Urogenital Pathogens Flashcards
(88 cards)
1
Q
What is the general make up of the urogenital microbiome and why is it important?
A
- Normal microbiome in vagina/vestibule/prepuce/distal urethra
o Commensals: gram (+)/(-)/Mycoplasma/Ureaplasma
o Need to differentiate between contaminant/commensal vs. pathogen
2
Q
What is a common signalment for a UTI
A
- UTI: more common in females and older animals
3
Q
What is a UTI and what are the common causes
A
o Microbial colonization of urine or urinary tract organs
o Usually single bacterial infections
Gram (-): E. coli (main), Proteus/Klebsiella/Pseudomonas/Enterobacter
Gram (+): Staph/Strep/Enterococci
o Extraintestinal infections by uropathogenic E.coli (UPEC)
- Opportunistic infections
4
Q
What is a common route of infection for UTI and what are the consequences
A
- Ascending infections
o Ascending urethra: bladder infections = cystitis
o Ascending ureter: kidney infection = pyelonephritis
5
Q
List host factors contributing to UTI development
A
- Host Factors:
o frequent emptying of bladder is protective
o normal microbiota s protective
o age
o sex
o structure (ectopic ureters/obstruction/recessed vulva)
o function (spinal cord injury/physical injury due to catheterization)
o metabolic (diabetes/renal dysfunction/cushings)
o immunosuppression
6
Q
List bacterial factors contributing to UTI development
A
- Bacterial Factors
o Attachment and colonization of mucosa of mucosal orifice
o Transport up urethra
o Attachment of uroepithelium
7
Q
Compare the clinical signs of cystitis vs pyelonephritis
A
- Cystitis: dysuria/pollakiuria/stranguria/hematuria/caudal abdomen and back pain
- Pyelonephritis: kidney or flank pain/febrile/vomit/PU/PD
8
Q
How does treatment differ for cystitis vs pyelonephritis
A
Treatment
* Cystitis: higher breakpoint for abx (can use less drug for the same effect)
o Should concentrate active drug in bladder
* Pyelonephritis: need abx to penetrate the tissue of the kidney
9
Q
How to obtain a sample for UTI analysis? How to store it?
A
- Sample: urine
o Cystocentesis mainly (reduce contamination)
o Catheterization (males, or if blocked)
o Free catch – more contamination
o Store at 4C
10
Q
What testing do you use for UTI analysis?
A
- Urinalysis
- Culture:
o within 24 hr: red or white top (no additives)
o within 24-72hr: grey top (preservatives)
11
Q
What are tthe general features of Corynebacterium
A
Corynebacterium (genus)
Features
* gram (+)
* pleomorphic
* rod
* opportunistic
12
Q
What species are commonly affected by Corynebacterium UTI? What species of bacteria? What is the pattern of infection?
A
Host: cattle
* prevelance: C. cystitidis > C. renale > C. pilosum
* Normal microbe in bull – lower urogenital tract/prepuce
* Sporadic (not common as a herd level problem
13
Q
What are the clinical signs of Corynebacteriuam UTI?
A
Clinically:
* Cystitis: old cows
* Pyelonephritis: ascending infection from vagina
* 25-30% case fatality – because cattle are good at hiding clinical signs
14
Q
What are the risk factors of Corynebacteriuam UTI?
A
Risk Factors:
* Short female urethra/anatomic anomalies
* Stress: peak lactation/dystocia
* High protein diet and high pH
* Physical damage/obstruction of urinary tract
15
Q
What are the virulence factors of Corynebacterium UTI?
A
Virulence
* Pili: bind urethral epithelium and colonization
* Urease: produce ammonia = mucosal inflammation and increasase pH
* Environmentally resistant – shed in urine
* Can ascend from environment to kidney
16
Q
What are the clincal signs of Corynebacterium UTI?
A
Clinical Signs: blood tinged urine in healthy cows
* Cystitis progresses to pyelonephritis
* Frequent urination attempts
* Anorexia
* Pyrexia
* Anemia
* Reduced milk production
17
Q
What are the gross lesions of Corynebacterium UTI?
A
Gross Lesions
* Thickened and inflamed bladder
* Thick ureters
* Purulent exudate in bladder/ureters
* Kidney lesions/abscesses = blood/exudate in bladder = hematuria/pyuria
18
Q
How to dx Corynebacterium UTI?
A
Dx
* Rectal palpation of the left kidney: enlarged/lack of lobulation/pain
* U/S – kidney/bladder/ureter
* Urinalysis: free catch (cattle) – hematuria/proteinuria/pyuria
* C/S: urine from sterile catheterization
19
Q
How to tx Corynebacterium UTI?
A
Tx
* Abx only in acute phase and prolonged (3-4 weeks) – later stages it is harder for abx to penetrate pus
* Chronic = kidney irreversibly damaged
20
Q
List 4 types of bacterial reproductive infections and the common associated pathogens
A
Infections
* Abortion - brucellosis
* Metritis
* Endometritis – equine strep. zooepidemicus
* Pyometra – E. coli
21
Q
List 6 types of bacteria causing reproductive infections
A
- S. equi subsp. Zooepidemicus
- Brucella
- Leptospira
- Taylorrella equigenitaliss
- Listeria monocytogenes
- Campylobacter fetus subsp. Venerealis
- Usually opportunistic
22
Q
When does canine pyometra usually occur? What is a predisposing factor?
A
- Luteal (1-3 mo post estrus)
- Cystic endometrial hyperplasia – due to persistent increased progesterone
o Fluid accumulation in endometrial glands and uterine lumen
o Low leukocyte activity
o Favour ascending infection
23
Q
What is the main causative agent for canine pyometra
A
- Usually E. coli
24
Q
What are the clinical signs associated with canine pyometra
A
- Clinically:
o Lethargy
o Depression
o Pyrexia
o v/d
o PU/PD
o Open cervix: vaginal discharge (serosanguinous-mucopurulent)
Better prognosis
o Closed cervix: no discharge
More severe
o +/- enlarged uterus
25
Compare prognosis of open and closed canine pyometra
o Open cervix: vaginal discharge (serosanguinous-mucopurulent)
Better prognosis
o Closed cervix: no discharge
More severe
26
How to diagnose canine pyometra and what samples to take?
* Dx: history/clinical signs
o U/S
o Radiographs
o Lab: CBC/Biochem/Urinalysis/Cytology + (C/S)
o Sample: urine/vaginal discharge/uterine fluid
27
How to treat canine pyometra?
* Tx: prompt and aggressive
o Fluids/abx/address underlying problems
o Sx: OVH is curative
o Medical management with prostaglandins and anti-progestins
No anesthesia but relapse rate is high
28
How to prevent canine pyometra?
o Prevent with early OVH or pregnancy
Risk of stump pyometra with OVH
29
What are the common agents causing metritis
* Agents: Brucellosis/Leptospirosis/Campylobacteriosis
o Common polymicrobial disease
o Imbalance of microbiome – more anaerobes
Truperella pyogenes
Fusobacterium necrophorum
Bacteroides spp.
30
When does metritis most commonly occur? Why?
* When: 2-3 weeks post partum
o Compromised barrier of cervix/vagina/vulva
31
List 3 main risk factors for metritis
* Risk factors
o Dystocia
o Fetal membrane retention
o Subclinical hypoCa
32
What is the emergent form of metritis? When does it occur?
* Emergency = acute puerperal metritis
o Within 21 days of parturition
33
What are the clinical and gross signs of acute puerperal metritis?
o Abnormally enlarged uterus
o Systemic: low milk production/inappetence/depression/fever
o Fetid, watery, reddish-brown uterine discharge
o Looks like a toxemia on labwork
34
How does clinical metritis compare to acute puerperual metritis?
o No fever
acute puerperual metritis has fever/systemic effect
35
What are the clinical signs of clinical metritis?
* Clinical metritis: delayed involution
o Mucopurulent-Purulent discharge
36
When does clinical endometritis occur? What is it characterized by?
* Clinical: >21d post partum
o Mucopurulent
o Purulent
37
When does subclinical endometritis occur and what is it characterized by?
* Subclinical: >21d post partum
o Macrophages
o No purulent material
38
What are the common causative agents of endometritis
* Agents: similar to metritis – opportunistic
* Agents: Brucellosis/Leptospirosis/Campylobacteriosis
o Common polymicrobial disease
o Imbalance of microbiome – more anaerobes
Truperella pyogenes
Fusobacterium necrophorum
Bacteroides spp.
39
What is an important sequelae of endometritis (especially in production animals)
* Causes fertility problems:
o more open days
o Longer calving to conception days
o Longer calving interval
40
Where is Strep. equi subsp. zooepidemicus found? How does it contribute to the disease manifestations it causes?
* Commensal of upper resp and caudal repro of horses
o Opportunistic
Resp: rhinitis/bronchitis/pneumonia
Repro: endometritis/placentitis
41
What species does Strep. equi subsp. zooepidemicus affect?
horses but lots of other species too
* Mainly isolated from equine joints/LN/nasal cavity/lung
42
What are the clinical presentations of Strep. equi subsp. zooepidemicus
o Endometritis – ascending infection from clitoral fossa/vagina
o Epididymitis
o Cause infectious abortion and placentitis
43
How is Strep. equi subsp. zooepidemicus diagnosed? What samples are used?
* Dx: cytology + C/S
o Sample: uterine swab/flush/biopsy
44
How is Strep. equi subsp. zooepidemicus prevented
* Prevent: difficult
o Vaccine – difficult because lots of strains
o Reduce stress and treat predisposing
45
What are the main features of Taylorella equigenitalis
Taylorella equigenitalis
* Gram (-)
* Pleomorphic
* Coccobacillus
* Obligate symbiotic facultative pathogenic
46
What is the primary disease manifestation of Taylorella equigenitalis
o Venereal – contagious equine metritis
o No clinical signs in stallions
o Also T. asinigenitalis as been isolated from stallion
47
How is Taylorella equigenitalis transmitted
* Transmit: semen/live breeding/movement and import
o fomites
48
What is the clinical signs and incubation period for contagious equine metritis
* Contagious equine metritis
o 2-13d incubation
o Clinically:
Endometritis
Cervicitis
Vaginitis
Infertility
Lots of vaginal discharge up to 14d post mating – highly neutrophilic
Abortion
o Some can spontaneously recover and be chronic carriers
49
Where is Taylorella equigenitalis found as a reserviour
o Reservoir: clitoral sinus/fossa/uterus
50
How does Taylorella equigenitalis present in stallions?
o Stallion: no clinical signs
No immunity
Carry on external genitalia
From fossa glandis and urethral sinus
* Distal urethra/prepuce/penis surface/testes/epididymis/seminal vesicles
51
How is Taylorella equigenitalis diagnosed? What sample is used?
o Dx: bacterial isolation = gold std
PCR
No serology
Sample: clitoral fossa/prepuce/penis/fossa glandis/urethral swab
* Reportable!
52
How is Taylorella equigenitalis treated
o Tx: flush and scrub genital surfaces
Topical abx
53
What are the general features of campylobacter
* Gram (-) rod
o Curved or spiral or slender
o Flagella
* Obligate pathogen
54
How is campylobacter transmitted
* Transmit: venereal or fomite
o Older bulls are carriers
55
What are the 2 types of campylobacter
* Types
o C. fetus subsp. Venerealis
o C. fetus subsp. Fetus
56
What are the clinical signs of campylobacter infection
o Endometritis
o 25% cases have vaginitis
Ascending to mucopurulent endometritis = acute embryonic dealth/abortus
Persistant vaginal infection – may recover but can carry to next breeding season
o Temporary infertility
Return to estrus
Irregular estrus
Repeat breeding
Prolonged calving
o Embryonic death
57
How is campylobacter diagnosed? What samples are used?
* Dx: PCR
o Difficult to culture
o Fluorescent Ig
o Sample: preputial scrape/wash
58
How is campylobacter prevented
* Prevent: vaccinate
o Heifer 3-4 wk before breed + boost half way through breeding season
o Bull/cow: annual
59
What are the general features of brucella
* Cocci/coccobacilli/short rods
* Obligate symbiotic
* Obligate pathogen
* Environmentally resistant (especially in organic matter)
* Replicate in macrophages
`
60
How is brucella bacteria identified/cultured?
* Special stain: modified acid fast (Koster)
* Difficult to culture
o Need complex media and high CO2
61
What is an important consideration when diagnosing Brucella? How does it differ between brucella species?
* Reportable
o B. abortus
o B. melitensis
o B. suis
* Non reportable
o B. canis
o B. ovis
* Zoonotic
62
How is Brucella transmitted
* Transmit
o Direct contact (contaminated fluid/abortus/water/feed/urine)
Vaginal shedding up to 6 weeks post abortion
o Late term abortion = carrier status = cow shedding
o Ingest: colostrum/milk/human food
o Dog: mucosal contact (B. canis)
o Most at risk = vets/animal handlers
63
What virulence factors does brucella have? What is its mechanism of virulence?
* Virulence factors
o Can invade phagocytes
Engulfed and form brucella containing vacuole – fuse with lysosomes – 90% of vacuoles = brucella degrade
* 10% live and go to ER and do intracellular replication
o No classic virulence factors
64
What is the pathogenesis of brucella
o Induce inflammatory cell response
o Placenta: trophoblastic necrosis and vasculitis = abortion/weak calves
o Infected animals can remain carriers
65
What are the clinical signs of brucella infection
* Clinically
o Seminal discharge – epididymitis
o Hyperglobulinemia
o Persist in spleen/lever/LN/mammary gland
66
How to treat brucella infection
* Tx: no practical tx
67
How to prevent brucella infection
* Prevent: serology
o No vaccine in CA
Can interfere with diagnostic tests/residual virulence/may cause abortion in pregnant animals
68
How does B. canis infection manifest in males and females
o Female = abortion
Late term: 45-60d, partially autolyzed pups
Puppies may be born but die soon after
Subsequent litters may be normal but can have intermittent repro failure
o Male = testicular abnormalities – usually subclinical
Tail of epididymis enlarged
Orchitis/epididymitis
Diffusely enlarged LN/spleen
+/- polyarthritis/meningoencephalitis/uveitis
69
How is brucella diagnosed? What samples do you use? What features of infection are you looking for in your diagnostics?
o Dx: CBC/Biochem/urinalysis/cytology and C/S
See > hyperglobulinemia/hypoalbuminemia/bacteriuria/lymphoid hyperplasia/pleocytosis in CSF/discospondylosis
Rads
Culture is gold std
* Sample: aborted fetal tissue/placenta/LN/uterus/vaginal discharge/blood
PCR
Serology
70
What are the features of leptospira? What are 2 main serovars
* Gram (-)
* Long/thin/spiral/hooked ends
* Not host specific - Each serovar has one host that is a main reservoir
* 2 species:
o L. biflexa = non pathogenic
o L. interrogans = pathogenic
71
What is the pathogenesis of leptospira infection
o 7d incubation
o Disseminate and replicate in kidney/liver/spleen/CNS/eye/genitals
* Replication
o Kidney tubules > shed > mild infection > occasional intrauterine infection > abortion
o LPS stimulate neutrophil and platelet activation = inflammation and coagulation
o Sphingomyelinases/hemolysin/porins = endothelial damage/vaascultitis
Renal/liver/spleen
72
How is leptospirosis transmitted
* Transmit: zoonotic
o Maintained in subclinical hosts
o Environmental resistant; viable for many months
o Urine/moist soil/slow water
o Direct: bite/venereal/placental/milk
73
How does leptospira infection differ if you are vaccinated/have Ig vs if you don't
* If vaccinated/moderate Ig = clear disease and no shedding
* No circulating Ig = chronic shedding
o Clinical disease: leptospiruria and urine shedding
74
What are the clinical signs of leptospirosis
o Acute renal fail
o Hepatic dysfunction
o Repro infection
Placentitis
Abortion
Epididymitis/orchitis
75
Describe the 3 stages of leptosporosis disease
Peracute: sudden death
Acute: hepatic and renal failure (fever/v+/weakness/tachypnea)
Subacute: intrahepatic cholestatis and necrosis of liver
* Renal fail/hepatic encephalopathy/icterus
76
How does lepto infection manifest in horses?
o Incidental host
Lower susceptibility
o Develop acute/severe disease
o Short shedding
o Clinically: recurrent uveitis (blindness)/abortion/stillbirth/neonate disease
77
How does lepto manifest in cattle and what serovars are associated with disease?
Sporadic abortion and infertility = Hardjo
Abortion storm = Pomona
Hemoglobinuria/jaundice/fever = Pomona/grippotyphosa/icterohemorrhagiae
78
How does lepto manifest in dogs and what are the associated serovars
Renal fail – Canicola/Bratislava/grippotyphosa
Hepatic disease – ictreohemorrrhagiae/pomona
o Serovar drift due to vaccine. – less common serovars causing disease
79
How is leptosporosis diagnosed?
o Dark field microscopy
o Immunofluorescence = higher sensitivity
o Culture = gold std but low sensitivity
o PCR
o Serology – look for Ig 5-7d after clinical sign onset
Need paired serum samples with 4 fold increase
80
How is lepto prevented
o Limit exposure
o Isolate affected animals
o Remove abortion tissues
o Vaccine – cow and dog
81
Describe the efficacy of the leptosporosis vaccines in dogs
Dogs: protect against clinical disease but not infection or carrier
Protect against: Pomona/grippotyphosa/icterhemorragiae/canicola
82
What are the general features of listeria
* Short rod with peritrichous flagella
* Psychrotolerant – low temp grow (4-45C
* Facultative intracellular
83
What are the 2 main virulence factors that listeria uses
o Listeriolysin: lyse phagosome membrane
o Phospholipase C: mediatte cell – cell spread
84
What is the pathogenesis of listeria monocytogenes
* Pathogenesis:
o Ingest
o Cross oral mucosa
o Ascend to brain steem
o Can also invade intestine mucosa = hematogenous spread = septicemia/abortion/mastitis/eye
85
What are the clinical signs of listeriosis
* Clinical
o Visceral – septicemia, young
o Repro: abortion (2nd half pregnancy), sheep/goat/cattle
o Neural: CNS meningoencephalitis
Circling disease
Cattle/sheep/goat/human
86
What is an important consideration to have when diagnosing listeriosis
zoonotic
87
How is listeria diagnosed and what samples are used?
* Dx: culture and C/S
o Sample: CSF/brainstem tissue/placenta/fetal tissue
88
How is listeriosis treated and prevented?
* Tx: procaine penicillin G or oxytetracycline
o Supportive care
* Prevent: +/- autogenous vaccines and remove soiled silage
