Vetreckon 15 december, Issue 4

VETRECKON – DIGITAL VETERINARY MAGAZINE Issue #4
33

VETRECKON DIGITAL VETERINARY MAGAZINE | Issue #4 2
Publishing Director
Sara Naqvi
+91-8800939109
axonvet@gmail.com
Editor
Dr Ibne Ali, M.V.Sc. IVRI
+91-9557907955
ibnester@gmail.com
Design & Circulation
Rahul Thakkar
+91-9540121922
thakkarrahul@axonvet.com
Contents
 Acute Diahhrea in Dogs –
Clinical Approach
 Recent Trends in Dairy
Farming – Corporate
Scenario
 Caseous Lymphadenitis in
Goats
 Amitraz - uses
 Centre proposes strict rules
to regulate pet shops in
VETRECKON
Vetreckon magazine is the magazine
and web/digital resource for the Indian
community of veterinary students,
teachers and field veterinarians which
provide latest up to date information
and new technology developments.
Hemorrhagic gastroenteritis (HGE) is a diarrheal syndrome
of unknown etiology that has a predilection for small breed
dogs; it has not been reported in cats. Speculation regarding
pathogenesis includes type-1 hypersensitivity reaction to
food components, CPE, and C difficile toxins A/B. HGE is
distinctively characterized by peracute onset of bloody
diarrhea and vomiting accompanied by marked
hemoconcentration. Packed cell volume of an affected dog
can reach 75% or higher within hours of onset of signs, yet
total plasma protein often remains within reference range.
Symptomatic therapy, primarily aggressive IV fluid therapy
and gastroprotectants, results in marked clinical
improvement within 24 to 48 hours. Antimicrobial therapy
is usually administered, although in a recent study, clinical
response was not improved in dogs that received antibiotics
(amoxicillin/clavulanic acid).With appropriate therapy,
mortality is low despite severity of signs.
Ibne Ali

Peer Review – collected from various
excerpts by P. Jane Armstrong, DVM, MS,
MBA, Diplomate ACVIM
Diarrhea can be defined as increased
fecal fluidity, usually accompanied by
increased defecation frequency and
volume of feces. Most cases of diarrhea
are mild and self-limiting, requiring
minimal diagnostics and therapy. Life-
threatening cases can occur, however,
that require greater diagnostic efforts
and intensive care.
ACUTE VERSUS CHRONIC
Diarrhea is considered:
• Acute if it lasts for less than 14 days
• Chronic if it persists for longer than 14
days.
Historical and clinical findings and
appearance of the feces are used to
differentiate whether the diarrhea is of
small bowel or large bowel origin (Table
1). This differentiation is most important
in cases of chronic diarrhea, when
selection of diagnostic tests is influenced
by the presumed location of enteric
pathology. Additionally, many pets with
acute diarrhea display signs of
enterocolitis (mixed small and large
bowel signs).
PREVALENCE & INCIDENCE
While diarrhea is a very common
presenting problem in companion animal
practice, it is either more common in
dogs than cats, or dogs with diarrhea are
more likely to be examined by a
veterinarian. A report of diagnoses from
over 2 million dogs and almost 430,000
cats in 2011 indicated that
“gastroenteritis (GI upset)” and “colitis”
both ranked in the top 19 diagnoses for
dogs, but were not among the most
common diagnoses in cats.
Incidence of diarrhea and vomiting was
investigated prospectively in a study of
585 large-breed dogs followed from birth
to 2 years of age.
Most dogs had only one episode of
diarrhea and/or vomiting during the
study period; those suffering from
several episodes demonstrated relatively
long periods between episodes.
There was a positive association between
occurrence of diarrhea and vomiting in
the same dog, but episodes of diarrhea
and vomiting did not usually occur at the
same time. Diarrhea and vomiting had a
much higher frequency in young puppies
despite complete vaccination and
deworming protocols. Risk for diarrhea
decreased from 16% in 7-to-12-weekold
puppies to 5.4% in 12-to 18-month-old
dogs.
An early study showed that frequency of
both vomiting and diarrhea were highest
in puppies and declined with increasing
age4; this is supported by Banfield data
demonstrating that “gastroenteritis (GI
upset)” was common in dogs up to 3
years but much less common in dogs
above that age.
OWNER IDENTIFICATION
Diarrhea is generally recognized by
owners, as long as the feces are
observed. Most owners realize that
diarrhea is usually self-limiting and may
be more prone to “wait and see” when
pets develop gastrointestinal (GI) signs,
compared to
clinical
signs
that
are not as familiar.
In a study of 772 pet dogs in England,
70% of the reports of diarrhea involved
only 1 or 2 episodes, and 78% lasted 2
days or less. Veterinary attention was
sought for only 10% of dogs with diarrhea
(and 5% of vomiting dogs). 5 All dogs
with diarrhea persisting for 7 days or
longer were presented to a veterinarian.
PATHOPHYSIOLOGY
Four major pathophysiologic
mechanisms can cause diarrhea.
Osmotic forces and changes in mucosal
permeability are the most important
mechanisms in dogs and cats. In most
small animal diseases, multiple
mechanisms contribute to diarrhea, and
it can be difficult to determine the
predominant mechanism.
1. Osmotic diarrhea: The number of
osmotically active particles in feces
determines water content, and presence
of increased numbers of these particles
within the intestinal lumen leads to
osmotic diarrhea.
Osmotic diarrhea occurs with many
malabsorptive disorders, such as
exocrine pancreatic insufficiency, in
which poorly digested nutrients are
malabsorbed, remain within the GI
lumen, and attract water. It can also
occur with overeating and dietary
indiscretion if poorly absorbed nutrients
are ingested.
Retention of nutrients in the GI tract can
also lead to dysbiosis (see below) and
fermentation of carbohydrates, which
further increases the number of
osmotically active particles. A hallmark
of osmotic diarrhea is that it resolves
when the patient stops ingesting poorly
absorbable solute.
2. Secretory diarrhea: Stimulation of
crypt enterocytes results in secretion of
large volumes of fluid that exceeds the
absorptive ability of the intestine. This

occurs most commonly with infectious
diseases, such as enteropathogenic
Escherichia coli and salmonellosis, but is
also a mechanism of diarrhea related to
inflammatory bowel disease (IBD). By-
products of dysbiosis can also stimulate
intestinal secretion. One distinguishing
feature of secretory diarrhea is its
persistence despite fasting, which is due
to abnormalities in ion transport not
related to food.
3. Increased mucosal permeability:
Increased permeability of the intestinal
mucosa causes loss of fluids, electrolytes,
proteins, and blood into the intestinal
lumen. It commonly accompanies
erosive, ulcerative, neoplastic (intestinal
lymphoma), and inflammatory
processes, such as IBD and hookworm
infection.
4. Abnormal motility: Deranged motility
is often secondary to disorders that cause
diarrhea. Decreased segmental
contractions result in transport of ingesta
at a rate too fast for normal digestion and
absorption. Platelet-activating factor,
synthesized and released from several
immunocytes, may be one of the
inflammatory response mediators that
stimulates giant aboral contractions, the
powerful contractions that propagate—
uninterrupted—from the small intestine
to the ileum or colon.
Tremendous fluid loss can occur when
the small and/or large intestine are not
functioning normally. Mild diarrhea
causes few metabolic consequences;
however, moderate or severe diarrhea
can lead to profound dehydration,
hypovolemic shock, electrolyte
abnormalities (hypokalemia,
hypochloremia, and hyponatremia), and
acid–base disturbances. Metabolic
acidosis typically develops secondary to
loss of intestinal bicarbonate and
dehydration leading to hypovolemia,
anaerobic metabolism by tissues, and
production of lactic acid.
ACUTE DIARRHEA: CAUSES
There are many causes of acute diarrhea
in dogs and cats. In many cases of acute
diarrhea, signs resolve spontaneously or
with symptomatic therapy without a
specific cause being discovered.
In animals with chronic diarrhea, a
thorough diagnostic evaluation and
appropriate dietary and therapeutic trials
for diagnostic purposes are much more
important. It is beyond the scope of this
review to discuss causes and diagnostic
approach to pets with chronic diarrhea;
however, watch for evidence of
chronicity even at first presentation of a
pet with diarrhea.
Endoparasites
It is well documented that
endoparasitism is primarily a concern in
young animals. Batchelor, et al,
documented that dogs with GI signs had
a higher prevalence of intestinal
parasites, including Giardia and
Toxocara. In a referral population,
however, dogs with GI signs had no
greater odds of endoparasitism than
healthy animals; instead, age and
median household income were the
strongest predictors of endoparasitism,
and dogs from heavily populated ZIP
codes had the greatest risk for
endoparasitism
.
Dietary Indiscretion
Dietary indiscretion is a common cause
of acute diarrhea. One study reported
that feeding a home-cooked diet, recent
history of scavenging, or change of diet
all increased the risk for diarrhea in dogs.
Another study found a positive
correlation between development of
diarrhea and/or vomiting and reports of
scavenging behavior (stealing food;
eating trash; or eating feces from horses,
farm animals, or cats). No correlation was
found between GI signs and eating table
food.
Bacterial Enteritis
A variety of bacteria are known or
suspected to cause enteritis in dogs and
cats. Establishing a diagnosis of bacterial
enteritis creates a significant challenge
due to:
• Limitations in understanding the
complex intestinal microflora
• Inadequate investigation of many
potential pathogens.
The fact that the microorganisms
responsible for enteritis can be found in
healthy individuals, and may not be
found at a higher prevalence in animals
with diarrhea, confounds diagnosis,
treatment decisions, and assessment of
infection control and zoonotic risk.
Cytology. Microscopic examination of
fresh feces has been used by some
clinicians for presumptive diagnosis of
disease by evaluating pathogen
appearance. However, fecal cytology is
now considered of no diagnostic utility
for bacterial enteropathogen
identification because:
• These bacteria can be present in normal
animals
• Appearance does not differentiate
between pathogenic strains and
harmless commensal species
• In the case of Clostridium perfringens,
no studies have reported a correlation
between presence or number of spores
and signs of disease.
Enterotoxin has received the most
attention in relation to C perfringens, and
some association has been found
between the presence of C perfringens
enterotoxin (CPE) and diarrhea in dogs.
Intestinal Microbes. Intestinal microbes
play a crucial role in maintenance of host
health. They:

• Act as a defending barrier against
transient pathogens
• Support the host in digestion and
energy harvest from the diet
• Stimulate the immune system
• Provide nutritional support for
enterocytes.
The total microbial load in the intestine is
estimated at 1012
to 1014
organisms,
about 10× the number of host cells in the
entire body. New technologies have
enhanced our understanding of the
microorganisms harbored by
mammalian GI tracts. Massive parallel
16S rRNA gene pyro sequencing has
provided the tool for molecular-
phylogenetic characterization of the GI
tract’s complex microbial community.
The gene content of these microbes is
defined as the intestinal microbiome.
There is mounting evidence that changes
in microbial populations play an
important role in pathogenesis of acute
and chronic enteropathies of dogs. In a
recent study, dogs with acute diarrhea,
especially those with acute hemorrhagic
diarrhea, had the most profound
alterations in their fecal microbiome
compared to healthy dogs, and observed
changes differed between acute and
chronic disease states.
Recognition of fecal biome alterations
(dysbiosis) in pets with various GI
disorders opens the door to future
studies that evaluate the ability of
probiotics, prebiotics, antibiotics, and
other therapies to restore the balance of
bacterial flora.
ACUTE DIARRHEA: HISTORY &
PHYSICAL EXAMINATION
Signalment and history often contain the
information necessary to make a
tentative diagnosis or help rank
differential diagnoses.
Puppies and kittens, especially from
shelters, are prone to viral diseases and
GI parasites.
Physical examination may detect:
• Abdominal masses • Dilated loops of
bowel
• Foreign bodies • Intussusception
• Abdominal pain.
When patient size permits, routinely
performing digital rectal palpation aids
recovery of feces for observation of the
presence of
blood (digested
[melena] or
fresh) and/or
mucus.
Dehydration (at
least 5% to be
clinically noted)
may be evident
by dry mucous
membranes,
loss of skin
turgor,
prolonged
capillary refill
time, or
enophthalmos.
More
pronounced alterations in these
parameters indicate moderate
dehydration (7%–9%); extreme
alterations denote severe dehydration
(10%–12%) approaching hypovolemic
shock (tachycardia with poor peripheral
perfusion and weak peripheral pulses).
ACUTE DIARRHEA: DIAGNOSTICS
The most important initial step in
evaluating animals with acute diarrhea is
to determine if they have a self-limiting
or potentially life-threatening problem
(Table 2). This distinction is crucial as it
guides the level of diagnostics and
therapy indicated, and should be based
on a thorough history, careful physical
examination, clinical experience and
judgment, and a sound understanding of
the differential diagnoses for acute
diarrhea.
Initial Diagnostics
Fecal Flotation. Animals with suspected
self-limiting diarrhea should always be
tested for GI parasites by centrifugation
fecal flotation using zinc sulfate, paired
with indirect fluorescent antibody testing
for Giardia cysts and Cryptosporidium
oocysts.
Cytology. Fecal cytology, a low-yield
diagnostic test, is not useful for detection
of potential bacterial enteropathogens
(Figure). In contrast, exfoliative rectal
cytology can be useful in dogs and cats
with signs of colitis, especially when
chronic, to identify fungal organisms or
colonic neoplasia.
Laboratory Analysis.
Measuring total plasma protein and
hematocrit will help assess hydration
and provide a baseline for reference if
clinical signs persist or progress.
Symptomatic Therapy
• If dietary indiscretion has occurred,
removal of the incriminating factors
and/or feeding a highly digestible diet
for 3 to 5 days usually helps resolve
diarrhea.
• If parasites are detected, diarrhea
should improve 2 to 3 days after
appropriate treatment
• If an etiology is not found, a
presumptive diagnosis of
acute idiopathic self-limiting diarrhea
may be made.
Symptomatic therapy usually relieves
clinical signs in 1 to 3 days. If diarrhea
persists or other clinical signs develop
or intensify, a more serious problem may
exist, requiring thorough evaluation and
more intensive therapy.
Additional Diagnostics

Laboratory Analysis. Laboratory
evaluation helps rank differential
diagnoses as well as assess severity of
dehydration and electrolyte disorders; it
may include:
• Complete blood count
• Serum biochemistry profile
• Urinalysis
•Baseline cortisol (to exclude
hypoadrenocorticism)
• SNAP Parvo Test.
In chronic or recurrent cases of diarrhea,
serum concentrations of cobalamin and
folate and canine or feline trypsin- like
immunoreactivity (cTLI or fTLI) can be
measured. Depending on clinical signs,
patients may be evaluated for
hyperthyroidism (cats) and pancreatitis.
Radiography.
Survey abdominal radiographs may
demonstrate an abdominal mass, dilated
loop of bowel, ileocolic intussusception,
foreign body obstruction, or linear
foreign body requiring surgical
intervention.
Specific Identification.
Additional diagnostic tests may be
indicated to definitively diagnose a
specific organism or disease or to pursue
diagnosis if a cause is not yet evident
(eg, abdominal ultrasound).
• Identification of Tritrichomonas foetus;
several diagnostic tests are available
• Serologic testing for feline leukemia
and immunodeficiency viruses may be
warranted in diarrheic cats based on
housing and origin
• Partial analysis for enteric pathogens,
usually reserved for diarrheic pets that
are systemically ill or in contact with an
immunosuppressed person:
»» Fecal enteric panel:
Gram-stained fecal smear, CPE
enterotoxin enzyme-linked
immunosorbent assay (ELISA), C difficile
toxin A/B ELISA
»» Fecal culture or polymerase chain
reaction (PCR):
For potential bacterial pathogens, such
as Salmonella and Campylobacter. It is
very difficult to establish evidence for a
causal association between the presence
of a specific bacterium in the feces and
occurrence of diarrhea.
ACUTE DIARRHEA: MEDICAL
THERAPY
Most cases of self-limiting diarrhea
resolve within 1 to 5 days, following
correction of the underlying cause and/or
symptomatic treatment. Nonspecific
symptomatic therapy may include one or
more of the following:
• Nutritional management
• Therapeutic deworming
• Antidiarrheal
• Antiemetic and/or gastroprotectant
• Probiotic
• Antimicrobial (selected
cases)
• Fluid therapy.
Nutritional Management
Administration. Animals with acute
diarrhea often benefit from withholding
food for 6 to 12 hours followed by
frequent (3–6 small meals/day) feeding of
small amounts of a highly digestible, so-
called “bland,” diet; amount fed per meal
can be slowly increased.
• Such diets for dogs should have a low or
modest fat content; fat restriction is not
required for cats.
• Useful choices include boiled rice with
lean chicken, low-fat cottage cheese.
When diarrhea resolves, the animal’s
usual diet can be slowly reintroduced
over a 2- to 3-day period by adding 25%,
50%, 75%, and finally 100% of the usual
diet. If vomiting is concurrently present,
an antiemetic can be administered.
High-fiber diets. For pets with signs of
acute large bowel diarrhea, a high-fiber
diet is often used instead of a bland diet
as fiber may be beneficial in reducing
tenesmus and facilitating colonic
epithelial repair. Commercial products
with increased mixed (soluble and
insoluble) fiber are ideal. Soluble fiber
(psyllium mucilloid, 1 tsp/10 kg body
weight) may be added to a bland diet.
Therapeutic Deworming
Parasite Identification. If a GI parasite is
identified on fecal examination, the
appropriate antiparasiticide should be
prescribed.
In many dogs and cats with acute
diarrhea, parasitic infection remains a
possibility despite negative test results
because:
• Testing is not 100% sensitive
• Not all parasites shed ova continuously.
Antiparasiticide Selection. For these
reasons, a good therapeutic strategy to
consider is administration of a broad-
spectrum dewormer, such as
fenbendazole, which is also an excellent
choice for treating giardiasis, showing
better efficacy and a greater safety
margin than metronidazole.
If a response to therapeutic deworming is
seen, a second course of fenbendazole in
3 months is needed for some parasites,
such as whipworms.
Antidiarrheals
Indications. If diarrhea is frequent
enough to interfere with the animal’s (or
sometimes the owner’s) ability to rest,
causes apparent pain or discomfort, or
results in large fluid losses, an opioid may
be given to alter intestinal motility.
Mechanism of Action. Opioids prolong
intestinal transit time, allowing increased
fluid absorption and reduction in the
frequency of diarrhea. They act by:
• Increasing colonic segmentation, fluid
absorption, and anal tone
• Decreasing propulsive peristaltic
contractions and secretion
These drugs are particularly effective in
patients with large bowel diarrhea
(colitis).
Specific Drugs.

Diphenoxylate or loperamide is very
effective in reducing frequency of
diarrhea.
• Both are available as elixirs, making
dosing convenient for small dogs and
cats.
• Loperamide is more potent and has
faster onset and longer duration of action
than diphenoxylate.
• In dogs, both drugs—at recommended
doses—are safe and have few side
effects.
• In cats, excitatory behavior can occur,
but appears to be rare; for this reason,
though, these drugs should be used
with caution in cats. If a toxin or possibly
pathogenic bacteria are the suspected
cause of acute diarrhea, opioids are
contraindicated because they may
increase toxin absorption or time for
bacterial proliferation.
Probiotics
Definition. Probiotics are live
microorganisms that, when
administered in adequate amounts,
confer a health benefit on the host
(World Health Organization definition).
Probioticsinclude a wide variety of
organisms, such as various species of
Lactobacillus, Bifidobacter, Bacillus, E
coli, Streptococcus, and Saccharomyces.
Mechanism of Action. Both live and dead
cells in probiotic products can generate
beneficial biological responses.
• Live probiotic cells influence both GI
microbiome and the immune response.
• Components of dead cells may have
anti-inflammatory effects in the GI tract.
In the case of live probiotic organisms,
bacterial levels in feces disappear within
days when supplementation ceases.
Clinical Evidence. To date, limited clinical
trials with probiotics have been
performed in dogs and cats with GI
disorders.
Antimicrobial Therapy
Nonspecific Use. Routine use of
antibiotics in cases of acute
uncomplicated diarrhea is strongly
discouraged. If an antibiotic is selected
for nonspecific use in such cases,
metronidazole or tylosin is an
appropriate choice.
Specific Use. In acute intestinal diseases,
antimicrobials are specifically indicated
only in animals with:
• Confirmed bacterial infection (eg,
positive blood culture and/or presence of
enteropathogenic bacteria on fecal
culture, along with signs of sepsis)
• Predisposition for bacterial
translocation (eg, disruption of intestinal
epithelial barrier)
• Increased risk for sepsis
Pets with acute bloody diarrhea of
unknown cause are usually treated with
an antibiotic, such as
amoxicillin/clavulanic acid, or monitored
very closely because:
• Ruling out enteric bacterial infection is
challenging
• Bacterial translocation is a potentially
life-threatening complication.
Markedly hemorrhagic diarrhea is often
interpreted as evidence of a breach of
intestinal integrity, justifying use of
antimicrobials, although no studies
document an increased risk for bacterial
translocation or sepsis in these patients.
Fluid Therapy
Administration. An animal’s deficit due
to dehydration can be calculated by
multiplying the percent of estimated
dehydration (from physical examination)
times body weight (kg). Maintenance
fluids (44–66 mL/kg/day) should be
added to this deficit. Continued losses
from diarrhea should be estimated and
added to the fluid volume administered.
If mild dehydration is present, a balanced
isotonic polyionic fluid (lactated Ringer’s)
can be administered subcutaneously,
but animals with severe dehydration
caused by life-threatening acute diarrhea
require intravenous fluid therapy.
Further Diagnostics. If diarrhea worsens
or other clinical signs develop, the animal
should be re-evaluated and further
diagnostics considered. Any underlying
conditions should be specifically treated.
If further diagnostic testing is needed,
fluid therapy consisting of crystalloids
and possible addition of colloids should
be instituted prior to obtaining a
definitive diagnosis.
Feeding. Food should be withheld for no
more than 12 hours and an antiemetic
administered if vomiting occurs to allow
feeding as soon as possible. Puppies with
parvoviral diarrhea treated by early
enteral feeding showed more rapid
clinical improvement than puppies held
off food.
Monitoring. Careful monitoring is
required during fluid therapy.
• Physical examination findings that
indicated dehydration should gradually
improve as the patient is rehydrated
during the first 24 hours of therapy.
• Hematocrit and total protein should
decrease.
• Body weight should be measured
frequently, as changes accurately reflect
hydration.
»» After hydration has been
reestablished, body weight should
remain relatively stable throughout the
treatment.
SUMMARY
• Dogs and cats frequently develop
diarrhea that starts abruptly and lasts for
less than 7 days.
• Most cases are mild and self-limiting,
and likely associated with changes to the
intestinal microbiota.
• In mild cases, in which there is no
indication for antimicrobial therapy,
nutritional management, therapeutic
deworming, and probiotic therapy,
sometimes in conjunction with an
antidiarrheal agent, should be
considered.
• In cases with more severe, sometimes
life-threatening, signs, a thorough and
logical diagnostic plan must be followed
to obtain an accurate diagnosis and guide
appropriate therapy

By Darshnik Bhateja, B.Tech, Dairy
Tech, NDRI
The country's dairy market will
continue to grow at about 13-15 per
cent annuallytill 2019-20,onincreasing
consumption of value added products
(dahi, paneer, ghee etc) and the value
chain becoming more and more
organised, according to a report by
Rabobank. Rabobank expects value
added dairy products such as yogurt,
paneer, cheese, ice cream and baby
food to grow at a CAGR (compound
annual growth rate) of 20 to 30 per cent
in the next four to five years.
• The country's total organized
diary sector is about USD 10 billion in
2012-13, comprising cooperatives and
private players who control the supply
chain linkages.
• "For years, the Indian dairy
market has remained an enigma for
global dairy players," said Rabobank
Analyst Shiva Mudgil, adding that
currently, however, the market is in a
transition phase.
• High market growth and
favorable market conditions may make
now the right time for global players to
engage with the Indian dairy sector, he
pointed out.
Demand Supply scenario is very
encouraging for the dairy farmers and
processing industries. it imperative
that no big player want to enter in
production system but everybody
wants milk for processing because
there is huge demand in the urban
areas. So production burden will
remain with farmers who are ultimate
producers. Cost of milk is increasing
due to lack of supply. In figure 1, above,
shows that annual increase in
production is 3.7 MT while demand
increasing at the rate of 6 MT per year.
That’s why cooperatives luring farmers
by giving most competitive prices and
incentives for quality milk production.
Multinational Scenario in Dairy
Industry in India “Apart from Danone
Food and Beverages (India), no one has
yet set up production base in India.
Danone, too, is outsourcing parts of its
production, while New Zealand’s
Fonterra is exploring possibilities of
tying up with local partners.
Outsourcing of production would only
help local players.” The foreign players
would opt for a partnership model with
local ones, and not go for direct
procurement from farmers. “They
would focus on high-end value-added
products like flavoured yogurt, very
popular in the international market. It’s
vital to think that engaging local
production facilities with big players
and helping them in procurement will
setup long lasting businesses in this
growing sector.
Most local entities feel foreign dairy
players taking interest in the market
would help open it further and gave
them competition. However, it should
be noted here that most foreign
players are not keen on backward
integration (not interested in
establishing their own dairy farms);
they would prefer tying up with local
players for production and focus on
marketing and distribution.
Right now, 90-95 per cent of the Indian
market is traditional liquid milk and the
remaining is value-added products.
Entry of foreign players will drive
demand in this segment and open the
value-added products segment for
Indian players as well.
Thanks to the rise in disposable
income, there is heightened consumer
interest in higher protein diets. With
entities paying attention to this
segment, the sector is set to grow
further over the years. Currently, 70-80
per cent of milk is procured from small
and marginal farmers. Rabobank
expects this procurement pattern of
milk to continue over the next decade
as well. Foreign players might find this
challenging and it will take some time
for them to be successful in India.

Formulations: Topical: 12.5% w/v
concentrated liquid;
Action: Increases neuronal activity
through its action on octopamine
receptors of mites.
Use:
1. To treat generalized mite infestation,
specifically canine demodicosis and
sarcoptic acariasis.
2. Dip to be left on coat.
3. Clipping long hair coats will improve
penetration.
4. Monthly application of the spot-on
product for demodicosis is not uniformly
effective. Concurrent bacterial skin
infections should be treated
appropriately.
5. Treatment and prevention of fleas and
ticks, and treatment of lice and
demodicosis in dogs & calves.
6. Use with care in small dogs.
7. Used for generalized demodicosis in
ferrets and hamsters and for acariasis in
rodents.
Safety and handling: Do not store
diluted product.
LD50:
Oral LD50, rat, acute: 800 mg/kg
Dermal LD50, rat, acute: >1600 mg/kg
Mechanism of action of amitraz
The acaricidal activity of amitraz is due to
its antagonistic effect on octopamine
receptors of the nerve cells in the brain.
Parasites become hyperexcited,
paralyzed and eventually die. This mode
of action is different from those of
synthetic pyrethroids,
organophosphates and other
ectoparasiticides.
Contraindications: Do not use in dogs
and calves <3 months (<8 weeks for spot-
on product), in Chihuahuas, diabetic
animals.
WARNING !!!: Never use on cats collars
approved only for dogs.
Adverse reactions: Sedation and
bradycardia; Antidote - alpha-2
antagonist, e.g. atipamezole. Can cause
irritation of the skin.
Drug interactions: No information
available.
DOSES
Large and small ruminants:•
1. Tick control / Earsore / Humpsore – 2ml
per liter of water
2. Mites – 4ml per liter of water
3. Sheep & Goat seasonal dipping – 2ml
per liter of water
Dogs:•
1. Generalized demodicosis: 2 ml Amitraz
per liter ofwater q5–7d until two negative
skin scrapings/hair plucks are achieved 2
weeks apart.
2. Sarcoptic acariasis: 1 ml Amitraz per
liter of water weekly for 2–6 weeks.
3. Prophylactic: spot-on product: 20
mg/kg each amitraz and metaflumizone
monthly.
Cats: Avoid in Cats
Small mammals: Ferrets, Guinea Pigs,
Rats and Mice: (1 ml Amitraz
concentrated liquid in 1 liter water)
applied topically to skin q14d for 3–6
treatments;
Birds, Reptiles: No information available.
Brands in market: Demonil, Virtraz,
Note: This article IS NOT A PRODUCT
LABEL. It offers complementary
information that may be useful to
veterinary professionals and users that
are not familiar with veterinary
antiparasitics.

Caseous
Lymphadenitis
in Goats
Introduction
Caseous Lymphadenitis (CL) is a
chronically infectious disease of
sheep and goats that is caused by the
bacterium Corynebacterium
pseudotuberculosis. Prevalent on all
continents throughout the world, CL
causes ulcerative lymphadenitis in
horses and superficial abscesses in
bovines, swine, rabbits, deer,
laboratory animals, and humans.
Some economic losses due to CL are
caused when breeding stock is no
longer marketable, when carcasses
are condemned due to internal
abscesses,when animalsdie, or when
abscesses devalue animal hides.
The disease is characterized by
abscess formation in or near major
peripheral lymph nodes (external
form) or within internal organs and
lymph nodes (internal form).
Although both the external and
internal forms of CL occur in sheep
and goats, the external form is more
common in goats, and the internal
form is more common in sheep.
Once established on a farm or region
(endemic), it is primarily maintained
by contamination of the environment
with active draining lesions, animals
with the internal form of the disease
that contaminate the environment
through nasal discharge or coughing,
the ability of the bacteria to survive
harsh environmental conditions, and
lack of strict biosecurity necessary to
reduce the number and prevent
introduction of new cases.
Causes and Reasons of
Caseous Lymphadenitis
C pseudotuberculosis is a
gram-positive,
facultative, intracellular
coccobacillus. Two
biotypes have been
identified based on the
ability of the bacteria to
reduce nitrate: a nitrate-
negative group that
infects sheep and goats,
and a nitrate-positive
group that infects
horses. Isolates from
cattle are a
heterogeneous group.
There are 2 main
factors of disease
1. Production of
Phospholipase D
2. Second virulence
factor
Pathogenesis
All strains produce an exotoxin called
phospholipase D that enhances
dissemination of the bacteria by
damaging endothelial cells and
increasingvascularpermeability. The
bacterium has a second virulence
factor which is an external lipid coat
that provides protection from
hydrolytic enzymes in host
phagocytes.
Replication of bacteria occurs in the
phagocytes, which then rupture and
release bacteria. The ongoing
process of bacterial replication,
followed by attraction and
subsequent death of
inflammatory cells, forms the
characteristic abscesses associated
with CL. To establish infection, C
pseudotuberculosis must penetrate
skin or mucous membranes. The
most common site of entry is the skin
after an injury that may result from
shearing, tagging, tail docking,
castration, or other environmental

hazards resulting in skin trauma.
Contact with purulent material
draining from open, active lesions
most commonly serves as the source
of bacteria through these breaches in
the skin. Although less common,
entry across mucous membranes
from inhalation or ingestion of the
bacteria also serves as a means of
infection. Once the bacteria have
entered the body, they move to the
lymph nodes via the regional draining
lymphatic system. Internally, the
bacteria establish infection not only
in the lymph nodes but also in the
viscera.
The incubation period varies from 1
to 3 months, culminating in
development of encapsulated
abscesses. C pseudotuberculosis is
hardy in the environment and can
survive on fomites such as bedding
and wood for 2 months and in soil for
8 mo. The presence of organic
material, shade, and moisture favor
and enhance survival.
Clinical Findings
The hallmark clinical finding in cases
of external CL is the development of
abscesses in the region of peripheral
lymph nodes. Common sites of
development include the
submandibular, parotid, prescapular,
and prefemoral nodes. Less
commonly, abscessation of
supramammary or inguinal lymph
nodes occurs, in addition to an
occasional ectopic location along the
lymphatic chain. If left untreated,
these lesions eventually mature into
open draining abscesses. The
purulent material from these lesions
has no odor and varies in consistency
fromsoft andpasty(morecommon in
goats) to thick and caseous (more
common in sheep).
Once naturaldraining occurs,the skin
lesion healswith scarring.Recurrence
is common, which can be months
later. CL should be highly suspected
in a sheep or goat with abscessation
in these regions. Although other
bacteria may also cause abscessation
in these locations (and in other
animals), because of the
ramifications of the presence of this
disease within a herd or flock, these
cases should be handled as CL until
proved otherwise. The internal form
of CL most commonly presents as
chronic weight loss and failure to
thrive. The presence of other clinical
signs depends on the organs of
involvement, which may include any
of the major organ systems.
Lung abscessation is a common site
of visceral involvement in internal CL;
therefore, signs of chronic ill thrift
with cough, purulent nasal discharge,
fever, and tachypnea with increased
lung sounds may be noted. The
internal form is more common in
sheep and has been termed the “thin
ewe syndrome.” The incidence of
abscesses and development of
clinical disease with either the
external or internal form increases
with age.
Lesions:
In sheep, abscesses often have the
classically described laminated
“onion-ring” appearance in cross
section, with concentric fibrous
layers separated by inspissated
caseous exudate. In goats, the
abscesses are less organized, and the
exudate is usually soft and pasty.
Diagnosis
The presence of an external abscess
on a small ruminant is highly
suggestive of CL, especially in

locations of peripheral lymph nodes.
However, the only definitive
diagnosis is bacteriologic culture of
purulent material from an intact
abscess. Although other pyogenic
organisms such as Truperella
pyogenes (formerly Arcanobacter
pyogenes), Staphylococcus aureus,
Pasteurella multocida, and
anaerobes such as Fusobacterium
necrophorum can cause
abscessation, affected animals
should be kept isolated pending
culture results. Animals with visceral
abscesses pose a greater diagnostic
challenge. Radiography and
ultrasonography can be useful to
detect internal lesions. Culture of a
transtracheal aspirate obtained from
an animal with pneumonia can help
determine whether CL is the cause.
Excluding other causes of chronic
weight loss and ill thrift in the face of
proper nutrition and good appetite
such as Johne's disease, parasitism,
and poor dentition further raise
suspicion. A synergistic hemolysin
inhibition (SHI) test that detects
antibodies to the phospholipase D
exotoxin is available at many
diagnostic laboratories. Positive
titers indicate past resolved
infections, recent exposure, recent
vaccination, or active lesions or their
development. Titers of 1:256 or
higher have been correlated in past
studies with the presence of active,
developing abscesses; however, in a
recent study, a high titer was poorly
correlated with presence or
development of abscesses over an
18-mo period. False-negative results
can occur if testing is done in the first
2 wkafterexposure beforethe animal
has seroconverted.
Treatment and Control
Once a diagnosis of CL has been
established, owner education
stressing the persistent, recurrent
nature of the disease is necessary.
The most practical approach for
commercial animals infected with CL
is to cull them from the herd or flock.
However, animals with draining
abscesses should not be sent through
sale barns until draining has ceased
and the wound has healed.
This disease is somewhat curable and
elite animals could be put on
treatment. Animals with genetic or
emotional value are treated mainly
for aesthetic reasons and to limit
their infectivity to the rest of the herd
or flock. Treatment options have
included lancing and draining,
surgical excision, formalin injection
of lesions, systemic antibiotics, and
intra-lesional antibiotics. If external
abscesses are lanced anddrained,the
cavity should be lavaged with dilute
iodine solution and the animal
isolated in an area that can be
disinfected until the lesion stops
draining and heals. Drained purulent
material should be carefully collected
and disposed of. Dilute bleach
(bleaching powder) and
chlorhexidine solutions (Dettol) are
effective disinfectants of hard
surfaces and fomites, but the
presence of organic material on these
surfaces inactivates them and
drastically reduces or prohibits
effectiveness. Injection of formalin
into the lesions are sometimes viable
and inexpensive but it should be done
with utmost care in food animals
because formalin is potent
carcinogenic. When we inject it into
lesions it will kill the bacteria but after
that it will not degrade but diffuse
into the bodywhere it resides for long
in internal tissues.
The efficacy of systemic
antimicrobial therapy and more
recently, intra-lesional antimicrobial
therapy has been investigated.
However, use of any antimicrobial for

treatment of CL is extra-label;
therefore, strict adherence to
published guidelines on withdrawal
times and an established
veterinarian-client-patient
relationship are mandatory. Penicillin
shows very good in-vitro efficacy but
in-vivo conditions its efficacy is
doubtful because it is poorly lipid
soluble and less penetrative in
lesions. However, administration of
penicillin with tissue softening agents
like serratiopeptidase could bear
more fruitful results in such cases.
However, recent studies have shown
that administration of one dose of
tulathromycin at 2.5 mg/kg, either SC
directly into the abscess cavity, or
two doses at 2.5 mg/kg, administered
at the same time, one SC and one
intralesionally) can resolve the
lesions without lancing the abscess.
Tulathromycin is not available in
India and same class antibiotic called
tylosin is good substitute for
tulathromycin.
Prevention
Because of the nature of the
causative organism, common means
of exposure, chronicity of the
disease, and difficulty in completely
eliminating the organism from
individual animals, control of CL
revolves around strict biosecurity
measures. The overriding goals of
any control program are to eliminate
the disease fromthe herdor flock and
to reduce the number of new cases
either from the spread of disease or
introduction to the farm. Ideally,
animals identified as infected should
immediately be culled. If immediate
removal is not possible, infected
animals should be isolated from the
rest of the herd or flock. Diligence in
this practice will eventually result in
decreased prevalence as animals that
develop active cases are identified
and removed, and given there are no
new animals incubating the disease
introduced to the premises.
Dividing the herds or flocks into
“clean” and “infected” groups and
eliminating older and less genetically
valuable animals over time is one
control strategy. Lambs and kids
from infected dams can be raised on
pasteurized colostrum and milk away
from infected animals. However, the
internal form of CL and animals
incubating the disease can maintain
infection within the “asymptomatic
clean” group and limit the success of
this approach. No vaccine for CL is
available in India. The risks of disease
transmission among animals should
be recognized when shearing or
dipping, and management practices
should be adjusted accordingly.
Animals with noted lesions should be
shorn last, and clipper blades
disinfected between animals.
Shearers should recognize the
hazards associated with contact with
purulent material and the possibility
of acting as mechanical vectors,
either on clothing or via equipment,
for spread of the bacteria to new
animals. Further, dipping tank
solutions should be kept as fresh as
possible, because C
pseudotuberculosis can survive
within them and serve as a source of
infection of freshly shorn sheep that
have skin abrasions. Owners should
remove hazardous items (barbed
wire, exposed nails, rough feeders)
from the environment to decrease
injury and potential CL transmission
from the presence of bacteria on
these fomites.
One of the most common ways CL
can be introduced into a previously
“clean” herd or flock, or reintroduced
to one in which CL has been reduced
or eliminated, is through the addition
of replacement stock. Often, animals
from other farms that are
asymptomatic on arrival are
incubating the disease and then
manifest infection weeks to months
later. Purchasing animals from
sources with unknown histories is
hazardous to maintaining a "clean"
herd or flock. Newly arrived animals
should be examined thoroughly for
signs of CL such as abscesses or scars
near peripheral lymph nodes. They
should remain isolated from the rest
of the herd or flock until their
serologic status is determined, and
only animals that are seronegative
with no evidence of present or past
CL lesions should be allowed to enter
the herd or flock.

Dr Zeenat, V.O., Dept. of Animal of
Animal Husbandary, Jharkhand
Dairy cattle require vitamins A, D, E, and
K; however, vitamins A and E are the only
ones with an absolute dietary
requirement. Vitamin K is synthesized by
ruminal and intestinal bacteria. Vitamin
D is synthesized by ultraviolet radiation
of the skin. Many natural feedstuffs
contain vitamin A precursors and vitamin
E, and under certain situations these will
not need to be supplemented. However,
relying solely on vitamins contained
within feedstuffs and on synthesis of
vitamin D via exposure to sunlight has
risk because of the large variability in
vitamin concentrations in feeds and
exposure to sunlight.
Vitamin A
SOURCES
Vitamin A activity is defined in retinol
equivalents. An IU of vitamin A
corresponds to 0.3 µg of all-trans retinol
(0.344 µg of all-trans retinyl acetate or
0.550 µg of all-trans palmitate). Retinol is
not found in plants, but many feeds
contain β -carotene (provitamin A).
Other carotenoids can be converted to
vitamin A by animals, but conversion
efficiency appears to be poor and most
common feeds do not contain substantial
amounts of those carotenoids.
Most of the β-carotene in plants is found
in vegetative material; therefore, forages
can contain substantial amounts of β -
carotene but most grains and grain
byproducts are practically void of β -
carotene (corn gluten meal contains
moderate concentrations of β -
carotene). Beta-carotene concentrations
decrease as forages mature. Beta-
carotene is easily oxidized
and once plants are cut,
concentrations
decrease quickly so
that stored forages
(silage and hay) have
significantly lower
concentrations of β -carotene
than do fresh forage. The length of time
forages are stored is negatively
correlated with β-carotene
concentrations. Even when known
sources of variation are considered, the β
-carotene concentrations in feedstuffs
are highly variable.
BIOAVAILABILITY
Studies on the bioavailability of various
forms of vitamin A and β -carotene for
dairy cattle are extremely limited.
Bioavailability of vitamin A is dependent
upon the degree of ruminal destruction
and on absorption efficiency by the small
intestine. In addition to those factors, the
bioavailability of β-carotene also
depends on the efficiency of converting it
to retinol. Beta-carotene is converted to
retinol by enzymes located in intestinal
mucosal cells. Dairy cattle also absorb
and store β -carotene. Blood and milk of
Guernsey and Jersey cattle contain more
β -carotene than that from other breeds
because they are either more efficient at
absorbing β-carotene or less efficient at
converting β -carotene to retinol. The
vitamin A activity of β –carotene for
cattle is defined as 1 mg of β -carotene =
400 IU of vitamin A (equivalent to 120 ug
of retinol), and is much lower for cattle
than for rats (1 mg β -carotene =1800 IU
of vitamin A). The defined activity of β -
carotene for cattle is based largely on
experiments using lambs fed corn silage.
Ruminal destruction
of vitamin A can be extensive.
Approximately 60 percent of
supplemental vitamin A was destroyed in
the rumen of steers fed hay and corn
grain diets. Similar values have been
obtained using in vitro rumen systems. In
vitro data suggest that ruminal
destruction of vitamin A was
approximately 20 percent when cattle
were fed high forage diets, but it
increased to about 70 percent when
cattle were fed diets with 50 to 70 percent
concentrate. Limited studies with β –
carotene suggest that between 0 and 35
percent of dietary β -carotene is
destroyed in the rumen.
FUNCTIONS AND ANIMAL
RESPONSES
Vitamin A (retinaldehyde) is necessary
for the production of rhodopsin (a vision
pigment) that is necessary for low light
vision. Vitamin A also is needed for
normal growth and development
(including fetal growth),
spermatogenesis, and for maintenance
of skeletal tissue and epithelial tissue.
Abortions, increased prevalence of
retained fetal membranes, and increased
calf morbidity and mortality are
indicators of vitamin A deficiency in
gestating cows.
Ross and Ternus reported that retinoic
acid indirectly regulates gene expression

which may explain the many diverse
functions of vitamin A. Vitamin A also
increases disease resistance and has
stimulatory effects on cell-mediated
immunity. A deficiency of vitamin A
often results in increased prevalence of
infectious diseases. Beta-carotene,
independent of its provitamin A function,
is an antioxidant and can enhance the
killing ability of neutrophils. In some but
not all studies, supplementing between
150,000 and 250,000 IU/day of vitamin A
or feeding 300 to 600 mg of β -
carotene/day reduced the incidence of
intramammary gland infections and
mastitis. These studies were conducted
with cows at dry-off or peripartum cows.
Vitamin A is clearly needed for good
reproduction and some data suggests
that β-carotene also may be involved
with reproduction. Supplemental β -
carotene (usually at 300 to 400 mg/day)
improved some measure of reproductive
efficiency in various studies.
FACTORS THAT AFFECT
REQUIREMENTS
Since the actual β -carotene content of
diets is highly variable and almost never
known in commercial situations, the
vitamin A requirements presented in this
publication are for supplemental vitamin
A, not total dietary vitamin A. Fresh
forage (e.g., pasture) has relatively high
concentrations of β -carotene. Therefore
the amount of supplemental vitamin A
needed when fresh forage is fed will be
less than for cattle consuming conserved
forages. The
requirements presented
below assume
conserved forages are
fed and are probably in
excess of requirements
for grazing cattle.
Based on a reevaluation
of older data, the
vitamin A requirement
for growing dairy
animals was increased to 80 IU/kg of
body weight (BW). In the previous
Nutrient Requirements of Dairy Cattle
(National Research Council, 1989), the
requirement for vitamin A of growing
dairy animals was 42 IU/kg of BW. That
requirement for growing cattle was
based on the amount of vitamin A
needed to maintain cerebrospinal fluid
pressure below 120 mm Hg in calves
(Rousseau et al., 1954). Other data
(Rousseau et al., 1954; Eaton et al., 1972)
using different criteria (i.e., a statistically
significant increase in cerebrospinal fluid
pressure or the presence of papillary
edema of the eye) suggests that the
vitamin A requirement for growing dairy
animals was between 60 and 100 IU/kg of
BW. The subcommittee decided that
rather than discounting these studies, a
compromise using all the data was
appropriate.
The vitamin A requirement for adult dairy
cattle has been increased to 110 IU/kg of
BW. In Nutrient Requirements of Dairy
Cattle (National Research Council, 1989),
the vitamin A requirement for adult
animals (76 IU/kg of BW) was based
largely on a long-term reproduction
study. Furthermore, in a more recent
study, milk production increased from
about 35 kg/day to 40 kg/day when cows
in early lactation were fed diets that
provided approximately 280 IU of
vitamin A/kg of BW compared with cows
fed approximately 75 IU/kg of BW
(Oldham et al., 1991). The new
requirement for lactating cows (110 IU/kg
of BW) was based on data used by the
previous Nutrient Requirements of Dairy
Cattle (National Research Council, 1989)
and on data showing that the
bioavailability of vitamin A (retinyl
esters) may be as much as 50 percent less
than that of β-carotene when fed in high
concentrate diets because of ruminal
destruction. Dry cows are typically fed
diets with lower amounts of concentrate
and bioavailability of vitamin A should be
higher than for lactating cows. The
previous National Research Council
requirement for dry cows (76 IU/kg of
BW) may be adequate, but in light of
potential improvements in mammary
gland health and data showing increased
milk production after dry cows were
supplemented with vitamin A in amounts
greater than National Research Council
(1989) requirements, the vitamin A
requirement for dry cows was kept the
same as that for lactating cows (110 IU/kg
of BW).
Presently available data are not adequate to define
a specific requirement for β -carotene for any class
of dairy cattle. Conditions that may warrant
additional supplementation of vitamin A include:
• low forage diets (more ruminal
destruction and less consumption of β -carotene);
• dietsthatcontainlargeramountsofcorn
silage and smaller amounts of haycrops (lower
concentrations of β -carotene and potentially lower
bioavailability of basal β -carotene);
• diets that contain lower quality forages
(lower basal concentrations of β -carotene);
• increased exposure to infectious
pathogens (increased demands on the immune
system); and
• Times when immunocompetence
maybe reduced (peripartum period).
• Vitamin A toxicosis should not be a
problem under most practical situations. The
presumed safe limit for vitamin A is 66,000 IU/kg of
diet for both lactating and non lactating cattle
(National Research Council, 1987).

Check Your Knowledge with Vetreckon
Veterinary Question bank – issue #4
1. Koster stain used
for?.............................
2. Fungal cell wall doesn’t contain?
A)chitin b)ergosterol c)muramic acid
d)polysaccharide
3. Which is an example of non-
segmented virus?.....................
4. Ag binding site on Ab?.................
5. Germinal center of lymph node
mainly contains?................
6. In late fetal life which are the organs
of haemopoises?................
7. Which Ab is present in maximum
conc. in milk?...............
8. Which Ab is present during allergic
reaction?......................
9. Pearl eye is associated with which
disease?..........................
10. Substance added to enhance the
immunity by using inactivated
microbes?.............
11. Which of the following is not an
innate factor of immunity?
A)age b)sex c)species d)infection
12. Exotoxins are mainly secreted
by?.............
13. Leechy disease also known
as?................
14. Russell body is present
in?......................
15. Coggin’s test is done
for?...........................
16. Humoral immunity is
associated with...........
17. Which one is known as
scavenger cells?.................
18. Mycolic acid is present in cell wall
of?....................
19. Lumpy jaw is caused
by?....................
20. Protein which is specific for viral
infection?................
21. Strangles in horses is caused
by?...............
22. Cell membrane of bacteria
includes?.........
23. Which one of the virus not comes
under paramyxo? ....
A)R.P b)C.D c)PPR d)Reovirus
24. which of the following is a
segmented virus?...........
25. In which animal preovulatory
leuteinisation of ova noticed?.......
26. Bimanual pregnancy diagnosis
mainly used for?.........................
27. Amniotic vesicle can be palpated for
pregnancy diagnosis in cattle
on?......................
28. Uterine inertia can’t be treated
by?.......... A)oxytocin b)PGf2α
c)Clenbuterone d)ergosterone
29. Example for induced
ovulator?.................................
30. Breech presentation is?..........
31. Still birth means?..............
32. Accumulation of pus in uterus is
called?....................
33. Write name of one is semen
extender?..............
34. Expulsion of placenta comes under
which stage of pregnancy ?................
35. Uterine involution
means?.................
36. Foetus covered with muconium at
time of parturition indicate?........
37. Which polar body is released during
ovulation in cattle?.......
Answers of issue #3
1. Histoplasma farciminosum
2. 100-105 days
3. Oxyspirura mansoni
4. Lymph node
5. Hypovitaminosis- E
6. Cat
7. Glycine
8. 1.34 ml
9. 35 mg
10.Listeria and Coxiella
11. Corynebacterium pyogenes
12. Moribili virus (paramyxovirinae)
13. 20 mm of Hg
14. HMGCOA lyase
15. Albumin
16. 6:1
17. Streptococcus pneumoniae
18. Buparvaquone (BUTALEX)
19. Vibrio parahaemolyticum
20. 8-12 mm of Hg
21. d-penicillamine
22. Shock
23. Isoproterenol
24. 64
25. Myasthenia gravis
26. Mandelic acid
27. Dermatophilus congolensis
28. 0.05-.25mg/Kg
29. Tetracyclins
30. Allopurinol
31. Chitinase and esterases
32. Ascaris suum
33. A. galli belongs to Family heterakidae
34. Anisakis
35. Phoconema
36. Oxyuris equi
37. Oxyspirura mansoni
38. Haebronema megastoma
39. Stephanurus dentatus
40. Oxyuris equi

HUDDLED beside a lion to take a
sample from a lump on its body is
all part of a day's work for a Sarina
vet.
There's no 'typical day' for Dr Bec
Bannan, who could be out
pregnancy testing 570 head of
cattle one day and on the road at
2am the next after a call-out to
help someone's pet.
"That day that I did 570 head...
that took four hours," she said.
"But you won't do that at most
set-ups, they had a lot of help."
Dr Bannan, who has been a vet for
16 years, also worked in Emerald
and it was there she encountered
the larger than usual cat.
"There was a circus in town and
they had a lion that had a big lump
on it," she said. "We had to go in
beside the crate and grab the
lump and put a needle in it. That
was pretty cool."
In Sarina about 80% of the
surgery's work involves small
animals including native birds,
echidnas, kangaroos, possums
and koalas.
"We would see probably five or six
wildlife cases a day," Dr Bannan
said. "We do all the wildlife stuff
for free. We work pretty closely
with Australian Wildlife here in
Sarina."
Inseminating dogs with semen
from overseas is one of the more
unusual tasks undertaken by the
Sarina Veterinary Surgery.
"We've inseminated dogs with
semen from the Netherlands,
Ireland, the (United) States," Dr
Bannan said.
"They (the dogs' owners) organise
for the semen to get to us and we
do a heap of testing to determine
the exact time to inseminate the
bitch... you've only got a six-hour
window.
"So if we need to do it at 2 o'clock
in the morning that's when we do
it.
"It's a surgical insemination so you
have to inject it directly into the
uterus."
Dr Bannan has co-owned the
Sarina Veterinary Surgery with
officer manager and veterinary
nurse Stephanie Sleeman for 10
years. While it has set opening
hours, someone is on call 24/7.
If her husband is away working Dr
Bannan has to take her three
children along with her to jobs,
sometimes in the middle of the
night.
"They usually sleep in the car," she
said. "They're used to it, they've
been brought up with it."

She also owns two dogs, three
cows and a horse which share the
family's 15-acre property near
Sarina.
Becoming a vet wasn't Dr
Bannan's first career choice.
"I was going to be a lawyer," she
said. "I said to Mum, I don't think I
can sit in an office all day, and
Mum said "why don't you be a
vet?" and that's the story.
"I really enjoy it. But it can be very
challenging and heartbreaking at
times."
When she has the time,Dr Bannan
enjoys photography.
"Some people do poetry and write
but photography is my creative
outlet," she said.
"When you drive around you don't
'see'... but when you stop and take
a look... we live in a really beautiful
part of the world."
TOI: NEW DELHI: Seeking to
regulate pet shops in the country,
the Centre on Friday issued draft
rules having multiple provisions to
prevent cruelty inflicted on
animals kept in such shops.
The rules, once notified by the
environment ministry after
analyzing suggestions of
stakeholders, will regulate,
among other practices, the
capture, housing, breeding and
transportation of animals sold in
the pet trade.
"The entire sector is unregulated.
Now, the state animal welfare
boards will register them after
inspections. The rules also define
space requirements and other
basic amenities tokeep the pets. It
will also be mandatory tomaintain
records of sales, purchase, sick
animals and death of animals in
the pet shops", said environment
minister Anil Madhav Dave.
Announcing the move, Dave said
the rules will be notified under the
existing Prevention of Cruelty to
Animals Act, 1960, factoring in the
need to rein in pet business which
is mushrooming with "little or no
accountability".
He said states and stakeholders,
including common people and
experts can come up with
suggestions over the rules
uploaded on the environment
ministry's website, for the
consideration within 30 days.
Once the rules are notified, non-
compliance will lead to
cancellation of registration of pet
shop and pet animals, so
confiscated, will be handed over
to an Animal Welfare
Organisation, or a rescue centre
recognized by the Board.
"We commend the environment
ministry for their foresighted
policy that will prevent tens of
thousands of animals from abuse
in the pet shop industry. We urge
the Centre to notify these rules
soon and duly implement them to
ensure that animals are not
subjected to cruel treatment at
the hands of illegal pet shop
owners," said Gauri Maulekhi,
trustee at the People for Animals
(PFA) and government liaison for
the Humane Society
International/India (HSI/India).
Both these animal rights
organisations have played a
significant role in drafting the
rules. These groups have
constantly been highlighting the
trauma the animals go through in
the pet trade, while being
transported in small cages, often
without adequate water, food or
any other form of relief.
"De-beaking, tail-docking, feather
plucking, nail clipping, de-clawing
and other cruel practices are
rampant in pet shops. Pet stores
often sell un-weaned pups, and
house animals in deplorable
conditions with no veterinary
attention for fatal illness or even
for the general well being of these
animals", said the HSI/India in a
statement.
It highlighted that the pet shops
also violate the Wildlife Protection
Act, 1972 as many exotic and
native wild animals are openly
sold there.
KEY POINTS OF THE
PROPOSED RULES:
It will be mandatory for all pet
shop owners to register
themselves with the State Animal
Welfare Board of the respective
State governments/Union
Territories.

Such shops will be registered only
after inspection by the
representatives of State Board, a
veterinary practitioner and a
representative of Society for
Prevention of Cruelty to Animals.
The rules define space
requirement for birds, cats, dogs,
rabbits, guinea pig, hamster, rats
and mice in the pet shops.
It defines the basic amenities,
power back-up, general care,
veterinary care and other
operational requirement for
animals kept in pet shops.
The rules make it mandatory to
maintain proper records of sale,
purchase, death of animals in pet
shops.
Every pet shop owner is required
to submit yearly report to the
State Board regarding animals,
sold, traded, bartered, brokered,
given away, boarded or exhibited
during previous year, or any other
information asked for by the State
Board.
TOI: TRICHY: Thanks to two
animal medical mobile
ambulances that have become
operational in Trichy, livestock
and cattle can get treatment at
their doorstep free of cost. These
vehicles are being operated by the
Veterinary University Training and
Research Centre (VUTRC) in
Trichy and will service the entire
district.
The objective of the animal
medical mobile ambulance is to
provide emergency medical
services to animals in rural areas
under the 'animal mobile medical
ambulance for rural veterinary
care in Tamil Nadu scheme' with
funds from Tamil Nadu and the
Centre. Farmers can call the
ambulance by dialling toll free
number 1962 from 8am to 8pm on
all days except Sunday.
Animals in rural areas are
vulnerable to poisonous bites
from insects. Sometimes, they
may invite danger by consuming
poisonous plants. They are also
prone to meet with accidents
while crossing roads.
Previously, when cattle needed
treatment, the farmers either
took them to the veterinary
hospitals or waited for private
veterinary doctors to visit the
spot. Sometimes, the animal died
before the vet visited the spot.
District level coordinator,
professor and head at VUTRC in
Trichy, Dr PN Richard
Jagatheesan, said the ambulance
facility could save the lives of
animals in times of emergency.
"The ambulance would reach the
spot in a timely manner and
provide treatment because the
vehicle is equipped with all the
necessary facilities," Dr Richard
told TOI.
The vehicles are equipped with
ultrasound scanner and animal
lifting facility. If the animal
requires further treatment at the
veterinary hospital, the vehicle
can transport it to government
veterinary hospital in Namakkal,
veterinary college and research
institute in Orathanadu,
Thanjavur and veterinary poly
clinic in Palakkarai in Trichy.
The scheme has been
implemented in Kancheepuram,
Trichy, Thanjavur, Namakkal and
Madurai under National
Agriculture Development Project
(NADP).
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.

i. The most likely cause is paramyxovirus 1 infection which can result in the sudden onset of watery
diarrhoea in a high proportion of susceptible birds. As shown in fig, the faeces consists of a clear pool of
urine with a central core of green material originating from the digestive tract. When this becomes mixed
by the movement of birds, a ‘green diarrhoea’ results. Also, affected birds are usually thirsty and a
proportion develop a range of nervous signs including torticollis, inability to fly, circling, ataxia and inability
to pick up feed. When the birds are stressed the severity of the nervous signs increases. Mortality is usually
low except in young birds, but some do not fully recover from the nervous signs and must be culled.
The diagnosis can be confirmed by combinations of: Isolating paramyxovirus 1 from tissues such as brain
and intestine; Demonstrating high antibody titres to paramyxovirus 1 in unvaccinated birds;Detecting
histological changes consistent with a viral encephalitis and interstitial nephritis.
ii. Although pigeons must now be vaccinated prior to racing or showing, young latebred pigeons, which
are too young to race, may be left unvaccinated with the intention of vaccinating them along with adult
birds later in the year. Should the racing teams of pigeons encounter paramyxovirus during transportation
or racing, they may bring the organism back into the loft resulting in infection and clinical disease in the in-
contact, unvaccinated late-bred birds. An increased incidence of paramyxovirus from August to November
has been observed, over several years.
iii. Other conditions to be considered include infections with Salmonella typhimurium, inclusion body
hepatitis associated with a herpesvirus or adenovirus, the motile protozoa Hexamita columbae and
Trichomonas gallinae, and rotavirus and circovirus. Nematodes, cestodes and trematodes may also cause
diarrhoea, and chlamydiosis as a cause of diarrhoea in young birds is not uncommon.
83 i. The clinical signs of profound depression and weakness following a period of severe diarrhoea are
consistent with acidosis caused rota virus/coronavirus infection.There is no evidence of septicaemia such
as injected scleral vessels, fever, or other organ system involvement such as polyarthritis, pneumonia,
pan ophthalmitis or meningitis.
ii. Treatment must correct the acidosis. The calf is estimated to be no more than 5% dehydrated. Fluid
replacement requirements are 45 kg × 0.05 = 2 L plus daily requirement of 75–150 mL/kg (equal to 3–6
L/day). The base deficit for recumbent/stuporous calves is estimated to be 20 mmol/L. The total base
deficit (or negative base excess) is calculated as: base deficit × bicarbonate space × dehydrated calf
weight = 20 × (0.5) × 40 = 400 mmol bicarbonate (400 mEq); 16g sodium bicarbonate = 200 mmol of
bicarbonate; 16 g sodium bicarbonate (200 mmol bicabonate) are dissolved in 1 L of isotonic saline and
infused over the first 20 minutes and the remaining 200 mmol bicarbonate are dissolved in 3 L and given
over the next 3 hr. Oral fluids should be offered at a rate of 1 L eight times daily. A bottle and teat is
preferred to an orogastric tube to gauge the calf’s mental state and appetite. This calf was not treated with
antibiotics.
iii. All cows should be vaccinated with rotavirus/coronavirus vaccine when such aetiology is confirmed.
Passive antibody transfer should be ensured. The remaining pregnant cows should be moved to a clean
environment.

Vetreckon
Digital
Veterinary
Magazine
NFC, Okhla, New Delhi
Delhi – 110025
This is our fourth issue with
the sole aim to serve the
veterinary education in
India. With time and your
precious suggestions we
will improve in future. For
the same, your articles,
suggestions & ads are
invited. Please write us on
following address
ibnester@gmail.com
+91-9557907955
113 A 6-month-old weaned Blackface lamb is brought to the veterinary surgery by a member
of the public, having been found near the roadside on open (unfenced) hill ground. The lamb
is dull and unable to use its pelvic limbs and adopts a dog-sitting position (113a). There is
flaccid paralysis of the pelvic limbs with absent reflexes. There is no tail or rectal tone.
Ultrasound exam ination reveals distension (>8 cm diameter) of the bladder and the rectum
is distended with faeces.
i. What is the extent of the spinal lesion?
ii. What treatments would you administer?
iii. What tests could be undertaken?
31. The 18-day-old duck embryo on the left is normal while on the right is an embryo of the same age that
was exposed to low levels of insecticide applied to the shell during incubation.
i. Describe the pathology exhibited.
ii. With what group of insecticides are these lesions commonly associated?

Vetreckon 15 december, Issue 4

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