1.1 Immunoprophylaxis or
minimum disease prevention
- Enhancement of a specific immune response
in an attempt to protect it against an infectious disease.
- Active induction of an immune response
requires exposure to the antigens of the infectious agent
- Passive disease prevention involves the
use of humoral or cellular factors obtained from a previous
- Vaccination is more commonly used in the
prevention of viral and bacterial diseases.
1.2 Passive Immunizations
- Protection of colostrum deprived
neonates (< 2 days old).
- Protection of dogs and cats receiving
cancer chemotherapy and exposed to infectious agents during
- Prophylactic or therapeutic use in
treating litters of puppies clinically affected with neonatal
- Used in the initial treatment of dogs
and cats with tetanus.
- May be used in other emergency
situations in which the rapid onset of protection is necessary.
- Antibody titer to the specific agent
- Importance of serum antibody in
controlling the particular infection involved
- The time of administration of antibody
compared with exposure
- Protection is low and of shorter
duration than that generated from vaccination.
- Allergic reactions are more likely with
- Transfer of infectious agents is more
likely with administration of serum when non-commercially
prepared products are used.
- The administration of immunoglobulins
also delays the ability to stimulate active immunity in the host
- Commercial preparations are available. (From
Laboratories, 703 Lake Shore Road, Grafton, WI 53024)
- Immune serum derived from healthy
individuals or from groups of animals that have recovered from
the disease in question.
- Hyperimmune serum is obtained from
animals that have been hyperimmunized by repeated vaccination
against specified infectious agents.
- Oral administration with serum alone or
in milk substitute most effective in neonates.
- Parenteral administration routes that
are accepted are intramuscular (IM), subcutaneous (SQ) and
- Dose is 2-4 ml/kg depending on the titer
of the preparation.
1.2.6 Maternal immunity and immunoprophylaxis
- Amount of immunoglobulin absorbed give
the neonate a titer almost equal to that of the dam.
- Decline of serum antibody in the neonate
is similar to that for passively administered imunoglobulins.
- Quantity of immunoglobulin in the serum
of the dam depends on the disease considered.
- The titer of maternal antibody in the
serum of the neonate determines the susceptibility to both
virulent and vaccine virus.
- This titer depends upon the quantity of
immunoglobulin received during nursing and the absolute titer of
- Due to the variability of individual
animals direct measurements of antibody titer of the puppy or
dam is required but not practical.
- Veterinarians use multiple vaccination
schedules in young puppies or kittens over a certain range of
- Vaccines are given at 2-4 week intervals
in an attempt to break through maternal immunity prior to
exposure with virulent virus.
1.3 Active Immunization
1.3.1 General principles
- The vaccine must induce the right type
of immune response.
- The vaccine should induce an immune
response in the right place.
- The vaccine should induce an immune
response to the right antigens.
- The disease should be serious enough to
1.3.2 Types of vaccines
188.8.131.52 Live vaccines
- must be modified (attenuated)
adaptation to unusual hosts prolonged storage serial passage
- retain antigenicity
- able to replicate in the intended
- heterotypic vaccines developed
- quality control essential
- lyophilization increases stability
and storage lifespan
- usually contain excess antigen
184.108.40.206 Inactivated vaccines
- subjected to various forms of
denaturation without destroying antigenicity formalin
- adjuvants are added increase vaccine
duration and level of immunity emulsified water in oil
preparations mineral gels containing alum, aluminum phosphate
or aluminum hydroxide
- do not replicate in the host
- antigenic mass determines the
efficacy of a particular product
- must be given twice to get the
anamestic response equal to 1 modified live vaccine
220.127.116.11 Subunit vaccine
- purified products containing bacterial
antigenic determinants or viral structural components
important for the immune response
- efficacious for diseases in which key
structural proteins have been identified from the infectious
agent that enable the host to recognize the organism and
- used if sufficient attenuation
cannot be achieved or the agent has the potential for
1.4 Vaccination failures
1. Host factors
- Hereditary or acquired
- Maternal immunity
- Concurrent immunosuppressive therapy
- Body temperature
- Anesthesia or surgery
2. Vaccine factors
- storage and handling
- strain differences
3. Human factors
- veterinary hospital procedures
- concurrent administration of
- improper use of disinfectants
- vaccine interference
- mixing of products
- route of administration
1.5.1 Immunological complications
18.104.22.168 Type I hypersensitivity
- associated with inactivated products
containing large amounts of foreign proteins
- local or systemic reactions
- occur within an hour after
- should not repeat vaccination with
the same antigen in single or combined vaccines
- revaccination may be attempted after
puppy reaches maturity
- IgE response may be generated in
22.214.171.124 Type II hypersensitivity
- reported following the use of MLV
- autoimmune hemolytic anemia
- autoimmune nonregenerative anemia
- occur within 1-2 weeks following
- transient thrombocytopenia or
autoimmune thrombocytopenia may require glucocorticoid therapy
for several weeks subsequent boosters must be avoided or
minimized to prevent a recurrence of the problem
126.96.36.199 Type III hypersensitivity
i. immune complex formation involved with
anterior uveitis (CAV-1 vaccine) local Arthus reaction
results from antibody antigen complex in eye secondary glaucoma
ii. generalized serum sickness widespread
immune complex deposition microvasculature of certain structures
such as renal glomeruli, joints and uveal tract are affected
usually seen with large amounts of passively given immunoglobulin
188.8.131.52 Type IV hypersensitivity
- seen in two incidences
- BCG as an immunostimulator (granuloma
- use of suckling mouse brain
inactivated rabies vaccine (postvaccinal encephalomyelitis)
1.5.2 Nonimmunologic complications
184.108.40.206 local reactions
- local irritation
- abscess formation
- noticed with inactivated products
- seen with bacterial vaccines
containing large amounts of tissue culture proteins
220.127.116.11 Systemic illness
- characterized by fever, malaise and
- result of self-limiting infection of
- usually does not last longer than
1-2 days following vaccination
18.104.22.168 Prenatal and neonatal infections
- if given during pregnancy can cause
fetal death and abortion particularly MLV vaccines
- neonatal infection can occur
following the use of MLV canine and feline paroviral vaccines
in puppies and kittens less than 4-5 weeks of age
22.214.171.124 Respiratory disease
- can occur as an expected postvaccinal
- usually occurs with intranasal
- mild clinical symptoms are usually
- immunity superior to parenteral
- can get the same reaction from
parenteral products inadvertently or accidentally released
into the environment
126.96.36.199 Shedding of vaccine agent
- occurs with MLV intranasal products
- occurs with administration of
- canine parvoviral vaccine (feces)
- CAV-1 vaccine (urine)
- CAV-2 vaccine (respiratory
- shedding may serve to vaccine other
- reversion to virulence a potential
188.8.131.52 Postvaccinal encephalomyelitis
- low passage MLV Rabies vaccine in dogs
- high passage MLV Rabies vaccine have
produced clinical disease in cats
- disease begins with paralysis in
vaccinated limb 7 to 21 days after vaccination
- progresses bilaterally and in an
- cats - progressive lower motor neuron
paralysis with an unusual extensor rigidity of the limbs
- pain and reflex function decrease in
an ascending fashion
- recovery after 1-2 months in dogs
have been reported
- do not present health hazard
because vaccine is attenuated and is not shed in the saliva
- Public health and expert virologists
should be consulted
- Other causes of postvaccinal
combined distemper virus and CAV-1 vaccine
MLV measles vaccine feline or canine parvoviral vaccines used in
animals less than 4-5 weeks of age
1.6 IMMUNIZATION SCHEDULE
Any immunization schedule must be tailored to the
specific needs of the individual. If a healthy puppy
is presented with no history of disease exposure, and the puppy is
not from a high risk area (i.e. pet shop, animal shelter, etc.) the
following schedule may be used for the convenience of the owner in
Age of Puppy When First Presented
Less than 6 weeks
Vaccination not usually recommended. Bordetella products
may be used.***
1st Distemper-Measles (D-M) intramuscular (IM).If D-M is used, a Distemper-CAV-2-parainfluenza-leptospirosis vaccine is administered when pup is 14 weeks old. Parvovirus vaccine may also be given at that time;
*lst Parvovirus vaccination.
1st D-M, (IM), D-CAV2-P-L at 14-16 weeks.
*lst Parvovirus vaccination.
1st D-M, (IM) D-CAV2-P-L at 14-16 weeks
1st D-CAV2-P-L 2nd D-CAV2-P-L at 10-11 weeks 3rd D-CAV2-P-L at 12-13 weeks
*lst Parvovirus vaccination
1st D-CAV2-P-L 2nd D-CAV2-P-L at 11-12 weeks 3rd D-CAV2-P-L at 12-13 weeks
*lst Parvovirus vaccine 2nd at 12-13 weeks 3rd at 16 weeks
1st D-CAV2-P-L 2nd D-CAV2-P-L at 12-13 weeks
*lst Parvovirus vaccine 2nd at 13-14 weeks 3rd at 16 weeks
1st D-CAV2-P-L 2nd D-CAV2-P-L at 13-14 weeks
*lst Parvovirus vaccine 2nd at 14-15 weeks 3rd at 17-18 weeks
Over 12 Weeks
1st D-CAV2-P-L (no booster needed)
**lst Rabies vaccination (intramuscular)
*lst Parvovirus vaccination
2nd at 3-4 weeks after these 2 doses of
parvovirus vaccine should be given (at 3-4 week intervals)
after the puppy is 14 weeks of age. Yearly revaccination (single
dose) with parvovirus vaccine is recommended. If a dog is
entering a high risk area (i.e. boarding kennel, dog shows,
- ii. swelling
- iii. abscess formation
- iv. noticed with inactivated products
- v. seen with bacterial vaccines containing
large amounts of tissue culture proteins
b. Systemic illness
i. characterized by fevfield trial, etc.) for
exposure to parvovirus that dog should be re vaccinated if his last
parvovirus vaccination was more that 6 months earlier.
D-CAV2-P-L (or D-H-P-L) is
**Rabies vaccine given at 3-4 months of age (or
up to 1 year of age) is repeated one year later. After the first
yearly booster, vaccination may be good for 3 years (see
Compendium of Rabies Vaccines and Local Ordinances).
***Under certain circumstances in high risk
area, Bordetella bacterins by either the systemic or intranasal
route may be indicated. In infected kennels puppies may be
vaccinated as early as 3 weeks of age with parenteral Bordetella
bacterin which should be repeated 3-4 weeks later (2 doses are
needed). The intranasal Bordetella product (a live avirulent
product) may be given to pups as young as 2 weeks of age. Only
one dose is given and protection lasts for 6 months.
1.7 MINIMUM DISEASE
PREVENTION RECOMMENDATIONS FOR CATS
Weaning to Physical examination
6-7 weeks Feeding instructions - grooming
and care instructions Fecal examination for internal parasites;
worming if needed. Panleucopeneia passive immunization with
hyperimmune or normal serum (1&endash;2ml/lb) in high risk area.
Repeat in 10-14 days, Intranasal feline herpes-calici virus
vaccination in high risk areas.
9-10 weeks Panleucopenia
vaccination with either (l) TCO inactivated vaccine repeat in 2-4
weeks and for maximum protection a third dose is given at 16 weeks of
age. or (2) TCO modified live (MLV) virus with a second vaccination in
2&endash;4 weeks. Herpes Calici virus vaccine with either: (l)
Parenteral (SQ or IM) inactivated or attenuated (MLV) virus vaccine.
Repeat in 2&endash;3weeks and again 2-3 weeks later (May be
combined with MLV or inactivated panleucopenia virus vaccine). or (2)
Intranasal (MLV) herpes&endash;calici virus vaccine. The
intranasal vaccine may be repeated in 2&endash;3weeks. Pneumonitis
vaccination (SQ or IM) in high risk areas. May be repeated in
Feline Leukemia (sub&endash;unit) vaccine
IM. This vaccination is repeated in 2-3 weeks and again 2
months after the first vaccination.
3-4 months Rabies vaccination
with a vaccine (inactivated) which will provide three years
protection. The rabies vaccine should be repeated in one year and
again every three years.
MLV, intranasal, herpes-calici virus
given at this time requires only a single dose, it is repeated yearly
MLV TCO panleucopenia vaccine if given at this
time requires only a single dose and should then be repeated yearly.
If parenteral herpes calici virus vaccine (attenuated
or inactivated) is used, it should be repeated in
2&endash;3weeks and yearly thereafter.
- Annually Panleucopenia vaccination
- Rabiea vaccination (if necessary)
- Feline Herpes-calici virus
- Feline Pneumonitis vaccine (in high risk
- Feline leukemia vaccination
- Physical examination with particular
attention to teeth, ears, and urinary system.
- In cats over 8 years of age an annual
physical examination is recommended with urinalysis, CBC, SGP-T,
creatinine, and 3UN evaluation.
1.8 IMMUNIZATION SCHEDULE
Any immunization schedule must be tailored to
the needs of the individual. If a healthy kitten is
presented, with no history of disease exposure, and the kitten is not
from a high risk area (i.e. animal shelter, pet shop, etc.),
the following schedule may be used for the convenience of the owner in
Less than 6 weeks Vaccination not usually
recommended. (May need panleucopenia antiserum if entering a high
Age of Kitten When First Presented
1st Panleucopenia vaccine (2nd vaccine given at 9-10 weeks, 3rd at 12-13 weeks). Either inactivated or MLV, feline cell culture origin (TCO).
*lst IN Herpes-calici vaccine (2nd at 9-10 weeks)
*lst IM Herpes-calici vaccine (2nd at 9-10 weeks)
1st Panleucopenia vaccine )2nd at 10-11 weeks,3rd at 13-14 weeks)
*lst IN Herpes-calici vaccine (2nd at 10-11 weeks)
*lst IM Herpes-calici vaccine (2nd at 10-11 weeks)
1st Panleucopenia vaccine (2nd at 11-12 weeks,14-15 weeks)
*lst IN Herpes-calici vaccine (2nd at 11-12weeks)
*lst IM Herpes-calici vaccine (2nd at 11-12 weeks)
1st Panleucopenia vaccine (2nd at 12-13 weeks)
*lst IN Herpes-calici vaccine (2nd at 12 weeks)
*lst rM Herpes-calici vaccine (2nd at 12 weeks)
1st rM Pneumonitis (if used) (2nd at 12 weeks)
1st Panleucopenia vaccine (2nd at 13-14 weeks)
1st IN Herpes-calici vaccine (2nd at 12-13 weeks)
1st IM Herpes-calici vaccine (2nd at 13-14 weeks)
1st IM Pneumonitis (2nd at 12-13 weeks)
1st Panleucopenia vaccine (2nd at 14 weeks)
1st IN Herpes-calici vaccine (no booster needed)or:
1st IM Herpes-calici vaccine (2nd at 14-15 weeks)
1st IM Pneumonitis vaccine (no booster needed)
Over 12 Weeks
1st Panleucopenia vaccine (no booster needed)
1st IN Herpes-calici vaccine (no booster needed)or:
1st IM Herpes-calici vaccine (2nd 3 weeks later)
1st IM Pneumonitis vaccine (no booster needed)
1st Rabies vaccine IM
All vaccines (Panleucopenia, Herpes-calici,
Pneumonitis and Rabies are repeated (one dose) yearly.
*Intramuscular herpes-calici virus vaccine is
available as an MLV or inactivated vaccine.
Intramuscular herpes-calici virus vaccine may be
administered as a combined vaccine with either MLV or inactivated
panleucopenia vaccine. Intranasal herpes-calici virus vaccine may be
administered as a combined vaccine with MLV panleucopenia vaccine.
Lyssa, hydrophobia, sylvatic plague, campesterol
The virus that causes rabies is in the family
rhabdovirus. Rhabdoviruses are enveloped ssRNA virus with a
characteristic bullet shape. Virus replication results in the
formation of intracytoplasmic inclusions. Free virus infects new or
adjacent cells by fusing their envelopes with the host cell membrane
allowing direct entry into the host cell. Easily destroyed by most
The primary mode of infection is deep exposure
to virus infected saliva (bite of a rabies infected animal).
Aerosol exposure (transmission by droplets in caves heavily
populated by bats) and and ingestion of infected material have
also been documented as a mode of transmission.
All mammals - highest incidence for dogs and
cats is in areas where wildlife rabies is epizootic.
Variation in incubation period is based on:
- the site of bite
- the amount of virus introduced
- the species that is bitten
Average incubation periods are:
- Dogs 3 to 8 weeks
- Cats 2 to 6 weeks
- Humans 3 to 8 weeks
Experimental variation in pathogenesis is
based on the mode on inoculation.
After intramuscular inoculation the virus
replicates in myocytes of infected muscle. Viral spread occurs
centripetally via neuromuscular junctions to the peripheral nerves
and then to brain. The greater the innervation at the site of the
bite the shorter the incubation time.
After intranasal inoculation, the virus enters
trigeminal nerves or cribriform plate and olfactory bulbs and travels
to the brain.
In oral inoculation the virus infects cells of
the oral mucosa, taste buds, pulmonary and intestinal mucosa. It
travels via the cranial nerves to the brainstem.
Once in the brain or spinal cord, virus
replicates in neuronal perikaryon. Interneuronal spread corresponds
with the progression of clinical signs. Following replication within
the CNS the virus moves to other body tissues via peripheral,
sensory and motor nerves and to the nerves to the salivary glands.
The spread of the virus to the saliva indicates that the brain has
already been infected.
1.9.6 Clinical signs
Clinical signs are divided into 3 phases.
Prodromal phase (2 to 3 day duration) is
associated with changes in behavior such as apprehension, anxiety,
and solitude. Other signs infrequently seen are; fever, pupillary
dilation, sluggish palpebral reflex, and pruritis at site of the
bite causing self mutilation. In cats the prodromal stage is shorter
(1 day) and signs are more erratic.
Furious phase (duration 1 to 7 days) is
characterized by restlessness and irritability. The infected animal
becomes hype-excitable, photophobic, and hyperesthetic.
Disorientation and a loss of muscle coordination may lead to ataxia.
Generalized grand mal seizures may develop and usually lead to the
death of the dog. Cats more consistently develop the furious form of
Paralytic phase develops within 10 days after
the first clinical signs are noted. The paralytic phase is
associated with lower motor neuron dysfunction that leads to
paralysis of certain muscle groups. Change in the bark, dropped jaw
and excessive salivation are all clinical signs of the paralytic
phase in dogs. In cats the paralytic phase begins at about the 5th
day of clinical illness. There is generalized paralysis and coma
resulting in death.
History and Physical exam - Rabies should be
considered in any case where there are characteristic signs of
behavior change and/or lower motor neuron paralysis.
- Hematology and biochemistry - no abnormal
- Cerebrospinal fluid - increase protein
- Virus isolation and identification - Tests
used for the detection of viral antigen
- Direct immunofluorescence
- Intracellular inclusions
- Mouse inoculation
- Monoclonal antibody
- Serology - Tests used for the detection of
antibody to virus
- Neutralization tests
- Indirect immunofluorescence
- Rapid Fluorescent-Focus inhibition test
- Pathologic findings
No gross lesions detectable in CNS. Histologic
lesions are acute polioencephalitis, neuronophagia, neuronal
degeneration and non-suppurative inflammation seen early.
Necrotizing encephalitis seen later as titer
to rabies rise in CSF. The longer the course of illness, the more
pronounced is the non-suppurative inflammatory response in the brain
and spinal cord.
Supportive care and symptomatic treatment of
- Zoonotic potential
- Human vaccines
- Canine and Feline vaccines
- Vaccine recommendations
- Postvaccinal Reactions
- Control of Epizootic Rabies in Dogs and
- Postexposure management of dogs and cats
mad-itch, Aujeszky's disease, infectious
An enveloped ds DNA virus of the herpesvirus
family. The virus is antigenically related to the infectious bovine
rhinotracheitis virus. Many strains have been found. Strains differ
in ability to cause cytopathic effect. Since viral DNA is
incorporated into host cell genome there is a potential for latent
infection. The virus is resistant to environmental factors and can
survive outside the host for several months.
Many mammalian species are susceptible. The
virus is predominantly a problem in pigs. It does not appear to
affect humans. The main reservoir is the pig where the infection is
often subclinical. Dogs have developed pseudorabies after biting
infected pigs. Direct spread from dog to dog has not been shown to
Incubation period in dogs and cats
irrespective of inoculation site is 3 to 6 days. Pseudorabies virus
enters the nerve endings at the inoculation site and travels in a
retrograde fashion via the axoplasm of the nerve fibers to the
brain. This mode of viral spread has been demonstrated in the cow.
The virus replicates in the tonsils and travels from the oral mucosa
via the sensory branches of the ninth and tenth cranial nerves to
1.10.5 Clinical findings
The onset of clinical illness is very acute
and progress rapidly until death occurs. Total course of disease
rarely lasts longer than 48 hours. Pseudorabies is always fatal in
dogs. Cats are more resistant. The initial sign is a change in
behavior (inactivity, lethargy, indifference). Eating of
inanimate objects may be observed (pica). Dyspnea, diarrhea
and vomiting are sometimes seen. Hypersalivation is a common
finding. The most characteristic sign is intense pruritus which
usually occurs in the head region. Excoriations of the face and neck
may be seen due to self-mutilation.
- Laboratory findings
- Hematology and Biochemistry - no abnormal
- Viral isolation and identification
- a. Animal Inoculation
- b. Fluorescent antibody testing
- c. Virus Isolation
- Pathologic Findings
No gross necropsy findings are pathognomonic
for pseudorabies. Skin lesions are present from intense pruritis and
abnormalstomach contents due to pica. Pulmonary edema and congestion
and focal myocarditis are
reported findings. Histological lesions in the
CNS are exclusively located in the brainstem and involvecranial
nerve nuclei. These lesions consist of perivascular cuffing with
mononuclear cells and proliferation of astrocytes and microglia
cells. Microabcesses and severe necrolysis and degenerative changes
in neurons. Inflammatory changes may also be seen in ganglia at site
of entry of virus (alimentary myenteric plexus).
Heavy sedation and anesthesia to lessen the
itching and convulsions.
Contact with pigs and eating raw pork avoided
in endemic areas. Vaccination of dogs and cats in endemic areas.
Vaccination efficacy questionable and postvaccinal reactions occur.
1.11 CANINE DISTEMPER
An enveloped ss RNA virus of the family
paramyxovirdae and the genus moribillivirus. The virus is
antigenically related to measles and rinderpest viruses. There are
numerous isolates that vary in virulence and ability to cause
neurological disease. The virus is rapidly inactivated by heat and
light. Many chemical are lethal to the canine distemper virus but
the virus is more protected in body secretions. The virus survives
in the environment longer at lower temperatures.
Direct and indirect transmission is possible.
Portal of entry is respiratory tract. Virus is shed in all
secretions and excretions. Recovering dogs may shed the virus for
Young dogs become susceptible when they lose
maternal antibody, usually between 6-12 weeks of age. Young dogs
between 3 to 6 months of age are thus more prone to infection. Most
infections are subclinical. Sub-clinically or clinically diseased
dogs are responsible for maintenance of virus in environment.
Other susceptible species are:
- family felidae: cat, lion, tiger*
- family viverridae: bintotong, civit
- family hyaenidae: hyenas
- family canidae: dog, fox, dingo, coyote,
- family procyanidae: kinkajou, raccoon,
coati mundi, badger, lesser and greater panda
- family mustelidae: mink, ferret, skunk,
- family ursidae: bears *
*canine distemper vaccination not recommended
Incubation period is variable (3 to 8 days
with an average of 5 days). Following natural exposure the virus
in droplets contacts the epithelium of the upper respiratory tract.
Within 24 hours it multiplies in the tissue macrophages and spreads
in these cells, via local lymphatics to tonsils and bronchial lymph
nodes. Two to 4 days postinoculation virus numbers increase in
tonsils and retropharyngeal and bronchial lymph nodes. By days 4 to
6 the virus multiplication occurs within lymphoid follicles in the
spleen, lamina propria of the stomach, small intestine, mesenteric
lymph nodes, and Kuppfer`s cells in the liver. This widespread
proliferation corresponds with a rise in temperature and leukopenia
mainly affecting lymphocytes (B and T lymphocytes affected
equally). Hematogenous spread of canine distemper occurs 9 days
postinoculation. Virus is spread to central nervous system and
epithelial surfaces. Severe clinical signs are associated with
viremic spread of virus and lack of protective antibodies provided
by vaccination program. There is an inverse relationship between the
development of antibodies and the severity of infection.
Central nervous system infection differ
according to whether signs develop before or after development of an
immune response. Acute encephalitis develops due to entry of virus
into CNS and direct damage to neuronal cells with secondary
demyelination. Chronic encephalitis develops due to the local immune
response with anti-myelin antibodies and primary demyelination.
1.11.6 Clinical signs
Clinical signs are related to involvement of
some or all of the major epithelial sites with eventual progression
to the central nervous system. Common early signs are fever which
persists for 1-2 days then subsides for 1-2 days and then recurs.
Later there is the development of serous ocular and nasal
discharges. These discharges may become mucopurulent with secondary
bacterial infection. Progression to interstitial and
bronchopneumonia occurs and coughing develops. Other related
clinical signs are mild dyspnea and crackling lung sounds on
thoracic auscultation. Diarrhea and vomiting unassociated with
feeding reflect gastrointestinal involvement. The diarrhea is watery
and may contain blood. Tenesmus and subsequent intussusception may
occur with severe gastrointestinal disease. Diarrhea leads to
dehydration, depression and weight loss. Sudden death may occur if
animal does not receive treatment.
Dermal lesions occur and consist of a skin
rash (impetigo, or pustular dermatitis) occurring on thinly
haired areas of the body. The pustular dermatitis is found with
early clinical disease. A thickening of the dermis of the footpads (hardpads
disease or hyperkeratosis of the foot pads) and nose may occur
after systemic illness. Hard pads disease is found with chronic
Neurological signs usually occur late in the
course of the disease. Neurological signs seen are paresis or
paralysis, myoclonus (clonic-tonic convulsions, chewing gum fits),
or convulsions may occur and the disease course is weeks to months.
The neurological signs are more associated with chronic encephalitis
and the development of immune-mediated demyelination of large axons.
- Clinical signs
- Hematology - related to secondary infection
- Biochemistry - elevated BUN, slightly
elevated liver enzymes
- Inclusion bodies
- Virus isolation and identification
Gross pathology consists of thymic atrophy,
interstitial pneumonia, bronchopneumonia, catarrhal enteritis,
hyperkeratinizedfootpads, pustular dermatitis, conjunctivitis,
rhinitis, meningealcongestion, and dilation of ventricles of the
Histological lesions are lymphoid depletion,
thickened alveolar septa, proliferation of respiratory epithelium,
swelling of transitional cell epithelium of the bladder,
degenerative changes in the adrenal gland, necrosis and cystic
degeneration of ameloblasticepithelium, perivascular
lymphoplasmacytic infiltration of CNS. Characteristic eosinophilic
inclusions may be present in cells of the bladder, conjunctiva,
brain, respiratory tract, renal pelvis, and lymphoid tissue.
Inclusions typical for canine distemper virus have been identified
in the bladder of normaldogs.
1.11.8 Treatment and prophylaxis
Treatment is supportive and non-specific. The
treatment is aimed at making the dog comfortable, correcting fluid
imbalances and aiding the immunosuppressed dog in combating
secondary bacterial infections. Canine distemper causes a secondary
1.12 CANINE INFECTIOUS
CIT, CITB, Kennel cough
CIT is caused by multiple etiological agents.
These agents may act singly or in groups to cause disease. Some are
considered to be contributing causes of disease. The etiological
agents associated with CIT are:
- Canine parainfluenza virus - A
paramyxovirus (enveloped ss RNA virus) in which strains
2,4, and 5 are found in respiratory infections in dogs. Local
replication has been demonstrated experimentally. The virus has
the ability to spread rapidly from direct exposure.
- Canine adenovirus 1 and 2 -
Adenoviruses are naked ds DNA viruses. CAV-2 (Toronto,
A26/61) is also called infectious laryngotracheitis virus.
CAV-2 is more significant than CAV-1 in causing respiratory
disease. Rapid spread by direct exposure occurs.
- Canine reovirus (respiratory-enteric-orphan)
- Reo viruses are naked ds RNA viruses. Three serotypically
different species have been found. Types I and II are found in
the U.S. This virus has potential for zoonoses. Commercial
vaccines are not available in the U.S.
- Canine herpesvirus - enveloped ds
DNA virus, has been isolated from dogs with respiratory disease.
- Mycoplasma cynos - Ten different
other species of mycoplasma have been isolated from clinically
normal and affected dogs. The organism is more of a contributing
than a causal agent.
- Bordetella bronchiseptica - most
common bacterial agent isolated from dogs with upper respiratory
tract disease. In certain instances can cause primary
Portal of entry is the respiratory tract. The
primary mode of transmission is direct (aerosol or airborne).
Indirect transmission via fomites possible.
Canidae, type and severity of disease varies
- age and resistance of the host
- type and severity of infection
1.12.5 Incubation period
Incubation period varies with etiological
agent (usually 8-10 days). Canine parainfluenza has an
incubation period of 4 days, canine adenovirus-2 2-4 days, and
bordetella bronchiseptica 4-5 days. Clincal course of disease is
usually 2-3 weeks.
1.12.6 Clinical signs
Paroxysms of coughing is the primary sign. The
cough is a dry non-productive cough followed by retching of phlegm.
It may be elicited on tracheal palpation. A serous nasal and ocular
discharge may also be present. With multiple infectious agents the
disease may be more severe with fever, anorexia, depression, and
lung sounds on thoracic auscultation.
1.12.7 Differential diagnosis
Therapy is symptomatic. Mild coughs may be
treated by keeping animal in a warm, well-ventilated area. Feeding
the dog a palatable diet is advocated. Avoiding situations that may
cause the onset of the paroxsyms of coughing is also advised. In
more severe cases antibiotics are used.
1.13 FELINE UPPER
RESPIRATORY VIRAL DISEASES
URI (upper respiratory infection), FURD
(feline upper respiratory disease), Coryza, Feline influenza,
Feline distemper, Pneumonitis
There are many etiological agents that may
cause upper respiratory disease of the cat. Of these respiratory
pathogens viruses comprise the majority of clinical cases of upper
respiratory infections. Diagnosis of a particular pathogen may be
difficult due infection with multiple pathogens or subclinical
infection. The following are the most common etiological agents of
upper respiratory infections in cats:
184.108.40.206 Feline rhinotracheitis virus
etiology - enveloped ds DNA virus, found
mainly in the respiratory and urogenital tract, rapidly
inactivated out side of host, easily destroyed by most
disinfectants, antigenically similar serotypes.
epizootiology - felidae only, multiplies
mainly in upper respiratory tract, transmission may be direct or
indirect, chronic carrier cats responsible for maintenance of
virus in environment, rapid spread under conditions where cats are
confined, virus present in saliva and nasal secretions.
clinical course - incubation period 2-10
days, course and severity variable, virus shed 1-3 weeks, virus
has an affinity for sites of osteogenesis (sequellae -
persistent frontal sinusitis).
symptoms - fever, depression,
paroxysmal sneezing, serous nasal and/or ocular discharge that may
become mucopurulent with secondary bacterial infection,
conjunctivitis, corneal lesions, ulcerative keratitis, ulcerative
glossitis, coughing, bronchopneumonia, abortions in infected
queens, keratoconjunctivitis neonatorum in kittens born to
220.127.116.11 Feline calicivirus
etiology - naked ss RNA virus, more stable
than FVR, remains infective for 10 days at room temperature,
resistant to ether and chloroform, inactivated by hypochloric acid
(Clorox), numerous serological strains exist
epizootiology - all Felidae (not as
common in exotic cats as FVR), shed continuously in
oropharynx, pathogenecity limited to oral mucosa and respiratory
tract, carrier cats (shed virus continuously up to one year),
transmission occurs direct or indirect.
clinical course - incubation period
1-2 days, clinical signs persist 3-5 days, severity of disease
varies due to presence of many strains, shed from oropharynx,
urine and feces, clinical signs vary according to virus strain.
symptoms - fever, depression, ulcers,
dyspnea, pneumonia (more of a potential than FVR for development
of lower respiratory and lung lesions, oculonasal discharge (infrequent),
transient fever and lameness associated with FCV, urologic
syndrome (manx calicivirus).
18.104.22.168 Chlamydia Psittaci
Etiology - classification bacteria,
rickettsiae, and viruses, propagated in yolk sac suspension,
remains infective for 1 week at low temperatures.
epizootiology - mice, hamsters, guinea pigs,
rabbits, man (Public health consideration), transmission
direct contact with secretions or contaminating organism, shed in
ocular and nasal discharges, present in lungs also, chronic
carrier state shed organism 1-2 months.
clinical course and symptoms -
incubation period 3-10 days, variable clinical signs, generally
mild, rapid recovery, recurrences common, conjunctivitis and
rhinitis, discharge serous or mucopurulent, fever uncommon.
Naked ds DNA viruses cause mild
conjunctivitis in affected cats.
Secondary invader causes conjunctivitis
- Clinical signs - difficult to diagnose
- based on clinical signs
- Conjunctival smears - cytology
- Viral isolation
- Serology - paired serum samples from acute
Treatment varies according to clinical
symptoms and causative agent. Antibiotics used are tetracycline,
chloramphenicol for mycoplasma. The common ophthalmic preparations
used are those containing tetracycline for mycoplasma, and
idoxuridine for FVR corneal ulcers. Decongestants (Phenylephrine
HCl) have also been used to dry nasal discharges. Supportive
care with fluid therapy is necessary with severe disease. Other
supportive care consists of keeping the cat in a warm and well
ventilated area, keeping nose and eyes free of discharge, force
feeding or placement of a nasal gastric tube may be necessary.
1.13.5 Prevention and control
- Good husbandry for breeding kennels
- isolation of new cats
- separation of young and older cats
- separation of pregnant queens
- adequate space between cages
- culling of affected cats
- vaccination of young and new cats
1.14 FELINE INFECTIOUS
PERITONITIS AND ENTERIC CORONAVIRUS
FIP, FEC, FECV
An enveloped ssRNA virus of the coronaviridae
family antigenically related to coronaviruses of other species (transmissible
gastroenteritis, canine coronavirus, and human coronavirus 229E).
There are 5 antigenically similar strains that vary both in
pathogenicity and rate of replication in tissue culture. The virus
is inactivated by most disinfectants. The virus of FIP is
antigenically indistinct from the virus of FEC.
Exotic and domestic cats are affected. The
incidence of disease shows age variation. High incidence is seen in
cats less than 2 years of age and those 13 years and older. Young
cats are extremely susceptible to disease with whole litters often
affected from infected queens. Mortality rate is 100% in clinically
diseased animals. Natural incubation period and route of infection
is unknown. Virus is shed in urine, saliva, and feces. Viral
infection has been associated with immunosuppression caused by
feline leukemia virus.
Two routes of infection are considered
important (in utero and ingestion). After ingestion the virus
replicates in the mature apical epithelium of the intestine. For
feline enteric coronavirus this replication is associated with
gastroenteritis. For FIP there is no associated gastroenteritis the
virus is phagocytized by macrophages. The macrophages are
responsible for a cell-associated viremia. Viremia leads to the
dissemination of virus to target organs (liver, peritoneum,
pleura, uveal tract, meninges and ependyma of brain and spinal
The immunity that develops after dissemination
determines the course of disease. A good humoral and cell-mediated
immune response leads to complete recovery or development of a
latent infection. There are no clinical signs associated. A good
humoral immune response with a partial cell-mediated immune response
leads to the development of the dry (non-effusive) form of
FIP. A good humoral immune response without any cell-mediated immune
response leads to the development of the wet (effusive) form
of FIP. The wet form of FIP is an immune vasculitis (pyogranulomatous
reaction) around small venules in target organs. This vasculitis
is responsible for the outpouring of protein and fibrin rich fluid
into body cavities. In the dry form of FIP,the cell mediated immune
response is sufficient to contain virus infection in target organ
but cannot abort viral infection therefore there is pyogranuloma
formation in the organ. The presence of high antibody titer does not
protect the cat from development of disease. Often the signs of
disease are more severe and occur more rapidly in cats with high
antibody titer (experimental evidence with vaccine to FIP).
1.14.5 Clinical signs
General signs - fever, gradual weight loss,
Signs of effusive FIP - abdominal distention,
ascites, dyspnea, muffled heart sounds, decreased exercise
tolerance, and fluctuating bouts of diarrhea and constipation
Signs of noneffusive FIP - organ specific and
varies in manifestation according to the organ affected. CNS
involvement seen more commonly with this form of the disease. signs
- paralysis, paresis, incoordination, hyperesthesia, nerve palsies,
dementia, personality changes, tremors, nystagmus, headtilt,
circling. Liver involvement - icterus, enlarged liver,
bilirubinuria. Ocular involvement - hyphema, keratitic plaques.
Kidney involvement - proteinuria, small kidneys with an irregular
Kitten mortality Syndrome - FIP and other
infectious diseases have been associated with a clinical entity
reproductive problems in cats and less
vigorous kittens. The syndrome is associated with reproductive
failures, endometritis, pyometritis, repeat breeders, fetal
resorptions, abortions, stillbirths, congenital malformations,
neonatal deaths and weak small kittens that fade away due to
Differential for wet form - cardiomyopathy,
chylothorax, pyothorax, trauma with hemothorax or diaphragmatic
hernia. Dry form may mimic primary liver or kidney disease. CNS
lesions may mimic rabies, toxoplasmosis or other infectious diseases
that may affect the brain.
- Clinical diagnosis
- Clinical signs and history often not
- Pleural or Abdominal centesis and cytology
of fluid - fluid high in proteins and cells
- Hematology - elevated white blood
cell count with a neutrophilia and lymphopenia
Biochemistry - elevated plasma proteins,
elevated plasma fibrinogen levels, elevated bilirubin, slight
elevation of liver enzymes, slight elevation of BUN. disseminated
intravascular coagulation in some cats may lead to prolonged
prothrombin and partial thromboplastin times.
- Urinalysis - proteinuria
- CSF - elevated protein concentration and
elevated amount of cells
- FeLV test
FIP titer - please know that a positive titer
means that the cat has been exposed to FIP and that it is only
important if the titer is negative. If the titer is negative then
the disease process is not FIP. If the titer is positive then FIP
must be kept on the rule out list. Many cats without clinical
disease will have high titers to FIP. Since there is crossreactivity
with FECV it is not known whether the titer is to FIP or FECV.
1.14.7 Treatment and Prevention
Therapy for FIP patients rely on the use of
immunosuppressive agents. Due to the infectious nature of this
disease longterm remissions have not been achieved. Successful
therapy using prednisolone or prednisone 5 mg/kg divided twice a day
combined with melphalan (Alkeran) tablets 0.2mg/kg every 3rd day has
Due to the nature of FIPV to cause more rapid
disease in some antibody positive cats vaccines to date have been
unsuccessful. Since the test used to detect FIPV also detects FECV
the use of programs to detect antibody positive animals and cull is
Feline infectious enteritis, infectious
agranulocytosis, cat plague, cat fever, and feline distemper
A naked ss DNA virus of the Parvoviridae
family demonstrating an affinity for rapidly dividing cells. The
virus is very stable but may be inactivated by chlorox, formaldehyde
and paraformaldehyde. The virus is antigenically related to
parvovirus of mink and dog but not parvoviruses of other species.
All felidae are affected. Other species
affected are coati mundi, kinkajou, racoon, ferret, mink, skunk,
otter, sable, badger, etc. (all procyonidae and mustelidae).
The virus is constantly encountered and maintained in the
environment due to its stability. Transmission occurs by direct
contact and may be transmitted by contaminated fomites. Virus is
present in all body secretions during active infection. The virus
may be shed for up to 6 weeks postinfection. The virus can cross the
placenta barrier in pregnant queens. It causes lesions in tissues
with the greatest mitotic activity due to its affinity for rapidly
Direct or indirect contact in the cat leads to
replication of the virus in the lymphoid tissue of the oropharynx (18-24
hours). Afterwards the cat becomes viremic (2-7 days). If
the cat is not vaccinated the antibodies do not prevent the spread
of the virus to tissues with the greatest mitotic activity.
Therefore the virus is spread to the intestinal crypt cells, bone
marrow, and lymph nodes. Spread to intestinal tract leads to signs
of gastroenteritis exhibited in clinically affected cats. Spread to
lymph nodes leads to lymphoid depletion or thymic atrophy in very
young cats making the cat more susceptible to other infection.
Spread to bone marrow leads to myeloid depletion leading to
susceptibility to infection. This is why panleukopenia is considered
to be a causative agent of secondary immunodeficiency in the cat.
Infections that occur in utero may lead to
infertility, fetal death, and resorption if the queen is infected
early in gestation. Infections that occur mid to late gestation lead
to abortion or mummified fetuses. Infections that occur in late
gestations have effects on either the fetus or the early neonate and
may lead to optic nerve atrophy, retinopathy, hydranencephaly,
cerebellar hypoplasia, bone marrow depression and lymphoid
depletion. Direct or indirect contact with the virus in the early
neonate (2-3 weeks of age) may also lead to cerebellar
hypoplasia, lymphoid depletion, and bone marrow depression.
1.15.5 Clinical findings
The clinical findings were related to the age
of the animal, vaccination status and pregnancy status of queens.
Clinical signs range from subclinical to mild and consist of
elevated temperatures, dehydration, depression, anorexia, and
diarrhea (less common).
In kittens less than 3 months of age the
symptoms are more severe. These symptoms consist of fever, anorexia,
depression, dehydration, vomitting, and diarrhea. Kittens with
peracute infections may develop fever, depression, become prostrate
and dies within 8-12 hours of clinical onset of disease.
Pregnant queens suffer abortions, still births
and resorption infertility. Prenatal or neonatal infections lead to
cerebellar hypoplasia. Clinical signs shown are a wide base stance,
ataxia, incoordination, and intention tremors. These signs may not
be seen until the kittens began to try to walk.
The febrile response in panleukopenia is
biphasic. The first febrile response lasts about 24 hours. Two days
later the animal may become febrile again. The first febrile
response may be related to the viremia and the second due to
secondary infection as the virus causes immunosuppression.
The diarrhea that develops is fluid
feces dark brown in color. It may become blood-tinged later with
shreds of intestinal mucosa. Loops of gas and fluid filled
intestines may be palpated on physical examination. Elevation of the
third eyelids may be seen along with tenting of the skin.
Differential diagnosis - Feline leukemia,
enteritis caused by other enteric viruses (rotavirus, reovirus,
feline enteric coronavirus), intestinal parasitism (ascarids,
giardia, coccidia), acute toxoplasmosis
Diagnosis is made on
- Physical examination
- Hematology - low WBC count
- Biochemistry - elevated BUN, elevated total
proteins, and slight elevation of liver enzymes
- FeLV test
- Toxoplasmosis titer
- FIP titer
- Complement fixation
- Hemagglutination inhibition
- Viral isolation and identification
Pathology - gross lesions of dilated loops of
bowel particularly the jejeunum and ilium are seen. There are
enlarged mesenteric lymph nodes. Fetid fluid feces is found in the
intestinal tract. Prenatal or early neonatal infection a small
cerebellum may be seen. Prenatally hydrocephalus and hydrancephaly
may be observed. Neonatal infection thymic atrophy may occur.
Histological lesions consist of
shortening of the villi in the intestines. The intestinal crypts are
dilated and there is sloughing of cells into the lumen. Lymphocyte
depletion is observed in the lymphoid follicles of the Peyer's
patches. In the cerebrum there may be dilation of the ventricles and
necrosis of ependymal cells. Cerebellar degeneration is noted by
reduced population of the granular and Purkenje cell layers.
Eosinophilic intranuclear inclusions maybe seen in panleukopenia
infections but are usually transient.
Supportive therapy consist of replacement of
fluid loss to counteract dehydration. Withholding oral intake of
food and water acts to decrease vomiting and slows bowel mitotic
activity. Plasma or blood transfusion therapy may be needed with
severe anemia, panleukopenia, hypotension and hypoproteinemia. Broad
spectrum antibiotics may be used for secondary bacterial infections.
Combination B vitamin therapy may be used for decreased food intake.
Gastric protectorants may be used to decrease toxins absorbed by the
intestinal tract and to coat the mucosal lining.
1.15.8 Prevention and Prophylaxis
Colostral antibodies last for about 3 weeks or
longer depending on the antibody titer in the queen. Passive
immunization may be used in which homologous antisera from cats with
a high titer to infection may be locally or commercially produced.
Commercial preparations vary in titer and therefore vary in amount
that should be given. The administered immunoglobulin persists for
up to 4 weeks. If passive immunization is given subsequent
vaccinations must be delayed due to interference from passive
immunoglobulins. Passive immunization should only be administered to
unvaccinated kittens or cats that have had prior contact with known
infected animals or fomites.
1.15.9 Active immunization
- inactivated vaccines - given to febrile
kittens less than 4 weeks of age
- Modified live vaccines - best to use
vaccines of feline origin. Mink enteritis vaccines have been
used in the past with success.
1.16 CANINE VIRAL ENTERITIS
Minute virus of canine (MVC, Parvovirus-1),
canine adeno-associated virus (CAAV, incomplete parvovirus),
Parovovirus-2 (variation of feline parvovirus responsible for
outbreak of hemorrhagic diarrhea in 1978).
Other viral causes of diarrhea - adenovirus,
picornaviruses, paramyxovirus, coronavirus, rotavirus, canine
Parvoviruses are naked ssDNA viruses. The
virus is very stable and may be inactivated by chlorox and
formaldehyde. It has an affinity for rapidly dividing cells.
Believed to be a strain variant of FPV or MEV. Canine parvovirus is
antigenically related to both.
Dogs are the primary reservoir for infection.
Other canidae that may be infected are coyotes, bush dogs,
crab-eating foxes, maned wolves. In cats this is a self-limiting
infection in which disease is not produced. Maintenance in the
environment is due to the stability of the virus. The most common
route of transmission is fecal contaminated fomites. Feces is the
primary mode of spread. Predisposing factors are increased crowding,
stress and concurrent disease.
After oral inoculation the virus replicates in
local lymphoid tissue and then is spread throughout the body in a
non-cell associated viremia (2-5 days PI). The viremia may be
terminated at this time by serum neutralizing antibodies or may be
spread to other sites of rapidly dividing cells. Clinical signs
occur 5-10 days PI.
The course of disease depends on the age and
the immune status of the dog affected. In puppies less than 8 weeks
of age the virus may infect intestinal crypt cells, bone marrow,
lymphoid tissue, and myocardium. In dogs and puppies 3 months or
older, the virus may infect the intestinal crypt cells, lymphoid
tissue, and bone marrow. Acute death is common in generalized
disease in neonates.
1.16.4 Clinical signs
Mild disease is characterized by depression,
anorexia, fever, diarrhea (mucoid), and enlargement of
superficial lymphoid tissue. Severe disease is characterized by
bloody diarrhea, vomiting, endotoxemia, dehydration, and weight
loss. There may be neurological signs such as seizures that are
associated with a septicemia/endotoxemia due to secondary bacterial
infection (lymphoid and myeloid depletion makes dog very
susceptible to infections). A reflux of gastric material vomited
may lead to a nasal discharge.
Myocardial disease is distinct from
gastrointestinal disease and occurs in two clinical forms. Acute
sudden death may occur in the neonate due to acute myocarditis.
Clinical signs noted are continuous crying, dyspnea, seizures, and
non-productive vomiting. Death may occur after excitement, stress,
or eating. Subacute form of myocardial disease may lead to
subclinical arrhythmias, decompensated heart failure, stunted
growth, and poor body condition. Clinically the myocardial disease
may be indistinct from other causes of decompensated heart disease.
Clinical signs seen are increase pulse rate, enlarged liver, jugular
pulse, and increased respiratory sounds.
- Clinical signs
- Hematology - leukopenia which is primarily
- Biochemistry - hypoproteinemia, increase in
LDH, SGOT, and CPK
- Electrocardiography - premature ventricular
contractions, ventricular tachycardia, decreased R wave
- Radiography - left sided heart enlargement
- Serology - IgM, or specific for parvovirus
- Virus neutralization
- Indirect immunofluorescence
- Virus Detection
- Electron microscopy
- Direct Fluorescence
- Enzyme linked immunosorbent assay
- Tissue culture
Pathology - Gross pathology of dogs with
gastrointestinal signs only show a dog that is thin, pale, and
dehydrated. The intestinal lumen may be filled with a hemorrhagic
watery exudate. The intestinal lumen is red and may be covered with
a pseudomembrane. In puppies with acute myocarditis, the lungs may
be heavy and wet with frothy fluid in the trachea. The enlarged
heart is characterized by pale streaks and dilated ventricles. In
older dogs gross pathology is indistinguishable from decompensated
Microscopic lesions - blunting of the villi
and denuding of the intestinal epithelium. Necrosis and depletion of
lymphoid tissue may also be seen. Degeneration and necrosis of
myocardial cells may also be seen.
Fluid therapy should be vigorous and potassium
supplementation may be needed. Glucose supplementation is also
advised. Whole blood or plasma may be used to combat
hypoproteinemia. Antibiotics commonly used are kanamycin,
gentamycin, and penicillin. Gastric protectorants are also
- Maternal immunity
- Inactivated feline and canine origin
- Mink enteritis vaccines
- Modified live vaccines of canine and feline
1.17 FELINE LEUKEMIA VIRUS
AND OTHER RETROVIRUSES OF THE CAT
1.17.1 Viral Properties
- Doubleanded rna virus, of the
retrovirus family and oncovirinae subfamily.
- Order of genes left to right
proteins encoded by genes; group specific
antigen (gag), reverse transcriptase (pol), envelope proteins (env).
The LTR serve as promoters for the transcription of the genes into
Group specific antigen p 27 accumulates in the
cytoplasm of viremic cats. This antigen is the primary antigen used
in detection of the virus.
The major envelope protein gp 70 is the
subgroup or type specific antigen. There are three subgroups of Felv
that differ due to the gp 70 protein. This causes a difference in
infectivity, host range, and pathogenecity. This protein is also
responsible for the attachment of virus to cells therefore virus
neutralizing antibodies are directed against gp 70.
The minor envelope protein is p 15E. This
protein causes intense immunosuppression by direct action on T cells
and by complement activation.
Viral replication involves the
attachment of virus to the cell. After penetration the virus sheds
its envelope and using its reverse transcriptase produces a
complementary strand of dna. This dna integrates into cellular dna.
This integration event can only occur following dna synthesis
therefore cycling cells are highly susceptible to Felv.
After integration disease can occur due
- productive infection
- latent infection
- insertional mutagenesis
Even if the virus fails to integrate disease
may occur because failure of integration causes an accumulation of
unintegrated viral dna in the cytoplasm of the infected cell which
is toxic. This the mechanism of disease in immunodeficiency caused
by Felv or the FAIDS syndrome seen in cats.
1.17.2 Felv Subgroups
Felv A - most common, responsible for latent
infection, causes disease slowly by itself, mutation leads to other
Felv variant A - directly lyses bone marrow
and lymphoid cells, leads to lymphopenia, nodal depletion,
immunosuppression, causes Felv-FAIDS, variant virus is defective,
finding of this viral form in cats indicates a grave prognosis and
short life span for the infected cat.
Felv B - recombinant virus, created each
time Felv A recombines with endogenous Felv, replicates well in
fibroblasts but poorly in cat leukocytes, incorporates into Felv A
envelope to infect cat leukocytes, associated with fatal
hemolymphatic disease, thymic lymphomas, myeloproliferative disease,
Felv C - derived from Felv A by
recombination or mutation, associated with fata erythroid aplasia,
close antigenically to feline oncornavirus associated cell membrane
FOCMA - present on Felv and Fesv induced
neoplastic lymphoid cells, rarely found in non-neoplastic cells, get
regression of lymphoid tumors containing FOCMA when antibodies are
mounted to these antigens, antigenically crossreactive with Felv C
subgroup gp 70.
Felv is not very stable in the
environment due to its envelope. It is easily destroyed by most
detergents. Therefore it is safe to place an uninfected cat in the
cage of an infected cat immediately after adequately cleaning that
cage. Also transmission is difficulty indirectly.
Saliva is the major source of infection.
Susceptible cats may be infected during grooming, fighting or eating
from the same bowl with an infected cat. Prolonged exposure leads to
The incidence of Felv infection is
higher than the incidence of Felv disease. The highest incidence of
Felv related disease is due to immunosuppression and subsequent
infections. Tumors that are Felv related have the lowest incidence
Six stages of Felv infection:
- 1. Replication in lymphoid tissue around
- 2. Infection of small numbers of
circulating lymphocytes and monocytes.
- 3. Felv replication amplified in spleen,
lymphnodes and gut- associated lymphoid tissue.
- 4. Replication progresses to involve bone
marrow neutrophis and platelets, and intestinal crypt epithelial
- 5. Peripheral viremia occurs via bone
marrow-derived neutrophils and platelets.
- 6. Widespread epithelial infection causes
excretion of virus in saliva and urine.
Cats undergoing transient infections usually
develop a virus neutralizing antibody response by stages 3 or 4.
Cats undergoing persistent viremia are unable to develop
neutralizing antibody by stage 4. Therefore stage 4 is considered
the pivotal stage.
1.17.4 Consequences of persistent
- 1. Recognizable signs of disease
attributable to Felv infection that occur only after a long
- 2. After a long induction period there is
- 3. About 50% of persistently viremic
cats will die within 6 months of detection of infection, and
about 80% will succumb within 3 years.
1.17.5 Latent infections
In 30-80% of cats undergoing transient Felv
infections, virus is not immediately eliminated from cat. The latent
infection may be abnormal stage of the recovery process. These
latent infection are probably maintained by virus-neutralizing
antibody. There is no difference in antibody titer between cats with
latent infection and those which recover completely. The duration of
latency is short in most cats and elimination of virus occurs within
30 months of exposure. Cats with true latent infections test
negative on the ELISA and IFA tests. Latent infection may be
responsible for persistently high anti-gp70 and anti-FOCMA antibody
titers seen in some cats. Latent infections may be reactivated by:
stress, immunosuppressive therapy, complement depletion, and serious
concurrent disease. Reactivated latent infections may result in
relapsing or persistent viremia with shedding of virus in the
saliva. If virus neutralizing antibody levels are high at the item
of reactivation, immune complexes may be formed. If these are
phagocytized and removed form the circulation the ELISA test may be
negative while the cats tests positive on the IFA test. Although
cats with true latent infections are not considered infectious to
other cats, the latent state is a fragile phase of infection.
A subgroup of cats has been identified which
are nonviremic, yet remain persistently ELISA (+) for p27 antigen.
These patients are defined as "persistently discordant".
They are thought to be immune carriers of Felv. Transmammary
transmission may occur in these cats. It is inadvisable to allow
persistently discordant cats to breed or live communally with other
1.17.6 Felv-associated diseases
Diseases caused by Felv is related to the cell
type infected. These diseases are in the text and are not very
different than those that are now published. There are at least
three clinical syndromes that occur alone or in combination in
persistently infected cats.
- 1. Uncontrolled proliferation of
virus-transformed cell (tumor).
- 2. Degeneration of progenitor (blast) cell (atrophy,
- 3. Generalized immunosuppression.
1.17.7 Diagnostic Tests for Felv
Presently 3 tests are available for detection
of p27 antigen
1.17.8 Indirect immunofluorescence test
This test detects p27 in infected leukocytes
and platelets. There is a strong correlation between positive IFA
results and ability to isolate infectious virus from blood and
saliva. About 97% of IFA (+) cats remain viremic for life. False (-)
IFA results may occur if smears are prepared poorly or low numbers
of infected cells are present. False (+) results may arise from
nonspecific immunofluorescence in eosinophils or in platelet clumps.
There has bee a subgroup of cats identified that are IFA and ELISA
(-) on blood samples, yet is strongly IFA (+) on bone marrow smears.
1.17.9 ELISA test
This test uses antibody-linked enzymatic color
change to detect p27 antigen. Most of antigen detected is a soluble
form. This test is more likely to detect weak, early or transient
infections. False (+) ELISA reactions are usually due to inadequate
washing of the test wells at each stage of the test. False (+) ELISA
reactions may result from the presence of anti-mouse antibodies in
the cat being tested. Healthy ELISA (+) cats should be evaluated
with an IFA test before a long term prognosis is given.
Healthy cats which ELISA (+) and IFA (-) on a
single examination may be:
- 1. Undergoing a transient regressive
- 2. Undergoing the early stages of a
- 3. Immune carriers of a localized
- 4. May have a false (+) ELISA test.
- 5. May have a false (-) IFA test.
Differentiation of the first 3 groups is
accomplished by repeating both tests 12 weeks after the initial
detection of the discordant state.
1.17.10 Noninvasive ELISA tests
- 1. ClinEase-VIRASTAT from Norden
Laboratories detects p27 in saliva.
- 2. Tear strip ELISA for home sampling
1.17.11 FelV Antibody Assays
- 1. Anti-gp70 antibodies - ELISA test,
maintenance of protective levels requires periodic exposure to
Felv. Single titer is of little prognostic value, but may be
useful to detect recent infection.
- 2. Anti-FOCMA antibodies - Indirect
immunofluorescence test, cats with titers >1:32 may be
protected against the neoplastic effects of Felv, high levels of
anti-FOCMA antibody do not protect against viremia or the
development of the more common non-neoplastic diseases caused by
- 3. Virus neutralization - ability of
cat serum to prevent replication of a standardized quantity of
Felv in an indicator cell line, available through specific
laboratories. Subgroup neutralization can be detected with this
test. This test is not cost effective for the practicing
1.17.12 Treatment of Felv infections
Palliative and symptomatic at the present
time. No readily available methods to reverse persistent viremia.
Experimental protocols have involved the use of extracorporeal
removal of immune complexes, passive immunotherapy, biological
response modifiers (fibronectin, blood constituent therapy),
bone marrow transplantation, macrophage activation and macrophage
transfer, reverse transcriptase inhibitor therapy (suramin,
3'azido-3' deoxy thymidine [AZT], dideoxycytidine]. In addition
to specific therapy for any neoplastic or degerative disorders that
may be present, the persistently viremic cat should receive
aggressive therapy for opportunistic microbial infections which may
be present. Bactericidal antimicrobials are preferred due to
underlying immunosuppression. Corticosteroids should be used with
great caution in viremic cats.
1.17.13 Felv vaccination
Two vaccines are presently available for the
prevention of Felv infection (leukocell [Norden laboratories],
covenant [Diamond Scientific]). The efficacy of both of these
vaccines remains to be determined. A screening ELISA test should be
taken before or at the time of first vaccine. Peripheral blood or
buffy coat smears are reserved for an IFA test, should the ELISA
test be positive. The vaccination of persistently viremic cats
offers no benefits.
1.18 EHRLICHIA PLATYS
Infectious Cyclic Thrombocytopenia
Ehrlichia platys, ricketsial organism that
specifically infects platelets. It does not cross react with E.
canis serologically although it is similar to E canis in
ultrastructural appearance. Megakaryocytes donto seem to be
parasitized therefore organism enters platelets after adhering. Thus
far attempts to culture organism have been unsuccessful.
Experimental transmission experiments have been successful.
Natural mode of transmission unknown. It is
thought to be transmitted by the tick. There has been one reported
case of a dog that was infected, therefore the host range is
The incubation period is 8-15 days. Afterwards
parasitized platelets are seen followed by a drop in platelet number
to 20,000 cells/microliter. When the platelet count drops the
parasite disappears from peripheral blood smears this is followed by
an increase in platelets numbers. The parasite again becomes evident
in platelets and the whole cycle of platelet decrease, parasite
absence and platelet increase begins again. The parasitemia and
thrombocytopenia continue to recur at 1-2 week intervals. The
percentage of platelets infected decreases with each cycle but the
thrombocytopenia remains as severe due to immune mechanisms. After a
time the cyclic nature disappears and the animal become mildly
thrombocytopenic, sporadic episodes of severe thrombocytopenia
1.18.5 Clinical findings
The disease is believed to exist as a
co-infection with E. canis or Babesia. If this occurs more severe
clinical signs occur than those listed below. As a single infection
there is an increase in rectal temperature, blood in the feces,
bleeding tendencies (extra bleeding on venipuncture or after
surgical procedures). While the clinical signs may not be life threatening
it should always be considered in a differential
list for thrombocytopenia.
This is based on finding the organism in
platelets of infected animals on stained blood films. An IFA
serological assay has been explored
Therapy - Possibly tetracyclines are
effective but experimental therapy has not been evaluated.
1.19 RICKETTSIA RICKETTSI
Rocky Mountain Spotted Fever, RMSF
Rickettsia Rickettsi - There are two other
antigenically related rickettsia that must be tested for
serologically when rickettsia rickettsi is suspected.
This organism is transmitted by three ticks
Dermacentor andersoni, D. variablis, Rhipicephalus sanguineous. The
susceptible tick becomes infected while feeding side by side with an
infected. There is not usually enough organisms in the blood to
infect an adult tick unless the dog is infested with ticks carrying
the organism. However since the organism is transovarially
transmitted the offspring of the tick may have enough organisms in
it to transmit infection. The sylvan cycle between immature ticks
and small rodents is important in outbreaks and maintenance of
organism in the environment. Dogs are important carriers of infected
ticks for other dogs and humans. Outbreaks are sporadic. The tick
requires high humidity, warm temperatures, and increased vegetation.
Disease when seen is seen in April-September. During the periods of
cold the rickettsial organism becomes inactive. Therefore after a
cold winter an infected tick cannot immediately infect a new host
unless attached for a minimum reactivation period of 5-20 hours.
Dogs may be affected subclinically. These dogs are probably present
in households in which there is a clinical human infection.
Infected tick transmits the organism while
feeding on a susceptible host. There is replication of the
rickettsia in the endothelial cells of small blood vessels. This
leads to a vasculitis and subsequent vasoconstriction. Endothelial
damage leading to increased vascular permeability and increased
plasma loss. The damaged endothelium leads to microvascular
hemorrhage thrombocytopenia, and disseminated intravascular
coagulation. This process is enhanced by immune complex formation.
The end result is hypotension leading to shock, petechial hemorrhage,
decreased renal perfusion, azotemia, and organ damage.
1.19.5 Clinical findings
The disease is usually subclinical. Severe
clinical signs are associated with a high innoculum of rickettsiae.
Clinical signs occur more rapidly than E. canis. Signs of severe
disease include fever, vomiting, diarrhea, and depression occurring
2-3 days following tick inoculation, later during the course of
illness then scleral injection, conjunctivitis, mucopurulent
oculonasal discharges, non-productive coughing, weight loss
dehydration, lymphadenopathy, depression and muscle or joint
tenderness. Signs related to the thrombocytopenia are petechia and
ecchymotic hemorrhages of the mucous membranes and depigmented areas
of the body, epistaxis, melena, and hematuria. Ocular lesions
consist of retinal hemorrhages and anterior uveitis. Early cutaneous
lesions consist of edema, hyperemia of lips, sheath of penis,
scrotum and dependent portions of the body. Neurologic signs consist
of lethargy, confusion stupor, convulsions, coma, paraparesis,
ataxia, and hyperesthesia. Shock, cardiovascular collapse, oliguria
are apparent during terminal stages of the disease.
Hematology and Biochemistry - Mild leukopenia
that progresses to severe leukocytosis as the disease progresses.
Thrombocytopenia is the most consistent finding. There is a
normocytic normochromic anemia and an elevated erythrocyte
sedimentation rate. Hyperfibrogenemia occurs in dogs with DIC. There
is an increase in SAP, SGPT, SGOT, cholesterol and a decrease in
albumin, Na, and Cl. There is an associated metabolic acidosis.
Clotting abnormalities occur in the face of DIC. In terminal stages
there is an increase in the BUN with proteinuria and oliguria. In
the CSF there is an increase in protein and PMN's. In dogs where
there the muscle is affected there may be an increase in the CPK.
1.19.7 Electrocardiographic changes
ST segment and T wave depression
1.19.8 Thoracic radiographic changes
diffuse interstitial infiltration pattern
1.19.9 Differential diagnoses
Same as E. canis
Weil Felix test is not specific but may be
used as screening test. For this test the antibodies increase the
second week of infection and remain high.
Complement fixation is the primary test in
human. This requires paired serum samples titers with a four fold
rise over 2-3 week post infection sample.
1.19.11 Microimmunofluorescence test
MIF test is a IFA test that can distinguish R.
rickettsi from the other two antigenically similar rickettsiae. It
also has the advantage that it classifies the antibody on the basis
of IgM or IgG. Paired serum samples must be run at the same time.
Unaffected dogs have titers of <1:64. Infected dogs have titers
> 1:128. Active infection is indicated by an increase in titer
from > 1:128 to >1:32,768. High titers decrease after 3-5
months but may remain above exposed levels for at least 10 months.
1.19.12 Rickettsial isolation
Monocyte cultures on clotted blood, liver,
spleen, and brain can be performed. These tissues may also be used
to infect chick embryo culture to detect rickettsial organism.
Organisms in culture can be detected by direct immunofluorescence.
This detection is usually accompanied by paired serum samples for
Tetracyclines 22mg/kg tid. Chloramphenicol
15-20 mg/kg tid. Clinical improvement occurs within 12-48 hours,
organ failure, lymphadenopathy, and spleenomegaly takes longer to
resolve. Therapy is aimed at decreasing the amount of organism until
the immune response is able to clear the organism. Supportive
care - Intravenous fluid therapy must be used with caution due to
increase vascular permeability. Expanded fluid volume may lead to
pulmonary and cerebral edema.
Avoidance of tick infested areas, rapid
removal of ticks from animal, repeated dips during April to
September, and application of insecticides or dust to surrounding
vegetation to decrease tick population. A new experimental tissue
culture origin vaccine shows some promise in laboratory animals.
Dogs recovering are immune to infection for 6-12 months later.
Increase possibility of infection due to
increase contact with infected ticks on dogs. Infection is known to
also occur through intact of abraded skin and conjunctiva. Effluents
from ticks are highly infectious so handling of ticks should be
avoided as removed from pets.
Canicola fever, Weils Disease, Stuttgarts
disease, Canine typhus
A gram negative spirochete is the causative
agent of leptospirosis. All pathogenic letospires are classified as
Leptospria interogans. This species includes 16 serogroups and 150
serovars. The serovars of importance in the dog are Leptospira
canicola, and L. icterohemorrhagiae within U.S. Outside U.S. L.
ballum, L. gryptyphosa, L. autumnalis, L. bataviae, L. janvanica and
others. L. pomona rarely ever involved in the canine disease.
Both direct and indirect transmission can
occur. Routes of direct transmission are venereal, bite wounds and
ingestion of infected meats. The most common portals of entry are
the nasal mucosa and conjunctival sac. Oral ingestion of Leptospira
is a less common route of entry. Infected dogs can shed Leptospira
in their urine for up to 3 years (more commonly 6-18 months).
The rat is an asymptomatic carriere of L. icterohemorrhagiae but not
L. canicola. Indirect transmission can occur from contaminated
vegetation, oil, food , water, and bedding. The organism can survive
for several weeks under optimal conditions. Optimal conditions are a
warm wet environment with neutral or alkaline water. Incidence is
higher in summer and early fall. The organism is susceptible to
iodine based disinfectants.
The dog is obviously susceptible as are many
specieis of animals (including cattle, sheep, pigs and wild
animals, etc) The cat very rarely suffers from clinical
Leptospirosis and some feel the cat possesses a species immunity.
The dog can serve as a reservoir host for Leptospirosis of man. The
disease is most common in young adult (18 mo.-3 years) male
Incubation Period: Experimental and probably
natural infections have an incubation period of 7-19 days; however,
Leptospira may be cultured from the blood prior to the appearance of
The majority of dogs infected with Leptospira
species show no clinical signs (inapparent infection). The
early signs of Leptospirosis - fever, depression, anorexia - cannot
be differentiated from those of CD, ICH, and many other canine
diseases. Leptospirosis may be acute, subacute, or chronic and a
wide variety of clinical signs may be seen. In addition to fever,
depression and anorexia an infected and ill dog may show any one or
several of the following signs: vomiting, diarrhea, dehydration,
petechial to ecchymotic hemorrhages on visible mucous membranes,
iritis, conjunctivitis, coughing, hematuria (not hemoglobinuria),
1.20.6 Course of disease:
In fatal cases, death may issue in 4 days or
the patient may linger for 7-10 days. Recovery is never rapid and
although the patient may show signs of improvement in 7-10 days, it
will take 4 months for kidney function to return to normal.
A wasted carcass with signs of dehydration.
Hemorrhagic lesions on all serous and mucous surfaces plus a
hemorrhagic enteritis from cardia to anus. Fatty degeneration of the
liver and acute or chronic nephritis.
Kidney function tests and urinalysis are
important guides to diagnosis and prognosis. Liver function tests
are less reliable for this purpose. Early leucopenia followed by
leucocytosis on 4th to 5th day of illness. Rapid sedimentation rate.
Thrombocytopenia, specific tests include darkfield examination of
the urine, animal inoculation, blood and urine culture,
agglutination, agglutination-lysis, and fluorescent antibody tests.
Supportive fluids and perhaps blood
transfusions. Specific treatment includes penicillin (50,000 IU/lb
body weight/day). Tetracyclines are perhaps better for some species
of Leptospira as L. sejoe, gryptyphosa, and mitis. Streptomycin (7-10
mg/lb/bid) is used to eliminate the carrier state and should be
given for at least 7-10 days.
Commercial bacterins. One, two or three doses
at two week intervals followed by annual revaccination.
- 1. Leptospirosis is thought to be the most
- 2. Contaminated urine is highly infectious
to humans and animals.
- 3. Contaminated areas should be washed with
detergent and treated with iodine-based disinfectants.
- 4. Animals that are shedding organisms
should be treated wit dihydrostreptomycin of streptomycin.
1.21 CANINE BRUCELLOSIS
Canine abortion, Epizootic Canine abortion,
Contagious Abortion of dogs, Beagle fever
Brucella canis a small, gram negative
coccobacillus. The organism is relatively short-lived outside the
dog and is readily inactivated by common germicidal disinfectants.
Both direct and indirect. Venereal
transmission occurs. The seminal fluid of the male dogs has been
incriminated as a vehicle of venereal transmission. Oral infection
as a result of ingestion of aborted feti, mammary secretions,
placental tissues of vaginal discharges of infected female is most
frequent a mode of transmission.
Dogs of all breeds and mixed breeds (infection
is significantly higher in stray dogs than in single dog households).
Man is mildly susceptible. Foxes are susceptible to experimental
Difficult to evaluate. Dog or bitch may
demonstrate a bacteremia 1-3 weeks after oral infection yet bitch
may not show signs (abortion) until bred 6 months to a year
1.21.6 Clinical Signs:
Abortion, without precursing signs, at 30th to
57th day of pregnancy (85% of abortions fall with the 44th-55th
day of pregnancy) in the bitch. Persistent vaginal discharge for
1-6 weeks after abortion. Males may show scrotal swelling,
epididymitis and painful, swollen testicles plus a scrotal
dermatitis. Testicular atrophy may occur. Abnormal sperm (80-90%)
appear in ejaculate of males 2-20 weeks post infection.
1.21.7 Course of disease:
Infection is prolonged, likely for 1-2 years,
Recovered animal are immune to reinfection.
Lymphadenitis, testicular atrophy in males.
Plate (slide) and tube agglutination test and
blood culture. Plate test is set to record only as positive those
animals with a tube agglutination of 1:200 or more. A negative slide
agglutination test is 99.7% specific; however, a positive slide
agglutination test is only 62.5% accurate and a diagnosis therefore
should not be based on a positive slide agglutination test.
Treatment is of questionable value and may
produce a false sense of security insofar as potential transmission
to dogs or man is concerned. The following regimen has been reported
as successful in some instances.
Tetracyclines 60mg/kg/day divided tid for 3
weeks rest 3-4 weeks and then repeat Tetracycline dosage and include
Streptomycin at 40mg/kg/day (IM) divided bid and sulfadimethoxine
50mg/kg sid for 14 days.
To control the disease in a kennel or colony.
- 1) Culture and tube test monthly until 3
consecutive clean tests occur. Eliminate all animals with
positive blood cultures plus all positive tube tests with titers
above or equal to 1:400.
- 2) Once kennel is clean, keep it that way.
Do not take in untested dogs or ship for breeding to an untested
- 3) Heavily used males should be bred only
to test-negative females and checked twice yearly by the slide
- 4) Bitches should be screened by the slide
test several weeks before their expected estrus. It is important
to screen dogs prior to proestrus so that if a suspicious result
is obtained, there is time to complete additional laboratory
tests before the onset of estrus.
The exotoxins (tetanospsmin and
tetanolysin) of Clostridium tetani, a gram positive, anaerobic,
spore forming rod. C. tetani is ubiquitous in nature.
Wound contamination plus something (as a
deep closed wound) which prevents normal tissue
oxidation-reduction activity and allows C. Tetani to vegetate.
Toxins travel centrally along nerve trunks to spinal cord. vascular
spread may be involved.
The horse and perhaps sheep are frequently
affected. Man may be infected. The dog, on the basis of body weight,
is 300 times more resistant than the horse to tetanus. The cat
appears to be even more resistant than the dog.
3 to 20 days. Common is 5-8 days.
Spasms of facial muscles, erect carriage of
ears with wrinkling of skin of forehead, trismus, protrusion of
nicititating membrane, hypersensitivity to external stimuli,
"sawhorse" posture, opisthotonus.
1.22.7 Course of disease:
3-30 days. Death, if it occurs is usually
within a week of the onset of signs.
May find the "wound" of
origin. No characteristic gross or microscopic lesions.
Meningitis of non-tetanus origin is most
frequently confused with tetanus.
- (a) Relief of muscle spasms: keep in dark,
quite quarters. Phenobarbital to sedate or pentobarbital to
anesthetize if needed. Muscle relaxants and-or tranquilizers may
be of value.
- (b) Neutralization of Free toxin:
25,00-50,00 units of tetanus antitoxin (TAT) in 250-500 cc
saline by slow IV drip. Repeat in 72 hours. Give test dose of
0.1-0.2 ml ID or subq and observe animal for 30 minutes for
untoward signs before giving large doses IV.
- (c) Removal of Toxin Source: Open wounds,
if found, and clean. Can use 10,000 units of TAT here. Put
patient on penicillin or tetracyclines systematically.
- (d) Supportive therapy as fluids,
pharyngostomy tub or oral alimentation etc.
Tetanus toxoid will provide a strong immunity;
however, it is seldom used. TAT following tetanus prone wounds may
The disease is caused by ingestion of
preformed neurotoxin produced in rotting carcasses and in food by
Clostridium botulinum. C. botulinum is a gram-positive spore-forming
saprophytic anaerobic rod. The spore is quite resistant to heat (can
boil for an hour and not destroy the spore). The toxin is
destroyed at 176 degrees Fahrenheit after 20-30 minutes.
Ingestion of the toxin in meat products or
Dog is said to be quite resistant to natural
infection. Cats are susceptible to subcutaneous injection of toxin
but resistant to oral ingestion (natural disease).
Very short in the dog. Twelve hours from
ingestion of toxin to signs of disease.
Rapid onset of flaccid paralysis. Mucous
membranes are injected; hear slow an weak. Thoracic respiration if
present is shallow and weak; abdominal type breathing may be seen
due to paralysis of muscles or respiration. Paralytic ileus with gas
in intestinal tract.
Short. 12-24 hours.
No characteristic gross or microscopic
pathology. May find ingesta in stomach such as chicken bones an
feathers that owner has no recollection of feeding.
Must be differentiated from all paralytic
diseases (tick paralysis, polyradiculoneuritis, etc) Can run mous
inoculation form blood of suspected case.
Ambivalent (Polyvalent) antitoxin. Not
much good once signs are seen. Five ml of polyvalent antitoxin
administered intravenously or intramuscularly has been used in dogs.
Antitoxin can be obtained rapidly from Mink cooperatives. Penicillin
has been used in dogs and humans to reduce any intestinal
populations of clostridia. This possibly could make the condition
worse by release of more toxin. Also penicillins cannot eradicate C.
botulinum in the intestine. Neuromuscular potentiators such as
guanidine hydrochloride may be tried especially in severe cases with
respiratory muscle paralysis. Supportive therapy is most important
since recovery is spontaneous if the amount of toxin ingested is not
too large. Affected animals should be assisted to eat and drink.
Waterbeds or cage padding should be used to reduce the incidence of
decubital sores. The ability to urinate should be monitored and the
bladder expressed as needed. Enemas or stool softeners should be
used for constipation. Parenteral fluids should be used as necessary
to avoid dehydration, especially if swallowing is impaired.
Antibiotics can be used if infection develops but aminoglycosides
should be avoided since they also have the potential to block
Toxoid is available. Disease is so rare in the
dog, its use is rarely indicated. Preventing access to carrion and
thorough cooking of any food fed to dogs will prevent the disease.
Salmonella. Motile, gram negative, aerobic,
non-sporulating rods. All members of the group have an antigenic
structure by which they can be identified. All known types are
pathogenic for man, animals or body. About 50 serotypes (of
approximately 900) of Salmonella have been isolated from dogs
and at least 23 serotypes have been isolated from cats. It is common
to find 3 to 12 serotypes in one outbreak.
Can be direct or indirect. Seemingly, indirect
transmission from contaminated food (dry dog food, frozen horse
meat, dried egg or milk products which may be contaminated by
exposure to mouse or rat feces from infected rodents) is most
sommon. direct dog to dog transmission (fecal-oral route) can
occur. The susceptible animal is infected by ingestion.
Dogs are susceptible ias is the cat. Both dogs
and cats can be asymptomatic carriers. In the dog, the disease
usually is more severe in the very young or the old and debilitated.
Short. 24-48 hours
Characterized by fever, gastroenteritis with
vomiting and diarrhea (may be blood stained), dehydration and
Four clinical syndromes (plus
asymptomatic carrier) are described:
- 1) Acute - Pups 4wks-4mos of age. Severe
signs of fever, rapid dehydration and sever depression. May or
may not show a diarrhea but have a sever gastroenteritis on post
- 2) Enteric Fever - also seen in young or
debilitated old animal. Fever, vomiting and diarrhea (often
blood stained) and dehydration. Long course of 2wks to 2mos or
- 3) Food Poisoning type: Exposive diarrhea
in a mature dog. Lasts 1-2 days. No fever, no loss of appetite,
no severe dehydration or depression.
- 4) Septicemic form: May follow any of
above. Pneumonia, peritonitis, and local abscesses.
- 5) Asymptomatic carrier - No signs. May
follow nay of the aobe forms or may be independent of them.
Carrier state in dogs seems to be short, i.e. months
Initial leukopenia then sever leukocytosis
with left shift. If no antibiotics have been used, blood cultures
may be positive during first 48 hours of illness. Stool cultures an
serology are not of great benefit in diagnosis of disease since
these do not differentiate the carrier form the diseased dog.
Drug resistance in Salmonella is emerging.
Parenteral broad spectrum antibiotics (chloromycetin,
tetracyclines, ampicillin) early if dog is vomiting. When
vomiting ceases these drugs can be used orally or can use neomycin,
ntirofurans, etc. Anticholinergics and intestinal protectives may be
indicated to control diarrhea. Fluids are indicated if dehydration
Sanitation. Autogenous Salmonella bacterins
can be prepared.
- 1. Dogs and cats have the greatest
potential for infecting humans through contaminated feces.
- 2. Infected animals have been shown to shed
the organisms either in the feces or in conjunctival secretions.
- 3. Unrestricted and indiscriminate use of
antibiotics has selected for increasingly resistant animal
strains of salmonellae, which are correspondingly more difficult
to treat in infected humans.
Gram-negative spirochete Borrelia burgdoferi.
Unstained cells are visualized by phase contrast or darkfield
microscopy techniques. The organism is microaerophilic and optimal
growth is obtained by 34-37 degrees Centigrade. Several strains have
been isolated. The organism is susceptible to routine disinfecting
The primary vectors are various species of
hard ticks. Principal vectors in U.S. Ixodes damini and Ixodes
pacificus. Transmission has also been shown to occur in dogs by
direct contact in the absence of an arthropod vector. This
transmission is considered to occur by infected urine. Adult ticks
are abundant during the spring and fall. These are the seasons
during which the majority of clinical cases in dogs occur.
The principal host for Borrelia is the
white-tailed deer (adult ticks) and white-footed mouse (larval
and nymphal stages). Other hosts are other small rodents ,
opossums, horses, dogs, cats, and human. All three stages of the
ticks feed on human.
The exact mechanism is unknown. It is
postulated that direct and indirect effects are involved. Parasites
remain active in the host even in face of a good antibody response.
A. Direct effects
- 1. Spirochetal lipopolysaccharide
producing a pyrogenic reaction.
- 2. Possible endotoxin
- 3. Possible that cell wall peptidoglycans
may induce persistent joint inflammation
B. Indirect Effects
- 1. Immune complexes are present in serum
and synovial fluid in abnormal amounts. These complexes may
localize and produce inflammatory joint disease.
- 2. Interleukin-1 production by
macrophages increases collagenase and PGE2 secretion by
synovial cells. Collagenase may play a role in digestion of
- 3. Spirochetes may cause mast cell
degranulation an release of mast cell mediators.
1.25.6 Clinical course:
The highest incidence occurs in dogs 0-5 years
of age. There is no breed predilection, but, hunting and sporting
breeds tend to have greater exposure and therefore higher incidence.
The most common clinical signs listed in order of observed frequency
- 1. fever
- 2. inappetence
- 3. Acute onset of lameness
severe pain without associated swelling
some dogs will develop swollen joints
lameness may be intermittent an migrate
from one leg to another
- 4. Recurrence of lameness weeks to months
- 5. Swollen lymph nodes
- 6. Generalized apin
- 7. Skin lesions
- 8. Atrioventricular block
- 9. Secondary glowmerulonephritis and
- 1. History
- a. travel to a Lympe disease endemic
- b. Acute onset of lameness with no
history of trauma
- c. History of past or current tick
- 2. Serology
- a. IFA or ELISA
- b. IgG antibody titers 1:1024 or
greater are positive. Titers below 1:64 should be considered
- c. Can monitor antibody titer to
determine effectiveness of treatment.
- 3. Culture: Blood or synovial fluid can be
used but organism is very difficult to culture
- 4. Clinical laboratory data
- a. CBC sometimes WBC is elevated
particularly neutrophils and monocytes.
- b. Normally there is joint pain without
radiographic evidence of disease. Dogs are usually ANA
- 1. Tetracycline 25mg/kg/day per os tid fo
minimum of 14 days
- 2. Erythromycin and ampicillin also
- 3. If joint pain is severe dexamethasone can be used at 0.25mg/kg but only in conjunction with antibiotic therapy
Prevention: Limit tick exposure, Use tick collars, remove ticks promptly.
1.25.10 Public Health Consideration:
The most common route of infections in human
is the bite of an infected tick. Tick-infested dogs could bring
infected ticks into close association with humans and indirectly
contribute to human infection. Urine from infected dogs can also
serve as a source of spirochetes. Care should be taken when handling
blood and urine samples from any dog from a Lyme disease endemic
Pathogenesis and Transmission
- I. The causative of agent is Toxoplasma
gondii. The life cycle of this parasite in fields may be
summarized as follows:
- A. Ingested sporulated oocysts excyst in the wall intestine
- B. Zoites released from the oocysts or zoites ingested from infected intermediate hosts penetrate intestinal epithelial cells and initiate asexual multiplication.
- C. Zoites later initiate a sexual cycle and form gamonts.
- D. Microgametes escape from microgaetocytes and fertilize macrogametes.
E. Resistant walls form around the zygotes to reproduce an
- F. Some zoites pass through intestinal cells and multiply in the lamina propria. These zoites then spread to extraintestinal cells via the lymphatic channels and bloodstream and initiate division.
- G. Infected cats usually become immune and recover; the parasites begin a resistant stage and form cysts in various organs.
- II. Transmission is effected by ingestion
of oocysts in feces, by ingestion of zoites from infected
intermediate hosts (e.g., rodents, uncooked meat), and by
- III. This parasite is cosmopolitan in
- IV. Oocysts are resistant to most common
disinfectants. They can be killed, however, by exposure to 10%
aqueous ammonia (the concentration found in most household
ammonia preparations) for 30 minutes.
1.26.2 Clinical Signs
- Most infection with T. Gondii are
- When clinical toxoplasmas occurs, signs
seen can include fever, hepatitis, bilirubinemia, pneumonia,
anemia, encephalitis, myositis, myocarditis, enteritis, and
- The degree of clinical illness
and type of infection depends on the animals age at time of
infection, the immune status, and the strain of infecting
- Clinical toxoplasmosis is most
commonly seen in the immunodeficient neonate or the
- Cats usually develop subclinical
infections. Diarrhea and central nervous system disease can
cause death in neonatal and unweaned kittens.
- Dogs with acute infections
develop systemic disease with clinical signs based on the organ
- Chronic infections are usually
of the ocular or CNS forms.
Tropical canine pancytopenia, canine typhus,
canine hemorrhagic fever, idiopathic hemorrhagic syndrome
Ehrlichia canis, tribe ehrlichieae, family rickettsiaceae, order
ricketsiales. It is an obligate intracellular
parasite. It is found intracytoplasmic in leukocytes particularly
monocytes and lymphocytes. A strain that has been found to infect
neutrophils is considered to be a variant of ehrlichia equi. The
organism is gram negative and pleomorphic.
Infection restricted to canidae (coyote,
jackal, fox, dog). Transmission occurs through tick vector
and/or contaminated blood. The tick vector is rhipicephalus
sanguineous or the brown dog tick. In the tick vector ehrlichia
exist and replicate in the gut epithelium and hemolymph of the
infected tick. Infected nymphs can transmit disease for at least 155
days. Infected unfed ticks are considered to be the prime reservoir
of E. canis. Since E. canis can be transmitted by whole blood
inoculation, blood donor dogs should be confirmed E. canis free
prior to their use. Differences in incidence of `e. canis infection
varies in endemic areas according to season, vector density,
awareness of disease, ability to identify disease, and stress of
other related diseases. The majority of cases are found in western,
southwestern and southeastern regions.
There are three phases of the disease acute,
subclinical, and chronic. The acute phase occurs 8-16 days following
the bite of an infected tick or after inoculation of infected blood
and lasts 2-4 weeks. The clinical signs associated are mild. The
subclinical phase occurs after the acute phase. In this phase the
dog is clinically normal with occasional episodes of clinical
disease. Chronic or terminal phase occurs 60-100 days after the
acute febrile phase. The clinical signs associated with this phase
are very severe. The degree of severity is dependent on the breed of
Pathological manifestation consists of an
extensive plasmacytosis and perivascular cuffing in parenchymatous
organs (particularly lung, meninges, kidney and spleen).
These lesions suggest an immunopathological basis of the disease
process. This is substantiated by the finding that lymphocytes from
infected dogs exert a cytotoxic effect upon autologous monocytes.
This cytotoxicity bears a temporal relationship to the
thrombocytopenia. Further evidence that thrombocytopenia in E. canis
is immunologically mediated is provided by the evidence that serum
from diseased dogs inhibits platelet migration.
1.27.5 Clinical signs
In the acute phase the signs are
lymphadenopathy, spleenomegaly, and fever. Clincopathologically the
animal may have a normal leukocyte count, leukopenia, or
leukocytosis. In the chronic phase clinical symptoms are the same as
the acute phase. In addition there is anemia, evidence of
thrombocytopenia, leukopenia, and plasmacytic infiltration of
various organs. Clinical signs are better divided into system
In hemorrhagic cases, there is severe bleeding
evidenced by petechial or echymotic hemorrhages on the mucous
membranes of the eye, mouth prepuce, vulva, hairless area on skin,
abdomen, pinna or iris. Frank bleeding may be evidenced by
epistaxis, hematuria, hemataemesis, hematochezia, and melena.
Bleeding in joints may be evidenced by sudden onset of lameness.
There may be prolonged bleeding from injection sites, minor surgical
procedures, or routine surgery. Thrombocytopenia in the acute and
chronic phase is due to thrombocytopenia. Bone marrow biopsy will
differentiate between the two phases.
In neurological cases, the involvement of the
CNS is due to hemorrhage. Clinical signs seen are an arched back,
severe pain in the neck or back, unilateral or bilateral hindleg
paresis, paraplegia, and/or sudden collapse. No abnormalities of the
spinal column will be detectable by plain radiography. Spinal
hemorrhage may be difficult to confirm by CSF tap. Diagnosis may be
made from E. canis cultured from the blood or improvement with
Breeding disorders may be associated with E.
canis are prolonged bleeding during estrous, inability to conceive,
abortion, neonatal death. This is circumstantial however.
In uremic cases, the clinical signs are
associated with cellular infiltration in the kidney. The signs vary
according to the amount of kidney affected. Clinical signs seen are
polyuria/polydipsia, depression, anorexia, emesis, pale or congested
mucous membranes, edema of limbs, halitosis, and/or oral ulceration.
Clinicopathologically there is an elevation of the BUN and an
increase in inorganic phosphorus. With treatment the damage may be
reversible. In some cases the damage is not reversible and with
treatment there is improvement of clinical signs but the BUN and
phosphorus remain high. In these cases the dog is treated for
chronic renal failure and placed on a low protein diet.
In subclinical cases, signs of disease may be
manifested under situations of stress such as major surgery,
malnutrition, pregnancy, extensive neoplasia, and other concomitant
disease. Clinical signs may be nonspecific such as weight loss,
selective appetite, intermittent lethargy. In these cases it is
difficult to find E. canis in blood smears and therefore monocytes
need to be cultured to identify the organism.
A carrier state may occur. The healthy carrier
state differs from subclinical E. canis because these dogs do not
develop clinical signs when stressed. In these dogs E. canis is
rarely found and must be identified by cell culture test.
Rocky mountain spotted fever, brucellosis,
blastomycosis, salmon poisoning, immune-mediated thrombocytopenia,
systemic lupus erythematosus, lymphosarcoma, and other causes of
specific organ dysfunction and lymphadenopathy.
The most prominent clinicopathological
manifestations of ehrlichiosis are an increase sedimentation rate,
thrombocytopenia, and slight to severe pancytopenia. The acute and
chronic phases may be differentiated by bone marrow aspirates. In
acute disease the bone marrow is normal cellularity. The bone
marrow becomes hypocellular in the chronic phase of disease. There
is a hypergammaglobulinemia that develops during the acute phase
of disease and may persists during subclinical and terminal phase
Clinical diagnosis is made on the
basis of history, physical examination, lab analysis, or necropsy.
Diagnosis by laboratory analysis is made by identifying organism
in thin blood smears, buffy coat samples from whole blood, or
culture of monocytes (cell culture test). Antibodies may be
identified by indirect fluorescent antibody testing (not always
Tetracycline total daily dose of 66mg/kg/day
divided into 2-3 doses for 14 days. Supportive care consists of
administration of fluids and other antibiotics for secondary
bacterial infection. Blood transfusions may be given but steroid
treatment should be advised in case of adverse reactions. Antibody
titers decline to non-detectable levels after elimination of E.
There is no vaccine available for E. canis.
Proper control of insect vectors is advised. Chemoprophylaxis is
advised in endemic areas. This consists of tetracycline at a dosage
of 6.6mg/kg/day. In some areas a four point program has been
established. This program consists of initiating and maintaining
strict tick control; the use of IF A testing to identify infected
dogs; maintain susceptible dogs on prophylactic levels of
tetracyclines; treatment of infected dogs followed by
1.28 CARE OF PUPPIES AND
Most of the care of puppies is done by the
mother. Therefore it is first important to take care of the bitch with
proper nutrition, immunization, housing and sanitation. Nursing care
of newborn puppies consists of protection from drought and cold;
stimulation of urination and defecation; and feeding of puppies. In
caring for puppies it is important to know the normal physiological
parameters so that the client may be advised of whether or not the
puppy is normal.
1.28.1 Physiological values in the puppy
- Newborn Two weeks
- Heartrate 160-200 180-210
- Respiratory rate 40 40
- Temperature 95-98.6 98.6-100.4
- Hematocrit 55 27-32
- Hemoglobin 17 10
- Erythrocytes (106) 6 3.2
There are limitations associated with treating
very young puppies and kittens. The main limitations are size and
the financial concern of the owner. Another limitation for the
clinician is the narrow response range of the neonate (i.e.
whining and crying to indicate discomfort of any kind). It may
be important that the veterinarian be able to observe the whole
litter rather than one puppy that seems to be showing the sign. This
may require a house call as breeders may be unwilling to bring in
all of the puppies. Often on the phone consultation is possible if
the owner is able to give accurate information and if you are
familiar with the owner's pet (i.e. regular clients in which the
veterinarian is aware of the history of the mother of the puppies).
The veterinarian in any case is usually able to give the owner
prognostic information allowing for a more satisfying and better
informed decision on the part of the owner. General care is aimed at
evaluating the puppy for physical abnormalities and making the owner
aware of behavioral abnormalities associated with disease.
1.28.2 Environmental Conditions
Fluctuations in temperature and humidity,
ventilation air exchanges, drafts, and moisture all are important in
the care and well being of the neonate. Protection from drought and
cold is important because the ability to nurse effectively is
dependent on both the maturity and body temperature of the newborn.
Adequate pulmonary function is also important for effective nursing.
Ineffectual nursing and lack of body fat lead to hypoglycemia. Death
may occur in 6-36 hours. The normal temperature in a newborn puppy
is 95-96.8 degrees Fahrenheit. The temperature may fall to 86*F
during drying. After drying there is reversal of the temperature.
The temperature rises over the first seven days to about 100.4*F. A
puppy that is chilled to 68-93.4 degrees Fahrenheit will whine
excessively. There will be an increase in both respiratory and heart
rate. The whining will cease if the puppy is placed beside the bitch
or another warm object. A puppy that is chilled to 60 degrees
Fahrenheit will become lethargic and uncoordinated. The respiratory
rate may decrease to 20-25 bpm and heart rate to 50 bpm.
This is to be differentiated from a puppy that
is too warm. This puppy will also become lethargic but not
uncoordinated and decreases in heart and respiratory rates will not
be seen. Environmental temperature is important in order to maintain
normal physiological temperature in the puppy. In the first week
environmental temperature is most optimum at 84.2-90 degrees
Fahrenheit. The second week the environmental temperature may be
lowered to 78.8-84.2 degrees Fahrenheit. The third week the
environmental temperature may be lowered even further to 73.4-78.8
degrees Fahrenheit. The fourth week the environmental temperature
may be a comfortable 73.4 degrees Fahrenheit.
1.28.3 Physiological conditions
The neonates eyes do not open until about 14
days after birth. Even after the eyes have opened the neonate can
see little but shadows until about 4 weeks of age. The ears of the
neonate do not open until 21 days after birth. Eventhough it is
difficult to determine the neonate seems to be more adept to
development of the sense of hearing and seems to be able to hear
soon after the ears open. Voluntary control of urination and
defecation begins at days 16-21 after birth. Prior to this time,
urination and defecation is stimulated by the bitch licking the
perennial region. Orphaned puppies may be stimulated to urinate and
defecate by gently wiping the perennial region and abdomen with a
warm damp cloth. Often the lack of response to this stimulus may
cause the mother to neglect the puppy and push it out of the
whelping box. This is considered as inability to thrive by the
1.28.4 Nutritional Factors
Adequate nutrition and the prevention of
malnutrition begins with the feeding of the pregnant bitch. The
bitch must be fed to the optimum level to produce enough milk for
feeding of the puppies. In addition to malnutrition some other
causes of inadequate milk production in the bitch are parasitism,
metritis, mastitis, and under developed mammary gland. Normally milk
production decreases 5 weeks after parturition.
Puppy vigor correlates directly with intake of
protein. The survival of puppies is related to rate of growth. Good
nutrition and normal growth in puppies may be monitored by a rule of
a daily gain of one gram for each pound of adult weight for that
breed. The puppy should double its birth weight by the tenth day
after birth. Puppies with sufficient milk should be pear-shaped with
the heavier part downward. In puppies gaining weight from the
beginning of nursing the prognosis of survival is good. In those
losing less than 10% of their birth weight and then gaining weight
again the prognosis of survival is good. In puppies losing greater
than 10% of their birth rate the prognosis is poor unless suitable
therapy is instituted. Puppies that do not gain as anticipated
should receive supplemental feeding with simulated bitch's milk. The
puppies are fed individually according to age.
Daily amount of milk substitute according to
age and bodyweight
percent of body weight age (days)
Feedings should be divided to be given 3 times
a day or more if gastric overload occurs. One of the signs of
gastric overload is diarrhea.
If a puppy is too weak to suck it may need to
be tube fed. The esophageal gastric tube should be measured so that
it reaches the stomach. This can be adequately performed by
measuring from the nose to the last rib. Puppies fed in this manner
should be fed every 8 hours. After each feeding the puppy should be
stimulated to urinate and defecate. Orphaned puppies and weak
puppies do not gain as fast a puppies suckled by their dam. In these
puppies the body weight should double in 2 weeks.
At the age of 4 weeks the puppies should begin
to be weaned. At this time weaning may be encouraged by supplemental
feeding. After weaning the puppies should be fed a commercial puppy
chow 4 times a day until 3 months of age. After which the feedings
can decrease to 3 times a day until 6 months of age. Then the puppy
can be fed twice a day.
- Viral Infections
- Those viruses that are of concern
especially in the neonate are;
- Canine Herpesvirus
- Canine Distemper
- Infectious Canine Hepatitis
- Feline Panleukopenia
- Coronaviruses and Rotaviruses
- Feline Leukemia Virus
1.28.6 Bacterial Infections
Septicemias are transmitted transplacentally,
via the umbilicus, orally, and as puppy passes through birth canal.
The most common bacterial causes of septicemias in the neonate are
E. coli and beta-hemolytic streptococci. Other less common causes
are staphylococci and other gram negative enteric organisms.
Treatment are usually with penicillins and cephalosporins.
Aminoglycosides, Chloramphenicol, and Trimethoprim-sulfas can be
used but should only be used in extreme cases and then with caution.
Bacterial respiratory infections in the
neonate are caused by poor sanitation and other environmental
factors (i.e. drafts, poor ventilation and humid conditions).
The most common respiratory pathogen in the neonatal dog is
Bordetella. In kittens the most common respiratory pathogen is
Pasteurella. These are sensitive to Tetracyclines, Trimethoprim-sulfa,
and Aminoglycosides. All of these antibiotics are toxic to the
Common bacterial pathogens in the neonate are
Salmonella (tx Trimethoprim-sulfa), Campylobacter (tx -
Erythromycin), and E coli (oral polymixin, and neomycin).
Treatments for enteric bacterial infections are also toxic to the
neonate particularly neomycin.
Urinary tract infections in the neonate are
best determined by gram staining the urine. Treatment with
Amoxicillin-Clavolonic acid is usually adequate for both
gram-negative and gram-positive infections.
"Toxic milk" or "Acid
milk" syndrome can also occur this is considered to occur
from the consumption of milk from a bitch with metritis or
subinvolution of the placenta. Clinical signs in the puppies are
bloating, crying, redness and edema of the anus, green diarrhea and
dehydration. Treatment consists of removal from the bitch for at
least a week and supporting the puppy with glucose fluid, incubator
to keep puppy warm, and antibiotics.
Brucellosis is transferred to the puppies
through the mother. Puppies that survive are infectious for 2 months
after birth. These puppies are a potential hazard to other dogs and
Tetracyclines bond to calcium and deposit in
newly formed bones and teeth causing yellow staining. It also causes
renal and hepatic toxicity.
Chloramphenicol is retained for excessive
lengths of time because the neonate is unable to conjugate it with
glucoronic acid for excretion (particularly kittens). It also
inhibits protein synthesis and therefore may lead to maturation
Aminoglycosides are both nephrotoxic and
ototoxic. Like chloramphenicol they inhibit protein synthesis.
Trimethoprim-sulfas cause anemia,
leukopenia, and thrombocytopenia in the neonate because of
antifolate properties. Cholestasis can also result from the use of
Roundworms - Toxocara canis are encysted
in the tissues of pregnant bitch and reactivated during the last
trimester of pregnancy. These parasites are able to cross the
placenta into the fetus in utero. Afterwards they go to the lungs
and liver where they remain until birth. After birth the parasites
move to the gut. The parasites can also be transferred through the
milk. Infection leads to an enteritis, poor growth and poor nutrient
utilization. Toxocara cati is the roundworm in the cat. It is
transferred only transmammary.
The most severe helminth parasite infection is
hookworms. Ancylostoma caninum is more pathogenic than other
hookworms because they ingest more blood. Ancylostoma tubaformae is
found more in cats. Hookworms are passed both transplacentally and
transmammary in the neonate. In older puppies and kittens the
transmission is by ingestion or cutaneous migration.
The parasite burden in the bitch can be
decreased by treatment with Fenbendazole from day 40 of pregnancy
until the second week of lactation.
1.29 CANCER THERAPY
The objective of cancer therapy is the
destruction of all cancer tissue and concomitant maintenance of the
host's normal cells. The modalities of cancer therapy are surgery,
radiotherapy, chemotherapy, and immunotherapy.
Surgery is used if the tumor is localized or in
an area where total surgical excision is feasible. It may be a
valuable adjunct for reducing the size of a tumor mass allowing for
greater success with chemotherapy or immunotherapy. The various types
of surgery in cancer therapy is prophylactic, diagnostic, adjunctive,
palliative, and curative.
Prophylactic surgery is the excision of a
potentially malignant or permalignant lesion such as a retained
testicle or rectal polyp.
Diagnostic surgery is performed to establish the
presence of cancer. Total excision is best or preferable to invasive
techniques and may be curative. If total excision is not possible
other methods may be used such as incisional biopsy, punch biopsy,
needle biopsies, fine needle aspiration, trephination, and core
biopsy. Vigorous manipulation of tumor tissue is more apt to cause
metastasis than sharp probing of tissue.
Adjunctive surgery is the use of surgery to
assist another therapeutic mode such as radiotherapy, chemotherapy or
hyperthermia. Adjunctive surgery may used for cytoreduction, organ
exposure, or second-look procedures.
Palliative surgery is selected when two criteria
are met. A histological diagnosis is known. Curative therapy is
impossible. It is used to improve the pets quality of life and
decrease clinical signs so that the owner can prepare for impending
death of the pet.
Curative surgery is used to remove or destroy
all gross tumor at primary and metastatic sites. Some tumors that lend
themselves to curative surgery are squamous cell carcinoma,
osteosarcoma, parosteal osteosarcoma, prostatic adenocarcinomas,
lipomas, transitional cell carcinoma, melanoma, mastocytoma, perennial
adenomas, mammary adenocarcinomas, and soft tissue sarcomas.
Radiotherapy is the use of ionizing radiation
for the treatment of cancer. It may be used if the tumor mass cannot
be completely removed by surgery . It may be an adjunct to
chemotherapy or immunotherapy. Radiotherapy is delivered in multiple
doses. This is due to the phenomenon that occur in normal and tumor
tissue after radiation that affects sensitivity. This phenomenon is
called the 4 R's of fractionated radiotherapy. They are
repopulation, redistribution, and repair.
Re-oxygenation is a rapid process that occurs
with in a few hours of irradiation. The process is the improvement of
oxygenation to hypoxic cells due to improvement of tumor vascularity.
Hypoxic cells are resistant to radiotherapy. Re-oxygenation probably
accounts for the benefits of fractionated radiotherapy in the
treatment of tumors. It also allows the use of dose levels below the
tolerance of normal tissue.
Repopulation is cellular regeneration after
injury. This known to occur in tumors and rapidly dividing normal
tissues after radiotherapy. In tumor accelerated growth occurs after
irradiation in some instances. This is thought to be due to improved
nutrient supply to previously non-proliferating areas. Repopulation
does not occur to any appreciable extent in slow dividing tissue.
Redistribution is a process of re-assortment of
cells into different phases of the cell cycle. It occurs because of
the variation in radiosensitivity during the cell cycle. Cells
synthesizing dna are most resistant and cells in mitosis are most
radiosensitive. Radiation induces a delay in cell cycle allowing cells
to pile up in one phase of the cell cycle. This may allow more tumor
cells to be dosed after the first radiation dose. Exploration of the
therapeutic gain of redistribution is difficult because it is
difficult to determine how to synchronize for optimal dose. It is
unknown which part of the cells cycle that cells have piled up.
A portion of the radiation damage to tissue is
repairable. The repair occurs in both rapidly and slowly dividing
tissue. Since evidence for lack of repair mechanism in tumor cells is
lacking, it is unknown whether repair from radiation damage may be
used for therapeutic gain. It may however help in normal tissue
In radiation the time and dose are important.
Time dose schemes must be determined to deliver therapy in multiple
doses instead of one large dose. Tumors that amend themselves to
radiation therapy are tumors of the face, gingiva, and perennial
regions such as squamous cell carcinoma, acanthomatous epuli,
fibrosarcoma, perennial adenoma, transmissible venereal tumor,
mastocytoma, and oral malignant melanoma.
Chemotherapy is used if the tumor is
multicentric in origin or if there are widespread metastasis. It may
also be used as an adjunct to surgery if total surgical excision is
The general principles of chemotherapy
- The body burden of tumor cells usually far
exceed clinically apparent disease.
- The proportion of tumor cells actively
dividing may fall from a level higher than normal to a relatively
low level as tumor size increases.
- Chemotherapeutic agents are more effective
in dividing cells than resting cells.
- Chemotherapeutic agents have maximal
effect following reductive surgery or radiation therapy.
- Tolerance to chemotherapy is often better
when tumor cell burden is low and associated with less organ
impairment, better nutrition, and greater resistant to infection.
- Chemotherapy may reduce tumor cell burden
to levels at which immunologic mechanisms are considered more
likely to be effective.
- Chemotherapy for regionalized tumor may be
delivered locally by direct application or intraarterial infusion.
The timing of chemotherapy may be critical.
Intermittent high dose therapy with cycle specific agents produces
therapeutic benefits with less cumulative toxicity. Better host
tolerance results from intermittent therapy. There is greater tumor
cell kill as a result from the high gradients of drugs produced by
intermittent high dose therapy.
A combination of anti-neoplasic agents may be
more effective than single agents. This is because an anti-tumor effect
may be additive on the tumor cell without being additive on host
cells. Multiple sublethal lesions in a tumor cell may kill that cell
whereas one lesion from one agent might be repaired. Tumor resistance
to drugs may be delayed by avoiding selection and growth advantaged
clones of tumor cells that are resistant to a single agent.
Classification of Antineoplastic Agents
- Alkylating agents
- Vinca Alkaloids
- Miscellaneous agents