Virology (week 5 and 6)

Relatively stable in environment

Persistent infection common

Narrow host ranges

Causes respiratory and gastroenteric diseases

Labile in the environment

Rarely a persistent infection

Can infect a variety of hosts

Siadenovirus

Atadenovirus

Mastadenovirus

Aviadenovirus

Betaherpesviridae

Panleukopaenia virus

Orbivirus

Infection through nasopharyngeal, oral and conjunctival route of entry

Vector transmission

Ingestion of urine, faeces or saliva from an infected animal

Transdermal infection

Peracute disease: pup found dead, often with short lived (3‐4 hours) or no apparent illness

Acute disease: may be fatal. Fever, vomiting, bloody diarrhoea, pettechial haemorrhages of gums, pale mucous membranes

Mild or inapparent disease

Chronic disease: Chronic fever, vomiting, bloody diarrhoea, pettechial haemorrhages of gums, pale mucous membranes

Peracute disease: may be fatal. Fever, vomiting, bloody diarrhoea, pettechial haemorrhages of gums, pale mucous membranes

Acute disease: pup found dead, often with short lived (3‐4 hours) or no apparent illness

Can lead to bronchitis and bronchiolitis

Causes localised respiratory
disease (part of kennel cough complex)

No systemic infection

CAV2 provides complete homologous protection and cross protection against disease caused by CAV1 without side effects

Convalescing animals can develop corneal oedema (Blue eye)

Causes haemorrhage and necrosis, especially of liver, kidneys, spleen and lungs

Isolated worldwide

Isolated from young horses with and without respiratory disease (can be symptomatic or asymptomatic)

Always causes symptomatic disease

Latent infection

Virus is endemic only to South East Asia and Africa

Mostly asymptomatic or mild disease

Isolated from lymph nodes and faeces of foals with respiratory disease and diarrhoea

Mostly asymptomatic or mild disease

Latent infection

Isolated worldwide

Endemic only to Africa and North America

May give rise to carcinomas, usually with appropriate co‐factors

Papillomavirus replication linked to growth and differentiation of stratified squamous epithelium of skin and some mucous membranes

Resistant in the environment

Resistant to solvents, disinfectants, low pH and high temperature

Resistant to solvents, disinfectants, high pH and low temperature

Labile in the environment

Usually regress after several weeks

Lesions are typically finger‐like projections of proliferating epithelium supported by a thin core of fibrous connective tissue

Transmission by fomite transfer (eg. contaminated equipment and facilities)

Sexual transmission

Vector transmission

Respiratory droplet transmission

Ingestion of faeces and urine

Cause aural plaques and cutaneous papillomas

Regression occurs in 1‐9 months

Generally occur around the muzzle of young horses

Can lead to equine sarcoids

Associated with enzootic haematuria

Superficial ulceration and secondary trauma are common

Do not metastasize

Locally aggressive

Occur singly or in groups

Head, ventral abdomen and limbs affected most commonly

More common in animals <4 years of age

Metastatic

Hyperaemia of oral and buccal cavities (salivation / frothy mouth)

Oedema (head and neck)

Hyperaemia of the coronary bands

Cyanosis of the tongue

Nasal discharge (serous – mucopurulent – blood flecked)

Abortion of lambs or lambs born with congenital abnormalities (hydranencephaly)

Severe cases have a protracted recovery (may lose part of the fleece)

Death occurs in up to 30% of cases, but more commonly 2 – 8%

Sheep experience asymptomatic infection

Course of disease is variable from sub-clinical to death (eg. Mild cases recover rapidly)

Incubation period ~ 1 week (time between infection and clinical signs)

Incubation period ~ 1 day (time between infection and clinical signs)

Viraemia lasts 14-28 days (cows up to 10 weeks)

It is an arbovirus transmitted by Culicoides spp.

It is an arbovirus transmitted by Lucilia spp.

Associated with red blood cells and leukocytes

Viraemia lasts 7-10 days (cows up to 6 weeks)

Replicate in nucleus

Very resistant to detergents, drying, heat, solvents, pH changes, disinfectants

Very stable in the environment

Require rapidly dividing cells (S‐phase)-- eg. intestinal cells

Easily killed by detergents, drying, heat, solvents, pH changes, disinfectants

Labile in the environment

Replicate in the cytoplasm

Highly contagious, systemic and enteric disease of cats

Causes bone marrow suppression, GIT signs, cerebellar hypoplasia (foetus)

Causes generalised disease of cats (domestic and wild cats)

Many infections are sub‐clinical

Onset of disease associated with profound panleukopaenia + fever

Incubation period ~5 days

Prefers mitotically active cells (S‐phase) (eg. Intestinal crypt cells, Lymphopoietic cells of bone marrow, Foetal cells (cerebellum, retina, death))

Acute cases progress to vomiting, (bloody) diarrhoea, dehydration while severe cases die in peracute stage

Distributed by free and cell associated viraemia

Virus enters via oropharynx, replicates in pharyngeal lymphoid tissue

One serotype with worldwide distribution

Endemic infection in vaccinated cat populations: unvaccinated cats at most risk

Endemic disease in unvaccinated cat populations: young cats affected

Two serotypes both with worldwide distribution

Seasonal disease pattern (kitten season)

Cats of all ages susceptible (Primarily see disease in kittens as maternal antibody wanes)

Incubation period ~5 days

Incubation period ~10 days

Causes generalised disease of cats (domestic and wild cats)

Causes generalised disease of cats and dogs (domestic and wild)

Trans‐placental infection in susceptible queens

Virus excretion in faeces (several weeks after clinical recovery), also in saliva, urine, vomit (acute stages)

Vector transmission

Direct contact required for transmission (eg. open wounds)

Supportive therapy (eg. Fluid therapy, blood / plasma transfusion, broad spectrum antibiotics)

Catteries: strict hygiene, quarantine and disinfection required

Vaccination (Inactivated and live‐virus vaccines available)

Antivirals are often used

Cleaning with bleach

Endemic worldwide

3 variants recognised (2a, 2b, 2c)

All members of Canidae family susceptible

High morbidity and mortality in initial outbreak situation (all ages affected)

High spread

Only endemic to Australia

Only domestic dogs are susceptible

Severe disease in pups between 6 weeks and 6 months of age (waning maternal immunity)

Myocarditis (but uncommon)

Haemorrhagic gastroenteritis and vomiting

Disease may be mild or sub‐clinical if sufficient immunity

Severely affected animals die

Causes CNS symptoms

Severe disease in adult dogs most often

Myocarditis (very common)

Myocarditis in pups infected late gestation or first 2 weeks of age due to rapid proliferation of myocytes in the perinatal period

Maldigestion and malabsorption and often severe haemorrhage (foetid smell, diarrhoea)

Mucosal collapse with contraction and fusion of villi of small intestine

Rapidly dividing cells in intestinal crypts are infected

Infection of the upper respiratory tract, mucosal cells (oronasal discharge)

Myocardial inflammation and necrosis

PCR assays

Haemagglutination

Presumptive diagnosis based on sudden onset of foul smelling haemorrhagic diarrhoea

Faecal immunoassays (virus shedding is transient: 3‐7 days after infection)

Bacterial culture

Supportive therapy (Fluid therapy, blood / plasma transfusion, broad spectrum antibiotics)

Kennels and shelters: strict hygiene, quarantine and disinfection\required

Vaccination (Inactivated and live‐virus vaccines available)

Antivirals are used often

Disinfection using sodium hypochlorite

Disinfection using Formalin, β‐propiolactone and oxidising agents

Most significant if virus is introduced into seronegative herd

Enzootic in many herds

Virus stable in environment for months

Morbidity reduced by vaccination

In endemic situation: disease seen in seronegative gilts infected in the sow herd when pregnant

Endemic only to the UK

Clinical signs in foetus depend on stage of gestation – apparent at farrowing

First clinical sign is often increased number of young sows returning to oestrus 3‐8 weeks after breeding

Some sows remain “endocrinologically pregnant” and don’t come back into oestrus until expected farrowing date

Reproductive failure

Death of young sows/gilts

Lifelong infertility in sows

<30 days gestation: foetal death and resorption

Local replication in tonsillar lymphoid tissue precedes viraemia and trans‐placental

Takes ~ 15 days for virus to reach foetus after infection

Takes ~ 2 days for virus to reach foetus after infection

Takes ~ 24 days for virus to reach foetus after infection

>70 days gestation: stillbirth or normal piglet (depends on immune response)

30‐70 days gestation: foetus fail to develop (mummification/stillbirth

>70 days gestation: foetal death and resorption

Difficult to diagnose early infections as embryonic death and resorption not obvious and no specimens

Serology (but limited usefulness)

Haemagglutination assays

PCR assays

Infected foeti contain high levels of virus

Ultrasound

Odd behaviour of sows when virus is infecting the placenta

Vaccination (inactivated vaccine) is available (however, limited opportunity to vaccinate gilts as they are bred at 7 months of age (waning maternal antibody)

Exposure of gilts prior to mating induces immunity (so that they do not become infected while pregnant)

Gilts should not be mated until they are 2yrs old

Abortion should be forced for the gilts first litter so she can become pregnant again quickly

Require actively dividing cells

Persistent infections

Stable at pH 3‐9

Resistant to disinfectants

Resistant to heating at 60oC, 30 minutes

Very stable in environment

Labile in the environment

Latent infections

Stable at pH 7-9

Psittacine beak and feather disease

Porcine circovirus

Chicken anaemia virus

Feline panleukopaenia

African horse sickness

First identified in Australian parrots in captivity

Birds under 5 years at greater risk

Disease in cockatoos, parrots and budgerigars

Disease in pigeons

Endemic to Africa only

In wild birds, malformed feathers and beak lead to difficulty feeding and death. In care, these birds can live for months/years if fed

Basophillic intracytoplasmic inclusions in follicular epithelium

Virus replicates in basal epithelial layer of feather follicles, beak and claws

Lymphoid depletion

Progressive disease

Virus replicates in the intestinal crypts

Virus causes death in less than 3 months due tp destruction of the intestinal crypts

Strict hygiene and quarantine protocols needed to keep infection out of breeding aviaries

There is only an experimental vaccine

Vaccination

Hard to eradicate when in the environment

Widespread in most pig populations

6 week old pigs present with weight loss, enlarged lymph nodes and dyspnoea

Progressive wasting disease

Causes a variety of clinical disease syndromes: Post‐weaning multisystemic wasting syndrome is most important

Causes infertility and abortions

Endemic only to Asia

Horizontal transmission by direct contact and contaminated fomites

Vertical transmission (into eggs)

2‐3 weeks of age: anorectic, anaemic, bone marrow aplasia, atrophy of thymus, bursa and spleen

Virus shed in faeces and feather dander

Virus shed in oronasal discharge

Young birds develop aplastic anaemia and generalised lymphoid atrophy

Only affects chickens

Affects all species of poultry