bite of an infected tick. The
vector tick is Amblyomma (bont) tick
Pathogenesis:
The rickettsia causes damage to the lining of the blood vessels
resulting in leakage of plasma or sometimes whole blood.
HEARTWATER (COWDRIOSIS)
Clinical signs:
Incubation period of 10-14 days.
In cattle from endemic areas, calves less than 6 months are not
usually affected.
The disease is characterised by sudden deaths,
fever 41- 430C,
anorexia,
depression and dyspnoea.
HEARTWATER (COWDRIOSIS)
Clinical Signs
Exaggerated blinking of eyelids,
walking in circles,
high stepping gait,
salivation & occasionally aggressiveness.
Animal lies on lateral recumbency (on side), with limbs making
running movements.
Convulsions, coma and death.
HEARTWATER (COWDRIOSIS)
PM findings:
Straw coloured protein rich fluid is found in various cavities:-
Hydrothorax, hydropericardium, pulmonary oedema, froth in the
trachea & occasional some ascites (fluid in the abdominal cavity)
Samples:
Brain crush smear
HEARTWATER (COWDRIOSIS)
Treatment:
Oxtetracycline injections
Prevention & control:
Tick control through regular dipping, spraying or use of pour-
ons.
Vaccination
ANAPLASMOSIS (GALL
SICKNESS)
Anaplasmosis (Gall sickness)
It is a tick-borne haemoparasitic disease mainly of cattle.
Aetiology:
Anaplasma marginale (cattle), Anaplasma ovis (sheep & goats)
(also a rickettsia)
Transmission:
 By the bite of an infected tick.
The vector is the blue tick (Boophilus).
Can also be transmitted mechanically by insect bites or
contaminated needles
ANAPLASMOSIS (GALL
SICKNESS)
Pathogenesis:
 Following entry into the blood, there is multiplication in the red
blood cells and destruction of the rbcs by the reticulo endothelial
system leading to haemolytic anaemia.
Clinical signs:
Fever up to 410C,
anorexia, weakness, incoordination,
laboured breathing (dyspnoea),
complete ruminal stasis, anaemia & jaundice.
ANAPLASMOSIS (GALL
SICKNESS)
Clinical Signs
There is drop in milk production,
loss of body condition,
increased frequency of urination.
Pregnant cows may abort.
Death in untreated cases
ANAPLASMOSIS (GALL
SICKNESS)
PM Findings:
Thin watery blood.
Anaemic and jaundiced carcass.
Splenomegally (enlargement of the spleen)
 hepatomegaly (enlargement of the liver) , liver is yellowish
in colour, enlarged gall bladder and thickened bile.
Samples:
Blood smear
ANAPLASMOSIS (GALL
SICKNESS)
Treatment:
Oxytetracycline injection (terramycine, hi-tet, coppermycine,
chanacycline etc). Imizol injection.
The above may be combined with a laxative e.g molasses
Prevention & control:
 Tick control through regular dipping, spraying or use of pour-
ons.
Vaccination
BABESIOSIS (RED WATER)
Babesiosis (Red Water)
A protozoan disease of ruminants, characterised by fever,
anaemia, jaundice, haemoglobinuria and sometimes CNS signs.
Aetiology:
 Babesia species (mainly B bigemina & B bovis for cattle, and B
ovis & B motasi for sheep and goats.
Transmission:
By the bite of an infected tick. The vector is the blue tick
(Boophilus). Can also be transmitted mechanically by insect bites
or contaminated needles or surgical instruments.
BABESIOSIS (RED WATER)
Pathogenesis:
Following entry into the blood, there is multiplication in the red
blood cells and intravascular haemolysis leading to anaemia and
haemoglobinuria.
Clinical signs:
 Incubation period of 2-3 wks. Fever (410C),
anorexia, depression & weakness.
Fall in milk production, increased respiration and heart rates.
Constipation initially and later diarrhoea.
BABESIOSIS (RED WATER)
Clinical Signs
Haemoglobinuria (red water/urine), anaemia & jaundice.
Pregnant cows may abort.
A cerebral form due to B bovis leads to incordination, posterior
paralysis, convulsions, coma and death.
BABESIOSIS (RED WATER)
PM Findings:
Enlarged spleen & liver. Watery blood, jaundice and urinary
bladder contains red brown urine.
Samples:
Blood smear, spleen smear or brain smear Treatment: Imidocarb
(imizol), Berenil or phenamidine
Prevention & control:
Tick control through regular dipping, spraying or use of pour-
ons. Vaccination of cattle over 6 months of age.
DISEASES OF THE YOUNG
ONES, METABOLIC &
POISONING DISORDERS
DISEASES OF THE YOUNG
ANIMALS
These are diseases which occur usually within the first month of
life in animal born alive at term.
These animals are especially sensitive to the environment
because they are immunologically incompetent.
They depend on readily available carbohydrates for energy and
are inefficient in maintaining body temperature.
COLIBACILLOSIS
Calves, piglets, kids and foals are affected.
It is characterised by diarrhoea from 1-3 days of age.
Aetiology:
The bacteria, Escherichia coli

Transmission:
Ingestion of contaminated food or water

Predisposing factors:
Inadequate intake of colostrums, unhygienic environment.
Stress caused by being born in inclement weather.
Use of inferior milk replacers.
COLIBACILLOSIS
Pathogenesis:
Bacteria colonise in the small intestine and produces enterotoxin
that results in net secretion of fluids into the intestines leading to
diarrhoea and dehydration.
Clinical signs:
Sudden onset.
Profuse watery diarrhoea, soiled buttocks,distended abdomen,
dehydration, severe weakness, coma and death.
COLIBACILLOSIS
PM Findings: Enteritis and fluid filled intestines.
Samples: Faeces
Treatment:
Antibiotics especially sulphonamides.
Fluid and electrolyte replacement therapy.
 Use of antidiarrhoeal drugs and intestinal protectants e.g kaolin.
 Withhold milk for 24-48 hrs or until recovery.
COLIBACILLOSIS
Prevention and control:
 Ensure that calves get colostrums within 6 hrs of birth.
 Maintenance of hygienic conditions.
 Calves and other young animals should be protected against adverse
weather conditions.
NAVEL/JOINT ILL
It is an infection of the umbilicus and associated structures. Infection occur soon
after birth and leads to inflammation of the umbilical cord.
Aetiology:
Mixed bacterial infection (may include E coli, staphylococcus, proteus etc)
Pathogenesis:
Infection leads to localised swellings, bacteraemia and localisation in the joints,
urinary bladder and meninges.
NAVEL/JOINT ILL
Clinical signs:
Umblicus si enlarged and painful on palpation.
 Calf is depressed and may not suckle.
May be draining pus.
Space occupying mass may be felt on palpation of the abdomen. Swollen joints my be
seen.
PM Findings:
Abscesses along umbilical vein.
Hepatic abscesses.
Cystitis and arthritis.
NAVEL/JOINT ILL
Treatment & control:
Antibiotic treatment (penicillin).
Surgical removal of abscesses.
Good sanitation and hygiene at the time of birth.
Apply drying agent of tincture of iodine on umbilicus
SALMONELLOSIS
A disease charecterised by septicaemia (blood poisoining by poison) and
enteritis (inflammation of the intestines)
Aetiology:
Salmonella typhimurium, sometimes S Dublin.
Transmission:
Ingestion of contaminated food and water
Predisposing factors:
As with E coli
SALMONELLOSIS
Clinical signs:
Calves are dull and feverish.
Anorexia but thirsty, pasty to fluid yellow or brown faeces.
Diarrhoea or dysentery with a fetid smell.
Marked weight loss. Nervous signs may occur due to septicaemia.

PM Findings:
Haemorrhage and congestion of the intestines
SALMONELLOSIS
Samples:
 Faeces, liver and spleen

Treatment & control:

Treatment is usually not very successful.
Use potentiated sulphonamides.
Fluid & electrolyte therapy.
Purchase animals from farms known to be free of the disease.
 Identify carriers and cull or isolate.
Prophylactic use of antibiotics in food or water.
 Feed and water must be protected from faecal contamination.
Contaminated buildings must be cleaned and disinfected.
Avoid stress.
COCCIDIOSIS
A protozoan disease mainly of the small intestines, charecterised
by varying degrees of diarrhoea.
Can affect calves, lambs, kids, piglets and foals.
Aetiology:
Cryptosporidium species
Transmission:
ingestion of contaminated material
COCCIDIOSIS
Pathogenesis:
Stunting of the villi especially in caecum and colon. Loss of surface
enzymes.eg lactase leading to maldigestion, malabsorption & diarrheoa.
Clinical signs:
Signs are not characteristic. Mild to moderate diarrhoea. Faeces are yellowish
and contain some mucus. Dehydration, decreased feed intake. Some cases are
self limiting. In severe cases the calf may collapse.
COCCIDIOSIS
PM Findings:
Haemorrhage and congestion of large intestines
Samples:
Faeces, sections of large intestines.
Treatment & control:
Sulphonamides. Fluid & electrolyte therapy. Avoid introduction of
infected animals into the property.
METABOLIC DISORDERS
METABOLIC DISORDERS
Importance of metabolic disorders:
They cause mortalities.
Higher prevalence in high producing cows.
Incidence is highest at calving to peak lactation (there is high
turnover of fluids, salt and organic materials).
There is genetic predisposition and are subject to management
practices.
MILK FEVER
It is also known as parturient paresis and is a metabolic disease of
ruminants commonly encountered at parturition in adult cows.
Aetiology:
Hypocalcaemia (depression of levels of calcium in body fluids).
There are generally low serum calcium levels at calving and
lactation due to disturbances of GIT calcium absorption and
mobilisation from bone at parturition due to high levels of
oestrogen.
 Amount of calcium in milk is directly proportional with volume
of milk secreted.
Coliform mastitis decrease serum calcium levels.
MILK FEVER
Predisposing factors:
 High calcium diet during dry season.
 High levels of phosphorous inhibit formation of 1,25 Dihydro-
cholecalciferol (Vit D) resulting in decreased intestinal calcium absorption.
 Age also decrease intestinal ca++ absorption
Pathogenesis:
Low calcium levels result in reduced cardiac output and
decreased blood pressure, ruminal/abdominal tone and motility.
MILK FEVER
Clinical signs:
 Common in mature cows of 5-10 years age group (3rd + calvers).
 Jerseys are most susceptible.
 Excitement and hypersensitivity.
 Temperature is normal or subnormal, muscle tremors and disinclination to
move.
 Sternal recumbence and lateral kink of neck.
 Animal is anorectic, has total ruminal stasis and loss of anal reflex.
Increased heart rate but decreased intensity and weak pulse.
 Low venous pressure and extremities may be cold.
MILK FEVER
Treatment:
Calcium borogluconate 200-500ml given slowly intravenously or
subcutaneously.
May give together with magnesium chloride.

Control:
Avoid feeding high protein & high phosphorous diet in late pregnancy.
Vitamin D injection about 8 days before calving is an effective preventive
remedy (repeat if cow does not calve on due date).
Give high calcium diet after calving.
BOVINE KETOSIS
A metabolic disease that occurs in lactating cows from 1-6 weeks
after calving resulting from impaired carbohydrate and fatty acid
metabolism.
Aetiology:
Energy drain to partitioning of glucose by mammary glands.
Common in high producing cows.
Predisposing factors:
Excessive feeding of silage (high butyric acid content).
Decreased excercise and obesity. Anorexia due other diseases
BOVINE KETOSIS
Pathogenesis:
Demand for glucose of milk supercedes the ability to synthesise it (from
glycerol and amino acids). Leads to depletion of hepatic storage and
increased fatty metabolism.
Clinical signs:
Gradual loss of appetite for silage but eat hay. Drop in milk yield, loss of
body condition and smell of ketones in breath and milk. Nervous signs
include aimless walking, apparent blindness, hyperasthesia and bellowing,
leg crossing and staggering.
BOVINE KETOSIS
Treatment:
 500ml of 50% glucose intravenously. Propylene glycol. Glycerine, nicotinic
acid
OTHER METABOLIC DISEASES
OF IMPORTANCE
Pregnancy Toxaemia (Ovine ketosis) (ewes0
Bovine Ketosis
Bloat
Acidosis
POISONING DISEASES
Chemical poison
Urea Poisoning
Organophosphate poisoning (pesticides0
Other chemical poisoning
Lead
Arsenic
POISONING DISEASES
Plant Poisoning
 Lantana camara (cherry-pie or tick berry)
 Dichapetalum cymosum (Umkauzan)
 Prussic acid in sorghum
 Nitrate Poison (amaranthus, sorghum and cynodon)
 Aflatoxin poison or Aflatoxicosis (groundnuts, maize, cotton seed, sorghum, sunflower seeds)
OTHER IMPORTANT DISEASES
MASTITIS
it is inflammation of the udder almost always due to bacterial
infection (also fungi).
3 major factors are involved; microorganisms, the cow (heredity,
increased incidence with age, teat shape-best is round) and the
environment (stress, injury, nutrition, hygiene).
Many different microorganisms can cause mastitis.
Cows vary in their ability to resist infection.
Environment influences the numbers & types of bacteria to
which the cow is exposed.
MASTITIS
Predisposing factors:
Poor milking hygiene, milking machine faults, teat sores &
injuries.
Environmental population of pathogens and drying off (flushing
of milk through teat which removes bacteria is terminated,
increased udder pressure induces teat duct dilation allowing entry
of bacteria, udder washing and dipping is discontinued), stress
towards calving and also dilation of teats.
Most common organisms involved are Streptococcus agalactiae
and Staphylococcus auereaus. Also E coli, Enterobacter
aeruginosa and Corynebacterium pyogenes
MASTITIS
Clinical signs:
May be clinical (observable mastitis) or subclinical where there
is no readily detectable abnormalities or change in milk.
Subclinical is the most common.
Major effects are swelling of affected quarters, decrease in milk
production, presence of clots in milk, dicolouration of milk and
fever
MASTITIS
Treatment:
Typically when clinical mastitis is detected, the cow is milked
out and then given an intramammary infusion of antibiotic, ie.
infused directly into the infected gland.
Give an injection of a long acting penicillin and oxytocin
MASTITIS
Control:
Check machine function and milking procedures & correct where necessary
Observe and correct hygiene
Detect infected cows, isolate and milk last (ie clean heifers-clean cows-recently
treated cows-infected cows)
Treat clinical cases as they occur.
Treat cows on drying with long acting antibiotic
Cull any cows that have had more than 3-5 attacks of mastitis during a lactation
Examine all introductions to the herd by udder palpation and culture
Treat teat cracks and sores
AGALACTIA
 This is partial or complete abscess of milk flow which may affect one or
more mammary glands.
 More common in sows but has also been seen in cattle. The exact aetiology
is unknown but there is failure of milk let down or absence of milk
secretion.
 This could be due to painful condition of teats, udder oedema, infection,
hysteria or hormonal defects (high oestrogen & low prolactin have been
found in cases).
AGALACTIA
Clinical signs:
Partial or complete absence of milk flow affecting one or more
mammary glands. Refusal to allow piglets to suckle.
 Piglets show sign of starvation and apathy, hypoglycaemia and
death.
Treatment:
Oxytocin and broad spectrum antibiotic injections