Canine and Feline parvovirus

Cause :
The genetic sequences of CPV and FPV differ by only around 2% and antigenically they are
very similar.The virus makes use
of the transferrin receptor to gain entry to cells and polymorphisms in this receptor are
responsible for host specificity. FPV replicates in feline cells in vitro and in vivo but not in
canine cell cultures. CPV replicates in feline and canine cells in culture and in dogs in vivo
The fecal-oral route is the traditionally understood means of transmission, but fomite
transmission also is very efficientmaternally derived titers mean that neonates are almost
never affected. Approximately 90% of maternally derived antibody is from colostrum and it
has a half-life of around 10 daysSusceptibility increases as maternal immunity wanes at
around 12-14 weeks of agefactors that contribute to infection include intestinal parasites,
overcrowding, and unsanitary and stressful environmental conditions

Pathogenicity and clinical signs :

CPV and FPV share a very similar pathogenesis and clinical presentation. The virus is unable
to induce mitosis in the cells it infects and hence it relies on the rapidly multiplying cells of
the body for its success. The virus thus shows a tropism for cells of the thymus, bone marrow,
spleen, and crypt cells of the gut epithelium. Stress factors, in particular parasitic and other
nonspecific factors such as weaning, can predispose dogs to infection by increasing mucosal
cell activity. FPV disease has been documented to be enhanced by feline leukemia virus
(FeLV), Clostridium piliforme, and feline coronavirus. Because a robust antibody response is
very protective, parvoviral infections are almost exclusively a disease of animals under a year
of age that are past the age at which maternally derived antibodies provide protection, or are
unvaccinated or inadequately vaccinated. For both CPV and FPV, vaccination status plays a
very important role in susceptibility.
Following oral infection, the virus disseminates to the regional lymph nodes of the pharynx
and the tonsils. In an experimental study in dogs, fecal shedding was present from day 3
following oral infection, peaked on days 3 and 4, and was greatly reduced by day 7. Shedding
could well occur for a day or 2 before clinical signs are apparent. The incubation period of
this disease varies from around 4 days (under experimental conditions) to the more typical 1
to 2 weeks usually seen under natural conditions. Following infection of lymphoid tissues of
the upper gastrointestinal (GI) tract, including the tongue, a cell-free viremia ensues.
Under experimental conditions, this lasts from day 1 to day 5 post-infection, with the first
signs of serum antibodies developing on day 5 and peaking from day 7 onwards. Thymic and
lymphoid tissue infection leads to thymic atrophy, lymphoid depletion, lymphopenia, and
immunosuppression. Viral antigen is detectable in the proliferative zone of the crypt
epithelium of the intestinal tract from day 4. Very little antigen remains in either the
lymphoid tissues or gut epithelium from day 7 onward. Subclinical infection probably is
common, especially in older, immune-competent animals.
The earliest clinical signs include fever, depression, and a loss of appetite. This is followed by
diarrhea and vomiting. This is true of CPV and most cases of FPV. The diarrhea initially is
clinically characteristic of small bowel disease. It may quickly become melenic and then
frankly hemorrhagic, and take on the character of a mixed small and large bowel type
diarrhea . These puppies carry a very characteristic fetid odor.

The vomiting usually increases in frequency and can become very severe and frequent
with little more than foam produced. Hematochezia can be present and ascarids also can be
observed in the vomitus. In peracute FPV, young cats can die within 12 hours of showing
depression, due to profound septic shock, dehydration, and hypothermia, and vomiting and
diarrhea may be minimal or absent. Bone marrow infection can lead to bone marrow necrosis
in both dogs and cats. This leads to leukopenia and also can contribute to the anemia seen in
some cases. In most cases of CPV and FPV, leukopenia is present by the time hemorrhagic
diarrhea and vomiting are present. Thrombocytopenia, however, is not a feature of the
disease. An increased concentration of granulocyte-colony stimulating factor (G-CSF) has
been documented in dogs with CPV and this is likely to be a response to the neutropenia. The
neutropenia also is partially due to an overwhelming demand in the gut. The
immunosuppression associated with CPV does mean these dogs are very susceptible to acute
secondary infections. The most common of these are bacterial bloodstream infections, which
manifest clinically as endotoxic shock; on recovery some puppies develop skin necrosis ,
bacterial polyarthritis, and discospondylitis
(R. Kirberger, personal communication). The immune-suppressed condition also means that
barrier nursing practices should be strictly enforced. Puppies with other infectious diseases
should not be kept within the same facility. The most important differential diagnosis for
systemic CPV-like signs is canine distemper virus infection. Every effort must be made to
exclude this highly contagious disease from being cared for in a facility that admits CPV-
infected puppies or by the same caregivers. Viral infection of the gut leads to crypt necrosis
and villous collapse; loss of the normal gut barrier function
has serious consequences, as elements of the gut content can no longer be kept out of the
bloodstream.
Escherichia coli was recovered from the lungs and liver of 90% of 98 CPV-infected puppies
in one study. Blood loss into the gut may be significant, resulting in melena, hematochezia,
and anemia (which can be masked in dehydrated animals). Ascarid infestations can result in
additional blood loss and are known to aggravate the disease. This comorbidity is common.
Less common are concurrent giardiasis and coccidiosis.
Devastating fluid and electrolyte losses can be caused by vomiting and diarrhea. This leads
to dehydration and electrolyte deficiencies, the most notable of which is hypokalemia. The
dehydration would be classified as isotonic or hypotonic (due to hypertonic fluid loss) and it
results in dry mucous membranes, increased skin turgor, increased capillary refill time,
tachycardia, hypotension, collapse, and reduced urine production. The acid-base
disturbances have been shown to be complex and heavily influenced by chloride, free water,
and albumin. Severely affected animals tend to demonstrate hypochloremic alkalosis,
whereas mildly affected puppies typically have a hyperchloremic acidosis.
Viral infection of the gut leads to crypt necrosis and villous collapse; loss of the normal gut
barrier function has serious consequences, as elements of the gut content can no longer be
kept out of the bloodstream. Escherichia coli was recovered from the lungs and liver of 90% of
98 CPV-infected puppies in one study.
Blood loss into the gut may be significant, resulting in melena, hematochezia, and anemia
(which can be masked in dehydrated animals). Ascarid infestations can result in additional
blood loss and are known to aggravate the disease. This comorbidity is common. Less
common are concurrent giardiasis and coccidiosis. Devastating fluid and electrolyte losses
can be caused by vomiting and diarrhea. This leads to dehydration and electrolyte
deficiencies, the most notable of which is hypokalemia. The dehydration would be classified
as isotonic or hypotonic (due to hypertonic fluid loss) and it results in dry mucous
membranes, increased skin turgor, increased capillary refill time, tachycardia, hypotension,
collapse, and reduced urine production. The acid-base disturbances have been shown to be
complex and heavily influenced by chloride, free water, and albumin. Severely affected
animals tend to demonstrate hypochloremic alkalosis, whereas mildly affected puppies
typically have a hyperchloremic acidosis.
The typical clinical presentation of advanced parvovirus infection in a young German
Shepherd Dog puppy. The dog is moribund (A) and in hypovolemic shock, with hemorrhagic diarrhea
(B) and pale, dry mucous membranes (C).

A young Basset Hound puppy that recovered from parvoviral diarrhea

complicated
by secondary Salmonella bacteremia. The bacteremia resulted in ear-tip skin
necrosis, probably due to
micro-embolization of the peripheral vasculature.
A 12-week-old Labrador
crossbreed puppy was
treated for parvovirus
infection and
discharged. It was
returned 3 days after
discharge with spinal
pain. Radiographs
showed a collapsed
lumbar 4-5 disc space
with mild subluxation
(A). Follow-up
radiographs up taken 2
weeks later showed
findings typical of
discospondylitis with
subluxation (B, arrow)

Diagnosis :
The diagnosis of parvoviral disease is not problematic and is usually based on combining
a cluster of findings that include the presentation of the typical signalment (young and un- or
inadequately vaccinated), classic chief complaints of depression, anorexia, vomiting and
diarrhea (which can be hemorrhagic) and the typical clinical findings of fever, dehydration,
fluid-filled and gassy intestine on abdominal palpation, and leukopenia on peripheral blood
smear

Treatment :
The level of care strongly affects outcome. There is no specific antiviral treatment available
and hence supportive care is the mainstay of therapy. Outpatient-based treatment is not
recommended as the standard of care, because in most cases owners are unable to maintain
hydration orally. It might be necessary to provide subcutaneous or intraperitoneal fluids and
oral antibiotics in some cases because of the financial constraints of some owners. Preliminary
results of an outpatient-type protocol, consisting of intravenous fluid resuscitation followed
by cefovecin (8 mg/kg SC once), maropitant (1 mg/kg SC q 24 h × 5 days) and SC fluids PRN,
showed a survival rate rivaling that of inpatient treatmentIntensive treatment with crystalloid
fluids, synthetic and natural colloids, correction of hypoglycemia and any electrolyte
disturbances, and a combination of antimicrobials, antiemetics, analgesics, enteral nutritional
support, and anthelmintics, usually form the basis of the treatment plan. Fluid therapy to
treat dehydration, re-establish effective circulating blood volume, and correct electrolyte and
acid-base disturbances is the mainstay of managing more severely affected puppies.
 Fluid therapy in these patients can be complex, and careful attention should be paid to
physical examination in addition to electrolyte and acid-base status. The preferred route of
administration is intravenous, but intraosseous administration, although rarely used, can be
useful in patients that need rapid fluid administration when intravenous access is impossible.
All intravenous catheters should be replaced every 72 hours. The initial fluid of choice is a
balanced electrolyte solution that is isotonic to blood (e.g., lactated Ringer's solution). The
initial rate of fluid administration will depend on the condition of the patient. IV fluid boluses
can be necessary in patients with hypovolemic shock. Fluid deficits should be replaced as
soon as possible (within 1 to 6 hours of presentation). Once perfusion is restored, the
intravenous fluid rate is reduced to a maintenance rate plus estimated ongoing losses.
Hypokalemia is common and potassium chloride (KCl) should be added to the IV fluids until
serum potassium concentrations have normalized. Hypoglycemia also is common, and in
severe cases, 25% dextrose should be given as a bolus to correct this Following this, the IV
fluid infusion can be supplemented with 2.5-5% dextrose to maintain
normoglycemia.Hypoalbuminemia is common as a result of protein-losing enteropathy.
Colloid oncotic pressure could require support with a synthetic colloid such as hydroxyethyl
starch if the serum albumin concentration should drop below 2 mg/dL (20g/L) or if there is an
obvious third space fluid loss.
The most commonly used antiemetic drugs for CPV enteritis are metoclopramide (0.2-0.4
mg/kg SC q 8 h or1 mg/kg/day IV constant rate infusion [CRI]), prochlorperazine (0.1 mg/kg
IV q 8-12 h), ondansetron (0.1-0.5 mg/kg IV q 12 h), or maropitant (1 mg/kg SC q 24 h × 5 days
maximum). In cases of intractable vomiting,and when intestinal obstruction has been ruled
out, combination therapy and continuous intravenous infusions of these drugs could be more
effective than monotherapies or boluses. A retrospective study
showed that in a high number of cases, antiemetics did not completely control vomiting, and
puppies that received antiemetics generally required longer hospitalization. Although this
study demonstrated an association between antiemetic use and prolonged hospitalization, a
cause-and-effect conclusion cannot be drawn, and antiemetics are definitely indicated in the
management of this disease.
Treatment with intravenous, broad-spectrum, bactericidal antibiotics is warranted in
puppies suffering from CPV enteritis, due both to the disruption of the intestinal barrier and
to severe leukopenia. A combination of a beta-lactam antibiotic (e.g., ampicillin, 20 mg/kg IV
q 8 h) or a beta-lactamase-resistant penicillin (e.g., amoxicillin/clavulanate, 20 mg/kg IV q 8 h)
with an aminoglycoside (e.g., amikacin, 20 mg/kg IV, IM, or SC q 24 h once the dog has been
rehydrated; used for a maximum of 5 days) will provide broad coverage. Metronidazole (15-
20 mg/kg PO q 12 h for up to 10 days) is indicated in cases where motile protozoa are found
on fecal wet preparation.
Analgesia is an important component of case management in almost all cases, as the enteric
pain can be severe; even in very depressed dogs, abdominal palpation can elicit immediate
abdominal splinting due to pain. The most commonly used drugs include buprenorphine
(e.g., 0.005-0.02 mg/kg IV q 8-12h) and fentanyl
Various hematological variables have been negatively associated with prognosis, including
leukopenia, lymphopenia, monocytopenia, and neutropenia. The presence of a systemic
inflammatory response syndrome at the time of admission also is a negative indicator.Other
factors that have been correlated with outcome include season of presentation, pure breed,
body weight, vomiting, hypercoagulability, hypercortisolemia, hypothyroxinemia,
hypoalbuminemia, elevated C-reactive protein, increased tumor necrosis factor,
hypocholesterolemia, and hypocitrullinemia.
 Canine distemper

Cause :
Canine distemper is an acute to subacute systemic disease with high mortality rate in dogs
and other carnivores worldwide. Affected dogs frequently develop neurologic
manifestations. The causative agent, canine distemper virus (CDV), is an enveloped, single-
stranded RNA virus belonging to the family Paramyxoviridae.
All ages and breeds are susceptible to CDV infection. CDV is transmitted by oronasal
exposure to viruscontaminated respiratory secretions, vomitus, feces, urine, and
environmental fomites. CDV also is spread efficiently by aerosols generated by coughing and
sneezing, as well as aerosols of other excretions. The incubation period typically ranges from
1 to 3 weeks. Virus shedding starts within 7 to 10 days of exposure, coinciding with the
hematogenous spread of the virus to epithelial and central nervous system (CNS) tissues
irrespective of the severity of clinical signs. Virus is shed in all body excretions during the
acute systemic disease. Dogs with subclinical infections also shed virus. Infected dogs can be
contagious for up to 3 months, although shorter periods of shedding are more typical.

Pathogenesis :
CDV causes systemic infection of epithelial tissues in many organ systems. Initially, the virus
replicates locally in macrophages and monocytes in the tonsils, upper respiratory tract
epithelium, and regional lymph nodes, reaching peak virion production by 2 to 4 days after
inoculation. The signaling lymphocyte activation molecule (SLAM, CD150) is the cellular
receptor that is expressed on the surface of the cells of the immune system. Viremia occurs 4
to 6 days later, with systemic spread of virus to the stomach, small intestine, spleen and
hepatic macrophages, bone marrow, and other lymphoid tissues. The widespread
increase in virus production is associated with fever, lymphopenia caused by lymphocytic
apoptosis, and immunosuppression. Further hematogenous spread of the virus is responsible
for infection of epithelial cells in multiple organs, including the eyes, skin, and CNS. Virus
shedding from the respiratory, gastrointestinal, and urogenital tracts coincides with epithelial
infection. Virus persists for long periods of time in the uvea, uroepithelium, epidermis, and
CNS.
After 9 to 14 days, the clinical outcome of infection depends on the host's immune
response. Viral infection in bone marrow and other lymphoid tissues can result in profound
and protracted immunosuppression due to T-cell depletion and other undefined mechanisms.
In convalescing puppies, cell-mediated immunosuppression can persist after CDV infection
for more than 10 weeks. Dogs with poor immune responses develop viral infection of several
additional tissues, including skin and other glandular and epithelial organs. These animals
generally exhibit severe clinical signs and are likely to die. Animals that do
recover from the initial clinical signs maintain virus in tissues and are likely to develop
clinical signs of CNS disease subsequently. In animals that mount an intermediate level of
immune response, mild or clinically silent infection may develop, with virus persisting in the
lungs, skin, or CNS. These animals can develop signs of CNS disease or can undergo
complete recovery. Animals that mount strong immune responses are unlikely to develop
signs of systemic infection but still can develop signs of CNS disease.
Hematogenous spread of CDV into the CNS results in infection of choroid plexus
epithelial cells, astrocytes, and neurons, which in general coincides with MHCII and
proinflammatory cytokine upregulation. Dogs, especially the young or immune-suppressed,
can develop acute demyelination attributed to direct viral injury in the absence of
inflammatory reactions. Subacute to chronic CDV encephalitis appears to be a consequence of
inflammatory responses to viral antigens in the CNS, with macrophage activation and release
of cytotoxic mediators playing a role in destruction and demyelination of CNS cells.

Brain stem of a dog with canine distemper. Perivasculitis consisting of mononuclear

cells surrounding an arteriole (asterisk). Bar = 50 microns. Inset: Immunohistochemical demonstration
of canine distemper virus antigen located in the cytoplasm of neurons (arrows). Bar = 20
microns.

Clinical signs :
The severity of the clinical course is a function of the animal's age, pathogenicity patterns for
different viral strains, and immune responses. Many dogs, particularly those that are older or
have partial immunity, have asymptomatic infection or mild disease. Puppies are more likely
to suffer from severe and
protracted illness and have the
highest mortality rate.
The severity of the clinical course
is a function of the animal's age,
pathogenicity patterns for different
viral strains, and immune
responses. Many dogs,
particularly those that are older or
have partial immunity, have
asymptomatic infection or mild
disease. Puppies are more likely to
suffer from severe and protracted
illness and have the highest
mortality rate.
2506Within the first week of
infection, systemic virus spread in lymphoid organs corresponds to a rise in body
temperature and lymphopenia affecting both B- and T-cells.
Affected dogs can be lethargic, anorexic, and dehydrated, and frequently develop
conjunctivitis and respiratory signs. These include serous or mucopurulent oculonasal
discharge and cough that progressively worsens if no adequate immune response
develops. Viral infection of the lower respiratory tract results in pneumonia that might or
might not be evident clinically but can be documented via radiographs. Viral pneumonia
complicated by secondary bacterial infections can be life-threatening. Infected dogs with mild
clinical signs can be indistinguishable
from those with other causes of
kennel cough. Depending on viral
strain, affected dogs also can have
vomiting and mucoid or hemorrhagic
diarrhea from viral replication in
epithelial cells of the gastrointestinal
tract. Viral infection of ocular tract
epithelium can cause photophobia,
anterior uveitis, and chorioretinitis.
Recovered animals can have
hyperreflective retinal lesions that
develop from retinal atrophy and
scarring, as well as
keratoconjunctivitis sicca from
scarring of the lacrimal glands. Optic neuritis
can cause blindness or mydriasis; blindness
also can result from serous retinal
detachments.
Production of large amounts of virus occurs in
uroepithelium, including the kidneys and
lower urinary tract, which can causeclinical
signs associated with kidney and bladder
dysfunction. Viral infection of the epidermis
can result in a pustular rash and
hyperkeratosis or “hardening” of the nasal
planum and footpads. Infection of developing enamel buds in
young puppies prior to eruption of the permanent dentition results in dental enamel
hypoplasia. Some dogs, especially young large-breed dogs, are susceptible to metaphyseal
osteosclerosis of long bones, which typically is not associated with lameness.
Neurologic signs can develop starting 1 to 3 weeks after recovery from systemic signs or
can develop months later. Neurologic signs can develop in dogs that had no noticed evidence
of systemic disease. Neurologic signs, whether acute or chronic, typically are progressive, and
are the most significant factors affecting prognosis and recovery from infection. Curiously,
certain features of clinical disease tend to correlate with the likelihood of developing
neurologic disease. Dogs that develop pustular skin lesions are less likely to develop CNS
disease, but hyperkeratosis of the nasal planum and digital footpads frequently is
associated with the development of neurologic signs. Neurologic abnormalities can reflect
lesions in any CNS site and include seizures, ataxia, hypermetria, paraparesis or tetraparesis,
and severe cervical pain . Myoclonus, either generalized or focal, is a common clinical sign
and is strongly suggestive of CDV infection. Hippocampal alterations can progress to the
point of causing status epilepticus . Puppies infected in utero or as neonates can develop CNS
signs during the first 4 to 6 weeks of life.
Abortion and neonatal death have been observed.

Diagnosis :
Due to the systemic infection and the variety of respiratory, gastrointestinal, and/or
neurological signs, a firm diagnosis of CDV based solely on clinical signs can be difficult to
achieve. Poor vaccination history might support a suspicion, but CDV also has been
described in vaccinated dogs. Intranuclear and intracytoplasmic viral inclusions can be seen
in monocytes, lymphocytes, neutrophils, or erythrocytes during examination of a stained
blood smear, but inclusions often disappear within 1 to 2 weeks after the onset of
clinical signs. There are no pathognomonic laboratory abnormalities. Lymphopenia is the
most consistent abnormality on the complete blood count. Biochemical profile abnormalities
can include hypoalbuminemia and hypoglobulinemia. The cerebrospinal fluid (CSF) can have
increased numbers of lymphocytes and monocytes and varying protein concentrations. Dogs
with respiratory disease can have interstitial or alveolar patterns on thoracic radiographs.
Radiographs of long bones in lame animals can show metaphyseal lesions consistent with
hypertrophic osteodystrophy. Animals with CDV-associated neurologic disease can be
diagnostic challenges if there is no history or evidence of systemic signs. Abnormalities on
magnetic resonance imaging (MRI) of the brains of dogs with acute CDV have been described
and, though not specific, potentially could help support a diagnosis in dogs with few or no
systemic signs.
A definitive diagnosis of CDV hinges on the detection of viral antigen or nucleic acid in
antemortem or postmortem samples, virus isolation, and serologic titers. Demonstration of
viral antigen in cells on blood smears, smears from nasal, conjunctival, or pharyngeal swabs,
or postmortem tissues by immunological methods such as fluorescent antibody or
immunohistochemical testing confirms the diagnosis. CDV titers might not be sufficiently
sensitive because they decrease beyond 3 weeks of infection. Reverse-transcription–
polymerase chain reaction (RT-PCR) assays are highly sensitive and specific for detection of
CDV in clinical cases and can be performed on virtually any sample type, including
conjunctival, nasal, and pharyngeal swabs; whole blood; feces; urine; CSF; and postmortem
tissues, particularly the urinary bladder.
However, CDV PCR assays offered by commercial laboratories do not discriminate between
vaccine and field CDV strains in samples collected from dogs recently vaccinated with
modified-live CDV. Duration of post-vaccine interference is variable but could be as long as 3
weeks. An exception to vaccine interference with PCR testing is a recombinant canarypox-
vectored CDV vaccine. Sequence analysis can discriminate between vaccine and CDV field
strains.Serologic tests are widely available for documentation of CDV specific antibodies.
However, due to profound immunosuppressive effects during acute CDV infections, the
amount of antibody can be low or even remain below the detection limit for serological tests.
Immunofluorescent assays (IFA)are used for measuring immunoglobulin M (IgM) and IgG
antibodies to CDV; detection of IgM antibodies,which can persist for 3 months, is supportive
of CDV infection. The serum neutralization assay is considered the “gold standard” for
quantifying total CDV antibodies. Diagnosis of recent active infection by this assay requires
collection of paired acute and convalescent sera to determine seroconversion, defined as at
least a fourfold increase in the antibody titer from the acute to the convalescent sample.
Infection also is supported by demonstration of higher concentrations of CDV antibody in the
CNS as compared with the serum, although not all animals will have CSF antibodies.

Treatment :
Treatment of dogs with CDV is largely supportive. Parenteral administration of fluids can be
necessary in dogs with vomiting or severe diarrhea. Animals with secondary bacterial
bronchopneumonia or other bacterial infections are candidates for antibiotics. In puppies,
resolution of bronchopneumonia could require combinations of broad-spectrum bactericidal
antibiotics administered for several weeks. Seizure control with anticonvulsant drugs can be
necessary. Ribavirin inhibits CDV replication in vitro, 15 but its use has not been described in
dogs. The prognosis for dogs with neurologic disease is considered guarded to poor.
 Canine herpes virus
Cause :
CHV is considered part of a complex of pathogens causing the canine infectious
respiratory disease complex (CIRD) or “kennel cough” (see ch. 227). The virus has
been isolated repeatedly from dogs with respiratory disease and was found to replicate
in the respiratory tract of dogs. However, clinical signs were not seen after
experimental exposure. CHV might have a secondary role, with activation of viral
replication induced by infection with more virulent respiratory pathogens.
The virus is transmitted by oronasal contact with infectious respiratory or genital
secretions and transplacental transmission also can occur. The source of infected
material can be body excretions from young puppies, respiratory secretions from
infected older dogs, or vaginal secretions from infected bitches. The incubation period
for primary infection is 6 to 10 days. Virus shedding occurs for 7 to 10 days after
primary infection or reactivation of latent infection. 25,26 In newborn pups, infection
spreads rapidly and all puppies in an infected litter usually die. Spread of infection
among older dogs appears to be slower and, even in close contact, not all dogs
become infected. Fetuses can be infected in utero during primary infection of the
pregnant bitch.
Pathogenesis :
Transplacental infection during primary infection of dogs results in fetal resorption,
abortion, stillbirths, or birth of weak puppies that die within days. Immunity following
primary infection protects future litters. Infection of naïve puppies younger than 2
weeks old causes fatal generalized necrotizing and hemorrhagic disease. Neonatal
puppies are infected by oronasal contact with the dam's infectious birth canal
secretions with actively replicating virus, or via grooming by the dam. CHV first
replicates in the epithelial cells of the oropharynx and tonsils. Virus subsequently
enters macrophages, which allows spread to other tissues hematogenously, including
the lymph nodes, spleen, adrenal glands, kidneys, lungs, liver, and CNS. The lower
body temperature of neonates, in conjunction with a limited capacity to mount a
febrile response, facilitates systemic spread of the virus. Infection of older pups and
adults is confined to the respiratory, ocular, or genital tract without systemic spread.
Most infections are subclinical or can present as mild and self-limiting respiratory,
ocular, or genital disease. Following a short replication period, CHV establishes latent
infection in neurons of the trigeminal and lumbosacral ganglia, lymphocytes in the
retropharyngeal lymph nodes and tonsils, and epithelial cells in the parotid salivary
gland. Reactivation of viral replication can be provoked by stress or
immunosuppressive disease/therapy.
Clinical signs :
The incubation period appears to be 4 to 6 days. Bitches remain overtly healthy and
milk production continues unchanged. The disease course in puppies is rapid. Infected
neonatal puppies exhibit persistent crying, anorexia, signs of abdominal pain,
dyspnea, and petechial hemorrhages. Most puppies in affected litters die between 1
and 4 weeks postpartum, 24 to 48 hours after onset of clinical signs. Petechial
hemorrhages in the liver, kidneys, and lungs are typical lesions observed on necropsy.
Older puppies develop mild signs of respiratory disease (rhinitis, pharyngitis) with
spontaneous recovery, but latent infections can emerge later as a cause of neurologic
disease, with signs of ataxia, blindness, or central vestibular disease being most
common. Puppies with maternal antibodies are readily infected by CHV. The
infection, however, remains localized and there is no systemic clinical disease.
Infection in adult dogs usually remains subclinical, but some dogs have rhinitis,
pharyngitis, vaginal or preputial hyperemia, hyperplasia of vaginal mucosal lymphoid
follicles, and sometimes submucosal hemorrhages. Corneal ulceration has been
reported in adult dogs during natural infection with CHV, while conjunctivitis
occurred in experimentally infected dogs. The clinical significance of CHV infections
in ocular diseases is not defined, but CHV should be considered a potential cause of
conjunctivitis or corneal disease after more common causes have been excluded.
Diagnosis :
The diagnosis is made by observation of clinical signs in puppies of susceptible age in
conjunction with necropsy lesions. Viral inclusion bodies can be observed in cells
surrounding areas of necrosis and hemorrhage. A definitive diagnosis of CHV
infection centers on demonstration of virus, viral antigen, or nucleic acids by PCR,
electron microscopy, or immunohistochemical techniques. PCR assays also can be
performed on ocular, nasal, pharyngeal, vaginal, or preputial swabs collected from
older puppies and adults. Serologic testing for neutralizing antibodies confirms
exposure but not necessarily active infection.
Treatment :
Treatment is supportive but often ineffective at preventing neonatal losses. Injection
of immune sera pooled from bitches that have had recent losses of litters might help
reduce mortality during outbreaks. Keeping puppies warm and hydrated can lessen
mortality in affected litters, primarily by limiting the spread of infection among
uninvolved puppies

infectious canine hepatitis

Cause :
Canine adenovirus type 1 (CAV-1),Infection occurs after oronasal exposure to virus-
contaminated body secretions and excretions and environmental fomites. Unlike
canine distemper virus, CAV-1 is not airborne. The incubation period is 4 to 9 days.
Virus shedding occurs during acute infection in all body secretions (saliva,
respiratory) and excretions (feces, urine) and is shed in the urine of dogs that have
recovered from clinical disease for up to 6 to 9 months. Infected urine therefore seems
to be the most important source of virus transmission.
Pathogenesis:
CAV-1 causes systemic infection, with a tropism for endothelial cells, epithelial cells,
and hepatocytes. After exposure, CAV-1 replicates in lymphoid tissue of the tonsils
and regional lymph nodes. Viremia follows 3 to 4 days post-infection, leading to
infection of other tissues. Direct cytopathic effects of the virus in the liver, eyes, and
kidney contribute to early clinical signs, which can become apparent in naïve dogs 4
to 9 days after exposure. Hemorrhages, which can be seen in many tissues, are the
result of vascular damage after viral replication in endothelial cells. The extent of
hepatic necrosis is a function of the level of antiviral antibody present at the time of
infection: animals with minimal antibody exhibit extensive necrosis that often is fatal;
those with high levels of antibody exhibit minimal clinical signs; and those with
intermediate antibody levels are susceptible to persistent hepatic inflammation.
Clinical signs of corneal edema and anterior uveitis (“blue eye”) initially develop as a
consequence of the inflammation following infection of corneal endothelial cells and
the deposition of immune complexes (hypersensitivity reaction type III) as the
antibody response to the virus increases.
Clinical signs :
Dogs of all ages are susceptible to CAV-1 infection and disease; however, most dogs
are infected early in life. Initial clinical signs include fever, depression, and lethargy.
Later, development of signs of abdominal discomfort, mucous membrane pallor, and
inflammation of the tonsils and pharynx with tonsillar and cervical lymph node
enlargement occur. Leukopenia develops and persists until the febrile period is
over.Abdominal fluid and hepatomegaly can be detected in some dogs. Laryngitis,
tracheitis, pneumonia, coughing, vomiting, and diarrhea occur in some. In severe
cases, petechial and ecchymotic hemorrhages and epistaxis can develop from
coagulation abnormalities secondary to hepatic dysfunction and disseminated
intravascular coagulation (DIC). Icterus is uncommon despite the presence of hepatic
necrosis. Neurologic signs can be seen as a consequence of hepatic encephalopathy or
CNS infection; serum bile acid or plasma ammonia concentrations, if elevated, would
support hepatic encephalopathy as a cause of neurologic signs. Dogs with severe
disease can die within hours of showing clinical signs, whereas dogs with less severe
disease can exhibit clinical improvement 5 to 7 days after onset of clinical signs.
Anterior uveitis and glomerulonephritis from deposition of immune complexes can
occur within a month of recovery.
Diagnosis :
The diagnosis of ICH usually is based on finding evidence of acute hepatic disease in
a dog with a poor vaccination history. No specific laboratory abnormalities are
pathognomonic for CAV-1 infection. There can be leukopenia or leukocytosis
depending on whether the patient is seen early or later in the course of disease,
respectively. Thrombocytopenia is possible and could contribute to bleeding disorders
in the setting of DIC or abnormal platelet function. Increases in serum alanine
aminotransferase (ALT) and alkaline phosphate (ALP) activities are expected, but the
magnitude of activity will depend on the extent of hepatic necrosis and the timing of
sample collection. Prolongations of activated partial thromboplastin time (aPTT) and
prothrombin time (PT) are common as a result of decreased hepatic synthesis of
coagulation factors, DIC, or both. Proteinuria also is expected as a sequel to renal
injury during viremia or immune complex injury later in the course of disease.
Definitive diagnosis of CAV-1 infection can be established by PCR performed on
secretions or excretions; ocular, nasal, and pharyngeal swabs; and tissues. PCR assays
are sensitive and can differentiate CAV-1 from CAV-2. Serologic titers and tissue
staining by immunofluorescent antibody and immunohistochemistry cannot
distinguish between CAV-1 and CAV-2. Intranuclear inclusion bodies observed
during cytologic or histologic examination of tissue, particularly the liver, can be
strongly supportive of the diagnosis.
Treatment :
Therapy is directed at provision of supportive care and management of clinical signs
and complications. Intravenous fluid therapy to replace losses from vomiting or
diarrhea is important, as is administration of blood products to manage the
complications of hemorrhage and DIC. In patients with neurologic signs from hepatic
encephalopathy, administration of lactulose via enema (or orally if the patient is not
vomiting) can help reduce circulating concentrations of encephalotoxins.

Canine infectious respiratory disease

Kennel cough
 ( infectious tracheobronchitits )
Etiology :
Several pathogens have been associated with the disease complex, with canine
parainfluenza virus (CPIV), canine adenovirus type 2 (CAV-2) and canine
herpesvirus 1 (CHV-1) traditionally considered the main viral causes, often in
conjunction with or preceding Bordetella bronchiseptica infection. 1-3 Clinical signs
such as coughing, nasal discharge and dyspnea are rarely associated with a single
pathogen and more often attributed to multiple agents which act sequentially or
synergistically to cause disease.
Pathogenesis :
ll the described respiratory viruses are transmitted by oronasal exposure through
direct contact with viruscontaminated respiratory secretions and environmental
fomites. Transmission can follow inhalation of aerosolized respiratory droplets
generated by sneezing or coughing. CHV-1 is also transmitted in genital secretions
and transplacentally. The incubation period ranges from 3 to 10 days, and virus
shedding in respiratory secretions generally ceases within 10 days of primary
infections, or in the case of CHV-1, reactivation of latent infection. In most dogs with
CIRD, initial infection takes place in the ciliated epithelial cells (and sometimes
goblet cells) of the upper respiratory tract and, for most uncomplicated viral
infections, seldom spreads further than the nasal cavity, sinuses, trachea and perhaps
bronchi, . Viral replication causes loss of coordinated beating of cilia, followed by
ciliostasis, and later loss of cilia, In primary viral infections, dogs can be
asymptomatic or have mild clinical disease consisting of rhinitis, sinusitis, tracheitis,
and bronchitis, or a combination of these. CIV is an exception in that it also seems to
result in a greater incidence of lower respiratory tract involvement and infected dogs
develop necrotizing tracheitis, bronchitis and in some cases also bronchiolitis and
pneumonia.
In uncomplicated viral infections, ciliated cells are replaced from a reserve stem cell
population. This process takes time and often the ciliated cells are replaced initially by
goblet cells (hyperplasia) before the differentiation pathway allows production of
ciliated epithelium. It is during this early phase of the viral infection that the main
defense of the upper respiratory tract, the “mucociliary escalator,” is rendered
ineffective. This can allow secondary pathogens, principally bacteria, to invade and
establish infection.
bronchiseptica produces a range of toxins to aid colonization and infection, such as
tracheal cytotoxin that induces ciliostasis, and adenylate cyclase that inhibits
neutrophil phagocytosis. Infection with CPIV or CRCoV creates an environment in
which Bordetella, which may be carried harmlessly in the upper tract, colonizes and
invades.
Clinical signs :
cough that can be very loud, persistent, and usually has been noted for a few days,
Appetite can be decreased slightly but anorexia of 24 hours' duration or longer is very
uncommon except in patients showing other, more serious abnormalities to suggest
systemic inflammation and/or complications such as pneumonia.Pulmonary
auscultation can reveal increased bronchovesicular sounds but wheezes and crackles
are very uncommon. Tracheal sensitivity is a frequent finding, and a cough often can
be elicited with mild tracheal palpation. if it does not occur spontaneously during the
exam. The intensity and sound of the cough often are much more severe (and of
greater concern to the owner) than any other respiratory, or any systemic, effects of
the disease. Likewise, ocular discharge is usually limited to a mild serous discharge if
there is one at all. Mucopurulent discharges warrant further evaluation. Mucopurulent
nasal discharge is not expected in uncomplicated cases; its presence suggests canine
distemper infection (see ch. 228), secondary bacterial pneumonia (see ch. 242), or
virulent disease with or without immunosuppression. Coughing is usually not
associated with significant phlegm or material produced at the end of tussive gagging.
Occasionally, a small amount of white phlegm is produced. Increased expectoration
suggests a deeper or more serious problem that could warrant further evaluation.
Diagnosis :
. A complete blood count can be evaluated for a left shift and/or toxic changes to
neutrophils, which would suggest systemic inflammation.Advanced diagnostic testing
to isolate the causative pathogen rarely is undertaken in mild cases without systemic
signs. In patients with radiographic evidence of pneumonia, sampling for bacterial
culture and sensitivity is warranted.
patients showing no other abnormalities beyond a cough are treated empirically
without diagnostic testing, and the owner is instructed to return if the cough does not
resolve after 7 days or at any time if additional clinical signs emerge.
Treatment :
Therapeutic options likewise are
selected based on the severity of
the patient's signs. Cough that is
distressing to the owner and/or the
patient can be treated with
antitussives (e.g., hydrocodone
0.25 mg/kg PO q 6-8 h PRN) if no
other clinical signs are present.
Over-the-counter antitussive
agents or antihistamines can
behelpful in making the owner
cognizant of the problem and
occasionally alleviate some of the
more racking efforts at coughing,
perhaps via sedation. Antibacterial
therapy is controversial because
Bordetella and Mycoplasma often
are present in healthy dogs; their
roles as pathogens in a specific
case, the need for their eradication,
and their susceptibility profiles,
often are unproven. Doxycycline
(10 mg/kg PO q 12 h × 14-21 days in adults, 7-9 days in puppies to reduce risk of
dental discoloration) has efficacy against both Bordetella and Mycoplasma;
minocycline, amoxicillin-clavulanate, or trimethoprim-sulfa also have been used for
Bordetella, whereas fluoroquinolones have been used for Mycoplasma. The usual
precautions regarding antibiotics should be recognized and fluoroquinolone use in
growing puppies is contraindicated. Supportive care and monitoring are implemented
if needed for dogs with pneumonia or other complications.
Feline Upper Respiratory Infections
Causes :
Feline viral respiratory disease is most commonly seen where cats are grouped
together, such as in breeding and boarding catteries, and in rescue shelters. The two
main causes of viral respiratory disease in cats are feline herpesvirus (FeHV-1) (feline
rhinotracheitis virus) and feline calicivirus (FCV). FeHV-1 generally induces a more
severe disease than FCV, but FCV appears to be more common. Bacterial pathogens
such as Bordetella bronchiseptica, Chlamydia felis, and possibly Mycoplasma felis,
are also involved in infectious respiratory and ocular disease in cats.cats are
susceptible to highly pathogenic and zoonotic avian influenza H5N1.
Clinical signs :
FeHV-1 causes upper respiratory tract (URT) disease, with oculonasal discharges,
conjunctivitis, sneezing, and sometimes hypersalivation and coughing. Occasionally,
more severe signs including pneumonia and generalized disease may be seen,
particularly in young or debilitated animals. Viral replication can also lead to
osteolytic changes in the turbinate bones that are believed to predispose some cats to
develop more chronic rhinitis. Abortion occurs rarely, and is probably due to severe
systemic disease and not to the virus itself. The role of FeHV-1 in conjunctivitis and,
in some cases, ulcerative keratitis, has
long been known. However, improved
viral detection using polymerase chain
reaction (PCR) has led to increasing
recognition of this role in the acute
disease as well as in more chronic
ocular lesions such as stromal keratitis.
The role of FeHV-1 in other ocular
conditions such as eosinophilic
keratitis, corneal sequestration, and
uveitis is less clear. Skin ulcers and an
ulcerative facial and nasal dermatitis
characterized by eosinophilic
infiltration.
In FCV infection, considerable strain
diversity may lead to some variation in
clinical signs. The most characteristic
sign is oral ulceration, typically on the
tongue, but lesions may also occur
elsewhere in the mouth or on the skin.
Classic URT disease signs, such as
sneezing, ocular and nasal discharges
and conjunctivitis, also commonly
occur, but these are generally milder than those seen with FeHV-1. With some strains
of FCV, lameness and pyrexia may be a feature, with or without respiratory/oral
disease; other strains may induce an interstitial pneumonia with infection of alveolar
macrophages, and some appear apathogenic. In addition, FCV infection is associated
with chronic stomatitis, although its precise role in the condition is not clear and other
factors are likely to be involved.
bronchiseptica can be a primary pathogen of cats, inducing mild clinical signs
consisting of fever, coughing, sneezing, oculonasal discharge and submandibular
lymphadenopathy. In addition to the above, field infection may also lead to more
severe disease, usually in younger kittens, including pneumonia with dyspnea,
cyanosis and death. It is likely that factors such as overcrowding and poor hygiene
may lead to higher challenge doses and more severe disease.
Infection with C. felis is generally associated with both acute and chronic
conjunctivitis, though upper and lower respiratory signs may sometimes also be seen.
Cases that start in one eye can rapidly progress to become bilateral. Affected eyes can
be markedly painful with profound conjunctival hyperemia, chemosis,
blepharospasm, and watery followed by mucoid or mucopurulent ocular discharges.
In some cases adhesions of the conjunctiva may develop although keratitis and
corneal ulcers, and other systemic illness, are not common and this can help
differentiate C. felis from FeHV-1. Whilst it is best considered an ocular pathogen
and not a respiratory pathogen, it is mentioned here as part of the differential for FCV
and FeHV-1, both of which can cause ocular as well as respiratory disease.
Diagnosis :
Diagnosis of FeHV-1 and FCV infection has classically been confirmed by virus
isolation in cell culture from oropharyngeal or conjunctival swabs, although
immunofluorescence has also been used, particularly for FeHV-1. In many
laboratories, PCR is used for diagnosis of FeHV-1, because it is significantly more
sensitive than traditional methods, especially in the chronic stages of the disease.Such
PCRs also allow an estimate of viral quantity, thereby allowing some laboratories to
stage disease and predict whether FeHV-1 is likely to be the cause of any acute signs,
or a more chronic infection. A comparison of PCR tests available does show
considerable differences in sensitivity between the published assays.
Diagnosis of B. bronchiseptica can be by isolation or PCR. As with FCV and FeHV-
1, recovered cats can continue to shed the organism, so care must be taken when
interpreting a positive result. The demonstration of B. bronchiseptica in samples
obtained by bronchoalveolar lavage from cats with lower respiratory signs is
considered to be diagnostic.
A PCR is the preferred method of diagnosing acute C. felis infection.
Treatment :
Primary treatment involves supportive therapy. Care should always be taken when
using antimicrobials in order to minimize the risk of resistance—the use of
antimicrobials should therefore be reserved for the more severe cases where bacterial
infection is clearly evident, and best follows local or national guidelines. For general
treatment of severe cases a broad spectrum antimicrobial may be indicated (e.g.,
potentiated amoxicillin) ; other drugs should be restricted to those cases where
resistance testing indicates their use. Tetracyclines are generally indicated if B.
bronchiseptica or C. felis is involved; in the youngest kittens, potentiated amoxicillin
may be preferred to avoid potential side-effects. For C. felis, treatment should be
continued for two weeks after resolution of clinical signs to reduce the likelihood of
recrudescence.

Coronavirus infections
Coronaviruses are classified into 3 different antigenic groups. Group 1 contains,
among others, the canine enteric coronavirus (CECoV) and the feline coronavirus
(FCoV), while the canine respiratory coronavirus (CRCoV) belongs to group 2.
Coronaviruses mutate easily, and mutation can result in more virulent strains; this has
been shown for CECoV and FCoV, resulting in fatal pantropic canine coronavirus
(pantropic CCoV) infection or feline infectious peritonitis (FIP), respectively.
Canine Enteric Coronavirus, Including Pantropic
Coronavirus :
CECoV first was isolated in dogs with acute enteritis in a canine military unit in
Germany,and experimental administration of the isolated strain to young dogs
reproduced the gastrointestinal (GI) signs.
CECoV is widespread in the dog population, primarily in kennels and
shelters.However, the true importance of CECoV as a pathogen is unknown, since
many clinically healthy dogs shed CECoV.
Clinical Signs:
differentiation of CECoV from other infectious causes of enteritis is difficult, since
many healthy dogs shed CECoV. Therefore, concurrent presence of CECoV infection
and diarrhea is not proof of causation. 22 Infection usually is restricted to the
alimentary tract, with sudden onset of signs typical of GI involvement, including loss
of appetite, vomiting, diarrhea, dehydration, and rarely death. Fatal disease can occur
as a consequence of mixed infections, e.g., with canine parvovirus or canine
distemper virus.
Although CECoV usually is restricted to the enteric system, mutations can result in
systemic spread, leading to high mortality in puppies.
“pantropic CCoV” because it had acquired the ability to spread to other tissues. In
addition to GI signs, pantropic CCoV infection caused severe leukopenia, neurologic
signs (ataxia, seizures), and death within 2 days.At necropsy, lesions in lung, liver,
and renal tissues also were found in affected dogs.
Treatment and Prevention :
Treatment is supportive and needs to resolve dehydration , acidosis , and hypovolemic
shock .
Canine Respiratory Coronavirus
CRCoV is very closely related to the bovine coronavirus (BCoV)
Clinical signs :
CRCoV can be responsible for mild respiratory signs and it is one of the etiological
agents of canine infectious respiratory disease (CIRD), together with Bordetella
bronchiseptica, canine adenoviruses type 1 and type 2, canine parainfluenzavirus,
canine herpesvirus, reoviruses, canine pneumovirus, and influenza viruses.
CRCoV RNA was detected only in the respiratory tract of dogs with respiratory
signs, but not in healthy dogs, 44 confirming its pathogenicity. In addition, replication
in the respiratory epithelium can damage the mucociliary system, 4 and this can lead
to a more severe clinical course of infections caused by other respiratory pathogens.
Treatment and Prevention
Symptomatic treatment usually leads to complete cure.
 Feline Coronavirus Infection and Feline Infectious
Peritonitis ( FIP )
. FCoV is transmitted by the fecal-oral route between felids, but is not infectious for
other species (including humans). FCoV usually does not cause clinical signs, and
only rarely is considered to be responsible for transient and mild diarrhea with or
without vomiting, 48 due to replication of FCoV in enterocytes.. Occasionally, the
virus can be responsible for severe, acute or chronic vomiting and/or diarrhea with
weight loss, which can be unresponsive to treatment and continue for months.
FIP is a fatal, immune-mediated disease and it is the most common infectious cause of
death of cats.There is increasing evidence that FIP develops after spontaneous
mutations of the genome of nonpathogenic FCoV within infected cats.These
mutations allow for successful virus replication in macrophages, 58 which is regarded
as a key event in the pathogenesis of FIP.

If a cat fails to eliminate the cells infected with the mutated virus, the presence of the
virus within macrophages initiates the ultimately fatal immune-mediated reaction that
defines FIP. In this aberrant modulation of the immune system, overproduction of
proinflammatory cytokines plays an important role, such as through activation of the
p38 MAPK pathway that regulates production of tumor necrosis factoralpha (TNF-
alpha) and interleukin-1-beta.Granulomatous lesions in the target organs also are
caused by overproduction of cytokines by infected macrophages, including neutrophil
survival factors (TNF-alpha, GMCSF, G-CSF), that lead to systemic activation of
neutrophils (such as increased expression if the alpha-chain of macrophage-1 antigen
[Mac-1]) causing them to extravasate and form granulomas. In addition, cats with FIP
have a severe suppression of natural killer cells and regulatory T cells, leading to a
decreased capacity of the immune system to battle the virus and suppress
immunopathologic functions. Granulomatous lesions can occur in the central nervous
system, eyes, and parenchymatous organs (including the intestine, commonly at the
ileocecal junction, appearing as masses in the abdominal cavity). Vasculitis leads to
fluid accumulation in body cavities, including the pleural and peritoneal spaces and
even the pericardium. In addition, some unusual manifestations have been described,
such as a mediastinal cyst-like mass in the thorax, skin fragility syndrome, 82 and
other skin lesions (e.g., skin papules and nodules, pododermatitis), orchitis or
priapism (with FCoV antigen immunohistochemically being detected in penile tissue).

Diagnosis :
Once the clinical disease FIP develops, it almost always leads to death within a few
days or weeks, and currently there is no treatment with proven efficacy.
At present, necropsy or immunostaining of FCoV antigen (immunohistochemistry) in
tissue samples obtained by laparotomy are considered the gold standard for the
diagnosis of FIP. 91-94 Thus, the definitive diagnosis can only be achieved with
invasive laparotomy and biopsies of multiple organs, or might not be possible at all.
Laboratory values often are altered in cats with FIP, but the changes are not
pathognomonic. Lymphopenia often is present, but in combination with neutrophilia
in sick cats, it commonly is part of a typical stress leukogram. A common finding in
cats with FIP is an increase in total serum protein concentration caused by a rise in
globulins, mainly gamma-globulins. 93,95-98 One mechanism leading to this massive
antibody production is an overproduction of B cell differentiation/survival factors by
virus-infected macrophages that promote B cell differentiation into plasma cells. 99
The hyperglobulinemia, together with the commonlyobserved hypoalbuminemia,
leads to a low albumin-to-globulin ratio. A low albumin-to-globulin ratio should raise
the suspicion of FIP, but is never diagnostic by itself.

Analysis of Effusion Fluid

Whenever effusion can be detected somewhere, the next diagnostic step always is to
sample and analyze the fluid, because tests on effusion have a much higher diagnostic
value than tests performed on blood. In general, half of cats with body cavity effusion
suffer from FIP. Although effusions of clear yellow color and sticky consistency often
are considered “typical,” the presence of this type of fluid alone is not diagnostic.
Sometimes the fluid has a totally different appearance and, for example, cases of FIP
with pure chylous effusion have been reported. The effusion's protein content usually
is high (>3.5 g/dL [>35 g/L]) and consistent with an exudate, whereas the cellular
content is rather low and resembles that of a modified transudate. Other diseases
causing similar effusions include lymphoma, heart failure, cholangiohepatitis, and
bacterial peritonitis or pleuritis. Cytologic evaluation of the effusion in cats with FIP
usually shows a pyogranulomatous inflammation with a predominance of
macrophages and neutrophils. Cytologic findings can appear similar in cats with
bacterial serositis (although in these cases, cell counts usually are higher) or with
lymphoma (although in these cases, malignant cells usually are present). A simple,
inexpensive, and very robust method (fluid can be stored in the refrigerator for at least
weeks before performing the test) for evaluating the effusion,
 the “Rivalta's test,” can help to differentiate FIP from effusions of other origins.
Positivity is caused by not only the high protein content, but also other components,
such as high concentrations of fibrin and inflammatory mediators. The Rivalta's test
had a sensitivity of 91.3% and a specificity of 65.5% in a recent study of 851 cats,
with a high positive predictive value of almost 90% in cats. Thus, a negative Rivalta's
test makes FIP very unlikely; a positive Rivalta's test at least increases the likelihood
of FIP, especially in a young cat. Falsepositive Rivalta's test results can occur in cats
with bacterial serositis or lymphoma; those effusions, however, can usually be
differentiated through cytologic evaluation and/or bacterial culture.
Treatment and Management
Virtually every cat with confirmed FIP dies from the disease. However, some cats
can survive for several months and enjoy some quality of life with symptomatic
treatment.
Supportive Treatment
As FIP is an immune-mediated disease, supportive treatment is aimed at controlling
the immune response to FCoV, and the most successful approach consists of high
dosages of immune-suppressive and antiinflammatory drugs that slow down disease
progression, such as prednisolone (2-4 mg/kg PO q 24 h). Although glucocorticoids
have been used in nearly every published case, their effect never has been
substantiated in controlled studies. If effusion is present, some cats benefit from daily
centesis for removal of the fluid (see ch. 90 and 102), and injection of dexamethasone
into the abdominal or thoracic cavity (1 mg/kg q 24 h until effusion is no longer
produced). Cyclophosphamide (2-4 mg/kg PO 4 times/week), alone or in combination
with glucocorticoid, sometimes is used but there are no data available on its efficacy.
Cats should also be treated with broad-spectrum antibiotics and supportive therapy
(e.g., fluids; see ch. 129) in addition to the immunosuppressive treatment. A
thromboxane synthetase inhibitor (ozagrel hydrochloride) that inhibits platelet
aggregation and cytokine release has been used in 2 cats with some improvement of
clinical signs. 127 Propentofylline has been used because it appears to down-regulate
proinflammatory cytokines, which in turn can reduce vasculitis. However, in a
placebo-controlled, double-blind study in cats with confirmed FIP, there was no
significant difference in survival time, quality of life, or any clinical or laboratory
parameter in cats treated with this drug versus cats receiving placebo.
 Liptospirosis
It is caused by spirochetes of the genus Leptospira. Leptospires are thin, elongated,
highly motile, helically coiled organisms that can be differentiated from other
spirochetes by their distinct hooked ends, Leptospires have Gram-negative staining
properties but have phenotypic features of both Gram-negative and Gram-positive
bacteria. Genotypic classification based on DNA hybridization has defined 20 species
of Leptospira including 9 pathogenic, saprophytic, and intermediate species,
Small rodents are considered the most important reservoir hosts, but it is likely that a
large spectrum of animals, including dogs and cats and also humans, can act as
reservoir hosts for pathogenic Leptospira. Hosts become infected either by direct
contact of mucous membranes or broken skin with urine from infected animals, or
indirectly, via contact with contaminated soil or surface water.In contrast to reservoir
hosts, which typically show no clinical signs of illness, incidental hosts can develop
acute, severe, and potentially lethal disease.
Leptospirosis is a seasonal disease, with peak incidence during the warmer parts of
the year and a link to rainfall or flooding. As a consequence, seasonal patterns of
leptospirosis are dependent on regional climate. Dogs living in proximity to outdoor
water, who swim or drink from outdoor water sources, and who are exposed to
wildlife, have a higher risk of infection.Males, herding dogs, hounds, working dogs,
and mixed breeds have been reported to be at increased risk, no sex, age , breed

predisposition.

Pathogenic mechanisms :
After entering the host, pathogenic leptospires quickly establish a systemic infection
via hematogenous spread. Unlike bloodstream infections with other Gram-negative
bacteria, leptospires do not cause fulminant septic disease shortly after the onset of
infection. This has been attributed to the low endotoxic potential of leptospiral
lipopolysaccharide. During this initial phase, leptospires evade the host immune
response by binding inhibitors of complement activation on their surface.
Leptospiremia continues until the host mounts an effective acquired immune
response, which clears the organism from the bloodstream and most tissues.
Thereafter, leptospires can persist in immune-privileged sites, such as the eye and the
renal tubules. Leptospirosis is a multisystemic disease, particularly affecting the
kidneys and liver, but also many other organs, such as the lungs, spleen, endothelial
cells, uvea/retina, skeletal and heart muscle, meninges, pancreas, and the genital tract.
The exact mechanisms through which pathogenic leptospires cause organ dysfunction
and tissue damage are not known and can vary among different organ systems. While
vasculitis can be a feature in some cases of leptospirosis, most studies in humans and
experimental animals do not support vasculitis as a consistent primary event
responsible for tissue damage.
During the acute phase, the predominant renal lesions are those of an acute interstitial
nephritis, with tubular cell necrosis, apoptosis, and regeneration.Tubular lesions are
assumed to be due to direct effects of the organisms because they are generally
associated with the presence of Leptospira,Glomerular abnormalities have been
described in both dogs and experimental animals with leptospirosis and indicate
structural and functional glomerular involvement. Leptospires can cause a specific
hypokalemic, nonoliguric form of acute kidney injury due to inhibition of the tubular
Na + -K + ATPase. Hyposthenuria can occur due to an acquired vasopressin
resistance of the inner medullary collection ducts.
Hepatic lesions described in humans and animals with leptospirosis include a
cholestatic hepatitis with complete or partial liver-plate disruption, hepatocellular
necrosis, binucleation of hepatocytes, periportal edema with inflammatory cell
infiltration, and proliferation of Kupffer cells along the sinusoidal lining.
Hyperbilirubinemia does not appear to be correlated with hepatocellular necrosis in
humans. In experimentally infected hamsters, hyperbilirubinemia coincided with the
invasion of hepatic intercellular junctions by migrating leptospires and subsequent
disruption of bile canaliculi. In human patients, both icteric and nonicteric forms of
leptospirosis have been described, the icteric form being considered more severe and
rapidly progressive. Similarly, a serum bilirubin of ≥0.6 mg/dL (≥10 micromole/L;
reference range 0.03-0.2 mg/dL [0.5-4.0 micromole/L]) was strongly associated with
death or euthanasia in a cohort of 254 dogs with acute leptospirosis.
Leptospiral pulmonary hemorrhage syndrome (LPHS) increasingly has been
recognized in humans, dogs, and many other species in recent years and has become a
major cause of mortality. 16,33 LPHS lung tissue shows various degrees of intra-
alveolar hemorrhage in the absence of a marked inflammatory cell infiltrate or
vasculitis. Intra-alveolar edema, fibrin, and hyaline membranes, which are
characteristic of disorders with diffuse alveolar damage, such as acute respiratory
distress syndrome (ARDS), also can be present but are not a predominant feature. In
contrast to what is seen in liver and kidney, few leptospires are observed in affected
lung tissue in immunocompetent hosts and they do not colocalize with the pulmonary
lesions. Several hypotheses, including systemic inflammatory, immune-mediated,
and direct leptospiral effects, currently are under investigation. It is likely that the
pathogenic mechanisms of LPHS are multifactorial, with both host- and pathogen-
related factors playing a role. It has been suggested that introduction of clones with
enhanced virulence might be a contributing factor to the recent emergence of LPHS.
However, at present, available evidence to link specific leptospiral serovars with
particular clinical manifestations in both humans and animals is weak.This might be
partially due to the limitations of current serological tests to correctly identify the
infecting serogroup or serovar in acutely infected patients.
Clinical findings :
The clinical signs of leptospirosis are nonspecific and most commonly relate to acute
renal and hepatic injury. The most common clinical signs reported in dogs are
anorexia, vomiting, lethargy, abdominal pain, diarrhea, jaundice, dehydration,
stiffness and musculoskeletal pain, fever or hypothermia, dyspnea and tachypnea,
weakness, and weight loss. Polyuria and polydipsia are common, while oliguria or
anuria were present in approximately 30% of dogs with acute leptospirosis in a
referral population. 16 In a recent study of a large cohort of dogs with acute
leptospirosis, the predominant clinical syndromes were renal (99.6%), hepatic (26%),
and pulmonary (76.7%). Signs consistent with disseminated intravascular coagulation
(DIC) were present in 18.2% of dogs. This study reflects the recent emergence of
LPHS as a common complication in acute canine leptospirosis. Isolated hepatic
involvement was very uncommon in this cohort but has been described in 14% of
dogs diagnosed with acute leptospirosis by others. Other clinical abnormalities can
include ventricular tachyarrhythmias, abdominal pain due to intussusception, ocular
signs, and skin calcifications. In contrast to large animal species, dogs rarely appear to
develop reproductive disorders associated with leptospiral infection. The role of
chronic leptospiral infection as a cause of chronic kidney disease in both cats and
dogs requires further studies. Progression of tubulointerstitial nephritis to tubular
atrophy and renal fibrosis has been described in dogs infected with serovar Canicola
and rats infected with serovar Icterohaemorrhagiae. In a recent study, cats with kidney
disease (acute and chronic) were more likely to have antibodies against Leptospira
spp. and to shed pathogenic leptospires in their urine than were cats without kidney
disease.

Hematology, Clinical Biochemistry, Urinalysis :

Mild to moderate anemia is present in approximately half of dogs with leptospirosis.
Causes of anemia can be 2338 blood loss via the respiratory or gastrointestinal (GI)
tract and anemia of inflammatory disease. Hemolysis due to the effect of leptospiral
toxins on erythrocytic membranes appears to be less common in dogs compared to
cattle. Neutrophilic leukocytosis, with neutrophilia, left shift, lymphopenia, and
monocytosis are often present. Mild to severe thrombocytopenia is common in dogs
with leptospirosis and can be caused by platelet or endothelial activation, immune-
mediated destruction, or splenic sequestration. Blood urea nitrogen and creatinine
concentrations are increased in the majority of dogs at presentation or during the
course of disease. Hepatic injury as evidenced by increases in the activity of serum
alanine aminotransferase (ALT), aspartate aminotransferase, alkaline phosphatase
(ALP), and hyperbilirubinemia occurs almost exclusively in conjunction with
azotemia. Increases in serum activity of ALP and total bilirubin are more frequent
than are increases in serum ALT activity. Electrolyte abnormalities, such as hypo- and
hyperkalemia, hyper- and hypophosphatemia, hyponatremia, and hypochloremia, are
common in canine leptospirosis and usually parallel the degree of renal and GI
dysfunction. Hypokalemia can occur due to renal and/or GI losses, as well as
potassium wasting due to the leptospiral-induced inhibition of Na + -K + -ATPase.
Hemostatic disorders in dogs with leptospirosis vary widely in severity and are
multifactorial. Hypocoagulable conditions from DIC, failure of coagulation factor
synthesis, thrombocytopenia, and thrombocytopathy compete with prothrombotic
conditions associated with inflammation and renal disease. Urinalysis reveals
isosthenuria in the majority of dogs with leptospirosis, but hyposthenuria also has
been described. Glucosuria, hematuria, pyuria, and granular casts can be present.
Proteinuria is present in many affected dogs and can be due to glomerular and/or
tubular dysfunction. The width of leptospires is below the resolution of light
microscopy and therefore, the organisms are not typically visible by routine urinary
sediment examination.
Diagnostic Imaging :
Radiographic and computed tomographic changes in dogs with LPHS have been
described. Initially, pulmonary changes appear in the caudodorsal parts of the lung
fields and range from a mild interstitial to severe reticulonodular pattern with focal
alveolar infiltrates. Mild mediastinal and/or pleural effusion can be present. The most
common abdominal sonographic findings relate to the kidneys and include cortical
hyperechogenicity, renomegaly, mild pyelectasia, a medullary band of
hyperechogenicity, and mild perirenal fluid accumulation.Other findings can include
hepatomegaly, splenomegaly, ascites, enlargement and hypoechogenicity of the
pancreas, thickening of the gastric and (rarely) intestinal walls, and mild
lymphadenomegaly.
Microscopic Agglutination Test (MAT)
Despite marked limitations, the MAT still is considered the gold standard test for
confirmation of acute leptospirosis. The MAT is based on determining the ability of
serial dilutions of patient serum to agglutinate live leptospiral serovars in vitro. MAT
reactivity to a serovar suggests exposure to a serovar within the broader serogroup,
but not necessarily to the serovar tested. The panel of serovars ideally should be based
on antibody prevalence data in the relevant geographic location, as failure to include
the infecting serogroup can lead to false-negative results. MAT results are strongly
dependent on quality control in the laboratory, with considerable interlaboratory
variability, The MAT has marked limitations with regards to sensitivity, specificity,
and repeatability, especially if single titers are interpreted. Infected dogs can be
antibody negative in the acute phase of the disease, due to the normal delay in
appearance of serum antibodies. On the other hand, noninfected dogs vaccinated with
bi- or quadrivalent whole-cell antileptospiral vaccines can have postvaccinal titers of
1: 6400 or higher to both vaccinal and nonvaccinal serovars. While the majority of
vaccinated dogs has been shown to become antibody-negative by week 15
postvaccination, vaccinal titers can persist for 12 months in a small percentage of
dogs. 75 Reactivity of antileptospiral antibodies with multiple serogroups often
prevents the determination of the infecting serogroup. Moreover, the serogroup with
the highest MAT titer can vary over time, indicating that the MAT does not reliably
predict the infecting serogroup in acutely infected animals.
However, the best way to confirm a recent infection using MAT is to test paired
samples, collected one or two weeks apart, which greatly increases the sensitivity of
the MAT.

Treatment :
Effective treatment of canine leptospirosis consists of appropriate antimicrobial
therapy and supportive care for the different organ systems involved. Leptospires are
susceptible to a wide range of antibiotics in vitro, but the capacity of antibiotics to
completely eradicate infection in vivo, in particular renal carriage, varies.Penicillin
and its derivatives have been shown to reduce leptospiremia but fail to reliably clear
the organisms from the kidney.Doxycycline has been shown to clear leptospires from
blood and organs including kidneys in rodent models. 83 Therefore, currently it is
recommended to treat dogs with leptospirosis with oral doxycycline (5 mg/kg PO q 12
h or 10 mg/kg PO q 24 h) for 14 days. Unfortunately, doxycycline often is not well
tolerated in the early phase of treatment because GI signs are common in acute
leptospirosis. In these cases, initial therapy with an intravenous penicillin derivative
(e.g., penicillin G, ampicillin, amoxicillin) often is recommended until doxycycline
can be used. Macrolide antibiotics such as azithromycin and thirdgeneration
cephalosporins have been assessed in animal models and have been proposed as
alternative treatment in humans who cannot tolerate doxycycline treatment.
Treatment of LPHS largely is supportive. Radiographic screening is recommended
even in the absence of respiratory signs, in order to detect early lesions and implement
precautionary measures. These include avoidance of stress and
overhydration/hypervolemia and control of systemic hypertension. Depending on the
severity of pulmonary hemorrhage, oxygen therapy and in severe cases, mechanical
ventilation may be required . Based on the hypothesis of an immune-mediated
mechanism of LPHS, the efficacy of immunomodulatory treatments has been
assessed. Results of small and often not well-controlled clinical trials in humans
suggest that immunosuppressive treatment with methylprednisolone, dexamethasone
alone or in combination with desmopressin, or plasmapheresis, can improve survival
in patients with LPHS. Further studies have to be performed in order to determine
whether immunosuppression is an effective treatment for LPHS in dogs.
After initial stabilization, renal recovery can continue for several months. A follow-up
study of dogs with leptospirosis indicated that ≈50% of dogs surviving the acute
phase of the disease displayed impairment of renal function more than one year after
hospital discharge. Long-term monitoring of renal function therefore is strongly
recommended in these dogs. Concurrent infection of other dogs that reside in the
same household can occur, probably following infection from the same environmental
source. Treatment of dogs living with dogs diagnosed with leptospirosis with
doxycycline for 2 weeks therefore is currently recommended.

Leptospirosis in Cats
Cats can become infected with leptospires and can shed leptospires in their urine, but
clinical signs of acute disease are rarely described. In experimentally and naturally
infected cats, interstitial nephritis is the most consistent histopathologic finding, and
in one study, cats with kidney disease (acute and chronic) were more likely to have
serum antibodies against Leptospira spp. and to shed pathogenic leptospires in their
urine.Therefore, the role of healthy cats as reservoir hosts, as well as the role of
leptospirosis as a clinical disease in cats, deserves further study and might have been
underestimated in the past.
 Clostridial enterotoxicosis
A syndrome characterized by diarrhea in dogs and cats associated with the production
of enterotoxin by normal bacterial flora in the GI tract.

Cause :
Clostridium perfringens—common enteric inhabitant generally found in the
vegetative form living in a symbiotic relationship with the host
■ Certain strains of C. perfringens (generally type A based on PCR analysis)—
produce enterotoxin that binds to the enteric mucosa, alters cell permeability, and
results in cell damage with subsequent local enterocyte death, but no systemic illness
■ C. perfringens enterotoxin—probably associated with enteric sporulation
■ Enterotoxin production—a number of intrinsic host-related factors influence
enterotoxin production and pathogenicity of C. perfringens
■ Pathogenicity of C. perfringens—may depend on the metabolic, mucosal, and
immunologic integrity of the GI tract
■ IgA deficiency—possibly
■ Alkaline intestinal luminal environment—promotes C. perfringens sporulation and
enterotoxin production
■ Incidence—unknown
■ Chronic large bowel diarrhea—suspected that up to 20% of cases of chronic large
bowel diarrhea in dogs are C. perfringens–related
■ Cats—infection less common than in dogs.
Signalment / history :
■ Most animals tend to be middle-aged or older
■ No sex or breed predilections
■ Historically, large-bowel diarrhea with mucus
■ Small amounts of fresh blood
■ Tenesmus with increased frequency commonly reported
■ Small-bowel diarrhea signs (large volume of watery stool) also reported
■ Vomiting
■ Flatulence
■ Abdominal discomfort
■ Stress factors to the GI tract, dietary change, concurrent disease, or hospitalization
may precipitate signs.

■ Signs usually associated with either:

■ An acquired acute, self-limiting large-bowel diarrhea lasting for 5–7 days
■ Chronic intermittent diarrhea
■ Signs associated with other GI or non–GI tract disease
■ Chronic disease—often characterized by intermittent episodes occurring every 2–4
weeks that may persist for months to years
■ The syndrome may develop from a nosocomial (hospital-acquired) infection, with
signs developing during or shortly following hospitalization or kennel boarding.
■ C. perfringens—occasionally associated with cases of parvovirus and acute
hemorrhagic gastroenteritis.
Fecalcytology—high numbers of C. perfringens endospores in the feces do not always
correlate with clinical disease or fecal enterotoxin assay
Cytologic examination—performed by making a thin fecal smear on a microscope
slide, air-drying or heat-fixing, and staining with Diff-Quick or Wright’s stain
Treatment :

■ High-fiber diets—either soluble (or fermentable) or insoluble fiber, often result in

clinical improvement
■ High-fiber diets—reduce enteric clostridial numbers, acidify the distal intestine,
thus limiting C. perfringens sporulation and enterotoxin production

Tylosin is drug of choice in long-term management ( chronic cases ).

 Bordetellosis
A contagious bacterial disease of cats primarily causing respiratory abnormalities and
establishing chronic infections.
Causes :
■ Bordetella bronchiseptica—a small,
aerobic gram-negative coccobacillus
■ Infections spread rapidly—usually by
direct contact from seemingly healthy cats to
others in the same environment
■ Infected queens may not shed organisms
prepartum but serve as a source of infection
to newborn kittens when shedding begins
postpartum.
■ Stress may serve as a cause of shedding.
Clinical signs :
Most severe in kittens less than 6weeks
Occurs at all ages and often with pre-
existing, subclinical airway disease
■ Signs—usually begin ∼5 days after
exposure to infecting agent
■ Bacterial agent—spreads rapidly from apparently healthy cats to others in the same
environment
■ Fever ■ Sneezing ■ Nasal discharge ■ Mandibular lymphadenopathy
■ Spontaneous or induced cough—characteristic of uncomplicated disease.
Severe Disease
■ Fever—may note constant, low-grade, or fluctuating fever (39.4–40◦C [103–
104◦F])
■ Cough—usually moist and productive
■ Nasal discharge ■ Lethargy ■ Anorexia
■ Dyspnea as a result of severe pneumonia that can lead to death
■ Lung sounds—often normal, but may detect increased intensity of normal sounds,
crackles, or (less frequently) wheezes.
Diagnosis :
■ CBC—neutrophilic leukocytosis with a left shift in cases of severe pneumonia
■ Radiologic examination—useful for ruling out noninfectious causes; may
demonstrate an interstitial and alveolar lung pattern with a cranioventral distribution
typical of bacterial pneumonia; a diffuse interstitial lung pattern typical of viral
pneumonia; a mixed lung pattern (combination of alveolar, interstitial, and
peribronchial lung patterns)
Treatment :
■ Antibiotic therapy—Ideally, antibiotic should be selected based on culture and
sensitivity results.
■ Amoxicillin/clavulanic acid—good for kittens
■ Doxycycline—very effective, and is the drug of choice
■ Tetracyclines—organism usually very susceptible

Salmonellosis
A bacterial disease that causes enteritis, septicemia, and abortions in both cats and
dogs
Causes :
■ Salmonella spp.—gram-negative bacteria of many different serotypes
■ The bacterium colonizes the small intestine (ileum), then invades enterocytes before
entering and multiplying in the lamina propria and local mesenteric lymph nodes.
■ Cytotoxin and enterotoxin are produced, causing inflammation and prostaglandin
synthesis and leads to the development of a secretory diarrhea and mucosal sloughing.
■ In uncomplicated enteritis, organisms are prevented from spreading from the
mesenteric lymph nodes—Patients develop diarrhea, vomiting, and dehydration as a
result of secretory diarrhea.
■ Focal extraintestinal infections—can result in abortion, joint disease, or
endotoxemia with organ infarction, generalized thrombosis, DIC, and death
Dogs
■ Most clinical disease seen in young or pregnant animals
■ Common in racing greyhounds and sled dogs due to raw meat diets; presence of
Salmonella does not necessarily imply infection but could reflect transient pass-
through.
Cats
■ Have a high natural resistance—especially older cats
■ Shelter cats—more likely to have Salmonella spp. in feces
■ Pandemics of salmonellosis in migrating songbirds (usually S. typhimurium) in
spring—create epidemics in bird-hunting cats.
Pathogenesis
Salmonella infections begin with ingestion of organisms in contaminated food or
water, followed by invasion of M-cells in the Peyer's patches. Salmonella express
several fimbriae that contribute to their ability to adhere to intestinal epithelial cells.
29 Salmonella pathogenicity islands (SPI-1 and SPI-2) encode the genes necessary for
the invasion of intestinal epithelial cells, induction of intestinal secretory and
inflammatory responses, intracellular replication, and establishment of systemic
infection. 30 Salmonella spp. inject an array of bacterial effector molecules into host
cytoplasms, triggering reorganization of actin cytoskeletons and resultant membrane
ruffling. Cell internalization of Salmonella occurs within minutes of bacterial contact.
Invasion is followed by inflammation, influx of neutrophils and macrophages, and
consequent secretory diarrhea. This is likely mediated by activation of inositol-
signaling pathways within affected host cells. The presence or absence of additional
virulence factors plays an important role in determining whether septicemia occurs
Clinical signs :
Environmental factors:
■ Coprophagia spreads infection
■ Dehydrated (dry) pet food can harbor organism (semimoist not as likely) ■
Contaminated foods (pig ear dog treats)
■ Dense populations (research colonies, boarding facilities)
■ Hunting/stray animals—scavenge for food (exposure to organism in food, dead
animals, infected raw meat, song birds)
■ Historically—Patients may have diarrhea, vomiting, fever, and anorexia.
■ Vaginal discharge/abortion—may occur in dogs

Dogs
■ Most infections—subclinical (carrier state: Salmonella spp. shed in feces)
■ Clinical forms—varying from mild, to moderate, to severe are seen in
neonatal/immature puppies and pregnant bitches
■ Most adult carrier dogs—clinically normal
■ Gastroenteritis:
■ Anorexia ■ Malaise/lethargy ■ Depression
■ Fever ■ Diarrhea containing mucus and blood
■ As disease progresses—the patient becomes more dehydrated, with:
■ Abdominal pain ■ Tenesmus ■ Pale mucous membranes
■ Mesenteric lymphadenopathy ■ Weight loss
■ Gastroenteritis with bacteremia and septicemia, septic shock, or endotoxemia:
■ Pale mucous membranes ■ Weakness ■ Cardiovascular collapse
■ Tachycardia ■ Tachypnea.■ Death preceded by multiple organ failure
■ Focal extraintestinal infections—Conjunctivitis, metritis/abortion, cellulitis, and
pyothorax have been reported.

Cats
■ Adult cats—highly resistant to clinical disease
■ Neonatal/immature and immunocompromised animals—susceptible to disease
■ May exhibit a syndrome of a chronic febrile illness (without gastrointestinal signs):
■ Persistent fever
■ Prolonged illness with vague, nonspecific clinical signs and leukogram with a left
shift
■ Recovering patients—may exhibit chronic intermittent diarrhea for 3–4 weeks; may
shed Salmonella spp. in stool for 6 weeks or longer

Diagnosis :
CBC—variable; depends on stage of illness
■ Initially neutropenia—often with left shift and toxic neutrophils
■ Nonregenerative anemia ■ Lymphopenia ■ Thrombocytopenia
■ Serum biochemical profile—hypoalbuminemia and electrolyte abnormalities with
secretory diarrhea (metabolic acidosis, hypokalemia)
Treatment :
Neonates, Aged, and Debilitated Animals
■ Antimicrobials—indicated, but important to base selection on culture and
sensitivity results because Salmonella spp. are notoriously resistant to many agents
■ TMS ■ Amoxicillin ■ Enrofloxacin ■ Chloramphenicol
Asymptomatic Carrier State ■ Antimicrobials—contraindicated because: ■ Increases
the risk of resistance developing to the drugs
■ Prolongs the convalescent excretion period