Lecture #4
Infections of the Skin - II (Lecture #4)
Presenter Information
Dr. Ashutosh Verma, BVSc, MVSc, PhD, DipACVM
Professor of Microbiology
Richard A. Gillespie College of Veterinary Medicine
Lincoln Memorial University, Harrogate, TN
Disclaimer
Material for the presentation sourced from various resources intended for educational purposes.
Influential texts included:
Veterinary Microbiology and Microbial Diseases, Quinn et al., 2nd ed.
Veterinary Microbiology, Songer and Post
Clinical Veterinary Microbiology, Markey et al., 2nd ed.
Infectious Diseases of the Dog and Cat, Greene, 5th ed.
Veterinary Microbiology, Hirsh et al., 2nd ed.
Learning Objectives
Determine types of skin infections: primary or secondary.
Identify predisposing factors/conditions leading to skin infections.
Select appropriate diagnostic tests for skin infection diagnosis.
Discuss virulence factors and mechanisms of bacteria causing skin infections.
Explore characteristics of bacteria related to skin infections.
Identify suitable antibiotic and non-antibiotic treatment measures for skin infections.
Specific Infections of the Skin
Staphylococcus spp.
Important Characteristics of Staphylococcus:
Facultative anaerobic, Gram-positive cocci forming grape-like clusters.
Contains at least 20 species, mostly host-specific.
Common pathogens in both animals and humans:
Staphylococcus aureus
Staphylococcus pseudintermedius
Staphylococcus hyicus
Staphylococcus epidermidis
Coagulase Positive/Negative:
S. aureus, S. pseudintermedius, and S. hyicus: Coagulase positive.
S. epidermidis: Coagulase negative.
Encounter
Common Flora:
Found in skin and mucous membranes:
S. aureus: Transient in humans and various domestic animals.
S. pseudintermedius: Transient; known to cause disease specifically in dogs.
S. hyicus: Transient; primarily in pigs causing greasy pig disease.
S. epidermidis: Resident in most animals; rarely causes skin infections; may initiate deeper infections.
Environmental Resilience:
Long-lived in the environment; resistant to heat and dehydration.
Easily spread, e.g., S. pseudintermedius prevalent at the recto-anal junction.
Entry
Colonization Resistance:
Low resistance to superficial colonization by Staphylococcus spp. but high resistance to deeper invasion.
Predisposing Factors:
Injury, use of catheters, disruption of normal flora, concurrent infections, sub-optimal immune function are key factors for invasion.
Infection Process:
Once epidermis is compromised, Staphylococcus spp. can penetrate the dermal layer by binding to the extracellular matrix using ECM-binding proteins.
Multiplication and Spread
Virulence Mechanisms:
Resistance to Phagocytosis:
Depending on capsule and ability to form clots, allowing survival within phagocytic cells.
Tissue Damage:
Proteases digest host tissue; contribute to the spread of infection.
Exotoxins:
Leukocidin: Kills leukocytes, decreasing immune response.
Hemolysin: Causes vasoconstriction and dermonecrosis.
Coagulase: Facilitates clot formation protecting bacterium from immune attack.
Points to Consider Regarding Virulence
Clinical presentation varies based on species and strains involved.
Not all strains express all identified virulence factors.
Host immunity plays a critical role in infection progression and resolution.
The interplay between bacterial growth and host clearance via opsonization and phagocytosis.
Immunity
Innate Immunity:
Opsonization by complement, phagocytosis by neutrophils, and macrophages.
Humoral Immunity:
Limited role in clearing organisms; crucial for antibody opsonization and toxin neutralization.
Cell-Mediated Immunity:
Involves killing of intracellular bacteria by activated macrophages.
Diagnosis
Methods include:
Gram's stain and cytology on smears.
Culture and sensitivity tests.
Surgical biopsy and histopathology for diagnosing primary issues.
Notably, mixed bacterial infections are common; Staphylococcus spp. often act as the primary invader allowing secondary invaders due to exotoxin production.
Treatment
Address underlying predisposing issues to prevent recurrence.
Antibiotics:
Decisions based on culture and antimicrobial susceptibility (AMS).
Long courses may be necessary, considering rampant antibiotic resistance.
Exudative Epidermitis (Greasy Pig Disease)
Etiology:
Caused by Staphylococcus hyicus; found worldwide in suckling and weaned pigs (up to 3 months old).
Highly contagious, characterized by excessive sebaceous secretion, exfoliation, and exudation on the skin.
Clinical Signs:
Affected pigs: Anorexia, depression, fever, widespread non-pruritic dermatitis with greasy exudate.
Young piglets (<3 months): High mortality (24-48 hrs post infection).
Pathophysiology:
S. hyicus typically retrieved from the vaginal mucosa and skin of healthy sows.
Entry through small abrasions, often via bite wounds.
Further Insights on Exudative Epidermitis
Virulence Factors:
Linking of bacterial virulence is through the production of exfoliative toxins, hindering keratinocyte cell adhesion.
Infection typically follows injuries from fighting or abrasions from rough surfaces.
Predisposing Factors:
Factors influencing disease severity: immunity, hygiene, nutrition, and skin damage by environment.
Colostrum provides piglets immunity from mature sows that had previous exposure.
Epidemiology:
Higher incidence in gilt litters and newly established SPF herds.
Management of Exudative Dermatitis
Examine areas of abrasion:
Identify injury sources like rough surfaces and manage appropriately.
Use hydrated lime with disinfectants to clear poor surfaces.
Treatment Protocol:
Daily disinfect the udder skin with iodine skin antiseptics.
Implement strict disinfectant protocols between farrowing episodes.
Ensure scrupulous care in tail and tooth removal to avoid injuries.
Control humidity levels; conditions above 70% are ideal for bacteria multiplication.
Conduct bacteriological checks post-cleaning and disinfection.
Dermatophilosis
Etiological Agent:
Dermatophilus congolensis is responsible; induces exudative epidermitis presenting with scab formation.
Affects a wide range of animals including ruminants and horses.
Common Names include:
Cutaneous streptothricosis, rain scald/rot, scratches, greasy heel, lumpy wool, strawberry foot rot.
Physical Presentation
Severe lesions in cattle due to Dermatophilus congolensis infection typically feature crust/scab formation and wart-like lesions.
Morphology
D. congolensis Profile:
Gram-positive, facultative anaerobe.
Characteristic morphology involves longitudinal and transverse division forming parallel rows resembling "railroad tracks".
Encounter and Transmission
Obligate parasite residing in hair follicles; has a global presence, with a higher incidence in tropical regions.
Reservoirs:
Carrier animals in endemic areas.
-Transmission: Via direct contact, mechanical vectors (ticks, flies), and fomites (clippers, brushes).
Survival: Does not thrive in soil but can persist for 42 months in crusts.
Entry and Pathogenesis
Infection likely if spores reach weakened skin:
Local debilitation due to wet conditions or injuries.
Infection Process:
Spores migrate to epithelial layers, leading to extended bacteria without traditional divisional replication.
These bacteria can cause exudative epidermitis and activate complement leading to tissue necrosis.
Diagnosis
Diagnosis relies on:
History of predisposing conditions; clinical signs usually sufficient for diagnosis in common animals.
Laboratory testing including fresh lesion impressions stained for characteristic “railroad track” structures.
Treatment
Eliminate predisposing factors (provide shelter, treat insects, avoid wet conditions).
Topical treatments and antibiotics (penicillin, long-acting oxytetracycline) for severe cases.
Presenter Information
Dr. Ashutosh Verma, BVSc, MVSc, PhD, DipACVM
Professor of Microbiology
Richard A. Gillespie College of Veterinary Medicine
Lincoln Memorial University, Harrogate, TN
Disclaimer
Material for the presentation sourced from various resources intended for educational purposes.
Influential texts included:
Veterinary Microbiology and Microbial Diseases, Quinn et al., 2nd ed.
Veterinary Microbiology, Songer and Post
Clinical Veterinary Microbiology, Markey et al., 2nd ed.
Infectious Diseases of the Dog and Cat, Greene, 5th ed.
Veterinary Microbiology, Hirsh et al., 2nd ed.
Learning Objectives
Determine types of skin infections: primary or secondary, distinguishing characteristics that define each type to better understand their origins and impacts on animal health.
Identify various predisposing factors and underlying conditions that lead to skin infections, including environmental stressors, poor hygiene practices, and genetic predispositions.
Select appropriate diagnostic tests for skin infection diagnosis, tailored to both the type of infection and the species affected.
Discuss virulence factors and mechanisms of bacteria causing skin infections, focusing on how they enable the pathogen to establish infection and resist host defenses.
Explore characteristics of bacteria related to skin infections, including their morphology, growth patterns, and unique metabolic processes relevant to their pathogenicity.
Identify suitable antibiotic and non-antibiotic treatment measures for skin infections, ensuring that considerations such as resistance patterns and side effects are included in treatment planning.
Specific Infections of the Skin
Staphylococcus spp.
Important Characteristics of Staphylococcus:
These bacteria are facultative anaerobes, demonstrating a Gram-positive cocci morphology and capable of forming grape-like clusters, a feature that aids in their identification.
Among the at least 20 different species, many are highly host-specific, which underscores the importance of species identification in clinical settings. Common pathogens include:
Staphylococcus aureus: notorious for a variety of infections in both humans and animals.
Staphylococcus pseudintermedius: frequently associated with canine infections.
Staphylococcus hyicus: primarily impacting swine, especially young pigs, leading to severe skin conditions.
Staphylococcus epidermidis: often regarded as a saprophytic organism, but can lead to opportunistic infections in compromised hosts.
Coagulase Positive/Negative:
Coagulase positive strains like S. aureus and S. pseudintermedius are more virulent compared to the coagulase negative species like S. epidermidis, which are typically less pathogenic.
Encounter
Common Flora:
The presence of Staphylococcus spp. is common in the skin and mucous membranes, where they can act as commensals or pathogens based on the host's condition:
S. aureus: usually transient; presents as a risk factor due to its pathogenic potential.
S. pseudintermedius: identified as a significant canine pathogen, with studies highlighting its role in pyoderma.
S. hyicus: serves as an opportunistic pathogen primarily affecting pigs, often in conditions of environmental stress.
S. epidermidis: while generally benign, can become pathogenic in immunocompromised cases by initiating deeper infections.
Environmental Resilience:
Staphylococcus spp. display remarkable resilience; they can survive in harsh environments, remaining infectious even after prolonged periods of heat and desiccation. Their ability to adhere to various surfaces, including skin and medical devices, facilitates their transmission.
Entry
Colonization Resistance:
Superficial colonization by Staphylococcus spp. is low; however, upon breaches in skin integrity, their ability to invade deeper tissues becomes significant.
Predisposing Factors:
An extensive range of factors can predispose individuals to infection, which includes but is not limited to:
Trauma or injuries that compromise skin integrity.
Medical interventions requiring catheterization that disrupt normal flora.
Concurrent infections that diminish local defenses.
Host factors such as age, nutrition, and overall immune status, which dictate susceptibility to infections.
Infection Process:
Infection begins once the epidermal barrier is compromised, with Staphylococcus spp. employing ECM-binding proteins to adhere and penetrate the dermal layer, thus establishing infection.
Multiplication and Spread
Virulence Mechanisms:
Resistance to Phagocytosis: S. aureus can evade the immune response thanks to its capsule and fibrin clot formation, allowing survival within phagocytes.
Tissue Damage: The production of various proteases facilitates the destruction of host tissues, aiding in the spread of infection through damaged areas.
Exotoxins: Such as Leukocidin, which targets leukocytes, impairing the immune response; Hemolysin, causing localized tissue necrosis; and Coagulase, aiding in the formation of clots which can protect bacteria from immune detection.
Points to Consider Regarding Virulence
The clinical presentation of infections varies, influenced by the strains involved and the specific virulence factors they express.
Not all bacterial strains will express the full array of known virulence factors, making strain identification crucial for effective treatment.
Host immunity plays a critical role in infection progression, with conditions like opsonization and phagocytosis determining the outcome of infections.
Immunity
Innate Immunity: Consists of mechanisms such as opsonization facilitated by complement proteins and phagocytosis predominantly involving neutrophils and macrophages, which are essential for the initial defense against Staphylococcus spp.
Humoral Immunity: While its role is limited in the direct clearing of organisms, it is crucial for the opsonization and neutralization of toxins produced by the bacteria, facilitating better immune responses.
Cell-Mediated Immunity: Activated macrophages play a significant role in targeting and eliminating intracellular bacteria, emphasizing the importance of this immune aspect in chronic infections.
Diagnosis
Diagnostic methods encompass a range of techniques including:
Gram staining and cytological examination of smears to visualize bacterial presence and morphology.
Culture and sensitivity testing to ascertain the specific pathogens involved and their antibiotic susceptibilities.
Surgical biopsy and histopathological examination for a definitive diagnosis, particularly in complex or severe cases.
It's important to recognize that mixed infections are common; Staphylococcus spp. frequently act as primary invaders, paving the way for secondary invaders owing to exotoxin production and tissue damage.
Treatment
Addressing Underlying Issues: A critical first step in treatment is to resolve predisposing factors to avert recurrence of skin infections.
Antibiotic Therapy:
Treatment decisions should be informed by culture results and antimicrobial susceptibility profiles. Given the rise in antibiotic resistance, long courses may be required, and selection of appropriate antibiotics must take into account resistant patterns observed in clinical isolates.
Exudative Epidermitis (Greasy Pig Disease)
Etiology: Caused by Staphylococcus hyicus; found globally, particularly affecting suckling and weaned pigs (up to 3 months old).
This disease is highly contagious, characterized by excessive sebaceous secretion leading to exfoliation and exudative dermatitis, necessitating stringent biosecurity measures in affected herds.
Clinical Signs: Anorexia, depression, fever, and widespread non-pruritic dermatitis marked by greasy exudate are hallmarks of the disease. Young piglets usually face a high mortality risk (24-48 hours post-infection).
Pathophysiology: S. hyicus is typically isolated from the vaginal mucosa and skin of healthy sows, with disease transmission occurring through small abrasions, often accentuated by fighting or rough environmental surfaces.
Further Insights on Exudative Epidermitis
Virulence Factors:
The pathogenicity is largely mediated by exfoliative toxins that disrupt keratinocyte adhesion, significantly contributing to infection stability and severity.
Predisposing Factors:
Factors influencing severity include host immunity, overall herd hygiene, nutritional status, and environmental conditions conducive to skin damage. Colostrum rich in antibodies can aid in providing passive immunity to piglets, particularly in sows previously exposed to S. hyicus.
Epidemiology: The disease shows a higher incidence in gilt litters and newly established SPF (Specific Pathogen Free) herds, necessitating monitoring and management strategies to limit outbreaks.
Management of Exudative Dermatitis
Ongoing assessment of areas prone to abrasions is crucial:
Identifying sources of injury, such as rough surfaces, and implementing corrective measures (e.g., using hydrated lime and disinfectants) to minimize environmental risks.
Treatment Protocol:
Daily disinfection of affected areas with iodine-based skin antiseptics is essential. Strict disinfectant protocols are mandatory between farrowing episodes, alongside meticulous care during tail docking and tooth trimming to prevent additional injuries.
Keeping humidity levels controlled below 70% can effectively limit bacterial multiplication. Post-cleaning bacteriological checks should be routinely conducted to ensure effective disinfection measures.
Dermatophilosis
Etiological Agent: Dermatophilus congolensis, associated with exudative epidermitis, manifests with scab formation; it infects a diverse array of animals including ruminants and horses.
Common Names: This condition is known by various names such as cutaneous streptothricosis, rain scald/rot, scratches, greasy heel, lumpy wool, and strawberry foot rot.
Physical Presentation
Severe lesions caused by D. congolensis typically exhibit crust/scab formation and prominent wart-like lesions on the affected animals, indicating a significant infection.
Morphology
D. congolensis Profile: A Gram-positive, facultative anaerobe that uniquely displays a morphology characterized by longitudinal and transverse divisions, resembling parallel rows akin to "railroad tracks" - a key identifier in laboratory diagnostics.
Encounter and Transmission
As an obligate parasite residing predominantly in hair follicles, D. congolensis has a distinct global distribution with higher prevalence observed in tropical regions.
Reservoirs: Carrier animals in endemic regions pose a continual risk for transmission.
Transmission Risks: Occurs via direct contact, facilitated by mechanical vectors (e.g., ticks, flies) and fomites such as clippers and brushes.
Survival: D. congolensis has shown resilience, capable of persisting in crusts for up to 42 months, thus presenting a prolonged hazard for reinfection.
Entry and Pathogenesis
Infection typically occurs when spores infiltrate damaged skin, particularly under wet and compromised conditions.
Infection Process: Spores can migrate to epithelial layers, leading to prolonged bacterial colonization without typical replication patterns, facilitating extensive tissue necrosis and exacerbating exudative conditions.
Diagnosis
Diagnosis is generally based on:
A thorough history of predisposing conditions and clinical signs, often sufficient for recognition in commonly affected animals.
Laboratory testing may include fresh lesion impressions stained for characteristic structures indicative of D. congolensis, enhancing the diagnostic accuracy.
Treatment
Effective management necessitates the elimination of predisposing factors, which includes:
Providing adequate shelter, treating external parasites, and mitigating exposure to wet conditions.
Application of topical treatments and antibiotics (such as penicillin and long-acting oxytetracycline) for cases of severe infection, making timely intervention pivotal to improve recovery chances.