:: The Immune System :: Vaccinations & Minimum Disease Prevention ::
:: Nutrition & the Immune System :: Immune Deficiencies & Autoimmunity ::
:: Immune-Mediated Thrombocytopenia (IMTP) :: 

1.1 Immunoprophylaxis or minimum disease prevention

  1. Enhancement of a specific immune response in an attempt to protect it against an infectious disease. 
  2. Active induction of an immune response requires exposure to the antigens of the infectious agent
  3. Passive disease prevention involves the use of humoral or cellular factors obtained from a previous sensitized donor.
  4. Vaccination is more commonly used in the prevention of viral and bacterial diseases. 

1.2 Passive Immunizations

1.2.1 Indications

  1. Protection of colostrum deprived neonates (< 2 days old). 
  2. Protection of dogs and cats receiving cancer chemotherapy and exposed to infectious agents during hospitalization. 
  3. Prophylactic or therapeutic use in treating litters of puppies clinically affected with neonatal herpesvirus infections.
  4. Used in the initial treatment of dogs and cats with tetanus.
  5. May be used in other emergency situations in which the rapid onset of protection is necessary.

1.2.2 Efficacy

  1. Antibody titer to the specific agent involved
  2. Importance of serum antibody in controlling the particular infection involved
  3. The time of administration of antibody compared with exposure 

1.2.3 Complications

  1. Protection is low and of shorter duration than that generated from vaccination.
  2. Allergic reactions are more likely with passive immunization.
  3. Transfer of infectious agents is more likely with administration of serum when non-commercially prepared products are used.
  4. The administration of immunoglobulins also delays the ability to stimulate active immunity in the host by vaccination.

1.2.4 Source

  1. Commercial preparations are available. (From Laboratories, 703 Lake Shore Road, Grafton, WI 53024)
  2. Immune serum derived from healthy individuals or from groups of animals that have recovered from the disease in question.
  3. Hyperimmune serum is obtained from animals that have been hyperimmunized by repeated vaccination against specified infectious agents. 

1.2.5 Administration

  1. Oral administration with serum alone or in milk substitute most effective in neonates.
  2. Parenteral administration routes that are accepted are intramuscular (IM), subcutaneous (SQ) and intraperitoneal (IP).
  3. Dose is 2-4 ml/kg depending on the titer of the preparation.

1.2.6 Maternal immunity and immunoprophylaxis

  1. Amount of immunoglobulin absorbed give the neonate a titer almost equal to that of the dam.
  2. Decline of serum antibody in the neonate is similar to that for passively administered imunoglobulins.
  3. Quantity of immunoglobulin in the serum of the dam depends on the disease considered.
  4. The titer of maternal antibody in the serum of the neonate determines the susceptibility to both virulent and vaccine virus.
  5. This titer depends upon the quantity of immunoglobulin received during nursing and the absolute titer of the dam.
  6. Due to the variability of individual animals direct measurements of antibody titer of the puppy or dam is required but not practical. 
  7. Veterinarians use multiple vaccination schedules in young puppies or kittens over a certain range of ages.
  8. 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

  1. The vaccine must induce the right type of immune response.
  2. The vaccine should induce an immune response in the right place.
  3. The vaccine should induce an immune response to the right antigens.
  4. The disease should be serious enough to justify vaccination. 

1.3.2 Types of vaccines Live vaccines

  1. must be modified (attenuated) adaptation to unusual hosts prolonged storage serial passage
  2. retain antigenicity
  3. able to replicate in the intended host
  4. heterotypic vaccines developed (cross-protection)
  5. quality control essential
  6. lyophilization increases stability and storage lifespan
  7. usually contain excess antigen Inactivated vaccines

  1. subjected to various forms of denaturation without destroying antigenicity formalin
    • ethyleneimine
    • betapropriolactone
  2. adjuvants are added increase vaccine duration and level of immunity emulsified water in oil preparations mineral gels containing alum, aluminum phosphate or aluminum hydroxide
  3. do not replicate in the host
  4. antigenic mass determines the efficacy of a particular product
  5. must be given twice to get the anamestic response equal to 1 modified live vaccine Subunit vaccine

  1. purified products containing bacterial antigenic determinants or viral structural components important for the immune response
  2. efficacious for diseases in which key structural proteins have been identified from the infectious agent that enable the host to recognize the organism and eliminate it
  3. used if sufficient attenuation cannot be achieved or the agent has the potential for producing disease 

1.4 Vaccination failures

1. Host factors

  1. Hereditary or acquired immunodeficiencies
  2. Maternal immunity
  3. Age
  4. Pregnancy
  5. Concurrent immunosuppressive therapy
  6. Body temperature
  7. Anesthesia or surgery 

2. Vaccine factors

  1. manufacture
  2. storage and handling
  3. strain differences

3. Human factors

  1. veterinary hospital procedures
  2. concurrent administration of antimicrobials
  3. improper use of disinfectants
  4. vaccine interference
  5. mixing of products
  6. route of administration 

1.5 Postvaccinal complications

1.5.1 Immunological complications Type I hypersensitivity

  1. associated with inactivated products containing large amounts of foreign proteins
  2. local or systemic reactions
  3. occur within an hour after administration
  4. should not repeat vaccination with the same antigen in single or combined vaccines
  5. revaccination may be attempted after puppy reaches maturity
  6. IgE response may be generated in atopic dogs Type II hypersensitivity

  1. reported following the use of MLV
  2. autoimmune hemolytic anemia
  3. autoimmune nonregenerative anemia
  4. occur within 1-2 weeks following parvoviral vaccinations
  5.  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 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 may occur

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 Type IV hypersensitivity

  1. seen in two incidences 
  2. BCG as an immunostimulator (granuloma formation) 
  3. use of suckling mouse brain inactivated rabies vaccine (postvaccinal encephalomyelitis)

1.5.2 Nonimmunologic complications local reactions

  1. local irritation
  2. swelling
  3. abscess formation
  4. noticed with inactivated products containing adjuvants
  5. seen with bacterial vaccines containing large amounts of tissue culture proteins Systemic illness

  1. characterized by fever, malaise and inappetence
  2. result of self-limiting infection of MLV
  3. usually does not last longer than 1-2 days following vaccination Prenatal and neonatal infections

  1. if given during pregnancy can cause fetal death and abortion particularly MLV vaccines
  2. 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 Respiratory disease

  1. can occur as an expected postvaccinal complication
  2. usually occurs with intranasal vaccines
  3. mild clinical symptoms are usually self-limiting
  4. immunity superior to parenteral counterpart
  5. can get the same reaction from parenteral products inadvertently or accidentally released into the environment Shedding of vaccine agent

  1. occurs with MLV intranasal products
  2. occurs with administration of parenteral vaccines
    • canine parvoviral vaccine (feces)
    • CAV-1 vaccine (urine)
    • CAV-2 vaccine (respiratory secretions)
  3. shedding may serve to vaccine other susceptible animals
  4.  reversion to virulence a potential Postvaccinal encephalomyelitis

  1. low passage MLV Rabies vaccine in dogs
  2. high passage MLV Rabies vaccine have produced clinical disease in cats
  3. disease begins with paralysis in vaccinated limb 7 to 21 days after vaccination
  4. progresses bilaterally and in an ascending fashion
  5. cats - progressive lower motor neuron paralysis with an unusual extensor rigidity of the limbs
  6. pain and reflex function decrease in an ascending fashion
  7. recovery after 1-2 months in dogs have been reported
  8. do not present health hazard because vaccine is attenuated and is not shed in the saliva
  9. Public health and expert virologists should be consulted
  10. Other causes of postvaccinal encephalomyelitis

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 


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 rescheduling visits.

Age of Puppy When First Presented A Vaccination
Less than 6 weeks Vaccination not usually recommended. Bordetella products may be used.***
6-7 Weeks 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; see below
*lst Parvovirus vaccination.
7-8 Weeks 1st D-M, (IM), D-CAV2-P-L at 14-16 weeks. 
*lst Parvovirus vaccination.
8-9 Weeks 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
9-10 Weeks 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
10-11 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
11-12 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 containing adjuvants
  • 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 repeated yearly.

**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. 


Age Recommendations

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 2&endash;3weeks.

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 thereafter.

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 vaccination
  • Feline Pneumonitis vaccine (in high risk areas)
  • 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. 


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 rescheduling visits.

Less than 6 weeks Vaccination not usually recommended. (May need panleucopenia antiserum if entering a high risk area.)

Age of Kitten When First Presented

A Vaccination

6-7 Weeks

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)

7-8 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)

8-9 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)

9-10 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)

10-11 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)

11-12 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. 


1.9.1 Synonyms

Lyssa, hydrophobia, sylvatic plague, campesterol plague 

1.9.2 Etiology

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 disinfectants. 

1.9.3 Transmission

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. 

1.9.4 Susceptibility

All mammals - highest incidence for dogs and cats is in areas where wildlife rabies is epizootic. 

1.9.5 Pathogenesis

Variation in incubation period is based on:

  1. the site of bite
  2. the amount of virus introduced
  3. 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 rabies.

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. 

1.9.7 Diagnosis

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 findings
  • Cerebrospinal fluid - increase protein content
  • 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. 

1.9.8 Therapy

Supportive care and symptomatic treatment of seizures. 

1.9.9 Prevention

  • Zoonotic potential
  • Human vaccines
  • Canine and Feline vaccines
  • Vaccine recommendations
  • Postvaccinal Reactions
  • Control of Epizootic Rabies in Dogs and Cats
  • Postexposure management of dogs and cats 


1.10.1 Synonyms

mad-itch, Aujeszky's disease, infectious bulbar paralysis 

1.10.2 Etiology

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. 

1.10.3 Epizootiology

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 occur. 

1.10.4 Pathogenesis

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 the nucleus. 

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. 

1.10.6 Diagnosis

  • Laboratory findings
  • Hematology and Biochemistry - no abnormal findings
  • Viral isolation and identification
    • a. Animal Inoculation
    • b. Fluorescent antibody testing
    • c. Virus Isolation
  • Serology
  • 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). 

1.10.7 Therapy

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. 


1.11.1 Synonyms

Carre's disease 

1.11.2 Etiology

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. 

1.11.3 Transmission

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 several weeks. 

1.11.4 Susceptibility

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, wolf
  • family procyanidae: kinkajou, raccoon, coati mundi, badger, lesser and greater panda
  • family mustelidae: mink, ferret, skunk, weasel
  • family ursidae: bears *

*canine distemper vaccination not recommended 

1.11.5 Pathogenesis

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 disease.

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.

1.11.7 Diagnosis

  • History
  • Clinical signs
  • Hematology - related to secondary infection elevated WBC
  • Biochemistry - elevated BUN, slightly elevated liver enzymes
  • Inclusion bodies
  • Virus isolation and identification
  • Serology
  • Pathology

Gross pathology consists of thymic atrophy, interstitial pneumonia, bronchopneumonia, catarrhal enteritis, hyperkeratinizedfootpads, pustular dermatitis, conjunctivitis, rhinitis, meningealcongestion, and dilation of ventricles of the brain.

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 immunodeficiency state.


1.12.1 Synonyms

CIT, CITB, Kennel cough 

1.12.2 Etiology

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: 

  1. 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.
  2. 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.
  3. 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.
  4. Canine herpesvirus - enveloped ds DNA virus, has been isolated from dogs with respiratory disease.
  5. 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.
  6. Bordetella bronchiseptica - most common bacterial agent isolated from dogs with upper respiratory tract disease. In certain instances can cause primary respiratory infection.

1.12.3 Transmission

Portal of entry is the respiratory tract. The primary mode of transmission is direct (aerosol or airborne). Indirect transmission via fomites possible. 

1.12.4 Susceptibility

Canidae, type and severity of disease varies with:

  1. age and resistance of the host
  2. type and severity of infection
  3. vaccination 

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

  • Canine distemper Systemic fungal disease
  • Allergic bronchitis Trauma
  • Bronchiectasis Lungworms
  • Bronchialforeign bodies Congestive heart failure
  • Neoplasia of bronchialtree
  • Clinical Diagnosis
  • History
  • Clinical signs
  • Physicalexamination
  • Symptomatic therapy
  • Hematology*
  • Radiograph*
  • Transtracheal wash* Serology - paired serum from acute and convalescent phases *may be necessary only with severe disease

 1.12.8 Therapy

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. 


1.13.1 Synonyms

URI (upper respiratory infection), FURD (feline upper respiratory disease), Coryza, Feline influenza, Feline distemper, Pneumonitis 

1.13.2 Etiology

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: 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 infected queens. 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). 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. Reoviruses

Naked ds DNA viruses cause mild conjunctivitis in affected cats. Mycoplasma

Secondary invader causes conjunctivitis 

1.13.3 Diagnosis

  • History
  • Clinical signs - difficult to diagnose causative agent
  • based on clinical signs
  • Hematology
  • Conjunctival smears - cytology
  • Viral isolation
  • Serology - paired serum samples from acute and convalescent
  • phases

1.13.4 Treatment 

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 


1.14.1 Synonyms


1.14.2 Etiology

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. 

1.14.3 Epizootiology

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. 

1.14.4 Pathogenesis

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 cord).

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, partial anorexia

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 shape. 

Kitten mortality Syndrome - FIP and other infectious diseases have been associated with a clinical entity involving

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 congestive cardiomyopathy.

1.14.6  Diagnosis 

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 helpful
  • 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 been reported. 

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 not advisable.


1.15.1 Synonyms

Feline infectious enteritis, infectious agranulocytosis, cat plague, cat fever, and feline distemper 

1.15.2 Etiology

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. 

1.15.3 Epizootiology

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 dividing cells. 

1.15.4 Pathogenesis

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. 

1.15.6 Diagnoses 

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  

  • History
  • Physical examination
  • Hematology - low WBC count
  • Biochemistry - elevated BUN, elevated total proteins, and slight elevation of liver enzymes
  • FeLV test
  • Toxoplasmosis titer
  • FIP titer
  • Serology
  • 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.

1.15.7 Therapy

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.


1.16.1 Etiology

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 herpesvirus, reoviruses

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. 

1.16.2 Epizootiology

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. 

1.16.3 Pathogenesis

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. 

1.16.5 Diagnosis

  • History
  • Clinical signs
  • Hematology - leukopenia which is primarily a lymphopenia
  • Biochemistry - hypoproteinemia, increase in LDH, SGOT, and CPK
  • Electrocardiography - premature ventricular contractions, ventricular tachycardia, decreased R wave amplitude
  • Radiography - left sided heart enlargement
  • Serology - IgM, or specific for parvovirus
  • Hemagglutination-Inhibition
  • Virus neutralization
  • Indirect immunofluorescence
  • Virus Detection
  • Electron microscopy
  • Hemagglutination
  • 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 heart failure. 

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. 

1.16.6 Therapy

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 suggested.

  • Prophylaxis
  • Maternal immunity
  • Vaccines
  • Inactivated feline and canine origin vaccines
  • Mink enteritis vaccines
  • Modified live vaccines of canine and feline origin  


1.17.1 Viral Properties 

  • Doubleanded rna virus, of the retrovirus family and oncovirinae subfamily.
  • Order of genes left to right
  • LTR-gag-pol-env-LTR

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 mrnas. 

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 to

  • 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 subgroups. 

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, myelopdysplastic disease.

 Felv C - derived from Felv A by recombination or mutation, associated with fata erythroid aplasia, close antigenically to feline oncornavirus associated cell membrane antigen (FOCMA)

 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 disease.

 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 of occurrence.

1.17.3  Pathogenesis

 Six stages of Felv infection:

  • 1. Replication in lymphoid tissue around exposure site
  • 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 cells.
  • 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 viremia

  •  1. Recognizable signs of disease attributable to Felv infection that occur only after a long induction period. 
  • 2. After a long induction period there is tumor development.
  •  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 cats. 

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, aplasia).
  • 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 infection.
  • 2. Undergoing the early stages of a progressive infection.
  • 3. Immune carriers of a localized infection.
  • 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 the virus.
  •  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 veterinarian. 

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.  


1.18.1 Synonym:

Infectious Cyclic Thrombocytopenia 

1.18.2 Etiology

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. 

1.18.3 Epizootiology

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 unknown. 

1.18.4 Pathogenesis

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 occurs occasionally. 

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.

 1.18.6 Diagnosis

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.


 1.19.1 Synonyms

Rocky Mountain Spotted Fever, RMSF

1.19.2  Etiology

Rickettsia Rickettsi - There are two other antigenically related rickettsia that must be tested for serologically when rickettsia rickettsi is suspected. 

1.19.3 Epizootiology

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. 

1.19.4 Pathogenesis

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 

1.19.10 Serology

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 MIF.

1.19.13  Therapy

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.

1.19.14 Prevention

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.

1.19.15  Public Health Considerations

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. 


1.20.1 Synonyms:

Canicola fever, Weils Disease, Stuttgarts disease, Canine typhus 

1.20.2 Etiology:

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. 

1.20.3 Transmission:

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. 

1.20.4 Susceptibility:

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 dogs. 

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 clinical signs. 

1.20.5 Signs:

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), jaundice, death.

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.

1.20.7 Lesions:

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.

1.20.8  Differential diagnosis:

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. 

1.20.9 Treatment:

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.

1.20.10  Prophylaxis:

Commercial bacterins. One, two or three doses at two week intervals followed by annual revaccination.

1.20.11  Public Health Considerations

  • 1. Leptospirosis is thought to be the most widespread zoonosis.
  • 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. 


1.21.1 Synonyms:

Canine abortion, Epizootic Canine abortion, Contagious Abortion of dogs, Beagle fever

1.21.2 Etiology:

Brucella canis a small, gram negative coccobacillus. The organism is relatively short-lived outside the dog and is readily inactivated by common germicidal disinfectants.

1.21.3 Transmission:

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.

1.21.4 Susceptibility:

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 infection.

1.21.5  Incubation period:

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 post infection. 

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.

1.21.8 Lesions:

Lymphadenitis, testicular atrophy in males.  

1.21.9 Diagnosis:

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. 

1.21.10 Treatment:

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. 

1.21.11 Prophylaxis:

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 stud.
  • 3) Heavily used males should be bred only to test-negative females and checked twice yearly by the slide test.
  • 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. 


1.22.1 Synonym:


1.22.2 Etiology:

The exotoxins (tetanospsmin and tetanolysin) of Clostridium tetani, a gram positive, anaerobic, spore forming rod. C. tetani is ubiquitous in nature.

1.22.3  Transmission:

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.

1.22.4 Susceptibility:

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.

1.22.5  Incubation Period:

3 to 20 days. Common is 5-8 days. 

1.22.6 Signs:

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.

1.22.8  Lesions:

May find the "wound" of origin. No characteristic gross or microscopic lesions.

1.22.9 Differential Diagnosis:

Meningitis of non-tetanus origin is most frequently confused with tetanus.

1.22.10 Treatment:

  • (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. 

1.22.11 Prophylaxis:

Tetanus toxoid will provide a strong immunity; however, it is seldom used. TAT following tetanus prone wounds may be indicated.


1.23.1 Etiology:

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. 

1.23.2 Transmission:

Ingestion of the toxin in meat products or vegetables. 

1.23.3 Susceptibility:

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).

1.23.4 Incubation Period:

Very short in the dog. Twelve hours from ingestion of toxin to signs of disease.

1.23.5 Signs:

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.

1.23.6 Course of Disease:

Short. 12-24 hours.

1.23.7  Lesions:

No characteristic gross or microscopic pathology. May find ingesta in stomach such as chicken bones an feathers that owner has no recollection of feeding.

1.23.8  Differential Diagnosis:

Must be differentiated from all paralytic diseases (tick paralysis, polyradiculoneuritis, etc) Can run mous inoculation form blood of suspected case.

1.23.9  Treatment:

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 neuromuscular transmission.

 1.23.10 Prophylaxis:

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.


1.24.1 Etiology:

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.

1.24.2 Transmission:

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.

1.24.3 Susceptibility:

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.

1.24.4 Incubation period:

Short. 24-48 hours

1.24.5 Signs:

Characterized by fever, gastroenteritis with vomiting and diarrhea (may be blood stained), dehydration and depression.

 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 mortem.
  • 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 more.
  • 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 

1.24.6 Lesions:

See above. 

1.24.7 Diagnosis:

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. 

1.24.8 Treatment:

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 is present. 

1.24.9 Prevention:

Sanitation. Autogenous Salmonella bacterins can be prepared.

1.24.10  Public Health Considerations

  • 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. 


1.25.1 Synonym:

Lyme disease 

1.25.2 Etiology:

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 procedures.

 1.25.3 Transmission:

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.

 1.25.4 Susceptibility:

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.

 1.25.5 Pathogenesis:

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 articular cartilage.
  • 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 are:

  • 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 later
  • 5. Swollen lymph nodes
  • 6. Generalized apin
  • 7. Skin lesions
  • 8. Atrioventricular block
  • 9. Secondary glowmerulonephritis and associated symptoms 

1.25.7 Diagnosis

  • 1. History
    • a. travel to a Lympe disease endemic area
    • b. Acute onset of lameness with no history of trauma
    • c. History of past or current tick bites
  • 2. Serology
    • a. IFA or ELISA
    • b. IgG antibody titers 1:1024 or greater are positive. Titers below 1:64 should be considered negative.
    • 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 negative 

1.25.8 Treatment

  • 1. Tetracycline 25mg/kg/day per os tid fo minimum of 14 days
  • 2. Erythromycin and ampicillin also effective
  • 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 area. 


1.26.1 Etiology

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 oocyst.
    • 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 transplacental transfer. 
  • III. This parasite is cosmopolitan in distribution. 
  • 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 

  1. Most infection with T. Gondii are asymptomatic. 
  2. When clinical toxoplasmas occurs, signs seen can include fever, hepatitis, bilirubinemia, pneumonia, anemia, encephalitis, myositis, myocarditis, enteritis, and lymphadenitis.
  3. 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 parasite.
  4. Clinical toxoplasmosis is most commonly seen in the immunodeficient neonate or the immunocomprimised adult.
  5. Cats usually develop subclinical infections. Diarrhea and central nervous system disease can cause death in neonatal and unweaned kittens.
  6. Dogs with acute infections develop systemic disease with clinical signs based on the organ affected.
  7. Chronic infections are usually of the ocular or CNS forms.


1.27.1 Synonyms

Tropical canine pancytopenia, canine typhus, canine hemorrhagic fever, idiopathic hemorrhagic syndrome

1.27.2 Etiology

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. 

1.27.3 Transmission

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. 

1.27.4 Pathophysiology

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 the dog.

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 affected.

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 treatment. 

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. 

1.27.6 Diagnosis 

Differential diagnoses 

Rocky mountain spotted fever, brucellosis, blastomycosis, salmon poisoning, immune-mediated thrombocytopenia, systemic lupus erythematosus, lymphosarcoma, and other causes of specific organ dysfunction and lymphadenopathy.

Clinical pathology 

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 of disease.

 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 available).

1.27.7 Treatment

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. canis. 

1.27.8 Prevention

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 chemoprophylaxis. 


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 bitch. 

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)

15-20 3
22-25 7
30-32 14
35-40 21 

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 newborn. 

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 human.

1.28.7 Antibiotic considerations 

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 defects. 

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 trimethoprim-sulfas 

1.28.8 Parasites

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.


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 re-oxygenation, 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 restoration.

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 unfeasible.

The general principles of chemotherapy 

  1. The body burden of tumor cells usually far exceed clinically apparent disease.
  2. The proportion of tumor cells actively dividing may fall from a level higher than normal to a relatively low level as tumor size increases.
  3. Chemotherapeutic agents are more effective in dividing cells than resting cells.
  4. Chemotherapeutic agents have maximal effect following reductive surgery or radiation therapy.
  5. 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.
  6. Chemotherapy may reduce tumor cell burden to levels at which immunologic mechanisms are considered more likely to be effective.
  7. 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

  1. Alkylating agents
  2. Antimetabolites
  3. Vinca Alkaloids
  4. Antibodies
  5. Hormones
  6. Enzymes
  7. Miscellaneous agents 

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