Exam 1 Flashcards
What is an obligate pathogen?
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 does the Establishment of infection occur?
- Encounter
- Entry
- Multiplication and spread
- Damage
- 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
Bacterial Shape and arrangement
Coccus: spheric Coccobacillus: longer spheric Bacillus: rod Vibrio: curved rod Spirillum: spirochete-like
Terminology
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.
Clinical case example
- History, Physical exam
- Create a problem list
- What are the differentials?
- Diagnostic plan
- Treatment decision and prevention plan.
Establishment of bacterial and fungal infections
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.
Virulence
Why do some animals develop disease while others do not?
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.
Definitions
-Infection: presence and replication of an obligate pathogen within a host, implies overt disease or capability of causing disease.
- 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 - 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. - Carrier infection: persistent infection with a pathogen that may have previously caused disease, may later progress to apparent infection, Ex: Anaplasma marginale in cattle
Events in Establishment of Infection
1. Encounter
- 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* - 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.
- Entry: microorganism or toxin enters the host body
- Multiplication and spread: microorganism and or toxin multiplies and spreads inside the host.
- Damage: host’s immune response and damage due to invasion
- Entry
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.
- Multiplication and spread
What determines multiplication and spread?
-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).
- Damage
Three ways microbes damage host
- 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. - 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. - 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.
Infections of the skin I-II
Anatomy of the skin
- 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
Normal Flora of the Skin
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.
Bacterial infections of the skin
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.
Diagnosis of Bacterial skin Infections
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).
Classification of Skin Infections (Pyodermas = pus).
- 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**
Infection of the Skin, Fungal
Dermatophytosis
Seborrheic dermatitis
Sporotrichosis
Phythiosis
Dermatophytosis (Ringworm infections)
What genera causes the infection?
- Microsporum: 17 conventional species.
- The most significant are M. canis, M. gypseum, M. nanum and M. gallinae. - Trichophyton: 20 species, The most common are T. mentagrophytes, T. equinum, T. verrucosum.
- Epidermophyton: people
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
- 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.
Clinical signs of dermatophytosis
- 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.
Canine ringworm
- 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)
