Circoviridae and Anelloviridae Flashcards
Family Circoviridae
Genus: circovirus
Psittacine beak and feather disease virus
Porcine circovirus type 1- non pathogenic
Porcine circovirus type 2- post-weaning multisystemic wasting syndrome
Viruses with circular single-stranded DNA genomes
-genus circovirus has a circular, single-stranded ambisense DNA
Virus replication occur in actively dividing cell
Virions are v stable. resisting 60C for 30 min and pH3 to 9
Genus: circovirus
Post weaning multisystemic wasting syndrome
Post weaning multisystemic wasting syndrome: etiology
Caused by porcine circovirus 2
Post weaning multisystemic wasting syndrome: host
Pigs. Most common at 4-6 wks of age or 2-3 wks post weaning
Post weaning multisystemic wasting syndrome: transmission
Virus is widespread in most pig pops
Fecal-oral transmission appears to be most common method of spread
Virus is found in all secretions, such as feces, urine, nasal secretions, saliva, etc
Vertical transmission (transplacental infection) occurs in swine
Stable and can survive on fomites for long periods
Post weaning multisystemic wasting syndrome: pathogenesis
Characterized by individual to coalescing foci of granulomatous inflammation in lymphoid tissue, lungs, liver, kidney, heart, and intestines, sometimes with prominent “botryoid” (grapelike) intra-cytoplasmic inclusion bodies in virus infected macrophages
Post weaning multisystemic wasting syndrome: pathogenesis- lymphoid depletion
Lymphoid depletion and lymphopenia in peripheral blood is a consistent feature in pigs that develop clinical PMWS
Loss of B cell and T cells. There appears to be no direct effect of PCV2 on lymphocytes and how this lymphopenia is caused is unknown
Post weaning multisystemic wasting syndrome: transplacental infection
Infection during the first and second trimester results in fetal death and resorption or aborted fetuses with severe cardiac congestion
Infection during last trimester has minimal effect on fetuses
Post weaning multisystemic wasting syndrome: Clinical signs
Subclinical infection most common
Lethargy, progressive weight loss, cough, dyspnoea, slow growth, lymphadenopathy (swollen inguinal lymph nodes), diarrhea, skin discoloration, congenital tremors, less commonly icterus (jaundice)
Post weaning multisystemic wasting syndrome: Co-infection
With porcine parvovirus, procine reproductive and resp virus, SIV, mycoplasma hyopneumoniae and/or a variety of opportunistic bact may cause severe disease and more pronounced lesions
Post weaning multisystemic wasting syndrome: diagnosis
Serological assays: most pigs are seropositive, therefore antigen detection is not of much value
Detection of PCV-2 nucleic acids by PCR
Post weaning multisystemic wasting syndrome: Vaccination
Chimeric vaccines: new generation chimeric vxns have been developed that utilize the non-pathogenic porcine circovirus 1 (PCV-1) as a genetic backbone for expression of the immunogenic capsid protein of PCV-2
Inactivation or baculovirus-expressed vxns: virus-like particles that include the capsid protein of PCV-2 are also available as vaccines
Sow vaccination: antepartum
Porcine Dermatitis and Nephropathy Syndrome
Associated with PCV2 Sporadic Reported in older piglets Findings: -necrotizing skin lesions -necrotizing vasculitis -necrotizing and fibrinous glomerulonephritis
Family: Anelloviridae
Genus: gyrovirus
Chicken infectious anemia virus
Genus: gyrovirus
Has a circular, single-stranded negative sense DNA
Chicken infectious anemia virus having 12 trumpet life structures that are less obvious in the other circoviruses
Chicken infectious anemia: host
Highly contagious disease of young chickens (2-4 wks)
Older chickens are more resistant to clinical disease
Chicken infectious anemia: transmission
Virus is shed in feces and feather dander
Horizontal transmission is through inhalation or oral exposure
Virus is also transmitted vertically through egg
Environmentally stable virus, remains in contaminated fomites for long periods
Chicken infectious anemia: pathogenesis
Principal sites of replication= hemocytoblasts in BM, precursor T cell in thymus cortex, dividing CD4 and CD* cells in spleen
Replication in hemocytoblasts=anemia, which rep in T cells= immunosuppression
Apoptin protein of virus induces apoptosis and cause destruction of infected lymphocytes
Immunosuppression and aplastic anemia. Blood may be watery and clot slowly as a result of thrombocytopenia
Birds= vulnerable to secondary bact and fungal infections
Virus rep in oviduct may be regulated by estrogen, allowing more efficient vertical transmission
Chicken infectious anemia: Clinical signs and lesions
Chicks are anorexic, lethargic, depressed, reduced body weight gain, pale
Blood may be watery and clot slowly as a result of thrombocytopenia
PCV low (in chicks, anemia= PCV<27)
SubQ hemorrhages and skeletal hemorrhages, pale muscles
CAV-induced thymic atrophy
Femur with pale aplastic bone marrow
Pale carcass
Atrophies bursa
Pall bone marrow and watery blood
Chicken infectious anemia: Diagnosis
CS
Examination of blood: low PCV, exam of blood for total erythrocyte count will reveal anemia, thrombocytopenia, blood watery and will clot slow
Necropsy
Histopathology
Serology: ELISA, neutralization test, FAT test
Virus isolation
PCR, RTPCR
Chicken infectious anemia: Vaccination
Immunity to chicken anemia virus is complex
Presence of Abs in breeders greatly reduced vertical as well as horizontal transmission
Aim of Vxn is to protect progeny from vaccinated breeders from early infections by means of maternally derived Abs
Live Vxns available for Ab negative breeder flocks before start of egg production
Administration is by injection or by addition to the drinking water depending on type of vxn
Bc of the synergism between CAV and other immunosuppressive viruses, such as marek’s disease virus, control of latter also important
