Infectious Diseases of Skin, Eye, Nervous Sys Summer 2020 PDF
Document Details
Uploaded by VerifiableTrust
Houston Community College
2020
Tags
Related
- PATHOLOGY 375 Lecture 11 Female Reproductive System, Breast, and Skin Pathology PDF
- Lecture 9 - Skin, Eyes and Central Nervous System Diseases PDF
- Infectious Skin Infections PDF
- Lecture 7: Chapter 30.1-30.2 Pathogenesis and Control of Viral Diseases PDF
- Phytotherapy to Skin Disorders Lecture 1 PDF
- Odos ligų skaidrės PDF
Summary
This document is a chapter about infectious diseases of the skin, eye, and nervous system from a Summer 2020 course.
Full Transcript
Chapter 19 Infectious Diseases Affecting the Skin Skin • Epidermis – Stratum corneum (dead cells are sloughed off) • Keratin (protein) – Waterproof the skin – Protects from microbial invasion – Replaced every 25-45 days – No nerve endings or blood vessels Skin continued • Dermis – Source for ep...
Chapter 19 Infectious Diseases Affecting the Skin Skin • Epidermis – Stratum corneum (dead cells are sloughed off) • Keratin (protein) – Waterproof the skin – Protects from microbial invasion – Replaced every 25-45 days – No nerve endings or blood vessels Skin continued • Dermis – Source for epidermis cells – Connective tissue (fibers) – Nerves, blood vessels, lymphatic – Hair follicles, glands (sebum, lysozyme) • Subcutaneous layer The different layers of the skin are important defenses of the skin. Fig. 18.1 A cross-section of skin Normal flora • Survive dry and salty conditions • Dense populations in the skin folds • Types – Diphtheroids (Propionbacterium acnes) – Micrococci (Staphylococcus epidermis) – Yeast (Candida albicans) Structure of the Skin • Wounds – Trauma to any tissue of the body • Cuts, scrapes, surgery, burns, bites, etc. – Allow microbes to infect the deeper tissues of the body • In most cases other body defenses eliminate infection • Can result in severe or fatal diseases © 2012 Pearson Education Inc. Skin Diseases • • • • • • • • • Acne Impetigo Cellulitis Staphylococcal Scalded Skin Syndrome (SSSS) Gas gangrene Hansen’s Disease Skin rashes Warts Large skin lesions Acne • Most common skin disorder • Proprionibacterium acnes, actually part of normal flora • Increased sebum production, ducts become blocked, rupture of follicle lining. • Prevention: good skin hygiene, genetic. • Rx- antibiotics, Accutane, topicals with benzoyl peroxide, Retin-A. • New treatment uses blue-light wavelength to destroy bacteria Figure 19.7 The development of acne Normal skin Pore Oily sebum produced by glands reaches the hair follicle and is discharged onto the skin surface via the pore. Bacteria Sebum Sebaceous gland Hair follicle Whitehead Inflamed skin swells over the pore when bacteria infect the hair follicle, causing the accumulation of colonizing bacteria and sebum. Blocked pore Blackhead Pus Pustule formation Dead and dying bacteria and sebum form a blockage of the pore. Severe inflammation of the hair follicle causes pustule formation and rupture, producing cystic acne, which is often resolved by scar tissue formation. Boils: Furuncles and Carbuncles Carbuncles- multiple heads, Furuncles- one head • • • • AKA Folliculitis, boils, sty (eyelash follicle) Infection of hair follicles Caused by S. aureus most often Spread by direct contact through micro abrasions • Complications; septicemia, pain, pressure • Prevent with cleanliness, no sharing of fomites • Rx- drainage, antibiotics Figure 19.2 Staphylococcus Impetigo • Caused by S. pyogenes and S. aureus • Direct/indirect contact through breaks in the skin, easily spread through fomites • Most common in school age children • Symptoms: superficial, pus filled blisters covered by yellowish brown crust, weepy. “brown sugar crusts” • Highly contagious • Prevention; hand washing, clean towels, bedding etc. • Rx- topical antibiotics, oral antibiotics for more severe cases Scalded skin syndrome • Caused by exfoliative exotoxin released by lysogenized strains of S. aureus • More common in infants, local infection spreads through the blood. • Skin blisters, then begins to peel. Red moist, tender skin revealed underneith – 20-100% of epidermis peels off in sheets, – Fatigue, fever, malaise, irritability – Rx- antibiotics, fluid & electrolyte replacement. Bacterial Diseases of the Skin and Wounds • Necrotizing Fasciitis – Pathogen and virulence factors • Most cases caused by S. pyogenes • Various enzymes facilitate invasion of tissues • Exotoxin A and streptolysin S are also secreted – Pathogenesis and epidemiology • S. pyogenes enters through breaks in the skin • Usually spread person-to-person – Diagnosis, treatment, and prevention • Early diagnosis is difficult because symptoms are nonspecific © 2012 Pearson Education Inc. • Treat with clindamycin and penicillin Figure 19.6 Necrotizing fasciitis Bacterial Diseases of the Skin and Wounds • Cat Scratch Disease – Pathogen and virulence factors • Caused by the Gram-negative bacterium Bartonella henselae • Endotoxin is the primary virulence factor – Pathogenesis and epidemiology • Transmitted by cat bites or scratches – Diagnosis, treatment, and prevention • Diagnosed with serological testing • Treated with antimicrobials © 2012 Pearson Education Inc. Bacterial Diseases of the Skin and Wounds • Pseudomonas Infection – Pathogen and virulence factors • Pseudomonas aeruginosa is the causative agent – Found in soil, decaying matter, moist environments • Virulence factors – Adhesins, toxins, and a polysaccharide capsule – Pathogenesis • Infection can occur in burn victims – Bacteria grow under the surface of the burn • The bacteria kills cells, destroys tissue, and triggers shock © 2012 Pearson Education Inc. Figure 19.8 Pseudomonas aeruginosa infection Gangrene • Gas gangrene, caused by Clostridium perfringens toxin. (anaerobic bacteria) • Often associated with crushing, or dirty wounds, extensive tissue damage, C. perfringens is transferred into wound. • Acute onset of pain, fever, skin turns bluish and tight because of gas production, brown frothy rotten smelling fluid in wound. Sepsis is likely. Necrosis of tissue. Crackling sound. • Prevention- prompt cleaning of wounds. • Rx- antibiotics, hyperbaric oxygen treatments, debridement, amputation. Bacterial Diseases of the Skin and Wounds • Gas Gangrene – Pathogenesis and epidemiology • Traumatic event must introduce endospores into dead tissue • Mortality rate exceeds 40% – Diagnosis, treatment, and prevention • Appearance is usually diagnostic • Rapid treatment is crucial – Surgical removal of dead tissue – Administration of antitoxin and penicillin • Prevent with proper cleaning of wounds © 2012 Pearson Education Inc. Leprosy, Hanson’s disease • Caused by Mycobacterium leprae. Slowly grows at cooler temperatures (30o C.) (what body parts does it strike?) • After several years of infection symptoms finally develop, skin lesions. Develops into tuberculoid, or lepromatous variety. • Tuberculoid destroys tissue, but mostly lose of nervous sensation in those areas. • Lepromatous destroys a lot of tissue. Underlying bone and cartilage often destroyed. Loss of sensation patchy. • Rx- Dapsone, rifampin, clofazimine, Hawaii treatment Chicken Pox • Varicella zoster virus • Highly contagious, direct/indirect transmission through respiratory droplets, and weepy lesions. • Pathology – Macules (red spots) become papules (bumps) turn into vesicles (blisters) become infected and turn into pustules. – Itchy rash spreads from head, down to trunk, then out to extremities. Concentrated on trunk. – Rx.- Vaccination, supportive therapy, calamine lotion Viral Diseases of the Skin and Wounds • Chickenpox and Shingles – Signs and symptoms • Chickenpox characterized by lesions on the back and trunk that spread across body • Shingles lesions localized to skin along an infected nerve – Pathogen • Varicella-zoster virus (VZV) causes both diseases – Pathogenesis • Infected dermal cells cause rash characteristic of chickenpox • Virus becomes latent in nerve ganglia © 2012 Pearson Education Inc. – Reactivated VZV causes shingles Viral Diseases of the Skin and Wounds • Chickenpox and Shingles – Epidemiology • Chickenpox occurs mostly in children – Disease is more severe in adults • Risk of shingles increases with age – Diagnosis, treatment, and prevention • Diagnosis based on characteristic lesions • Treatment based on relief of symptoms • Vaccine available against chickenpox © 2012 Pearson Education Inc. Cold sores Figure 1. The herpes simplex virus life cycle. (a) Herpes simplex virus (HSV) is shown undergoing the lytic cycle (entry, uncoating, viral transcription and DNA replication in the nucleus, particle assembly, exit from the cell) in epithelial cells of the skin to cause a primary infection. (b) Some virus enters the sensory neuron terminals and travels retrogradely to the nucleus where it establishes latency. (c) Periodic reactivation results in anterograde transport of viral particles, shedding from the neuron, and re-infection of epithelial cells, which leads to asymptomatic shedding or recurrent lesions. • Herpes simplex I, Cold sores, fever blisters, oral herpes • Majority of population infected, only 15% have outbreaks • Transmission- fomites, and direct contact • Virus remains in dorsal root ganglia, reactivated by several factors; stress, excessive sun, heat, immunodeficiency. • Prevention, avoid close contact with someone who has an outbreak • Rx-acyclovir reduces length and severity of outbreaks Figure 19.12 Sites of events in herpesvirus infections Ophthalmic branch Trigeminal (V) nerve ganglion Site of viral latency Ocular herpes Maxillary branch Mandibular branch Brachial ganglia Site of viral latency Fever blisters Sacral ganglia Site of viral latency Genital herpes Whitlow Smallpox • Variola virus (overall fatality 30%) • Transmission - Fairly prolonged face to face contact, as well as contact with body fluids or infected items like bedding. • Fever, headache, body ache, then rash appears in the mouth. Rash moves to head and extremities. Red spots become umbilicated bumps with thick fluid inside. Then pustules with hard bump inside, then scab over. • Infectious until scabs have all fallen off. • Last case in U.S. 1949, last case in the world 1977 eradicated through vaccination. • Cidofovir possible drug for treatment Measles, rubeola Measles, Rubeola (red measles) • Rubeola virus • Transmitted by respiratory droplets • More common and less severe in school aged kids vs, infants or adults. • Pathology – Fever, runny nose cough swollen weepy eyes – Koplik spots appear on tongue and inside of mouth (salt grains) – Eruption of fine red rash on the forehead and spreads to the trunk of body. – Rx- MMR vaccine 95-99% effective, could be eradicated if not for unvaccinated population. Cases Cases (thousands) Figure 19.15 Measles cases in the United States since 1950 Attenuated vaccine licensed Year Rubella, German measles • Rubella virus • Transmission respiratory droplets • Mild childhood disease, headache fever, malaise, rash on face, chest, abdomen, NO koplik spots • Serious complication for pregnant women, – Infection during 1st 6 weeks minor deafness, crosses the placenta can affect, ears, eyes, heart and brain. Rx- MMR vaccine very effective, 3 months before pregnancy test your titer. Figure 19.14 The efficacy of immunization against rubella Cases Cases (thousands) Attenuated vaccine licensed Year Features for measles, rubella, fifth disease, and roseola. Checkpoint 18.8 Maculopapular rach diseases Viral Diseases of the Skin and Wounds • Warts – Benign epithelial growths on the skin or mucous membranes • Can form on many body surfaces – Various papillomaviruses cause warts – Most warts are harmless – Transmitted via direct contact and fomites – Diagnosed by observation – Various techniques to remove warts • New warts can develop due to latent viruses © 2012 Pearson Education Inc. Figure 19.13 Various kinds of warts--lesions caused by papillomavirusesoverview Features of papillomas and molluscum contagiosum. Checkpoint 18.9 Wart and wart-like eruptions. Features of leishmaniasis and cutaneous anthrax. Checkpoint 18.10 large pustula skin lesions Superficial mycoses Mycoses of the Hair, Nails, and Skin • Mycoses are diseases caused by fungi • Most are opportunistic pathogens • Mycoses are classified by infection location – Superficial – occur on the hair, nails, and outer skin layers; most common fungal infections – Subcutaneous – in the hypodermis and muscles – Systemic – affect numerous systems © 2012 Pearson Education Inc. • Tinea corporis (skin/ring worm), capitis (scalp), cruris (groin), pedis (foot) - Caused by various dermatophytes • Transmission through breaks in the skin, spread with contact. • reddened raised area with itchy, scaly sometimes flaking skin. Hair loss, or cracks in skin can occur. • Prevention; reduce body surface moisture, wear loose breathable clothing, regularly change socks, wear flip flops at the gym! • Rx – prescription and OTC fungal medications, miconazole. Figure 19.19 Dermatophytosis (ringworm) Parasitic Infestations of the Skin • Leishmaniasis – Signs and symptoms • Cutaneous: Produces large painless skin lesions • Mucocutaneous: Skin lesions enlarge to encompass mucous membranes • Visceral: Parasite is spread by macrophages throughout body – Pathogen and virulence factors • Leishmania is the causative agent – Protozoan transmitted to humans by female sand flies © 2012 Pearson Education Inc. Figure 19.24 Mucocutaneous leishmaniasis Chapter 20 Microbial Diseases of the Nervous System and Eyes Eye • Conjunctiva – Thin membrane that covers the eye, except the cornea – Secretes oil and mucous-containing fluids • Best defense • Cornea – Covers the iris – Several layers of epithelial cells – Epithelial cells can regenerate if damaged • No lymphocytes, no inflammation – Immune privilege The main parts of the eye that are important eye defenses. Fig. 18.2 The anatomy of the eye. The best defense of the eye is the film of tears, which originates from the lacrimal apparatus of the eye. Fig. 18.3 The lacrimal apparatus of the eye. Conjunctivitis “Pink eye” Many organisms: Neisseria, Chlamydia, Staph. & Strep. Various viruses Direct contact transmission Inflammation of the conjunctiva, itching, burning, swelling of lids, redness of eyes and eyelid, and crusty exudates. Treatment: antibiotic therapy/ self resolution Often associated with ear / respiratory infections Otitis media • Middle ear infection • Variety of bacteria, S. pneumoniae, S. pyogenes, S. aureus • Associated with pink eye, and sinusitis • Pressure pain in ear, rupture of eardrum • Mastoiditis and meningitis • Treatment with antibiotics tubes (kids) Summary of diseases of the skin and eye. Taxanomic organization of microorganisms causing diseases of the skin and eyes. Infectious Diseases Affecting the Skin and Eyes. Fig. 18.p573 Nervous system • Central nervous system (CNS) • Peripheral nerves (PNS) CNS • Brain • Spinal cord • Neurons – cells that make-up the brain and spinal cord • Defenses Defenses • Meninges – surround the brain and spinal cord • Cerebrospinal fluid (CSF) • Bone casing • Blood-brain barrier • Immunologically privileged A diagram of the central nervous system and the peripheral nerves. Fig. 19.1 Nervous system. Important structures of the brain and spinal cord that are associated with defenses. Fig. 19.2 Detailed anatomy of the brain an spinal cord. Normal flora • Absent • Viruses can exist in a dormant state in the nervous system Structure of the Nervous System • Portals of Infection of the Central Nervous System – CNS is an axenic environment • It has no normal microbiota – Pathogens may access the CNS several ways • Breaks in the bones and meninges • Medical procedures • Travel in peripheral neurons to the CNS • Infect and kill cells of the meninges, causing meningitis © 2012 Pearson Education Inc. Nervous System Diseases • • • • • • • • • • Meningitis Neonatal meningitis Meningoencephalitis Acute encephalitis Subacute encephalitis Rabies Poliomyelitis Tetanus Botulism African sleeping sickness Bacterial Diseases of the Nervous System • Bacteria cause disease in two ways – Infect cells of the nervous system • Meningitis • Leprosy – Bacteria growing elsewhere release toxins that affect neurons • Botulism • Tetanus © 2012 Pearson Education Inc. Meningitis • Five species cause 90% of bacterial meningitis cases – Neisseria meningitidis (most severe) – Streptococcus pneumoniae (most common in adults) – Haemophilus influenzae – Listeria monocytogenes – Streptococcus agalactiae Also caused by various fungi and viruses. Acute onset of fever, headache, painful or stiff neck, increased number of white blood cells in CSF. Confused or disturbed brain function. Transmission – Mostly respiratory droplets Meningococcal meningitis causes the most severe Acute forms of meningitis. Associated with epidemic forms of meningitis. Petechiae, ecchymosis, shock and coma. Death can occur within a few hours Treatment – Suspicion of bacterial meningitis is a medical emergency and treatment begins immediately. 15% mortality rate for treated cases. Penicillin is given in large doses via IV. Vaccination is available for bacterial forms. Viral forms: Generally milder than bacterial or fungal forms. Usually resolves in 2 weeks. Prevention – good hygiene, no treatment. Meningitis Bacterial Diseases of the Nervous System • Bacterial Meningitis – Pathogenesis • S. agalactiae acquired during birth • Listeria transmitted via contaminated food • Other species transmitted via respiratory droplets – Epidemiology • S. pneumoniae present in throat of 75% of humans • Not spread by casual contact • Meningococcal meningitis can become epidemic © 2012 Pearson Education Inc. Features of meningitis caused by different species of bacteria, and viruses. Checkpoint 19.1 Meningitis Viral Diseases of the Nervous System • Viruses more readily cross the blood-brain barrier • Occur more frequently than bacterial and fungal infections • Include meningitis, polio, rabies, and encephalitis © 2012 Pearson Education Inc. Acute encephalitis • • • • Viral infection Arboviruses Herpes simplex 1 or 2 JC virus Viral Diseases of the Nervous System • Arboviral Encephalitis – Arboviruses are arthropod-borne viruses • Transmitted via blood-sucking arthropods (e.g., mosquitoes) – Mosquito-borne arboviruses can cause arboviral encephalitis – As zoonotic diseases, they rarely affect humans – Arboviruses usually cause mild, coldlike symptoms • Can cause if cross the blood-brain barrier © 2012 Pearson Education Inc. Table 20.2 Characteristics of Arboviral Encephalitis Diseases and Viruses in the United States Figure 20.16 Human West Nile virus encephalitis in the United States Reported cases Number of reported cases Annual deaths (299) (124) (264) (84) (86) (9) Time (months/years) (43) (30) Viral Diseases of the Nervous System • Arboviral Encephalitis – Diagnosis based on signs and symptoms • Confirmed by presence of arbovirus-specific antibodies in CSF – Treatment is supportive – Prevention involves limiting contact with mosquitoes • Use netting and insect repellents • Eliminate stagnant water – Vaccines for horses available against EEE, WEE, VEE, and WNV © 2012 Pearson Education Inc. Subacute encephalitis • • • • Mostly a protozoan infection Viral infection Prion infection Symptoms develop slowly Kuru - a rare and fatal brain disorder - occurred at epidemic levels during the 1950s-60s among the Fore people in New Guinea. -practice ritualistic cannibalism: relatives consumed the tissues (including brain) of deceased family members. Brain tissue from individuals with kuru was highly infectious Comparison between a normal and prion infected brain tissue sample. Fig. 19.14 The microscopic effects of spongiform Encephalopathy. Prion Disease • A prion is an infectious protein • Spongiform encephalopathies • A class of diseases that includes scrapie and mad cow disease • Leave the brains of victims full of holes • Humans can contract by eating meat from infected cattle © 2012 Pearson Education Inc. Prion Disease • Variant Creutzfeldt-Jakob Disease – Signs and symptoms • Insomnia, weight loss, and memory failure • Progressive worsening of muscle control – Pathogen, pathogenesis, and epidemiology • Caused by abnormal form of prion • Prions may remain formant for many years – Diagnosis, treatment, and prevention • Diagnosed by characteristic signs and symptoms – Confused with other forms of dementia in elderly • No treatment is available • Prevented by avoiding prion contaminated meat © 2012 Pearson Education Inc. Rabies - rabies virus Transmission – contact with infected body fluids, usually animal bite. Incubation of 1-2 months (depending on wound site). - Virus replicates in muscle cells and then moves into neurons (Postmortem detection of Negri bodies in the brain) Symptoms – Anxiety, nervousness, impaired swallowing, coma, then death. Furious rabies - agitation, disorientation, seizures, severe pain during swallowing = hydrophobia Dumb rabies – paralyzed, disoriented, stuporous Both result in coma, death from cardiac or respiratory arrest Prevention/treatment – immunizing pets and people. Post exposure antibody therapy and immunization. Immunizing wild populations. Figure 20.12 Predominant wildlife reservoirs for rabies in the U.S. Skunk Fox Raccoon Figure 20.13 Negri bodies Negri bodies Poliomyelitis - Poliovirus Transmission – Fecal to oral route (Transmitted most often by drinking contaminated water) Symptoms are dependent upon destruction of nervous tissue. – Signs and symptoms • Asymptomatic infections – almost 90% of cases • Minor polio – nonspecific symptoms; fever, headache, nausea • Nonparalytic polio – muscle spasms and back pain • Paralytic polio – produces paralysis; causes degrees of flaccid paralysis over a few hours to several days. – Unused muscles begin to atrophy, growth slows and deformities can develop. Limbs are often painful. Treatment – alleviate pain, artificial ventilator if needed, prompt physical therapy. Prevention: 1955 Salk vaccine IPV (inactivated) 1961 Sabin OPV (attenuated) has been discontinued in the U.S. WHO is fighting hard to eradicate polio. Only 4 countries left with wild virus. 1988 – 350,000+ cases in 125 countries. 2005 – 1,951 cases in 4 countries. Figure 20.11 Poliomyelitis-overview The poliovirus has a unique icosahedral capsid shell. Fig. 19.18 Typical structure of a picornavirus. Tetanus - Clostridium tetani toxin (tetanospasmin) Symptoms: Toxin blocks the inhibition of muscle contraction. Clenching of the jaw, extreme arching of the back. Flexion of the arms, extension of legs. Rigid “spastic” paralysis, death occurs because of paralysis of respiratory muscles. Clostridium tetani, the causative agent of tetanus, have a unique tennis racket morphology. Fig. 19.21 C. tetani Transmission – wound infection, Anaerobic conditions, necrotic tissue, poor blood supply, a dirty puncture wound. Prevention/treatment – toxoid vaccination, antitoxin antibodies, antibiotics, muscle relaxants Botulism - Clostridium botulinum toxin 3 types – food borne (intoxication), infant, or wound (infections) Prevents the release of acetylcholine, thus prevents muscle contraction. Symptoms – Double vision, dizziness, difficulty in swallowing. Descending muscular paralysis. Death comes from respiratory arrest. Flaccid “rag doll” paralysis. . Transmission – 20-25% of cases associated with low acid vegetables and fruits improperly canned Prevention/treatment – Proper food prep. Treat with antitoxin and cardiac and respiratory supportive care. Recovery takes weeks. Infant botulism – 80% of cases. Normal flora is undeveloped. Raw honey is one suspected culprit. Botulin can prevent the release of acetylcholine, thereby muscle contractions do not occur. Fig. 19.24 The physiological effects of botulism toxin. African Trypanosomiasis (sleeping sickness) 2 protists, Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense cause the disease. Transmitted by the Tse Tse fly in equatorial Africa. Migrate from bite site to secondary lymph tissue, and multiply – fever, malaise, enlarged nodes, joint pain. Enter CNS, damage blood vessels as well as brain tissue. Symptoms- above malaise, then change in personality or behavior, decreased ability to concentrate, walk, talk. Extreme tiredness during the day, insomnia at night. Eventually coma, then death. Easier drug treatment before CNS is involved, afterward, highly toxic arsenic based drug. Antigenic shifting of protozoan makes a vaccine extremely difficult. Controlling tse tse flies is best option in decreasing the disease Protozoan Diseases of the Nervous System • Primary Amebic Meningoencephalopathy – Signs and symptoms • Same as those of meningitis and encephalitis caused by other microbes – Pathogen, pathogenesis, and epidemiology • Caused by Acanthamoeba and Naegleria • Enter host through abrasions on the skin or the eyelid or by inhalation of contaminated water – Diagnosis, treatment, and prevention • Drugs have limited success • Prevented by avoiding possibly contaminated water supplies © 2012 Pearson Education Inc. Infectious Diseases Affecting the Nervous System. Fig. 19.p608