C.

FAMILY ADENOVIRIDAE

Conventional Adenovirus
2 genera:
1. Mast adenovirus – Affects both animals & humans
2. Aviadenovirus - Affects birds
• Many produces mild or subclinical respiratory diseases.
• Some produces mild or subclinical intestinal infection
• Few produce severe systemic diseases
• Contains double – stranded DNA
• Non enveloped
• Icosahedra symmetry
• 70 to 90 nm
• 252 capsomeres, 7nm each
Pentons – 12 vertex capsomeres that are antigenically distinct from other
240 capsomeres (hexons). Each penton carries a filamentous
Projection of fiber.
• Resistant to ether but can be inactivated by many disinfectants
• Viral assembly takes place in the nucleus of the cell, where IB are seen.
• Oncogenic – under certain conditions
- produces cytopathological pattern in monolayer cell cultures
with marked rounding of cells that form aggregates in grapelike
clusters

DISEASES CAUSED BY GENUS MASTADENOVIRUS

1. Infectious Canine Hepatitis – hepatitic & hemorrhagic

• Caused by Canine Adenovirus Virus 1 (CAV-1), the first canine
adenovirus officially recognized
• ICH (Abbreviation)
• Synonyms: Canine Adenovirus I Infection
Fox Encephalitis
Hepatitis Contagiosa canis
Rubarth’s disease
● Acute disease of young dogs (newly weaned puppies) with severe
hepatitis, edema of gallbladder, tonsillitis, multifocal vasculitis and
hemorrage
- Less effect on respiratory tissues
● Characteristic forms of the disease:
a. Per acute Course/Form
- Dogs become moribund within hours of the first signs of
clinical illness.
- Resembles poisoning
 b. Typical Case/ Form
- Biphasic febrile response (39.4-40.7oC)
- Apathetic
- Inappetent/anorectic
- Shows intense thirst
- Sometimes exhibit edema of head, neck & lower portion of
abdomen
- Vomiting & diarrhea are common
- Painful abdomen
- Leucopoenia and early febrile state
- Transient opacity of cornea (BLUE EYE) due to edema &
anterior uveitis. Afghan Hound has predilection to eye lesions.
- Mucous membranes are usually pale and petechial or
ecchymotic hemorrhages may appear on the gums or other
mucous membranes.
- albuminuria
c. Encephalitic form - occurs among wild foxes
- Loss of appetite is noted a day or 2 before other signs
- Violent convulsions - initial sign
- Lethargy with common watery nasal and eye discharge
- Feces is soft & filled with mucus- sometimes with profuse
diarrhea w/ blood streaks
- Rapid course- 1 hour or usually less than 24 hours
- Few cases last for 3 days.

● Properties of Virus
- Resistance: a.) Survives well when frozen or dried
b.) Survives between ph 3-9 at room temperature
c.) Ether & chloroform resistant
d.) Survives for days in 0.5% phenol
- Susceptibility: a.) 0.2% formal in at 24 hrs
b.) 50oc after 150 minutes
c.) 60oc in 3-5 minutes

● Cultivation
- Successfully cultivated in roller-tube cultures of dog kidney

● Epizootiology & Pathogenesis:

-Unlike canine distemper, ICH is not transmitted by droplet
inhalation
- Transmitted by: a) Direct contact of infected & susceptible dogs
b) Indirect contact with urine-contaminated
environment eg. fomites - food & water
dishes
- Transmitted via oro-nasal exposure
- Short course of disease
- Progress is more rapid than Canine Distemper (CD)
- 10 – 25% mortality

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 - Natural Infection ( oro-nasal exposure)
↓
Tonsils (localize & replicate)
↓

Regional Lymph Node

↓ (through lymphatic)

Blood stream → liver,

kidney main target areas for
eye replication and
endothelium pathological damage
- Tissue injury is caused by cytolysis as virus replicates
- Has predilection for endothelial cells; vascular damage results to
petechial & ecchymotic hemorrhages as in Disseminated
Intravascular Coagulation (DIC)

● Necropsy Findings:
- No evidence of emaciation
- Liver - somewhat swollen & light in color with stiff capsule;
more prominent than normal lobule
- Blood vessels and sinusoids – greatly dilated and blood
content is increased
- Endothelial cells & kupffer cells – greatly swollen with Cowdry
Type inclusion bodies
- Gall bladder is thickened
- Spleen is enlarged

● Immunity:
CAV-1 – protects dogs against itself & CAV-2
CAV-2 – protects dogs against itself & CAV-1

● Diagnosis:
1. Presumptive – a. Clinical signs
b. Clinic pahological findings
* Difficult to distinguish from Canine Distemper clinically
2. Confirmative – a. Virus isolation in cell culture
b. Serologic tests
c. Gross & microscopic lesions @ necropsy
At necropsy, ICH can be readily distinguished from CD:
a. Characteristics liver and gallbladder lesions &
effusions in body cavities with ICH
b. ICH – intranuclear Inclusion Bodies
CD – intracytoplasmic Inclusion Bodies

● Treatment:
- Basically symptomatic & supportive
a. Fluid therapy – lV, slowly

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 b. Fresh whole blood- counter the effects of DIC
c. Hypertonic glucose infusion – counter hypoglycemia
associated with neurological signs in fox
● Prevention:
1. Active Immunization – using inactivated or attenuated CAV-1
or CAV-2 vaccines
2. Passive Temporary Maternal Immunity
3. Hyper immune homologous serum

2. Canine Adenovirus 2 Infection- Respiratory type

● caused by Canine Adenovirus-2 (CAV-2), one of several viruses
involved in respiratory disease complex of dogs known as Canine
Infectious Tracheobronchitis or Kennel Cough

● Character of the Disease:

- Mild to in apparent respiratory disease of young dogs
- Signs include: rhinitis, tonsillitis, pharyngitis and
Tracheobronchitis
- Virus has strict affinity for epithelial cells lining the respiratory
tract; it fails to produce hepatitis in dogs
- severity of the disease is frequently increased by the presence
of Bordetella bronchiseptica
- Incubation period is 3-5 days
- Starts with mild fever for short time. Then followed by
tonsillitis for few days, harsh dry hacking cough for 6–7 days,
then fatal pneumonia
- Other signs include: depressions, dyspnea, anorexia, muscular
trembling and serous to mucopurulent nasal discharge

● Properties of the Virus

- DNA of CAV- 2 is distinct from CAV-1
- CAV-2 cross reacts antigenically with CAV-1

● Epizootiology & Pathogenesis

- Viral replication produces severe narcotizing & proliferate
bronchitis & brochiolitis
- Lesions are confined in the respiratory tract:
a. Atelectasis and congestion in the lung
b. Congestion and hemorrhages in the bronchial
lymph nodes
c. Cowdry type A inclusion bodies in bronchial
epithelium, alveolar septa and turbinate
epithelium
- No lesion (no IB, edema or hemorrhage) in liver and gallbladder
- No corneal opacities

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 ● Diagnosis
1. Clinical signs
2. Laboratory tests for identification
Specimens: a. nasal swab
b. Pharyngeal swab
c. Tracheal wash sample
- Easily isolated and identified in cell cultures

● Treatment- not specific

a. Warm environment and rest – usually sufficient for natural recovery
b. CNS-suppressing antitussives – suppress dry, hacking cough
c. Antibiotics – for secondary bacterial infection via aerosol or
intratracheal administration, twice a day for 3 days:
i. Kanamycin sulfate (250 mg)
ii. Gentamycin sulfate (50 mg)
iii. Polymyxin B sulfate (166,666 IU)
● Prevention
1. Attenuated and inactivated vaccines of either CAV-1 or CAV-2
- given at 8 to 10 weeks old and 4 weeks later
- annual revaccination

3. Bovine Adenovirus Infection

• caused by Bovine Adenovirus (BAdV)
• produce mild or subclinical respiratory disease and enteric disease

• Character of the Disease:

- affects 2-16 weeks old calves, especially those that are
colostrum-deprived.
- natural disease is enhanced by cold weather and other agents
such as viral diarrhea virus
● Necropsy Findings:
- Lung is collapsed and emphysematous – very prominent
- histologic findings:
a. proliferative bronchitis with necrosis
b. bronchiolar occlusion, resulting in alveolar collapse
c. nuclear inclusion bodies in bronchiolar epithelium, septal
cells and bronchial lymph nodes.
● Properties of BAdV:
- similar in morphology and size to human and avian adenovirus
- can be cultivated in calf kidney and calf testes cell monolayers, where
they show cytophatic effect characteristics of adenovirus

• Epizootiology and Pathogenesis

- primarily transmitted by:
a) direct contact of infected and susceptible animals
b) indirectly by contact with contaminated excretions
- via: a. aerosol transmission thru oral, nasal or conjunctival
b. transplacental infection

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 Mouth → oropharyngeal lymph nodes → intestinal epithelium = Enteritis
Nose → epithelial cells of respiratory tract → downward infection
=Pneumonia
Conjunctiva → conjunctival epithelium = Conjunctivitis or
Keratoconjunctivitis

• Immunity
- neutralizing antibodies are developed within 10-14 days
- strong and lasting immunity after vaccination or natural disease

• Diagnosis:
- Requires laboratory isolation & identification of virus
- Materials/ Specimens:
a. exudates from nasal passages from acutely
b. exudates from conjunctiva ill animals
c. feces
d. trachea & lung tissues
- The ability of most serotypes to hemagglutinate rat erythrocytes
provide an especially convenient & quick identification
- ELISA- an excellent way to diagnose disease

● Treatment:
- no specific treatment
- antibiotics are used to control secondary bacterial invaders
- appropriate supportive measures is recommended

● Prevention and Control

- Vaccines for BAV-1 or BAV-3 in combination with vaccines for
IBR or Bovine Parainfluenza 3 is safe and very effective.
- Single vaccine – unlikely to play a prominent role in the control
of disease due to numerous serotypes with no cross-
protection.
- Difficult to control due to persistence of the virus.
- The severity of the disease can be reduced by:
a. good management
b. health care
c. housing

4. Equine Adenovirus Infections

• Caused by Equine Adenovirus (EAdV)
- common virus of horse which generally produce asymptomatic
or mild respiratory infections
- the cause of fatal pneumonia of Arabian Foals with combined
immunodeficiency disease, where 27 out of 28 Arabian foals
died.
● Occurrence
- Common in horses but clinical signs would accompany infection only in
unusual cases.

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 - In neonates, signs developed are: a) fever
b) nasal & ocular discharge
c) dyspnea
- Older foals are less affected. Colostrum-fed foals had milder illness than
colostrums-deprived foals.
- Lesions in older foals are: a) hyperplasia
b) swelling
c) necosis
d) intranuclear 1B in epithelial cells of
respiratory tract

5. Porcine Adenovirus Infections

• caused by Porcine Adenovirus (PAdV), a widespread virus of swine that
generally produce symptomatic infections that may be associated with
a) pneumonia
b) enteritis
c) kidney lesions
d) transplacental infections ,&
e) encephalitis
● 4 recognized serotypes
- Serotype 4 – isolated in natural cases of diarrhea or encephalitis
- produce meningoencephalitis in gnotobiotic pigs
● Experimental studies reveal the following information:
- Incubation Period is 3-4 days
- Primary sign is diarrhea
- Lesion: Shortened villi of terminal jejunum & ileum w/
typical intranuclear IB
- Virus persist in altered cells for 45 days

6. Ovine Adenovirus Infections

• Caused by Ovine Adenovirus (OAdV), where 6 serotypes are identified
• Produce mild or inapparent infection associated primarily with the
respiratory tract but occasionally with the intestinal tract

7. Other Mammalian Adenovirus Infections

a. Murine Adenoviruses – occur in some mouse colonies
- eliminated in the urine over extended periods
- disseminated pathological lesions: a) brown fat in heart and
adrenals
b. Opossum Adenovirus – has the ability to produce disease that has not
been determined
c. Simian Adenovirus – with 16 recognized serotypes

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DISEASES CAUSED BY GENUS AVIADENOVIRUS

1. Avian Adenovirus Infections

• Synonyms are: Egg Drop Syndrome (EDS)
Fowl Adenovirus Infection
Hemorrhagic Enteritis (HE)
Inclusion Body Hepatitis (IBH)
Marble Spleen Disease (MSD)
• Caused by Avian Adenovirus (AAdV), with 12 serotypes
• Commonly manifested by respiratory disease
- either clinical or subclinical
- multifocal interstitial or diffuse pneumonia

● MSD is characterized by:

- pulmonary congestion and edema
- splenomegaly
- hepatomegaly

● IBH is characterized by: Sudden increase in mortality of birds 5-7

weeks old
- Few birds appear to be sick.
- Findings are:
a. hemorrhages
b. pale and friable livers
c. hepatomegaly
d. anemia
-Inclusion Bodies (IB) are present in hepatocytes

● EDS – clinical disease of fowl characterized by soft or thin-shelled eggs

or eggs with no shell at all
- Birds are healthy, sometimes with edematous uterus
- Change in Na pump mechanism of epithelial cells in uterine
mucosa increases Na concentration and decreases
concentration of K, Ca, Mg and glucose in uterine fluid
- Incubation Period is 10-24 days
- The degenerative epithelial cells contain IB intranuclearly
- Causative agent, Adenovirus 127 is antigenically
indistinguishable from hemagglutinating adenovirus of ducks
which is non pathogenic to laying hens but protects the birds
against subsequent infection from adenovirus 127.

● HE – caused by HE virus in turkey

- a subclinical infection in chicken that produces intranuclear IB

● Other conditions attributed to avian adenovirus infection:

a. Atrophy of Bursa of Fabriciuos
b. Hemorrhagic Aplastic Anemia Syndrome
c. Tenosynovitis and leg weakness, where Avian reovirus is also

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 involved

● Properties of the Virus

- lacks common complement-fixing antigen shared by all
mammalian adenoviruses
- Can be isolated in:
1. cell cultures
2. embryonated eggs

● Immunity
- long-lasting, solid immunity is conferred with monovalent virus
- Maternal antibodies confer temporary protection to young
chicks
- Inactivated vaccine is used in breeder flocks

2. Turkey Adenovirus Infections

- caused by 3 classes of viruses:
a. Fowl adenovirus
b.Turkey adenovirus
c. Turkey hemorrhagic enteritis virus

- manifested by:
a. Respiratory Illness – severe in day-old poults
b. Hemorrhagic Enteritis - affects young turkeys
- show bloody diarrhea
- acute death – occur in large number of
dark red, bloody clots in intestinal tract,
many petechiae in the mucous membrane
of small intestine, atrophy of spleen and
cecum.
c. Marble Spleen Disease – described in young poults and ring-
necked pheasant

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