Infectious diseases of

the dog and cat

 The Respiratory tract
 Canine Distemper
 Canine Adenovirus type 2

 Parainfluenza virus 2

 Canine Herpesvirus 1
 Distemper
 Paramyxovirus

 Disease of Canidae, seals, dolphins…

 Serologically unique

 Virus strains differ in virulence

 Not very resistant

 Patogenesis
 Respiratory infection - aerosol
 Primary replication in macrophages of
upper respiratory tract (within 24 hours)
and subsequently in macrophages and
lymphocytes (lymph nodes, tonziles)
 6 days following infection, first wave of
fever and lymphopenia
 Critical period: 8-10 days p.i.

 Virus dissemination in epithelial cells and

CNS
 Critical period

Ab titre > 100: absence of Ab:

Till 10 – 18 days

 Virus elimination  Infection of epithelial

 End of viremia cells
 Long lasting immunity  Secondary replication
 2nd wave of fever
 Lymphopenia
 Clinical signs
 Distemper – forms:
 Systemic Distemper
 Gastroenteritis
 Conjunctivitis
 Bronchitis, pneumonia
 Nervous form
 Hematogenous spread of the virus
 Demyelinisation

 Old dog encephalitis

 Hyperkeratosis (hard pad)
 Transplacental transmission
 Immunosupression, secondary infections
 Diagnostics
 Conjunctival swab
 pharyngeal swab

 urine, blood, serum

 Cerebrospinal fluid

 Postmortem: lungs, tonzils, lymph

nodes, urinary bladder, brain
 Diagnostics
 IFA - yes

 Isolation on tissue cultures – no

 Isolation on embryonnated eggs – no

 Intracytoplasmatic and intranuclear

inclusions (in epithel. cells, neuronal
cells, leukocytes)
 Failure of IFA

 Virus masking by antibodies

 Virus occurrence in focuses

 Time limited occurrence

 Detection of Antibodies
 VNT (paired samples)
 Indirect IFA

Immune status
(after 2nd. viremia)

 Prognosis non favourable < 1:20

 Protection > 1:100
 Protection incertain 1:20 – 1:100
 Analysis of cerebrospinal
fluid

 Used to confirm CDV encephalopathy

 Detection of specific IgM and IgG in
the CSF-acute Distemper
 Kennel cough
 Viruses:
– Parainfluenza virus 2
– Adenovirus type 2

 Replicationin the lower part of the

respiratory tract
 Bacterial and fungal infections in
the respiratory system (RS)
 Nasalinfections (acute/ chronic diseases,
mycoses)
 Upper RT (kennel cough)

 Lower RT
 Diagnosis of RS infections
 Localizing diseases
 Imaginig the RT (endoscopy, tomography,
magnetic resonance imaginig)
 Obtaining material for microbiological
examinations:
– Swabing of RS
– Washing (nasal, transtracheal aspiration,
endotracheal w., bronchoalveolar lavage)
 The upper RS


 B.bronchiseptica prim. doxycycline p.o.

 S.intermedius co-amoxicillin p.o.
 cephalosporins 1.g. p.o.

 Escherichia coli flumequin p.o.

 Pasteurella multocida cephalosporins 1.g. p.o.
 amox./ampicillin p.o.

 Klebsiella pneumoniae flumequin p.o.
 Aspergillus spp.

 The lower RS: Bronchopneumonia I.

 B.bronchiseptica prim. doxycycline p.o.


 S.intermedius co-amoxicillin p.o.
 cephalosporins 1.g. p.o.

 Escherichia coli flumequin p.o.

 Pasteurella multocida cephalosporins 1.g. p.o.
 amox./ampicillin p.o.

 Klebsiella pneumoniae flumequin p.o.
 Bronchopneumonia II.


 P.aeruginosa enro/difloxacin s.c.,p.o.

 Pseudomonas spp. amikacin i.v.,i.m.,s.c.
 piperacilllin/tikarcillin i.v.,i.m.
 gentamicin i.v.,i.m.,s.c.

 Obligate anaerobes co-amoxicillin i.m.,s.c.,p.o.
 clindamycin i.m.,s.c.,p.o.
 Streptococcus spp. amox./ampicillin i.v.,i.m.,s.c.,p.o.
 benzylpenicillin s.c.,i.m.

 Mycobacterium spp.
 Pyothorax/pleuritis


 Escherichia coli enro/difloxacin s.c.,p.o.
 Klebsiella pneumoniae enro/difloxacin s.c.,p.o.

 Enterobacter spp. cephalosporins 2.-3.g.
i.v.,i.m.,s.c.,p.o.
 P.multocida co-amoxicillin i.m.,s.c.,p.o.
 cephalosporins 1.g. i.v.,i.m.,s.c.,p.o.
 Obligate anaerobes co-amoxicillin i.m.,s.c.,p.o.
 klindamycin i.m.,p.o.
 S.intermedius co-amoxicillin i.m.,s.c.,p.o.
 cephalosporins 1.g. i.v.,i.m.,s.c.,p.o.
 Enteric tract - viruses
 Canine parvovirus CPV-2
 Canine coronavirus

 Distemper

 Canine Adenovirus type 1 (CAV-1)

 Parvovirosis
 Canine Parvovirus
 Hosts – Canidae

 Originated by mutations from Feline

panleukopenia virus
 Three antigennic types CPV-2a,b,c

 Very stable and resistant

 Disease of 6 – 8 weeks old puppies

 Pathogenesis
 Oral infection
 Primary replication in the regional lymph-nodes
and tonziles (1 – 2 days)
 Replication in enterocytes, myocardium
 Virus is disseminated by blood
 Virus could be isolated from all tissues

Significant affinity to replicating cells (mitosis)!!

 Enteritis
 Myocarditis
 Transplacental infection

Acute myocarditis in 3 – 8 weeks

Mortality 20 – 100%
 Pathogenesis

 Virusreplicates in non-mature
enterocytes
 Transient lymphodepletion and
neutropenia….. bacterias (sepsis)
and viruses.
 Diagnosis
 Hemmaglutination test (porcine
erytrocytes)
 Virus isolation on A72, CRFK – no!

 Rapid immunochromatographic tests

 Serological tests
 Hemmaglutination inhibition test
 titres >80 are protective

 Colostral antibodies persist till 8 – 16

weeks of age
 4 fold rise is significant
 Canine Coronavirus
 Mild infection, often asymptomatic
 70% Ab positive dogs

 Age: 1-3 months

 Incubation period 3-4 days

 Involvement of small intestine, replication

in mature enterocytes on the apical
surface of intestinal villi, virus shedding up
to 2 weeks
 Watery yellow-green diarrhea
 Diagnosis
 Serology -meaningless- low titre of
systemic IgG
 Paired samples

 EM, FA, Cell cutures

 Inaktivated vaccine – interference with

colostral antibodies
 The alimentary tract infections
 The oral cavity, pharynx

 The stomach

 The intestine
 The alimentary tract
 stomatitis , periodontitis

 Obligate anaerobes clindamycin p.o.
 co-amoxicillin p.o.,s.c.,i.m.
 gastritis
 Helicobacter spp. amoxicillin-+metronidazole p.o.
 Acute enterokolitis

 Salmonella spp. flumequin p.o.
 Y.enterocolitica potenc.sulfonaides p.o.
 amox./ampicillin p.o

 Campylobacter spp. erythromycin p.o.
 C.perfringens .amox./ampicillin i.v.,i.m.,s.c.,p.o.
 E.coli (EHEC,EAEC) potenc.sulfonamides p.o.
 E.coli sultamicilin i.v.,i.m.
 (neonatal sepsis) cephalosporins 2.-3.g s.c.,i.v.,i.m.


 The urinary tract


 Escherichia coli potenc.sulfonamides p.o.,i.m.

 Proteus mirabilis. amox./ampicillin p.o.,i.m.,i.v.,s.c.

 Proteus vulgaris potenc.sulfonamides p.o.,i.m.,s.c.
 S.intermedius co-amoxicillin p.o.
 cephalosporins 1.g. p.o.
 Klebsiella pneumoniae cephalosporins 1.-3.g. p.o.,i.m.,i.v.,s.c.
 Pseudomonas aeruginosa tetracycline p.o.

 Enterococcus spp. amox./ampicillin p.o.

 Streptococcus spp. amox./ampicillin p.o.

 Urogenital tract and viruses
 Canine Herpesvirus CHV-1
 Distemper

 Parvovirus
 Canine Herpesvirus

 Opportunistic pathogen

 Period of increased sensitivity:

 last 3 weeks of pregnancy
 3 weeks after birth
 stress
 Pathogenesis
 Infection:
 transplacental
 during parturition – oronasal infection

 Primary replication in oronasal region

 Infection of mononuclear cells

 Spread in organs and tissues

 Latency
 Diagnosis
 PCR

 Isolation
on tissue culture???
(primary canine fibroblasts) CPE
within 48 hours

 Neutralization test
 paired samples
 The skin
(pyoderma)


 S.intermedius cephalosporins 1.g. p.o.
 co-amoxicillin p.o.
 oxacillin p.o.
 Escherichia coli potenc.sulfonamides p.o.
 Proteus mirabilis cephalosporins 1.g. p.o.
 Pseudomonas spp. enro/difloxacin p.o.
 Streptococcus canis cephalosporins 1.g. p.o.
 Bacillus cereus co-amoxicillin p.o.
 CNS - viruses
 Distemper

 Rabies
The cat
 Enteric Infections

 Feline Panleukopenia
 Feline infectious peritonitis - FIP
 Felina Panleukopenia
 Parvovirus

 Ag related with other parvoviruses

 Oronasal infection

 Newborn kittens– systemic or CNS

infection
 Later – panleukopenia and enteritis
 Feline Infectious Peritonitis
(FIP)
 Coronavirus
 Susceptible hosts: felidae
 Antigenniv relationship with other
coronaviruses (TGEV, CCoV)
 FIP – mutation of ubikvitous feline
enteral coronavirus (FeCV)
 Both viruses differ by macrophage
tropism
 Pathogenesis

 Primary replication – epithelium of

tonziles
 Replication in enterocytes

 Infection of macrophages allows

virus spread in the organism
 Pathogenesis
 Antibodies enhance infection (Fc
receptors allows entry into
macrophages)
 Immunocomplex

 Cell mediated response is protective

 Effusive - wet form
 Non-effusive – dry form (immunity is
partially preserved)
 Diagnosis
FeCV complicates diagnosis:

 Cross reactivity of antibodies

– FeCV IFA titre: 25 – 3200

– FIP IFA titre: 100 - 64000

 Titre >3200 evidence of FIP infection

 Similarity of genomes– complicates PCR

diagnostics
 FIV
 Retrovirus

 Host – felidae
 Main route of infection– bite
 Pathogenesis
 Target cells
monocytes / macrophages
lymfocytes T , B
astrocytes
 perzistent, life-long infection
Provirus integration into host cell
chromosome
Expression of virus proteins is
restricted
antigennic drift
 Pathogenesis
 Acute phase (several weeks)
 fever
 neutropenia
 asymptomatic phase (3 – 5 years)
 ARC (AIDS related complex)
 generalized lymphadenopathy
 chroni secundary infection of mouth and
upper respiratory tract
 5 - 10% infected animals
 tumors
 Involvement of CNS
 Diagnosis
 Antibody detection
 ELISA

 IFA

 Rapid tests
 Serological latency- several weeks

 PCR – in some laboratories

 Feline leukosis virus (FeLV)

 Retrovirus

 Disease of stray animals (1 - 7% of

population)
 Infection occurs in the first 5 years of
life (age resistence)
 transmission– salive (bite), urine,
feces, in utero
 Pathogenesis
3 biotypes
 FeLV-A – Immunosupression, oportunistic
infection
 FeLV-B – Viremia, immunosupression,
neoplasia, lymphomas
 FeLV-C –thymus atrophy, lymphodepletion

 permissive cells: macrophages,

lymphocytes, non-mature
enterocytes
 Antibodies are able to eliminate
infection
 Pathogenesis
 Primary replication in macrophages and B
lymphocytes in tonziles
 Primary viremia (1-2 weeks), virus is
associated with mononuclear cells
 Infected cells are in bone marrow,
intestine, oesophagus, stomach, kidney,
pancreas, urinary bladder
 Virus is spread by saliva, urine, tears,
feces
 Early phase
4 – 16 weeks following infection (persistent
viremia or regression)

 latent phase - up to 3 years

 Terminal phase
lymphoid tumors, anemia, immunodeficiency
(secondary infection)

83% of cats die during 3,5 years

 Diagnosis
 p25 antigen detection in blood,
saliva…
 ELISA

 IFA

 Rapid immunochromatographic tests

 Antibody detection – no!