Exam 3 Flashcards
(106 cards)
1
Q
General Features of Mycobacterium
A
o aerobic, “Gram-positive rods” o Facultative intracellular specific to macrophages o non-spore forming, non-motile o mycolic acids & lipids in cells wall o must be acid-fast stained o grow very slowly o Complex egg-based media is required for growth o Chronic/progressive dz
2
Q
Major Pathogenic Mycobacteria
A
M. bovis:
• Primarily infects cattle
• Can affect others
M. tuberculosis
• Primarily Human, but dogs, rodents, swine can get infected
M. avium (paratuberculosis )
• Cattle, sheep and goats
Non-tuberculous Mycobacterium (NTMs)
• Several species
3
Q
Bovine Tuberculosis (M bovis) source of infection & survival in environment
A
- Infected animals are source of infection.
- Bacteria are in exhaled respiratory droplets, sputum, milk, feces, urine, vaginal discharge.
- Survives in environment for 4 - 28 days
- May survive longer in presence of organic material.
4
Q
Bovine Tuberculosis (M bovis) Entry, Multiplication, Spread, Damage
A
- Bacteria inhaled or ingested ->
- taken up by macrophages.
- multiply intracellularly and travel inside of macrophages to regional lymph nodes ->
- May enter lymphatics and blood and disseminate widely ->
- Two possible outcomes:
- Latency
- tuberculosis & systemic granulomas (Pathognomonic Lesion)
5
Q
Bovine Tuberculosis (M bovis) Clinical Signs, Diagnosis, Treatment
A
Clinical Signs
• Respiratory signs:
moist cough, dyspnea, weight loss
• Rarely mastitis
• Enlarged bronchial, mediastinal and mesenteric nodes
Diagnosis
• Caudal fold test (cross-reactivity common)
• tubercles on necropsy
• culture (time consuming)
• PCR (definitive & fast but difficult if no clinical signs)
Treatment & Control
• No treatment = slaughter
• Test new animals
• No Vx
6
Q
Bovine Paratuburculosis or Johne’s (M. avium) Encounter, Entry, Multiplication, Spread
A
Encounter
• Environment contaminated w/ fecal material from infected animals
Entry, Multiplication, Spread
• Feces Ingested shortly after birth ->
• Invades macrophages in Peyer’s patches ->
• Multiply & kill macrophages ->
• Spread to adjacent cells ->
• Inflammatory response ->
• Thickened intestine & loss of absorption
7
Q
Bovine Paratuburculosis or Johne’s (M. avium) Clinical Signs, Diagnosis, Treatment
A
Clinical Signs
• Perinatal period
• reduced milk production, diarrhea, weight loss, normal appetite.
• shedders are often not clinically ill
Diagnosis • Direct microscopy • DNA based PCR test • Johnin test • Culture of organisms from manure or ileal node (good, takes long time, need multiple samples)
Treatment/Control
• No treatment = slaughter
• Do not accept new animals
8
Q
Non-Tuberculous Mycobacterium (NTM) Clinical Signs & Diagnosis
A
Clinical Signs
• Granulomatous inflammation in dogs & cats
• Localized or systemic
• Skin infections, pneumonia, or GI infection
Diagnosis of NTMs
Histology
• Acid fast stain
• Pyogranulomatous inflammation
PCR
• On tissue sections or culture
Culture & Sensitivity
• Use for treatment w/ antibiotics
9
Q
Basics of Mycoplasma
A
o Facultative anaerobes o Smallest self-replicating bacteria o obligate parasites o no cell walls o need giemsa stain o resistant to penicillin, cephalosporin o Extremely fragile o “fried egg” colonies o “fastidious bacteria” (must use special media w/ penicillin to ward off gram (+) & thallium acetate to ward off gram (+) )
10
Q
Encounter/Entry Mycoplasma
A
Encounter
o introduced by clinically healthy carrier animals
o Prefer upper respiratory, intestinal, genital tract, joints, conjunctiva and mammary glands
Entry
• direct droplet of oral, ocular, or genital secretions
• contaminated equipment or blood transfusion)
• Some transmitted via tick bite (mechanical)
11
Q
4 Virulence Factors of Mycoplasma
A
Adhesins
• used for binding of bacteria to
the host cells
Capsules
• For biofilm = impede host defense & persist in environment
Hydrogen peroxide
• Affects ciliary movement in trachea and induces hemolysis
Biofilm
• resistance for dessication, heat and complement mediated lysis
12
Q
Chronic Respiratory Disease caused by M gallisepticum Basics, Encounter, & Entry
A
o Affects chickens, turkeys, game birds
o Localized mycoplasma infection
o exogenous
Encounter/Entry
• Infection via respiratory route or thru infected eggs
• Stress = asymptomatic carriers become sick & shed in respiratory aerosols
13
Q
Chronic Respiratory Disease caused by M gallisepticum Multiplication/spread, damage, symptoms
A
Multiplication / Spread
• attaches ciliated epithelium of trachea & multiplies
Damage
• Damages cilia
• Sinusitis, tracheitis, airsacculitis
Symptoms
• coughing, sneezing, nasal discharge, dyspnea, reduced growth, decreased egg production
• high morbidity, low mortality
14
Q
Chronic Respiratory Disease caused by M gallisepticum Diagnosis, Treatment, Control
A
Diagnosis • Culture • FA • PCR from exudate & tissue • ELISA on serum
Treatment
• Tylosin, tiamulin, chlortetracycline, lincomycin
Control
• Depopulation & disinfection
15
Q
Basics of Invasive Mycoplasma Infections; two outcomes
A
o penetrate epithelial barriers and enter the blood stream
infection / acute septicemia
o fever and sudden death
Brief period of inapparant mycoplasmemia
o localization in serosal cavities and joints ->
o chronic inflammation
16
Q
Feline hemotrophic mycoplasmosis Basics & mycoplasmas involved
A
- cause of hemolytic anemia in cats
- can be endogenous or exogenous
Mycoplasmas involved
• M hemofilis (clinical symptoms)
• M hemominutum
• M turicensis
17
Q
Feline hemotrophic mycoplasmosis Predisposing Factors & Encounter for Exogenous infection
A
Predisposing factors:
o Surgical stress, FIV/FelV, abscess, corticosteroids
Encounter for Exogenous • Arthropod vectors? • Biting and fighting • queens to new borne • blood transfusion
18
Q
Feline hemotrophic mycoplasmosis 4 Phases
A
Pre-parasitemic phase
o Lasts 1-3wk post infection
o Bacteria not detectable
o Mild reduction HCT
Acute Phase
o ~30 days
o cyclic high number of bacteria in blood
o Parasitized RBCs sequestered in spleen w/ release of non-parasitized RBCs
o rapid decrease in HCT followed by rapid increase
o W/o treatment, 1/3 die of anemia
Recovery Phase
o time from last bacteremia until HCT has stabilized
o sufficient immune response or treated w/ antibiotics & recover
o regenerative bone marrow response
Chronic/Carrier Phase
o recovery from acute infections = clinically normal & chronically infected
o Low numbers of organisms may/may not be detectable
19
Q
Feline hemotrophic mycoplasmosis Damage & Clinical Signs
A
Damage • Regenerative anemia w/ polychromasia & reticulosytosis • Precipitous drop in HCT Clinical Signs Acute o Fever, o marked mental depression, o tachypnea, o weakness, o anorexia, o pale mucous membranes, o dehydration
Chronic
o Mild anemia
20
Q
Feline hemotrophic mycoplasmosis Diagnosis, Treatment
A
Diagnosis • No culture • Reduced HCT, reticulocytosis, icteric plasma • Blood smear may show mycoplasma on RBC • PCR highly sensitive
Treatment
• Tetracycline / doxycycline (gold standard)
• Enrofloxacin (alternative)
• Antibiotic does not clear parasite
21
Q
Defense Mechanisms of Mammary Glands
A
Physical Barrier • Sphincter muscle tightens teat canal • Keratin plug • Keratinized squamous epithelium (prevents adherence) • Flushing milk
Innate & Adaptive Immune Response
• Macrophages (normal 66-88%)
• Neutrophils (normal should not have many)
• Abs neutralize bacteria/toxins
• B & T cells enhance immune response & kill infected cells
Soluble mediators
• Lactoferrin: iron binding protein prevents bacterial iron usage
• Lysozyme: cleaves peptidoglycans in gram (+) cell wall
22
Q
Risk Factors for Mastitis
A
Host
• Age, stage of lactation, teat lesions, genetics
Environment
• Poor milking hygiene, milking technique, contaminated env
Microbial
• Contagious Vs environmental agent, virulence factors, habitat
23
Q
Entry of Pathogens in Mastitis
A
o Systemic infection with localization in mammary gland
o Lymphatic spread
o Direct penetration
Breakdown of teat sphincter barrier (most COMMON)
• Teat sphincter open 2hrs post milking
• Bacteria ascend during this period
24
Q
Pathogenesis of Mastitis
A
o If not eliminated by immune response -> multiply in mammary ->
Produce virulence factors • Adhesins: help adhere to mammary epithelial cells • Capsule: Anti-phagocytic • Exotoxins: produced by Gram (+) & (–) • Endotoxin: Released by Gram (-)
Induce leukocytes and epithelial cells to release chemo-attractants, including cytokines ->
Infiltration of polymorphonuclear neutrophils (PMNs) to the site of infection
• engulf/destroy bacteria
• destroy few epithelial cells = reduced milk production & release of enzymes
PMNs destroyed by macrophages ->
Dead epithelial cells & leukocytes secreted into milk = high milk somatic cell counts (SCCs) ->
Bacteria may spread into deeper mammary ductal system (eg., Staphylococcus aureus) or may float in milk secretion (eg., E. coli).
• Systemic signs from system infection OR endotoxin
25
Damage in Mastitis
o No persistent damage w/ proper treatment
```
Persistent infection
• Damage to mammary gland alveoli
• Breach of blood-milk barrier
• Extensive damage can result in leakage of blood in milk
• swelling w/in mammary epithelium
```
Chronic Dz due to uncleared infection
• Abscessation and gangrenous reaction
• Atrophy of mammary alveoli
• Fibrosis of mammary tissue leading to further damage
26
Clinical Signs & Diagnosis of Mastitis
Clinical Signs
o Clinical
• Inflammation (SHARP)
• Abnormal milk (flecks, clots, off color)
o Subclinical
• No visible signs
• (+) SSC, CMT, & sterile milk culture
Diagnosis
o Direct Tests
• Multiple samples of Sterilely collected milk & gram’s stain or bacterial culture
• Biopsy (uncommon)
o Indirect Tests
• Somatic cell count (milk tank)
• California mastitis test (MST) – increased DNA = gel
• Electrical conductivity of milk to look for Na & Cl
27
Contagious Pathogens in Mastitis
```
o Obligate parasites
o Obligate pathogens
o Subclinical mastitis more common
o Mycoplasma bovis
o Staph aureus
o Strep agalactiae
```
28
Clinical significance of mycotic infections & fungal structure
Clinical Significance
o mimic other types of diseases
o frequently associated with local debilitation or immune deficiency
Fungal Structure
o Eukaryotes (antibiotics don’t work)
o cells have ergosterol and zymosterol
(target for antifungal)
o cell walls high in polysaccharide (used for diagnosis w/ histochemical stain)
o anti-phagocytic capsule
29
Growth/Repro of Fungus
Molds
• Multicellular
• Hyphal elongation & division
• Mycelium: tangled hyphae (cottony) seen on agar for diagnosis
Yeasts
• Unicellular
• Reproduce by budding & form moist colonies
```
Dimorphic
• Yeast in tissue
• Mold in environment
• Transition mediated by temp change
• Exception: Candida albicans forms pseudo hyphae in tissue but yeast in culture
```
Important Fungi not Dimorphic
• Aspergillus fumigatus = mold in environment and tissue
• Cryptococcus neoformans is always yeast.
30
Types of Fungal Dz's
cutaneous mycoses (ringworm)
subcutaneous mycoses (sporotrichosis, Rhinosporidium)
systemic mycoses
• opportunists (Candida albicans)
• primary pathogens (Blastomyces dermatitidis, Histoplasma capsulatum)
31
Encounter for Fungal Dz
```
o Most free living in environment
o Some specific in animals
• H. capsulatum : bat or chicken feces
• Cryptococcus neoformans: pigeon feces
• Microsporum canis: obligate paraiste
• Candida albicans: skin & mucous membranes
o inhalation or traumatic implantation from an exogenous source
o usually not contagious
o some have carriers
```
32
What Allows Entry of Fungal Dz
o Innate resistance from skin barrier (low pH, fatty acids, normal flora)
o Infection usually self-limiting
o Weakly virulent
```
Requires diminished host resistance
• Loss of cutaneous barrier
• Loss of normal flora
• Local Immunosuppression
• Decreased systemic resistance (malnuitrition or immunosuppression)
```
33
Multiplication/Spread & Damage for Fungal Dz
```
Multiplication/Spread
o Most are aerobes
o Don’t multiply well in body temp
o Growth limited due to need for Fe++
o First line of defense is phagocytosis
o 2nd line defense = T lymphocytes
```
Damage
o No toxins
o destruction of tissue by fungal multiplication & host inflammatory response
o granuloma formation is hallmark
34
Diagnosis of Fungal Dz; why pursue? presumptive & difinitive
Why pursue etiologic diagnosis?
• differentiate from other diseases characterized by loss of functional tissue by cellular infiltration
• differentiate between opportunistic and pathogenic fungi
• selection of appropriate drugs
presumptive diagnosis
• identification of hyphae or yeast on smear & cytology or histo & biopsy
• serology or skin tests
definitive diagnosis
• Saboraud's Dextrose Agar (with antibiotics)
• Blood Agar
• up to 3-4 weeks for diagnosis
35
Antifungal Therapy basics; therapeutic index, dosing strategy
o Some may not need treatment
o opportunistic infections resolve when underlying problem corrected
o anti-fungal drugs toxic to host
o limited anti-fungal drugs
o fungi can develop resistance but sensitivity testing not done
therapeutic index:
• ratio between antimicrobial efficacy and toxic effects to host animal
```
dosing strategy
• target organ
• lowest effective dose
• schedule
• combination therapy
```
36
Polyene Anti-fungal Drug; compounds, mechanism, uses, notes
Compounds
• amphotericin B, nystatin
Mechanism
• Disturbs cell membrane (higher affinity for ergosterol than cholesterol)
Uses
• systemically (IV) for systemic infections
• topically for superficial infections (candidiasis)
```
Notes
• Not water soluble
• must be given IV for systemic infections
• poorly penetrate CSF
• nephrotoxic
```
37
Allylamines Anti-fungal Drug; compounds, mechanism, uses,
Compounds
• Terbinafine
Mechanism
• inhibits ergosterol biosynthesis
Uses
• Broad spectrum
• oral or topical for superficial & sub-cutaneous infections
• less toxic than amphotericin B
38
Azoles Anti-fungal Drug; compounds, mechanism, uses,
Compounds
• clotrimazole, miconazole, itraconazole, fluconazole, ketoconazole
Mechanism
• inhibits ergosterol biosynthesis
```
Uses
• Broad spectrum
• PO, IV for systemic infections
• topically for superficial infections (ringworm),
• less toxic than amphotericin B
```
39
Pyrimidine Anti-fungal Drug; compounds, mechanism, uses, notes
Compounds
• 5-fluorocytosine (5FC)
Mechanisms
• inhibits DNA and RNA synthesis
Uses
• PO for systemic infections
Notes
• Narrow spectrum
• resistance develops rapidly (use combo w/ other)
• enters CSF in high concentration
40
Grisines Anti-fungal Drug; compounds, mechanism, uses, notes
Compounds
• griseofulvin
Mechanisms
• inhibits microtubule assembly
Uses
• PO for superficial infection
Notes
• Not effective topically
• Teratogenic especially in cats
41
Cutaneous Mycoses; common name. 3 main sources
o Ringworm
Geophilic:
• dermatophytes that live (grow & replicate) in soil.
• prefer warm and humid climate
• poorly transmitted in animals
Zoophilic:
• dermatophytes that are obligate parasites
• spread rapidly among animals
• zoonotic
Anthropophilic:
• dermatophytes that are obligate animal parasites but predominately found on humans
• Ex: Athlete's foot
42
Ringworm Host-parasite relationships in domestic animals
Microsporum canis
o natural host is the cat (is zoophilic)
o 15% human ringworm = zoonotic
o children very susceptible
```
Microsporum gypseum
o reservoir is soil (is geophilic)
o 1-10% cat infections
o 25% dog infections
o most common ringworm in horses in southern U.S.
o poorly zoonotic
```
43
Virulence Factors Mycoplasma Bovis (Mastetitis)
Adhesins:
• adhere to epithelium, hematogenous spread, proliferation in lact ducts
Phospholipase:
• Breaks connective tissue = purulent interstitial inflammation & abscess
44
Virulence Factors Staph Aureus (Mastetitis)
Hemolysins:
• lyse erythrocytes -> paralysis & necrosis of blood vessels -> gangrene
Toxic Shock Syndrome Protein
• Cytokine release & systemic shock
Capsule
• Antiphagocytic
Adhesins
• help in adherence
• Protein A aids evasion from immune response
45
Virulence Factors Staph agalactiae (Mastetitis)
Hemolysins:
| • lyse erythrocytes
46
E. coli role in Mastatitis
* Most common environmental mastitis pathogen
* usually cause clinical mastitis of short duration
* rarely have systemic signs.
* does NOT adhere to the mammary epithelium
* Does NOT commonly spread into the mammary parenchyma.
* Spontaneous resolution common
release of ENDOTOXIN
• edema and necrosis of mammary tissue
• endotoxemia
• Bacteremia may in up to ~50% of cases
47
Why do Microbiological Diagnosis of Mastitis?
o Required for clinical and subclinical mastitis
o differentiation between contagious vs environmental
o Important determinant of treatment and control practices
48
Strategy for Microbiological Diagnosis of Mastitis
```
o gram stain ->
o (-) rods -> MacConkey
o lactose (-) = salmonella, proteus, pseudomonas
o lactose (+) -> idole
o indole (+) = E coli
o indole (-) = klebsiella
```
o gram stain ->
o (+) cocci -> catalase test
o catalase (-) = strep
o catalase (+) = staph
o CAMP test for strep species
o coagulase test for staph species
49
3 Treatments for Mastitis
Intra-mammary
• Infusion of antibiotics into udder
• Streptococcus - Penicillin
• Staphylococcus - Penicillin, cephalosporin classes
• Antimicrobials may fail to reach location of infection due to abscessation or fibrosis
• Antimicrobial resistance due to β-lactamase production or altered penicillin binding
proteins
```
Systemic therapy
• Needed if systemic signs
• Staphylococcus – exotoxins
• E. coli - endotoxin
• Antibiotics IV or IM
• Supportive therapy
• Remove toxins by Frequent milking
```
Dry Cow Therapy
• stop milking
• contagious mastitis
• Larger dose, longer acting product
50
Prevention of Mastitis
o hygiene to prevent cow-cow transmission at milking
o Teat dipping pre- and post- milking (Iodines, Chlorhexidine)
o Identification of chronic/subclinical cases
o Antibiotic therapy
o Detection and segregation of infected animals
o Culling chronically infected cows
o Quarantine/testing of new herd additions
o Adequate nutrition
Vaccines
• No Vx for S. agalactiae
• Mycoplasma bovis: Vx efficacy questionable.
• Lysigin, a S. aureus bacterin Vx helpful in prevention of chronic infection but not in prevention of new infections
51
Important Pathogens of Mastitis in Sheep & Goats
```
o Staphylococcus aureus
o Coagulase-negative Staphylococcus sp.
o Streptococcus agalactiae
o Pasturella multocida
o Mannheimia haemolytica
```
52
Entry & Multiplication/Spread of Cutaneous Mycoses
Entry
• normal skin has fungicidal fatty acids
• requires debilitated skin barrier
• exacerbated by high humidity and low sunlight
• primarily outbreaks in young animals in close contact
Multiplication & Spread
• Arthroconidia enter abraded skin
->
• arthrospores germinate to hyphae in the stratum corneum
(adjacent to hair follicles) ->
• limited to epidermis by temperature range (25-32C) and dependence on keratin
53
Damage, Diagnosis, Treatment of Cutaneous Mycoses
Damage
• inflammation due to contact dermatitis
• chronic inflammation results in loss of hair and hyperkeratosis
• most infections self-limiting due to cell-mediated immune response
Diagnosis
• puritic or non-pruritic, non-healing focal lesions
• vary from red, moist lesions (acute) to dry, flaky lesions (chronic)
• detection with UV light (M. canis)
• KOH digestion and examination
• skin biopsy and histo
• in house cultivation
to diagnose ringworm
• lab cultivation to determine species
Treatment
• Self-limiting in large animals (increase sun)
• Clipping & topical iodide or miconazole
• Oral ketoconazole, terbinafine(choice) or grisans (toxic)
54
Pythiosis Basics
* Pythium insidiosum
* Subcutaneous mycoses
* Not considered true fungi
* Affects horses in Gulf Coast states
* Also affects dogs and rarely cats, cattle and humans
* Wet environments essential for reproduction of fungi
* Enters via skin wounds (common) or by ingestion
* Chronic, non-healing, severe granulation tissue lesions
* rapid tissue destruction due to allergic response to presence of fungal hyphal element
55
Pythiosis Diagnosis
Isolation
o definitive diagnosis
o grow on agar or blood agar
Serology ELISA
o common in labs
Microscopy
o typical, wide, sparsely septate,
branching filamentous hyphal elements
Histology
o Tissue section stained with PAS
PCR
o DNA extracted from tissue samples; rapid & specific
56
Pyhtiosis Treatment
Surgical removal
Systemic antifungals
o Amphotericin B and azoles
Therapeutic vaccine
o Effective in acute lesions
57
Sporotrichosis Basics, Encounter, Entry
* Sporothrix schenckii
* subcutaneous abscesses in horses and dogs occasionally cats
```
Encounter
• dimorphic
• free-living hyphae in soil
• worldwide distribution
• more common in hunting dogs and male cats
```
Entry
• requires implantation of conidia or mycelia in wounds
• most common in head, neck, paws
58
Sporotrichosis Multiplication/Spread/Damage & Diagnosis
Multiplication/ Spread/Damage
• yeast form grows in subcutaneous tissue
• spreads via lymphatics
= lymphangitis
• resolves via T-lymphocyte mediated macrophage activation
Diagnosis:
• clinically suspect with recurrent, non-healing nodules
• may underlie chronic Staphylococcus infection
• deep pyoderma that is non-responsive to antibiotics
• cytology or biopsy by histopathology
• indirect fluorescence on tissue detects Ag in tissues
59
Sporotrichosis Treatment & Zoonotic Potential
Treatment
• surgical excision
• supersaturated KI
for 30 days PO (Monitor signs of toxicity - esp. cats)
• ketoconazole or itraconazole
Zoonotic
• Cats to people
60
Cryptococcosis; fungus, encounter, entry, Multiplication/spread
• Cryptococcus neoformans = most common systemic mycotic infection in cats
Encounter
• Free living in soil where there is pigeon feces
```
Entry
• Inhaled as spore
• Most infections inapparent
• Penetrates respiratory epithelium
o Upper – cats
o Lower – dogs & cats
```
Multiplication & Spread
• Proliferates as yeast
• Polysaccharide capsule = avoid phagocytosis
• Systemic spread
61
Cryptococcosis; damage, clinical disease in cats Vs dogs
• replicates and replace host tissue
immunosuppressed patients
o no/minimal response
immunocompetent patients
o granulomatous response
o nasal mass
o meningoencephalitis
```
clinical disease in cats:
o >50% have rhinitis, sinusitis, or nasal mass
o ~40% have pulmonary lesions
o ~40% have cutaneous lesions
o ~25 have ocular lesions
o ~25% have CNS lesions
```
```
clinical disease in dogs:
o 75% have CNS lesions
o 65% have ocular lesions
o 42% have disseminated visceral lesions
o 20% have cutaneous lesions
```
62
Cryptococcosis; Diagnosis & Treatment
```
Diagnosis
• Cytology of skin lesions, nasal discharge, tracheal wash, CSF = high leukocyte count
& encapsulated organisms
• histopathology
• cultivation (48hrs-6wks)
• detection of Ag
```
Treatment
o Itraconazole or Fluconazole
o Amphotericin B
(Does not cross bbb well)
o 5-fluorocytosine (use w/Amphotericin B)
• Ag test to evaluate therapeutic efficacy
63
Aspergillosis; fungus, animals affected, encounter, entry
* Aspergillus fumigatus
* respiratory disease in closely housed young birds
* sporadic occurrence in all animals
* guttural pouch mycosis in horses
Encounter
• soil contaminant
• found on skin and feathers of normal animals
• multiplies in moist environment
Entry
• Inhaled as conidia
• Must be immunosuppressed or high organism count
64
Aspergillosis; multiplication/spread, damage, diagnosis, treatment
Multiplication/Spread
• conidia vegetate and form hyphae in the nasal cavity, lungs, and air sacs
• in pregnant ruminants, may spread systemically to the placenta and fetus
Damage
• Granulomatous response
Diagnosis
• branching septate hyphae on cytology or histo
• cultivate on Saboraud's Dextrose Agar
Treatment
• control predisposing causes
• ketoconazole or amphotericin B
65
Candidiasis; fungus, animals affected, encounter, entry
* Candida albicans
* stressed captive birds
* sporadically in all species of animals
Encounter
• Normal flora on skin, oral cavity, genital tract
```
Entry
• poor nutrition
• prolonged antibiotic therapy
• overcrowding
• immunosuppression
```
66
Candidiasis; multiplication/spread, damage, diagnosis, treatment
Multiplication/Spread
• Yeast germinate into hyphae above 37 degrees C
Damage
• Shallow ulcers on mucosal surfaces & GI
Diagnostics
• appearance of white-pseudomembrane on epithelial surfaces
• cultivation on Saboraud's Dextrose Agar (1-2 days at room temperature)
• Gram stain to identify budding yeast
• grow on Blood Agar
Treatment
• control predisposing causes
• topically = Nystatin
• systemically = Amphotericin B, 5-
fluorocytosine
67
Fungal Otitis; basics, encounter, spread, damage, diagnosis, treatment
* Malassezia pachydermatis
* otitis externa in dogs w/ chronic bacterial otitis
* likes warm moist environment
encounter
• normal flora of canine skin in small numbers
multiplication/spread
• secondary problem to bacterial otitis externa
damage
• no specific damage, contributes to the chronicity of the problem
diagnosis:
• direct cytology w/ identification of budding yeast
treatment
• clean ears
• resolve bacterial otitis
68
Mycotic Abortion in Cattle; most common fungi & diagnosis
• 5-25% of abortions in cattle
most common fungi
• Aspergillus fumigatus
• other Aspergillus
• Mucor spp.
diagnosis:
• fungal hyphae in the placenta and fetal stomach contents
69
Mycotic Mastitis in Cattle; basics & most common fungi
* positive correlation with use of intramammary antibiotics
* due to direct inoculation from needle
most common fungi
• Candida sp.
• Cryptococcus neoformans
70
Mycotic Rumenitis; predisposition & most common fungi
predisposition:
• antibiotic use in calves
• lactic acidosis in older cattle
most common fungi
• Candida albicans
• Mucor spp.
• Rhizopus spp.
71
Fungi tht Cause Systemic Infections
* Blastomyces dermatitidis (blastomycosis)
* Coccidioides immitis (coccidioidomycosis)
* Histoplasma capsulatum (histoplasmosis)
72
Basics of Systemic Fungal Infections
* strong geographic distribution
* entry by inhalation
* most infections subclinical
* slow onset with granulomatous response
* once established, are life-threatening
* no vaccines
* are not true zoonoses
* therapy is long-term
73
Coccidiomycosis, basics, encounter, entry
* Coccidioides immitis
* severe pneumonia and systemic disease in dogs
Encounter
• enzootic in soil in desert southwest and central valley of California
• fecal contamination by burrowing rodents may enhance growth
• sporulation following rainfall
Entry
• inhalation by dogs and humans
• outbreaks during dust storms
• requires few (<10 in dogs) arthrospores
• arthrospores lodge in bronchioles and then alveoli
74
Coccidiomycosis, Spread, Dz in dogs, Damage
Multiplication/ Spread
• arthrospores -> large spherules
```
Dz in dogs
• 58% seroconvert without signs
• mild upper respiratory signs
• severe pneumonia
• disseminate to bone, CNS, skin, abdominal viscera
also joints, heart, pericardium, testicles, eyes
• course of months to years
• high case fatality
```
Damage
• pyogranulomatous response
• chronic and progressive
75
Coccidiomycosis, Diagnosis, Treatment, Human Dz
Diagnosis
• radiographic evidence of granulomatous pneumonia or osteomyelitis
• serology – (+) 2 wks after exposure, (-) after 4-5 weeks, may become (+) again
• titer: <16 early or focal disease, >16 disseminated disease (does not consistently rise 4x)
• ID of Coccidioides immitis spherules on TTW & cytology = confirmatory
• culture: 72 hrs & risk to humans
Treatment
• surgical curettage
• itraconazole and fluconazole are drugs of choice
Human Dz
• rare zoonosis mot cases from the environment
76
Blastomycosis; basics, geo distribution, encounter, entry, spread
• Blastomyces dermatitidis
• dimorphic
• mycelia in environment
• yeast in tissue
• severe morbidity and high case fatality in dogs
geographic distribution:
• most frequently in central & eastern US
encounter:
• appears to be located in old buildings and soil.
entry:
• organism is inhaled and invades via the lungs
multiplication/spread:
• spread to skin, subQ tissue, CNS, bone
• disseminates to viscera
77
Blastomycosis; Damage, Diagnosis, Treatment
damage:
• inapparent
primary infection in lung
• epithelioid granulomas to chronic suppuration, necrosis, and fibrosis
• epithelial hyperplasia
• Large budding yeast cells with broad bases in microabscesses.
diagnosis:
• geographic predisposition
• pulmonary radiography
• organism in lesion (cytology or histopathology)
• cultivation on Saboraud's Dextrose Agar (days)
• serology
Treatment
• ketoconazole is drug of choice
78
Histoplasmosis; basics, geo distribution, encounter, entry, syndromes
* Histoplasma capsulatum
* dimorphic
* mycelia in the environment
* budding yeast in tissue
* affects dogs, rarely cats and horses
geographic distribution:
• Ohio and Mississippi River valleys
• Other countries
encounter:
• free-living in soil enriched with bird or bat excreta
entry:
• inhaled & enters lower respiratory tract
```
Syndromes:
• inapparent infection (90%)
• mild upper respiratory disease
• severe bronchopneumonia
• disseminated disease (CNS, skin, bone, viscera)
```
79
Histoplasmosis; Spread & Damage
```
Multiplication/Spread
• phagocytosis by alveolar macrophages
• multiply within macrophages
• macrophage activation -> organism eliminated -> small granuloma formation -> calcification OR
• disseminates via infected macrophages
```
Damage
• Acute: many yeast found in macrophages
• Over time: epithelioid granulomas that contain plasma cells, lymphocytes, macrophages, neutrophils and giant cells
• resolved disease: calcification may be prominent.
80
Histoplasmosis; Diagnosis & Treatment
diagnosis:
• geographic predisposition
• pulmonary radiography
• organism in lesion (cytology or histopathology)
• cultivation on Saboraud's Dextrose Agar (days)
• serology
treatment
• ketoconazole is the drug of choice
81
Basics of Anaerobic Infections & Pathogens involved
o O2 is toxic
o Can be in sites exposed to ambient air
o Endogenous opportunistic infections
Gram (+)cocci
• Peptococcus,
• Peptostreptococcus
```
Gram (+) rods
• Clostridium spp.,
• Actinomyces spp.,
• Bifidobacterium,
• Eubacterium,
• Lactobacillus,
• Proprionibacterium
```
Gram (-) rods
• Bacteroides
• Fusobacterium
82
Anaerobic Infections; encounter, entry/multiplication
Encounter
• Normal flora of mucous membranes & skin
• Can be found in soil
Entry/Multiplication
• Breakdown of host defense barriers
• Damage to blood supply or necrosis = low O2
• facultative help obligates by reducing O2, producing necrosis & beta-lactamases
• obligates help falcultative by destroying tissue & impairing host defenses
83
Anaerobic Infections; Damage, Clinical Signs, Diagnosis
Damage
• tissue destruction
collageases
• digest stroma, allow extension of infection
lecithinases
• dissolve cell membranes
leukocidins
• impair host defenses
```
Clinical Characteristics
• foul, putrid odor
• gas in lesion
• black discoloration
• "sterile" culture
```
Diagnosis
• Preserve anaerobic environment
• Direct gram stain of initial sample
• Requires special equipment to culture
84
Anaerobic Infections; Treatment & Resistance
```
Treatment
• Surgery for drainage & debridement
• Prolonged antibiotic therapy necessary
• Antibiotics to use
• penicillin (Gram (+) anaerobes)
• metronidazole (only works on anaerobes)
• clindamycin (resistant strains of B. fragilis; no horses!)
• Chloramphenicol (not in food animals)
```
Resistance
• plasmid-mediated resistance can occur
• sensitivity testing can be done
85
Contagious Ovine Foot Rot bacteria involved
```
Fusobacterium necrophorum
• anaerobe
• gram (-)
• normal flora
• present in feces
• survives on pasture ~10 months
• requires damaged tissue to multiply on skin
```
```
Dichelobacter nodosus
• gram (-)
• Obligate parasite
• Obligate pathogen
• survives less than 14 days on pasture
• infected animals act as reservoir
```
86
Entry, Virulence Factors, & helper of F. necrophorum in Contagious Ovine Foot Rot
Entry
• Any damage to skin & hoof allows multiplication
dermotoxin
• lyses cells
leukotoxin
• kills phagocytic cells
exotoxin and endotoxin
• inflammation
```
Helper
• Trueperella pyogenes
• Gram (+) facultative anaerobe
• secretes growth-enhancing molecule
• scavenges free oxygen
• growth facilitated by necrophorum leukocidal activity
```
87
Entry & Virulence Factors of D. nodosus in Contagious Ovine Foot Rot
• invades inflamed interdigital area
Pili
• binds hoof epithelium
exotoxin
• protease dissolves hoof matrix
factor
• enhances infectivity and invasiveness of F.
necrophorum
88
Treatment of Contagious Ovine Foot Rot
• Hoof trimming
Topical
• 5% oxytetracycline, 20% cetrimide or 5% formaldehyde
Foot bath
• 5% copper sulfate, 10% zinc sulfate or 5% formaldehyde)
89
Immunity Control for Ovine Foot Rot
• no immunity to F. necrophorum
Antipilus Ab blocks D. nodosus binding to hoof epithelium
• requires high titer
• recovered sheep immune for limited period
vaccine available for D. nodosus
• not much cross-protection
• used w/ other management practices
90
Basics & Classifications of Wounds
* All wounds have potential to become infected
* Endogenous or exogenous infections
* Usually opportunistic anaerobes or aerobes
* Anaerobes usually always involved
Causal types
o Traumatic wounds
o Bite wounds
o Surgical wounds
Clinical Types
o Clean wound
o Clean-contaminated wound
o Contaminated wound
91
Predisposing Factors for Wound Infection
* extent of tissue damage
* presence of clotted blood
* devitalized tissue
* duration of wound exposure -“golden period”
* presence of foreign bodies
* type, number, dose and resistance of bacteria
* factors influencing host defense
92
Diagnosis & Treatment of Infected Wounds
```
Diagnosis
• Surgical biopsy
• Syringe aspirate
• Swab may be contaminated
• Gram stain (presumptive)
• Culture (definitive)
```
```
Treatment
• Clean
• Lavage w/ sterile saline
• Suture depending on wound
• Systemic or topical antibiotics depending on deepness
```
93
4 Protective Barriers for Skin
Physical
• Hair, stratum corneum, temp
Chemical
• Fatty acids, inorganic salt, transferrin
Normal Flora
• Influenced by:
• Hydration, health, environment
• Resident & transient
Lymphocyte/Ag interaction
94
Resident Vs Transient Flora on Skin
```
Resident Flora
o Live & replicate on skin
o Obligate parasites
o Permanent
o Normally harmless
```
```
Transient flora
o from environment or mucous membranes
o do NOT multiply on skin
o are transient, CAN be removed
o may be pathologic = secondary invaders
```
95
Primary Vs Secondary Skin Infections
Primary Infections
• bacteria initiate and cause most of the pathology
• occurs in "healthy" skin
• single bacterial species is dominant
• characteristic disease pattern
• antibacterial therapy alone is effective
Secondary infections
• most common
• secondary to other, primary, skin disease
• diseased, non-healthy skin
• multiple species of bacteria
• disease pattern comprised of several diseases
• must treat of underlying cause
96
Surface Pyoderma
* epidermis only
* sequelae to self-trauma and allergic skin disease
* EX: hot spots, early skin fold dermatitis
97
Superficial Pyoderma
o skin down to and including intact hair follicles (folliculitis)
o pustules
o usually secondary to other disease
o recurrence is common and long term management may be difficult
o Ex: puppy pyoderma
98
Deep Pyoderma
```
o tissues deeper than hair follicles - dermis and subcu
o ALWAYS secondary to other conditions
o not common
o VERY difficult to treat
o EX: bacterial cellulitis
```
99
Conditions that lead to secondary skin infections
o Skin infected w/ parasites, virus, fungi
o systemic disease
o physical or chemical trauma
o immunosuppression
100
Diagnosis of Bacterial Infections
Bacterial culture
o distinguish infection from colonization
o Gram or wright’s stain
o Histo & biopsy of intact pustules
101
Staph Infection; basics & encounter for S. aureus, pseudintermedius, hyicus, epidermidis
```
o Facultative anaerobe
o Gram (+) cocci
o Aureus, pseudintermedius, hyicus, epidermidis
```
Encounter
o Long lived in environment
S. aureus
• transient flora
S. pseudintermedius
• transient flora
• disease in dogs
S. hyicus
• transient flora
• exudative epidermitis in pigs
S. epidermidis
• resident flora,
• rarely a skin pathogen
• can cause deeper opportunistic infections
102
Staph Infection; Entry, Immunity, Diagnosis, Treatment
Entry
o Little resistance to staph colonization
o High resistance to deeper infection or dz
o Colonizes by binding to fibronectin on damaged epidermis
Immunity
o Opsonization by Abs
o phagocytosis by neutrophils and macrophages
```
Diagnosis
o smears – Gram’s stain and cytology
o culture and sensitivity
o surgical biopsy and histopathology
o commonly see mixed bacterial infections
```
Treatment
o must correct underlying/predisposing causes
o antibiotics
o need sensitivity test
103
Staph Infection; virulence factors
o not all strains produce all virulence factors
o host factors play a major role
o balance btwn staph growth and opsonization/phagocytosis
Capsule
• resist phagocytosis
proteases
• enzymes aid spread by digesting tissue & damaging skin
exotoxins
• leukocidin kills leukocytes
• alpha hemolysin causes vasoconstriction & dermonecrosis
• coagulase forms clot & protects from phagocytosis
104
Dermatophilus congolensis; basics & encounter
o Gram (+)
o Facultative anaerobe
o obligate parasite
o divides longitudinally, then transversely
o forms parallel rows of coccoid cells (railroad tracks)
Encounter
• On skin of carrier animals
• Does not survive in soil but can persist in scabs for up to 42Mo
• Motile bacteria spores (zoospores)
• Direct contact btwn animals
• Indirect contact via mechanical vectors
105
Dermatophilus congolensis; Entry & Damage
Entry
• Motile bacteria spores invade debilitate epidermis ->
• migrate to epidermal surface beneath stratum corneum due to increased [CO2]
->
• bind to epidermal cells ->
• colonize at epidermal-dermal junction
->
• form elongated bacteria (hyphae) ->
• hyphae divide into motile cocci (zoospores)
Damage
• exudative epidermitis
• activates alternative complement pathway ->
• neutrophils
->
• acute inflammation and dermal cell necrosis ->
• new layer of epidermis forms below damaged upper layer
->
• separation and scab formation ->
• organisms remain primarily in scab
106
Dermatophilus congolensis; diagnosis, treatment, prevention
Diagnosis
• clinical signs
• most commonly seen in cattle, sheep, horses
• rarely seen in dogs, cats, humans
• painful, but NOT pruritic
• impression smear of fresh lesion
• Wright-Giemsa or Gram's
stain
• visualize cocci and "hyphal” structures
• bacterial cultivation (rarely necessary)
Treatment
• Eliminate predisposing conditions
• Remove crusts and treat w/ iodine or dyriung agent
• Penicillin
Prevention
• Vx w/ D. congolensis in tropical countries
