MEDICINE 1 – MIDTERMS
intestinal tract lining
General systemic state
TOXEMIA
 Caused by the presence of toxins deriving from
bacteria or produced by body cells. It does not
include the diseases caused by toxic substances
produced by plants or insects or ingested
organic or inorganic poisons.
 Etiology: toxins can be classified as being
metabolic or antigenic toxins
ANTIGENIC TOXINS
 These are produced by bacteria and to a less
extent by helminth parasites. Both groups of
parasites act as antigens and stimulates the
development of antibodies
 Antigenic toxins is divided into exotoxins and
endotoxins
Exotoxins
 These are protein substances produced by
bacteria which diffuse into surrounding medium
 They are specific in their pharmacological
effects and in the antibodies that they produced
 The most important bacterial exotoxins are
those produced by Clostridium spp.
Enterotoxins
 These are exotoxins that exert their effect
principally on the mucosa of the intestine,
causing disturbances of fluid and electrolyte
balance
 The most typical example is the enterotoxin
released by enterotoxigenic E. coli which causes
hypersecretory diarrhea in neonatal farm
animals
Endotoxins
 The endotoxins of several species of Gram-
negative bacteria are major cause of morbidity
and mortality in farm animals
 Endotoxins are lipopolysaccharides found in the
outer wall of the bacteria
 Gram negative bacteria are present in the
METABOLIC TOXIN
 This may accumulate as a result of incomplete
elimination of toxic materials normally
produced by body metabolism, or by abnormal
metabolism
 Normally toxic products produced in the
alimentary canal or tissues are excreted in the
urine and feces or detoxified in the plasma and
liver
 Example of abnormal metabolism causing
toxemia is Ketonemia
 Ketonemia due to a disproportionate fat
metabolism, and lacticacidemia caused by acute
ruminal impaction
Pathogenesis of Toxemia:
 The relationship between the toxins of bacteria
and the lesions they produce are specific to the
particular bacteria
 Classified as toxemia, they remain non-specific
and relates to carbohydrate metabolism
 Carbohydrate metabolism wherein there is a a
fall in blood sugar level, the rate and degree
varying with the severity of the toxemia, a
disappearance of liver glycogen and a
decreased glucose is not used rapidly
 These combined effects of hypoglycemia
interference with tissue enzymes and
degenerative changes are reduce the functional
activity of those tissues eg. Myocardium is
weaken and response to a cardial stimulants is
diminished. There is a similar loss of tone in
skeletal muscles and is manifested by weakness
and terminally by frustration
 There is a general depression of function such
as depression, dullness and coma
Clinical findings:
 Depression, Lethargy, Separation from the
group, anorexia, failure to grow or produce,
emaciation
 Most toxemia is due to bacterial infection or
tissue destruction produce fever but not in
metabolic toxin which is in terminal cases there
 is mascular weakness, collapse and death
occurs due to coma and convulsion
Clinical pathology:
 There is a low blood sugar level
 Highblood non-protein nitrogen (NPN)
 Aplastic anemia
 Leukocytosis
 Albuminuria
Necropsy findings:
 Gross findings at necropsy are limited to those
of the lesion which produces the toxin
 Microscopically there is degeneration of the
parenchyma of the liver, the glomeruli and
tubules of the kidney and of the myocardium
 There may also be degeneration or necrosis in
the adrenal gland
Diagnosis:
 Rather base on ill-defined syndrome mentioned
in the clinical findings
Treatment:
 If possible, it must be directed at removal of the
origin if the toxin, the provision of specific
antitoxins and supportive treatment to
counteract the effects of the toxemia
Examples:
 Provide intensive fluid and electrolytes
theraphy by continuous intravenous infusion is
essential until the animal begins to eat and
drink
 Give glucocorticoids or steroids IV every 4hrs
 *these is a universally accepted procedure in
treatment of toxemia especially when shock is
part of pathogenesis and this is most commonly
use in acute cases and large doses
 Adrenocorticoid-like activity is acetyl salicylic
acid and phenylbutazone
HYPERTHERMIA (heat stroke)
 Elevation of the body temperature due to
excessive heat production or absorption, or the
deficient heat loss when the causes of these
abnormalities are purely physical
 Caused by high environmental temperature
especially during summertime
 Severe muscular exertion
 Damage to the hypothalamus which is refer to
neurogenic hyperthermia or because of
dehydration hyperthermia and excessive heat
production due to muscular or metabolic
activity
OTHER CAUSES OF HYPERTHERMIA
 Neurogenic hypothermia
 due to spontaneous hemorrhage though
poikilothermia occurs (body temp is higher than
the environment)
 Dehydration hyperthermia
 due to insufficient tissue fluids to accommodate
heat loss by evaporation
 Excessive muscular activity
 eg. Strychnine poisoning
 Miscellaneous poisoning including levamisole
(anthelmintic drugs)and dinitrophenols
 Malignant hyperthermia in the porcine stress
syndrome with rare occurrence in other species
including horses
 Cattle with hereditary bovine syndactyly
 Administration of tranquilizing drugs to sheep in
hot weather
 Specific mycotoxins
Eg.
 Claviceps purpurea
 Acremonium coenophialum - the cause of
epidemic hyperthermia
*These poisonings represents one of the most
interesting new discoveries in a food-animal medicine
of recent times
 Iodism
 Sylade poisoning
Pathogenesis of hyperthermia:
 Unless the body temperature reaches the
critical level of point, a short level of
hyperthermia is advantageous in an infectious
disease because of phagocytosis and immune
body production are facilitated and viability of
most embedding organisms is impaired
  Slight fever is a normal reaction of cells, if the
fever stays longer that’s the time to act
 The metabolic rate maybe increased by 40-50%
 Liver glycogen stress are rapidly depleted
 Extra energy is derived from increase
endogenous metabolism of protein
 Anorexia occurs due to respiratory
embarrassment and dryness of the mouth
resulting to considerable loss of body weight
and lack of muscle strength companied by
hypoglycemia and arise in non-protein nitrogen
 Increase thirst due to dryness of the mouth. An
increase heart rate occurs due directly the rise
in body temperature and indirectly to the fall of
blood pressure resulting from peripheral
vasodilatation
 Respiration increases in rate and depth due to
high temperature in respiratory center
*if the period oh hyperthermia is unduly prolonged
rather than excessive in degree, the deleterious effects
are:
- increased endogenous metabolism and efficient food
intake
- extensive degenerative change in most body tissues
but this is more likely to be due to metabolic changes
than to the direct effects of elevation of the body temp
Clinical findings:
 The animals rectal temperature exceeds 39.5
degrees centigrade
 Increase heart rate and respiratory rates with a
weak pulse of large amplitude
 Sweating and salivation occurs initially followed
marked absence
 Affected animals may soon becomes dull,
 Stumbles while walking and tends to lie down
 In early stages, increase thirst and the animal
seeks cool places often lying water or
attempting to splash itself
 When the temperature 41% centigrade
respiration is labored and general distress is
evident
 Respiration becomes shallow and irregular, the
path becomes very rapid and weak
 Signs: Collapse, convulsion and terminal coma
 Death occurs in most species when a
temperature reaches
41.5-42.5 degrees celsius (106-108 degrees
Fahrenheit)
 Abortion may occur if the period of
hyperthermia is prolonged in Sows
HYPOTHERMIA
 Occurs when excess heat is loss or insufficient is
produced so that the body temperature falls
Common causes of Hypothermia:
 Excessive exposure to the cold air temperature
 Increase metabolic activity, muscle tone and
peripheral vasoconsctriction
 Decrease in muscle tone as in parturient paresis
and acute ruminal impaction and during
anesthesia and sedation, associated with
profuse diarrhea in the ‘cold cow syndrome’.
Peripheral vasodilatation shock, and reduction
of metabolic activity in the terminal stages of
many diseases
In man consciousness fails at rectal temperature of:
29.5-26.6 degrees celsius (85-87degrees F)
Hypothermia is recommended as an anesthetic
procedure in small size animals
 In cattles and sheep, prolong exposure to cold
environment down to -10 to -20 degrees C
result to a reduction in apparent digestibility of
the diet
 To offset the lower digestibility the animals
would accordingly need to consume more feed
FEVER
 A syndrome in which hyperthermia and toxemia
are produced by substances circulating in the
bloodstream
Etiology:
Fevers may be septic, the more common type
Aseptic, depending on whether or not infection is
present
Septic
These include infection with bacteria, viruses, protozoa
or fungi is
 Localized infection such as abscess, cellulitis,
empyema
 Intermittently systemic as in bacteremia
 Consistently systemic as in septicemia
Aseptic
 Chemical fevers, caused by injection of foreign
protein, intake of dinitrophenols
 Surgical fever due to breakdown of tissue and
blood
 Fever from tissue necrosis eg:
Breakdown of muscle after injection of
necrotiIng material
Severe intravascular hemolysis
Extensive infarction
Extensive necrosis in rapidly growing neoplasms
Immune reaction – anaphylaxis, angioneurotic
edema
Fevers are mediated through the action of endogenous
or leukocytic pyrogen produced by granulocytes,
monocytes and macrophages
Pathogenesis:
- The effect of bacterial and tissue pyrogens is
exerted on the thermoregulatory center of the
hypothalamus so that the thermostatic level of
the body is raised
Parenchymatous organs:
Liver, Adrenal glands, kidneys, pancreas
Diagnosis of fever:
- Sudden onset
- High fever 39.5-41 degrees centigrade
- Anorexia, dullness, depression, not interested
to move
- Vomiting or diarrhea
- Lymphadenopathy, possibly splenomegaly
- Marked changes in the total differential
leukocyte (CBC test)
- The isolation of a pathogen from a blood by or
excreta
Treatment:
The general principles of treatment of fever are to
remove the source of toxin and to treat the toxemia and
hyperthermia if the fever is excessive or prolonged
Removal of the toxin necessitates control of infections
by antibacterial drugs and removal of necrotic materials
in aseptic fevers
Antipyretics in large animals for symptomatic release of
fever but little value
Sept 11
SEPTICEMIA/VIREMIA
- Septicemia is the disease state compounded if
toxemia, hyperthermia and the presence of
large numbers of infectious microorganisms,
including viruses, bacteria and protozoa in the
bloodstream
Etiology:
There are many infectious agents that may produce
septicemia
The difference between septicemia and bacteremia is:
- In bacteremia, bacteria are present in the
bloodstream for only transitory periods and do
not produce clinical signs
- In septicemia, the causative agent is present
throughout the course of the disease and its
directly responsible for the signs that appears
Pathogenesis of septicemia:
There are two mechanisms that operate in septicemia
1. Exotoxins
2. Endotoxins
- Produced by the infectious agets produce a
profound toxemia and high fever because of the
rapidity with which they multiply and their rapid
spread to all body tissues
- Localization occurs in many organs, it also cause
direct endothelial damage and hemorrhages
into tissues
 - The same general principle apply also to viremia
except toxin is not produce by the virus it is
more likely that the general signs that occurs
are cause by the product of tissue cells killed by
the multiplying virus
Clinical findings:
- Toxemia and hyperthermia
- Fever and presence of submucosal and
subepidermal hemorrhages usually petechial or
occasionally ecchymotic
Clinical pathology:
- Isolation of causative bacteria from the
bloodstream
- Presence of leukopenia or leukocytosis which
aid in diagnosis
Necropsy findings:
- there is subserous and submucosal
hemorrhages and embolic foci of infection in
various organs but these are usually
overshadowed by the lesions specific to
causative agents
Diagnosis:
- isolation of the causative agent from the
bloodstream can a positive diagnosis of
septicemia be made
Treatment of septicemia:
- IV or parenteral treatment with antibacterial
drugs or sera and antitoxins
Prevention:
- Strict hygiene precaution to avoid spread of
diseases
DISTURBANCE OF BODY FLUIDS ELECTROLYTES AND
ACID BASE BALANCE
A disturbance of body water balance in which more
fluid is loss from the body than is absorbed results in
reduction in circulating volume of blood and in
dehydration of tissues
2 major causes of dehydration: (ETIOLOGY)
1. Failure of water intake
2. Excessive loss
Common causes of dehydration:
1. Diarrhea
2. Vomiting
3. Polyuria
4. Loss of fluid from extensive skin wound
5. Copious sweating
6. Deprivation of water
7. Lack of thirst due to toxemia
8. Inability to drink water as in esophageal
obstruction
9. Acute carbohydrate engorgement in ruminants
10. Acute intestinal obstruction and diffuse
peritonitis in all species
11. Dilatation and torsion of abomasum
Two factors involve in the pathogenesis of dehydration
 Depression of tissue fluid levels with resulting
interference in tissue metabolism
 Anhydremia (decrease amount of water in the
plasma) with reduction in the fluid content of
the blood (oligamia)
Dehydration may cause death especially in acute
intestinal obstruction, vomiting, and diarrhea but it’s a
chiefly contributory cause of death when combined
with other systemic states such as:
Acidosis, Electrolyte imbalances, toxemia, and
septicemia
Clinical findings:
- The most important sign of dehydration is
dryness and wrinkling of the skin giving the
body the shrinking appearance
- Eyeballs recede in the socket and the skin
subsides slowly after being picked up into a fold
- The skin of the upper eyelid and neck gives one
of the best indication of the degree of
dehydration
Degree of dehydration
4-6% degree of dehydration – mild dehydration, barely
detectable clinically
6-8% dehydration – manifested in the eyes which
appear sunken and the skin fold or tempting of the skin
will remain elevated for 2-4 seconds
8-10% dehydration – the eyes are markly sunken and
the skin fold will remain elevated for 6-10 seconds
10-12% dehydration – manifest the eye skin fold can
remain elevated for 20-45 seconds
TYPES OF DEHYDRATION:
Hypertonic dehydration – simple deprivation of water
resulting to simple dehydration w/o sodium loss
classidied as mild dehydration
Isotonic dehydration – exemplified by loss of isotonic
fluid, as in copious sweating, necrosis, simple enteritis
and there is isotonic fluid and sodium loss. Considered
as mild dehydration and anhyponatremia
Hypotonic dehydration – enterotoxigenic collibacillosis
and salmonellosis in horse, there is a a consequent
which occurs hypotonic sodium low. Classified as severe
dehydration plus severe hyponatremia
ELECTROLYTE IMBALANCE
- The most electrolyte imbalances is due to net
loss of electrolytes due to the disease of
alimentary tract
- Sweating, exudation from burns, excessive
salivation and vomiting
- Horse
- The electrolytes of major concerns are:
Sodium, potassium, chloride, bicarbonates
HYPONATREMIA
- Reduce or subnormal sodium levels
- Sodium is the most abundant iron in the
extracellular fluid and is chiefly responsible for
maintenance of osmotic pressure of the
extracellular fluids
- Common cause of hyponatremia is increase loss
of sodium through the intestinal tract in case of
enteritis which is particularly marked in the
horse with acute diarrhea
Effect of hyponatremia
- It increases in the renal excretion of water in an
attempt to maintain normal osmotic pressure or
its result in a decrease in extracellular fluid
space leading to decrease circulating blood
volume, hypotension, peripheral circulatory
failure, ultimate renal failure and muscular
weakness, hyperthermia and marked
dehydration
Clinical findings in hyponatremia:
- Dehydration, muscular weakness, mental
depression which occurs with the disturbances
of both water and electrolytes and with acid
base imbalance
HYPOCHLOREMIA
- Reduction in the amount of blood chlorides, it
occurs as result of an increase in the net loss of
the ion in the intestinal tract in acute intestinal
obstruction, dilatation, impaction, and torsion
of the abomasum and in enteritis
- No clinical signs
- Clinincal findings are those of anorexia, wet
nose, lethargy, mild polydipsia and polyuria
- Promotes the reabsorption of bicarbonates and
further development of alkalosis
HYPOKALEMIA
- Occur as a result of decrease dietary intake,
increased renal excretion, abomasal stasis,
intestinal obstruction and enteritis
- It can be due to prolonged administration of
mineralocorticoids and prolong used of
potassium soln in fluid therapy for dieric
animals that may result in excessive renal
excretion of potassium and hypokalemia
- In horses, this hypokalemia is due to loss of
electrolyte due to competition, and likewise
hypokalcemia and alkalosis (potassium leaves
the extracellular space and become
concentrated in the cell)
Effects of hypokalemia is

- Reduction of the potassium

- Muscular weakness
- Muscular tremors
- Depression
- Cardiac arrhythmia
- Coma

HYPERKALEMIA

- Excessive amount of potassium in the blood

- Occurs most commonly in severe metabolic
acidosis which can be seen in calves suffering in
severe diarrhea wherein potassium leaves the
cell and moves in the etracellular fluids
- Results in bradycardia, cardiac arrhythmias,
convulsion and death

ACID BASE IMBALANCE

- pH of the blood
- maintained at normal range of 7.35-7.45 by its
buffer system, in which the bivarbonate system
is most important
- other buffers blood are hemoglobin (which has
the greatest buffer capacity), plasma protein
and phosphates
- Clinical findings in acidosis is related chiefly to
respiratory system
1. Increase in the depth and the rate of
respiration by simulation of the respiratory
center which is called cosmol breathing as a
result of carbon dioxide tension in the
blood and depletion of bicarbonate
2. Depress respiratory function resulting in
additional accumulation of hydrogen ions in
severe bolemic shock and weakness,
lassitude (state of feeling tired or
listlessness and terminally coma)

ALKALOSIS

- Caused by increased absorption of alkali and

also excessive loss of acid or defeciet in carbon
dioxide and in cattle because of abomasal
atony?? Due to dilatation, impaction or torsion
of the abomasum
 DISEASES OF THE NEWBORN
Newborn – first month of life of the animal. Born alive
at term
3 General classification of diseases of the
newborn
 Fetal diseases
- refers to the diseases of the fetus during the
intra uterine life
Eg. During forum gestation, congenital defect,
abortion, fetal death with amification and goiter
 Parturient diseases or Perinatal diseases
- Occurs at birth at first 24hrs of life
- Associated with dystocia difficulty of giving
birth, causing cerebral anoxia, injury to the
skeleton or soft tissues
 Postnatal diseases
Divided into 3 aspects:
1. Early postnatal disease – within 24hrs of birth
- Due to malnutrition
- Poor mothering of the dam
- Because of hypothermia due to exposure to
cold
- Navel infection and collibacillosis
Navel infection – septicemia disease
Collibacillosis – involvement of interotoxigenic
eschericia coli
2. Delayed postnatal disease
- The fetus/neonates is about 2-7 days of age
- Reasons of delayed postnatal disease
- Desertion or abandoning of the dam
- Mammary incompetence resulting in starvation
- Increase susceptibility to infection due to
hypogammaglubinemia due to collibacillosis,
land messentry and foal septicemia
3. Late postnatal disease
- 1-4wks of age neonates
- This is exemplified by white muscle disease,
enterotoxemia
All animals must be born close to term if they are to
survive in a normal farm environment
Calf - should be born atleast 240 days of pregnancy
Foal - 300 days of pregnancy
Lamb – 138 of pregnancy
Piglets – 108 days of pregnancy
GENERAL EPIDEMIOLOGY
Conginetal defects
- There are abnormality of structure or function
present at birth and this can be due to
inheritance like cliff palate, or because of virus
infection such as classical swine fever, glutam in
sheep or bovine virus diarrhea or because of
nutritional deficiencies
- Iodine deficiency, Selenium deficiency, Vitamin
E deficiency – resulting to muscular dystrophy,
conginetal cardiomyopathy
- Copper deficiency – enzootic ataxia in lambs
- Manganese deficiency – limb deformities and
condrude dystrophy in cows
- Vit. A – eye defect, hair lip
- Vit. D – neonatal rickets
- Chemical poisons – selenium, tetanus toxins,
sulfonamides in treating bacterial infections in
animals
- Physical insults – severe exposure in beta and
gamma ray infection
Pathogenesis:
Structural malformation and deformations
Viral keratogenesis like tremors and blindness
Inhirited congenital defects because of conditions
like maple
Lysosomal storage disease – excessive accumulation of
undigestive substrate in cells
Factor IX and XI deficiency – bleeding tendency or
bleeding problem
Myocydosis – accumulation of saccharides
ENVIRONMENTAL INFLUENCES AS A CAUSE OF
CONGINETAL DEFECTS
- This usually due to noxious influences in
environment such as accidental release of
plybrominate biphinils
Diagnosing neonatal disease/diseases of the newborn
- Base on pedigree analysis (ancestors)
- Nutritional history
- Disease history of dams
- History of drugs used
- Movement of dams during pregnancy
- Season of the year
- Introduction of the animals to the herd
Physical and environmental influences that can result in
illness and death in neonates
1. Malnutrition – it can be associated to
antepartum malnutrition of dam reducing milk
flow, inclement weather, inadequate maternal
behavior, and too much human interference
and dam is too old for satisfactory milk flow
Neonatal infection is common caused of morbidity and
mortality in domestic animals. It can be caused of the ff.
- In cattle, it can be caused by bacteremia or
septicemia due to organisms or bacteria like
Escherichia coli, listeria monocytogens,
pasteurella, streptococci and salmonella spp.
- Enteritis caused by clostridium perfringens
- Respiratory tract disease due to infectious
bovine rhinotrachitis
- In pigs, the neonatal infection can be due to
septicemia with localization in joints,
endocardium, meninges caused by streptococci
spp
- Bacteremia, septicemia and enteritis caused by
E.coli, transmissible gastroenteritis (TGE),
vomiting and wasting disease by viruses
- Arthritis and septicemia – erysipelas
- In horses, septicemia with localization in joints
caused by ecoli, salmonella aboti equine,
Salmmonella typimorium
- Lungs
- Enteritis – perfringens
- Sheep, septicemia localization in joints, caused
by streptococci, micrococci, and erysipilotrix,
gas gangrene in the navel
POSTNATAL INFECTION
- Acquired after birth from the enteric or
respiratory tract flora of the dam from the
environment or close contact with other
infected neonates
PRENATAL INFECTION
- Acquired in utero
- Majority of these are agents that cause abortion
and neonatal septicemia
- Eg. Septicemic infections – actinobacillus ecoli,
Escherichia coli
When it comes to the route of transmission, we should
know the entry point or portal of infection
If the infection is intra-uterine in origin, the infection
gains an entrance via the placenta and probably by
means of placentitis in infection and endometritis
If the disease is postnatal, the portal of entry of the
infection may be thru the navel or thru ingestion which
can be through contamination of the environment from
soiling of the other or by bedding, by uterine discharges
by the dam, or previous parturition
Intra-uterine infection are more common associated
with death of the fetus or with abortion
All newborn farm animals are more susceptible to
infection than the adult counterpart. Due to the
reasons:
The calf, lamb, piglets and foals are born without
significant levels of gamma aglobulin and they are born
agammaglobinemic and possess almost no resistance
to infection until after they have ingested colostrum
and absorbs efficient quantities of lactoglobulins from
the colostrum.
Colostrum immune responsiveness is dependent but
also varies with the antigen in colostrum fed animals,
however part of the inefficiency of newborn to produce
humoral-antibodies following ingestion of antigens is
the interference by circulating colostrum antibody