exam 2 Flashcards
Upper urinary tract
the ureters and kidneys
lower urinary tract
the batter, urethra, and prostate
Cystitis
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
Natural defenses against urinary tract infections
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
Uncomplicated infectious cystitis
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
Complicated infectious cystitis
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
What kind of bacteria is typically manifested in urinary tract infections
facultative anaerobes
The majority of infectious agents that cause UTI in small animals include
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.
What are some less common causes of UTI in small animals
Corynebacterium urealyticum (fac anaerobe gram + rod)
Non enteric gram - rods (Pseudomonas aeruginosa)
Mollicutes- Mycoplasma spp and ureaplasma spp
Fungal (typically C. albicans)
What is the main pathogen that causes UTIs in large animals
Corynebacterium renale
Corynebacterium renale
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
Urease role
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)
What UTI pathogens produce urease and predispose the animal to urolithiasis?
Staphylococcus spp.
Proteus spp.
Enterobacter spp.
Corynbacterium Renale/urealyticum
What single pathogen is the most common cause of UTI in humans and dogs?
UPEC (uropathogenic E.coli) that is a type of ExPEC
UPEC
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
Is the presence of bacteriuria an indication to treat the animal?
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
What drugs go to the urine and are helpful to treat UTIs?
Penicillin (Amoxicillin)
Cephalosporins (Cephalexin)
Fluoroquinolones (Enrofloxacin)
Trimethoprim- Sulfamethoxazole
Tetracyclines (Doxycycline)
Aminoglycosides (Amikacin)
Nitrofurantoin
How should you diagnose UTIs?
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
In-clinic cultures
small incubator with standard plate media and commercial kits for UTI culture, most are gram + and show up overnight
How do you prevent against UTIs?
-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
Cranberry’s role in UTI treatment
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
Empirical therapy for UTI
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)
Targeted therapy for UTI
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
Pyelonephritis
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
How should you treat pyelonephritis
antimicrobial agents with high tissue penetration is best: fluoroquinolones, Trimethoprim Sulfa
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
What is the most common causative agent of prostatitis?
the same as UTI, E coli is the most common overall
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)
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)
Are mammary glands in quarters connected?
NO there is 1 mammary gland per quarter and there is no physical connection to the other quarters
What is the milk vein?
Subcutaneous abdominal vein (milk vein)
What ligaments support the mammary gland
Median suspensory ligament, lateral suspensory ligament, and intermammary groove
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
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
What SCC indicates an animal is uninfected with mastitis?
SCC less than 100,000 cells/mL
What SCC indicates an animal has mastitis (subclinical or clinical) or early lactaction (colostrum)
SCC of more than 200,000 cells/mL
What is the target of bulk tank SCC
SCC of less than 250,000 cells/mL
What is the US legal limit of SCC in milk?
SCC of 750,000 cells/mL
What is the EU legal limit of SCC in milk?
SCC of 400,000 cells/mL
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
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
Mastitis Physical Exam Signs
decrease in feed intake, decrease in milk production, lethargy, depression, tachypnea, tachycardia, weakness, recumbency, fever, pale mucous membranes, dehydration, shock
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)
Composite mastitis testing
multiple quarters of the cow into one sample, used for screening for contagious pathogens, not recommended for identifying quarter infections
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
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
What are the contagious mastitis pathogens?
Streptococcus agalactiae
Mycoplasma bovis
Staphylococcis aureus
Corynebacterium bovis
(Contagious Mastitis Sucks Severely)
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
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
Corynebacterium bovis
*Highly contagious mastitis pathogen
gram +, rod club shaped, facult anaerobe
manifest in the teat canal
curable with intramammary antibiotic
What do all the contagious mastitis pathogens have in common
facultative anaerobes and gram + (except for mycoplasma bovis- no cell wall)
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
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
What are the environmental mastitis pathogens
1) Environmental Streptococcus
2) Coagulase Negative Staphylococcus
3) Coliform Mastitis
4) Trueperella pyogenes
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
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
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
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
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
IS Brucella zoonotic?
Yes
Brucella spp.
aerobic gram negative bacteria
non spore forming and intracellular
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
Brucella virulence
LPS with smooth a rough
Smooth (O antigen)
Rough (only core polysaccirdge)
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
Brucella abortus human applications
causes Malta/ Undulant fever leading to flu-like febrile syndrome, almost eradictated in US, issue with raw milk consumption
What zoonotic pathogen is a problem with raw milk consumption leading to Malta/Undulant fever?
Brucella abortus
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
Which of the following urease-producing organisms is most often associated with “pizzle rot” in the ram
Corynebacterium renale
What of the organisms has a rough colony phenotype?
Brucella canis
What tests is used to initially screen cattle for B. abortus?
CARD test
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
What is the classic agent associated with calf diphtheria (necrotic laryngitis)?
Fusobacterium necrophorum
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
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
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
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
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
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
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
What bacterial agents are on your differentials for abortion in sheep/goats
Coxiella burnetti
Camylobacter jejuni
Brucellosis (ovis, abortis)
Chlamydia abortus
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
abortifacient Campylobacter spp.
Gram - curved rod, darting motility
Campylobacter fetus subsp fetus & veneralis
Campylobacter jejuni
Campylobacter coli
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
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
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
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
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
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
Adult Cattle Leptospirosis
Abortion (primarily L. Hardjo, also Pomona, Canicola, Icterohemorrhagiae, Grippotyphosa)
Clinical signs: Hemoglobinuria, Icterus, Fever, Aborted feti
Calf Leptospirosis
-Hemolytic Anemia via hemolysis virulence factor and IgM agglutins induced causing complement fixation and MAC formation, Hemoglobinuric animals
-Acute renal failure
Pig Leptospirosis
Reproductive disease from uterine colinization, SMEDI, mastitis, often subclinical
younger pigs- fever, anorexia, jaundice, hemoglobinuria
Horse Leptospirosis
Causes recurrent iveitis (Moon blindness) - often L. Pomona, grippotyphosa, correlated with elevated titers ,
Abortion 6months-term
Acute renale failure in foals
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
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
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)
