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exam 2 Flashcards

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1
Q

Upper urinary tract

A

the ureters and kidneys

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2
Q

lower urinary tract

A

the batter, urethra, and prostate

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3
Q

Cystitis

A

urinary bladder inflammation, the most common form of UTI, primarily bacterial causes
more common in dogs than cats
ascending infections is wayyyyy more common than descending infection
Cause: opportunistics that overcome normal host defenses

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4
Q

Natural defenses against urinary tract infections

A

1) Urethral length (males longer, harder to establish an infection)
2) Sphincters
3) Urine flow flushes out bacteria
4) Healthy urine has an osmolarity and urea concentration that is difficult for bacteria to establish
5) Location innate immunity of urothelium- glucosaminoglycans and antimicrobial peptides

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5
Q

Uncomplicated infectious cystitis

A

sporadic urinary tract infections that are common in dogs and humans, presumptive diagnosis is reasonable if there are no predisposing causes and an animals has had less than 3 times in a year

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6
Q

Complicated infectious cystitis

A

frequent urinary tract infections that are a cause of predisposing causes
1) normal micturition interference (obstruction, upper motor neuron injury to detrusor, etc)
2) anatomic defects (ectopic ureter- embryonic origin, juvenille vulvar conformation, urachal diverticula, etc.
3) urothelium changes (traumatic catherization, neoplasia of urothelium, urolithiasis)
4) Metabolic/Immunological causes (Chronic Kidney disease- dilute urine, diabetes mellitus, corticosteroids, hyperadrenocortism, congenital immunodeficiency- IgA or SCID)
5) Decreased kidney function

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7
Q

What kind of bacteria is typically manifested in urinary tract infections

A

facultative anaerobes

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8
Q

The majority of infectious agents that cause UTI in small animals include

A

Gram - enteric organisms (fac anaerobes)
1) E. coli
2) Proteus spp.
3) Enterobacter spp
4) Klebsiella spp

Gram + cocci (fac anaerobes)
1) Coagulase positive Staphylococcus sp. (S. pseudointermedius, S. aureus)
2) Enterococcus spp.

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9
Q

What are some less common causes of UTI in small animals

A

Corynebacterium urealyticum (fac anaerobe gram + rod)
Non enteric gram - rods (Pseudomonas aeruginosa)
Mollicutes- Mycoplasma spp and ureaplasma spp
Fungal (typically C. albicans)

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10
Q

What is the main pathogen that causes UTIs in large animals

A

Corynebacterium renale

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11
Q

Corynebacterium renale

A

a facultative gram + rod that is a part of the normal urogenical flora and causes ascending UTI infections in cattle, sheep, and goats
often reach the kidney (pyelonephritis) and cause balanoposthitis (pizzle rot)
have pili that attach to the urothelium

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12
Q

Urease role

A

Produced by Staphylococcus spp, Proteus sp, enterobacter, and corynebacterium renale

converts urea to ammonia which raises urine pH and forms struvite crystals and causes a predisposition to urolithiasis (stones)

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13
Q

What UTI pathogens produce urease and predispose the animal to urolithiasis?

A

Staphylococcus spp.
Proteus spp.
Enterobacter spp.
Corynbacterium Renale/urealyticum

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14
Q

What single pathogen is the most common cause of UTI in humans and dogs?

A

UPEC (uropathogenic E.coli) that is a type of ExPEC

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15
Q

UPEC

A

Uropathogenic E. Coli that is the cause of most UTIs in dogs and humans have P-fimbrae- pili that attach to the urothelium and alpha-hemolysin, siderophores for iron uptake

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16
Q

Is the presence of bacteriuria an indication to treat the animal?

A

NO, dont treat aniamls that dont have urinary signs (straining, increased frequency, and discomfort)
the simple presence of bacteriuria is not an indication to treat and infection

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17
Q

What drugs go to the urine and are helpful to treat UTIs?

A

Penicillin (Amoxicillin)
Cephalosporins (Cephalexin)
Fluoroquinolones (Enrofloxacin)
Trimethoprim- Sulfamethoxazole
Tetracyclines (Doxycycline)
Aminoglycosides (Amikacin)
Nitrofurantoin

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18
Q

How should you diagnose UTIs?

A

Collect using cystocentesis, catherization, or midstream voided and do an aerobic culture as most are facultative anaerobes

use quantitative plating that measures the number of colony forming units per mL of urine (varies on collection technique- midstream gives the most organisms and cystocentesis gives the least amount
(guidelines for contamination, suspicious, and significant infection

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19
Q

In-clinic cultures

A

small incubator with standard plate media and commercial kits for UTI culture, most are gram + and show up overnight

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20
Q

How do you prevent against UTIs?

A

-Address anatomic defect (vulvoplasty)
-Control primary metabolic diseases (diabetes mellitus)
-good catheter management
-Pulse dosing (not really helpful)
Methenamine- used to prevent recurrence after treatment, hydrolyzed to formaldehyde only in acidic urine, not effective in urease + bacteria, no efficacy studies in animals

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21
Q

Cranberry’s role in UTI treatment

A

Theoretically might prevent some infections caused by UPEC, prevents p-fimbriae attachment to the urothelia, works in humans well to reduce the incidence of infection

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22
Q

Empirical therapy for UTI

A

Therapy for a UTI that is on the basis of clinical diagnosis (signs and abnormal urinalysis)
NO CULTURE
Reasonable if it is the first time with clinical signs but not optimal for recurrent cases
Drug choice: Beta lactam drug (amoxicillin or amoxicillin/Cluvulanic acid, or cephalexin)

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23
Q

Targeted therapy for UTI

A

Basis of significant culture result and antimicrobial susceptibility testing
typically used for 2nd, 3rd, 4th, 5th, etc presentation
or in suspect hospital acquired infections (onset of greater than 48 hours in the hospital

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24
Q

Pyelonephritis

A

an ascending infection (can be sequelae to cystitis)
-Dogs and cats are common
challenging to diagnose
-Ultrasound (dilated renal pelvis)
-Elevated blood urea nitrogen (BUN) and creatinine
-flank pain on palpation
-+/- fever, +/- leukocystis
can lead to bacteremia and sepsis

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25
How should you treat pyelonephritis
antimicrobial agents with high tissue penetration is best: fluoroquinolones, Trimethoprim Sulfa
26
Prostatitis (dogs)
a disease that can occur in both intact and neutered males cysts occur in intact males (14% males) approx half of cysts become infected Acute: fever, depression/lethargy, anorexia, +/- urethral discharge Chronic: infection is often silent and you should diagnose baced of infertility and recurrent UTI or hematuria, only enlarged if concurrent benign hyperplasia
27
What is the most common causative agent of prostatitis?
the same as UTI, E coli is the most common overall
28
How should you treat prostatitis in dogs?
-Surgical approach in cases of abscesses (drainage and omentalization) Use antimicorbial drugs (only a few options bc acidic acini pf prostatic acini and you can only use lipophilic/weakbases (Enrofloxacin, Trimethoprim-Sulfamethoxazole, Clindamycin, Chloramphrenicol)
29
Describe the pathway of milk to ejection
1)Alvelous with myoepithelia and capillaries with tight junctions 2) Interlobular ducts 3) Intralobular ducts 4) Lactiferous ducts 5) Gland Cistern (where it is help) 6) Annular ring 7) Teat cistern 8) Sphincter muscle (sm. that allows milk leltdown) 9) Streak canal (Papillary canal)
30
Are mammary glands in quarters connected?
NO there is 1 mammary gland per quarter and there is no physical connection to the other quarters
31
What is the milk vein?
Subcutaneous abdominal vein (milk vein)
32
What ligaments support the mammary gland
Median suspensory ligament, lateral suspensory ligament, and intermammary groove
33
Defense mechanisms of the mammary gland?
Physical factors (Keratin plug, stratified squamous epithelium) Cellular factors (WB: neutrophils, macrophages, lymphocytes) and epthelial cells Innate Immunity: lactoferin- bind iron to prevent iron depended bacteria from binding, cytokines, complement, acute phase proteins acquired immunity: immunoglobulins, T lymphocytes
34
Mastitis pathogenesis
compromised defense mechanisms (teat milking, post milking, and immune suppression lead to inflammation of the mammary gland teat end exposure and invasion, pathogens multiply in the milk leading to an inflammatory response and induced signs
35
What SCC indicates an animal is uninfected with mastitis?
SCC less than 100,000 cells/mL
36
What SCC indicates an animal has mastitis (subclinical or clinical) or early lactaction (colostrum)
SCC of more than 200,000 cells/mL
37
What is the target of bulk tank SCC
SCC of less than 250,000 cells/mL
38
What is the US legal limit of SCC in milk?
SCC of 750,000 cells/mL
39
What is the EU legal limit of SCC in milk?
SCC of 400,000 cells/mL
40
Subclinical mastitis
milk is normal grossly and no systemic signs elevations in the SCC which lead to reduced quality, increased plasmin bc of inflammatory cells- off flavors, and reduced shelf-life with coagulation
41
Clinical mastitis
Mild: Increased SCC, milk abnormal color, thick and water viscosity and bad consistency Moderate: Same as above and inflammed mammary gland Severe: Same as above and systemic signs present
42
Mastitis Physical Exam Signs
decrease in feed intake, decrease in milk production, lethargy, depression, tachypnea, tachycardia, weakness, recumbency, fever, pale mucous membranes, dehydration, shock
43
California Mastitis Test (CMT)
Milk and regent swirled in the well and creates a gel after the cell membranes are broken down. 4 wells for each teat. Negative (N): No inf. or thickening, less than 200,000 SCC , indicates a healthy quarter Trace (T): Possible inflammation- slight thickening. 200K to 400K SCC (Subclinical Mastitis) Weak Positive (1): Infected, distinct thickening -> no gel formation, 400K to 1.2 SCC (Subclinical/ Clinical Mastitis) Distinct Positive (2): infected, immediate thickening with slight gel formation, 1.2 to 5 million SCC (clinical mastitis) Strong Positive (3): infected amd gel formed of milkex elevated (like a fried egg) central peak remains even after paddle rotation is stopped, >5 million SCC (clinical mastitis- severe)
44
Composite mastitis testing
multiple quarters of the cow into one sample, used for screening for contagious pathogens, not recommended for identifying quarter infections
45
Bulk tank masitits testing
a stanrdard plate count, bulk tank somatic cell count may test for coliforms *Agitate milk for 5 min prior to sampling, collect at bottom with sanitized dipper, place samples on ice immediately or refrigerate
46
How should you culture milk samples for diagnosis?
Use a blood/MacConkey agar that is incubated aerobically (can identify multiple bacteria, cheaper) or use a PCR to identify some trains
47
What are the contagious mastitis pathogens?
Streptococcus agalactiae Mycoplasma bovis Staphylococcis aureus Corynebacterium bovis (Contagious Mastitis Sucks Severely)
48
Contagious mastitis
spread due to infected equipment, fomites, bedding Milk affected, cow is rarely affected, strong ability to colonize the gland and high cow transfer. caused by CMSS -Corynbacterium bovis, Mycoplasma bovis, Staphylococcus aureus, and Streptococcus Agalactiae
49
Streptococcus agalactiae
an obligate pathogen of the mammary gland Gram + , chain forming cocci, factul. anaerobe Responsive to Beta lactam (intramammary treatment) leads to transient, abnormal milk and decreased milk production *Contagious mastitis pathogen
50
Corynebacterium bovis
*Highly contagious mastitis pathogen gram +, rod club shaped, facult anaerobe manifest in the teat canal curable with intramammary antibiotic
51
What do all the contagious mastitis pathogens have in common
facultative anaerobes and gram + (except for mycoplasma bovis- no cell wall)
52
Mycoplasma bovis
a contagious mastitis pathogen cocci, fried egg appearance, no cell wall and pleomorphic highly contagious with a predilection for cells lining serous cavities hard to cure, cause pneumonia, swollen joints, head tilts, mastitis, and vulvovaginities
53
Staphylococcus aureus
a contagious mastitis pathogen gram + with grape like clusters facultative anaerobe associated with a very high SCC (1 million + cells/mL Loss cure rate (<40%) with ceftiofur and prilimycin combo peracute: high fever, depression, swollen quarter chronic: fibrosis of the mammary gland source: commensal skin organisms, found in upper respiratorym GI, and GU tracts
54
What are the environmental mastitis pathogens
1) Environmental Streptococcus 2) Coagulase Negative Staphylococcus 3) Coliform Mastitis 4) Trueperella pyogenes
55
Environmental mastitis pathogens are:
found in the water, maure, bedding, mud. feces and impact the milk with or minus the cow impacted fair ability to colonize the gland can last days to weeks poor potential for cow to cow transfer
56
Environmental Streptococcus
gram - cocci, chain forming facultative anaerobes (some obligate anaerobes) 14-26% of mastitis cases in US Commensal in GI tract and on skin Treatment: dry off therapy for subclinical infections with high SCC includesL S. uberis, S. dysgalactiae, S. bovis, Enterococci spp
57
Coagulase Negative Staphylococcus
gram + cocci clumps that have a variety of species often found on the teats, nasal tissue, and hands of people who milk Typically subclinical mastitis, treatment not usually warranted *Environmental mastitis pathogen
58
Coliform Mastitis
environmental pathogens causing mastitis, typically gram - rods include E. coli, Klebsiella, Enterbacter, Serratia Facultative anaerobes Bedding, manure, water milk equipment Culture on macconkey agar
59
Trueperella pyogenes
gram +, pleomorphic rod found on the skin and muscles of upper respiratory tract, GI, or urogenital tracts opportunistic, associated with summer mastitis need to amputate affected quarters
60
IS Brucella zoonotic?
Yes
61
Brucella spp.
aerobic gram negative bacteria non spore forming and intracellular
62
How does Brucella replicate?
Invasion with zipper mechanism, phagosomes fuse with the lysosomes, and replication in ER via T4SS, leaves cell membrane Intracellularly, it replicates in epithelial endothelial cells, dendritic, macrophages, and microglia leading to a pyogranulatous responece and persistant infection through living quissentally in the reticulendothelial system
63
Brucella virulence
LPS with smooth a rough Smooth (O antigen) Rough (only core polysaccirdge)
64
Brucella abortus
Aerobic gram -, non spore forming, intracellular Bang's disease after ingestion infection is localized at lymphoid tissue and carried in macrophages can be vaxed using modified live vaccines utilizing TH1, CD4+ via MHC II Strain 19- may cause abortion (pregnant), orchitis, arthritis's, interferes with serological testing RB51: less virulent and doesnt interfere with testing, rapidly cleared, doesnt cause abortion
65
Brucella abortus human applications
causes Malta/ Undulant fever leading to flu-like febrile syndrome, almost eradictated in US, issue with raw milk consumption
66
What zoonotic pathogen is a problem with raw milk consumption leading to Malta/Undulant fever?
Brucella abortus
67
Brucella canis
Aerobic gram - , non spore forming intracellular pathogenesis same as B. abortus but associated with puppy mills and central US important to screen for pre-breeding (diskospondylitis, orchitis, abortion, lymphadenopathy, uveitis managed by spay/neuter, dual antimicrobial therapy, doxycyclin, can never say animal is negative, they can still shed Diagnostics: RSAT (w mercaptoethanol step is needed) , TAT, IFA, Cornell multiplex antibody test, AGID, blood cultures False positive common
68
Which of the following urease-producing organisms is most often associated with "pizzle rot" in the ram
Corynebacterium renale
69
What of the organisms has a rough colony phenotype?
Brucella canis
70
What tests is used to initially screen cattle for B. abortus?
CARD test
71
A dog with back pain and fever is evaluated radiographically and there is evidence of vertebral endplate lysis with disc space narrowing L7-S1. This is diskospondylitis until proven otherwise. What two additional tests are appropriate immediately?
B. canis tube agglutination test Blood culture
72
What is the classic agent associated with calf diphtheria (necrotic laryngitis)?
Fusobacterium necrophorum
73
Listeria
Gram + rods, motile, facultative anaerobes, motile, non spore former, intracellular lifestyle invades using zipper mechanism and spreads systemically to cause Visceral listeriosis, abortion, meningoencephalitis, micro abscesses, meningitis a human public health risk
74
Listeria pathogenesis
1) Ingestion (foodborne/ soil) or ocular route 2) Cellular invasion via Zipper Mechanism 3) Escape for the vacuole to the cytoplasm via listeriolysis O: takes over actin and spreads to neighnoring sights via protruding cell membrane, also immune invasion 4) Spread to extraintestinal sites to lymphnode then, bloodstream Th1 dependent spread 5) Replication in the liver and spleen 6) spread to the fetus and placenta
75
How might a patient present with Listeria infection?
1) Visceral listeriosis: septicemia with localization in the parenchymous organs (Liver and spleen) 2) Abortion (necrotic placentitis) from localization in the placenta and fetus, common in cattle, sheep, typically last trimester 3) Meningoencephalitis (Neuronal form from localization in the pons, medulla via the axon of the trigeminal nerve or meninges via bacteremia) leading to Circling disease (Rhomoboencephalitis) 4) Microabscesses: Perivascuar ciffing with infiltrate of leukocytes 5) meningitis
76
Circling Disease
Rhomboencephalitis, inflammation of the brainstem and cerebellum leading to circling manifestions, most common in ruminants caused by localization of Listeria in the pons, medulla via the axon of trigmeinal nerve or meninges via bacteremia
77
How do you diagnose Listeria
Typically postmortem through histopathology (Brain, liver, spleen, fetal tissues, and placenta) Aerobic bacterial culture- send in brainstem sample, use cold incubation with periodic subculture (takes several weeks) and specialized enrichment media is used
78
How do you treat for Listeria?
needs to be prompt and aggressive Penicillin is drug of choice, erythromycin, and trimethoprim/ sulfonamide high pencillin dose needed to achieve effective concentration in the brain via blood brain barrier
79
Coxiella burnetti
"Q-fever" - reportable to CO state vet, CDC select agt Gram - , aerobic rod, obligate intracellular lifestyle reservoirs: cattle, sheep, goats Asymptomatic in non-pregnant animals, causes placentitis (trophoblast infection) in pregnant animals Humans: highly infectious (High fever, chills, headache, pain) Diagnose using Serology, PCR (CDC approved labs), culture is not practical
80
What bacterial agents are on your differentials for abortion in sheep/goats
Coxiella burnetti Camylobacter jejuni Brucellosis (ovis, abortis) Chlamydia abortus
81
Chlamydia spp.
Gram - (but no peptidoglycan wall) , aerobic, short coccobacilli, obligate intracellular lifestyle shed in high numbers at parturition and weeks before and after in vaginal discharge, inhalation, ingestion, venereal infects epithelial cells and proliferates causes abortion (placentitis with cotyledonary necrosis)- ewes/does most susceptible in 3 months and causes polyarthritis and conjunctivities in lambs diagnosed: ELISA, placental histopath- cant culture *zootnotic risk to pregnant women
82
abortifacient Campylobacter spp.
Gram - curved rod, darting motility Campylobacter fetus subsp fetus & veneralis Campylobacter jejuni Campylobacter coli
83
Campylobacter fetus subsp veneralis
very important abortion causing agent in cattle (federally reportable) *resevoir in preputial crypts and carrier bulls (same as Tritrichomas foetus) transmission: through coital interactiong cause bovine genital campylobacteriosis -mild endometritis makes it inhospital for implantation to occur -cow returning to estrous and several pregnancies required
84
Campylobacter fetus subsp foetus
abortifactant in all ruminants (sheep most important) use zipper, trigger, to cause suppurative inflammation cause abortion through placentitis Diagnosis using a special transport media (weybridge mediuym or clarks medium) which will get you to the species level, subspecies level is determined by PRC or glycin tolerance test take sample for tritichomas at same time
85
Taylorella equigenitalis
gram - coccobaccilus (short rod), microaerophilic causes contagious equine metritis spread through venereal transmission, AI, fomites, frozen semen, asymptomatic carriers causes: infection of endometrium leading to mucopurelence, failure to conceive Diagnosis: culture by USDA approved lab, transport media must have charcoal, highly fastidious and may take up to 2 weeks to culture
86
Leptospirosis
gram - rods (spriochetes), aerobic has different species disease manifestations with different serovars (ex: pigs-SMEDI, horses-abortion and ocular disease, Dogs- renal and hepatic disease) virulence mechanisms: lipopolysaccharide, lipoprotein, hemolysins, induction of autoantibodies high prevalence of infection animal to animal and shed in urine
87
Leptospirosis pathogenesis
entry through the broken skin or mucous membrane leading to leptospiremia in the blood, vascular damage and vasculitis plis thrombocytopenia, leading to CNS/Ocular/spleen/Repro, hepatic dysfunction, and renal damage
88
Can you detect lepto in the urine?
Yes it is shed in the urine because of replication association with the tubular epithelial microvilli of the kidneys
89
Adult Cattle Leptospirosis
Abortion (primarily L. Hardjo, also Pomona, Canicola, Icterohemorrhagiae, Grippotyphosa) Clinical signs: Hemoglobinuria, Icterus, Fever, Aborted feti
90
Calf Leptospirosis
-Hemolytic Anemia via hemolysis virulence factor and IgM agglutins induced causing complement fixation and MAC formation, Hemoglobinuric animals -Acute renal failure
91
Pig Leptospirosis
Reproductive disease from uterine colinization, SMEDI, mastitis, often subclinical younger pigs- fever, anorexia, jaundice, hemoglobinuria
92
Horse Leptospirosis
Causes recurrent iveitis (Moon blindness) - often L. Pomona, grippotyphosa, correlated with elevated titers , Abortion 6months-term Acute renale failure in foals
93
Dog Leptospirosis
-Uremic disease (all serovars) causing severe azotemia (elevated BUN, creatine), chemistry (Ca2+, PO3- elevated), and urinalysis showing renal dysfunction -Icteric disease (Icterohemoorhagiae, pomono, Grippotyphosa ) Multifocal hepatic necrosis leading to icterus, mild to moderate hypoalbuminemia, chronic active hepatitis, fibrosis
94
What is the preferred method for lepto diagnosis?
Microscopic Agglutination Test (MAT) for the detection of Leptospira antibodies. vax history is very important and results expressed as titers. Single titer result okay if there is a greater than 1:800 result. If you do acute and convalescent titers 7 to 14 days apart, it is significant if the is greater than a 4 fold increase you can also use Fluorescent antibody test, PCR, ELISA (snap), and Histopath
95
How do you treat acute oliguric renal failure with lepto in your differential?
First manage the systemic complications with IV fluids then cover for Lepto with antimicrobials Cattle/Horses: Oxytetracycline, Ceftiofur, Penicillin Dogs: Parenteral Antimicrobials- Ampicillin and oral antimicrobials (Doxyclicine)
96

bacteriology & myocology (3 decks)

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