mixed Flashcards
1
Q
anthrax
A
OIE listed
2
Q
aetiology anthrax
A
- ¬bacillus anthracis, G+, aerobic, spore forming,
- Spores extremely resistant – survive in environment for decades. Spores form when bacteria exposed to air
- Capsule = 1o virulence factor – inhibits phagocytosis, protective antigens, lethal factor + oedema factor combine to form lethal toxin + oedema toxin
- Colonies grow wo CO2 = “medusa head”
3
Q
GD anthrax
A
- GD: Central + South America, sub-Saharan Africa, Asia, southern + eastern Europe, Caribbean.
4
Q
SOI anthrax
A
- SOI: contaminated environment, feed, soil/hides/wool. In water for 2y + 10y in milk
5
Q
MOT anthrax
A
- MOT: ingestion/inhalation of spores, via wounds. Birds/flies can mechanically transmit
6
Q
HS anthrax
A
- HS: cattle, sheep + goat highly susceptible, horses less
7
Q
risks anthrax
A
- Risks = flooding/drought concentrate spores. Neutral, alkaline or calcareous soil
8
Q
anthrax pathogenesis
A
- wound inoculation/ingestion/ inhalation spores infect macrophages, germinate+ proliferate.
- proliferation at the site of infection + draining Ln
- Lethal + edema toxin = necrosis + oedema
- multiply in LN toxaemia bacteremia
- increase toxin tissue destruction = organ failure
- death vegetative bacilli released + sporulate on contact + w air. Rapid pH changes after death = bacteria die without sporulating
9
Q
signs of anthrax
A
- incubation = 1-14d, clinical course = peracute-chronic
- peracute = ruminants, death w no signs, pyrexia, trembling, <2h, dyspnoea, collapse, convulsions, bloody exudate
- acute = rum + equids. Fever, excitement, lethargy, stupor, resp + cardiac distress, staggering seizures, death, rumination + milk production stops, abortion, bloody discharge
- horses = colic, fever, anorexia, weakness. Oedema of neck, sternum, lower abdo + perineum (fly bites) death in 2-3d
- pigs. Dogs = sudden death + oropharyngitis – swelling of throat. Mild chronic = systemic illness + recovery
- chronic = 3+ d till death. Oedema of pharynx, face, asphyxia
10
Q
PM anthrax
A
- Rigor mortis is absent or incomplete. Blood from orifices. Bloating, rapid decomp
- DON’T OPEN CARCASS – septicaemic lesions, blood dark + not clotting
- Haemorrhage on serosa of abdo + thorax + GI tract. Ulcers on peyer’s patches, enlarged, semifluid black spleen. Gelatinous LN
11
Q
treatment anthrax
A
- Atb to stop incubation then vaccine 7-10d after treatment. Retreat if sick + revac in IM penicillin or oxytetracycline
12
Q
diagnosis anthrax
A
- Swab dipped in blood + dried. Nasal turbinate swab (spores), PCR, Ascoli test to find antigens in decayed samples. IF but cross reactivity common. Culture from plsene. MacFaedes stain of blood to see capsule
13
Q
differential anthrax
A
- Lightening strike, clostridial infection, lepto, lead poisoning, colic, bacillary haemoglobinuria, CSF, ASD, acute EIA,
14
Q
immunoprophylaxis anthrax
A
- Vaccination of grazing animals in endemic area. Non-encapsulated s
terne-strain vaccine (live)
o Give 2-4w before expected outbreak. Don’t give ATB within 1w of giving
15
Q
prevent anthrax
A
- Remove animals from pasture. Burning/burial of carcasses
16
Q
control anthrax
A
- Notify regulatory officials. Quarantine, disposal of bedding/carcass etc. cleaning + disinfection of equipment. Insect + bird repellents. Formaldehyde treatment of soil/removal
17
Q
public health antrhax
A
Public health
- Potential bioweapon – fatal human illness
18
Q
botulism
A
- Intoxication not infection
- If untreated, ends in death from paralysis of the respiratory muscles
19
Q
aetiology botulism
A
- Toxin produced by Clostridium botulinum, anaerobic, Gram+, spore-forming, Types A-G
- Spores highly resistant
- ABE = humans, C= animals, D = cattle
- 4 genotypically + phenotypically distinct groups
- 1= proteolytic, 2 = non-proteolytic, 3 = in animal
20
Q
SOI botulism
A
- SOI = decaying carcasses/ food, spoiled silage
21
Q
MOT botulism
A
- MOT = indigestion of toxin (only produced in anaerobic), wound contaminated with bacteria toxin when no oxygen
22
Q
HS botulism
A
- HS = diff species have different susceptibility. Dog, cat + pig. Relatively resistant. Birds v susceptible
23
Q
risk botulism
A
- Risk = phosphorus def soil = cattle chew bones with toxin
24
Q
toxic-infectious
A
- Toxico infectious = bacteria grows in tissues + forms
25
Q
pathogenesis botulism
A
- Toxin ingested carried in blood to neuromuscular junction blocks release of acetylcholine flaccid paralysis + death due to resp muscle paralysis
26
Q
signs botulism
A
- incubation period 2 hours - 2 weeks; mostly appear in 12 to 48 hours.
- progressive motor paralysis (hind first), disturbed vision, dysphagia, weakness, incoordination
- cattle = drooling, dysphagia, not urinating, recumbency, death. Skin sensation normal, withdrawal, reflexes weak
- horses = restlessness, dysphagia, decreased tone of tail/tongue. 90% mortality
27
Q
PM botulism
A
no pathognomonic lesions
28
Q
treatment botulism
A
- have to know toxin as antiserum doesn’t work for all
- binding of toxin to endplate is irreversible but axon can form new one if kept alive long enough – w/m of intensive care, mechanical ventilation, fluids, etc. GI lavage if ingested. Surgical debride + atb + hydrogen peroxide for aerobic conditions if wound
29
Q
diagnosis botulism
A
- exclusion of other differentials. Mouse inoculation test. ELISA to detect toxin, false +ve possible. For toxicoinfectious culture from tissue but caution-spores can be found in healthy
30
Q
differentials botulism
A
- parturient paresis, hypocalcaemia, rabies, carbamate poisoning, equine grass sickness, hepatic encephalopathy, encephalomyelitis
31
Q
prevent botulism
A
- remove feed, destroy carcasses, fly control (toxic maggots)
- type specific toxoid vaccines. Survivors not protected
32
Q
shaker foal syndrome
A
- ulcers, navel abscesses + wounds = growth of bacteria <4w old, death wo signs or stilted gait, tremors, constipation, dysphagia, frequent urination, neck extension, dyspnoea. PM = pul oedema, excessive pericardial fluid w fibrin. Death in 24-72h
33
Q
immunoprophylaxis botulis
A
- areas where botulism is common, vaccines in animals: horses, cattle, sheep + goats.
34
Q
public health botulism
A
- non-communicable, foodborne intoxication or wound contamination (drug users)
- In babies – spores germinate + produce toxin in GI tract. They have immature flora + decrease bile acids. Clostridial organisms can grow
- Botox = neurotoxin from Cl. Botulinum
35
Q
tetanus
A
- ubiquitous neurologic disease, characterized by spastic paralysis + not a transmissible disease.
36
Q
aetiology tetanus
A
- Neurotoxin from Cl. Tetani. G+ anaerobic rod with terminal spores (drumstick)
- Found in soil + GI tract of healthy animals. Spores survive moderate heating. Prevalence increases in warm (75–80°C for 10min), humidity (1 h at 100°C) (iodine and chlorine kill spores)
37
Q
GD tetanus
A
worldwide distribution
38
Q
SOI tetanus
A
contaminated soil
39
Q
POE tetanus
A
wounds (deep puncture), castration
40
Q
MOT tetanus
A
wound
41
Q
HS tetanus
A
all species – horses, human, sheep most susceptible. Birds resistant, cattle/dog more resistant
42
Q
pathogenesis tetanus
A
- Inoculation = production of Tetanolysin + TeNT
- Toxins produce intracellularly + released on autolysis + Tetanolysis = necrosis
- Toxin absorbed by motor nerves, retrograde travel to spinal cord ascending tetanus
- TeNT blocks release of inhibitory neurotransmitter GABA + glycine muscles can’t relax
- If more toxin released than nerves an absorb, excess is carried in blood + lymph to CNS descending tetanus
- Incubation = usually 10-14d
- Generalised disease = usually starts at jaw + spreads
- Localised = muscles of infected region become painful then spastic (more resistant eg cat + dog)
43
Q
signs tetanus
A
- Trismus = rigidity of masseter + temporal muscles
- Increases reflexes, easily excited, violent spams with noise/sudden movement. Difficulty eating -lockjaw
- Horses = erect ears, stiff tail, nares dilated, 3rd eyelid prolapsed, hard to turn/walk, sweating “saw horse”
- Increased HR + RR, congestion of MM. consciousness not affected
- Sheep + pigs = fall to ground + opisthotonus when startled
- Temp slightly increased, then 43oC in fatal attack. Death due to paralysis of larynx/diaphragm resp failure
44
Q
PM tetanus
A
- No pathognomic signs, fast autolysis, try to find POE – if minimal autolysis can try to find G+ rods in wound
45
Q
diagnosis tetanus
A
- Signs, history of trauma. PCR from wound/serum to confirm toxin. Try culture from wound but hard
46
Q
treatment tetanus
A
- Eliminate bacteria (Penicillin G and metronidazole), clean wound
- Antitoxin – prevent free TeNT from entering neurones
- Control spasms – diazepam, phenobarbital
- Fluids, urinary catheter, ear plugs, dark room
- Animals that recover – no protect immunity
47
Q
prevent tetanus
A
- Inactivated toxin vaccine 2 in 3-4w interval then q1y? mares in last 6w of preg + foals at 5-8w old. Good hygiene of wounds, sterilised equipment
48
Q
aijesky
A
- in swine signs and lesions vary among different age groups
- it’s characterised by 3 overlapping syndromes: CNS, respiratory or reproductive system infection
49
Q
aujeskzy aetiology
A
- suid herpesvirus-1, single stranded DNA, enveloped – inactivated in sun, drying = heat
- survives 2d in soil + faeces, 4d in straw bedding. Travels 2km in aerosol
50
Q
MOT aujeszky
A
oronasal (most common), feco-oral, aerosol, transplacental, venereal in feral pigs, AI w contaminated
51
Q
HS aujeszky
A
horses resistant, fatal in rums, dogs + cats, pigs survive. Young pigs v. susceptible
52
Q
SOI aujeszky
A
= inapparent shedders – secreted for 2w in all secretions. Dead end host (dog, wildlife)
53
Q
pathogenesis aujeszky
A
- Tropism for CAN + resp tract
- 1o replication in nasal, pharynx + tonsillar epithelium spreads via lymph to LN + by nervous tissue to brain replicates in pons + medulla. Becomes latent in trigeminal + paravertebral ganglia
- Inflam + necrosis of resp epithelium
- Repro = endometritis, vaginitis + necrotic placentitis
54
Q
signs aujeszky
A
- Pigs = <7d old = sudden death with no signs
- 2-10w = CNS signs predominate, tremors, paddling, ataxia, paralysis, death in 24-36h, fever
- 10w-market = resp sign predominate, fever, dyspnoea, sneezing, anorexia, weight loss
- Breeding herd = little signs, recover. Repro failure, abortion etc
- Non pigs = sudden death, intense sudden pruritus’, circling, manic behaviour, fever, resp distress, excessive drinking. Death in 24h
55
Q
PM aujeszky
A
- Maybe serous rhinitis, necrotic tonsilitis, haemorrhagic LN, pulmonary oedema, necrotic foci on liver
- Micro = nonsuppurative meningoencephalitis, thickened meninges, intranuclear inclusion bodies in neurones
56
Q
diagnosis aujeszky
A
- suspect if repro failure, high mortality + CNS signs in young
- Serum neutralisation = standard (8-10d antibodies appear)
- DIVA ELISA possible, virus isolation. Brain/spleen/lung
- PCR of nasal swabs
57
Q
differential aujesky
A
- TGE, E.coli, SI, CSF, NaCl poisoning, rabies (not aggressive to man in pseudo)
58
Q
treatment aujeszky
A
- No treatment, but vaccination = alleviate signs
- OIE
59
Q
present aujesky
A
- MLV- intranasal young, IM old. Breeding q3m
60
Q
rabies
A
- Acute viral encephalomyelitis that can affect any mammal. The disease is almost invariably fatal once the clinical signs develop.
- ZOONOSIS!!!!!!!
- Public heath risk = highly fatal
- OIE
61
Q
rabies aetiology
A
- Rabies virus, Family: Rhabdoviridae, Genus: Lyssavirus
- 16 other rabies related
- lyssaviruses (nonrabies lyssaviruses)
- single strand RNA, envelope
- urban cycle = dogs main reservoir (Africa, Asia)
- sylvatic cycle = skunk, racoon, fox (Europe)
- virus adapted to reservoir host + antigenically distinct
- Variants maintained within reservoir species
62
Q
rabies GD
A
worldwi
63
Q
rabies SOI
A
reservoir host
64
Q
MOT rabies
A
bite from rabid animal, aerosol in lab+ via transplatns
65
Q
HS rabies
A
all mammals
66
Q
pathogenesis rabies
A
- Eclipse phase= Replicates in non-nervous tissue at site of inoculation enters peripheral nerves goes to CNS via retrograde flow in axons. Reaches brain salivary glands + other organs
67
Q
incubation rabies
A
- Variable 10d-6m
- Saliva in dogs can be infectious + shed virus 10d before signs
- Cats for 1 to 5 d, Dogs for 1-5 (13) d, Cattle for 1 to 2 d, Skunks < 14 d Bats for 2 weeks
68
Q
signs rabies
A
- Acute behaviour changes + unexplained progressive paralysis, anorexia, apprehension, nervousness, irritability, hyperexcitability, altered phonation, ataxia, aggressiveness, loss of fear of humans, nocturnal walking in day
- Prodromal = 1-3d. acute excitive – paralytic end stage
- Furious = excitive stage pronounced. Attacking, eat foreign objects, wandering, seizures. Death in 4-8d due to paralysis
- Paralytic = ataxia, paralysis of throat + masseter, salivation, inability to swallow, death in 2-6d due to resp failure
69
Q
PM rabies
A
- no characteristic signs, abnormal stomach contents.
- Histo: multifocal, mild, polioencephalomyelitis w mononuclear perivascular infiltrates
o Negri bodies can be seen in some but not all cases.
70
Q
treatment rabies
A
- Symptomatic rabies is almost always fatal.
71
Q
diagnosis rabies
A
- IF microscopy on fresh brain tissue. Official lab. No definitive AM test – euthanasia
- RT-PCR in some modern labs, VN, ELISA to test seroconversion before travel
72
Q
prevention rabies
A
- Inactivated vaccine in domestic. PO MLV in mild animals q3y. after initial series of 2 vaccines 1y apart
- Disinfection = v. susceptible to disinfectant, heat + UV
73
Q
brucellosis
A
- Brucellosis is chronic infectious disease of domestic animals + humans caused by bacteria of the genus Brucella
- It is manifested by abortion and retained placenta in female animals and by orchitis and epididymitis in male animals.
- Occur in ruminants, pigs, dogs, and rarely horses.
- ZOONOSES + OIE
74
Q
aetiology brucellosis
A
- Genus: Brucella, G-, non-motile, facultative intracellular bacteria
- Survives in foetuses + faeces >2m in cold, pH >4 but susceptible to pasteurisation
75
Q
SOI brucella
A
carrier animals, aborted foetus, contaminated food, water + environment
76
Q
MOT brucella
A
direct + indirect contact, mating, per oral, etc
77
Q
POE brucella
A
MM of resp, GI tract, genital tract (B.suis/canis/ovis) skin abrasions
78
Q
HS brucella
A
o abortus – rums, pig, horse, human
o melitensis – rums, humans, dogs, poultry
o suis-biovar 1-3 = pig + boar, biovar 2 = pig + hare
o ovis = sheep
o canis = dog + human
79
Q
pathogenesis brucella
A
- enters via conjunctiva + MM in to macrophages + neutrophils LN cell associated bacteraemia (6-36m)
- intervertebral disc, eye, kidney
- MPS cells multiply + persist in spleen, liver, LN reticuloendothelial hyperplasia
- Genital tract prostate, epididymis sperm
- Agglutination + macrophage activation inflam
80
Q
signs brucella
A
- In cattle (bang’s disease)
o Late term abortion, REM, decreased milk. Bulls = asymptomatic, orchitis etc
o Inflam of joints, subcut abscess - In sheep and goats – B. melitensis
o Abortion storm – last 3rd pregnancy
o Goat = carrier for 5m PI, udder infected for years
o Sheep = carrier for 3m after abortion
o Goat = articular hygroma localisation - Infectious epididymitis in sheep – B.ovis
o Sheep. Oxidase + urease negative. Rarely abortion, manifestation on testes + epididymitis, not zoonotic - Brucellosis in swine – B. suis
o Cows = asymptomatic
o Abortion, infertility, spondylitis, abscess - Brucellosis in dogs – B.canis
o Bitches = abortion (consecutive cycles too) dogs = epididymitis, prostatitis, fever, lymphadenopathy, discospondylitis, glomerulonephritis, uveitis - Brucellosis in horses- B. abortus, B. suis
o Abortio rare, inflam of bursae, fistulas
81
Q
pathology brucella
A
- Abortus = changes on foetus/placentan/genitalia
- Melitensis = non-specific
- Suis = abscesses on LN, liver, bones, joints, spleen, kidney, testes. Brucellomas
- Canis = discospondylitis
- Ovis = orchitis, epididymitis
82
Q
diagnosis brucella
A
- epizootiology, signs, bacteriology + molecular
- ID + typisation of brucella (PCR), serum agglutination, rose Bengal, ELISA, milking test
83
Q
differentials brucella
A
Trichomoniasis, Vibriosis, Leptospirosis, Listeriosis, IBR, Various mycoses
84
Q
treatment brucella
A
- NO TREATMENT!!! – by law (eradication)
- Mandatory measures!
- Positive B. melitensis herd – stamping out!.
- Positive B. abortus and B. suis – slaughter under special condition.
- Vaccination in certain circumstances approved by OIE.
85
Q
zoonosis brucella
A
- Occupational disease – through skin, raw milk, foetus
- Waxing + waning flu, multisystemic
- Treat = atb, can be fatal/need surgical intervention
86
Q
ringworm
A
- Ringworm – superficial fungal infection of skin + hair self-limiting disease
87
Q
aetiology ringworm
A
- Microsporum sp or trichophyton esp
- anthropophilic, zoophilic or geophilic
- arthrospores = parasitic phase. Saprophytic stage produced on media.
- Spores remain viable for years if cool + dry
88
Q
SOI ringworm
A
carriers animals (asymptomatic carriers are cats), premise + harnesses etc
89
Q
MOT ringworm
A
direct contact + w carriers + environment if skin trauma
90
Q
risks ringworm
A
young/free roaming/hunting dogs + warm environment
- High incidence in winter + spontaneous recovery in spring
- they’re sensitive to UV lights, chlorine also will
91
Q
pathogenesis ringworm
A
- viable spores/hyphae on animal
- attack stratum corneum + hair fibre autolysis of fibre structure hair breaks alopecia
- exudation, debris + hyphae = dry crust
- centrifugal progression (die in middle of lesions leaving periphery active)
- 2nd bacterial infection common
92
Q
signs ringworm
A
- Hair loss, scaling, crust, erythema, papules, nodular reaction in some dogs + persians
93
Q
diagnosis ringworm
A
- take from the edge between healthy + diseased area + take hair that stays between your fingers
- Microsporum grows the fastest (can be 5-6 days) other fungi’s 2-6 weeks
- PCR – not the choice as can catch DNA from dead saprophyte
- gold standard = skin scrape
- woods lamp = green m.canis pluck hair/scrape on edge of lesions for microscopy (decontam skin w alcohol) false positives due to other things showing up like m.canis infection, only 40-50% produce the fluorescence
- fungal culture to know if spores present (2-6w)
- PCR confirms presence of fungal DNA (non-viable spore)
94
Q
PM ringworm
A
- dermatohistopathology – suppurative luminal folliculitis + pyogranulomatous furunculosis
95
Q
differential ringworm
A
- dermatitis, bacterial pyoderma, parasites, allergies
96
Q
treatment ringworm
A
- spontaneous recovery in 90 days – culture 1x/m during treatment + stop after 2 neg cultures
- isolate from pets during treatment
- itraconazole 5mg/kg PO 1x1d week-on-week off, usually resolved after 3-4 cycles
- topical enilconazole/chlorhexidine wash 2x/w until mycologic cure
- stop when clinical + mycological cure
97
Q
prevent ringworm
A
- disinfectant environment, clean bedding + grooming equipment etc
- decreased stocking density
- ringval vaccine (live attenuated) for cows
- ensure adequate vitamin A, selenium and zinc status
98
Q
public health ringworm
A
zoonotic
99
Q
causative agent ringworm
A
- horses = t. equinum, t. mentagrophytes, m. gyspneum etc
- cattle = t. verrucosum, t.mentagrophytes
- pigs = m.nanum , t.mentagrophytes
- small rum = t.mentagrophytes
100
Q
papillomatosis
A
- international occurrence in all animal species and sarcoid and urogenital tumours occur in almost all population
101
Q
aetiology papillomatosis
A
- PVs, papillomaviridae family, double-stranded DNA - 6 open reading frames
- 24 bovine, 15 canine, 7 equine, 4 feline
102
Q
MOT papillomatosis
A
direct contact, fomites, insects. Through TB testing, rectal exams etc
103
Q
POE papilloamtosis
A
cutaneous/mucosal abrasions
104
Q
HS papillomatosis
A
all species. Most common in young cattle, dogs + horses. Uncommon in pigs + sheep. PV in cat rare
105
Q
pathogenesis papillomatosis
A
- infects basal keratinocytes + replicates in differentiating spinous + granular layers extra growth (wart)
- contains epithelial and CT – papilloma/ fibropapilloma,
- basal-cell hyperplasia without viral antigen production
106
Q
horses papilomatosi
A
- nose, lips, eyelids, distal legs, penis, vulva + mam gland 2o to abrasions – 1km
- young then regress as immunity increases
- aural plaque, SCC of penis
- DD = verrucous sarcoid
107
Q
cattle papillomatosis
A
- Head, neck, shoulders. Appear 2m after exposure + can last >1y. immunity 3-4w after infection. Cauliflower like pedunculated proliferation of epidermis with keratotic surface
- BPV1+2 = paponodule with warty surface on venereal region – pain etc but no decrease repro
- Persistent cutaneous papillomatosis in older herd
- Bladder + GI tumours – co-carcinogen
108
Q
dogs papillomatosi
A
- Canine MM papillomatosis, cutaneous papillomas + cutaneous inverted papillomas
109
Q
diagnosis papillomatosis
A
- Signs, biopsy to differentiate from SCC, PCF to detect virus/serology to see PV exposure
110
Q
PM papillomatosis
A
- micro –hyperplastic epidermis wi scant dermal tissue
111
Q
treatment papillomatosis
A
- self-limiting
- surgical removal at max size to prevent growth stimulation
- azithromycin in canine MM
- aural plaque = imiquimod 5% cream 3x1 w every other week for 6w-8m. remove crusts first
112
Q
vaccination papillomatosis
A
- cattle, autogenous vaccines of ground wart tissue
- inactivated with formalin
- calves at 4-6w old 0.4ml intradermal at 2 sites again after 4-6w + 1yo
- vaccines continued for 1y after last war
- clean and disinfection
113
Q
haemomycoplasmosis
A
- epierythrocytic parasites. Rare, sporadic, noncontagious, blood-borne disease in sheep, swine, cattle
114
Q
haem aetiology
A
- haemotrophic mycoplasma (previously eperythrozoon species) G-
- M. suis, M. ovis, M. hemofelis, M.hemocanis, M.wenyonii
- Obligate intracellular, can’t be grown, in culture
115
Q
MOT haem
A
- MOT: transfer of infected blood (transfusion/contaminated equipment) + arthropod vectors
- Vertical in cats, swine + camelids. Direct – fighting in cats (present in saliva)
116
Q
HS haem
A
- HS: M. suis – associated with stress in young pigs, increase in summer due to management/other diseases etc. rums - min infective dose = 1 parasitised RBC
117
Q
pathogenesis haem
A
- Pigs – extravascular anaemia – regenerative. No haemoglobinuria
- Rums – intravascular haemolysis +erythrophagocytosis macrocytic anaemia
118
Q
signs haem
A
- Pigs – anorexia, weakness, pale MM, icterus, hypoglycaemia – convulsions -death, chronic = poor growth, decreased reprod, lesions on ears
- Sheep – asymptomatic or severe in young with worms. Incubation 1-3w, episodic hyperthermia, weakness, anaemia. Chronic = exercise intolerance, death, decreased wool
- Cattle – asymptomatic, mammary gland, scrotum + hindlimb, oedema, decreased milk, fever, lymphadenopathy
- Dogs – acute haemolysis if splenectomised. Asymptomatic healthy
119
Q
diagnosis haem
A
- PCR whole blood or aspirate of spleen
- Microscopy of wright-stained blood smear – take when animal has fever. Parasitaemia can be cyclic in chronic + can die if in EDTA too long
120
Q
treatment haem
A
- IM tetracycline/ oxytetracycline – improve within 24hrs
- Maybe blood transfusions on cats. Can remain carriers
121
Q
prevent haem
A
- Screen blood donors, sterilised equipment, control arthropod vectors
122
Q
health haem
A
- Potential for zoonosis – immunocompromised but most species are host specific
123
Q
black leg
A
- acute, highly ftal necrotising myositis
124
Q
aetiology black leg
A
- clostridium chauvoei – gram +, spore-forming, anaerobic, motile
- natural in GI tract spores remain viable in soil for years
125
Q
SOI black leg
A
- SOI: soil-borne infection
126
Q
MOT black leg
A
- MOT: contaminated soil, food, water
127
Q
POE black leg
A
- POE: ¬alimentary tract, wounds (shearing sheep)
128
Q
HS black leg
A
- HS: ¬cattle 6m - 2y, healthy bull breeds, sheep of all ages (not horse + pig)
129
Q
GD black leg
A
- GD: worldwide, most common in warm/wet months
130
Q
path black leg
A
- ¬recent excavation/flooding
- Spores ingested bloodstream muscle, spleen, liver + GI tract dormant
- Cattle = endogenous infection (no trauma)
- Sheep = tissue laceration + trauma
- Returns to vegetative state + produces haemolysis, DNAase, hyaluronidase + neuromidase severe necrotosing myositis + systemic toxaemia death
131
Q
signs black leg
A
- ¬incubation 1-3 days
- Cattle = sudden onset/death wo signs. Acute severe lameness, depression, fever, oedematous + crepitant swellings – hot + painful. Swelling increased, skin becomes cold + insensitive. Tremors + prostration. Death in 24-48hr, dyspnoea
- Sheep = similar to cattle but oedema + crepitation uncommon. Local lesion of vagina/skin. Death in 24-60h
132
Q
PM black leg
A
- ¬often in characteristic position: lying on the side with the affected hindlimb stuck out stiffly
- bloating + putrefaction v fast. Blood stained froth from nostrils + anus. Blood clotting fast
- rancid odour, serosanginous fluid with bubbles of gas. Muscle dark red/black + swollen. Check tongue, myocardium + diagraphm
133
Q
diagnosis black leg
A
- anaerobic culture + Biochem ID from muscle ASAP
- IF = fast + reliable. PCR unreliable for environment
134
Q
differentials black leg
A
malignant oedema, anthrax, lightning strike, bacillary haemoglobinuria
135
Q
treatment back leg
A
- penicillin + surgical debridement, recovery low
136
Q
prophylaxis black leg
A
- multivalent clostridium vaccine at 2m old. 2x 4 w apart then q1y before danger period
- if outbreak – vaccinate + penicillin for 14d + move from pasture
- sheep = vaccinate naïve ewe 1m before lambing then yearly Lambs before out on pasture. Immunity is short
- burn or deep bury + fence off carcasses
137
Q
enterotoxaemia
A
clostridium
138
Q
clostridium species
A
- Enteropathogenic = C. perfringens (A-G), C. difficle, C. coliform, C. spiriform
- Neurotoxic = C.tetani, C. botulinum (A-G)
- Atypic = C. piliform
- Histiotoxic = C. chauvoei, C. septicum, C. novyi type A, C. perfringens Type A, C. histiolyticum, C. haemolyticum
- C. perfringens - type A = enterotoxemia, malignant oedema, Type B= enterotoxemia, lamb dysentery, Type C= enteroxaemia, struck, Type D = enterotoxemia, pulpy kidney disease
- C. chauvoei = black leg
- C. haemolyticum = bacillary hemoglobinuria
- C. septicum = malignant oedema
- C. novyi = type B = necrotising hepatitis
- C. sordelli = sudden death syndrome
139
Q
clostridium perfringens aetiolgoy
A
- clostridium perfringens exotoxins, G+, non-motile, sporulating bacteria
- 7 types = A-G
- Colonies are grey/yellow, normal inhabitant of the intestine of animals and humans
- When environment altered (sudden diet changes) it proliferates + produces exotoxins. Spores v resistant in environment
140
Q
alpha toxin (CPA)
A
- hydrolyses phospholipids, damages membranes of RBC, endothelial cells, myocytes
- lethal
141
Q
beta toxin (CPB)
A
damages epithelial cells SI
142
Q
epsilon toxin (ETX)
A
- damages vascular endothelial cells
143
Q
iota toxin (ITX)
A
alters intestinal permeability
144
Q
enterotoxin (CPE)
A
disturbs electrolyte + water resorption (pigs)
145
Q
cytotoxic beta-2 toxin (CPB-2)
A
important in foals and adult horses
146
Q
c. perfringens type A
A
- main toxin = alpha
- causes: equine intestinal Clostridiosis, enteritis in piglets, enterotoxemic jaundice (lambs), abomastitis/enteritis calves, haemorrhagic enterotoxaemia ruminants
147
Q
C. P type A horses
A
- found in 8% of healthy horses + >90% foals so important to find toxin producing strains
- risk = atb, stress, food deprivation
- signs = sudden death, diarrhoea, colic, fever, decreased feed intake, lethargy, sepsis
- diagnosis = isolation + ID of toxigenic clostridia from faeces, reflux, tissue, blood, PCR for toxins. ELISA for enterotoxin
- treat = supportive care, metronidazole, polymyxin B (toxin binder)
- prevent = good farm hygiene
148
Q
c. perfringens type A pigs
A
- <5d old piglets
- Watery, yellow diarrhoea, self-limiting 5d
- High morbidity, low mortality
- No specific diagnosis (exclusion)
- Prevent = good farm hygiene
149
Q
c. perfringens type a ruminants
A
- Haemorrhagic enterotoxaemia + haemolytic disease
- Acute severe depress, pale MM, dyspnoea, abdo pain, collapse
- Death within 12h
150
Q
c. perfringens type A sheep
A
- Yellow lamb disease (enterotoxemic jaundice)
- Diet predisposes to bacterial overgrowth
- Signs = depress, anaemia, icterus, haemolysis (alpha toxin)
- Death in 6-12h
151
Q
c. perfringens type b
A
lamb dysentry
enterotoxaemia calves + foals
152
Q
c. perfringens type c
A
necrotic enteritis piglets
struck
enterotoxamiea
153
Q
c. perfringens type d
A
pulpy kidney disease
154
Q
lampy dysentry aetiology
A
morbidity 30%, mortality 100%
- C. perfringens Type B, alpha, beta and E toxins
- MOT – ingestion
- HS - <3w old lambs
155
Q
lamb dysentry pathogenesis
A
- In young due to immaturity of GI tract no trypsin to inhibit beta toxin bacteria colonise
- Alpha toxin = haemolysis + cytotoxic
- Beta toxin = increase capillary permeability
- E toxin = neuro signs
156
Q
signs lamb dysentry
A
- Peracute sudden death
- Stop nursing, listless, recumbent, fetid blood tinged diarrhoea
157
Q
PM lamb dysentry
A
- Haemorrhagic enteritis w ulceration of mucosa. Dark red/purple intestine
158
Q
treatment lamb dysentry
A
no treatment as course too shrot
159
Q
struck
A
- Aetiology = c. perfringens Type C
- HS = adult sheep on good pasture in spring
- Signs = sudden death with no signs
160
Q
necrotic enteritis in pigs
A
- Aetiology = c. perfringens type C
- SOI = environment, sow skin, faeces
- MT = during suckling PO
- HS = <7d old piglets. Can become endemic in unit
- Signs = diarrhoea, reddening of anus, depression, watery yellow haemorrhagic faeces death in 12h
161
Q
pulpy kidney aetiology
A
- cl. Perfringens Type D. toxins esp E toxin. Part of normal microbiota
162
Q
epizoo pulpy kidney
A
- HS: ruminants, mostly <2 w old lambs or fatten lots – ‘overeating disease’
- Risks: excessive grain/single lamb so too much milk (lots of starch in duodenum = overgrowth of bacteria to toxin production)
163
Q
path of pulpy
A
- E toxin causes vascular damage, esp in capillaries of brain
164
Q
signs pulpy
A
- Sudden death, excitement, seizures + incoordination, opisthotonus, circling, head pressing, hyperglycaemia, greeny, pasty diarrhoea
165
Q
PM pulpy
A
- Peracute no lesions
- Intestinal hyperemeia, fluid in pericardial sac, pulmonary oedema, petechiae of heart. Undigested feed in ileum+ Soft pulpy kidneys (rapid autolysis)
- Micro – oedema + malacia in cerebellum
166
Q
diagnosis pulpy
A
- Signs, detection of E toxin in SI fluid (PCR)
167
Q
treatment pulpy
A
too acute to treat
168
Q
control pulpy
A
- Vaccinate ewes w type D toxoid 1x then 4-6w before lambing
- Vaccinate lambs on entrance to feedlot (cold abscesses common post) decrease concentration in feed
169
Q
malignant oedema
A
acute generally fatal toxaemia affecting all species
170
Q
aetiology of malignant oedema
A
- clostridium septicum (mixed Cl infection), gram +, spore forming, anaerobic (perfringens A)
- found in soil + GI tract
171
Q
SOI malignant
A
contaminated soil
172
Q
MOT malignant oedema
A
wound contamination
173
Q
POE malignant
A
wounds: accident, castration, docking, insanitary vaccination and parturition
174
Q
Hs malignant
A
various animal species of all ages
175
Q
path of malignant
A
- infection through contaminated wounds or activation of dormant spores
- exotoxins inflammation severe oedema, necrosis and gangrene
- necrotoxin animals death (septicaemia and toxaemia)
176
Q
signs malignnat
A
- incubation 6-48hr
- high fever, anorexia, depress, tremor, lame soft, pitted swelling, extremely painful, muscle = brown/black, subcut oedema
- systemic toxaemia, sloughing of skin
- severe oedema of head in rams (fighting) oedema of vulva, death in 24-48h if infection at parturition
177
Q
PM malignant
A
- ¬tissue changes occur rapidly after death
- gangrene of skin, subcutaneous oedema, subserosa haemorrhages + serosanguineous fluid in cavities
- rams – spread to lungs = pleural/pulmonary oedema
178
Q
diagnosis malignant
A
- IF from tissue smear. Cl. Septicum rapidly invades from intestine so not reliable if dead >24hr. PCR. FNA + G stain shows G+ rods + confirms w anaerobic culture
179
Q
differential malignant
A
- anthrax (pigs + horse), blackleg, photosensitivity (sheep) cl. Septicum = braxy in sheep – fatal toxaemia with inflammation of abomasal wall
180
Q
treatment malignant
A
- emergency – penicillin high dose IV a4-6h, NSAIDs
- fluids, surgical incision + drainage
181
Q
prophylaxis malignant
A
- hygiene at lambing, shearing, castration and docking
- bacterins for immunisation. Specific or multivalent
- vaccine before castration/docking
- prophylactic penicillin to at risk
- bravoxin 10-
o cl. Perfringens A,B, C + D toxoid
o cl. Chauvoci whole culture
o cl. Novyi, septicum, tetani, sordelli + haemolyticum toxoid
182
Q
infectious foot rot in sheep
A
- contagious bacterial infection of sheep and goats
- most common cause of lameness in sheep
- initial infection involves the skin between claws
- survives indefinitely in lesions of foot, outside in environment – couple of days, 2 weeks at most (dichelobacter)
- fusobacterium – normal inhabitant of rumen stomach
183
Q
aetiology foot rot
A
- dichelobacter nodosus – gram -, anaerobic, obligate pathogen + 1o agent, 20 strains, variable pathogenicity
- fusobacterium necrophorum – gram - ,anaerobic , synergistic in pathology, survive 2w in environment + lifelong in cracks + deformities of affected sheep
184
Q
SOI foot rot
A
- SOI: carrier sheep + contaminated environment
185
Q
POE foot rot
A
- POE: moist interdigital skin
186
Q
MOT foot rot
A
- MOT: most rapidly in warm + moist condition
187
Q
HS foot rot
A
- HS: sheep mostly, rare cattle + goats. Merino most, susceptibility increased with age
188
Q
risks foot rot
A
- Risks = overcrowding, pasture types (abrasion)
189
Q
pathogenesis foot rot
A
- f. necrophorum colonises moist, macerated interdigital skin + provides conditions for d. nodosus
- D.N liquified cells of stratum granulosum + spinosusm (proteanes) separation of hoof wall + basal epithelium
- Progresses from interdigital horn heel sole lat side of hoof
- Virulence of D.N depends on keratinolytic capacity – heat stable elastase + protease
190
Q
signs foot rot
A
- score 1 and 2 = benign foot rot, related to mild or more severe interdigital dermatitis. beginning of virulent form
o 1 = limited, mild interdigital dermatitis
o 2= more extensive, interdigital dermatitis - score 3 and 4 = virulent footrot
o 3 = severe interdigital dermatitis and underrunning of the horn of the heel and sole
o 4 = similar to 3, but with underrunning extended to the walls of the hoof - most common in both digits in more than one leg
- smell is characteristics
- goats and cattle – more mild
191
Q
diagnosis foot rot
A
- clinical suspicion, bad odour
- swabs of feet for PCR - best place for swab – skin -horn junction
- D.N in gram stain or culture (Difficult)
- Virulence determined by extracellular proteases. Type IV fimbriae
- Virulent strains identified by RT-PCR of genes- aprB2 + aprv2 = benign + virulent respectively
192
Q
differential foot rot
A
- ovine contagious interdigital dermatitis, foot abscess, orf, FMD, strawberry footrot, laminitis)
193
Q
treatment foot rot
A
- temp control (wet season) or total eradication
- foot trimming – remove all of necrotic material + exposure to air
- topical solutions: sprays
- foot-bathing of atb – 6cm deep for 10 min dry + clean after
- parenteral long acting oxytetracycline
- check treated 1x/w not responding – cull
194
Q
control foot rot
A
- vaccine with certain strains – immunity lasts 2-3m
- vaccine reactions common
- selective breeding for resistance, quarantine
195
Q
control phase - foot rot
A
- during periods of active spread or to decrease affected
- vaccination, footbaths + parenteral antimicrobials used
196
Q
eradication phase foot rot
A
- during dry season
- not until w after meds stopped + 10-12 w after vaccination
- extremities inspected every 3-4w
- infected treated w atb on first inspection only – after infected culled
- continued until 2 consecutive negative flock inspection
197
Q
surveillance phase foot rot
A
- all lame sheep examined immediately
- if foot rot – go back to phase 1 or 2
198
Q
blue tongue disease
A
- OIE
- non-contagious, vector-borne, viral disease of domestic and wild ruminants
199
Q
aetiology of blue tongue
A
- Orbivirus, family reoviridae (AHSV), 28 serotypes + 8 typical strains
- Non-enveloped, double stranded RNA
- very stable in presence of protein in blood for years stored at 20oC
- inactive by 50oC/3hours; 60oC/15minutes, pH <6.0 and >8.0, iodophors + phenols
200
Q
GD blue tongue
A
- GD: prallel to distribution of culicoides in uk
201
Q
SOI blue tongue
A
- SOI: sub clinically infected ruminants + infected vectors: small midges from colicoides family
202
Q
MOT blue tongue
A
- MOT: culicoides bite, in contact BTV serotype 26 in goats. Transplacental in cattle
203
Q
HS blue tongue
A
- HS: fine wool + mutton breed sheep – 100% morbidity + 30-70% mortality, wild ruminants + cattle
- Vectors infected by biting infected animal. BTV has high affinity for RBC = long viraemia in presence of neutralising antibody. Up to 11w viraemia in cattle = yer round transmission where water is short
204
Q
pathogenesis blue tongue
A
- Bite of midge BTV spreads + replicates in regional LN viraemia + systemic spread replication is haematopoetic + endothelial cells cytokine storm, DIC, thrombosis, sloughing of epithelium, cyanosis etc
205
Q
signs blue tongue
A
- Sheep – peracute to chronic. Cattle usually subclinical incubation 4- 6 d, peracute die in 7-9d due to pulmonary oedema. Chronic die in 3-5w due to bacterial complications + exhaustation
- Fever, listlessness, oedema of face, congestion of mouth, nose, coronary bands, lameness, depression
- Serous nasal discharge mucopurulent. Cyanotic tongue ulcers o fmouth, torticollis due to skeletal muscle damage, abortion, abnormal wool growth – dermatitis
- Cattle = fever, increased RR, salivation, stiffness, dermatitis
206
Q
PM blue tongue
A
- Highly characterist = petechiae, ecchymosis/ haemorrhage in wall of base of pulmonary artery
207
Q
diagnosis blue tongue
A
- Signs, PM, PCR, VI on eggs – EDTA blood from febrile comp ELISA – 7-14d after infection + serology lifelong – good as doesn’t detect cross reactivity antibody to others
- no cross immunity
208
Q
differentials blue tongue
A
- contagious ecthyma, FMD, vesicular stomatitis, MCF, BVD, sheep pox, etc
209
Q
prevention and control blue tongue
A
- attenuated + inactivated vaccines. 3 polyvalent, eaech with 5 serotypes available in south Africa
- monovalent (BTV 10) MLV in US
- vaccines with different seroyypes don’t provide consistent cross protection
- live attenuated vaccines don’t use in culicoides season as can transmit vaccine viruses to non-vaccinated new strains
- passive immunity in lambs = 2-4m
- in non-endemic – use of vaccines strains other than ones causing infection = not recommended
- vector control
- econ losses = morbidity + mortality, trade restrictions, surveillance, vaccine etc
210
Q
treatment blue tongue
A
none
211
Q
listeria
A
- circling disease - affects humans + animals (ruminants)
- proper pasteurisation will eliminate listeria from milk
- 3 different clinical forms
o encephalitis – lethality is high
o abortion – occur in large numbers in small ruminants, cattle it’s sporadic
o septicaemia: less common, monogastric animals - 2 things that destroy listeria: high acidity, proper pasteurisation (high temperature)
212
Q
aetiology of listeria
A
- listeria monocytogenes, G+, motile, non-spore forming, extremely resistant, 16 serotypes
o grows at 4-45oC, 10% salt, >2y dry soil, >200d on straw, ubiquitous saprophyte in soil
213
Q
SOI listeria
A
- SOI: alkaline spoiled silage, reservoir = soil + mammal GI tract, faeces
214
Q
MOT listeria
A
- ¬MOT: ingestion, inhalation (milk)
215
Q
GD listeria
A
- GD: worldwide, temperate/colder climates
216
Q
HS listeria
A
- HS: winter-spring disease of feedlot animals (ruminants)
217
Q
risk listeria
A
- Risks: post nutrition, overcrowding, stress etc
218
Q
pathogenesis listeria
A
- Swallowed, invade mm migration via trigeminal nerve microabscesses on brain stem meningoencephalitis
- Intestinal MM circulation damage to placental barrier or through to foetus abortion + stillbirth or born infected
- Facultative intracellular – can survive in macrophages = nucleated cells disseminate in host tissues, sheltered from humoral response
219
Q
sings listerai
A
- encephalitis, anorexia, depression, circling, facial paralysis, lack of menace, recumbent
- abortion = in last trimester, no clinical signs. Up to 30% of sheep. Cattle = retained placenta
- septicaemia = monogastric animals (calves), depress, weakness, pyrexia, diarrhoea
- chinchillas = septicaemia with aborton + encephalitis
220
Q
PM listeria
A
- small necrotic foci on organs esp liver. Calves = haemorrhagic gastroenteritis. Foetus = autolysied, necrotic foci on liver, bloody fluid in serous cavity
- micro = perivascular cuffing and multifocal micro abscesses in pons + medulla oblongata
221
Q
diagnosis listeria
A
- ¬clinical suspcision (CSF – increased protein + large mononuclear cells)
- No serology – healthy have titres
- Isolation from brain or aborted foetus/placenta
- Anton test (not done anymore) = put on conjunctiva of rabbit conjunctivitis
222
Q
differentials listeria
A
- Ketosis, preg toxaemia, BSE, rabies, brucellosis, coenurosis, polioencephalomalacia)
- abortion (brucella, lepto, Q fever)
223
Q
treatment listeria
A
- early, aggressive ATB treatment (penicillin q12h for 1-2 w high dose as hard to reach conc in brain)
224
Q
control listeria
A
- isolation and treatment, check silage, decrease risk, cost v benefit of vaccine?
225
Q
public health listeria
A
- all material but esp aborted foetus + necropsy of septicaemic animals at greater srisk
- fever, Gi signs, sepsis, flu, meningitis, abortion
- infected milk = hazard
- 15-30% lethality in at risk group even with atb
226
Q
paratuberculosis (John’s disease)
A
- Chronic, contagious granulomatous enteritis
- National control programmes
- Listed = priority for international trade OIE
227
Q
aetiology of Johne’s disease
A
- Mycobacterium avium, subspecies paratuberculosis (MAP)
- Survives in soil >1y, water, and manure, resistant to many disinfectants
- Can be killed by crescylic acid compounds
228
Q
SOI Johne’s disease
A
- SOI = faeces (feco-oral transmission)
229
Q
HS John’s disease
A
- HS = ruminant + foxes, pigs, wild rabbits + non-human primates. Highest prevalence in dairy (20-90%) Can also be found in several wild and captive exotic species
230
Q
path Johne’s disease
A
- Infection soon after birth but signs don’t develop until after puberty
- Enters SI + engulfed by macrophages in intestinal wall multiples in cell + macrophage dies
- Chronic granulomatous enteritis with thickening + distortion of intestinal wall
- Can take m-y to develop
231
Q
signs Johne’s disease
A
- Emaciation (wasting disease), diarrhoea in late stage of disease
- Diarrhoea increase in severity weight loss, coat colour can fade, good appetite still
- Ventral + submandibular oedema (bottle jaw) due to PLE
- Unresponsive to wormers + Atb
232
Q
PM Johne’s disease
A
- None thickened + corrugated intestine w enlarged + oedematous local LN. no correlation between signs + severity of lesions
- Micro = diffuse granulomatous enteritis, progressive accumulation of epithelioid macrophages + giant cells In mucosa + submucosa of gut
233
Q
diagnosis Johne’s disease
A
- PCR – more sensitive + specific than serology
- ELISA
- Gold Standard – necropsy with culture + histopath of various tissue (8-24w for colonies to show)
234
Q
treatment John’s disease
A
none
235
Q
control and prevention johnes
A
- Good sanitation, limit exposure of young to organism. Vaccine but subject to regulatory approval
- clean udders on dams before nursing
- move to “clean” pasture
- Do not graze sheep on contaminated pasture
- Slaughter of positive reactors
- Potential zoonosis – chron’s in people
236
Q
actinomycosis (lumpy jaw)
A
- Lumpy jaw
- Localised, chronic, progressive, granulomatous abscess
237
Q
aetiology lumpy jaw
A
- Actinomyces bovis, Gram +, anaerobic, filamentous/branching
- Difficult to culture – blood media, 37oC
- Actinomyces = normal in mouth + nasopharynx
238
Q
SOI lumpy jaw
A
- SOI= pus discharged from lesion
239
Q
POE lumpy jwa
A
- POE: wounds of buccal mucosa/dental alveoli
240
Q
risks lumpy jaw
A
- Risks = sharp feed, foreign bodies, young cattle when teeth erupting
241
Q
HS lumpy jaw
A
- HS: cattle, A.suis in pigs, A. viscosus/hordevulneris in dogs, horses
242
Q
MOT lumpy jaw
A
- MOT: through wounds/abrasions
243
Q
signs lumpy jaw
A
- Slow growing, painless mass on mandible/maxilla near central molars
- Increase in size ulceration + fistulation
- Pus = sticky, honey like, small amount. Containing sulfur granules
- Severe = spreads to muscle + fascia of throat
o Oesophageal groove reticulum = impaired digestion periodic diarrhoea + bloat - Facial distortion, loose teeth, dyspnoea
244
Q
diagnosis lumpy jaw
A
- Signs = presumptive
- Culture = confirmatory
o Specific media, anaeoribc conditions, often negative - Cytology = G+ rods + filaments (sulfur grain)
- X-ray = osteomyelitis, periosteal new bone + fibrous tissue
- Biopsy for histopathology
245
Q
treatment lumpy jaw
A
- IV sodium iodide 70mg/kg 10-20% solution 1x then repeated q7-10d
- Stop if signs of iodine toxicity start
- Atb – oxytetracycline, florfenicol, penicillin
246
Q
botryomycosis
A
- It is a chronic granulomatous infectious disease of equine, caused by Staphylococcus sp., characterized by development of granuloma commonly located on the limbs near the point of elbow or scrotum (spermatic cord fistulae).
247
Q
aetiology botryomycosis
A
- Staphylococcus species. Saprophytic bacteria – opportunistic infection (horses w PPID/EMS)
248
Q
MOT botryomcysosi
A
- MOT: after trauma/contamination of wounds (post castration)
249
Q
GD botryomycosis
A
- GD: The disease present where equine is raised
250
Q
HS botryomycosis
A
- HS: Horses, donkeys and mules
- Morbidity and mortality rates are low.
251
Q
signs botryomycosis
A
- Granuloma on limbs (near point of elbow) or scrotum – spermatic cord fistula
- Skin = papules/nodules that are non-pruritic + non-healing. Crusts w ulcers + draining tracts
- 10-20cml, looks like a tumour
- Yellow, sticky mucoid pus with white ish seeds/granules of clumped masses of staphylococcus
- Spermatic cord = scirrhous cord. Chronic discharging sinus at scrotum with fibrosis + abscessation of cord + testes
o Possible metastatsis of purulent lesions to internal organs (liver, lung, spleen, kidney)
252
Q
diagnosis botryomycosis
A
- History + signs
- Lab samples: Pus, skin biopsy, blood and serum.
- Direct microscopic of stained pus to see Staph sp.
- Culture of pus samples
253
Q
treatment botryomycosis
A
- Complete surgical excision of lesion
- local dressing with prolonged course of systemic antibiotic.
254
Q
control botryomycosis
A
- Early diagnosis, isolation and treatment of infected animals,
- Prophylactic treatment of all cutaneous wound and abrasions
- Adequate hygiene to prevent spread of infection.
255
Q
tularaemia
A
- Bacterial septicaemai, category A, bioterrosim agent
- Reportal to public health authorities in some jurisdictions - OIE
- Infective dose low – 10-50bacteria for disease
- cats, sheep (show clinical problem more often)
- natural foci – circulates in certain area in certain biome
256
Q
aetiology tularaemia
A
- francisella tularensis, gram -, aerobic, non-spore forming, nonmotile coccobacillsus
- facultative intracellular
- killed by heat + disinfection but survives w/m in moist environment
- 4 sub species: differ in virulence in biochemical properties, ecology + geographical spread
o Type A = most pathogenic – in North America type A = subsp tularensis
o type B = subsp. Holarctica, subsp. Mediasiatica, subsp. novicida
257
Q
SOI infected animals tularaemia
A
- SOI: ¬infected animals – rodents + horses = reservoirs, vectors – mechanical, biological = ticks + deer fly, contaminated environment/ food and water
258
Q
MOT tulaearemia
A
aerosol pneumatic form. Direct contact/ingestion ulceroglandular, oculoglandular, oropharyngeal or typhoid forms. Waterborne (in amoeba)
259
Q
POE tularaemjia
A
skin and mucous membranes, per orally, respiratory tract
260
Q
HS tularaemia
A
sheep, cat, dog, pig, horse, human. Cats increase risk due to predatory behaviour, cattle are resistant
261
Q
SOI for people
A
bite of infected tick
262
Q
path tularaemia
A
- facultatively intracellular + multiplies in almost all host cell tytpes disseminates via blood to all organs
- bacteria + cell debris from capillary endothelium necrotic foci in liver, splene, LN + bone marrow due to thrombotic development
- incubation = 2-10d, signs v. variable
263
Q
signs tularaemia
A
- cats – most susceptible, viraemia diagnosed only after they die from systemic infection so via PM or because their owner develops viraemia, fever + lymphadenopathy, anorexia, lethargy, ulcers in mouth
- sheep: fever + lymphadenopathy, progressive weakness, decreased BW, diarrhoea, subclinical
- hare = lethargy, altered mental status, excitation
- prostration + death in few hours - days
264
Q
PM tularemia
A
- yellow/white foci of necrosis on spleen, liver and lungs
- hepatomegaly/splenomegaly or both
265
Q
diagnosis tularaemia
A
- culture, PCR, serology – IF/antibody titres take care during necropsy – ZOOTNOTIC
- bacteriology – CAUTION – not allowed to do isolation if you don’t have certain biosecurity level (BSL3) as can spread from plate into air to people working
- conventional and RT-PCR: relatively safe for people doing it
- in cats seroconversion 2-3 after infection
266
Q
differentials tularaemia
A
tick paralysis, other septicaemia, anthrax
267
Q
treatment tularaemia
A
- early atb – streptomycin, gentamicin, quinolones, streptomycin for 10d, tetracyclines
- chloramphenicol for 14d to decrease relapse risk
o need to be aware that domestic animals are important source of infection for their families - lambs – oxytetracycline (6-10mg/kg)
268
Q
control tularaemia
A
difficult – insect + tick control + prevent contact
269
Q
leptospirosis
A
- likes water and high humidity
- disinfection – standard alcohols, contact time a few minutes
- rodents
270
Q
aetiology leptospirsos
A
- leptospiraceae, order: spirochaetales
- old clasisficaiton = L.biflexa (non-pathogenic) + L.interogans (250 pathologic serovars)
- new = L. interogans sensu lato + 10 pathogenic = L. interogans, L. kir schneri, L. borgpeter senii
271
Q
leptospirosis SOI
A
- SOI: sick + carrier domestic + wild animals (rats, mice, voles = reservoirs)
272
Q
leptospirosis MOT
A
- MOT: direct contact with infected urine, placental fluids or milk. Venerally + transplacentally. Indirect with urine contam environment
273
Q
leptospirosis HS
A
- HS: all mammals – esp cattle, swine, dogs, horses
- Maintence host:: high prevalent, low antibodies, mild signs + persistent
- Incidental = low prevalence, severe signs, marked atb response eg grippotyphosa in dogs
- Where = warm, moist climates – endemic in tropical. Croatia = sporadic seasonal disease, l.pomona, Bratislava, grippotyphosa
- Doesn’t live long in dry soil or temp <10oC + <>24oC
- Killed by freezing, drying or direct sunlight
274
Q
pathogenesis leptospirosis
A
- Penetrate MM or damaged skin circulate in blood replicate in liver, kidney, lungs, genital tract + CNS for 7-10d (acute lepto)
- Antibodies form, clear from blood + signs decrease
- Incidental host = remain in kidney tubules + shed for d-ws
- Maintanence = in kidney, genital tract + eye for m-years
275
Q
signs dogs - leptospirosis
A
- L. interogans canicola, Pomona, grippotyphosa, icterohaemorrhagiae + Bratislava
- Acute kidney injury – lethargy, anorexia, vomit, abdo pain, poly/olig/anuria
- Acute liver probl = jaundice, increased ALP, ALT, azotaemia, hyperphosphataemia, hyponat
- Mouth ulcers, haemorrhagic gastroenteritis
- New form = pulmonary haemorrhage
- Treat = fluids, correct acid-based etc, doxy 5mg/kg PO q/2h for 2w, penicillin then doxy
- Prevent = vaccines against canicola + icterohaemorrhagiae, Pomona + grippotyphosa. Immunity up to 6m. no cross protection among reservoars
276
Q
signs swine - lepto
A
- Maintenance host for Pomona + Bratislava
- Repro problems – abortion in last 2w, avital piglets
277
Q
signs horse lepto
A
- Bratislava, Grippotyphosa, Pomona, Saxkoebing, Icterohemorrhagiae
- Abortion (late term), foal born infected. Fever + acute renal failure. Uticaria
- 2-8m post infection = equine recurrent uveitis – IM against antibodies for some leptospira antigen
- FAT or placenta, PCR
- Treat = enrofloxacin, penicillin etc. intravitreal low dose genta to decrease uveitis
278
Q
signs cattle lepto
A
- Hardjobovoirus (main host), Pomona, grippotyphosa, icterohaemorrhagie
- Abortion at any time of pregnancy or chronic silent infection w repro failure. Rarely severe disease w GI signs, hepatorenal syndrome, mastitis
279
Q
signs human lepto
A
- acute septicaemia - generalized vasculitis
- Intensity depends on serovar, age, immune status.
- Incubation period -2-30 (5-14) days.
- headaches, fever, muscle pain, episcleral injection and photophobia.
- severe = fatal, non-icteric cases last 3-6weeks,
- chronic = headaches, neurologic signs, months or years
280
Q
diagnosis lepto
A
- Leptospires in blood (first 7-10 d) dark field microscopy (direct), Haemoculture (non-direct) on selective media (EMJH, Korthof), Urinoculture –7 days of disease + reconvalescence
- PCR – detect specific DNA sequence of leptospires in blood, urine, CSF or tissue PM (no serovar)
- MAT = mix dilutions of serum w serovars. If antibodies, will agglutinate, titre = highest dilution causing 50% agglutination. Often cross reactions. Paradoxical reactions is early acute infections. Paired titres to discriminate vaccine + infection
- Post-mortem – in parenchymatous organs –liver, kidney (if patient was not treated with atb)
- Histopathology: kidney/liver stains with silver based stains
281
Q
differential lepto
A
- to exclude – all other septicaemic disease, all other causes of abortion in different animals
- in horse – influenza, EIA, piroplasmosis, enzootic hepatitis
- in dog – infectious hepatitis, piroplasmosis
282
Q
treatment lepto
A
- ¬dogs: aggressive fluid therapy (to support kidney azotaemia), ATB (penicillin)
- at beginning bacteria is in blood so treat with penicillin, they “hide” in kidneys (nephrons) and the penicillin wouldn’t sort problems in the kidneys and then it will release leptospirae in urine and oxytetracycline (for the bacteria in kidneys)
- fluids 10ml/kg/h (for severe azotaemia) and important to monitor urination
283
Q
immunoprophylaxis lepto
A
- commercial vaccine (dogs) protect against serovars canicola and icterohaemorrhagiae – immunity last up to 6 months: Pomona and grippothyphosa
- no cross protection among serovars
284
Q
Q-fever
A
- mostly latent infectious disease of domestic and wild animals, manifested with abortion of gravid animals, retention of placenta, mastitis, bronchopneumonia, keratoconjunctivitis and arthritis
- in humans – it’s manifested as septicaemic infectious disease with occurrence of atypical interstitial pneumonia
- causative agent is bacteria (previous rickettsia) Coxiella burnetti
285
Q
aetiology Q-fever
A
- ¬Coxiella burnetti, G- bacteria, obligate intercellular microorganism
- Large cell variant = vegetative form found in infected cells
- Small cell variant = extracellular infectious form shed in milk, urine, faeces, semen. Resistant to heat, drying + disinfectant. Viable weeks-years in environment. Susceptible to ethanol + formaldehyde
- V. virulent
286
Q
SOI Q-fever
A
- SOI: sick reconvalescent carriers, ticks ixodes (1o), contaminated environment; products (2o)
287
Q
MOT Q-fever
A
- MOT: ¬aerogenic, contact, alimentary, vertically
288
Q
POE Q-fever
A
- POE: ¬mucous membranes of nasopharynx
289
Q
HS Q-fever
A
- HS: cattle, sheep, goat, dog, cat, human
290
Q
pathogen q-fever
A
- entry local LN blood generalisation organ dissemination uterus, udder excretion of causative agent (months p.i)
- bacteria enters to cells passively, grows in vacuoles degen + destruction of cells
291
Q
signs Q-fever
A
incubation: not known
- Usually subclinical infection or anorexia + late term abortion, retained placenta, endometritis, keratitis, arthritis
292
Q
PM Q-fever
A
- Necrotic changes on cotyledons
- Micro: hyperaemia, desquamation, lympholeucocytic infiltration, bacteria in cotyledons
293
Q
diagnosis Q-fever
A
- ¬Epizootioloigcal: lots of problems in reproduction (sterility, abortion, retention of placenta)
- Culture – carefully biosecurity level 3
- PCR – but shedding variable through year
- IF on paired sera 2w apart. ELISA but not in first 7d post infection
294
Q
differentials Q-fever
A
- all other disease with reproductive disturbances
295
Q
treatment Q-fever
A
- NONE
- eradication by law, OIE
- very important in med countries, carriers slaughtered under special conditions + meat conditionally usable
296
Q
public health - Q-fever
A
- incubation 2-4w, sudden onset GI signs w fever, headache, sweating, cough – interstitial pneumonia – doxycycline/ TMPS
- very important disease in Croatia and Mediterranean countries (it’s a professional disease)
- carriers should be slaughtered under special condition
- meat of slaughtered animals are conditionally usable
level 2 – working in lab, all windows should be closed, no food/water In lab
level 3 – closed system circulation of air
level 4 – working, completely covered like astronauts, in closed boxes, only hands inside
