BIO 208 - Microbiology - Unit 4 - Diseases of Skin ...

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This outline is intended to facilitate your preparation for lecture. This web outline will NOT substitute for regular lecture attendance.For the rest of Unit 4 we will discuss:Significant or Interesting Human DiseasesKey to Understanding Infectious Diseases:Microbes are as old as the planetHumans evolved under the selective pressure of microbesMicrobes see our bodies as just another habitatIn all the vast diversity of microbial life, only the smallest fraction of microbes are capable of causing illnessFor any infection with a potential pathogen, there are a wide variety of possible outcomesA. Diseases of the skinGeneral backgroundMain pathogens of the skinStaphylococcus aureusStreptococcus pyogenesGPC, cat + GPC, cat -Skin diseases caused by S. pyogenesGroup A Strep (GAS)1. impetigo2. erysipelas – infection of dermal layer of skin3. invasive GAS - 10,000-15,000 cases/yr; 2,000 deaths/yra. streptococcal toxic shock syndrome (TSS) 2,000-3,000/yr; 60% fatalThe class vote --Disease - necrotizing fasciitis (a.k.a. flesh-eating strep)Agent – phage-infected strain of group A Streptococcus pyogenes (bacterium, GPC, cat-) frequently initiates the infection, but infection often becomes “polymicrobial” with aerobic and anaerobic pathogens, including Bacteroides, Clostridium, Peptostreptococcus, Enterobacteriaceae, coliforms, Proteus, Pseudomonas, and Klebsiella. Similar clinical course may be seen with Clostridium perfringens and some strains of S. aureus (e.g., MRSA).Virulence factors (what factors does this strain have that other strains do not, that makes this one capable of causing disease)Only strains of. S. pyogenes that are parasitized by lysogenic bacteriophages are virulent – lysogenized strains produce a phage-encoded streptococcal pyrogenic exotoxin (SPE) that is responsible for tissue destruction. A second toxin called exotoxin A interferes with a coordinated immune response.Transmission - direct contact through some minor wound (community-acquired) or through a surgical incision (hospital-acquired)Medical description of disease - “a progressive, rapidly-spreading, inflammatory infection located in the deep fascia, with secondary necrosis of the subcutaneous tissues”.Clinical picture – very rapid progression from trivial wound to gangrene and shock. Take a few notes off the powerpointTreatment – must be aggressive – life support, IV antibiotics, surgical debridement and amputation.Frequency – More rare. - Since 2004, increasing number of cases due to MRSA.Mortality – overall 70-80%; lowered to 20% with aggressive treatment.Prevention - wash hands, keep wounds clean and watch them.B. Diseases of the nervous systemGeneral backgroundNervesBrainEncephalitis - inflammation of the encephalon (the brain itself)Encephalitis is usually caused by viruses or, in rare cases, by protozoa. Always serious, often fatal.The class vote –Disease - RabiesAgent – Lyssavirus (Family Rhabdoviridae; ss RNA virus, enveloped)Virulence factors – evades immune detection in the nervous system. Spreads cell to cell in brain,, causes dysfunction in infected cells.Transmission – direct contact with saliva of an infected animalClinical Picture –Take a few notes off the powerpointTreatment – within 14 days of bite (the sooner the better) - post-exposure prophylaxis. Once clinical signs begin, there is no treatment. Frequency – very rare in humans in the U.S.Mortality – 100% (due to paralysis of respiratory/cardiac systems)Prevention – vaccinate people at high risk (veterinarians, animal control, etc)C. Diseases of the cardiovascular and lymphatic systemsGeneral backgroundThe class vote –Disease – plagueAncient – described in Old Testament3 great historical plague pandemicsJustinian’s plague – 6th century – lasted 60 years, killed 100 millionBlack Death – 14th century – killed 25 million in Europe alone (add in Asia, etc, unknown #)Modern Pandemic – 1896-1930Agent – bacterium Yersinia pestis (GNR, ox-; an Enterobacteriaceae (as is E. coli).Virulence factorsVery complex3 different plasmids carrying multiple virulence genes, the products of which are used for invading host tissue, evading host immune responses, and producing toxinsTransmissionNatural disease of rodents; rats are classic primary reservoir; in US it is wild rodents. Humans are accidental hosts and are not critical for maintenance of disease.Rat fleas are intermediate hosts and vectors, carrying bacteria from one mammalian host to another while feeding.Flea-borne, from infected rodents to humans Direct contact with infected tissues or fluids from handling sick or dead animals Respiratory droplets from cats and humans with pneumonic form of plague Clinical picture 1. Bubonic plague - a very painful, usually swollen, and often hot-to-the touch lymph node, called a “bubo”.2. Pneumonic plague - characterized by development of an overwhelming pneumonia with high fever, cough, bloody sputum, and chills.3. Septicemic plague – characterized by bacterial spread in the bloodstream and necrosis of the tissues (“Black death”)Treatment – antibiotics (streptomycin or tetracycline) if early.Frequency – In US, last urban outbreak was Los Angeles, 1924-25. Now about 18 cases/year. Mortality – Mortality 50-90% if untreated; 15% when diagnosed and treated. Prevention – surveillance of infected animals, vectors, and human contacts. Destruction of plague-infested animal populations.FYI 1 (additional nervous system disease)Disease - Epidemic bacterial meningitisAgent - Neisseria meningitidis (bacterium, GNC, ox+)Virulence factors - 3capsule - evade phagocytosis by host immune cellslipopolysaccharide (lps) – induces inflammationfimbriae – allows for attachment to meningesTransmissionHumans are only host 5-20% of population are asymptomatic carriers – higher end on college campuses Transmitted through the air by respiratory droplets resulting from sneezing and coughing and from direct contact, such as kissing or sharing items with an infected person. College students may have an increased risk of meningitis related to features in campus life. These include active and passive smoking, going to bars, consuming alcohol, and living in close quarters (residence halls). Freshmen living in dormitories are at the greatest risk -- more than 7 times higher than undergraduates in general.Clinical Picture – very rapid progression from flu-like to death (within hours) – can kill more rapidly than any other infectious disease. Take a few notes off the powerpointTreatment – must be aggressive – IV antibiotics, life-supportFrequency - The disease strikes nearly 3,000 Americans each year, and results in 300 deaths annually (100-125 college students are infected yearly, resulting in 5-15 deaths). Of those who survive, one in five suffers a permanent disability due to amputation, brain damage, hearing loss, and seizures.Mortality - The mortality rate is approximately 5% in children and 5-10% in adults; however, meningococcemia associated with DIC (disseminated intravascular coagulation) has a mortality rate of greater than 90%.Prevention – Vaccine for some strainsFYI 2 (additional cardiovascular disease)Viral Hemorrhagic Fever Syndromewidespread vascular damage, leaky small RNA viruses, lipid envelope zoonotic persist in nature most infectious via aerosol4 families – All are RNA viruses!Arenaviridae - Machupo, Lassa Bunyviridae – hantavirus (same as in our epidemiology mystery case), Rift Valley Flaviviridae - dengue, yellow fever Filoviridae - Marburg, EbolaDisease – Ebola hemorrhagic feverAgent – Ebola virusTwo main human infectious strains:Ebola ZaireEbola SudanVirulence factors – still under investigation? ability to evade host interferon? (a chemical produced by infected host cells that interferes with viral replication)? ability to evade immune defenses that are normally activated early against viral infectionsTransmission – blood, aerosol (candidate biowarfare agent)History of the Emergence of EbolaClinical PictureIncubationneedle transmitted 5-7 days; person-person transmission 6-12 daysEarlysudden onset fever, severe headache, severe muscle/body aches – resembles bad case of Influenza at this stageLaternausea, abdominal pain, vomiting, diarrhea5-7 daysfocal necrosis of vascular endothelium leading to hemorrhaging7-16 daysdeath due to shock (severe drop in blood volume)Treatment – No specific treatment for the virus (i.e., no anti-viral drugs) – supportive care only (fluids, electrolytes, comfort care)Frequency – 4 outbreaks of Ebola Sudan (1976-2004); 11 outbreaks of Ebola Zaire (1976-2004)Mortality – 65%-89%Prevention – Interruption of person-person spread*Interesting note - Semen from men recovering from Ebola infection has been shown to contain infectious virus, and Ebola has been transmitted by sexual intercourse involving recovering men and their sex partners.FYI 3 (additional disease that can target skin, nervous, and/or cardiovascular system)Disease - Lyme Disease – emerged in 1975Agent - Borrelia burgdorferi – bacterium, GN spirocheteTransmission - Transmitted to humans through bite of infected deer tickClinical Picture - 3 phases1. 7-10 days post bite - local reaction -expanding ring-shaped lesion (bull’s eye rash), flu-like symptoms2. Weeks - months later – disseminated, spreads throughout the body - neurological abnormalities, heart inflammation, arthritis3. Years later - late stage – nervous system degeneration = neuroborreliosis – why?? Perhaps triggers and autoimmune response that attacks the nervous system?Treatment - Antibiotics early in illnessFrequency - Most common tickborne disease in U.S. 10,000+ cases/yrNatural hosts - deer and field mice Prevention1. Highest transmission May-July 2. Light colored pants with pant legs tucked into socks3. Insecticide for ticks4. Examine your body for ticks, shower w/ lots of soap 5. Prompt removal of ticks ................
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