Herpesvirus Flashcards
(115 cards)
1
Q
Herpesvirus
General Characteristics
A
- dsDNA
- Icosahedral
- Enveloped
- Replicates in nucleus-> Nuclear inclusion bodies!
- Strongly immunosupressive , strong CPE
- Weak antigenicity-> weak immune response-> Lifelong carriers and latency
- Cross reaction withim the genera - cross protection
- Weak resistance (exc. Marke’s disease virus)
2
Q
Infectious Bovine Rhinotracheitis
Species affected
A
Ru
3
Q
Infectious Bovine Rhinotracheitis
Most susceptible
A
All age groups
- Respiratory form: 1-6mo
- Calves encephalitis <5mo
- Genital form: adults
4
Q
Infectious Bovine Rhinotracheitis
Spread
A
Slow spread
- Carrier animal introduction
- Semen
- contact
- Airborne
5
Q
Infectious Bovine Rhinotracheitis
Pathogenesis
A
- Aerogenous: Respiratory Mucosa —> Inflammation —> Viraemia —> Other organs —> Encephalitis in calves and Abortion
- Ascending inflammation in the nose —> nerves —> calf encephalitis
- Genital form —> Degeneration and inflammation of the mucosal epithelium and nodule formation
6
Q
Infectious Bovine Rhinotracheitis
Primary replication
A
- Aerogenous: respiratory mucosa
- Genital: genital mucosal epithelium
- Incubation: 2-5d
7
Q
Infectious Bovine Rhinotracheitis
Target organs
A
Respiratory & Genital organs
8
Q
Infectious Bovine Rhinotracheitis
Clinical signs
A
Febrile disease!
*Respiratory form: conjunctivitis, coughing, nasal discharge, encephalitis, interstitial pneumonia, abortion(in resp form, not genital), red nose disease(necrotic mm), calf encephalitis (<5mo)
*Genital form: adults,
Vulvoginits& Balanoposthitis
Greyish yellow nodules, vaginal discharge
*no fertilization& abortion in acute
9
Q
Infectious Bovine Rhinotracheitis
Pathology
A
- Inflammation, hemorrhages and erosions in upper respiratory
- Intranuclear inclusion bodies
10
Q
Infectious Bovine Rhinotracheitis
Diagnosis
A
CS
PCR
ELISA
11
Q
Infectious Bovine Rhinotracheitis
Treatment
A
No effective treatment
Ab
12
Q
Infectious Bovine Rhinotracheitis
Prevention and immunity
A
- AI tested bulls
- closed groups according to age
- Marker vaccines
- Live&inactivated vaccine - inactivated- breeding, cow before parturition, 2-3mo calves, heifers in fertlization
13
Q
Bovine Herpesmamillits
Species affected
A
- Cattle, Buffalo (other ru might be seropositive)
* Humans —> Zoonotic!
14
Q
Bovine Herpesmamillits
Most susceptible
A
Milking Cows
15
Q
Bovine Herpesmamillits
Occurrence
A
- Africa, Australia and USA
* Rare in Europe
16
Q
Bovine Herpesmamillits
Spread
A
- Infected animal
- Spread within the herd via milking
- Arthropod vectors
17
Q
Bovine Herpesmamillits
Clinical Signs
A
- After first parturition: teat edema, suffusion, pustules
- Hu: lesions on the hands
- Subclincial infection is common
- Secondary infection -> mastitis
- Reduced production
- Teat scarring
18
Q
Bovine Herpesmamillits
Primary Replication
A
- Teat epithelium
* Incubation: 3-7d
19
Q
Bovine Herpesmamillits
Target Organs
A
Teat
20
Q
Bovine Herpesmamillits
Pathogenesis
A
- Epithelial damage, inflammation —> pustules, scabs, lacerations, erosions —> recovery within 1-2 weeks
21
Q
Bovine Herpesmamillits
Pathology & Histopathology
A
Intranuclear inclusion bodies
22
Q
Bovine Herpesmamillits
Diagnosis
A
Histopathology
Virus isolation
PCR
Serology
23
Q
Bovine Herpesmamillits
Treatment
A
Local, symptomatic treatment
24
Q
Bovine Herpesmamillits
Prevention & Immunity
A
No vaccine available!
25
Malignant Catarrhal Fever
Species Affected
* Reserviors: Wildbeest, Sheep (asymptomatic,the only oneswho can infect)
* Ru - dead end hosts
26
Malignant Catarrhal Fever
Most susceptible
Elderly Animals!
27
Malignant Catarrhal Fever
Occurrence
* Africa —> Wildebeest associated MCF
| * Rest of World —> Sheep associated MCF
28
Malignant Catarrhal Fever
Spread
* Carrier animal introduction, thier secretion (respiratory)
| * Cattle are unable to shed and transmit the virus
29
Malignant Catarrhal Fever
Pathogenesis
Aerogenous Infection —> Cell associated viraemia —>immunopathological process
* Lifelong infection in surviving animals
* Systemic febrile disease
30
Malignant Catarrhal Fever
Primary Replication
Latent infection -Incubation: 2w-couple of months
31
Malignant Catarrhal Fever
Target Organs
* All organs
* Lifelong infection in surviving animals
* Systemic febrile disease
32
Malignant Catarrhal Fever
Clinical Signs
* Peracute: fever, hemorrhagic enteritis, convulsions, Urinary bladder wall oedema death.
* Acute: keratitis, conjuctivitis, laboured breathing, laminitis, odema, severe hemorrhagic enteritis, CNS
33
Malignant Catarrhal Fever
Pathology & Histopathology
Peracute:
* Inflamed mucosa, haemorrhages, without erosions
* Urinary bladder wall oedema
Subacute:
* Eye lesions, *Hemorrhagic pneumonia and enteritis
* Arteritis
34
Malignant Catarrhal
Fever
Diagnosis
History, CS, PM, histopathology, PCR, ELISA
35
Malignant Catarrhal Fever
Treatment
Poor prognosis
| No effective treatment
36
Malignant Catarrhal Fever
Prevention & Immunity
No vaccine available!
37
Aujeszky’s Disease (Pseudorabies)
Species Affected
Pigs: natural hosts&reservoir
| Other mammals - dead end hosts
38
Aujeszky’s Disease (Pseudorabies)
Most susceptible
All age groups
39
Aujeszky’s Disease (Pseudorabies)
Spread
*infected swine, semen (vertical transmission), fomites, mechanical vectors (rodents), raw pork!!
40
Aujeszky’s Disease (Pseudorabies)
Pathogenesis
PO/inhalational-> haemolymph->nerves->encephalitis> Secondary lung multiplication->fever& respiratory
Pigs may be lifelong carriers& shedders
41
Aujeszky’s Disease (Pseudorabies )
Primary Replication
Tonsils, Nasal & Pharyngeal mucosa
2-8d incubation
Placental crossing!
42
Aujeszky’s Disease (Pseudorabies)
Target Organs
All organs (lungs, brain)
43
Aujeszky’s Disease (Pseudorabies)
Clinical Signs
*Febrile& systemic
*Vertically infected piglets will be asymptomatic
*Piglets usually have febrile general disease, CNS (~100% mortality), sometimes die without CNS cs
*Gilts mostly recover after 5-6d(resp& CNS symp)
*Pregnant: abortion, stillbirth, infertility
*Adults are usually subclinical
*Ru- mad itch disease, acute lethal encephalitis, death in 1-2s, recovery is rare
Ca- febrile& general, acute lethal encephalitis
44
Aujeszky’s Disease (Pseudorabies)
Pathology & Histopathology
* Lung edema
* suckling piglets- necrotic foci on pharyngeal mucosa& tonsils, spleen and liver
* hemorrhages in Ln
* Nuclear inclusion bodies
* Meningitis
45
Aujeszky’s Disease (Pseudorabies)
Treatment
No effective treatment
| Ab
46
Aujeszky’s Disease (Pseudorabies )
Prevention & Immunity
Epidemiology measures
* No feeding with raw pork to carnivores
* Maternal protection until 8-14w
* modified live vaccine at 10-121wo, 6mo, at fertilization and 70-904 pregnant
* The virus can maintain in vaccinated pigs!
47
Inclusion Body Rhinitis
Most susceptible
Nestlings/newly weaned/ pregnant
48
Inclusion Body Rhinitis
Spread
Airbonre/direct contact
49
Inclusion Body Rhinitis
Pathogenesis
PO/Inhalational Infection —> Viraemia —> Lymphocytes & alveolar macrophages —> latency in lacrimal gland, nasal mucosa & kidney
*Shed in nasal&ocular secretion, urine, aerosol
50
Inclusion Body Rhinitis
Target organ
Upper Respiratory Tract
| Placental Crossing!
51
Inclusion Body Rhinitis
Clinical Signs
Piglets < 3weeks of age:
* Fever, appetite loss, sneezing, serous or bloody nasal discharge
* Up to 25% mortality
Piglets > 6 weeks of age: Inapparent
*Infection of foetus weak, SMEDI
52
Inclusion Body Rhinitis
Pathology & Histopathology
* Mucopurulent exudate in nasal passages
* SC odema & in larynx, pharynx , lungs
* serum accumulation in body cavities , pleura, pericardium
* Intranuclear inclusion bodies in mucous
* cytomegaly
53
Inclusion Body Rhinitis
Treatment
No effective treatment
54
Inclusion Body Rhinitis
Prevention & Immunity
Maternal immunity up to 4wo
55
Equine Rhinopneumonitis / Epizootic Abortion
Species Affected
Equids are the hosts & reservoirs
56
Equine Rhinopneumonitis / Epizootic Abortion
Most susceptible
Foals (<2yo) , pregnant mares
57
Equine Rhinopneumonitis / Epizootic Abortion
Spread
quick, aerosols, direct contact, ingestion, semen, aborted fetus ,placenta - infective sources
58
Equine Rhinopneumonitis / Epizootic Abortion
Pathogenesis
PO/inahalational -> viraemia via lymphoid cells
59
Equine Rhinopneumonitis / Epizootic Abortion
Replication& Target Organs
Respiratory mucosa
3-5d incubation
placental crossing!
60
Equine Rhinopneumonitis / Epizootic Abortion
Clinical Signs
1. interstitial pneumonia: <2yo foals- ,fever (risk of co-infection with R.equi - laminitis)
2. abortion:(weak, dying foals) , usually >5m of pregnancy, abortion storm (30-40%). After recovery, mares return cycling and fertility
3. CNS: neural degeneration- paresis(lysis) tail& anus paralysis - euthanasia
61
Equine Rhinopneumonitis / Epizootic Abortion
Pathology
* Pneumonia
| * aborted fetus: yellow, SC edema, lung edema and necrotic foci, hemorrhages in mm and brain
62
Equine Rhinopneumonitis / Epizootic Abortion
Treatment
Rest, supportive therapy
| *Prevent abortion: hyperimmune serum and acycloguanosine
63
Equine Rhinopneumonitis / Epizootic Abortion
Prevention & Immunity
Early dx.- > vaccination
* ongoing abortion storms are difficult to eradicate
* maternal immunity until 3-6mo
* vaccination with weak Ag - only effective for respratory form, foals from 3mo and 5m pregnant mare, new horses in quarantine
64
Equine Multinodulary Pulmonary Fibrosis
Most susceptible
Few week old foals
65
Equine Multinodulary Pulmonary Fibrosis
Clinical Signs
* Fever
* Mild respiratory symptoms (serous nasal discharge, coughing) - recovery after 1 week/ secondary bacterial infection (R.equi!)
* Keratoconjunctivitis,
* swollen lymph nodes
* Can also be isolated from clinically healthy horses!
66
Equine Multinodulary Pulmonary Fibrosis
Prevention & Immunity
Hyperimmune serum
67
Coital Exanthema of Horses
Pathogenesis
Mating , iatrogenically (rectal/genital exam.)
| foals - from teat suckling
68
Coital Exanthema of Horses
Clinical Signs
* venereal->nodule, vesicle and pustule formation on epithelium of vagina,
* prepuce and penis -> erupts to become erosions -> scab
* Recovery usually within 2-3 weeks but unpigmented spots and scars will remain
* DOESN'T affect pregnancy!
* No viraemia
* Lifelong latency&persistant
69
Coital Exanthema of Horses
Primary Replication
Genital mucosa
| 6-8d incubation
70
Coital Exanthema of Horses
Histopathology
Intranuclear inclusion bodies
71
Coital Exanthema of Horses
Prevention & Immunity
No mating during signs and one month thereafter
72
Canine Herpes
Most susceptible
All age groups
73
Canine Herpes
Spread
Close contact with secretion and infected animals, replicates in leukocytes->generalized infection
* Venereal
* Intrauterine
* optimal temp for the virus: 33-35c
74
Canine Herpes
Clinical Signs
* Intrauterine infection: generalized& fatal death/recovery with CNS
* <2wo: death/recovery with CNS signs( vision and motion) necrotising vasculitis, fever, rash, death if opisthotonus
* >2wo+adults: localized infection in respiratory/reproductive tract-> latency, reactivation in stress.
* adults are usually asymptomatic/ vesicular vaginitis or posthitis, abortion, transient infertility
75
Canine Herpes
Pathology & Histopathology
* Generalized haemprrhages&odema
* Necrosis in spleen, liver, brain, lungs
* Nuclear inclusion bodies
76
Canine Herpes
Treatment
Hyperimmune sera IP, antivirals
77
Canine Herpes
Prevention & Immunity
keep warm, vaccinate 2x in pregnancy
78
Infectious Rhinotracheitis of Cats
Most susceptible
all age groups
| predisposing factors: <6mo, old, pregnant , weak
79
Infectious Rhinotracheitis of Cats
Spread
very contagious, contact, airborne, vertical
shed in nasal discharge
80
Infectious Rhinotracheitis of Cats
Pathogenesis
PO/Inhalational —> Replicates in respiratory mucosa (necrosis& inflammation) —> Viraemia —> foetus —> Abortion
81
Infectious Rhinotracheitis of Cats
Primary Replication
Respiratory mucosa
3-6d incubation
*Latency in pharynx lymp and trigiminal ggl.
82
Infectious Rhinotracheitis of Cats
Clinical Signs
* Serous->mucopurulent conjuctival &nasal discharge, *Corneal ulcers,KCS, epiphora.
* In young age: permanent damage to nasal and sinus tissue - disruption of cillary clearance -> chronic bacterial infection
* Abortion in 6th week
83
Infectious Rhinotracheitis of Cats
Histopathology
intranuclear inclusion bodies
84
Infectious Rhinotracheitis of Cats
Treatment
Symptomatic treatment: IV, feeding tube, oxygen ,hyperimmune serum
85
Infectious Rhinotracheitis of Cats
Prevention & Immunity
* Attenuated (intranasal) or inactivated vaccines in 7wo, 2x, then yearly only protects from CS, doesn't prevent infection
* Maternal immunity 7-10wo
86
Infectious Laryngotracheitis of Chicken
Species Affected
Mainly Chicken.
| But also Pheasant, Turkey, Peacock, Quail
87
Infectious Laryngotracheitis of Chicken
Most susceptible
Growers and Adults
88
Infectious Laryngotracheitis of Chicken
Spread
Very contagious , Airborne
89
Infectious Laryngotracheitis of Chicken
Pathogenesis
Airborne —> Upper airways, conjunctiva —> Local multiplication in the upper respiratory epithelium —> endothelium damage —> exudates, oedema, haemorrhage
* No viraemia
* Lifelong carriers & shedders
90
Infectious Laryngotracheitis of Chicken
Clinical Signs
* Mild form: mild respiratory symptoms, seconday bacterial infection
* Classic virulent form: dyspnoea, conjuctivitis, almond shaped eyes, cheesy plugs in trachea recovery in 2-6w
91
Infectious Laryngotracheitis of Chicken
Pathology & Histopathology
* inflammed, necrotised tracheal mucosa, pseudomembrane , bleeding, cheesy plugs
* Nuclear inclusion bodies
92
Infectious Laryngotracheitis of Chicken
Treatment
No effective treatment
| Slaughter affected birds if sporaic
93
Infectious Laryngotracheitis of Chicken
Prevention and Immunity
Eye drop with attenuated vaccine
| *Broilers 2-4wo, 12-16wo, protected for 1 laying period, doesn't last long
94
Duck Plague / Duck Viral Enteritis
Most susceptible
Layer ducks
Adults
Wild ducks are main reservoirs
Notifiable!
95
Duck Plague / Duck Viral Enteritis
Spread
Contact with wild duck& thier secretion
| Notifiable!
96
Duck Plague / Duck Viral Enteritis
Pathogenesis
PO —> primary replication -->viraemia —> endothelia damage of blood—> necrosis, haemorrhage, fibrin precipitation in mucosa
*lifelong carriers and shedders
Notifiable!
97
Duck Plague / Duck Viral Enteritis
Primary Replication
*Intestines —> Bloody diarrhoea
*Upper Respiratory Tract —> Rhinitis
*Eye —> Conjunctivitis
*Incubation 3-7 day
Notifiable!
98
Duck Plague / Duck Viral Enteritis
Target Organs
Blood Vessel Walls
| Notifiable!
99
Duck Plague / Duck Viral Enteritis
Clinical Signs
*Bloody diarrhea, rhinitis, conjuctivitis death within 4-6d(15-25%)
*Eye: photophobia, eyelid edema
*CNS signs: ataxia, tremors, droopiness, floating on water
*Ducklings: blue beaks, blood-stained vents, changed voice.
*adult may die while appear healthy or with prolapsed penis blood in cavities,
*paint brush heart,
*large patchy diphteric membrane hepatomegaly, brass, gray and hemorrhagic.
Notifiable!
100
Duck Plague / Duck Viral Enteritis
Treatment
No effective treatment
Slaughter affected birds if sporadic
Notifiable!
101
Duck Plague / Duck Viral Enteritis
Prevention & Immunity
* Avoid contact with wild waterfowl
| * Modified live virus vaccine available >3wo, 2x , immunize layers 2x before laying season
102
Pigeon Herpes
Most susceptible
2-6 month old
103
Pigeon Herpes
Pathogenesis
Airborne/ PO from mother
104
Pigeon Herpes
Clinical Signs
* Adults are asymptomatic
* Young are asymptomatic when maternal ab protection
* co-infection with chlamydia, E. coli mycoplasma, pasteurella
* Acute: conjuctivits, pharyngitis, rhinitis, diarrhoea, death(10%)
* Chronic: sinusitis, dyspnoea, co-infection
* latent infection and periodic shed
105
Pigeon Herpes
Pathology & Histopathology
* Hepatomegaly, bloody intestine, conjunctival edema, enlarged pancreas
* Nuclear inclusion bodies
106
Pigeon Herpes
Treatment
No effective treatment
107
Pigeon Herpes
Prevention & Immunity
Attenuated or inactivated vaccines (may be with other viruses- polyvalent) 50do&2w after
108
Marek's Disease
Species Affected
Chicken
109
Marek's Disease
Most susceptible
1-2 weeks old, hens are more susceptible
110
Marek's Disease
Spread
very resistant virus, airborne, quick spread
* In feather follicular epithelial cells and in dust —> Over 1 year
* In litter for about 4 months
111
Marek's Disease
Clinical Signs
*Severity is strain dependant
* 1. Neurological form: the classical, chronic, low virulence, long lasting, recovery >1yo. growers &young hens, one sided leg paralysis, wing and claw paralysis, convulsions, Grey eye disease, blindness , enlarged plexus brachialis and ischiadicus
2. Transient paralysis: more virulent, quick (24h), may lead to visceral form. 6-7wo &unvaccinated
* 3. Visceral form: acute, CNS in vax, 100% morbidity in unvaccinated, high mortality! tumours in all parenchymal organs, red leg disease, T cell tumour, MATSA
4. Peracute/anaemia: 4-6 yo
112
Marek's Disease
Pathology & Histopathology
* microtumours in skin, CNS signs, small focal tumours in organs, grey eye disease, in very virulent -> mononuclrar cell tumours(T)
* Neurological: Enlarged plexuss brachialis&Ischiadicus
113
Marek's Disease
Diagnosis
*No differentiation between Avian Leucosis and Marek’s
disease based on clinical signs!
*PM, histo, PCR
114
Marek's Disease
Prevention and immunity
*Prevent early infection:
• Frequent egg collection, shell disinfection, hatching hygiene
• Cleaning, disinfection of stables and ventilators
• Overpressure ventilation, filtered air, separate stuff
• Cleaning and disinfection and destroying fomites
• Breeding genetically resistant
chicken lines
*Immunisation
• In ovo vaccination - 18do embryo
• Vaccinate the day of hatching
• Vaccine does not protect from infection
115
Marek's Disease
Treatment
No effective treatment
