Week 8

• Asfarvirida (African Swine fever)


  Only known DNA arbovirus

  OIE list A disease

  Endemic to sub-saharan africa, island of sardinia, italy

  Recent outbreaks in eastern europe and russia
• African Swine fever hosts

  • All breeds and types of domestic pigs and european wild boar
  • Warthogs
  • Bush pigs
  • Giant forest hogs
• Warthogs, bush pigs, and giant forest hogs have inapparent infection and act as reservoirs
• Asfarviridae stability

  • Survive at least 30 days in pens
  • Very resistant to wide range of ph
  • Survive chilled carcass
  • Highly resistant to putrefaction
  • Remains viable for long period
• Asfarviridae transmission

  • Blood
  • Feces
  • Tissues
  • Uncooked or undercooked pork products
• Asfarviridae

  • Can multiply in vectors
  • Hemadsorption
  • Doesn't hemagglutinate
  • Pig erythrocytes will adhere to surface pig monocyte/macrophage cells infected with african swine fever
  • Attributed to virus specific protein
  • Appears on plasma membrane of infected cells during late infection
• Asfarviridae Transmission

  1. Vector: Ornithodoros spp. (soft ticks)

  2. Biological vectors: Replicates in tick (tick to tick transmission), Trans-stadial, transovarial, sexual transmission

  3. Reservoir hosts (sylvatic cycle): Transmission between warthogs and soft ticks
• Asfarviridae domestic cycle

  • Primary outbreaks in domestic swine
  • Bite of infected tick
  • Direct contact with infected animal (oronasal spread)
  • Indirect contact with fomites
  • Virus spreads to new areas when pigs are fed uncooked scraps that contain infected pork
  • Aerosol
  • Mechanical transmission: Biting flies
• All body fluids and tissues contain large amounts of infectious african swine fever
• Pigs that survive african swine fever infection

  • Become carriers
  • Shed virus in secretions and excretions
• Asfarviridae Pathogenesis

  1. Primary hemorrhages - Vascular damage from degeneration of vascular endothelium, DIC, Infection and necrosis of megakaryocytes, Activation and extensive destruction of monocytes/macrophages, Thrombocytopenia & coagulation defects in many organs and tissues (edema, infarction, exudation, hemorrhages)

  2. Apoptosis: p54 protein directly induced apoptosis of host cells, Infected macrophages release cytokines and apoptotic mediators, Apoptosis of lymphocytes and mononuclear phagocytic cells

  3. Leukopenia, lymphopenia, thrombocytopenia
• African swine fever clinical signs

  • Peracute: Pigs may die suddenly
  • Acute form: High fever, Cyanotic skin blotching, Respiratory distress, Diarrhea (initially mucoid, later may become bloody), Abortion
  • Chronic form: Emaciation & stunting, Swollen joints, Ulcers & reddened or raised necrotic skin foci, Pneumonia, Enlarged friable spleen, Fibrinous pericarditis & myocardial hemorrhage
• Asfarviridae Immunity

  • Infected pigs produce virus-specific antibodies, Sera from infected pigs don't neutralize the virus, Humoral immunity response doesn't seem to have substantial protective value, Attempts to develop a vaccine have been unsuccessful
• Asfarviridae Prevention

  1. Pigs should be kept in well constructed pig sites, Hygienic conditions, Controlled entry to the piggery

  2. Movement of pigs inside the country and across international borders, Pigs should not be fed swill that might contain remains of pigs (should be boiled for 30 minutes and cooled before feeding)
• Papillomaviridae

  Can transform cultured cells

  Produce papillomas on skin and mucous membranes of most animals species

  Warts are benign neoplasms that may progress to malignancy as a property of specific virus strains, viral DNA is integrated into that of the host

  DNA is episomal, not integrated into host-cell DNA, persists as an autonomously replicating episome

  Hyperplastic epithelial outgrowths generally regress spontaneously

  Species and site specific

  Serological cross-reactivity has not been detected among papillomaviruses of different species
• Papillomaviridae replication

  Linked intimately to growth and differentiation of cells in stratified squamous epithelium, Skin and some mucous membranes
• Bovine papillomatosis

  • Warts more commonly seen in cattle than any other domestic animal
  • Natural infection of horses may occur after exposure of horses to cattle
• Transmissionof bovine papillomatosis

  • Contaminated fomites: Milking equipment, Halters, Nose leads, Grooming and earmarking equipment
  • Sexual transmission: Venereal warts
• Fibropapilloma

  Mostly caused by bovine papillomavirus 1, 2, and 5

  Fibroid core covered to variable depth with stratified squamous epithelium (outer layer are hyperkeratinized)

  Lesions vary from small firm nodules to large cauliflower-like growths

  Grayish to black in color, Rough and spiny to the touch

  Common on udder and teats; head, neck, and shoulders, Omasum, vagina, penis, anus
• Cutaneous papillomas

  Bovine papillomaviruses type 3

  Lesions lack fibrous core

  Usually flat with broad base
• Bracken fern and bovine papillomavirus

  Bovine papillomavirus 4

  Transient papillomas in alimentary tract

  Ingestion of bracken fern can result in transition to invasive carcinoma of alimentary tract, Syndrome of enzootic hematuria (Papillomavirus 1 and 2 may also contribute, charaterized by hematuria and/or urinary bladder cancer)
• Treatmentof bovine papillomatosis

  • Surgical excision or cryosurgery with liquid nitrogen
  • Topical agents: Podophyllin, Undiluted medical grade DMSO
  • Bovine interferon-ɑ
  • Wart vaccine: Killed virus
• Canine oral papillomatosis

  Contagious

  Self-limiting disease

  Warts usually benign on the lips - Can spread to buccal mucosa, tongue, palate, and pharynx, May become roughened and cauliflower-like, Don't extend below epiglottis or into esophagus

  Lesions typically regress spontaneously

  Progression to squamous cell carcinoma occurs rarely
• Clinical signsof canine oral papillomatosis

  • Halitosis, hemorrhage, hypersalivation, discomfort
  • Numerous warts may interfere with mastication and deglutition
  • Secondary bacterial infection and ulceration may occur
  • Ocular warts - conjunctiva, cornea, eyelid margins
  • Recovered dogs are refractory to reinfection
• Treatmentof canine oral papillomatosis

  • Surgical excision, cryosurgery, electrosurgery
  • Autogenous vaccines
• Equine sarcoids

  Commonly occur in horses, donkeys, mules, 1-6 years of age, Most common neoplasia in horses

  Locally invasive benign fibroblastic skin tumors

  Associated with bovine papillomavirus 1 or 2

  Sarcoids don't metastasize, May persist for life, Locally invasive, Recur after surgical removal
• Transmissionof equine sarcoids

  • Not yet confirmed
  • Flies may act as vectors
  • Fomites - stable management practices
• Equine sarcoid Lesions

  • Commonly occur in traumatized areas
  • Single or multiple
  • May reach size of man's fist
  • Bulge under skin
  • May become ulcerated
• Treatmentof equind sarcoids

  • Cryotherapy
  • Surgical or laser excision
  • Local immune modulation
  • Local radiotherapy
• Parvoviridae

  Viruses are very stable, Disinfection of contaminated premises is difficult

  Replication occurs in nucleus of dividing cells, Infection leads to large intracellular inclusion bodies
• Parvovirus

  Replication occurs only in cells that pass through mitotic S phase, Can't replicate in stationary cells, Rely on enzymes of actively dividing cells
• Human parvovirus B19 is different from parvovirus seen in dogs and cats, No evidence of transmission of B19 from dogs or cats or vice versa
• Feline panleukopenia (feline distemper; feline infectious enteritis)


  Etiology: Feline parvovirus, Highly contagious, often fatal disease of cats, Severe in kittens, Ubiquitous disease, Virtually all cats are exposed and infected within first year of life, Unvaccinated kittens acquire maternal antibodies, Protected up to 3 months of age, Most infections subclinical, Up to 75% of all unvaccinated healthy cats have demonstrableantibody titers by 1 year of age, Shed virus in urine or feces, Maximum of 6 weeks after recovery, Maintained in population by environmental persistence
• Owners losing a kitten to feline panleukopenia shouldn't introduce new kitten into household without having it vaccinated
• Transmissionof feline panleukopenia

  Oronasal, Exposure to infected animals, Feces, secretions, Contaminated fomites

  In-utero

  Mechanical - flies
• Enteritis in feline panleukopenia

  1. Virus selectively damages replicating cells deep in the crypts of intestinal mucosa

  2. No replacement of lost absorptive cells at tips of villi

  3. Shortening of intestinal villi

  4. Marked villous blunting and fusion

  5. Malabsorption and diarrhea
• Central nervous system infection in feline panleukopenia

  • CNS, optic nerve, and retina susceptible to damage
  • Cerebellar damage most commonly reported
  • Cerebellar hypoplasia
• Cerebellar hypoplasia in feline panleukopenia

  1. infected during last 2 weeks of pregnancy of first 2 weeks of life
  2. Lysis of mitotic cells of external germinal layer
  3. Impaired cerebellar development
• Disseminated intravascular coagulation in feline panleukopenia

  • Susceptible to secondary bacterial infection
  • Gram-negative endotoxemia common sequelae of systemic FPV infection
  • Endotoxin induces expression of tissue factor on endothelial cells
  • Potent activator of coagulation
  • Resulting in DIC followed by hemorrhages
• Clinical manifestations of feline panleukopenia

  • Diarrhea
  • Lymphopenia
  • Neutropenia, thrombocytopenia and anemia
  • Loss of pregnancy
  • Cerebellar ataxia