Overview Flashcards
Parvo topics
Foetopathy of swine caused by parvoviruses (SMEDI).
Canine enteritis caused by parvoviruses.
Feline panleukopaenia.
Parvovirus diseases of the mink.
Derzsy’s disease of geese, parvoviral disease of ducks
Parvo general
- Strong resistance and antigens.
- stenoxen
- ssDNA
- dividing cells - cellular polymerse
Circoviral topics
Circoviral disease of swine (PMWS, PDNS).
Avian diseases caused by circoviruses, chicken infectious anaemia.(anello)
Circovirus general
- Small circular ssdna
- resistant, good ag
- dividing cells
- ## NA also infective
Parvo pathogenesis
PO -> lymphoid throat –> small int –> blood –> thymus, foetus, spleem ln, crypt, myocardial cells, bm (cross placenta cat(cerebellar hypopl) su(myoclon gongenita/shaking piglets
Circo pathogenesis
Oronasal -> macrophages -> viraemia -> lymphoid, lung, GI, liver, brain, heart, kidney
Anello pathogenesis
PO -> intestines/resp -> viraemia -> bm -> anemia
Papilloma pathogenesis
Animals rubbing against eachother causing small abrasions, Spread to lesions - mainly direct contact or mechanic vector eg fly, mosquito. Iatrogenic spread -> infection
Have to infect in str. Basale to replicate
=need opening
Then move to str corneum -> sheds from here!
1-2month incubationperiod bc longer process
Papilloma general
Resistant non-enveloped, dsDNA, Stenoxen and oncogenic Latency Hidden ag Autovax!
Polyoma topics
Haemorrhagic nephritis and enteritis of geese.
Polyoma pathogenesis
Oronasal -> lymhoid tissue in throat -> viraemia -> repl in endothelial cells, bursa, kidney, GI mm, b-cells
Polyoma general
Resistant, dsDNA, good ag but hidden, stenoxen, latent, oncogenic
Adeno topics
- Pneumoenteritis of ruminants caused by adenoviruses.
- Canine infectious hepatitis and infectious laryngotracheitis.
- Adenoviral diseases in poultry.
Adeno in general
Resistant, good ag, mastadeno most imp, dsDNA, oncogenic effect but NEVER tumors!
Cowdry A inclusion bodies
Adeno pathogenesis
Oronasal -> tonsilla -> viraemia -> resp, enteral mm, liver, kidney
Herpes topics
- Characteristics of herpesviruses, groups, epidemiological features.
- Infectious bovine rhinotracheitis (aetiology, epidemiology, pathogenesis, clinical signs, post mortem lesions).
- Infectious bovine rhinotracheitis (diagnosis, prevention, control, eradication). - Bovine herpesmamillitis, inclusion body rhinitis of swine.
- Malignant catarrhal fever.
- Aujeszky’s disease (aetiology, epidemiology, pathogenesis, clinical signs, post mortem lesions). - Aujeszky’s disease (diagnosis, prevention, control, eradication).
- Diseases of horses caused by EHV-1 and EHV-4 viruses.
- Diseases caused by EHV-2, EHV-3 and EHV-5 viruses in horses.
- Canine herpesviral disease.
- Feline infectious rhinotracheitis.
- Infectious laryngotracheitis of chicken.
- Marek’s disease.
- Duck plague, herpesviral disease of pigeons.
Herpes in general
Latency
Weak antigens, short lasting immunity, stenoxen (exc aujesky, malignant catarrhal fever.) immunosuppr reactivates latency -> always potential shedding!
Alpha: broad sprectrum, short repl, neuron latency
Beta: narrow spectrum, long repl, gland, lymphoid
Gamma: narrow spectrum, B/T cell tumor, immunosuppression, lymphoid cell latency
Duck plague is unassigned!
Herpes pathogenesis
Alpha: aerogenic -> resp mm -> viraemia -> brain, genitals, foetus, udder
Beta: aerogenic -> lymphocytes, alveolar macroph -> viraemia -> foetus (incl body rhinitis)
Gamma: aerogenic -> macrophages anemia -> immunosuppression (malign cath fever, EHV-2,5)
Pox topics
- Bovine diseases caused by poxviruses. - Contagious pustular dermatitis of sheep and goat. Swine pox. - Sheep and goat pox. - Myxomatosis. - Fowl pox.
Pox general
DNA, enveloped.
Epitheliotrop virus, acute, mammals, birds, may be widespread lesions or localized.
Poxv.
Resistant viruses! enveloped, but decades = protected in scabs. = once present hard to eradicate!
Often can infect more than one spp, and several are zoonotic! (Euryxen)
In general: cytopl IC (repl) –>guarnieri (mammal), bollinger (bird) = diagnostic value (DNA virus but repl in cytopl! Red/eosinoph.). After repl they exit cell. Very contagious - can use several cell surface rec to enter cells.
Pox pathogenesis
Aerogenic/contact/percutan/vector -> erythema -> papule -> vesicle -> crust -> scar -> generalization
Asfarviridae pathogenesis
ASF!
ASF (arbo/PO) - tonsilla - ln - viraemia, attack endothel
ASF tricks the immune system with trick ag,
can cause viremia and shedding fast - 2d shedding in incubation period!!
Picorna topics
- Teschovirus encephalomyelitis.
- Swine vesicular disease and vesicular exanthema of swine.
- Avian encephalomyelitis.
- Duck viral hepatitises.
- Encephalomyocarditis.
- Foot and mouth disease (aetiology, epidemiology, pathogenesis, clinical signs, post mortem lesions).
- Foot and mouth disease (diagnosis, differential diagnosis, prevention, control).
Picorna general
Smallest rna, resistant, maternal immunity, more severe young, carriers, infection from gut (FMD)
Picorna pathogenesis
PO -> gi mm/GALT (FMD: lar/phar mm) -> viraemia, CNS, skin, mm, liver, spleen, kidney
Calici topics
- Feline calicivirus infections.
- Rabbit haemorrhagic disease, European brown hare syndrome.
Calici general
(Similar to picorna) ssRNA
- resistant, (not enveloped)
- isolation hard - vax tricky(cant culture)
- good ag (immunity), no cross immunity/reactions btw strains loads of strains and mutations - reinfection!
- rel stenoxen
Calici pathogenesis
Oronasal -> pharynx -> viremia -> lung, mouth, throat, joint, pads, PO, (high virulence: liver, vasculitis)
Hepeviridae
+ssRNA, non-enveloped, good resistance BUT CANNOT STAND COOLING!
Hepatitis E viruses diseases,
Orthohepe A, C: underestimated food safety risk!! Zoonosis
Avian hepatitis E: (orthohepe B), Usually confused farmers - everything else looks normal but incr mortality and lower egg prod
Astroviral diseases
Winter gastroenteritis: mamastrovirus genus (ho, bo, su, fe)
Avastrovirus genus
- Avian nephritis is the major disease
- duck astroviruses, duck hepatitis minor causative agents, other topic (duck viral hepatitis)
- turkey astrovirus - diarrhoea
Astrovirus general
Similar to picorna!
Po -> gut -> kidney
Toga topics
Equine encephalomyelitis caused by togaviruses (Zoon.).
Toga general, pathogenesis
Enveloped, arbo
Arbo -> Ln -> 1st viraemia -> PO -> 2nd viraemia (-> BBB)
Arterivirus topics
Equine infectious arteritis.
Porcine reproductive and respiratory syndrome.
Arteri general, pathogenesis
Enveloped, poor resistance, RNA
Oronasal/veneral ->lymph tissue (macroph) -> macrophages, endothelium, sm vascular –> foetus (small virus!)
Flavi topics
- Louping ill and tick-borne encephalitis (Zoon.).
- West Nile fever, disease caused by Usutu virus and other mosquito-borne flaviviral diseases. - Bovine viral diarrhoea.
- Border disease of sheep.
- CSF
Flavi general
Weak resistance, some are arbo (biological), above/below 37C loose infectivity…, euryxen, many zoonotic
Flavi pathogenesis
Arbo//PO -> local repl ->viraemia (lymphoid - immunosuppr, endoth - vasculitis) -> PO, BM, CNS, foetus,
Corona topics
- Transmissible gastroenteritis of swine.
- Porcine epidemic diarrhoea, haemagglutinating encephalomyelitis of pigs.
- Coronaviral diarrhoea of cattle and dogs.
- Diseases of cats caused by coronaviruses.
- Infectious bronchitis of chicken, coronaviral enteritis of turkey.
Corona general
- Big spherical, enveloped, +ssRNA virus
- Good ag - endemic in eu mostly (naive herd outbreaks..)
- long shedding
- Mutations common
- Alpha, beta, gamma, delta genuses
- AGE DEPENDANT!
Corona pathogenesis
Oronasal -> resp/enteral mm (on villus!) (pns nerve to cns) –> viraemia -> udder, oviduct, kidney, liver
Reo topics
- Diseases of farm animals caused by orthoreoviruses and rotaviruses.
- Reoviral diseases of poultry.
- Bluetongue.
- Epizootic haemorrhagic disease.
- African horse sickness, equine encephalosis.
Reo general
- Resp Enteric Orphan :-(
- age related resistance
- non-enveloped, resistant (exceptions! Arbo)
- must hide dsRNA alien! (Several capsid layers, not all removed during decaps. To hide genome!
- segmented rna - re-assortments common = live vax prohibited
Reo pathogenesis
Arbo, poor res (bluetongue, african horse sickness, equine encephalosis)
BITE -> lymphatic tissue –> viraemia -> endothel damage, mm, skin, muscle damage, foetus, (AHS - lung too)
Avian orthoreo: (good res)
(Trypsin res: PO -> enterocytes->
Trypisin sens: aerog/skin -> mm–>
=> -> viraemia -> bursa, joint, PO
Mammalean orthoreo: (good res)
PO/aerogenic ->mm -> viraemia (-> CNS su)
Birna topics, general
Infectious bursal disease (Gumboro-disease).
Bi - RNA (dsRNA), resistant (both dsrna are)
Birna pathogenesis
Oronasal -> gut macroph -> viraemia -> fabricii -> GALT/ConjALT/BrochiALT etc lymphoid tissue -> immunosuppression, immunocomplexes, necr Parench organs!
Rota general
(Reo, rota genus, RV A-J)
Basically all birds, mammals can be infected…
V resistant in environment. Frequent recombinations -> tricky to prevent with immunization. Fluid loss due to diarrhoea. HU susc. Too. Common, worldwide
Affect to epithelial cells covering the villus - temporarily shortened villi
Basal cells intact - repair within a week, full recovery within 2w (if no severe exiccosis or secudnary infections)
Hygiene important. Frequent coinfections = worse outcome!
MATERNAL IMMUNITY IS ONLY DEFENSE AGAINST ROTA!
We see sudden diarrhoea in 1-2w olds, mortality may occur in secundary infections.
Orthomyxo topics
- Characteristics of influenza viruses, epidemiology of influenza (Zoon.).
- Swine influenza.
- Equine influenza.
- Avian influenza.
Orthomyxo general
(Alpha/beta/gamma/deltainfluenza genuses)
- Introduced with infected animal aerogenic/fomites - ssRNA, enveloped!
- not germinative, but:
- good ag - maternal! (Until new mutations… yearly…)
- disease dep a lot on host!
(Subacute, acute, mild..)
Similar to corona in resistance, envelope, good ag but mutations
Orthomyxo pathogenesis
Resp/enteric mm -> viraemia
Paramyxo topics
- Rinderpest, peste des petits ruminants.
- Canine distemper.
- Diseases caused by Henipa viruses.
- Diseases caused by bovine respiratory syncytial virus and parainfluenza-3 virus.
- Newcastle disease (aetiology, epidemiology, pathogenesis, clinical signs).
- Newcastle disease (post mortem lesions, diagnosis, prevention, control).
- Avian metapneumovirus infections.
Paramyxo general
Morbilli
- sterile healing
- good antigens
- uniform
- ssRNA, enveloped
Paramyxo pathogenesis
Morbilli (rinderpest, PPR, distemper)
Po > Ln > viraemia > spleen, Ln, bm, mm -> leukopenia,
(Henipa: endothel resp/cns vasculitis)
Penumo (BRSV, PI3)
Aerog -> alv mm -> alveolitis, bronchitis, interst edema -> hyaline membr -> pneumonia -> emphysema, allergic reaction
Avula (Newcastle)
Po/Aerog -> resp mm -> viraemia -> generalise (lung, int, CNS)
Metapneumo (rhinotrach.. SHS)
Arogenic -> resp mm -> viraemia -> oviduct
Bunya topics
- Diseases caused by Orthobunyaviruses (Zoon.).
80. Rift Valley fever and Nairobi sheep disease.
Bunya general
- Segmentet genome!
- poor resistance - arbo biological + amplifier/reservoid: (hu is dead end!)
- zoonotic
- good antigens
- In europe schmallenberg is present
- Abortion, fetal abnormalities
Bunya pathogenesis
Bite -> viraemia -> endoth, cns, foetus
Rhabdo topics
- Vesicular stomatitis, ephemeral fever.
- Rabies (aetiology, epidemiology, pathogenesis, clinical signs, post mortem lesions, zoon.).
- Rabies (diagnosis, prevention, control, zoon.).
Rhabdo general
Bullet shaped, Low resistance, enveloped
Can neutralized cell mediated response
Good immunity, sterile healing (if healing)
Some cross protection btw serotypes! (Ephemeral fever is uniform)
Generalization!, arbo/wounds/saliva!
Genuses: lyssa, vesico, ephemero
Rhabdo pathogenesis
Contact/wound/arbo -> lesion -> generalization no bloor OR blood/leuco/endothel
Borna topics
Borna disease, avian diseases caused by bornaviruses
Borna general
Uniform, good immunity, round shape
Poor resistance - enceloped. Spread is not really known - discharges, feces possibly!
Slow - travel along ns, high mortality low morbidity
Borna pathogenesis
Oronasal mm -> n. Olfactorius > CNS -> generalize from nerve to nerve
Retro topics
- General characteristics and grouping of retroviruses.
- Enzootic bovine leucosis.
87. Ovine pulmonary adenomatosis.
88. Feline leucosis and acquired immune deficiency of cats. - Avian leucosis and reticuloendotheliosis.
90. Maedi-visna.
91. Caprine arthritis-encephalitis.
92. Equine infectious anaemia.
Retro general
- insert into host genome
- lymphocytes (bm , fabricii) -> immunosupression
- Persistent infection (latent/repl) -> STAMP OUT
- oncogenic (fast/slow)
- mutations (variable signs)
- intrauterine
- no vax/treatment
- frequrent seropos - no signs
- immune system cant form VN abs (but ab is formed tho!
- SLOW - incr seropos with age!
- We like to use serological methods (exc 87) bc latency, carrier, hiding in certain tissue…
Retro pathogenesis
Infected lymphocytes in discharges, milk -> integrade into genome of host -> replication/latent (vertical!)
Direct/Oronasal/intrauterine
Leukosis: (tonsils) -> lymphoid cells (other bm cells)
Maedi/visna, cap enceph: ln, myeloid, bm -> lung, cns
EIA: arbo - lymohoid (bm…) - anemia
Adenomatosis (endothelial cells, resp!)
Clostridia topics and their agents (that I wouldnt remember:-))
G+
- Malignant oedema (septicum, novyi, histolyticum)
- Blackleg. (Chavoei)
- Bradsot of sheep and Köves-disease of swine. (Septicum)
- Infectious necrotic hepatitis, bacillary haemoglobinuria caused by Clostridium
haemolyticum. (First is novyi B)
- Lamb dysentery (B) and struck (C).
- Necrotic enteritis of piglets. (C)
- Enterotoxaemia of sheep and goats. (D)
- Necrotic enteritis and ulcerative enteritis of chicken. (A/C, colinum)
- Tyzzer disease and gangrenous dermatitis of poultry. (Piliforme)
Streptococcus topics
Streptococcosis of swine.
Strangles.
Streptococcus general
G+ chains Medium resistance Virulence factors (capsule phag, surf proteins attach, ec enzymes lesions(not as many as staph)) Found on mm Purulent!
Local: dermatitis, inflammation MM, cellulitis; arthritis; mastitis (S uberis, agalactiae, dysgalactiae), metritis; abscesses
Generalised:
o Swine: streptococcosis
o Horse: strangles
o Calf: S. pneumoniae - bronchopneumonia (can cause disease in humans as well)
o Pigeon: S. bovis - septicaemia (can cause mastitis in cows)
Streptococcus pathogenesis
Wound, po, aerogenic -> local repl at mm -> (bacteremia)
Eg strangles throat -> lymphatic vessels and ln
Staphylococcus topics, erysipelas
- Diseases of farm animals caused by staphylococci (rabbit, swine, poultry).
(Local purulent, rabbit bronchopneumonia, swine ex dermatitis hyicus, poultry septicemia of young)
Erysipelothrix rhusiopathiae, Erysipelas Zoonotic
o Gram+rods, facultative
o Worldwide, summer, sporadic, small farms
Staphylococcus general
G+ cocci, grape bunch!
Coag pos - aureus
Coag neg - hyicus
Virulence factors (EC encymes like coagulase, hyaluronidase, lectinase), toxins like hemolysins, leukocidins (WBC memb),
Staphylococcus pathogenesis
Good resistance
Found on mm, skin, soil, water, environment, food
Lesion on skin/mm -> purulent lesions! (Predisposing)
Listeria
G+. Sheep most susceptible. Super wide repl range (4-42C), silage, puddles, ivanovii/monocytogenes, fac IC bacterium (hide!). Gut-soil cycle -> blood -> brain, foetus -inflammation and microabcesses (purulent!) (microscopic abcesses in placenta and brain). Signs = too late. Treat the rest.
Other bacteria often present - U-tube (flagella, temp!!)
Corynebacteria general
G+. Similar aetiology to listeria (soil, mm, skin, water,… fac bact mostly, cell wall lipoids incr resistance, fac IC (in host).
C. Pseudotuberculosis (caseous lymphadenitis of sheep and goat, ulcerative lymphangitis of horse and edematous skin disease of buffalo. (Travel along lymphatics from PO/wound to Ln(onion). May generalize!! (In blood, abcesses)
Some ascending pyelonephritis bact of cattle (c. Renale, cystidis and pilosum)
(Campylo)(:
Mycobacterium general
Polymorphic, G+(cant be stained due to high lipid content in cell wall), attach together
ZN+ (acid and alcohol fast - pink)
Fac IC (macrophages), decent resistance, in environment too!
Slow spread tuberculosis (PTB too!)
Which spread slowly
Tuberculosis Borna Retro Salmonella typhisuis Corynebacteria Mycoplasma … not done
Actinomycses, nocardia general
G+
Similar lesions. Ddx ZN, nocardia is partially acid fast (pink!)
Actinomycosis: On skin, mm -> lesion -> pyogranulomatous infection (cattle - lumpy jaw, sulphur granules, swine - pyelonephritis, ca/fe - SC pyogran. lesion, fistulation!
Nocardia: dog basically same thing (pyothorax) or if inhaled in lung, or in young disseminated in PO. Cattle skin, SC (like dog) mastitis too!
(Vs dermatophilus more only skin lesions… but similar morph, pyo..)
R. Equi and dermatophilosis
G+
RHODOCOCCUS EQUI - Suppurative bronchopneumonia (ic macroph - lysis) of 1-4 months old foals, abscesses in the lungs,( granulomatous ulcerative enterocolitis(peyer patches), mesenteric lymphadenitis, arthritis) - zoon.! But from swine:-)
Dermatophilus: zoon, Very characteristic morph: Small G+ cocci forms filaments, falgellated
Very resistant in environment, years, = “zoospores” (?)
Causing exudative, pustular dermatitis of eq and ru, may be lethal
- zoonotic!
E coli topics (that doesnt have e coli in name :-))
Oedema disease of swine
E coli general
Enterobact family, escherichia genus.
Gut flora, mostly saprophytes, fecal contamination indicators.
Lab ddx!!! Huge genetic variability - plasmids! Surface antigens (PCR to ddx serotype), pathotypes based on virulence factors (disease groups(PCR)
(Enteric, septicemic, mastitis, uti)
Entero: -pathogenic, -toxogenic, -invasive, -adhesive-aggregative, -haemorrhagic strains, verotoxigenic and necrotoxic strains..
Extra-enteric: septicemic, uropathogenic, avian pathogenic strains
Coryne pathogenesis
Oronasal(ov)/wound(Eq, Bo - arbo)
–> travel along lymph vessels -> ln (repl in phagocytes, lysed, attract wbc) -> blood -> generalization -> abcesses
Salmonella topics
- Salmonella diseases of swine.
- Salmonellosis of cattle.
- Salmonellosis of small ruminants and horses.
- Fowl typhoid.
- Fowl paratyphoid (Zoon.).
- Reduction of Salmonella carriage of poultry, salmonella reduction programs, and their control.
Salmonella general
Enterobacteria familiy, genus salmonella.
Spp s. Enterica subsp enterica cause the diseases. The “spp” named in topics are different serovars belonging to this species!
Serovar-animal species specific severity (=murium mice kill mice but diarrhorea in other animal eg)
G- rods.
- Zoonosis, loads of asympt carriage.
- germinative infection!! Will always get to next generation.
- ab/vax only for signs, carry still whole life basically
Salomnella pathogenesis
From Environment or animal -> oronasal/vertical infection -> gut -> blood -> PO -> ab response -> hide in joints, tendon sheath, foetus giving chronic signs!
Yersinioses: rodentiosis and diseases caused by Yersinia enterocolitica (Zoon.).
Y. Pseudotuberculosis. Mostly PO infection from facal contamination - poor food/water source! Small rodents and hares most imp, but birds and mammals too predisposing needed! GI -> septicemia with focal inflammation and necrosis in PO. General signs and diarrhoea in rodents, swine, eq, car, while cattle may present with diarrhoea, mastitis and abortion, and birds diarrhoea and arthritis!
Enterocolitica. More common than rodentiosis, common asympt, signs in young, common crossreactions with brucella bc O9 serotype, swine shed in feces and maintain + other is susceptible. The disease is similar. Rodents can be infected too, so imp when improving management. Most eu countries are free from so importance of maintenance! Humans must wash fruit and veg!
Necrobacillosis and panaritium of ruminants.
Necrobacillosis: Weak invasion capacity, anaerobe. Need predisposing!! (Entry way), most common in YOUNG (lamb, calf, rabbit). Infection form skin, mm, naval infection or rumen parakeratisos. We recognize by necrosis in oral cavity, slaivation, pain, general signs. If naval inf/rumen parakeratosis we see liver necrosis (rare!) due to toxin prod (proteases). Mucous memb of oral cav, pain - clean necrotic tissue and good disinfection surgically needed (oxidizing disinfection)
Footrot:
Warm, wet. Dichelobacter nodosus, strict anaerobe! Stand long time, warm, rainy(spring/autumn) -> softer hoof and plac of entry! Or poor ground causing wound. Shed from feces - hygiene omp. 100% morbidity!! Suffolk sheep more susceptible, hoof not as hard as other races. Other bacteria present in lesions, eg. F. Necrophorum! (Necrobacillosis) can lead to footrot), strept, staph help create anaerobe environment. Sheep! (Suffold soft hoof) Aerobe consume ox (stap, strept, entero), local environment for fuso necrophorum to join aswell, further reduce ox, synergistic effect help dichelobacter nod –> repl –> virulence facto prod –> fibria, can now attach to arget cells -> protease, keratinase damage hoof and tissues –> local cap damage, decr circ –> further help detachement of hoof.. interdig derm -> extended necrosis. Benign - footbath, virulent - surgical + local and parenteral ab.
Diagnosis of INDUVIDUAL ANIMALS!
Pasturella topics
- Respiratory pasteurellosis of cattle.
- Haemorrhagic septicaemia of cattle.
- Pasteurellosis of sheep and goats.
- Pasteurellosis of swine and rabbits.
- Atrophic rhinitis of swine.
- Fowl cholera.
Pasturella general
On mm, gut flora
Anaerobe, (bipolar stained) rods G-
Not uniform (inact serotype specific vax)
Not vertical
Respiratory-, septicemic, -matitic pasturellosis
Mannheimia - leukotoxin
Multocida (dermonecrotoxin(su!, -B), capsule, surf proteins, hyaluronidase)
Trehalosi (goat, sheep)
Pasturella pathogenesis
Aerogenic -> upper resp -> lung -> m hemolytica leukotoxin (alv macroph) -> uninhibitied replication!
Or tonsils -> septicemia
(Non-resp pasturellosis)
Anatipestifer disease and disease caused by Ornithobacterium rhinotracheale.
(Weeksellaceae family) no germinative, non-enveloped, G-, mm?
Infectious serositis: rimiella anatipestifer. Large flocks, facultative - predisposing, loads of serotypes, many birds susceptible but most severe in ducklings under 2m - LARGE SCALE DUCK FARMS.
Low resistance - survive in water. Long shedding. Wild bird spread, no vertical (like last, prev pasturella but re-classified) resp, gi(green), cns. 50%mortality
OR: Growers(no vertical) - broiler, turkey (farm mammals, wild birds), facultative, many serotypes, low resistance, need predisposing, no vertical. Young - peracute, acute, older - asympt
Resp signs, mucous suffocate, serositis, + decr egg no in layer
Tularaemia (not pathogenesis)
Franciella tularensis. First seen in norway in 1653(lemmen), mainly rodent and wild rabbit (but super wide host range, bioterrorism) - zoonosis! Maintenance btw bloodsucking - wild rabbit and bird. Mainly in northern hemisphere! Uniform, tricky to culture.
Number of cases depend on rodent population, from urine (christmas tree workers). Either acute septicemic (tular-emia) of chronic disease - inflamm necrotic foci in parench organs. Can be lethal.
Long immunity! Eg a lot of sheep affected, loads of ticks - think of this!
Tularemia pathogenesis
G- cocci
Decent resistant; carcass, soil, water, tick (biological vector! Rest is mechanical).
Po/arbo/inhalation (urine) –> macroph –> ln –> septicemia –> POrgans
Actinobacillus general
Mm, gut flora G- rod Low resistance Fac pathogens Purulent Cytotoxin su! Alv macr + endothel
Actinobacillus pathogenesis
Local or septicemia \+: Bo: wound (torus linguae) Cap/Ov: ascending genit Eq: intrauterine (sleepy foal) Su: aerog -> resp tract (cytotoxin damage alv macrhop)
Hemophilus topics
- Porcine polyserositis (Glässer’s disease).
- Infectious coryza of poultry.
- Diseases of cattle and sheep caused by Histophilus somni.
Hemophilus general
- G- rods
- On mm
- low resistance, close contact! Facultative!
Hemophilus pathogenesis
Glassers: Aerogenic -> resp tract -> septicemia -> serofibrinous, joints, CNS
Only upper resp in coryza: serofibrinous upper resp
H somi: aerogenic -> resp -> septicemia -> inflamm, vasculitis, thrombus, necrosis in: CNS, resp, joints, foetus
Contagious equine metritis.
Taylorella equigenitalis. On genital mm, G-
Late 70s, big problem, now sporadic, only eq, low resistance, veneral both genders. Cervix+uterus inflamed, carriers - mare longer(fossa clitoridis) = imp to treat!. Stallion asympt, mare repeat breeders, loads of discharge(can just hold cup under..). Isolate and treat, test new horses.
Bordetella general
G-, good resistance, mm
Common on mm resp of birds and mammals. Trachea (kill ciliated cells), dermonecrotoxin (skin necrosis, stop osteogenesis) and osteotoxin killing osteoblasts toxin cause signs.(only osteoclast activity…)
Moraxella
On mm! Infectious keratoconjuctivitis of cattle.
M. Bovis.
Irritation in eye -summer, dusty pasture, fast spread, EC enzymes causing lesions (proteases…), flys can transmit, rubbing eye transmit mostly. May or end with keratitis and blindness. Secundary purulent infections may also cause blindness. Ointment AB - vax if common.
Brucella general
Fac IC, mm
ABORTION
Stamp out
OIE, ND! (Many)
Brucella pathogenesis
Aerogenic -> upper resp -> ln -> macroph to blood -> septicemia -> uterus, placenta, udder (hide here + semen, joints!)
Burkholderia
Glanders and melioidosis (Zoon.). Fac IC.
Malleus/farcy: ND, zoonotic - Glanders, an often fatal contagious disease of equidae (donkey v susc), now found in remote areas of the world, eradicated in europe, is caused by Burkholderia mallei. The disease is characterized by purulent nasal discharge(help spread of poor res), nasal mucosal ulceration, lung lesions, and ulcerating nodules along the subcutaneous lymphatics. Diagnosis is based on presence of nasal ulcers, complement fixation test reaction, positive mallein test(allergic test in conjunct), and culture and PCR. Ddx STRANGLES (enlarged LNs can be moved, here ct proliF!),Control is based on isolation and culling of affected animals.
Pseudomallei: Zoonotic, sporadic import to europe, su, bo, cap, eq, camel - pigs carry often! Warm, rainy and stress may cause infection - NO SPREAD BTW ANIMALS - SOIL BACTERIA! So rain, warm… predisp.
Abcesses are seen, resp signs, (diarrheoa, CNS) - varying, depending on lesion!
Burkholderia pathogenesis
Oronasal -> pharynx -> not pseudo(lymph vessel -> ln) -> blood
Campylobacter general, pathogenesis
Fac IC
On mm - low resistance
Enteric(thermophilic, 42C), genital, hepatic
Genital:
Bo: Ascending infection!
Ov, Cap: PO/veneral -> gut(asympt) -> foetus, semen
(Dont mix with actinobacillus! Sleepy foal, cap ascending, torus)
Enteric (av, su, ca, fe, (bo)
Colonize gut, asympt or mild diarrhoea
Av Hepatitis:
PO -> gut(no lesion) -> liver(repl) -> septicemia
Lawsonia intracellularis
Obli IC, G-, poor resistance
Wide host range, but we focus on pig bc here we see signs. Obl IC pathogen of enterocytes. Poor resistance, but survive alright in feces - carriers or rodents as source of infection! (Water, feed, environment) Economic impact of growers (more common) - decr gain, more feed needed. More severe in young. (But rarer)
All forms related to repl of enterocytes - thickening (gyri like, like paratuberculosis)
Degen/reparation?: fibrin ppt, necrosis, bleeding - LOCAL ONLY!
Acute: young 1-5m, A, Chronic: older 4-12m, B, C, D
A) Intestinal adenomatosis (adenoma - edema!, necrosis, tube like, ddx paratuberculosis)
B) Necrotic enteritis - necrosis
C) Regional ileitis - hypertrophy of muscular layer
D) Proliferative haemorrhagic enteropathy - blood, black feces, anemia!
Spirocheates general
- Long incubation
- slow spread (not Lepto su)
- serotypes not spp!!
- borrelia: arbo, blood
- Lepto: water
- Treponema: rabbit syphilis
- brachysp: varying..
Mycoplasma topics without mentioning mycoplasma in title :-)
Contagious bovine pleuropneumonia.
Mycoplasma general
Huge economic impact, widespread, large scale farmes
- fast spread, low resistance, found on mm. (Vs. Mycobact resistant, slow spread, fac IC) -> aerogenic, direct contact
(Slow: (bo)mycoides, (su) hyopneumoniae, gallisepticum) - host specific! (Exc gallisepticum, canis)
- growers!! (After weaning, early laying..)
- vertical! (But often local in lung) Eg bovis, gallisepticum born with resp signs
- No cell wall - polymorphic, G- but stain dont work. (Vs. Mycobact G+, no stain bc high lipid in cell wall)
- Smallest bacteria. Neep special tp media!
- Some are easy to culture, someone hard… the easy might overgrow the hard ones. Haemotrophic cant becultured!
- Most are stenoxen (gallisepticum several bird spp, canis: ru mainly + other).
- Immunosuppression - Hide -> tricky eradication, prevention
- remain carriers
- usually infect older than suckling… (but still young!)
Diagnosis: saprophytes in mm - 16ssRNA ddx!
Mycoplasma pathogenesis
- Cell level pathogenicity! Damage cells, cilia, hides amongh them, and blocks receptors (delayed ab production, wbc activity) –> immunosuppression!) –> hard to eradicate!
- Haemotrophic damage rbc, lower lifespan so we see anemia and jaundice!
Often stays in resp, septicemia - arthritis is typical.
often 100% morbidity!
(Immunosuppr - v contagious, aerog)
- MAKePS (mastitis, arthitis, keratitis, pneumonia, septicemia (anemia- haemotr)
Chalmydia general
- Obl ic bacterium, G-, great res
- biphasic form; EC elementary body and IC as reticulate body. They form IC vesicle from cytopl memb of host for extra ic protection.
- Super resistant, can survive dehydrated for a month! They replicate on mm of gi and resp. Intermittent shedding
- Isolation tricky bc need live cells (embr egg eg, and serological methods expensive!
- Occur in birds and mammals. Asympt carriage is common!
- Remember no peptidoglycan in cell wall so cant use ab that acts on this! wide spectrum ab is needed, eg. TTC or macrolides!
Chlamydia pathogenesis
Oronasal -> gut/resp mm -> blood -> foetus, lung, CNS, joints, conjunctiva
Coxiella
- Coxiella burnetii - Q fever!
- obl IC, 2 forms like chlamydia, great resistance
- Q comes from query fever, meaning unknown fever. Occurance is underest. Often, asympt frewuently
- infection widespread in ru herds! Has a wide host range, but mainly signs in ru, and humans are imp too bc zoonosis (susceptible!).
- Aetiology similar to chlamydia (small(infectiouus) cell variant, and large (met. Active) - inside phagolysosomes ic it inhibits maturation of phagolysosome - cant be lysed!
- Most imp sign is the abortion, seen most in small ru, not so often in cow (dog).
- Typiical pm lesion is haemorrh necrotic placentitis in foetus. (We dont see lesions in cow)
Coxiella pathogenesis
We see a natural focal infection, where we have maintaining host (ru most imp) + ticks - disease circulate btw them (like lyme disease!) the tick has a special characteristic as a biological vector, the virulence can incr in next gen.
- spread by discharges that are aerosolized, dust, ticks.
- humans most imp is excretions, milk.
- Dogs can eat.
- Repl –> blood –> lung, liver (this repl lead to death), lymphoid tissue, udder, uterus.
- The immune system kicks the bacteria out of blood, hides in gut, udder! and foetus.
Rickettsia ORDER (not fam) general
Rickettsia and anaplasma family
Similar to coxiella. Obl ic, narrhow host range, poor resistance - ticks, G- rod. (biol and mech)!
Natural focal infection - wild living and ticks usually. Rickettsia fam is mostly human importance with cell wall (peptidoglycan and LPS), while for us anaplasmosis (anaplasma, ehrlichia, neorickettsia genus) most imp. Due cell wall missing (mycoplasma!) we cant use gram stain, giemsa is used!
Rickettsia pathogenesis
BITE -> Ln -> septicemia
Ehrichia:
lymphoid - immunosuppression, endothel - anemia
BO anaplasma
A marginale, centrale: RBC
A bovis: monocytes
BO/EQ: A phagocyticum: granulocytes
Neorickettsia: monocytes
What are basic epi rules for prevention?
- closed population,
- separation of different age groups
- All in all out if possible (su, av)
- immunization
- import from free herd
- quarantine
- regular serological monitoring
What are basic eradication methods
o 1) Replacing: quick, safe, but expensive
o 2) Raising free generation: time-consuming, vaccination of whole herd, seclusion of calves on day 3, after colostrum consumption, isolated raising
o 3) Selection: remove seropositive. DIVA is helpful to ddx vaxed/nonvaxed.
- Under 10% remove +tive animals.
- Over 10% seropos selection with the help of marker vaccines
o Basic immunization of whole herd with marker vaccine
o Repetition in every 6 months - reduced virus shedding frequency
and intensity
o Isolation of offspring from the adults, vaccinations in every 6 months -> eg heifers
at parturition are already atleast 4 times vaccinated
- Regular control: repeated, discriminative ELISA (DIVA)
- DIVA - when sero+ is low in no., we remove them from herd. Then we have a vaxed free herd. Then we stop vax = becoming seroneg.
Maintenance of virus-free status: closed farm, virus-free semen and bull, regular controls
Facultative vs obligate pathogen, what influences the infection?
Facultative:
Disease is influenced by virulence of the agent, resistance of the host and nature & severity of predisp. factors
Obligate:
Balance btw the host and the agent determines the course of infection and severity of signs (eg. TB exudative vs. Proliferative infections, generalization or latent…)
- can only replicate in host, but the agent may still have good resistance to survive outside host!
