Exam 1 Flashcards

(56 cards)

1
Q

What is an obligate pathogen?

A

One that if present causes disease. Example, Bordetella bronchiseptica.

Upper respiratory infection: Kennel cough - Bordetella bronchiseptica, Infectious coryza (chickens) Avibacterium paragallinarum, Strangles Streptococcus equi.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the Establishment of infection occur?

A
  1. Encounter
  2. Entry
  3. Multiplication and spread
  4. Damage
  5. Outcome

Each event requires breach in the host-defense and the way a bacteria combats host-defense decides the outcome of the infection.

Infection in balance with immunity
Disease = bolus of infection * virulence/ host immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Bacterial Shape and arrangement

A
Coccus: spheric
Coccobacillus: longer spheric
Bacillus: rod
Vibrio: curved rod
Spirillum: spirochete-like
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Terminology

A

Gram Staining

  • Gram positive: purple. Retain crystal violet stain, thick peptidoglycan wall
  • Gram negative: pink/red, do not retain the crystal violet stain. Thin peptidoglycan wall.
  • Strain: genetic variant
  • Serotype: serologically and antigenically distinct, like a subgroup.
  • Serovar: synonym for serotype.
  • Oxidase positive/negative: Positive (when the color changes to dark purple within 5-10 secs). Bacteria that produce cytochrome c oxidase, an enzyme of the bacterial electron transport chain, which oxidizes the test reagent. Mostly Aerobic bacteria.
  • Catalase positive/negative: Some bacteria have the enzyme Catalase, which facilitates cellular detoxification, it neutralizes H2O2.
  • Coagulase: clotting reaction. It clots plasma in the presence of its activator. As a result of coagulase-activator reaction, a substance similar to Thrombin is produce, which converts fibrinogen to fibrin. S. aereus is coagulase positive.
  • CAMP test: (Christie–Atkins–Munch-Peterson) test to identify group B Beta-hemolytic streptoccocci. Zone of Co-hemolysis phenomenon on sheep blood agar.
  • Blood agar: hemolytic activity detection
  • MacConkey agar: selective and differential media for non-fastidious gram negative rods, particularly Pseudomonas spp. Gram-negative enteric bacteria and the differentiation of lactose fermenting from lactose non-fermenting gram-negative bacteria.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Clinical case example

A
  1. History, Physical exam
  2. Create a problem list
  3. What are the differentials?
  4. Diagnostic plan
  5. Treatment decision and prevention plan.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Establishment of bacterial and fungal infections

A

Pathogen: organism that causes disease in an immunocompetent host

Pathogenicity: the ability of an organism to cause disease in an immunocompetent host

Virulence: is a relative measure of pathogenicity. For example, a highly virulent vs. weakly virulent strain of a pathogen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Virulence

Why do some animals develop disease while others do not?

A

Virulence can be measured in a few different ways

  • ID50 or infectious dose 50: is the number of bacteria needed to cause an infection in 50% of exposed animals.
  • LD50 or lethal dose 50: number of bacteria needed to cause death in 50% of exposed animals.
  • MLD or minimum lethal dose: for example, MLD of botulinum toxin for mice is <0.01 ng (1mg would kill 100 billion mice).
  • Differences in the susceptibilities of individual animals: for example, the ID50 is 1000 for one animal, but 10 for another.
  • Differences in the immune status of the host: immunocompromised vs. immunocompetent
  • Differences in the breed susceptibilities: some breed are predisposed to some diseases due to genetic differences.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Definitions

A

-Infection: presence and replication of an obligate pathogen within a host, implies overt disease or capability of causing disease.

  1. Apparent infection: infection with overt disease.
    - Acute: SHORT time course, outcome may be death, recovery or progression to chronic. Ex: E. coli in canine
    - Chronic: PROLONGED time course. Ex: Tuberculosis
  2. Inapparent infection: infection without the presence of overt disease, generally results in colonization
    - Colonization: presence of an organism without clinical or subclinical disease. However, it is replicating.
  3. Carrier infection: persistent infection with a pathogen that may have previously caused disease, may later progress to apparent infection, Ex: Anaplasma marginale in cattle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Events in Establishment of Infection

1. Encounter

A
  1. Encounter: microorganism meets the host
    - Begins at birth
    - Challenge with exogenous organisms: possible outcomes:
    - Most common: do not gain entry or eliminated
    - Less common: colonize to form normal flora
    - Very few cases: cause disease
    * Disease is more of the exception than the rule*
  2. All neonates receive immunologic protection at birth: example, ETEC (enterotoxigenic E. coli) in calves due to failure of passive transfer of IgG, also calves have receptors in intestine that allow organism to bind.

LATER ENCOUNTERS
-Exogenous: obtained from an external source. Ex, food-borne Salmonella infection.
Control: modification of external source in some way, disinfectants, decreased contact, etc. The goal is to eliminate from host tissue.
-Endogenous: due to normal flora that is present in or on the host’s body. Ex: Pseudomonas aeruginosa infection in immunosuppressed patients.
Control: difficult. The goal is to eliminate from tissue NOT from host.

  1. Entry: microorganism or toxin enters the host body
  2. Multiplication and spread: microorganism and or toxin multiplies and spreads inside the host.
  3. Damage: host’s immune response and damage due to invasion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. Entry
A

Several routes: Inhalation, ingestion, etc.

A. Ingress: pathogen enters without crossing epithelial barrier. Inhalation, ingestion, infection of mucus membranes.

  • Inhalation: protection by constitutive host defenses. Any kind of damage (cilia/mucus) predisposes to bacterial infection. Ex: BRSV M. hemolytica infection in cattle.
  • Ingestion: High concentration of bacteria (resident microflora) competes with invader and prevent infection/colonization. Ex: Enterotoxigenic E. coli in calves.
  • Direct infection of mucus membranes: Examples, conjunctivitis, UTI, Keratoconjunctivitis in cattle Moraxella bovis (pink eye)

B. Penetration: pathogen penetrates deeper into tissues

  • Pathogen dependent: specific bacterial structures bind to receptors and facilitate penetration. These structures are considered virulence factors as they contribute to the virulence of the pathogen. Ex: S. aureus adhesins, invasins, toxins.
  • Pathogen independent: vector-borne transmission, cathaters, blood transfusions.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. Multiplication and spread

What determines multiplication and spread?

A

-Inoculum size: is a prime determinant in outcome of exposure.
-Surgical prep goal is to decrease or eliminate inoculum size. 99% of neutralization of 10^5 organism still leaves 10^3 organisms. Pseudomonas aeruginosa (non-pathogenic) at high dose 100 billion/L enough to overwhelm skin defenses and cause infection in immunocompetent people.
E. coli 0157:H7 is highly pathogenic, 10-100 organisms can cause serious illness.

  • Incubation period: time between exposure and onset of disease/symptoms. During this time bacteria are multiplying to get large enough in number to cause disease.
  • Nutritional requirements of bacteria: can become a limiting factor, most bacteria need iron. Host increases transferrin levels -binds free iron.
  • Temperature: some organisms can’t grow at certain temperatures. Som ringworm fungi can’t survive at 37C
  • Some bacteria spread via blood: bacterimia. Transient bacteria is common, but rapidly cleared by host’s immune defenses.
  • Bacteria in blood may be cell-associated: Brucella abortus is found in monocytes, hidden to some extent from immune system.
  • Some bacteria spread via lymphatics: Streptococcus equi spreads from tonsils to submandibular LN (results in strangles) and can spread to medialstinal LN (bastard stangles).
  • Some bacteria spread via fascial plane: Pseudomonas aeruginosa is highly motile and spreads this way (Hot tub folliculitis).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. Damage
A

Three ways microbes damage host

  1. Release of endotoxin: the constitutive part of gram negative cell wall. Also called Lipopolysaccharide (LPS) Lipid A component is responsible for endotoxin activity.*
    - Action is non-specific and dose-dependent. It can have physiological and or pathological effects, very harmful at high dose levels.
  2. Production of exotoxin: Secreted bacterial proteins, may be from gram positive or gram negative.
    Have very specific and often different actions. Most are encoded by plasmids or bacteriophages.
  3. Damaging hist response: Inflammation, immune scape, immunopathology.

-Inflammation: beneficial in moderation, but harmful in excess.
-Immune scape: Streptococcus pneumoniae or Klebsiella carry capsule.
Rickettsia escape from phagosome and Ehrlichia inhibit phago-lysosomal fusion.
Bacillus anthracis produces toxins that damage phagocytes.
-Immunopathology: Immune complexes- Purpura hemorrhagica (S. equi)
Granuloma formation- Rhodococcal pneumonia, Tuberculosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Infections of the skin I-II

Anatomy of the skin

A
  • Hair
  • Sebaceous Gland
  • Sensory nerve ending
  • Epidermis
  • Dermis
  • Subcutaneous tissue
  • Capillaries, sweat glad, muscle, fat, collagen, fibroblasts, arteriole.

Physical barriers:

  • Hair/fur: prevent direct contact
  • Stratum corneum: inert and impermeable layer
  • Temperature and pH: too cold/unfavorable pH for optimal growth or many. Skin pH acidic in healthy tissue.

Chemical Barriers:

  • Fatty acids: bacteriostatic
  • Inorganic salts: high salt concentration
  • Transferrins: bind iron needed for bacterial growth

Immunological defense

  • Site for interactions between immune cells and antigens
  • Prevent deeper invasion

Normal Flora

  • Bacteria and fungi
  • Protective
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Normal Flora of the Skin

A

Number and species affected by several factors, including:
-Hydration, general health, physical and chemical environment, salt-transferrin, other bacteria nutrients, antibiotic production.

Resident Flora

  • Live and multiply in the skin (obligate parasites)
  • Form a permanent population
  • Cannot be eliminated
  • Normally are harmless
  • Examples: Coagulase-negative Staphylococcus, alpha-hemolytic Streptococcus, Micrococcus spp. etc.

Transient flora

  • Acquired from environment or mucous membranes
  • Most do NOT multiply efficiently on skin - just there
  • Are transient - CAN be remove or eliminated
  • May be involved in pathological processes as secondary invaders
  • Examples: Coagulase-positive Staphylococcus, E. coli, Proteus, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Bacterial infections of the skin

A

A. Primary: Initiate and cause most of the pathology.

  • Occur in otherwise “healthy” skin - predisposing factor, if any, is minor.
  • Single bacterial species is dominant
  • Characteristic disease pattern evident - consistent disease syndrome.
  • Antibacterial therapy is effective - underlying problem is less significant.
  • Grease pig disease: Staphylococcus hyicus
  • Dematophilosis: Dermatophilus congolensis (horses). Train rail-like morphology.

B. Secondary: associated with other conditions or infections. They join the party later.

*Demodectic mange and Staphylococcus pseudintermedius causes pyoderma.

-Predisposing conditions for secondary skin infections: parasites, viruses, fungi, etc.
Other local predisposing factors: humidity, skin folds, systematic disease.
-Hypothyroidism, Cushing’s disease.
-Physical or chemical trauma: surgical incisions, catheter placement, etc.
-Immunosuppression, corticosteroid therapy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Diagnosis of Bacterial skin Infections

A

Bacterial Culture

  • Must distinguish between colonization and infection.
  • Identification of bacteria in primary and secondary infection is useful if also consider the presence of normal flora. Ex: isolation of Staphylococcus pseudintermedius alone is not enough.

Need Correlation

  • History: predisposing (underlying) factors
  • Clinical signs: Pustules, prulent exudate, crusts.
  • Bacterial isolates: virulence

Diagnostic work up considerations

-Sampling for bacterial culture: Do not sample open tracts or erosions (use unopened pustule).
Punch biopsy of lesion - NOT into formalin for culture.

-Direct smears: Gram’s and Wright’s stains
Gram’s stain: number and type of bacteria, presumptive ID; initiation of therapy
Wright’s stain: presence/type inflammatory cells, degenerate neutrophils with bacteria within cell is indicative of infection

Histopathology and surgical biopsy

  • When to biopsy: any dermatosis that is unresponsive to treatment for 3 weeks or any recurrent dermatosis
  • Advantages of early biopsy: avoids nonspecific, masking, and misleading changes of chronicity; allows rapid institution of specific therapy.
  • What to biopsy: intact pustules, take multiple biopsies, try to obtain primary lesions (avoid those marked by excoriation and chronicity).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Classification of Skin Infections (Pyodermas = pus).

A
  • Based on the depth of skin involvement: depth of infection
  • Distinctions are clinically useful: deeper the lesions, more likely to be significant problem.

Surface Pyoderma: involves the epidermis only. Including intact hair follicles.

  • Often sequelae to self-trauma or allergic skin disease. Examples, hot spots and early skin fold dermis.
  • Pustules are present (mini abscesses)
  • Recurrence is common and long-term management may be difficult.
  • *Epidermis, maybe dermis

Deep Pyoderma: involves tissues deeper than hair follicles.

  • Almost always secondary to other contributing factors
  • Not common, but VERY difficult to treat.
  • *Epidermis, dermis, and subcutaneous layer involvement**
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Infection of the Skin, Fungal

A

Dermatophytosis
Seborrheic dermatitis
Sporotrichosis
Phythiosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Dermatophytosis (Ringworm infections)

What genera causes the infection?

A
  1. Microsporum: 17 conventional species.
    - The most significant are M. canis, M. gypseum, M. nanum and M. gallinae.
  2. Trichophyton: 20 species, The most common are T. mentagrophytes, T. equinum, T. verrucosum.
  3. Epidermophyton: people
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Characteristics and other information about Microsporum canis and Trichophyton (dermatophytes).

  • Hyphae: supports spore-bearing structures.
  • Conidia: types of spores (asexual reproduction) formed on conidiophores.
  • Sporangiospores: formed within sporangium
  • *Mycoses: tissue invasion
A
  • Large, rough, thick-walled multiseptae macroconidia (large multi-celled conidia).
  • Macroconidia vary in shape from fusiform to a obavate.
  • Microconidia are sessile or stalked, clavate, and usually arranged singly along the hyphae.
  • M. canis: spindle-shaped
  • M. gypseum: Boat-shaped
  • M. nanum: Pear-shaped or ovoid macroconidium.

Trichophyton

  • Macroconidia are cylindrical, clavate to cigar-shaped, usually thin-walled and smooth.
  • Rarely produced and in small numbers
  • Both genera attack skin, hair, nails, horns, and claws.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Clinical signs of dermatophytosis

A
  • Vary according to immune status of host and strain.
  • Alopecia, erythema (abnormal redness of the skin), scaling, crusting, annular-ringed lesions, and vesicles or papules.
  • Trichophyton spp. infections generally more severe due to inflammation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Canine ringworm

A
  • Circular lesions up tp 2.5cm in diameter, commonly on face, elbows, and paws.
  • Intense inflammation caused by T. mentagrophytes KERION, swelling, ulcerations, and purulent exudation.
  • M. gyseum (compulsive burying of objects in soil)
  • T. mentagrophytes (good rat catchers)
  • T. erinacei (avid hedgehog-worriers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Feline Ringworm

A
  • Usually caused by M. canis and cats are reservoirs.
  • Often asymptomatic, public health risk.
  • Cs: alopecia, mild scaling, folliculitis and generalized hair loss.
  • Most common in kittens or immunocompromised
24
Q

Bovine Ringworm

A
  • Common disease, calves most susceptible
  • Incidence higher in winter
  • Mostly Trichophyton verrucosum.
  • Severe inflammation, pruritis, and secondary bacterial infection may occur.
  • Spontaneous resolution of infection follows
25
Porcine ringworm
- large breeds most commonly affected - Higher incidence due to humidity, stocking density, and poor sanitation - M. nanum most common followed by M. gyseum, M. canis and T. mentagrophytes (geophilic). - Lesions: located anywhere in body, circular, roughened, mildly inflamed, usually no loss of hair.
26
Equine ringworm
- Trichophyton equinum and M. gypseum most common - Lesions: multiple dry scaly raised lesions on any part of body. - Inflammation and production of exudates cause hair to mat together, and enlarged lesions create a moth-eaten appearance. - infection often become chronic and subclinical, but recur during stress.
27
Ringworm of poultry
- M. gallinae - Called 'favus' or "white comb" - White patches in comb of infected males. May enlarge and coalesce to entire comb is thick and white. - Occasionally spread to feathers
28
What is the more infective fungal stage?
- Spores are the major infectious form - They are shed by infected animals in to the environment and may remain liable for months - Transmission direct contact or by exposure to arthroconidia (arthrospores: spores formed during the process of hyphal fragmentation) in the environment or on fomites.
29
How does entry occur?
- Enters the skin through abrasions - They do not invade or survive on living cells or areas of intense inflammation - Spores germinate and the fungus grows on the stratum corneum of the skin and nails - Crusty skin, bridle hair
30
How does multiplication occur? Spread?
- Virulence factors: proteases, keratinases and elastases * **Infection with dermatophytes evokes intense inflammatory response. As a result fungal growth stops and moves to the next follicle. This continues and leads to circular lesions with a healing center*** - Most infections clear within weeks or months
31
Diagnosis
1. Wood's lamp examination of lesions. - Not very sensitive (50-60%) - Fluoresce green 2. Direct microscopic examination - Use 10-20% KOH to examine hair and scales from lesions. - Better results - Ectothrix arthroconidia on hair - Hyaline: clear, Dots outside hair: ectothrix 3. Culture: clean area with alcohol - Hair clipped to quarter of an inch - Sample from the periphery of a lesion - scrape skin and pluck hair - Dermatophyte test medium (DTM) for culture
32
DTM: dermatophyte test medium Microscopic Morphology
- Cultures best incubated at 25C (spores, fungi) 37C, yeast form. - T. verrucosum in cows 37C - Growth in red slant before 10 days = dermatophyte - Growth with yellow slant that turns red after 10 days = non-dermatophyte - Dermatophytes utilize peptones in a DTM producing alkaline (RED) reaction. - Most contaminant fungi utilize sugars first produce acid (yellow) then utilize protein (RED) * *Nicotinic acid: required for T. equinum * *Inositol and thiamine: T. verrucosum Microscopic morphology - Lactophenol cotton blue wet mounts of fungal growth - Trichophyton may develop few macroconidia and are more difficult to identify - Nutritional requirements, temperature tolerance, urase production, and in vitro hair perforation help identify Ectothrix.
33
Treatment, control and prevention | Zoonotic Potential
-Removal of hair, shampoos, dips, sprays, topical antifungal. Systematic: - Griseofulvin - Azoles: Ketoconazole, clotrimazole, and itraconazole. - Terbinafine - Treat until 3 negative weekly cultures. Control and Prevention - Clipping, topicals, sprays, etc. - Clean up environment and fomites - Wash bedding. - 10% bleach solution - Vaccination Zoonotic potential -Most common zoonoses: M. canis, T. verrucosum
34
Seborrheic dermatitis
Dogs - Lipophilic yeast belonging to genus Malassezia (normally present in ears) - Malassezia furfur, M. pachydermatis, M. sympodialis, M. globosa, M. obtusa, M. restricta, M. dermatis, M. nana, and M. slooffiae. - M. pachydermatis also causes OTITIS EXTERNA. Encounter/entry - Normal in cutaneous flora, anus, lips, skin, vagina, anal sacs, external ear canal of dogs. - Opportunistic pathogen - High humidity and excessive wax accumulation - hairy and pendulous ears - Neoplasm - Allergies - Change in quality or quantity of sebum; presence of other dermatoses. - Recent antibiotic or glucocorticoid therapy - Trauma Clinical Signs - Superficial: regionalized, face, feet, perineum, etc. - Face rubbing, licking - Skin erythematous and scaly - Secondary alopecia and excoriation (when animal bites due to itch) - Hyperpigmentation and lichenification with seborrhea as infection becomes chronic. - Overgrowth due to predisposition factors (e.g., allergies, Seborrhea) - Maybe allergic reaction to metabolic by-products of the yeast. Diagnosis - Consistent clinical signs - Poor response to antibiotics, glucocorticoid and immunotherapy - Demonstration of the typical yeast cells on skin scrapings or swabs - SHOE PRINT or peanut-shape cells, impression smears. Treatment and control - Aimed at reducing number of organisms and identification plus removal of predisposing factors. - Local/mild: selenium sulfide (shampoos), chlorhexidine, miconazole, ketoconazole. - Systematic: ketoconazole, plus itraconazole daily Zoonotic potential - Malassezia pachydermatis is emerging zoonotic pathogen - outbreak in neonatal care unit
35
Sporotrichosis
SUBCUTANEOUS -Sporothrix schenckii: humans and animals affected. Dogs - Cutaneous, multicentric - Lymphocutaneous: predominant syndrome, nodules along lymphatics - Disseminated: rare, potentially fatal * *Lesions begin at the point of entry and consists of subcutaneous nodules that ulcerate and heal. - Disease may follow the course of lymphatic vessels and lymph nodes - NOT PAINFUL NOT PRURITIC Sporothrix schenkii - Thermally dimorphic dematiaceous fungus -Mold at 25C, yeast at 37C -Most common in tropical and sub-tropical America "Rose handler's disease" -Isolated from soil, peat moss, and wood, vegetation. IN HORSES -cutaneous nodules that develop along the lymphatics, usually medial surface. 1-5cm in diameter and may ulcerate. Zoonotic Encounter/Entry/Spread - Conidia or mycelia through broken skin - INSIDE the host: mycelial form changes to yeast form - Lymphocutaneous manifestations, erythematous nodules at the site of entry - Microabscesses and granulomas - Spreads along lymphatics - Regional lymph node may be involved Virulence factors: - Thermotolerance - Acid phosphatase, proteinases I and II - Adhesion to the host's body somewhere Diagnosis - Direct microscopic examination (feline specimens) - exudate or aspirate from lesion - Cigar-shaped yeast cells, may be seen in macrophages or extracellularly - Lesions from cats tend to have large numbers of yeast cells. - FAT on impression smears - Cultures: 2-7 days Sabouraud dextrose agar at 25C. Mold colonies colored, wrinkled, leathery and turn black/grey with age. - In brain-heart infusion agar 5% blood incubated 37C, 5-7% CO2 for 3-5 days. Yeast colonies are soft and white to cream colored Treatment - Iodide in humans and animals - Azole also effective - Cats sensitive to iodide, recommended itraconazole - 3-4 mts for resolution Zoonosis from cats: lesion exudates and feces contact
36
Pythiosis
- Chronic granulomatous disease - Phytium insidiosum pathogen, fungal-like organism - Lack chitin and ergosterol - Gulf Coast states - Horses and dogs most affected Equine Pythiosis (Bursatti, Swamp fever, leeches) - Cutaneous and subcutaneous mycosis - Limbs and ventral abdomen - Ulcerative lesions - Pruritic, discharge, mucosanguineous exudate, self-mutilation/trauma from itchiness. - Lesions contain 'kunkers' or 'leeches' which are irregular, yellowish concretions that form in sinus tracts - Necrotic coral-like seen inflammation Pythium insidiosum in horses Diagnosis - Direct exam and/or histopathology - Large, hyaline, non-septate hyphae - Culture needed for definitive diagnosis to distinguish from zygomycosis - PCR, ELISA - Lateral pegs or perpendicular branches Treatment - Radical excision is best, if possible - Poor response to therapy Caninie pythiosis - GI disease, cutaneous, and subcutaneous - Infiltrative pyrogranulomatous enteritis - Subcutaneous lesions do occur in days - Poor prognosis - Surgical excision best NO zoonotic potential
37
Buccal Cavity Infections | What are the two buccal cavity infections and pathogens?
1. Wooden Tongue: antinobacillosis = soft tissue getting harder 2. Lumpy Jaw = antinomycosis = hard tissue getting softer.
38
Wooden Tongue | What is the pathogen? Treatment? characteristics? Clinical signs?
-Soft tissue of mouth primarily in adult cattle, but sheep, pigs, horses and dogs can become infected - Antinobacillus lignieresii * *Gram Negative coccobacilli** Clinical sigs - Very hard, diffusely swollen tongue - Excessive salivation - Inability to prehend food normally - Visible enlarged tongue that protrudes from the mouth - On palpation, the tongue will feel very hard and it is painful - Rare: large granulomas embedded in the tongue - Pathogen is always present in the GI tract. Encounter/Entry - Part of normal mucosal flora upper GI tract - Wound or trauma usually caused by straw or barley awns Symptoms - Localized infections, but can spread via lymphatics to other tissues. - Can be confused with lumpy jaw - Inability to prehend food - Loss of condition - May die from starvation - Chronic infection may result in large abscesses with granules, creamy pus discharge Diagnosis - Clinical signs, lesions, history (rough feed) - Confirmatory Dx: Culture, Gram-negative bacteria Rod. - PCR, 16S gene - MacCokey media growth - Biochemical analysis - Pus from abscesses crushed between two slides: club-like spicules of calcium phosphate. - Granulomatous abscesses - Club colonies (calcium phosphate around bacteria) - No reliable serological tests Antinobacillus lignieresii characteristics - Gram negative - Rod shape - Facultative anaerobe - Small, sticky, non-hemolytic colonies in BAP (blood agar plate) Treatment - Sodium iodide: IV 1-2 times per week. - Systematic antibacterial: ceftiofur, penicillin, ampicillin, florfenical, and tetracyclines. - Surgical removal of granulomatous if necessary Prevention -Avoid straw, coarse stemmy feedstuffs.
39
Lumpy Jaw = Antinomycosis = hard tissue getting softer
Pathogen: Actinomyces bovis -It has also been isolated from nodular abscesses in the lungs of cattle, infrequently in other mammals Clinical sigs - Mandibular lesion of suppurative (formation and conversion to pus discharge )and proliferative osteomyelitis. - Distortion, loose teeth (difficulty chewing), dyspnea from swelling into the nasal cavity - At first lesion small growing, firm mass - With or without drainage, purulent exudate - Enlargement of the mandible Encounter/Entry - Actinomyces bovis: part of the normal flora of ruminants - Via penetrating wounds from wire or coarse hay/sticks - Gram positive - Anaerobic bacteria Diagnosis - Based on clinical signs - Gram-positive - Culture from lesion sample - Cytology - Club-shaped rods filaments (sulfur granules) - Radiography also useful Treatment - Sodium iodide: IV 1-2 per week - Concurrent administration of oxytetracycline, penicillin or florfenicol recommended Prevention -Avoid course, rough, stemmy feedstufs
40
Wooden tonge vs. lumpy jaw
Wooden tongue: - Gram negative - Actinobacillus lignieresii - Granulomatous abscesses - Granules in exudates: greyish-white - Club Colonies - Spreads via lymphatics - No bone involvement - Facultative anaerobe Lumpy Jaw - Gram-positive - Actinomyces bovis - Bone involvement - Jaw region - Yellow 'sulphur' granules 1-3 mm - No spread via lymphatics - Anaerobic (O2 kills it)
41
Buccal cavity infections Candida albicans Aspergillus spp.
Fungal: Candidiasis, Aspergillosis | -Necrotic stomatitis/pharyngitis bacterial
42
Candidiasis
- Localized mucocutaneous disease - Pathogen: Candida albicans Candida albicans - Normal inhabitant of flora in nasopharynx, GI tract, and external genitalia. - Opportunistic Encounter/Entry - Disruption of mucosal integrity - Urinary catheters - Antibiotic use - Immunosuppression **Most frequently in birds** Thrush, Crop mycosis, Sour crop. -Disease of GI tract in chickens, turkeys, young chicks and poults are most susceptible Clinical signs - Lesions in the crop - Thickened mucosa - Whitish, raised pseudomembranes - Lesions in esophagus, mouth - Swallow ulcers and sloughing of necrotic epithelium may be present - Listlessness and inappetence Control/Prevention/treatment - Minimizing antibiotic use - Nystatin and fluconazole Tx Dogs and cats - Exfoliative dermatitis - Muzzle, inguinal area, scrotum, dorsal or lateral aspect of feet - Otitis externa in foxhounds - GI candidiasis associated with gastric ulceration in foals and calves - Pigs cutaneous and mucocutaneous infection Diagnosis -Scrapings or biopsy specimens from mucocutaneous lesions C. albicans - Void, budding yeast cells with thin walls - Pseudohyphae and true hyphae may be seen in the same specimen - Culture in Sabourad's dextrose agar colonies white to cream color looks like Staph, but a lot larger. - Culture 2-3 days at 25-30C * *Germ tube test: differentiation from other Candida spp. Several colonies grown in animal serum at 37C for 3 hours = Short term tubes unique - Biochemical and Molecular test commercially available
43
Aspergillosis | Guttural pouch mycosis, infection of nasal and paranasal tissue
Pathogen: Aspergillus spp. - A. fumigatus, A. terreus - Primarily a respiratory infection - Opportunistic - Careful when taking samples, wear gloves - Deep into tissue to get sample Guttural Pouch mycosis - Caudo-dorsal aspect of medial guttural pouch, over the internal carotid artery - Damage to cranial nerves and the arteries within the mucosal lining of the pouch - Mycotic plaques cause fungal erosion of the wall of internal and or external carotid arteries - Hemorrhage is spontaneous and severe may be fatal - Cranial nerves IX, X. Aspergillus spp. - Periodic acid-Schiff (PAS) stain - Characteristic filamentous hyphae present in large numbers, biopsy. Diagnosis -Endoscopic examination of the guttural pouch Treatment -topical and systematic antifungal therapy, based on sensitivity testing
44
Canine nasal Aspergillosis
- Can lead to bone loss - The mucosa of the nasal and paranasal sinuses may be covered by a layer of gray-black necrotic material and fungal growth. - Loss of bone definition on radiographs - Lethargy, nasal pain, ulceration of the nares, sneezing, unilateral or bilateral sanguinopurulent nasal discharge, frontal sinus osteomyelitis and epistaxis (nose bleeding). Diagnosis - clinical signs - Rhinoscopy - presence of fungal plaques - Biopsy for histopathology or cytology and culture - Radiology - Microscopy of tissue samples : wet mount using KOH * *Hyaline, septate hyphae that branch dichotomously with a 45 degree angle - Easy to identify via characteristic conidial arrangement - Remember that this is a ubiquitous and common fungus!! - Phyloconidia: pretty bulbs Treatment -Topical azole (clotrimazole) delivered as 1-hour infusion Health risk -Immunosuppressed individuals at risk
45
Necrotic stomatitis/laryngitis/pharyngitis | Calf Diphtheria
- Infectious disease affecting pharynx, larynx, and oral cavity - Pathogen: fusobacterium necrophorum Fusobacterium necrophorum (gram-negative) - part of the normal flora - Inhabits mouth, intestines, genital tract of herbivores and omnivores. - widespread in the environment - Considered as a secondary invader - Gains access through traumatic injury of the oral mucous membranes - Diphtheria often occurs as necrotic dermatitis in calves <3mts of age ``` Clinical sigs -difficulty nursing -Diarrhea -Painful swallowing -Odor in breath (necrotic stomatitis) -Swollen cheeks -Lump in neck -Excessive salivation (necrotic stomatitis) -Fever (necrotic stomatitis) -Tachypnea -Loud wheezing -Pharyngeal edema -Continuous bawling Untreated calves usually die within 2-7 days from toxemia and pneumonia ``` Diagnosis - Based on clinical signs - Lesions on necropsy identified - Ulcers may extend into nasal cavity, trachea, or lungs Fusobacterium necrophorum (gram-negative) - Smear from deep tissue in the lesions - Filamentous, beaded, gram-negative bacteria. - culture in blood agar in anaerobic environment - irregular staining, long, non-branching filamentous forms Treatment - sulfonamides or procaine penicillin G - Flunixin meglumine or aspirin may be given to reduce fever and inflammation - supportive care IV fluids, shelter, adequate ventilation. - The prognosis is good if the infectious disease is detected very early and aggressive treatment is administered
46
Eye and Ear Infections Moraxella bovis (IBK: infectious bovine keratoconjuctivitis) Moraxella bovoculi Moraxella ovis
Infectious bovine keratoconjuctivitis (IBK) "Pink Eye or New Forest Disease" -Pathogen: Moraxella bovis Moraxella bovis - Gram-negative rods, usually in pairs. - Aerobic, non-motile - Growth in enriched media - Catalase positive and oxidase-positive - Proteolytic (Hydrolysis of proteins), unreactive with sugar substrates. - virulent strain are firmbriated and hemolytic - Short-lived in environment - Survives in salivary organs and on flies for 72 hours - Age related immunity - Asymptomatic carriers harbor M. bovis in nasolacrimal ducts, nasopharynx and vagina. - Transmission via direct contact, aerosols, and through vector flies. - Highly contagious - Affects superficial structures of the eyes - Affects mostly animal <2 years of age - Causes economic losses - Decreased weight gain - Decreased milk production - Short-term disruption of breeding programs - Treatment costs M. bovoculi -Isolated from animals affected by IBK. Possess RTX toxin but pathogenicity unproven M. ovis -Isolated from a number of sites in farm animals but pathogenicity uncertain Clinical Signs of IBK - Blepharospasm, lacrimation, conjunctivitis, photophobia - Keratitis, corneal opacity and ulceration; occasionally panophthalmitis and permanent blidness - In mild cases cornea heals but there may be permanent scaring. - Incidence lower in cattle with darker ocular pigmentation Predisposing factors - Age: <2 years of age - Breed: Bos taurus - Fly activity: increase vector activity - Ocular irritants: dust, tall grasses, grass seeds, wind, cold ambient temperatures - Concurrent infections: Herpesvirus 1 or Thelazia spp. - Vitamin deficiency: Vitamin A Virulence Factors: - Fimbriae (Q fimbriae, I fimbriae): adherence to the cornea, stimulate type-specific protective immunity - Hemolysin: (Mbx A) a calcium dependent, pore-forming cytolysin which damages the cell membrane of neutrophils. This is a RTX toxin with hemolytic and cytotoxic activity. - Fribrolysin - Phosphatase - Hyaluronidase - Aminopeptidase Diagnosis - Clinical signs - Isolation of organism via cultural swabs or lacrimal secretions - Organism is extremely fragile, so process samples quickly - Blood and MacConkey agar: aerobically at 37C for 48-72 hours - Rod small shiny friable colonies - Catalase, oxidase positive; pitting of Loeffler's agar M. bovoculi can be differentiated from M. bovis based on positive phenylalanine deaminase test Treatment and control - Use antimicrobials, prevention of ocular irritation - Long-acting oxytetracycline at 72 hours apart - Eye patches - Control flies - Vitamin A supplement - Fimbriae-derived bacterins are of uncertain efficacy
47
Otitis Externa
- Inflammation of the external ear canal - Common problem in dogs and cats Clinical signs - head shaking - Pain - Malodor - Erythema - Erosion - Ulceration - Swelling - Ceruminous gland inflammation Diagnosis - Otoscopic examination - Cytology - Culture Primary cause - allergy - parasites (otodectes, demodex, sarcoptes) - Autoimmune - Foreign bodies - Viral (distemper) - Miscellaneous Secondary causes - Bacteria (Staphylococcus, Streptococcus, Enterococcus, Pseudomonas, etc.) - Yeast: Malassezia - Medication reactions - Overcleaning Predisposing factors - Excessive moisture - Systematic disease - Conformation: excessive hair, pendulous pinna, etc. - Obstructive ear disease - Changes in normal flora
48
Otitis externa in dogs due to Yeast infection
Pathogen: lipophilic yeast belonging to the genus Malassezia -M. furfur, M. pachydermatis, M. sympodialis, M. globosa, M. obtusa, M. restricta, M. dermatis, M. nana, M. slooffiae ***In dogs M. pachydermatis also causes Seborrheic dermatitis*** Clinical signs - Head shaking - Pruritis - Odor - In chronic cases, external ear canal may become filled with a thick waxy brown discharge Encounter/Entry - Malassezia spp. are part of normal flora - Opportunistic pathogens - Normally resides in skin, lips, anus, vagina, anal sacs, and external ear canal of dogs. Predisposing factors - High humidity and excessive wax accumulation - Hairy and pendulous ears - Neoplasm - Allergies - Change in quantity or quality of sebum; presence of other dermatoses; increased moisture - Recent antibiotic or glucocorticoid therapy - Trauma Multiplication/Damage -Overgrowth due to predisposing factors. Seborrhea, allergic reactions to metabolic by-products of the yeast. Malassezia spp. - Shoe-print or peanut-shaped cells - Cytologic exam of affected areas (impression smears) - Broad-based yeast cells, oval elongated. Treatment and control - Therapy to reduce number of organisms and identification - Removal of predisposing factors - Systematic disease: KETOCONAZOLE. Pulse administration and daily administration of itraconazole **Diff-Quick stained smear can quickly determine whether microbial overgrowth is present - Coccal organims usually staphylococcus or streptococcus - Rod-shaped: Pseudomonas aeruginosa, E. coli, or Proteus mirabilis - If a gram stain is not available, ulceration of the ear canal, a slimy green discharge, and cytology that shows rods only is highly suggestive of Pseudomonas infection - Otitis externa with primarily gram-negative rod infection may also be associated with a particular pungent odor - Polymyxin B and fluoroquinolone antibiotics have most successfully controlled Pseudomonas infections.
49
Chlamydial Conjunctivitis
Pathogen Chlamydiaceae family bacteria - Intracellular bacteria - GI tract, repro tract, conjunctiva - Shedding usually from conjunctiva - Spherical intracellular - Unique developmental cycle - Stain with MZN and Giemsa - Energy parasites are able to synthesize ATP - Cell walls lack peptidoglycan but contain LPS family specific - Elementary bodies (EBs): Infectious extracellular form: small, metabolically inactive, NOT MULTIPLY. - Reticulate bodies (RBs): Non-infectious intracellular reproductive: Large, metabolically active, MULTIPLY. -Several members of the family: Chlamydia caviae guinea pigs, Chlamydia suis pigs, Chlamydia psittaci birds sheep, Chlamydia pecorum cattle sheep Most common cause of pink eye in sheep. Clinical Signs -Acute or chronic purulent inflammation of the conjunctiva with or without the presence of keratitis Treatment - Tetracycline-class antibiotics - Systematic administration of antibiotics is preferred because infection may arise from or involve other anatomic sites.
50
Feline Chlamydiosis
- Chlamydia felis (formely Chlamydia psittaci) - Conjunctivitis and rhinitis (less common) - Feline pneumonitis original name, rare lower respiratory tract infection Epidemiology - Direct contact or fomites - Nasal secretions or conjunctival secretions - May shed from repro tract - Most susceptible <1 year of age Clinical signs - Incubation period ~ 5 days - Uni or bilateral conjunctival congestion, clear ocular discharge - Chemosis (swelling of the conjunctiva tissue around the cornea) and blepharospasm (involuntary winking) evident - Secondary infection with Mycoplasma felis, Staphylococcus spp. - Ocular discharge mucopurulent - Conjunctivitis accompanied by sneezing and nasal discharge - Resolves without treatment in a few weeks when animal is healthy Diagnosis - Conjunctival swab - Giemsa-stained smears may reveal intracytoplasmatic inclusions - Isolation of organism in cell lines or embryonated eggs - RBs (reticular bodies) intracellular, non-infectious, metabolically active - EBs (elementary bodies) extracellular, infectious, small. Not active. - ELISA kits, lipopolysaccharide antigen - Conventional and real-time PCR - Complement fixation test, ELISA, immunofluorescent test to detect Chlamydia antibodies Treatment - Tetracyclines antibiotics of choice - Live vaccines available reduce clinical effects but does not prevent infection - Zoonotic, small number of cases from guinea pigs - **Wear gloves**
51
Guinea Pigs inclusion Conjunctivitis
- Chlamydia caviae - Susceptible 1-2 mts of age - Subclinical disease may occur - Rhinitis, lower respiratory tract disease, genital infections causing salpingitis and cystitis in female guinea pigs, urethritis in males may also occur
52
Leptospiral uveitis in horses
-Water-borne Leptospira spp. - Motile, tightly coiled spiral organism with hooked ends - Gram-negative - Stain poorly, need dark field or phase contrast microscope - Serologically and epidemiologically diverse > 250 serovars - Can persist in renal tubes or genital tract - Worldwide zoonosis - Carriers mice, asymptomatic - Enter body through abraded skin or intact mucous membranes - Humans infected via contact with infected urine
53
Leptospiral uveitis
Inflammation - Ciliary body - Iris - Choroid body - Late complication = reversible or irreversible blindness in humans and horse - Inflammation of the uveal tract of the eye; iris, ciliary body, choroid
54
Human Leptospiral uveitis
- Weil 1886 - Acute and non-granulomatous pan-uveitis - Timely treatment = good prognosis - 10% of total uveitis endemic in India, one-third infectious cases - Hypopyon and cataract - Vitreous membranes attached to the dis - Hyperemic disc with retinal vasculitis - Retinal vasculitis
55
Equine Recurrent Uveitis (ERU)
- Leptospira interrogans serovar POMONA is the most common in the US - The Appaloosa breed and horses with MHC class I haplotype ELA-A9 increased risk Pathogenesis - Autoimmune responses to ocular tissue components play a significant role in pathogenesis - Antigenic relationship between equine lens and L. interrogans components has been suggested
56
Which leptospiral proteins are expressed in the eye? what do they do?
- LruA, LruB: lens proteins identified to react with antisera raised against LruA and LruB - They may cross-react with resulting antibodies, leading to inflammation and or disruption of protein function "MOLECULAR MIMICRY" damages eye Diagnosis - Microscopic Agglutination test (MAT): Gold standard, paired samples - PCR (targeting lipl32) very sensitive and specific. - IHC and Dark-field: low sensitivity - Culture: requires special media and takes several weeks