Infections of the Integumentary CM 109 PDF

` CM 109: INTEGRATED BASIC SCIENCES II (MICROBIOLOGY & PARASITOLOGY) INFECTIONS OF THE INTEGUMENTARY DR. KIMBERLY TRISHA R. CONCEPCION | 15 OCTOBER 2024 TABLE OF CONTENTS...

` CM 109: INTEGRATED BASIC SCIENCES II (MICROBIOLOGY & PARASITOLOGY) INFECTIONS OF THE INTEGUMENTARY DR. KIMBERLY TRISHA R. CONCEPCION | 15 OCTOBER 2024 TABLE OF CONTENTS Pustule Scar → < 1 cm, pus-filled Hypertrophic wir I. PRIMARY AND SECONDARY LESION 1 → Within the border II. OUTLINE OF INFECTIONS 1 Keloid extend- A. BACTERIAL SKIN INFECTIONS 1 → Extending border B. VIRAL INFECTIONS 1 II. OUTLINE OF INFECTIONS C. FUNGAL SKIN INFECTIONS 1 A. BACTERIAL SKIN INFECTIONS D. PARASITIC INFECTIONS 1 Impetigo E. TICK BORNE DISEASE 1 Cellulitis III. BACTERIAL SKIN INFECTIONS 1 Folliculitis, Furuncle, Carbuncle A. IMPETIGO 1 Acne B. CELLULITIS 2 B. VIRAL INFECTIONS Measles C. FOLLICULITIS, FURUNCLE, CARBUNCLE 2 German Measles D. ACNE 3 Mumps IV. VIRAL INFECTIONS 3 Chickenpox A. MEASLES 3 Smallpox Monkeypox B. GERMAN MEASLES 4 Molluscum Contagiosum C. MUMPS 5 Fifth Disease D. CHICKEN POX 5 Roseola Infantum Hand Foot Mouth Disease E. SMALLPOX 6 Dengue F. MONKEYPOX 6 C. FUNGAL SKIN INFECTIONS G. MOLLUSCUM CONTAGIOSUM 7 Candidiasis H. FIFTH DISEASE/ERYTHEMA INFECTIOSUM 7 Superficial Mycoses: Tinea Versicolor I. ROSEOLA INFANTUM 7 Other Superficial Mycoses Cutaneous Mycoses J. HAND FOOT MOUTH DISEASE 8 Subcutaneous Mycoses: Sporothrix Schenckii K. DENGUE 8 D. PARASITIC INFECTIONS IV. FUNGAL SKIN INFECTIONS 9 Scabies A. CANDIDA 9 E. TICK BORNE DISEASE B. SUPERFICIAL MYCOSES 9 Lyme Disease C. CUTANEOUS MYCOSES (DERMATOPHYTES) 11 III. BACTERIAL SKIN INFECTIONS D. TINEA 11 A. IMPETIGO epidermis - E. SUBCUTANEOUS MYCOSES 11 It is an infection of the surface of the epidermis V. PARASITIC SKIN INFECTIONS 11 Most common skin infections in children Organisms: catalase & coagulase (t) A. SCABIES 11 = cluster Laurita-cluster of mony) → S. aureus a wmus GABHS-chain sair B. TICKBORNE (LYME DISEASE) 12 ▪ Gram (+) cocci in clusters hemoly / & bacitracin sensitive VI. REFERENCES 12 → Group A Beta-hemolytic streptococci (GABHS) pyogenes group & - A ▪ Gram (+) cocci in chains or pairs I. PRIMARY AND SECONDARY LESION Table 1. Primary Lesion vs Secondary Lesion Primary Lesion Secondary Lesion Macule Scales - kratinizat → Flat, non palpable ≤ 1 cm → Rapid process of normal Patch keratinization → Flat, non palpable > 1 cm Example: Seborrheic dermatitis → Yellowish greasy scales Psoriasis → Thick adherent silvery scales Papule Crust -deposit → Superficial, elevated, → Hardened deposits palpable ≤ 1cm Nodule → Superficial, elevated, palpable > 1cm Plaque Excoriations → >1cm, “like patch na → “Kamot” Figure 1. Gram-Positive Bacteria Lineage matambok na may kaliskis” Retrieved from Dr. Concepcion’s PPT (2024). → Example: Psoriasis PRECEPTOR NOTES Cyst Fissure S. aureus is both catalase (+) and coagulase (+) → Fluid filled → "Crack" Group A Beta-hemolytic Streptococcus → Firm, movable → Complete hemolysis and bacitracin sensitivity Vesicle Erosions → < 1 cm, fluid-filled → "Natuklap", epidermis Bullae Ulcer → >1 cm, fluid-filled → Dermis Trans # 08 B2: Jusi, Llorente, Machitar, Malonzo, Meneses, Millena, Olayes, Ong, Pangan, Pendras, Rañola, Sinogba TH: Manzanares 1 of 20 Table 2. S. aureus vs Group A Streptococcus Diagnosis Staphylococcus Aureus Group A Streptococcus Gram Stain → Gram (+) cocci in grapelike clusters Catalage (+) Catalase (-) Culture of the lesion Coagulase (+) Beta hemolytic PCR → mecA gene for MRSA Sensitive to Bacitracin Treatment (B-BRAS) Topical mupirocin or retapamulin 2-3 times a day for 10-14 days Possesses M Protein Systemic therapy for lesions near the mouth, or widespread or deep Produces Streptolysin S and O involvement → Ex. Cephalexin 25-50mg/kg/day in 3-4 divided doses for 7-10 Virulence Factors: Virulence Factors: days → If no response in 7 days, do a culture and give clindamycin, Protein A Hyaluronidase doxycycline or cotrimoxazole for 7 days especially if Prevents complete Degrades hyaluronic acid considering MRSA activations, binds IgG, (spreading factor) Methicillin sensitive SA (MSSA) preventing opsonization and → Penicillinase resistant penicillins (2nd gen penicillins): Nafcillin, phagocytosis Streptokinase (Fibrinolysin) Oxacillin, Dicloxacillin Opposite of coagulase Methicillin-resistant SA (MRSA) Coagulase → Vancomycin Allows insoluble fibrin DNASE (Streptodornase) Vancomycin resistant SA (VRSA) formation, protecting it from Degrades DNA in exudates → Linezolid phagocytosis B. CELLULITIS C5a Peptidase Infection of loose connective tissue with limited dermal involvement Hemolysin (Cytotoxins) Inactivates complement C5a and sparing of the epidermis Toxic to hematopoietic cells Area of edema, warmth, erythema, and tenderness with indistinct margins Leukocidin Organisms: S. aureus and S. pyogenes Specific for WBCs Catalase Detoxifies hydrogen peroxide Penicillinase Secreted of beta-lactamase, disrupts beta lactam portion of the penicillin molecule PRECEPTOR NOTES Mnemonic: “B-BRAS” Bacitracin - B Resistant A Sensitive Figure 3. Cellulitis → Group B is Resistant Retrieved from Dr. Concepcion’s PPT (2024). → Group A is Sensitive Diagnosis Take note of the virulence factors (common board exam questions) Usually done clinically Impetigo usually occurs near the mouth Blood culture not recommended Bullous vs Non Bullous Impetigo The Infectious Disease Society of America (IDSA) doesn’t recommend routine collection of cultures, including: Table 3. Bullous vs Non Bullous Impetigo → Biopsies, blood, cutaneous aspirates, swabs Bullous Non Bullous When culture is recommended Culture may help when atypical pathogens are suspected Flaccid, transparent bullae Preceded by insect bite, Recommended by the IDSA for: developing into the skin abrasion, or laceration → Animal bites → Immersion injuries Tiny vesicles or pustules rapidly → People with immunocompromised status developing into honey colored crusted plaque Treatment Penicillinase-resistant penicillin (Cloxacillin) or first generation cephalosporin (Cephalexin) Parenteral therapy (ex. Oxacillin) should be initiated if: → Disease progresses significantly within 1-2 days of antibiotic → No improvement noted on oral antibiotics → With fever, lymphadenopathy Table 4. Cellulitis Treatment Oral Antibiotics IV Antibiotics Cephalosporins (eg. Cefalexin cephalexin) Ceftriaxone Impetigo Contagiosa Clindamycin Clindamycin Dicloxacillin Penicillin Penicillin C. FOLLICULITIS, FURUNCLE, CARBUNCLE Folliculitis, Furuncle, and Carbuncle → Causative agent: Staphylococcus aureus Folliculitis → Most superficial type of inflammation of the hair follicles → Pyoderma that begins within the hair follicle Furuncle → Infection of the hair follicle that goes into the deeper layers of skin → A deep seated nodule that develops around a hair follicle Carbuncle → A group of infected hair follicles with pus → Extremely painful Figure 2. Impetigo Infection caused by Staphylococci. This infection is characterized by isolated pustules that become crusted over. Retrieved from Dr. Concepcion’s PPT (2024). CM 109 Infections of the Integumentary 2 of 20  → Presence and activity of Propionibacterium acnes → Inflammation and immune response Clinical features → Comedones (whiteheads and blackheads) → Papules → Pustules (face, chest, back) → Nodules (face, chest, back) Figure 4. Folliculitis, Furuncle, and Carbuncle Retrieved from Dr. Concepcion’s PPT (2024). Diagnosis Use diagnostic and management algorithm for Staphylococcus aureus under localized dermal or subcutaneous infections Figure 7. Clinicopathologic correlation of acne lesions. A. Closed comedone. B. Open comedone. C. Inflammatory papule. D. Nodule. Retrieved from Fitzpatrick's Dermatology in General Medicine (8th Ed.) Chapter 30, pg. 901. Note: Information was directly taken from Fitzpatrick's Dermatology in General Medicine 9th Ed. (2019). A. Closed comedone The follicular infundibulum is distended, filled with keratin and sebum, and the follicular epithelium is attenuated The follicular ostium is narrow B. Open comedone Resembles the closed comedone with the exception of a patulous follicular ostium C. Inflammatory papule Acute and chronic inflammatory cells surround and infiltrate the follicle, which shows infundibular hyperkeratosis D. Nodule The follicle is filled with acute inflammatory cells With the rupture of the distended follicle, there is a foreign body granulomatous response Diagnosis Clinical history and physical exam Laboratory work up: → Serum DHEAS (dehydroepiandrosterone sulfate) ▪ 4000-8000 = Congenital Adrenal Hyperplasia ▪ >8000 = Adrenal Tumor → Total testosterone ▪ >150 = Ovarian source of excess androgens ▪ 150-200 or Increased LH to FSH ratio = found in PCOS → Free testosterone (most sensitive for PCOS) ▪ PCOS: increased likelihood for acne Figure 5. Diagnostic and Management Algorithm for Staphylococcus aureus LH to FSH ratio or serum 17-hydroxyprogesterone Retrieved from Dr. Concepcion’s PPT (2024). → To identify adrenal source of androgens Refer to Appendix for a larger view ▪ Increased androgens can cause acne PRECEPTOR NOTES Treatment Clinical Examination: Medication → Inspect the wound → Topical retinoid Recalls: → Clindamycin → Erythema: Cellulitis → Adapalene → Honey colored crusts: Impetigo → Salicylic acid → Corticosteroid Treatment → Benzoyl Peroxide (BPO) Therapy Table 5. Folliculitis, Furuncle, and Carbuncle Treatment → Extraction Infection Treatment → Laser/Light Therapy → Photodynamic Therapy Folliculitis, Furuncle, and Incision and drainage (consider Carbuncle (Simple) oral antibiotics in below row) Refer to Table 6 on Appendix for the detailed treatment algorithm for acne vulgaris. Furuncle, Carbuncle, abscesses Clindamycin, that are not drainable and are IV. VIRAL INFECTIONS Trimethoprim/sulfamethoxazole associated with cellulitis (TMP-SMX), Doxycycline, A. MEASLES Minocycline, and Linezolid Also known as Rubeola, First Disease, Red Measles Tagalog: Tigdas Refer to Figure 6 on Appendix for the dosing and duration of Folliculitis, Causative agent: Furuncle, and Carbuncle Treatment or refer to Fitzpatrick’s Dermatology → Paramyxovirus (Measles Virus) 9th Ed. Chapter 150, pg. 2731. Incubation period: 10-14 days Transmission: Airborne D. ACNE Period of Communicability: 4 DAYS BEFORE TO 4 DAYS AFTER Common disorder of the pilosebaceous unit ONSET OF RASH Causative agent: Symptoms → Propionibacterium acnes High grade fever with 3 C’s: 4 elements of pathogenesis → Cough → Follicular epidermal hyperproliferation → Conjunctivitis → Sebum production CM 109 Infections of the Integumentary 3 of 20  → Colds for 3-5 days Treatment Photophobia Supportive Care Rashes usually appear at the height/peak of the fever Vitamin A: Pathognomonic enanthem: → Oral once a day for 2 days (24 hrs apart) → Koplik’s Spot → Essential for the maintenance of normal epithelial tissue ▪ Bright red lesions with white central spots found on the inner throughout the body buccal mucosa → The measles virus damages the epithelial tissue, reduces Maculopapular Rash complications and mortality → Rash appear and disappear in cephalocaudal direction → Vitamin A deficiency ▪ Face → Trunk → Extremities → Palms & Soles ▪ Affects the severity of measles and delays the recovery and can lead to measles related complications including blindness PRECEPTOR NOTES Recalls for Measles (Emphasized by lecturer) → Cephalocaudal direction → 3Cs ▪ Cough, Cold, Conjunctivitis → Pathology: ▪ Multinucleated Giant Cells → Other names: ▪ Rubeola, First Disease, Red Measles Prevention Table 7. Prevention for Measles Figure 8. Measles rash MEASLES MMR VACCINE POST Retrieved from https://www.nhsinform.scot/illnesses-and-conditions/ VACCINE EXPOSURE infections-and-poisoning/measles/. PROPHYLAXIS Type of Live Attenuated Measles Vaccine vaccine Immunoglobulin (Ig): may be given within 6 days of being exposed to Measles Age 9 months 12-15 months given 2nd Outbreak: 6 2nd doses Dose/ months recommended Boosters Figure 9. Measles with Koplik Spots. Red papules on buccal mucosa 2nd dose: 4-6 opposite premolars prior to the appearance of exanthema. years old (can Retrieved from Fitzpatrick's Color Atlas pg. 651. be earlier as long as it is 28 PRECEPTOR NOTES days after the During History and PE: 1st dose) → Ask for other associated symptoms → Look out for the key detail about rashes appearing at the peak Route Subcutaneously Subcutaneously of the fever B. GERMAN MEASLES Complications Also known as Rubella Blindness Tagalog: Tigdas Hangin Otitis Media 3-day measles → Most common Causative agent Pneumonia → Togavirus (Rubella Virus) → Most common cause of mortality Incubation period Subacute Subsclerosing Panencephalitis (SSPE) → 14-21 Days → Dawson Disease Transmission → Fatal neurodegenerative disease → Droplet or Transplacental ▪ Caused by persistent infection of the brain by an altered form Period of communicability of measles virus ▪ Manifest after 7-10 years → 7 days before to 7 days after the appearance of rash Bronchiolitis obliterans Symptoms → Final common pathway to a fatal outcome Fever Diagnosis Most characteristic sign Pathology: → Postauricular lymphadenopathy → Warthin-Finkeldey Giant Cells/Bodies No photophobia ▪ Multinucleated giant cells/fusion of infected cells Enanthem → Forchheimer Spots Maculopapular rash → Cephalocaudal and centrifugal ▪ Centrifugal: from trunk to extremities ▪ Centripetal: periphery to midline → The rash looks red or pink on the white skin → It can be harder to see on brown or black skin, but might feel rough or bumpy Figure 10. Slide illustrating a Warthin-Finkeldey Giant Cells Retrieved from https://step1.medbullets.com/microbiology/ Figure 11. Maculopapular Rash 104100/rubeola-measles. Retrieved from Dr. Concepcion’s PPT (2024). CM 109 Infections of the Integumentary 4 of 20  C. MUMPS Causative agent → Paramyxovirus (Mumps Virus) Incubation period: → 12-25 days Transmission: → Respiratory Droplets Period of communicability: → 1-2 days before to 5 days after onset of parotid swelling Signs and Symptoms Fever Figure 12. Maculopapular Rash on Dark Skin → 1-2 days Retrieved from Dr. Concepcion’s PPT (2024). Headache Vomiting Parotitis Figure 13. Forchheimer Spots Retrieved from Dr. Concepcion’s PPT (2024). Figure 15. Comparison of parotid glands between healthy patient and mumps patient Retrieved from Dr. Concepcion’s PPT (2024). Figure 14. Postauricular Lymphadenopathy Retrieved from Dr. Concepcion’s PPT (2024). PRECEPTOR NOTES Postauricular lymphadenopathy → Look at the back of the ear Figure 16. Swollen parotid glands in a child with mumps → Lymph nodes will be evidently swollen Retrieved from Dr. Concepcion’s PPT (2024). → Accompanied by fever → Will usually begin 24 hours before rash appears, and remains Complications for 1 week Ends with “itis” denoting inflammations Enanthem → Orchitis → Not pathognomonic for german measles → Meningitis → Forchheimer spots → Pancreatitis ▪ Discrete spots on the soft palate → Myocarditis ▪ Appears at the same time of rash → Optic neuritis → Conjunctivitis Complications → Nephritis Thrombocytopenia → Thrombocytopenia → 2 weeks after the rash Diagnosis Arthritis of small joints of hands Enzyme immunoassay from mumps IgM → Especially adult women Serum IgG from acute and convalescent serum specimens Encephalitis Reverse Transcriptase PCR → Post infectious syndrome → Using buccal swab specimen → Rare → Laboratory testing method of choice to confirm mumps Congenital Rubella Syndrome → Peak at 1st trimester Treatment → Demonstrate chromosomal breakage and inhibition of mitosis Supportive care is most often indicated → Often demonstrated with: Prevention ▪ Patent Ductus Arteriosus MMR vaccine ▪ Cataracts There is no post-exposure prophylaxis for mumps ▪ Mental retardation ▪ Sensorineural defects D. CHICKEN POX ▪ Blueberry muffin appearance Also known as Varicella Causative agent PRECEPTOR NOTES → Varicella Zoster Virus (HHV-3) Child is blind, deaf (bingi), with heart defects (butas sa puso) and Incubation period has brain problems → 14-21 days → All “B” Transmission → Direct contact or airborne spread Diagnosis Period of communicability Rubella IgM and IgG testing → 7 days before to 7 days after appearance of rash → Fourfold increase in antibody Signs and Symptoms Treatment Fever then pruritic exanthem Supportive care is most often indicated Vesicular rash Prevention → Dewdrop on a rose petal appearance MMR vaccine → Centrifugal pattern → Given 12-15 months ▪ Begins on trunk then spreads to face and extremities → Not given in pregnant women and immunocompromised patients Intensely pruritic red macules ▪ Reliant on herd immunity → Becomes papules then become vesicles ▪ Rapid progression CM 109 Infections of the Integumentary 5 of 20 PRECEPTOR NOTES Congenital Varicella Varicella zoster causes chickenpox Fetus infected with VZV at 6-12 weeks AOG Zoster sounds like “rooster” = chicken → Short and malformed limb Rash begins on the trunk Fetus infected at 16-20 weeks AOG → Imagine the biggest part of the body of the chicken: trunk → Eye and brain involvement Diagnosis Varicella-zoster antibody titers Pathology → Multinucleated giant cells with intranuclear inclusions Treatment IV Acyclovir → For severe disease and immunocompromised Oral Acyclovir → Best started on the first day, shortens duration of symptoms PRECEPTOR NOTES Oral Acyclovir 800 mg - 400 mg if what’s available Figure 17. Chickenpox rashes showing the characteristic evolution of → 800 mg lesions from papule, to blister, then ulcer Retrieved from Dr. Concepcion’s PPT (2024). ▪ Every 4 hours 5 times a day for 7 days → 400 mg Complications ▪ Take 2 tablets every 4 hours 5 times a day Pneumonia Varicella is self-limiting Encephalitis Reye’s Syndrome E. SMALLPOX Glomerulonephritis Causative agent: Herpes Zoster-Shingles → Variola virus Secondary reactivation of chickenpox Only disease that has been eradicated from face of the earth Unilateral painful vesicular eruption with dermatomal distribution (year 1967) → Thoracic and lumbar Incubation period Occurs in patient with latent virus → 7-14 days → Once reactivated, it will appear as painful rash or shingles Transmission → Trunk and back are usual areas → Aerosol; contact Symptoms Prodrome of fever and malaise followed by centrifugal rash Classic smallpox lesion: → Deep-seated, firm, hard, round well-circumscribed vesicles or pustules Figure 18. Shingles lesions that reactivated in an adult patient Retrieved from Dr. Concepcion’s PPT (2024). Ramsay-Hunt Syndrome Also referred to as Herpes Zoster Oticus Reactivation of latent varicella zoster virus residing within geniculate ganglion Triad → Ipsilateral facial paralysis ▪ Geniculate ganglion are near the facial nerve, hence the facial paralysis → Ear pain Figure 21. Smallpox → Vesicles on the face Retrieved from Dr. Concepcion’s PPT (2024). Diagnosis Pathology: → Guarnieri bodies (intracytoplasmic eosinophilic inclusion) Prevention Smallpox vaccine has been developed F. MONKEYPOX Causative agent: → Monkeypox virus ▪ Species of the genus Orthopoxvirus Mode of transmission: → Close contact with someone who has monkeypox → With contaminated materials → With infected animals During pregnancy, the virus may be passed to the fetus, or to the newborn during or after birth Incubation period: → From the time between the infection and the onset of symptoms Figure 19. Ramsay-Hunt Syndrome 3-17 days Retrieved from Dr. Concepcion’s PPT (2024). Duration of illness: → 2-4 weeks Symptoms Monkeypox is an infectious disease that can cause: → Painful rash → Enlarged lymph nodes → Fever → Headache → Muscle ache → Back pain → Low energy Refer to Table 8 on Appendix for the Symptoms of Monkeypox, Chickenpox, and Measles. Figure 20. Ramsay-Hunt Syndrome in an elderly woman Retrieved from Dr. Concepcion’s PPT (2024). CM 109 Infections of the Integumentary 6 of 20  Screening Checklist for Monkeypox Virus Infection (Yes or No) Diagnosis 1. Do you have any rash? Their appearance is diagnostic 2. Is the rash associated with any of the following: Molluscum bodies a. Headache → Characteristic finding in scrapings stained with Giemsa or iodine, b. Fever or history of fever or by electron microscopy of expressed material c. Swollen lymph nodes d. Muscle and body pains, including back pain e. Weakness 3. Do you have any travel history to other countries 4. Do you have any history of contact with another person with rash? 5. Do you have any history of prolonged or close physical (skin-to-skin, mouth-to-skin) contact with other individuals in the past 21 days? 6. Do you have any unprotected exposure to respiratory secretions, or items used by confirmed or suspected cases of monkeypox? Note: An answer of YES to Number 1 PLUS any of the other items should make one consider the possibility of monkeypox Figure 24. Molluscum Contagiosum virus Retrieved from Dr. Concepcion’s PPT (2024). Treatment Healthy people usually recover from molluscum without treatment Lesions can be removed by → Curetting, ablated by freezing, or 'killed' ▪ By inserting the point of an orange-stick dipped in 80% phenol solution into the umbilicated center Extensive skin lesions in HIV patients often respond well to cidofovir 10% topical ointment → Monkeypox is quite confusing because it resembles other infections H. FIFTH DISEASE/ERYTHEMA INFECTIOSUM Causative agent: → Parvovirus B-19 Incubation period: Figure 22. Monkeypox → 4-14 days Retrieved from Dr. Concepcion’s PPT (2024). Transmission: → Large droplet spread from nasopharyngeal shedding Diagnosis → Blood/blood-borne products Polymerase chain reaction (PCR) Period of communicability: → Preferred laboratory test for monkeypox via detection of viral DNA → Before onset of rash until after the onset of rash Best diagnostic specimens are taken directly from the rash → Skin, fluid, or crusts Symptoms Prevalent in 5-15 years old ▪ Collected by vigorous swabbing Mild fever & facial rash Treatment Hallmark sign: Goal is to take care of the rash, manage pain, and prevent → Rash with erythematous facial flushing ("slapped cheek complications appearance") Early and supportive care ▪ Spreads rapidly to trunk & proximal extremities as a diffuse → Important to help manage symptoms and avoid further problems macular erythema Some antivirals have received emergency use authorization in some countries and are being evaluated in clinical trials. No proven effective antiviral treatment for monkeypox Isolation → For at least 21 days or until skin lesions have healed and scab fall off G. MOLLUSCUM CONTAGIOSUM Causative agent: → POX virus Transmission: → Skin contact → By fomites such as clothing and towels → Autoinoculation to other skin sites is common Figure 25. Fifth Disease Lesion: Retrieved from Dr. Concepcion’s PPT (2024). → Flesh-colored dome-shaped papules with central umbilication PRECEPTOR NOTES Remember fifth disease because the hands have five fingers “HIGH PARV B-19”, sounded like “High Five” Complications Transient aplastic anemia → For sickle cell patients Arthritis Pancytopenia Diagnosis Serum IgM antibodies PCR - most sensitive Treatment Supportive Figure 23. Molluscum Contagiosum showing the central umbilication Retrieved from Dr. Concepcion’s PPT (2024). CM 109 Infections of the Integumentary 7 of 20  I. ROSEOLA INFANTUM Treatment Also known as Sixth Disease Supportive Causative agent → Human Herpes Virus (HHV) 6 PRECEPTOR NOTES Incubation period: Symptoms: Seen on the hand and foot externally, and nowhere → 9-10 days else Transmission Diagnosis: Most viral rashes can be diagnosed through physical → Saliva examination and history taking Period of communicability K. DENGUE → Unknown Dengue Virus Symptoms → Refers to 4 serotypes of RNA viruses Most often among < 3 years old, peak at 6-15 months old → From the genus FLAVIVIRIDAE Fever for 3-5 days ▪ DEN-1,2,3,4 Rash appears within 12 - 24 hrs after fever resolution Transmitted through the bite of Aedes Aegypti mosquito → Rose colored macules Incubation period Nagayama spots: → 1 - 7 days → Erythematous papules on soft palate and base of uvula Period of communicability → In mosquito: DENV replication for 8-12 days and remains infectious for life PRECEPTOR NOTES Aedes Mosquito: white stripes Incubation period: usually seen in stagnant water Symptoms Transient, macular, generalized rash that blanches under pressure → Seen during the first 24 - 48 hours of fever Figure 26. Roseola Infantum Hermann Rash Retrieved from Dr. Concepcion’s PPT (2024). → 1-2 days after defervescence PRECEPTOR NOTES → Generalized maculopapular rash appears which spares palms Remember: Rashes after Fever and soles → Disappears in 1-5 days and may desquamate Diagnosis PRECEPTOR NOTES HHV-6 serology, PCR, virus culture Hermann Rash: Isles of white in a sea of red Low WBC count, neutrophils, lymphocytes Treatment Refer to Table 9 on Appendix for the Phases of Dengue. Supportive Criteria for Dengue & Warning Signs J. HAND FOOT MOUTH DISEASE Probable Dengue Causative agents: → Live in / travel to dengue endemic area, fever and 2 of the → Coxsackie A 16 following criteria: → Enterovirus 71 ▪ Nausea, vomiting Incubation period: ▪ Rash → 4-6 days ▪ Aches and pains Transmission: ▪ Tourniquet test positive → Fecal-oral and respiratory routes ▪ Leukopenia Period of communicability: ▪ Any warning sign → Viral shedding from respiratory tract 1-3 weeks & fecal → Laboratory-confirmed dengue shedding up to 7-11 weeks post infection ▪ Important when no sign of plasma leakage PRECEPTOR NOTES Warning Signs* Entero → Abdominal pain or tenderness → Mostly associated with fecal route because it enters in the → Persistent vomiting mouth → Clinical fluid accumulation → Cause: putting hands in the mouth → Mucosal bleed → Lethargy, restlessness Symptoms → Liver enlargement ≥2cm Commonly affects