Midterms - L3.1 - Microbial Agents Causing Skin Infection 4 PDF

MICROBIOLOGY AND PARASITOLOGY MICROBIAL AGENTS OF SKIN INFECTIONS 4 Dr. Josephine Bandalan | September 25, 2024 Mucocutaneous Manifestation...

MICROBIOLOGY AND PARASITOLOGY MICROBIAL AGENTS OF SKIN INFECTIONS 4 Dr. Josephine Bandalan | September 25, 2024 Mucocutaneous Manifestation OUTLINE Viral Agents of Skin Infection Koplik spots: small white lesions on buccal A. Measles (Rubeola) mucosa appearing 2-3 days prior to appearance of B. Rubella (German measles) rashes C. Herpes virus type 6 (Roseola infantum) Generalized maculopapular rash: initially in the D. Parvovirus B19 (Erythema infectiosum) head progressing to the limbs E. Herpes simplex virus I F. Varicella-Zoster virus G. Variola (Smallpox) H. Monkeypox I. Molluscum contagiosum J. Human papillomavirus Figure 1. Koplik spots and maculopapular skin rash K. Hand-foot-and-mouth disease Source: Dr. Bandalan’s PPT Parasitic Skin Infestation II A. Scabies B. Pediculosis APA References Figure 2. Branny desquamation and Warthin-Finkeldey I. VIRAL AGENTS OF SKIN INFECTION cells taken from lungs of patient with measle pneumonitis Measles (Rubeola) Source: Dr. Bandalan’s PPT Rubella (German measles) Dr. Bandalan: Herpes virus type 6 (Roseola infantum) Primarily a childhood infection (although this can Herpes simplex virus happen in adults also) Varicella-Zoster virus Characterized by high grade fever, coryza (watery Human papillomavirus nasal discharge, increase in lacrimation ), cough, and Variola (Smallpox) conjunctivitis Monkeypox Koplik spots Parvovirus B19 (Erythema infectiosum) ○ Typical lesion, considered as a Hand-foot-and-mouth disease pathognomonic sign clinically for measles A. MEASLES (RUBEOLA) infection. RNA enveloped Paramyxoviridae ○ Found in the mucosa of the inner cheek Transmitted by droplet inhalation ○ Described as small wide lesion that are Respiratory mucosa → lymphoid organs → surrounded by erythema systemic circulation → skin ○ Characteristically, this appears about 2-3 High fever, coryza, cough, conjunctivitis days prior to the appearance of skin rash Maculopapular skin rash Dr. Bandalan: Maculopapular skin rash Measles also referred as rubeola ○ Hairline One of the most common infection in pediatric age The first area where you are able to group see maculopapular skin rash “Tipdas” Spread into the face, neck, upper RNA, Paramyxoviridae family, enveloped, single extremities, trunk, and abdomen stranded until the lower extremity. Mainly transmitted through respiratory droplets Occur about 3-5 days ○ So initial infection starts in the respiratory ○ While skin rashes are there, fever becomes tract continuously high. ○ From the respiratory tract, the virus is ○ Fever will start to subside when the skin rash transported to the lymphoid organs, reaches the lower extremities. particularly the regional lymph nodes. ○ When skin rash heals, they leave branny ○ From regional lymph nodes, the virus is desquamation of the skin brought into the blood circulation/systemic Temporary, after several weeks the circulation until it reaches skin and skin will return to normal produce the characteristic skin lesions Warthin-Finkeldey cells ○ Typical cytopathic effect produced by measles infected cells ○ Syncytia formation, fusion of infected cells NMD2027  Lesson 3: Microbial Agents of Skin Infections 4 NMD2027 Rubeola Clinical Significance 3 categories of congenital rubella syndrome Immune suppression—most important in the 1. Transient effects in the infants cell-mediated arm (anergy) 2. Permanent manifestations that may be apparent at Lifelong immunity birth or become recognized during first year Complications: 3. Developmental abnormalities that appear and ○ Otitis media progress during childhood and adolescence ○ Pneumonia (life-threatening) CLASSIC TRIAD: ○ Acute encephalitis and postinfectious ○ Congenital cataracts encephalomyelitis (serious) ○ Cardiac abnormalities ○ Subacute sclerosing panencephalitis ○ Deafness (SSPE): late complication ADDITIONAL INFORMATION: CONGENITAL RUBELLA Dr. Bandalan: Crosses placenta when mother has acute infection Anergy The earlier the fetus is infected → more serious ○ Temporary suppression of the immune disease system particularly the cell mediated May result in serious congenital abnormalities: immunity. ○ Intrauterine growth retardation ○ Hepatosplenomegaly ○ Seen in patient with measle infection ○ Cataracts ○ That is why in most instances there are ○ Mental retardation clinicians/consultants that usually give ○ Sensorineural hearing loss INH prophylaxis in the pediatric patients ○ Heart-Patent Ductus Arteriosus especially with histories of primary ○ Pulmonary stenosis complexes. ○ Thrombocytopenic purpura Primary complex or initial Classic Triad: infection of mycobacterium tuberculosis Because the immune system is suppressed especially the cellular immunity part, it may cause reactivation of a primary complex In the primary complex (first exposure to the organism), the child may even recover from the infection even if not treated. Figure 3. Classic Triad: However, the organism becomes (1) PDA dormant in the macrophages of (2) Cataracts and deafness the lungs. They will become (3) +/- “Blueberry Muffin” Rash reactivated. Source: Dr. Bandalan’s PPT INH prophylaxis - prevent flare up or reactivation of previous C. HUMAN HERPESVIRUS 6 primary complex (ROSEOLA INFANTUM) When you recover from measles, this will confirm a DNA enveloped Herpesviridae prominent immunity Cause roseola infantum or exanthem subitum Subacute sclerosing panencephalitis (SSPE) (Sixth disease) ○ Late complications - months or years Occur in infancy Vaccine for measles: live attenuated virus, similar Transmitted via oral secretions to MMR Fever and erythematous macular rash on neck and trunk that resolves after a few days without sequelae B. GERMAN MEASLES (RUBELLA) RNA enveloped Togaviridae 3-day measles, mild, self-limited Transmitted via droplet inhalation Cutaneous lesions ○ Accompanies a mild subclinical syndrome, including lymphadenopathy (suboccipital, post-auricular, cervical) ○ Generalized maculopapular rash Dr. Bandalan: Rubella Clinical Significance Roseola Infantum clinical presentation: Congenital anomaly FEVER → 3rd day: FEVER SUBSIDES → ○ Infection of pregnant woman in first APPEARANCE OF SKIN RASH trimester results in abnormalities in infants in about 85% of cases 2 of 8  Lesson 3: Microbial Agents of Skin Infections 4 NMD2027 D. HUMAN PARVOVIRUS B19 Site of latency: Dorsal root ganglia ○ Oropharyngeal Infection latent in (ERYTHEMA INFECTIOSUM) Trigeminal Ganglia ssDNA nonenveloped Parvoviridae ○ Genital infection in Sacral Ganglia Parvovirus B19 - only species pathologic to men ○ Infect immature red cells in erythroid Recurrent infections lineage ○ HSV is a lifetime disease ○ Transmission by: HSV 1 – oropharyngeal lesions Respiratory route HSV 2 – genital herpes; neonatal herpes Blood transfusion Disease: Vertical from mother to fetus ○ Gingivostomatitis Infection of oral cavity (Gingivo: gums; stoma: tongue) Dr. Bandalan: Gingivitis (swollen, tender gums) MODES OF VERTICAL TRANSMISSION: is the most striking and common ○ PLACENTAL lesion. ○ PERINATAL ○ Pharyngitis → most common form Sometimes extend to esophagus → the baby will pass thru the infected especially in vaginal canal immunocompromised patients ○ NEONATAL ○ Herpes Labialis (most common) → child is exposed to the mother’s Infection in mucocutaneous secretions (breast milk) junction of the lips → RECALL: ○ Genital infection All DNA viruses are DOUBLE STRANDED (DS) except Sexually transmitted Parvovirus All RNA viruses are SINGLE STRANDED (SS) except Both serotypes causes genital Reovirus herpes but often, it is caused by All DNA viruses are enveloped except: HSV-2 “PaPaAdPo” (naked) Characterized by → Parvovirus vesiculoulcerative lesions of the → Papillomavirus penis of the male or of the cervix, → Adenovirus vulva, vagina, and perineum of → Polyomavirus All RNA viruses are enveloped except the female “naked at a Picnic in Rio, California, & Australia” Lesions are very painful and may (naked) be associated with fever, malaise, → Picornavirus dysuria, and inguinal → Reovirus lymphadenopathy → Calicivirus ○ Conjunctivitis → Astrovirus Inflammation of conjunctiva Table 1. Human Parvovirus B19 ○ Keratitis Syndrome Host/Conditions Clinical Features Inflammation of cornea Erythema Children Cutaneous rash ○ Keratoconjunctivitis infectiosum Adults Arthralgia-arthritis Recurrent eye lesions are Transient Underlying Severe acute common and appear as: aplastic hemolysis anemia Dendritic keratitis crisis Corneal ulcers Pure red cell Immunodefi Chronic anemia Eyelid vesicles aplasia ciencies Recurrent keratitis can cause: Hydrops Fetus Fatal anemia fetalis Progressive corneal Source: Dr. Bandalan’s PPT stroma involvement Permanent opacification Blindness HSV infections are a leading cause of corneal blindness in the United States, second only to trauma. Figure 4. Clinical manifestations of diseases caused by ○ Herpetic whitlow Human Parvovirus B19 Herpes skin infection of the finger Source: Dr. Bandalan’s PPT ○ Encephalitis HSV: most common cause of E. HERPES SIMPLEX VIRUS (HSV) 1 & 2 encephalitis in US Herpesviridae Japanese encephalitis Virus: ○ Alpha group most common cause of dsDNA, enveloped, icosahedral encephalitis in Asia Transmission: Direct contact with infected ○ Disseminated disease secretions 3 of 8  Lesson 3: Microbial Agents of Skin Infections 4 NMD2027 ○Neonatal Herpes Additional Information: most commonly caused by HSV-2 PATHOLOGY may be acquired in utero, during Primary Infection: birth, or after birth 1. The virus must encounter mucosal Most common route of infection: surfaces or broken skin for an infection to during birth by contact with be initiated (unbroken skin is resistant) herpetic lesions in the birth canal 2. Viral replication occurs first at the site of To avoid infection: delivery by infection. cesarean section has been used 3. Virus then invades local nerve endings and in pregnant women with genital is transported by retrograde axonal flow to herpes lesions. dorsal root ganglia. Cowdry type A inclusions 4. After further replication, latency is ○ Intranuclear Inclusions established. Review on Tzanck test Latent infection ○ Multinucleated giant cell in syncytia ○ Virus resides in latently infected ganglia in formation a nonreplicating state. ○ Stained scrapings obtained from base of ○ Only a few viral genes are expressed vesicle during latency. Treatment: Acyclovir ○ Viral persistence in ganglia lasts for the ○ Drug of choice host’s lifetime. ○ Same for Varicella-Zoster Infection ○ No virus is found between recurrences near the usual lesion site. Dr. Bandalan: ○ Provocative stimuli can reactivate the latent Infections are usually mild, usually asymptomatic. virus, including axonal injury, fever, stress, Systemic disease rarely developed. and UV exposure. Transmitted by direct contact with infected ○ The virus travels through axons to secretions: peripheral sites, where replication occurs. ○ Infected saliva in patients with ○ Spontaneous reactivations can happen oropharyngeal lesions despite host immunity. ○ Genital secretions of patients with genital ○ Immunity limits local viral replication during herpes recurrences. Once you are infected with HSV, you will have it for ○ Many recurrences are asymptomatic, only life. detectable through viral shedding. 2 serotypes: HSV 1 & 2 ○ Symptomatic recurrent episodes often ○ HSV 1 manifest as cold sores near the lip. Transmitted by contact, usually ○ Over 80% of humans carry latent HSV-1, involving infected saliva but not all experience recurrences. associated with oropharyngeal ○ The reason for reactivation in some lesions individuals remains unknown. Recurrent fever blisters or cold sores ○ HSV 2 Transmitted sexually or from a maternal genital infection to a newborn Associated with genital infections Most common cause of Neonatal Herpes (Neonatal Herpes is also caused by HSV 1) ○ Similar in organization and exhibit Figure 5. HSV 1 & 2 Lesions substantial sequence homology Source: Dr. Bandalan’s PPT ○ Can be distinguished by sequence analysis or by restric- tion enzyme Dr. Bandalan: analysis of viral DNA Herpes Lesions ○ Cross-react serologically, but some A: Herpes Labialis unique proteins exist for each type B: Herpes in the trunk ○ Patterns of transmission are becoming C. Herpes in the Eye less distinct, and both viruses can cause ○ Can involve the cornea either presentation ○ Eventually, it can cause blindness if the lesions are not treated D: Genital Herpes ○ Can be found in vulva and cervix 4 of 8  Lesson 3: Microbial Agents of Skin Infections 4 NMD2027 Table 2. Herpesviridae Chickenpox lesions are more prominent in the Mnemonics trunk “Simple, Simple ○ Have different stages of development Herpesviridae lang niyan. Very dsDNA It is infectious to others as long as the skin rash is Group Easy like enveloped Chicken na there or if the lesions are not yet healed. icosahedral Roasted in Varicella pneumonia Kenny’s” ○ rare in healthy children HHV 1 HERPES SIMPLEX 1 Simple HHV 2 ○ most common complication in neonates, HERPES SIMPLEX 2 Alpha Simple HHV 3 VARICELLA ZOSTER Very adults, and immunocompromised patients HHV 4 EPSTEIN BARR Gamma Easy Reactivation: When infected and healed from HHV 5 CYTOMEGALOVIRUS Chicken Chicken pox (Varicella), the virus will stay dormant HHV 6 Beta Roasted in the neurons of sensory nerve ganglia. Later on, ROSEOLA INFANTUM triggers will cause reactivation of virus causing HHV 7 In HHV 8 KAPOSI SARCOMA Gamma Kenny’s Herpes Zoster infection (a.k.a Shingles) Dr. Bandalan: Take note of the Herpesviridae groups Chickenpox can still reoccur even if previously infected or vaccinated with one dose of Varicella F. VARICELLA-ZOSTER VIRUS (VZV) vaccine Herpesviridae ○ Alpha group Shingles (Herpes Zoster) dsDNA, enveloped, icosahedral There is a particular distribution of the skin lesions Transmission: Close personal contact, especially because it usually follows the nerve innervation of respiratory the area. Incubation period of 14-16 days ○ Most common nerve involved: Thoracic Respiratory mucosa → regional lymph nodes → Nerve blood → endothelium →skin ○ trunk, head, and neck are most commonly ○ Skin: macules→vesicles→crusting affected. Site of latency: sensory nerve ganglia/neurons ○ In many instances, unilateral. in sensory ganglia ○ Myth: Bilateral lesions are deadly. Disease Extreme painful lesion ○ Primary infection: Chicken pox (Varicella) ○ Elderly: They cannot be relieved by usual ○ Reactivation: Shingles (Herpes zoster) analgesics. Anesthetics are used Treatment: Acyclovir sometimes for pain relief. ○ Same for HSV Infection Postherpetic neuralgia: most common Vaccine complication of zoster in elderly adults. ○ Live, attenuated varicella vaccine Can be the source of Chicken pox infection, ○ Before, the recommended dose for especially in children. Varicella vaccine was only one dose. Nowadays, 2 doses of vaccine is recommended for complete protection. Figure 6. Varicella-Zoster Virus Lesions Source: Dr. Bandalan’s PPT Dr. Bandalan: Chicken Pox (Varicella) Figure 7. Pathogenesis of Primary Infection with Varicella-Zoster Virus infection is a childhood Varicella-Zoster Virus disease Source: Jawetz Medical Microbiology, 28th Ed. There are individuals who did not develop chickenpox during childhood but rather developed it when they reached adulthood. G. SMALLPOX (VARIOLA) Not as contagious like measles DNA enveloped Poxviridae Skin lesions: Complex symmetry 1. Start as macule like a pimple, Generalized infection with pustular rash that leaves 2. Become a vesicle deep-seated scars 3. Vesicle ruptures Inclusion body called Guarnieri bodies 4. Lesion will be covered by a crust Eradicated since 1980 Biological weapon 5 of 8  Lesson 3: Microbial Agents of Skin Infections 4 NMD2027 Dr. Bandalan: ○ 1-5 days of fever & malaise → exanthem Completely eradicated due to smallpox vaccine, no (macules → papules → vesicles → natural smallpox infection since 1980 pustules) → crust falls after 2 weeks → Lesion starts as papule → vesicle → pustular rash pink scars Usually leaves permanent scars ○ In each affected area, the lesions were generally found in the same stage of development (in contrast to chickenpox). Immunity: ○ Infection with one virus w/in the Orthopoxvirus genus induces an immune response that reacts with all other members of the group. Laboratory Diagnosis: ○ Identification of viral DNA or antigen from the lesion ○ Direct microscopic examination of material from skin lesions ○ Recovery of virus from the patient ○ Demonstration of antibody in the blood Treatment: Figure 7. Smallpox Rash ○ Primarily supportive Source: Dr. Bandalan’s PPT ○ Methisazone - chemotherapeutic agent, effective as prophylaxis only ADDITIONAL INFORMATION: ○ Cidofovir - nucleotide analog, also been Comparison of Vaccinia and Variola Viruses: used to treat molluscum contagiosum ○ Vaccinia virus and orf virus infections agent used for smallpox vaccination species of Orthopoxvirus H. MONKEYPOX product of genetic Orthopoxvirus of Poxviridae recombination, a new species Zoonotic derived from cowpox virus or Primary reservoir host is not known but squirrel, rabbits, variola virus by serial passage, and rodents can be infected or the descendant of a now Central and West Africa extinct viral genus Transmission: Direct contact with infected person or Has a broad host range that animals or contaminated materials includes rabbits and mice Human monkeypox similar to smallpox but less severe ○ Variola virus: Incubation period: 5-21 days Has a narrow host range (only Fever, intense headache, lymphadenopathy, back pain, humans and monkeys) myalgia Pathogenesis and Pathology of Smallpox: Pronounced lymphadenopathy occurs in most patients, a ○ The portal of entry of variola virus was feature not seen with smallpox or chickenpox. the mucous membranes of the upper Skin rash appear 1-3 days of fever: face, palms and respiratory tract. soles, oral mucosa, genitalia ○ After viral entry, the following are believed ○ Macule to papule to vesicles to pustules to to have taken place: crust/scab which dry up and fall off (1) primary multiplication in the Self-limited; 2-4 weeks lymphoid tissue draining the site Complications are common and often serious: of entry; ○ pulmonary distress (2) transient viremia and ○ secondary bacterial infections infection of reticuloendothelial ○ encephalitis cells throughout the body; Vaccination with vaccinia either protects against (3) a secondary phase of monkeypox or lessen the severity of disease multiplication in those cells, leading to Dr. Bandalan: (4) a secondary, more intense Gibasa lang ni doc ang ppt for this part. viremia; and (5) the clinical disease ○ By the 6th-9th day, lesions in the mouth tended to ulcerate and discharge virus. Clinical Findings: Figure 8. Monkeypox (Microscopic) ○ Incubation period of variola: 10–14 days Source: Dr. Bandalan’s PPT ○ Onset was usually sudden 6 of 8  Lesson 3: Microbial Agents of Skin Infections 4 NMD2027 Oncogenic: Cervical and penile carcinoma (especially HPV types 16 and 18) Treatment: ○ Spontaneously disappear ○ Surgical or chemical removal Prevention Figure 9. Monkeypox Rash ○ Avoid contact with infected person Source: Dr. Bandalan’s PPT ○ Active vaccine I. MOLLUSCUM CONTAGIOSUM Molluscipoxvirus genus of Poxviridae The viral DNA resembles vaccinia but antibodies to the virus do not cross-react with any other poxviruses. Occurs only in humans Figure 12. HPV vaccine: Gardasil More frequent in children than in adults. Source: Dr. Bandalan’s PPT Transmitted by ○ Direct (including sexual contact) Dr. Bandalan: ○ Indirect contact (by barbers, common use HPV of towels, swimming pools) We have more than 100 serotypes of HPV Benign tumors described as small, pinkish, wart-like however only those associated with genitals can lesions on the face, arms, back buttocks cause transformation of cells Incubation period: may extend for up to 6 months Types 16 and 18 have the highest form of The virus is a poor immunogen malignancy and now have become serotypes for ○ 1/3 of patients never produce antibodies Anti-HPV vaccine against it. Condylomata Acuminata are the anogenital warts ○ second attacks are common occurs in the genital area and anus Inclusion body called Molluscum bodies of Chronic and repeated infections of HPV will Henderson-Patterson bodies increase the risk of development of carcinoma esp. in the vulva, penis and even larynx Koilocytes/ Koilocytosis - referred to as the epithelial infection of HPV. Taken via Pap’s Smear which shows the atypical change in the epithelial cell. Figure 10. Molluscum contagiosum The virus CANNOT PENETRATE THE INTACT Source: Dr. Bandalan’s PPT SKIN AND MUCOUS MEMBRANE BUT ONLY THROUGH ABRASIONS WHERE IT CAN ENTER AND SELF INOCULATES. J. HUMAN PAPILLOMAVIRUS (HPV) Serotypes 6,11,16,18 are also carcinogenic types DNA non enveloped Papillomaviridae which can prevent malignancy to those who are Transmission: sexually active. ○ Direct contact US recommends vaccination at 9 yrs ○ Sexual contact for genital warts Philippines recommends vaccination at 12-14 yrs ○ Autoinoculation Site of latency: Epithelial tissue Disease ○ Induce hyperplastic epithelial lesions of K. HAND-FOOT-AND-MOUTH DISEASE skin and mucous membranes Coxsackievirus A ○ Warts: skin warts, plantar warts, flat warts, Oral and pharyngeal ulcerations and a vesicular anogenital warts, laryngeal papillomas rash on the palms and soles that may spread to the ○ Cancers of the cervix, vulva, penis, anus, arms and legs oropharyngeal cancers Vesicles heal without crusting Figure 11. HPV infections Source: Dr. Bandalans PPT Figure 13. Hand-Foot-and-Mouth Disease Source: Dr. Bandalan’s PPT 7 of 8  Lesson 3: Microbial Agents of Skin Infections 4 NMD2027 Dr. Bandalan: B. PEDICULOSIS (LICE) Coxsackievirus A ○ belongs to Picornaviridae Table 3. Lice in the body ○ belongs to the enterovirus group along Pediculus humanus with Coxsackievirus B capitis – head louse ○ It can also cause: Herpangina - lesions produced in the oral cavity; many lesions involved can be: (1) bacterial, (2) viral, or (3) fungal Pediculus humanus Head-Foot-and-Mouth Disease usually occurs in corporis – body louse children. II. PARASITIC SKIN INFESTATION Phthirus pubis (crab Scabies louse) – pubic louse Pediculosis Source: Dr. Bandalan’s PPT A. SCABIES Life Cycle: Caused by a mite Sarcoptes scabiei ○ Adult lice lay eggs (nits) → nymphs → adult Suck blood for nutrition Treatment: Permethrin VII. APA REFERENCES [Bandalan, J.]. (2023). Microbial Agents Causing Skin Figure 14. Sarcoptes scabiei Infections Part 4 [Powerpoint Slides]. College of Source: Dr. Bandalan’s PPT Medicine, Davao Medical School Foundation, Inc. Jawetz, Melnick and Adelberg’s Medical Microbiology (28th ed.). McGrawHill. Intense local itching and is caused by the mite Dr. Bandalan Audio Recording burrowing under the skin to lay its eggs Mite transmitted by intimate contact including sexual contact Treated by topical application of Permethrin Difficult cases may be treated with oral Ivermectin Figure 15. Scabies Source: Dr. Bandalan’s PPT Dr. Bandalan: Scabies are produced by the migration of the mite, and produce lesions as it burrows under the skin to lay their eggs. Belongings and beddings can be sources of infestation. 8 of 8