General Microbiology MICR 210
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This 97 page Class Notes was uploaded by Emmy Thiel on Monday October 26, 2015. The Class Notes belongs to MICR 210 at University of Tennessee - Knoxville taught by E. McPherson in Fall. Since its upload, it has received 28 views. For similar materials see /class/229875/micr-210-university-of-tennessee-knoxville in Microbiology at University of Tennessee - Knoxville.
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MICRBIOLOGY WITII DISEASES BY BODY SYSTEM SECOND EDITION Chapter 23 U 9 mser Structures of the Digestive System Structures of the digestive system divided into two groups Gastrointestinal tract GI tract The pathway from the mouth to the anus Most organs of the GI tract protected by a membranous covering called the peritoneum Accessory digestive organs Organs involved in grinding food or providing digestive secretions The Gastrointestinal Tract Digests food absorbs nutrients and water into the blood and eliminates waste Components of the gastrointestinal tract Mouth site where food is moistened and chewed Esophagus tube leading to the stomach Stomach secretes chemicals that work to digest foods Small intestine responsible for the majority of digestion and absorption of nutrients Large intestine colon completes absorption of nutrients and water Rectum and anus store and eliminate waste The Accessory Digestive Organs Components of the accessory digestive system Tongue and teeth chew food into small pieces Salivary glands secrete saliva that moistens food to allow it be swallowed Liver neutralizes or removes harmful substances from the body and produces bile that aids in digestion Gallbladder concentrates and stores bile that is made in the liver Pancreas produces pancreatic juice that neutralizes stomach acid as it enters the intestine and further digests food Defenses that Protect the Digestive System o A seamless surface of epithelial cells coated with secretory lgA Peristalsis movement of food in the esophagus Stomach acid Microbial antagonism Rapid transport of food through stomach amp duodenum Bile helps slow the growth of some organisms because it is acidic Normal Microbiota of the Digestive System Esophagus Stomach Duodenum These regions are almost free of microbes Tongue Teeth Jejunum Ileum Colon Rectum Tongue and teeth Viridans streptococci are most prevalent in this region Lower small intestine amp colon heavily colonized Bacteroides rod gram anaerobe is the dominant organism in the intestines Lactobacillus Escherichia Enterobacter Proteus and Klebsiella Candida yeast and Entamoeba protozoan Bacterial Gastroenteritis A general terms that refers to the inflammation of the stomach or intestines due to the presence of bacteria Associated with contaminated foods or water and poor living conditions Bacterial Gastroenteritis General Features Signs and symptoms similar despite different causative agents Include nausea vomiting diarrhea abdominal pain and cramps Some cases are asymptomatic or involve mild diarrhea only Dysentery diarrhea containing mucus and blood Diagnosis based on signs and symptoms Causative agent can be identified but generally is not Treatment involves fluid and electrolyte replacement May need antinausea medication May need IV fluid replacement Antidiarrheal drugs may prolong symptoms Bacterial Gastroenteritis General Features Prevention involves proper handling storage and preparation of food Clean food before consuming or cooking Cook foods at a temperature that is high enough to kill bacteria Clean utensils Use only pasteurized milk and juices Good sanitation and personal hygiene Proper handwashing is essential Cholera Pathogen and Virulence Factors Caused by Vibrio cholerae Slightly curved Gramnegative Curved rods 1 restate a Epidemic strains 01 El Tor W f 5 7 Q frhd a a 6 5lt P 7 pandemics and 0139 533 3 z xg l Ben al 33 3 1534 9 are 439 quot 3 at at o Envnronment Within human 323 a tig fivzg g 25 3 13 3 273 3 body activates some genes so l gla fwgm u w it becomes more virulent in g g 39g gg ufg if og 3353 if g 35 c 39 71 Q Q humans versus in the S 39r environment 7 20am Cholera Pathogenesis Humans become infected by ingesting contaminated food and water High infective dose because most cells die in the stomach Those who use antacids have a lower infective dose Environment within a human body activates virulence genes Most important virulence factor is a plasmid encoded cholera toxin five B subunits and one A subunit B subunit binds to receptor on surface of intestinal epithelial cell A1 enters cell s cytosol and activates adenylate cyclase Adenylate cyclase converts ATP gt cAMP cAMP stimulates secretion of electrolytes into intestinal lumen Water follows electrolytes via osmosis Cholera Pathogenesis Intestinal lumen 6 03 A o Cholera toxin B a Water follows binds to electrolytes membrane 1 into lumen of epithelial H20 cell Cl Na C R f quotV V 4W V E 71 l or pit eia 933 em stimulates part of cell to A enters secrete cell Cl Nah 2 and other a electrolytes A1 activates r adenylate u 0 cyc39aseAc39 ATP 3 synthesize Z c g1 r quot39 Cholera Signs and Symptoms Infections may be asymptomatic or cause mild diarrhea but in 5 of patients it can result in rapid severe and fatal fluid and electrolyte loss Explosive watery diarrhea and vomiting 23 days after infection Stool becomes increasingly watery colorless and odorless Rice water stools Some patients lose 1 liter of fluid an hour Dehydration metabolic acidosis hypokalemia loss of K and hypovolemic shock can result Muscle cramping irregular heartbeat kidney failure coma and death can result Mortality is 60 in untreated patients Cholera Epidemiology Reservoir is marine zooplankton Multiplies within shellfish Attaches to chitincontaining shells 7 cholera pandemics since 1817 o 7th pandemic began in 1961 and reached South America in 1991 o October 21 2010 cholera was confirmed in Haiti I Initial epidemics January 1991 I August 1991 B February 1992 l 1 November 1994 Cholera Diagnosis Treatment and Prevention Diagnosis Diagnosed by manifestations including ricewater stools Treatment Supportive care with fluid and electrolyte replacement Must be administered promptly Doxycycline reduces the production of cholera toxin Prevention Adequate sewage and water treatment can limit the spread and prevent epidemics Oral vaccine against the 01 El Tor strain Antimicrobial prophylaxis not effective Infective dose is high so proper hygiene is usually sufficient Shigellosis Pathogens and Virulence Factors Shigella dysenteriae S exneri S boydii and S sonnei S sonnei most common species in industrialized nations S exneri most common species in developing nations Genetic evidence indicates that Shigella are within the genus of Escherichia coli and diverged 35000 270000 years ago Diarrheaproducing enterotoxin o S dysenteriae produces an exotoxin known as Shiga toxin that stops protein synthesis in host s cells Cells will die If they can t make new proteins Shigellosis Pathogenesis Pathogen initially colonizes cells of the small intestine and causes an enterotoxinmediated diarrhea Organism attaches to and invades epithelial cells in large intestine Bacteria multiply in cytosol Organisms directly invade neighboring cells and evade host s immune system Organisms kill host cells resulting in holes in intestinal mucosa V Shigella I QShigeIla attaches to l I l epithelial cell of colon Epitheliai cell I a Shigella triggers l r endocytosis Y i 39 oShigelIa multiplies l 39 l in cytosol l l l l Actin fibers o Shigella invades neighboring epithelial cells thus avoiding immune defenses l Mucosal abscess 9An abscess forms as epithelial cells are killed by the infection 39r39 Phagocyte 39 7 r a Shigella that quot enters the blood is quickly phagocy zed and destroyed Blood vessel l V V 7 r r Shigellosis Signs and Symptoms o All species cause a severe form of dysentery called shigellosis which is characterized by abdominal cramps fever diarrhea and purulent pus bloody stools Shigellosis Epidemiology Humans are reservoir People become infected by ingesting bacteria on their own contaminated hands and by consuming contaminated food direct contact and foodborne Little affected by stomach acid so an infective dose may be as few as 200 cells Persontoperson spread is possible Groups at highest risk are children in daycare centers and persons in custodial settings where personal hygiene is difficult to maintain 14000 cases per year in the US but actual case numbers are estimated to be 280000 Not diagnosed and underreported Shigellosis Diagnosis Treatment and Prevention Diagnosis Based on symptoms and presence of Shigella in stool Treatment Involves fluid and electrolyte replacement Disease is usually selflimiting Administration of antimicrobials such as ciprofloxacin sulfonamides penicillin or cephalosporin can reduce the spread of Shigella to close contacts Prevention Live attenuated vaccine recently developed against S exneri Prevents dysentery but recipients experienced mild diarrhea and fever as a result of immunization Work continues Campylobacteriosis Pathogen and Virulence Factors Campyobacterjejuni Gramnegative slightly curved rod with polar flagella Virulence factors include adhesins cytotoxins endotoxins that enable colonization and invasion of the jejunum ileum and colon Nonmotile strains are avirulent Survives inside cells after being endocytosed Campylobacteriosis Pathogenesis Normally founds in cattle birds and pigs where it is nonpathogenic zoonosis common in chicken and turkeys Spreads to humans in contaminated meat Fewer than 500 cells can cause illness Virulence factors enable colonization and invasion of jejunum ileum and colon Organism produces bleeding lesions and trigger inflammation In immunocompromised patients the organism can spread to the bloodstream and cause a lifethreatening infection Campylobacteriosis Signs and Symptoms Infections commonly produce malaise fever abdominal pain and bloody and frequent diarrhea 10 or more bowel movements per day is not uncommon Disease is selflimiting bacteria are expelled from the intestinal tract Campylobacteriosis Epidemiology One of the most common causes of diarrheal illness in the US Vast majority are isolated sporadic events and are not epidemics Most cases are due to consumption of raw or undercooked poultry or from crosscontamination of other foods by these items Infants can become infected by contact with poultry packages in shopping carts One drop of juice from raw chicken can infect humans Outbreaks are also associated with unpasteurized milk or contaminated water supplies Estimated to infect 24 million people per year Isolated from infants and young adults more frequently than other groups Isolated from males more frequently than females Campylobacteriosis Diagnosis Treatment and Prevention Diagnosis Based on signs and symptoms and demonstration of organism in stool Treatment Most cases resolve without treatment Severe cases require supportive therapy and antimicrobial drugs Prevention There is no vaccine so preventative practices should focus on minimizing contamination of kitchen surfaces and utensils from raw chicken or turkey Communities should prevent contamination of drinking water from feces from stockyards feedlots and slaughterhouses Food Intoxication Pathogen and Virulence Factors Staphylococcus aureus common causative agent Gram positive cocci in clusters Normal flora of skin and upper respiratory system Salt tolerant Possesses several virulence factors Five enterotoxins that stimulate intestinal muscle contractions trigger nausea amp cause intense vomiting Heat stable Food Intoxication Pathogenesis Food preparers contaminate foods with S aureus during cooking Organism grows well at room temperature in foods containing high concentrations of protein Processed meats custard pastries potato salad and ice cream Organism must grow at room temperature or warmer for several hours before enterotoxins secreted Warming or reheating food does not inactivate enterotoxins although it does kill the bacteria Toxin consumed Toxin crosses mucous membranes of intestinal tract Incubation period 16 hours Food Intoxication Signs and Symptoms Nausea severe vomiting diarrhea headache sweating and abdominal pain Most cases are selflimiting and last 24 h Food Intoxication Epidemiology Outbreaks usually associated with picnics school cafeterias or large social functions where food stands unrefrigerated or where food preparation is less than optimal Number of cases unknown Mild and selflimiting s MICRBIOLOGY WITII DISEASES BY BODY SYSTEM SECOND EDITION Chapter 24 on Structures of the Urinary System Kidneys Remove waste from the blood and excrete it in urine Nephrons are the functional unit of the kidneys Responsible for filtering the blood to form urine Ureters urine travels via these to the urinary bladder Urinary bladder stores urine until it can be eliminated Urethra site of urine excretion Structures of the Female Reproductive System In females the urinary and reproductive systems are distinct Ovaries site of egg production Uterine fallopian tubes eggs travel toward the uterus through the uterine tubes Uterus develops a bloodrich wall in preparation for pregnancy Vagina unfertilized eggs pass through the vagina during menstruation External genitalia includes the clitoris and labia Microorganisms can enter the reproductive tract through the vagina Structures of the Female Reproductive System Uterine tube Ovary Uterus Urinary bladder Urethra Clitoris G Copyrighl Cc 2009 Pearson Education inc publishing as Pearson Benjamin Cummings Structures of the Male Reproductive System In males the urinary and reproductive systems share some components Testes site of sperm production Scrotum external structure that contains the testes System of ducts pass sperm to the prostate gland Accessory glands such as the prostate gland add fluid to sperm to form semen Penis semen passes from the penis out of the body Microorganisms can enter the reproductive tract through the urethra skin of the penis Structures of the Male Reproductive System Ureter opening Urinary bladder Ductus Rectum deferens w Seminal Prostate vesicle land 9 Urethra Anus Penis us 7 Prepuce Testis foresmn d Copyright 2009 Pearson Education lnc publishing as Pearson Benjamin Cumminga Defenses that Protect the Reproductive and Urinary Systems Urethra may be portal of entry in females Females 4 cm Males 20 cm Flow of urine pee hard Acidic pH of urine Mucosal epithelial cell layer Normal flora of vagina maintain pH 45 Normal Microbiota of the Urinary and Reproductive Systems Urethra Supports colonization by some microorganisms Primary species include Lacfobacillus and Staphylococcus Remainder of the urinary organs are sterile Male reproductive system The regions above the prostate are sterile Female reproductive system The vagina is colonized by various microorganisms depending on hormone levels Microorganisms infecting the urethra can move up to infect the kidneys Opportunistic and sexually transmitted microbes can infect the reproductive system Gonorrhea Pathogen and Virulence Factors Neisseria gonorrhoeae Gram negative diplococci with adjacent sides flattened Fimbriae Polysaooharide capsule Lipooligosaccharide LOS containing lipid A Cells that lack fimbriae a capsule and LOS are typically avirulent lgA protease Survive and multiply within neutrophils l l Susceptible to drying and 1 m extremes of temperature Gonorrhea Pathogenesis As few as 100 pairs of cells can result in disease Gonococci adhere to mucous membranes of genital urinary and digestive tracts of humans Fimbriae and capsules mediate Cannot attach to cells in vagina Attach to sperm via fimbriae or LOS Can result in pelvic inflammatory disease leading to ectopic pregnancies or sterility Urethritis in women Oral and anal infections can occur More common in men who have sex with men Gonorrhea Pathogenesis As organisms multiply they invade deeper connective tissues Organisms phagocytosed but survive and multiply within neutrophils Travel throughout the body Can enter blood and travel to joints meninges or heart Arthritis meningitis and endocarditis Infection during childbirth ophthalmia neonatorum or blindness Gonorrhea Signs and Symptoms Men Begin after 25 day incubation penod Urethritis Thick purulent creamy yellow discharge from penis Organism can invade prostate or epididymis Scar tissue can result in infertility epididymitis a comMication of gonorrhea Gonorrhea Signs and Symptoms Women Begin after 25 day incubation pedod 5080 asymptomatic Lack of treatment results in infertility or pelvic inflammatory disease 25 Mistaken for vaginal yeast infection or bladder infection Burning and frequency of urination Yellow or bloody vaginal discharge Gonorrhea Signs and Symptoms Opthalmia neonatorum inflammation of the conjunctiva in newborns Gonorrhea Epidemiology Humans are the only reservoir Transmitted by direct contact with an infected host Any sexually active person can be infected Most cases in adolescents who engage in a promiscuous sexual lifestyle in several southeastern states Infection 19X more common among blacks than nonblacks More common among females Women have a 50 chance of becoming infected during a single sexual encounter with an infected man 20 chance for men Risk increases with increasing frequency of sexual encounters Infection of children strong evidence of sexual abuse Gonorrhea Epidemiology Gonorrhea Rates by state United States and outlying areas 2008 VT 60 NH 76 MA 330 RI 290 CT 800 NJ 610 623 DE 1203 MD 1186 DC 4515 Rate per 100000 population D 5190 n7l l 19l 1000 0124 gt1000 3123 Puerto Rico 69 9 C31 Islands 1093 I 39 V Gonorrhea Epidemiology Gonorrhea Age and sexspecific rates United States 2008 Men Rate per 100000 populatlon Women 750 600 450 300 150 0 Age 0 150 300 450 600 750 I I I I I 58 10 14 I I 154 9 20 24 25 29 30 34 35 39 40 44 45 54 55 64 65 l l I 6368 6086 Total Gonorrhea Diagnosis and Treatment Presence of Gramnegative diplococci in pus from an inflamed penis from symptomatic male patient is diagnostic Asymptomatic men and women diagnosed by commercially available genetic probes Treatment is complicated by spread of multidrug resistant strains CDC currently recommends broadspectrum oral cephalosporins Gonorrhea Prevention Immunity does not exist reinfection is common Surface antigens are highly variable o No gonorrhea vaccine available due to existence of many different strains Control difficult except in newborns Preventative strategies Abstinence Monogamous relationships Consistent use of condoms during intercourse Prompt identification and treatment of all sexual contacts of diagnosed patient Chlamydia Pathogen and Virulence Factors Chlamydia trachomatis Obligater intracellular and nonmotile Gram negative Only grow and multiply within vesicles in host cells Were once thought to be viruses but are cellular and do have DNA RNA and functional 708 ribosomes Lack cell walls no peptidoglycan All strains pathogenic for humans Infect conjunctiva lungs urinary tract or genital tract Unique developmental cycle EBs RBs Chlamydia Pathogen and Virulence Factors RB EB 0 EB attaches to receptor 7 rev on host cell 0 hour a EBs are released e E8 enters host cell from host cell via endocytosis 39 40 hours Vesicle a Most FlBs convert back into EBs 21 hours EB lt inside 39 vesicle EB converts into R8 in in vesicle 10 hours 0 FIB divides rapidly resulting in multiple RES in an inclusion body Inclusion body b Chlamydia Pathogenesis Organism enter body through abrasions or lacerations Infects cells of conjunctiva or cells lining mucous membranes of trachea bronchi urethra uterus uterine tubes anus or rectum Clinical manifestations result from destruction of infected cells at infection site Also from inflammatory response Chlamydia Signs and Symptoms Known as a silent disease because majority of people do not experience signs and symptoms f signs and symptoms do occur they appear 13 weeks following infection Cervix and urethra initially infected in women May have abnormal vaginal discharge or burning upon urination Organisms can spread to fallopian tubes Some still have no signs and symptoms Some have lower abdominal pain low back pain nausea fever pain during intercourse or bleeding between menstrual periods Infection can spread to the rectum or can be acquired by receptive anal intercourse Rectal pain discharge or bleeding Chlamydia Signs and Symptoms Men may have a discharge from the penis or experience burning upon unna on May have burning or itching around opening of penis Infection can be acquired by receptive anal intercourse Rectal pain discharge or bleeding Organisms can be found in the throats of men and women having oral intercourse with an infected partner 1015 of women with untreated chlamydia will develop pelvic inflammatory disease some women have a silent infection in the fallopian tubes Can result in permanent damage to fallopian tubes uterus and surrounding tissue Chronic pelvic pain infertility and ectopic pregnancies Complications among men are rare Chlamydia Epidemiology Most frequently reported bacterial sexually transmitted disease in the US 1210523 cases reported in 2008 but it is estimated that 2291000 civilians ages 1439 are infected Highest infection rates in Native and AfricanAmericans Most prevalent in women lt20 physiologically more susceptible Cervix is not fully matured and is probably more susceptible Women with chlamydia have a 3 to 5 fold increased risk of acquiring HIV Humans are the reservoir Transmission is via direct contact Chlamydia Diagnosis Treatment and Prevention Diagnosed by demonstration of bacteria inside cells from the site of infection Treatment with tetracycline or azithromycin for 21 days Prevented by abstinence or faithful mutual monogamy Condoms may provide some protection however som warn that irritation by condoms and their lubricants actually increases the likelihood of infection Infections are often asymptomatic and frequently occur among populations that have limited access to medical care Genital Warts Pathogen and Virulence Factors Family Papillomaviridae Nonenveloped DNA viruses of which there are several hundred speCIes Highly host and tissuetropic and are rarely transmitted between speCIes Replicate exclusively in the basal layer of the keratinocytes Various strains infect either cutaneous or mucosal tissues Shed through release of skin cells desquamination to help avoid an inflammatory response Majority cause no symptoms in most people but some cause warts and others can lead to cancers of the cervix vulva vagina anus and penis Genital Warts Pathogen and Virulence Factors Human papillomavirus HPV More than 40 HPVs spread through sexual contact and are classified as high risk or low risk Low risk Do not cause cervical cancer Do cause genital warts strains 6 and 11 are linked to 90 of all cases of genital warts High risk 13 strains integrate into human chromosomes Believed to cause cervical anal vaginal penile amp oral cancers especially if patient is coinfected with herpesvirus Types 16 and 18 cause about 70 of cervical cancers 8090 of all cervical cancers are due to HPV infection Genital Warts Pathogenesis Very contagious Can be acquired during oral vaginal or anal sex with infected partner May be contracted by skintoskin contact during vaginal anal or rarely oral sex with infected partner 67 who have sexual contact with infected partner will develop warts usually within 34 months of infection Viruses gain access to lower portion of epithelium by local trauma Infect basal epithelial cells and replicate in the nucleus Causes infected epithelial cells to proliferate Genital Warts Signs and Symptoms Genital warts condylomata acuminata or veneral warts most easily recognized sign Soft moist or fleshcolored may appear in cauliflowerlike bumps condylomata acuminata and may be raised or flat small or large Appear in genital area weeks to months after infection May be painful or itchy and can bleed and increase vaginal discharge Women may appear on vulva and cervix and inside and surrounding vagina and anus Men may appear on scrotum and penis Many have HPV infection without presence of warts Genital Warts Signs and Symptoms Genital Warts Epidemiology Transmitted via direct contact and via fomites stable outside the body HPV is the most common causes of sexually transmitted disease in the US mostly in young adults Approximately 62 million new cases of sexually transmitted HPV infections are reported each year in the US At least 20 million Americans currently infected with genital HPV gt50 of sexually active adults infected By age 50 at least 80 of women will have acquired genital HPV infection Genital Warts Epidemiology Several types of cancer are associated with HPV Cervical cancer the most common HPVassociated cancer almost all cervical cancer is caused by HPV Vulvar cancer about 40 are linked to HPV Vaginal cancer about 70 are linked to HPV Penile cancer about 40 are linked to HPV Anal cancer about 85 are linked to HPV Cancers of the head and neck are mostly caused by tobacco and alcohol but recent studies show that about 25 of mouth and 35 of throat cancers may be linked to HPV Genital Warts Diagnosis and Treatment Diagnosis usually by observation Abnormal results from PAP smear test that indicates cancerous or precancerous cells in cervix DNA probes can determine exact strain of HPV involved Cytotoxic T lymphocytes eventually recognize and destroy infected cells Warts disappear over time Treatment Genital warts removed with surgery freezing burning laser or caustic chemicals but viruses may remain in surrounding tissues Laser surgery causes viruses to become airborne Duct tape MICROBIOLOGY WITII DISEASES BY BODY SYSTEM SECOND EDITION Chapter 19 Structure of the Skin Two main layers Dermis Epidermis Functions of the skin I H Prevents excesswe water loss a Important to temperature regulation Assists in the formation of vitamin D Involved in sensory phenomena Barrier against microbial invaders Dendritilt Stratum 0 V comeurn i A Hair 39 Nails Stratum 39 granulosum Skin Sweatpores Stratum 31 spinosum air shaft i 22 I JEpidermi5 Stratum1quot basale llHypodermis quot Nerve Sweat gland Microbiota in sweat gland Hair erector Pacinian corpuscle muscle pressure receptor Microbiota H Blood vessels In hair follicle 3quot root Hair Oil gland l quot39 39es Hair follicle receptOr rmuniLymahemmtinuivun l wrmmm nnnnnn m Defenses That Protect the Skin Outermost layer of skin flattened dead dry keratinized Covered with salt and sebum Contain antimicrobial chemicals Sloughing of skin removes microbes Wounds 0 Trauma to any tissue of the body Cuts abrasions scrapes surgery inoculations bites and other penetrating wounds as well as burns Allow microbes to infect the warm moist deeper tissues of the body Dirty wounds provide substrates for growth of biofilms Body forms a clot and then neighboring cells multiply and grow into the clot may or may not scar In most cases other body defenses including phagocytosis complement and inflammation eliminate the infection Wound infections can result in severe or fatal diseases Normal Microbiota of the Skin Normal flora compete with potential pathogens for nutrients and space and produce chemicals that interfere with the growth of other microbes Cannot be completely removed through cleansing Typically grow in small clusters in moist areas Waste products produce body odor Prominent members Malassezia a yeast eukaryotic organism Staphylococcus gram cocci Micrococcus gram cocci Diphtheroids a rod that can be many shapes Pathogenic microbes can still produce diseases particularly if they penetrate the epidermis through wounds or when the immune system is suppressed Folliculitis Pathogen and Virulence Factors Most commonly caused by members of the genus Staphylococcus Facultatively anaerobic Gram positive cocci in clusters Tolerant of bc they grow on skin Salt Desiccation Radiation Heat 6065 degree heat Folliculitis Pathogen and Virulence Factors Two species commonly found on the skin and mucous membranes Staphylococcus epidermidis Staphylococcus aureus S epidermidis Accounts for up to 90 of bacteria on skin Major member of microbiota o S aureus More virulent Often grows in nasal passages Produces variety of disease conditions and symptoms Folliculitis Pathogen and Virulence Factors Have at least three categories of virulence factors Enzymes CellFree Coagulase immunological disguise Hyaluronidase promotes spread through the degradation of cartilage Staphylokinase promotes spread through degrading blood clots Lipases provides source of nutrition on surface of skin Blactamase resistance to some antibiotics Structural Defenses Against Phagocytosis Polysaccharide slime layer inhibits chemotaxis and phagocytosis by WBC facilitates attachment Protein A inhibits opsonization and complement cascade Bound Coagulase immunological disguise Folliculitis Pathogen and Virulence Factors Toxins Cytolytic toxins damage cytoplasmic membranes Leukocidins provides some protection against phagocytosis bc they directly kill WBC Exfoliative toxin dissolution of epidermal desmosomes promotes spread Toxic shock syndrome toxin activates T cells and leads to problems Enterotoxins stimulate intestinal muscle contractions nausea and vomiting associated with staphylococcal food poisoning Folliculitis Pathogen and Virulence Factors Comparison of Virulence Factors of Two Staphylococcal Species Enzymes Coagulase Staphylokinase Lipase BLactamase Present in 90 of strains Factors That Inhibit Phagocytosis Polysaccharide slime layer Protein A on cell surface Toxins Cytolytic toxins Leukocidin A Exfoliative toxin Present in some strains Toxic shock syndrome toxin Present in some strains Folliculitis Pathogenesis Transmitted S aureus or epidermidis among humans via direct contact and via fomites Organism grows into hair follicles and invades sebaceous glands inflammation develops Follicles enlarges and fills with pus Organisms can cause bacteremia and be carried around the body Endocarditis Pneumonia Osteomyelitis Folliculitis Signs and Symptoms Infection of the hair follicle Often called a pimple Called a sty when it occurs at the eyelid base Spread of the infection into surrounding tissues can produce furuncles boils Carbuncles occur when multiple furuncles grow together Fever may occur in severe cases Folliculitis Epidemiology S epidermidis is ubiquitous on human skin whereas S aureus is commonly found only on moist skin folds nostrils Both grow in the upper respiratory gastrointestinal and urogenital tracts of humans o S epidermidis seldom causes disease though it can be an opportunistic pathogen o S aureus often transferred from the face to other locations on the body Both transmitted through direct contact as well as via fomites Proper handwashing and aseptic techniques are essential in preventing their transfer in health care settings Folliculitis Diagnosis Detection of Grampositive bacteria in grapelike arrangements isolated from pus blood or other fluids Positive coagulase test for S aureus Coagulase negative staphylococci are usually S epidermidis and not indicative of a staphylococcal infection Folliculitis Treatment Critical to clean amp drain abscesses of pus Hot moist compresses may promote drainage of extensive folliculitis Vancomycin is drug of choice Oct 2010 o Drugresistant S aureus is major health problem MRSA methyl resistant VRSA vancomycin resistant Folliculitis Prevention Health care workers should take precautions against contaminating patients Organism is ubiquitous Large inoculum required to establish infection Proper cleansing of wounds and surgical openings attention to aseptic use of catheters and indwelling needles and appropriate use of antiseptics will prevent infections in most healthy patients Those with staphylococcal lesions should refrain from working with food patients with open wounds immunocompromised patients and women in labor and they should not work in nurseries or operating rooms The most important measure for protecting against nosocomial infection is frequent handwashing Scientists currently testing vaccine Rocky Mountain Spotted Fever Pathogen and Virulence Factors Rickettsia rickettsii Small aerobic Gramnegative intracellular Cell wall of peptidoglycan and outer a membrane of LPS with little endotoxin 0 activity Loosely organized slime layer Enters host s cells by stimulating t v endocytosis and escapes endosome 3 394 1 v prior to fusion with lysosome It f Reproduces slowly 812 h generation time Daughter cells release via exocytosis Organisms are unstable outside host s cells requires biological vector for transmission Photo CDC Atlanta GA Rocky Mountain Spotted Fever Pathogenesis Typically dormant in salivary glands of tick Become active and infective only when tick feeds for at least 610 hours Organism transmitted to mammals via Bites Biological vector Crushed ticks or tick feces Organisms released from salivary glands of tick and travel into host Spreads through host via circulatory and lymphatic systems Infect cells lining small blood vessels No toxins produced Disease follows damage to blood vessels Loss of intravascular fluid into tissue spaces Low blood volume Reduced blood flow to organs Disordered function of tissues with damaged blood vessels Attempted plugging of blood vessel walls consumes platelets Thrombocytopenia in 50 of patients Rocky Mountain Spotted Fever Signs and Symptoms One week after infection patients experience fever headache chills muscle pain nausea and vomiting 90 of patients develop a nonitchy spotted rash on trunk and appendages 50 of cases rash develops into petechiae subcutaneous hemorrhages blood leaks out of cells and causes bruises Resembles many other diseases during the early stages of infection when antibiotics are most effective Severe cases respiratory CNS GI and renal systems fail Encephalitis may also occur language disorders delirium convulsions coma and death 5 mortality rate even with treatment Recovering patients may experience paralysis hearing loss and secondary infections necessitating amputation Rocky Mountain Spotted Fever Signs and Symptoms Rocky Mountain Spotted Fever Epidemiology Hard ticks in genus Dermacentor transmit organisms among humans and rodents Rodents are reservoirs zoonosis Male ticks infect female ticks during mating direct contact and females transmit the bacteria to eggs forming in their ovaries transovarian transmission direct contact Rocky Mountain Spotted Fever Epidemiology Disease more prevalent in Appalachian Mountains Oklahoma and southeastern US Among most severe of human diseases Mortality rate 2025 unless treated with appropriate antibiotic Frequency is highest among males Caucasrans and chrldren 67 of cases occur in children under the age of 15 Typically occurs as isolated cases 1393 cases in 2009 319 cases In Missouri Rocky Mountain Spotted Fever Diagnosis Initial diagnosis based on rash on soles or palms sudden fever and headache following exposure to hard ticks Serological tests required test for antibodies Early diagnosis crucial because prompt treatment often makes the difference between recovery and death Rocky Mountain Spotted Fever Treatment Careful removal of tick Treatment with doxycycline tetracycline or chloramphenicol If treatment is initiated within the first 45 days of the disease fever generally subsides within 24 72 hours Rocky Mountain Spotted Fever Prevention No effective vaccine available Wear tightfitting clothing Light colors enable one to see a crawling tick Tick repellants permethrin and DEET Frequent body checks and promptly remove attached ticks Avoid tickinfested areas especially spring amp summer ChickenpoxShingles Pathogen Human Herpesvirus 3 Varicella Zoster virus Icosahedral enveloped DNA virus Related to Herpes simplex virus and EpsteinBarr virus ChickenpoxShingles Signs and Symptoms Highly infectious Two to three weeks after infection characteristic skin lesions on back and trunk appear may spread to face neck and limbs Slight fever Severe cases lesions spread into mouth pharynx amp vagina Lesions begin as macules Progress in 12 days to papules Become thinwalled fluidfilled vesicles on red bases dewdrops on rose petals Vesicles turn cloudy dry up amp crust over Successive crops of lesions appear over 35 day period Viruses are shed through respiratory droplets and fluid in lesions Dry crusts are not infective Not lifethreatening but may be to newborns ChickenpoxShingles Signs and Symptoms ChickenpoxShingles Signs and Symptoms Virus can become latent in sensory nerves Stress aging or immune suppression cause virus to reactivate in 1520 of infected individuals Stress aging or immune suppression Viruses reactivate and travel down nerve they inhabit Produce an extremely painful skin rash near distal end of nerve Lesions localized and on same side of body as nerve May affect eye ear or other part of head Temporary vision problems Hearing loss Paralysis of face Scabs fall off Most have no further symptoms Pain may remain months to years after lesions heal ChickenpoxShingles Signs and Symptoms Shingles ChickenpoxShingles Pathogenesis Infection begins in mucous membrane of respiratory tract Spreads to liver spleen and lymph nodes via blood and lymph Two weeks later second wave of viruses spreads via blood throughout body and to skin lnfects cells of dermis ChickenpoxShingles Epidemiology Disease is usually mild Can rarely be fatal especially if associated with secondary bacterial infection Chickenpox is most often seen in children but is more severe in adults Much of the tissue damage results from immune response Adults have more developed immune system 1520 of those who had chickenpox as children develop shingles Usually after age 50 4 develop second case of shingles Shingles patient can spread virus to person who has never had chickenpox ChickenpoxShingles Diagnosis Chickenpox characteristic appearance of lesions Shingles more difficult localization of lesions within band of skin on one side of body Antibody tests available ChickenpoxShingles Treatment Chickenpox general selflimiting no treatment required Relief of symptoms acetominophen and antihistamines Do not give aspirin to children Reye s syndrome Shingles management of symptoms amp bedrest Loosefitting clothing and nonadherent dressings Acyclovir provides relief but is not a cure
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