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Canine distemper
presented by : salam elayh DVM
2013,5,6
Urmia university
Veterinary medicine faculty
overview
• Canine distemper virus (CDV) is a highly contagious, incurable and often deadly disease. The virus occurs
worldwide and is a leading cause of death in unvaccinated puppies and dogs.
• Besides domestic dogs, this viral disease infects other wild carnivores such as fox, wolves, coyotes, coati,
raccons, skunks, badger, bear, and ferrets.
• Recently (2007), a university of leads study linked CDV to the death of African lions, emphasizing the deadly
threat of this disease to a wide variety of carnivorce animal species.
• The CDV can infect dogs of any age but puppies between 3 and 6 months of age are most likely to become ill
and die. Older dogs which have never been vaccinated are also very susceotible to infection and pregnant
mothers can pass the infection to her unborn pups.
overview
• Canine distemper virus (CDV) is a highly contagious, incurable and often deadly disease. The virus occurs
worldwide and is aleading cause of death in unvaccinated puppies and dogs.
• Besides domestic dogs, this viral disease infects other wild carnivores such as
fox, wolves, coyotes, coati, raccons, skunts, badger, bear, and ferrets.
• Recently (2007), a university of leads study linked CDV to the death of African lions, emphasizing the deadly
threat of this disease to a wide variety of carnivorce animal species.
• The CDV can infect dogs of any age but puppies between 3 and 6 months of age are most likely to become ill
and die. Older dogs which have never been vaccinated are also very susceptible to infection and pregnant
mothers can pass the infection to her unborn pups.
Etiology and
transmission
canine distemper is caused by a paramyxovirus closely related to the viruses of measles and riderpest. The
enveloped virus is sensitive to lipid solvents and most disinfectants and is relatively unstable outside the host.
Infected dogs shed the virus through all body secretions (such as urine) and excretions.
Transmission commonly occurs in unvaccinated dogs that come into contact with infected animals.
The main methods of disease transmission is by the dog breathing in airborn viral particles emitted by
barking, sneezing, and coughing or by licking contaminated surfaces.
A dog recovering from distemper can shed the virus ( can spread disease) for 60 to 90 days after all symptoms
have disappeared
Transmission
Despite the fact that CDV particles are present in many enviroments, not every dog will become infected.
This is because several factors influence the effectiveness of the virus:
Host vitality (overall health of the dog, immune experience, vaccination status)
Virulence of the virus ( the number of viral particles in a given area)
 and other environmental factors (stress, dry and hot weather, cold weather, pH)
 though the most important factors seem to be the immune level of the dog and the number of viral
particles the dog is exposed to, if each factor is just right, a dog will become infected.
when this occurs, a specific sequence of events is initiated as the virus attacks the body.
pathogenesis
CDV travels about as aerosol particles and enters the body through the nose or mouth as the body breathes.
There is then a latent period of approximately 10 t0 14 days during which the virus is replicating and spreading
thoughout the body, but no clinical symptoms have yet become visible.
Once in the respirating tract, the virus makes its way to the nearby lymph nodes in the neck
(tonsils,retropharyngeal & brontial lymph nodes).
Virus multiplication occurs within lymphoids follicles in the spleen, the gut-associated lymphoid tissue of the
lamina propria of the stomach and small intestines, the mesenteric lymph nodes, and the kupffer’s cell in the
liver.
Widespread virus proliferation in lymphoid organs coreesponds to an initial rise in body temperature and
leukopenia between day 3 and 6 PI.the leukopeniasis primarily a lymphopenia caused by viral damage to
lymphoid cells, affecting both T and B cells.
pathogenesis
o Once secure within the nods, viral particles begin replicating and gradually spread through the lymphatic
system, generally infecting all lymphatic tissue within 5 days.
o By the ninth day post infection the virus has invaded the blood, from which it will spread into the respirating
and GI tracts and eventually the CNS
o Canine distemper is estimated to be fatal in 50% of cases affecting adult dogs, and in 80% of cases affecting
puppies.
o The degree of viremia and extent of spread of virus to various tissues is moderated by the level of specific
humoral immunity and cell-mediate cytotoxicity in the host during the viremic period.
Signs and symtoms
 Clinical signs of canine distemper vary depending on the virus strain, environmental conditions, and host age and
immune status.
 Canine distemper causes symptoms in multiple body systems, including the gastrointestinal tract, respiratory tract,
urogenital epithelium, optic nerve, and the brain and spinal cord.
 Early symptoms during the incubation period ( 3 to 6 days after infection) include: fever, loss of appetite, and mild
eye inflammation. These early symptoms are usually not noticed, but as the disease progresses the symptoms
increase in severity.
Respiratory signs:
 Nasal discharge ( usually a thick green and yellow discharge)
 Coughing
 Dyspnea (difficulty breathing)
 Pneumonia ( lower airway disease)
Signs and symptoms
Gastrointestinal signs:
Anorexia (loss of appetite)
Vomiting
Diarrhea ( may be bloody)
Clinical signs of upper or lower respiratory infection and GI disease are non-specific, a
diagnosis of distemper should not be made based on these signs alone.
Respiratory and GI symptoms are exacerbated by secondary bacterial infection which is
the reason some ill dogs appear to improve temporarity when olaced on antibiotics.
Signs and symptoms
Ocular signs:
 Anterior uveitis ( inflammation of the front chabber of the eye, may cause the cornea to appear cloudy and / or cause changes in
the appearance of the iris)
 Keratoconjunctivitissicca ( KCS = dry eye )
 Optic neuritis ( inflammation of the optic nerve – may cause sudden blindness)
 Retinal degeneration or separation ( may cause vision impairment)
Dermatological signs:
 Pustular dermatitis (skin rash – associated with a favorable prognosis)
 Nasal and digital hyperkeratosis ( thickening of the nose and footpads – associated with a poor prognosis and progression to
neurological signs)
 Distempre has sometimes been called hardpad disease.
Signs and symptoms
Ocular signs:
 Anterior uveitis ( inflammation of the front chabber of the eye, may cause the cornea to appear cloudy and / or cause changes in the
appearance of the iris)
 Keratoconjunctivitissicca ( KCS = dry eye )
 Optic neuritis ( inflammation of the optic nerve – may cause sudden blindness)
 Retinal degeneration or separation ( may cause vision impairment)
Dermatological signs:
 Pustular dermatitis (skin rash – associated with a favorable prognosis)
 Nasal and digital hyperkeratosis ( thickening of the nose and footpads – associated with a poor prognosis and progression to
neurological signs)
Distempre has sometimes been called hardpad disease.
Signs and symptoms
Bone lesions:
 young, growing dogs with experimentally and naturally induced CDV infection develop metaphyseal
osteosclerosis of the long bones.
 Large-breed dogs between 3 and 6 months of age are most commonly affected.
 Studies have not shown animals with systemic distemper to develop overt clinical signs related to these
long bone disease.
 Howevere CDV RNA transcripts have been seen in the bone cells of young dogs with hypertrophic
osteodystrophy (HOD), a metaphyseal bone disease that can be similar to and confused with
metaphyseal osteomyelitis.
Signs and symptoms
Neurological signs:
o May occur in dogs with no or only a mild history of other signs.
o Usually occur within 1-3 weeks after systemic signs, but may occur at the somtime or weeks to months later.
o Once the nervous system ( brain and spinal cord) of puppies and dogs in infected, the animal usually dies.
o Are highly variable and may include:
 Seizures
• Local or generalized
• Of any part of the body, but seizure look as if the dog is chewing gum are uniqe to distemper
• Convulsions characterized by salivayion and often chewing movements of the jaw (“chewing – gum
fits”)
Signs and symptoms
Weakness or paralysis
Uncoordinated movements
Myoclonus (muscle twitching, involuntary contraction)
Hyperkinesia
Increased sensitivity to touch or pain
Neck pain / rigidity
Vestibular signs (head tilt, loss of balance or walking in circles)
Behavioral changes
Diagnosis
 Diagnosis of this disease is challenging but is usually done based on the dogs vaccination history, clinical symptoms and results of
various laboratory tests to support a probable diagnosis
 Unfortunately, laboratory tests frequently provides false results
 Because signs are variable and may take time to appear, and secondary infections are common, diagnosis can be complicated
addtionally, other infections can produce similar signs to distemper
RT – PCR ( reverse transcription polymerase chain reaction)
 Can detect viral RNA in respiratory secretions, nasal or ocular discharge, cerebrospinal fluid, feces, and/ or urine (depending
on localization of virus)
 A negative result does not rule out distemper, especially when samples are obtained late in the course of disease when virus
may no longer be shed.
 False positives are possible within 1-3 weeks of vaccination.
Diagnosis
Real PCR test
This test provides a quantitative measure of the CDV viral load, which is typically much higher
during active infection compared to the level detected due to recent vaccination.
Immunofluorescence assay ( IFA )
To detect inclusion bodies & viral antigen on conjunctival scrape, buffy coat, urine
sediment, traumatic bladder catheterization, trans-tracheal wash, or cerebrospinal fluid.
This test is most useful early in the course of disease
A positive result is very likely to indicate infection rather than vaccination
Negative result dose not rule out diseaae, as false negative are very common.
Diagnosis
o Serology test
 Vaccination generates antibody titers indistinguishable from natural infection, there fore
serology has limited application in most shelter populations.
 however, it may be helpful in dogs known not to have been recently vaccinated.
o IgM: serum antibody measured by ELISA
 Positive results possible within 3 weeks of vaccination. Otherwise, a positive result is a good
indicator of distemper infection. IgM antibodies persist for approximately 5-12 weeks in natural
dis.
 False negative results can occur in dogs that die acutely without developing an antibody
response and can also occur in subacutely or chronically infected dogs.
Diagnosis
IgG
Serial titers on 2 serum samples taken to weeks apart to detect rising titers
Positive IgG titers are expected in vaccinated dogs, so a single positive IgG result can not be used to
diagnose distemper.
In a dog known to not have been vaccinated within the past month, rising titers are indicative of
infection and an increase of greater than four-fold is indicative of infection even in a recently
vaccinated dog
False negative are possible as within IgM
Less dramatic increases in IgG titers may be caused by infection or recent vaccination.
Diagnosis
Necropsy / histopathology findings:
If distemper is a concern and a definitive diagnosis has not been reached by other testing
methods, a necropsy is a worthwhile investment in a dog believed to have died of the
disease to establish whether or not distemper is present in the shelter.
spleen, tonsil, lymph node, stomatch, duodenum, bladder and brain should be submitted
for examination by a pathologist in order to detect distemper, since it can localize in many
different tissues.
Pathologic findings
Lymphoid depletion is a typical histologic findings in a dog with systemic illness, (thymic atrophy in young dogs).
Pneumonia & catarrhal enteritis & rhinitis & inflammation of the tracheobrontial tree in infected puppies.
Meningealcongestion, ventricular dilation, and increased CSF pressure resulting from brain edema in a acute
encephalitis.
Epididymitis and orchitis (causing decrease in spermatogenesis, prostate fluid, and testosterone that occurs in
recovering animals.
Inclusions can be found in the nucleus or cytoplasm of astrocytes (mostly intranuclear) and neurons (mostly
intracytoplasmic), and its contains viral nucleocasid and heat shock protein.
Treatment
 At present there is no specific drug or treatment to kill the distemper virus.
 Treatment consist of supportive care, and may include:
 Intravenous fluid therapy can alleviate dehydration ( lactate ringer’s solution)
 Anti – emetic therapy for vomiting and prolonged anorexia
 Nebulization, expectorants and coupage for pneumonia
 Seizures may need to be controlled with anti-seizure medication (phenobarbital for maintenance prevention & parenteral
diazepam for status epilepticus. Primidone or potassium bromide are alternative choices).
 Antibiotic therapy
 Broad spectrum antibiotics are indicated to treat secondary bacterial infection
 Antibiotic with good activity against bordetella bronchiseptica and mycoplasma (e.g doxycycline, ampicillin, amoxicillin,
cephapirin, tetracycline, chloramphenicol) may also be indicated if these pathogens are suspected or confirmed.
 Parenteral florfenicol might be considered if this is a concern, ( is essential when GI signs are present).
Treatment
Single dose of dexamethasone (steroid) may be considered in a attempt to control CNS edema.
Dogs having difficulty with their vision may be administered glucocorticoid therapy in an attempt
to prevent blindness.
Even if a dog survives and recovers from about with canine distemper, it should be noted that
many animals continue to suffer long term effects.
Enamel hypoplasia or lack of tooth enamed is a common affliction of CDV survivors, and is
relatively pathognomonic for prior infection with CDV).
Also there is abnormal body walking gaits, decreased eyesight. This deficiency, untreated, cases
severe tooth decay.
Treatment
Dogs with some of the more chronic progressive or vaccine-induced forms of neurologic disease may respond to
immunosuppressive therapy with anti-inflammatory or greater dosages of glucocorticoids.
Specific antiviral therapy against CDV has not been evaluated in infected dogs, however ribavirin to have antiviral
efficacy in vitro.
B vitamins should be administered as non-specific therapy to replace vitamins lost from anorexia and diuresis and
to stimulate the appetite.
Anecdotally, intravenous administration ascorbic acid can be beneficial.
Experimentally infected ferrets, A vitamins can be effective.
Once an animal develops neurological symptoms of the disease, such as seizures or paralysis its chances of surviving
are slim and its quality of life is bound to become progressively worse. Thus, these animals are usually “put to
sleep”, euthanized, in order to ensure a human death.
Prevention
Vaccination and avoiding contact with infected animals or contaminated enviroments are the best strategies
for disease prevention.
Following vaccination protocols based on the age of the dog is essential for adequate protection against
infection.
Vaccination schedules can start at about 6 weeks of age and continue until 12 or 16 weeks of age, with a 2 to
4 week interval between shots.
Vaccination should be repeated a year later, then at regular intervals.
As with other vaccines, presence of antibodies received from the mother can interfere with vaccines so a
puppy is not considered fully protected until the final vaccine in the series has been given.
Prevention
Until the vaccination series is completed, the pup or dog is at risk to contract this deadly disease.
Avoid taking a pup or unvaccinated dog to places where dogs congregate (parks, obedience classes, pet day
care, grooming). If absolutely necessary, visit only reputable establishments and training places which require proof
of vaccination and practice appropriate sanitation procedures.
The use of appropriate disinfectants such as quaternary ammonium disinfectants and chloroform, dilute (less than
0.5%) formalin solution, phenol (0.75%) is effective in killing the canine distemper virus in kennels, hospital, or other
potentially infected areas.
Further, contaminated objects and areas may be disinfected using a 1:30 bleach-water solution
Sanitation is very important in preventing the spread of any infectious disease.
Prevention
Thankfully, the canine distemper virus is not as tough as the canine parvovirus and can not
survive for long outside the dog’s body.
The viral particles may be killed by exposure to heat, sunlight, various detergents and
soaps, and un assortment of chemicals.
Once the sick dog has recovered or has left the home, pet owners should wait one month
before introducing a new animals.
A dog recovering from distemper can shed the virus ( can spread disease) for 60 to 90 days
after all symptoms have disappeared.
References
Veterinary internal medicine diseases of the dog and cat
sixth edition [Stephan J. Etinger, DVM & Edward C. Feldman, DVM]
Infectious diseases of the dog and cat
Fourth edition [Craig E. Greene, DVM, MS, DACVIM]
Emergenacy protocols dog and cat
First edition [Maureen Mcmichael, John DeBiasio, Christopher G. byers]
manual of small animal practice
Third edition [Stephen J. Birchard, Robert G. sherding]
Salam elayh
2013.5.6
Any question?
Thanks for your
attention

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Canine distemper signs, diagnosis, treatment and prevention.antibiotics, analgesic and vaccination in dogs.by salam elayh

  • 1. Canine distemper presented by : salam elayh DVM 2013,5,6 Urmia university Veterinary medicine faculty
  • 2. overview • Canine distemper virus (CDV) is a highly contagious, incurable and often deadly disease. The virus occurs worldwide and is a leading cause of death in unvaccinated puppies and dogs. • Besides domestic dogs, this viral disease infects other wild carnivores such as fox, wolves, coyotes, coati, raccons, skunks, badger, bear, and ferrets. • Recently (2007), a university of leads study linked CDV to the death of African lions, emphasizing the deadly threat of this disease to a wide variety of carnivorce animal species. • The CDV can infect dogs of any age but puppies between 3 and 6 months of age are most likely to become ill and die. Older dogs which have never been vaccinated are also very susceotible to infection and pregnant mothers can pass the infection to her unborn pups.
  • 3.
  • 4. overview • Canine distemper virus (CDV) is a highly contagious, incurable and often deadly disease. The virus occurs worldwide and is aleading cause of death in unvaccinated puppies and dogs. • Besides domestic dogs, this viral disease infects other wild carnivores such as fox, wolves, coyotes, coati, raccons, skunts, badger, bear, and ferrets. • Recently (2007), a university of leads study linked CDV to the death of African lions, emphasizing the deadly threat of this disease to a wide variety of carnivorce animal species. • The CDV can infect dogs of any age but puppies between 3 and 6 months of age are most likely to become ill and die. Older dogs which have never been vaccinated are also very susceptible to infection and pregnant mothers can pass the infection to her unborn pups.
  • 5. Etiology and transmission canine distemper is caused by a paramyxovirus closely related to the viruses of measles and riderpest. The enveloped virus is sensitive to lipid solvents and most disinfectants and is relatively unstable outside the host. Infected dogs shed the virus through all body secretions (such as urine) and excretions. Transmission commonly occurs in unvaccinated dogs that come into contact with infected animals. The main methods of disease transmission is by the dog breathing in airborn viral particles emitted by barking, sneezing, and coughing or by licking contaminated surfaces. A dog recovering from distemper can shed the virus ( can spread disease) for 60 to 90 days after all symptoms have disappeared
  • 6. Transmission Despite the fact that CDV particles are present in many enviroments, not every dog will become infected. This is because several factors influence the effectiveness of the virus: Host vitality (overall health of the dog, immune experience, vaccination status) Virulence of the virus ( the number of viral particles in a given area)  and other environmental factors (stress, dry and hot weather, cold weather, pH)  though the most important factors seem to be the immune level of the dog and the number of viral particles the dog is exposed to, if each factor is just right, a dog will become infected. when this occurs, a specific sequence of events is initiated as the virus attacks the body.
  • 7. pathogenesis CDV travels about as aerosol particles and enters the body through the nose or mouth as the body breathes. There is then a latent period of approximately 10 t0 14 days during which the virus is replicating and spreading thoughout the body, but no clinical symptoms have yet become visible. Once in the respirating tract, the virus makes its way to the nearby lymph nodes in the neck (tonsils,retropharyngeal & brontial lymph nodes). Virus multiplication occurs within lymphoids follicles in the spleen, the gut-associated lymphoid tissue of the lamina propria of the stomach and small intestines, the mesenteric lymph nodes, and the kupffer’s cell in the liver. Widespread virus proliferation in lymphoid organs coreesponds to an initial rise in body temperature and leukopenia between day 3 and 6 PI.the leukopeniasis primarily a lymphopenia caused by viral damage to lymphoid cells, affecting both T and B cells.
  • 8. pathogenesis o Once secure within the nods, viral particles begin replicating and gradually spread through the lymphatic system, generally infecting all lymphatic tissue within 5 days. o By the ninth day post infection the virus has invaded the blood, from which it will spread into the respirating and GI tracts and eventually the CNS o Canine distemper is estimated to be fatal in 50% of cases affecting adult dogs, and in 80% of cases affecting puppies. o The degree of viremia and extent of spread of virus to various tissues is moderated by the level of specific humoral immunity and cell-mediate cytotoxicity in the host during the viremic period.
  • 9. Signs and symtoms  Clinical signs of canine distemper vary depending on the virus strain, environmental conditions, and host age and immune status.  Canine distemper causes symptoms in multiple body systems, including the gastrointestinal tract, respiratory tract, urogenital epithelium, optic nerve, and the brain and spinal cord.  Early symptoms during the incubation period ( 3 to 6 days after infection) include: fever, loss of appetite, and mild eye inflammation. These early symptoms are usually not noticed, but as the disease progresses the symptoms increase in severity. Respiratory signs:  Nasal discharge ( usually a thick green and yellow discharge)  Coughing  Dyspnea (difficulty breathing)  Pneumonia ( lower airway disease)
  • 10.
  • 11. Signs and symptoms Gastrointestinal signs: Anorexia (loss of appetite) Vomiting Diarrhea ( may be bloody) Clinical signs of upper or lower respiratory infection and GI disease are non-specific, a diagnosis of distemper should not be made based on these signs alone. Respiratory and GI symptoms are exacerbated by secondary bacterial infection which is the reason some ill dogs appear to improve temporarity when olaced on antibiotics.
  • 12. Signs and symptoms Ocular signs:  Anterior uveitis ( inflammation of the front chabber of the eye, may cause the cornea to appear cloudy and / or cause changes in the appearance of the iris)  Keratoconjunctivitissicca ( KCS = dry eye )  Optic neuritis ( inflammation of the optic nerve – may cause sudden blindness)  Retinal degeneration or separation ( may cause vision impairment) Dermatological signs:  Pustular dermatitis (skin rash – associated with a favorable prognosis)  Nasal and digital hyperkeratosis ( thickening of the nose and footpads – associated with a poor prognosis and progression to neurological signs)  Distempre has sometimes been called hardpad disease.
  • 13.
  • 14. Signs and symptoms Ocular signs:  Anterior uveitis ( inflammation of the front chabber of the eye, may cause the cornea to appear cloudy and / or cause changes in the appearance of the iris)  Keratoconjunctivitissicca ( KCS = dry eye )  Optic neuritis ( inflammation of the optic nerve – may cause sudden blindness)  Retinal degeneration or separation ( may cause vision impairment) Dermatological signs:  Pustular dermatitis (skin rash – associated with a favorable prognosis)  Nasal and digital hyperkeratosis ( thickening of the nose and footpads – associated with a poor prognosis and progression to neurological signs) Distempre has sometimes been called hardpad disease.
  • 15.
  • 16. Signs and symptoms Bone lesions:  young, growing dogs with experimentally and naturally induced CDV infection develop metaphyseal osteosclerosis of the long bones.  Large-breed dogs between 3 and 6 months of age are most commonly affected.  Studies have not shown animals with systemic distemper to develop overt clinical signs related to these long bone disease.  Howevere CDV RNA transcripts have been seen in the bone cells of young dogs with hypertrophic osteodystrophy (HOD), a metaphyseal bone disease that can be similar to and confused with metaphyseal osteomyelitis.
  • 17.
  • 18. Signs and symptoms Neurological signs: o May occur in dogs with no or only a mild history of other signs. o Usually occur within 1-3 weeks after systemic signs, but may occur at the somtime or weeks to months later. o Once the nervous system ( brain and spinal cord) of puppies and dogs in infected, the animal usually dies. o Are highly variable and may include:  Seizures • Local or generalized • Of any part of the body, but seizure look as if the dog is chewing gum are uniqe to distemper • Convulsions characterized by salivayion and often chewing movements of the jaw (“chewing – gum fits”)
  • 19. Signs and symptoms Weakness or paralysis Uncoordinated movements Myoclonus (muscle twitching, involuntary contraction) Hyperkinesia Increased sensitivity to touch or pain Neck pain / rigidity Vestibular signs (head tilt, loss of balance or walking in circles) Behavioral changes
  • 20. Diagnosis  Diagnosis of this disease is challenging but is usually done based on the dogs vaccination history, clinical symptoms and results of various laboratory tests to support a probable diagnosis  Unfortunately, laboratory tests frequently provides false results  Because signs are variable and may take time to appear, and secondary infections are common, diagnosis can be complicated addtionally, other infections can produce similar signs to distemper RT – PCR ( reverse transcription polymerase chain reaction)  Can detect viral RNA in respiratory secretions, nasal or ocular discharge, cerebrospinal fluid, feces, and/ or urine (depending on localization of virus)  A negative result does not rule out distemper, especially when samples are obtained late in the course of disease when virus may no longer be shed.  False positives are possible within 1-3 weeks of vaccination.
  • 21. Diagnosis Real PCR test This test provides a quantitative measure of the CDV viral load, which is typically much higher during active infection compared to the level detected due to recent vaccination. Immunofluorescence assay ( IFA ) To detect inclusion bodies & viral antigen on conjunctival scrape, buffy coat, urine sediment, traumatic bladder catheterization, trans-tracheal wash, or cerebrospinal fluid. This test is most useful early in the course of disease A positive result is very likely to indicate infection rather than vaccination Negative result dose not rule out diseaae, as false negative are very common.
  • 22.
  • 23. Diagnosis o Serology test  Vaccination generates antibody titers indistinguishable from natural infection, there fore serology has limited application in most shelter populations.  however, it may be helpful in dogs known not to have been recently vaccinated. o IgM: serum antibody measured by ELISA  Positive results possible within 3 weeks of vaccination. Otherwise, a positive result is a good indicator of distemper infection. IgM antibodies persist for approximately 5-12 weeks in natural dis.  False negative results can occur in dogs that die acutely without developing an antibody response and can also occur in subacutely or chronically infected dogs.
  • 24. Diagnosis IgG Serial titers on 2 serum samples taken to weeks apart to detect rising titers Positive IgG titers are expected in vaccinated dogs, so a single positive IgG result can not be used to diagnose distemper. In a dog known to not have been vaccinated within the past month, rising titers are indicative of infection and an increase of greater than four-fold is indicative of infection even in a recently vaccinated dog False negative are possible as within IgM Less dramatic increases in IgG titers may be caused by infection or recent vaccination.
  • 25. Diagnosis Necropsy / histopathology findings: If distemper is a concern and a definitive diagnosis has not been reached by other testing methods, a necropsy is a worthwhile investment in a dog believed to have died of the disease to establish whether or not distemper is present in the shelter. spleen, tonsil, lymph node, stomatch, duodenum, bladder and brain should be submitted for examination by a pathologist in order to detect distemper, since it can localize in many different tissues.
  • 26. Pathologic findings Lymphoid depletion is a typical histologic findings in a dog with systemic illness, (thymic atrophy in young dogs). Pneumonia & catarrhal enteritis & rhinitis & inflammation of the tracheobrontial tree in infected puppies. Meningealcongestion, ventricular dilation, and increased CSF pressure resulting from brain edema in a acute encephalitis. Epididymitis and orchitis (causing decrease in spermatogenesis, prostate fluid, and testosterone that occurs in recovering animals. Inclusions can be found in the nucleus or cytoplasm of astrocytes (mostly intranuclear) and neurons (mostly intracytoplasmic), and its contains viral nucleocasid and heat shock protein.
  • 27.
  • 28. Treatment  At present there is no specific drug or treatment to kill the distemper virus.  Treatment consist of supportive care, and may include:  Intravenous fluid therapy can alleviate dehydration ( lactate ringer’s solution)  Anti – emetic therapy for vomiting and prolonged anorexia  Nebulization, expectorants and coupage for pneumonia  Seizures may need to be controlled with anti-seizure medication (phenobarbital for maintenance prevention & parenteral diazepam for status epilepticus. Primidone or potassium bromide are alternative choices).  Antibiotic therapy  Broad spectrum antibiotics are indicated to treat secondary bacterial infection  Antibiotic with good activity against bordetella bronchiseptica and mycoplasma (e.g doxycycline, ampicillin, amoxicillin, cephapirin, tetracycline, chloramphenicol) may also be indicated if these pathogens are suspected or confirmed.  Parenteral florfenicol might be considered if this is a concern, ( is essential when GI signs are present).
  • 29. Treatment Single dose of dexamethasone (steroid) may be considered in a attempt to control CNS edema. Dogs having difficulty with their vision may be administered glucocorticoid therapy in an attempt to prevent blindness. Even if a dog survives and recovers from about with canine distemper, it should be noted that many animals continue to suffer long term effects. Enamel hypoplasia or lack of tooth enamed is a common affliction of CDV survivors, and is relatively pathognomonic for prior infection with CDV). Also there is abnormal body walking gaits, decreased eyesight. This deficiency, untreated, cases severe tooth decay.
  • 30.
  • 31. Treatment Dogs with some of the more chronic progressive or vaccine-induced forms of neurologic disease may respond to immunosuppressive therapy with anti-inflammatory or greater dosages of glucocorticoids. Specific antiviral therapy against CDV has not been evaluated in infected dogs, however ribavirin to have antiviral efficacy in vitro. B vitamins should be administered as non-specific therapy to replace vitamins lost from anorexia and diuresis and to stimulate the appetite. Anecdotally, intravenous administration ascorbic acid can be beneficial. Experimentally infected ferrets, A vitamins can be effective. Once an animal develops neurological symptoms of the disease, such as seizures or paralysis its chances of surviving are slim and its quality of life is bound to become progressively worse. Thus, these animals are usually “put to sleep”, euthanized, in order to ensure a human death.
  • 32. Prevention Vaccination and avoiding contact with infected animals or contaminated enviroments are the best strategies for disease prevention. Following vaccination protocols based on the age of the dog is essential for adequate protection against infection. Vaccination schedules can start at about 6 weeks of age and continue until 12 or 16 weeks of age, with a 2 to 4 week interval between shots. Vaccination should be repeated a year later, then at regular intervals. As with other vaccines, presence of antibodies received from the mother can interfere with vaccines so a puppy is not considered fully protected until the final vaccine in the series has been given.
  • 33. Prevention Until the vaccination series is completed, the pup or dog is at risk to contract this deadly disease. Avoid taking a pup or unvaccinated dog to places where dogs congregate (parks, obedience classes, pet day care, grooming). If absolutely necessary, visit only reputable establishments and training places which require proof of vaccination and practice appropriate sanitation procedures. The use of appropriate disinfectants such as quaternary ammonium disinfectants and chloroform, dilute (less than 0.5%) formalin solution, phenol (0.75%) is effective in killing the canine distemper virus in kennels, hospital, or other potentially infected areas. Further, contaminated objects and areas may be disinfected using a 1:30 bleach-water solution Sanitation is very important in preventing the spread of any infectious disease.
  • 34. Prevention Thankfully, the canine distemper virus is not as tough as the canine parvovirus and can not survive for long outside the dog’s body. The viral particles may be killed by exposure to heat, sunlight, various detergents and soaps, and un assortment of chemicals. Once the sick dog has recovered or has left the home, pet owners should wait one month before introducing a new animals. A dog recovering from distemper can shed the virus ( can spread disease) for 60 to 90 days after all symptoms have disappeared.
  • 35. References Veterinary internal medicine diseases of the dog and cat sixth edition [Stephan J. Etinger, DVM & Edward C. Feldman, DVM] Infectious diseases of the dog and cat Fourth edition [Craig E. Greene, DVM, MS, DACVIM] Emergenacy protocols dog and cat First edition [Maureen Mcmichael, John DeBiasio, Christopher G. byers] manual of small animal practice Third edition [Stephen J. Birchard, Robert G. sherding]