CLIN101B: INTRODUCTION TO VETERINARY CLINICS

COMMON DISEASES IN SMALL ANIMALS

Dr. JAMES MIRANDILLA, DVM

TOPIC OUTLINE LESIONS

● Canine Distemper ● Thymic atrophy is a consistent postmortem finding in young puppies

● Infectious Canine Hepatitis infected with canine distemper virus.
● Canine Leptospirosis ● Hyperkeratosis of the nose and footpads is often found in dogs with
● Canine Parvoviral Infection neurologic signs.
● Canine Parainfluenza ● Depending on the extent of secondary bacterial infection,
● Canine Coronaviral Diarrhea bronchopneumonia, enteritis, and skin pustules also may be
● Rabies present.
● Kennel Cough ● In cases of acute to peracute death, exclusively respiratory
● Feline Viral Rhinotracheitis abnormalities may be found.
● Feline Caliciviral Infection ● Histologically, canine distemper virus produces necrosis of
● Feline Panleukopenia Virus lymphatic tissues, interstitial pneumonia, and cytoplasmic and
● Feline Chlamydiosis intranuclear inclusion bodies in respiratory, urinary, and GI
epithelium.
● Lesions found in the brains of dogs with neurologic complications
CANINE DISTEMPER include:
→ neuronal degeneration
● Canine distemper virus is a paramyxovirus closely related to the → gliosis
viruses of measles and rinderpest. → noninflammatory demyelination
● The fragile, enveloped, single-stranded RNA virus is relatively unstable → perivascular cuffing
outside the host. → nonsuppurative leptomeningitis
→ intranuclear inclusion bodies, predominantly within glial cells
MODE OF TRANSMISSION

● Infection is transmitted mainly via aerosol droplet secretions from DIAGNOSIS

infected animals.
● Some infected dogs may shed virus particles for several months. ● Preliminary diagnosis: clinical evaluation
● Confirmation: reverse transcriptase PCR (RT-PCR) and antibody
detection tests
CLINICAL SIGNS, SYMPTOMS, LESIONS
TREATMENT AND CONTROL

CLINICAL SIGNS AND SYMPTOMS

● Transient fever usually occurs 3–6 days after infection with canine
distemper virus, and there may be leukopenia (characterized by
lymphopenia) at this time; these clinical signs may go unnoticed or
may be accompanied by anorexia.
● The fever subsides for several days before a second fever occurs,
which may be accompanied by serous nasal discharge,
mucopurulent ocular discharge, lethargy, and anorexia.
● GI and respiratory signs, typically complicated by secondary
bacterial infections, may follow; rarely, pustular dermatitis may be
observed.
● TYPICAL NEUROLOGIC SIGNS
→ localized involuntary muscle twitching (myoclonus, chorea, flexor
spasm, hyperkinesia)
→ seizures, including salivation and chewing movements of the jaw
(chewing-gum fits)
● OTHER NEUROLOGIC SIGNS
→ Circling
→ head tilt
→ nystagmus
→ paresis to paralysis
→ seizures ranging in type from focal to generalized
● Supportive care
Treatment includes:
→ administration of prophylactic broad-spectrum antimicrobials
→ provision of balanced electrolyte solutions
→ provision of parenteral nutrition
→ administration of antipyretics, analgesics, and anticonvulsants
→ excellent nursing care
INFECTIOUS CANINE HEPATITIS
● Infectious canine hepatitis is due to a nonenveloped DNA virus,
canine adenovirus 1 (CAV-1), which is antigenically related to CAV-
2 (one of the causes of canine infectious tracheobronchitis).
MODE OF TRANSMISSION
● Oronasal exposure to urine, feces, or saliva from infected dogs is the
main route of infection.
● Transmission via either fomites or ectoparasites is also possible.
Recovered dogs shed virus in their urine for ≥ 6 months.
● Initial infection occurs in the tonsillar crypts and regional lymph nodes,
followed by viremia and disseminated infection.
● Vascular endothelial cells are the primary target; hepatic and renal
parenchyma, spleen, and lungs become infected as well.

CLIN101B PULIDO, JIANNE DAPHNE 1 of 7

 CLINICAL SIGNS, SYMPTOMS, LESIONS
CLINICAL SIGNS AND SYMPTOMS
● The first sign is commonly fever of > 40°C (104°F), which lasts 1–6
days and is usually biphasic. If the fever is of short duration,
leukopenia may be the only other sign; if fever persists for > 1 day,
however, acute illness develops.
Clinical signs may include:
→ nonspecific signs such as lethargy, thirst, or anorexia
→ conjunctivitis, serous oculonasal discharge, or corneal clouding
(blue eye)
→ abdominal pain and vomiting, including hematemesis
→ signs consistent with coagulopathy or vasculitis, such as
petechia of the oral mucosa
● In some cases, the tonsils may be enlarged, and tachycardia out of
proportion to the fever may occur. There may be subcutaneous
edema of the head, neck, and trunk. Despite hepatic involvement,
there is a notable absence of icterus in most acute clinical cases.
LESIONS
● Endothelial damage results in “paint brush” hemorrhages on the
gastric serosa, lymph nodes, thymus, pancreas, and subcutaneous
tissues.
● Hepatic cell necrosis produces a variegated color change in the liver,
which may be normal in size or swollen.
● Histologically, there is centrilobular necrosis, with neutrophilic and
monocytic infiltration, and hepatocellular intranuclear inclusions.
● The gallbladder wall is typically edematous and thickened; edema of
the thymus may be found.
● Grayish white foci may be evident in the kidney cortex.
DIAGNOSIS
● Clinical Evaluation
● Testing
● Although clinical signs of infectious canine hepatitis can be
nonspecific, any young puppy with evidence of severe hepatic
dysfunction, coagulopathy or disseminated intravascular coagulation,
or corneal clouding should be considered a suspect for ICH.
● Commercially available ELISA, serologic, and PCR tests are available
to obtain an antemortem diagnosis.
TREATMENT AND CONTROL
● Supportive care
● The treatment for infectious canine hepatitis is supportive care, which
includes the following goals:
→ to provide fluid support (balanced IV electrolyte solutions and
dextrose supplementation as necessary)
→ to maintain adequate nutrition
→ to address coagulopathy (plasma and/or whole blood transfusions
and/or anticoagulant therapy)
→ to limit secondary bacterial invasion (IV antimicrobials)
● PREVENTION
→ Injectable modified live virus (MLV) vaccines are available and
are often combined with other vaccines.
→ Live, attenuated CAV-1 vaccines have produced transient
unilateral or bilateral opacities of the cornea, and the virus may be
shed in urine.
▪ For these reasons, live, attenuated CAV-2 strains, which provide
cross-protection against CAV-1, are preferentially
administered because they have very little tendency to
CLIN101B DISEASES OF SMALL ANIMALS
produce corneal opacities or uveitis, and the virus is not shed
in urine.
CANINE LEPTOSPIROSIS
● Leptospirosis in dogs is an infectious disease caused by bacteria in
the genus Leptospira.
● Dogs are the maintenance host for Leptospira interrogans serovar
Canicola
MODE OF TRANSMISSION
● The true infecting serovar is unknown in most cases. However, it is
likely that the serovars that cause disease in dogs are those
circulating in local wildlife
CLINICAL SIGNS, SYMPTOMS, LESIONS
CLINICAL SIGNS AND SYMPTOMS
● Acute kidney injury has been the most common presentation for
canine leptospirosis in recent years.
● Dogs affected by leptospirosis might show clinical signs that
include lethargy, anorexia, vomiting, abdominal pain, and polyuria,
oliguria, or anuria.
● Serum biochemistry or serum blood gas analysis might
show abnormalities such as azotemia, hyperphosphatemia,
metabolic acidosis, hyponatremia, and hypo- or hyperkalemia.
● Urinalysis might show abnormalities such as hyposthenuria,
isosthenuria, or minimal concentration; proteinuria; glucosuria
(with normal blood glucose); cylindruria; hematuria; or pyuria.
LESIONS
● Thoracic radiographs might show diffuse or caudodorsal
reticulonodular pulmonary opacities, likely because of pulmonary
hemorrhage.
● Abdominal radiographs might be normal or might show renomegaly
or hepatomegaly.
● Gross necropsy findings can include jaundice, effusions, and
petechial or ecchymotic hemorrhages on any organ, pleural, or
peritoneal surface.
→ The kidneys and liver might be enlarged, and lungs can be wet,
heavy, and discolored.
→ The liver is often friable with an accentuated lobular pattern and
might have a yellowish-brown discoloration.
→ The kidneys might have white foci on the subcapsular surface.
● Microscopic findings in the liver could include mild random
hepatocytic necrosis, nonsuppurative hepatitis, and intrahepatic bile
stasis, while swollen tubular epithelial cells, tubular necrosis, and a
mixed inflammatory reaction can occur in the kidneys.
DIAGNOSIS
● Combination of the following findings: acute azotemia, cholestatic
liver disease, mild to moderate thrombocytopenia, and glucosuria
with normal blood glucose
● Serologic testing to detect antibodies, combined with PCR assay to
detect organisms
TREATMENT AND CONTROL
● Supportive care, together with specific antimicrobial therapy
● Doxycycline to eliminate both the leptospiremic and carrier phases
of infection
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● Supportive measures for acute kidney injury and liver disease might
include: fluid therapy, with electrolyte supplementation as
necessary; correction of acid-base disorders; antiemetics;
phosphate binders; hepatic support medications; or appetite
stimulants.
● Renal replacement therapy with intermittent hemodialysis or
continuous renal replacement therapy should be considered for dogs
that are anuric or oliguric despite appropriate supportive therapy.
● Current recommendations are to treat with doxycycline (5 mg/kg,
PO, every 12 hours, for 2 weeks).
→ For dogs that cannot tolerate doxycycline, initial therapy with a
penicillin is appropriate; however, this course of therapy should
be followed by a 2-week course of doxycycline treatment to
eliminate the renal carrier phase of infection.
● In general, currently available vaccines provide good protection
from disease for at least one year, and also reduce renal colonization
and urine shedding.
CANINE PARVOVIRAL INFECTION
● Canine parvovirus (CPV) is a highly contagious and relatively
common cause of acute, infectious GI illness in young and/or
unvaccinated dogs.
● Although its exact origin is unknown, it is believed to have arisen from
feline panleukopenia virus.
● It is a nonenveloped, single-stranded DNA virus, resistant to many
common detergents and disinfectants, as well as to changes in
temperature and pH.
MODE OF TRANSMISSION
● Virus is shed in the feces of infected dogs within 4–5 days of exposure
(often before clinical signs develop), throughout the period of illness,
and for ~10 days after clinical recovery.
● Infection is acquired through direct oral or nasal contact with virus-
containing feces or indirectly through contact with virus-
contaminated fomites (eg, environment, personnel, equipment).
CLINICAL SIGNS, SYMPTOMS, LESIONS
CLINICAL SIGNS AND SYMPTOMS
● Clinical signs of parvoviral enteritis generally develop within 5–7
days of infection but can range from 2–14 days.
● Initial clinical signs may be nonspecific (eg, lethargy, anorexia,
fever) with progression to vomiting and hemorrhagic small-bowel
diarrhea within 24–48 hours.
● Physical examination findings can include depression, fever,
dehydration, and intestinal loops that are dilated and fluid filled.
● Abdominal pain warrants further investigation to exclude the
potential complication of intussusception.
● Severely affected animals may present collapsed with prolonged
capillary refill time, poor pulse quality, tachycardia, and
hypothermia—signs potentially consistent with septic shock.
LESIONS
Gross necropsy lesions of canine parvovirus can include:
→ a thickened and discolored intestinal wall
→ watery, mucoid, or hemorrhagic intestinal contents
→ edema and congestion of abdominal and thoracic lymph nodes
→ thymic atrophy
→ in the case of CPV myocarditis, pale streaks in the myocardium
CLIN101B DISEASES OF SMALL ANIMALS
DIAGNOSIS
● Suspected based on signalment, history, and clinical signs
● Confirmation by fecal parvoviral antigen testing or viral PCR
● Commercial ELISAs for detection of antigen in feces are widely
available and have good to excellent sensitivity and specificity, even
for the more recently evolved CPV-2c strain.
TREATMENT AND CONTROL
● Dogs suspected or confirmed to have canine parvovirus should be
immediately isolated from other dogs to prevent spread of infection
● Treatment is based on supportive care, including fluid and
electrolyte therapy, nutritional support, anti-emetics, and
antibiotics
● To prevent and control CPV, vaccination with a modified-live
vaccine is recommended at 6–8, 10–12, and 14–16 weeks of age,
followed by a booster administered 1 year later and then every 3
years.
CANINE PARAINFLUENZA
● The disease is cause by parainfluenza virus
MODE OF TRANSMISSION
● CPIV is excreted from the respiratory tract of infected animals for up to
2 weeks after infection and is usually transmitted through the air.
● The virus spreads rapidly in kennels or shelters where large numbers of
dogs are kept together.
CLINICAL SIGNS, SYMPTOMS, LESIONS
CLINICAL SIGNS AND SYMPTOMS
● Dogs of any breed or age can be affected.
● Most exposed dogs (approximately 80%) develop mild infection, with
a cough that persists 1–3 weeks that may be similar to the cough
of canine infectious tracheobronchitis.
● Other possible clinical signs include ocular and nasal discharge,
sneezing, fever, lethargy, and anorexia.
● Some dogs become severely ill, with high fever (104º–
106ºF), pneumonia, and secondary bacterial infection. The mortality
rate is 1–5%.
LESIONS
● Thoracic radiographs may or may not have changes unless there is a
secondary bacterial pneumonia.
DIAGNOSIS
● Clinical signs
● Serologic testing
● There is no rapid test for specific diagnosis of canine influenza. Nasal
or pharyngeal swabs from dogs ill for < 3 days can be submitted for
PCR testing.
● After 4 days of illness, PCR testing may result in false-negatives,
because the time of maximal virus shedding has passed.
● Serum antibodies to CIV may be detected as early as 7 days after
onset of clinical signs.
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 TREATMENT AND CONTROL
● Supportive care
● Infection control practices
● Vaccination
● Routine infection control practices and good hygiene within
facilities are key to preventing spread.
● Proper isolation precautions should be used, such as keeping
animals at a minimum of 20 feet from other animals, as well as
using proper handwashing techniques.
CANINE CORONAVIRAL DIARRHEA
● Canine coronavirus disease, known as CCoV, is a highly infectious
intestinal infection in dogs, especially puppies.
● Canine coronavirus is usually short-lived but may cause considerable
abdominal discomfort for a few days in infected dogs.
● The virus is from the Coronaviridae family.
MODE OF TRANSMISSION
● Most cases of canine coronavirus are contracted by oral contact with
infected fecal matter.
● A dog may also become infected by eating from contaminated food
bowls or by direct contact with an infected dog.
● Crowding and unsanitary conditions lead to coronavirus transmission.
● The incubation period from ingestion to clinical signs is one to four
days.
● The duration of illness is two to ten days in most dogs.
● Secondary infections by bacteria, parasites, and other viruses may
develop and prolong illness and recovery.
● Dogs may be carriers of the disease for up to six months (180 days) after
infection.
CLINICAL SIGNS, SYMPTOMS, LESIONS
CLINICAL SIGNS AND SYMPTOMS
● Main idea
● The most typical sign associated with canine coronavirus is diarrhea,
typically sudden in onset, which may be accompanied by lethargy and
decreased appetite.
● The stool is loose, with a fetid odor and orange tint. It may contain blood
or mucus.
● If a puppy has a mixed infection, for instance both coronavirus and
parvovirus, the illness will be more severe.
LESIONS
● Lesions in the intestinal tract are present
DIAGNOSIS
● Basis of clinical signs
● Definitive diagnoses can be made by performing PCR tests, but the
procedure is complicated and rarely performed.
TREATMENT AND CONTROL
● Supportive treatment can be done since antibiotic are not effective
against the disease
● Canine coronavirus vaccines are available.
● This vaccine is not recommended for all dogs and will be administered
based on your dog's lifestyle and risk assessment.
● This vaccine will only work for the CCoV type of coronavirus.
CLIN101B DISEASES OF SMALL ANIMALS
RABIES
● Rabies is caused by viruses in the genus Lyssavirus in the family
Rhabdoviridae.
Rabies virus has a nonsegmental single-stranded negative-sense RNA
genome (~12 kb) encoding five viral proteins:
● nucleocapsid protein (N)
● matrix protein (M)
● glycoprotein (G)
● large protein (L), the enzymatically active RNA-dependent RNA
polymerase
● phosphoprotein (P), L protein's cofactor
MODE OF TRANSMISSION
● Transmission of rabies virus almost always occurs via introduction of
virus-laden saliva into tissues, usually by the bite of a rabid animal.
● Although much less likely, virus from saliva, salivary glands, or neural
tissues can also cause infection by entering the body through fresh
wounds or intact mucous membranes.
CLINICAL SIGNS, SYMPTOMS, LESIONS
CLINICAL SIGNS AND SYMPTOMS
● Clinical signs of rabies are suggestive but rarely definitive. Rabid
animals of all species usually exhibit typical signs of CNS
disturbance, with minor variations among species.
● The most reliable clinical signs, regardless of species, are acute
behavioral changes and unexplained progressive paralysis.
Behavioral changes may include:
● sudden anorexia
● signs of apprehension or nervousness
● irritability
● hyperexcitability (including priapism)
LESIONS
● Signs are more behavioral and no definitive lesions
DIAGNOSIS
● Immunofluorescence microscopy on fresh brain tissue
● Molecular testing
● When rabies is suspected and definitive diagnosis is required,
laboratory confirmation is indicated
● The brain (including the brainstem) is removed as the preferred organ
for testing. Immunofluorescence microscopy on fresh brain tissue,
which allows direct visual observation of a specific antigen-antibody
reaction, is the current test of choice.
TREATMENT AND CONTROL
● Rabies vaccination and registration of cats and dogs
● Promotion of responsible animal ownership
● Management of stray populations
● Oral vaccination of wildlife reservoirs
● Education to avoid exposure to suspect animals
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 KENNEL COUGH
● Kennel cough has multiple etiologies, including Bordetella
bronchiseptica, canine parainfluenza virus (CPIV), canine adenovirus 2
(CAV-2), canine influenza, and less likely canine distemper virus.
MODE OF TRANSMISSION
● Kennel cough should be suspected whenever the characteristic
cough suddenly develops 5–10 days after exposure to other
susceptible or affected dogs.
CLINICAL SIGNS, SYMPTOMS, LESIONS
CLINICAL SIGNS AND SYMPTOMS
● The prominent clinical sign of kennel cough is a cough that sounds
like a "goose honk" that may be followed by retching and gagging.
● The cough is easily induced by gentle palpation of the larynx or
trachea.
● Development of more severe signs, including fever, purulent nasal
discharge, depression, anorexia, and a productive cough, is
indicative of bronchopneumonia.
● Stress, particularly due to adverse environmental conditions and
improper nutrition, may contribute to a relapse during
convalescence.
LESIONS
● Tracheal trauma
● Alveolar disease
DIAGNOSIS
● History and clinical signs
● Radiography
TREATMENT AND CONTROL
● TREATMENT
→ The antibiotics recommended include amoxicillin/clavulanic acid
12–25 mg/kg, PO, every 12 hours; trimethoprim-sulfa drugs 15–30
mg/kg, PO, every 12 hours (schirmer tear test should be performed
before starting medications); enrofloxacin 10 mg/kg, PO, every 24
hours; and doxycycline or minocycline 5–10 mg/kg, PO, every 12
hours for 7–14 days.
● PREVENTION
→ Dogs should be immunized with modified-live virus vaccines
against distemper, parainfluenza, and CAV-2, which also provides
protection against CAV-1.
→ An initial vaccination should be given at 6–8 weeks and repeated
twice at 3- to 4-week intervals until the dog is 14–16 weeks old.
Revaccination should be performed annually .
FELINE VIRAL RHINOTRACHEITIS
● The principal disease, feline viral rhinotracheitis (FVR; feline
herpesvirus type 1)
MODE OF TRANSMISSION
● Feline rhinotracheitis is spread between cats through direct contact
with the eyes or nose of an infected cat or through contaminated
objects, such as food and water bowls.
CLINICAL SIGNS, SYMPTOMS, LESIONS
CLIN101B DISEASES OF SMALL ANIMALS
CLINICAL SIGNS AND SYMPTOMS
● The onset of illness is marked by fever, frequent sneezing, nasal
discharge (mucopurulent or serous), conjunctivitis, rhinitis, and
salivation.
● The fever may reach 105°F (40.5°C) but subsides and tends to
fluctuate from normal to 103°F (39°C).
● The cat may become anorectic and hypersalivate.
● Signs may persist for 5–10 days in milder cases and as long as 6
weeks in severe cases.
● Generally, the mortality is low and prognosis good because the
disease is usually self-limiting.
LESIONS
● Cats may develop ulcerative keratitis, epiphora, chemosis,
blepharospasm, or conjunctival hyperemia; severely debilitated cats
may develop ulcerative stomatitis.
● Lesions generally are confined to the respiratory tract, conjunctivae,
and oral cavity.
● In FVR infection, the conjunctivae and nasal mucous membranes are
reddened, swollen, and covered with a serous to purulent exudate.
● In severe cases, focal necrosis of these membranes may be seen.
● The larynx and trachea may be mildly inflamed.
● The lungs may be congested, with small areas of consolidation;
however, pulmonary changes are rarely remarkable in FVR infection
except possibly in stressed, young kittens.
DIAGNOSIS
● The presumptive diagnosis is based on such typical signs as
sneezing, conjunctivitis, rhinitis, lacrimation, salivation, oral ulcers,
and, if severe enough, respiratory distress and pneumonia.
● Cytologic examination of Giemsa-stained conjunctival scrapings is of
value for the identification of chlamydiae and mycoplasmas.
● A definitive diagnosis is based on isolation and identification of the
agent.
TREATMENT AND CONTROL
● If corneal ulcers develop in FVR infections (herpetic keratitis), topical
antiviral ointments containing idoxuridine, trifluridine, or vidarabine
every 4 hours should be considered. Lysine (250 mg, PO, 2 to 3 times
a day) interferes with herpetic viral replication and may reduce the
severity of FVR infection.
● If dyspnea is severe, the cat may require oxygen supplementation in
an oxygen cage.
● Fluids may be indicated to correct dehydration, and assisted feeding
may be necessary, either by syringe feeding or, in severely affected
cats, by a feeding tube (nasoesophageal, nasogastric, or
esophagostomy).
● Several intranasal modified-live virus FVR-FCV vaccines are
available. Cats >9 weeks old should be vaccinated twice, with a 3-
week interval. Kittens should be vaccinated at intervals of 3–4 weeks
until they are ≥12 weeks old. In adult cats, revaccination with a single
dose every 1–3 years is indicated.
FELINE CALICIVIRAL INFECTION
● The principal disease feline calicivirus (FCV)
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 MODE OF TRANSMISSION
● infected cats sneeze occasionally. Fever may develop as the disease
progresses beyond serous lacrimal discharge to mucopurulent
conjunctivitis, lymphoid infiltration, and epithelial hyperplasia.
Convalescent cats may undergo relapses.
CLINICAL SIGNS, SYMPTOMS, LESIONS
CLINICAL SIGNS AND SYMPTOMS
● The onset of illness is marked by fever, frequent sneezing, nasal
discharge (mucopurulent or serous), conjunctivitis, rhinitis, and
salivation.
● The fever may reach 105°F (40.5°C) but subsides and tends to
fluctuate from normal to 103°F (39°C).
● The cat may become anorectic and hypersalivate.
● Cats may develop ulcerative keratitis, epiphora, chemosis,
blepharospasm, or conjunctival hyperemia; severely debilitated cats
may develop ulcerative stomatitis.
● Signs may persist for 5–10 days in milder cases and as long as 6
weeks in severe cases.
● Generally, the mortality is low and prognosis good because the
disease is usually self-limiting.
● There are many serologically related strains of feline caliciviruses.
They appear to have a predilection for the epithelium of the oral cavity
and the deep tissues of the lungs.
● Some caliciviruses are nonpathogenic.
● Some induce little more than salivation and ulceration of the tongue,
hard palate, or nostrils; others produce pulmonary edema and
interstitial pneumonia.
LESIONS
● Calicivirus has also been found in cats with lymphocytic-plasmacytic
gingivitis and stomatitis.
● The superficial lesions heal rapidly, and appetite returns 2–3 days
after onset.
● The clinical course usually is 7–10 days. An acute febrile response,
inappetence, and depression are common signs.
● Serous rhinitis and conjunctivitis also can occur.
● Persistent calicivirus infections have been linked to chronic
ulcerative and proliferative lymphoplasmacytic stomatitis.
DIAGNOSIS
● Clinical signs
● Conjunctival scrapings
● Isolation and identification of the agent(s)
● The presumptive diagnosis is based on such typical signs as
sneezing, conjunctivitis, rhinitis, lacrimation, salivation, oral ulcers,
and, if severe enough, respiratory distress and pneumonia.
TREATMENT AND CONTROL
● Antimicrobial treatment for secondary bacterial infection
● Treatment is largely symptomatic and supportive, but broad-
spectrum antimicrobials are useful against secondary bacterial
infections (eg, amoxicillin with clavulanic acid, cephalosporins,
trimethoprim-sulfa, fluoroquinolones, tetracyclines,
chloramphenicol)
● Nebulization or saline nose drops may aid in removal of tenacious
secretions.
● Nose drops containing a vasoconstrictor (eg, two drops of ephedrine
sulfate [0.25% solution] in each nostril, twice a day) and antibiotics
may help reduce the amount of nasal exudate.
CLIN101B DISEASES OF SMALL ANIMALS
● Modified-live virus FVR-FCV vaccines intended for parenteral
administration are available in combination with either chemically
inactivated or modified-live virus feline panleukopenia vaccines.
● A parenterally administered vaccine composed entirely of
inactivated viruses also is available.
FELINE PANLEUKOPENIA
● Feline parvovirus (FPV; synonymous with feline panleukopenia virus)
is closely related to mink enteritis virus and the type 2 canine
parvoviruses (CPV) that cause canine parvoviral enteritis.
● All are now designated as members of the species Carnivore
protoparvovirus 1.
MODE OF TRANSMISSION
● Virus particles are abundant in all secretions and excretions during
the acute phase of illness and can be shed in the feces of survivors
for as long as 6 weeks after recovery.
● Being highly resistant to inactivation, parvoviruses can be
transported long distances via fomites (eg, shoes, clothing).
CLINICAL SIGNS, SYMPTOMS, LESIONS
CLINICAL SIGNS AND SYMPTOMS
● Physical examination typically reveals profound depression,
dehydration, and sometimes abdominal pain.
● Abdominal palpation—which can induce immediate vomiting—may
reveal thickened intestinal loops and enlarged mesenteric lymph
nodes.
● In cases of cerebellar hypoplasia, ataxia and tremors with normal
mentation are seen. Retinal lesions, if present, appear as discrete
gray foci.
LESIONS
● Bowel loops may be segmentally dilated and may have thickened,
hyperemic walls.
● There may be petechiae or ecchymoses on the intestinal serosal
surfaces.
● Perinatally infected kittens may have a noticeably small cerebellum.
● Histologically, the intestinal crypts are usually dilated and contain
debris consisting of sloughed, necrotic, epithelial cells.
● Blunting and fusion of villi may be present.
● Eosinophilic intranuclear inclusion bodies are seen only occasionally
in formalin-fixed specimens
DIAGNOSIS
● Typically based on clinical signs and leukopenia on a CBC
TREATMENT AND CONTROL
● Supportive care, prompt IV fluid treatment, and antibiotics are the
primary treatments
● Effective vaccines are available
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 FELINE CHLAMYDIOSIS environments where infections associated with clinical signs of
chlamydiosis have been confirmed.
● Chlamydiosis is an infection in animals due to bacteria in the family
Chlamydiaceae (Chlamydia psitacci).
● Chlamydial disease ranges from subclinical infections to death
depending on the chlamydial species, host, and tissue infected.

MODE OF TRANSMISSION

● Organisms may be transmitted by handling infected animals and

tissues directly, breathing in aerosolized dried feces or respiratory
secretions, or other exposure.

CLINICAL SIGNS, SYMPTOMS, LESIONS

CLINICAL SIGNS AND SYMPTOMS

● In cats, infections with C felis result in rhinitis, conjunctivitis, or

bronchopneumonia, and seropositive cats can be subclinically
affected. Although C felis has been found in dogs, the clinical
importance is unknown because many dogs are clinically normal.

LESIONS

● Acute pulmonary lesions include bronchiolitis, severe focal

pneumonia, and dystelectasis. Dissemination of chlamydial bodies
in lung tissue is usually accompanied by an influx of macrophages,
granulocytes, and activated T cells.
● Bronchointerstitial pneumonia and alveolitis may be accompanied
by progression to type II pneumocyte hyperplasia and interstitial
thickening due to ingress of mixed inflammatory cells. Lymphocytic
aggregates are frequently seen around airways and pulmonary
vessels.
● In chronic (often subclinical) chlamydial infections, lesions may
include neutrophil inflammation, follicular bronchiolitis, and active
lymphoid tissues (tonsils, tracheobronchial and pulmonary lymph
nodes, etc) and can be more lobular in distribution.
● Small intestinal lesions can be characterized by mild to severe villus
atrophy with occasional villus necrosis.
● Hepatic lesions include hepatocyte necrosis, lymphohistiocytic
infiltrates, and inclusion bodies within hepatocytes and sinusoidal
histiocytes.

DIAGNOSIS

● Collection of samples
● Laboratory testing
● In vivo, swabs (nasal, ocular, rectal, vaginal, choanal, or cloacal),
tracheal washing or bronchoalveolar lavage fluid, and biopsies are
useful.
● Serologic testing can demonstrate that an animal was infected by a
chlamydial species but might not indicate an active infection.
● False-negative results in animals with acute infection can also result
from specimens being collected before seroconversion.

TREATMENT AND CONTROL

● Varies by species
● Doxycycline for birds
● Limited vaccination
● Vaccines against C felis are available for pet cats.
● This vaccine has been shown to decrease the severity and incidence
of clinical signs but is not completely protective.
● This is considered a noncore vaccine and may potentially be
considered part of a control regime for cats in multiple-cat

CLIN101B DISEASES OF SMALL ANIMALS 7 of 7