dogs Flashcards

1
Q

campylobacteria zoonoses

A
  • It’s manifested with watery diarrhoea, +/- vomiting > chronic disease
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2
Q

aetiology of campy

A
  • Campylobacter jejuni, Gram negative, curve bacilli
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3
Q

SOI of campy

A

sick animals which excrete bacteria in faeces 4 months PI, poultry meat, milk

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4
Q

MOT of campy

A

direct and indirect contact (food, water, faecal/oral, ubiquitous in environment)

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5
Q

HS of campy

A

puppies + kittens up to 6m (rarely older), predisposing = stress (overcrowding kennels) parasites

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6
Q

pathogenesis of campy

A
  • Ingestion  multiplication in intestines  produces mucinase  enables penetration of mucosa  adhere to and invade enterocytes  produce enterotoxin  secretory diarrhoea
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7
Q

signs of campy

A
  • Anorexia, depression, diarrhoea 9lasting 5-15d), vomiting is rare
  • Fever, leucocytosis (when faced with bacteria, leukocytes always rise)
  • Recovery in 1-2 weeks, occasionally chronic for several weeks
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8
Q

diagnosis of campy

A
  • Based on signs
  • Confirm = stain faeces with gram staining + see bacteria culture faeces/intestinal scrape on special media 42oC microaerophilic, PCR
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9
Q

treatment of campy

A
  • Supportive care
  • Erythromycin 20mg/kg bid P/O for 5-7d, 10-14d for chronic
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10
Q

public health of campu

A
  • Dogs could excrete C. jejuni through faeces up to 4 months PI, manifests as self-limiting watery diarrhoea with fever and abdominal cramping
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11
Q

aetiology of clostridia

A
  • C. perfringens: 4 main toxins: alpha, beta, gamma, e
  • C. difficile: toxin A and toxin B
  • C. perfringens in 67%
  • C difficile in 21% of dogs with acute haemorrhagic diarrhoea
  • In cats it’s less frequent, only 5-7%
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12
Q

pathogensis of clostridia

A
  • Enterotoxins – virulence factors, induce fluid accumulation and consequently diarrhoea occur
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13
Q

signs of clostridia

A
  • Enteritis/enterocolitis, Haemorrhagic diarrhoea, Intestinal tenesmus – is very important
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14
Q

diagnosis of clostridia

A
  • ELISA test for toxin in faeces, faecal culture (in healthy too), PCR
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15
Q

treatment of clostridia

A
  • Metronidazole 8-10mg/kg/ tid P/O due to protozoal interaction
  • Amoxicillin + clavulanic acid
  • Mild form not complicated can only give amoxicillin and clavulanic acid around 10 days – it’s enough
  • Chronic form – add metronidazole is not nice as it destroys the stomach so have problem with stomach acid so need to add antiacid
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16
Q

yersinia

A
  • Gastroenteritis and enterocolitis in puppies
  • In faeces of healthy dogs and cats
  • Very common in high intensive swine production
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17
Q

aetiology of yersinia

A
  • Yersinia enterocolitica in dogs
  • Yersinia paratuberculosis in cats, gram +, coccobacilli
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18
Q

SOI of yersinia

A
  • Sick animals, Asymptomatic carriers, raw/undercooked pork meat + slaughter waste
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19
Q

signs of yersinia

A
  • dogs: tenesmus, frequent defecation with traces of mucus and blood in softened faeces
  • Y. pseudotuberculosis in cats: diarrhoea, vomiting, fever and icterus
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20
Q

treatment of yersinia

A
  • Trimethoprim sulphonamide 12-15mg/kg P/O or IV bid
  • Tetracycline 20mg/kg P/O tid
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21
Q

zoonoses yersinia

A
  • Systemic illness
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22
Q

aetiology of salmonella

A
  • salmonella enterica spp. (s. typhimurium, S. enteritidis)
  • Gram negative, bacillus, facultative intracellular. Can survive months in wet, warm areas (poultry/pig barn), </w in composted manure
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23
Q

SOI of salmonella

A

faeces of sick animal, faeces of carriers (small rodents, birds)

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24
Q

MOT of salmonella

A

direct and indirect contact (faecal contamination of food, water and fomites)

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25
POE of salmonella
faecal oral, in utero infection (always a risk of abortion), inhalation, through conjunctiva
26
HS of salmonelal
<1 yr old. Stress increases incidence. Dogs and cats
27
pathogenesis of salmonella
- Ingestion  invasion + multiplication in enterocytes + tonsillar lymphoid tissue attachment by fimbriae + intracellular injection  fluid secretion  strong inflam response usually enough to restrict to GI sepsis can occur  brain, uterus, joints + tips of ears + tails - Shed in faeces 3-6 w PI - If treatment is too late, may not be enough to cut off the sepsis – kill bacteria but not toxins, rest in the circulation which block all metabolic pathways
28
signs of salmonella
- Dogs + cats often asymptomatic carriers, Acute diarrhoea with septicaemia (brutal diarrhoea) - Fever, anorexia, maybe pneumonia or neuro signs - Leukopenia = terminal phase of sepsis - Sometimes the toxin can penetrate the CNS: o excitations, incoordination, blindness and convulsions (may look like rabies, but it’s terminal phase of sepsis) - animals with acute GI usually recover within 3-4 weeks
29
diagnosis of salmonella
- repeated culture from faeces to determine carrier state (low sensitivity due to intermittent shedding of low number of bacteria) - check feed and water etc - PCR (also finds non-viable bacteria), serology (agglutination in serum/milk for surveillance and control) - isolation of bacteria from faeces and blood – haemoculture (if have sepsis)
30
treatment of salmonelal
- probiotics, metabolic stimulators, fluids, NSAIDs - Bacteriemia – enrofloxacin, cephalosporins (3rd generation IV) (ATB controversial: can achieve clinical cure but maybe not bacteriologic  increase number of carrier animals + resistant bacteria)
31
public heath of salmonella
- High zoonotic significance – faeces of clinically healthy dogs + cats + contaminated pet food
32
intestinal spirochaetosis
- Spirochetes colonise colon of human and animals (colitis)
33
aetiology of intestinal spirochaetosis
- Genus Brachyspira  7 genomic species - Commensal + pathogenic species. In 6-66% of dogs - B. pilosicoli – causes disbalance of microflora in colon  diarrhoea - Invades lamina propria of colon  chronic inflammation + blocks passive resorption of water
34
diagnosis of intestinal spirochaetosi
- faecal samples (gram stains) intestinal scratches to the TSA agar + PCR
35
treatment of intestinal spirochaetosis
- Amoxicillin + clavulanic acid, In vitro: metronidazole and cephtriaxone
36
public health intestinal spirochaetosis
- Infected dogs can be SOI for humans
37
aetiology of canine distemper
- Canine distemper virus (CDV), Genus: morbillivirus, Family: paramyxoviridae - Similar to measles + rinderpest - Fragile, envelope single strand RNA - Lasts 1d outside host - Routine disinfection procedures mostly effective (phenols, ethers + 4 ammonium compounds)
38
MOT of distemper
aerosol droplets (direct contact) also urine
39
HS of distemper
Dogs, ferrets etc
40
risk of distemper
3-6m old and unvaccinated
41
pathogenesis of distemper
- Replication in lymphatic tissue of resp tract (tonsil, LN, thymus)  cell-associated viraemia (in mononuclear cells in blood)  adequate immunity = inapparent illness - inadequate w no antibody response = severe multisystemic illness death or recover with CNS signs - Inadequate low antibody response = milder illness  lungs and skin affected - Recovery but can shed for 60d
42
signs of distemper
- Incubation period: 3-6 days - Diphasic fever, anorexia, lethargy, ocular nasal discharge, cough, diarrhoea, vomiting, hyperkeratosis of nose + foot pads, pustular dermatitis - Neonatal = enamel hypoplasia - neuro = twitching, salivation, seizures, circling paresis, paralysis (w-m later appear)course can be as short as 10d
43
old dog encephalitis
- chronic, rare progressive disease in unvaccinated adults. Not infectious ataxia, head pressing, hypermetria
44
inclusion body polio encephalitis
- Variant form of CDV encephalitis. It can occur after vaccination or in dogs with sudden onset of only neurological manifestation of distemper
45
diagnosis of distemer
- RT-PCR of conjunctiva/nasal/vaginal epithelium, urine, buffing coat - Qualitative RT-PCR to distinguish vaccine from natural infection. Compare ELISA of blood and CSF + IF
46
PM of distemper
- Thymic atrophy in young. Hyperkeratosis. Broncho-pneumonia, enteritis, skin pustules - Micro: necrosis of lymphoid tissue. Inclusion bodies in resp, urinary + GI epithelium. Gliosis, neuronal degeneration, perivascular cuffing
47
treatment of distemper
- Supportive- ATB, electrolytes, food, antipyretics, analgesics, anticonvulsants
48
prevention of distemper
- MLV at 6w + 3-4w intervals until 16w (immunity normally >3y) - Don’t give MLV to late gestation/early lactation bitches - Recombinant canarypox vector vaccine for ferrets
49
prognosis of distemper
- acute neuro = poor + CNS signs can persist after resp + GI gone (steroids may help)
50
aetiology of infectious canine hepatisi
- canine adenovirus 1 (CAV 1), nonenveloped double-stranded DNA virus - antigenically related to CAV-2 (tracheobronchitis) - very resistant to disinfection + environment (w-m) – steam cleaning/bleach kills it - inactivated after 5 minutes at 50-60oC
51
HS of ICH
dogs <1y, foxes, wolves, bear, lynx, recovered dogs shed virus in urine for >6 m
52
MOT of ICH
direct contact, oronasal
53
SOI of ICH
saliva, faeces, urine, fomites, ectoparasites
54
pathogenesis of ICH
- Tonsils + LN  viraemia + dissemination - Primary target = vascular endothelial cells  vasculitis - Immune complex rection  uveitis + corneal oedema (blue eye) + nephritis - Liver = centrilobular necrosis  hepatitis starts in tonsils and cervical lymph nodes  to blood, via thoracic duct  inside blood  dissemination  virus is extremely fast  into liver and all endothelium (including, eye, kidney, and CNS)
55
signs of ICH
- incubation period is 4-9 days, mortality rate 10-30% - clinically inapparent infections are common - Peracute death - fever (transient or biphasic), apathy, polydipsia, anorexia, corneal clouding, abdo pain, vomiting, increased HR, petechia of oral mucosa - hepatic encephalopathy, intracranial vasculitis, increased AST + ALT, proteinuria. Clotting time correlated with severity of injury (longer = worse)
56
PM of ICH
- “paint-brush” haemorrhages on the gastric serosa, LN, thymus, pancreas, + subcut tissues, hepatomegaly with colour change (thickened, oedematous gallbladder) - Micro: centrilobular necrosis, hepatocellular intranuclear inclusions – Cowdry type A.
57
diagnosis of ICH
- Signs + history (coagulopathy, eyes + liver problems) - Serology: VN test, IHA, CF, ELISA (VI or PCR Of liver at PM) - PCR – nasal, rectal an ocular swabs, blood, tissue obtained at necropsy, urine - Immunofluorescent technique – confirmation of virus within various tissues
58
differential of ICH
distemper
59
treatment of ICH
- Supportive (fluids, electrolytes, nutrition) plasma for clotting - Maybe ATB maybe atrophic for eye
60
prevention of ICH
- MLV vaccine of CAV-2 preferred over live attenuated CAV-1 (can cause eye reaction + shedding in urine). Immunity = >3y (annual revac)
61
canine herpes virus aetiology
- Canine herpes virus (CHV-1), enveloped DNA, very fragile, inactivated readily by most disinfectants, solvents and heat >40oC + latent infectious lifelong
62
HS herpes
canids (dogs, wolves, coyotes), neonatal puppies first 3w of life (colder), immunologically naïve pregnant at risk + can pass to puppies (in utero)
63
MOT of herpes
direct contact (with oral, nasal or vaginal secretions of infected dog),
64
herpes
- seroreactivity of 30 -100% (higher in kennels than in individually kept dogs) - optimal replication at temperatures < 37ºC so pups more at risk as can\t maintain body temp - persistence in ganglionic and lymphoid tissues of the oronasal and genital mucosae - stress (overcrowding, transport, pregnancy, immunosuppressive therapy) - activation shedding
65
pathogensis of herpes
- replication in surface cells of nasal mucosa, pharynx + tonsils - in utero/ <1 w = leukocyte associated viraemia  lymphoid hyperplasia  gen infection + vasculitis - adult = localised infection + persistence  latency (reactivated by stress)
66
signs of herpes
- death in <24h in 1-3w old pups. If signs, then crying, lethargy, decreased sucking, diarrhoea, nasal discharge - X-ray = unstructured interstitial pattern. Leucocytosis - older = mild upper resp signs, vaginitis, posthitis - acute infected pregnant = abortion/stillbirth with no other signs + future breeding good
67
diagnosis of herpes
- signs, PCR, antibody ELISA, necropsy of a puppy in litter - seronegative in latency possible - PCR, VI from lung, liver, kidney
68
differentials of herpes
- ICH (no thickened gall bladder), distemper (is sudden death), neosporosis/hepatitis (kidney lesion)
69
PM of herpes
- Disseminated focal necrosis + haemorrhages, esp lung, kidney cortex, adrenals, liver + GI tract - Enlarged LN + spleen
70
treatment of herpes
- Supportive – fluids, antiemetic, oxygen, warming, food - Usually, unrewarding + surviving puppies often too much damage to survive, intraperitoneal serum in exposed adults usually self-limiting
71
prevention of herpes
- Application of hyperimmune serum - inactivated CHV-1 for pregnant 10 days post-coitus and near-term booster - isolate 3w before birth + good hygiene
72
aetiology of kennel cough
- canine parainfluenza virus (CPIV), CAV-2, canine influenza virus (CIV), (CHV-1), (CDV) - pseudomonas, E.coli, Strep, B. bronchiseptica (bacteria normally secondary) - B. bronchiseptica can be primary in < 6m old
73
HS of kennel cough
All ages, puppies more prone to severe, spreads v quickly in kennels, shelters, etc
74
MOT of kennel cough
aerosol
75
pathogenesis of kennel cough
- Virus damages upper resp tract epithelium  2ndary bacterial infection - Immune response initiated + spread to lower resp tract prevented - Adverse condition = spread to lower resp tract  pneumonia + chronic
76
signs of kennel cough
goose-honk” cough. Retching/gagging, easily induced cough - Fever, purulent nasal discharge, anorexia etc = bronchopneumonia
77
diagnosis of kennel cough
- Cough 5-10d after exposure. Severity usually decreases during 1st 5d but disease lasts for 10-20d - Aetiologic diagnosis if severe/rapidly progressing, signs lasting 7-10d+ or multiple animals affected - Bacterial culture: false – if atb or low burden (nasal, oropharyngeal, BAL) - Many sp = opportunistic 2ndary infection/contamination - PCR: resp panels for mycoplasma cynos + viruses o False – if transient/low shedding, false + if recently vaccinated with live attenuated - Serology = can’t distinguish vaccine from infection
78
treatment of kennel cough
- Supportive usually self-limiting, antitussives (hydrocodone) - If hospitalised: keep in isolation - If pneumonia, then ATB (culture + sensitivity from tracheal wash/bronchoscopy). Antitussives contraindicated if pneumonia as decrease bacterial clearance
79
prevention of kennel cough
- MLV vaccine with distemper, parainfluenza + CAV-2 at 6-8w + q3-4w until 16w, revac q1y - Intranasal/ PO vaccine for B. bronchiseptica if risk high - Vaccines decrease clinical signs + amount of shedding, doesn’t provide total immunity
80
aetiology of parvo
- ¬CPV2, non-enveloped, single strand DNA, resistant to disinfectants, temp + pH (room oC 2m) - Outside 6m – y. highly contagious (likes young cells or cells that multiply quickly) - 2 syndromes: Haemorrhagic enteritis and Acute myocarditis
81
MOT of parvo
direct oral/nasal contact with faeces or contaminated environment
82
HS of parvo
all ages but 2-6m old unvaccinated most susceptible. If >6m – intact males
83
parvo
- Breeds = Dobermans, rottweilers etc more likely to be vaccine non-responders - More severe if: stress (weaning etc), parasites or other enteric pathogen infection too - Colostral antibodies protect for 2m ish + problem occurs if improper/irregular vaccine/ exposed to other dogs during vaccines
84
pathogensis of parvo
- Tonsils  virus reproduces in lymphocytes within 3-4 days  lysis of cells  viremia - (multiplies until overcomes the border and goes to the blood and causes viremia) - Bone marrow (stem cells) and GIT - Virulence factors (enzyme DNase)  virus enters into young cells  DNase can degredate cell proteins apoptosis - Impaired absorption, gut microbiome lost  bacterial translocation  sepsis, shock, dehydration  death
85
signs of parvo
- Myocarditis, sudden death in >8 w old puppies, born to unvaccinated bitch/infected in utero - Signs appear 5-7d after exposure, lethargy, anorexia, fever, vomiting, haemorrhagic diarrhoea  abdo pain, tachycardia, decreased CRT (septic shock), CNS signs due to hypoglycaemia + sepsis, lympho+ neutropenia - > 6 weeks GIS (general infected syndrome), fever, lethargy, anorexia
86
death mechanism in parvo
1. Diarrhoea and vomiting  extreme dehydration  shock a. no absorption GI, acidosis + shock due to loss of electrolytes, high proteinemia in blood 2. Lost of protective barrier in the gut  bacterial penetration  septic shock a. Lamina propria “naked” has a hole for bacteria to go through to go into the blood. 3. Myocarditis  acute heart failure a. Virus thinks heart cells are fast multiplying myocardial cells have a lot of nucleus
87
diagnosis of parvo
- History and signs - ELISA (rapid test’s – Ag prove in stool) o false positive 4-10d post MLV, false negative before shedding if large vol of diarrhoea - PCR faeces, Mod-severe leukopenia. 4x increase serology (rare)
88
PM of parvo
- Thickened discoloured intestinal wall, thymic atrophy - Micro = necrosis of SI crypts, bone marrow hypoplasia
89
differential parvo
- Distemper, CIH, corona, Salmonellosis, Campyobacteriosis, Poisoning
90
treatment of parvo
- Fluid therapy – 70ml/kg/day and more, electrolyte balance, Fresh frozen plasma - Atb – amoxicillin 10-20mg/kg, Metoclopramide/maropitant. No food for 12-24h then bland, low-fat + Parenteral if >3d anorexia. Faecal transplantation rectally
91
prognosis of parvo
- 7-90% survive if ICU and early treatment
92
aetiology of corona
- Canine coronavirus, RNA
93
MOT corona
PO, direct + indirect contact (faeces)
94
HS of corona
all ages, puppies most susceptible
95
SOI corona
= sick animals that shed virus through faeces in the environment (up to 2 weeks. P.i)
96
pathogenesis corona
- attacks mature cells in the gut wall  replaced immature cells that are not affected
97
signs of corona
- Anorexia, depression, diarrhoea (vomiting is rare), Mucosal diarrhoea, with putrid odour lasts 2-4 days + Asymptomatic infection in older dogs - Usually, dogs recover 1-2 weeks following onset of clinical signs - Secondary bacterial infection is possible
98
diagnosis of corona
- Milder than parvo, ELISA for antigen in faeces, IFA, PCR
99
treatment of corona
- Symptomatic – fluid therapy, metabolic stimulators
100
prevention of corona
- Attenuated vaccine 2x in 3-4w interval, first in age of 7-8 weeks - Not good to administer the 2 vaccines at the same time because of the competition of the virus
101
aetiology of rotaviral
- Causative agent rotavirus, 7 serogroups A-G, most common = A
102
MOT of rotavirus
Orofecal infection (faeces up to the 3 weeks PI)
103
HS of rotavirus
severe in puppies, mild/asymptomatic in older. Possible zoonosis
104
diagnosis of rotavirus
- ELISA – Ag detection in a stool, Electronic microscopy of faecal content + PCR
105
treatment of rotavirus
- Symptomatic – pups possible severe haemorrhagic mucosal diarrhoea
106
prevention of rotavirus
- There’s no effective vaccine