Transcript Lecture 5

FELINE INFECTIOUS
PERITONITIS
INTRODUCTION
 Affects both domestic and wild cats.
 Highly fatal and characterized by prolonged
progressively debilitating course, anorexia,
depression, weight loss and anemia.
 Usually refractory to treatment.
 It is an immulogical reaction to some viral
diseases manifesting as either effusive (wet or
serositis) or non-effusive granulomatous form.
Etiology – RNA virus 70-94nm
Cats usually have both leukemia virus and FIP
virus.
Transmission:Oral,
nasal
and
ectoparasites
Transplacental transmission
• All age groups and sex can be infected but
young animals are more susceptible.
Clinical Signs:
There are two forms:
 Effusive (wet)
 Noneffusive form (Parenchymal or dry and granulomatus form)
Clinical Signs:
There are two forms:
 Effusive (wet) form characterized
 Ascites
 Hydrothorax
 Pleuritis Dyspnoea.
Affected cat dies within 1-8 weeks
Clinical Signs:
Noneffusive form (Parenchymal or dry form and granulomatus)
characterized by the involvement of specific organs e.g.
 The brain (causing pyogranulomatous meningoencephalitis)
 The eye causing pyogranlomatous uveitis, bilateral iritis, ocular
discharges, keratic precipitates in the anterior chamber of the
eye.
 Kidney
 Spleen,
 Liver
 Pancreas.
Several clinical forms may coexist in young adults, 6 months – 3 years
are mostly affected. There is Fluctuating fever, progressive anorexia,
depression, weight loss and dehydration. Non regenerative anaemia.
A few patients may vomit or have diarrhea.
Diagnosis: Hemogram – moderate to marked
leukocytosis increase in icterus index 10-50
units (normal 2.5 – 7.5 units), non
regenerateive anaemia
 Hyperproteinaemia due to hypoglobulinaemia
peritoneal fluid can clot because it contains
high concentration of protein and flecked
fibrin.
 Radiography.
Treatment:
Temporary remission may occur, seemingly
recovered cats relapse and ultimately die.
1. Peritoneal lavage with balanced electrolyte
solution.
2. Administration of chloramphenicol or tylosin
and flumethasone.
3. Oral antibiotic and steroid combined with
lavage.
4. Most effective is a combination of oral
tylosin and prednisolone.
Prevention:Difficult. Vaccine not presently available.
Prevent contact between susceptible and ill cats.
FELINE
LEUKEMIA
INTRODUCTION
Malignant proliferative or degenerative
disease of the hematopoietic tissue of the
domestic cat
Etiology: caused by feline leukemia virus
(RNA) an RNA retrovirus
Transmission:- The virus is present in the
saliva, urine, feces, milk and nasal discharges
of the affected cat. Transmission is both
horizontal (cat to cat) and vertical (mother to
foetus)
Clinical signs:
Variable because of the various body systems
that might have been affected.
The proliferative forms (Myelo-proliferative)
always affect the bone marrow resulting in
pallor of mucous membranes, enlargement of
liver and spleen and fluctuating fever, anorexia,
malaise.
In non-regenerative anaemia
panluekopenia like syndrome, thymic atrophy.
Diagnosis
1. Clinical signs
2. Cytologiy of the body fluid and histological
examination at post mortem.
Treatment
Not advisable because they constitute a
distinct hazard to cats, other species and man.
CANINE ADENOVIRUS
INFECTIONS (Double straded
DNA cubic sysmetry)
(Infectious canine hepatitis)
Synonyms:
Contagious canine Hepatitis or Rubarth’s
Disease.
INTRODUCTION
 It is a multisystemic acute viral disease
which primarily affects the liver of dogs
and other canids.
 Characterized by very rapid course,
tonsillitis, oedema of the subcutaneous
tissues (especially of the neck regions).
Aetiology
There are two serologically distinct
adenoviruses responsible for disease of dogs.


CAV-1
CAV-2
Aetiology
Epizootiology and Dermology
 Adenoviruses are more stable than canine
distemper virus under moist condition and out of
direct sunlight. One strain of CAV-ICH in urine can
survive up to 5-6 days on soil or concrete floor.
 The disease is widely spread but only a small
proportion of dogs come down with the disease.
Clinical signs may be so slight that they pass
unnoticed, while definite clinical signs may be
diagnosed in some dogs.
 A small minority come down with severe clinical
signs in that case there is high mortality. In endemic
areas sporadic epidemics may occur. Young puppies
3-6 months are most susceptible. About 20% occur
in 18 months and above old dogs.
Transmission:Ingestion of food or water contaminated
with infected urine but the respiratory form can
be transmitted through aerosol during
coughing.
Clinical Signs
1.
2.
3.
4.
Liver
GIT
Cardiovascular
Eye
Clinical signs
 Acute fulminating, high temperature, (1060F).
Death may occur within a few hours. This
condition may be severe and acute that it can be
confused with poisoning.
 The mucus membrane of the tonsil is
inflamed.
 High temperature becomes subnormal just
before death.
Clinical signs
Extreme apathy depression, sudden onset of
anorexia, vomiting, which may be severe and contains
blood terminally, as a result of liver damage in about
35% of the cases.
Bilirubinuria, increase in liver enzymes (ALP, ALT)
Damage to the vascular endothelium manifest as
perivascular haemorrhage cardiovascular system,
thymus, brain, lungs, epi and endocardium, lymph
nodes, spleen and subsutaneous tissues.
Vomiting and diarrheoa may become haemorragic.
Clinical signs
 Presence of blood in faeces signifies grave prognosis.
 There is an intense thirst
 The mucous membranes may be extremely pale.
Jaundice may occur in 25-34% cases. In some cases
there may be petichial haemorrhage on the mucous
membrane of the mouth.
 Tenderness and pain in the abdominal region which
can be induced by palpation especially toward the
xiphisternum.
 There is hepatomegaly. The abdomen contains some
fluid.
 There may be tachypnoea in some cases.
Clinical signs
 There is cornea opacity which may be unilateral or bilateral
referred to as “hepatitis blue eye”. When this occurs it is diagnostic
and prognosis is good.
 Subcutaneous oedema of the head region i.e. head, neck and
sternum.
 CNS involvement is low (5%) showing signs such as restlessness
(moving, pacing around the room) and posterior incoordination.
Excitability and hyper asthesia may be evident. Sometimes
epileptiform convulsions progressing to coma.
 The pulse is usually fast and weak.
 High temperature (105-1060F) and remains so until the animal
collapses when it becomes subnormal.
 There is high protein in the urine.
 Superficial lymph nodes are enlarged, tonsil is swollen and
inflamed. The course is usually rapid therefore no room for weight
loss.
Diagnosis:Clinical signs
Sudden onset, pallor of mucous membrane,
palpable enlarged liver, corneal opacity, leucopenia,
increase
coagulation
due
prothrombinemia
thromibocytopenia, increased liver enzymes.
Virus isolation from tonsil, swab or clotted blood
samples. Serum assay – paired sera.
Serum
neutralization test CFT.
Immunofluorescence
and
histopathology,
intranuclear inclusion bodies in liver and spleen.
Material becomes useless 48 hours after death.
Treatment:Antibiotic to control 20 bacterial infection.
Supportive treatment: Blood transfusion,
vitamins, Vit K. i/v glucose saline, specific
antiserum.
If nervous signs appear, administer primidone.
Prognosis:In clinically diagnosed cases the prognosis is
poor but good when corneal opacity occurs.
Prophylaxis:Vaccination, hygiene.
FELINE RESPIRATORY
DISEASE
INTRODUCTION
• Respiratory disease is common among cats. The
term “cat flu” is widely used to describe the
clinical signs associated with infection.
• Feline respiratory disease is a syndrome that may
be cause by one or a number of infectious agents.
It is thus similar to Kennel cough of dogs.
• Morbidity of viral respiratory disease in cats is high
but the mortality is low.
• Severity of the disease varies, with subclinical or
mild infections being more common, though more
serious cases may occur.
AETIOLOGY
are
The two major causes of upper respiratory disease (URD) in cats
1.) Feline viral rhinotracheitis (FVR), virus, also known as feline
herpersvirus 1 (FHV 1)
2.) Feline calicivirus (FCV).
Together, these two viruses are responsible for majority of cases of
URD.
Others are
Feline reovirus, Feline poxvirus
 Bacteria such as Clamydia psitacci, staphylococci, haemolytic
stereptococci, pasteurella spp, coliforms and mycoplasmas have been
isolated from causes of URD.
 Their main importance may be as secondary invaders following
primary viral damage.
 Bordetella bronchiseptica has been isolated in some cases of feline
URD but its significance has not been determined.
EPIZOOTIOLOGY
 Feline viral respiratory disease is more common in
colony cats than individual house pets.
 The disease appears commonly in situations
where cats have been brought together e.g. catteries,
breeding colonies, stray-cat homes etc.
 Feline upper respiratory disease (URD) is
widespread worldwide. Most cases are due to
infection by FHV and FCV.
 In endemic situations, URD is generally acute in
young kittens especially after weaning.
 Older cats usually suffer a milder disease which is
characterized by persistent, or recurrent rhinitis,
sinusitis.
TRANSMISSION
Occurs from sick or carrier cats to susceptible
ones through transfer of virus-containing oral or
nasal secretions.
Close contact, rather than aerosol, is
responsible for virus spread.
The viruses persist in cat populations in 3 ways:
1. Direct transmission from acutely infected to
susceptible cats.
2. In the environment for short periods of time.
3. Persistence through a carrier state in recovered
cats.
PATHOGENESIS
FVR
Following infection, upper respiratory tract
secretions carry the virus into the nasal
passages, oropharynx, and trachea.
FCV
Infection leads to growth of the virus in the
epithelia of the tongue, palate, external nares
and lungs.
CLINICAL SIGNS
FVR
The incubation period is usually 2-4 days but may be up
to 10 days depending on the virus dose. PHV infection
generally produces a severe disease. The initial stages are
characterized by depression, anorexia, pyrexia (400C) and
sneezing. Conjuctival oedema occurs commonly.
In the later stages, ocular and nasal discharge become
more copious and are often purulent. Drooling of saliva
due to hypersalivation is common. Mouth breathing occurs
as a result of obstruction of the nasal passages.
Recovery begins 7 to 10 days after the initial clinical signs
but complete recover may take several weeks. In a few
cases chronic rhinitis and sinusitis may persists. Recovered
cats are resistant to re-infection and do not develop clinical
signs.
FCV
The incubation period is short, 1-3 days. FCV usually
produces a milder disease than FHV though severe cases
may be similar to FVR. General malaise, coughing and
oculo-nasal discharges are less copious. Nasal discharges
usually occur with sneezing.
Initially there is usually depression and anorexia
associated with pyrexia. The characteristic sign is
ulceration of the anterior border and dorsum of the
tongue, hard palate and external nares.
Since there is a large number of strains of feline
calicivirus, the pathogencity and clinical signs may vary
slightly.
Some strains produce primary interstitial
pneumonia, others pyrexia, myalgia and limping, while
infection with some strains may be subclinical.