Lectures of systemic Medicine-1
(Med 404)
(Mid Term Examination)
Terminologies
Medicine:
It is an art of healing. It diagnoses, treats and prevents the disease.
Allopathic Medicine:
Purely on scientific bases. These drugs hit specific targets like penicillin is effective
against G +ve bacteria. Disprin causes vasodilatation and relieves pain.
Homeopathic Medicine:
These drugs slowly hit the target; improve the immune system of the host. They control
different factors. They use different phenomena. It is scientifically not proved.
Holliastic medicine:
Relief may come from anything like spiritual activities etc.
Epidemiology:
It is the study of disease in a population. We have to collect data about the presence of
diseases in an area. We also study the frequency of diseases in area or country.
Epidemic:
Disease with high spread or increases in occurrence of disease with temporarily high
frequency.
Pandemic:
Disease spread worldwide.
Endemic:
Disease spread in a population with specific frequency. It is applied to the diseases which
are present constantly.
Prevalence:
No. of cases at any time in population
% prevalence = total no. of cases/total no. of animals × 100
Incidence:
No. of newly diagnosed cases during a specific time period.
Incidence = no. of new cases/total no. of animals × 100
Epidemiological Triad:
Disease is related to three things: host, environment and agent. If any one is missing there
will be no disease.
Population at risk:
This means the subset of original population selected for sampling. This shows the total
no. of animals in region or population which are considered to be having disease.
For example in Faisalabad abortion occurs in cattle. Now we will not focus the females
which are not capable of reproducing (heifers) and males because population at risk is all
those females which are capable of reproducing.
Determinants:
Factors which affect the frequency of disease in a population e.g. environment, host,
agent.
(a): Intrinsic Determinants:
May be physical or physiological (inherent characteristics of host) e.g. two types of
bacteria: Pathogenic and non pathogenic.
(b): Extrinsic Determinants:
Include some environmental influences e.g. low or high temperature, bacteria grow better
at high temperature while virus grow better at low temperature.
Infectivity:
It refers to speed of spread.
Virulency:
It is related to the cause of disease.
Pathogenesis:
Pathological changes caused by the agent.
Host immunity relationship:
Strong immunity, less chances of disease.
Antigenic shift:
It is minor change in genome.
Antigenic drift:
It is major change in genome.
Transboundary diseases:
Diseases spread to different countries. Like RP, FMD.
Contagious:
Which spread through direct or indirect contact.
Non contagious:
In which no need of contact for spread. Whenever opportunity is there, disease will be
developed.
Types of Carriers
(a): True carriers:
Animals that have organism in their body and also have the ability to disseminate the
agent but show no sign of disease e.g. virus of rabies in bat.
(b); Incubatory carriers:
Animal is having infection but organism is in incubatory phase and cause physiological
changes slowly.
(c): Convalescent carriers:
The animals which have agent into the body even after recovery and this agent is shed
into the environment.
Transmission
(a): Direct Transmission:
Transmission by physical contact.
(b): Indirect Transmission:
Transmission by means of some agent. Agent goes to environment through secretion and
excretion of body.
(c): Vertical Transmission:
From dam to offspring transmission. Salmonellosis is transmitted to chicks through egg
in poultry.
(d): Horizontal Transmission:
From one individual to other.
(e): Mechanical transmission:
A vector shifts agent from infected animal to healthy one. No multiplication in vector.
The animal which is involved in the transmission of infection is called as reservoir. It has
no clinical signs.
(f): Biological transmission:
Agent completes its few steps of multiplication in vector.
(G):Transovarian Transmission:
It is vertical type of transmission. Infection is from dam to offspring by ovary. It is
shifted to offspring by eggs.
Role of Veterinarian
To increase the production of livestock in the form of milk, meat, eggs, hides etc.
Pakistan is on the 5th number in milk production, even then there is great potential to
increase the production.
Major Issues in Livestock
Disease:
If animals are healthy, there will be more production. So Veterinarian must diagnose and
treat the disuse. Diseases should be prevented and less expense should be spent on
management.
Best breeds of buffalo:
Niliravi, Kundi
Best breeds of cattle:
Red sindhi and Sahiwal
Rinderpest:
In 2007 Pakistan was declared free of RP. This is morbillivirus infection. Stomatitis, high
fever, diarrhea, and nasal discharge are its signs.
Foot & Mouth Disease:
In FMD production reduces. Signs of vesicles are there. First it was seasonal: Sep – Oct
and March – April. But now it is seen throughout the year due to exotic breeds.
Vaccination schedule should be followed but not enough available. The cold chain for the
vaccination is not available to maintain the antigenecity of vaccine. Vaccine is expensive.
A, O, Asia Ι, and Iran 2005 are serotypes of FMD. This disease came from Iran.
PRP:
Mainly it is disease of sheep and goat with very typical signs. Digestive and respiratory
systems are involved. Typical sign is oral lesion.
It is newly emerging disease and work is being done on it. It emerged from Africa. In
Asia first time seen in India & Bangladesh. Zoonotic importance and ultimately human
health is affected.
Bovine Spongiform Encephalitis (mad cow disease):
Due to prion.
Avian Influenza:
Swine flue:
It is an acute, highly contagious respiratory disease that results from infection with type
A influenza virus. Pig is the principal host of this disease. It is an orthomyxovirus of
influenza A group with haemagglutinating antigen. H1 and neurominidase antigen N1 (i.e.
H1N1). Recently new subtypes have been reported (H3N2 & H1N2).
Role of Host in Infection
There is a certain no. of bacteria required to produce infection in host. If agent
acquires suitable environment for multiplication then agent has more chances of
infection. If environment is not suitable although bacteria are in required number
infection will not be there.
Certain species are agent specific. Like FMD is present in cattle but absent in dog
and cat. Some diseases affect early age, some middle age, and some late age e.g. HS in
young calves is high due to weak immunity as compare to adult one. Similarly some
problems are found in male which are absent in females and vice versa e.g. abortion.
Mastitis
It is a major problem in dairy industry throughout the world. Price of dairy animal
is based in its milk production. If one teat is lost it loses 25-30% production.
In cow front teats produce more milk (60%) than rear teats (40%) and vice versa
in case of buffalo. If cow loses its front left or front right teat then there will be a huge
loss. This disease causes huge economic losses to farmers in terms of production and
price of milk. Udder health has effect on animal health also. So loss of udder means the
loss of animal. Mastitis causes severe pain. So always give pain killer while treating
mastitis.
Human is getting poor quality milk of low protein, fat and minerals and cause
malnutrition in human beings. The dairy products of mastitic milk will have low quality
and short half life. These will become rancid early.
Mastitis is an inflammation of mammary glands that happens in response to the
injury for purpose of neutralizing infectious agent to prepare way for healing and turned
to normal function. (National Mastitis Council)
In case of clinical mastitis there will be redness, pain, swelling, and hotness. In
severely infected cases necrosis and sloughing of tissue is found.
In case of subclinical mastitis there is no obvious change in udder but change in
the composition of milk; increased no. of bacteria and increased somatic cell count.
Mostly subclinical mastitis persists for months due to Staph aureus and slowly affects
udder and alveoli for months and years and sometimes within weeks.
In Pakistan every 3rd or 4th cow or buffalo (20-25 %) is mastitic. Overall there is
an incidence of 20-25 % in cow and 14-17 % in buffalo. Prevalence of clinical and
subclinical mastitis in cow is 7.08 % and 48.7 % respectively. In buffalo prevalence of
clinical and subclinical mastitis is 3.7 % and 23.9 % respectively.
Loss caused by mastitis was 5.4 billion dollars of farmers in 2001 in India. Loss
of 1.7-2 billion dollars to dairy industry of America. There is a loss of 240 billion dollars
annually in India. There is shortness of 57 days in lactation period due to mastitis. On
average 30% reduction in production of one cow and 15% loss in whole lactation.
Normal somatic cell count in milk is 200,000 and in mastitis it goes to several
thousands. If more than 200,000 cells then consider mastitis. In America standard is
100,000 cells. There are two methods: individual Somatic cell count and bulk somatic
cell count (recently named as milkscan.). Fossometer is another one and it is mostly used.
Increased number of somatic cells show severity of infection. In USA, they pay premium
to farmer if farmer has milk with 1000 cells. Similarly if increased no. of somatic cells,
they put penalty. In some areas penalty is 30-60 %.
Whenever mastitis, there is chance of losses of quarter in dairy animal. They have to be
culled from herd. 22.5 % animals are culled 10-18 % lactations are terminated due to
mastitis.
Somatic cell count in buffalo is 50,000 to 375,000 in buffalo. Bacterial count
varies from 100,000 to 10,00,000 in cows. Mastitic milk has 90 % neutrophils and 10%
somatic cells. If 40 % neutrophils, there will be mild mastitis. In case of 90 %
neutrophils; there will be severe mastitis.
Mastitis was first time known in 1940 due to some bacterial involvement.
Major pathogens: Staphylococcus aureus, streptococcus aglectai, E.coli
Minor pathogens: Mycoplasma, Klebsella.
Effect of Mastitis on Milk
Mastitis affects the quality of milk and there is increase in the number of bacteria.
Common sources of bacteria are inadequate cleaning of milking utensils, hands not
properly washed, skin of udder not properly cleaned and contamination of the teat skin.
There is a direct relationship between skin and mastitis. If dirty skin then more chances of
mastitis. By providing hygienic conditions mastitis can be controlled and quality of milk
and its byproducts can be improved.
Increased somatic cell count:
Increased somatic cell count and increased neutrophils and macrophages also
deteriorate the quality of milk. Increased somatic cell count claims mastitis. So there is
direct relationship between mastitis and somatic cell count. But in late lactation and
newly parturating animals, somatic cell also increases.
Whenever there is rise in somatic cell count, casein content falls down (which is
very important protein).Similarly leakage of certain proteins from serum like albumin,
immunoglobulin and transferring into milk also occurs. Na and K ions also increase.
Calcium level decreases with fall in level of casein because it has binding capacity with
casein. Normal pH of milk is 6.6 but it may raise upto 6-9 or more in the milk collected
from subclinically mastitic animal and even more in clinically mastitic animals. There is
release of proteolytic enzyme from blood like plasmin. Plasmin is excessive in blood but
low in milk. It cannot be destroyed at 140 oC. If it is high in milk then deteriorate the
quality of milk. Milk heated at 140 oC for 1.5 minute destroys the Plasmin and some
other enzyme like lipase which attack triglycerides to convert them into FFA, which
produce offensive smell in milk and rancid flavour is developed in milk.
Watery milk shows chronic type of inflammation. If watery secretion present in
first few streaks (about 10 streaks) then normal but if more than it then chronic mastitis.
Flaques present in milk show severe infection. If present at start of milking then shows
infection due to S. aureus. If at the end of milking then indicates animal having TB.
These flakes are normally present in milk in 1-2 days of lactation and in last 2-3 days of
lactation.
Types of Mastitis
No pathological lesions, no swelling, no pathological organism and normal cell
count upto 500,000 cells in milk is considered normal udder
Latent Mastitis:
Pathological organism present in milk but no swelling of udder and normal cell count.
Sub Clinical Mastitis:
Bacteria and somatic cells present in milk and change in composition of milk but no
gross lesion.
Clinical Mastitis:
It is divided into three categories depending upon severity:
(a): Acute: There are obvious symptoms of inflammation present on udder, change in
colour and composition of milk and increased temperature.
(b): Subacute: No obvious change in udder but clots and plaques present in the milk.
(d): Chronic: Every acute infection develops into chronic infection if not treated. In this
phase major changes are fibrosis of udder, very tough hard mass of fiber, the quarter may
be atrophied which may persist for rest of life. There may be fibrotic mass particularly in
teat canal.
Aseptic/non specific Mastitis:
It is due to trauma or injury to the udder.
Major Pathogens Involved in Mastitis
Contagious Pathogens:
They spread from quarter to quarter through contamination by hands, flies,
wounds etc. They always require host e.g. Staph aureus, Mycoplasma, Pasteurella. They
have very limited life in environment. In Pakistan mastitis caused by Staph aureus and
Streptococcus agalectia is 70-80 % of mastitis and rest of it is caused by environment
(E.coli).
Environmental opportunist:
Coliform species like E.coli, Klebsella), Streptococcus uberis, etc.
Opportunist pathogens:
Staph other than Staph aureus
Endogenous pathogens:
Etiological agents of systemic diseases with mammary gland involvement like
Leptospira, Mycobacterium bovisetc.
Etiology of Mastitis
Due to various endogenous pathogens. Staph aureus is the most common bacteria.
70-80 % cows are infected by this. Streptococcus has been controlled 100 % and Staph
aureus 10 %. E.coli major (-ve) mastitis causing bacteria. Americans are facing
environmental mastitis.
Staph aureus
Staph means clusters and coccus means spheres. In blood agar culture they are in
the form of clusters of spheres. Staph aureus is the most common causative agent of
mastitis.
Milk in udder, teat tips, rectum, eyes, teat orifice, udder, vagina, naries of animal,
gut of flies, even milker’s hand, throat and naries are different sources of Staph aureus.
Similarly the contaminated milking machine cups are good source of Staph aureus.
Infected animals serve as reservoir for infection.
Pseudocapsules, α and ß toxins (produced during infection), Protein A (a part of
cell wal), Clumping factor C, and fibronectin binding protein are virulence factors of
Staph aureus.
Pseudocapsule provides protection to S. aureus and makes it inaccessible to neutrophils,
so no phagocytosis. α toxin causes cytotoxicity of neutrophils so killing defense cells of
the body. ß toxin causes the hemolysis. Protein A, part of cell wall, is very good character
and make the bacteria safe from the attack of host defense mechanism. Protein A binds
IgG at the Fc region (neutrophils attachment region) instead of the Fab (specific antigen
attachment of region) and interferes with antibody presentation region to neutrophils.
Correct attachment of IgG to the S. aureus cell wall is required in order to attract
neutrophils to the bacteria and trigger phagocytosis and bacterial killing. Clumping factor
C is required to attach the bacteria with host cells or gland cells or the protein surface of
mammary gland. Most common factor is A1. Fibronectin binding protein is also a source
of attachment of bacteria to host cell and after adhesion start multiplication and
multiplication develops infection.
S. aureus is transmitted through contact at the time of milking when milking man
moves from infected to healthy animal. The quarters of udder are separated. One quarter
if affected cannot affect the other quarter. Only the way of infection of other quarter is
contamination by milker’s hand.
S. aureus causes fibrosis and scar formation and it is defensive mechanism but
antibiotics cannot reach the udder due to scar formation.
In acute mastitis quarter may be swollen, temperature of animal 103-104 oF, and rarely
quarter become gangrenous and cold to touch. This condition is called as blue bag.
Streptococcus agalectia
It is the second most important pathogen. Broad zone hemolytic colonies, narrow
zone hemolytic colonies, and non hemolytic colonies on blood agar. Non hemolytic is
non pathogenic.
It is transmitted through contamination. It is controllable by using antibiotics
particularly penicillin is drug of choice. This bacterium affects the lower part of udder i.e.
duct system of mammary gland. It can also affect the tissue of udder as it blocks the duct
channels due to which milk stays in udder and causes scaring, involution, low production,
and clotting and accumulation of milk
Toxin produced by it may cause severe inflammation of udder and as a result of
this there is less milk production. It rarely affects generalized health but may cause
infection in humans and can enter in fetal body and affect in 0-7 days of pregnancy
(pneumonia, meningitis, hypotension, abdominal distension, fever, and jaundice).In late
stages meningitis and non specific bacteremia may lead to immunological disorder in
fetus and mostly abortion occurs. Mortality rate is 5-15 %. In America antibiotics are
used to control it in pregnant women.
Coliform Bacteria
Coliforms bacteria can be engulfed by neutrophils due to O, K, and H antigen,
recognized by phagocytes. Primary virulence factor is lipopolysaccharide present in cell
wall of G –ve bacteria (causes endogenous toxins production from LPS which destroys
the vessels and cause endotoxic shock.
E.coli has three sorts of antigen: somatic antigen present on cell wall i.e. ‘O’ Ag
(thermostable and lipopolysaccharide), K Ag (capsular), and H antigen (flageller Ag).
This organism does not require adhesion. It multiplies and survives in milk. It particularly
requires iron. So infection occurs in lactation phase due to availability of iron. In dry
period iron binding protein increases and the availability of iron is decreased. In case of
this organism infection is sudden.
LPS is present in cell wall of G –ve bacteria and that causes endogenous toxin
production and endotoxemia and bacteremia occur. LPS cause severe damage to blood
vessels and endotoxic shock. Severe inflammation and there is sudden appearance of
clinical signs and sometimes skin of udder may be ruptured and fluid may ooze out.
Sources of Mastitis
a. Hands of milker. Staph aureus is present on skin, naries of human if no proper
bath. He will shift from one herd to other.
b. Lack of proper management i.e. proper teat dipping is not carried out, no
antiseptic solution is used and no sanitation measures are taken.
c. Trauma during sitting posture or due to kicking udder or teats may be injured;
leading to mastitis.
d. Folded thumb milking particularly in villages damages the teat and causes
adhesion and increases the chances of mastitis.
e. In old animals teat canal is fragile and immune system is weak. So more chances
of infection.
Side Effects of Mastitis
It causes huge economic loss to dairy industry in the form of milk loss, medicine
charges, and discarded milk.
Pathogenesis of Mastitis
There are three phases of mastitis:
1. Invasive/invasion Phase:
It depends upon no. of bacteria; bacteria enter, multiply and increase in
population. So certain no. of bacteria is required for invasion. This determines the
infection rate. More no. of bacteria, severity increases. Any damage to teat canal provides
opportunity to bacteria to invade and multiply. Loose sphincter will also provide the
opportunity of entrance and adhesion to bacteria.
2. Infection Phase:
1. Whenever bacteria enter, the infection depends upon the nature of bacteria. If
highly pathogenic, then sever infection.
2. Some bacteria are susceptible to antibiotics and some are resistant. Staph aureus if
capsulated it resists and more chances of infection.
3. If less immunoglobulins present in udder or teat canal then more chances of
infection.
4. Pre existing leukocytes if more in no. less chances of infection. They cause
phagocytosis of bacteria. Cow having increased somatic cell count mean less
infection but low quality of milk.
5. Stages of lactation also help in the severity of infection e.g. in lactating phase
milk flow does not allow bacteria to attach. Similarly during lactation treatment is
difficult because antibiotics may flow in milk. Dry period is the best time to treat
mastitis because antibiotics will stay for longer time in udder. The best time for
infection is also the dry period; bacteria once entered, remain there and cause
infection.
3. Inflammation Phase:
Inflammation depends upon the pathogenecity of bacteria and the production of
endotoxins, particularly the endotoxins of S. aureus (α and ß) and E.coli that cause
damage to the capillaries of udder and cause the release of fluid in s/c parenchyma tissue.
In E.coli there is huge number of endotoxins and huge damage and inflammation. But in
S. aureus endotoxins cause less damage to the vessels. They cause chronic mastitis and
more fibrosis. Their ultimate target is to damage milk alveoli.
Clinical Findings of Mastitis
Abnormality in milk and udder. Milk colour and taste may be changed. There
may be plaques, clots, and blood in milk.
There is change in udder size; size increases in acute cases while in chronic cases
it decreases due to fibrosis and atrophy. Udder and teat will be small in size. Consistency
of udder is soft in acute and hard in chronic due to fibrosis. In case of endogenous spread
(like E.coli) systemic reaction may occur and cause temperature, anorexia, depression
and whenever increase in fever animal is off feed.
In acute mastitis udder is soft and hot. In S. aureus infection there is rise in
temperature in early stages. In case of streptococcus no rise in temperature while in case
of E.coli high temperature.
Forms of Mastitis on the Basis of Severity
Per acute: Generalized infection, temperature etc.
Acute: Severe inflammation but no temperature e.g. Staph
Subacute: Mild inflammation of udder and changes also in milk but no systemic
reaction. In buffalo mostly this type of mastitis is found.
Chronic: Acute may convert to chronic. S. aureus etc. cause it and there will be fibrosis,
hardness of udder and atrophy of udder and teat canal.
Forms of Mastitis on Clinical Basis
Subclinical: No gross changes. Increased number of somatic cell but no changes in
udder.
Clinical: changes in milk and udder
.
Diagnosis of Mastitis
Direct microscopic Method:
Make a slide and observe under microscope. Put 0.1 ml of milk sample on slide,
dry it and stain it with Newman Lampert’s Stain and then count somatic cells with the
help of microscope in certain area. Multiply the cell counted with a working factor of
microscope, it will give the number of cells per ml of milk. Normal milk contains 1 × 105
SCC/ml
Fossometer:
It counts the cells in the milk. It actually counts the wavelength of the cells.
NAGase Assay:
It is N-acetyl glucosamide enzyme (lysosomal enzyme). Its level increases due to
mastitis.
Indirect Method:
(a): California Mastitis Test:
A reagent is used in California test which is alkaline in nature. Whenever mastitis
occurs, there will be destruction of leukocytes due to phagocytosis. As a result DNA
content increases in milk which is acidic in nature and causes the increase in the acidity
of milk. Any alkaline reagent if added, it will neutralize the milk. The reagent added has
alkyl aryl sulfoxide which will cause the precipitation or gel formation in milk.
(b): Surf field Test:
Make 3 % surf field solution: add 6 teaspoons of surf in half litre water, mix it,
filter the solution and heat it. Then take equal volume of milk and solution, wait for
reaction.
Mild precipitation +
Flakes ++
Mild gel +++
Strong gel ++++
(c): Strip Cup Method:
It is the simplest method. Take few streaks in cups with black background and
observe the flakes or any other abnormality.
Take few streaks on ground. If the absorbance of streak is quick in ground then animal is
–ve for mastitis but if the absorbance is slow then milk is mastitic. Late absorbance is due
to pus. Mastitic milk is pus containing milk.
Treatment of Mastitis
We have to target three things:
(a): Specific treatment according to the cause
(b): Symptomatic treatment
(c): Supportive treatment.
First of all consider etiology. It is due to multiple causes. If want to treat S. aureus, it is
very difficult infection because it is intracellular and capsulated due to which antibiotics
do not reach the target it.
As early as you treat the animal you will get quick result but as you delay it, there
will be problem. Animal having mastitis of less than 2 weeks, there are more chances of
recovery i.e. 70 % but after two weeks there are fewer chances. Treatment depends upon
the severity or type of organism involved.
Veterinarian does not want to treat the chronic mastitis because chances of
recovery are very less as in case of chronic hepatitis. You cannot do anything.
Surf test or any other test should be repeated after two weeks. It is desirable to check after
every week. Animals which have three or four +ve should be treated as soon as possible.
Before giving antibiotic, culture sensitivity should be performed. Muller Hilton Agar is
used, inoculate the bacteria and put antibiotic disc on it containing different antibiotics.
Incubate it and transparent zones will be formed where bacteria are killed. The best
antibiotic disc is that whose MIC level is low i.e. the potency of antibiotic is low but
effectiveness is large.
S. aureus produces ß- lactase which is penicillinase enzyme. So for this purpose
although penicillin is drug of choice but with it we use anitpencillinase enzyme i.e.
Clavulenic acid e.g. Augmentin (clavulanic acid + Amoxycilline).
Some antibiotics are poorly distributed in udder like sulpha, amoxicillin,
gentamycin, kenamycin. Whenever given through I/M rout the best drugs to be given are
Macrolides (erythromycin, tilosin), oxytetracyclin, Cephlosporin, chlorofluracin, quinolin
(nor floxacin) (activity against intracellular bacteria). Tribersen (Sulpha and
trimethoprim) is also good.
The best approach is to give antibiotics through intramammry rout.
Intramammary tubes are also available like of tetracycline, chloromphenicol, tetradelta.
Short needle is best.
500mg valosef and cephradine (in powder form), add 40 ml distilled water and 3
or 4 ml dexamethasone (if animal not pregnant) and prednisilone. Take 30 ml syringe,
butterfly branulla no. 22 (plastic part) and put on needle and inject in mammary gland.
Above was for G +ve.
For G –ve Bacteria: First two generation of quinolone, enrofloxacin, flobiuon, nilidixic
acid, flimiquine, gentamycin but do not in udder. A new drug is cefquinone is highly
effective and use in E.coli.
For subsiding inflammation you may use steroids in acute inflammation otherwise
NSAIDS (diclofanic Na, cubixin, ketoprufin, flunixin meglumin, proxican)
Vitamins A, D3, E to increase immunity, vitamin C. AD3E (50 ml vial) (Fornet Pharma
Company), lysovit (immune enhancer), 50mg daily for 4-6 days
Zn, Cu, I: 2 g daily for 10 days. (Immunity enhancer trace elements).
Ground copper sulfate and dissolve in 250 ml water. Add it to ¼ litre of vinegar. Now
add these to 1 Kg wheat flour and add zink sulphate while heading. Make 15 boluses of
wheat dough. Give one bolus daily for 15 days.
Biotechnological products like Interleuken.1 and 2 are also used
Vaccination is also used in treatment because chances of reoccurrence and long
term
Usually the therapy is given for 5-7 days. As you increase the time duration of therapy
more the animal will recover. More chances or recovery if treatment for 7-8 days.
Treatment is most effective in dry period.
Principles/pharmacokinetics of Drug while Treating Mastitis
a. Drug should have low MIC (minimum inhibitory concentration)
b. Drug should have bioavailability through IM injection.
c. Drug should be basic, weakly acidic or none ionized in the serum so that may not
bind with the serum protein.
d. Drug should be lipophilic.
e. It should have long half life in udder.
f. It should be active/ penetrate well and active well when inflammatory reaction
should reach inflammatory secretion.
g. It should not remain for longer time in the body; complete plasma clearance.
Udder Toilet
It refers to infusing larger quantity of weak antiseptic solution into udder e.g. KMNO4,
acriflavin (1:10000). Remove milk from the udder and infuse 50 ml of KMNO4 and
remain there for 5 minutes and then remove out with the help of syringe cure has been
60-70%.
Permanent dry/block of Affected Quarter
If quarter do not respond to antibiotic. Infuse tincture iodine into that quarter, it will
cause irritation and block that quarter permanently. 50 ml of chlorhexadene (norbaseen)
can also be used.
BASIC REMEDIES
Garlic, lemon , ginger, red chilies, black pepper, black zera, dried ginger….dry for 5
days.Mix them sprinkle water and mix flour or wrap in newspaper. Give for 5 days.
250 ml lemon and 500 gram sugar may also be given.
250 gram garlic and 1000 ml milk is cooked and given to animal for 2-3 days.
Homeopathic Treatment
For fibrosis inject fibronil 5 ml
Belladona, Bryonia alba, SSC 30 c
Control of Mastitis
Two main objectives of control:
1. Prevention of new infection in the herd
2. Duration of existing infection should be reduced.
5 different plans to control mastitis devised by NMC (National Mastitis Council) in 1990.
a. Post milking teat dipping.
b. Pre milking teat dipping
c. Dry cow therapy
d. Prompt treatment of clinical cases.
e. Culling of chronic mastic animals from the herd
Post milking teat dipping:
Organism presents in environment and teat skin. In order to avoid it we go for post
milking dipping. After milking teat sphincter remain open for 30 minutes to 2 hours. It is
ideal time for entry of organism to teat canal. Teat cups are available having antiseptic in
it like iodofores (0.1-1 % iodine). Dip the teats one by one for 2-3 seconds.
Quarernary NH4 compound:
Chlorhixadine, sodium hypochlorite. Long term use of it may cause cracks in teat. To
recover it use Vaseline and some Vaseline mixed preparation but it helps to attach
organism to the teat.
Hand milking:
Person going to milk should also use lubricant for hands.
Pre Milking Teat Dipping:
With the same solution as above. Pre dipping is important but dry the teats after pre
dipping by towel or tissue.
Dry cow Therapy:
Infuse long action antibiotics persist for few days in udder. In dry period wax formation
occur and it will not allow the entry of any organism but if organism entered before wax
formation it will cause mastitis
Prompt Treatment of Clinical Cases:
Two ways of therapy routs:
Intramammary route antibiotics: cephradin, cephrapyrine.
Intramuscular route: Norfloxacin injection (14 days of parturition).
Combination of IM and intramammary injection.
Culling of Chronic Mastitic Animals:
Culling should be done of chronic mastitic animals if not possible then strategy is to milk
such animal at the last.
Managemental control:
Flies should be avoided; there should be balanced diet supplement with Zn, Cu, and
minerals; and proper disposal of mastitic milk.
Vaccination
Plane Staph aureus bactrin Dr. Shakoor
Polyvalent plain bactrin Dr. Athar
Oil based polyvalent vaccine Dr. Asif Yousif
Oil based montinide adjuvant Dr. Irfan Yousef
Bivalent Aluminium hydroxide adjuvant vaccine Dr. Tanveer
Mastivac (commercial vaccine) in USA
They provide protection for 6 months.
Dr. Irfan used Montinide adjuvant, ability to provide protection for one year. So people
are going for this.
Actinobacillosis
It is a disease of soft tissues, lymph node, and skin of oral or nasal region. Mostly
infection is on the tongue especially pharyngeal lymph nodes are involved. Tongue
becomes hard painful so also called as wooden tongue.
In sheep and goat LN will become swollen, hard, and ultimately burst and release pus.
Pus opens outside through many openings. Abscess formed varies from pea size to tennis
ball size.
Etiology:
Actinobacillus lignieressi is involved. It is normal inhabitant of nasal mucosa and oral
cavity. In any trauma of mucous membrane, this organism enters the body of animal
through nasal or oral mucosa. Rough fodder feeding lead to trauma of oral cavity.
Pathogenesis:
Organism enters the mucous membrane and multiplies there. It is localized infection and
may be multiplied and cause destruction of mucous cells and lymphocytes. So there is
accumulation of pus. When abscess mature this pus comes out through several openings.
When tongue is involved, it becomes hard and shrunken. Ultimately tortion of tongue
may occur. Animal will feel pain during mastication and prehention.
Clinical findings:
Severe inflammation of tongue, hyper salivation, anorexia, gentle chewing of tongue,
hard swollen tongue particularly at the base. Neck may be swollen. Nodule and ulcer
formation on lateral side of tongue. Nodules are replaced by fibrosis of tongue so it will
be shrunken and immobilized leading to permanent disorder. Parotid and submaxillary
LN will be swollen particularly in sheep goat. LN rupture and pus comes out. This pus
does not have smell. For small ruminants tongue involvement is not must. LN of lower
jaw, face and nose are swollen. Diameter of lesion is 8 cm (too large than tennis ball).
In small ruminants LN of cranial and cervical regions are swollen and have pus of yellow
green color containing small granules. Removal of pus from LN may lead to fibrosis,
making tissue hard.
Clinical Pathology:
Pus containing sulfur granules.
Post mortem:
No need to slaughter only take pus and nodule.
Treatment:
Decide those antibodies which should penetrate otherwise use iodine. NaI or KI will kill
pus.
KI
Oral rout 10g daily for 10 days in large animals. 2-3g/day till iodism develop. There may
be coughing, anorexia, dandruff, exudation, dry and scaly skin, and alopecia; it is iodism.
NaI:
1 g/12 Kg of body weight as 10 % solution I/V. It can not be given I/M, S/C or orally
because it is highly irritant and causes sloughing. Make sure needle is in the vessel. In
pregnant NaI may cause abortion. Give therapy after 24-48 hours of disappearing signs.
NI should be given in 2 doses. Repeat same dose after 10-14 days. If this condition
persists it could be given for 4-5 days.
Antibiotics:
Sulfonamide can be given for 3-5 days. Penicillin and streptomycin (5g streptomycin +
40 lac pencillin) may be given which may help in quick response. Inject 5 gram
streptomycin directly into the abscess. It may help in quick of animals.
Actinomycosis
Actinomyces bovis is involved. Main difference is of tissue. It affects hard tissue.
Pus formation on the bone of mandible but can develop on any other part. Lead to
formation of hard mass.
Same treatment as of actinobacillosis. Pus has focal smell. Problem is with mastication. It
is rare but bacillosis is common.
Tuberculosis
It is progressive disease in which emaciation of body occurs. Previously this
disease was diagnosed in 1890 due to Tubercle bacilli but now named as Mycobacterium
bovis. It can affect almost all species but sheep and horses are resistant to this infection.
In human it is caused by Mycobacterium tuberculosis.
Predisposing Factor:
Main factor is close contact in closed area. Large family in small areas, more chances of
infection. If ten animals reside and closely packed, chances are more.
Debilitating Factor:
Factors which cause emaciation: poor feeding, poor housing, lack of ventilation.
Sources of Disease:
Exhaled air, secretion of infected animals i.e. sputum, urine, semen, uterine discharges,
and milk, discharges from open peripheral LN.
Reingestion of sputum and excreted in feaces. So feaces contain organism. Wild animals
e.g. deer are the reservoir.
Mode of transmission:
Through inhalation and ingestion. In most of the cases lesions are present on lungs or
intestine. During grazing animal my ingest sputum of infected animal. Under natural
conditions animal having T.B drinks water from the pond of stagnant water and goes
away. That water remains contaminated for 80 days. Then other animals drink from that
water and get infection. In running water no such problem. Drinking infected milk, it is
more common in calves. Swelling of retropharyngeal lymph nodes by suckling infected
milk and due to this swelling calves are not able to swallow.
Intrauterine infections occur through coiter either from infected female or male. Zebu
cattle are more resistant particularly Sahiwal cow than Fresian. Incidence of T.B. in goats
is 70 %.
Zoonosis:
Milk man and men taking raw milk are more prone to this infection. 5-10 % cases have
been reported in human beings but in human the condition is not as severe as in animals.
Taking boiled and pasteurized milk has reduced it.
Pathogenesis:
Entry point → lesion → post primary complex dissemination
When animal inhales →. organism in lungs → necrotic fossi formation within 8 days →
calcification of lesions ( monocytes, granulocytes, plasma cells and they make a tubercle
at primary site). About 90-95 % dissemination occurs through this tubercle present in the
respiratory tract.
If organism ingested → no lesion at entry point → but ulceration of tonsils and intestinal
mucosa → in calves particularly swelling of retropharyngeal L.N.
If infection through intestine then first lesion form on liver → this primary complex leads
to milliory lesion on various organs of the body. It is typical sign of chronic T.B.
Clinical Signs:
Progressive emaciation, capricious appetite (goat like appetite), and fluctuating
temperature.
If respiratory tract: initially cough is low (once or twice a day) but with time loudness
increases, nasal discharge. Cough is more in morning and cold. Coughing can be induced
by palpating pharynx.
In case of digestive tract: rarely but if involve diarrhea, ingestion, swelling of L.N. lower
jaw becomes immoveable.
In reproductive tract abortion may occur.
In udder flakes present in last of milking streams in early phase but in later stage milk
becomes thin, watery and may have yellow flakes.
Diagnosis:
Single Intradermal Tuberculin Test:
Tuberculin is purified protein derivative of Mycobacterium bovis. It is more potent and
specific. Reaction time is 48-72 hours.
Test is more sensitive at 48-72 hours but more specific at 96 hours and if not after 96
hours then infection. 0.1 ml of tuberculin is injected to each animal of herd in cervical
fold of skin in centre of neck or anal and caudal region.
Inject 2 ml of tuberculin If animal is positive for T.B then; there will be diffused
swelling at injection site. It means animal is infected.
Disadvantage of this test is that it can not differentiate between M. avian and M. bovis
and M tuberculosis.
Short Thermal Test:
Inject 4 ml of tuberculin s/c in neck of animal having temperature 102.5 oF. Check
temperature after 2, 4, 6, and 8 hours. If increase in temperature after 2 hours of infection
then animal is positive. After 2 hours temperature may reach upto 104.5 F and it remains
upto 6 hours.
Store Mount Test:
Same as Short Thermal Test. Inject 0.1-0.2 ml of tuberculin and at the same place inject
second dose after 7 days. If increase in thickness of skin upto 5 cm within 24 hours then
animal is positive.
Comparative Tuberculin Test:
For comparison with Johne’s Disease which is number one killer in bovines. Inject avian
tuberculin at upper side of neck and inject bovine tuberculin 12 cm apart at lower side of
first injection at neck. Where is more swelling after 4-48 hours that is positive.
Avian tuberculin is used because it is antigenically similar to Jhone’s Disease. The
Johne’s organism i.e. Mycobacterium paratuberculosis and it is present intracellulary and
does not give good response to antibiotics.
Treatment:
No specific treatment available because very much expensive and time consuming. So
people prefer to slaughter but in humans available and 1-2 year therapy. There are
chances of reoccurrence of this disease as the organism is intracellular. Huge quantity of
antibiotics are required and for long term. It could be 2 months to 1 year.
Rifamyicin , erythromycin are the antibiotics used in human.
Supportive treatment: Good protein (eggs), poultry meat, & fruits (apple etc.) for 2
months.
Control:
Mainly it is based on the culling of infected animals. The animals which give +ve test for
tuberculin; start program to slaughter or cull the animals by burning or buried. In
slaughtering you have to keep in mind if calcified lesions more pronounced on pleura,
peritoneum, and liver extensive in nature; this animal should be burned or buried.
Test policy of herd should be adopted in all area until you achieve an incidence below 0.5
%. If incidence is higher than 0.5 % then test each and every animal every year until
incidence becomes 0.5 %. This incidence is not disease incidence but it is positive reactor
percentage.
Hurdles in control:
Wild animals and feral animals carry this organism. Feral buffaloes, cows and wild
animals may harbour this infection. Incidence of TB in buffalo is 10 %. If you do not
adopt the testing procedure then 10-20 % of total infected animals may die.
Hemorrhagic Septicemia/Pasturellosis
It also causes heavy losses in Livestock.
In NWFP: Peshawer Madran, Abottabad, Mansehra, DI Khan, Bannu, & Swat where it is
reported. (1988-89 survey).
Punjab:
Attock, Rawalpindi, Jehlum, Gujrat, Sergodha, Mianwali, Faisalabad, Jhang, Lahore,
Shekhupura, Gujranwala, Sialkot, Multan, Sahiwal, Muzafargarh, D. G. Khan and
Rahimyar Khan.
Sindh:
Karachi, Jacobabad, Sukher, Nawabshah, Hyderabad, Larkana, Kherpur.
Balouchistan:
Not reported.
In 1992, in Gujrat study showed that HS is the most important disease. In terms of
morbidity and mortality HS is one of the most important disease of buffalo and cattle in
Pakistan and it is considered no. 1 killer of buffalo. HS is caused by two serotypes of G
–ve, non motile, coccobacillus bacteria named as Pasteurella multocida (two serotypes
B: 2 & E: 2)
B indicates capsular Ag and no. 2 indicate somatic Ag. All manifestation of
disease is due to release of endotoxins of bacteria. Another factor is change in weather
like monsoon and low nutrition level and the pressure of work load.
In Asia B: 2 serotype is prevalent but in Africa E: 2 is also reported.
Disease is associated with humid weather; increase incidence of disease is
reported in wet season. It is evident that out breaks do occur in all times of the year but
those occurring during wet season spread rapidly because of the longer survival of
organism in the moist conditions. The disease is spread by direct or indirect contact. The
source of infection is infected animals or carriers. The causative agent does not survive
for more than 2-3 weeks in soil or pastures. Majority of cases are acute or peracute in
nature with death occurring from 6-24 hours in cattle and buffalo after the appearance of
signs.
Signs:
Dullness, reluctant to move, high body temperature, serous nasal discharge, salivation,
edematous swelling starts in throat region and then spread to parotid region and to the
neck. Mucous membranes are congested, difficult respiration and animal dies within few
hours. Recovery in buffalo is very rare than in cattle.
Diagnosis:
Field or clinical diagnosis is usually based on history, clinical signs, pathological lesion
observed on postmortem, previous occurrence of HS in the herd, endemicity of the area,
species affected, and vaccination history. For lab diagnosis, blood from the heart, liver,
lungs and spleen for smear and culture and staining can be done with Giemsa stain and
methylene blue stain. Pasteurella grows on common laboratory media like blood agar.
Haemagglutination test detecting somatic Ag.
Treatment:
It is caused by G –ve bacteria. So antibiotics affected for G –ve. In acute HS endotoxins
(component of cell wall) is the main cause of pathological changes and death of the
animal because endotoxins start arachidonic acid pathway resulting in production of
inflammation mediators like prostaglandins, leukotrienes which cause vasodilatation,
hypotension and other circulatory disturbances. So non steroidal anti-inflammatory
(dichlophanic Na) and steroids are given which have beneficial effects for stoppage of
endotoxins.
Bacteriostatic antibiotics: chlorotetracyclin, oxyclor P
Detoxifying agents: Novococc Forte (100 ml) it is given in diluted form through IV. If
direct then give s/c at different places.
Non steroids and steroids, dichlophanic Na,
Norfloxacin 5 % 25 ml (IM),
Enrotil (cephalosporin)
Vaccination program: alum precipitated vaccines are widely used. Oil adjuvant is used in
Pakistan
Chlostridial Myonecrosis or Black Quarter or
Black Leg Disease, Quarter Ill
It is an important disease of small ruminants. It affects skeletal muscles.
Chlostridium chouvei is anaerobe. This condition starts when tissue damage occurs.
It is acute bacterial, emphysematous, myonecrotic, highly fatal disease. Wide
range of ruminants are susceptible to this condition but cattle and sheep are more
susceptible of age of 6 months – 2 yeas but cattle below this age and above 6 years are
also susceptible.
This disease is more in summer and fall. It is widely distributed all over the world
occurring in all the countries mostly in hilly areas, sandy regions, more prevalent and this
is one of the most important causes of cattle mortality in sandy and hilly regions.
According to epidemiological survey it is an economically important disease of
livestock. When pasture or grazing grounds once become affected, the disease will
reappear regularly in susceptible animals year after year. Cl. chouvei is G +ve, spore
forming, anaerobic bacillus and spores are highly resistant to environmental influence
and disinfectants.
Transmission:
First entry is through alimentary mucosa after ingestion of contaminated feed or
eruption of teeth. Bacteria are found in spleen, liver and elementary tract of normal
animals. Contamination of soil and pasture occurs from infected feacal material or
decomposition of carcasses of animals dieing of this disease. Black quarter develops
when spores proliferate after the trauma or anoxia like conditions
Pathogenesis:
Spores are ingested though soil contaminated forage and localized in muscles,
they remain latent for indefinite period. Latent spores are not virulent and must be
activated to become pathogenic organism. Black quarter tissue damage creates a focal
anaerobic environment in which spores become activated and transform into vegetative
bacterial cells that proliferate locally in the host tissue. Pathogenesis is similar to the
other chlosrtidial disease. No. of toxins are produced like α toxins (necrotizing
leukosidin), ß toxin (doxyribonuclease enzyme), γ toxin (hyluronidase), and delta toxin
(hemolysin). These toxins are liberated by Cl. chouvei into tissue and resulting in muscle
necrosis and septicemia occurs. Exotoxins also cause hemolysis of RBCs and release Hb
which produces muscle lesions with dark red appearance. The characteristic rancid odour
is due to formation of butyric acid as an end product of Chlostridial fermentation and
finally toxemia is the cause of the death of the animal.
Clinical signs:
In small ruminants in black leg lesions occur in limb musculature and results in
stiffness of gait. Animal is disinclined to move because of severe lameness in one or
more limbs. S/C edema and gaseous creptation develops. They develop just before the
death of animal. Discoloration of the skin occurs but skin necrosis and gangrene develop
in the later stages. In cases where infection occurs through the wounds of the skin or
lesions are present on the head there will be severe local swelling due to edema, bleeding
from nose, high fever, anorexia, depression and in later stages death due to toxemia.. In
sheep and goat death is due to development of cardiomyositis. In cattle there will be high
fever, gaseous swelling under skin mainly on hind quarter and shoulder. Stiffness or
limping of one leg. Gaseous swelling may develop in other parts of the body as well like
neck, chest and flanks. At the beginning swellings are hot, painful and limited later they
become larger, cold and painless. Skin over the swellings becomes dry, hard to dark in
colour and on palpation, creptation is felt.
Other symptoms include less appetite, cessation of rumination, rapid breathing,
depression and death of animal within 24-48 hours. Affected animal may die without
showing signs.
Diagnosis:
On the basis of age, season, swelling on specific area. Make smear, gram staining
and observe clostridium.
Treatment:
Treatment must be in time within 24-48 hours. For specific treatment provision of
oxytetracyclin 10 mg/kg b.w. (IV).
(Oxytetracyclin is very irritant in small ruminants and usually not given but in this case
given. Now a days oxytetracyclin and lignocane or xylocane in combination are available
to avoid pain but when given IV, it should not be with lignocane . It can cause cardiac
arrest.
Multivitamins: biodil (injection) IM/IV/SC/ 2-4 ml with 24 hours interval, 3-4 injections
are sufficient (sheep, goat), in cattle 20 ml with 48 hours interval.
Metabolase: 20-40 ml/10 Kg s/c, IV, intraperitoneal (sheep, goat), in cattle 250 ml
Vitamin AD3E 2-4 ml (small ruminants) I/V, s/c, I/P
Aini vicom: 1-1.5 ml/ 5Kg (small ruminants), 0.3-0.5 ml/Kg fpr ;afge animal.
Butadine (good in equine) 15-20 ml on alternate day (large ruminants),1 ml/10 Kg (small
ruminants)
Solon- M injection (prednisilon + antihistamin) 5 ml small, 10 ml large. It is anti-
inflammatory, analgesic and antipyretic.
Prednicorol D: (prednsilon and dexa)
Prevention:
Dead animals are potential source of it. So dead animals should be burned.
Vaccination:
Alum precipitated formalized vaccine prepared from Cl. Chouvei in first week of April.
First injection conquers immunity for 6 months but if boost injection is given after 15
days of first infection then it will provide immunity for one year. Dose rate: 5 ml for 275
Kg b.wt.
Allergic reaction can develop so for it adrenalin (2-5 ml s/c) and prednisilone (4-10 ml
I/M in non pregnant)
Ultra filtered toxoid of local Cl. Strain but it is not used in our country. Vaccine is
prepared by VRI.
Enterotoxaemia
Toxemia originating from intestine. Cl. perfringens present in intestine. It is G
+ve anaerobic bacteria. Enterotoxemia vaccination 1 cc for lamb, 5 cc for sheep. Now a
days multivalent vaccine is used internationally. Acute diarrhea and sudden death. This
disease mostly occurs in highly fed animals and mostly this disease is seen in lambs and
calved fed on high lactating animals.
This bacteria is normally expelled from intestine when peristaltic movements occur but if
highly fed peristaltic movements become slow and bacteria get chance to stay and
anaerobic conditions will favour to grow and multiply. Toxins are released. Mostly affect
capillaries, permeability is increased. If does not cause bacteremia, it will only cause
toxemia. Only toxins came in blood and cause diarrhea and pulpy kidney disease.
Control:
Avoid excessive feeding. In winter give oil (20-100 ml). Vegetable oil in adult animals
after every 15 days.
(Solution of pollution is dilution)
Treatment:
Ringer lactate D, dextrose
Give fluid and diuretics (manitol is best diuretic because it has no effect on kidney) for 2-
3 days. Penicillin 5 g orally.
Contagious Caprine Pleuropneumonia
Mycoplasma capricolum sub species capripneumonia. It is very fatal disease in goats and
have incubation period of 6-10 days. Its infectivity is high with 100 % morbidity. Illness
is acute and severe with mortality rate from 60-100 %. Transmission of this infectious
agent is by inhalation. Organism does not survive outside the body for long time and
infection is brought into the flock by a carrier of infected animal.
Clinical findings:
Coughing, dyspnea, animal lies down on the ground; temperature may raise upto 104-106
o
F, mouth breathing, tongue protrusion, and frothy salivation.
Clinical Pathology:
Ag is detected by polymerase chain reaction. Sample is taken from lung tissue and
pleural fluid. Serological tests include CFT, ELISA, & Latex agglutination test.
Postmortem finding:
Lesions are restricted to the lungs and pleura. Freeze dry method should be used for
storage or when sent to lab.
Differential Diagnosis:
Mycoplasma capricolum infection, M mycoides. These infections have similar signs.
Treatment:
When you are confirm that it is mycoplasma infection. Then drug of choice is tylosine 10
mg/Kg. b.wt. Oxytetracycline 15 mg/ Kg b. wt. is also given.
Treated animals after recovery remain carrier of it. Vaccination is done in Oct-Nov (0.5-
1cc)
Tick pyemia of Lambs
Enzootic Staphylococcosis of Lamb
From septicemia produce by Staphylococcus aureus. Pre disposed by infection of
Ehrlichia phagocytophilum which is transmitted by Ixodes ricinus. It causes tick borne
fever which in turn creates factors favoring the development of pyemia.
Pathogenesis:
Ticks transmit the Ehrlichia and lymphocytopenia develops six days after infectin. T and
B lymphocytes are affected and neutropenia remain for 2-3 weeks. There will be severe
thrombocytopaenia. 70 % of neutrophils are parasitized. Lambs with parasitemia have
high susceptibility to Staphylococcus infection.
Clinical Findings:
Lambs 2-10 weeks of age are more susceptible. Infection is localized in joints, muscles,
tendon sheaths, and CNS. (Arthritis and meningitis)
Post mortem finding:
Abscess formation on tendons, muscle, skin, joints and other viscera.
Treatment & control:
Long acting antibiotic like Oxytetracyclin is given.
Ticks should be controlled. Dipping of animals should be done regularly. e.g.
Cypermethrin preparation (Ecofleece)1 ml for 1 litre water. Ivomec like preparation.
Corynibacterium Paratuberculosis
This organism has two biotypes. Biotype 1 is responsible for condition in small
ruminants. Biotype 2 is responsible for condition in equines and cattle.
The condition caused by it is called as Ulcerative lymphangitis in equines and cattle.
Corynibacterium paratuberculosis is involved. Infection is of skin wounds, lymphatic
vessels. In cattle s/c abscess are seen in summer, and in winter ulcerative dermatitis of
foot heel. In coetaneous form there will be single or multiple painful abscesses even on
s/c tissue on head, flanks, shoulder, neck region, hind legs and ruptured abscess. It will
discharge blood stained yellowish pus. Necrotic and ulcerative dermatitis of heels of feet
will create lameness and edematous swelling on digital part of the leg.
In horses initial wound infection is followed by swelling of pastern region causing severe
lameness. There will be involvement of lymphatic and abscess formation.
In sheep and goat it is termed as caseous lymphadenitis of sheep also called as cheesy
glands or pseudotuberculosis. It is rare in goats as compared to sheep.
It is a chronic sheep disease characterized by greenish yellow abscess in lymph nodes
with little effect on health. Biotypes are caprine biotype and ovine biotype. These
biotypes produce exotoxins. Phospholipidase-D, and toxic lipid cell wall are the factors
which stop phagocytosis.
Sources of infection:
Infected animals are primary habitat of the micro organism. Source of infection is
discharge from ruptured, abscessed, superficial lymph nodes and the nasal or oral
secretion from animal with pulmonary abscess drainage into brachial tree.
Microorganism can survive in the pus, infected soil for eight months, in infected shearing
shed for four months, on straw, hey for two months. Low temperature and moisture
prolong its survival time.
Transmission:
Infection of the animal is facilitated by skin wound. Transmission is by direct contact
with infected discharges, by shearing equipments, contaminated dipping fluid and dust of
the shed area.
Clinical Signs:
Abscesses are easily palpable and abscess on lymph nodes and green pus. Inflammation
of superficial L.N, submixillary, prescapular, pre crural (in flank region), inguinal LN,
supra mammary LN. Abscess may occur on any organ like lung, liver, kidney and is
palpable easily. Abscess is commonly ruptured with creamy caseated pus and there is no
foul smell. In cases where systemic involvement occurs, here will be chronic pneumonia,
polynephritis and other complications depending upon site of infection. Local infection
from supra mammary gland to mammary tissue results in low production, poor growth
and death in lambs. In rams development of intrascrotal lesions.
Treatment:
Surgically remove pus form lymph nodes. Locally inject the penicillin at various sites.
Aminoglycosides should not be given in it like gentamycin; penicillin and tetracycline
should be given.
Listeriosis
Its causative agent is Listeria monocytogenes.
Susceptible:
Mostly sheep but also in other ruminants. It has 16 serotypes on the basis of flageller or
somatic Ag. Virulent strain multiply in macrophages and monocytes and produce
Lesteriolysin O (major virulent factor) and can grow on wide range of pH i.e. from 4.5 to
9.6.
Organism is susceptible to almost all common disinfectants. It is wide spread in nature.
Primarily the disease of ruminants, there may be development of encephalitis, pregnant
animal may abort, spinal myelitus, septicemic disease, ophthelmitis, gastroenteritis and
rare chances of development of mastitis.
Sources f Infection:
Organism is common in environment and infection is not limited jut to the animals, but
mammals, birds, insects, fish. Organism can be isolated from animal fecal material, soil
water trough, animal feed, walls and floor of farm, animal itself can be source of Listeria.
Most of its complication is due to presence of this organism in silage. It is commonly
present in silage but do not multiply in properly fermented silage whose pH is below 4.5.
Transmission:
Lambs can ingest contaminated feed, or it may be congenital disease is due to naval
infection. Encephalitis form of disease results from the infection of the nerves after some
injury to the buccal mucosa from feed or infection of the tooth cavities and browsing.
Spinal myelitus occurs due to involvement of spinal nerves; there are certain risk factors
that help in multiplication of microorganism. Weak the host resistance mechanism. Poor
nutrition of the animal Sudden change of weather.
Spinal mellitus: weakness of hind limb, paralysis of forelimb, constriction of pupil, iris
swelling, and corneal ulceration of mostly found dead. If survive, green colour feaces.
Animal is weak lethargy.
Differential Diagnosis:
Encephalitis, middle ear disease, polioencephalomaletia, rabies, nervous ketosis on cattle,
gid , pregnancy toxemia in sheep if enteritis problem then differentiate from
salmonellosis..
Zoonosis:
Listeriosos is a feed born disease in humans e.g. milk products and raw milk
contaminated with Listeria through feacal material or valerians aim treating dystokia may
get dermatitis. Conjunctivitis may occur in humans.
Pathogenesis:
Ingestion of microorganism… penetration in musosa of intestine…. Inapparent infection
with prolong faecal excretion of microorganism to a subclinical bacteremia which clears
with the development of immunity, bacteremia is subclinical and microorganism is
excreted in milk. Splenic Listeriosis with or without menegitis occurs in new born
ruminants and pregnant sheep and goats. Listeria monocytogenes is a facultative
intracellular pathogen that can infect cells including intestinal cells by direct endocytosis.
It can survive in macrophages and monocytes. Bacterial superoxide dismutase protects
against bactericidal activity of phagocytes and listereolysin O damages the lysosomal
membrane allowing the microorganism to grow in cytoplasm. In pregnant animals,
invasion of placenta and fetus occur within 24 hours of onset of bacteremia, edema and
necrosis of placenta leads to abortion, 5-10 days post infection or newly born young ones
they may suffer from fetal septicemia. Encephalitis occurs due to acute inflammation of
brain stem and is unilateral. Portal of entry is ascending infection is on the nerves (cranial
and trigeminal nerves). Spinal myelitus mastitis.
Necropsy finding:
Microabscesses in intestine
Clinical pathology:
CFT, agglutination test.
Clinical signs:
Flock depressed, fever (104-107), in coordination, head deviation (tilting), walking in
circles, unilateral facial hypelgesia (pain sensitivity decreased), facial paralysis, dropping
of ears, lips paralysis, third eye lid paralysis (ptoris), panopthalmitis (pus in anterior
chamber of one or both eyes), prehention and mastication become slow, drooling of
saliva, food hanging from mouth.
Duration of disease in cattle is 2-3 weeds while in sheep and goat is 2-4 days. If Listerial
abortion in last trimester, retention of placenta, fever 107 0F, abortion assert soon after
commencement of silage feeding, retained placenta, blood stained vaginal discharge for
several days.
Septicemic Listeriosis::
Depression, weakness, fever, diarrhea, death within 12 hours. In case of mastitis single or
both quarters are involved, somatic cell count increased but milk remains normal.
Treatment:
Chlorotetracyclin 10 mg per Kg body weight.
Penicillin 44000 IU/Kg b. wt I/M for 7 days or may continue upto 14 days.
Fluid therapy. Atropine, corticosteroid.
Diseases caused by Pasteurella spp.
Pasteurella spp. Occurs in many animal and act as primary cause and in some condition
as secondary cause e.g. in viral pneumonia like condition and it converts the condition in
major economic loss to farmer.
Diseases caused by Pasteurella multocida
Menengeoencephalitis of calves and young cattle: nervous signs, coma like condition and
death within few hours.
Lymphadenitis: in lambs. Enlargement of submendibular, cranial, cervica land pre
scapular lymph nodes.
Mastitis: secondary cause
Diseases caused by Pasteurella hemolytica
Incoordination, paralysis of tongue and blindness and death within 1-7 days after
commencement of illness. Also causes fatal septicemia in equines.
Pneumonic Pasteurellosis of Cattle:
Caused by P.hemolytica biotype A. P. multoicda biotype A (fibrinopurulent
bronchopneumonia), coagulation, necrosis demarcated by leukocytes considered to be a
pathignomonic lesion.
Pasteurella of sheep and goat:
P. hemolytica. it causes pneumonia and septicemia in lambs
Vaccines from VRI
Sheep/goat pox:
Twice a year first in first week of March. Second vaccine in first weed of September.
Sheep/goat cell culture vaccine: it is an attenuated like virus cell culture vaccine. It is
grown on prime kid kidney. Vaccine is safe for pregnant goat as well Strain is RM-65.
100 doses packing. 1 ml s/c. use within 1-2 hours.
Listeriosis:
It is a formalized bactrin of a local strain. Vaccine twice a year in March and September.
300 ml packing. 5ml s/c (60 doses)
Caprine pleuropneuminia:
Formalized culture of mycoplasma mycoids. 1 ml s/c. prepare in 20 % serum
mycoplasma broth. 100 doses.
HS:
VRI, NIAB
Alum precipitated bactrin of local strain of P. multocida Robert type 1
300 ml packing 60 doses
5ml for 300 Kg body s/c
Booster dose is necessary for calves after 4 weeks of first vaccination. Second one is oil
adjuvant.
Bacillary Haemoglobinuria
Its causative organism is Chlostridium haemolyticum it provides hemolytic toxin
(lysis of blood). These are spore forming, G +ve, anaerobic bacteria. In infected animal,
organism is found in liver of healthy animal. Whenever animal ingest organism it is
lodged in liver. Association of this disease is with poorly drained pasture or more
irrigated pasture because of presence of liver fluke or snails and in summer and in
autumn.
Pathogenesis:
Organism is ingested through contaminated feed. It enters into animal, lodges in liver,.
Liver fluke invasion: infarct areas due to necrosis of liver tissue or portal vein thrombus
or due to Fusebacterium necrobacillosis or due to cysticercus. These infarct areas are site
for proliferation of Clhlostridium. They produce hemolytic toxin and go into blood and
cause systemic toxemia and also cause vascular damage.
Clinical signs:
There is fever (106 oF) but in terminal stages sub normal temperature, off feed, anorexia,
week and anemic animal, jaundice, abortion. Blood in urine (haemoglobinuria); dark red
colour urine.
Treatment:
First specific/immediate treatment: antitoxic serum, penicillin, tetracycline (6-10 mg/Kg),
20,000-40,000 IU/Kg in large animals. By this treatment haemoglobinuria disappear
within 12 hours.
In supportive treatment: blood transfusion, fluid therapy, haemopiotic drugs (iron or
copper), liver tonic (hepamer).
Control:
Vaccination: 4-6 week before expected season, pasture management.
Differential Diagnosis:
Hematuria (intact blood in urine). This condition develops in kidney infection or in
trauma of urinogenital tract. In this case RBCs will settle down at bottom.
Lysed blood mostly in parturient hemoglobinuria, babisiasis, theleriasis. But in parturient
haemoglobinuria: no toxemia, deficiency of phosphorus, oxidants are more in amount in
feed, fever does not occur, non responsive to antibiotics.
In babesiasis and theleriasis parasite present is seen in blood smear, staining with Giemsa
stain. If red water haematuria due to phosphorus deficiency then urine colour will be
chocolate coloured. In haemoglobinuria temperature remains increased. If phosphorus
deficiency then wall of RBC will become fragile as phosphorus is required for the
formation of cell wall. When it breaks down the RBCs will be lysed and come to urine.
Theleria and babesia: dark yellow colour. When parasites are present in RBC then animal
suffer fever and when RBCs burst, fever falls down. So intermittent fever and they are
not treated with antibiotics. Animal will not respond to antibiotics.
Pseudotuberculosis/Johne’s Disease
It is chronic infection of intestine, mostly present in cattle, sheep, and goat.
Disease named after Henry Johne in
Transmission:
By nursing of calf by infected dam. Organism shed directly in colostrums and milk and
through contaminated feed. It also have oral feacal route. Also transmitted from dam to
fetus also present in genitalia.
Most important is infection occurs under thirty days of age and incubation period is very
long so clinical signs appear at 3-5 years of age.
Organism is also transmitted by trade.
Pathogenesis:
Organism → ingestion → localized in small intestine → phagocytosized by microphages
→ do not able to change in phagolysosome, so organism remain viable in microphages
(infected macrophages) → immune system fight against macrophages as a result injuries
to epithelium of intestine due to which malbsorption, hypoproteinemia and diarrhea
occur. This disease is also called the tuberculosis of intestine.
Clinical Findings:
Stage one is silent stage in which no clinical signs and occur in younger animals, carrier
but healthy.
In subclinical stage animal becomes carrier and potential source of infection. It is at adult
stage.
In clinical stage chronic diarrhea with presence of air bubbles and no odour, feed intake is
normal, all other parameters normal but more thirst.
In advanced clinical stage emaciation, dehydration and ultimately death.
Treatment:
No treatment is recommended. But in this disease streptomycin (50 mg/kg b. wt.) or
isoziazid (for T.B) (20 mg/Kg b. wt. for 100 days.
Losses:
Low milk production, low feed efficiency, more chances of infertility and mastitis, pr
mature culling
Diagnosis:
Blood test, ELISA, faecal examination.
There is a tuberclin like test in which Mycobecterium is injected in the neck of animal. If
swelling occurs after 48-72 hours, test is positive.
Zoonosis:
Chronic inflammatory disease 7.5-38 %, Corhen disease. Mycobacterium avium is
isolated from the patient of Corhen Disease. It may be due to consumption of
unpasteurized milk.
Botulism
Botulism is and intoxication (infection of perform toxin) not an infection. It is caused by
the ingestion of toxin in food
Etiology:
Cl. botulinum is anaerobic spore forming. clostridium spores are lethal in vdgetation
form.
Strain of Cl. Botulinum: there are seven types A, B c1, E, F, and G. Most susceptible type
is Type A. it is found in neutral and alkaline soil. Type D is found in alkalinesoil while
type B & E are found in damp soil. Type G is found in acidic soil.
Sources: the usual source of the toxin is decaying carcasses or vegetable materials such as
decayng grass, hay,grain, spoiled silage, and cane food.
Toxificatious Botulism
this name is given to the disease in which C. botulinum grows in tissues of a living
animal and produces toxins there. The toxins are liberated during the Shaker foal
syndrome.
Pathogenesis:
Toxin is the neurotoxic.
Prefoemed toxin → Blood → Neuromuscular junction → block of ACH → flaccid
Paralysis
There will be paralysis of hind quarter
Chances of hind quarter → fore quarter → neck → movement of eye ball and head and
medriasis is frequent.
Diagnosis:
History.
Treatment:
We give drug which counteract the blockage of ACH Guanidine HCl (11 mg/Kg).
Antiserum is also given
Control:
Dietary deficiency should be fulfilled, and carcass should be disposed off.decaying grass
and spoiled silage should not be offered.
Anthrax
Anthrax is originated from Greek word means coal. Other names are spleenic
fever, woolsorter’s disease. Locally it called as golle or sut.
It is an acute, contagious and septicemic disease. Highly fatal and affecting a wide
range of mammalian species including human beings. Before the availability of an
effective vaccine, anthrax was one of the most important causes of death in livestock
throughout the world. It became available in late 1930. The western countries have
controlled but fatal in underdeveloped countries. The results of national epidemiological
survey of important diseases of livestock in Pakistan has indicated that anthrax is one of
the leading causes of death among sheep, goat cattle in hilly and desert areas. Anthrax
occurs in all vertebrates but it is more common in cattle and sheep and less frequent in
horses and goats. Humans occupy an intermediate position. Dogs and cats are relatively
resistant.
Anthrax is caused by a bacterium known as Bacillus anthracis. The organism is G
+ve, non motile, aerobic, facultative anaerobe and spore forming. There are two forms of
this organism: vegetative and spore forming. Vegetative form occurs inside the body of
affected animals and is responsible for producing clinical signs and pathological lesions.
The spore formation occurs outside the body of host and is the result of exposure of
vegetative form to oxygen.
When disease is septicemic (usually in herbivores); blood secretion, excretion
(urine and feaces) and tissues of affected animals are filled with vegetative form of B.
anthracis. If carcass is not opened, the vegetative form of organism will die within few
hours.
Transfer:
Mostly animals are infected while grazing in areas that have previously
experienced anthrax.
The spores are also transmitted through the consumption of contaminated water,
hay, and fodder.
Eating of bone meal and blood meal of infected animals also cause transmission.
Eating of dry fodder or spiky grass produces lesions in gastrointestinal mucosa,
and the chances of infection are increased.
Flies are also a source of transmission.
Zoonosis:
In developing countries it is a major cause of human illness. It is a serious cause
of mortality in humans who eat infected meat and develop alimentary form of disease.
Cutaneous form occurs in veterinarian following postmortem examination of carcass
infected with anthrax and lesions are mostly restricted to fore arms and neck.
Pathogenesis:
Upon ingestion of spores, infection occurs through intact mucous membrane,
through defects in epithelium around erupting teeth or through scratches form tough and
fibrous food materials. Organism is resistant to phagocytosis due to Poly D glutamic acid
in capsule. It proliferates in regional draining lymph nodes passing through lymphatic
vessels into blood stream, causing septicemia. Bacillus anthracis produces lethal lesions
that cause edema and tissue damage. Death occurs due to shock, acute renal failure and
anorexia.
Clinical Findings:
Its incubation period is 1-2 weeks, some says 7 weeks. Most common sign of
disease is sudden death. In cattle and sheep there are three forms of disease:
Peracute: It is most common at the beginning of out break. Animals are found dead
without signs. Course of disease is only two hours. Signs may be fever, dyspnia,
congestion of mucosa and muscle tremor and animal dies after convulsion. After death
there is discharge of blood from natural orifices (mouth, nostrils, anus, vulva etc.).
Acute: Course of disease is 48 hours. There is severe depression, increased body
temperature upto 107 oF, rapid and deep respiration, and congested mucosal lining.
Pathogenic signs are congestion of mucous membrane, hemorrhage from natural orifices,
increased heart rate, animal off feed, ruminal stasis, abortion in pregnant cows, blood
stained or deep yellow milk, diarrhea, dysentery, and local edema of tongue
Chronic: Chronic infection is characterized by localized, subcutaneous, edematous
swelling that can be quite extensive. Areas most frequently involved are ventral neck,
thorax, and shoulders.
Diagnosis:
It is based on the history of the occurrence of disease in an area, then clinical
signs, necropsy findings.
Post mortem is not allowed. But if by mistake the carcass is opened, septicemic
lesions are seen. Blood is dark, thickened, and hemolysed and fails to clot readily. Dark
clotted blood in spleen. Spleen is enlarged, soft and hemorrhagic. The apparent petechial
hemorrhages may be visible throughout the organs. Intestinal mucosa is dark red and
edematous with areas of necrosis. The carcass undergoes rapid purification. Small
hemorrhages are detectable in mucosa of serous membranes and subcutaneous tissues.
There is accumulation of blood stained fluid in serous cavities and gelatinous fluid in
loose connective tissue.
To prepare blood smear, blood is obtained from ear by giving incision. Blood film
should be dried and fixed by heat or immersion for one minute in absolute methanol and
stained with polychrome methylene blue. Then it is washed after thirty seconds into
hypochlorite solution. After drying the slide, it is examined under microscope for reddish
purple capsular material and deep blue Bacilli. This reaction is termed as M- Fadyean
reaction.
Treatment:
Because it is rapid in onset and with large mortality rate upto 90 %, this is
insufficient to initiate treatment before death. If anthrax is suspected, segregation of
animal should be done. Early supportive and antimicrobial therapy is useful and Bacillus
anthracis is highly susceptible to a wide range of antibiotics including benzylpenicillin @
200,000-400,000 IU / Kg, tetracycline, and ciprofloxacin.
First dose of antibiotic should be administered I/V and then I/M for 5 days. Serum is also
available with dose rate of 50-100 ml s/c 2-4 times per day. Prognosis is not favourable
and no time to treat the animal.
Differential Diagnosis:
In cattle and buffalo differentiate it from acute fatal blot, per acute babesiasis,
gross tetany, black quarter, acute poisoning, and enteritis. Anthrax should be considered
in differential diagnosis when an animal dies after having observed apparently good
health during the preceding 24 hours.
Control Strategy for Anthrax:
Control measure aim is to break the cycle of infection. The important thing is to
correct the disposal of carcasses. When a cow or buffalo dies inside a shed, paddle or
barn, its carcass should be received for burial incineration.
Plug the natural orifices properly before disposing carcass. Burial should be away from
water supply and pasture.
The pit should be 180 cm deep. The top layer after burying should be covered with
unslacked lime. Decontaminate the area, bedding, unconsumed feed, and room. Dip the
equipments in 4 % formaldehyde solution for 12 hours.
Vaccination:
VRI has developed anthrax spore vaccine. It is a suspension of live, attenuated
spores of non-capsulated Bacillus anthracis in glycerin saline. It imparts solid immunity
for one year. Packing contains 300 ml. Its shelf life is one year. Its dosage in cattle,
buffalo, and horse is 1 ml s/c; in sheep and goat it is 0.5 ml.
Lectures of Systemic Medicine-1
(Med 404)
(Final)
Peste Des Petits Ruminants
This is most common in sheep and goats. Its name is of Latin and petits means small
ruminants. It is highly contagious viral infection. Virus is genetically close to
Morbillivirus (rinderpest) and called as PPR virus. First time reported in 1942 in Africa,
now in Turkey, Saudi Arabia, Pakistan, Bangladesh, India, and Nepal. In Pakistan it was
started in 1990; first time cases were reported in Lahore in 1994. This condition is
prevalent in all four provinces and Azad Kashmir but locally no name in these provinces
except Kata in Punjab.
Transmission:
Disease is transmitted from diseased animal to healthy animals through saliva, milk,
feacal material; when healthy and diseased animal are kept together or fed together. So
isolate the diseased animal from healthy animals.
Pathogenesis:
Virus penetrates retropharyngial mucosa, causes viremia and finally damages the
alimentary tract, respiratory tract, and lymphoid system. Necrosis starts in cells and death
of animal occurs due to diarrhea and dehydration.
Symptoms:
At a time whole herd may be affected. Mortality may reach upto 50 %; high in young
animals. There is 50 % loss in weight and low production in survived animals. Signs of
disease appear 4-6 days after viral attack. Temperature may raise upto 106 oF. Animal
seems sleepy. Animal is under stress, isolated from herd, off feed, and drinks more water
than normal. There is mucoid discharge from eyes and nostrils. There is conjuctivitis.
Gums, palate, and tongue have small wounds initially and foamy salivation; with the
passage of time necrotic lesions on tongue and gums develop. There is swelling of the
lips. There is heavy deposition of necrotic mass on gums which can be removed with
finger. Foul odour from the mouth. Watery feaces sometimes blood mixed. Respiratory
rate increases and there is coughing. Pregnant animal may abort. Death may occur due to
dehydration after 6-10 days.
Post Mortem Findings:
Sunken eyes, dry and loose skin, wounds in oral cavity and nostrils; mucopurulent
material in nostrils and respiratory tract; inflammation of large intestine; zebra strips (it is
characteristics of post mortem findings of RP and PPR); and necrotic lesions on spleen.
Serological Tests:
Serological tests, signs and symptoms.
Treatment:
No specific treatment; but rely on symptomatic treatment. Give antibiotics (broad
spectrum) which are related to digestive system and respiratory system.
Enrofloxacin: 5-12 mg/Kg b. wt for example:
Encure: 1 ml for 40 Kg b. wt for 5 days
Enrotil (10 %): 0.5 ml/20Kg b. wt I/M, s/c
Tyslosine (20%): 0.02-0.05 ml/Kg b. wt. I/M (specific for respiratory system)
Gentamysine: 2 ml/50 kg b. wt. e.g. Gentalin.
Scour-x syrup (antidiarrheal) 6 ml/5 Kg.
Anti inflammatory drugs like loxin, avil, NSAIDS.
For fluid therapy give ringer solution, ORS, normal saline etc. (Never give
dextrose in case of diarrhea).
Separate healthy animals from diseased animals.
Foot & Mouth Disease
It is an infectious disease; known throughout the world due to economic loses. It is
causing more losses in cattle as compared to buffalos. After recovery the production of
animal decreases.
NWFP: Peshawar, Swat.
Punjab: Attack, Rawalpindi, Gujrat, Sargodha, Mianwali, Faisalabad, Lahore,
Sheikhupura, Sialkot, Multan, DG Khan, Muzaffargarh and Rahim Yar Khan.
Sindh: Karachi, and Hyderabad.
There are four types of virus causing FMD. Type A, type C, type Asia 1, and type O have
been identified in Pakistan; the antigenic difference among various types and sub types is
the main problem in the control of the disease. So regular typing and sub typing of virus
should be done and field strains should be added into vaccine. Mostly cattle and exotic
breeds are susceptible. Mouth lesions are more severe in cattle and foot lesions are more
severe in buffalo. In 1992 study showed that cattle are more susceptible. Disease is not
fatal but cause economic losses.
Some Factors due to Which FMD is not Controlled in
Pakistan
o In Pakistan numerous natural and socio-economic problems made the control of
FMD very difficult.
o Occurrence of different serotypes, subtypes and frequent mutation is one of the
major problems in control of FMD. Apart from 7 serotypes there are several
subtypes that are ontogenetically and immunologically different and do not
provide cross protection. About 80-88 subtypes have been identified.
o New antigenic subtypes are constantly emerging. Animals which are immune
against one subtype remain susceptible to the emerging subtype.
o Quality of vaccine: in our area trivalent (A, O, Asia 1) vaccine is given having
three serotypes but most of the times FMD contains newly emerging strains which
lead to failure of vaccine.
o Lack of comprehensive vaccination program.
o FMD virus is quite resistant even to commonly used disinfectants.
o There is lack of quarantine measures in case of entry and exit of animal at farm.
(isolate diseased from healthy one)
o Nomadic animals move from one geographical area to another area carrying
infection.
o Some non susceptible animals like birds, dogs, and cats are potential agencies of
spread. These species are not infected with FMD. Virus passes unchanged from
GIT of birds so birds play important in dissemination of virus from one area to
another. Similarly dogs and cats fed on died animals of FMD also becomes the
source of spread.
o Carrier animals (recovered from FMD, non diseased vaccinated and non
vaccinated) and these animals carries the virus in nasopharyngeal region. About
50 % of recovered animals act as FMD carriers. So it is more beneficial to keep
recovered animals separate from healthy animals.
o Lack of communication between farmers and veterinarian.
o Non certification of freedom from disease before introducing them to the farm.
o Nosocomial spread (from hospital, veterinarian and para veterinary staff) by
syringes, crush, thermometer etc.
o Common grazing and watering and common and not properly disinfected utensils.
o Socio economic factor: farmers can not afford the vaccination
o Farming with multiple animal species.
o Lack of effective reporting system.
Researchers use a formula to know the field strains
r= titre of reference antiserum against field virus
titre of reference antiserum against vaccine strain
Antigenic relationship is determined by this
If r is 0 - 0.19 then there is need to change vaccinal strain
If r is 0.2 - 0.39 it means protection may be satisfactory.
If r is 0.4 - 1.0 it shows that vaccinal and field strains are not significantly different and
will protect against field strain.
FMD is a viral disease of all cloven fitted animals e.g. buffalo, cattle, sheep and goat.
It is characterized by high fever, vesicle formation in the oral cavity, on the feet and in
female animal on the teats. In terms of economic loses it is one of the most important
diseases of livestock by drastic fall in meat and milk production. Death in adult animal is
rare; more in young animals and affected females become infertile for long periods. Pure
exotic breeds and cross bred animals that have been recovered form FMD start panting
and become useless for farmers in case of transport or other work.
Long and rough hair coat, milk production declines especially in summers and cracks
develop in hooves of animals. In calves high mortality leads upto 70 %. FMD is
worldwide in distribution. Japan, Korea, USA, Canada, Australia, and European countries
are apparently free from FMD. In 2001 Pan Asian O strain of FMD invaded United
Kingdom and then to France and other European countries but now they are free from it.
Etiological Agent:
Picornaviridae, genus Aphthovirus. There are 7 types A, O, E, Asia l, SAT 1, SAT 2, and
SAT 3.
One of the important characteristic of FMD is that the virus is produced in large amount
in infected animal and present in all secretions and excretions of animals including urine,
feaces, and exhaled air; that is why it is contagious disease. Virus is also present in the
products from infected animals e.g. meat, milk, hides etc.
Pathogenesis:
The primary site of infection and replication is usually the mucosa of pharynx although
the virus can enter through skin abrasions or the GIT. Virus is distributed through the
lymphatic system to sites of replication in the epithelium of the mouth, muzzle, feet and
teats and also to areas of damaged skin (e.g. the knees and hocks of pigs kept on
concrete). Vesicles develop at these sites and rupture, usually within 48 hours. Viremia
persists for three days.
Signs:
High rise in body temperature that generally do not respond to antibiotics, heavy stringy
salivation, occurrence of vesicles and ulcers in the mouth, on feet and teats of the
animals, reduction in feed intake and milk production, teat infection may lead to mastitis,
lameness due to lesions on feet, high death rate in young animals, deformities in hooves,
50 % weight loss.
Diagnosis:
FMD viral antigenic serotype is identified in tissue and body fluid. ELISA. For lab test
epithelium of ruptured or non ruptured vesicle on feet is best sample (at least 1 g).
Vesicles of buccal mucosa and udder, blood sample, and esophageal pharyngeal fluid
(OP fluid) are also used.
Treatment:
As it is a viral infection so no specific treatment but purpose is to shorten the disease.
Isolate the sick animal with separate feeding and watering utensils.
Wash the mouth of animal with 2 % alum solution or 1:1000 dilution of
potassium per magnate.
Ointment for vesicle:
Alum: 1 tea spoon
Potassium chlorate: 1 tea spoon smear on vesicle (mouth) three times a day
Boric acid: 1 tea spoon
Xylocain injection with 2 % adrenalin: 15 ml
Antibiotics:
Tribacteril (trimethoprin + sulphadiazine) 20ml I/M for four days in adult buffalo and
cattle.
Dipyrone (antipyretic) 25 ml (I/M). Cold water therapy for fever.
2 % solution of CuSO4, wash feet lesions and then smear with piodine or tincture
iodine.
Multivitamins (AD3E) 15 ml (I/M)
Soft diet (leafy) should be given.
Protect lesion from flies to avoid maggots because maggots can produce in
lesions.
Ethnoveterinary practice:
Hot bread (roti) with butter is offered which will rupture the vesicles.
Walk on hot sand or floor.
Water from tanneries is applied on vesicles. It will dry the vesicles.
Rinderpest/Cattle Plague
It is a transboundary disease (the disease which spread in a large area without any
discrimination of boundaries of countries). Pakistan was declared free from rinderpest in
2003. Before this, it was reported in Sindh. Vaccination of RP is not allowed in Pakistan.
Family of virus is Morbillivirus (Paramyxoviridae), many strains having similar genetic
make up. Animals of all the ages can be affected. Large animals, sheep, goat, camels are
affected.
Pathogenesis:
Virus is inhaled in infected droplets and it penetrates through the epithelium of upper
respiratory tract, multiplies in tonsils and regional lymph nodes, from these sites virus
enters the blood in mono nuclear cells and disseminated throughout the body because
virus have high affinity for lymphoid tissues and alimentary mucosa. So it replicates in
monocytes, lymphocytes and epithelial cells. Destruction of leukocytes results in
leukopenia. Local necrotic stomatitis and enteritis result after proliferation in epithelial
cells in alimentary tract and death occurs due to severe dehydration. In less acute cases
death occurs due to activated latent parasitic or bacterial infection because the animal is
immunosuppressd due to destruction of lymphoid organs by virus.
Clinical signs:
Incubation period is 6-9 days and temperature may raise upto 105-107 oF. There are
chances of absence of mucosal lesion. There is anorexia, decrease in milk yield and
lacrimation.
In mucosal phase inflammation of buccal mucosa, nasal mucosa, conjuctiva, hyperemia
of vaginal mucosa, swelling of genitalia and lacrimation becomes purulent. Blephropasm
(spasm of eyelids), blood stained salivation, purulent salivation, halitosis (fowl odour
from breathing of animal). Serous nasal discharge that later becomes purulent. Grayish
raised necrotic lesions first appear inside the lower lip, adjacent gums, lower surface of
the tongue, and mucosa at commissures. Later they become general including dorsum of
tongue. Small lesions unite and become large which cause the sloughing. After sloughing
of necrotic material red areas are left that form shallow ulcers. Severe diarrhea,
sometimes dysentery. Skin becomes moist and red and later it is covered with scab.
After period of 3-5 days temperature decreases, dyspnea, cough, diarrhea, dehydration
and abdominal pain may be observed. Pregnant animas may abort and discharge infective
virus in fetus and vaginal secretions for 24 hours.
Necropsy Findings:
Carcass will be dehydrated, emaciated, soiled with feacal material. Small necrotic areas
found on oral mucosa; ulcers can be seen. These lesions extend to pharynx, upper
esophagus, and abomasums; payer’s patches become swollen and hemorrhagic. Necrotic
zones of hemorrhage running transversely across the colon mucosa produce characteristic
strips called zebra strips. Mucopurulent exudates in respiratory tract.
Tissues for Sampling:
Fixed sections of lymph nodes, tonsils, alimentary tract, fresh spleen and blood.
Treatment:
No treatment is given in this disease but left over and surroundings of animal are burnt.
Control:
Slaughter the infected animals. Proper cleaning and disinfection of premises. Adopt
proper quarantine measures. Vaccination is not recommended in diseased animals.
Vaccine:
Universal vaccine is used; Tissue culture Rinder pest vaccine. It gives life long immunity.
It is cultured on calf kidney cells. It should be used within 2-3 hours otherwise it will be
destroyed.
Attenuated vaccine: virus is passaged in goats, rabbits, chicken eggs.
Vaccination failure occurs due to lack of cold chain in Pakistan.
Scabby Mouth/ Contagious
Echthyma/ORF/Sore Mouth/ Contagious
Pustular Dermatitis
There is zoonotic importance of this disease for the people who work in wool and hide
industry.
This is caused by Paramyxovirus or ORF virus which belongs to Poxviridae. This disease
occurs in sheep and goat and causes pain to animal and economic losses to owners.
Lips and face of animals are more affected and in female udder also. Morbidity may
reach upto 100 % but mortality is 15-20 %.
Transmission:
1. Natural infection: if any sharp object in fodder or dry roughages and causes
wound then provide the rout to virus to enter.
2. Scab: vesicles dry and become the scab. After healing scab is shed off that is an
important source of virus. So scabs must be burnt (potential source of spreading
of virus).
3. Common feed and water troughs and common grazing places.
Pathogenesis:
After viral challenge of mildly abraded skin. The virus does not replicate in the damaged
epidermis but in cells of underlying replacement epidermal layer and this layer is derived
from the walls of wool follicles.
Lesions have different stages:
Macule: First stage of spot formation is. These are not raised but colourless spot.
Papule: A small circumscribed skin elevation (solid consistency)
Vesicle: Elevated area containing liquid and having soft in consistency.
Pustule: Small circumscribed skin and elevated but soft in consistency.
Scab: Pustule ruptures within few days and ulcer will form on the red area and after
healing of it formation of scab will occur which is a rich source of virus.
Clinical findings:
First lesions develop at oral muco-cutaneous junction/oral commissures accompanied by
lip swelling. Then the lesions spread to muzzle, nostrils, nearby hairy skin, and buccal
mucosa. Lesions may appear as thick scabs that are soft to touch and difficult to remove
from underlying granulation. There will be accumulation of fluid in scrotal sac that may
cause temporary infertility. Ears and anal area is rarely involved. If alimentary tract is
involved then gastritis and if respiratory system is involved then bronchopneumonia.
Autogenous vaccination:
Remove scab from animal and mix it in normal saline (5 ml); tirturate the solution and
inject it in the muscle.
Scarification:
Vaccine fork is used which has sharp ends like needle. Dip it in solution and apply on
inner side of thigh in cross form. Mild bleeding occur, virus enter the body and create
immunity.
Clinical Diagnosis:
PCR, Viral DNA gene sequencing, recombinant DNA technology, restriction enzyme
analysis. Neutralizing antibodies in serum are detected by gel diffusion test.
Necropsy findings:
Typical proliferative lesions and ulcers. If observe microscopically hyperplastic epithelial
tissue containing swollen degenerative cells and in some cells eosinophilic cytoplasmic
inclusion bodies will be present. Formalin fixed lesion are used as samples for histology.
For virology vesicle fluid and scrapping from lesions are taken.
Differential Diagnosis:
Ulcerative dermatitis, mycotic dermatitis, facial eczema, pappilomatosis, blue tongue,
sheep pox.
Vaccine:
Vaccine used is formed from live virus so do not recommended because sign of disease
may occur.
Treatment:
As it is viral disease so there is no specific treatment. Chloromphenicol and
oxytetracyclin are given.
Chloromphenicol 20 % injection s/c I//m, I/v Dose in sheep and goat is 5-10 ml.
Ooxy-5 injection: 4-5 ml for 50 Kg b. wt.
Oxychlor P: (oxytetracyclin, lidocain, prednisolone and chloromphenicol); for sheep and
goat 1-1.5 ml/30Kg b. wt.
Soft palatable diet due to oral lesions.
Mostly animal is off feed so give fluid therapy. If enteritis not present then give dextrose.
Multivitamins
Somogel like preparations or glycerin for oral lesions.
Viral disease will take 7-10 days for healing.
Fly repellents like pink spray, neem oil.
Blue Tongue
Blue tongue virus is an arthropod born virus related to genus Orbivirus and family is
Reoviridae. At least 24 serotypes are found and it infects domestic livestock population
throughout all tropical and sub tropical countries.
Distribution and intensity of infection is determined by climate and geography of area
because these facts affect the occurrence and activities of Culicoides and presence of
susceptible mammalian host. Sheep is mostly susceptible. Cattle are major reservoir.
Transmission:
Not contagious. Disease is transmitted by saliva of Culicoides mosquito (female).
Pathogenesis:
In sheep there is vascular endothelial damage that results in change of capillary
permeability with disseminated intravascular coagulation and necrosis of tissues supplied
by the damaged capillaries. This results in edema, congestion, hemorrhages,
inflammation and necrosis. Following infection into the skin there is replication in the
draining lymph nodes and dissemination in mononuclear cells to secondary sites of
infection and replication in lymphoid tissues and lungs. Viremia is detected by day three
and peak viremia is associated with fever and leukopenia. Leukopenia usually occurs 6-7
days after infection. Circulating virus concentration falls with the appearance of
circulating interferon and specific neutralizing antibodies. With viremia there is
localization of virus in vascular endothelium that causes endothelial cell degeneration,
necrosis, thrombosis and hemorrhages. The distribution of lesions is influenced by
mechanical stress, lower temperature of the area.
In cattle infection of endothelial cells is minimum. Viremia in cattle is highly cell
associated particularly with erythrocytes and platelets. Virus does not replicate in
erythrocytes so it is protected from circulating neutralizing antibodies. In cattle, type 1
hypersensitivity reaction depends upon the virus specific immunoglobin E (IgE) and
happens due to repeated exposure.
Clinical Findings:
Incubation period is of one week with severe febrile condition, temperature may raise
upto 105-106 oF. Fever remains for 5-6 days. About 48 hours after rise in temperature.
There is nasal discharge, salivation, reddening of buccal and nasal mucosa. Nasal
discharge is mucopurulent and blood stained and saliva is frothy in nature. Swelling and
edema of lips, gums, dental pads and tongue occur. Involuntary movement of lips,
excoriation (sloughing) of buccal mucosa, and blood stained saliva, and offensive smell
from mouth. Necrotic ulcers develop on lateral aspects of tongue that may become
swollen and purple in colour. Hyperemia and ulceration are also common on
commissures of lips around the anus and external genitalia. Swallowing is difficult for
animals and respiration rate may increase upto 100/minute.
Diarrhea and dysentery may occur. There is coronitis and lameness. Animal is in
recombancy. There are dark red purple band in skin just above coronet. There is twisting
of head and neck to one side due to direct action of virus on muscle tissue. There will be
muscle stiffness and weakness, facial swelling, drooping of ears, hyperemia of non
wooled skin, and conjunctivitis with severe lacrimation, colonitis and vomiting.
Aspiration pneumonia may develop due to difficult eating and drinking so it is its
complication.
Death occurs usually 6 days after the appearance of signs in severe cases. In recovery
phase partial or complete loss of wool, cracking of hooves, cracking of skin around the
lips and muzzle.
Clinical Pathology:
Virus agar gel immunodiffusion, competitive or blocking ELISA.
Necropsy Finding:
Mucosal lesions, hemorrhages and necrosis of skeletal and cardiac muscles. Hemorrhagic
lesions at the base of pulmonary artery.
Treatment:
As far as its treatment is concerned no so specific treatment. Treatment is according to
signs and symptoms. To prevent secondary infection, you can use antibiotics like
tribursin, anrofloxacine, tetracycline, chloromphenicol.
Washing of lesions with mild antiseptic.
Fluid therapy.
Control vector.
Differential Diagnosis:
FMD, contagious ecthyma and sheep pox or goat pox.
Sheep/Goat Pox
Causative agent of goat pox is Capripox virus, collectively the infection by this virus is
called as Capripox infection.
Transmission:
Sheep pox is highly contagious condition. Virus enters through respiratory tract, through
aerosol. Virus is present in nasal and oral secretions for several weeks and live in the
scabs for several months that is why it is important to burn the scabs. Spread is also
possible through contaminated material and skin abrasions. Capripox is also transmitted
by tsetse fly.
Pathogenesis:
Initially viremia, virus deposits in tissues including skin and start replication.
Clinical findings:
Incubation period is 12-14 days. One form is malignant and second one is benign.
Malignant form is more common in lamb. There will be depression, high temperature,
discharge from eyes and nose. Infected lambs die before the appearance of lesions.
Lesions develop on unwooled skin, buccal mucosa, respiratory mucosa, digestive mucosa
and urogenital tract mucosa.
Papules → Nodules → Vesicles → Pustules → Scab.
Some lesion may progress from nodules to tumour like masses.
Benign form is common in adult. Only skin lesions occur particularly under the tail and
there is no systemic reaction.
Treatment:
No specific treatment, only palliative (soothing). Ointment/antiseptic/neem oil on lesions
is applied. ZnO powder mixed in Vaseline can be applied on lesions topically. Parentally
antibiotics can be given.
Vaccine:
Cell culture sheep vaccine is used in sheep pox. It is an attenuated live virus cell culture
vaccine. Strains used in it are RM-65 strain. Vial consists of 100 doses. Its shelf life is
two years. 100 ml distilled water or normal saline is used. Vaccine should be used within
1-2 hours. Its dose rate is 1 ml s/c. Vaccination in first week of March and first week of
September (twice a year).
Goat pox cell culture vaccine is live attenuated cell culture vaccine grown on prime kid’s
kidney cell culture. It is safe for pregnant goats. Shelf life is 24 months. Dose rate is 1 ml
s/c it with normal saline. 100 ml distilled water or normal saline is used. Vaccine should
be used within 1-2 hours.
Cow pox
It is caused by Orthipox virus family Poxviridae. Pox lesions are on teats and udder.
Papules are formed with hyperemia around the base. Vesiculation, pusturlar lesions and
finally scab formation. Treatment is palliative.
Pseudo Cow Pox/Milker’s Nodules
It is caused by Parapox virus.
There is formation of vesicles, pustules and thick scabs. Scabs are horse shoe shaped
surrounded by granulation tissue. It has zoonotic importance as it can be transmitted to
human/milkers. Treatment is palliative.
Borna Disease
It is infectious encephlomalitis in horses, cattle and small ruminants caused by single
stranded RNA virus. It may cause disease in humans including lymphocyte
manengioencephalitis.
Transmission:
Unknown but most probably by inhalation or indigestion.
Pathogenesis:
Infection of cells of CNS. Virus enters into CNS through nerves (olfactory, trigeminal)
with subsequent dissemination of infection to brain. Virus transmission and replication
occurs within cell nucleus and the cell mediated immune response starts by the host;
immune response destroys the infected cell.
Signs:
Anorexia, ataxia, paresis (mild form of paralysis), pharyngeal paralysis, and circling
movements, death occurs within 1-6 weeks.
Intranuclear inclusion bodies within neurons. Virus is also detected in formalin, paraffin
embedded brain tissue by PCR. Control measures are not recommended due to lack of
knowledge of transmission.
Dermatophilosis/Mycotic Disease/ Cutaneous
Streptotrichonosis/Lumpy Wool of
Sheep/Senkobo Disease
In central Africa named Senkobo, also present in equines, collectively in all species
termed as dermatophilosis.
Etiology:
Dermatophilus congolensis is an infective agent but not invasive until skin damages.
Organism is dimorphic and grows as branched filament and dormant zoospores which are
transformed by moisture to infective stage of motile cocci. Animals of all ages are
susceptible to this infection.
Sources:
There are no. sources:
Minor active lesions on face and feet.
Infection in scabs, still carried in hair and wool from healed lesions.
D. congolensis normally does not reach the healthy skin; barriers are:
Stratum corneum
Wax produced by sebaceous gland
Feet and face are the areas where these barriers are easily broken because of
thorny and spiny feed stuff or forage.
Transmission:
It is a contagious disease. Transmission occurs from the carriage lesions by contact from
the face of one animal to other animal, through flies and ticks, and from feet during
dipping; dip also becomes the source of infection. In sheep if wool remains wet for long
time.
Pathogenesis:
Minor trauma, exaggerate by wetting in sheep. Infection establishes where multiplication
of organism starts and pyramidal crusts are formed by repeated cycles of infection into
the epidermis by hyphae. Bacterial multiplication in epidermis. Rapid infiltration of
neutrophils and regeneration of epithelium. Lesions remain expanding until immunity
develops and healing start. The scab then separate from healed lesion but held loosely in
placed by hair or wool fibers. Secondary bacterial infection occurs and gives rise to
suppuration and severe toxemia.
Clinical findings:
In sheep lesions are commonly not visible due to presence of wool but crust can be
palpated as hard masses at the surface of skin that is why called as lumpy wool disease.
Lesions are distributed irregularly over the dorsal midline with ribs spreading laterally
and ventrally. Crust are roughly circular and thick upto 3 cm. Pyramidal concave base,
pigmented and underlying scab will be moist and red area. Muzzle, face and ears and
scrotum of rams are involved. Heavy mortality in rams occurs due to cutaneous myiases
and secondary pneumonia.
In cattle the lesion is first pustule, hairs of the infected site become erect and give a paint
brush like appearance with greasy exudates forming hard crust that is hard to remove.
These developed into scabs of white brown colour, 2-5 cm in diameter and will give
mosaic appearance. Pus is formed in secondary infection. In cattle mostly neck, legs and
udder of animal is involved. If calves come in contact with udder, muzzle of calves will
be affected.
Clinical Pathology:
Skin scraping: zoospores are found. Serological evidence by ELISA, counter
immunoelectrophorosis.
Differential Diagnosis:
Fleece rot in sheep, Corynebacterium pseudo tuberculosis in horse.
Treatment:
Penicillin: 70,000 IU/Kg b. wt. + streptomycin: 70 mg/Kg b. wt.
Erythromycin: 10 mg/Kg b. wt.
Lincomycin + spectinomycin: 5 mg/Kg b. wt. + 10 mg/Kg b. wt. respectively.
Tetracycline in large animal: (20 mg/Kg b. wt.), in small animal 5 mg/Kg b. wt.
Prevention:
Healthy animal should be dipped separately.
Dermatomycosis / Ring worm
Its causative agent: Trichophyton and Microsporum canis
T. verrucosum (sub specie: album and discoides) T. mentagrophyte, T. megninii
In sheep T. verrucosum and M.canis
In goat T. verrucosum
Most common where animals are kept indoor and congested. Direct contact with infected
animals or infected objects like bedding. Young animals are more susceptible, incidence
is more in winter, healing spontaneously in spring but humidity is main factor.
Zoonosis:
Human acquires ring worm infection from equine and cattle, also from dogs.
Pathogenesis:
Ring worm fungus attack keratinized tissue, stratum corneum, and hair fibers. There will
be breaking of hairs; alopecia develops. Exudation from infected epithelial layer starts.
Epithelial debris and fungal hyphae produce crust that is characteristics of this disease.
Warm and humid environment is favourable for mycillial group and alkaline pH of skin.
Ring worm fungus is strict aerobes and dies under the crust. Living on the peripheral site
active but die in centre. Due to this mode of growth it produces centrifugal progression
(because animal requires oxygen for growth) and characteristic ring form of lesion.
Secondary bacterial infection to hair follicle is common.
Clinical Findings:
Crust is heavy and grayish white, raised above skin. Lesions are circular and 3 cm in
diameter. In early stages surface below crust is moist. In older lesions the scab becomes
detached and alopecia develops. Lesions are commonly on neck, head but general
distribution over whole body particularly in calves. Itching does not occur. In sheep
lesions are mostly present on head and very rare on wooly and fleece areas and disappear
in 4-5 weeks. But disease may persist in flocks for some months. Lesions are normal
patches covered with grey crust. Similar lesions are seen in goat.
Clinical Pathology:
Skin scrapping: first defat with alcohol or ether. Then put a drop of 20 % potassium
hydroxide or sodium hydroxide, warm it and make slide, observe polyhedral rounded,
irregular spores in the form of chains or hair follicles.
Differential diagnosis:
Mycotic dermatitis, sarcoptic mange.
Treatment:
Crusts are removed by soft brushing and burnt.
Apply weak solution of iodine, quaternary NH4 compound.
Bourdeoux mixture (CuSO4 + lime + water), it is basically used in paint.
10 % solution of NaI 1g/14 Kg.
Greseofulvin.
Aminoglycosides if bacterial infection.
Control:
Isolation and treatment of infected animals.
Disinfectant: 5 % formalin, 5 % Na hypochlorite.
2 % formaldehyde + 1 % Caustic soda are used for walls.
Nematodes
Parasitic Gastroenteritis in Ruminants
Ostertagia cooperia
Transmission:
Transmission is by ingestion of infective larvae. Disease risk is determined by factors
influencing the susceptibility of the host, the numbers of infective larvae accumulating on
pastures and the numbers of larvae undergoing hypobiosis. Lambs and calves are more
prone to this.
Hypobiosis:
Adaptive mechanism is according to favourable environment.
Signs:
Weight loss, low production, and diarrhea.
Clinical Pathology:
High fecal egg count, high plasma pepsinogen and gastrin in abomasal infections.
Differential Diagnosis:
Malnutrition, Coccidiosis, John’s disease, Chronic Fascioliasis.
Treatment:
Ivermectin: 0.2 mg/Kg s/c, albendazole: 10 mg/Kg, levamisole: 5.5-11 mg/Kg. orally,
levamisole s/c is also available: 3.3-8 mg/Kg.
Hemonchosis
It is caused by Hemonchus contotrus. It is common in sheep and goat. Animal is anemic,
anorexic and there is acute sudden death.
Clinical Pathology:
Anemia, Hypoproteinemia, increased fecal egg count.
Diagnosis:
Barber pole appearance of female worm.
Differential Diagnosis:
Cobalt deficiency, Cu deficiency, Coccidiosis, babesiasis, anaplasma, anemia.
Treatment:
Same as above.
Bunostomiasis
It is Hook worm disease.
Transmission:
Through skin, warm and humid environment is favourable.
Signs:
Anemia, diarrhea, and anasarca (subcutaneous edema).
Clinical Pathology:
Eggs in feaces, hypoproteinemia.
Necropsy Findings:
Red worms attached to mucosa of small intestine nearby ingesta often blood stained.
Clinical Findings:
Diarrhea, paleness, weakness, anasarca along belly or under jaws, death under 2-3 days.
Blood suckers cause severe anemia. 100 worms may cause illness, may cause death if no.
is 2000.
Loss of blood, mild intermittent diarrhea, mild irritation.
Lung Worm Infestation in Cattle
(Bovine Verminous Bronchitis)
This disease has different local names as Parasitic bronchitis, Husk/Hoose in America,
bovine infectious bronchitis.
Dictyocaulus viviparus causes it.
Transmission:
When cattle ingest third stage larvae by grazing. The third stage larvae migrate to
intestinal wall to reach mesenteric lymph nodes. From here they pass via the lymphatics
to venous blood stream and through heart to lungs in alveoli. They migrate up the
bronchioles to their predilection site in the larger air passages and start to lay eggs 3-4
weeks after infestation.
There are four phases:
Penetration Phase: Ingestion to arrival of larvae in lung, 1-7 days.
Prepatent Phase: Larvae in lung, 7-25 days.
Patent Phase: Mature worms in lung, 25-55
Postpatent: Lung worm disappear from lungs, 55-70 days.
Signs:
Coughing, dyspnea, rapid shallow abdominal breathing, 60-100 breaths/min, slight nasal
discharge, breathing through mouth, temperature raise 104-105 oF
Treatment:
Ivermectin, albendazole: 7.5 mg/Kg, oxfandozole: 4.5 mg/Kg, levamisole: 7.5 mg/kg,
antihistaminic drugs like NSAIDS, loxin.
Diagnosis:
Baermann technique (funnel like worms in bottom after one night).
Ascariasis/Calf Hood Disease
It is caused by nematode Toxocara vitulorum. It has complex life cycle. Transmission is
by ingestion of highly resistant and ling lived larvated eggs. It is also transferred by
colostrums.
They settle in somatic cells and activate near parturition and migrate to udder. They
transfer to calf in colostrums and grow to the adult stage in intestine. When animal is of
3-4 weeks, problem start and there is diarrhea and effect to growth (calf hood disease).
Clinical Signs:
Rough coat, diarrhea, if lungs involved fever and cough, mucopurulent nasal discharge,
anemia and steatorhea (fat along with feaces) specially in young ones.
Differential Diagnosis:
Pneumonia in young animals, malnutrition, chronic enteritis.
Treatment:
Ivermectin, levamisole, benzinidazole group (alfendazole, albandazole). First week
before parturition deworming is done. After one month of calving again deworming is
done. Then after every 2 or 3 month (3 or 4 times/year). Albandazole is not given in first
trimester of pregnancy and when animal is in estrous.
Parasite resistance: when under dosing and repeated use of same anathematic. So
change rotation of anthelmentics.
Thelaziasis (Eyeworm Disease)
It causes eye infection. All mammalian are susceptible. It is a thin worm up to 2 cm long.
Lacrimation starts in animal; there is photophobia, conjuctivitis, keratitis, corneal
ulceration, and abscess formation on eyelids. It is indirect transmission by fly.
Intermediate host is face fly (Musca autumnalis). It mostly occurs in summer and autumn
when flies are more active. Flies lay eggs on conjuctiva while feeding from eyes. Larva
feed on secretions of eye. Adult worm is found in conjuctiva. First stage larva is found in
eye washing.
Treatment:
Ivomec injection.
Trematodes
Hepatic Fascioiasis/ Liver Fluke Disease
F. hepatica and F. gigantica are responsible for it. It is caused by ingestion of
metacercariae. Intermediate host is snail (Lymnaeid snail).
Life Cycle:
Adult liver flukes live in bile duct where they lay eggs which are excreted in feaces.
Hatching occurs in moist condition only after first larval stage, the meracidium, has
formed and when ambient temperature rises above 5-6 oC. Meracidium invades the tissue
of intermediate host snail within 24-30 hours. After asexual multiplication fluke leaves
snail as cercariae. They attach to herbs and transform into metacercariae by secreting a
tough cyst wall i.e. protective. After ingestion by final host each metacercariae releases
an immature fluke which crosses the intestinal wall and migrates across the peritoneal
cavity to the liver. F. hepatica migrates thorough hepatic parenchyma for about 4-5 weeks
and after entering the bile duct start laying eggs about 10-12 weeks after infestation.
Adult sheep and cattle may remain carrier.
Pathogenesis:
Acute hepatic fascioliosis cussed by the passage of young liver fluke through liver
parenchyma. Clinical signs occur 5-6 weeks of infestation of large no. of metacercariae.
Environment becomes favorable for Cl. novyi and develops infection known as infectious
necrotic hepatitis also termed as black disease in sheep and goats. It provides suitable
environment for Bacillray hemoglobinurea in cattle.
Chronic hepatic fascioliosis develops only after the adult flukes establish in the bile duct
causing colengitis, biliary obstruction, fibrosis, leakage of plasma protein (albumin),
hypoalbumenemia, loss of whole blood due to sucking activity of flukes and leads to
anemia. Chronic infection limits the growth rate.
Clinical Findings:
Acute Fascioliasis: Sudden death and if signs observed animal is dull, weak, anorexic,
pallor and edema of mucosa and conjuctiva and animal feels pain when pressure excreted
on liver. Death occurs with passage of blood stained discharges from mouth and anus and
most death within 2-3 weeks.
Subacute Fascioliasis: Submandibular edema (bottle jaw), weight loss, pallor mucosa.
Chronic Fascioliasis: Submandibular edema (bottle haw), weight loss, pallor mucosa. In
case of sheep there is shedding of wool. Duration of disease may be 2-3 months. In case
of cattle there is loss in milk production, edema and chronic diarrhea.
Clinical Pathology:
Development of anemia, increased serum glutamate dehydrogenase concentration
increases, eggs in feacal material, hypoalbumenemia.
Differential Diagnosis:
In acute fascioliosis: hemoncosis, anthrax, enterotoxemia.
Chronic: Cu or cobalt deficiency, other internal parasitism, johne’s disease.
Treatment:
Triclabendazole: (oral) Sheep (10 mg/Kg), cattle (12 mg/Kg).
Albendazole: sheep (7.5 mg/Kg), cattle (10 mg/Kg).
Oxychlozanide: (10-15 mg/Kg for sheep/cattle).
Levamisol: (5.5-11 mg/Kg)
Paramphistomiasis (Stomach Fluke Disease)
Infection by ingestion of metacercariae of Paramphistomum cervi.
Clinical Signs:
Severe enteritis and diarrhea
Clininal pathology:
Same as above.
Differential Diagnosis:
Same as above.
Treatment:
Same as above.
Control:
Biological control as snail is intermediate host: ducks, chemical control: CuSO4.
Deworming.
Tapeworm Infestations
Moniezia expansa, Moniezia benedeni
These infestations are important in livestock.
Life cycle:
Eggs passed in feaces of final host either singly or in tapeworm segments. These are
ingested by free living oribated mites and intermediate stage metacestode is formed.
Mature state develops when primary host accidentally swallow the infected mites while
grazing, and tapeworm in small intestine.
Pathogenesis:
Heavy infestation; then competition for nutrition. M. expansa causes enterotoxemia.
Clinical signs:
There is poor and rough coat, constipation, mild diarrhea, milk dysentery, and anemia.
Under the age of 6 months signs are more severe.
Clinical Pathology:
Tapeworms segments are macroscopically visible in skin, around tail base and in feacal
material.
Necropsy Finding:
Site of attachment of worm in small intestine; leads to formation of small ulcers and mild
inflammation.
Treatment:
Praziquental: 3.75 mg/Kg, albandazole, febendazole and oxibendazole.
Control:
Ticks should be controlled.
Ticks
Ticks are economically important in cattle and livestock species. These are
vectors for parasites like babeisia, theileria, anaplasma, rickettsia; virus like
Crimean Congo Hemorrhagic Fever; bacteria like pasterurella, brucella, listeria,
staphylococcus. Ticks are also blood suckers. Ticks belonging to genus Ixodes
and Ornithodorus are associated with tick paralysis because of toxin is released
from ticks. Important species of ticks are Boophilus, Hyaoloma, Rhipicephalous,
Amblyomma.
Ticks show a variety of host contact pattern during their life cycle.
One host tick: Boophilus, each developmental stage feeds upon same host.
Three host species: Hyalomma, complete different larval stages on different hosts.
Control Strategies:
Housing of animals in tick proof buildings. Cracks and crevices are big source of
ticks for this purpose caulking (tape) of wall and roof is done.
Herbage and wastage of farm (dung) should be burned slowly and by the smoke
produced the ticks are killed.
Separate housing of cattle and buffalo. Cattle are more susceptible but if kept
together, buffalo may also get infestation due to stress.
Sahiwal cattle is resistant to ticks due to some factors like its skin moves, hairs are
short, and straight and secretion from skin (sebaceous).
Pasteur of grazing of cattle and buffalo should also be separated.
Quarantine measures; new animal in herd should be kept separately first and
observed for any disease.
Manual removal of ticks but do not twist it in hand because it causes Crimean
Cango Hemorrhagic Fever in humans. Always remove ticks with forceps in anti-
clock wise direction.
Clearance of vegetation.
Use of Acaricides, in the form of dip, injection, pour on, ear tags etc
For dips different preparations like Ecofleeece: 2 ml/2 litres water, Cypermethrin:
2 ml/2 litres water, delta 25 (deltamethrin 2.5 %): 2 ml/litre, Negovan
(organophosphate),
Ivomec: 1 ml/50 Kg or 200 µg/Kg s/c.
Tick vaccines are available but not in Pakistan. Tick guard vaccine prepared in
Australia, Endosymbiotic relationship can be broken down. Some fungus if grown
in Pasteur then the larval stages of tick can be controlled. Similarly in body there
are some microorganisms which are useful for ticks; if we control them, we can
control ticks.
Development of resistant tick breeds.
Ethnoveterinary Practices:
Salt is applied on body of animal. Taramira oil mixed in simple oil and applied on body
or 250 mg of terpentine is soaked in water and next morning mix with ice or cold water
and 100 g salt is added and applied to animals.
Micronutrients/Microminerals
Mineral imbalance is quite common in our situations. Mineral deficiency causes severe
effect on reproductive and productive performance of animal. Immune status also
reduced due to deficiency.
Minerals play important role in nutritional and metabolic disease of dairy that are
responsible for catalytic, physiological and structural functions. Minerals are classified
into macro and micro minerals.
Macro minerals: Ca P Mg, Na, K, Flouride and Sulfer.
Micro minerals: required in small quantities i.e. ppm and found 0.01 % of the total mass
of an organism.
Essential Trace Minerals: Cu, iodine, iron, Mn, Zn, cobalt, fluorine, selenium, and
cromium, molybdenum (excessive Mo, low Cu).
Possible essential trace minerals: Al, Ni, lead.
Problems are first observed in areas of health and production. Many mineral deficiencies
are noticed after a prolong period of underfeeding. It may take time to appear clinical
symptoms for mineral deficiency. These include less growth rate, late maturity, anemia,
longer inter-calving period, reproductive disorders. Mild deficiencies or subclinical
differences are of great importance because these are difficult to diagnose and clinically
manifested by unsatisfactory growth rate, production and fertility.
Farm animals derive high portion of mineral portion from fodder they consume. The
extent of problem varies from locality to locality between geographical areas depending
upon soil type, climate conditions, farming, practices, quality and quantity of fertilizers,
and water used.
Alkaline soil leads to increased availability of some trace elements like selenium and
molybdenum. In acidic soil (decrease soil pH), selenium is less available and uptake of
Cu is said to be increased. The concentration of mineral in the crops and forage plants
depends upon the variety of the fodder, type of the soil, climatic conditions, stage of
maturity of plant and conditions imposed by humans.
Copper
It plays important role in metabolism of plant, animals and humans. It is one of the
important trace elements for the natural resistance to diseases and fertility in dairy
animals. It is part of hemoglobin and used in its formation. It has significant role in iron
metabolism, cross linking of connective tissue, pigmentation and characterization of hair
and wool, CNS and other metabolic function. Cu deficiency in buffalo is a complicated
process because it can result from very low Cu in diet that is the primary Cu deficiency or
interference with absorption of Cu due to high quantity of sulphate and molybdenum.
The most commonly observed results of Cu deficiency in cattle and buffalo are diarrhea,
poor weight gain. Particularly in young one diarrhea will be seen. Growth is severely
affected by Cu deficiency. Non infectious leukoderma also occurs due to deficiency of
Cu in which there is depigmentation of the skin mainly on back, face, abdomen, and hind
limbs. Other signs are broken bones, infertility and anemia.
Cu deficiency lowers immune response and makes animal more susceptible to disease.
Cu may affect the tissue damage resulting from infectious disease. Reproductive problem
is commonly observed in animals fed on Cu deficient diet. Anemia, hemorrhage, and
mortality of embryo is caused by defect in RBC and connective tissue formation in early
embryonic development.
Diagnosis:
Trace element status of Cu is determined by its concentration in liver because most of the
Cu in body is stored in liver but at farm level it is determined from serum. Liver is
authentic but difficult. If below 0.5 part per million in serum, it is diagnosis of Cu
deficiency. It is late diagnosis. Liver diagnosis is early.
Treatment:
Cu and Zn also part of catalytic activity. Superoxide dismutase is an enzyme that
converts suuperoxide into hydrogen peroxide. So these minerals also related to cellular
antioxidant system. Cu is also a part of an antioxidant protein ceruloplasmin that may
prevent Cu from participating in oxidation reaction. In treatment of mastitis Cu and zink
is also used to repair damage due to inflammation and to enhance immunity. CuSO4 18
g, ZnSO4 5 g.
CuSO4 is mixed in 250 ml water and then mix it in flour and then add 250 ml of vinegar
if not acidified Cu and then make 15 equal size bolus and give to animal daily 1 or 2
according to weight of animal. Acidified Cu has good absorption. Copper glycinate is
also used. It is an injectible preparation s/c but not available in Pakistan. Give 5 g Cu to
cattle and 1 g to sheep in one week as preventive measure.
Zink
It is essential for all animal and play significant role in metabolic activity, numerous
enzymatic reactions, nucleic acid metabolism, protein synthesis and carbohydrate
metabolism. It is found in all body tissues which are rich in protein. Higher concentration
is in skin hair, wool, and in internal organs like pancreas. It is required for mobilization
of vitamin A from liver. Concentration of Zn is high in forages found in soil of high pH
level. Early effects of Zn include reduced feed intake, reduced skin disorder, in most
severe cases infection of nose and mouth, stiffness of joint, soft edematous swelling of
feet in front of fetlocks, and many of these symptoms are because of problem in protein
synthesis and metabolic processes.
Severe Zn deficiency in cattle and buffalo, reduced feed intake. loss of hair, and lesions
are more severe on neck, head, legs, around nostrils, excessive salivation, swollen feed
with scaly lesions and reproductive problem. Quantity of zink is assessed in serum and
liver.
Treatment:
2 g ZnSO4 orally in large animals. 1 g ZnSO4 parentrally in deficient animals. Zink and
copper balance is 4:1. If it is disturbed, synthetic and metabolic function will be affected.
Managanese
Required for normal reproduction, bone structure, CNS function. Its highest
concentration is found in bone, liver, kidney, pancreas, and pituitary gland. Its deficiency
is associated with poor reproductive system, reduced production, and skeletal
abnormality in calf.
Treatment:
4 g MnSO4 in large animals orally, 1 g to calves, 2 g to heifer. MnO is used but sulphate
is better due to its availability.
Ratio of zink and manganese is 1:1
Pox
It is caused by Orthopox virus belonging to family Poxviridae. Orhtopox viruses are
antigenically similar.
Occurrence and Transmission:
Pox can come from pets to human beings. They may carry the virus. Spreads of this virus
from animal to animal is may be by direct or indirect contact: milker’s hands or infected
milking teat cups. Similarly infection travel from one herd to another by carrier or
infected animals. It is also transmitted by ticks, flies, and mites. It comes from one herd
to other by milkers and gwalas. This disease is sporadic.
If any injury on udder, it allows other bacteria to grow; then chances of mastitis. Teat or
udder lesions cause discomfort to animal during milking. Spread of this infection is very
rapid in the herd. Strong immunity develops in the animal because mammary teat cells
develop nodules and remain in whole life.
Pathogenesis:
There are five stages:
Erythema → papule (raised area) → vesicle → pustule → scab or scar.
In cattle you may observe all five stages. Erythema is filled raised pustules light in colour
but soon hyperemia around it. True scab in cattle may be 1-2 cm in diameter. It is thick,
tenacious, and yellow brown or red in colour.
Clinical Findings:
Severe itching. Pain in scab stage. Lesions are particular on teat to treat specially near
orifice. These lesions disappear after two weeks normally but on teat may be upto 1
month or more due to milking. So wounds on teats take more time to heal. Suckling
calves may develop lesions in oral cavity and moth. In bulls lesions may present on
scrotum.
Diagnosis:
It is based on clinical picture. Whenever formation of scar, central depression in the
lesion is present. Star coating appearance of scar on skin of cattle.
Differential Diagnosis:
Pseudocowpox, bovine ulcerative mammilitus, teat fibropapilloma. In case of pseudocow
pox spread is very slow and healing also slow (10 months). Bovine ulceration persists for
6-14 weeks and self limiting (viral disease). Teat fibropapilloma disappear in 2-3 months.
Lesions are vat like.
Anaplasmosis
Blood born disease due to protozoa. This disease is transmitted through ticks which act as
mechanical vectors.
Buffalo, cattle, sheep and goat are susceptible. There is marked anemia. Anaplasma
organism is present as intraerythrocytic bodies; lysis leads to anemia. They could be
centrally or marginal. If present in centre, anaplasma cenrtrale; if in periphery, anaplasma
marginale.
Anaplasma centrale is less pathogenic and used for vaccine which is available in
Australia, South America and Middle East.
This disease is present throughout the world in all tropical, subtropical, and other climatic
regions. 60 % of transmission occurs through tick and others through lice, Culicoid
mosquitos and mites. Transmission is also through contamination of instruments,
syringes and blood transfusion. Cross breeder more prone to this disease and foreign
breeds like Fresian. Local animals are resistant but low frequency.
Pathophysiology:
Enter in RBCs, this enhance within 24 hours. High production of anaplasma and more
RBC affected and persists for 5-7 days → spleen. There is low supply of oxygen to vital
organs and hypoxic condition. More RBCs release so more hemoglobin and more paling
of mucous membrane.
Clinical findings:
High rise in body temperature 104-108 oF or 42 oC. When RBCs destroyed, there is
release of RBCs in urine.
Anemia, pale mucous membrane, abortion in pregnant anima, decrease in milk
production, edematous swelling of limbs, mortality may be upto 10-30 %. Recovered
animal becomes carrier for the rest of life. Ticks can bite and transmit it.
Diagnosis:
Clinical findings and microscopic examination, ELISA, PCR, and DNA probing.
Treatment:
Imidocarb diproprionate (imizole) drug of choice is 2.5 ml for 100 Kg.
Oxytetracyclin (oxy-5 20 % or 5 %) 20 mg/Kg, deep intramuscular for 5 days.
Carrier animals should be given oxytetracycline for 3-4 days.
Babeisiasis
It is found in equine, bovine, and humans. It is transmitted by ticks. There is high
morbidity and high mortality. It causes huge economic losses in term of low productivity
and mortality.
B. bovis (in cattle and buffalo) and B. bigemina (buffalo and cattle but mostly in buffalo)
are main culprits other are B. divergens, B. major, B. jakimovi, B. ovata (in cat).
Present in tropical and tick populated areas. Mosquitoes, flies and contaminated
instruments also transmit the disease.
B. bovis is transmitted by larval stage of tick. B. bigemina is transmitted by nymph stage
of tick (Boophilus tick). Incubation period varies from species to species.
B. bovis: 1 % of total RBC infected and animal show clinical signs.
B, bigemnia: 10 % of total RBCs infected (more dangerous damage) then animal shows
signs; Damage occurs in less time.
Clinical Findings:
Elevated temperature, jaundice, anemia, more removal of RBCs from spleen,
hemoglobinurea is more pronounced in this case. Hemoglobin is free and come in urine
via filtration through kidney. Hematuria (fresh blood, settlement of RBCs). Hburea
(destructed RBCs do not settle). Abortion, low milk production, photosensitization.
Animal shows nervous signs due to hypoxic injury to brain. Most problematic condition
is DLC (disseminated intravascular coagulopathy). This is coagulation defects, sometime
thromboembolism also develop so you have to give anti coagulants like heparin or
sodium citrate (mostly heparin).
Postmortem Lesions:
Intravascular hemolysis, congestion and edematous lungs, petechial hemorrhages on
heart, brown to red colour fluid present in bladder.
Differential Diagnosis:
Hemoglobinurea: due to phosphorus deficiency and no temperature and seasonal
(winter), metabolic disorder, no presence of parasites.
Babesia: in hot summer when ticks present, do not respond to antibiotics.
Leptospirosis: response to antibiotics.
Diagnosis:
Blood examination, PCR, ELISA, CFT, DNA probing.
Treatment:
Imidocarb dipropionate (immizole) s/c 1-3 mg/kg b. wt.
It is dangerous so you have to keep emergency measures, allergic reaction may occur. So
steroids are used and preferable to use steroid 5-10 minute before injecting immizole.
High dose of immizole can remove parasites but high dose can not be given. You can use
it as prophylactic measure. If injected once it provides protection for 36 days.
Diamizine (Diaceturate) for example Pronil by Selmon: 3-5 mg/Kg I/M
Cold therapy to lower temperature otherwise at high temperature these drugs can not
work.
Supportive therapy: Fluid, blood transfusion, vitamins mainly B-complex.
Control:
Control ticks, mosquitoes, and flies. Avoid contaminated instruments. In Australia make
areas free zone of ticks.
1906: huge economic loss by ticks in America and Australia.
1943: made a program to eradicate particularly in young farms.
Main problem is coagulation of blood and you can not stop coagulation of blood due to
which death occurs.
Biological Control:
By keeping pet birds they are good pickers of ticks.
Dipping by Acricides
Burning of shed
By blocking cracks and crevices.
Scrapie
Disease of sheep and goat; characterized by pruiritis. It has long incubation period.
Causative agent is viroid, the protein particle which effect ventrolaterla side of the spinal
cord. This particle causes degeneration of neurons. This particle multiplies in host and
look as it is virus but it is not virus. Similarity to virus is that it can survive boiling for 30
min, survive antivirals, freezing and thawing. Jerk can not kill. There is no effect of either
and 20 % formalin. Viroid is an agent which has no antigenecity. So there is no antibody
production. No serotype and can not be cultured and no immunity against scrapie.
Occurrence:
Most common in Europe and less in Australia, Canada, Newzeland, USA and India.
Susceptible:
Foreign breeds of sheep and goat. 20-30 % morbidity and 100 % mortality.
Transmission:
Direct from and animal to another and can transmit from dam to offsprings. It is
genetically inherited.
Pathogenesis:
This particle multiplies in lymphatic tissues and then transfer to the spinal cord and brain
through sympathetic nervous system. This particle causes vacuolation in medulla,
ventrolateral and dorsal spinal cord and also in brain. Lesions are bilateral. It also causes
the degeneration of optic and ophthalmic nerves. There is imbalance of cerebellum.
Clinical Findings:
2-12 months and in some cases average within 6 months. Effected animal show changes
in behavior; tremor, pruiritis, and locomotory disorder. In early stages nervous signs for
weeks. It may be confused with BSE. Signs occur at different intervals for several weeks.
These episodes show collapse, and sudden change of behaviour. Sheep charge at walls,
doors or closed gates. Rubbing and biting at skin. Most of time nervous signs may not be
observed. There is pruritis on rum, thighs and base of the tail where animal bites usually.
Upper portion of head and dorsum of the neck may also involve. But ribs behind the
elbow are less commonly involved. You will see the bilateral symptoms (both on left and
right). In advance cases there is severe pruritis, muscular tremors and abnormality of gait
and emaciation. Persistent rubbing can result in loss of wool on the area. Hematoma of
ear and swelling of face may occur due to rubbing. Whenever application of heat or cold
or pressure then animal will show nibbling (pleasant feelings), light or deep pressure, and
pricking needle may cause nibbling and scrapie reaction (elevate the head and nibbling
movement of tongue and lips). This reaction shows that animal feels pleasant.
Impairment of locomotion, hind limb abnormality appears first and there is incomplete
flexion of hock, shortening of steps jump. Weakness and lack of balance and hyper
excitability present. Nodding or jerking of head. Other clinical signs: no proper
swallowing, pretension, vomiting, loss of vision due to optic nerve damage. Anorexia not
present upto 4-5 weeks but after that anorexia.
Goat:
Pruiritis, hyperexcitability, same as in sheep but less loss of body conditions. Clinical
course period is 2-24 weeks.
Diagnosis:
There is vacuolation in optic nerve, medulla, spinal cord. Vacuolation is more visible at
microscopic level.
Differential diagnosis:
Looping ill: it is short term and affect young and old but scrapie affect aged animals.
Pseudo rabies: very rare
Photosenstization.
Pregnancy toxemia: have ketourea.
Treatment:
No specific treatment so animal should be slaughtered.
Control:
Adopt strict quarantine measures. No vaccination.
Parturient Paresis or Milk Fever
Usually it develops due to deficiency of Ca in serum. Whenever there is less Ca there is
loss of normal body tone and muscles become flaccid. It happens in high producing
animals. Hypocalcemia, general weakness, collapse, depression of consciousness.
Factors:
Inability to absorb Ca from intestine or unavailability of ionized calcium ions in serum
e.g. in severe inflammation of intestine and sometimes calcium is bind to some other
elements.
Excessive secretion of Ca in colostrum so excessive loss of Ca from body.
Malabsorption, malnutrition, deficiency of thyroid hormone which helps in Ca
reabsorption from bone.
When calcium level decreases in serum PTH becomes active and provides Ca by
reabsorption of Ca from bones.
If calcitonin level is increased in body then it binds ionic Ca and makes it unavailable for
body for normal functioning.
Aminoglycosides like kenamycin etc. bind the Ca when given I/v rout. EDTA and
oxytetracyclin also bind the Ca. So we can not use these drugs during pregnancy,
parturition and lactation.
Sheep and goat are also prone to milk fever. In sheep it is due to prolonged starvation,
rarely lambing related milk fever but in cattle related to pregnancy.
20-30 % of cows are prone to it and usually 5-10 years old cows having 3rd, 4th, 5th, 6th, or
7th calving. Incidence at first calving is less. There are three phases of milk fever in cattle:
o Prior to parturition (animal may fall on ground)
o During parturition
o After parturition
Maximum care right after 48 hours and occasionally occurs after 6-8 weeks. Suddenly
animal may fall. Most of time during pregnancy estrogen level is increased due to which
loss of appetite; animal does not take feed properly due to which Ca deficiency occurs
and leads to milk fever. Burseem fodder cause increase in estrogen level and leads to
starvation.
Pathogenesis:
Ca level falls in serum which is required from normal body tone, it will cause decreased
heart rate, high pulse rate, flaccid paralysis, hypothermia due to decrease heart rate, and
periphery becomes cool and leads to uterine prolapse and dystokia. Sometimes Mg level
falls but in some cases it shoots up and muscular tetany will be seen. Ca and phosphorus
ratio is disturbed. Ca low and phosphorus high, it is milk fever. Sometimes Ca and P
simultaneously low in serum it is more dangerous.
Clinical Findings:
Mild/Prodormal/subclinical stage:
Animal is in standing position, brief state of excitement, muscle tremors (head and neck),
animal can not move and eat, slight shaking of head, tongue protrudes out, teeth grinding,
temperature normal or slightly high, animal ataxic, anorexia. Agalactia (no milk
production), ruminal stasis, normal temperature, respiration, and heart rate.
All this happens due to loss of Ca and loss of body tone. It may remain for several hours
and at this time animal response very well to the calcium therapy. So early diagnosis is
important.
Sternal Recumbancy Stage:
Unable to stand, cow is drowsy, turned head towards the flank. No tetany, flaccid
muscles, muzzle dry, skin and periphery cooled, rectal temperature 99-101.5 oF,
increased heart rate but intensity very low, pulse also weak, ruminal stasis, constipation,
tympany, and blot.
Lateral Recombancy Stage:
Complete flaccidity, cow can not resume sternal recumbancy, can not move, heart sounds
inaudible, heart rate is increased upto 120 beats/min, pulse almost can not be palpated,
can not raise the jugular vein by putting pressure. This stage can not be retrieved.
Drenching pneumonia is common complication of this stage.
Clinical Pathology:
The Ca level falls from 8 mg to 5 mg/dl of blood and in severe cases upto 2 mg/dl that is
critical level. Calcium and Mg ratio also varies. Normal level of Mg is 1-2 mg but it may
increase upto 4-5 mg/Kg. Normal Ca to Mg ratio is 6:1 but in this condition it is 2:1. in
mild cases it is 5:2.
Phosphorus level may remain normal or may change. Normally it is 1.5 mg/dl and
increase upto 4.5 mg/dl. Consider these values for diagnosis. Treat animal as soon as
possible within 48 hours.
Treatment:
Usually 400-800 ml 25 % calcium borogluconate is given in large animals,
Calcivet.
Melfone-C
While giving Ca note all parameters, high doses may cause Ca toxicity and low dose
causes relapse of Ca. to avoid heart attack give Ca in different doses.
Calcium borogluconate 20-25 ml I/V, 100 ml s/c in small animals.
If slight high dose, immediate death may occur. Ca should be given in combination with
5 % dextrose. Absorption of Ca in tissue is increased due to dextrose because it
emulsifies the Ca. To avoid reoccurrence give 20-30 ml of vitamin D (AD3E).
Increased absorption of calcium from intestine.
Other multivitamis through I/V like B complex. If aspiratory pneumonia, then give
calcium through s/c or intraperitonial route. If you give I/V it will lead to edema,
pulmonary hypertension.
Never inject Ca in summer season in direct sunlight it increases heart rate and chances of
heart attack in animal, so bring animal in shade and give.
Facts:
70-75 % case recovered by calcium therapy, therapy fails in under doing false diagnosis.
Low PTH, Ca therapy you can diagnosis by level of Ca in serum. 100 % animals
recovered in first stage. 30 % in second stage. 26 % in third stage.
Control:
Avoid excessive Ca therapy before parturition. As Ca level increases, calcitonin increases
and parathyroid hormones decreases and whenever pregnancy, high negative pressure
and Ca fall in serum and release in milk so Ca not reabsorbed from bone to serum.
In milk fever diet rich in estrogen level also cause change in Ca level.
You can use testosterone derivatives, they have anabolic action, it not only increas3e
appetite of animal but also decrease estrogen level and improve the calcium metabolism.
Dietary phosphorus can also exert negative pressure on parathyroid hormone. In this
disease if animal getting low P then ratio becomes 6:1 and then there are 30% chances of
milk fever.
If Ca P ratio is 1:3.3 then no chances of milk fever during pregnancy it will create
negative pressure on PTH less chances of milk fever but bad impact is osteoporosis of
bones in animals and it is more common in older animals. To avoid this you can give 5 %
of monosodium phosphate (add it in concentrate as control measure) because our soil is
deficient in phosphorus. P deficiency also leads to post parturient hemoglobinurea.
Managemental Practices:
Avoid excessive Ca feeding in parturition.
Ca is 100-150 g/day can be given in diet, avoid over feeding and also avoid stress during
parturition
CaCl2 can be used by and after 24 hours of parturition this can minimize chances of milk
fever (150 g cacl2 given 1-2 hour before, 1-2 hours during and 1-2 after parturition and
after 10-15 hours of parturition to avoid jerk of negative pressure. CaCl2 has bitter/bad
taste. So you have to give through stomach tube.
Vitamin D3 should be given it helps in absorbance of calcium, vit. D changes to 2,5
dihydropolycalciferol and in kidney 1,25 dihydropolycalciferol and liver converts to
precursor which reabsorbs calcium.
Vitamin D2 @ dose of 200000 IU/oral 4-5 day prior to parturition. Vitamin D3 10-12
days prior to parturition.
Avoid vitamin D3 therapy during lactation or dry period because it absorbs more
calcium. So lead to decrease calcium.
Vitamin AD3E injection 50 ml (20 ml, 15 ml, 15 ml) for three days.
Vitamin D3 2-3 million, 8-10 million units can be given one week prior to parturition.
Vitamin D2 used for one or two week can cause excessive calcification. So D3 should be
used.
We can give PTH hormone but therapy not feasible because we can not give so much
parathyroid hormone (costly)
NH4Cl 20-100g, increased acidity in stomach/rumen having basic environment but Ca
require acidic environment for absorption. So it will keep in absorption of Ca.
Theileriases
There are two types of Theileria:
Caused by Theilaria parva: East cost fever
Caused by Theleria annulata: Tropical or Mediterranean.
T. annulata is more common in the subcontinent (Indopak). These parasites can infect all
types of cattle, buffalo, and yak.
Transmission:
Transmission is through ticks so control is very difficult. Ticks involved in transmission
of T. parva are Rhipicephalous. T. annulata is transmitted by Hyaloma. Both these
organism remain in tick for life span. Do not multiply in tick and comes in saliva. When
bite, it transfer organism to animal. High temperature and high humidity is required for
tick growth. These organisms complete their life cycle in lymphocytes (Schizonts) and in
RBCs (piroplasm).
Clinical Signs:
Incubation period is 10-25 days. Swelling of L.N so locally called (giltyon ka bukhar)
Prescapular L.N prominently swollen and visible in young calves. More deadly disease in
young calves high rise in temperature, anorexia, emaciation, anemia, nasal discharge,
corneal opacity. Sometimes Schizonts and piroplasm block the capillaries and cause
hypoxic injury to the brain and you will see the nervous signs. Poor growth.
Annulata cause anemia, jaundice (destruction of RBC), prescapular L.N swelling and
hemogloninurea.
Postmortem Findings:
Myocardial degeneration, hemorrhages on liver and spleen. If lungs involve thins
exudates in lungs (bronchia, trachea). If not treated 100 % mortality occurs.
In endemic area severity of disease is less but in Theleria free region where if infection
comes then severity is more. Death in summer. Animal becomes carrier after recovery.
Diagnosis:
Based on blood smear examination, stained with Geimsa stain, bluish bodies present in
RBCs. Mostly sample is taken by absorption from swollen LN or micro capillaries of tip
of ear. PCR, ELISA, CFT.
Treatment:
Most effective drug is buparvaquone/Butalex 1 ml for 20 Kg, 2 - 2.5 mg/ Kg I/M
Repeat after two days because animal may not respond to first infection but may quickly
respond to second.
Oxytetracyclin and butalex: 10-20 mg/Kg for 4-6 days regularly.
Antipyretics/anti inflammatory drugs.
Fluid therapy/blood transfusion depends upon severity. 6-8 litres blood can be infused in
cattle. If sever jaundice then give dextrose 5%. Prophylactic treatment is given when
ticks are present. For this purpose inject Butalex 1 cc at the age of 7 days and repeat it
after 1 month.
Post Parturient Hemoglobinurea
It is disease of high producing animals. It occurs after parturition and is characterized by
straining during defecation, red urine, hemoglobinurea, anemia; and death may occur in
this disease. It is more common in buffalo because RBCs are sensitive to saponins e.g.
Brassica compestrus.
Etiology:
This disease occurs due to hypophosphotemia is major cause. It is more common in
buffalo as compared to cattle because plants like Crusiform that contain saponin that
cause fragile RBC, destruction of RBC in buffalo. This plant is deficient in phosphorus
e.g. Brassica compestris, turnip, reddish, and cucumber.
Predisposing factors:
The diet deficient in phosphorus leads to post parturient hemoglobin urea.
If deficiency of phosphorus in soil.
There is deficiency of phosphorus in plants like turnips, brassica, reddish leaves
and beat pulp.
Usually animal in 3rd – 4th lactation are more prone to this disease as compared to
in first, second lactations.
Deficiency of Cu in soil. Cu is essential part of an enzyme dismutase which is
necessary for hemopoiesis.
Animal in dry period have normal P. But lactating animals have deficiency of P
and Ca. So more prone to it. It is metabolic disorder.
It is more common after 2-4 weeks after parturition. Incidence of this disease is
low but mortality upto 50 %. This disease does not occur in beef cattle.
Ingestion of cold water also leads to hemolysis.
Pathogenesis:
Due to phosphorus, as it is essential element in cell wall of cells. If deficient, makes the
RBCs fragile and more chances of hemolysis. But more chances that RBCs are intact in
urine; if RBC are intact then no relation PPH.
Diagnosis:
Through clinical pathology, signs and symptoms.
Clinical Findings:
Hemoglobinuria, inappetence and weakness develop suddenly and there is a severe
depression of the milk yield, although in some acute cases. Dehydration develops
quickly, pale mucous membrane, temperature 103.5 oF. Feaces dry and firm. Low oxygen
carrying capacity of RBCs will not fulfill the requirement of oxygen; there will be
increase heart rate and respiration. So there will be dyspnea and tachycardia. In later
stages there is jaundice. Pica may be present. Course of disease is 3-5 days. Animal
becomes stagger, weak and recombinant.
In non fetal cases this duration may extend upto three weeks. When animal is off feed,
there are chances of ketosis as animal will utilize its own proteins (due to which
emaciation occur and animal becomes woody) and after protein starts utilization of fat
due to which production of ketone bodies.
Clinical Pathology:
Change in normal values. Normal phosphorus level is upto 1.5 - 4 mg/dl but may fall to
0.4-1.5 mg/dl in serum. No RBC in urine. Red brown color and turbid urine.
Treatment:
Best treatment is blood transfusion upto 5 litres. You can get from healthy animals.
Add 4 % Na citrate in blood with ration of 1:10. You can take blood from donor and
recipient on glass slide. Gross match blood on slide. If clotting occurs, avoid infusion.
There is huge variation. Once a while it is acceptable, you cannot repeat it.
Sodium acid phosphate Na2H2PO4 60 g/300 ml water of which is given through I/V or
s/c. Repeat after 12 hours.
Route of administration depends upon the severity of disease. 100 g Na2H2PO4 orally can
be given for 5 days. I/V is given once or twice a day as well as s/c and orally but
maintenance dose is orally for 5 days. Inorganic p also present like injection of
phosphone at rate of 20 ml + 15 ml + 15 ml.
CuSO4 (acidified) 1-2 g orally for 10-15 days. It helps in hemopoiesis.
B-complex, dextrose (if dehydration)
Bone meal containing calcium phosphorus 120 g (1 +1) for 3 days.
Control:
Avoid feeding Crusiferous plants. But if have to be given then also give wheat bran
(phosphorus rich diet) along with it. PPH is third largest problem right after FMD and
HS. Very difficult if there is constipation.
Ketosis
Acetonemia in cattle and pregnancy toxemia in sheep,
Ketosis occurs when glucose is not fed from outside. There is high incidence in high
producing animals because they have negative energy balance as energy is utilized for
milk synthesis. They require balanced diet for producing good milk. So whenever glucose
is utilized in the form of lactose and no glucose available then hypoglycemia. Then
protein and fat of body will be utilized and there will be formation of ketone bodies.
There are three types of ketone bodies: acetoacetic acid, β hydroxyl butyric acid, and
acetone. These produce ketonemia and ketouria.
Normally animals use carbohydrates and in ruminants it is much complex. They get from
cellulose which is converted to fructose and then glucose production which is provided to
body. This glucose is utilized by microbes in rumen to produce VFAs: propionic acid,
butyric acid and acetoacetic acid. Propionic acid is more safe and more glucogenic while
butyric acid and acetoacetic acid are more ketogenic. Microflora converts propionic acid
to oxalic acid which will be converted to glucose. Butyric acid and acetoacetic acid are
converted to acetate in the presence of oxaloacetate. Acetate is further converted in into
glucose. If oxaloacetate is less then they rapidly change into ketone bodies.
Most of time propionic acid no. is high and other two less. Oxaloacetic acid is deficient
then start formation of ketone bodies. If more protein is fed there will be more chances of
butyric acid production and more chances of ketosis.
Diagnosis is difficult in live animals but kits are available strips kip in colour changes
from yellow to red. Huge shift of energy from dam to offspring, after parturition goes in
negative energy balance. Normal ketogenic and glucogenic ratio is equal. In ketosis
ketogenic acids are 4 times higher than propionic acid.
Some other factors like adrenal gland disfunction that leads to deficiency of glucose due
to lack of glucocorticosteroids and cortisole.
Hypothyroidism leads to increased metabolism of glucose, protein and fat causing
hypoglycemia and ultimately ketosis. Hay and silage also have ability to produce VFAs
but hay is less ketogenic and silage is more. Silage contains more butyric acid. Starvation
also leads to ketosis. If chronic disease and off feed for longer time or deficiency of
fodder. Morbidity is 1-10 % rarely occurs.
Primary Ketosis:
Predisposing Factors:
High producing animals fed on barns or stall fed, animal fed inadequate rations, some
nutritional deficiency of soil, complications of PPH, genetic, any defect in TDN,
deficiency of vitamin B12.
Secondary ketosis:
Predisposing Factors:
Right after disease.
Metritis and off feed.
Any disease in which fever act for long time can provide condition.
Ketosis more common in first month after lactation. Less in second month.
More chances in sheep in last month of pregnancy.
Pathogenesis:
No entry of glucose from outside → hypoglycemia → utilization of protein (liver and
muscle), β oxidation of fat → ketone bodies → ketouria
Clinical Findings:
Wasting form: it is the most common form. It is manifested by moderate decrease in
diet, milk yield low for 2-4 days, refuse silage but accept hay and then totally deprived of
hay, rapid loss in body weight, body coat becomes thin, due to loss of s/c fat there is no
elasticity, zero s/c fat may occur and you can name it as woody appearance feaces are
firm and dry
Utilization of protein and fat. Animal may have constipation but not as severe as in PPH.
Cow is depressed and gives appearance of hang lock, hypoglycemia is the cause of it.
Cow is unable to move and can not eat properly. Temperature and respiration are normal
but have low ruminal movements. 25 % loss in milk production. In wasting form mild
type of nervous signs may found in some cases like staggering gait and partial blindness.
Nervous form: Animal walk in circle, may cross its legs, head pushing, apparent
blindness, animal move aimlessly and may wander, licking of skin and inaminate objects
(pica), loss of appetite, chewing movement with salivation. Animal may be off feed but
still chew with salivation, hyperesthesia (animal may become excited), ballowing, muscle
tremor, tetany, and incoordinate gait. Nervous signs last for 2 hours and after that become
normal and reoccur after 8-10 hours of first onset of nervous signs. During this cow may
injure itself by falling on ground.
Clinical Pathology:
Ketonemia, ketouria, hypoglycemia. Blood glucose level reduced form normal i.e. 50
mg/dl to 20-40 mg/dl. In secondary ketosis its level is more than 40 mg/dl or normal (no
sharp change in blood glucose level).
Blood ketones level of 10 mg/dl is acceptable but in this case 10-100 mg/dl which is
toxic. In secondary ketosis it never exceeds 50 mg/dl.
In urine normal ketone level may be as high as 70 mg/dl but most of time it is 10mg/dl.
80-1300 mg/dl level indicates ketosis. (normal range is 10-70 mg/dl). Urine color remains
normal in ketosis but if more ketone bodies then smell may change. Its smell becomes
gur (sugar) like (sweetish)
Milk ketones values are less than 10 and exceed upto 40 mg/dl. 10-40 mg/dl in milk
indicate ketosis.
Diagnosis:
It is based on clinical findings , 100 findings kit, strips available in the form of Rhoter’s
reagent. Normal color is yellow; if changed to red, ketosis.
Weight loss, fall in glucose level indicates ketosis. In secondary ketosis abomasal
displacement, partial anorexia and pass less feaces.
Subclinical Ketosis:
High in high producing animals. Ketone bodies are 20-40 mg/dl. Pure ketosis, ketone
bodies upto 100 mg/dl. No signs are shown.
Treatment:
50 % solution of glucose (glucose-D is saturated).
500 g/litre of N.S or ringer lactate.
Glycerin (oral) 220 g/day (1+1) for two days.
NaHCO3 or ringer to lessen acidosis. Excessive glucose may cause acidosis.
Deg Nala Disease
It is more common in rice growing areas. This disease is still confusing. Some believes
that it is due to fungus. It was introduced in 1930 in the rice growing areas. Name came
from Nala deg which is a monsoon drain. It starts from Sialkot and pass through Sialkot,
Gujranwala, and Lahore.
In this area more crop of rice. It affects buffalo which is fed on rice straw.
Clinically it is characterized by gangrenous lesions on hoof, ears and tails. Initially
necrosis and later affected area shed off.
Etiology:
There are two basic theories about cause:
According to Indian workers it is due to excessive ingestion of toxic amount of selenium
contaminated fodder grown on selenium rich soil. Feeding of rice straw for long period is
associated with it. Selenium is accumulated in rice straw. Its concentration is 8-11.6 times
high in straw rice than grains and grains may contain 5.2-9.8 times higher concentration
of Se than soil.
In Pakistan Dr. Irfan pointed out that this disease is due to mycotoxin produced on rice
straw. Whenever stored in moist condition these may chances of growth of fungus and
there will be production of mycotoxins.
An antidote Degcure developed at National Research Institute of India, Kernel. It
contains MgSO4 1 Kg, FeSO4 166g, CuSO4 24 g, ZnSO4 75 g, CoSO4 15 g. Two doses of
30 grams are given orally/day. After 1-2 days you repeat dose and local ASD of lesions
so that flies do not sit and do not produce maggots. Recovery after 10-15 weeks but not
possible if hooves have shed.
Arsenic improves immunity. Arsenic preparation @ 10 ml/animal for 2-3 days intervals
3-5 injections can be given. Acetyllarson: cnontains 23.6 % arsenic.
Along with it orally give sodium arsenate: 60 mg/animal s/c by Star Labs (on alternate
days).
Locally available toxin binders like myco-ad product of aerobina 60 g myco-ad in ½ litre
of water for five days.
After ten day to treatment animal may show normal sign. In our area condition has
improved by giving mycotoxin binders. Advise formers to use supplement of Cu and zink
in rice growing areas. 1-2 g to large animals for 10-15 days. Leave for 1 month and again
for 15 days. ½ g in small animals for 10-15 g. It is mixed in water and flour for 15.
Raw Cu not pure. Buffalo can tolerate upto 5 g Cu.
Hypomagnesemia
(Lactation tetany, Grass Tetany, Grass Staggers, Wheat
pasture poisoning)
o Hypomagnesemia is mainly related to nerves. There is nervous disorder of cattle
which is due to low level of Mg. Animal would be excited, there is muscle spasm
and death may occur and most commonly occurs as complex entity e.g. acidosis.
o Chances of this are more common in beef animal as compared to dairy animals
because animal fed on high protein diet will have more conversion into NH3. This
high production of ammonia may hamper absorption of Mg from rumen. So
animals on proteinaceous diet are more prone to Mg deficiency. Incidence of
hypomagnesemia is 0.5-1.5 %.
o Diet rich in K, which is antagonist with Mg (lower absorption from intestine). N2
and K contents in plants; this occurs antagonist to Mg.
o It is a complex, hormonal and physiological function. Normal value of Mg is 1.8-
3 Mg/ 100 ml of blood. Affected animal has 0.9 mg/100 ml.
o Normally Mg improves Ca and P absorption. So has role in building of strong
skeleton.
o In a study it was observed that 88 % cases of hypocalcemia also having
hypomagnesemia in lactating animals.
o Other causes may be renal insufficiency. Level of Mg is antagonist to level of K.
Mixture of in 3 liters of water and about 280 g of KCl can kill a cow within 10
min. Excessive K can shift Mg level sharply and can shift to nervous signs and
even death. Hyperkelemia can also lead to heart failure.
o If fed on high lush green Pasteur. Leguminous plants like lucern are rich in Mg
but avoid giving because they also contain saponin and cause blot. Similarly in
estrus there is low Mg because demand of Mg increases.
o During spring lush green pasteur available; there are more chances. But it mostly
occurs in winter and late autumn. If fed animal 83 % proteins there are chances of
deficiency of Mg.
o If deficiency of Na salts in ration K level increases and antagonism with Mg; so
Mg level decreases. Secretion of Mg in milk is also the cause of low Mg level.
Cow producing 20 litres of milk is 3 times deficient in Mg than cow in dry period.
Lactating cow should give Mg supplement. Fasting cows also have Mg
deficiency.
o There are two types of hypomagnesemia:
It could be hypomagnesemia along with hypocalcemia. Signs are tetany,
stiffness, neck and legs.
Hypomagnesemia with normal Ca level. It is acute and rarely happens.
Sudden convulsions and death occurs.
o Old animals are more prone to Mg deficiency. These are metabolic disorder.
Signs and Symptoms:
Nervous type, staggering gait, stiffness of fore limbs, grinding teeth, neck, muscle
tremors are common signs. Convulsions, collapse, padding of feet and death may occur.
In most cases cow suddenly collapse and no clinical signs.
Two forms in dairy animals:
Peracute Lactation Tetany:
Animal is off feed, tends to be more alert due to excitability and twitching of muscles and
ear followed by uneasiness, ballowing, champing of jaws and salivation, temperature
could be 107.6 oF, and more audible heart sounds. There is increased heart rate. Animal
died if untreated.
Sub Acute Lactation Tetanus.
Less sever signs off feed with low milk production, staggering gait, stiffness of neck
muscles, twitching, pupil dilated, and grinding of teeth.
Postmortem Findings:
No postmortem findings.
Lab findings:
Low lever of Mg 0.9 mg/100 ml.
Differential diagnosis:
o Lead poisoning: it does not respond to Mg therapy.
o Ketosis: ketone bodies in blood
o Tetanus: more stiff and prolapse of third eye lid.
o Nitrate poisoning: urine color is of coffee color.
Treatment:
o 30 g of Mg SO4 in 300 ml of water in caution. It causes bradycardia and may lead
to heart arrest. It can be given through I/V but safer if given through s/c.
o If complex situation, Ca, Mg deficiency. Calcium borogluconate 60 g along with
30 g of MgSO4.
o Mixture of Ca borogluconate (200 g) and Mg borogluconate (50 g): 250-500 ml
I/V.
o Mg licks: MgO 35.7 % in molasses which lowers incidence.
Prevention:
You can give hay right after parturition. Epsom salt 3-6 g/liter of water given. Dust the
Pasteur with MgO (12-14 Kg/hector). You can also give carbohydrate supplements in the
form of molasses particularly animal going toward calving and peak production; this will
dilute the protein level. Similarly young calves fed on milk upto 3 months (all milk diet)
may have deficiency of Mg. These sorts of calves are apparently blind, there is
convulsions and death may occur. So give 10 g of Mg SO4 in 100 ml through s/c route
and shift all milk diet with concentrate and add 5 g of MgSO4. This will lower the
incidence of Mg deficiency.
Phosphorus, Calcium and Vitamin D
Their imbalance and ratio play important role.
Phosphorus Deficiency or Pica:
This is condition of deprived appetite in which animal starts eating objects that they
normally do not eat. This condition is normally seen in cattle and buffalo particularly
pregnant and lactating animals and also in horses and goats. Affected animals have the
tendency to lick with anything with which they come into contact. They eat sand, soil,
bone and even excreta. Some affected animals start licking walls and floors.
Cause is not well understood and it is more probably due to indigestion and insufficiency
of Na and phosphates in the field. It may be due to some nervous problems. In lactating
buffalos pica may be a sign of sub-clinical ketosis where animal refuses to eat
concentrate and continue eating roughages. When the condition is first noted animal is in
good health, good state of nutrition but soon there is loss of conditions. Animal becomes
restless, uneasy, and depressed. The patient will almost at any time eat the abnormal
substances. Then in late stages animal becomes quite thin and waited and shows various
intermittent sighs of indigestion like tympany, partially suspended rumination. Fecal
material becomes dry and firm. Sometime diarrhea with offensive odour. Mucous
membrane becomes pale. Skin becomes rough and dry. If untreated the animal may die
from malnutrition after a varying period that may extend over months. This depraved
appetite leads to osteomalacia and there is development of fracture.
Treatment:
Carbonate of iron: 120 g
Finely ground bone meal: 500 g
Common salt: 240 g
Powdered gention: 140 g
Fenugreek 140 g
Equally mix these and a full table spoon is given 3 times daily.
Vitomineral D is given.
Calcium Deficiency
Dietary deficiency or disturbance of metabolism of Ca, P or vitamin D including
imbalance of Ca and P ratio is the principle cause of osteodystrophies. Different factors
involved.
o Calcium deficiency; it may be primary or secondary
1. Primary: an absolute deficiency in diet
2. Secondary: when deficiency is conditioned by some other factors like
excessive intake of phosphorus.
o P deficiency also primary and secondary
1. Secondary: due to excessive intake of Ca
o Vitamin D deficiency is also primary and secondary
1. Primary: when no intake or reduced intake
2. Secondary: when deficiency conditioned by other factors in which
carotene intake
Ca:P ratio should be 2:1 or 1:1 but in livestock 2:1 is best for absorption.
Ca functions in bone formation, milk production, blood clotting, maintenance of
neuromuscular excitability. Lack of appetite, poor growth, loss of condition, infertility,
low milk flow, osteodystrophies, dental defects and tetany may develop due to Ca
deficiency.
Vitamin D Deficiency
Lack of ultraviolet solar radiations and due to dietary deficiency. Signs are reduced
productivity, poor weight gain, and rickets in young, osteomalacia in adult. Vitamin D
assessed in plasma; Ca and phosphorus in serum.
Postmortem:
Lack of mineralization
Osteomalacia due to another reason.
Treatment:
Vitomineral D 120 g in cattle and 20-30 g in sheep and goat orally. It includes vitamin E,
Ca, vitamin D, selenium and P.
Vitamin E and Se are best antioxidants.
Bone phosphate (DCP) 100-120 g in cattle, 20 g in goat (Ca and P)
Cal-C-Con (inj) 200-300 ml I/V and s/c in cattle, 30-60 ml in goat sheep. It is given in
case of milk fever, P and Ca metabolism abnormalities, and rickets.
Melfon C 200-300 ml cattle I/V and s/c and 30 -60 ml I/V, s/c in sheep and goat. In
hypocalcemia and osteomalacia.
Selfos (Vitamin E, Se) inj. 10-20 ml in cattle, 10 ml in small animals.
Fat soluble vitamin:
Vitamin A
All vitamins enhance immune system. Rumen synthesizes vitamin A and B complex.
Vitamin B12 have to be supplemented in diet if cobalt deficiency in diet.
Deficiency signs:
Night blindness, xenthophahalmia (thickening and clouding of cornea specially in calves
and ulceration and serous mucoid discharge from eyes with corneal keratinization,
ulceration and phosphobia. Rough dry coat of body, growth rate low, reproductive
efficiency reduced.
Dose rate 440 IU/Kg of vitamin
Water Soluble Vitamin
Vitamin C and B complex
These are of secondary importance. B-complex: niacin, folic acid, vitamin B12
(synthesized in rumen). When animal is in stress or disease, supplement these vitamins.
Mycotoxins
Important one is Aspergillus. Filaments and spores are present in roughages and
concentrate. Vegetative from causes mycosis. It usually develops when immune status is
weak. Lungs, udder, intestine are affected. Mycotoxins of importance in veterinary is
aflatoxin. Other toxins are Deoxynivelenol, T-2 toxin, and ochratoxins. Molds also
present in silage.
Symptoms of aflatoxin are weak, anorexic, depression, rough coat, and low production.
In chronic case jaundice like signs.
Treatment:
No such treatment but toxin binders are used. Universal antidote i.e. activated charcoal is
given. Purgative is given along with it. Charcoal 1g per Kg b. wt. orally.
Other proportions aluminosilicate, clay, bentonite, xeolite, complex indigestible
carbohydrate like cellulose, polysaccharide.
Supportive therapy as blood therapy, liver tonic.
Above was to avoid absorption from rumen. If absorbed, give antitoxins. Aflatoxin not
more than 20 ppb in lactating feed. Aflatoxin no more than 0.5 ppb in milk.
.
Disaster Management
Different sort of disaster which can affect human beings and animals as some natural
desaster like earthquake, flood or there could be severe weather conditions, extreme hot
or extreme cool.
As regards non natural and man made disaster it includes atomic explosions, wars, huge
destruction of buildings, roads, construction and in atomic war conditions as worst as it
can destroy every thing in world. We should manage ourselves for disaster.
Natural Disaster
Earthquake:
If area is prone to earthquakes then buildings should be earthquake proof.
Flood:
If flood, there will be destruction of animals, crops etc. You can predict flood by level of
water in river and alarm the people and farmers. In case of flood veterinarians are
assigned as there is contagious disease spread like FMD, anthrax, and enteric diseases. In
case of humans there is spread of cholera.
Snakebite:
Snakebite is common. So there should be emergency measures for it also.
Measures for in Case of Natural Disaster
o One measure you can adopt during disaster earthquake and particularly flood is
open all the animas and let them move.
o Vaccinate each and every animal before flood season.
o Deworm the animas.
o Place your animas on higher place where flood water has no access.
o
Fire
Fire can also cause alarming situation. Fire in forest affect plants as well as wild life for
that we have to use modern control measures. We can use water and CO2 foam. If fire is
on wood then use water. If fire of oil origin, do not use water. Sand or CO2 in can be
used.
By timely and quick action you can save the life. Animals have very good sense of
disaster specially earthquake.
War Conditions
Very much problem is that no veterinary service is available. So animals become off feed
firstly. First measure is to open animals so that they can move, eat and save their life.
In war area most of casualties of animal is due to lack of food. So best solution is to make
your animal free.
Atomic War
Shelters are available in USA and Russia. You can make shelters that avoid radiations
which have any harmful effect.
Before 2005 there was no concept of disaster management in Pakistan but now we have
good equipments, ambulances and fire fighters. We had not the machinery which can
remove concrete blocks but now we have.